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GIR Test 2 > B5.024 - Big Case TML > Flashcards

B5.024 - Big Case TML Flashcards

1
Q

Describe the synthesis and metabolism functions of the liver

A

Synthesis - albumin, coagulation factors Metabolism - cholesterol synthesis/uptake, glucose production, glycogen storage, conversion of ammonia to urea, endogenous hormones, lipoproteins, AAs (non essential)

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2
Q

Biotransformation functions of the liver

A

Bilirubin - conjugation and excretion Drugs Ethanol

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3
Q

Immune function of normal liver

A

Reticule-endothelial formation Clearance of damaged cells, proteins, drugs, activated clotting factors Clearance of bacteria and antigens from portal circulation

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4
Q

What is stored in the liver

A

Glycogen Fats Iron Copper Vitamins A,D,K, B12

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5
Q

What are the two types of liver injury

A

Hepatocellular Coolest attic

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6
Q

What measures liver function

A

Albumin PT/INR Bilirubin

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7
Q

Liver function tests

A

Serum albumin - quantitative PT/INR - liver synthesizes the majority of coagulation factors (1, 2, 5, 7, 9, 10) so its an excellent predictor of liver dysfunction but NOT bleeding tendency Bilirubin

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8
Q

What tests suggest hepatocellular injury

A

ALT/AST Tells you about injury to hepatocytes

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9
Q

What tests suggest cholestatic injury

A

Alkaline phosphatase/bilirubin

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10
Q

What is cholestatic injury

A

Decrease bile flow to impaired secretion by hepatocytes Or Obstruction of bile flow through Indra or extra hepatic bile ducts

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11
Q

Acute causes of hepatocellular injury

A

Viral hepatitis Ischemia Autoimmune hepatitis Acetaminophen/toxins Drugs

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12
Q

Causes of acute cholestatic injury

A

Any biliary obstructive process PBC/PSC Drugs Sepsis

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13
Q

Markers of liver injury

A

ALT/AST Alk phos GGT Bilirubin

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14
Q

What is ALT

A

Alan in aminotransferase More specific for liver Located in hepatocyte cytosol

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15
Q

What is AST

A

Aspartate aminotransferase Present in liver, heart, skeletal muscle, kidney, brain, lungs, leukocytes In hepatocyte cytosol and all Mitochondria

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16
Q

What are ALT and AST markers for

A

Hepatic necrosis

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17
Q

What are normal values for AST/ALT

A

10-50

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18
Q

What causes highest elevation of AST/ALT

A

Over 1000 Acute viral hepatitis Toxin induced necrosis Ischemia Autoimmune hepatitis

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19
Q

What causes serum levels moderately elevated of AST/ALT

A

Chronic liver disease, neoplasms

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20
Q

Describe AST/ALT levels in acute biliary obstruction

A

Most have high levels initially which rapidly decline in 24-72 hours

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21
Q

Who gets alcoholic hepatitis

A

10-35% of drinkers who consume 30-50g of alcohol daily >5 years

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22
Q

Characterize alcoholic hepatitis

A

Inflammation and injury to liver; disease ranges from mild to severe More severe in females, European descent

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23
Q

Histo characteristics of alcoholic hepatitis

A

Ballooned hepatocytes Mallory desk hyaline Steatosis

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24
Q

What is the main enzyme responsible for the breakdown of ethanol

A

Alcohol dehydrogenase converts NAD—NADH and ethanol —Acetaldehyde

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25
Q

Increased ratio of NADH/NAD leads to what

A

Alcoholic fatty liver

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26
Q

What is the MEOS pathway

A

Microsomes ethanol oxidizing pathway - inducible p450 pathway CYP2E1: implicated in tolerance of various drugs in alcoholics and increased susceptibility to toxicity

27
Q

What is perixosomal catalase

A

<2% of overall in Vito alcohol oxidation

28
Q

What is alkaline phosphatase

A

Found in or near canalicular membrane Mainly present in liver, bone, placenta, intestine

29
Q

Normal level of alkaline phosphatase

A

70-150 Less than 3x elevation in liver diseases 3-4x higher in infiltrative liver diseases or disease of bile duct

30
Q

When is GGT useful

A

To determine if Alk phos is high from liver issues or bone/placenta

31
Q

Where is GGT found

A

in bile duct epithelium and endoplasmic reticulum NOT IN BONE Sensitive indicator of cholestasis and poor specificity

32
Q

Causes of acute liver injury

A

Drugs Toxins Ischemia Viral hepatitis

33
Q

What are causes of chronic liver injury

A

Alcohol Autoimmune NAFL PSC/PBC Chronic viral hepatitis

34
Q

What is jaundice

A

A medical condition with yellowing of the skin or whites of the eyes arising from excess of the pigment bilirubin and typically caused by obstruction of the bile duct, by liver disease or excessive breakdown of RBCs

35
Q

Normal bilirubin v elevated

A

Normal 1 mg/dL Over 2-3 mg/dL needed to cause jaundice

36
Q

How does blood flow through these structures

A

hepatic artery comes from aorta

portal vein brings nutrient rich blood from the GI tract

bile duct transports bile derived from hepatocytes to the gallbladder

37
Q

Describe the flow of broken down RBCs through the circulation to excretion

A
38
Q

What is the main enzyme responsible for the breakdown of bilirubin

A

Heme oxygenase breaks down heme into biliverdin

39
Q

What do you need to know when evaluating jaundice

A

Is it conjugated or non conjugated

40
Q

What are causes of pre hepatic and hemolytic jaundice

A

extrinsic causes external to blood cells

intrinsic defects in red blood cells

41
Q

Differential for genetic causes of pre hepatic hyperbilirubinemia

A

indirect

spherocytosis

sickle cell

thalassemia

G6PD deficiency

wilsons disease

42
Q

Autoimmune causes of indirect hyperbilirubinemia

A

hemolytic anemia

drug induced

43
Q

Infectious, trauma, drug causes of indirect hyperbilirubinemia

A

Malaria

extravascular blood loss

dapsone

rifampin

44
Q

What is G6PD deficiency

A

genetic x linked disorder

mutation in G6PD gene

normal function is to produce compounds which prevent ROS build up in RBCs

in deficiency, ROS build up can cause hemolytic anemia

45
Q

Explain the epidemiology of G6PD deficiency

A

makes it more difficult for malaria to infect RBCs

46
Q

Hepatitis A transmission, incubation period, natural Hx

A

fecal oral

28 days

98% chance complete recovery

symptoms and biochemical abnormalities should resolve over the next few days

in one or 2 months, her anti-HAV should convert from IgM to IgG

47
Q

Management of hepatitis A

A

supportive care

good handwashing

close household contacts should receive serum immune globulin

48
Q

What is physiologic jaundice

A

increased enterohepatic circulation of bilirubin

lack intestinal flora to convert bilirubin conjugates

decreased hepatic levels of UDP glucuronosyltransferase actvity

meconium has a lot of bilirubin

49
Q

Breast milk jaundice

A

unknown cause, persists after physiologic

from 2-12 weeks

dont stop breastfeeding

50
Q

Breast feeding jaundice

A

decreased hepatic levels of UDP glucuronosyltransferase activity, more pronounced in premature infants

not enough milk: keep trying or supplement

51
Q

Treatment of physiologic jaundice

A

hydration

adequate nutrition

bili lights

exchange transfusion

52
Q

How does phototherapy work

A

bili lights change the internal hydrogen bonds of the bilirubin molecule to create forms that can be excreted into bile or urine without glucuronidation

53
Q

What is kernicterus

A

severe unconjugated hyperbilirubinemia

yellow staining of the basal ganglia, hippocampus, cerebellum, and nuclei of the floor of the fourth ventricle

clinically: high pitched cry, hypotonia, vomiting, hyperpyrexia, sluggish, seizures, paresis of gaze, death

54
Q

Differential for post hepatic hyperbilirubinemia

A

congenital - biliary atresia

malignancy - HCC, pancreatic, lymphoma, cholangiocarcinoma

infectious - clonorchis, opisthorchis

antatomic obstruction - mirizzi syndrome, gallstones

55
Q

What is mirizzi syndrome

A

when a gallstone in the cystic duct becomes so large it obstructs the common hepatic duct

56
Q

Risk factors for HCC

A

Cirrhosis - 80%

HBV

HCV

NAFLD

M>W

57
Q

Dx and treatment of HCC

A

CT or MRI

AFP

treatment ; TACE, tumor ablation, surgical resection, liver transplant

58
Q

What is cirrhosis

A

the end result of chronic hepatic inflammation

defined histologically by hepatic fibrosis, regenerative nodule formation

59
Q

Complications of cirrhosis

A
  1. Loss of hepatocytes
  2. Portal hypertension and portal systemic shunting
  3. Hematologist abnormalities
60
Q

Portal hypertension manifestations

A

ascites

verices

hepatic encephalopathy

hepatorenal syndrome

61
Q

What is hepatic encephalopathy

A

derangment of mental function caused by acute liver failure or by cirrhosis with portal systemic shunting

cirrhotic liver fails to detoxify portal blood toxins, which then interact with the CNS

62
Q

Grades of hepatic encephalopathy

A

1 - trivial lack of awareness, euphoria/anxiety, shortened attention

2 - lethargy or apathy, minimal disorientation, subtle personality changes, inappropriate behavior

3 - somnolence to semi stupor but responsive to verbal stimuli, confusion

4 - coma

63
Q

Hepatorenal syndrome

A

oliguria, increased BUN and Cr, concentrated ruin in a patient with decompensated chronic liver disease

ascites

tubular function INTACT

no glomerular injury

similar to intravascular volume depletion

64
Q

Hematologist complications of cirrhosis

A

anemia

thrombocytopenia

leukopenia

GIR Test 2 (17 decks)

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