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Med School > Liver > Flashcards

Liver Flashcards

1
Q

Role of hepatocytes in anabolic vs. catabolic states

A

anabolic - hepatocytes store energy rich nutrients from portal circulation

catabolic - hepatocytes release glucose from glycogen/gluconeogenesis into the systemic circulation

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2
Q

How do hepatocytes make glycogen?

A
  • import glucose via GLUT2
  • phosphorylated into G6P via glucokinase (polymer of this is glycogen)
  • G6P can also be made into pyruvate via glycolysis
  • pyruvate can then enter the Krebs cycle and feed into lipid synthesis

*hepatocytes also import a.as for hepatocyte and plasma protein synthesis

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3
Q

How does glycogenolysis occur in hepatocytes?

A
  • G6P converted back into glucose via glucose 6 phosphatase, then exported
  • G6P can also be created from pyruvate via gluconeogenesis (precursors include lactate, a.a.s, glycerol from lipid catabolism)
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4
Q

When does ketogenesis occur?

A
  • occurs during catabolism, comes from acetyl-CoA and is exported
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5
Q

Describe the Cori Cycle

A
  • In the liver, lactate becomes pyruvate via LDH and pyruvate becomes glucose (also from gluconeogenesis)
  • In muscle, glucose becomes pyruvate and pyruvate becomes lactate via LDH
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6
Q

Lactic Acidosis

A
  • occurs when pyruvate enters the Krebs cycle and the ETC and conversion of pyruvate to glucose is inhibited
  • this is caused by a lack of O2 (hypoxia, ischemia), impaired gluconeogenesis (liver failure), ETC disorder (HAART, ASA, genetics)
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7
Q

What are the plasma proteins made in the liver?

A
  • albumin, transferrin, ceruloplasmin (transport)
  • fibrinogen (coagulation)
  • IgG (immunity)
  • C3 (complement)
  • alpha1-antitrypsin (protease inhibitor)
  • miscellaneous peptide hormones
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8
Q

How are plasma proteins made in the liver regulated?

A
  • all plasma proteins are produced at a faster rate with decreased plasma oncotic pressure
  • Acute phase Reaction (IL-6 regulated) - positive regulation for A1AT/ceruloplasmin/C3, and negative regulation for albumin/transferrin
  • estrogen increases A1AT, ceruloplasmin, coagulation proteins
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9
Q

Storage of nutrients in the liver

A
  • carbohydrates (glycogen)
  • lipids (triglycerides)
  • vitamins (B12, folate, A)
  • trace metals (iron, copper)
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10
Q

Lipid Metabolism

A
  • uptake from intestine, synthesis with hepatocytes (FFAs, PGs, cholesterol), export into blood via lipoproteins (VLDLs, LDLs, HDLs), oxidation for energy
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11
Q

Diff between chylomicrons, VLDLs, LDLs, HDLs

A

Chylomicrons - intestine generated, deliver TGs to tissues, remnants deliver cholesterol to the liver

VLDLs - export TGs and cholesterol from liver to tissues
LDLs - derived from LDLs after they deliver TGs
HDLs - reverse transport of cholesterol from tissues to liver

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12
Q

Ammonia (NH4)

A
  • byproduct of a.a. metabolism
  • toxic but detoxified in the urea cycle (which produces urea, a non-toxic water soluble compound that can be excreted by the kidneys)
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13
Q

Bilirubin
- explain metabolism

A
  • end product of heme metabolism, mainly made in RE cells from old erythrocytes, metabolized only in the liver
  • transported in blood via albumin
  • free bilirubin is TOXIC to cells
  • uptake into hepatocyte, conjugated to glucuronic acid and excreted in bile
  • enters SI via common bile duct, glucuronic acid is hydrolyzed, conversion to urobilinogens, reabsorbed from SI mostly taken up by the liver (enterohepatic circulation), re-excreted by the liver
  • eventually eliminated in the urine/ feces
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14
Q

3 Categories of Jaundice Causes

A

pre-hepatic (unconjugated) - hemolysis, hematoma, inherited metabolic abnormality

hepatic (conjugated) - viral, drug, alcohol, cirrhosis, Gilbert’s

cholestatic (conjugated) - sex hormones, gallstones, bile duct or pancreatic cancer, drugs, alcohol, viral, sepsis, PBC

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15
Q

Heaptic Metabolism of Drugs

A
  1. Chemical modification (hydroxylation, oxidation, P450 system)
  2. Conjugation (sulfate, glucuronic acid)
  3. Excretion (water-soluble conjugate leads to biliary and renal excretion)
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16
Q

Bile
- production
- 3 main functions
- composition

A
  • yellow/green/brown fluid excreted into bile canaliculi by hepatocytes
  • drained by the hepatic duct and stored in the gallbladder
  • digestion, excretion, hepatic cell signalling
  • mainly bile salts, then electrolytes, phospholipids, cholesterol, bilirubin
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17
Q

Bile salts

A
  • derived from cholesterol (conjugated to glycine and taurine)
  • both hydrophilic and phobic surfaces to solubilize lipids
  • reabsorbed in the terminal ileum and returned to the liver (enterohepatic circulation)
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18
Q

Risks for gallstone disease

A
  • older age
  • female, pregnant
  • DM, dyslipidemia, obesity
  • rapid weight loss
  • family history
  • SCI
  • cirrhosis, hyperbilirubinemia
  • Crohn’s
  • Meds (ceftriaxone, fibres, OCPs)
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19
Q

Definition of:
Cholelithiasis
Choledocolithiasis
Cholecystitis
Cholangitis
Biliary Colic

A
  • stones in the gall bladder or cystic duct
  • stones in the common bile duct or SI opening
  • inflammation of the gallbladder
  • inflammation of the bile duct system
  • abdominal pain often due to stone obstruction
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20
Q

Signs and symptoms of gallstones in the gallbladder vs. in the common bile duct

A

Gallbladder - asx, dull URQ/epigastric pain, nausea, diaphoresis, vomiting, fever, leukocytosis
- can see gallstones and sludge on U/S

CBD - fever, jaundice, pain, increased bilirubin/lipase/amylase/AST/ALT, mental changes, acute pancreatitis
- may see intrahepatic duct dilation on U/S along with gallstones and sludge in CBD

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21
Q

Which tests are more helpful for cholelithiasis vs. choledocolithiasis?

A

Cholelithiasis - HIDA scan helpful for cholecystitis, U/S

Choledocolithiasis - MRCP helps with anatomy and stones, ERCP helps with dx AND tx of stones

*only 10-15% of all gallstones have enough calcium to be visible on x-ray

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22
Q

Pros and Cons of U/S and CT for gallstones

A

U/S pros: cheap, no radiation, high sp/sn, can detect 1.5-2mm stones
U/S cons: operator dependent, scarring can lead to false negatives, can miss stones under 3mm, poor sensitivity in distal CBD

CT pros: useful to rule out other Dx, assess complications like perforation/cancer

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23
Q

What would you see on CT for acute cholecystitis? What is considered a dilated CBD on U/S?

A
  • gallbladder distension, wall thickening, gallstones, mucosal hyper enhancement, pericholecystic fat stranding
  • 6mm or more is considered dilated for CBD
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24
Q

HIDA Scan
MRCP
ERCP

A

HIDA Scan - use if diagnosis is unsure after U/S
- technetium label HIDA is IV injected and taken up via hepatocytes –> excreted into bile (allows tracing)

MRCP - magnetic resonance cholangiopancreatography and MRI with liver contrast
- helps evaluate biliary tree, non-invasive, no radiation
- good for CBD stones if no ECRP available or cancer

ERCP - scope, can diagnose and remove CBD stones
- can help stent and brush the CBD to rule out cancer
- could lead to bleeds, perforation, pancreatitis

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25
Q

What are indications for cholecystectomy?

A
  • biliary colic, cholecystitis, cholangitis, pancreatitis

*most gallstones do not need to be treated unless they are symptomatic

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26
Q

Courvoisier’s Sign

A
  • jaundice with non-tender palpable RUQ mass
  • unlikely to be a stone
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27
Q

General investigation steps for jaundice

A
  • CBC/ liver panel/ lytes/ kidney/ blood
  • CT and U/S as initial imaging
  • biopsy/brush
  • stage with CT chest/abdo/pelvis and possibly MRI/PET
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28
Q

Pancreatic Adenocarcinoma

A
  • often too far gone by diagnosis
  • vascular invasion and extra pancreatic spread common
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29
Q

Gallbladder Cancer
- tx

A
  • incidence is about as common as the prevalence of cholelithiasis
  • often found late as an incidental finding
  • tx - cholecystectomy and resection of the gallbladder fossa
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30
Q

Cholangiocarcinoma
- sx
- tx

A
  • arises from the epithelial cells of bile ducts
  • mostly extrahepatic
  • biliary obstruction, abdominal pain, weight loss, fever
  • tx - NO chemo, liver transplant
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31
Q

Whipple Surgery

A
  • remove most of pancreas, gallbladder, part of stomach and SI, bile duct
  • some pancreas left for digestion and insulin
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32
Q

Gallstone Ileus

A
  • fistula from the biliary tract to intestine (most commonly the duodenum)
  • obstruction if stone is over 2.5cm (often terminal ileum)
  • will see distended SI loops, SBO, ectopic calcified gallstone, nausea, vomiting, pain, constipation
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33
Q

Mirizzi Syndrome
- sx
- dx
- tx

A
  • obstructive jaundice from stone in the neck of gallbladder or CD, narrowing CHD
  • epigastric pain, jaundice, increased enzymes on liver fxn test
  • Dx: ERCP
  • Tx: open cholecystectomy
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34
Q

These clinical pictures point to:

  1. RUQ pain, high WBC, normal liver function, presence of cholelithiasis on U/S w or w/out CBD dilation
  2. Fever, Jaundice, Hypotension, Upper Abdominal Pain, Tachycardia
    - also: biliary duct dilation w shadowing in the CBD on U/S
A
  1. Cholecystitis
  2. Reynold’s Pentad (Cholangitis)
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35
Q

When would gallbladder resection not be appropriate?

A
  • metastases, involvement of vital structures (portal vein), other comorbidities (HF, CKD)
36
Q

Risks of chronic alcohol abuse?
How is alcohol metabolized?

A
  • fatty liver, cirrhosis, cancer, acute hepatitis
  • alcoholic hepatitis has high mortality if severe
  • acetaldehyde causes cell injury, oxidative stress, mitochondrial dysfunction due to increased NADH/NAD ratio, hypoxia of centrilobular area
  • ADH is primary if lower [EtOH], CYP2E1 is induced by higher [EtOH]
  • metabolized from EtOH - acetaldehyde - acetate - CO2 and water
37
Q

What is the common presentation of alcoholic liver disease?

A
  • history of alcohol use
  • RUQ pain
  • increased AST compared to ALT (alcohol inhibits pyridoxal 5-phosphate which is more important for ALT synthesis) *BUT if AST over 400 consider other causes
  • hyperbilirubinemia
  • hepatic encephalopathy
  • coagulopathy
  • leukocytosis
38
Q

What would you see on biopsy for someone with alcoholic liver disease?

A
  • macro vesicular steatosis
  • hepatocellular ballooning
  • neutrophil/lymphocyte infiltration
  • Mallory-Denk bodies (condensed cytokeratin filaments/ ubiquitin)
  • cholestasis
  • bile duct proliferation
  • fibrosis with perivenular/sinusoidal/ cellular distribution (chicken wire)
39
Q

What are tx options for someone with alcoholic liver disease?

A
  • prednisone
  • pentoxyfilline
  • nutritional support and abstinence
40
Q

Intrinsic vs. Idiosyncratic Drug-Induced Liver Injury (and three subtypes of idiosyncratic)
*worsened by alcohol and malnutrition

A

Intrinsic - predictable, prototype is acetominaphen but also alcohol, tetracycline

Idiosyncratic - variable presentation, affects susceptible individuals, most common

  1. Non-immune - no features of hypersensitivity, metabolites bind and cause oxidative stress, bad metabolism
    - amiodarone, diclofenac, isoniazid
  2. Immune - rash, fever, joint pain, eosinophilia, SJS, prompt recurrence after rechallenge, covalent binding of drugs with protein, activation of immune cells
    - amoxicillin, diclofenac, phenyotin
  3. Autoimmune-Like - increased IgG/ANA/ASMA, eosinophilia or granulomas on biopsy, responds to corticosteroids, NO relapse
    - minocycline, nitrofurantoin
41
Q

Hepatocellular Injury (i.e. hepatitis) vs. Cholestatic Injury

A

Hepatocellular - transaminases (ALT/AST) much higher than alkaline phosphatase
- acetaminophen, macrolides, isoniazid

Cholestatic - alkaline phosphatase much higher than transaminases
- amoxicillin, chlorpromazine

*bilirubin may be increased in both cases
* a mixture of both can be caused by anabolic steroids, amiodarone, flavocoxib

42
Q

What is the R value?

A
  • ALT/ULN divided by ALK/ULN
  • if over 5, hepatocellular
  • if under 2, cholestatic
43
Q

Liver biopsy will rarely show a pathognomonic pattern, but what do these suggest?
- Steatosis
- Acute cholestasis
- Chronic cholestasis

A

Steatosis - methotrextae
Acute cholestasis - amoxicillin/ OCPs
Chronic cholestasis - amoxivcillin

44
Q

What are management options for drug-induced liver disease?

A
  • stop offending agent
  • supportive
  • do not suggest a rechallenge
  • antidotes (i.e. acetaminophen is N-acetylcysteine)
45
Q

Acetaminophen Injury
- signs
- what is fatal?
- nomogram

A
  • will see severe transaminitis (ALT > 1000)
  • fatal if over 15g, unless also an alcoholic then 2-6g
  • also at higher risk if fasting, CYP promoter medications
  • nomogram is used to determine [serum] related to time since ingestion
46
Q

Drugs of Concern:
Anabolic Steroids
Antibiotics
Methotrexate

A

Steroids - cholestasis without hepatitis, bilirubin more than 20x ULN, very slow resolution to normal

  • ABX - cholestasis WITH hepatitis, onset of sx can be delayed by weeks
  • amox-clav, fluoroquinolone
  • MTX - increased risk if over 60/ alcoholic/ obesity/ DM/ NSAIDs/ vitamin A
  • possibly greater in psoriatic arthritis

*also need to worry about “-Mabs” and herbal supplements

47
Q

Lab Values and Signs of:
- transaminitis
- acute hepatitis
- acute severe hepatitis
- acute liver failure
- acute on chronic liver failure

A

Transaminitis - high enzymes

Acute hepatitis (under 6 months) - very very high enzymes, high bilirubin

Acute severe hepatitis - high enzymes, high bilirubin, high INR (coagulopathy), jaundice

Acute Liver Failure - high enzymes, high bilirubin, high INR (over 1.5), altered mentation (encephalopathy)

Acute on Chronic Liver Failure - high enzymes, high bilirubin, high INR, possible altered mentation, pre-exisiting liver disease

*only see encephalopathy with failure, NOT hepatitis
* acute hepatitis can be managed outpatient, failure needs hospital

48
Q

What can cause cirrhosis?
What can cirrhosis lead to?
What is the pathophys?

A
  • inflammation, infections (HAV/BV/CV/EBV/CMV), hereditary (hemochromatosis), toxins (EtOH, acetaminophen), vascular (Budd-Chiari)
  • portal HTN, which (if decompensated) can lead to fluid overload, variceal bleeds, hepatic encephalopathy, heptocellular carcinoma
  • hepatocellular damage - macrophages - hepatic stellate cells - myofibroblasts - fibrosis - cirrhosis
49
Q

Portal HTN
- pathophys
- consequences

A
  • destruction of sinusoidal architecture leading to increased resistance in the portal vein/ feeding venous structures
  • as resistance increases through the liver, there is development of venous collaterals for blood to return to the heart
  • systemic vasodilation (ascites, hyponatremia, edema)
  • hematemesis, hemorrhoids
  • splenomegaly, anemia (will have low platelet count)
  • gynecomastia, testicular atrophy
  • jaundice, asterixis, fetor hepaticus
  • coma
50
Q

How to manage varices?

A
  • want to decrease portal pressures
  • ABCs (IV fluids)
  • IV octreotide and PPI
  • correct coagulopathy (platelet infusion), transfuse RBCs ub to Hb100
  • endoscopy
  • ABX to prevent spontaneous bacterial peritonitis (Ceftriaxone and Cipro)
51
Q

Ascites
- different forms and their causes

A
  • presinusoidal - portal vein thrombosis
  • post sinusoidal - heart failure, Budd-Chiari
  • sinusoidal - cirrhosis, liver metastases
  • portal HTN - splanchnic vasodilation –> low ECF –> RAAS –> ascites and renal vasoconstriction leads to hepatorenal syndrome
52
Q

What is SAAG?
- what do diff values mean?

A
  • serum ascites albumin gradient
    = serum albumin - ascites albumon
  • if over 11, portal HTN or cardiac cirrhosis
  • if under 11, hypoalbuminemia (malnutrition, nephrotic syndrome) or interruption of peritoneal lining (infection, malignancy, pancreatitis)
53
Q

Managing ascites

A
  • restrict sodium to under 2g/day
  • spironolactone, furosemide, amiloride
  • paracentesis, TIPS if refractory
54
Q

Spontaneous Bacterial Peritonitis
- sx
- tx
- prophylaxis

A
  • infection of ascitic fluid, growth of bacteria
  • often asx but can have pain/ Lower LOC/ AKI
  • Tx - paracentesis to dx, cefotaxime/ceftriaxone
  • prophylaxis - cipro/septra, do if presenting with GI bleed/ prior SBP/ fluid protein under 10g/L
55
Q

Hepatic Encephalopathy

A
  • altered mentation from cirrhosis due to toxins in blood
  • precipitants include infection, acidosis, constipation, GI bleeds, opioids/benzos/NSAIDs, hypoNA/hyperK/hyperCa, renal failure, dehydration
56
Q

Hepatic Encephalopathy
- precipitants
- sx
- tx
- prophylaxis

A
  • altered mentation from cirrhosis due to toxins in blood
  • precipitants include infection, acidosis, constipation, GI bleeds, opioids/benzos/NSAIDs, hypoNA/hyperK/hyperCa, renal failure, dehydration
  • lowered memory/concentration, confusion, somnolence, day/night reversal, coma (grade IV)
  • tx - lactulose (acute), flatly, PEG, CANNOT DRIVE
  • prophylaxis - lactulose, rifaximin, avoid opioids/ benzos/ NSAIDs
57
Q

Clues for Advanced Liver Disease

A
  • AST > ALT (AST is found more in extra hepatic tissues)
  • more than 1g increase (less Kuppfer cell mass, increased liver vascular shunting)
  • leukopenia and thrombocytopenia (due to splenomegaly)

*dupuytren’s contractions can be a sign of chronic liver disease

58
Q

What do these suggest?
- ANA+, ASMA+, anti LKM+, higher IgG
- higher IgA
- very high GGT
- very high ferritin
- AMA+, ANA+, higher IgM
- increased ferritin, increased TSAT
- low ceruloplasmin, increased urinaey copper
- decreased alpha-1 antitrypsin

A
  • autoimmune hepatitis
  • fatty liver
  • induced by drugs/alcohol/fat
  • induced by steatosis, alcohol, inflammation
  • primary biliary cholangitis
  • hemochromatosis/alcohol/fatty liver
  • Wilson’s
  • alpha1 antitrypsin deficiency
59
Q

Alcoholic Hepatitis

A
  • active inflammation and hepatocyte damage
  • non-cirrhotic portal hypertension (inflammation around central veins)
  • presents as acute severe dysfunction
  • women have less ADH
  • abstinence is the only determinant of longterm survival, steroids and nutrition for longterm
60
Q

Metabolic Associated Fatty Liver Disease (MAFLD)
Non Alcoholic Fatty Liver Disease (NAFLD)
Secondary Fatty Liver Disease

A
  • visceral fat (not peripheral) is the problem - waist circumference over 35 for women and 40 for men
  • treat by losing 10% weight in one year
  • PNPLA3 gene, often have features of metabolic dysfunction, exclusion of other causes
  • genetic syndromes, rapid weight loss, celiac’s, drugs
61
Q

Primary Biliary Cholangitis
- tx

A
  • chronic progressive cholestatic liver disease
  • more common in women
  • destruction of small and medium intrahepatic bile ducts
  • tx: ursodeoxycholic acid (#1), obeticholic acid, bezafibrate/fenofibrates
62
Q

Autoimmune Hepatitis

A
  • inflammation affecting hepatocytes of an unknown cause
  • more common in women
  • IgG, ANA, ASMA are most common markers, anti-LKM if pediatrics
  • tx: prednisone, budesonide (if no cirrhosis or portal HTN), tacrolimus, azathioprine
63
Q

Primary Sclerosing Cholangitis
- screening?

A
  • chronic inflammation/ fibrosis of intra and extra hepatic bile ducts, leads to strictures/ cirrhosis/ portal HTN
  • likely immune (common with IBD), ANCA in 80%
  • increased risk of cancers
  • every 5 years with a colonoscopy if no IBD
  • every 1-2 years with a colonoscopy if IBD
  • multiphase MRI+MRCP annually if no cirrhosis
  • alternate US/MRI 6 months if cirrhosis
64
Q

Hereditary Hemochromatosis
- tx

A
  • type I autosomal recessive (over 90% homozygous C282Y mutation of HFE gene), high incidence in celtic
  • systemic iron overload, leads to hepatitis/cirrhosis/ risk of HCC and many other co-morbidities
  • will see increased ferritin, TSAT over 45% if female or over 50% if male, echogenic liver in U/S, ferriscan (MRI)

tx: phlebotomy until ferritin 50mcg/L, avoid vitamin C supplements

65
Q

Wilson’s Disease

A
  • uncommon autosomal recessive
  • excessive copper deposition in organs
  • neuropsychiatric symptoms, Kayser Fleisher ring in eyes, low ceruloplasmin, increased 24 hour urine copper, increased hepatic copper on biopsy
  • tx: D-penicillamine (chelation), zinc, low copper diet
66
Q

Liver Cysts

A
  • common, may be multiple, bile duct origin
  • usually asymptomatic, but can be large
  • simple - smooth, thin walls, solid (no internal septa/nodules)
  • complex - separations, nodules, thick walls (i.e. daughter cysts within a main cyst is suggestive of parasites)
67
Q

Hemangioma

A
  • most common liver tumor
  • endothelial origin, may be multiple, collagen scaffold
  • usually asymptomatic
  • peripheral in-filling is diagnostic on radiology
68
Q

Focal Nodular Hyperplasia

A
  • second most common liver tumor
  • hyperplasia of normal liver cells, possible due to AVM/scar
  • usually of no clinical significance and rarely symptomatic
69
Q

Liver Cell Adenoma

A
  • benign neoplasm, less common
  • hepatocyte origin, may be symptomatic/large/fleshy, risk of rupture (especially in pregnancy) which can lead to death, treat with surgery if large
  • will look the same throughout contrast imaging
  • more common in women (may regress with cessation of OCPs)
  • hard to distinguish from well-differentiated hepatocarcinoma
70
Q

Hepatocellular Carcinoma
- dx
- tx

A
  • may be multifocal, usually associated with cirrhosis (hepB/C/hemochromatosis)
  • may arise from dysplastic regenerative nodules
  • Dx: tumor marker is alphaFP, tumor will have less contrast than liver later on
    -Tx: surgical resection (#1), treat underlying disease, ablate if small tumor/ radiate (chemo injected directly into tumors)/ transplant
71
Q

Cholangiocarcinoma
- risk factors
- tx

A
  • less common and harder to treat (close to portal triad so can spread easily), malignant
  • from bile duct epithelium (usually major ducts)
  • risk factors: PSC, choledochal cysts, clonorchis infection
  • tx: surgical resection, stenting, biliary bypass
  • poor results with chemo!
72
Q

Liver Metastasis

A
  • more common than primary cancers in the west
  • will see alpha FP increase (tumor marker)
  • can be hypo OR hyper vascular

tx: resection, ablation, chemo
transplant is not an option

73
Q

When is systemic chemo a viable treatment option?

A
  • metastases (5-FU, oxaliplatin, bevacizumab)
  • moderate benefit for HCC (sorafenib, lenvatinib)
  • do NOT give for cholangiocarcinoma
74
Q

What are considered markers of liver cell injury?

A
  • AST (90% released from liver)
  • ALT (small amounts also in kidney and muscle)
    *both key for converting a.a.s into high energy molecules for gluconeogenesis
    *both intracellular enzymes - means cells are DYING (markers of hepatocellular injury)
75
Q

What are considered markers of hepatic secretory function?

A
  • ALP (also see rise in GGT), mostly on canalicular membrane of the hepatocyte, induced by bile acids due to duct obstruction or hepatocyte injury
  • total bilirubin - increases due to over production (hemolysis), under secretion (obstruction, liver injury), or impaired metabolism (Gilbert’s)

*known as cholestatic enzymes, markers that something is wrong post-hepatically

76
Q

What are considered markers of impaired synthetic function?

A
  • albumin - only made in the liver, half life of 14-21 days, production inhibited by physiological stress (surgery, infxn, disease, advanced chronic liver disease)
  • INR (PT) - extrinsic clotting pathway (2,5,7,10) all made in liver, increased INR suggests deficient production of at least one of the cofactors
  • factor 7 has shortest half-life so reasonable measure of immediate liver function
77
Q

What is a broad differential of things that can cause elevated AST or ALT?
Elevated ALP or GGT?

A
  • AST/ALT - viral, bacterial, fungal, parasites, toxins (drugs, alcohol), shock, right heart failure, hepatic vein thrombosis, Wilson’s, Celiac’s, hemochromatosis, sacred/amyloidosis, fat
  • ALP/GGT - stones, strictures, malignancy (CCA/HCC), drugs, lymphoma, metastases, viral
78
Q

What you test for with:
- Hep C
- Hep B
- Hemochromatosis
- Wilson’s Disease
- A1AT

A

Hep C - anti-HCV Ab, HCV RNA by PCR and genotype if positive

Hep B - HBsAg, anti-Hb core, HBeAg/HBeAb/HBV-DNA by PCR if positive

Hemochromatosis - Fe TIBC, ferritin, HFe genetic testing if positive

Wilson’s - ceruloplasmin, 24h urine copper, ATP7b genetics if positive

A1AT - A1AT, A1AT phenotypic if positive

79
Q

NASH

A
  • non-alcoholic steatohepatitis (happens if you have NAFLD)
  • ALT over 150, dyslipidemia, obesity, DM2
  • check ferritin, IgA, U/S
80
Q

What is Hy’s law?

A
  • serum bilirubin over 2x ULN with transaminases over 3x ULN will have a worse prognosis than isolated increased transaminases
81
Q

DDx of high ferritin

A
  • hemochromatosis
  • HCV
  • NASH
  • alcoholic liver disease
  • any inflammatory disease (acute hepatitis)

*high ferritin and high enzymes is NOT always indicative of hemochromatosis (need genetics and biopsy)

82
Q

How are Hep A/B/C/D/E transmitted, and what are risks of longterm infection?

A

Hep A/E - food-borne, usually no long-term infection

Hep B/C/D - body fluids, can cause a chronic infection

83
Q

Hepatitis C
- what kind of virus?
- sx
- consequences
- dx
- staging

A
  • RNA virus (cannot integrate in our genome)
  • only 15% are symptomatic - malaise, fever, abdominal pain, jaundice, dark urine, clay stools
  • increase in ALT/AST 6-8 weeks after exposure
  • 75% develop chronic exposure, 20% of those develop cirrhosis after 20 years and further risk of ascites/encephalopathy/HCC/variceal bleeds
  • Dx: HCV Ab - if positive either an ongoing or resolved infection
  • order additional HC RNA PCR
  • repeat in 6m for spontaneous clearance
  • can stage using fibroscan - measures liver stiffness via vibration velocity (slow if more fibrous)
  • can also stage with APRI:

((AST/AST ULN)/platelet count) x 100
- if over 0.7, significant fibrosis
- if over 2, cirrhosis

84
Q

Treatment for Hep C

A
  • Direct-Acting Antiviral (DAA) therapy
  • anyone with detectable RNA is eligible, goal is HCV clearance (RNA negative 3 and 6m after therapy)
  • target NS3/4A protease inhibitors, NS5A inhibitors (replication and assembly), NS5B inhibitors (polymerase)
  • different combos of sofosbuvir/velpatasvir/ ledipasvir depending on pa-genotype/ genotype 1 specific, re-tx
85
Q

Hepatitis B
- type of virus
- consequences
- tx

A
  • enveloped DNA virus, can form mini-chromosome in nucleus
  • 30-50% have sx, only 5-10% progress to chronic (unless infant, then 90%)
  • 20-30% of chronic get cirrhosis/HCC/failure within 5 years
  • tx: only intervene if signs of inflammation/damage (follow enzymes and fibroscan)
  • nucleoside analogues
  • lamivudine, entecavir, tenofovir (most potent) are all first line
  • goal is longterm viral suppression and reversal of liver damage (can rarely get seroconversion)
  • HBV vaccine (synthetic surface Ag) - part of standard BC vax at 0/2/6m
  • immunity is lifelong, better response if young
86
Q

Process of Diagnosing Hep B

A
  1. HBV surface Ag (HBsAg) - marker of active infection (acute or chronic)
  2. HBV surface Ab (antiHBs) - marker of immunity (infection or vaccine)
  3. HBV Core Ab (anti HBc) - suggests acute infection or re-activation of viral replication
  4. HBV eAg - seen in active infection, marker of viral replication and infectivity
  5. HBV eAb - marker of some degree of immunity, usually recovery phase
  6. HBV DNA - measuring replication in active infection/ response to tx
  7. Hep Delta Ab - check for co-infection

*HBsAG (+) antiHBc (+) IgM antiHBC (+) antiHBs (-) –> acutely infected
(igm only rises in acute phase)

*HBsAG (+) antiHBc (+) IgM antiHBC
(-) antiHBs (-) –> chronically infected

  • HBsAG (-) antiHBc (+) antiHBs (+) –> immune from natural infection
  • HBsAG (-) antiHBc (-) antiHBs (+) –> immune due to vaccination

Med School (21 decks)

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