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Postoperative ileus should be suspected when a patient has nausea/vomiting, abdominal distension and failure to pass flatus for at least 3-5 days following abdominal surgery. Before making the diagnosis of postoperative ileus, bowel obstruction must be ruled out. Postoperative ileus is thought to occur due to inflammation caused by surgical manipulation of the bowel. The muscarinic receptors in the bladder and gastrointestinal tract stimulate contraction of the bladder and expulsion of urine, and increased gastrointestinal motility, respectively. Bethanechol is a cholinomimetic agent that can be used to treat postoperative ileus and urinary retention. It should be used to treat these disorders only after mechanical obstruction is ruled out as a possible cause.<br/>
'''Educational Objective:''' Bethanechol is a cholinomimetic agent that can be used to treat postoperative ileus and urinary retention.<br/>
'''References:''' Smith AJ, Nissan A, Lanouette NM, Shi W, Guillem JG, Wong WD, Thaler H, Cohen AM. Prokinetic effect of erythromycin after colorectal surgery: randomized, placebo-controlled, double-blind study. Dis Colon Rectum. 2000;43(3):333.<br>
Myrhöj T, Olsen O, Wengel B. Neostigmine in postoperative intestinal paralysis. A double-blind, clinical, controlled trial. Dis Colon Rectum. 1988;31(5):378.<br>
First Aid 2013 page 233 +
The drug described is able to cause a right-shift in the concentration-response curve to endothelin, meaning that higher doses of endothelin-1 are required to achieve the same response in the presence of Ro47-0203. Endothelins are the most potent vasoconstrictors known. Because Ro47-0203 acts antagonistically to endotelin-1, it is likely to be an enothelin receptor antagonist. The only endothelin receptor antagonist among the answer choices is Bosentan. Futhermore, the decrease in potency depicted by a right-shift in the concentration-response curve of endothelin demonstrates that Bosentan is a competitive (rather than a non-competitive) antagonist of endothelin-1 receptors.<br/>
'''Educational Objective:''' Bosentan is a competitive antagonist of endothelin-1 receptors that is used to treat pulmonary hypertension.<br/>
'''References:''' Véniant M, Clozel JP, Hess P, Clozel M. Endothelin plays a role in the maintenance of blood pressure in normotensive guinea pigs. Life Sci. 1994;55(6):445-54.
First Aid 2013 page 564 +
Children are the most frequent victims of ethylene glycol poisoning. Ethylene glycol can be found in items such as antifreeze, and has a sweet taste which can cause children to drink it. Ethylene glycol itself is not toxic, but its metabolites are. Ethylene glycol is first metabolized to glycolaldehyde, which then undergoes further oxidation to glycolate, glyoxylate, and oxalate. It is glycolate and oxalate that are primarily responsible for the metabolic acidosis and renal damage that accompany ethylene glycol poisoning. The antidotes to ethylene glycol poisoning are ethanol and fomepizole, both of which inhibit the metabolism of ethylene glycol. Ethanol competitively inhibits the metabolism of ethylene glycol by alcohol dehydrogenase. Fomepizole is also a competitive inhibitor of alcohol dehydrogenase. Hemodialysis should be initiated in any patient with known ethylene glycol or methanol poisoning.<br/>
'''Educational Objective:''' Fomepizole acts as an antidote to ethylene glycol poisoning by competitive inhibition of alcohol dehydrogenase.<br/>
'''References:''' Leth PM, Gregersen M. Ethylene glycol poisoning. Forensic Sci Int. 2005;155(2-3):179-84. +
Non-selective beta-blockers such as propranolol interfere with the binding of catecholamine stress hormones such as epinephrine to beta-adrenergic receptors at most sites (β1-adrenergic receptors are located mainly in the heart and in the kidneys; β2-adrenergic receptors are located mainly in the lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and skeletal muscle; β3-adrenergic receptors are located in fat cells). Because beta blockers decrease activity in the SA-node, they can lead to bradycardia and first degree heart block. In addition to arrhythmias, beta-blocker overdose may cause CNS depression and seizures. At the molecular level, beta-blockade causes a decrease in intracellular levels of cAMP. Glucagon binds to its G protein-coupled receptor, which then activates adenylate cyclase to increase intracellular levels of cAMP. This cascade counteracts the effects of beta-blocker overdose.<br/>
'''Educational Objective:''' Glucagon counteracts beta-blocker toxicity by increasing intracellular cAMP.<br/>
'''References:''' Weinstein RS, Cole S, Knaster HB, Dahlbert T (February 1985). "Beta blocker overdose with propranolol and with atenolol". Ann Emerg Med14 (2): 161–163 +
The patient in this vignette most likely has anal squamous cell carcinoma (SCC). The dentate or pectinate line divides the upper 1/3 and lower 2/3 of the anal canal. The line marks the transition from columnar epithelium to squamous epithelium; and demarcates the meeting point of ectoderm (distal anal canal) and endodermal hindgut (proximal anal canal). Cancers of the anal canal are relatively uncommon and account for 2% of colorectal cancers. Anal SCC progresses from a locally confined lesion, to a cancer that invades the basement membrane, to lymphatic spread and finally metastasis. This set of steps is the basis for the TNM staging system. Because of the location of this particular tumor, the most likely site of spread from the primary site is via the lymphatics to the superficial inguinal lymph nodes. Above the pectinate line, the tumor would most likely be a colorectal adenocarcinoma and would first reach the mesenteric lymph nodes.<br/>
'''Educational Objective:''' The most likely route of spread of a distal rectal tumor (squamous cell carcinoma most common) is via the lymphatics to the superficial inguinal lymph nodes.<br/>
'''References:''' Bullard Dunn KM, Rothenberger DA. Colon, Rectum, and Anus. In: Brunicardi F, Andersen DK, Billiar TR, Dunn DL, Hunter JG, Matthews JB, Pollock RE. eds. Schwartz's Principles of Surgery, 10e. New York, NY: McGraw-Hill; 2014. +
The patient in this vignette has a direct inguinal hernia, in which the contents of the abdomen protrude through a weakened area in the transversalis fascia. This region lies superior to the inguinal ligament, medial to the inferior epigastric vessels and lateral to the rectus abdominus. It is often referred to as Hesselbach’s triangle. The inferior border of the Hesselbach triangle, the inguinal ligament, is formed by the external abdominal oblique aponeurosis. Direct hernias are capable of exiting via the superficial inguinal ring but, unlike indirect inguinal hernias, they cannot move into the scrotum. Direct inguinal hernias occur 10x more often in males than in females. In contrast, indirect hernias protrude lateral to the inferior epigastric vessels and passes through the deep inguinal ring into the scrotum. The pathophysiology of indirect hernias is due to failure of closure of the processus vaginalis, and outpouching of the peritoneum into the scrotum.<br/>
'''Educational Objective:''' The aponeurosis of the external abdominal oblique gives rise to the inguinal ligament.<br/>
'''References:''' Moore KL, Agur AM, (II) AF. Essential Clinical Anatomy. Lippincott Williams & Wilkins; 2014. +
The patient in this vignette has the classical signs of a migraine headache. Migraines are often preceded by an aura, or a perceptual disturbance that may include an unpleasant smell, a visual disturbance, or unconventional thoughts. Migraines can have variable presentations but are classically described as moderate to severe headaches that are unilateral and localized most commonly to the frontotemporal areas. Several hypotheses have been suggested for the causes of migraines including irritation of CN V and release of substance P. Although non-opioid analgesics and NSAIDS are considered a first line therapy, sumatriptan is a more effective therapy for more severe migraine headaches. Sumatriptan is a serotonin 5-HT<sub>1B/1D</sub> agonist. Although the mechanism of action of sumatriptan is not clearly understood, the 5-HT1B receptors it activates are present in the cranial arteries and veins, suggesting a vascular mechanism (vasoconstriction). For patients with severe debilitating migraines that are not controlled by abortive therapies and lead to medication overuse (NSAIDS, triptans, analgesics), prophylaxis should be considered with either a non-selective beta-blocker, such as propranolol or timolol, or an antiepileptic agent, such as valproate or topiramate.<br/>
'''Educational Objective:''' Sumatriptan is a serotonin analogue that acts as a 5-HT<sub>1B/1D</sub> agonist to relieve migraine headaches.<br/>
'''References:''' Silberstein SD, Holland S, Freitag F, et al. Evidence-based guideline update: pharmacologic treatment for episodic migraine prevention in adults: report of the Quality Standards Subcommittee of the American Academy of Neurology and the American Headache Society. Neurology. 2012;78(17):1337-45.<br>
Diagnosis and management of headaches in young people and adults. NICE clinical guideline 150 (2012). +
The patient in this vignette has a combination of cytokine storm and tumor lysis syndrome (TLS). The most likely explanation is the activation of the administered anti-tumor T-cells and release of copious amounts cytokines such as IL-6 (cytokine storm). Patients with cytokine storm present with high grade fever, erythema, and elevated levels of TNF-alpha, IL-1, and IL-6. At the same time, the patient's lab demonstrate signs of tumor lysis syndrome secondary to rapid destruction of tumor cells. TLS is caused by the breakdown products of dying cancer cells and is characterized by hyperkalemia, hyperphosphatemia, hyperuricemia, hypocalcemia, and hyperuricosuria leading to consequent acute uric acid nephropathy and acute kidney injury. Treatment of tumor lysis syndrome consists primarily of managing uric acid levels and electrolytes. In all cases of suspected TLS, patients should receive IV hydration. When TLS is confirmed, patients should receive allopurinol or in more serious cases, rasburicase (a recombinant enzyme that degrades uric acid). In severe cases, patients must be started on hemodialysis.<br/>
'''Educational Objective:''' Allopurinol is a xanthine oxidase inhibitor that decreases the production of uric acid; it is essential in the treatment of tumor lysis syndrome.<br/>
'''References:''' Coiffier B, Altman A, Pui CH, Younes A, Cairo MS. Guidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based review. J Clin Oncol. 2008;26(16):2767-78. +
Keratoacanthoma (KA), a common low-grade skin tumour that is believed to originate from the neck of the hair follicle. The defining characteristic of KA is that it is dome-shaped, symmetrical, surrounded by a smooth wall of inflamed skin, and capped with keratin scales and debris. It always grows rapidly, reaching a large size within days or weeks, and if untreated will starve itself of nourishment, necrose (die), slough, and heal with scarring. Approximately 6% of KA progress to squamous cell carcinoma when left untreated.<br/>
'''Educational Objective:''' Keratoacanthoma is a low-grade skin tumor characterized by a dome-shaped growth with a keratin-filled central dimple. It grows rapidly over several weeks, then spontaneously regresses.<br/>
'''References:''' Schwartz RA. Keratoacanthoma: a clinico-pathologic enigma. Dermatol Surg. 2004;30(2 Pt 2):326-33.<br>
Image Attribution: The Dermatology Atlas. 2014. http://www.atlasdermatologico.com.br/ +
The patient in this vignette has a urinary tract infection caused by ''Staphylococcus saprophyticus''. ''S. saprophyticus'' is a catalase-positive, coagulase-negative, gram-positive coccus with novobiocin resistance. It is the second most common cause of urinary tract infections among sexually active women (10-20%) following ''E. coli''.<br/>
'''Educational Objective:''' ''S. Saprophyticus'' is a catalase-positive, coagulase-negative, gram-positive coccus with novobiocin resistance. It is the second most common cause of urinary tract infections among sexually active women.<br/>
'''References:''' Hovelius, Birgitta, and Per-Anders Mardh. Staphylococcus saprophyticus as a common cause of urinary tract infections. Review of Infectious Diseases. 1984; 6(3):328-337.<br>
First Aid 2015 page 174. +
The patient in this vignette has suffered a spontanoues pneumothorax. Spontaneous pneumothorax tends to occur among tall, thin young males (M:F ratio is 8:1). It is thought to arise from the rupture of apical "blebs" (small air-filled lesions under the pleural surface), which are presumed to be more common in those classically at risk of pneumothorax (tall males) due to mechanical factors. In spontaneous pneumothorax, blebs can be found in approximately 77% of cases, compared with only 6% in the general population without a history of spontaneous pneuomothorax.<br/>
'''Educational Objective:''' Spontaneous pneumothorax typically occurs among tall, thin young males. It is thought to arise from the rupture of apical "blebs" (small air-filled lesions under the pleural surface).<br/>
'''References:''' Light, Richard W. "Management of spontaneous pneumothorax." Am Rev Resp Dis. 1993;148: 245-245.<br>
First Aid 2015 page 615 +
This patient has a high anion gap metabolic acidosis due to salicylate toxicity. The criteria for high anion gap metabolic acidosis is pH < 7.35 and an anion gap >16 (anion gap limit differs with age). The anion gap is defined by the following equation:
<br>
Anion Gap = Na - Cl - Bicarbonate
<br>
In this case, the anion gap equals 140-100-15= 25. The oxygen-hemoglobin dissociation curve is right shifted by a decrease in pH (increasing acidity). The following factors result in a right shift of the oxygen-hemoglobin dissociation curve:<br>
*CO2<br>
*BPG (2,3-BPG)<br>
*Exercise<br>
*Acidic pH<br>
*High altitude<br>
*High temperature<br/>
'''Educational Objective:''' The following factors result in a right shift of the oxygen-hemoglobin dissociation curve:<br>
*CO2<br>
*BPG (2,3-BPG)<br>
*Exercise<br>
*Acidic pH<br>
*High altitude<br>
*High temperature<br/>
'''References:''' First Aid 2013 page 548 +
Maple syrup urine disease (MSUD) is an autosomal recessive genetic disease characterized by the deficiency of alpha-keto acid dehydrogenase. Patients with MSUD often appear normal at birth. However, plasma concentrations of branched-chain amino acids (leucine, isoleucine, and valine) gradually increase, and the disease typically manifests during the 2nd or 3rd day of birth. Manifestations include irritability, poor feeding, convulsions, lethargy, opisthotonus, and a distinctive honey-like/burnt sugar urine odor. Patients may also exhibit stereotyped movements referred to as fencing or bicycling. If left untreated, patients die by the 10th day of birth from ketoacidosis and respiratory failure. The diagnosis of MSUD is confirmed by elevated urinary concentrations of branched-chain amino acid, hydroxyacid, and keto acid. In USA, newborn screening for MSUD is necessary for early treatment and prevention of complications. Management of MSUD involves thiamine supplementation (thiamine is a cofactor for alpha-keto acid dehydrogenase) and dietary restrictions, where patients are advised to avoid foods with branched-chain amino acids.<br/>
'''Educational Objective:''' Maple syrup urine disease (MSUD) is an autosomal recessive genetic disease characterized by the deficiency of alpha-keto acid dehydrogenase. Patients with MSUD often appear normal at birth. However, plasma concentrations of branched-chain amino acids (leucine, isoleucine, and valine) gradually increases, and patients initially manifest the disease during the 2nd or 3rd day or birth. The disease typically manifests with irritability, poor feeding, convulsions, lethargy, opisthotonus, and a distinctive honey-like/burnt sugar urine odor. Patients may exhibit stereotyped movements referred to as fencing or bicycling.<br/>
'''References:''' Strauss KA, Puffenberger EG, Morton DH. Maple Syrup Urine Disease. In: Pagon RA, Adam MP, Ardinger HH, et al., editors. GeneReviews®. Seattle (WA): University of Washington, Seattle; 2006. Available from: http://www.ncbi.nlm.nih.gov/books/NBK1319/<br>
First Aid 2014 page 112
Maple syrup urine disease (MSUD) is an autosomal recessive genetic disease characterized by the deficiency of alpha-keto acid dehydrogenase. Patients with MSUD often appear normal at birth. However, plasma concentrations of branched-chain amino acids (leucine, isoleucine, and valine) gradually increase, and the disease typically manifests during the 2nd or 3rd day of birth. Manifestations include irritability, poor feeding, convulsions, lethargy, opisthotonus, and a distinctive honey-like/burnt sugar urine odor. Patients may also exhibit stereotyped movements referred to as fencing or bicycling. If left untreated, patients die by the 10th day of birth from ketoacidosis and respiratory failure. The diagnosis of MSUD is confirmed by elevated urinary concentrations of branched-chain amino acid, hydroxyacid, and keto acid. In USA, newborn screening for MSUD is necessary for early treatment and prevention of complications. Management of MSUD involves thiamine supplementation (thiamine is a cofactor for alpha-keto acid dehydrogenase) and dietary restrictions, where patients are advised to avoid foods with branched-chain amino acids.<br/>
'''Educational Objective:''' Maple syrup urine disease (MSUD) is an autosomal recessive genetic disease characterized by the deficiency of alpha-keto acid dehydrogenase. Management of MSUD involves thiamine supplementation (thiamine is a cofactor for alpha-keto acid dehydrogenase) and dietary restrictions, where patients are advised to avoid foods with branched-chain amino acids.<br/>
'''References:''' Strauss KA, Puffenberger EG, Morton DH. Maple Syrup Urine Disease. In: Pagon RA, Adam MP, Ardinger HH, et al., editors. GeneReviews®. Seattle (WA): University of Washington, Seattle; 2006. Available from: http://www.ncbi.nlm.nih.gov/books/NBK1319/<br>
First Aid 2014 page 112 +
Non ST Segment Elevation Myocardial Infarction (NSTEMI) management is different in that there is no use of thrombolytic, heparin is used routinely, glycoprotein IIb/IIIa lower mortality particularly in those undergoing angioplasty.<br/>
'''Educational Objective:''' <br/>
'''References:''' +
The main difference between Internal mammary artery grafts and saphenous vein grafts is in the occlusion period. Vein grafts started to be occluded after 5 years, while internal mammary aretry grafts are often patent at 10 years. There is no difference in the medication needs between them.<br/>
'''Educational Objective:''' <br/>
'''References:''' +
The patient is exhibiting a type of defense mechanism called as Repression.<br/>
'''Educational Objective:''' <br/>
'''References:''' +
Amiodarone augment the anticoagulant effect caused by warfarin, and results in an increase in international normalized ratio (INR) and increased risk of bleeding. The enhanced anticoagulant effect that happens when amiodarone and warfarin are prescribed is due to amiodarone induced cytochrome P450 inhibition.
Coagulopathy might manifest as epistaxis, gingival bleeding, hematemesis, hematuria, hematochezia, menometrorrhagia, ecchymosis, petechial hemorrhages, intracranial hemorrhages, or bleeding that is disproportionate to the level of the injury
The effects of interaction with amiodarone do not peak until seven weeks after the initiation of concomitant therapy. A mean reduction of 35% in the dose of warfarin, and frequent follow up of INR and prothrombin time is needed when amiodarone used with warfarin.
'''Reference''': "The incidence, magnitude, and time course of the amiodarone-warfarin interaction.",journal = Arch Intern Med, volume = 148, issue = 8, month = Aug, year = 1988, PMID = 3401099.<br/>
'''Educational Objective:''' <br/>
'''References:''' +
Amiodarone is the ant arrhythmic agent of choice that is used to treat ventricular arrhythmias and atrial fibrillation. Amiodarone augment the anticoagulant effect caused by warfarin, and results in an increase in international normalized ratio (INR) and increased risk of bleeding.
The effects of interaction with amiodarone do not peak until seven weeks after the initiation of concomitant therapy. A mean reduction of 35% in the dose of warfarin, and frequent follow up of INR and prothrombin time is needed when amiodarone used with warfarin.
'''Reference''':"The incidence, magnitude, and time course of the amiodarone-warfarin interaction.", journal = Arch Intern Med, volume = 148, issue = 8, month = Aug, year = 1988, PMID = 3401099.<br/>
'''Educational Objective:''' <br/>
'''References:''' +