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BMED2405 > GIT Physiology > Flashcards

GIT Physiology Flashcards

1
Q

Parasympathetic innervation

A
  • Long preganglionic (ACh)

- short postganglionic (ACh/ peptides)

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2
Q

Sympathetic innervation

A
  • short preganglionic (ACh)

- Long postganglionic NE

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3
Q

Where is gastrin secreted

A

stomach

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4
Q

Where is secretin, cholecystokinin and gastric inhibitory peptide

A

duodenum/ jejunum

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5
Q

Function of saliva

A 
buffer
digests
dilutes
protects
cleanses
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6
Q

acinar cells move in which direction?

A

blood to lumen

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7
Q

duct cells move in which direction?

A

Blood to lumen or lumen to blood

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8
Q

What type of secretion is parotid

A

thin, watery (PNS)

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9
Q

what type of secretion is sublingual

A

serous, thick (SNS)

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10
Q

submandibular

A

mixed

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11
Q

Mechanism of salivary secretion

A

isotonic –> hypotonic
(Na, Cl, K, HCO3 enter)
(K + HCO3 secreted in lumen, while Na Cl secreted into blood and H20 can’t get into blood)

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12
Q

Neural control?

A

parasympathetic main controller –> initiates and maintains salvation

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13
Q

Mechanism of pancreatic secretion

A

isotonic –> isotonic

Na + K is same

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14
Q

what does cholecystokinin (CCK)

A

I cells

stimulates the release of enzymes

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15
Q

What does secretin do?

A

S cells
natural antacid
stimualtes the release of bicarbonate

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16
Q

Small intestine where does absorption and secretion occur

A

absorption in villi (Na)
secretion in cyrpts (Cl)
A>S

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17
Q

What is succus entericus

A
  • ions, water and mucus

- intestinal juice which is secreted in SI

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18
Q

gastric juice into lumen?

A
  • mucus
  • pepsinogen
  • HCl
  • intrinsic factor
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19
Q

secretions from paracrine into lamina propria

A
  • gastrin (stimulates acid secretion)
  • somatostatin (inhibits acid secretion)
  • histamine
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20
Q

What cells secrete Gastrin

A

G cells in pyloric region

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21
Q

what cells secrete somatostatin

A

D cells in pyloric region

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22
Q

what cells secrete pepsinogen

A

chief cells

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23
Q

what cells secrete histamine

A

Enterochomaffin-like cells

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24
Q

what cells secrete HCl and intrinsic factor

A

parietal cells

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25
Q

Resting vs stimulated parietal cell

A

resting:
- basal levels of acid production, SA lumen is reduced

active:

  • the lumen incr
  • no. of pumps
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26
Q

Parietal cell via vagus nerve (direct)

A
  1. vagus nerve release ACh
  2. ACh stimulates M3 receptors
  3. M3 receptor stimulates parietal cells –> incr. intracellular conc of ca
  4. As [Ca] incr. it then binds with Calmodulin which stimulates K pump
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27
Q

histamine stimulation of parietal cells

A
  1. Histamine stimulates H2 receptors on parietal cells
  2. Stimulation of H2 receptors cause on increase in cAMP in parietal cells
  3. cAMP combines with Protein Kinase A and stimulates the H/K ATPase pump
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28
Q

ECL via vagus nerve (indirect)

A
  1. The vagus nerve releases ACh
  2. ACh stimulates M3 receptors
  3. ECL cells release Histamine
  4. Histamine stimulates H2 receptors on parietal cells
  5. Stimulation of H2 receptors cause on increase in cAMP in parietal cells
  6. cAMP combines with Protein Kinase A and stimulates the H/K ATPase pump
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29
Q

G cell (indirect)

A
  1. G cells secrete gastrin
  2. Gastrin is an endocrine secretion which stimulates ECL cells
  3. ECL cells release histamine
  4. Histamine stimulates H2 receptors on parietal cells
  5. Stimulation of H2 receptors causes an increase in cAMP in parietal cells (ATP binds –> cAMP –.> AMP via phosphodiestrase)
  6. cAMP combines with Protein Kinase A and stimulates the H/K ATPase pump
30
Q

Feedback Regulation of HCl secretion

• G cells

A 
o	Gastrin (stimulates histamine release)
o	Incr. HCl production (mostly indirect)
31
Q

Feedback Regulation of HCl secretion

- D cells

A

o Somatostatin

o Inhibits HCl production

32
Q

Cephalic phase (30%)

A

thought/ smell of food

  • vagally mediated
  • stimulatory
  • incr. motility
33
Q

Gastric phase (50-60%)

A

part vago-vagal, part enteroendocrine

  • stimulatory
  • inc. motility
34
Q

intestinal phase (10-20%)

A

inhibitory (turn off acid production)
enteroendorcrine
- decr. motility

35
Q

vitamin B12 absorption steps

A
  1. cobalamin is bound to food
  2. pepsin and gastric acid release the cobalamin from food
  3. salivary and gastric glands to release haptocorrin which binds to cobalamin
  4. pariteal cells release IF
  5. the pancreas releases proteases and biocarbonates which degrades the haptocorrin and cobalamin is released
  6. IF-cobalamin complex forms
  7. IF cobalamin complex absorbed in terminal illeum
36
Q

absorption of non-polar

A

intestinal epithelium via simple diffusion

37
Q

absorption of polar substances occurs where and how

A

carrier mediated transport either active or passive

38
Q

what are the dissachrides and what they made of

A
  • Sucrose: fructose + glucose
  • lactose: glucose and galactose
  • maltose: glucose + glucose
39
Q

Digestive process for carbohydrates

A
  1. luminal

2. membrane

40
Q

intraluminal digestions - amalyase purpose?

A

to breakdown the polysacchrides down the middle, can’t cleaf the ends, can’t make glucose

Polysaccharides  disaccharides, oligosaccharides (a few sugars in a chain)

41
Q

membrane digestion

A
  • Small intestional brush border enzymes (apical membrane of villus epithelial cells)
  • Disaccharides, oligosaccharide  monosaccharides (absorbable units)
42
Q

SGLTI at brush border allow what to pass through

A

glucose/ galactose / Na

43
Q

GLUT5 what passes through

A

fructose - all products empt into blood

44
Q

Proteins to produce olipeptides and AA

A

Endopeptidases (aka proteases e.g. pepsin) –> can’t cleave off AA
exopeptidases –> can produce individual AA

45
Q

protein process

A
  1. luminal
  2. membrane
  3. cellular
46
Q

Luminal protein

A

gastric (pepsin) and pancreatic proteases (inactive form, as if active would be digested by pancreas)

47
Q

when is pepsin active and not

A

pepsin is active at acidic pH

Pepsin is denatured in the duodenum when the pH rises

48
Q

pancreatic exocrine secretion in protein luminal

A
  • proteases (inactive)

- amalyses/ lipases (Active)

49
Q

enzymatic component (acinar cells)

A

proteases (inactive)

  • trypsinogen –> trypsin (once activated other proteases activated)
  • Chymotrypsinogen  chymotrypsin
  • Procarboxypolpeptidase  carboxypolypeptidase (can cleave an individual peptide)
  • Proelastase  elastase
50
Q

cellular

A

AA absorption

51
Q

Lipids digestion

A

entirely luminal

52
Q

triglyceride

A

lipase –> FFA + Monoglycerides

53
Q

Bile salts synthesis

A
  1. liver conjugates the bile acid with glycine to form bile salts
  2. conjugation makes the bile acids more water soluble at dudodenal pH
    Thus bile salts are water soluble yet ampipathic
54
Q

luminal lipid digestion

A
  1. emulisfication
  2. lipase action
  3. micelle formation
55
Q

emulification

A

break up large fat drops to smaller ones

56
Q

Lipase action

A

digests lipids into absorbable units (creates SA to allow lipase action)

57
Q

micelle formation

A

transports products of digestion to luminal surface for absorption

hydrophillic shell outside and hydrophobic core inside

58
Q

bile salts are

A

recycles

59
Q

biliary secretion

A
  • Yellow-green “soapy” solution
  • Electrolytes – bicarbonate rich
  • Important components include
    o Bile salts (including bile acids) – 50%
    o Phospholipids (lecithin and others) – 40%
    o Bilirunin – 2% (to be eliminated)
    o Cholestrol – 4% (to be eliminated)
  • ONLY Bile salts and lecithin aid digestion
60
Q

Neural control of motility

A

PNS: motilin, increases motility
SNS: secretin, GIP, decrease motility, decr. acid secretion.

61
Q

Oesophagus

  • motility
  • function
  • control
A

Motility:
Swallowing
Peristalsis (progressive wave of SM contraction) – Primary and secondary

Function: move food –> stomach

Control:

  • Initially voluntary then reflex
  • Distention signals CNS to produce changes in muscle contraction
62
Q

Gastric motility:

  • motility
  • function
  • control
A

motility: relaxation (accomodates for food) and peristalis

Function: mixes and empties the stomach

control: cephalic, gastric, intestinal

63
Q

gastric motility - storage Receptive relaxation

A

oesophageal gastric reflex initiated by pharynx with each swallow

Even before food has entered stomach, it prepares to receive by relaxing stomach

64
Q

Adaptive relaxation (gastro-gastric reflex)

A

initiated by the stomach

65
Q

Enterogastric reflex

A

o Food in intestine  gastric relaxation
o food leaves stomach, control the rate of food entering into the intestine, if food enters too quickly it can affect fluid movement. Food enters intestines, decreases motility of the stomach

66
Q

Small Intestine – Interdigestive phase

A 
•	Fasting- interdigestive patterns 
o	MMC migrating myoelectric (motor) complex 
o	From stomach to terminal ileum 
o	Repeats every 90 minutes or so 
o	Mediated by Motilin 
o	Moving debris from stomach to LI
67
Q

Gastroileal reflex

A

a feedforward reflex
-pushes valve open and relaxes sphincter
illeocecal valve: pushes valve closed and contracts sphincter

68
Q

Feedback

A

slow organ above
o Enterogastric (neural) enterogastrone (hormonal)
 Inhibits gastric emptying when duodenum distended
o Ileogastric/ ileojejunal/ ileal brake
 Slows gastric or jejunal emptying when ileum distended
o Mostly achieved by increased sphincter tone; the stomach will not be emptying as quickly

69
Q

Feedforward

A

stimulates organ below
o Gastroileal, gastrocolic reflexes
 Stimulate ileal or colonic emptying when stomach is distended
o Most achieved by decreased sphincter tone

70
Q

defaecation relfex

A
  • rectal distention
  • rectum contracts
  • internal anal sphincter relaxes
  • increased tone in the external anal sphincter

BMED2405 (9 decks)

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