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GIR Test 2 > B5.024 Big Case: Jaundice/Abnormal LFTs/Dark Urine > Flashcards

B5.024 Big Case: Jaundice/Abnormal LFTs/Dark Urine Flashcards

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1
Q

major functions of the normal liver

A
  1. synthesis of plasma proteins
  2. metabolism
  3. biotransformation
  4. bile salt synthesis and bile formation
  5. immune: reticulo-endothelial function
  6. storage
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2
Q

what proteins does the liver primarily synthesize

A

albumin

coagulation factors

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3
Q

what metabolic functions does the liver participate in

A 
cholesterol synthesis and uptake
glucose production, glycogen storage
conversion of ammonia to urea
endogenous hormone balance
lipoproteins
synthesis of non-essential amino acids
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4
Q

biotransformative functions of liver

A

bilirubin conjugation
drugs
ethanol

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5
Q

immune functions of liver

A

clearance of damaged cells, proteins, drugs, and activated clotting factors
clearance of bacteria and antigens from the portal circulation

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6
Q

storage functions of liver

A 
glycogen: liver stores enough glucose in the form of glycogen to provide a day's worth of energy
fats
iron
copper
vitamins A, D, K, and B12
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7
Q

2 patterns of liver injurt

A
  1. hepatocellular

2. cholestatic

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8
Q

liver function tests

A

albumin
PT/INR (coagulation factors)
bilirubin

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9
Q

serum albumin measurement

A

quantitatively the most important plasma protein synthesized by the liver
serum levels are affected by: synthesis, distribution, catabolism

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10
Q

why is albumin important

A

provides osmotic pressure

acts as a transport system within the serum

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11
Q

PT/INR measurement

A

excellent test of hepatic synthetic capacity (liver makes coag factors 1,2,5,7,9, and 10)
predictor of liver dysfunction but NOT a predictor of bleeding tendency

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12
Q

hepatocellular injury

A

elevated ALT/AST

injury to hepatocytes

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13
Q

cholestatic injury

A 
elevated alk phos/bilirubin
decrease in bile flow due to
-impaired secretion by hepatocytes
OR
-obstruction of bile flow through intra- or extra-hepatic bile ducts
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14
Q

possible causes of acute hepatocellular injury

A 
viral hepatitis
ischemia
autoimmune hepatitis
acetaminophen/toxins
drugs
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15
Q

possible causes of acute cholestatic injury

A

any biliary obstructive process
PBC/PSC
drugs
sepsis

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16
Q

ALT test

A

more specific for liver

located in hepatocyte cytosol

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17
Q

AST test

A

present in liver, heart, skeletal muscle, kidney, brain, lungs, leukocytes
in hepatocyte cytosol and all mitochondria
not as specific as ALT, but equally as sensitive

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18
Q

discuss ALT/AST test results

A

elevated to some extent in almost all liver diseases
normal: 10-50
highest elevations (over 1000) causes by a few conditions
most other diseases give moderately elevated levels (50-200)

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19
Q

what are the causes of the highest ALT/AST elevations

A

acute viral hepatitis
toxin-induced necrosis (APAP, mushrooms)
ischemia
autoimmune hepatitis

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20
Q

acute biliary obstruction ALT/AST results

A

most patients have high levels which decline rapidly in 24-72 hours

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21
Q

features of alcoholic hepatitis

A

10-35% of drinkers who consume 30-50g alcohol daily > 5 years
characterized by inflammation and injury to the liver (mild to severe)
often underlying cirrhosis
mortality rate 30-60%

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22
Q

histologic characters of alcoholic hepatitis

A

ballooned hepatocytes
Mallory-Denk hyaline
steatosis

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23
Q

major alcohol metabolism pathway

A

ethanol>acetaldehyde via alcohol dehydrogenase
acetaldehyde > acetate via aldehyde dehydrogenase
acetate > H2O and CO2 via oxidation in peripheral tissues

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24
Q

2 alternative pathways from ethanol > acetaldehyde

A
  1. MEOS pathway (CYP2E1)

2. peroxisomal catalase

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25
alcohol dehydrogenase pathway
as alcohol is oxidized, NAD is converted to NADH | increased ration of NADH/NAD leads to alcoholic fatty liver
26
microsomal ethanol oxidizing pathway (MEOS)
inducible p450 pathway | CYP2E1: implicated in tolerance to various drugs in alcoholics and increased susceptibility to toxicity
27
peroxisomal catalase pathways
<2% of overall in vivo alcohol oxidation
28
alkaline phosphatase test
found in or near the canalicular membrane mainly present in liver, bone, placenta, intestine typically: 70-159 -less than 3 folds elevation in most liver disease -> 3-4 fold elevations are typically seen in infiltrative liver diseases or disease of bile ducts
29
GGT test
found in bile duct epithelium and in ER of cholangiocytes found in multiple organs but not in bone sensitive indictor of cholestasis with poor specificity
30
typical outcome of acute liver injury
may experience full recovery OR fulminant hepatic failure
31
typical outcome of chronic liver injury
often develop hepatic fibrosis/cirrhosis
32
causes of acute liver injury
drugs toxins ischemia viral hepatitis
33
causes of chronic liver injury
``` alcohol autoimmune hepatitis non-alcoholic fatty liver PSC/PBC chronic viral hep B or C ```
34
definition of 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 bile duct, by liver disease, or by excessive breakdown of RBCs levels normally 1 mg/dL and levels over 2-3 mg/dL are typically needed to cause jaundice
35
symptoms associated with jaundice
dark urine | light colored stool
36
overview of bilirubin processing
1. breakdown of RBCs heme to bilirubin occurs in macrophages of the reticuloendothelial system 2. unconjugated bilirubin is transported through blood (complexed to albumin) to the liver 3. bilirubin taken up via facilitated diffusion by the liver and conjugated with glucuronic acid 4. conjugated bilirubin secreted into bile and then intestine 5. in intestine, glucuronic acid is removed by bacteria and bilirubin is converted to urobilinogen 6. some of urobilinogen is reabsorbed and enters portal blood (some is excreted in kidneys) 7. remaining urobilinogen in GI is oxidized by bacteria to brown stercobilin
37
heme to biliverdin enzyme
heme oxygenase
38
total serum bilirubin components
conjugated (direct) + unconjugated (indirect)
39
pre-hepatic/hemolytic causes of hyperbilirubinemia
extrinsic causes external to blood cells OR intrinsic defects in RBCs
40
intra-hepatic/ hepatocellular causes of hyperbilirubinemia
pathology is located within the liver and due to disease of hepatic parenchymal cells
41
post hepatic/cholestatic hyperbilirubinemia
pathology is located after conjugation in the liver caused by an obstructive process
42
genetic causes of pre-hepatic hyperbilirubinemia
``` spherocytosis sickle cell thalassemia G6PD deficiency Wilson's disease ```
43
autoimmune causes of pre-hepatic hyperbilirubinemia
hemolytic anemia | drug induced
44
infectious causes of pre-hepatic hyperbilirubinemia
malaria
45
traumatic causes of pre-hepatic hyperbilirubinemia
extra vascular blood loss
46
drug causes of pre-hepatic hyperbilirubinemia
dapsone | rifampin
47
characteristics of a G6PD deficiency
genetic disorder, occurs almost exclusively in males (X-linked) affects 400 million worldwide (North Africa, Middle East, Mediterranean)
48
function of G6PD
normal function to produce compounds which prevent ROS build up in RBCs in deficiency , ROS build up and cause hemolytic anemia certain drugs/infections/foods can increase ROS
49
genetic causes of hepatocellular hyperbilirubinemia
hemochromatosis Wilson's disease Gilbert's syndrome crigler-najjar syndrome
50
autoimmune causes of hepatocellular hyperbilirubinemia
autoimmune hepatitis PBC PSC IgG4 cholangiopathy
51
infectious causes of hepatocellular hyperbilirubinemia
viral hepatitis | hepatic abscess
52
vascular causes of hepatocellular hyperbilirubinemia
impaired flow
53
drug/toxin causes of hepatocellular hyperbilirubinemia
APAP INH idiosyncratic drug reactions alcohol
54
malignant causes of hepatocellular hyperbilirubinemia
HCC cholangiocarcinoma lymphomas metastatic disease
55
50/50 ratio of direct to indirect bilirubin in lab testing
intra-hepatic cause of hyperbilirubinemia
56
physiologic jaundice of the newborn
increased enterohepatic circulation of bilirubin -lack of intestinal flora to convert bilirubin conjugates -decreased hepatic levels of UDP1A1 activity -inability to pass meconium (contains significant amount of bilirubin) impacts 60% of newborns
57
breast milk jaundice
cause unknown, persists after physiologic jaundice from weeks 2-12 don't stop breastfeeding
58
breast feeding jaundice
decreased hepatic levels of UDP1A1 activity, more pronounced in premature infants not enough milk: keep trying or supplement
59
treatment for physiologic jaundice of the newborn
hydration adequate nutrition bili lights (phototherapy) exchange transfusion
60
kernicterus
severe unconjugated hyperbilirubinemia | yellow staining of basal ganglia, hippocampus, cerebellum, and nuclei of the floor of 4th ventricle
61
clinical features of kernicterus
high pitched cry, hypotonia, vomiting, hyperpyrexia, sluggish Moro, seizures, paresis of gaze, and death survivors can have choreoathetosis, spasticity, and sensorineural hearing loss
62
congenital causes of post-hepatic hyperbilirubinemia
bilirary atresia
63
malignant causes of post-hepatic hyperbilirubinemia
``` HCC cholangiocarcinoma pancreatic cancer lymphoma ampullary cancer ```
64
infectious causes of post-hepatic hyperbilirubinemia
clonorchis | opisthorchis
65
anatomic causes of post-hepatic hyperbilirubinemia
biliary strictures mirizzi syndrome cholelithiasis
66
what is mirizzi syndrome
gallstone not in duct but in outflow portion of gallbladder | still causes obstruction
67
epidemiology of HCC
6th most common malignancy and leading cause of mortality in patients with cirrhosis risk factors: cirrhosis HBV, HCV, NAFLD, M>W
68
diagnosis of HCC
multi phase imaging with IV contrast | often secrete alpha-fetoprotein (AFP)
69
treatment of HCC
chemotherapy (TACE) tumor ablation surgical resection liver transplantation
70
histo findings of cirrhosis
hepatic fibrosis | regenerative nodule formation
71
etiologies of cirrhosis
``` viruses (hepatitis B and C) ethanol misuse NAFLD chronic biliary obstruction autoimmune hepatitis storage disease chronic CHF ```
72
primary complications of cirrhosis
1. loss of hepatocytes (decrease in liver function) 2. portal hypertension and portal-systemic shunting 3. hematologic abnormalities
73
portal venous system
begins in capillaries in the intestine and terminates as the hepatic sinusoids nutrients from the GI tract and hormones from pancreas are delivered to the liver
74
manifestations of portal hypertensions
ascites varices hepatic encephalopathy hepatorenal syndrome
75
development of ascites
sodium and water retention in conjunction with increased intrahepatic resistance and increased sinusoidal pressure
76
esophageal varices
portal systemic collaterals
77
hepatic encephalopathy
derangement of mental function caused by acute liver failure or by cirrhosis with portal system shunting cirrhotic liver fails to detox portal blood toxins which then interact with the CNS
78
compensated cirrhosis
1. increased intrahepatic vascular resistance, moderate portal hypertension 2. splanchnic arterial vasodilation 3. low effective arterial blood volume 4. increased cardiac output and plasma volume 5. restoration of effective arterial blood volume
79
decompensated cirrhosis (hepatorenal system) (HRS)
1. disease progression, severe portal hypertension, bacterial translocation 2. severe splanchnic arterial vasodilation 3. markedly reduced effective arterial blood volume, increased CO and plasma volume insufficient to normalize effective arterial blood volume, activation of sodium retaining and vasoconstrictor systems 4. sodium and water retention and ascites formation 5. further activation of vasoconstrictor systems & impairment in CO 6. renal failure
80
clinical picture of hepatorenal syndrome
oliguria, increased BUN and creatinine, concentrated urine in a patient with decompensated chronic liver disease - ascites - tubular function intact - no glomerular injury - similar to dehydration clinically
81
hematologic complications of cirrhosis
anemia thrombocytopenia leukopenia

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