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Flashcards in Hepatic Physiology Deck (73):
1

Ascites

Fluid accumulation in peritoneal cavity
- liver dysfunction is the major cause

2

Icterus

Elevated bilirubin levels
- aka: hyperbilirubinemia, jaundice

3

Cirrhosis

Condition in which normal cells are replaced by scar tissue
- end stage occurrence

4

Portal hypertension

Hypertension in the portal vein and its branches
- elevated bp in the portal vein or elevation in interstitial hydrostatic pressure

5

Metabolism

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

6

Liver functions

- 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

7

The liver makes every ____ in the body

Protein

8

_____ is relevant during ascities

Lymph formation
- excess lymph gets into the peritoneal cavity

9

Liver lobule

Basic functional unit of liver

10

Hepatocytes

Main liver cells
- produce bile, which is drained into bile canaliculi

11

Sinusoids

Protein, lymph production
- holes in between endothelial cells leak into lymphatics

12

Portal vein

Main blood supply to the liver

13

Hepatic artery

2nd main blood supply
- filters bacteria coming from portal vein (hepatocytes)

14

Kupffer cell

Macrophages, makes sure bacteria does not go into systemic circulation

15

Liver structure

Largest internal organ
- 2-5% total body weight
- receives 30% of cardiac output

16

Liver lobes

6 lobes
- right and left medial
- right and left lateral
- quadrate
- caudate

17

Venous sinusoids

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)

18

Lymph formation

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

19

Lymph flow

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

20

Increased sinusoidal pressure increases lymph production

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

21

Extramedullary hematopoiesis

Production of blood cells outside of bone marrow during times of need
- cytokine stimulation
- hypoxia

22

Liver blood flow breakdown

- 20% from hepatic artery
- 80% from portal vein

23

Liver oxygen supply breakdown

- 50% from hepatic artery
- 50% from portal vein

24

Portosystemic shunts

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

25

Congenital shunts

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

26

Consequences of congenital shunts

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

27

Portal pressures

- 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

28

Ascites

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

29

Causes of portal hypertension

- cirrhosis
- severe infection
- chronic biliary tract obstructions
- portal vein thrombosis (increase hydrostatic pressure)

30

Consequences of portal hypertension

- GI edema/ulceration
- severe GI signs and protein loss
- ascites
- acquired portosystemic shunts

31

Acquired shunts

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

Causes of congestion

Right sided congestive heart failure
- HW disease
- congenital disease
- cor pulmonale

33

Consequences of congestion

- GI edema/ulceration
- severe GI signs and protein loss
- ascites

34

Obstruction of lymph flow/congestion is due to ____

Right sided heart failure

35

Portal hypertension is due to ___

Increased resistance to blood flow thru the liver

36

Increased sinusoidal pressure in the liver is caused by ______

Anything that makes the liver sick enough

37

Hypoalbuminemia

<1.6 mg/dl = potential for effusion
- pure transudate (water like)

38

What is the main production site for albumin?

Liver!!

39

Can the liver repair itself?

Yes!
- insult>repair
- transforming growth factor B --> cytokine secreted by hepatocytes, stops liver cell proliferation

40

Instances where the liver is unable to repair itself

Injury > fibrosis > cirrhosis

41

Vitamins stored in the liver

A, D, B12

42

Iron

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

43

Role in coagulation

Makes most of proteins needed in this process
- fibrinogen
- prothrombin
- clotting factors: 2, 7, 9, 10 are vitamin K dependent

44

Role in drug/hormone/toxin metabolism

- detoxify antibiotics
- excrete antibiotics into bile
- chemical alteration of hormones
- excrete hormones
- calcium excretion

45

Bilirubin

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

46

Hemoglobin is split into _____ and ______

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

It what form is bilirubin transported throughout the body?

Unconjugated bilirubin joins with albumin
- reaches the liver and is absorbed through hepatocyte membrane

48

Conjugated bilirubin

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

49

Fate of bilirubin

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

Increased bilirubin

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

Hyperbilirubinemia causes

- 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

Hepatic metabolism

- high rate of metabolism
- shares substrates with other organs
- processing and transportation to other organs

53

Carbohydrate metabolism

- storage of glycogen
- conversion of galactose and fructose to glucose
- gluconeogenesis
- formation of other compounds from "byproducts" of CHO metabolism

54

Glycogen storage

Allows removal of excess glucose in blood
- released in times of need (stress, hypoglycemia)

55

Gluconeogenesis

Maintains normal blood glucose between meals
- uses amino acid from protein and glycerol from triglycerides to make glucose

56

Lipid metabolism

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

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

80%
- remainder is transported in lipoproteins in the blood to needy tissues
- cell membrane formation
- intracellular structure formation/reactions

58

Phospholipids are transported by ______

Lipoproteins
- cell membrane function
- intracellular structure formation/reactions
- second messenger systems

59

Lipid metabolism process

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

60

Where does acetyl CoA go?

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

Protein metabolism

- 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

Manifestations of liver disease

- decreased albumin --> decreased colloidal osmotic pressure = effusion and edema
- decreased glucose
- increased bilirubin

63

Hepatic encephalopathy

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

64

Coagulopathies

- increased prothrombin time
- increased partial thromboplastin time
- platelet dysfunction
- decreased fibrinolysis
- excessive fibrinolysis

65

Alanine aminotransferase

ALT
- most common/important
- leakage enzyme made inside hepatocyte
- indicators of hepatic injury (biomarkers of necrosis)

66

Aspartate aminotransferase

AST
- leakage enzyme made inside hepatocyte mitochondria
- indicators of hepatic injury (biomarker of necrosis)
- more of a muscle enzyme

67

Alkaline phosphatase

ALP
- induced enzyme made in lining of bile canaliculi
- elevated with cholestasis

68

Gamma glutamyl transpeptidase

GGT
- excellent marker for hepatobiliary disease especially biliary tract disease

69

What to look for on bloodwork

- increased bilirubin
- decreased albumin
- decreased cholesterol
- decreased glucose
- decreased BUN
= increased ALT/AST and ALP/GGT

70

Bile acid assay process

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

71

Bile acid assay results

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

Ammonia tolerance test process

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

73

Ammonia tolerance results

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