GI Physiology Flashcards

1
Q

What cells make up a gastric gland?

A

Surface mucous cells
Mucous neck cells
Parietal cells
Chief cells

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2
Q

What do mucous neck cells secrete?

A

Mucus

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3
Q

What do chief cells secrete?

A

Pepsinogen

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4
Q

What do parietal cells secrete?

A

HCl and intrinsic factor

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5
Q

What is the mechanism for HCl secretion from parietal cells?

A

CO2 + H2O -> H2CO3
H2CO3 -> H + HCO3
H pumped out across apical membrane
HCO3 pumped out across basolateral membrane in exchange for Cl ion
CL leaves cell via apical membrane
H and Cl are in lumen of stomach with H2O

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6
Q

What transporter is essential for HCl secretion?

A

H+/K+ ATPase

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7
Q

What 4 factors act on H+/K+ ATPase to control gastric acid secretion?

A

Gastrin
Histamine
Prostaglandins
Acetylcholine

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8
Q

What is the function of Gastrin?

A

Binding to receptor causes increase in intracellular calcium.
Calcium acts on protein Kinase C which increases activity of ATPase

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9
Q

What is the function of Histamine?

A

Coupled to adenylate cyclase to convert ATP → cAMP.
cAMP acts on Protein kinase A to increase activity of ATPase

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10
Q

What is the function of ACh?

A

Binding to receptor causes increase in intracellular calcium.
Calcium acts on protein Kinase C which increases activity of ATPase

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11
Q

What is the function of prostaglandins?

A

Coupled up to adenylate cyclase to inhibit production of cAMP and switch the mechanism off.

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12
Q

What is the neurocrine control of gastric acid secretion?

A

Vagus nerve/ local reflexes

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13
Q

What is the endocrine control of gastric acid secretion?

A

Gastrin

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14
Q

What is the paracrine control of gastric acid secretion?

A

Histamine

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15
Q

What cells release histamine?

A

Enterochromaffin like cell (ECL)

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16
Q

What is the stimulation for histamine release?

A

Increased Gastrin/ ACh levels

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17
Q

What is the stimulation for ACh and gastrin release?

A

Increased vagal activity

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18
Q

What is involved in the cephalic phase for stimulating gastric acid production?

A

Sight/smell/taste of food

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19
Q

What is involved in the gastric phase for stimulating gastric acid production?

A

Distention of stomach
Peptides in lumen

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20
Q

What is involved in the cephalic phase for inhibiting gastric acid production?

A

Stopping eating

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21
Q

What is involved in the gastric phase for inhibiting gastric acid production?

A

Low pH due to HCl causes gastrin levels to lower

22
Q

What is involved in the intestinal phase for inhibiting gastric acid production?

A

Acid in duodenum -> enterogastric reflex and secretin release
Fat/CHO in duodenum -> HIP release
The result is reduced activity of G cells and parietal cells

23
Q

What are enterogastrones?

A

Hormones released from gland cells in duodenal mucosa
- Secretin
- Cholecystokinin (CKK)
- GIP

24
Q

What is the stimulation of enterogastrones?

A
  • Acid in duodenum
  • Hypertonic solutions
  • Fatty acids or monoglycerides in duodenum
    All signs that the stomach is emptying its contents
25
Q

What is the action of enterogastrones?

A
  • Inhibit gastric acid secretion
  • Reduce gastric emptying
26
Q

What is intrinsic factor?

A

Glycoprotein released by stomach parietal cells to absorb vitamin B12

27
Q

What is gastric motility?

A

The process by which food travels through the digestive tract via a series of muscular contractions called peristalsis

28
Q

What produces gastric peristaltic waves?

A

Peristaltic rhythm (3/min) generated by pacemaker cells within longitudinal muscle layer

29
Q

What is the impact of gastrin on motility?

A

Increased contraction

30
Q

What is the impact of stomach wall distention on motility?

A

Reflexes cause increased contraction

31
Q

What is the impact of Fat/acid/amino acid/hypertonicity in duodenum on motility?

A

Reduced contraction

32
Q

What is the result of acid in the duodenum?

A

Vagal and ENS reflexes
Secretin release from S cells

The result is HCO3 secretion to neutralise the acid

33
Q

What cells is HCO3 secreted from in the duodenum?

A

Brunner’s glands in the submucosa

34
Q

What are long and short reflexes?

A

ENS- short
Vagal- long

35
Q

What is the endocrine portion of the pancreas?

A

Pancreatic Islets
Produce insulin, glucagon and somatostatin

36
Q

What is the exocrine portion of the pancreas?

A

Acini -> Lobules -> intralobular ducts -> Main pancreatic duct -> common bile duct -> hepatopancreatic ampulla

37
Q

What do acinar cells secrete?

A

Digestive enzymes

38
Q

What to duct cells secrete?

A

Bicarbonate

39
Q

What is the action of enterokinase?

A

Converts trypsinogen to trypsin

40
Q

What is the action of trypsin?

A

Converts all other zymogens to active forms

41
Q

What is secretin released in response to?

A

Acid in duodenum

42
Q

What is Cholecystokinin (CCK) released in response to?

A

Fat/amino acids in duodneum

43
Q

What is the mechanism for glucose transport?

A

SGLT1 undergoes conformational change when sodium and glucose bind
Secondary active transport
Creates osmotic gradient

44
Q

What is the mechanism for fructose transport?

A

Facilitated diffusion through GLUT-5 and GLUT-2
No sodium involvement
No water uptake associated

45
Q

What is the mechanism for sodium transport?

A

SAAT transports sodium and amino acid across apical membrane
Sodium independent transporter in basolateral membrane
Creates osmotic gradient

46
Q

What is PepT1?

A

Transports dipeptides and tripeptides via hydrogen ion dependant process

47
Q

What are the fat soluble vitamins?

A

A, D, E, K

48
Q

What are the water soluble vitamins?

A

B, C, folic acid

49
Q

What doe sDMT1 transport?

A

Iron into the duodenal enterocytes

50
Q

What do iron ions bind to?

A

Ferritin

51
Q

What do iron in blood bind to?

A

Transferrin

52
Q

What do iron in blood bind to?

A

Transferrin