Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

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

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what proteins does the liver primarily synthesize

A

albumin

coagulation factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

biotransformative functions of liver

A

bilirubin conjugation
drugs
ethanol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

2 patterns of liver injurt

A
  1. hepatocellular

2. cholestatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

liver function tests

A

albumin
PT/INR (coagulation factors)
bilirubin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

serum albumin measurement

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

why is albumin important

A

provides osmotic pressure

acts as a transport system within the serum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

hepatocellular injury

A

elevated ALT/AST

injury to hepatocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

possible causes of acute hepatocellular injury

A 
viral hepatitis
ischemia
autoimmune hepatitis
acetaminophen/toxins
drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

possible causes of acute cholestatic injury

A

any biliary obstructive process
PBC/PSC
drugs
sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

ALT test

A

more specific for liver

located in hepatocyte cytosol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the causes of the highest ALT/AST elevations

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

acute biliary obstruction ALT/AST results

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

histologic characters of alcoholic hepatitis

A

ballooned hepatocytes
Mallory-Denk hyaline
steatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

2 alternative pathways from ethanol > acetaldehyde

A
  1. MEOS pathway (CYP2E1)

2. peroxisomal catalase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

alcohol dehydrogenase pathway

A

as alcohol is oxidized, NAD is converted to NADH

increased ration of NADH/NAD leads to alcoholic fatty liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

microsomal ethanol oxidizing pathway (MEOS)

A

inducible p450 pathway

CYP2E1: implicated in tolerance to various drugs in alcoholics and increased susceptibility to toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

peroxisomal catalase pathways

A

<2% of overall in vivo alcohol oxidation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

alkaline phosphatase test

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

GGT test

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

typical outcome of acute liver injury

A

may experience full recovery OR fulminant hepatic failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

typical outcome of chronic liver injury

A

often develop hepatic fibrosis/cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

causes of acute liver injury

A

drugs
toxins
ischemia
viral hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

causes of chronic liver injury

A 
alcohol
autoimmune hepatitis
non-alcoholic fatty liver
PSC/PBC
chronic viral hep B or C
34
Q

definition of 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 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
Q

symptoms associated with jaundice

A

dark urine

light colored stool

36
Q

overview of bilirubin processing

A
  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
Q

heme to biliverdin enzyme

A

heme oxygenase

38
Q

total serum bilirubin components

A

conjugated (direct) + unconjugated (indirect)

39
Q

pre-hepatic/hemolytic causes of hyperbilirubinemia

A

extrinsic causes external to blood cells
OR
intrinsic defects in RBCs

40
Q

intra-hepatic/ hepatocellular causes of hyperbilirubinemia

A

pathology is located within the liver and due to disease of hepatic parenchymal cells

41
Q

post hepatic/cholestatic hyperbilirubinemia

A

pathology is located after conjugation in the liver caused by an obstructive process

42
Q

genetic causes of pre-hepatic hyperbilirubinemia

A 
spherocytosis
sickle cell
thalassemia
G6PD deficiency
Wilson's disease
43
Q

autoimmune causes of pre-hepatic hyperbilirubinemia

A

hemolytic anemia

drug induced

44
Q

infectious causes of pre-hepatic hyperbilirubinemia

A

malaria

45
Q

traumatic causes of pre-hepatic hyperbilirubinemia

A

extra vascular blood loss

46
Q

drug causes of pre-hepatic hyperbilirubinemia

A

dapsone

rifampin

47
Q

characteristics of a G6PD deficiency

A

genetic disorder, occurs almost exclusively in males (X-linked)
affects 400 million worldwide (North Africa, Middle East, Mediterranean)

48
Q

function of G6PD

A

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
Q

genetic causes of hepatocellular hyperbilirubinemia

A

hemochromatosis
Wilson’s disease
Gilbert’s syndrome
crigler-najjar syndrome

50
Q

autoimmune causes of hepatocellular hyperbilirubinemia

A

autoimmune hepatitis
PBC
PSC
IgG4 cholangiopathy

51
Q

infectious causes of hepatocellular hyperbilirubinemia

A

viral hepatitis

hepatic abscess

52
Q

vascular causes of hepatocellular hyperbilirubinemia

A

impaired flow

53
Q

drug/toxin causes of hepatocellular hyperbilirubinemia

A

APAP
INH
idiosyncratic drug reactions
alcohol

54
Q

malignant causes of hepatocellular hyperbilirubinemia

A

HCC
cholangiocarcinoma
lymphomas
metastatic disease

55
Q

50/50 ratio of direct to indirect bilirubin in lab testing

A

intra-hepatic cause of hyperbilirubinemia

56
Q

physiologic jaundice of the newborn

A

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
Q

breast milk jaundice

A

cause unknown, persists after physiologic jaundice
from weeks 2-12
don’t stop breastfeeding

58
Q

breast feeding jaundice

A

decreased hepatic levels of UDP1A1 activity, more pronounced in premature infants
not enough milk: keep trying or supplement

59
Q

treatment for physiologic jaundice of the newborn

A

hydration
adequate nutrition
bili lights (phototherapy)
exchange transfusion

60
Q

kernicterus

A

severe unconjugated hyperbilirubinemia

yellow staining of basal ganglia, hippocampus, cerebellum, and nuclei of the floor of 4th ventricle

61
Q

clinical features of kernicterus

A

high pitched cry, hypotonia, vomiting, hyperpyrexia, sluggish Moro, seizures, paresis of gaze, and death
survivors can have choreoathetosis, spasticity, and sensorineural hearing loss

62
Q

congenital causes of post-hepatic hyperbilirubinemia

A

bilirary atresia

63
Q

malignant causes of post-hepatic hyperbilirubinemia

A 
HCC
cholangiocarcinoma
pancreatic cancer
lymphoma
ampullary cancer
64
Q

infectious causes of post-hepatic hyperbilirubinemia

A

clonorchis

opisthorchis

65
Q

anatomic causes of post-hepatic hyperbilirubinemia

A

biliary strictures
mirizzi syndrome
cholelithiasis

66
Q

what is mirizzi syndrome

A

gallstone not in duct but in outflow portion of gallbladder

still causes obstruction

67
Q

epidemiology of HCC

A

6th most common malignancy and leading cause of mortality in patients with cirrhosis
risk factors: cirrhosis HBV, HCV, NAFLD, M>W

68
Q

diagnosis of HCC

A

multi phase imaging with IV contrast

often secrete alpha-fetoprotein (AFP)

69
Q

treatment of HCC

A

chemotherapy (TACE)
tumor ablation
surgical resection
liver transplantation

70
Q

histo findings of cirrhosis

A

hepatic fibrosis

regenerative nodule formation

71
Q

etiologies of cirrhosis

A 
viruses (hepatitis B and C)
ethanol misuse
NAFLD
chronic biliary obstruction
autoimmune hepatitis
storage disease
chronic CHF
72
Q

primary complications of cirrhosis

A
  1. loss of hepatocytes (decrease in liver function)
  2. portal hypertension and portal-systemic shunting
  3. hematologic abnormalities
73
Q

portal venous system

A

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
Q

manifestations of portal hypertensions

A

ascites
varices
hepatic encephalopathy
hepatorenal syndrome

75
Q

development of ascites

A

sodium and water retention in conjunction with increased intrahepatic resistance and increased sinusoidal pressure

76
Q

esophageal varices

A

portal systemic collaterals

77
Q

hepatic encephalopathy

A

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
Q

compensated cirrhosis

A
  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
Q

decompensated cirrhosis (hepatorenal system) (HRS)

A
  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
Q

clinical picture of hepatorenal syndrome

A

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
Q

hematologic complications of cirrhosis

A

anemia
thrombocytopenia
leukopenia

GIR Test 2 (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions