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DIG > Absorption of Ions and Water > Flashcards

Absorption of Ions and Water Flashcards

1
Q

Which part of the digestive system is exclusively responsible for the absorption of dietary nutrients?

A

The small intestine.

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2
Q

List 5 cells that can be found in the small intestine (in the crypts of Lieberkuhn).

A

1 - Enterocytes (absorptive cells).

2 - Goblet cells.

3 - Enteric endocrine cells.

4 - Stem cells.

5 - Paneth cells.

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3
Q

What are the two main intestinal glands?

A

Crypts of Lieberkuhn

Brunner’s Glands

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4
Q

Where are Brunner’s glands found and what is their function?

A
  • Only in the first few centimetres of the duodenum.

- Antacid function (alkaline secretion).

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5
Q

Where are crypts of Lieberkuhn found?

A

All over the surface of the small large intestines.

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6
Q

What is the function of Paneth cells?

A

Provide antimicrobial defence.

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7
Q

How do villous enterocytes differ from crypt enterocytes?

A
  • Villous enterocytes are mostly responsible for nutrient and electrolyte absorption.
  • Crypt enterocytes are mostly responsible for secretion.
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8
Q

List 5 differences between the histology of the large intestine and the small intestine.

A

1 - There are no villi lining the large intestine epithelium.

2 - Goblet cells are more prominent in the large intestine.

3 - Paneth cells are not usually present in the large intestine.

4 - The muscularis mucosae is more prominent in the large intestine.

5 - The outer longitudinal layer of the muscularis externa of the large intestine varies in thickness and forms three thick longitudinal bands, the taeniae coli.

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9
Q

What type of epithelium lines the small and large intestines?

A

Simple columnar epithelium (enterocytes).

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10
Q

What two layers comprise the muscularis externa of the small intestine?

A

An inner circular layer and an outer longitudinal layer.

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11
Q

List 3 features of the small intestine that increase surface area.

A

1 - Macroscopic folds of kerckring (plicae circulares).

2 - Villi.

3 - Microvilli.

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12
Q

What are plicae circulares?

A

Large circular folds of the small intestine’s mucous membrane that increase surface area.

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13
Q

Describe transcellular and paracellular movement.

A
  • Transcellular: the solute crosses the cell membranes and active transport implicated.
  • Paracellular: the solute moves passively between adjacent epithelial cells via tight junctions.
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14
Q

What does the absorption of water into enterocytes depend on?

A

Absorption of ions:

  • Transport of Na+, Cl- and HCO3 - into the intercellular spaces near the apical end.
  • Resulting hypertonicity causes osmotic flow of water from the lumen via tight junctions into intercellular spaces.
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15
Q

In the jejenum, ilium and colon, is Na+ absorbed or secreted?

Active or passive?

A

Actively absorbed in all three.

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16
Q

In the jejenum, ilium and colon, is K+ absorbed or secreted?

Active or passive?

A

Passively absorbed in the jejenum and ileum.

Both absorbed and secreted in the colon. Net secretion.

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17
Q

In the jejenum, ilium and colon, is Cl- absorbed or secreted?

A

Absorbed in all three.

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18
Q

In the jejenum, ilium and colon, is HCO3- absorbed or secreted?

A

Absorbed in the jejenum.

Secreted in the ileum and colon.

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19
Q

List 4 transport routes of entry for sodium.

A

1 - Na/Glucose transport or Na/Amino acid transport.

2 - Na-H exchanger.

3 - Parallel Na-H and Cl-HCO3- exchange.

4 - Epithelial Na+ channels.

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20
Q

Which protein is responsible for the cotransport of sodium and glucose into enterocytes?

A

SGLT-1

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21
Q

How is sodium ejected from enterocytes at the basal and lateral membrane?

How does this aid sodium absorption into enterocytes?

A

Via sodium-potassium pumps (3 Na+ out for every 2 K+ in).

  • Creates electrochemical gradient across enterocyte membrane.
  • Facilitates cotransport of Na and glucose / galactose / amino acids.
  • Facilitates Na / H exchange.
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22
Q

Where is the rate of absorption of Na+ highest?

Why is the rate of absorption high here?

A
  • In the jejunum.

- Na+ absorption in the jejunum is enhanced by the presence of glucose, galactose and neutral amino acids in the lumen.

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23
Q

What increases the rate of Na-H exchange?

A

Low intracellular pH or high luminal pH.

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24
Q

What can cause a high luminal pH?

A

HCO3- secretion by pancreatic, biliary or duodenal tissues.

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25
Q

Where does most Na / H exchange occur?

Where does it also occur to a lesser extent?

A

Mostly occurs in jejenum and to a lesser extent in duodenum.

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26
Q

What is the primary methods of Na+ absorption between meals (when fasting)?

A

Parallel Na-H and Cl-HCO3- exchange.

27
Q

Where does parallel Na-H and Cl-HCO3- exchange occur?

A

In the ileum and proximal colon.

28
Q

List 3 regulators of parallel Na-H and Cl-HCO3- exchange.

How does ach affect parallel Na-H and Cl-HCO3- exchange?

A
  • cAMP, cGMP and intracellular Ca2+.

- Increases in any reduce NaCl absorption.

29
Q

How do enterotoxins induce secretory diarrhoeas?

A

By elevating cAMP, inhibiting NaCl absorption.

30
Q

List the stages of parallel Na-H and Cl-HCO3- exchange.

A
  • H2O and CO2 enter the enterocyte through the basal membrane.
  • Carbonic anhydrase catalyses CO2 + H2O -> H2CO3.
  • H2CO3 -> H+ + HCO3-
  • H+ exchange occurs, causing Na+ influx.
  • Cl-HCO3- exchange occurs, causing Cl- influx.
31
Q

What are ENaCs?

Where in the digestive tract are they found?

A
  • Epithelial sodium channels.

- Found in the distal colon.

32
Q

Why is sodium absorption in the distal colon highly efficient?

A

ENaCs are capable of absorbing sodium against large concentration gradients.

33
Q

Where does Cl-HCO3- exchange occur in the absence of parallel Na-H exchange?

A

In the ileum and throughout the large intestine.

34
Q

What is congenital chloridorrhoea?

What are the main symptoms?

What treatment is available?

A
  • An autosomal recessive disorder causing the absence of apical Cl-HCO3- exchangers.
  • Causes diarrhoea with a high stool [Cl-].
  • Patients are alkalotic as HCO3- secretion is reduced.
  • PPI for treatment.
35
Q

Which chemical mediators promote absorption?

A

Absorptagogues.

36
Q

Which chemical mediators promote secretion?

A

Secretagogues.

37
Q

List 5 examples of absorptagogues.

A

1 - Angiotensin.

2 - Aldosterone.

3 - Somatostatin.

4 - Enkephalins.

5 - Noradrenaline.

38
Q

Which axis is stimulated in response to dehydration and a drop in effective circulating volume?

What is released as a result?

A
  • The renin-angiotensin-aldosterone axis.

- Angiotensin and aldosterone are released.

39
Q

How and where does angiotensin promote absorption?

A
  • In the small intestine.

- Upregulates NaCl absorption by upregulating Na-H exchange.

40
Q

Where does aldosterone promote absorption?

List 3 ways in which this is achieved.

A
  • In the colon.

1 - Increase in the opening of ENaCs.

2 - Translocation of ENaCs from vesicle pools to the apical membrane.

3 - Increased synthesis of apical ENaCs and basal Na-K pumps.

41
Q

What are the 4 categories of secretagogues?

A

1 - Bacterial enterotoxins.

2 - Hormones and neurotransmitters.

3 - Products of cells of the immune system.

4 - Laxatives.

42
Q

List 4 bacterial enterotoxins.

A

1 - Cholera toxin.

2 - E-coli toxins.

3 - Yersinia toxin.

4 - Clostridium difficile toxin A.

43
Q

List 3 hormones and neurotransmitters that can act as secretagogues.

A

1 - VIP.

2 - Acetylcholine.

3 - Bradykinin.

44
Q

List 2 immune cell products that can act as secretagogues.

A

1 - Histamines.

2 - Prostagladins.

45
Q

What effect do bile acids have on absorption?

A

Act as secretagogues (decrease absorption).

46
Q

Which second messenger is upregulated in response to cholera toxin?

A

cAMP.

47
Q

Which second messenger is upregulated in response to E-coli toxins?

A

cAMP.

48
Q

Which second messenger is upregulated in response to Yersinia toxin?

A

Ca2+.

49
Q

Which second messenger is upregulated in response to stimulation by VIP?

A

cAMP.

50
Q

Which second messenger is upregulated in response to stimulation by acetylcholine?

A

Ca2+.

51
Q

Which second messenger is upregulated in response to histamine?

A

cAMP.

52
Q

Which second messenger is upregulated in response to prostaglandins (an immune cell product)?

A

cAMP.

53
Q

Which second messenger is upregulated in response to bile acids?

A

Ca2+.

54
Q

What is the name of the bacterium that releases cholera toxin?

A

Vibrio cholerae.

55
Q

How does the upregulation of cAMP cause secretory diarrhoea?

A
  • cAMP increases Cl- and K+ secretion and inhibits parallel Na-H and Cl-HCO3- exchange.
  • NaCl absorption decreases.
56
Q

What is contained in diarrhoea relief medication?

Why does this work?

A
  • A solution of sodium and glucose.
  • Since enterotoxin reduces NaCl absorption by inhibiting parallel Na-H and Cl-HCO3- exchange, Na+ absorption can be increased using sodium-glucose cotransporters.
57
Q

What is Verner-Morrison syndrome?

A
  • A hormone/neurotransmitter mediated cause of diarrhoea.
  • Pancreatic tumours produce vasoactive intestinal peptide.
  • Causes diarrhoea through cAMP upregulation.
58
Q

How do prostaglandins and histamine cause diarrhoea?

What are the sources of postraglandins and histamine in the bowel?

A
  • Mast cells release histamine.
  • Macrophages release prostaglandins.
  • Both induce diarrhoea through cAMP.
59
Q

How does loperamide function as an anti-diarrhoeal?

A
  • Opioid receptor agonist which acts on the myenteric plexus in the large intestine.
  • Decreases smooth muscle motility.
  • Increases amount of time substances stay in the intestine.
  • More water absorbed out of fecal matter.
60
Q

Give an example of an anti-diarrhoeal other than loperamide.

A

Somatostatin analogues.

61
Q

How do the transport routes of passive Ca2+ absorption and active Ca2+ absorption differ?

A

Passive is paracellular whereas active is transcellular.

62
Q

List the three stages of active Ca2+ absorption.

What controls this process?

A

1 - Uptake via Ca2+ channels on the apical membrane of enterocytes (diffusion down electrochemical gradient).

2 - Cytosolic Ca2+ binds to calbindin, which acts as a buffer.

3 - A Ca2+ pump and a Na-Ca exchanger on the basolateral membrane extrude Ca2+ into itnerstitial fluid (establishes electrochemical gradient).

  • Active vitamin D (D-1,25-dihydroxy-vitamin D) stimulates all 3 steps by binding to VDR.
63
Q

What is rickets?

How is it treated?

A
  • Vitamin D deficiency which leads to hypocalcaemia.
  • Treatment involves increasing dietary intake of calcium, phosphates and vitamin D (exposure to ultraviolet (sunshine), fish oils are good sources of vitamin D).

DIG (20 decks)

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