https://www.wikidoc.org/api.php?action=feedcontributions&user=WikiBot&feedformat=atomwikidoc - User contributions [en]2024-03-28T17:16:25ZUser contributionsMediaWiki 1.40.0https://www.wikidoc.org/index.php?title=WBR9876&diff=1672426WBR98762020-10-28T03:02:35Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Anatomy<br />
|MainCategory=Anatomy<br />
|MainCategory=Anatomy<br />
|MainCategory=Anatomy<br />
|MainCategory=Anatomy<br />
|MainCategory=Anatomy<br />
|MainCategory=Anatomy<br />
|MainCategory=Anatomy<br />
|MainCategory=Anatomy<br />
|MainCategory=Anatomy<br />
|MainCategory=Anatomy<br />
|MainCategory=Anatomy<br />
|MainCategory=Anatomy<br />
|Approved=No<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR591&diff=1672425WBR5912020-10-28T03:02:25Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor= {{TS}}<br />
|ExamType=USMLE Step 2CK<br />
|MainCategory=Behavioral Science/Psychiatry<br />
|MainCategory=Behavioral Science/Psychiatry<br />
|MainCategory=Behavioral Science/Psychiatry<br />
|MainCategory=Behavioral Science/Psychiatry<br />
|MainCategory=Behavioral Science/Psychiatry<br />
|MainCategory=Behavioral Science/Psychiatry<br />
|MainCategory=Behavioral Science/Psychiatry<br />
|MainCategory=Behavioral Science/Psychiatry<br />
|MainCategory=Behavioral Science/Psychiatry<br />
|MainCategory=Behavioral Science/Psychiatry<br />
|SubCategory=Psychiatry<br />
|Prompt=A 35 year old man presented with right upper quadrant abdominal pain. Initial ultrasound confirmed the presence of gall stones and an elective cholecystectomy was performed. Post operatively he is stable with vitals BP 130/90, Pulse 100/min and RR 18/min, but complains of tremulousness, increasing anxiety and “bugs crawling on his hands”. On examination patient is confused and tremors are noted in both hands. Rest of the neurological examination is within normal limits. What is the most common cause of his present complaints?<br />
|Explanation=Mild to moderate alcohol withdrawal manifests as autonomic hyperactivity, insomnia, tremulousness, anxiety, sweating, hypertension, tachycardia and fever. Patients with chronic alcohol use can also present with hallucinations. Visual hallucinations are more common, but auditory and tactile hallucination can also be present. Severe alcohol withdrawal manifests with seizures and delirium tremens. Delirium tremens usually occurs after 2-4 days of alcohol abstinence. <br />
|AnswerA=Cocaine intoxication<br />
|AnswerAExp=Cocaine intoxication can present with tactile hallucinations and anxiety, however, tremors and hallucinations in a hospital setting is more specific for substance withdrawal than intoxication.<br />
|AnswerB=Brief psychotic disorder<br />
|AnswerBExp=Brief psychotic disorder is defined as presence of at least 2 of the 5 symptoms which define schizophrenia for more than one day and less than one month in absence of any other condition. Symptoms which define schizophrenia are: hallucinations, delusions, disorganized thought (speech), disorganized or abnormal motor behaviour (including catatonia), and negative symptoms. Presence of auditory hallucinations is more common than visual hallucinations in schizophrenia.<br />
|AnswerC=Schizophrenia<br />
|AnswerCExp=For diagnosis of schizophrenia, symptoms must be present for more than 6 months. If symptoms are present for more than one month but remits within six months, it is classified as schizophreniform disorder<br />
|AnswerD=Alcohol withdrawal<br />
|AnswerDExp=Alcohol withdrawal is the most probable reason for tremors and visual hallucinations in a hospital setting. Most commonly patient presents with these symptoms one day after admission<br />
|AnswerE=Post operative delirium<br />
|AnswerEExp=Post operative delirium is more commonly present in elderly patients. It manifests with agitation and a fluctuating level of consciousness. It is caused by wide range of etiologies such as infections, drugs, electrolyte disturbance, post operative pain, hypotension and dehydration. It is a diagnosis of exclusion, therefore a meticulous search for etiology is mandatory.<br />
|RightAnswer=D<br />
|WBRKeyword=Alcohol withdrawal<br />
|Approved=No<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR295&diff=1672424WBR2952020-10-28T03:02:15Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|MainCategory=Microbiology<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|Prompt=A 29-year-old man presents to the clinic with symptoms of abdominal pain, malaise, and watery diarrhea that begin a day after coming back from a travel to Bangladesh. He complains of orthostatic dizziness and has dry mucosa and decreased skin turgor. Few leukocytes are found in his fecal specimen. Growth of purple colonies on Eosin methylene blue agar is noted. Presence of the heat-labile enterotoxin is confirmed by enzyme-linked immunosorbent assay (ELISA). Which of the following events best describes the mechanism of action of this toxin?<br />
|Explanation=Enterotoxigenic ''Escherichia coli'' (ETEC) is a type of ''Escherichia coli'' and the leading bacterial cause of diarrhea in the developing world, as well as the most common cause of travelers' diarrhea. Enterotoxins produced by ETEC include heat-labile enterotoxin (LT) and heat-stable enterotoxin (ST). LT activates adenylyl cyclase and increases the amount of cAMP, and results in profound chloride efflux secondary to phosphorylation of CFTR by persistently activated protein kinase A. ST activates guanylyl cyclase in the signal pathway of the enteric epithelial cells and triggers fluid secretion.<br />
|AnswerA=Increase of intracellular cyclic GMP<br />
|AnswerAExp=Increase of intracellular cyclic GMP is mediated by heat-stable enterotoxin (ST).<br />
|AnswerB=Phosphorylation of CFTR by protein kinase A<br />
|AnswerBExp=Phosphorylation of CFTR by protein kinase A is mediated by LT.<br />
|AnswerC=Cytotoxicity to intestinal epithelium<br />
|AnswerCExp=Cytotoxicity to intestinal epithelium is mediated by EAEC toxins such as PET.<br />
|AnswerD=Adherence to intestinal epithelium<br />
|AnswerDExp=Adherence to intestinal epithelium may be mediated by colonizing factor antigen (CFA) of ETEC, Tir (translocated intimin receptor) of EPEC, or surface adhesins.<br />
|AnswerE=ADP ribosylation of Gi protein<br />
|AnswerEExp=ADP-ribosylation of Gi protein is mediated by pertussis toxin.<br />
|EducationalObjectives=Enterotoxins produced by ETEC include heat-labile enterotoxin (LT) and heat-stable enterotoxin (ST). LT activates adenylyl cyclase and increases the amount of cAMP, and results in profound chloride efflux secondary to phosphorylation of CFTR by persistently activated protein kinase A. ST activates guanylyl cyclase in the signal pathway of the enteric epithelial cells and triggers fluid secretion.<br />
|References=First Aid 2015 page 138.<br />
|RightAnswer=B<br />
|WBRKeyword=Escherichia coli, Gastroenteritis, Enterotoxins, Heat-labile enterotoxin, Heat-stable enterotoxin<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR294&diff=1672423WBR2942020-10-28T03:02:05Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|MainCategory=Microbiology<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|Prompt=A 28-year-old man presents to the clinic with abdominal cramps, general malaise, fever, and diarrhea 6 hours after consuming ground beef. Few leukocytes are found in his fecal specimen. Growth of colorless colonies on sorbitol-MacConkey agar is noted. The pathogen produces toxins which contain enzymatic subunits that interfere with protein synthesis. Which of the following antibiotics has a similar mechanism regarding to the toxin's action on translation?<br />
|Explanation=''E. coli'' O157:H7 (EHEC) is negative for invasiveness (Sereny test), adheres through the ''E. coli'' common pilus (ECP), and does not produce either heat-stable or heat-labile toxins. In addition, ''E. coli'' O157:H7 is usually sorbitol-negative, whereas other ''E. coli'' ferment sorbitol. Among the virulence factors, Shiga-like toxin (SLT-1) is an iron-regulated toxin that catalytically inactivates 60S ribosomal subunits of eukaryotic cells. It cleaves N-glycoside bond of adenine in 28S rRNA of the 60S ribosome unit to prevent EF-1-dependent aminoacyl tRNA binding, thereby inhibiting protein synthesis. This mechanism of action is similar to tetracyclines, which also inhibit protein synthesis by blocking the entry and binding of aminoacyl transfer RNA.<br />
|AnswerA=Linezolid<br />
|AnswerAExp=Linezolid and aminoglycosides block the formation of initiation complex, thereby inhibiting protein synthesis.<br />
<br />
|AnswerB=Tetracycline<br />
|AnswerBExp=Tetracycline blocks the entry and binding of aminoacyl transfer RNA, thereby inhibiting protein synthesis.<br />
|AnswerC=Quinupristin/dalfopristin<br />
|AnswerCExp=Quinupristin/dalfopristin and other streptogramins block peptidyl transferase which forms peptide bonds between adjacent amino acids using tRNAs during the translation process.<br />
|AnswerD=Clindamycin<br />
|AnswerDExp=Clindamycin and macrolides block translocation by binding to the 50S rRNA of the large bacterial ribosome subunit.<br />
|AnswerE=Chloramphenicol<br />
|AnswerEExp=Chloramphenicol blocks peptidyl transferase which forms peptide bonds between adjacent amino acids using tRNAs during the translation process.<br />
|EducationalObjectives=Among the virulence factors of ''E. coli'' O157:H7, Shiga-like toxin (SLTs) is an iron-regulated toxin that catalytically cleaves N-glycoside bond of adenine in 28S rRNA of the 60S ribosome unit to prevent aminoacyl tRNA binding, thereby inhibiting protein synthesis. This mechanism of action is similar to tetracyclines, which also inhibit protein synthesis by blocking the entry and binding of aminoacyl transfer RNA.<br />
|References=First Aid 2015 page 138.<br />
|RightAnswer=B<br />
|WBRKeyword=Protein synthesis, Shiga-like toxin, Tetracycline, Gastroenteritis<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR293&diff=1672422WBR2932020-10-28T03:01:55Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|MainCategory=Microbiology<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|Prompt=A 27-year-old man presents to the clinic with abdominal cramps, general malaise, fever, and diarrhea 5 hours after consuming hamburgers. He has dry mucosa and decreased skin turgor. Few leukocytes are found in his fecal specimen. Growth of colorless colonies on sorbitol-MacConkey agar is noted. Which of the following descriptions best explains the pathogenesis of the organism responsible for this patient's condition?<br />
|Explanation=''Escherichia coli'' O157:H7 (EHEC) is an enterohemorrhagic strain of ''Escherichia coli''. Infection may lead to hemorrhagic diarrhea and subsequent development of hemolytic-uremic syndrome (HUS). Transmission is via the fecal-oral route, and the majority of cases are associated with ingestion of undercooked, contaminated ground beef or pork.<br />
<br />
''E. coli'' O157:H7 is negative for invasiveness (Sereny test), adheres through the E. coli common pilus (ECP), and does not produce heat-stable or heat-labile toxins. In addition, ''E. coli'' O157:H7 is usually sorbitol negative, whereas other ''E. coli'' ferment sorbitol. ''E. coli'' O157:H7 also lacks the ability to hydrolyze 4-methylumbelliferyl-β-D-glucuronide (MUG) and does not grow at 45 °C in the presence of 0.15% bile salts (cannot be isolated by using standard fecal coliform methods that include incubation at 45 °C).<br />
<br />
Among the virulence factors are periplasmic catalase and shiga-like toxins. Shiga-like toxin (SLT-1) is an iron-regulated toxin that catalytically inactivates 60S ribosomal subunits of eukaryotic cells. It cleaves N-glycoside bond of adenine in 28S rRNA of the 60S ribosome unit to prevent EF-1-dependent aminoacyl tRNA binding, thereby inhibiting protein synthesis.<br />
|AnswerA=ADP-ribosylation of the Gs alpha subunit proteins<br />
|AnswerAExp=Cholera toxin involves ADP-ribosylation of the Gs alpha subunit proteins.<br />
|AnswerB=ADP-ribosylation of elongation factor 2 (EF-2)<br />
|AnswerBExp=Exotoxin A from Pseudomonas aeruginosa involves ADP-ribosylation of elongation factor 2 (EF-2).<br />
|AnswerC=Cleavage of N-glycoside bond of adenine in 28S ribosomal RNA<br />
|AnswerCExp=Shiga-like toxin-1 (SLT-1) of EHEC cleaves N-glycoside bond of adenine in 28S rRNA of the 60S ribosome unit to prevent EF-1-dependent aminoacyl tRNA binding, thereby inhibiting protein synthesis.<br />
|AnswerD=Attachment of epithelium and effacement of microvilli<br />
|AnswerDExp=In EPEC, attachment of epithelium and effacement of microvilli is mediated via phosphorylation of Tir and subsequent intimin binding.<br />
|AnswerE=Local invasion of colonic mucosa<br />
|AnswerEExp=In EIEC, diarrhea is caused by local invasion of colonic mucosa.<br />
|EducationalObjectives=''Escherichia coli'' O157:H7 (EHEC) is an enterohemorrhagic strain of ''Escherichia coli''. Transmission is via the fecal-oral route, and the majority of cases are associated with ingestion of undercooked, contaminated ground beef or pork. Shiga-like toxin-1 (SLT-1) of EHEC cleaves N-glycoside bond of adenine in 28S rRNA of the 60S ribosome unit to prevent EF-1-dependent aminoacyl tRNA binding, thereby inhibiting protein synthesis.<br />
|References=First Aid 2015 page 138.<br />
|RightAnswer=C<br />
|WBRKeyword=Escherichia coli, Gastroenteritis, Shiga-like toxin<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR292&diff=1672421WBR2922020-10-28T03:01:45Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|MainCategory=Microbiology<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|Prompt=A 26-year-old man presents to the emergency department with abdominal cramps, general malaise, fever, and profound diarrhea 3 hours after a potluck dinner. Three of his friends also have similar symptoms. Stool samples demonstrate numerous polymorphonuclear leukocytes and are positive for growth on a selective medium under CO2 incubation at 42 °C (108 °F). The microorganism responsible for this patient's condition is also found to possess an enzyme that catalyzes the transport of electrons from NADPH to oxygen. Which of the following descriptions best explains the pathogenesis of this microorganism?<br />
|Explanation=''Campylobacter jejuni'' is a curved, helical-shaped, non-spore forming, non-glucose-fermenting, microaerophilic, gram-negative bacteria. It is one of the most common causes of human gastroenteritis worldwide. Infection with ''C. jejuni'' occurs following invasion of the microorganism of the colonic mucosa with disruption of epithelial cells. ''C. jejuni'' has also been associated with subsequent development of Guillain-Barré syndrome, which usually develops two to three weeks after the initial illness. ''C. jejuni'' is commonly associated with ingestion of poultry as it naturally colonizes the digestive tract of many bird species. ''C. jejuni'' is grown on specially selective agar plates at 42°C, the normal avian body temperature, rather than at 37°C, the temperature at which the majority of other pathogenic bacteria are grown. Since the colonies are oxidase positive, they will usually only grow in scanty amounts on the plates. Microaerophilic conditions are required for abundant growth. A selective blood agar medium (Skirrow's medium) may also be used. <br />
The following include the mportant oxidase-positive pathogens:<br><br />
*''Campylobacter''<br />
*''Helicobacter''<br />
*''Legionella''<br />
*''Neisseria''<br />
*''Pseudomonas''<br />
*''Vibrio''<br />
|AnswerA=ADP-ribosylation of the Gs alpha subunit proteins using nicotinamide adenine dinucleotide (NAD)<br />
|AnswerAExp=''Cholera'' toxin involves ADP-ribosylation of the Gs alpha subunit proteins.<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
|AnswerB=ADP-ribosylation of elongation factor 2 (EF-2) thus inhibiting protein synthesis<br />
|AnswerBExp=Exotoxin A from ''Pseudomonas aeruginosa'' involves ADP-ribosylation of elongation factor 2 (EF-2).<br />
|AnswerC=Invasion of colonic mucosa with disruption of epithelial cells <br />
|AnswerCExp=''Campylobacter jejuni'' infection involves invasion of colonic mucosa with disruption of epithelial cells.<br />
|AnswerD=Activation of guanylyl cyclase that enhances intestinal secretion<br />
|AnswerDExp=Heat-stable toxin (STa) of ETEC involves activation of guanylyl cyclase that enhances intestinal secretion.<br />
|AnswerE=Preformed toxins in ingested food<br />
|AnswerEExp=''Staphylococcus aureus'', ''Bacillus cereus'', and ''Clostridium botulinum'' produce preformed toxins in ingested food.<br />
|EducationalObjectives=Campylobacter jejuni grows at 42°C and causes intestinal disease by invasion of the colonic mucosa.<br />
|References=First Aid 2015 page 138.<br />
|RightAnswer=C<br />
|WBRKeyword=Campylobacter jejuni, Bacteria, Gram negative, Gastroenteritis, Toxin<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR291&diff=1672420WBR2912020-10-28T03:01:35Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|MainCategory=Microbiology<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|MainCategory=Microbiology<br />
|MainCategory=Microbiology<br />
|SubCategory=Gastrointestinal<br />
|Prompt=A 25-year-old man presents to the clinic with abdominal cramps, general malaise, fever, and bloody diarrhea 6 hours after consuming undercooked poultry. Two of his family members also have similar symptoms. Laboratory studies identify the causal agent as microaerophilic, gram-negative, curved rods. Which of the following descriptions of the causative pathogen is true?<br />
|Explanation=''Campylobacter jejuni'' is a curved, helical-shaped, non-spore forming, non-glucose-fermenting, microaerophilic, gram-negative bacteria. It is one of the most common causes of human gastroenteritis worldwide. Infection with ''C. jejuni'' occurs following invasion of the microorganism of the colonic mucosa with disruption of epithelial cells. ''C. jejuni'' has also been associated with subsequent development of Guillain-Barré syndrome, which usually develops two to three weeks after the initial illness. ''C. jejuni'' is commonly associated with ingestion of poultry as it naturally colonizes the digestive tract of many bird species. ''C. jejuni'' is grown on specially selective agar plates at 42°C, the normal avian body temperature, rather than at 37°C, the temperature at which the majority of other pathogenic bacteria are grown. Since the colonies are oxidase positive, they will usually only grow in scanty amounts on the plates. Microaerophilic conditions are required for abundant growth. A selective blood agar medium (Skirrow's medium) may also be used. <br />
The following include the mportant oxidase-positive pathogens:<br><br />
*''Campylobacter''<br />
*''Helicobacter''<br />
*''Legionella''<br />
*''Neisseria''<br />
*''Pseudomonas''<br />
*''Vibrio''<br />
|AnswerA=Negative for glucose fermentation test<br />
|AnswerAExp=''Campylobacter jejuni'' is negative for glucose fermentation test.<br />
<br />
|AnswerB=Negative for catalase test<br />
|AnswerBExp=''Campylobacter jejuni'' is positive for catalase test.<br />
<br />
|AnswerC=Negative for nitrate reduction test<br />
|AnswerCExp=''Campylobacter jejuni'' is positive for nitrate reduction test.<br />
|AnswerD=Negative for oxidase test<br />
|AnswerDExp=''Campylobacter jejuni'' is positive for oxidase test.<br />
|AnswerE=Immotile on wet mount<br />
|AnswerEExp=''Campylobacter jejuni'' contains polar flagella and is motile on wet mount.<br />
|EducationalObjectives=''Campylobacter jejuni'' is a curved, helical-shaped, non-spore forming, non-glucose-fermenting, microaerophilic, gram-negative bacteria. It is one of the most common causes of human gastroenteritis worldwide. <br />
|References=First Aid 2014 page 138.<br />
|RightAnswer=A<br />
|WBRKeyword=Campylobacter jejuni, Gastroenteritis<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR290&diff=1672419WBR2902020-10-28T03:01:25Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=[[User:Gonzalo Romero|Gonzalo A. Romero, M.D.]] [mailto:gromero@wikidoc.org]<br />
|ExamType=USMLE Step 2 CK<br />
|MainCategory=Surgery<br />
|SubCategory=Cardiovascular, Surgery<br />
|MainCategory=Surgery<br />
|SubCategory=Cardiovascular, Surgery<br />
|MainCategory=Surgery<br />
|SubCategory=Cardiovascular, Surgery<br />
|MainCategory=Surgery<br />
|MainCategory=Surgery<br />
|SubCategory=Cardiovascular, Surgery<br />
|MainCategory=Surgery<br />
|SubCategory=Cardiovascular, Surgery<br />
|MainCategory=Surgery<br />
|SubCategory=Cardiovascular, Surgery<br />
|MainCategory=Surgery<br />
|SubCategory=Cardiovascular, Surgery<br />
|MainCategory=Surgery<br />
|MainCategory=Surgery<br />
|SubCategory=Cardiovascular, Surgery<br />
|Prompt=A 62-year-old-female is brought to the ER after getting involved in a high-speed motor vehicle accident. Her vitals upon admission to the hospital are T 36C, 82bpm, BP=100/60 mmHg, 20 respirations/min. She has multiple bruises on her anterior chest. Her sternum is tender to palpation. A CXR reveals a widened mediastinum. What is the next best step in management?<br />
|Explanation=The widened mediastinum following a trauma to the chest could be due to an aortic dissection or thoracic vertebral fractures. The best next step in management is performing a spiral CT scan to rule out these conditions. A sternal fracture can also cause a myocardial contusion, therfore an EKG, and troponins should be ordered in order to rule out arrythmias and myocardial damage. The real important test is the spiral CT to rule out aortic dissection, which could rupture if left untreated.<br />
The surrogate markers of aortic rupture are fractures of the following bones: sternum, scapula and of the first rib. A flail chest is also a surrogate marker of an aortic injury. A contained rupture hematoma due to an aortic dissection is different from an aortic rupture, which has inmediate mortality. Patients with aortic rupture, do not arrive to the hospital alive. <br />
<br><br />
<br />
<font color="MediumBlue"><font size="4">'''Educational Objective:''' </font></font><br />
<br><br />
'''References:''' Master the Boards for Step 2CK, surgery chapter<br />
{{See also|Traumatic aortic rupture}}<br />
|AnswerA=EKG<br />
|AnswerAExp=<font color="red">'''Incorrect.'''</font>This is an important step to rule out arrhythmias in case of a myocardial contusion. <br />
|AnswerB=Thoracic ultrasound<br />
|AnswerBExp=<font color="red">'''Incorrect.'''</font> <br />
|AnswerC=Repeat CXR<br />
|AnswerCExp=<font color="red">'''Incorrect.'''</font><br />
|AnswerD=Troponins<br />
|AnswerDExp=<font color="red">'''Incorrect.'''</font><br />
|AnswerE=Spiral CT<br />
|AnswerEExp=<font color="Green">'''Correct.'''</font> See overall explanation<br />
|RightAnswer=E<br />
|WBRKeyword=Aortic rupture, aortic dissection, thoracic trauma<br />
|Approved=No<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR289&diff=1672418WBR2892020-10-28T03:01:15Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=[[User:Gonzalo Romero|Gonzalo A. Romero, M.D.]] [mailto:gromero@wikidoc.org]<br />
|ExamType=USMLE Step 2 CK<br />
|MainCategory=Surgery<br />
|SubCategory=Respiratory<br />
|MainCategory=Surgery<br />
|SubCategory=Respiratory<br />
|MainCategory=Surgery<br />
|SubCategory=Respiratory<br />
|MainCategory=Surgery<br />
|MainCategory=Surgery<br />
|SubCategory=Respiratory<br />
|MainCategory=Surgery<br />
|SubCategory=Respiratory<br />
|MainCategory=Surgery<br />
|SubCategory=Respiratory<br />
|MainCategory=Surgery<br />
|SubCategory=Respiratory<br />
|MainCategory=Surgery<br />
|MainCategory=Surgery<br />
|SubCategory=Respiratory<br />
|Prompt=A 34-year-old male gets into a street fight. He is stabbed in the right chest. He develops shortness of breath and is brought to the ER. His vitals upon admission were T 37C, BP= 110/70mmH, 85 bpm, 18 respirations/min. His chest has an 1 cm entrance wound on the right mid-axillary line at the 9th rib level. His lungs have no breath sounds at the right base and distant apical breath sounds. There is dullness to percussion over the right base. The rest of the physical exam is unremarkable. The CXR reveals a hemothorax. A chest tube is placed at the right pleural base recovering 260mL of blood per hour during the first four hours and starts deteriorating. What is the most appropriate next step in management?<br />
|Explanation=This patient is presenting with a hemothorax which is draining 260mL/hr for the first four hours, a total of 1040mL during the first 4 hours. The criteria for thoracotomy is when the chest tube placed drains the following:<br />
# More than 250 mL/hr for 4 hours= 1 Liter in 4 hours<br />
# More than 2.5 Liters in 24 hours<br />
# 1.25 Liters at chest tube insertion<br />
This criteria is a sign that the bleeding comes from a high pressure, or systemic circulation or a '''major hemothorax''', therefore exploration through thoracotomy or thoracoscopy, and vessel ligation is necessary to stop the bleeding. The most likely source of bleeding is an intercostal artery. <br />
<br><br />
<font color="MediumBlue"><font size="4">'''Educational Objective:''' </font></font><br />
# A thoracotomy or thoracoscopy is indicated when there is more than 1 Liter of blood coming out of a chest tube in a 4 hour period.<br />
<br><br />
'''References:''' Master the Boards for Step 2CK, surgery chapter<br />
{{See also|Thoracotomy|Hemothorax}}<br />
|AnswerA=Chest tube replacement<br />
|AnswerAExp=<font color="red">'''Incorrect.'''</font><br />
|AnswerB=Thoracotomy<br />
|AnswerBExp=<font color="Green">'''Correct.'''</font> The patient has drained through the chest tube more than 250 mL/hr for 4 hours, therefore a thoracotomy or thoracoscopy is necessary to ligate the vessel.<br />
|AnswerC=Left chest tube insertion<br />
|AnswerCExp=<font color="red">'''Incorrect.'''</font> Bilateral chest tube placement is indicated in the case of a flail chest.<br />
|AnswerD=CT scan with contrast<br />
|AnswerDExp=<font color="red">'''Incorrect.'''</font> The patient is hemodynamically stable therefore he cannot be placed into a CT scanner.<br />
|AnswerE=Positive pressure ventilation<br />
|AnswerEExp=<font color="red">'''Incorrect.'''</font> This could be the next step in management if the patient starts desaturating.<br />
|RightAnswer=B<br />
|WBRKeyword=Thoracotomy, chest tube, hemothorax<br />
|Approved=No<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR288&diff=1672417WBR2882020-10-28T03:01:05Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=[[User:Gonzalo Romero|Gonzalo A. Romero, M.D.]] [mailto:gromero@wikidoc.org]<br />
|ExamType=USMLE Step 2 CK<br />
|MainCategory=Surgery<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Surgery<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Surgery<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Surgery<br />
|MainCategory=Surgery<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Surgery<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Surgery<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Surgery<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Surgery<br />
|MainCategory=Surgery<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|Prompt=A 72-year-old male falls at home and hits his right chest wall against the bed frame. He is brought to the ER after his wife called 911. His vitals are T 37C, 86 bpm, 21 respirations/min, BP: 126/80 mmHg. His head, eyes, ears, nose and throat are unremarkable. His carotid pulse is 2+ without bruits. His chest is symmetric with decreased expansion on the right side. Upon palpation he has exquisite tenderness over the eight right rib at the anterior axillary line level. His lungs are clear to auscultation and percussion bilaterally. The rest of the physical exam is unremarkable. A chest x-ray reveals a rib fracture and no other abnormal findings. Which of the following is the most appropriate management in this patient?<br />
|Explanation=This elderly patient following a fall presents with a right 8th rib fracture which is limiting his right hemithorax expansion due to pain. The most appropriate management is local pain relief by nerve block and epidural catheter. After this the patient should be observed for 24 hours. If left untreated, a rib fracture can cause splinting leading to hypoventilation in the affected area. The hypoventilation could lead to pneumonia.<br />
A rib fracture can be complicated also by atelectasis and a pulmnonary contusion.<br />
<br><br />
<font color="MediumBlue"><font size="4">'''Educational Objective:''' </font></font><br />
# A plain rib fracture is the most common chest injury<br />
# A rib fracture can cause hypoventilation due to pain (specially in the elderly) leading to pneumonia if left untreated<br />
<br><br />
'''References:'''Master the Boards for Step 2CK, Surgery Chapter <br />
{{See also|Rib fracture}}<br />
|AnswerA=Oral NSAIDs<br />
|AnswerAExp=<font color="red">'''Incorrect.'''</font> Oral NSAIDs may slightly control the pain associated with a plain rib fracture, but it is not enough to prevent the hypoventilation which could lead to pneumonia, specially in the elderly.<br />
|AnswerB=Positive airway pressure<br />
|AnswerBExp=<font color="red">'''Incorrect.'''</font> It is used primarily in the treatment of sleep apnea.<br />
|AnswerC=Observation<br />
|AnswerCExp=<font color="red">'''Incorrect.'''</font><br />
|AnswerD=Intercostal nerve block<br />
|AnswerDExp=<font color="Green">'''Correct.'''</font><br />
|AnswerE=Oral narcotic therapy<br />
|AnswerEExp=<font color="red">'''Incorrect.'''</font> This can worsen the hypoventilation caused by the pain which can increase the risk of developing pneumonia.<br />
|RightAnswer=D<br />
|WBRKeyword=Rib fracture, chest trauma, narcotics, intercostal nerve block<br />
|Approved=No<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR287&diff=1672416WBR2872020-10-28T03:00:55Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=[[User:Gonzalo Romero|Gonzalo A. Romero, M.D.]] [mailto:gromero@wikidoc.org]<br />
|ExamType=USMLE Step 2 CK<br />
|MainCategory=Surgery<br />
|SubCategory=Musculoskeletal/Rheumatology, Musculoskeletal/Rheumatology<br />
|MainCategory=Surgery<br />
|SubCategory=Musculoskeletal/Rheumatology, Musculoskeletal/Rheumatology<br />
|MainCategory=Surgery<br />
|SubCategory=Musculoskeletal/Rheumatology, Musculoskeletal/Rheumatology<br />
|MainCategory=Surgery<br />
|MainCategory=Surgery<br />
|SubCategory=Musculoskeletal/Rheumatology, Musculoskeletal/Rheumatology<br />
|MainCategory=Surgery<br />
|SubCategory=Musculoskeletal/Rheumatology, Musculoskeletal/Rheumatology<br />
|MainCategory=Surgery<br />
|SubCategory=Musculoskeletal/Rheumatology, Musculoskeletal/Rheumatology<br />
|MainCategory=Surgery<br />
|SubCategory=Musculoskeletal/Rheumatology, Musculoskeletal/Rheumatology<br />
|MainCategory=Surgery<br />
|MainCategory=Surgery<br />
|SubCategory=Musculoskeletal/Rheumatology, Musculoskeletal/Rheumatology<br />
|Prompt=A 24-year-old male gets involved in a school fight and is shot in the arm with a .38-caliber revolver. He is brought to the ER with the following vital signs: 88 bpm, T 37C, BP: 110/70mmHg, 22 respirations/min. Upon arrival to the hospital, the patient is exposed by the trauma team. The surgical resident on call observes an entrance wound in the medial aspect across the left extremity and an exit wound located on the lateral aspect of the left arm. He has a large hematoma in the medial aspect of the arm, radial pulse is non palpable. Fluid resuscitation is started and the radiologic bone survey reveals a shattered humerus fracture. Which of the following is the correct order in management?<br />
|Explanation=This patient is presenting with a gun shot wound involving the bone, nerve and artery, therefore he will need surgery. This question is asking what is the most appropriate order. Fist the bone should be stabilized (performing it last would damage the delicate and vascular and nerve repairs). After the fracture stabilization, the vessels (both artery and vein) are repaired. Lastly the nerve is repaired.<br />
<font color="MediumBlue"><font size="4">'''Educational Objective:''' </font></font><br />
# '''WikiDoc Mnemonic:''' The '''BANK:''' keeps the bones, artery and nerves in place. '''B'''one--> '''A'''rtery(vessel) --> '''N'''erve<br />
'''References:''' Master the Boards for Step 2 CK, surgery chapter<br />
{{See also|Humerus fracture}}<br />
|AnswerA=Vascular repair, followed by fracture stabilization, followed by nerve repair<br />
|AnswerAExp=<font color="red">'''Incorrect.'''</font><br />
|AnswerB=Nerve repair, followed by vascular repair, followed by fracture stabilization<br />
|AnswerBExp=<font color="red">'''Incorrect.'''</font><br />
|AnswerC=Fracture stabilization, followed by vascular repair, followed by nerve repair<br />
|AnswerCExp=<font color="Green">'''Correct.'''</font> See overall explanation.<br />
|AnswerD=Fracture stabilization, followed by nerve repair, followed by vascular repair<br />
|AnswerDExp=<font color="red">'''Incorrect.'''</font><br />
|AnswerE=Nerve repair, followed by fracture stabilization, followed by vascular repair<br />
|AnswerEExp=<font color="red">'''Incorrect.'''</font><br />
|RightAnswer=C<br />
|WBRKeyword=extremities trauma, humerus fracture, brachial artery, radial nerve palsy<br />
|Approved=No<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR286&diff=1672415WBR2862020-10-28T03:00:45Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=[[User:Gonzalo Romero|Gonzalo A. Romero, M.D.]] [mailto:gromero@wikidoc.org]<br />
|ExamType=USMLE Step 2 CK<br />
|MainCategory=Internal medicine, Surgery<br />
|SubCategory=Musculoskeletal/Rheumatology, Musculoskeletal/Rheumatology, Surgery, Electrolytes<br />
|MainCategory=Internal medicine, Surgery<br />
|SubCategory=Musculoskeletal/Rheumatology, Musculoskeletal/Rheumatology, Surgery, Electrolytes<br />
|MainCategory=Internal medicine, Surgery<br />
|SubCategory=Musculoskeletal/Rheumatology, Musculoskeletal/Rheumatology, Surgery, Electrolytes<br />
|MainCategory=Internal medicine, Surgery<br />
|MainCategory=Internal medicine, Surgery<br />
|SubCategory=Musculoskeletal/Rheumatology, Musculoskeletal/Rheumatology, Surgery, Electrolytes<br />
|MainCategory=Internal medicine, Surgery<br />
|SubCategory=Musculoskeletal/Rheumatology, Musculoskeletal/Rheumatology, Surgery, Electrolytes<br />
|MainCategory=Internal medicine, Surgery<br />
|SubCategory=Musculoskeletal/Rheumatology, Musculoskeletal/Rheumatology, Surgery, Electrolytes<br />
|MainCategory=Internal medicine, Surgery<br />
|SubCategory=Musculoskeletal/Rheumatology, Musculoskeletal/Rheumatology, Surgery, Electrolytes<br />
|MainCategory=Internal medicine, Surgery<br />
|MainCategory=Internal medicine, Surgery<br />
|SubCategory=Musculoskeletal/Rheumatology, Musculoskeletal/Rheumatology, Surgery, Electrolytes<br />
|Prompt=A 73-year-old male is brought to the ER after being involved in a car accident. The firemen and paramedics invested 30 minutes to get him out of the car. After removing him from the car, they noticed a crush injury on the right distal arm, forearm and arm. His vital signs upon arrival are Temp 37C, 20 respirations/min, 130/86 mmHg, 87bpm. The patient complaints of paresthesias and pain on the right upper extremity. Physical examination is remarkable for multiple bruises on the right upper extremity, pallor, radial and ulnar pulses 2+, muscle strength II/IV. An initial radiologic survey does not reveal any fractures or internal bleeding. An EKG is shown below. Which of the following is the best next step when managing this patient to improve survival?<br />
<br><br />
[[File:Hyperkalemia1.jpg|center]]<br />
|Explanation=This elderly patient was involved in a car accident getting his upper extremity injured in a crush accident. He is hemodinamically stable. He has signs of compartment syndrome: pallor, paralysis, paresthesias, paralysis. His distal radial and ulnar pulses are strong (2+), but this sign is not enough to rule out compartment syndrome; the pulse is the last sign that appears in a compartment syndrome. Following a crush injury, the muscles get injured releasing myoglobin and potassium, which leads to hyperkalemia and myoglobinemia. The myoglobin is filtered through the kidney causing myoglobinuria which can ultimately cause renal failure. The hyperkalemia suspected in this patient following the muscle injury should be treated with calcium gluconate to establize the cardiac membrane in order to prevent arrhythmia which can lead to death. <br />
<font color="MediumBlue"><font size="4">'''Educational Objective:''' </font></font> compartment syndrome manifests by pain, pallor, paresthesias, paralysis and pulseless. The pulse is last to disappear and is a sign of irreversible muscle damage. Management of the compartment syndrome include the following:<br />
# Treatment of hyperkalemia. The first initial step is to provide calcium gluconate to prevent arrythmias. The following steps are also included as the management of hyperkalemia: insulin, dextrose 50, beta-2 agonists. <br />
# Fasciotomy. This is the following step, which includes dissecting the skin through the fascia in order to release the pressure increased in the syndrome which is limiting the blood blow to the extremity.<br />
# Hydration to protect the kidney from the myoglobinemia/myoglobinuria<br />
# Osmotic diuretics (manitol)<br />
# Soidum bicarbonate to alkalinize the urine to protect the kidney<br />
# '''WikiDoc Mnemonic:''' 5 Ps within the comPartment syndrome: pain, pallor, paresthesia, paralysis and pulseless<br />
<br><br />
'''References:''' Master the Boards for Step 2CK<br />
{{See also|Compartment syndrome|Hyperkalemia}}<br />
|AnswerA=Calcium gluconate<br />
|AnswerAExp=<font color="Green">'''Correct.'''</font>Calcium supplementation (calcium gluconate 10% (10ml), preferably through a central venous catheter as the calcium may cause phlebitis) does not lower potassium but decreases myocardial excitability, protecting against life threatening arrhythmias.<br />
|AnswerB=Normal saline<br />
|AnswerBExp=<font color="red">'''Incorrect.'''</font>Hydration is the best initial step in any patient following trauma in order to maintain the cardiac output. This patient does not have any signs of bleeding and is hemodinamically stable.<br />
|AnswerC=Sodium bicarbonate<br />
|AnswerCExp=<font color="red">'''Incorrect.'''</font> Bicarbonate therapy (e.g. 1 ampule (45mEq) infused over 5 minutes) is effective in cases of metabolic acidosis. The bicarbonate ion will stimulate an exchange of cellular H+ for Na+, thus leading to stimulation of the sodium-potassium ATPase. It will not prevent acutely the development of arrhythmias.<br />
|AnswerD=Mannitol<br />
|AnswerDExp=<font color="red">'''Incorrect.'''</font>It is an osmotic diuretic used to force diuresis and protect from the myoglobinuria damage. It does not prevent arrhythmias following crush injury-related hyperkalemia.<br />
|AnswerE=Fasciotomy<br />
|AnswerEExp=<font color="red">'''Incorrect.'''</font> It is the surgical treatment of choice in compartment syndrome. However, following a crush injury, the rise in potasium could lead to fatal arrythmias, which should be treated initially with calcium gluconate.<br />
|RightAnswer=A<br />
|WBRKeyword=Compartment syndrome, hyperkalemia, fasciotomy<br />
|Approved=No<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR284&diff=1672414WBR2842020-10-28T03:00:35Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Pathology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pathology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pathology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pathology<br />
|MainCategory=Pathology<br />
|MainCategory=Pathology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pathology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pathology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pathology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pathology<br />
|MainCategory=Pathology<br />
|SubCategory=Cardiology<br />
|Prompt=A newborn boy is evaluated for vomiting when fed for the first time. Physical examination is remarkable for flat facies, an unusually large tongue, and prominent epicanthal folds. Upper gastrointestinal studies demonstrate gas in the stomach and the duodenal bulb. Which of the following cardiovascular defects is mostly associated with his newborn's underlying genetic disease?<br />
|Explanation=The patient is most likely diagnosed with Down syndrome (trisomy 21), as evidenced by the phenotypic profile, Down syndrome is associated with duodenal atresia, which is characterized by the congenital underdevelopment of parts of the duodenum and is suggested by the vomiting and the double bubble sign on imaging. Down syndrome is strongly associated with an increased risk of congenital cardiovascular disease, especially endocardial cushion defects (AV canal). Down syndrome is also associated with other congenital heart diseases (less commonly than with endocardial cushion defects), namely ventricular septal defects (VSD) and atrial septal defects (ASD).<br />
|AnswerA=Ectopic ductal tissue<br />
|AnswerAExp=Coarctation of the aorta, which is commonly associated with Turner syndrome, results from ectopic ductal tissue or from abnormal development of the fourth and sixth aortic arch.<br />
|AnswerB=Improper alignment of aorticopulmonary septum<br />
|AnswerBExp=Tetralogy of Fallot is caused by improper alignment of aorticopulmonary septum.<br />
|AnswerC=Failure of aorticopulmonary septum to twist<br />
|AnswerCExp=Transposition of the great vessels is caused by failure of aorticopulmonary septum to twist and is commonly present in children of diabetic mothers.<br />
|AnswerD=Inadequate formation of the septum secundum<br />
|AnswerDExp=Ostium secundum atrial septal defect (ASD) is the most common type of ASD. It arises from inadequate growth of the septum secundum and comprises up to 10% of all cases of congenital heart diseases. Although ASD is associated with Down syndrome, endocardial cushion defects are more common.<br />
|AnswerE=Inadequate migration of neural crest cells<br />
|AnswerEExp=Failure of migration of neural crest cells to the endocardial cushion is the most common congenital heart disease associated with Down syndrome.<br />
|EducationalObjectives=Down syndrome is strongly associated with endocardial cushion defects (formation of AV canal), which is characterized by failure of migration of neural crest cells to the endocardial cushion.<br />
|References=FIrst Aid 2015 page 290.<br />
|RightAnswer=E<br />
|WBRKeyword=Down syndrome, AV canal, Endocardial cushion defect<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR283&diff=1672413WBR2832020-10-28T03:00:25Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by Serge Korjian)<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Pharmacology<br />
|SubCategory=Cardiology<br />
|Prompt=A 32-year-old woman delivers a newborn at 33 weeks gestation. The newborn is found to have persistent pulmonary hypertension and is promptly administered high frequency ventilation and inhaled nitric oxide therapy. Six hours later, the newborn becomes cyanotic and lethargic and develops a seizure. What is the most appropriate initial therapy for this patient?<br />
|Explanation=Persistent pulmonary hypertension in the newborn may be either idiopathic or associated with prematurity, pulmonary hypoplasia, or premature closure of the ductus arteriosus. In hypoxemic newborns with pulmonary hypertension, inhaled nitric oxide reduces pulmonary vascular resistance and decreases the need for extracorporeal membrane oxygenation therapy. However, nitric oxide inhalation may result in elevations in methemoglobin leading to methemoglobinemia. In infants with PPH receiving nitric oxide, methemoglobin levels should be monitored every 4 hours and maintained below 5%. Infants with methemoglobinemia have signifcant cyanosis. Methemoglobin interferes with the regular pulse oximetry often giving a reading higher than the true available oxygen, and not in proportion to the level of cyanosis. A co-oximeter, able to differentiate oxyhemoglobin, methemoglobin, and deoxyhemoglobin, is the best way to monitor methemoglobin levels. Treatment should be initiated promptly in patients with elevated methemoglobin with or without clinical manifestations. Methylene blue is the optimal initial agent. Exchange transfusions are recommended when methylene blue is contraindicated (E.g.: G6PD deficiency). Methylene blue increases the rate of reduction of methemoglobin into hemoglobin by converting the iron moeity from a ferric ion (Fe<sup>3+</sup>) into a ferrous ion (Fe<sup>2+</sup>).<br />
|AnswerA=N-Acetylcysteine<br />
|AnswerAExp=N-Acetylcysteine replenishes the reduced form of glutathione, which neutralizes the oxidative stress associated with acetaminophen overdose. It is also used in reducing the mucus viscosity in patients with cystic fibrosis by isolating disulfide bonds.<br />
|AnswerB=EDTA<br />
|AnswerBExp=EDTA is a chelating agent for treating heavy metal poisoning. It is also an anticoagulant for keeping blood samples.<br />
|AnswerC=Methylene blue<br />
|AnswerCExp=Methylene blue and ascorbic acid (Vitamin C) have the ability to convert ferric ion into ferrous ion in hemoglobin and restores its oxygen-binding capacity to the proper state.<br />
|AnswerD=Amyl nitrite<br />
|AnswerDExp=Amyl nitrite is used in cyanide poisoning. It oxidizes iron to the ferric state and actually causes methemoglobinemia to decrease the binding of cyanide to hemoglobin.<br />
|AnswerE=Vitamin K<br />
|AnswerEExp=Vitamin K is required for gamma carboxylation of glutamate residues and is used in warfarin overdose.<br />
|EducationalObjectives=Methylene blue is the treatment of choice in methemoglobinemia. It increases the rate of reduction of methemoglobin into hemoglobin by converting the iron moeity from a ferric ion (Fe<sup>3+</sup>) into a ferrous ion (Fe<sup>2+</sup>).<br />
|References=Jaffe ER, Neurmann G. A comparision of the effect of menadione, methylene blue and ascorbic acid on the reduction of methemoglobin in vivo. Nature. 1964;202:607-8.<br><br />
Bizzarro M, Gross I, Barbosa FT. Inhaled nitric oxide for the postoperative management of pulmonary hypertension in infants and children with congenital heart disease. Cochrane Database Syst Rev. 2014;7:CD005055.<br><br />
Hamon I, Gauthier-moulinier H, Grelet-dessioux E, Storme L, Fresson J, Hascoet JM. Methaemoglobinaemia risk factors with inhaled nitric oxide therapy in newborn infants. Acta Paediatr. 2010;99(10):1467-73.<br />
|RightAnswer=C<br />
|WBRKeyword=Pulmonary hypertension, Methylene blue, Methemoglobinemia<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR282&diff=1672412WBR2822020-10-28T03:00:15Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by Serge Korjian)<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Pathology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pathology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pathology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pathology<br />
|MainCategory=Pathology<br />
|MainCategory=Pathology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pathology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pathology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pathology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pathology<br />
|MainCategory=Pathology<br />
|SubCategory=Cardiology<br />
|Prompt=A 29-year-old woman presents with a three-year history of increasing dyspnea on exertion associated with chest tightness and lightheadedness. Physical examination is notable for palpable double apical impulses, fourth heart sounds, and systolic murmurs at the left lower sternal border. Echocardiography demonstrates systolic anterior motion of the mitral valve. Which of the following disorders has the same pattern of inheritance as the disorder likely to be present in this patient?<br />
|Explanation=Familial hypertrophic cardiomyopathy (HCM) is an autosomal dominant disorder due to one or more of 11 identified missense mutations in genes that encode the thick and thin contractile myofilament protein components of the sarcomere (specifically the beta-myosin heavy chain and myosin-binding protein C) which are exclusive to the heart. Phenotypically, not all patients with the mutation manifest the disease, although phenotypic conversion is possible at any point in the disease. Diagnosis requires phenotypic confirmation with imaging, which demonstrates unexplained LV wall thickness >15 mm. Patients generally have a normal life expectancy-, but have a higher risk of sudden death, progressive heart failure, and paroxysmal or chronic atrial fibrillation. The typical murmur of HCM is a systolic ejection murmur that is intensified with conditions of decreased preload or after long cardiac cycles and softened with conditions of increased afterload. The hypertrophied interventricular septum with systolic anterior motion of the mitral valve among patients with phenotypically manifest disease may result in subaortic obstruction of the left ventricular outflow tract that produces a "double-tap" apical impulse as well as pulsus bisferiens (biphasic or beating twice). Treatment of HCM depends on the extent of symptoms. Beta-blockers are the first-line for outflow tract obstruction to decrease the flow gradient (same mechanism as decreased murmurs). Patients with siginificant obstruction may benefit from surgical septal myectomy. Implantable cardioverter-defibrillators are the only strategy shown to reduce the risk of sudden death.<br />
|AnswerA=Huntington disease<br />
|AnswerAExp=Huntington disease has an autosomal dominant mode of inheritance similar to familial hypertrophic cardiomyopathy (HCM).<br />
|AnswerB=Cystic fibrosis<br />
|AnswerBExp=Cystic fibrosis has an autosomal recessive mode of inheritance.<br />
|AnswerC=Kartagener syndrome<br />
|AnswerCExp=Kartagener syndrome has an autosomal recessive mode of inheritance.<br />
|AnswerD=Tay-Sachs disease<br />
|AnswerDExp=Tay-Sachs disease has an autosomal recessive mode of inheritance.<br />
|AnswerE=Leber hereditary optic neuropathy<br />
|AnswerEExp=Leber hereditary optic neuropathy has a mitochondrial mode of inheritance.<br />
|EducationalObjectives=Hypertrophic cardiomyopathy (HCM) is an autosomal dominant disorder due to one or more of 11 identified missense mutations in genes that encode the thick and thin contractile myofilament protein components of the sarcomere.<br />
|References=Maron BJ, Ommen SR, Semsarian C, Spirito P, Olivotto I, Maron MS. Hypertrophic cardiomyopathy: present and future, with translation into contemporary cardiovascular medicine. J Am Coll Cardiol. 2014;64(1):83-99.<br />
|RightAnswer=A<br />
|WBRKeyword=Hypertrophic cardiomyopathy, Huntington's disease, Autosomal dominant, Inheritance, Cardiomyopathy<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR281&diff=1672411WBR2812020-10-28T03:00:05Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by Serge Korjian)<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Microbiology, Pharmacology<br />
|SubCategory=Infectious Disease<br />
|MainCategory=Microbiology, Pharmacology<br />
|SubCategory=Infectious Disease<br />
|MainCategory=Microbiology, Pharmacology<br />
|SubCategory=Infectious Disease<br />
|MainCategory=Microbiology, Pharmacology<br />
|MainCategory=Microbiology, Pharmacology<br />
|MainCategory=Microbiology, Pharmacology<br />
|SubCategory=Infectious Disease<br />
|MainCategory=Microbiology, Pharmacology<br />
|SubCategory=Infectious Disease<br />
|MainCategory=Microbiology, Pharmacology<br />
|SubCategory=Infectious Disease<br />
|MainCategory=Microbiology, Pharmacology<br />
|SubCategory=Infectious Disease<br />
|MainCategory=Microbiology, Pharmacology<br />
|MainCategory=Microbiology, Pharmacology<br />
|SubCategory=Infectious Disease<br />
|Prompt=A 55-year-old man presents to the emergency department after being bitten by his brother during a domestic dispute. On physical examination, the physician notices a 3 by 3 inch wound on his arm lined by human teeth marks. What is the most appropriate agent to prevent infection of the wound in this case?<br />
|Explanation=Human bite wounds can be divided into 2 different types: occlusive injuries, defined as a wound from a direct bite, or clenched-fist injuries, defined as a wound from a fist striking teeth. Bacteria associated with human bite injuries are usually part of the oral flora and include viridans ''Streptococci'', ''Staphylococci'', anaerobic organisms (''Fusobacterium nucleatum'', ''Prevotella'', ''Peptostreptococci''), and ''Eikenella corrodens''. ''E. corrodens'' is a facultatively anaerobic, pleomorphic bacillus that requires ample carbon dioxide concentrations to thrive. ''E. corrodens'' is part of the normal flora of the oral cavity and the upper respiratory tract. ''E. corrodens'' infections are common in untreated human bite wounds, especially clenched fist injuries. ''E. corrodens'' infections typically progress slowly and can manifest clinically one to two weeks after inoculation. Complications include osteomyelitis, loss of joint function, and bacteremia with endocarditis. General treatment of human bite wounds includes irrigation and topical wound cleansing, however, unlike animal bites, prophylactic antimicrobials should be administered to all patients regardless of the wound appearance. Antibiotic regimens should cover: ''E. corrodens'', ''S. aureus'', ''Haemophilus'' species, and anaerobes. Notably, ''E. corrodens'' is resistant to first-generation cephalosporins, macrolides, clindamycin, and aminoglycosides. Adequate agents include amoxicillin-clavulanate, ampicillin-sulbactam, carbapenems, and doxycyline. Intravenous antibiotics are preferred in clenched-fist injuries.<br />
|AnswerA=Cefazolin<br />
|AnswerAExp=Agents that lack anaerobic coverage as well as coverage against ''Eikenella corrodens'', ''Haemophilus'' species, and ''Staphylococcus aureus'' are not appropriate for prophylaxis. Cefazolin does not cover anaerobic organisms or ''Eikenella'' species.<br />
|AnswerB=Dicloxacillin<br />
|AnswerBExp=Agents that lack anaerobic coverage as well as coverage against ''Eikenella corrodens'', ''Haemophilus'' species, and ''Staphylococcus aureus'' are not appropriate for prophylaxis. Dicloxacillin lacks ''Eikenella'' coverage.<br />
|AnswerC=Erythromycin<br />
|AnswerCExp=Agents that lack anaerobic coverage as well as coverage against ''Eikenella corrodens'', ''Haemophilus'' species, and ''Staphylococcus aureus'' are not appropriate for prophylaxis. Erythromycin lacks coverage for all three.<br />
|AnswerD=Clindamycin<br />
|AnswerDExp=Agents that lack anaerobic coverage as well as coverage against ''Eikenella corrodens'', ''Haemophilus'' species, and ''Staphylococcus aureus'' are not appropriate for prophylaxis. Although clindamycin has anerobic and staphylococcal coverage, it does not cover ''Eikenella''.<br />
|AnswerE=Amoxicillin-Clavulanate<br />
|AnswerEExp=Amoxicillin-Clavulanate may be used for post-exposure prophylaxis in cases of human bite wounds. It has adequate coverage for ''Eikenella corrodens'', ''Staphylococcus aureus'' (MSSA), and anaerobic organisms.<br />
|EducationalObjectives=Prophylactic antimicrobials should be administered to all patients with human bite injuries. Antibiotic regimens should cover: ''E. corrodens'', ''S. aureus'', ''Haemophilus'' species, and anaerobes. Adequate agents include amoxicillin-clavulanate, ampicillin-sulbactam, carbapenems, and doxycyline.<br />
|References=Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft-tissue infections. Clin Infect Dis. 2005;41(10):1373-406.<br><br />
Decker MD. Eikenella corrodens. Infect Control. 1986;7(1):36-41.<br />
|RightAnswer=E<br />
|WBRKeyword=Eikenella corrodens, Human bite injuries, Bite injuries, Clenched fist injuries, Antibiotics, Prophylaxis, Emergency,<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR280&diff=1672410WBR2802020-10-28T02:59:55Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by Serge Korjian)<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Microbiology, Pharmacology<br />
|SubCategory=Head and Neck, Hematology, Musculoskeletal/Rheumatology<br />
|MainCategory=Microbiology, Pharmacology<br />
|SubCategory=Head and Neck, Hematology, Musculoskeletal/Rheumatology<br />
|MainCategory=Microbiology, Pharmacology<br />
|SubCategory=Head and Neck, Hematology, Musculoskeletal/Rheumatology<br />
|MainCategory=Microbiology, Pharmacology<br />
|MainCategory=Microbiology, Pharmacology<br />
|MainCategory=Microbiology, Pharmacology<br />
|SubCategory=Head and Neck, Hematology, Musculoskeletal/Rheumatology<br />
|MainCategory=Microbiology, Pharmacology<br />
|SubCategory=Head and Neck, Hematology, Musculoskeletal/Rheumatology<br />
|MainCategory=Microbiology, Pharmacology<br />
|SubCategory=Head and Neck, Hematology, Musculoskeletal/Rheumatology<br />
|MainCategory=Microbiology, Pharmacology<br />
|SubCategory=Head and Neck, Hematology, Musculoskeletal/Rheumatology<br />
|MainCategory=Microbiology, Pharmacology<br />
|SubCategory=Head and Neck, Hematology, Musculoskeletal/Rheumatology<br />
|MainCategory=Microbiology, Pharmacology<br />
|MainCategory=Microbiology, Pharmacology<br />
|SubCategory=Head and Neck, Hematology, Musculoskeletal/Rheumatology<br />
|Prompt=An 8-year-old girl with a history of thalassaemia major presents to the emergency department with low-grade fever, leg pain, and malaise for the past week. Her blood pressure is 110/60 mm Hg, heart rate is 90/min, and temperature is 37.8 ᵒC (100 ᵒF). On physical examination, her anterior left shin is red, swollen, and tender to palpation. Following an extensive work-up, the diagnosis of tibial osteomyelitis is confirmed. Cultures from bone biopsies reveal gram-negative rods. Which of the following regimens is the most appropriate for the initial management of this patient?<br />
|Explanation=Beta-thalassemia major is and inherited autosomal-recessive blood disorder characterized by reduced or absent synthesis of beta hemoglobin chains resulting in severe anemia requiring transfusions, splenomegaly, and bone deformities due to marrow expansion. Beta-thalassemia major, and other hemoglobinopathies such as sickle cell disease, predispose patients to osteomyelitis secondary to ''Salmonella'' species. Among these patients, ''Salmonella'' osteomyelitis is more commonly observed than in the general population; however, ''S. aureus'' remains the predominant cause of osteomyelitis. Several hypotheses have been proposed to explain the higher incidence of ''Salmonella'' osteomyelitis in hemoglobinopathies. Given the impairment in effective oxygen delivery in these disorders, some have suggested that patchy ischemic infarction of the bowels may occur allowing transient mucosal barrier breakdown and passage of the bacteria into the bloodstream. Empiric treatment of hematogenous osteomyelitis in patients with hemoglobinopathies includes coverage for ''Salmonella'', ''E. coli'', and ''S. aureus'' species. Regimens should include [[ciprofloxacin]] and either [[oxacillin]]/[[nafcillin]]/[[ceftriaxone]] or [[vancomycin]]/[[linezolid]], depending on risk of MRSA. In patients with bone biopsy diagnosis of ''Salmonella'' osteomyelitis, treatment with ciprofloxacin is recommended if susceptibility is documented.<br />
|AnswerA=Ciprofloxacin<br />
|AnswerAExp=Empiric treatment of hematogenous osteomyelitis in patients with hemoglobinopathies includes coverage for Salmonella, ''E. coli'', and ''S. aureus'' species. Regimens should include ciprofloxacin and either oxacillin/nafcillin/ceftriaxone or vancomycin/linezolid depending on risk of MRSA.<br />
|AnswerB=Linezolid<br />
|AnswerBExp=Although linezolid provides adequate coverage for staphylococcal species, it does not cover ''Salmonella'' species, which are highly likely in this case given the history of thalassemia and the culture results.<br />
|AnswerC=Ampicillin<br />
|AnswerCExp=Although ampicillin provides adequate coverage for staphylococcal species, it does not cover ''Salmonella'' species, which are highly likely in this case given the history of thalassemia and the culture results.<br />
|AnswerD=Vancomycin<br />
|AnswerDExp=Although vancomycin provides adequate coverage for staphylococcal species, it does not cover ''Salmonella'' species, which are highly likely in this case given the history of thalassemia and the culture results.<br />
|AnswerE=Clindamycin<br />
|AnswerEExp=Although clindamycin provides adequate coverage for staphylococcal species, it does not cover ''Salmonella'' species, which are highly likely in this case given the history of thalassemia and the culture results.<br />
|EducationalObjectives=Empiric treatment of hematogenous osteomyelitis in patients with hemoglobinopathies includes coverage for Salmonella, ''E. coli'', and ''S. aureus'' species. Regimens should include ciprofloxacin and either oxacillin/nafcillin/ceftriaxone or vancomycin/linezolid depending on risk of MRSA.<br />
|References=Burnett MW, Bass JW, Cook BA. Etiology of osteomyelitis complicating sickle cell disease. Pediatrics. 1998;101(2):296-7.<br />
|RightAnswer=A<br />
|WBRKeyword=Salmonella, Osteomyelitis, Antibiotics, Thalassemia, Sickle cell disease<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR279&diff=1672409WBR2792020-10-28T02:59:45Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by Serge Korjian)<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Microbiology, Pharmacology<br />
|SubCategory=Dermatology<br />
|MainCategory=Microbiology, Pharmacology<br />
|SubCategory=Dermatology<br />
|MainCategory=Microbiology, Pharmacology<br />
|SubCategory=Dermatology<br />
|MainCategory=Microbiology, Pharmacology<br />
|MainCategory=Microbiology, Pharmacology<br />
|MainCategory=Microbiology, Pharmacology<br />
|SubCategory=Dermatology<br />
|MainCategory=Microbiology, Pharmacology<br />
|SubCategory=Dermatology<br />
|MainCategory=Microbiology, Pharmacology<br />
|SubCategory=Dermatology<br />
|MainCategory=Microbiology, Pharmacology<br />
|SubCategory=Dermatology<br />
|MainCategory=Microbiology, Pharmacology<br />
|MainCategory=Microbiology, Pharmacology<br />
|SubCategory=Dermatology<br />
|Prompt=A 15-year-old girl presents to the emergency department after being bitten by a stray dog in her neighborhood. On physical examination, she has a 5 by 3 inch wound on her calf with evidence of deep punctures. The wound is cleaned and sutured and the patient is sent home. The next day, she returns to the emergency department with fever and a swollen and erythematous wound. Which of the following antimicrobial agents is most likely indicated in this case?<br />
|Explanation=Pasteurella multocida is a non-motile, penicillin-sensitive, Gram-negative coccobacillus that causes zoonotic infections in humans following bites or scratches from pets (such as cats and dogs). Many mammals and fowl harbor it as part of their normal respiratory flora. Inflammatory signs of pasteurellosis are very rapid to develop. Classical presenting signs include severe pain, fever, swelling and exudation hours to a few days following a cat or a dog bite. Patients with more severe disease and bacteremia can present with vomiting, headache and diarrhea. Lymphangitis is common among infected patients. Untreated, the disease could lead to septic shock, septic arthritis, meningitis, endocarditis, or osteomyelitis. Depending on the stage of the infection, diagnosis is made by tissue or blood culture. Most cases of pasteurellosis can be prevented with a short-course of oral antibiotics following a cat or dog bite. Severe or progressing infections may require IV antibiotics, or surgical intervention. Pasteurella is generally susceptible to oral amoxicillin, amoxicillin/clavulanate, fluoroquinolones, trimethoprim-sulfamethoxazole, and tetracyclines. Most isolates are resistant to second generation cephalosporins, dicloxacillin, macrolides and clindamycin. <br />
|AnswerA=Amoxicillin-Clavulanate<br />
|AnswerAExp=Pasteurella multocida is sensitive to amoxicillin-clavulanate, which can be used in the prophylaxis and treatment of pasteurellosis. The disease may also be treated with fluoroquinolones or tetracyclines.<br />
|AnswerB=Cephalexin<br />
|AnswerBExp=P. multocida is reported to be resistant to dicloxacillin, cephalexin, and clindamycin; many strains are resistant to erythromycin.<br />
|AnswerC=Clindamycin<br />
|AnswerCExp=P. multocida is reported to be resistant to dicloxacillin, cephalexin, and clindamycin; many strains are resistant to erythromycin.<br />
|AnswerD=Dicloxacillin<br />
|AnswerDExp=P. multocida is reported to be resistant to dicloxacillin, cephalexin, and clindamycin; many strains are resistant to erythromycin.<br />
|AnswerE=Erythromycin<br />
|AnswerEExp=P. multocida is reported to be resistant to dicloxacillin, cephalexin, and clindamycin; many strains are resistant to erythromycin.<br />
|EducationalObjectives=Pasteurella multocida is sensitive to amoxicillin, amoxicillin-clavulanate, fluoroquinolones, and tetracycline. Most strains are resistant to second generation cephalosporins, dicloxacillin, macrolides and clindamycin.<br />
|References=Oehler RL, Velez AP, Mizrachi M, Lamarche J, Gompf S. Bite-related and septic syndromes caused by cats and dogs. Lancet Infect Dis. 2009;9(7):439-47.<br><br />
Weber DJ, Wolfson JS, Swartz MN, Hooper DC. Pasteurella multocida infections. Report of 34 cases and review of the literature. Medicine (Baltimore). 1984;63(3):133-54.<br />
|RightAnswer=A<br />
|WBRKeyword=Pasteurella multocida, Parteurellosis, Dog bite, Cat bite, Zoonotic infections, Antibiotics, <br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR278&diff=1672408WBR2782020-10-28T02:59:35Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor= {{Sapan}}<br />
|ExamType=USMLE Step 3<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Cardiovascular<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Cardiovascular<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Cardiovascular<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Cardiovascular<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Cardiovascular<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Cardiovascular<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Cardiovascular<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Cardiovascular<br />
|Prompt=A 68-year-old male is seen in the office for recurrent chest pain. He reports that he is getting substernal chest pain, without radiation, when he goes for a walk. The pain resolves with 12–15 minutes of rest. He has never had pain at rest. He has no other cardiac complaints and his review of systems is otherwise negative. He has an unremarkable medical history and takes only a baby aspirin a day. On examination, his blood pressure is 130/68, pulse 86, and respiratory rate 14. His cardiac examination is notable for a harsh, 3/6 systolic ejection murmur along the sternal border that radiates to the carotid arteries. His carotid pulsation is noted to rise slowly and is small and sustained. His lungs are clear. The remainder of his examination is normal. Which of the following would be the most appropriate test to order?<br />
|Explanation=EXPLANATION: Aortic stenosis is one of the most common valvular abnormalities found in adults. It can be congenital—such as a unicuspid or bicuspid valve—or acquired. In young adults, acquired aortic stenosis is often seen as a consequence of rheumatic fever. This is becoming less common in developed nations. In adults over the age of 65, the most common cause of aortic stenosis is age-related degenerative, calcific aortic stenosis. The valvular cusps are immobilized and the stenosis caused by calcium deposits along the flexion lines of the valves. Acquired aortic stenosis typically has a prolonged asymptomatic period. During this time the stenosis may be found incidentally by auscultation of the characteristic harsh, holosystolic murmur in the aortic valve area that radiates to the carotid arteries. There may also be a slow, small, and sustained arterial pulsation (pulsus parvus and tardus) due to the relative outflow obstruction. <br />
When considering the diagnosis of aortic stenosis, the initial diagnostic test of choice would be echocardiography. It would provide information on both the structure (bicuspid, tricuspid, and the like) and the function (valve area, pressures) of the valve. The size and function of the left ventricle can also be determined. <br />
<br />
EDUCATIONAL OBJECTIVE: Aortic stenosis is one of the most common valvular abnormalities found in adults. The initial diagnostic test of choice would be echocardiography.<br />
|AnswerA=Cardiac catheterization<br />
|AnswerAExp=Incorrect- If aortic stenosis is found on echocardiogram and the patient is symptomatic, the next test would be cardiac catheterization. This would allow for direct measurement of the pressure gradient across the valve. It would also allow for evaluation of the status of the coronary arteries in order to determine whether CABG would need to be performed along with valve replacement.<br />
|AnswerB=Electrophysiologic studies<br />
|AnswerBExp=Incorrect- Electrophysiologic studies would not play a role in the typical evaluation of aortic stenosis.<br />
|AnswerC=Exercise stress test<br />
|AnswerCExp=Incorrect- Exercise stress testing is relatively contraindicated in the setting of symptomatic aortic stenosis.<br />
|AnswerD=Echocardiogram<br />
|AnswerDExp=Correct- see explantion.<br />
|AnswerE=24-hour Holter monitor<br />
|AnswerEExp=Incorrect- Holter monitoring would only be useful if there were a concomitant arrhythmia.<br />
|RightAnswer=D<br />
|WBRKeyword=Aortic stenosis<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR277&diff=1672407WBR2772020-10-28T02:59:25Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor= {{Sapan}}<br />
|ExamType=USMLE Step 3<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Pediatrics<br />
|Prompt=Physician is called to see a newborn in the nursery because the nurse is concerned that the baby have single crease in the palm of the hand, small ears, small mouth, upward slanting eyes, wide space between the first and second toes, short hands with short fingers. Which of the following sign is most likely associated in this newborn?<br />
|Explanation=<br />
EXPLANATION: The most common finding in a newborn with Down syndrome is hypotonia. Other common findings include single palmar crease, flat facial profile, macroglossia, and wide space between the first and second toes. Hypotonia in the newborn period should prompt close evaluation and follow-up. <br />
<br />
EDUCATIONAL OBJECTIVE: The most common finding in a newborn with Down syndrome is hypotonia which should prompt close evaluation and follow-up.<br />
<br />
<br />
|AnswerA=Café au lait spots<br />
|AnswerAExp=Incorrect- This newborn is showing signs of Down syndrome. Café au lait spots are associated with neurofibromatosis.<br />
|AnswerB=High arched palate<br />
|AnswerBExp=Incorrect- This newborn is showing signs of Down syndrome. High arched palates are associated with fragile X syndrome.<br />
<br />
|AnswerC=Ambiguous genitalia<br />
|AnswerCExp=Incorrect- This newborn is showing signs of Down syndrome. Ambiguous genitalia are commonly seen in CAH.<br />
|AnswerD=Hypotonia<br />
|AnswerDExp=Correct- See explanation.<br />
|AnswerE=Club feet<br />
|AnswerEExp=Incorrect- This newborn is showing signs of Down syndrome.<br />
|RightAnswer=D<br />
|WBRKeyword=Down syndrome<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR271&diff=1672406WBR2712020-10-28T02:59:19Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor= {{Sapan}}<br />
|ExamType=USMLE Step 3<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Genitourinary, Genitourinary, Hematology, Pediatrics<br />
|Prompt=A 6-year-old child is brought to office because of a sudden onset of irritability, weakness, and pallor. The father provides history that both of his children have been experiencing episodes of vomiting and diarrhea. His physical examination reveals a blood pressure of 116/82, dry mucus membranes, petechiae, and diffuse abdominal pain. The following laboratory work is obtained:<br />
<br />
*Urinalysis: microscopic hematuria and proteinuria<br />
*Blood urea nitrogen (BUN)/creatinine (Cr): 20/1.0 mg/dL<br />
*Hemoglobin: 7 g/dL<br />
*Peripheral blood smear: fragmented RBCs<br />
*Prothrombin time (PT), partial thromboplastin time (PTT): normal<br />
*Coombs' test: negative<br />
<br />
What is the most likely diagnosis?<br />
|Explanation=HUS (Hemolytic Uraemic Syndrome) is the combination of a microangiopathic hemolytic anemia and acute renal failure. It is commonly associated with E. coli O157/H7 gastroenteritis. HUS is one of the most common causes of acquired renal failure in children.<br />
<br />
EDUCATIONAL OBJECTIVE: HUS is triad of gastroenteritis, microangiopathic hemolytic anemia and acute renal failure.<br />
|AnswerA=Idiopathic thrombocytopenic purpura<br />
|AnswerAExp=Incorrect- Idiopathic thrombocytopenic purpura is a bleeding disorder in which the immune system destroys platelets, which are necessary for normal blood clotting. Persons with the disease have too few platelets in the blood. But findings of gastroenteritis and acute renal failure are more suggestive of HUS.<br />
|AnswerB=Henoch Schonlein Purpura<br />
|AnswerBExp=Incorrect- Purpura, arthritis and abdominal pain are known as the "classic triad" of Henoch–Schönlein purpura. But finding of acute renal failure are more suggestive of HUS.<br />
|AnswerC=Evans syndrome<br />
|AnswerCExp=Incorrect- Evans syndrome is an autoimmune disease in which an individual's antibodies attack their own red blood cells and platelets. Both of these events may occur simultaneously or one may follow on from the other. But findings of gastroenteritis and acute renal failure are more suggestive of HUS.<br />
|AnswerD=Meningococcemia<br />
|AnswerDExp=Incorrect- Meningococcemia, like many gram-negative blood infections, can cause disseminated intravascular coagulation (DIC), which is the inappropriate clotting of blood within the vessels. DIC can cause ischemic tissue damage when upstream thrombus obstructs blood flow and haemorrhage because clotting factors are exhausted. But normal PT and PTT findings exclude this as a possibility.<br />
|AnswerE=Hemolytic Uraemic Syndrome<br />
|AnswerEExp=Correct- See explanation<br />
|RightAnswer=E<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR270&diff=1672405WBR2702020-10-28T02:59:14Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor= {{Ochuko}} (Reviewed by {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Biochemistry<br />
|SubCategory=General Principles<br />
|MainCategory=Biochemistry<br />
|SubCategory=General Principles<br />
|MainCategory=Biochemistry<br />
|SubCategory=General Principles<br />
|MainCategory=Biochemistry<br />
|MainCategory=Biochemistry<br />
|MainCategory=Biochemistry<br />
|SubCategory=General Principles<br />
|MainCategory=Biochemistry<br />
|SubCategory=General Principles<br />
|MainCategory=Biochemistry<br />
|SubCategory=General Principles<br />
|MainCategory=Biochemistry<br />
|SubCategory=General Principles<br />
|MainCategory=Biochemistry<br />
|MainCategory=Biochemistry<br />
|SubCategory=General Principles<br />
|Prompt=A 3-year-old boy is brought to the physician’s office with a 3-day history of fever, cough, and runny nose. The mother states that the child is not growing like his siblings before him. Physical examination is remarkable for generalized hypotonia, restricted joint movements, and coarse facial features. Radiographic findings include bullet-shaped phalanges, wedging of the vertebrae, and widening and thickening of the ribs. Which of the following statements is true regarding the impaired cellular organelle involved in this patient's condition?<br />
|Explanation=Inclusion cell disease (I-cell disease) is an inherited lysosomal storage disorder characterized by failure of addition of mannose -6- phosphate to lysosome proteins. It usually manifests with coarse facial features, clouded corneas, restricted joint movement, and in the majority of cases, it is fatal in childhood. The disease is caused by defective phosphotransferase enzyme that is located on the Golgi apparatus (involved cellular organelle). The Golgi apparatus is a distribution center of proteins and lipids from the endoplasmic reticulum (ER) to the plasma membrane, lysosomes, and secretory vesicles. It modifies N-oligosaccharides on asparagine and adds O-oligosaccharides to serine and threonine residues.<br />
|AnswerA=It is involved in the addition of O-oligosaccharides to serine and threonine residues<br />
|AnswerAExp=The cellular organelle involved in I-cell disease disease is the Golgi apparatus, which normally modifies N-oligosaccharides on asparagine and adds O-oligosaccharides to serine and threonine residues.<br />
|AnswerB=Modification of N-oligosaccharides on glycine<br />
|AnswerBExp=Modification of N-oligosaccharides is on asparagine.<br />
|AnswerC=It is involved in the addition of glucose -6-phosphate to proteins<br />
|AnswerCExp=The Golgi apparatus is involved in the addition of mannose-6-phosphate to specific lysosomal proteins.<br />
|AnswerD=It is a distribution center of proteins and lipids from the endoplasmic reticulum to the mitochondria<br />
|AnswerDExp=The Golgi apparatus is a distribution center of proteins and lipids from the endoplasmic reticulum to the plasma membrane, lysosomes, and secretory vesicles.<br />
|AnswerE=It is involved in proteoglycan assembly from prelysosomes<br />
|AnswerEExp=The Golgi apparatus is involved in proteoglycan assembly from core proteins.<br />
|EducationalObjectives=The cellular organelle involved in I-cell disease disease is the Golgi apparatus. It is a distribution center of proteins and lipids from the endoplasmic reticulum (ER) to the plasma membrane, lysosomes, and secretory vesicles. It modifies N-oligosaccharides on asparagine and adds O-oligosaccharides to serine and threonine residues.<br />
|References=Leroy JG, DeMars RI, Opitz JM. I-cell disease; Birth Defects Orig Art Ser. 1969;4:174-85.<br><br />
First Aid 2015 page 73.<br />
|RightAnswer=A<br />
|WBRKeyword=I-cell disease, Golgi apparatus, Organelle, O-oligosaccharides, Serine, Threonine<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR269&diff=1672404WBR2692020-10-28T02:58:28Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor= {{Sapan}}<br />
|ExamType=USMLE Step 3<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Cardiovascular, Preventive Medicine<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Cardiovascular, Preventive Medicine<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Cardiovascular, Preventive Medicine<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Cardiovascular, Preventive Medicine<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Cardiovascular, Preventive Medicine<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Cardiovascular, Preventive Medicine<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Cardiovascular, Preventive Medicine<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Cardiovascular, Preventive Medicine<br />
|Prompt=A 42-year-old female presents to your office for elevated blood pressure (BP). She has been having headaches for the last 2 weeks. She checks her BP at pharmacy and she presents with readings ranging between 162/106 and 154/92. After some research she did on her own, she has been exercising and following the "DASH (Dietary Approaches to Stop Hypertension)" diet for the past 2 months. Her BP in the office after more than 10 minutes of resting was 152/88 in her left arm and 146/92 in her right. She tells you that both her mother and father have hypertension. She denies chest pain, shortness of breath, dizziness, or blurred vision. She denies tobacco use, drinks 3–4 beers on weekends, and uses no recreational drugs. Your physical examination should include documentation of which of these?<br />
|Explanation=The seventh report of the Joint National Committee on the prevention, detection, evaluation, and treatment of high blood pressure (JNC 7) key recommendations classify this patient in hypertension stage 1, as most of her BP readings are systolic blood pressure (SBP) in the 140–159 range and diastolic blood pressure (DBP) between 90 and 99.<br />
<br />
*Category: SBP and/or DBP<br />
*Normal: <120 and <80<br />
*Prehypertension: 120–139 or 80–90<br />
*Hypertension stage 1: 140–159 or 90–99<br />
*Hypertension stage 2: >160 or >100<br />
<br />
The primary purpose of the initial physical examination is to look for causes of secondary hypertension and for early organ damage due to untreated hypertension. In physical examination for a newly diagnosed patient with hypertension, there are recommendations to include BP measurement in both arms, examination of the optic fundi, BMI calculation, auscultation for carotid, abdominal and femoral bruits, palpation of the thyroid gland, examination of the heart and lungs, and examination of the abdomen for enlarged kidneys, masses, and abnormal aortic pulsation. <br />
<br />
Educational objective: The primary aim of the initial physical examination is to look for causes of secondary hypertension and for early organ damage due to untreated hypertension.<br />
|AnswerA=Cranial nerve examination<br />
|AnswerAExp=Incorrect- It is not an essential part of physical examination for a newly diagnosed patient with hypertension.<br />
|AnswerB=Peripheral nerve examinations<br />
|AnswerBExp=Incorrect- It is not an essential part of physical examination for a newly diagnosed patient with hypertension.<br />
|AnswerC=Auscultation for carotid, abdominal, and femoral bruits<br />
|AnswerCExp=Correct- See explanation<br />
|AnswerD=Palpation of the abdomen for hepatosplenomegaly<br />
|AnswerDExp=Incorrect- It is not an essential part of physical examination for a newly diagnosed patient with hypertension.<br />
|AnswerE=Mental status examination<br />
|AnswerEExp=Incorrect- It is not an essential part of physical examination for a newly diagnosed patient with hypertension.<br />
|RightAnswer=C<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR267&diff=1672403WBR2672020-10-28T02:58:18Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor= {{Ochuko}} (Reviewed by {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Embryology, Pathophysiology<br />
|SubCategory=Vascular<br />
|MainCategory=Embryology, Pathophysiology<br />
|SubCategory=Vascular<br />
|MainCategory=Embryology, Pathophysiology<br />
|SubCategory=Vascular<br />
|MainCategory=Embryology, Pathophysiology<br />
|MainCategory=Embryology, Pathophysiology<br />
|MainCategory=Embryology, Pathophysiology<br />
|SubCategory=Vascular<br />
|MainCategory=Embryology, Pathophysiology<br />
|SubCategory=Vascular<br />
|MainCategory=Embryology, Pathophysiology<br />
|SubCategory=Vascular<br />
|MainCategory=Embryology, Pathophysiology<br />
|SubCategory=Vascular<br />
|MainCategory=Embryology, Pathophysiology<br />
|MainCategory=Embryology, Pathophysiology<br />
|SubCategory=Vascular<br />
|Prompt=A 4-week-old female infant is brought to the emergency room for rapid breathing, diaphoresis, and difficulty feeding. The girl's past medical history is significant for preterm birth. Her mother mentions that ever since the girl was born, she has not been feeding well and there has been little weight gain. On physical examination, the infant has a hoarse cry with with evidence of bilateral basal crackles on pulmonary auscultation. Doppler echocardiogram demonstrates a significant left-to-right shunt. Which of the following statements is true about the infant’s underlying condition?<br />
|Explanation=The patient is diagnosed with patent ductus arteriosus (PDA), which is characterized by significant postnatal left to right shunt. Pneumonia is a typical early manifestation of PDA, and PDA should be ruled out when infants are diagnosed with recurrent pneumonias shortly after birth. The ductus arteriosus (DA) is derived from the embryonic left sixth aortic arch. It connects the pulmonary artery to the aorta and it serves to shunt blood away from the lungs into the umbilical placental circulation, where gas exchange takes place. At birth, the closure of the DA is essential for postnatal adaptation. Its closure is initiated by an increase in oxygen and changes in both the pulmonary and systemic blood pressures. In full-term neonates, the DA typically closes within the first 5 days post-delivery. In preterm infants, however, failure of DA closure following birth is associated with an increased incidence of neonatal morbidity. The patency of the ductus arteriosus is primarily controlled by low fetal oxygen tension and the prostanoids in the blood produced from arachidonic acid metabolism.<br />
<br />
Oxygen-induced constriction of the ductus arteriosus fails in preterm infants potentially due to immaturity of oxygen-sensing receptors. Smooth muscle relaxation of the ductus arteriosus results from the activation of the G-coupled prostaglandin receptor EP4 by PGE2. Within 1 – 5 days after a full-term birth, the ductus arteriosus closes as a result of increased oxygen tension and decreased circulating PGE2 and prostacyclins (PGI2).<br />
<br />
Using either indomethacin or ibuprofen to trigger prostaglandin inhibition has been the standard of care to close the PDA in predisposed infants, who are particularly preterm. Surgical closure of the patent DA is often reserved to patients whose PDA fails to close following pharmacologic therapy.<br />
<br />
|AnswerA=The patency of the ductus arteriosus is primarily controlled by low fetal oxygen tension and the circulation of prostanoids produced from arachidonic acid metabolism.<br />
|AnswerAExp=Oxygen-induced constriction of the ductus arteriosus fails in preterm infants potentially due to immaturity of oxygen-sensing receptors. Smooth muscle relaxation of the ductus arteriosus results from the activation of the G-coupled prostaglandin receptor EP4 by PGE2. Within 1– 5 days after a full-term birth, the ductus arteriosus closes as a result of increased oxygen tension and decreased circulating PGE2 and prostacyclins (PGI2).<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
|AnswerB=Oxygen-induced constriction of the ductus arteriosus fails in preterm infants potentially due to maturity of oxygen-sensing receptors<br />
|AnswerBExp=Oxygen-induced constriction of the ductus arteriosus fails in preterm infants potentially due to immaturity (not maturity) of oxygen-sensing receptors.<br />
|AnswerC=The ductus arteriosus is thought to derive from the embryonic left fourth aortic arch<br />
<br />
|AnswerCExp=The ductus arteriosus is thought to derive from the embryonic left sixth (not fourth) aortic arch.<br />
|AnswerD=Smooth muscle contraction of the ductus arteriosus results from the activation of the G-coupled prostaglandin receptor EP4 by PGF2<br />
|AnswerDExp=Smooth muscle contraction of the ductus arteriosus results from the activation of the G-coupled prostaglandin receptor EP4 by PGE2 (not PGF2).<br />
|AnswerE=Within 1 – 5 days after a full-term birth, the ductus arteriosus closes as a result of decreased oxygen tension and increased circulating PGE2 and prostacyclins (PGI2)<br />
|AnswerEExp=Within 1 – 5 days after a full-term birth, the ductus arteriosus closes as a result of increased (not decreased) oxygen tension and decreased (not increased) circulating PGE2 and prostacyclins (PGI2).<br />
|EducationalObjectives=Oxygen-induced constriction of the ductus arteriosus fails in preterm infants potentially due to immaturity of oxygen-sensing receptors. Smooth muscle relaxation of the ductus arteriosus results from the activation of the G-coupled prostaglandin receptor EP4 by PGE2. Within 1– 5 days after a full-term birth, the ductus arteriosus closes as a result of increased oxygen tension and decreased circulating PGE2 and prostacyclin (PGI2).<br />
|References=Thebaud B, Lacaze-Mazmonteil T. Patent ductus arteriosus in premature infants: A never-closing act. Paediatr Child Health. 2010;15(5):267-70.<br><br />
<br />
|RightAnswer=A<br />
|WBRKeyword=PDA, Patent ductus arteriosus<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR266&diff=1672402WBR2662020-10-28T02:58:09Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor= {{Sapan}}<br />
|ExamType=USMLE Step 3<br />
|MainCategory=Emergency Room<br />
|SubCategory=Psychiatry<br />
|MainCategory=Emergency Room<br />
|SubCategory=Psychiatry<br />
|MainCategory=Emergency Room<br />
|SubCategory=Psychiatry<br />
|MainCategory=Emergency Room<br />
|MainCategory=Emergency Room<br />
|SubCategory=Psychiatry<br />
|MainCategory=Emergency Room<br />
|SubCategory=Psychiatry<br />
|MainCategory=Emergency Room<br />
|SubCategory=Psychiatry<br />
|MainCategory=Emergency Room<br />
|SubCategory=Psychiatry<br />
|MainCategory=Emergency Room<br />
|MainCategory=Emergency Room<br />
|SubCategory=Psychiatry<br />
|Prompt=The police bring a 22-year-old male into the emergency room after a disruption at the local college campus. According to his medical chart, he has been treated for a depressive episode in the past. He describes his mood as "great" but claims to have been awake for 4 days due to working on several inventions. He admits to rapid thoughts and believes that God has chosen him to be the next Messiah. In fact, angels have commanded him to steal from the student union in order to begin a new church. <br />
Which of the following drugs should be given to treat symptoms of this patient?<br />
|Explanation=This patient displays criteria for bipolar disorder, manic with psychotic features. Individuals intoxicated with cocaine classically show signs similar to mania. Frank psychotic symptoms can occur in up to 50% of individuals.<br />
<br />
Cocaine is a powerful nervous system stimulant. Its effects can last from 15–30 minutes to an hour, depending on dosage and the route of administration.<br />
<br />
Cocaine increases alertness, feelings of well-being and euphoria, energy and motor activity, feelings of competence and sexuality. Athletic performance may be enhanced in sports where sustained attention and endurance is required. Anxiety, paranoia and restlessness can also occur, especially during the comedown. With excessive dosage, tremors, convulsions and increased body temperature are observed.With excessive or prolonged use, the drug can cause itching, tachycardia, hallucinations, and paranoid delusions. Overdoses cause hyperthermia and a marked elevation of blood pressure, which can be life-threatening. <br />
<br />
Educational Objective: Lorazepam is used to treat manic symptoms associated with cocaine intoxication and it has relatively rapid course of action.<br />
|AnswerA=Divalproex sodium<br />
|AnswerAExp=Incorrect- It is an appropriate treatment for mania but it may take several days to weeks before significant therapeutic effects are achieved.<br />
|AnswerB=Lamotrigine<br />
|AnswerBExp=Incorrect- Lamotrigine is efficacious in bipolar depression and in the maintenance phase, but it is not particularly effective in treating the manic phase.<br />
|AnswerC=Lithium<br />
|AnswerCExp=Incorrect- It is an appropriate treatment for mania but it may take several days to weeks before significant therapeutic effects are achieved.<br />
|AnswerD=Mirtazapine<br />
|AnswerDExp=Incorrect- An antidepressant such as mirtazapine may worsen mania in a bipolar patient.<br />
|AnswerE=Lorazepam<br />
|AnswerEExp=Correct- Lorazepam or other high potency benzodiazepines are useful in the acute management of manic patients as the sedative effects are relatively rapid.<br />
|RightAnswer=E<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR265&diff=1672401WBR2652020-10-28T02:56:37Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor= {{Ochuko}} (Reviewed by Will Gibson and {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Microbiology<br />
|SubCategory=Pulmonology, Infectious Disease<br />
|MainCategory=Microbiology<br />
|SubCategory=Pulmonology, Infectious Disease<br />
|MainCategory=Microbiology<br />
|SubCategory=Pulmonology, Infectious Disease<br />
|MainCategory=Microbiology<br />
|MainCategory=Microbiology<br />
|MainCategory=Microbiology<br />
|MainCategory=Microbiology<br />
|SubCategory=Pulmonology, Infectious Disease<br />
|MainCategory=Microbiology<br />
|SubCategory=Pulmonology, Infectious Disease<br />
|MainCategory=Microbiology<br />
|SubCategory=Pulmonology, Infectious Disease<br />
|MainCategory=Microbiology<br />
|SubCategory=Pulmonology, Infectious Disease<br />
|MainCategory=Microbiology<br />
|MainCategory=Microbiology<br />
|SubCategory=Pulmonology, Infectious Disease<br />
|Prompt=A 4-year old boy is brought to the emergency department by his mother with complaints of fever, cough, runny nose, and a rash. The mother reports that the rash began on the forehead and progressively moved downwards. The patient's past medical history is unremarkable. Physical examination is remarkable for post-auricular lymphadenopathy. Which of the following is the most likely pathogen responsible for this patient's symptoms?<br />
|Explanation=The patient is most likely diagnosed with Rubella virus infection (German measles). The primary symptom of rubella virus infection is the appearance of a rash (exanthem) on the face which spreads to the trunk and limbs and usually fades after three days. Other symptoms include low grade fever, swollen glands (typically post-cervical/post-auricular lymphadenopathy), joint pains, headache, and conjunctivitis. The swollen glands or lymph nodes can persist for up to a week, and the fever rarely rises above 38 <sup>o</sup>C (100.4 <sup>o</sup>F). The rash disappears after a few days with no staining or peeling of the skin. <br />
|AnswerA=HHV-6<br />
|AnswerAExp=HHV-6 causes Roseola, a macular rash over the body that appears several days after a high-grade fever.<br />
|AnswerB=Varicella zoster virus<br />
|AnswerBExp=Varicella zoster virus (VZV) causes chicken pox, in which the rash typically begins from the trunk and then spreads to the face and extremities.<br />
|AnswerC=Mumps virus<br />
|AnswerCExp=Mumps virus causes mumps, which typically presents with no rash but with parotitis and/or meningitis (pancreatitis, orchitis/oophoritis in young adults).<br />
|AnswerD=Rubella virus<br />
|AnswerDExp=Infection with the Rubella virus is associated with the development of a descending rash and post-auricular lymphadenopathy.<br />
|AnswerE=Measles virus<br />
|AnswerEExp=Measles virus causes measles. The rash in measles is preceded by cough, coryza, conjunctivitis and blue-white (Koplik) spots on the buccal mucosa.<br />
|EducationalObjectives=Rubella virus causes German measles with the clinical presentation of post-auricular lymphadenopathy and rash.<br />
|References=First Aid 2015 page 163 <br><br />
|RightAnswer=D<br />
|WBRKeyword=Microbiology, Virus, Viruses, Rubella, Rash, Skin, Togavirus<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR263&diff=1672400WBR2632020-10-28T02:56:01Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor= {{Ochuko}} (Reviewed by Will Gibson and {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Embryology<br />
|SubCategory=General Principles<br />
|MainCategory=Embryology<br />
|SubCategory=General Principles<br />
|MainCategory=Embryology<br />
|SubCategory=General Principles<br />
|MainCategory=Embryology<br />
|MainCategory=Embryology<br />
|MainCategory=Embryology<br />
|MainCategory=Embryology<br />
|SubCategory=General Principles<br />
|MainCategory=Embryology<br />
|SubCategory=General Principles<br />
|MainCategory=Embryology<br />
|SubCategory=General Principles<br />
|MainCategory=Embryology<br />
|SubCategory=General Principles<br />
|MainCategory=Embryology<br />
|MainCategory=Embryology<br />
|SubCategory=General Principles<br />
|Prompt=A 12-month-old girl is brought to the physician’s office with complaints of fever, vomiting, and difficulty breathing. The mother is a chronic alcoholic and had consumed alcohol excessively throughout the child’s pregnancy. Physical examination is remarkable for microcephaly, facial abnormalities, a heart murmur, and developmental delay. Which one of the following errors most likely occurred during the embryonic period?<br />
|Explanation=Fetal alcohol syndrome is a leading cause of congenital malformation and intellectual disability in the United States. Newborns of mothers who consumed significant quantities of alcohol during pregnancy have an increased incidence of congenital abnormalities. These abnormalities include: <br />
* pre-and postnatal developmental retardation<br />
* microcephaly<br />
* holopresencephaly<br />
* facial abnormalities<br />
* limb dislocation<br />
* heart and lung fistulas.<br />
<br />
The child exhibits microcephaly, facial abnormalities, both of which are tissue malformations. The patient's heart murmur is likely also caused by tissue malformation, but echocardiography would be required for confirmation.<br />
Malformation refers to the intrinsic disruption of tissue structure, and it typically occurs during the embryonic period of development (3rd -8th week). Alcohol, a teratogen, exerts its effect during this stage of fetal development. Defective cell migration is thought to mediate a substantial fraction of alcohol's teratogenicity.<br />
|AnswerA=Aplasia<br />
|AnswerAExp=Aplasia refers to the failure of an organ to develop despite the presence of primordial tissue.<br />
|AnswerB=Hypoplasia<br />
|AnswerBExp=Hypoplasia is incomplete organ development with the presence of primordial tissue.<br />
|AnswerC=Agenesis<br />
|AnswerCExp=Agenesis refers to the failure of an organ to develop due to the absence of primordial tissue.<br />
|AnswerD=Deformation<br />
|AnswerDExp=Deformation is extrinsic disruption of an organ or tissue; it occurs after the embryonic period.<br />
|AnswerE=Malformation<br />
|AnswerEExp=Alcohol exposure during pregnancy causes tissue and central nervous system malformations. The effects of alcohol in the CNS appear to be due in part to the negative effects on cell migration.<br />
|EducationalObjectives=Fetal alcohol syndrome is caused by the teratogen alcohol which causes congenital malformations, an error in organ morphogenesis during the embryonic period (3rd – 8th weeks).<br />
|References=Riley, Edward P., M. Alejandra Infante, and Kenneth R. Warren. "Fetal alcohol spectrum disorders: an overview." Neuropsychology review 21.2 (2011): 73-80.<br><br />
First Aid 2015 page 561<br />
|RightAnswer=E<br />
|WBRKeyword=EtOH, Fetal Alcohol Syndrome, FAS, Alcohol, Teratogen, Substance abuse, Embryology, Embryo, Development<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR262&diff=1672399WBR2622020-10-28T02:55:51Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor= {{Sapan}}<br />
|ExamType=USMLE Step 3<br />
|MainCategory=Emergency Room<br />
|SubCategory=Psychiatry<br />
|MainCategory=Emergency Room<br />
|SubCategory=Psychiatry<br />
|MainCategory=Emergency Room<br />
|SubCategory=Psychiatry<br />
|MainCategory=Emergency Room<br />
|MainCategory=Emergency Room<br />
|SubCategory=Psychiatry<br />
|MainCategory=Emergency Room<br />
|SubCategory=Psychiatry<br />
|MainCategory=Emergency Room<br />
|SubCategory=Psychiatry<br />
|MainCategory=Emergency Room<br />
|SubCategory=Psychiatry<br />
|MainCategory=Emergency Room<br />
|MainCategory=Emergency Room<br />
|SubCategory=Psychiatry<br />
|Prompt=The police bring a 22-year-old male into the emergency room after a disruption at the local college campus. According to his medical chart, he has been treated for a depressive episode in the past. He describes his mood as "great" but claims to have been awake for 4 days due to working on several inventions. He admits to rapid thoughts and believes that God has chosen him to be the next Messiah. In fact, angels have commanded him to steal from the student union in order to begin a new church.<br />
Urine toxicology performed in order to rule out a substance of abuse as a cause of his symptoms would most likely reveal which substance?<br />
|Explanation=This patient displays criteria for bipolar disorder, manic with psychotic features. Individuals intoxicated with cocaine classically show signs similar to mania. Frank psychotic symptoms can occur in up to 50% of individuals.<br />
<br />
Cocaine is a powerful nervous system stimulant. Its effects can last from 15–30 minutes to an hour, depending on dosage and the route of administration.<br />
<br />
Cocaine increases alertness, feelings of well-being and euphoria, energy and motor activity, feelings of competence and sexuality. Athletic performance may be enhanced in sports where sustained attention and endurance is required. Anxiety, paranoia and restlessness can also occur, especially during the comedown. With excessive dosage, tremors, convulsions and increased body temperature are observed.With excessive or prolonged use, the drug can cause itching, tachycardia, hallucinations, and paranoid delusions. Overdoses cause hyperthermia and a marked elevation of blood pressure, which can be life-threatening.<br />
<br />
Educational objective: Individuals intoxicated with cocaine classically show signs similar to mania. Frank psychotic symptoms can occur in up to 50% of individuals.<br />
|AnswerA=Alcohol <br />
|AnswerAExp=Incorrect- While alcohol can present with psychotic symptoms, it more commonly creates a depressed picture.<br />
|AnswerB=Benzodiazepines<br />
|AnswerBExp=Incorrect- Benzodiazepine intoxication rarely causes manic or psychotic symptoms.<br />
|AnswerC=Cannabis <br />
|AnswerCExp=Incorrect- Although cannabis use is not infrequently associated with paranoia, it rarely displays frank psychosis.<br />
|AnswerD=Cocaine <br />
|AnswerDExp=Correct- See explanation<br />
|AnswerE=Opiates<br />
|AnswerEExp=Incorrect- Opiate intoxication will appear more as a depressed syndrome.<br />
|RightAnswer=D<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR261&diff=1672398WBR2612020-10-28T02:55:41Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor= {{Sapan}}<br />
|ExamType=USMLE Step 3<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Neurology, Psychiatry<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Neurology, Psychiatry<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Neurology, Psychiatry<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Neurology, Psychiatry<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Neurology, Psychiatry<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Neurology, Psychiatry<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Neurology, Psychiatry<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|MainCategory=Community Medical Health Center, Primary Care Office<br />
|SubCategory=Neurology, Psychiatry<br />
|Prompt=The patient is a 72-year-old man brought to the primary care clinic by his family over concerns that he has Alzheimer's disease. They have noticed a worsening of his memory over the past 6 months. He does not seem to want to get out of bed, and he appears to have difficulty providing for his basic needs such as cleaning, dressing, and cooking for himself. He is hesitant when talking, but it is unclear whether he is unable or unmotivated to speak. His family has also noticed that he appears depressed and is often seen crying. A MSE of the patient is performed to help determine whether he is suffering from a dementing illness or a depressive illness (pseudodementia).<br />
Further history, cognitive examinations, physical examination, and laboratory/radiographic studies are obtained. The results are consistent with Alzheimer's dementia. While the family had been able to take care of him initially, they have since returned to the clinic stating that they can no longer keep him at home. They feel that he is becoming much more agitated. He is staying up at night. Lately he has been rearranging the furniture, claiming to look for "the little people who are teasing me." They have noticed that he has difficulty walking, often moving slowly and dropping items. The family has pursued nursing home placement, but they wish to have something prescribed in order to help him sleep and keep him calm.<br />
Which of the following medications should be avoided in this patient?<br />
|Explanation=This patient displays characteristics of Lewy body disease, a dementia that may be related to [[Alzheimer dementia]]. The classic triad of Lewy body dementia is a fluctuating course, peduncular hallucinations (visual hallucinations of small people, animals, or objects), and parkinsonian features. These patients tend to be very sensitive to extrapyramidal side effects and, therefore, antipsychotics such as [[risperidone]] should be avoided or sparingly used.<br />
<br />
Educational objective:In patients with Lewy body dementia, antipsychotics such as [[risperidone]] should be avoided or sparingly used as they tend to be very sensitive to extrapyramidal side effects.<br />
|AnswerA=Buspirone<br />
|AnswerAExp=Incorrect- This drug should not be avoided as it does not have extrapyramidal side effects.<br />
|AnswerB=Donepezil<br />
|AnswerBExp=Incorrect- This drug should not be avoided as he has [[Alzheimer's disease]]. It is treatment of choice.<br />
|AnswerC=Lorazepam<br />
|AnswerCExp=Incorrect- This drug should not be avoided as it does not have extrapyramidal side effects.<br />
|AnswerD=Trazodone<br />
|AnswerDExp=Incorrect- This drug should not be avoided as it does not have extrapyramidal side effects.<br />
|AnswerE=Risperidone<br />
|AnswerEExp=Correct- See expanation<br />
|RightAnswer=E<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR259&diff=1672397WBR2592020-10-28T02:55:40Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Mahmoud Sakr M.D.<br />
|ExamType=USMLE Step 3<br />
|MainCategory=Inpatient Facilities<br />
|SubCategory=Infectious Disease, Neurology<br />
|MainCategory=Inpatient Facilities<br />
|SubCategory=Infectious Disease, Neurology<br />
|MainCategory=Inpatient Facilities<br />
|SubCategory=Infectious Disease, Neurology<br />
|MainCategory=Inpatient Facilities<br />
|MainCategory=Inpatient Facilities<br />
|SubCategory=Infectious Disease, Neurology<br />
|MainCategory=Inpatient Facilities<br />
|SubCategory=Infectious Disease, Neurology<br />
|MainCategory=Inpatient Facilities<br />
|SubCategory=Infectious Disease, Neurology<br />
|MainCategory=Inpatient Facilities<br />
|SubCategory=Infectious Disease, Neurology<br />
|MainCategory=Inpatient Facilities<br />
|MainCategory=Inpatient Facilities<br />
|SubCategory=Infectious Disease, Neurology<br />
|Prompt=89 y/o Caucasian male is admitted to the hospital due to altered mental status, lower back pain and development of a low-grade fever. His past medical history is remarkable for hypertension, hyperlipidemia, prior MI, prostate cancer and advanced dementia. Temperature is 99.6, Blood pressure is 109/67, Pulse is 95, Respiratory rate is 20. Physical exam is notable for absence of spontaneous movement of his lower extremities and loss of sensation from his waist downwards. He’s also unable to control neither his bladder nor his bowels. What is the most important next step in management?<br />
|Explanation=A spinal epidural abscess threatens the spinal cord or cauda equina by compression and also by vascular compromise (see images below). If untreated, an expanding suppurative infection in the spinal epidural space impinges on the spinal cord, producing sensory symptoms and signs, motor dysfunction, and, ultimately, paralysis and death. This patient is having cauda equina signs and immediate surgical consultation and operative decompression is the first step in management. All other answers are appropriate in the meantime, but after steps towards surgical release are taken.<br />
|AnswerA=Order an urgent MRI of the spine<br />
|AnswerAExp=This is an important diagnostic step and can be done, but after the surgical team is informed.<br />
|AnswerB=Start broad spectrum IV antibiotics<br />
|AnswerBExp=This answer is important and should be done after blood cultures are taken<br />
|AnswerC=Neurosurgical consultation. This patient is having cauda equina signs and immediate surgical consultation and operative decompression is the first step in management. All other answers are appropriate in the meantime, but after steps towards surgical release are taken.<br />
|AnswerCExp=Correct.<br />
|AnswerD=Start IV dexamethasone<br />
|AnswerDExp=IV steroids are used in clinical practice by neurosurgeons and often administered empirically if cauda equina is suspected, however this is not the first step in management.<br />
|AnswerE=Obtain 2 sets of blood cultures.<br />
|AnswerEExp=This step would be next after neurosurgical consult.<br />
|RightAnswer=C<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR258&diff=1672396WBR2582020-10-28T02:55:18Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Mahmoud Sakr M.D.<br />
|ExamType=USMLE Step 2 CK<br />
|MainCategory=Internal medicine<br />
|SubCategory=Cardiovascular<br />
|MainCategory=Internal medicine<br />
|SubCategory=Cardiovascular<br />
|MainCategory=Internal medicine<br />
|SubCategory=Cardiovascular<br />
|MainCategory=Internal medicine<br />
|MainCategory=Internal medicine<br />
|SubCategory=Cardiovascular<br />
|MainCategory=Internal medicine<br />
|SubCategory=Cardiovascular<br />
|MainCategory=Internal medicine<br />
|SubCategory=Cardiovascular<br />
|MainCategory=Internal medicine<br />
|SubCategory=Cardiovascular<br />
|MainCategory=Internal medicine<br />
|MainCategory=Internal medicine<br />
|SubCategory=Cardiovascular<br />
|Prompt=43 y/o female presents to her primary care physician for routine health examination. She denies any complaints and walks 2 miles 3 times a week. Initial evaluation reveals a Blood pressure is 127/77 mm Hg, Pulse is 82 /min, RR 14, oxygen saturation of 99% on room air. Physical examination is unremarkable except for a midsystolic click on cardiac auscultation. Which of the following mechanisms is likely responsible for this physical finding;<br />
|Explanation=Mitral valve prolapse (aka primary form of myxomatous degeneration of the mitral valve aka floppy mitral valve syndrome) is a valvular heart disease characterized by the displacement of an abnormally thickened mitral valve leaflet into the left atrium during systole. Upon auscultation of an individual with mitral valve prolapse, a mid-systolic click, followed by a late systolic murmur heard best at the apex is common. Echocardiography is the most useful method of diagnosing a prolapsed mitral valve. Two- and three-dimensional echocardiography are particularly valuable as they allow visualization of the mitral leaflets relative to the mitral annulus. This allows measurement of the leaflet thickness and their displacement relative to the annulus. Thickening of the mitral leaflets >5 mm and leaflet displacement >2 mm indicates classic mitral valve prolapse.<br />
|AnswerA=Rupture of a papillary muscle due to an ischemic event<br />
|AnswerAExp=This answer would relate an ischemic event.<br />
|AnswerB=Myxomatous degeneration of a heart valve<br />
|AnswerBExp=Correct answer. Mitral valve prolapse is due to of myxomatous degeneration of the mitral valve leading to a floppy mitral valve.<br />
|AnswerC=Congenital bicuspid anomaly of valvular leaflets<br />
|AnswerCExp=usually an abnormality of the aortic valve.<br />
|AnswerD=Lipid deposition and plaque formation in the arterial walls<br />
|AnswerDExp=This answer relates to an atherosclerotic process<br />
|AnswerE=Rheumatic heart disease<br />
|AnswerEExp=Rheumatic fever is an inflammatory disease that occurs following a Streptococcus pyogenes infection, such as streptococcal pharyngitis. Chronic rheumatic heart disease (RHD) is characterized by repeated inflammation with fibrinous resolution. It presents with polyarthritis, Carditis, subcutaneous nodules, erythema marginatum, fever, leukocytosis, ECG may show features of heart block, such as a prolonged PR interval.<br />
|RightAnswer=B<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR255&diff=1672395WBR2552020-10-28T02:55:07Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Pathology<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Pathology<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Pathology<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Pathology<br />
|MainCategory=Pathology<br />
|MainCategory=Pathology<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Pathology<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Pathology<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Pathology<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Pathology<br />
|MainCategory=Pathology<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|Prompt=A 48-year-old woman visits the clinic for evaluation of her skin conditions. She has patches of hardened skin on her face, elbows, and knees. She feels that her fingers are tight especially in cold weathers, and become pale and cyanotic. She also complains of difficulty swallowing of both solids and liquids and often regurgigates her food. Laboratory findings are remarkable detection of nucleolar pattern of anti-nuclear antibodies as well as elevated anti-centromere antibodies. Which of the following conditions is most likely to be associated with this patient's condition?<br />
|Explanation=Systemic sclerosis is usually classified by the extent of cutaneous manifestations and may be either limited (70%, less severe - positive anti-centromere antibodies) or diffuse (30%, more severe with visceral manifestations - positive anti-Scl-70 antibody). The limited cutaneous form of systemic sclerosis (lcSSc) may include characteristic vascular manifestations and is then termed CREST syndrome which is an acronym for the five main features: Calcinosis, Raynaud's syndrome, Esophageal dysmotility, Sclerodactyly, and Telangiectasia. The patient is most likely diagnosed with CREST syndrome, whereby she complains of hardened skin patches (calcinosis), tight pale fingers (Raynaud's phenomenon), difficulty swallowing (esophageal dysmotility), and has positive anti-centromere antibodies. The majority of patients with CREST syndrome do not have all 5 characteristic features of the disease, but often have variable manifestations. The association between CREST syndrome and vascular abnormalities predisposes to the development of pulmonary hypertension when the pulmonary vasculature is affected. While limited sclerosis is associated with pulmonary hypertension, the diffuse form is typically associated with pulmonary fibrosis.<br />
|AnswerA=Renal tubular acidosis<br />
|AnswerAExp=CREST syndrome is not typically associated with renal tubular acidosis.<br />
<br />
|AnswerB=Primary sclerosing cholangitis<br />
|AnswerBExp=CREST syndrome is not typically associated with primary sclerosing cholangitis.<br />
|AnswerC=Libman-Sacks endocarditis<br />
|AnswerCExp=CREST syndrome is not typically associated with Libman-Sacks endocarditis.<br />
|AnswerD=Membranous glomerulonephritis<br />
|AnswerDExp=CREST syndrome is not typically associated with membranous glomerulonephritis.<br />
|AnswerE=Pulmonary hypertension<br />
|AnswerEExp=CREST syndrome is associated with pulmonary hypertension.<br />
|EducationalObjectives=Systemic sclerosis is usually classified by the extent of cutaneous manifestations and may be either limited (70%, less severe - positive anti-centromere antibodies) or diffuse (30%, more severe with visceral manifestations - positive anti-Scl-70 antibody). Vascular involvement in limited forms of scleroderms is referred to as CREST syndrome (Calcinosis, Raynaud's phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasia). CREST syndrome may be associated with pulmonary hypertension.<br />
|References=Lonzetti LS, Joyal F, Raynauld JP, et al. Updating the American College <br />
of Rheumatology preliminary classification criteria for systemic <br />
sclerosis: addition of severe nailfold capillaroscopy adbnormalities <br />
markedly increase the sensitivity of limited scleroderma. Arthritis <br />
Rheum. 2001;44(3):735.<br><br />
Silman AJ. Scleroderma. Bailleres Clin Rheumatol. 1995;9(3):471-82.<br><br />
First Aid 2015 page 436.<br />
<br />
|RightAnswer=E<br />
|WBRKeyword=Systemic sclerosis, CREST syndrome, Pulmonary hypertension<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR254&diff=1672393WBR2542020-10-28T02:54:16Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Biochemistry, Pathophysiology<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Biochemistry, Pathophysiology<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Biochemistry, Pathophysiology<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Biochemistry, Pathophysiology<br />
|MainCategory=Biochemistry, Pathophysiology<br />
|MainCategory=Biochemistry, Pathophysiology<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Biochemistry, Pathophysiology<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Biochemistry, Pathophysiology<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Biochemistry, Pathophysiology<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Biochemistry, Pathophysiology<br />
|MainCategory=Biochemistry, Pathophysiology<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|Prompt=A 30-year-old woman presents with mild fever, malaise, and swollen hand and knee joints. Physical examination is remarkable for malar rash. Laboratory findings include lymphopenia with mild anemia and thrombocytopenia. A diagnosis is then made following the detection of a homogeneous pattern of anti-nuclear antibody as well as autoantibodies against RNA. Which of the following types of RNA is most likely to be the target of the antibodies?<br />
|Explanation=Antinuclear antibody (ANA) is a non-specific screening test to evaluate for the presence of rheumatic diseases. ANA screening often yields positive results in many connective tissue disorders and other autoimmune diseases, and may also be positive among normal individuals. Subtypes of antinuclear antibodies include anti-Smith (targets RNA) and anti-double stranded DNA (targets dsDNA) antibodies, both of which are associated with the diagnosis of systemic lupus erythematosus (SLE), and anti-histone antibodies (targets histones), which are associated with the diagnosis of drug-induced lupus.<br />
|AnswerA=Messenger RNA (mRNA)<br />
|AnswerAExp=Anti-Sm antibody does not target mRNA.<br />
<br />
|AnswerB=Transfer RNA (tRNA)<br />
|AnswerBExp=Anti-Sm antibody does not target tRNA.<br />
|AnswerC=Ribosomal RNA (rRNA)<br />
|AnswerCExp=Anti-Sm antibody does not target rRNA.<br />
|AnswerD=Small nuclear ribonucleic acid (snRNA)<br />
|AnswerDExp=Anti-Sm antibody is specific for SLE. Smith antigen is a group of proteins (B/D/E/F/G) without snRNA; it is metabolized by trypsin but not by RNase.<br />
|AnswerE=Heterogeneous nuclear RNA (hnRNA)<br />
|AnswerEExp=Anti-Sm antibody does not target hnRNA.<br />
|EducationalObjectives=Subtypes of antinuclear antibodies include anti-Smith (targets RNA) and anti-double stranded DNA (targets dsDNA) antibodies, both of which are associated with the diagnosis of systemic lupus erythematosus (SLE), and anti-histone antibodies (targets histones), which are associated with the diagnosis of drug-induced lupus.<br />
|References=Migliorini P, Baldini C, Rocchi V, et al. Anti-Sm and anti-RNP antibodies. Autoimmunity. 2005;38(1):47-54.<br><br />
First Aid 2015 page 213, 433.<br />
|RightAnswer=D<br />
|WBRKeyword=Small nuclear ribonucleic acid, snRNA, Antinuclear antibody, SLE, Systemic lupus erythematosus<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR253&diff=1672392WBR2532020-10-28T02:54:05Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Biochemistry, Pathophysiology<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Biochemistry, Pathophysiology<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Biochemistry, Pathophysiology<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Biochemistry, Pathophysiology<br />
|MainCategory=Biochemistry, Pathophysiology<br />
|MainCategory=Biochemistry, Pathophysiology<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Biochemistry, Pathophysiology<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Biochemistry, Pathophysiology<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Biochemistry, Pathophysiology<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|MainCategory=Biochemistry, Pathophysiology<br />
|MainCategory=Biochemistry, Pathophysiology<br />
|SubCategory=Musculoskeletal/Rheumatology<br />
|Prompt=A 37-year-old woman presents with malaise, proxmial muscle weakness, and swollen hand and knee joints. She also reports dry eyes and dry mouth. When exposed to cold temperatures, her fingers become pale and cyanotic and turn red and numb. Physical examination is remarkable for scaly erythematous eruptions overlying the knuckles and elbows. Laboratory findings demonstrate lymphopenia with mild anemia and thrombocytopenia. A diagnosis is then made following the detection of speckled anti-nuclear antibody as well as autoantibodies against extractable nuclear antigens. Which of the following structures is most likely to be the target of the antibodies?<br />
|Explanation=Mixed connective tissue disease (MCTD) combines features of scleroderma, myositis, systemic lupus erythematosus, and rheumatoid arthritis and is thus considered an overlap syndrome. MCTD commonly manifests with joint pain/swelling, malaise, Raynaud phenomenon, Sjögren's syndrome, muscle inflammation, and sclerodactyly. Distinguishing laboratory characteristics are a positive, speckled anti-nuclear antibody and an anti-U1-RNP antibody.<br />
|AnswerA=Transfer RNA (tRNA)<br />
|AnswerAExp=Anti-U1-RNP antibody does not target tRNA.<br />
|AnswerB=Small interfering RNA (siRNA)<br />
|AnswerBExp=Anti-U1-RNP antibody does not target siRNA<br />
|AnswerC=Small nuclear ribonucleoprotein (snRNP)<br />
|AnswerCExp=Anti-U1-RNP antibody targets snRNP, which is a complex of snRNA (produced by RNAP II) and multiple proteins.<br />
|AnswerD=Heterogeneous nuclear RNA (hnRNA)<br />
|AnswerDExp=Anti-U1-RNP antibody does not target hnRNA. The snRNP combines with hnRNA to form spliceosome and undergoes splicing.<br />
|AnswerE=Deoxyribonucleic acid (DNA)<br />
|AnswerEExp=Anti-U1-RNP antibody does not target DNA.<br />
|EducationalObjectives=Anti-U1-RNP antibodies are often elevated in patients with mixed connective tissue disease. Anti-U1-RNP antibody targets snRNP, which is a complex of snRNA (produced by RNAP II) and multiple proteins.<br />
|References=Ghirardello A, Doria A, Vesco P, et al. Blotting patterns of IgG anti-(U1)RNP antibodies in mixed connective tissue disease. Rheumatol Int. 1996;16(4):145-50.<br><br />
First Aid 2015 page 213.<br />
|RightAnswer=C<br />
|WBRKeyword=Anti-U1-RNP antibody, Mixed connective tissue disease, MCTD, Small nuclear ribonucleoprotein<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR252&diff=1672391WBR2522020-10-28T02:54:05Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Pathophysiology<br />
|SubCategory=Gastrointestinal, Neurology<br />
|MainCategory=Pathophysiology<br />
|SubCategory=Gastrointestinal, Neurology<br />
|MainCategory=Pathophysiology<br />
|SubCategory=Gastrointestinal, Neurology<br />
|MainCategory=Pathophysiology<br />
|MainCategory=Pathophysiology<br />
|MainCategory=Pathophysiology<br />
|SubCategory=Gastrointestinal, Neurology<br />
|MainCategory=Pathophysiology<br />
|SubCategory=Gastrointestinal, Neurology<br />
|MainCategory=Pathophysiology<br />
|SubCategory=Gastrointestinal, Neurology<br />
|MainCategory=Pathophysiology<br />
|SubCategory=Gastrointestinal, Neurology<br />
|MainCategory=Pathophysiology<br />
|MainCategory=Pathophysiology<br />
|SubCategory=Gastrointestinal, Neurology<br />
|Prompt=A 24-year-old woman gradually develops throbbing headache, pulsatile tinnitus, and blurred vision that are worse in the morning and often accompanied by nausea and vomiting. She is awake, alert, afebrile and has no other focal neruologic deficit on exmaination. She has a past medical history significant for acne vulgaris, for which she takes daily oral isotretinoin. Neuroimaging is negative for space-occupying lesions. Cerebrospinal fluid pressure is elevated with a normal composition. Accumulation of the culprit substance is most likely to be found in which of the following cell types in the liver?<br />
|Explanation=Pseudotumor cerebri is a neurological disorder that is characterized by increased intracranial pressure in the absence of a tumor or other diseases. The main symptoms are headache, nausea, and vomiting, as well as pulsatile tinnitus, double vision and other visual symptoms.<br />
Intracranial pressure may be increased due to medications such as high-dose vitamin A derivatives (e.g. isotretinoin), long-term tetracycline antibiotics, lithium, or hormonal contraceptives. Following ingestion, vitamin A, a lipid soluble vitamin, undergoes hepatic metabolism, whereby hepatic parenchymal cells absorb vitamin A in the form of retinyl esters. Parenchymal cells metabolize the retinyl esters, which is subsequently transferred to the stellate cells for either storage with other long-chain fatty acids or mobilization into the plasma (bound to RBP). The advantage of vitamin A storage in the stellate cells is the capacity of the liver to maintain adequate supply of vitamin A by metabolizing stored vitamin A during periods of low dietary intake. In cases of hypervitaminosis, vitamin A saturates in the hepatic stellate cells and leaks from the liver into the bloodstream beyond the blood brain barrier. The mechanism by which vitamin A excess results in pseudotumor cerebri is poorly understood.<br />
|AnswerA=Kupffer cell<br />
|AnswerAExp=Kupffer cells are specialized macrophages (reticuloendothelial cells) in the liver. They play a role in the hepatic response to toxic compounds but are not the main storage site of vitamin A metabolites.<br />
<br />
|AnswerB=Sinusoidal endothelial cell<br />
|AnswerBExp=A liver sinusoid is a type of sinusoidal blood vessel (with fenestrated, discontinuous endothelium) that serves as a location for the oxygen-rich blood from the hepatic artery and the nutrient-rich blood from the portal vein. <br />
|AnswerC=Perisinusoidal cell<br />
|AnswerCExp=Hepatic stellate cells, also known as either perisinusoidal cells or Ito cells (earlier lipocytes or fat-storing cells), are pericytes found in the perisinusoidal space of the liver also known as the space of Disse. Following ingestion, vitamin A, a lipid soluble vitamin, undergoes hepatic metabolism, whereby hepatic parenchymal cells absorb vitamin A in the form of retinyl esters. Parenchymal cells metabolize the retinyl esters, which is subsequently transferred to the stellate cells for either storage with other long-chain fatty acids or mobilization into the plasma (bound to RBP).<br />
|AnswerD=Cholangiocyte<br />
|AnswerDExp=Cholangiocytes are the epithelial cells of the bile duct. They are cuboidal epithelium in the small interlobular bile ducts, but become columnar and mucus secreting in larger bile ducts approaching the porta hepatis and the extrahepatic ducts.<br />
|AnswerE=Hepatocyte<br />
|AnswerEExp=Hepatocytes are involved in protein synthesis, protein storage, transformation of carbohydrates, synthesis of cholesterol, bile salts and phospholipids, and detoxification, modification, and excretion of exogenous and endogenous substances.<br />
|EducationalObjectives=Hepatic stellate cells, also known as either perisinusoidal cells or Ito cells (earlier lipocytes or fat-storing cells), are pericytes found in the perisinusoidal space of the liver also known as the space of Disse. Following ingestion, vitamin A, a lipid soluble vitamin, undergoes hepatic metabolism, whereby hepatic parenchymal cells absorb vitamin A in the form of retinyl esters. Parenchymal cells metabolize the retinyl esters, which is subsequently transferred to the stellate cells for either storage with other long-chain fatty acids or mobilization into the plasma (bound to RBP).<br />
|References=Penniston KL, Tanumihardjo SA. The acute and chronic toxic effects of vitamin A. Am J Clin Nutr. 2006;88(2):191-201.<br><br />
Morrice Jr, G, Havener WH, Kapetansky F. Vitamin A intoxication as a cause of pseudotumor cerebri. JAMA. 1960;173(16):1802-5.<br><br />
Toren G, Nilsson A, Norum KR, et al. Characterization of liver stellate cell retinyl ester storage. Biochem J. 1994;300:793-8.<br><br />
First Aid 2015 page 89, 468.<br />
|RightAnswer=C<br />
|WBRKeyword=Stellate cells, Hepatocytes, Retinyl esters, Perisinusoidal cells, Ito cells, Vitamin A, Isotretinoin, Acne, Pseudotumor cerebri, Headache, <br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR251&diff=1672390WBR2512020-10-28T02:53:43Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Pathology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pathology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pathology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pathology<br />
|MainCategory=Pathology<br />
|MainCategory=Pathology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pathology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pathology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pathology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pathology<br />
|MainCategory=Pathology<br />
|SubCategory=Cardiology<br />
|Prompt=A 75-year-old woman presents to the emergency department (ED) with an acute-onset substernal chest pain for the past 30 minutes. She explains she was asymptomatic earlier today, but she felt a sudden, unusual chest pressure sensation while she was walking her dog in the afternoon. She recalls she has recently had a history of intermittent chest pains that are worsened by physical activity and relieved by rest, but her current chest pain has been constant and is markedly more severe than her usual symptoms. Upon further questioning, she reports her chest pain is associated with cold sweating, shortness of breath, and left upper extremity numbness. Her past medical history includes diabetes mellitus, hypertension, and dyslipidemia. In the ED, her temperature is 37.5 °C (99.5 °F), blood pressure is 90/65 mmHg, and heart rate is 115/min. Electrocardiogram demonstrates ST-segment elevation in leads I, aVL and V5-V6. Which of the following events is most likely to underlie her clinical presentation?<br />
|Explanation=The patient is likely having an acute transmural myocardial infarction of the lateral wall, as suggested by the clinical findings (persistent, substernal chest pain) and as evidenced by the ECG changes (ST-segment elevation in the lateral leads I, aVL, V5-V6). Clinically, stable/unstable angina are differentiated from a myocardial infarction (MI) by the persistence and radiation of symptoms, hemodynamic changes, and the absence of relief with rest or with pharmacological therapy (e.g. sublingual nitroglycerin). In MI, patients typically report substernal chest pain, often felt as chest pressure, that radiates to either the jaw, the left arm, or the epigastric region. Given that a MI and other life-threatening conditions should always be ruled out when patients present with chest pain, clinical differentiation between angina and myocardial infarction is not very relevant since all patients end up with a diagnostic work-up.<br />
<br />
The fatty streak is the the earliest evidence of atherosclerosis. It is characterized by non-obstructive, yellowish lesions in the arterial lumen. Although asymptomatic, fatty streaks often predispose to endothelial dysfunction, which subsequently results in a pro-inflammatory state that allows the aggregation of inflammatory mediators (leukocyte recruitment and foam cell formation from monocytes) and the entry and modification of lipids in the subendothelial intima. As lipids accumulate within the intima, they are trapped and oxidized, forming reactive oxygen species. The plaque progression is highly dependent on the smooth muscle cell migration into the intima following the formation of the fatty streak and the subendothelial changes that ensue. As the plaque grows, it can obstruct luminal blood flow, resulting in myocardial ischemia and clinical manifestations (e.g. stable angina). As the plaque grows further, its fibrous cap may rupture, and prothrombotic molecules (originally in the subendothelial within the lipid atheroma) are exposed. Once exposed, thrombosis occurs and an occlusive clot develops, resulting in a myocardial infarction.<br />
|AnswerA=Atheromatous plaque with 80% stenosis of the lumen without thrombus<br />
<br />
|AnswerAExp=Coronary artery disease is defined as presence of a lesion that obstructs > 50% of at least one of the epicardial arteries. Symptoms of stable angina usually do not develop until the lesion obstrucs > 75% of the lumen.<br />
<br />
|AnswerB=Diffuse coronary artery vasospasm causing flow limitation is incorrect<br />
|AnswerBExp=Prinzmetal (variant) angina is caused by coronary vasospasm due to contraction of the vascular smooth muscle, rather than by atherosclerosis. It occurs more commonly among younger women and typically manifests as clustered angina that occurs nocturnally at rest rather than on exertion. Although approximately two-thirds of patients have concurrent atherosclerosis of a major coronary artery, this is often mild or not in proportion to the degree of symptoms. ECG changes may only be evident while the patient is experiencing an attack, where typically ECG of patients with Prinzmetal angina demonstrates ST-segment elevations (rather than depressions). Prinzmetal angina generally responds to calcium channel blockers.<br />
|AnswerC=Ruptured atheroma with fully obstructive thrombus<br />
|AnswerCExp=Ruptured atheroma with fully obstructive thrombus is the underlying pathophysiology of a myocardial infarction. The patient is likely to have acute transmural myocardial infarction of the lateral wall, as evidenced by the ECG changes.<br />
|AnswerD=Calcification and thickening of the coronary intima<br />
|AnswerDExp=Although fibrocalcific plaque with thickening of the coronary intima may be associated with nonocclusive thrombus, it does not typically cause symptoms of unstable angina.<br />
|AnswerE=Dissection of the coronary wall with intraluminal flap<br />
|AnswerEExp=Coronary artery dissection is most likely associated with percutaneous coronary interventions and is a rare cause of acute coronary syndrome and sudden death.<br />
|EducationalObjectives=As the atherogenic plaque grows, its fibrous cap may rupture, and prothrombotic molecules (originally in the subendothelial within the lipid atheroma) are exposed. Once exposed, thrombosis occurs and an occlusive clot develops, resulting in a myocardial infarction.<br />
|References=Libby P. Inflammation in atherosclerosis. Nature. 2002;420(6917):868-74.<br><br />
First Aid 2015 page 292.<br />
|RightAnswer=C<br />
|WBRKeyword=Myocardial infarction, STEMI, Atherogenesis, Atheroma, Plaque, Thrombosis, Coronary artery disease<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR250&diff=1672389WBR2502020-10-28T02:53:33Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Pathology<br />
|SubCategory=Vascular<br />
|MainCategory=Pathology<br />
|SubCategory=Vascular<br />
|MainCategory=Pathology<br />
|SubCategory=Vascular<br />
|MainCategory=Pathology<br />
|MainCategory=Pathology<br />
|MainCategory=Pathology<br />
|SubCategory=Vascular<br />
|MainCategory=Pathology<br />
|SubCategory=Vascular<br />
|MainCategory=Pathology<br />
|SubCategory=Vascular<br />
|MainCategory=Pathology<br />
|SubCategory=Vascular<br />
|MainCategory=Pathology<br />
|MainCategory=Pathology<br />
|SubCategory=Vascular<br />
|Prompt=A 33-year-old woman presents to her physician's office with complaints of headache and shortness of breath. She denies any chest pain, weakness of the extremities, cough, runny nose, or abdominal symptoms. In the clinic, her temperature is 36.7 °C (98.2 °F), her blood pressure is 182/122 mmHg, her heart rate is 20/min, and her respiratory rate is 22/min. Physical examination is remarkable for an abdominal bruit upon auscultation in the left periumbilical region. Work-up demonstrates normal values for thyroid-stimulating hormone (TSH), cortisol, and 24-hour urinary excretion of catecholamines. Abdominal angiogram demonstrates a string-of-bead appearance of the left renal artery. Which of the following pathologic findings is most likely to be found on lesional biopsy from her left renal artery?<br />
|Explanation=Fibromuscular dysplasia (FMD) is a non-atherosclerotic, non-inflammatory vascular disease that most commonly affects the renal and internal carotid arteries. Nonetheless, FMD has been described in virtually all arterial beds. On abdominal angiogram, FMD is characterized by a string-of-bead appearance that is suggestive of arterial beaing, typically in the middle-to-distal segment of the renal artery. On histopathological analysis of the vascular lesion, FMD demonstrates involvement of the media, with preservation of other vascular layers such as the intima, internal elastic lamina, and adventitia. Renovascular fibromuscular dysplasia tends to affect women between the age of 15 and 50 years. In the majority of cases, individuals with FMD remain asymptomatic for many years, and fibromuscular dysplasia is often discovered incidentally. Management of renovascular FMD includes pharmacologic therapy to control blood pressure, especially ACE-inhibitors. Percutaneous balloon angioplasty is usually reserved for patients who have uncontrollable blood pressure despite optimal pharmacologic therapy, patients who cannot tolerate pharmacologic therapy, or patients whose renal function is compromised.<br />
|AnswerA=Amorphous, proteinaceous material in the extracellular matrix<br />
|AnswerAExp=The pink material resembling fibrin in the wall of this arteriole is indicative of fibrinoid necrosis as a consequence of malignant hypertension. Hyaline arteriolosclerosis is a major morphologic characteristic of benign nephrosclerosis, in which the arteriolar narrowing causes impairment of renal blood supply and a reduction in glomerular filtration rate leading to increased renin secretion and decreased renal function.<br />
|AnswerB=Homogeneous dysplasia of elastic tissue at the media<br />
|AnswerBExp=Medial fibroplasia, which is characterized by its classic “string of beads” appearance, represents the most common type of fibromuscular dysplasia. Histologically, there is involvement of the media, whereas the intima, internal elastic lamina, and adventitia are preserved.<br />
|AnswerC=Nuclear debris from infiltrating neutrophils in and around the vessels<br />
|AnswerCExp=Leukocytoclastic vasculitis is an inflammation of small blood vessels characterized by palpable purpura. It is the most common vasculitis in clinical practice. Leukocytoclasis refers to the damage caused by nuclear debris from infiltrating neutrophils in and around the vessels.<br />
|AnswerD=Smooth muscle proliferation with lipid-laden foam cells<br />
|AnswerDExp=Atherosclerotic plaques are rich in extracellular matrix and smooth muscle cells. Foam cells are macrophages that engulf oxidized low-density lipoproteins by endocytosis via scavenger receptors and form the fatty streaks of atheroma in the tunica intima of arteries.<br />
|AnswerE=Thickened smooth muscle layer and duplicated basement membrane<br />
|AnswerEExp=Hyperplastic arteriolosclerosis is a type of arteriolosclerosis involving a narrowed lumen that may result from malignant hypertension. Thickened concentric smooth muscle cell layer and duplicated basement membrane on histopathological analysis is often termed onion-skin appearance. These changes are most prominent in the kidney and can lead to ischemia and acute kidney injury.<br />
|EducationalObjectives=Fibromuscular dysplasia (FMD) is a non-atherosclerotic, non-inflammatory vascular disease that most commonly affects the renal and internal carotid arteries. Medial fibroplasia, which is characterized by its classic “string of beads” appearance, represents the most common type of fibromuscular dysplasia. On abdominal angiogram, FMD is characterized by a string-of-bead appearance that is suggestive of arterial beaing, typically in the middle-to-distal segment of the renal artery. Histologically, there is involvement of the media, whereas the intima, internal elastic lamina, and adventitia are preserved.<br />
|References=Poloskey SL, Olin JW, Mace P, et al. Fibromuscular dysplasia. Circulation. 2012;125:e636-9.<br><br />
Slovut DP, Olin JW. Fibromuscular dysplasia. N Engl J Med. 2004; 350:1862-71.<br><br />
First Aid 2015 page 290.<br />
|RightAnswer=B<br />
|WBRKeyword=Fibromuscular dysplasia, Hypertension, String of beads<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR249&diff=1672388WBR2492020-10-28T02:53:24Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Pharmacology<br />
|SubCategory=Pulmonology<br />
|MainCategory=Pharmacology<br />
|SubCategory=Pulmonology<br />
|MainCategory=Pharmacology<br />
|SubCategory=Pulmonology<br />
|MainCategory=Pharmacology<br />
|MainCategory=Pharmacology<br />
|MainCategory=Pharmacology<br />
|SubCategory=Pulmonology<br />
|MainCategory=Pharmacology<br />
|SubCategory=Pulmonology<br />
|MainCategory=Pharmacology<br />
|SubCategory=Pulmonology<br />
|MainCategory=Pharmacology<br />
|SubCategory=Pulmonology<br />
|MainCategory=Pharmacology<br />
|MainCategory=Pharmacology<br />
|SubCategory=Pulmonology<br />
|Prompt=A 32-year-old man with a history of intravenous drug use is admitted with a worsening respiratory distress accompanied by fever and nonproductive cough. Arterial blood gas values are pH=7.52, PaCO2=28 mm Hg, HCO3=22 mEq/L, and PaO2=70 mm Hg when breathing room air. The patient's CD4+ count is 145 cells per microliter. Chest X-ray demonstrates bilateral perihilar interstitial infiltrates suggive of an infectious etiology. The causative organism is detected in bronchoalveolar lavage with silver stain. Two days following pharmacologic therapy, the patient returns to the emergency department with chest pain, dizziness, headache, cold extremities, and pale skin. Peripheral blood smear is remarkable for irregularly fragmented erythrocytes. Supravital stain of the smear demonstrates immature red blood cells with dark blue dots and curved linear structures in the cytoplasm. Which of the following drugs is most likely to be responsible for this patient's readmission?<br />
|Explanation=''Pneumocystis jiroveci''/''carinii'' pneumonia (PCP) is an opportunistic infection caused by ''Pneumocystis jiroveci''. The risk of PCP increases among HIV-positive patients when CD4+ cell concentrations are less than 200 cells/μl. Symptoms include fever, non-productive cough, shortness of breath, weight loss, and night sweats. Chest films typically demonstrate diffuse, symmetrical, perihilar interstitial infiltration that may progress to a homogenous, ground-glass opacification of the lung fields. <br />
<br />
Hypoxemia, the most characteristic laboratory abnormality, may range from mild (room air arterial oxygen ≥70 mm Hg or alveolar-arterial O2 difference <35 mm Hg) to moderate (A-a DO2 ≥35 and <45 mm Hg) to severe (A-a DO2 ≥45 mm Hg).<br />
<br />
TMP-SMX is the treatment of choice for PCP. For mild-to-moderate disease, alternative therapeutic regimens include either dapsone plus TMP, primaquine plus clindamycin, or atovaquone. For moderate-to-severe disease, either clindamycin-primaquine or pentamidine may be administered. Patients with moderate-to-severe disease should receive adjunctive corticosteroids as early as possible within 72 hours after starting specific PCP therapy. <br />
This patient's hospital course is complicated by hemolytic anemia due to increased oxidative stress, which typically occurs among patients with glucose-6-phosphate dehydrogenase deficiency. Heinz bodies, bite cells, spherocytes, and reticulocytes may be evident on peripheral blood smear.<br />
|AnswerA=Atovaquone<br />
|AnswerAExp=For mild-to-moderate PCP alternative therapeutic regimens include either dapsone plus TMP, primaquine plus clindamycin, or atovaquone. However, atovaquone generally does not cause hemolytic anemia.<br />
|AnswerB=Clindamycin<br />
|AnswerBExp=For mild-to-moderate PCP, alternative therapeutic regimens include dapsone plus TMP, primaquine plus clindamycin, or atovaquone. However, clindamycin generally does not cause hemolytic anemia.<br />
|AnswerC=Methylprednisolone<br />
|AnswerCExp=Patients with moderate-to-severe PCP should receive adjunctive corticosteroids as early as possible within 72 hours after starting specific PCP therapy. However, methylprednisolone generally does not cause hemolytic anemia.<br />
|AnswerD=Pentamidine<br />
|AnswerDExp=For moderate-to-severe PCP, either clindamycin-primaquine or pentamidine may be administered. However, pentamidine generally does not cause hemolytic anemia.<br />
|AnswerE=Primaquine<br />
|AnswerEExp=For mild-to-moderate PCP, alternative therapeutic regimens include either dapsone plus TMP, primaquine plus clindamycin, or atovaquone. Common triggers of hemolytic anemia include sulfonamides and other drugs such as chloroquine, isoniazid, nalidixic acid, nitrofurantoin, and primaquine.<br />
|EducationalObjectives=For mild-to-moderate PCP, alternative therapeutic regimens include either dapsone plus TMP, primaquine plus clindamycin, or atovaquone. Common triggers of hemolytic anemia include sulfonamides and other drugs such as chloroquine, isoniazid, nalidixic acid, nitrofurantoin, and primaquine.<br />
|References=Kaplan JE, Benson C, Holmes KK, et al. Guidelines for Prevention and Treatment of Opportunistic Infections in HIV-Infected Adults and Adolescents. Centers for Prevention and Disease Control. 2009;58(RR04);1-198.<br><br />
First Aid 2015 page 168, 170.<br />
|RightAnswer=E<br />
|WBRKeyword=Pneumocystis jiroveci, HIV, PCP, Pneumocystis carinii pneumonia, Dapsone, Antimicrobial therapy<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR248&diff=1672387WBR2482020-10-28T02:53:13Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Genetics<br />
|SubCategory=Endocrine, Oncology<br />
|MainCategory=Genetics<br />
|SubCategory=Endocrine, Oncology<br />
|MainCategory=Genetics<br />
|SubCategory=Endocrine, Oncology<br />
|MainCategory=Genetics<br />
|MainCategory=Genetics<br />
|MainCategory=Genetics<br />
|SubCategory=Endocrine, Oncology<br />
|MainCategory=Genetics<br />
|SubCategory=Endocrine, Oncology<br />
|MainCategory=Genetics<br />
|SubCategory=Endocrine, Oncology<br />
|MainCategory=Genetics<br />
|SubCategory=Endocrine, Oncology<br />
|MainCategory=Genetics<br />
|MainCategory=Genetics<br />
|SubCategory=Endocrine, Oncology<br />
|Prompt=A newborn male is evaluated for vomiting and failure to pass his first stool within 48 hours of birth. The vomit is approximately two teaspoons in volume, green-brownish in color, without bloody contents. On physical examination, the patient's abdomen is distended, and digital rectal examination elicits massive passage of gas and stools. Diagnosis is made by rectal biopsy that demonstrates lack of migration of ganglions due to mutation of a proto-oncogene. Genetic mutation of the proto-oncogene involved in this patient's condition is also responsible for the development of which of the following clinical manifestations?<br />
|Explanation=Meconium ileus is characterized by thickening meconium that is congested in the ileum. It is associated with abdominal distension and bilious vomiting that occur soon after birth. Failure of meconsium passage may be associated with either Hirschsprung's disease or cystic fibrosis. GIven that the two diseases may manifest similarly at birth, a rectal biopsy is usually indicated to differentiate between both conditions.<br />
<br />
During normal fetal development, cells from the neural crest migrate into the colon to form Auerbach's plexus and Meissner's plexus. Hirschsprung's disease (HD) is characterized by incomplete migration of the neural crest cells, which results in the lack of nerve bodies in the distal segments of the colon. The affected segment of the colon cannot relax and pass stool through the colon, and patients typically manifest with meconium ileus after birth.<br />
''RET'' is a proto-oncogene that codes for proteins that assist cells of the neural crest in their movement through the digestive tract during the development of the embryo. It encodes a receptor tyrosine kinase for members of the glial cell line-derived neurotrophic factor family of extracellular signalling molecules. Loss-of-function mutations are associated with Hirschsprung's disease, while gain-of-function mutations are associated with medullary thyroid carcinoma, pheochromocytoma, and multiple endocrine neoplasias type 2A and 2B.<br />
|AnswerA=Café au lait macules<br />
|AnswerAExp=Café au lait macules may be associated with several diseases, including neurofibromatosis type I, McCune–Albright syndrome, tuberous sclerosis, Fanconi anemia, ataxia telangiectasia, Bloom syndrome, Chediak-Higashi syndrome, Gaucher disease, Hunter syndrome, and Wiskott–Aldrich syndrome.<br />
|AnswerB=Cutaneous angiofibroma<br />
|AnswerBExp=Angiofibromas are reddish brown papules of 0.1 to 0.3 cm diameter that are typically located over the sides of the nose and the medial portions of the cheeks. Angiofibromas may be assoicated with type 1 multiple endocrine neoplasia.<br />
|AnswerC=Medullary thyroid carcinoma<br />
|AnswerCExp=Medullary thyroid cancer is a form of thyroid carcinoma, which originates from the parafollicular cells that produce calcitonin. Approximately 25% of medullary thyroid cancers are genetic in nature, caused by a mutation in the ''RET'' proto-oncogene. Medullary thyroid carcinoma may be associated with multiple endocrine neoplasias type 2A and 2B.<br />
|AnswerD=Pituitary prolactinoma<br />
|AnswerDExp=Pituitary prolactinoma is a benign tumor of the pituitary gland. It is the most common type of pituitary tumor. Symptoms of prolactinoma are either caused by hyperprolactinemia or by pressure of the tumor on surrounding tissues. Prolactinoma and other pituitary tumors may be associated with type 1 multiple endocrine neoplasia.<br />
|AnswerE=Vasoactive intestinal peptide tumor<br />
|AnswerEExp=A VIPoma is an endocrine tumor usually originating from non-beta islet cells of the pancreas that produce vasoactive intestinal peptide (VIP).The massive amounts of VIP cause profound, chronic watery diarrhea and dehydration, hypokalemia, achlorhydria, vasodilation, hypercalcemia and hyperglycemia. VIPoma may be associated with type 1 multiple endocrine neoplasia.<br />
|EducationalObjectives=''RET'' is a proto-oncogene that codes for proteins that assist cells of the neural crest in their movement through the digestive tract during the development of the embryo. It encodes a receptor tyrosine kinase for members of the glial cell line-derived neurotrophic factor family of extracellular signalling molecules. Loss-of-function mutations are associated with Hirschsprung's disease, while gain-of-function mutations are associated with medullary thyroid carcinoma, pheochromocytoma, and multiple endocrine neoplasias type 2A and 2B.<br />
|References=Edery P, Lyonnet S, Mulligan LM, et al. Mutations of the RET proto-oncogene in Hirschsprung's disease. Nature. 1994;367(6461):378-80.<br><br />
First Aid 2015 page 337<br />
|RightAnswer=C<br />
|WBRKeyword=Men syndromes, RET, Medullary thyroid cancer, MEN syndrome, Meconium ileus, Hirschsprung's disease<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR247&diff=1672386WBR2472020-10-28T02:53:04Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Pharmacology<br />
|SubCategory=Oncology<br />
|MainCategory=Pharmacology<br />
|SubCategory=Oncology<br />
|MainCategory=Pharmacology<br />
|SubCategory=Oncology<br />
|MainCategory=Pharmacology<br />
|MainCategory=Pharmacology<br />
|MainCategory=Pharmacology<br />
|SubCategory=Oncology<br />
|MainCategory=Pharmacology<br />
|SubCategory=Oncology<br />
|MainCategory=Pharmacology<br />
|SubCategory=Oncology<br />
|MainCategory=Pharmacology<br />
|SubCategory=Oncology<br />
|MainCategory=Pharmacology<br />
|MainCategory=Pharmacology<br />
|SubCategory=Oncology<br />
|Prompt=A novel chemotherapeutic pharmacologic agent of unclear mechanism is under investigation. Following intravenous administration of the investigational agent, hamster ovary cells are found to be arrested at metaphase. Further studies demonstrate that both the investigational agent and paclitaxel bind to beta-tubulins and promote stabilization of microtubules. Which of the following pharmacologic agents has the same mechanism of action?<br />
|Explanation=When hamster ovary cells are incubated with the investigational agent, cell division arrests at metaphase. In the absence of an intact mitotic spindle, duplicated chromosomes cannot correctly align along the division plate and may result in apoptosis. Paclitaxel is a microtubule-stabilizing agent that differs from the vinca alkaloids and colchicine derivatives in that it binds to a different tubulin site and promotes, rather than inhibits, microtubule formation. Paclitaxel blocks cell in the G2-M phase of the cell cycle by binding to the beta-subsunit of tubulin. Remarkably also, it has the ability to polymerize tubulin with the absence of any cofactor. The taxanes have a central role in the treatment of ovarian, breast, lung, gastrointestinal, genitourinary, and head and neck cancers. <br />
|AnswerA=Colchicine<br />
|AnswerAExp=Colchicine is a mitotic poison that inhibits microtubule polymerization by binding to tubulin. The mitosis-inhibiting function of colchicine has been utilized in karyotype studies. Arresting cells in metaphase by adding colchicine facilitates visualization of chromosomes under a light microscope. Apart from inhibiting mitosis, colchicine also inhibits neutrophil motility and produces an anti-inflammatory effect.<br />
<br />
<br />
<br />
<br />
<br />
|AnswerB=Estramustine<br />
|AnswerBExp=Estramustine is synthesized by coupling estradiol and mustard through a carbamate link. However, estramustine has a weak DNA-alkylating action. In fact, it binds to beta-tubulin and microtubule-associated proteins and leads to microtubule disassembly. Estramustine is used primarily for the treatment of metastatic or locally advanced, hormone-refractory prostate cancer.<br />
|AnswerC=Irinotecan<br />
|AnswerCExp=Irinotecan and topotecan are camptothecin analogs approved for clinical use in colorectal, ovarian, and small cell lung cancer. Camptothecins stabilize the normally transient DNA-topoisomerase I cleavable complex and cause an irreversible double-strand DNA break during replication. DNA topoisomerases are nuclear enzymes that reduce torsional stress in supercoiled DNA, allowing selected regions of DNA to become sufficiently untangled for replication, repair, and transcription. Camptothecin analogs inhibit topoisomerase I, while anthracyclines, epipodophyllotoxins, and acridines inhibit topoisomerase II.<br />
<br />
<br />
DNA topoisomerases are nuclear enzymes that reduce torsional stress in supercoiled DNA, allowing selected regions of DNA to become sufficiently untangled for replication, repair, and transcription. Camptothecin analogs inhibit the function of topoisomerase I, while anthracyclines, epipodophyllotoxins and acridines inhibit topoisomerase II.<br />
|AnswerD=Ixabepilone<br />
|AnswerDExp=The epothilones resemble taxanes in that they bind to beta-tubulin and trigger microtubule nucleation and cell-cycle arrest at the G2-M interface. Epothilones bind to a site distinct from that of taxanes. Ixabepilone is approved for metastatic breast cancer treatment.<br />
|AnswerE=Vincristine<br />
|AnswerEExp=Vinca alkaloids block cells in mitosis. Vincristine binds specifically to beta-tubulin, thereby blocking the polymerization of beta-tubulin with alpha-tubulin into microtubules. Vincristine does not stabilize the microtubule but rather inhibits its assembly.<br />
|EducationalObjectives=Paclitaxel is a microtubule-stabilizing agent that differs from the vinca alkaloids and colchicine derivatives in that it binds to a different tubulin site and promotes, rather than inhibits, microtubule formation. Paclitaxel blocks cell in the G2-M phase of the cell cycle by binding to the beta-subsunit of tubulin. The epothilones resemble taxanes in that they bind to beta-tubulin and trigger microtubule nucleation and cell-cycle arrest at the G2-M interface.<br />
|References=Cooper GM. The Cell: A Molecular Approach. 2nd edition. Sunderland (MA): Sinauer Associates; 2000. Microtubules. Available from: http://www.ncbi.nlm.nih.gov/books/NBK9932/<br><br />
First Aid 2015 page 411.<br />
|RightAnswer=D<br />
|WBRKeyword=Ixabepilone, Paclitaxel, Chemotherapy, Tubulin, Microtubules<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR246&diff=1672385WBR2462020-10-28T02:52:54Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Pathophysiology<br />
|SubCategory=Pulmonology<br />
|MainCategory=Pathophysiology<br />
|SubCategory=Pulmonology<br />
|MainCategory=Pathophysiology<br />
|SubCategory=Pulmonology<br />
|MainCategory=Pathophysiology<br />
|MainCategory=Pathophysiology<br />
|MainCategory=Pathophysiology<br />
|SubCategory=Pulmonology<br />
|MainCategory=Pathophysiology<br />
|SubCategory=Pulmonology<br />
|MainCategory=Pathophysiology<br />
|SubCategory=Pulmonology<br />
|MainCategory=Pathophysiology<br />
|SubCategory=Pulmonology<br />
|MainCategory=Pathophysiology<br />
|MainCategory=Pathophysiology<br />
|SubCategory=Pulmonology<br />
|Prompt=A 5-year-old boy is brought to the physician's office for routine evaluation. The patient was diagnosed with a congenital disease immediately after birth and has been followed up by his physician ever since. The patient's genetic analysis reveals a homozygous deletion of three nucleotides coding for phenylalanine at amino acid position 508. Which of the following pathophysiological changes in this patient does not result in clinical manifestations at his present age?<br />
|Explanation=Cystic fibrosis (CF) is an autosomal recessive genetic disorder that affects the lungs, pancreas, liver, and intestine. It is characterized by abnormal transport of chloride and sodium across an epithelium, leading to thick, viscous secretions. CF is caused by mutation of the gene CFTR (cystic fibrosis transmembrane conductance regulator) which encodes a member of the ATP-binding cassette (ABC) transporter superfamily. ABC proteins transport various molecules across extra- and intra-cellular membranes. The encoded protein functions as a chloride channel and controls the regulation of other transport pathways. ΔF508 is the most common type of mutation within the CFTR gene. The mutation is a deletion of the three nucleotides that comprise the codon for phenylalanine (F) at position 508. Individuals with the CFTRΔF508 mutation produce an abnormal CFTR protein that lacks this phenylalanine residue. This protein does not escape the endoplasmic reticulum for further processing and fails to be translocated to the epithelial surface, rendering epithelial membranes relatively impermeable to chloride ions. In sweat ducts, there is decreased absorption of chloride through CFTR with decreased absorption of sodium through epithelial sodium channel (ENaC) which results in production of hypertonic sweats. In the gastrointestinal tract, there is decreased secretion of chloride through CFTR with increased absorption of sodium through ENaC which leads to production of dehydrated mucus. In the airways, the absence of functional CFTR causes upregulation of the ENaC channel which further decreases salt and water secretion by reabsorbing sodium ions. As such, the respiratory complications in cystic fibrosis are not solely caused by the lack of chloride secretion, but instead by enhanced reabsorption of sodium and water.<br />
<br />
Cystic fibrosis is a multisystem disease that affects epithelial cells of virtually all organs. It is characterized by excessive salt loss via sweat glands, meconium ileus, bilious vomiting, intestinal obstructionm, malabsorption, steatorrhea, chronic pulmonary infections that result in pulmonary fibrosis, cardiac arrhythmias, pancreatic insufficiency, and male infertility (bilateral congenital vas deferens). Clinical manifestations often occur early during the course of the disease, and patients may develop clinical features of CF as early as day 1 of birth (e.g. meconium ileus). The thickened secretions from the pancreas block the exocrine movement of the digestive enzymes into the duodenum and result in irreversible damage to the pancreas. This causes atrophy of the exocrine glands and progressive fibrosis. The observed delay for pancreatic fibrosis to develop accounts for the delayed damage to the endocrine pancreas, whose manifestations often appear at an advanced stage of the disease. The median age at diagnosis of cystic fibrosis-related diabetes (CFRD) is 18-21 years.<br />
|AnswerA=Reduced chloride secretion by the sweat duct<br />
|AnswerAExp=Reduced chloride absorption in sweat ducts is observed in patients with CF. In the absence of chloride flow in cystic fibrosis, sodium ions do not flow through ENaC despite upregulation of the ENaC channel, leading to greater salt and water loss. As such, patients' skin tastes salty. A chloride sweat test, which detects the concentration of salt on the patient's skin, is a diagnostic test of CF.<br />
|AnswerB=Reduced chloride secretion by the intestinal epithelium<br />
|AnswerBExp=Reduced chloride secretion with augmented sodium absorption results in water retention in the intestinal epithelium of patients with CF. Colonic manifestations of CF, such as recurrent constipations, are often evident during childhood.<br />
<br />
|AnswerC=Decreased insulin release from the islets of Langerhans <br />
|AnswerCExp=The thickened secretions from the pancreas block the exocrine movement of the digestive enzymes into the duodenum and result in irreversible damage to the pancreas. This causes atrophy of the exocrine glands and progressive fibrosis. The observed delay for pancreatic fibrosis to develop accounts for the delayed damage to the endocrine pancreas, whose manifestations often appear at an advanced stage of the disease. The median age at diagnosis of cystic fibrosis-related diabetes (CFRD) is 18-21 years.<br />
|AnswerD=Loss of migration of neurons to submucosa and muscularis propria of the colon<br />
|AnswerDExp=During normal fetal development, cells from the neural crest migrate into the colon to form Auerbach's plexus and Meissner's plexus. In Hirschprung's disease, the migration is not complete, and part of the colon lacks these nerve bodies that regulate the activity of the colon. The affected segment of the colon cannot relax and may result in meconium ileus.<br />
<br />
|AnswerE=Reduced transepithelial chloride conductance of the airway cells<br />
|AnswerEExp=The "high salt" hypothesis suggests that patients with CF have a reduced transepithelial chloride conductance of the airway cells, which results in high salt concentrations in the surface liquid of the airways. Pulmonary manifestations of CF, including airway plugging and recurrent pulmonary infections, are often evident during early childhood.<br />
|EducationalObjectives=The thickened secretions from the pancreas block the exocrine movement of the digestive enzymes into the duodenum and result in irreversible damage to the pancreas. This causes atrophy of the exocrine glands and progressive fibrosis. The observed delay for pancreatic fibrosis to develop accounts for the delayed damage to the endocrine pancreas, whose manifestations often appear at an advanced stage of the disease. The median age at diagnosis of cystic fibrosis-related diabetes (CFRD) is 21 years.<br />
|References=Rowe SM, Miller S, Sorscher EJ. Cystic fibrosis. N Engl J Med. 2005;352:1992-1991.<br><br />
Ntimbane T, Comte B, Mailhot G, et al. Cystic fibrosis-related diabetes: From CFTR dysfunction to oxidative stress. Clin Biochem Rev. 2009;30(4):153-77.<br><br />
First Aid 2015 page 84.<br />
|RightAnswer=C<br />
|WBRKeyword=Cystic fibrosis, High salt hypothesis<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR245&diff=1672384WBR2452020-10-28T02:52:43Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Pathophysiology<br />
|SubCategory=Oncology<br />
|MainCategory=Pathophysiology<br />
|SubCategory=Oncology<br />
|MainCategory=Pathophysiology<br />
|SubCategory=Oncology<br />
|MainCategory=Pathophysiology<br />
|MainCategory=Pathophysiology<br />
|MainCategory=Pathophysiology<br />
|SubCategory=Oncology<br />
|MainCategory=Pathophysiology<br />
|SubCategory=Oncology<br />
|MainCategory=Pathophysiology<br />
|SubCategory=Oncology<br />
|MainCategory=Pathophysiology<br />
|SubCategory=Oncology<br />
|MainCategory=Pathophysiology<br />
|MainCategory=Pathophysiology<br />
|SubCategory=Oncology<br />
|Prompt=A 48-year-old woman with no past medical history presents to her physician's office with complaints of chronic watery diarrhea and occasional shortness of breath. She also complains of frequent abdominal pains that occasionally wake her up at night and intermittent facial flushing episodes which fail to respond to aspirin. Upon further questioning, she reports a 5 kg weight loss over the past 3 months and chronic fatigue. In the clinic, her blood pressure is 142/88 mmHg, heart rate is 90/min, and respiratory rate is 22/min. Cardiothoracic examination is remarkable for wheezing and a holosystolic murmur at the lower left sternal border that is intensified by applying pressure on her liver. Abdominal exam is remarkable for abdominal tenderness in the right lower quadrant, hyperactive bowel sounds, and mild hepatomegaly. Which of the following urinary findings are diagnostic of this patient's condition?<br />
|Explanation=Carcinoid syndrome is caused by a carcinoid tumor, which is a neuroendocrine tumor that is characterized by excessive production of serotonin and histamine. Carcinoid tumors are rare tumors that typically develop in the gastrointestinal tract. Carcinoid tumors are typically silent until hepatic metastasis occurs. Prior to metastasis, serotonin produced by the tumor undergoes first pass metabolism and is eliminated by the liver. Once hepatic metastasis occurs, the first pass metabolism is bypassed, the clinical manifestations develop. Clinical manifestations of carcinoid syndrome are multisystemic and include cardiac, pulmonary, GI, and cutaneous manifestations. Valvular involvement usually includes either tricuspid insufficiency or pulmonic stenosis (right-sided). Facial flushing observed in carcinoid syndrome is mediated primarily by vasodilatory actions of histamine, which is not affected by prostaglandin inhibition by aspirin. Pellagra (vitamin B3 deficiency) may occur when tryptophan is depleted by accelerated synthesis of serotonin, which is converted to 5-hydroxyindoleacetic acid (5-HIAA) and is excreted in the urine. Management of carcinoid syndrome is surgical resection, but pharmacologic therapy, such as octreotide, are usually administered to provide symptomatic relief.<br />
|AnswerA=Vanillyl mandelic acid<br />
|AnswerAExp=Increased urinary concentration of vanillyl mandelic acid (VMA) is diagnostic of [[pheochromocytoma]], which is a neuroendocrine tumor of the adrenal medulla. Typical symptoms of pheochromocytoma include increased sympathetic tone include paroxysmal palpitations, diaphoresis, anxiety, headache, and refractory hypertension.<br />
|AnswerB=5-hydroxyindoleacetic acid (5-HIAA)<br />
|AnswerBExp=5-hydroxyindoleacetic acid (5-HIAA) is a serotonin metabolite that is diagnostic of [[carcinoid syndrome]].<br />
|AnswerC=Cross-linked N-terminal telopeptides (NTX)<br />
|AnswerCExp=N-terminal telopeptides are biomarkers that reflect increased bone remodeling, which is commonly associated with [[hyperparathyroidism]], [[Paget disease of the bone]], and [[hypercalcemia]] of malignancy.<br />
|AnswerD=Cyclic adenosine monophosphate (cAMP)<br />
|AnswerDExp=Urinary cAMP concentration are typically elevated [[hyperparathyroidism]] and PTHrP-secreting tumors.<br />
|AnswerE=Porphobilinogen (PBG)<br />
|AnswerEExp=Increased urinary porphobilinogen is associated with [[acute intermittent porphyria]].<br />
|EducationalObjectives=Carcinoid syndrome is a neuroendocrine tumor that is characterized by excessive production of serotonin and histamine. Accelerated synthesis of serotonin by the carcinoid tumor is converted to 5-hydroxyindoleacetic acid (5-HIAA) and is excreted in the urine.<br />
|References=Zuetenhorst JM, Taal BG. Metastatic carcinoid tumors: a clinical review. Oncologist. 2005;10(2):123-31.<br><br />
First Aid 2015 page 336.<br />
|RightAnswer=B<br />
|WBRKeyword=5-hydroxyindoleacetic acid, HIAA, Carcinoid syndrome, Neuroendocrine tumor, GI tumor<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR244&diff=1672383WBR2442020-10-28T02:52:33Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Pharmacology<br />
|SubCategory=Vascular<br />
|MainCategory=Pharmacology<br />
|SubCategory=Vascular<br />
|MainCategory=Pharmacology<br />
|SubCategory=Vascular<br />
|MainCategory=Pharmacology<br />
|MainCategory=Pharmacology<br />
|MainCategory=Pharmacology<br />
|SubCategory=Vascular<br />
|MainCategory=Pharmacology<br />
|SubCategory=Vascular<br />
|MainCategory=Pharmacology<br />
|SubCategory=Vascular<br />
|MainCategory=Pharmacology<br />
|SubCategory=Vascular<br />
|MainCategory=Pharmacology<br />
|MainCategory=Pharmacology<br />
|SubCategory=Vascular<br />
|Prompt=A 24-year-old woman presents to her primary care physician with complains of finger discoloration and tingling sensations of her digits. She states that her fingers turn blue upon brief exposure to cold water, and 10 minutes later, the fingers appear pale and eventually become red and swollen. When her fingers are warmed up, their color returns to normal and the swelling disappears. She recalls that during winter time last year, she had similar complaints, and she had an ulcer on her left index finger that eventually healed. Upon further questioning, the patient denies fevers, recent weight changes, fatigue, skin changes, dysphagia, or joint pains or deformities. Which of the following pharmacologic agents is effective to manage this patient's condition?<br />
|Explanation=Raynaud's phenomenon is characterized by transient digital ischemia due to excessive vasoconstriction triggered by either cold temperatures or stressful situations. Clinical manifestations of Raynaud's phenomenon often include vasoconstrictive changes (well-demarcated areas of pallor or bluish (cyanotic) discoloration of the digits) followed by vasodilatory changes and reactive hyperemia (red skin). Raynaud's phenomenon may either be an isolated phenomenon (primary) or a manifestation of more serious, systemic diseases (secondary), such as CREST syndrome. Raynaud's phenomenon is typically managed by avoiding triggers, such as keeping warm hands during winter seasons, and possibly vasodilators. The addition of pharmacologic agents may be reserved to patients to experience severe vasoconstrictive changes, such as those who develop digital ulcers. Dihydropyridine calcium channel blockers (CCBs), such as nifedipine, amlodipine, or felodipine, are the first-line pharmacologic agents for Raynaud's phenomenon. Other pharmacologic agents include nitroglycerin, hydralazine, papaverine, minoxidil, prostaglandins, or niacin, all of which have not been as extensively studied as CCBs for the management of Raynaud's phenomenon. <br />
<br />
Triphasic discoloration of digits on exposure to cold environment is a typical presentation for Raynaud phenomenon. Among the drug classes that have been used are calcium channel blockers, vasodilators, sympatholytic agents, and prostaglandins<br />
|AnswerA=Nifedipine<br />
|AnswerAExp=Nifedipine is a dihydropyridine calcium channel blocker that is effective in the management of Raynaud's phenomenon. <br />
|AnswerB=Ramipril<br />
|AnswerBExp=ACE-inhibitors are not effective in the management of Raynaud's phenomenon. <br />
|AnswerC=Diltiazem<br />
|AnswerCExp=Non-dihydropyridine calcium channel blockers are not effective in the management of Raynaud's phenomenon.<br />
|AnswerD=Verapamil<br />
|AnswerDExp=Non-dihydropyridine calcium channel blockers are not effective in the management of Raynaud's phenomenon.<br />
|AnswerE=Metoprolol<br />
|AnswerEExp=Beta-blockers are not effective in the management of Raynaud's phenomenon.<br />
|EducationalObjectives=Raynaud's phenomenon is typically managed by avoiding triggers, such as keeping warm hands during winter seasons, and possibly vasodilators. The addition of pharmacologic agents may be reserved to patients to experience severe vasoconstrictive changes, such as those who develop digital ulcers. Dihydropyridine calcium channel blockers (CCBs), such as nifedipine, amlodipine, or felodipine, are the first-line pharmacologic agents for Raynaud's phenomenon.<br />
|References=Wigley FM. Raynaud's phenomenon. N Engl J Med. 2002;347:1001-8.<br><br />
First Aid 2015 page 301.<br />
|RightAnswer=A<br />
|WBRKeyword=Raynaud's phenomenon, Calcium channel blockers, Digital ischemia, Pharmacologic therapy<br />
|Approved=No<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR242&diff=1672382WBR2422020-10-28T02:52:33Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Pharmacology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pharmacology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pharmacology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pharmacology<br />
|MainCategory=Pharmacology<br />
|MainCategory=Pharmacology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pharmacology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pharmacology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pharmacology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pharmacology<br />
|MainCategory=Pharmacology<br />
|SubCategory=Cardiology<br />
|Prompt=A 58-year-old hypertensive woman presents to her physician's office for a routine check-up. Upon review of systems, the women states that she is asymptomatic and has no complaints. She reports that she was prescribed an antihypertensive drug by another primary care physician 6 months ago and has been taking one tablet each day. In the clinic, she is afebrile with a blood pressure of 118/80 mmHg, heart rate of 58/min, and respiratory rate of 14/min. Physical examination is unremarkable. Laboratory work-up demonstrates a total cholesterol concentration of 220 mg/dl, LDL-C of 100 mg/dl, HDL-C of 50 mg/dl, triglyceride concentration of 350 mg/dl. The patient is surprised and states that she never had abnormal lipid profiles in the past. The physician suspects the patient's abnormal findings are related to an adverse effect of the drug she has been prescribed. Which of the following antihypertensive drugs is the patient most likely receiving?<br />
|Explanation=The patient is most likely receiving a beta blocker. Beta-blockers are antihypertensive, sympatholytic agents that reduce the cardiac output by binding to beta-adrenoreceptors present in the cardiac nodal tissue, thereby decreasing the number of unoccupied receptors available for norepinephrine and epinephrine to bind to. Beta blockers bind to may be either cardioselective (B1 blockade > B2 blockade) or non-selective (both B1 and B2 blockade). They are indicated in hypertension as well as stable/unstable angina and in the acute phase of myocardial infarction (MI) among stable patients and for the long-term management of MI patients. Beta blockers are also indicated in arrhythmias, bleeding esophageal varices, migraine, and early/advanced heart failure, where some beta blockers have proven efficacy in reducing mortality in heart failure patients (metoprolol, bisoprolol, and carvedilol). Adverse effects associated with the undesired β2-adrenergic antagonism include bradycardia (heart rate < 60/min), bronchospasm, peripheral vasoconstriction, and alteration of glucose and lipid metabolism. These effects are typically observed with administration of non-selective beta blockers or at higher doses of cardioselective beta blockers.<br />
|AnswerA=Prazosin<br />
|AnswerAExp=Prazosin is an alpha-1 adrenergic antagonist (alpha blocker). Prazosin is typically associated with orthostatic hypotension and nasal congestion.<br />
|AnswerB=Lisinopril<br />
|AnswerBExp=Lisinopril is an angiotensin-converting enzyme inhibitor (ACE-I). ACE-I are typically associated with cough and hyperkalemia.<br />
|AnswerC=Clonidine<br />
|AnswerCExp=Clonidine is a centrally acting alpha-2 agonist. Clonidine is typically associated with lightheadednes, dry mouth, dizziness, constipation, and hypotension.<br />
|AnswerD=Atenolol<br />
|AnswerDExp=Atenolol is a non-selective beta blocker. Beta blockers are typically associated with bradycardia and dyslipidemia.<br />
|AnswerE=Verapamil<br />
|AnswerEExp=Verapamil is a non-dihydropyridine calcium channel blocker (CCB). Non-dihydropyridine CCBs are typically associated with constipation and GI distress.<br />
|EducationalObjectives=Beta-blockers are antihypertensive, sympatholytic agents that reduce the cardiac output by binding to beta-adrenoreceptors present in the cardiac nodal tissue, thereby decreasing the number of unoccupied receptors available for norepinephrine and epinephrine to bind to. Adverse effects associated with the undesired β2-adrenergic antagonism include bradycardia (heart rate < 60/min), bronchospasm, peripheral vasoconstriction, and alteration of glucose and lipid metabolism.<br />
|References=Helfand M, Peterson K, Christensen V, et al. Drug Class Review: Beta Adrenergic Blockers: Final Report Update 4 [Internet]. Portland (OR): Oregon Health & Science University; 2009 Jul. Available from: http://www.ncbi.nlm.nih.gov/books/NBK47172/<br><br />
First Aid 2015 page 256<br />
|RightAnswer=D<br />
|WBRKeyword=Atenolol, Beta blockers, Adverse effects, Drug class, Pharmacologic therapy, Bradycardia, Lipid profile<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR239&diff=1672381WBR2392020-10-28T02:51:50Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Pharmacology, Physiology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pharmacology, Physiology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pharmacology, Physiology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pharmacology, Physiology<br />
|MainCategory=Pharmacology, Physiology<br />
|MainCategory=Pharmacology, Physiology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pharmacology, Physiology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pharmacology, Physiology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pharmacology, Physiology<br />
|SubCategory=Cardiology<br />
|MainCategory=Pharmacology, Physiology<br />
|MainCategory=Pharmacology, Physiology<br />
|SubCategory=Cardiology<br />
|Prompt=A 35-year-old man with no past medical history presents to the clinic with acute-onset, recurrent headaches for the past 3 weeks. The patient states that his symptoms are strongest at the beginning of each business week and usually improve by Fridays and the weekends. The patient denies any allergies or intake of any medications. Upon further questioning, the patient also reports occasional fatigue and light-headedness. In the clinic, the patient's vital signs are within normal limits, and his physical examination is unremarkable. Following history-taking and physical examination, the physician suspects that the patient's symptoms are caused by an occupational exposure. Which of the following industries does the patient most likely work in?<br />
|Explanation=Monday disease is a form of nitrate tolerance that occurs among individuals who are exposed to high concentrations of organic nitrates, such as those who work in the manufacture of explosives, fireworks, and fertilizers. While healthy individuals may report clinical manifestations related to either the mechanism of action of nitrates (venodilation), such as light-headedness and fatigue, some may experience adverse reactions related to nitro exposure, such as severe, violent headaches. In contrast, patients with angina pectoris often report improved symptoms during the weekdays and recurring chest pains during the weekends. Workers are often exposed to nitrates during the weekdays, developing tolerance to the effects of nitrates. However, the tolerance effect is lost over the weekend, and patients typically re-experience symptoms the next Monday. The discovery of nitroglycerin tolerance was originally attributed to the observations of Monday disease among workers with occupational exposure.<br />
|AnswerA=Steel mill<br />
|AnswerAExp=Working in the steel mill may be associated with iron poisoning.<br />
|AnswerB=Vintage paint manufacturing<br />
|AnswerBExp=Vintage paint manufacturing may be associated with lead poisoning.<br />
|AnswerC=Pesticide manufacturing<br />
|AnswerCExp=Pesticide manufacturing may be associated with organophosphate poisoning.<br />
|AnswerD=Explosive manufacturing<br />
|AnswerDExp=Explosive manufacturing may be associated with nitroglycerin exposure, intoxication, and tolerance.<br />
|AnswerE=Cyanide processing<br />
|AnswerEExp=Cyanide processing may be associated with cyanide poisoning.<br />
|EducationalObjectives=Monday disease is a form of nitrate tolerance that occurs among individuals who are exposed to high concentrations of organic nitrates, such as those who work in the manufacture of explosives, fireworks, and fertilizers.<br />
|References=Ferreira JCB, Mochly-Rosen D. Nitroglycerin use in myocardial infarction patients: risks and benefits. Circ J. 2012;76(1):15-21.<br><br />
Mayer B, Beretta M. The enigma of nitroglycerin bioactivation and nitrate tolerance: news, views and troubles. Br J Pharmacol. 2008;155:170-84.<br />
|RightAnswer=D<br />
|WBRKeyword=Monday disease, Nitroglycerin, Nitrates, Occupational Exposure, Explosive manufacture, Fertilizers, Fireworks<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR235&diff=1672380WBR2352020-10-28T02:49:14Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor=Gerald Chi (Reviewed by {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Physiology<br />
|SubCategory=Cardiology<br />
|MainCategory=Physiology<br />
|SubCategory=Cardiology<br />
|MainCategory=Physiology<br />
|SubCategory=Cardiology<br />
|MainCategory=Physiology<br />
|MainCategory=Physiology<br />
|MainCategory=Physiology<br />
|SubCategory=Cardiology<br />
|MainCategory=Physiology<br />
|SubCategory=Cardiology<br />
|MainCategory=Physiology<br />
|SubCategory=Cardiology<br />
|MainCategory=Physiology<br />
|SubCategory=Cardiology<br />
|MainCategory=Physiology<br />
|MainCategory=Physiology<br />
|SubCategory=Cardiology<br />
|Prompt=A lab researcher develops a novel pharmacologic agent that preferentially targets smooth muscle cells in the coronary vessels. During her experiment, she accidentally sticks herself with a needle loaded with the novel agent, and she begins to have repeated attacks of profound substernal discomfort that prompt urgent evaluation in the emergency department (ED). In the ED, her vital signs are within normal range, and her physical examination is unremarkable. A 12-lead ECG demonstrates modest ST-segment elevation. Which of the following molecular events is most likely to be induced by the novel pharmacologic agent?<br />
|Explanation=The novel agent induces an acute vasoconstriction of the epicardial coronary arteries and may result in either near or complete arterial occlusions. Coronary artery spasm typically manifests in angina with ST-segment elevations (not depressions) on 12-lead ECG. Modulation of contraction and relaxation of vascular smooth muscles is mainly mediated by the phosphorylation and dephosphorylation of myosin light chain kinase (MLCK) and phosphatase (MLCP). In the classical muscle contraction pathway, stimuli (e.g. histamine) initially bind to Gq protein-coupled receptors located on the surface of vascular smooth muscle cells. The binding process activates phospholipase C, which mediates the synthesis of both 1,4,5-triphosphate (IP3) and diacylglycerol (DAG). IP3 then binds to receptors on the sarcoplasmic reticulum to mediate the mobilization of stored calcium into the cytosol. As cytosolic calcium concentration increases, calcium/calmodulin complexes form and activate MLCK, which result in the phosphorylation of myosin light chain and smooth muscle contraction.<br />
|AnswerA=Activation of protein kinase A<br />
|AnswerAExp=Protein kinase A mediates the phosphorylation of the myosin light chain kinase and subsequently inactivates it. Myosin light chain kinase inactivation results in vasodilation.<br />
|AnswerB=Activation of protein kinase G<br />
|AnswerBExp=Activation of protein kinase G activates myosin light chain phosphatase. Activation of myosin light chain phosphatase results in vasodilation.<br />
|AnswerC=Activation of phospholipase C<br />
|AnswerCExp=In the classical muscle contraction pathway, stimuli (e.g. histamine) initially bind to Gq protein-coupled receptors located on the surface of vascular smooth muscle cells. The binding process activates phospholipase C, which mediates the synthesis of both 1,4,5-triphosphate (IP3) and diacylglycerol (DAG). IP3 then binds to receptors on the sarcoplasmic reticulum to mediate the mobilization of stored calcium into the cytosol. As cytosolic calcium concentration increases, calcium/calmodulin complexes form and activate MLCK, which result in the phosphorylation of myosin light chain and smooth muscle contraction.<br />
|AnswerD=Inhibition of calcium binding to the troponin C subunit<br />
|AnswerDExp=Calcium binding to the troponin C subunit is involved in the contraction of cardiac muscles rather than smooth muscles.<br />
|AnswerE=Decreased expression of the gene that encodes phosphodiesterase 5<br />
|AnswerEExp=Phosphodiesterase 5 converts cyclic GMP to 5'-GMP. Cyclic GMP activates protein kinase G and causes vasodilation.<br />
|EducationalObjectives=In the classical muscle contraction pathway, stimuli (e.g. histamine) initially bind to Gq protein-coupled receptors located on the surface of vascular smooth muscle cells. The binding process activates phospholipase C, which mediates the synthesis of both 1,4,5-triphosphate (IP3) and diacylglycerol (DAG). IP3 then binds to receptors on the sarcoplasmic reticulum to mediate the mobilization of stored calcium into the cytosol. As cytosolic calcium concentration increases, calcium/calmodulin complexes form and activate MLCK, which result in the phosphorylation of myosin light chain and smooth muscle contraction.<br />
|References=Lanza GA, Careri G, Crea F. Mechanisms of coronary artery spasm. Circulation. 2011;124:1774-82.<br><br />
Kimura K, Ito M, Amano M, et al. Regulation of myosin phosphatase by Rho and Rho-associated kinase (Rho-kinase). Science. 1996;273(5272):245-8.<br><br />
Somlyo AP, Somlyo AV. Signal transduction and regulation in smooth muscle. Nature. 1994; 372(6503):231-6.<br />
|RightAnswer=C<br />
|WBRKeyword=Vasospasm, Coronary artery spasm, Muscle contraction, Pharmacologic agent, Phospholipase C, PIP2, IP3, DAG, Calcium, MLCK, MLCP, Classical muscle contraction pathway<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR234&diff=1672379WBR2342020-10-28T02:49:04Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor= {{Rim}} (Reviewed by Will Gibson)<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Physiology<br />
|SubCategory=Renal<br />
|MainCategory=Physiology<br />
|SubCategory=Renal<br />
|MainCategory=Physiology<br />
|SubCategory=Renal<br />
|MainCategory=Physiology<br />
|MainCategory=Physiology<br />
|MainCategory=Physiology<br />
|SubCategory=Renal<br />
|MainCategory=Physiology<br />
|SubCategory=Renal<br />
|MainCategory=Physiology<br />
|SubCategory=Renal<br />
|MainCategory=Physiology<br />
|SubCategory=Renal<br />
|MainCategory=Physiology<br />
|MainCategory=Physiology<br />
|SubCategory=Renal<br />
|Prompt=An experiment to measure the filtration fraction in healthy volunteers is conducted. One sample of the available urine and serum values is shown below. If the urine flow is 2.0 ml/min, what is the best approximate filtration fraction?<br />
<br />
[[Image:Screen Shot 2013-09-08 at 9.43.33 PM.png|600px]]<br />
|Explanation=Despite the presence of several parameters, utilization of only [[creatinine]] and [[PAH]] is required to calculate the filtration fraction. <br />
Filtration fraction (FF) is calculated by the following equation: FF (%) = (GFR / RPF) x 100<br />
<br />
GFR = (UCr x V)/PCr = (100 mg/dL x 2 ml/min ) / (1 mg/dL) = 200 mL/min<br />
RPF = (UPAH x V)/PPAH = (50 mg/dL x 2 ml/min ) / (0.2 mg/dL) = 500 mL/min<br />
FF (%) = (GFR / RPF) x 100 = (200/500) x 100 = 0.4 x 100 = 40%<br />
<br />
Abbreviations:<br><br />
* GFR: Glomerular Filtration Rate (mL/min)<br />
* UCr: Urinary creatinine concentration (mg/mL)<br />
* V: Volume of urine produced per unit time (mL/min)<br />
* PCr: Plasma creatinine concentration (mg/mL)<br />
* RPF: Renal plasma flow<br />
* UPAH: Urinary Para-aminohippurate (PAH) concentration (mg/mL)<br />
* PPAH: Plasma Para-aminohippurate (PAH) concentration (mg/mL)<br />
* FF: Filtration fraction<br />
|AnswerA=20%<br />
|AnswerAExp=One could obtain this number by using the ratio of the serum PAH to serum creatinine. However, this does not reflect any standard physiologic parameter.<br />
|AnswerB=30%<br />
|AnswerBExp=According to the calculation, this is an incorrect answer.<br />
|AnswerC=35%<br />
|AnswerCExp=According to the calculation, this is an incorrect answer.<br />
|AnswerD=40%<br />
|AnswerDExp=According to the calculation, this is a correct answer.<br />
|AnswerE=100%<br />
|AnswerEExp=This number could be achieved by dividing the renal creatinine concentration by the serum creatinine concentration. However, this measure does not reflect any normal physiologic parameter.<br />
|EducationalObjectives=The filtration fraction can be calculated by the following formula: FF (%) = (GFR/RPF) x 100<br />
|References=First Aid 2015 page 530<br />
|RightAnswer=D<br />
|WBRKeyword=Renal physiology, Renal plasma flow, Filtration fraction, Nephrology, Kidney, GFR, PAH, Creatinine,<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR233&diff=1672378WBR2332020-10-28T02:48:56Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor= {{YD}} (Reviewed by {{YD}})<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Microbiology<br />
|SubCategory=Dermatology<br />
|MainCategory=Microbiology<br />
|SubCategory=Dermatology<br />
|MainCategory=Microbiology<br />
|SubCategory=Dermatology<br />
|MainCategory=Microbiology<br />
|MainCategory=Microbiology<br />
|MainCategory=Microbiology<br />
|SubCategory=Dermatology<br />
|MainCategory=Microbiology<br />
|SubCategory=Dermatology<br />
|MainCategory=Microbiology<br />
|SubCategory=Dermatology<br />
|MainCategory=Microbiology<br />
|SubCategory=Dermatology<br />
|MainCategory=Microbiology<br />
|MainCategory=Microbiology<br />
|SubCategory=Dermatology<br />
|Prompt=A 20-year-old man presents to the physician’s office with complaints of several skin lesions for the past 2 days. He recently arrived to the United States from Iraq. In the clinic, the patient's temperature is 36.8 °C (98.2 °F), his blood pressure is 120/78 mmHg, his heart rate is 68/min, and his respiratory rate is 14/min. On physical examination, the patient has red cutaneous nodules and skin ulcers as shown in the figure below. Skin scraping with microscopic analysis and needle aspiration of the tissue fluid from the margin were performed. Which of the following organisms is most likely responsible for this patient’s condition?<br />
[[File:WBR233.jpg | 600px]]<br />
|Explanation=[[Leishmaniasis]] has a spectrum of cutaneous, mucocutaneous, and visceral manifestations. [[Cutaneous leishmaniasis]] is a [[parasitic disease]] that is characterized by multiple skin ulcerations. The disease is spread by the bite of sand flies. Diagnosis of cutaneous leishmaniasis is based on physical examination findings of characteristic non-healing scaling lesions that frequently ulcerate. The disease is endemic to several regions of the world, most commonly the Middle East region in Afghanistan, Algeria, Iran, Iraq, Saudi Arabia, and Syria and in the South American region in Brazil and Peru. Treatment of cutaneous leishmaniasis is pentavalent antimonials, such as [[sodium stibogluconate]] (Pentostam) and local care of ulcerating lesions that may be exposed to bacterial super-infections, commonly ''[[Staphylococcus aureus]]''.<br />
|AnswerA=''Toxoplasma gondii''<br />
|AnswerAExp=''[[Toxoplasma gondii]]'' is a parasitic infection that is clinically relevant in utero and among [[HIV]]-positive patients. Transmission of ''[[T. gondii]]'' cysts is usually via ingestion of cysts found in contaminated meat and cat feces. Skin lesions are not characteristic findings of [[toxoplasmosis]].<br />
|AnswerB=''Trypanosoma brucei''<br />
|AnswerBExp=''[[Trypanosoma brucei]]'' is the causative agent of African sleeping sickness, transmitted by the Tse Tse fly. The disease is characterized by somnolence, [[lymphadenopathy]] and recurrent fevers. Winterbottom’s sign is typically observed among patients with early trypanosomiasis and is characterized by swollen lymph in the posterior cervical region.<br />
|AnswerC=''Leishmania aethiopica''<br />
|AnswerCExp=Diagnosis of cutaneous leishmaniasis is based on physical examination findings of characteristic non-healing scaling lesions that frequently ulcerate.<br />
|AnswerD=''Loa loa''<br />
|AnswerDExp=''[[Loa loa]]'' (eye worm) is a [[nematode]] that rests in the subcutaneous layer of the [[skin]]. Before transmission to the human host, Loa loa larvae grow in horseflies, such as deer flies and yellow flies.<br />
|AnswerE=''Paragonimus westermani''<br />
|AnswerEExp=''[[Paragonimus westermani]]'' (lung fluke) is a [[trematode]] that is contaminates undercooked crab meat. It often causes either a subacute or a chronic lung disease and hemoptysis. Disseminated disease can spread to the [[spinal cord]] and may result in paralysis.<br />
|EducationalObjectives=Cutaneous leishmaniasis is a common form of leishmaniasis characterized by ulcerating red lesions. Leishmaniasis is endemic to the Middle East and South America. The causative organism is the ''Leishmania'' parasite. Sodium stibogluconate is an effective treatment for cutaneous leishmaniasis.<br />
|References=Markle WH, Makhoul K. Cutaneous leishmaniasis: Recognition and Treatment. Am Fam Physician. 2004; 15;69(6):1455-1460<br><br />
First Aid 2015 page 152<br><br />
Image Attribution: "Cutaneous Leishmaniasis.jpg" by user:Abanima licensed under the GFDL, released under the GNU Free Documentation License<br />
|RightAnswer=C<br />
|WBRKeyword=Microbiology, Parasites, Skin ulcer, Skin lesion, Zoonotic infection, Leishmania aethiopica, Cutaneous leishmaniasis, Leishmaniasis<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR232&diff=1672377WBR2322020-10-28T02:48:44Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor= {{Rim}} (Reviewed by Will Gibson)<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Pathology<br />
|SubCategory=Renal<br />
|MainCategory=Pathology<br />
|SubCategory=Renal<br />
|MainCategory=Pathology<br />
|SubCategory=Renal<br />
|MainCategory=Pathology<br />
|MainCategory=Pathology<br />
|MainCategory=Pathology<br />
|SubCategory=Renal<br />
|MainCategory=Pathology<br />
|SubCategory=Renal<br />
|MainCategory=Pathology<br />
|SubCategory=Renal<br />
|MainCategory=Pathology<br />
|SubCategory=Renal<br />
|MainCategory=Pathology<br />
|MainCategory=Pathology<br />
|SubCategory=Renal<br />
|Prompt=A 24 year old Caucasian male patient presents to the emergency department with back pain that radiates to the inguinal region. The pain started on the day of presentation. On further questioning, the patient reveals he has had recurrent kidney stones since the age of 11. The patient’s urine smells like rotten eggs. Appropriate work-up done prior to presentation has shown elevated levels of urinary arginine, ornithine, and lysine. Which of the following treatment modalities is the best option for this patient’s renal colic?<br />
|Explanation=[[Cystinuria]] is an autosomal recessive inherited disorder characterized by defect in intestinal absorption and renal reabsorption of cystine and dibasic [[amino acids]] across the luminal membrane of the renal proximal tubule. Elevated levels of urinary cystine will subsequently crystallize and form stones. <br />
The clinical symptoms of cystine stones are identical to other kidney stones (ie severe flank pain). Typically, patients with cystinuria complain of recurrent kidney stones starting the first 2 decades of life and often have a positive family history of stone disease. [[Urinalysis]] shows pathognomonic hexagonal crystals that contain sulfur amino acids due to the presence of cystine. Characteristic rotten egg urine smell is also attributed to the sulfur-containing compounds in cystine stones.<br />
<br />
Initial management of cystine stones includes increased fluid intake, urinary alkalinization with [[acetazolamide]], a carbonic anhydrase inhibitor, and thiol medications to reduce the urinary cystine concentration. However, once stones have formed, the kinetics of crystal dissolution are unfavorable. Extracorporeal shock wave lithotripsy or surgery are options for patients with symptomatic stones.<br />
|AnswerA=Parathyroidectomy<br />
|AnswerAExp=[[Parathyroidectomy]] would be an appropriate treatment option for patients with primary [[hyperparathyroidism]] who have recurrent calcium-containing stones.<br />
|AnswerB=Carbonic anhydrase inhibitor<br />
|AnswerBExp=Carbonic anhydrase inhibitors are used in the management of cystine stones.<br />
|AnswerC=Protein synthesis inhibitor that acts on bacterial 30S ribosomal subunit<br />
|AnswerCExp=[[Antimicrobial]]s are not helpful in cystine stones. Antimicrobials are helpful in urinary tract infections that might in turn predispose to magnesium ammonium phosphate (MAG) struvite stones. These bacteria precipitate struvite stones by splitting urea into ammonium.<br />
|AnswerD=Xanthine oxidase inhibitor<br />
|AnswerDExp=Xanthine oxidase inhibitors, such as [[allopurinol]], are helpful in the treatment of kidney stones with a uric acid component.<br />
|AnswerE=Na-K-2Cl co-transport inhibitor at the level of loop of Henle<br />
|AnswerEExp=[[Loop diuretic]]s are Na-K-2Cl inhibitors; they have no role in the treatment of cystine stones.<br />
|EducationalObjectives=Cystinuria is an autosomal recessive disorder characterized by impaired GI absorption and renal reabsorption of cystine and dibasic amino acids. Cystine stones contain sulfur containing compounds that give a characteristic rotten egg smell. Treatment includes alkalinization of urine by acetazolamide, a carbonic anhydrase inhibitor.<br />
|References=First Aid 2015 page 108<br />
|RightAnswer=B<br />
|WBRKeyword=Biochemistry, Genetics, Metabolism, Amino acids, Amino acid metabolism, Kidney stones, Nephrolithiasis, Cystine, Cystinuria<br />
|Approved=Yes<br />
}}</div>WikiBothttps://www.wikidoc.org/index.php?title=WBR231&diff=1672376WBR2312020-10-28T02:48:34Z<p>WikiBot: refreshing WBR questions</p>
<hr />
<div> {{WBRQuestion<br />
|QuestionAuthor= {{Rim}} (Reviewed by Will Gibson)<br />
|ExamType=USMLE Step 1<br />
|MainCategory=Histology, Pathology<br />
|SubCategory=Renal<br />
|MainCategory=Histology, Pathology<br />
|SubCategory=Renal<br />
|MainCategory=Histology, Pathology<br />
|SubCategory=Renal<br />
|MainCategory=Histology, Pathology<br />
|MainCategory=Histology, Pathology<br />
|MainCategory=Histology, Pathology<br />
|SubCategory=Renal<br />
|MainCategory=Histology, Pathology<br />
|SubCategory=Renal<br />
|MainCategory=Histology, Pathology<br />
|SubCategory=Renal<br />
|MainCategory=Histology, Pathology<br />
|SubCategory=Renal<br />
|MainCategory=Histology, Pathology<br />
|MainCategory=Histology, Pathology<br />
|SubCategory=Renal<br />
|Prompt=A 68 year old Caucasian male patient presents to his physician for his annual check-up. The patient’s past medical history is significant for hypertension controlled on lisinopril and advanced diabetes mellitus type II poorly controlled on daily insulin injections. Routine work-up reveals elevated serum creatinine. A renal biopsy is performed, the results of which are shown below. The histologic findings could be best explained by which of the following pathologic processes?<br />
<br />
[[File:Diabetic_nephropathy.png|300px]]<br />
|Explanation=[[Diabetic nephropathy]] is a common microvascular complication in advanced [[diabetes mellitus]]. Renal biopsy under light microscopy typically reveals characteristic eosinophilic nodules in the glomerular tuft called “Kimmelsteil-Wilson” lesion. Chronic hypercalcemia causes non-enzymation glycosylation (glycation) of proteins, which are collectively called advanced glycation end products (AGEs). Glycation is the irreversible attachment of reducing sugars to amino acids in proteins. The resulting AGEs trap extravasated [[immunoglobulin]]s, [[albumin]], [[LDL]], and other proteins via cross-linking to the extra vascular matrix. These accumulated products cause generalized cellular dysfunction and can initiate inflammatory cascades, leading to further tissue damage.<br />
|AnswerA=Amorphous pink deposits of amyloid in renal cortex<br />
|AnswerAExp=Amyloidosis is characterized by [[amyloid]] deposition that is positive for Congo red stain.<br />
|AnswerB=Immune response mediated by CD4 and CD8 lymphocytes<br />
|AnswerBExp=Immune response mediated by [[CD4]] and [[CD8]] [[lymphocytes]] describes the mechanism of renal rejection following [[transplantation]].<br />
|AnswerC=Cystic distribution throughout the renal parenchyma<br />
|AnswerCExp=[[Polycystic kidney disease]] is characterized by cystic distribution throughout the renal parenchyma.<br />
|AnswerD=Immune complex deposition activating the complement pathway<br />
|AnswerDExp=The pathogenesis of several primary glomerulonephritides, including post-infectious glomerulonephritis and membranoproliferative [[glomerulonephritis]], is characterized by immune complex deposition that activates the complement pathway.<br />
|AnswerE=Non-enzymatic glycosylation of proteins<br />
|AnswerEExp=Diabetic nephropathy is a common microvascular complication in advanced diabetes mellitus. Renal biopsy under light microscopy would reveal characteristic eosinophilic nodules in the glomerular tuft called “Kimmelsteil-Wilson” lesion. Chronic hypercalcemia causes non-enzymation glycosylation (glycation) of proteins. <br />
|EducationalObjectives=Diabetic nephropathy is a microvascular complication of uncontrolled [[diabetes mellitus]]. It is characterized by Kimmelsteil-Wilson lesions, which are eosinophilic nodules in glomerular tufts. The pathogenesis of diabetic nephropathy is believed to be due to accumulation of advanced glycation end products (AGEs).<br />
|References=Tan, Adeline LY, Josephine M. Forbes, and Mark E. Cooper. "AGE, RAGE, and ROS in diabetic nephropathy." Seminars in nephrology. Vol. 27. No. 2. WB Saunders, 2007.<br><br />
Kalia K, Sharma S, Mistry K. Non-enzymatic glycosylation of immunoglobulins in diabetic nephropathy. Clin Chim Acta. 2004;347(1-2):169-76.<br><br />
First Aid 2015 page 543<br />
|RightAnswer=E<br />
|WBRKeyword=Diabetes, Diabetes Mellitus, DM, Glucose, Glycosylation, Glycation, AGEs, Histology, Nephropathy, Renal, Kidney, Histology<br />
|Approved=Yes<br />
}}</div>WikiBot