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Medical School > Hepatology > Flashcards

Hepatology Flashcards

1
Q

Alcoholism

  1. Liver pathologies causes by alcoholism (3)
  2. USS finding (fatty liver), biopsy results
  3. Blood tests
  4. Withdrawal - symptoms
  5. Withdrawal - management
  6. Wernicke’s Encephalopathy - clinical features
  7. Korsakoff’s syndrome - cause and symptoms
  8. CAGE questionnaire (4)
  9. Questionnaire to decide level of alcohol dependence
  10. Advice if dependent
  11. Management - mild
  12. Medication to stop anxiety, insomnia, craving
  13. Medication causing acetaldehyde build up (N+V, flushing, headache, palpitations if drink)
  14. How to work out units
A
  1. Steatosis (fat in liver cells), hepatitis + cirrhosis
  2. Echogenicity up + mallory bodies, neutrophil infiltrates
  3. Macrocytic anaemia, high AST/ALT, very high YGT, high ALP in cirrhosis, high PT
  4. Tachycardia, HTN, tremor (6-12 hours), hallucination (12-24 hours), seizures (1-2 days), delirium tremens (1-3 days)
  5. Chlordiazepoxide, vit K, pabrinex (3 vitamins)
    Pabrinex contains thiamine (vit B1 - always give if AD), riboflavin (B2), vitamin C
  6. Confusion, ophthalmoplegia, ataxia
  7. Hypothalamic damage/cerebral atrophy from chronic thiamine deficiency (confabulation, no insight, apathy)
  8. Do you feel: should Cut down / Annoyed if drinking criticised / Guilty about drinking, ever have Eye opener
  9. AUDIT questionnaire
  10. No sudden stopping/NSAIDs/warfarin tell DVLA/work
  11. CBT +/- acamprostate
  12. Acamprostate
  13. Disulfiram
  14. % x ml / 1000 x no. of days
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2
Q

Cirrhosis

  1. Definition
  2. Causes
  3. Hand signs
  4. Face/neck signs
  5. Chest signs
  6. Abdominal signs
  7. Blood tests
  8. Further tests
  9. Decompensated definition
  10. Conservative management
  11. Screening required for
  12. Cirrhosis scores: severity, compensated mortality/need for transplant
A
  1. Hepatocellular degeneration, inflammation, + fibrous tissue thickening
  2. Alcohol, hepatitis (B/C), genetic (Wilson’s), drugs (methotrexate), autoimmune
  3. Clubbing, leukonychia, dupuytren’s contracture, palmar erythema, asterixis (flapping tremor if decompensated)
  4. Jaundice, raised JVP
  5. Spider naevi, gynacomastia, bruising (abnormal clotting)
  6. Hepatosplenomegaly, ascites, caput medusae
  7. AST/ALT/ALP/YGT/bilirubin up, U+E (deranges in HRS), platelets/albumin down, PT up, FBC (MCV high), IgA, cholesterol
  8. USS liver (nodular surface, corkscrew arteries, corkscrew portal vein), CT, biopsy if needed for extent of damage, MRCP/ERCP
  9. Cirrhosis with ascites/ bleeding / reduced GCS
  10. Alcohol abstinence, nutrition (low Na+, high protein)
  11. Varices development - OGD
  12. Child-Pugh (5-15), Meld (every 6 months)
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3
Q

Liver function tests (LFTs)

  1. Hepatic function tests

Aminotransferases (AST, ALT)

  1. Most specific for liver injury
  2. ALT - expressed in
  3. AST - expressed in
  4. ALP - expressed in
  5. yGT - expressed in
  6. Alcoholic liver disease
  7. Acute viral hepatitis
  8. Chronic viral hepatitis
  9. Fatty infiltration of liver
  10. Ischaemic hepatitis
  11. Cholestasis - blood results
  12. Bone - blood results
  13. Other causes for raised LDH
A
  1. Serum albumin, serum bilirubin, PT (INR)
  2. ALT
  3. Liver, kidney, muscle
  4. Liver, heart, skeletal muscle, RBCs
  5. Liver, bone (raised in growing children), placenta
  6. Liver, pancreas, renal tubules, intestine
  7. High AST:ALT is >2:1, high yGT, macrocytosis
  8. High ALT, maybe high AST, maybe normal bilirubin
  9. High ALT
  10. Mildly high AST/ALT
  11. Very high ALT, high LDH
  12. High ALP + yGT
  13. High ALP, normal yGT
  14. Liver metastases, obstructive jaundice
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4
Q

Jaundice

Causes

  1. Pre-hepatic
  2. Intra-hepatic
  3. Post-hepatic
  4. Unconjugated
  5. Conjugated
  6. Bilirubinuria - found in which types (2), appearance, why
  7. Urobilinogen - absent in which cause
  8. History - important points
  9. Examination
  10. Blood tests
  11. Further investigations
A
  1. Increased haemolysis e.g. sickle cell, malaria, spherocytosis, thalassaemia
  2. Hepatocellular damage
  3. Cholestasis
  4. Overproduction (haemolysis), impaired hepatic uptake (hepatitis from rifampicin, paracetamol, ischaemia), impaired conjugation (Gilbert’s), physiological neonatal (combination)
  5. Hepatocellular damage, cholestasis
  6. Intra and post, conjugated is water soluble, urine dark
  7. Cholestasis
  8. Blood transfusions, IVDU, piercings/tattoos, sex, travel, jaundice contacts, FH, alcohol, medication
  9. Chronic liver disease, hepatic encephalopathy, lymphadenopathy, hepatosplenomegaly, ascites, palpable gall bladder (not gallstones if painless jaundice - Courvoisier)
  10. FBC, clotting, film, reticulocyte count, Coombs/haptoglobin for haemolysis, malaria, Paul Bunnell (EBV), culture, hepatitis serology
  11. Ultrasound, then ERCP, or biopsy
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5
Q

Disorders of excretion (cholestasis) - blood tests

A

Bilirubin
ALP
Copper raised
Cholesterol

(all increased in cholestasis)

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6
Q

Synthetic liver function - which tests

A

Coagulation - prothrombin time and INR
Liver screen
Albumin

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7
Q

Which clotting factors are produced by the liver?

A

1,2,5,7,11 and 13

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8
Q

Which tests are done in a liver screen?

A 
Viral hepatitis
CMV and EBV
Autoantibodies
Ig
Ferritin
Copper

USS of the liver

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9
Q

Acute liver failure

  1. Definition
  2. Consequences (2)
  3. Main causes (3)
  4. Infectious causes
  5. Drug sauses
  6. ‘Other’ causes
  7. Important questions
  8. Bloods
  9. Imaging
  10. Immediate management
  11. Monitoring requirement
  12. Commonest mode of death
  13. Fulminant hepatic failure - definition
  14. Complications
A
  1. Acute liver injury (reduction in hepatic function <6m due to hepatocellular death) - hyperacute <7d, acute 8-21d, subacute 4-26 weeks
  2. Increased INR, hepatic encephalopathy
  3. Infections, drugs, malignancy
  4. Hepatitis (A, B, E), immunocompromised (EBV, CMV), foreign travel (dengue)
  5. Paracetamol, cocaine, iron, amoxicillin, rifampicin, isoniazid, phenytoin, valproate
  6. Autoimmune, Wilson’s, ischaemia, pregnancy related (acute fatty liver / HELLP)
  7. Recent new medication, travel history, unprotected sex, IVDU
  8. FBC, U+E, LFT, albumin, coagulation, copper, glucose, ABG, hepatitis screen, toxicology, autoantibodies, culture
  9. USS, CT, ascitic tap
  10. ABC, fluid resuscitation, vitamin support, IV N-acetylcysteine if paracetamol, discuss with transplant/ITU
  11. INR 6 hourly, urine output, creatinine
  12. Sepsis
  13. Sudden onset liver failure with hepatic encephalopathy within 2 weeks in a person with no underlying liver pathology
  14. Cerebral oedema (mannitol, hyperventilate), ascites, bleeding (Vit K, platelets, FFP + blood), infection (ceftriaxone NOT gentamicin), encephalopathy
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10
Q

Hepatic encephalopathy

  1. Due to build up of
  2. Precipitating events
  3. Microbiology (3)
  4. Imaging (2)
  5. Bloods
  6. General acute management
  7. First line ammonia-focussed management
A
  1. Ammonia
  2. Infection, GI bleed (protein absorption), constipation, dehydration, alcohol binge, TIPS
  3. Blood cultures, ascitic tap, urine dip
  4. USS, CT
  5. FBC, U+E, LFT, coagulation, CRP, ABG (including ammonia), glucose
  6. ABCDE, fluids, ABX (rifamixin), treat the cause
  7. Lactulose - thought to promote the excretion of ammonia and increasing the metabolism of ammonia by gut bacteria
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11
Q

Liver tumours

Primary

  1. Main causes
  2. Important diagnostic tests (2)
  3. Symptoms
  4. Signs
  5. Hepatocellular carcinoma (HCC) - commonest cause

Cholangiocarcinoma (biliary tree cancer)

  1. Main risk factor
  2. Elevated markers
  3. What symptom comes earlier than in HCC
  4. Test to do if suspected following USS/CT
  5. Benign tumours - types (2)

Secondary (commonest)

  1. Origins in men
  2. Origins in women
A
  1. Hepatocellular carcinoma (75%), cholangiocarcinoma
  2. Abdominal USS/CT (3 phase), alpha feto protein (HCC)
  3. Fever, malaise, weight loss, RUQ pain
  4. Hepatomegaly (hard and irregular if metastases / HCC / cirrhosis), decompensation (e.g. jaundice, ascites)
  5. Hepatitis B - monitor AFP for HCC recurrence
  6. Primary sclerosing cholangitis (PSC)
  7. CA 19-9 (normally pancreas), CEA (normally bowel), CA 125 (normally ovarian)
  8. Jaundice
  9. ERCP with biopsy
  10. Haemangioma (don’t biopsy), adenoma (caused by steroids, COCP, pregnancy)
  11. Stomach, colon, lung
  12. Stomach, colon, breast, uterus
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12
Q

Autoimmune hepatitis

  1. Types (2), autoantibodies present, age
  2. Other linked autoimmune diseases
  3. Presentation
  4. Bloods
  5. Bloods suggesting hypersplenism
  6. Invasive test, + result
  7. Diagnosis
  8. 1st line management
A
  1. 1 (Anti-smooth, ANA - adults <40); 2 (anti-LKM1 - children)
  2. SLE, UC, GN, haemolysis, DM, PSC, thyroid disease, pernicious anaemia
  3. Acute hepatitis (e.g. jaundice), autoimmune disease signs (e.g. fever, malaise, urticaria, pleurisy polyarthritis), amennorhoea
  4. Bilirubin, AST, ALT, ALP, IgG all raised
  5. Pancytopaenia
  6. Liver biopsy (mononuclear infiltrate of peri/portal areas, piecemeal necrosis, +/ fibrosis)
  7. IgG, autoantibodies, histology in absence of viral disease
  8. Prednisolone, then azathioprine
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13
Q

Primary biliary cholangitis

  1. Cause and result
  2. Antibody present
  3. Typical presentation
  4. Early blood results
  5. Late blood results
  6. Complications
  7. Management
A
  1. Autoimmune distruction of the lobular ducts, can lead to cholestasis and fibrosis/cirrhosis/portal HTN
  2. Anti-mitochondrial (AMA) - M2 subtype
  3. Age 50, asymptomatic, maybe lethargy, pruritis, then jaundice much later
  4. Raised ALP, yGT (mild AST/ALT)
  5. Raised bilirubin/PTT, low albumin
  6. Malabsorption of fat-soluble vitamins (A, D, E, K) from cholestasis and low bilirubin in gut lumen leads to osteomalacia, coagulopathy
  7. Symptoms (colestyramine for pruritis, codeine for diarrhoea), vits A/D/E/K, ursodeoxycholic acid (UDCA)
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14
Q

Primary sclerosing cholangitis

  1. Definition
  2. Associated condition
  3. Autoantibody present
  4. Associated cancer
  5. Other bloods
  6. Diagnostic imaging + findings
A
  1. Chronic liver disease leading due to fibrosis and inflammation leading to bile duct scarring, cholestasis and cirrhosis
  2. IBD
  3. p-ANCA
  4. Cholangiocarcinoma
  5. ALP, bilirubin, gamma globulins, IgM
  6. MRCP - duct stricture, damage/dilatation ‘beaded’ appearance
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15
Q

Liver disease - peripheral signs

A

Bruising - poor clotting
Malnourished
Oedema

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16
Q

Shunting of blood from the portal to systemic system leads to

A

Hepatic encephalopathy

17
Q

Portal hypertension

  1. Definition
  2. Pre-hepatic causes (2)
  3. Hepatic causes (2)
  4. Post-hepatic causes (2)
  5. Clinical features
  6. Medical management (3)
  7. Surgical management
  8. Complications (3)
A
  1. Abnormally high pressure in the portal vein
  2. Thrombosis (splenic/portal/mesenteric vein), extrinsic compression
  3. Cirrhosis, hepatitis
  4. Cardiac failure, thrombosis (hepatic vein)
  5. Ascites, bleeding, decreased GCS
  6. Anticoagulation for thrombosis, beta blockers, TIPS (transjugular intrahepatic portosystemic shunt)
  7. Shunt
  8. Varices, ascites, splenomegaly
18
Q

Hepatic / portal vein thrombosis - diagnostic imaging

19
Q

Ruptured varices

  1. Clinical presentation
  2. Bloods
  3. 1st line management (2)
A
  1. Haemodynamically unstable, haematemesis, melaena, may be signs of chronic liver disease (e.g. jaundice, ascites, encephalopathy)
  2. ABG, FBC, LFT, U+E, clotting, group and save
  3. Endoscopy, banding
20
Q

Best guide as to whether ascites due to portal hypertension

A

SAAG - Serum ascitic albumin gradient

<11 g/L

21
Q

Ascites

  1. Transudate - protein count
  2. Causes
  3. Exudate - protein count
  4. Causes
  5. Examination findings
  6. Straw coloured fluid aspirate - meaning
  7. Orange
  8. Turbid
  9. Blood
  10. Management - conservative
  11. Medical
  12. Surgical
  13. Serious complication
A
  1. <25 g/L
  2. Liver failure, renal failure
  3. > 25 g/L
  4. Infection, malignancy, pancreatitis
  5. Swelling, full flanks, shifting dullness
  6. Normal
  7. Bilirubin
  8. Infection
  9. Malignancy
  10. Monitor fluid input and output, reduce sodium input
  11. Diuretics (spironolactone)
  12. Paracentesis, TIPS
  13. Spontaneous bacterial peritonitis
22
Q

Spontaneous bacterial peritonitis

  1. Causative organisms
  2. Bloods
  3. Signs
  4. Main diagnostic investigation
  5. Medical management
A
  1. E.Coli, klebsiella, gram-positive cocci
  2. High WBC, CRP, creatinine or metabolic acidosis
  3. Fever, abdominal pain, ileus, hypotension
  4. Gram stain and cell count of ascitic tap
  5. IV cefotaxime / tazocin 5 days
23
Q

Gilbert’s Syndrome

  1. Definition
  2. LFT results
A
  1. Genetic syndrome of mild unconjugated hyperbilirubinaemia

2. Liver function is otherwise normal

24
Q

Liver damage/decompensation - causes

  1. Pre-hepatic
  2. Hepatic
  3. Systemic/post-hepatic
A

Pre-heptatic

  • Haemolytic anaemia e.g. sickle cell or autoimmune
  • Gilbert’s syndrome

Hepatic

  • Hepatitis - infective / autoimmune
  • Alcohol
  • Fatty liver disease
  • Haemochromatosis / Wilsons
  • Primary biliary sclerosis

Post / systemic

  • Gall bladder disease
  • Pancreatic cancer
  • Congestive heart failure
25
Q

Hepatomegaly

  1. Associated symptoms
  2. Family history questions
  3. Social history questions
  4. Causes - mild
  5. Causes - moderate (‘MR HAM HIFI’)
  6. Causes - massive (‘MR HAM’)
  7. Smooth
  8. Craggy
A
  1. Nausea, pruritis, abdominal distention, weight loss, pyrexia, jaundice, dark urine, pale stool
  2. Sickle cell, carcinoma, autoimmune disease
  3. Travel history, alcohol, tattoos/needles/sex
  4. Hepatitis, biliary obstruction, HIV
  5. MR HAM, + Haematological disease, Iron (haemochromatosis), Fatty liver, Infiltration
  6. Metastases, Right heart failure, Hepatocellular cancer, Alcoholic liver disease, Myeloproliferative disorders
  7. Hepatitis, CCF, sarcoid, early cirrhosis, tricuspid incompetence (pulsatile)
  8. Secondaries, primary hepatoma
26
Q

Hepatorenal syndrome

  1. Triad of signs
  2. Diagnosis only if
  3. Pathophysiology
  4. Type 1 - progression rate
  5. Management
  6. Type 2 - progression rate
  7. Management
A
  1. Cirrhosis, ascites, renal failure
  2. Other causes of renal impairment excluded
  3. Splanchnic/systemic vasodilation, renal vasoconstriction
  4. Quick, median survival <2 weeks
  5. Terlipressin for hypovolaemia, haemodialysis
  6. Steady, median survival 6 months
  7. TIPS, transplant
27
Q

Drug-induced jaundice

  1. Haemolysis
  2. Hepatitis
  3. Cholestasis
A
  1. Antimalarials (dapsone)
  2. Paracetamol, TB drugs, MAOIs (selegiline), valproate, statins
  3. Fusidic acid, co-amoxiclav, nitrofurantoin, anabolic steroids, sulfonylureas, antipsychotics (prochlorperazine, chlorpromazine)
28
Q

Viral hepatitis

Hep A

  1. Type
  2. Spread
  3. Symptoms
  4. Test
  5. Prognosis

Hep C

  1. Type
  2. Spread
  3. Symptoms
  4. Test
  5. Management

Hep D

  1. Type
  2. Test
  3. Prognosis

Hep E

  1. Type
  2. Spread
A
  1. RNA
  2. Faeco-oral (travellers)
  3. Fever, malaise, anorexia, jaundice, hepatosplenomegaly
  4. AST/ALT rise from day 20-40, IgM from day 25 (recent infection), IgG up for life
  5. Usually self-limiting
  6. RNA
  7. Blood, IVDU, sex
  8. Often mild/asymptomatic, cirrhosis after 20 years
  9. AST:ALT <1:1 until cirrhosis develops, anti-HCV antibodies (exposure), HCV PCR (ongoing infection)
  10. Ledipasvir/sofosbuvir
  11. Incomplete RNA (needs HBV)
  12. Anti-HDV antibody (only ask if HBsAg positive)
  13. Potential transplant
  14. RNA
  15. Faeco-oral, associated with pigs
29
Q

Hepatitis B

  1. Type
  2. Spread

Bloods - abnormal results

  1. Incubation
  2. Acute
  3. Carrier
  4. Recovery/immune post-natural infection
  5. Vaccinated
  6. What is the surface antigen for HBV
  7. Which antigen implies high infectivity
  8. What is positive post-vaccination
  9. Complications
  10. Management
A
  1. DNA
  2. Blood, IVDU, sexual
  3. HBsAg, HBeAg
  4. LFT very high, HBsAg, HBeAg, Anti-HBc IgM + IgG
  5. LFT slightly raised, HBsAg, Anti-HBc IgG,
    (maybe HBeAg, Anti-HBe, Anti-HBc IgM)
  6. Anti-HBs, Anti-HBc IgG
  7. Anti-HBs
  8. HBsAg
  9. HBeAg
  10. Anti-HBs
  11. Fulminant hepatic failure, cirrhosis, HCC, cholangiocarcinoma, membranous nephropathy, polyarteritis nodosa
  12. Avoid alcohol, immunise sexual contacts, antivirals if chronic liver inflammation (ALT >30), cirrhosis, or HBV DNA
30
Q

Wilson’s disease / hepatolenticular degeneration

  1. Inheritance pattern
  2. What it is
  3. Pathophysiology
  4. Presentation
  5. Signs
  6. Urine test + result
  7. Blood tests + results
  8. Diagnostic test
  9. Further investigations
  10. Management - lifestyle
  11. Management - other
A
  1. Autosomal recessive
  2. Disorder of copper secretion; excess builds up in liver and CNS (basal ganglia) instead of secreted into bile
  3. Copper transporting ATPase (ATP7B) doesn’t incorporate copper into caeruloplasmin
  4. Liver disease (children), CNS failure e.g. Parkinsonism (adults), low mood, low cognition
  5. Kayser-Fleischer rings, haemolytic anaemia, blue lunulae (nails), hypermobile joints, arthritis, grey skin, osteopaenia, renal tubular acidosis
  6. 24 hour copper secretion is HIGH
  7. Serum caeruloplasmin/copper LOW
  8. Molecular genetic testing
  9. Slit lamp, liver biopsy, MRI brain
  10. Avoid high copper foods (chocolate, nuts, mushrooms, legumes, shellfish), check water sources
  11. Lifelong penicillamine, transplant, screen siblings
31
Q

Hereditary haemochromatosis

  1. What is it (+ locations affected)
  2. Responsible genes
  3. Presentation (early) - in 40s
  4. Presentation (late)
  5. Blood tests
  6. Diagnostic test
  7. Imaging
  8. Management - 1st line
  9. Management - if cannot tolerate 1st line
  10. Complications
A
  1. High intestinal iron absorption, causing iron deposits in joints, liver, heart, pancreas, pituitary, adrenals + skin
  2. HFE (C282Y, H63D)
  3. Tiredness, arthralgia (including pseudogout), low libido
  4. Slate grey skin, signs of chronic liver disease, DM (iron in pancreas), hypogonadism (pituitary dysfunction)
  5. High LFT, ferritin + transferritin saturation, TIBC low
  6. HFE genotyping
  7. Joints (chondrocalcinosis), liver/cardiac MRI (iron overload)
  8. Venesection 0.5-2 units every 1-2 weeks until ferritin <50, then lifelong monthly venesection
  9. Desferrioxamine
  10. T1DM, liver cirrhosis/HCC, cardiomyopathy, hypothyroid
32
Q

Alpha 1 antitrypsin (A1AT) deficiency

  1. Organs affected and pathology
  2. What is A1AT
  3. Name for deficiency of this type
  4. Commonest cause of liver disease in which patient cohort
  5. Symptoms
  6. Blood tests
  7. Lung function tests
  8. Liver biopsy results
  9. Management
A
  1. Lungs (basal emphysema) from 30yo, liver (cirrhosis, HCC) from 50yo
  2. Serine protease inhibitor (control inflammatory cascades
  3. Serpinopathy
  4. Children
  5. Dyspnoea, cirrhosis, cholestatic jaundice
  6. Low serum A1AT (but part of acute phase response so may rise to normal in inflammation)
  7. FEV1 low - obstructive, high-res CT diagnoses emphysema
  8. Periodic acid schiff (PAS) positive, diastase-resistant globules
  9. Stop smoking, lung/liver transplant, maybe IV A1AT
33
Q

Non-alcoholic fatty liver disease (NAFLD)

  1. Stages 1-4
  2. Risk factors (same as CVD/T2DM)
  3. Investigations - 1st and 2nd line
  4. Management - conservative
  5. Management if fibrosis (stage 3)
A
  1. NAFLD, non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis
  2. Obesity, diet, T2DM, cholesterol, age, smoking, HTN
  3. 1st: Enhanced Liver Fibrosis (ELF) blood test, then NAFLD fibrosis score
  4. Weight loss, exercise, no smoking, no alcohol, DM/BP/cholesterol control
  5. Vitamin E / pioglitazone (via liver specialist)

Medical School (28 decks)

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