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GI / Hepatology > 2 - Hepatic Physiology > Flashcards

2 - Hepatic Physiology Flashcards

1
Q

If the liver is too big

A

It will shrink

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2
Q

If the liver is too small

A

It will grow

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3
Q

Bilirubin Produced By

A

Oxidation of Heme and Reduction of resultant bilverdin

Heme oxygenase converts Heme to Biliverdin
Biliverdin Reductase converts Bilverdin into Bilirubin

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4
Q

After C-Glycine Administration Early Peak

A

Ineffective Erythropoiesis

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5
Q

Conjugation of Bilirubin

A

To make it more soluble

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6
Q

Bilirubin

A

Delivered in sinusoid
Uptaken into hepatocyte
Biotransformed and secreted into biliary flow

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7
Q

Glucuronyl Transferase

A

Does something I don’t know he did not use enough words

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8
Q

Bilirubins

A

Unconjugated (UCB)
Mono-Glucuronide (BMG)
Diglucuronide (BDG)

These are progressive steps

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9
Q

Bacterial Breakdown of Bilirubin

A

In color

Gives stool brown color

Deconjugation
Reduction
Oxidation

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10
Q

No bilirubin in stool

A

Clay colored stool

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11
Q

Biliary Atresia

A

Agenesis of common bile duct

Treat with “Cuh-sai” procedure
Sew intestine into intrahepatic bile ducts
Stool color doesn’t matter much actually. Stool swatches were more for parents. What more counts is bilirubin in serum.

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12
Q

Enterohepatic Circulation of Bilirubin - In Hepatocyte dysfunction (hepatocellular)

A

Increased urobilinogen in urine because it is less efficiently reabsorbed by hepatocytes

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13
Q

Enterohepatic Circulation of Bilirubin - In Biliary Obstruction

A

Stools appear white

No urobilinogen detected in urine

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14
Q

Measurement of bilirubin in blood

A

=

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15
Q

Hyperbilirubinemia and Jaundice

A

Occur when liver fails or when other steps of the metabolism are abnormal.
Bilirubin >35μM can begin to detect jaundice clinically.
Coca Cola urine

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16
Q

Beefy Red Liver

A

Bile getting stuck in liver

Leads to micronodules too

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17
Q

Cause of Unconjugated Hyperbilirubinemia

A

Overproduction: Hemolysis or Ineffective Erythropoiesis
Impaired Uptake: Fast, Sepsis, Drugs (eg probenecid)

Impaired Conjugation:
Inherited Mutations in UGT1 - Grigler-Najjar Syndrome (Type I and Type II)
Inherited polymorphisms in UGT1 - Gilbert Syndrome

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18
Q

Cause of Conjugated Hyperbilirubinemia

A

Hepatocellular Diseases Cause Decreased Secretion:
Cirrhosis
Acute Hepatitis (drugs, viral, alcohol)

Pregnancy

Drugs

Inherited Diseases:
Dubin-Johnson Syndrome (ABCC2 mutation)
Rotor Syndrome (SLCO1B1 and SCLO1B3 mutations)

Biliary Obstruction:
Gallstones
Tumors
Primary Biliary Cirrhosis
Sclerosing Cholangitis
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19
Q

“Physiological Neonatal Jaundice”

A

Results from immaturity of ALL steps in bilirubin metabolism

Increased Production
Decreased Delivery
Decreased Uptake

High bilirubin level
BBB not great yet
Bilirubin in brain leads to kernicterus

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20
Q

Kernicterus

A

Brain damage due to bilirubin deposition

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21
Q

Treatment of Neonatal Jaundice

A

Phototherapy
Biliblankets or Bililight
Convert Natural Bilirubin to Photobilirubin (can pee out)

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22
Q

Jaundice

A

At “50”, you can glow in the dark

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23
Q

Plasma proteins secreted by liver

A 
Albumin
Clotting Factors
Antithrombin III
α-1-antitrypsin
Ceruoloplasmin
Complement C3
C-reactive protein
α-1-fetoprotein
fibrinogen
Haptoglobin
Hemopexin
α-lipoprotein
β-lipoprotein
α-2-macroglobulin
Orosomucoid
Other clotting factors
Prothrombin
Transferrin
IL-6
24
Q

Factor VIII Level tells us

A 
High = Liver Failure
Low = DIC
25
Q

Clotting Factor tests

A

PTT or INR
Responsive to Vitamin K
II, VII, IX, X, Protein C & Protein S

Gotta start heparinizing and coumadinizing them because the tests will hypercoagulabilize them? I don’t understand.

26
Q

IL-6

A

Regulates body temperature

27
Q

Pathway of protein Secretion

A

Synthesized in ER
Golgi Network
Secretion into bloodstream

28
Q

Prolonged Prothrombin Time

A

Bleeding Tendency

29
Q

Low Serum Albumin

A

Edema or maybe ascites but that can be portal hypertension as well

30
Q

Blood Supply of the Liver

A

Hepatic Artery - Directly from the Heart

Portal Vein - Drains the gut (FIRST PASS METABOLISM)

31
Q

Drug and Toxin Metabolism

A

Oxoreductases (Cytochrome P450) - Phase I
Lead to more polar metabolites, generate active groups for transferases

Hydrolases (Phase I)
Lead to more polar metabolites for transferases

Transferases (Phase II)
Addition of groups

32
Q

Decreased Clearence of Toxins from portal circulation

A

Buildup of vasodilatory molecules (NO)
Decreased systemic vascular resistance
Increased Cardiac Output

After a liver transplant, you can go into heart failure because your spotter is gone

These mechanisms relate to trying to bypass cirrhosed liver

33
Q

Ethanol Metabolism

A

Acetyl Acohol to Acetate

With chronic drinking, P450 catalyzed oxidation more active
Hella hypotheses on how alcohol damages tissues

34
Q

Carbohydrate Metabolism

A

Glycogen Storage & Glycolysis

Portal Circulation contains high levels of insulin and glucagon

35
Q

Glycogen

A

Polymerized glucose
Stored in liver
Glycogen phosphorylase cleaves glyocgen to make glucose available during fasting

36
Q

Epinephrine

A

Stimulates glycogen degradation

37
Q

Glucagon

A

Stimulates glycogen degradation

38
Q

Insulin

A

Stimulates glygogen synthesis

39
Q

Gluconeogenesis

A 
You've exhausted your glycogen storage
Form new glucose from non-carbohydrate carbon sources
Lactate
Glycerol
Most amino acids
40
Q

Acute read-out on how well liver is doing

A

Lactate is the marker

Maybe acid/base metabolism too

41
Q

Transamination

A

ALT and AST

Indicators of hepatocyte damage

42
Q

Urea Cycle

A

Elimination of Excess Nitrogen (Urea)

Occurs in Liver, Kidney, Striated Muscle

43
Q

When you don’t clear ammonia and nitrogenous metabolites

A

Hepatic Encephalopathy
Build-up of neurotoxins (nitrogen-based)
Patients become confused, obtunded, brain swelling, herniation, death

44
Q

Physical exam - Sign of hepatic encephalopathy

A

Asterixis!

45
Q

Fatty Acid Synthesis

A

Happens in cytosol

46
Q

Fatty Acid β-Oxidation

A

Happens in mitochondria

47
Q

Carnitine palmitoyl transferase 1A (CPT1)

A

Conjugates fatty acids to carnitine for transfer into inside mitochondria)

48
Q

LDL Uptake by Hepatocytes

A

Decreased HMG CoA Reductase (target of Statins)
Increased ACAT
Decreased LDL receptors

LDL Binding > Internalization > Lysosomal Hydrolysis > Regulatory Actions

49
Q

Familial Hypercholesterolemia

A

Transplant the kids before soft cheesy plaque lesions become calcified
LDLapheresis

50
Q

Synthesis of bile salts in liver

A

Derive from cholesterol

51
Q

Bile salts reabsorbed

A

Terminal ileum

Need it out before it hits the colon

52
Q

Bile Salts

A

Start with cholesterol, end with bile salts

53
Q

Enterohepatic Circulation

A

Important pathway he explained too fast

54
Q

Primary Bile Acids

A

Converted to secodnary bile Acids in the intestin, and secondary to tertiary in the liver again

55
Q

PFIC

A

Progressive Familial Intrahepatic Cholestasis
Hella itchy
Treat by bypassing terminal ileum through resection or through connecting gall bladder to skin so bile drains out of body. Gotta watch fat soluble vitamins ADEK if you do that though

56
Q

BSEP

A

Important in 2 situations:

Dysfunction in sepsis - reason for elevated bilirubins
PFIC Type 2 - Increased bile salts and de

57
Q

Other important metabolic activities of the liver

A 
Heme biosynthesis (in infancy)
Hematopoiesis in utero
Iron metabolism
Copper metabolism
Vitamin A storage
Vitamin D metabolism

GI / Hepatology (28 decks)

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