Brainscape's Knowledge GenomeTM

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


See full index

GI > Bilirubin, Jaundice and Gallstones > Flashcards

Bilirubin, Jaundice and Gallstones Flashcards

1
Q

Describe bilirubin transport and liver absorption

A

Insoluble unconjugated bilirubn is transported in blood by binding to albumin.

At hepatocyte membrane, albumin separates allowing bilirubin absorption

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

Describe process of bilirubin conjugation

A

Bilirubin is transported by ligandin in cytosol and is conjugated with glucorinade by UDP glucuronosyltransferase in ER

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

Describe process of bilirubin secretion

A

Secreted mostly as diglucuronide (conjugated) into canaliculus against concentration gradient

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

Bile formation process: what are the transporters for movement into canaliculi

A

MDR3 for phospholipids
MRP2 for glucuronides (bilirubin)
SPGP for bile salts

On basolateral membrane: ion exchangers and bile salt channels

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

What are major components of bile?

A

Bile salts=66%
Phospholipids=22%
Protein=5%
Bilirubin= only 1%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Conjugation produces what change in bilirubin?

A

Glucuronidation makes molecule more water soluble

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

What is toxic effect of unconjugated bilirubin? How is this prevented?

A

Unconjugated bilirubin is a neurotoxic lipid

Protective mechanisms: Albumin binding, blood-brain barrier, conjugation, excretion in bile

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

What is delta bilirubin

A

Conjugated bilirubin that is covalently bonded to albumin

It is only found in patients with protracted presence of conjugated bilirubin and its size prevents passage into urine

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

What is effect of bacteria on bilirubin?

A

Bacteria convert bilirubin to colorless water soluble urobilinogen– some is absorbed and some reaches urine via serum

Bacteria act on urobilinogent o produce payrolls which are excreted

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

What is the difference between indirect and direct jaundice?

A

Indirect: unconjugated hyperbilirubinemia– hydrogen bonding to albumin prevents passage into urine

Direct: mixture of conjugated/unconjugated bilirubin in serum– conjugated can pass into urine, may see delta bilirubin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe difference in urine in unconjugtaed vs. conjugated jaundice

A

Unconjugated: yellow urine (negative on urine dipstick)
Conjugated: dark red urine (positive on dipstick)

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

Main etiologies of unconjugated hyperbilirubinemia: (3)

A

Overproduction of bilirubin: hemolysis, extravasation into tissue, ineffective erythropoiesis
Reduced uptake of BR by liver: altered circulation or drug-induced
Defects of BR conjugation: inherited or acquired (drugs, hep, hyperthyroidism), newborns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is cause of jaundice in the newborn and how is it treated?

A

Jaundice in newborn is result of immature transport and conjugation of bilirubin as well as hemolysis

Treat with phototherapy (breaks hydrogen bonds allowing excretion) to prevent CNS injury

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

What is Gilbert’s Syndrome?

A

A benign autosomal recessive defect in promoter gene for glucuronosyltransferase leading to elevated unconjugated bilirubin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is effect of fasting in Gilbert’s syndrome?

A

Exaggerated increase in unconjugated bilirubin that may cause jaundice

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

How is Gilert’s Syndrome diagnosed

A

Exclusion: unconjugated bilirubinemia with no other uses

Normal LFTs, no bilirubine in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are main causes of conjugated hyperbilirubinemia? (3)

A 
Inherited secretory defect
Disease of hepatocytes: necrotizing hepatocellular, cholestatic (intrahepatic cholestasis), mixed
Biliary obstruction (extrahepatic cholestasis)
18
Q

What are Dubin-Johnson & Rotor syndromes?

A

Inherited secretory defect– normal LFTs and normal bile salt excretion

Liver in Dubin-Johnson syndrome is black because of pigment

19
Q

What is necrotizing hepatitis?

What are some observations (3)

A

Acute disease associated with high serum transaminase and decreased synthetic function

Observe low serum prothrombin not corrected by intramuscular vitamin K as well as fatigue and anorexia

20
Q

What is chronic hepatitis?

A

Scarring and destruction of liver cells due to variety of causes (viral, alf, drugs, toxins, autoimmune)
Poor synthetic function (serum prothrombin not corrected by IM VitK)

21
Q

What is the difference between intrahepatic and extra hepatic cholestasis?

A

Intrahepatic: hepatocellular disease (i.e chronic hepatitis)

Extrahepatic: biliary obstruction ( can see dilated ducts)

22
Q

What is the histological appearance of cholestasis?

A

Canalicular bile plugging with little necrosis

Looks similar for both intrahepatic and extra hepatic causes

23
Q

What are biochemical findings of cholestasis? (2)

A 
Alkaline phosphatase>3x normal 
Increased GGT (more specific)

Note: can have elevated alkaline phosphates or GGT without jaundice for partial biliary obstruction or intrahepatic cholestasis

24
Q

What are major symptoms in cholestasis? (3)

A

Pruritis (itchy skin)
Malabsorption of fat/fat-soluble vitamins (ADKE)
High serum cholesterol leading to xanthelasma (deposits in tissue)

25
Q

What are causes of extra hepatic cholestasis: both benign (3) and malignant (3)

A

Benign: gallstones, strictures, pancreatitis

Malignant: Pancreas, bile duct or gallbladder

26
Q

What are intrahepatic causes of cholestasis (big list)

A

Alcohol, drugs, hepA, sepsis, pregnancy, estrogens, TB, primary biliary cirrhosis, malignancies, primary sclerosing cholangitis

27
Q

What is effect of ursodeoxycholic acid in cholestasis?

A

Prolongs life in primary biliary cirrhosis

May be useful in other forms of cholestasis

28
Q

Describe maximum serum bilirubin in following conditions:

Hemolysis, Gilbert’s, complete obstruction, obstruction+hemolysis, obstruction+renal failure

A

Very high in complete obstruction

Even higher in obstruction with hemolysis or renal failure

29
Q

What lab signs are visible in acute obstruction? Transaminase, bilirubin and alkaline phosphatase

A

Transaminase immediately dramatically increases and declines rapidly once stone passed

Bilirubin increases then falls

Delayed increase and fall in alkaline phosphatase levels

30
Q

What is etiology of gallstones?

What are predisposing factors? (3)

A

Gallstones may form when cholesterol or BR precipitate from bile

Predisposing factors: supersaturation, stasis, nucleation factors

31
Q

What are the different types of gallstones (2)

A

Cholesterol: >50% (form in gallbladder

Pigment: unconjugated bilirubin

32
Q

What is the significance of black vs. brown pigment gallstones?

A

Black=form in gallbladder

Brown: form in bile ducts

33
Q

What are risk factors for cholesterol gallstones?

A

Female, age>30, multiparity, obesity, lack of exercise
Rapid weight loss
Family history, Native Americans, whites, blacks
Drugs: estrogens, clofibrate, somatostatin
Parenteral feeding

34
Q

Cholesterol Stone Composition

A

50-90% cholesterol with small amounts of mucin, Ca and bilirubin

35
Q

What is cholesterol supersaturation? What is result of it?

A

Supersaturation: low phophoslipid+bile salts/ cholesterol

Supersaturation consistent with cholesterol stones (but not pigment stones)

36
Q

What is the medical treatment for cholesterol stones/sludge

A

Ursodeoxycholic acid or chenodeoxycholic acid may be effective for cholesterol stones (but not pigment stones)

37
Q

Black gallstones: What is composition? Where do they form and what are the risk factors (3)?

A

50-80% Calcium Bilirubinate (85% radio-dense)

Form only in gallbladder; risk factors include old age, hemolysis and cirrhosis

38
Q

Brown gallstones: composition, formation and risk factors (2)

A

Brown gallstones are mostly calcium bilirubinate, but also contain fatty acids, bacteria
Form mainly in bile duct
Risk factors: old age, post cholecystectomy

39
Q

What are complications of gallstones? (6)

A

Intermittently obstructs cystic duct==>Intermittent biliary colic (20%)
Impacts in cystic duct==>acute cholecystitis (10%)
Compress common bile duct==>Mirizzi syndrome (.1%)
Impact in distal common bile duct==>jaundice, colic pain, cholangitis/ acute biliary pancreatitis (5%)
Erode thru gallbladder into duodenum==>cholesystenteric fistula (.1%)
Chronic cholelithiasis==>gallbladder carcinoma (.1%)

40
Q

Describe the pathophysiology for acute cholecystitis

A

Persistent blockage of cystic duct by gallstone leads to increase in mucosal prostaglandins, which causes inflammation

Superimposed infection can develop

GI (41 decks)

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