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
Clotting Factor tests
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
IL-6
Regulates body temperature
27
Pathway of protein Secretion
Synthesized in ER Golgi Network Secretion into bloodstream
28
Prolonged Prothrombin Time
Bleeding Tendency
29
Low Serum Albumin
Edema or maybe ascites but that can be portal hypertension as well
30
Blood Supply of the Liver
Hepatic Artery - Directly from the Heart | Portal Vein - Drains the gut (FIRST PASS METABOLISM)
31
Drug and Toxin Metabolism
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
Decreased Clearence of Toxins from portal circulation
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
Ethanol Metabolism
Acetyl Acohol to Acetate With chronic drinking, P450 catalyzed oxidation more active Hella hypotheses on how alcohol damages tissues
34
Carbohydrate Metabolism
Glycogen Storage & Glycolysis | Portal Circulation contains high levels of insulin and glucagon
35
Glycogen
Polymerized glucose Stored in liver Glycogen phosphorylase cleaves glyocgen to make glucose available during fasting
36
Epinephrine
Stimulates glycogen degradation
37
Glucagon
Stimulates glycogen degradation
38
Insulin
Stimulates glygogen synthesis
39
Gluconeogenesis
``` You've exhausted your glycogen storage Form new glucose from non-carbohydrate carbon sources Lactate Glycerol Most amino acids ```
40
Acute read-out on how well liver is doing
Lactate is the marker | Maybe acid/base metabolism too
41
Transamination
ALT and AST | Indicators of hepatocyte damage
42
Urea Cycle
Elimination of Excess Nitrogen (Urea) | Occurs in Liver, Kidney, Striated Muscle
43
When you don't clear ammonia and nitrogenous metabolites
Hepatic Encephalopathy Build-up of neurotoxins (nitrogen-based) Patients become confused, obtunded, brain swelling, herniation, death
44
Physical exam - Sign of hepatic encephalopathy
Asterixis!
45
Fatty Acid Synthesis
Happens in cytosol
46
Fatty Acid β-Oxidation
Happens in mitochondria
47
Carnitine palmitoyl transferase 1A (CPT1)
Conjugates fatty acids to carnitine for transfer into inside mitochondria)
48
LDL Uptake by Hepatocytes
Decreased HMG CoA Reductase (target of Statins) Increased ACAT Decreased LDL receptors LDL Binding > Internalization > Lysosomal Hydrolysis > Regulatory Actions
49
Familial Hypercholesterolemia
Transplant the kids before soft cheesy plaque lesions become calcified LDLapheresis
50
Synthesis of bile salts in liver
Derive from cholesterol
51
Bile salts reabsorbed
Terminal ileum | Need it out before it hits the colon
52
Bile Salts
Start with cholesterol, end with bile salts
53
Enterohepatic Circulation
Important pathway he explained too fast
54
Primary Bile Acids
Converted to secodnary bile Acids in the intestin, and secondary to tertiary in the liver again
55
PFIC
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
BSEP
Important in 2 situations: Dysfunction in sepsis - reason for elevated bilirubins PFIC Type 2 - Increased bile salts and de
57
Other important metabolic activities of the liver
``` Heme biosynthesis (in infancy) Hematopoiesis in utero Iron metabolism Copper metabolism Vitamin A storage Vitamin D metabolism ```