GI: Physiology of GIT Flashcards

1
Q

Function of the GI tract

A

Injestion, secretion, mixing, digestion, absorption and excretion

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2
Q

Layers of the GI tract (out to in)

A

Mucosa (epithelium, NAV), submucosa (loose CT), muscularis (circular and longitudinal), serosa (peritoneum)

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3
Q

What are villi used for

A

Absorption

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4
Q

What are crypts used for

A

Secretion. ECF released into lumen, water follows. (Fluid derived from plasma)

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5
Q

What is involved in the coordination if GI tract?

A

Nervous system, local (physical stretch or chemical), hormone

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6
Q

Difference between enteric nervous system and ANS

A
  • Enteric, short reflexes, communications in the gut.
  • Enteric signals go up to CNS and become ANS. (long reflexes)
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7
Q

Stomach motility stimulation and inhibition

A

Stimulated by stomach distension and peptides
Inhibited by dudodenal lumen, high peptides, high pressure, high osmolarity, low pH and high fat

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8
Q

Process of stomach motility/ contractions

A

Meal-> acetylcholine + gastrin -> High threshold -> stomach contracts

Slow wave contractions (3-4mins)

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9
Q
  1. Cephalic phase (seeing food)
A

Release gastrin. Chief cells to pepsinogen and parietal cells to HCL.

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10
Q

Phases of gut secretions

A

Cephalic phase, gastric phase, intestinal phase

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11
Q
  1. Gastric phase (food in stomach)
A

Through stretch receptors. Gastrin release, peptides stimulate gastrin release.

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12
Q

Parietal cell secretions

A

Secretes HCl.
Stimulation: Vagus, Gastric, Histamine
Inhibition: Somatostatin + Low pH

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13
Q

Alkaline tide

A

HCO3- by pancreas into duodenum to neutralize stomach H+ from stomach.

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14
Q

What is the pancreatic mucus secretion used for

A

Protective layer against stomach acids

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15
Q

How are the sphincters of the of the GIT controlled?

A

Controlled by enteric NS/ stretch (except external anal sphincter) and regulated by stretch. Found between each organ.

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16
Q

Causes of vomiting (3)

A

Physiology, drugs and chemicals (through chemical trigger zone) and pathology

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17
Q

Stages of vomiting (6)

A
  1. Postural adaptation
  2. Saliva stimulated (protect against acidity)
  3. Respiratory (inspiration inhibited), glottis closed, larynx raised, increased SP
  4. Diaphragm + abdominal muscles contract
  5. High intragastric pressure, retching
  6. Lower oesophageal sphincter relaxes, gastric contents expelled.
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18
Q
  1. Intestinal phase (What is secreted?)
A

Parietal cell secretions and mucus secretions

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19
Q

What controls salivary secretion?

A

Complete neural control

20
Q

What comprises enteric NS? (2 nerve plexuses)

A
  • Myenteric plexus (sensory, found btw and regulates muscles)
  • Submucosal plexus (regulates mucosal gland secretions)
21
Q

Gastrin

A

Stimulation of HCl production and supports growth of mucosa. (distal stomach)

22
Q

Secretin

A

Stimulates production of bicarbonate by pancreas and Brunner’s glands. (duodenum)

23
Q

Cholecystokinin (CCK)

A

Stimulates enzyme production in pancreas and gall bladder by contraction. (duodenum)

24
Q

Gastric inhibitory polypeptide (GIP)

A

Reduces HCl production and stomach emptying. Stimulates insulin release. (Proximal small bowel)

25
Q

Somatostatin

A

Reduces acid secretion, gastric motility and stomach emptying. (intestines and pancreas)

26
Q

Leptin

A

Stimulates satiety

27
Q

Ghrelin

A

Stimulates feeding centre

28
Q

Peptide YY (PYY)

A

Stimulates satiety, inhibits eating.

29
Q

Small intestine function

A

Secretes fluid, mucus and HCO3- (from Brunner’s glands)

30
Q

S.intestine motility (2)

A
  • Segmentation: Alternating contractions, squeezing back and forth to mix
  • Peristalsis: Initiated at a point, contraction of circular muscles on oral side and relaxing on aboral side.
31
Q

Control of s.intestine motility

A
  • Local distension, enteric peristalsis
  • Extrinsic: parasymp increase, sympathetic decreases
32
Q

Standing- gradient osmosis (how water is absorbed)

A
  • Dependent on Na+
  • Pump Na/Cl into lateral space between cells. Water follows
  • Pressure build and pushed out into tissue
33
Q

L. intestine function

A
  • Absorbs remaining water and Na, vitamins produced by commensal bacteria, eliminates metabolic waste, etc.
34
Q

What happens in the rumen? (Carb and proteins) (2)

A
  • Anaerobic bacteria fermenting carbs into short chain fatty acids
  • Microbes use ammonia (by-product) for protein. Flushed through, protein from dead bacteria
35
Q

Reticuloruminal motility

A

2nd rumenal wave
- Antiperistalsis and eructation voided through nares

36
Q

Primary ruminal contractions

A
  • Rumen fill = strength of mixing
  • Peristaltic to reticulum
37
Q

Secondary ruminal contractions

A
  • Eructation of gas
  • Anti-peristaltic and follows half of primary ruminal contractions
38
Q

What do the Short chain fatty acids become? (Ruminant digestion)

A

Acetate > Proprionate > Butyrate (and ketone bodies)

39
Q

Acetate, proprionate or butyrate; which one directly produces glucose

A

Propionate

40
Q

Lactation ketosis

A

Ketone bodies replace glucose due to high energy demand and low oxaloacetates in Krebbs.
- Acetyl-CoAs diverted to produce ketone bodies
- Very acidic conditions

41
Q

Grain overload

A
  • High fermentation rate, acidic rumen, high lactate, lactophiles thrive
  • High rumen osmolarity, low BP and dehydration
  • Renal and respiratory comprimise + metabolic acidosis.
42
Q

Uses of saliva (ruminant)

A
  • pH buffer
  • plant wetting agent
  • anti-frothing proteins (to prevent bloat)
43
Q

Salivary glands (4)

A

Parotid, mandibular, zygomatic and sublingual

44
Q

Control of saliva

A

Parotid and sublingual nerve + food :)

45
Q

Chemical compound that provides energy when there isn’t enough glucose (result of ketosis)

A

B-hydroxybutyrate