liver!! Flashcards
fatty liver patho
1st stage of liver disease d/t alcohol consumption - >30% of hepatocytes w/ TG accumulation
**reversible quickly w/ abstinence! no fibrosis / necrosis!
fatty liver pres
- most asx
- may have vague malaise, fatigue, RUQ pain
fatty liver labs
- w/ alcohol, expect AST:ALT 2:1 or more
- *mild elevation - AST rarely >300-500 and ALT rarely >300!
- can have normal labs!!
NAFL patho
fatty liver due to metabolic complications - a/w insulin resistance w/ increased lipolysis, TG accum in liver and FA uptake!
***does NOT progress and NOT a/w sig inflammation!
NASH patho
progressive NAFLD w/ >50% of hepatocytes w/ TG accumulation with inflammation and fibrosis!
*progresses to cirrhosis (1-5%) and hepatocellular carcinoma!
RF NAFL & NASH
- insulin resistance, metabolic syndrome, diabetes, obesity, dys/hyperlipidemia, hypothyroidism
- can see NAFLD acutely w/ pregnancy - confusion, RUQ pain, jaundice - must deliver to correct!
when to suspect NAFLD and NASH…
Asx patient with elevated AST and ALT, espeically w/ diabetes / obesity / hyperlipidemia!
workup for NAFLD
- CMP to see elevated LFT
- AST < ALT = NONALCOHOLIC!
- AST: ALT = 2:1 or more…ALCOHOLIC!
- check RF - lipids, glucose, AIC and check meds (methotrexate, glucocorticoids, tetracyclines, tamoxifen)
- acute changes: LDH, AST, ALT, lactate
- chronic changes: PT, bilirubin, albumin - R/o hepatitis!! w/ serology!
- r/o autoimmune w/ ANA, gammaglobulin, antismooth muscle antibody
- r/o hemochromatosis w/ iron studies!
- often have elevated alk phos and ferritin
- u/s is best imaging
- biopsy only for severe - only way to differeentiate NAFLD AND NASH
NAFLD diagnostic criteria
- evidence (imaging / histology) of steatosis
- r/o alcohol consumption
- r/o other causes of steatosis
labs c/w alcoholic liver dz
- ast: ast >2 and moderately increased (hundreds)
- increased ggt
- macrocytic anemia
- increased carbohydrate-deficient transferrin
* always check bili, alk phos and GGT, albumin and coag tests
diagnosis of alcoholic liver dz…
- consistent hx, PE findings
1. labs -elevated ast: alt 2:1 or more, elevated ggt, macro anemia
2. r/o hepatitis, hemochromatosis, autoimmune
3. steatosis on imaging: u/s (cannot distinguish from nonalcoholic steatosis!) - may need biopsy if unclear after imaging
distinguishing NAFL and NASH…
LIVER BIOPSY then calculate NAFLD score -
<3 = NAFL
3-4 = borderline NASH
5+ = NASH
NAFLD management
- WEIGHT LOSS!!! most beneficial!
- control other CVD risk factors - statin for lipids, diabetes
- vitamin E in non-diabetics
- avoid alcohol!
- monitor labs q 1 year and u/s q 1 year
metabolic syndrome - criteria
3 or more of:
- blood glucose 100+ or on tx
- bp 130/85 or more or on antihypertensives
- triglycerids of 150 or more or on tx
- hdl < 50 women
- waist circum 102cm or more in men or 88 cm or more in women
cirrhosis! patho and causes
chronic liver dz/ w/ fibrosis and nodules, most due to alcohol and hep c/b
- irreversible!
- 2 major effects:
- portal HTN: ascites, edema, caput medusa, hemorroids, splenomegaly, varicosities
- biochem changes w/ hepatocyte death: low albumin, increased conjugated bili, abnl coags
- always look at meds, family hx (think about alpha 1 antitrypsin def, hemochromatosis, wilsons..)
cirrhosis - whats used to classify severity?
child classification - a (best) and c (worst)
- assesses ascites, albumin, bili, encephalopathy and nutrition status
cirrhosis pres
- lots asx
- nonspecific malaise, fatigue, RUQ discomfort, anorexia, bleeding
- stimata: caput medusa, ascites, palmar erythema, spider angiomatas, peripheral edema, fluid wave, gynecomastia, testicular atrophy
whats considered “decompensated cirrhosis?”
once a patient has complications of cirrhosis = decompensated
complications of liver dz
AC, 9H:
- ascites
- coagulopathy
- high ammonia
- hepatic encephalopathy
- hypoalbumin
- hepatorenal syndrome
- high bilirubin
- hypoglycemia
- portal hypertension
- hepatocellular carcinoma
- hyperestrinism (vascular changes)
portal htn - liver dz
- pres: bleeding, ascites
- dx: paracentesis can help if ascites present
- tx: TIPS, nonselective BB for varices if present
ascites - liver dz
MOST COMMON COMPLICATION! MUST HAVE PORTAL HTN TO HAVE ASCITES! then also have low albumin!
- pres: shifting dullness, fluid wave, distension
- dx: paracentesis indicated w/ new-onset / changing, suspect SBP, SOB/tense abdomen
- *serum ascites albumin gradient >1.1 suggests portal htn! (transudate, while <1.1 suggests exudate d/t inflam / pancreatitis/ biliary / CA)
- confirm w/ ultrasound
- tx: bed rest, salt restriction and diuretics: lasix + aldactone! may need abx if suspect SBP
hepatorenal syndrome - liver dz
- seen w/ advanced liver disease - renal failure d/t poor perfusion and arterial vasoconstriction that does NOT respond to fluids!
- often precipitated by infection or diuretics!
sx: azotemia, oliguria, hypotension, hyponatremia and low urine sodium - tx: liver transplant - poor prognosis!
SBP - liver dz
- infection of ascitic fluid most d/t E coli
- pres: abdominal pain, rebound, fever
- suspect in anyone w/ ascites w/ new onset fever or change in mental status
- dx: paracentesis w/ wbc >500 and PMN <250, culture
- tx: for prophylaxis: rocephin, tailor to culture and repeat paracentesis 2-3 days later to doc decreased PMN
cirrhosis tx
- avoid alcohol and toxic meds!
2. monior labs q 3-4 mo, endoscopy for varices (nonselective BB for prophylaxis), CT biopsy if suspect HCC
ascites - medications
- spironolactone (aldactone): 100-400 mg PO qd
alt: amiloride, tiramterene- monitor K
- lasix -2nd line / adjunct w/ aldactone
- if intractable: paracentesis, replace albumin and 1/2 dose of diuretic
- TIPS and shunt
* *stop diuretics if sodium 2
1 cause of intractable ascites…
EXCESS SODIUM!!
hepatic encephalopathy - patho
reversible mental status changes, ASTERIXIS, neuromuscular twitching in liver dz d/t ammonia accumulation
-often in pt w/ liver dz w/ insult (hemorrhage, infection, fluid or electrolyte disturbance)
hepatic encephalopathy stages
- mild confusion, changes in speech / sleep
- marked confusion, lethargy, asterixis
- stuporous, incoheret, asterixis, arousable
- coma
- fetor hepaticus: musty breath
hepatic encephalopathy - dx
- r/o tox, hypoglycemia
2. EEG - symmetric slowing of basic rhythm
hepatic encephalopathy tx
- lactulose - titrate to 2-3 bm/d
- if worsening or no change after 2 days add rifaximin (very expensive, not long-term tx)
- neomycin / FQ / flagyl - will help decrease ammonia production by decreasing bowel flora
- reduce protein to 30-40 g/day
LFT abnormalities…
ALT is more specific!!
- with mild increase (hundreds) think about chronic viral hepatitis (BCD), alcoholic
- moderate increase: acute viral
- severe (thousands): shock liver, ischemic, severe acute viral hepatitis
cause of increased LFT + asx
- autoimmune
- hep B
- hep C
- drugs
- ethanol
- fatty liver
- growths (ca)
- hemodynamic dz (CHF)
- iron, copper
acute and chronic hepatitis
acute: 6 mo
* can be caused by EBV, CMV and HSV in immunosuppressed
hepatitis transmission
A and E: fecal-oral, most in developing countries
NO CHRONIC FORMS!!!
B: parenteral and sexual; perinatal in asia and africa
C: parenteral - IV DRUG USERS
D: only as coinfection w/ B or superinfection in chronic B
**chronic forms of b,c,d!!
acute hepatitis pres
wide range from asx to fulminant!
- often have jaundice, N/V, anorexia, aversion to smoke, RUQ pain, dark urine (d/t increased conjugated bili), malaise
- *polyarteritis nedosa w/ B and cryoglobulinemia w/ C
acute liver failure
- fulminant: develop hepatic encephalopathy within 8 weeks of acute liver disease onset. all have coagulopathy (INR 1.5 and up)
- subfulminant: develop hepatic enceph 8 weeks-6 mo w/in onset of acute liver disease
- *most d/t tylenol tox, idiosyncratic drug rxns (abx, AED, anti-TB meds)
- death most commonly d/t cerebral edema and sepsis
acute liver failure tx
aimed at correcting metabolic disturbances - lactulose for encephalopathy, acetylcysteine for tylenol tox, GI prophylaxis, mannitol for cerebral edema
hep a testing
-elevated AST and ALT, then increased alk phos (not seen w/ hep b)
-serum IgM anti-HAV with clinical symptoms= gold std for diagnosis of acute infection
-peaks in 1st week, gone in 3-6 mo
IgG indicates exposure - positive after 1 mo, persists for years-decades
hep a prognosis
expect recovery! supportive tx and bed rest. most recover in 3-6 months!
only see symptoms in adults! kids = asx!
hep b testing
- higher ast and alt than in hep a, no signs of cholestasis
1. HBsAg: 1st sign of acute infection before biochemical changes- if positive >6 mo = chronic infection
- if negative = virus cleared!
- anti-hbs: appears once surface antigen is gone! 1-3 mo after infection
* pos = sign of RECOVERY, NONINFECTIOUS, IMMNUNE - Anti-HBc = IgM and IgG - after surface antigen, before antibody
- pos = acute or chronic
- IgM pos in acute and flares of chronic
- IgG pos in acute and persists - hbeag: indicates replication and infectivity
- hbv dna - mimics hbeag - if positive >6 weeks - risk of chronic!
- anti-hbs: appears once surface antigen is gone! 1-3 mo after infection
hep b tx / prognosis
- chronic form more in KIDS and immunocompromised! most clear in 3-6 mo
- tx: interferon alpha (alt = lamivudine) for CHRONIC
- potential exposure / neonate: immune globulin w/in 7 days then vaccinate!
hep c testing
- hep c antibody: positive in 2-6 mo
- more indicative of exposure
- hep c RNA - positive 1st w/in 2 weeks!
- always check genotype - changes treatment!
- w/ positive antibody, check RNA or if suspect acute / known exposure automatically get RNA at same time as antibody!
- w/ positive RNA, marked increase in enzymes and neg antibody = likely ACUTE infection!
- RNA often lower in acute
- w/ positive RNA, positive antibody and moderate elevated enzymes = more likely chronic
- higher more stable RNA levels, fibrosis
- pos antibody + neg RNA = CLEARED previous infection
hep c tx - chronic
peginterferon and ribaviron - longer for genotype 1
hep d testing
-to infect, must have positive Hbsag and Igm Anti HBc and then check for HDV antibodies!
hep e testing
test for Igm HEV #1 cause of acute hep worldwide!
hepatocellular adenoma - RF , a/w…
benign liver tumor most in young women (15-40) a/w steroid use and OCPs!!
hepatocellular adenoma pres
- asx or RUQ pain / fullness
- dx: often single mass seen on imaging - ct or u/s
hepatocellular adenoma tx
-stop OCP
-resect if >5 cm d/t risk of RUPTURE!
10% risk of malignant transformation!
cavernous hemangioma
MOST COMMON BENIGN LIVER TUMOR! vascular tumor d/t dilation of vessels
cavernous hemangioma pres
most asx, may have RUQ pain (r/o other causes if present)
- dx w/ imaging: u/s or ct w/ iv contrast!
- *BIOPSIES ARE CONTRAINDICATED!!!
cavernous hemangioma tx
-most dont need treatment unless symptomatic or high risk of rupture!
focal nodular hyperplasia
second most common benign tumor of liver - NO MALIGNANT POTENTIAL!!!
-NOT a/w OCP and has a CENTRAL SPOKE WHELL SCAR!
focal nodular hyperplasia pres
most asymptomatic!
-usually nodular mass in both R and L lobes w/ fibrous scar w/ radiating septa!
focal nodular hyperplasia workup
- can dx w/ imaging (ct / mri) w/ characteristic scar and asx
- if painful, r/o other causes of pain
- if uncertain / no scar, must dx histiologically
focal nodular hyperplasia tx
- w/ central scar and asx - no treatment
- if growing / persistent sx - resection
liver cancers…
mostly metastatic!
most common primary = hepatocellular carcinoma!!! (>80% primary)
hepatocellular carcinoma
1 primary tumor (most liver tumors= mets!) - rare in u.s. but #1 cause of cancer deaths worldwide!!
hepatocellular carcinoma types
- nonfibrolammelar - more common
- a/w hep B, C, cirrhosis!
- typically NOT resectable and SHORT survival (less than 1 year)
- fibrolamellar - less common
- NOT a/w hep b, c or cirrhosis
- more in teens / young adults
- more likely resectable w/ longer survival
HCC risk factors
- cirrhosis (develops in 10%)
- liver carcinogens
- hepatocellar adenoma
- inheritied liver dz - wilsons, AAT, hemocrhomatosis
- smoking
HCC pres
-male, 50s-60s w/ PAINFUL HEPATOMEGALY w/ constitutional fever, weight loss fatigue and signs of cirrhosis
HCC workup
- check hep b, c, lft, coags
- check AFP - elevated in 40-70%
- for diagnosis and treatment monitoring
- imaging - u/s or CT
- *positive for hypervascular mass >2cm w/ elevated AFP in pt w/ cirrhosis is DIAGNOSTIC for HCC!!!!
- biopsy - only done for non-operative patients!!
HCC tx
tx of choice: resection - done for child class A
- if non op- ablation, percutaneous ethanol injection, embolization
- systemic chemo not effective!
- mets: bone, lung, peritoneum
