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| | ==Physical examination== |
| | ==References== |
| | {{reflist|2}} |
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| | {{WH}} |
| | {{WS}} |
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| ==Physical Examination== | | ==References== |
| | {{Reflist|2}} |
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| *Physical examination of patients with [disease name] is usually remarkable for:[finding 1], [finding 2], and [finding 3].
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| *The presence of [finding(s)] on physical examination is diagnostic of [disease name].
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| *The presence of [finding(s)] on physical examination is highly suggestive of [disease name].
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| ===Appearance of the Patient=== | | ===Pathophysiology prev=== |
| *Patients with [disease name] usually appear [general appearance].
| | <div style="-webkit-user-select: none;"> |
| | {| class="infobox" style="position: fixed; top: 65%; right: 10px; margin: 0 0 0 0; border: 0; float: right;" |
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| | | {{#ev:youtube|https://https://www.youtube.com/watch?v=5szNmKtyBW4|350}} |
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| | |} |
| | __NOTOC__ |
| | {{Cirrhosis}} |
| | {{CMG}} {{AE}} |
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| ===Vital Signs===
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| *High-grade / low-grade fever
| | ===Pathophysiology prev=== |
| *[[Hypothermia]] / hyperthermia may be present
| | <div style="-webkit-user-select: none;"> |
| *[[Tachycardia]] with regular pulse or (ir)regularly irregular pulse
| | {| class="infobox" style="position: fixed; top: 65%; right: 10px; margin: 0 0 0 0; border: 0; float: right;" |
| *[[Bradycardia]] with regular pulse or (ir)regularly irregular pulse
| | |- |
| *Tachypnea / bradypnea
| | | {{#ev:youtube|https://https://www.youtube.com/watch?v=5szNmKtyBW4|350}} |
| *Kussmal respirations may be present in _____ (advanced disease state)
| | |- |
| *Weak/bounding pulse / pulsus alternans / paradoxical pulse / asymmetric pulse
| | |} |
| *High/low blood pressure with normal pulse pressure / [[wide pulse pressure]] / [[narrow pulse pressure]]
| | __NOTOC__ |
| | {{Cirrhosis}} |
| | {{CMG}} {{AE}} |
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| ===Skin=== | | == History and Symptoms == |
| *[[Cyanosis]]
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| *[[Jaundice]]
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| *[[Pallor]]
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| *Bruises
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| <gallery widths=150px>
| | * History should include: |
| | ** Appearance of bowel movements |
| | ** Travel history |
| | ** Associated symptoms |
| | ** Immune status |
| | ** Woodland exposure |
| | ==References== |
| | {{reflist|2}} |
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| UploadedImage-01.jpg | Description {{dermref}}
| | {{WH}} |
| UploadedImage-02.jpg | Description {{dermref}}
| | {{WS}} |
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| </gallery>
| | ==Other Imaging Findings== |
| | * [[Endoscopy]] |
| | * [[Barium enema]] |
| | * [[Colonoscopy]] |
| | * [[Sigmoidoscopy]] |
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| ===HEENT=== | | ==Other diagnostic studies== |
| * Abnormalities of the head/hair may include ___
| | == Other Diagnostic Studies == |
| * Evidence of trauma
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| * Icteric sclera
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| * [[Nystagmus]]
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| * Extra-ocular movements may be abnormal
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| *Pupils non-reactive to light / non-reactive to accomodation / non-reactive to neither light nor accomodation
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| *Ophthalmoscopic exam may be abnormal with findings of ___
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| * Hearing acuity may be reduced
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| *[[Weber test]] may be abnormal (Note: A positive Weber test is considered a normal finding / A negative Weber test is considered an abnormal finding. To avoid confusion, you may write "abnormal Weber test".)
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| *[[Rinne test]] may be positive (Note: A positive Rinne test is considered a normal finding / A negative Rinne test is considered an abnormal finding. To avoid confusion, you may write "abnormal Rinne test".)
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| * [[Exudate]] from the ear canal
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| * Tenderness upon palpation of the ear pinnae / tragus (anterior to ear canal)
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| *Inflamed nares / congested nares
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| * [[Purulent]] exudate from the nares
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| * Facial tenderness
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| * Erythematous throat with/without tonsillar swelling, exudates, and/or petechiae
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| ===Neck===
| | * Breath hydrogen test |
| *[[Jugular venous distension]] | |
| *[[Carotid bruits]] may be auscultated unilaterally/bilaterally using the bell/diaphragm of the otoscope
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| *[[Lymphadenopathy]] (describe location, size, tenderness, mobility, and symmetry)
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| *[[Thyromegaly]] / thyroid nodules
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| *[[Hepatojugular reflux]]
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| ===Lungs===
| | * [[HIV test]]ing for those patients suspected of having HIV |
| * Asymmetric chest expansion / Decreased chest expansion | |
| *Lungs are hypo/hyperresonant
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| *Fine/coarse [[crackles]] upon auscultation of the lung bases/apices unilaterally/bilaterally
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| *Rhonchi
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| *Vesicular breath sounds / Distant breath sounds
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| *Expiratory/inspiratory wheezing with normal / delayed expiratory phase
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| *[[Wheezing]] may be present
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| *[[Egophony]] present/absent
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| *[[Bronchophony]] present/absent
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| *Normal/reduced [[tactile fremitus]]
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| ===Heart=== | | == |
| *Chest tenderness upon palpation
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| *PMI within 2 cm of the sternum (PMI) / Displaced point of maximal impulse (PMI) suggestive of ____
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| *[[Heave]] / [[thrill]]
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| *[[Friction rub]]
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| *[[Heart sounds#First heart tone S1, the "lub"(components M1 and T1)|S1]]
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| *[[Heart sounds#Second heart tone S2 the "dub"(components A2 and P2)|S2]]
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| *[[Heart sounds#Third heart sound S3|S3]]
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| *[[Heart sounds#Fourth heart sound S4|S4]]
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| *[[Heart sounds#Summation Gallop|Gallops]]
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| *A high/low grade early/late [[systolic murmur]] / [[diastolic murmur]] best heard at the base/apex/(specific valve region) may be heard using the bell/diaphgram of the otoscope
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| ===Abdomen=== | | ==Overview== |
| *[[Abdominal distention]]
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| *[[Abdominal tenderness]] in the right/left upper/lower abdominal quadrant
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| *[[Rebound tenderness]] (positive Blumberg sign)
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| *A palpable abdominal mass in the right/left upper/lower abdominal quadrant
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| *Guarding may be present
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| *[[Hepatomegaly]] / [[splenomegaly]] / [[hepatosplenomegaly]]
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| *Additional findings, such as obturator test, psoas test, McBurney point test, Murphy test
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| ===Back=== | | ==References== |
| *Point tenderness over __ vertebrae (e.g. L3-L4)
| | {{reflist|2}} |
| *Sacral edema
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| *Costovertebral angle tenderness bilaterally/unilaterally
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| *Buffalo hump
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| ===Genitourinary===
| | {{WH}} |
| *A pelvic/adnexal mass may be palpated
| | {{WS}} |
| *Inflamed mucosa
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| *Clear/(color), foul-smelling/odorless penile/vaginal discharge
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| ===Neuromuscular=== | | ===Pathophysiology prev=== |
| *Patient is usually oriented to persons, place, and time
| | <div style="-webkit-user-select: none;"> |
| * Altered mental status
| | {| class="infobox" style="position: fixed; top: 65%; right: 10px; margin: 0 0 0 0; border: 0; float: right;" |
| * Glasgow coma scale is ___ / 15
| | |- |
| * Clonus may be present
| | | {{#ev:youtube|https://https://www.youtube.com/watch?v=5szNmKtyBW4|350}} |
| * Hyperreflexia / hyporeflexia / areflexia
| | |- |
| * Positive (abnormal) Babinski / plantar reflex unilaterally/bilaterally
| | |} |
| * Muscle rigidity
| | __NOTOC__ |
| * Proximal/distal muscle weakness unilaterally/bilaterally
| | {{Cirrhosis}} |
| * ____ (finding) suggestive of cranial nerve ___ (roman numerical) deficit (e.g. Dilated pupils suggestive of CN III deficit)
| | {{CMG}} {{AE}} |
| *Unilateral/bilateral upper/lower extremity weakness
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| *Unilateral/bilateral sensory loss in the upper/lower extremity
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| *Positive straight leg raise test
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| *Abnormal gait (describe gait: e.g. ataxic (cerebellar) gait / steppage gait / waddling gait / choeiform gait / Parkinsonian gait / sensory gait)
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| *Positive/negative Trendelenburg sign
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| *Unilateral/bilateral tremor (describe tremor, e.g. at rest, pill-rolling)
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| *Normal finger-to-nose test / Dysmetria
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| *Absent/present dysdiadochokinesia (palm tapping test)
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| | |
| ===Extremities=== | |
| *[[Clubbing]]
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| *[[Cyanosis]]
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| *Pitting/non-pitting [[edema]] of the upper/lower extremities
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| *Muscle atrophy
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| *Fasciculations in the upper/lower extremity
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| Head to toe:
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| jaundice
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| spider angiomata
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| gynecomastia
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| ascites
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| splenomegaly
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| palmar erythema
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| digital clubbing
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| asterixis.
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| Decreasing blood pressure — normotensive or hypotensive. The decrease in mean arterial pressure contributes to the development of hepatorenal syndrome and is an important predictor of survival.
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| Skin findings — jaundice
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| spider angiomata
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| Jaundice is a yellow coloring of the skin and mucous membranes that results from increased serum bilirubin.
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| It is usually not detectable until the bilirubin is greater than 2 to 3 mg/dL. Hyperbilirubinemia may also cause the urine to appear dark or "cola" colored.
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| Head and neck findings — parotid gland enlargement and fetor hepaticus.
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| Chest findings — Gynecomastia
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| Men may also develop other features reflecting feminization,
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| loss of chest or axillary hair
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| inversion of the normal male pubic hair pattern
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| Gynecomastia is defined histologically as a benign proliferation of the glandular tissue of the male breast and clinically by the presence of a rubbery or firm mass extending concentrically from the nipple(s).
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| Abdominal findings — Findings on abdominal examination include hepatomegaly
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| Splenomegaly
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| Ascites
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| caput medusae
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| Cruveilhier-Baumgarten murmur.
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| Ascites —
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| Physical findings in patients with ascites include :
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| abdominal distension
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| a fluid wave
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| flank dullness to percussion.
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| approximately 1500 mL of fluid had to be present for flank dullness to be detected.
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| Hepatomegaly — The cirrhotic liver may be enlarged, normal sized, or small.
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| Splenomegaly — Splenomegaly is common, especially in patients with cirrhosis from nonalcoholic etiologies.
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| Caput medusae —
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| Cruveilhier-Baumgarten murmur — The Cruveilhier-Baumgarten murmur is a venous hum that may be auscultated in patients with portal hypertension. It results from collateral connections between the portal system and the remnant of the umbilical vein. It is best appreciated when the stethoscope is placed over the epigastrium. The murmur is augmented by maneuvers that increase intraabdominal pressure, such as the Valsalva maneuver, and diminished by applying pressure on the skin above the umbilicus
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| Genitourinary findings — testicular atrophy
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| Extremity findings —
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| palmar erythema on the thenar and hypothenar eminences,
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| nail changes: Muehrcke nails: paired horizontal white bands separated by normal color due to hypoalbuminemia
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| Terry nails, the proximal two-thirds of the nail plate appears white, whereas the distal one-third is red due to hypoalbuminemia
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| Clubbing: the angle between the nail plate and proximal nail fold is greater than 180 degrees.
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| severe, the distal finger has a "drum stick" appearance.
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| hypertrophic osteoarthropathy
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| Dupuytren's contracture causes flexion deformities of the fingers .
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| Neurologic findings — Asterixis (bilateral but asynchronous flapping motions of outstretched, dorsiflexed hands) is seen in patients with hepatic encephalopathy.
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| ==History==
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| === Psychosocial history ===
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| *Past history of abuse
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| === Past Medical history ===
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| *History of
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| === Menstrual history === | | ==Video codes== |
| *History of
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| === Family history === | | ===Normal video=== |
| *[[Family history]] of:
| | {{#ev:youtube|x6e9Pk6inYI}} |
| **
| | {{#ev:youtube|4uSSvD1BAHg}} |
| | {{#ev:youtube|PQXb5D-5UZw}} |
| | {{#ev:youtube|UVJYQlUm2A8}} |
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| === Medication history === | | ===Video in table=== |
| *History of [[medication]] use should be obtained as many [[:Category:Drugs|drugs]] such as [[Opioid|opioids]] cause [[constipation]] as a side effect.
| | <div style="width:350px">{{#ev:youtube|5ucSlgqGAno}}</div> |
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| ===Causes=== | | ===Floating video=== |
| {| class="wikitable"
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| ! style="background:#4479BA; color: #FFFFFF;" align="center" + |Drugs and Toxins
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| ! style="background:#4479BA; color: #FFFFFF;" align="center" + |Infections
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| ! style="background:#4479BA; color: #FFFFFF;" align="center" + |Autoimmune
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| ! style="background:#4479BA; color: #FFFFFF;" align="center" + |Metabolic
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| ! style="background:#4479BA; color: #FFFFFF;" align="center" + |Biliary obstruction(Secondary bilary cirrhosis)
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| ! style="background:#4479BA; color: #FFFFFF;" align="center" + |Vascular
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| ! style="background:#4479BA; color: #FFFFFF;" align="center" + |Miscellaneous
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| |-
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| |Alcohol
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| |Hepatitis B
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| |Primary Biliary Cirrhosis
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| |Wilson's disease
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| |Cystic fibrosis
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| |Chronic RHF
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| |Sarcoidosis
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| |-
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| |Methotrexate
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| |Hepatitis C
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| |Autoimmune hepatitis
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| |Hemochromatosis
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| |Biliary atresia
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| |Budd-Chiari syndrome
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| |Intestinal
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|
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| bypass operations for obesity
| | {| class="infobox mw-collapsible" id="floatvideo" style="position: fixed; top: 65%; width:361px; right: 10px; margin: 0 0 0 0; border: 0; float: right;" |
| | | Title |
| |- | | |- |
| |Isoniazid
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| |Schistosoma japonicum
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| |Primary Sclerosing Cholangitis
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| |Alpha-1 antitrypsin deficiency
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| |Bile duct strictures
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| |Veno-occlusive disease
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| |Cryptogenic: unknown
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| |- | | |- |
| |Methyldopa | | | {{#ev:youtube|https://https://www.youtube.com/watch?v=ypYI_lmLD7g|350}} |
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| |Porphyria
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| |Gallstones
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| |- | | |- |
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| |Glycogen storage diseases (such as Galactosaemia, Abetalipoproteinaemia)
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| |} | | |} |
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| ===Cirrhosis=== | | ===Redirect=== |
| | #REDIRECT[[Esophageal web]] |
| | |
| | ===synonym website=== |
| | https://mq.b2i.sg/snow-owl/#!terminology/snomed/10743008 |
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| Pathophysiology <ref name="pmid7932316">{{cite journal |vauthors=Arthur MJ, Iredale JP |title=Hepatic lipocytes, TIMP-1 and liver fibrosis |journal=J R Coll Physicians Lond |volume=28 |issue=3 |pages=200–8 |year=1994 |pmid=7932316 |doi= |url=}}</ref><ref name="pmid8502273">{{cite journal |vauthors=Friedman SL |title=Seminars in medicine of the Beth Israel Hospital, Boston. The cellular basis of hepatic fibrosis. Mechanisms and treatment strategies |journal=N. Engl. J. Med. |volume=328 |issue=25 |pages=1828–35 |year=1993 |pmid=8502273 |doi=10.1056/NEJM199306243282508 |url=}}</ref><ref name="pmid8682489">{{cite journal |vauthors=Iredale JP |title=Matrix turnover in fibrogenesis |journal=Hepatogastroenterology |volume=43 |issue=7 |pages=56–71 |year=1996 |pmid=8682489 |doi= |url=}}</ref><ref name="pmid7959178">{{cite journal |vauthors=Gressner AM |title=Perisinusoidal lipocytes and fibrogenesis |journal=Gut |volume=35 |issue=10 |pages=1331–3 |year=1994 |pmid=7959178 |pmc=1374996 |doi= |url=}}</ref><ref name="pmid17332881">{{cite journal |vauthors=Iredale JP |title=Models of liver fibrosis: exploring the dynamic nature of inflammation and repair in a solid organ |journal=J. Clin. Invest. |volume=117 |issue=3 |pages=539–48 |year=2007 |pmid=17332881 |pmc=1804370 |doi=10.1172/JCI30542 |url=}}</ref><ref name="pmid11984538">{{cite journal |vauthors=Arthur MJ |title=Reversibility of liver fibrosis and cirrhosis following treatment for hepatitis C |journal=Gastroenterology |volume=122 |issue=5 |pages=1525–8 |year=2002 |pmid=11984538 |doi= |url=}}</ref>
| | ===Image=== |
| * When an injured issue is replaced by a collagenous scar, it is termed as fibrosis.
| | [[Image: Normal versus Abnormal Barium study of esophagus.jpg|thumb|left|200px|Normal versus Abnormal Barium study of esophagus with varices]] |
| * When fibrosis of the liver reaches an advanced stage where distortion of the hepatic vasculature also occurs, it is termed as cirrhosis of the liver.
| |
| * The cellular mechanisms responsible for cirrhosis are similar regardless of the type of initial insult and site of injury within the liver lobule.
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| * Viral hepatitis involves the periportal region, whereas involvement in alcoholic liver disease is largely pericentral.
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| * If the damage progresses, panlobular cirrhosis may result.
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| * Cirrhosis involves the following steps: <ref name="pmid7737629">{{cite journal |vauthors=Wanless IR, Wong F, Blendis LM, Greig P, Heathcote EJ, Levy G |title=Hepatic and portal vein thrombosis in cirrhosis: possible role in development of parenchymal extinction and portal hypertension |journal=Hepatology |volume=21 |issue=5 |pages=1238–47 |year=1995 |pmid=7737629 |doi= |url=}}</ref>
| |
| ** Inflammation
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| ** Hepatic stellate cell activation
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| ** Angiogenesis
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| ** Fibrogenesis
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| * Kupffer cells are hepatic macrophages responsible for Hepatic Stellate cell activation during injury.
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| * The hepatic stellate cell (also known as the perisinusoidal cell or Ito cell) plays a key role in the pathogenesis of liver fibrosis/cirrhosis.
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| * Hepatic stellate cells(HSC) are usually located in the subendothelial space of Disse and become activated to a myofibroblast-like phenotype in areas of liver injury.
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| * Collagen and non collagenous matrix proteins responsible for fibrosis are produced by the activated Hepatic Stellate Cells(HSC).
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| * Hepatocyte damage causes the release of lipid peroxidases from injured cell membranes leading to necrosis of parenchymal cells.
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| * Activated HSC produce numerous cytokines and their receptors, such as PDGF and TGF-f31 which are responsible for fibrogenesis.
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| * The matrix formed due to HSC activation is deposited in the space of Disse and leads to loss of fenestrations of endothelial cells, which is a process called capillarization.
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| * Cirrhosis leads to hepatic microvascular changes characterised by <ref name="pmid19157625">{{cite journal |vauthors=Fernández M, Semela D, Bruix J, Colle I, Pinzani M, Bosch J |title=Angiogenesis in liver disease |journal=J. Hepatol. |volume=50 |issue=3 |pages=604–20 |year=2009 |pmid=19157625 |doi=10.1016/j.jhep.2008.12.011 |url=}}</ref>
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| ** formation of intra hepatic shunts (due to angiogenesis and loss of parenchymal cells)
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| ** hepatic endothelial dysfunction
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| * The endothelial dysfunction is characterised by <ref name="pmid22504334">{{cite journal |vauthors=García-Pagán JC, Gracia-Sancho J, Bosch J |title=Functional aspects on the pathophysiology of portal hypertension in cirrhosis |journal=J. Hepatol. |volume=57 |issue=2 |pages=458–61 |year=2012 |pmid=22504334 |doi=10.1016/j.jhep.2012.03.007 |url=}}</ref>
| |
| ** insufficient release of vasodilators, such as nitric oxide due to oxidative stress
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| ** increased production of vasoconstrictors (mainly adrenergic stimulation and activation of endothelins and RAAS)
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| * Fibrosis eventually leads to formation of septae that grossly distort the liver architecture which includes both the liver parenchyma and the vasculature. A cirrhotic liver compromises hepatic sinusoidal exchange by shunting arterial and portal blood directly into the central veins (hepatic outflow). Vascularized fibrous septa connect central veins with portal tracts leading to islands of hepatocytes surrounded by fibrous bands without central veins.<ref name="pmid18328931">{{cite journal |vauthors=Schuppan D, Afdhal NH |title=Liver cirrhosis |journal=Lancet |volume=371 |issue=9615 |pages=838–51 |year=2008 |pmid=18328931 |pmc=2271178 |doi=10.1016/S0140-6736(08)60383-9 |url=}}</ref><ref name="pmid15094237">{{cite journal |vauthors=Desmet VJ, Roskams T |title=Cirrhosis reversal: a duel between dogma and myth |journal=J. Hepatol. |volume=40 |issue=5 |pages=860–7 |year=2004 |pmid=15094237 |doi=10.1016/j.jhep.2004.03.007 |url=}}</ref><ref name="pmid11079009">{{cite journal |vauthors=Wanless IR, Nakashima E, Sherman M |title=Regression of human cirrhosis. Morphologic features and the genesis of incomplete septal cirrhosis |journal=Arch. Pathol. Lab. Med. |volume=124 |issue=11 |pages=1599–607 |year=2000 |pmid=11079009 |doi=10.1043/0003-9985(2000)124<1599:ROHC>2.0.CO;2 |url=}}</ref>
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| * The formation of fibrotic bands is accompanied by regenerative nodule formation in the hepatic parenchyma.
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| * Advancement of cirrhosis may lead to parenchymal dysfunction and development of portal hypertension.
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| * Portal HTN results from the combination of the following:
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| ** Structural disturbances associated with advanced liver disease account for 70% of total hepatic vascular resistance.
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| ** Functional abnormalities such as endothelial dysfunction and increased hepatic vascular tone account for 30% of total hepatic vascular resistance.
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|
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| Pathogenesis of Cirrhosis due to Alcohol:
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| * More than 66 percent of all American adults consume alcohol.
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| * Cirrhosis due to alcohol accounts for approximately forty percent of mortality rates due to cirrhosis.
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| * Mechanisms of alcohol-induced damage include:
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| ** Impaired protein synthesis, secretion, glycosylation
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| * Ethanol intake leads to elevated accumulation of intracellular triglycerides by:
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| ** Lipoprotein secretion
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| ** Decreased fatty acid oxidation
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| ** Increased fatty acid uptake
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| * Alcohol is converted by Alcohol dehydrogenase to acetaldehyde.
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| * Due to the high reactivity of acetaldehyde, it forms acetaldehyde-protein adducts which cause damage to cells by:
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| ** Trafficking of hepatic proteins
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| ** Interrupting microtubule formation
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| ** Interfering with enzyme activities
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| * Damage of hepatocytes leads to the formation of reactive oxygen species that activate Kupffer cells.<ref name="pmid11984538">{{cite journal |vauthors=Arthur MJ |title=Reversibility of liver fibrosis and cirrhosis following treatment for hepatitis C |journal=Gastroenterology |volume=122 |issue=5 |pages=1525–8 |year=2002 |pmid=11984538 |doi= |url=}}</ref>
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| *Kupffer cell activation leads to the production of profibrogenic cytokines that stimulates stellate cells.
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| *Stellate cell activation leads to the production of extracellular matrix and collagen.
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| * Portal triads develop connections with central veins due to connective tissue formation in pericentral and periportal zones, leading to the formation of regenerative nodules.
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| * Shrinkage of the liver occurs over years due to repeated insults that lead to:
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| ** Loss of hepatocytes
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| ** Increased production and deposition of collagen
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|
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|
| | ===Image to the right=== |
| | {| style="float: right; width: 350px;" |
| | | [[Image:Coxiella burnetii.JPG|right|400px|C. burnetii, the Q fever causing agent]] |
| | |} |
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| Pathology
| | ===Image and text to the right=== |
| * There are four stages of Cirrhosis as it progresses:
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| ** Chronic nonsuppurative destructive cholangitis - inflammation and necrosis of portal tracts with lymphocyte infiltration leading to the destruction of the bile ducts.
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| ** Development of biliary stasis and fibrosis
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| *Periportal fibrosis progresses to bridging fibrosis
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| *Increased proliferation of smaller bile ductules leading to regenerative nodule formation.
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| ===Classification===
| | <figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline>[[File:Global distribution of leptospirosis.jpg|577x577px]]</figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline> Recent out break of leptospirosis is reported in Bronx, New York and found 3 cases in the months January and February, 2017. |
| __NOTOC__
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| {{Cirrhosis}}
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| {{CMG}} {{AE}} {{CP}}
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| ==Overview== | | ===Gallery=== |
| Cirrhosis of the [[liver]] can be classified using two methods; classification based on [[etiology]], and classification based on [[morphology]]. Currently, classifying cirrhosis based on morphology is not used, as it requires an invasive procedure to examine the gross appearance of the liver, and it provides little diagnostic value. Classifying cirrhosis according to etiology is a more accepted form of classification, as it can be attained through non-invasive laboratory testing, and has a higher diagnostic value.
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| ==Classification Based on Etiology== | | <gallery widths="250px"> |
| Cirrhosis can be classified by its etiology. This is the most widely accepted method of [[classification]].
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| ===Alcoholic Cirrhosis===
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| This is the most common cause of cirrhosis, and is caused by continuous and prolonged [[alcohol abuse]]. The American Academy of Family Physicians estimate that 60-70 percent of all cases of cirrhosis are a result of [[alcohol abuse]].
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| ===Post-Necrotic Cirrhosis===
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| This type of cirrhosis occurs after a massive event causes liver [[cell death]]. [[Viral hepatitis]] is the most common cause for this type of cirrhosis. Agents that are [[toxic]] to the liver can also cause this type of cirrhosis, as well as certain types of [[carcinomas]].
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| ===Biliary Cirrhosis===
| | Pancreatic insulinoma histology 2.JPG|Histopathology of a pancreatic endocrine tumor (insulinoma). ''Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas''<ref name=aaa> Neuroendocrine tumor of the pancreas. Libre Pathology. http://librepathology.org/wiki/index.php/Neuroendocrine_tumour_of_the_pancreas</ref> |
| This type of cirrhosis results from any diseases that cause [[biliary obstruction]]. There is usually a blockage in the [[bile duct]] and there may also be [[inflammation]]. The excess [[bile]] in the liver causes tissue destruction. It commonly results in [[jaundice]].
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| ===Cardiac Cirrhosis===
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| This type of cirrhosis is caused by [[congestive heart failure]] causing poor circulation of [[oxygenated blood]] to the liver. This results in liver cell death, and the subsequent replacement of dead cells by [[fibrous tissue]].
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| ===Genetic Disorder===
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| This is when the cirrhosis is caused by a [[genetic disorder]] such as [[hemochromatosis]], [[Wilson's disease]], or [[alpha-1 antitrypsin deficiency]].
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| ===Malnutrition===
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| This category contains cirrhosis caused by various forms of [[malnutrition]], particularly chronic starvation.
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| ==Classification Based on Morphology==
| | Pancreatic insulinoma histopathology 3.JPG|Histopathology of a pancreatic endocrine tumor (insulinoma). Chromogranin A immunostain. ''Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas''<ref name=aaa> Neuroendocrine tumour of the pancreas. Libre Pathology. http://librepathology.org/wiki/index.php/Neuroendocrine_tumour_of_the_pancreas</ref> |
| [[Cirrhosis]] has historically been classified upon the [[Nodule (medicine)|nodular]] morphology that is seen on upon the gross appearance of the [[liver]]. Accurate assessment of the [[liver]] morphology can only be obtained through [[surgery]], [[biopsy]], or [[autopsy]], therefore more recently, more non-invasive means of classifying and determining the causes of [[cirrhosis]] are used.
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| {| class="wikitable"
| | Pancreatic insulinoma histology 4.JPG|Histopathology of a pancreatic endocrine tumor (insulinoma). Insulin immunostain. ''Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas''<ref name=aaa> Neuroendocrine tumour of the pancreas. Libre Pathology. http://librepathology.org/wiki/index.php/Neuroendocrine_tumour_of_the_pancreas</ref> |
| ! style="background:#4479BA; color: #FFFFFF;" |Micronodular
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| ! style="background:#4479BA; color: #FFFFFF;" |Macronodular
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| ! style="background:#4479BA; color: #FFFFFF;" |Mixed
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| |-
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| |Micronodular [[cirrhosis]] is characterized by [[Nodule (medicine)|nodules]] that are less than 3mm in diameter
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| |Macronodular [[cirrhosis]] is characterized by [[Nodule (medicine)|nodules]] that are more than 3mm in diameter
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| |Micronodular [[cirrhosis]] can often progress into macronodular [[Cirrhosis|cirrhosis.]] During this transformation, a mixed form of [[cirrhosis]] may be seen.<ref name="pmid6629323">{{cite journal| author=Fauerholdt L, Schlichting P, Christensen E, Poulsen H, Tygstrup N, Juhl E| title=Conversion of micronodular cirrhosis into macronodular cirrhosis. | journal=Hepatology | year= 1983 | volume= 3 | issue= 6 | pages= 928-31 | pmid=6629323 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6629323 }} </ref>
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| |Causes:
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| *[[Alcohol]]
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| *[[Hemochromatosis]]
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| *[[Cholestasis|Cholestatic]] causes of [[cirrhosis]]
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| *Hepatic venous outflow obstruction
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| *[[Nutrition|Nutritional]] causes of [[cirrhosis]]
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| Causes:
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| *Chronic [[viral hepatitis]]
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| *[[Hemochromatosis]]
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| *[[Wilson's disease]]
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| *Post-necrotic [[cirrhosis]]
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| |Mixed nodular [[cirrhosis]] is also seen in Indian childhood [[cirrhosis]]. <ref name="pmid47794">{{cite journal| author=Nayak NC, Ramalingaswami V| title=Indian childhood cirrhosis. | journal=Clin Gastroenterol | year= 1975 | volume= 4 | issue= 2 | pages= 333-49 | pmid=47794 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=47794 }} </ref>
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| |}
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| | </gallery> |
| ==References== | | ==References== |
| {{Reflist|2}} | | {{Reflist|2}} |
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| [[Category:Gastroenterology]]
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| [[Category:Hepatology]]
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| [[Category:Disease]]
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| {{WS}} | | {{WS}} |
| {{WH}} | | {{WH}} |
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| REFERENCES | | REFERENCES |
| <references /> | | <references /> |
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| | [[Category:Gastroenterology]] |
| | [[Category:Needs overview]] |
| | [[Category:Hepatology]] |
| | [[Category:Disease]] |
</figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline> Recent out break of leptospirosis is reported in Bronx, New York and found 3 cases in the months January and February, 2017.
![Histopathology of a pancreatic endocrine tumor (insulinoma). Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[1]](/images/2/2f/Pancreatic_insulinoma_histology_2.JPG)
![Histopathology of a pancreatic endocrine tumor (insulinoma). Chromogranin A immunostain. Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[1]](/images/a/a3/Pancreatic_insulinoma_histopathology_3.JPG)
![Histopathology of a pancreatic endocrine tumor (insulinoma). Insulin immunostain. Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[1]](/images/d/d5/Pancreatic_insulinoma_histology_4.JPG)
![Histopathology of a pancreatic endocrine tumor (insulinoma). Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[1]](/index.php/File:Pancreatic_insulinoma_histology_2.JPG)
![Histopathology of a pancreatic endocrine tumor (insulinoma). Chromogranin A immunostain. Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[1]](/index.php/File:Pancreatic_insulinoma_histopathology_3.JPG)
![Histopathology of a pancreatic endocrine tumor (insulinoma). Insulin immunostain. Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[1]](/index.php/File:Pancreatic_insulinoma_histology_4.JPG)