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GI Midterm > Bile, Cholesterol, Bilirubin, Lipoproteins > Flashcards

Bile, Cholesterol, Bilirubin, Lipoproteins Flashcards

1
Q

Criggler Najjar

Type 1

A

Complete absence of UDP-GT gene
Buildup of unconjugated bilirubin
Causes kernicterus in newborn

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2
Q

Criggler Najjar

Type II

A

Mutation in UDP-GT; allows for some activity
Buildup of unconjugated
Benign

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3
Q

Gilbert Syndrome

A

Reduction in transcription of UDP-GT
Buildup of unconjugated bilirubin
Appears in adolescence
See mild jaundice during periods of stress

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4
Q

Dubin-Johnson

A

Mutation in MRP2 (needed to move conjugated bilirubin from hepatocyte to canalicululs)
Deposits in hepatocytes
Appears at early adulthood
Jaundice

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5
Q

Rotor Syndrome

A

Mutations in OAT1B1 and OAT1B3 (needed move bilirubin from blood to hepatocyte)
Seen after birth or childhood
Unconjugated and conjugated hyperbilirubinemia

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6
Q

7-alpha hydroxylase

Function and feedback

A

Aka CYP7a
Only found in liver
Catalyzes rate limiting step needed to convert cholesterol to bile acids
Negative feedback by accumulation of bile acids
Activated when there is an accumulation of cholesterol

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7
Q

Primary bile acids

A

Chenodeoxycholic acid and cholic acid

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8
Q

Purpose of bile acid conjugation

A

Decrease the pKa so that more are present in ionized form, making them better detergents
Use glycine or taurine to produce glycohoilc acid and taurocholic acid, BILE SALTS

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9
Q

Production of secondary bile acids

Where are they found?

A

Done in colon by bacteria, which deconjugate and dehydroxylate primary bile acids

In feces

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10
Q

Secretion and reabsorption of bile acids

Channels

A

NTCP-sinusoidal space to hepatocyte
BSEP-hepatocyte to canaliculus
ASBT-absorption in ileum
OST-ileal cell to portal circulation

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11
Q

Morphological features with cholestasis

A
  1. Enlargement of hepatocytes
  2. Dilated canalicular spaces
  3. Apoptosis
  4. Kupffer cells with bile pigments

May see bile plugs

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12
Q

Pharmacological intervention with bile salts

A

Bile acid resins/sequestrates bind to bile acids to prevent reabsorption, to reduce cholesterol levels

Forces the liver to make more bile acids, which reduces cholesterol (takes away negative feedback mechanism

Can also use soluble fibers, which may also bind to bile acids to prevent reabsorption

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13
Q

Extravascular Erythrocyte Destruction

A

90%
Macrophages from reticuloendothelial system (spleen, liver, and bone) monitor RBCs to phagocytose them before they lyse
In macrophage, globin is broken down into AA, iron is recycled, and heme is broken down
SPHEROCYTES

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14
Q

Intravascular hemolysis

A

10%
Usually due to trauma
RBCs lyse in circulation, releasing hemoglobin into plasma
SCHISTOCYTES
Haptoglobin-hemoglobin: Hemoglobin binds to HAPTOGLOBIN, which takes into the macrophage, where it is then broken down into iron, heme, and globin
Hemopexin-heme: If haptoglobin saturated, free heme binds to hemopexin on macrophages of reticuloendothelial system to be engulfed

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15
Q

Heme degradation to bilirubin

Where and how?

A

Occurs in reticuloendothelial system (macrophage)

Heme converted to biliverdin by heme oxygenase; ONLY enzyme that produces carbon monoxide (here is cytoprotective)

Biliverdin converted to bilirubin by biliverdin reductase

Bilirubin released bound to albumin

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16
Q

Bilirubin fate in the liver

A

In circulation, bilirubin bound to albumin

Bilirubin enters the liver, and is bound to GST-b to prevent it from returning to circulation (which can happen when bilirubin is in its indirect form)

UDP-GT acts on bilirubin twice to make it direct (first time is the committed step to make BMG, second time is the rate limiting step BDG)

Direct bilirubin is excreted into small intestine

Acted on by bacterial enzymes to produce urobilinogen–>stercobilin (brown poop)
Some urobilinogen is reabsorbed and goes to kidney for excretion (stercobilinogen–>urobilin)

17
Q

MRP2

A

Movement of bilirubin from hepatocyte to canaliculus for secretion

Defect causes Dubin-Johnson-buildup of direct bilirubin in hepatocytes

18
Q

OAT1B1/3

A

Transporter of bilirubin from sinusoidal space to hepatocyte

Defect causes rotor syndrome (hyperbilirubinemia in both conjugated and unconjugated)

19
Q

Hemolytic Jaundice

A

“Pre-hepatic”
Massive lysis of RBCs exceeds liver capacity to process bilirubin
Increase in indirect bilirubin
Urobilinogen in blood and urine also increased

20
Q

Hepatocellular jaundice

A

Damage to liver cells causes increase in conjugated and unconjugated bilirubin

21
Q

Regulation of Cholesterol Synthesis (positive, negative, short term vs. long term)

A

+ regulators:
Insulin dephosphorylates HMG receptor with HMGR phosphatase to activate it

-regulators:
Glucagon phosphorylates HMG receptor with AMPK to inactivate it

Long term regulation:
Decreased cholesterol causes SREPB2 (TF) to move into golgi and increase transcription of LDL receptors and HMG CoA reducatse. In presence of cholesterol, SREBP2 stays in endoplasmic reticulum

22
Q

Statins

A

Inhibit HMG CoA reductase to reduce cholesterol synthesis

This then increases LDL removal from circulation by increases LDL receptors

23
Q

Hypertriglyceridemia
Diagnostic
Causes
Clinical features

A

TAG over 150 due to abnormally high chylomicrons, VLDL, or both

Could be caused by lipoprotein lipase or CII deficiency

Can cause pancreatitis, eruptive cutaneous xanthomas, tuberous xanthomas, lipemia retinalis

24
Q

Familial dysbetalipoproteinemia

A

Increased levels of IDL
(elevated VLDL:triglyceride)

Defective ApoE

Can cause xanthomas and atherosclerosis

25
Q

Treatment for hypertriglyceridemia

A

Statins
Omega-3 FA and fibrate that increase LPL activity
Niacin

26
Q

Hypercholesterolemia

A

Defect in LDL-R causes elevated LDL and normal VLDL

Increased serum cholesterol but normal TAGs

Leads to causes tendon xanthomas, xanthelsma (yellow pockets of cholesterol by eye), ischemic heart disease

27
Q

ApoA-1 deficiency

A

Low HDL; normal LDL and TAGs

Lack of ApoA1 causes reduction in half life of HDL

Leads to CAD; random deposit of cholesterol, corneal clouding

28
Q

LCAT deficiency

A

Can lead to low levels of HDL because LCAT is required for HDL maturation from HDL3 to HDL2.

Increase in cholesterol

Fish eye

29
Q

Tangier Disease

A

Absence of ABCA1 causes decrease in HDL levels

Cholesterol accumulation in tissues throughout the body, especially orange tonsils

30
Q

Ezetimbe

A

Inhibits absorption of cholesterol at the brush border and increases number of LDL receptors at liver

Decreases LDL

GI Midterm (6 decks)

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