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
Somatostatin
Reduces acid secretion, gastric motility and stomach emptying. (intestines and pancreas)
26
Leptin
Stimulates satiety
27
Ghrelin
Stimulates feeding centre
28
Peptide YY (PYY)
Stimulates satiety, inhibits eating.
29
Small intestine function
Secretes fluid, mucus and HCO3- (from Brunner's glands)
30
S.intestine motility (2)
- 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
Control of s.intestine motility
- Local distension, enteric peristalsis - Extrinsic: parasymp increase, sympathetic decreases
32
Standing- gradient osmosis (how water is absorbed)
- Dependent on Na+ - Pump Na/Cl into lateral space between cells. Water follows - Pressure build and pushed out into tissue
33
L. intestine function
- Absorbs remaining water and Na, vitamins produced by commensal bacteria, eliminates metabolic waste, etc.
34
What happens in the rumen? (Carb and proteins) (2)
- Anaerobic bacteria fermenting carbs into short chain fatty acids - Microbes use ammonia (by-product) for protein. Flushed through, protein from dead bacteria
35
Reticuloruminal motility
2nd rumenal wave - Antiperistalsis and eructation voided through nares
36
Primary ruminal contractions
- Rumen fill = strength of mixing - Peristaltic to reticulum
37
Secondary ruminal contractions
- Eructation of gas - Anti-peristaltic and follows half of primary ruminal contractions
38
What do the Short chain fatty acids become? (Ruminant digestion)
Acetate > Proprionate > Butyrate (and ketone bodies)
39
Acetate, proprionate or butyrate; which one directly produces glucose
Propionate
40
Lactation ketosis
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
Grain overload
- High fermentation rate, acidic rumen, high lactate, lactophiles thrive - High rumen osmolarity, low BP and dehydration - Renal and respiratory comprimise + metabolic acidosis.
42
Uses of saliva (ruminant)
- pH buffer - plant wetting agent - anti-frothing proteins (to prevent bloat)
43
Salivary glands (4)
Parotid, mandibular, zygomatic and sublingual
44
Control of saliva
Parotid and sublingual nerve + food :)
45
Chemical compound that provides energy when there isn't enough glucose (result of ketosis)
B-hydroxybutyrate