Liver Function Flashcards

1
Q

What are the main functions of the liver?

A
Vitamin synthesis 
Blood storage 
Metabolism
Clotting factor production 
Detoxification 
Bile production
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2
Q

What are kupfer cells?
What are stellate cells?
What are the 3 main functions of hepatocytes?

A

Kupfer cells = resident macrophages that of the sinusoidal lining
Stellate cells store Vitamin A in lipid droplets, they can become activated in liver cirrhosis to myofibroblasts which block the sinusoidal capillaries

Remove substances for blood or secrete substances into the blood via space of disse
chemically modify or degrade compound
secrete bile into compound

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3
Q

What is the space of Disse?

A

Space of Disse = subendothelial space that separates the endothelium lining of capillaries from the hepatocytes
Blood passes through the endothelial wall to have close contact with the hepatocytes
It allows for hepatocytes to secrete their components into the blood

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4
Q

What are the 3 sources of cholesterol?

A

Intestinal chylomicrons:
LDL
Self synthesis of cholesterol in the liver via negative feedback

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5
Q

What is enterohepatic circulation?

A
  • Liver produces cholesterol-> bile acids
  • Bile acids are reabsorbed in terminal ileum and colon to form secondary bile acids
  • Returned to the liver via the hepatic portal vein
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6
Q

Describe the role of insulin in the skeletal muscle, adipose tissue and liver

A

Anabolic hormone

Skeletal muscle: Promotes glycolysis, inhibits gluconeogenesis and glycogenolysis. Glucose uptake via GLUT4 into cells + glycogen storage

Adipose tissue: Promote glycolysis, uptake glucose and glycogen storage.

Liver: Glycogen storage, promote glycolysis and production of AA + fats.

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7
Q

Describe the role of glucagon in the skeletall muscle, adipose tissue and liver

A

Skeletal muscle: Proteolysis to produce amino acids for gluconeogenesis in the liver

Adipose tissue: Lipolysis so fatty acids can be used in hepatic gluconeogenesis

Liver: Glycogenolysis, inhibit glycolysis, promote gluconeogenesis. Oxidation of fat to produce ketone bodies.
- Activate fructose-1,6- bisphosphatase + glucose-6-bisphosphatase

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8
Q

What leads to ascites?

A
  • Liver cirrhosis causes damage
  • Stellate cells are activated -> myofibroblasts
  • myofibroblasts lay down collagen and block the sinusoidal capillaries -> decreased plasma albumin so reduced capillary osmotic pressure
  • myofibroblasts contract and compress capillaries so increases resistance to flow
    This causes portal hypertension
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9
Q

How does activation of the RAS system worsen ascites?

A

Portal hypertension = greater pressure in the splachnic circulation which cause NO to be released. There is vasodilation of arterioles upstream and so more blood is stored in the splachnic veins

  • Less blood is reaching the IVC
  • Decreased blood volume detected by baroreceptors
  • Cardiopulmonary baro receptors signal to the renal sympathetic nerve -> increase Na+ rebasorption
  • Renal baroreceptors cause renin secretion from the granular cells of the afferent arteriole
  • Activation of the RAS system
  • RAS: Aldosterone increases Na+ rebasorption directly, increase Na+ appetite, thirst
  • Less Na+ lost in the urine
  • Increased Na+ of the ECF -> Increased plasma osmolality
  • Larger blood volume to support the large scale loss of fluid into the peritoneal cavity
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10
Q

What are the 3 stages of fasting?

A

Post absorptive: Glucose in blood from glycogenolysis to supply glucose to the Brain, CNS + tissues

Gluconeogenic phase: Gluconeogenesis in the liver to supply the brain and CNS with glucose whilst other cells use ketones or fats as a fuel source

Protein conservation phase:
- Ketones supply the CNS and fatty acids supply all other tissues

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11
Q

Describe iron homeostasis

A

Small intestine reabsorbs iron to produce RBC
Macrophages recycle red blood iron from dead red blood cells to reuse it again in RBC production
When there is XS iron Fe2+ -> Fe3+ ( ferritin)
If iron is low then it can be released from the liver

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12
Q

How does diabetic ketoacidosis occur?

A
  • Glucose is high but insulin deficiencies or insensitivity means that the cells cannot take up the glucose via GLUT2 transporters
  • FFA are released from the liver to produce ketones
  • ketones accumulate in the blood stream causing nausea, vomiting and dehydration
  • Can cause coma = medical emergency
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13
Q

How does ascites worsen when pressure increase in the splachnic circulation?

A
  • Nitric oxide is produced which is vasodilatory
  • There is vasodilation of arterioles upstream of the splachnic circulation so increased blood flow and more blood is stored in the splachnic veins
  • low plasma albumin, resistance to blood flow and portal hypertension favour fluid filtration across the capillary bed into the peritoneal cavity
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