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Physiology > Hepatic Physiology > Flashcards

Hepatic Physiology Flashcards

1
Q

Ascites

A

Fluid accumulation in peritoneal cavity

- liver dysfunction is the major cause

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2
Q

Icterus

A

Elevated bilirubin levels

- aka: hyperbilirubinemia, jaundice

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3
Q

Cirrhosis

A

Condition in which normal cells are replaced by scar tissue

- end stage occurrence

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4
Q

Portal hypertension

A

Hypertension in the portal vein and its branches

- elevated bp in the portal vein or elevation in interstitial hydrostatic pressure

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5
Q

Metabolism

A

Sum of all anabolic and catabolic reactions as it relates to use of all nutrients

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6
Q

Liver functions

A
  • filtering and storage of blood (largest cardiac output)
  • metabolism of carbs, proteins, fats
  • metabolism of hormones, drugs, toxins
  • formation of cholesterol and bile (fat synthesis)
  • storage of vitamins and iron
  • production of coagulation factors
  • production of plasma proteins
  • lymph formation
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7
Q

The liver makes every ____ in the body

A

Protein

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8
Q

_____ is relevant during ascities

A

Lymph formation

- excess lymph gets into the peritoneal cavity

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9
Q

Liver lobule

A

Basic functional unit of liver

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10
Q

Hepatocytes

A

Main liver cells

- produce bile, which is drained into bile canaliculi

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11
Q

Sinusoids

A

Protein, lymph production

- holes in between endothelial cells leak into lymphatics

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12
Q

Portal vein

A

Main blood supply to the liver

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13
Q

Hepatic artery

A

2nd main blood supply

- filters bacteria coming from portal vein (hepatocytes)

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14
Q

Kupffer cell

A

Macrophages, makes sure bacteria does not go into systemic circulation

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15
Q

Liver structure

A

Largest internal organ

  • 2-5% total body weight
  • receives 30% of cardiac output
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16
Q

Liver lobes

A

6 lobes

  • right and left medial
  • right and left lateral
  • quadrate
  • caudate
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17
Q

Venous sinusoids

A

Lined by endothelial cells with large pores to allow movement of plasma proteins
- contains Kupffer cells that keep less than 1% of GI bacteria from entering systemic circulation (defense mechanism)

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18
Q

Lymph formation

A

50% of lymph is formed in the liver

  • sinusoidal endothelial cell leak fluid/proteins into “space of Disse”
  • lymph from liver has protein conc of 6 g/dl
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19
Q

Lymph flow

A

Lymph –> space of Disse –> lymph vessels –> lymphatic system

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20
Q

Increased sinusoidal pressure increases lymph production

A

Any disease of liver, especially chronic diseases

  • fibrosis, cirrhosis
  • once pressure rises enough, the liver sweats lymph (ascities)
  • liver lymph volume can increase by 1 liter or more
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21
Q

Extramedullary hematopoiesis

A

Production of blood cells outside of bone marrow during times of need

  • cytokine stimulation
  • hypoxia
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22
Q

Liver blood flow breakdown

A
  • 20% from hepatic artery

- 80% from portal vein

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23
Q

Liver oxygen supply breakdown

A
  • 50% from hepatic artery

- 50% from portal vein

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24
Q

Portosystemic shunts

A

Shunting of blood from portal circulation to systemic circulation without passing through the liver

  • congenital
  • acquired
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25
Q

Congenital shunts

A

Intrahepatic or extrahepatic vessel that does not allow blood to take a normal course thru the liver
- ex: portocaval shunt where portal vein empties directly into caudal vena cava

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26
Q

Consequences of congenital shunts

A
  • impaired liver development = stunted growth
  • liver dysfunction = build up of toxins (ammonia), poor ability to metabolize anesthetics
  • liver failure
  • end stage cirrhosis without repair
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27
Q

Portal pressures

A
  • pressure in portal vein: 9 mmHg
  • pressure in hepatic vein leading to vena cava: 0 mmHg
  • low pressure gradient gets blood from intestines and spleen, thru liver, into vena cava and back to right atrium
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28
Q

Ascites

A

Sweating from surface of the liver due to increased hydrostatic pressure in hepatic veins
- fluid similar to plasma in regards to protein content
OR: due to increased hydrostatic pressure in vena cava
- increases lymph flow

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29
Q

Causes of portal hypertension

A
  • cirrhosis
  • severe infection
  • chronic biliary tract obstructions
  • portal vein thrombosis (increase hydrostatic pressure)
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30
Q

Consequences of portal hypertension

A
  • GI edema/ulceration
  • severe GI signs and protein loss
  • ascites
  • acquired portosystemic shunts
31
Q

Acquired shunts

A

Multiple tortuous vessels outside of the liver develop due to high pressure in the liver (portal hypertension)

  • acts as a relief valve for portal vasculature
  • located all throughout the abdomen (often near the kidney)
  • worsens liver function
32
Q

Causes of congestion

A

Right sided congestive heart failure

  • HW disease
  • congenital disease
  • cor pulmonale
33
Q

Consequences of congestion

A
  • GI edema/ulceration
  • severe GI signs and protein loss
  • ascites
34
Q

Obstruction of lymph flow/congestion is due to ____

A

Right sided heart failure

35
Q

Portal hypertension is due to ___

A

Increased resistance to blood flow thru the liver

36
Q

Increased sinusoidal pressure in the liver is caused by ______

A

Anything that makes the liver sick enough

37
Q

Hypoalbuminemia

A

<1.6 mg/dl = potential for effusion

- pure transudate (water like)

38
Q

What is the main production site for albumin?

A

Liver!!

39
Q

Can the liver repair itself?

A

Yes!

  • insult>repair
  • transforming growth factor B –> cytokine secreted by hepatocytes, stops liver cell proliferation
40
Q

Instances where the liver is unable to repair itself

A

Injury > fibrosis > cirrhosis

41
Q

Vitamins stored in the liver

A

A, D, B12

42
Q

Iron

A

Stored as ferritin in hepatic cells by combining with apoferritin
- released from storage in times of need

43
Q

Role in coagulation

A

Makes most of proteins needed in this process

  • fibrinogen
  • prothrombin
  • clotting factors: 2, 7, 9, 10 are vitamin K dependent
44
Q

Role in drug/hormone/toxin metabolism

A
  • detoxify antibiotics
  • excrete antibiotics into bile
  • chemical alteration of hormones
  • excrete hormones
  • calcium excretion
45
Q

Bilirubin

A

Green/yellow pigment that is the major end product of hemoglobin degradation
- comes from old/sick RBCs that get phagocytosed by macrophages

46
Q

Hemoglobin is split into _____ and ______

A

Globin and heme

  • releases free iron and a substrate from which bilirubin is formed
  • biliverdin –> free bilirubin (unconjugated) is released from macrophages into circulation
47
Q

It what form is bilirubin transported throughout the body?

A

Unconjugated bilirubin joins with albumin

- reaches the liver and is absorbed through hepatocyte membrane

48
Q

Conjugated bilirubin

A

Conjugation with glucuronide, sulfate, etc occurs in the hepatocyte
- excreted into bile canaliculi and then into intestines

49
Q

Fate of bilirubin

A

Converted via bacteria to urobilinogen

  • urobilinogen is reabsorbed thru intestinal mucosa back into blood —> mostly goes back to liver for re-excretion into gut and is oxidized to stercobilin (feces)
  • remaining 5% is excreted by kidneys and oxidized to urobilin (urine)
50
Q

Increased bilirubin

A

Aka: hyperbilirubinemia, icterus, or jaundice

  • yellow tint to body tissues due to excessive build-up of conjugated or unconjugated bilirubin
  • normal range is 0.2-0.6 mg/dl
  • jaundice is noted at a bilirubin around 2 mg/dl
51
Q

Hyperbilirubinemia causes

A
  • hemolytic anemia (prehepatic)
  • liver failure/dysfunction
  • obstruction of biliary tracts in the liver
  • obstruction of posthepatic biliary system (gallbaldder, common bile duct, pancreas, etc)
52
Q

Hepatic metabolism

A
  • high rate of metabolism
  • shares substrates with other organs
  • processing and transportation to other organs
53
Q

Carbohydrate metabolism

A
  • storage of glycogen
  • conversion of galactose and fructose to glucose
  • gluconeogenesis
  • formation of other compounds from “byproducts” of CHO metabolism
54
Q

Glycogen storage

A

Allows removal of excess glucose in blood

- released in times of need (stress, hypoglycemia)

55
Q

Gluconeogenesis

A

Maintains normal blood glucose between meals

- uses amino acid from protein and glycerol from triglycerides to make glucose

56
Q

Lipid metabolism

A

Oxidation of fatty acids to supply energy for body functions

  • synthesis of cholesterol, phospholipids, and most lipoproteins
  • synthesis of fat from proteins and carbs
57
Q

______ of cholesterol made in the liver is converted to bile salts

A

80%

  • remainder is transported in lipoproteins in the blood to needy tissues
  • cell membrane formation
  • intracellular structure formation/reactions
58
Q

Phospholipids are transported by ______

A

Lipoproteins

  • cell membrane function
  • intracellular structure formation/reactions
  • second messenger systems
59
Q

Lipid metabolism process

A

Neutral fat –> glycerol + FA –> beta oxidation –> acetyl CoA

60
Q

Where does acetyl CoA go?

A

Citric acid cycle
Leftover CoA —> acetoacetic acid –> transported in circulation to other tissues –> conversion back to acetyl CoA for oxidation and energy production by needy tissue

61
Q

Protein metabolism

A
  • breakdown of amino acids for energy, conversion to CHO and fat
  • formation of urea for removal of ammonia from body fluids
  • formation of all plasma protiens
  • manipulation of amino acids and synthesis of other stuff from amino acids (non-essential FA formation)
62
Q

Manifestations of liver disease

A
  • decreased albumin –> decreased colloidal osmotic pressure = effusion and edema
  • decreased glucose
  • increased bilirubin
63
Q

Hepatic encephalopathy

A

Occurs due to accumulation of ammonia and hormones
= seizures, dullness, lethargy, etc
- worsened after a meal

64
Q

Coagulopathies

A
  • increased prothrombin time
  • increased partial thromboplastin time
  • platelet dysfunction
  • decreased fibrinolysis
  • excessive fibrinolysis
65
Q

Alanine aminotransferase

A

ALT

  • most common/important
  • leakage enzyme made inside hepatocyte
  • indicators of hepatic injury (biomarkers of necrosis)
66
Q

Aspartate aminotransferase

A

AST

  • leakage enzyme made inside hepatocyte mitochondria
  • indicators of hepatic injury (biomarker of necrosis)
  • more of a muscle enzyme
67
Q

Alkaline phosphatase

A

ALP

  • induced enzyme made in lining of bile canaliculi
  • elevated with cholestasis
68
Q

Gamma glutamyl transpeptidase

A

GGT

- excellent marker for hepatobiliary disease especially biliary tract disease

69
Q

What to look for on bloodwork

A
  • increased bilirubin
  • decreased albumin
  • decreased cholesterol
  • decreased glucose
  • decreased BUN
    = increased ALT/AST and ALP/GGT
70
Q

Bile acid assay process

A
  1. baseline BA
  2. feed small meal with protein/carb
  3. 2 hr post meal BA
71
Q

Bile acid assay results

A

If 2 hr post meal is elevated = liver failure or PSS

  • pro: can do in practice
  • cons: have to feed patient, cannot rely on results if bilirubin is elevated, determine if hepatic or post-hepatic
72
Q

Ammonia tolerance test process

A
  1. baseline ammonia
  2. give 100 mg/kg ammonia
  3. 30 minute post ammonia
73
Q

Ammonia tolerance results

A

If baseline, or post ammonia is elevated = liver failure or PSS

  • pro: can do if bilirubin is elevated
  • con: not able to do in practice, can cause hepatic encephalopathy/coma

Physiology (33 decks)

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