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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
Increased ratio of NADH/NAD leads to what
Alcoholic fatty liver
26
What is the MEOS pathway
Microsomes ethanol oxidizing pathway - inducible p450 pathway CYP2E1: implicated in tolerance of various drugs in alcoholics and increased susceptibility to toxicity
27
What is perixosomal catalase
\<2% of overall in Vito alcohol oxidation
28
What is alkaline phosphatase
Found in or near canalicular membrane Mainly present in liver, bone, placenta, intestine
29
Normal level of alkaline phosphatase
70-150 Less than 3x elevation in liver diseases 3-4x higher in infiltrative liver diseases or disease of bile duct
30
When is GGT useful
To determine if Alk phos is high from liver issues or bone/placenta
31
Where is GGT found
in bile duct epithelium and endoplasmic reticulum NOT IN BONE Sensitive indicator of cholestasis and poor specificity
32
Causes of acute liver injury
Drugs Toxins Ischemia Viral hepatitis
33
What are causes of chronic liver injury
Alcohol Autoimmune NAFL PSC/PBC Chronic viral hepatitis
34
What is jaundice
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
Normal bilirubin v elevated
Normal 1 mg/dL Over 2-3 mg/dL needed to cause jaundice
36
How does blood flow through these structures
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
Describe the flow of broken down RBCs through the circulation to excretion
38
What is the main enzyme responsible for the breakdown of bilirubin
Heme oxygenase breaks down heme into biliverdin
39
What do you need to know when evaluating jaundice
Is it conjugated or non conjugated
40
What are causes of pre hepatic and hemolytic jaundice
extrinsic causes external to blood cells intrinsic defects in red blood cells
41
Differential for genetic causes of pre hepatic hyperbilirubinemia
indirect spherocytosis sickle cell thalassemia G6PD deficiency wilsons disease
42
Autoimmune causes of indirect hyperbilirubinemia
hemolytic anemia drug induced
43
Infectious, trauma, drug causes of indirect hyperbilirubinemia
Malaria extravascular blood loss dapsone rifampin
44
What is G6PD deficiency
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
Explain the epidemiology of G6PD deficiency
makes it more difficult for malaria to infect RBCs
46
Hepatitis A transmission, incubation period, natural Hx
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
Management of hepatitis A
supportive care good handwashing close household contacts should receive serum immune globulin
48
What is physiologic jaundice
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
Breast milk jaundice
unknown cause, persists after physiologic from 2-12 weeks dont stop breastfeeding
50
Breast feeding jaundice
decreased hepatic levels of UDP glucuronosyltransferase activity, more pronounced in premature infants not enough milk: keep trying or supplement
51
Treatment of physiologic jaundice
hydration adequate nutrition bili lights exchange transfusion
52
How does phototherapy work
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
What is kernicterus
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
Differential for post hepatic hyperbilirubinemia
congenital - biliary atresia malignancy - HCC, pancreatic, lymphoma, cholangiocarcinoma infectious - clonorchis, opisthorchis antatomic obstruction - mirizzi syndrome, gallstones
55
What is mirizzi syndrome
when a gallstone in the cystic duct becomes so large it obstructs the common hepatic duct
56
Risk factors for HCC
Cirrhosis - 80% HBV HCV NAFLD M\>W
57
Dx and treatment of HCC
CT or MRI AFP treatment ; TACE, tumor ablation, surgical resection, liver transplant
58
What is cirrhosis
the end result of chronic hepatic inflammation defined histologically by hepatic fibrosis, regenerative nodule formation
59
Complications of cirrhosis
1. Loss of hepatocytes 2. Portal hypertension and portal systemic shunting 3. Hematologist abnormalities
60
Portal hypertension manifestations
ascites verices hepatic encephalopathy hepatorenal syndrome
61
What is hepatic encephalopathy
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
Grades of hepatic encephalopathy
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
Hepatorenal syndrome
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
Hematologist complications of cirrhosis
anemia thrombocytopenia leukopenia

GIR Test 2 (17 decks)

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