SCT III - Gastrointestinal Tract: Absorption & Liver Flashcards

1
Q

What coupling does the absorption in the small bowel use?

A

Na+-Coupled; secondary active transport

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2
Q

What drives nutrients to go to the enterocyte?

A

Low Na+ concentration in the enterocyte causes Na+ from interstitium to diffuse in, bringing with it nutrients (AA, FA, Vit, Bile salts, Carbs, etc.)

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3
Q

What happens to lipids once absorbed into the enterocyte?

A

They are formed back to their original form to form chylomicrons

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4
Q

What happens in water and electrolyte transport in the jejunum?

A
  • Absorption of nutrients & Na+ (Na+/K+ pump)
  • K+ leaves via leaky channels
  • H+ secretion
  • H2CO3 reabsorption
  • Cl- reabsorption (paracellular)
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5
Q

What happens in water and electrolyte transport in the ileum?

A
  • Absorption of nutrients & Na+ (Na+/K+ pump)
  • K+ leaves via leaky channels
  • H+ secretion
  • HCO3- secretion
  • Cl- reabsorption (paracellular)
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6
Q

What happens in water and electrolyte transport in the colon?

A
  • Na+ reabsorption via Aldosterone (adrenal cortex)
  • K+ secretion
  • Na+/K+ exchange
  • HCO3- (sec)/Cl- (reabs) exchange
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7
Q

Steps of iron absorption

A
  1. Fe2+ and Fe3+ enter stomach
  2. Fe3+ converts to Fe2+ due to HCl
  3. Fe2+ binds to Gastroferritin
  4. Gastroferritin bound iron gets to small bowel
  5. Absorption to bloodw
  6. Iron binds to transferrin in blood
  7. Iron binds to Apoferritin in liver and stored as Ferritin
  8. Iron distribution in the body
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8
Q

What is the main substance that Ca2+ absorption depends on?

A

Calcitriol-dependent adaptive Ca2+ absorption

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9
Q

What is Ca2+ absorption enhanced by?

A
  • Calcitriol
  • Ca2+
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10
Q

What is Ca2+ absorption decreased by?

A
  • Vit. D deficiency
  • Malabsorption of lipids
  • Precipitation of Ca2+ (oxalate)
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11
Q

What may cause hyperacidity (increased HCl secretion)?

A
  • Gastrinoma (gastrin-producing tumor)
  • Stress (stimulate G-cells/inhibit Brunner’s glands)
  • Infection (H. pylori)
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12
Q

Name all the possible ways of blocking hyperacidity (increased HCl secretion)

A
  • Carbonic anhydrase blockers
  • H+ pump blockers
  • Histamine receptor blockers
  • mAChR blockers (atropine)
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13
Q

What are the bile synthetic processes present in hepatocytes?

A

Cholesterol → Primary Bile Acids → Secondary Bile Acids

Primary Bile Acids → Bile Salts
In conjugation w/ GLYCINE & TAURINE

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14
Q

What are other synthetic processes present in hepatocytes?

A
  • Plasma protein synthesis
  • Globulin synthesis (NOT gamma)
  • Urea synthesis (Ammonia deg.)
  • Lipid metabolism
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15
Q

What is LDL?

A

Cholesterol Transport
Liver → Body
via LDL

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16
Q

What is HDL?

A

Cholesterol Transport
Body → Liver
via HDL

17
Q

Bilirubin metabolism pathway

A
18
Q

What happens in prehepatic hyperbilirubinemia?

A

Excessive hemolysis (RBC breakdown), overwhelming liver’s capacity to process bilirubin

19
Q

What happens in hepatic hyperbilirubinemia?

A

Impaired liver function, reducing conjugation and excretion of bilirubin

20
Q

What happens in posthepatic hyperbilirubinemia?

A

Bile duct obstruction, preventing excretion of conjugated bilirubin into the intestine

21
Q

How does the liver maintain blood-glucose concentration?

A

Glycogenesis

22
Q

How is Vitamin D3 activated?

A

Sunlight → Liver Enzyme → Kidney Enzyme → Activation

23
Q

What is HISS and what is its function?

A

Hepatic Insulin Sensitizing Substance
Makes tissue more sensitive to insulin

24
Q

What role does the liver have in ketoacids?

A

Production of ketoacids
Starvation stimulates ketoacid production in the liver for the brain and vital organs, prolonging survival

25
Q

What could be the coagulative problems that are faced due to posthepatic jaundice?

A

Vit. A, D, E, K deficiency

Vit. K is needed for factors II, VIII, IX, X of the coagulation cascade

26
Q

What is Wilson’s disease?

A

A mutation in a transporter which (when unmutated) pushes Copper into bile (for excretion)

Visible by a Kaiser-Fleischer ring (copper ring colored ring) around the eye