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#1 cause of alcoholic liver disease
chronic alcohol consumption
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most common hepatic manifestation
steatosis (fatty liver)
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fat accumulates in liver due to ethanol's interference with normal cellular metabolism
steatosis
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fat accumulation within hepatocytes leads to lysis and hepatocellular necrosis & inflammation
steatohepatitis (alcoholic hepatitis)
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- acetaldehyde stimulates synthesis of collagen w/in parenchyma of liver
- fibrous tissue is deposited around terminal hepatic venules and hepatocytes to cause obstruction of flow
chronic liver disease/cirrhosis
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mainstay of therapy for all stages of alcoholic liver disease
abstinence from alcohol
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causes fibrosis in chronic liver disease
synthesis of collagen
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types of ALD that are assoc'd with a possible genetic predisposition, and develop in only ~10-20% of alcoholics (2)
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risk factors for ALD (5)
- 1) amt of alcohol ingested (LT >30g/day)
- 2) drinking outside of meals/binging
- 3) type of alcohol (spirits)
- 4) women > men, AA & Hisp > Cauc
- 5) presence of HepC
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ratio of AST/ALT suggestive of alcohol abuse
2-3:1
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albumin lab result in ALD
DECREASED
(diminished hepatic synthesis of proteins, sequestration, malnutrition)
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PT or INR lab results in ALD
INCREASED
(decreased hepatic production of coagulation factors)
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bilirubin lab results in ALD
INCREASED
(decreased liver excretory capacity)
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3 medical conditions present in ALD
- 1) hyponatremia (inc ADH activity)
- 2) anemia (folate deficiency, typically megalycytic anemia)
- 3) thrombocytopenia (dec hepatic TPO prod)
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clinical manifestations of ALD (10)
- 1) jaundice
- 2) spider angioma
- 3) splenomegaly
- 4) caput medusae
- 5) white nails
- 6) finger clubbing
- 7) gynecomastia
- 8) hypogonadism
- 9) asterixis ("liver flap")
- 10) anorexia, weight loss, fatigue, muscle wasting
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small dilated blood vessels near the surface of the skin w/ radiating capillary branches
spider angioma, palmer erythema
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indicative clinical manifestation of hepatic encephalopathy
asterixis (liver flap)
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distended/engorged paraumbilical veins radiating from the umbilicus across the abdomen to join systemic veins
caput medusae
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low risk MDF score
 32
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low risk MELD score
18
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DF score for contraindication to prednisolone
>54
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first-line treatment of high risk AH
prednisolone
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when to use pentoxifylline
in high-risk AH, when there are steroid contraindications or signs of early renal failure
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prednisolone dosing for AH
- 40mg PO QD for 4 weeks
- taper off in 2 weeks
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pentoxifylline (PTX) treatment of AH
400mg PO TID x 4weeks
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MOA of PTX
PDE inhibitor that decreases TNF production
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Child-Pugh A score
<7 points
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Child-Pugh B score
7-9 points
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Child-Pugh C score
10-15 points
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MELD score for pts considered candidates for transplanation
 17
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Compensated Cirrhosis (2)
- 1) Child-Pugh A
- 2) median survival ~9years
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Decompensated Cirrhosis (3)
- 1) any: jaundice, encephalopathy, variceal hemmorhage, ascites
- 2) Child-Pugh B or C
- 3) 60% 5yr survival if abstain from EtOH vs 30%
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spectrum of neuropsychiatric sx due to liver disease (mainly a dx of exclusion)
hepatic encephalopathy
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recurrent encephalopathy
2 episodes w/in 1 year
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Mechanism for HE development
accumulation of gut-derived nitrogenous substances (mainly ammonia) that enter the CNS & cause alterations in neurotransmission
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what ammonia is normally converted to in the liver
urea
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how GI bleed can be a precipitating factor in increased nitrogen load
increased ammonia production through breakdown of Hb in gut
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how metabolic/electrolyte disturbances (alkalosis, hypokalemia) can be precipitating factors in increased nitrogen load
NH4+ -> NH3 conversion facilitation
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primary aim of HE therapy
reduction of blood ammonia levels
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possible drug therapies for HE (3)
- 1) lactulose
- 2) rifaximin
- 3) lactulose + rifaximin
(RARELY: neomycin or metronidazole)
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MOAs of lactulose in HE treatment (2)
- 1) degraded by colonic bacteria to acetic acid & lactic acid -> decrease colonic pH -> promotion of NH3 to NH4+ (ammonium ion)
- 2) acts as osmotic laxative
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acute dosing of lactulose for HE tx
30-45mL PO q1-2hrs until stool, then 15-30mL q8-12hr to maintain 2-3 soft stools/day
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MOA of rifaximin for HE tx
"non-absorbable" abx that eliminates urease-producing bacteria in colon which convert protein to ammonia
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acute dosing of rifaximin for HE tx
400mg PO TID or 550mg PO BID
(EXPENSIVE)
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1st-line tx for episodic HE and prevention of recurrent HE
lactulose
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extremely dilated sub-mucosal veins in the lower third of the esophagus
esophageal varices
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mechanism for development of esophageal varices
fibrosis -> portal hypertension -> inc collateral blood flow/backup into left gastric vein (innervates lower esophagus) -> varices
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when to screen for varices
any pt w/ a dx of cirrhosis
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primary prevention of variceal hemorrhage
non-selective  -blockers
(propranolol, nadolol, carvediol)
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MOA for non-selective -blockers w/ respect to variceal hemorrhage
- reduce portal flow & pressure by...
- 1) inhibiting 2-adrenergic Rs -> vasoconstriction of splanchnic capillaries/arterioles
- 2) inhibiting 1-adrenergic Rs -> dec cardiac output
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1st line option in med-large varices or pts that can't take non-selective beta-blockers
endoscopic variceal ligation
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endoscopic variceal ligation (EVL)
placement of rubber bands around the varices (q1-2weeks) until obliteration
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tx for acute variceal hemorrhage (3)
- 1) supportive fluids, blood transfusion
- 2) prophylaxis w/ antibiotics for 7 days
- 3) drug tx & endoscopic variceal ligation/sclerotherapy
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main drug used to treat variceal bleed
ocreotide (IV)
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ocreotide MOA
- decrease portal pressure & collateral flow by...
- 1) inhibited release of vasodilatory GI peptides (eg: glucagon)
- 2) local vasoconstrictor effects in splanchnic vasculature
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pathologic accumulation of free fluid w/in the peritoneal cavity
ascites
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most common complication of portal hypertension
ascites
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SAAG value that confirms ascites due to portal HTN
1.1 g/dL
(SAAG = serum-ascites albumin gradient = [albumin] in serum - [albumin] in ascitic fluid)
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#1 activation of the renin-angiotensin aldosterone system
ascites
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causes of moment of fluid out of vasculature into peritoneal cavity (3)
- 1) dec plasma oncotic P (low albumin)
- 2) inc capillary permeability
- 3) inc plasma hydrostatic P (Na/H2O retention)
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new-onset ascites drug treatment
- 1st line diuretic tx:
- spironolactone + furosemide (100:40)
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spironolactone MOA
acts by inhibiting aldosterone's effects on the distal tubule/cortical collecting duct, reducing Na+ & H2O retention
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furosemide MOA
acts on ascending limb of Henle to reduce Na+ & H2O retention
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when spironolactone should be used alone
only in the management of mild ascites
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when should furosemide be used alone for ascites management?
NEVER
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goal in random spot urine test during tx of ascites
urinary Na > urinary K
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therapeutic treatment used to relieve abdominal pain or respiratory difficulties when tense ascites is present
paracentesis (abdominal fluid tap)
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when paracentesis is appropriate (3)
- 1) when tense ascites is present
- 2) diuretic-resistant (refractory) ascites
- 3) to diagnose spontaneous bacterial peritonitis (SBP)
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infection in the peritoneal cavity in pt w/ ascites
spontaneous bacterial peritonitis (SBP)
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tx of SBP
PO or IV abx for 5days, then consider LT PO abx prophylaxis
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complication of cirrhosis due to thiamine (Vit. B1) deficiency
Wernicke-Korsakoff Syndrome
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how to treat Wernicke-Korsakoff Syndrome
- high dose IV thiamine for 3-5days
- (100mg PO QD for prevention)
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progression of Wernicke-Korsakoff Syndrome
Wernicke Encephalopathy (WE) -> continued thiamine deficiency -> Korsakoff Dementia (KD)
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bleeding from an esophageal varice into the esophagus, or bleeding of collateral varices into the stomach
variceal hemorrhage
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