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🚌 GI Flashcards

i ignored the notes part

1
Q

What happens after a vagotomy?

A

vagal nerves cut ∮ ↓accommodation + gastric compliance

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2
Q

What happens to food after accommodation?

A

moved from gastric reservoir ➩ antral pump –> Stomach thrown➩ folds –> mix/grind of chyme–>squirt food via sphincter

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3
Q

How is food moved ➩ antral pump?

A
  • Tonic contraction = produced by fundus pacemaker cells mins-hrs
  • Peristaltic 🌊 in body
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4
Q

What does proximal stomach do?

A

relaxes to store food at low p whilst broken down acid, enzymes, đ”Œ,mechanically

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5
Q

Why is gastric emptying regulated?

A

Coordinates mechanical/chemical breakdown with absorption
Reduces swamping of duodenum with acidic chyme
Particles that are large cannot pass the pylorus

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6
Q

What’s gastric stasis (gastroparesis)?

A

chronic condition when stomach cannot empty normally –>food pass slowly

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7
Q

How’s gastric motility/emptying regulated?

A

Excitatory reflex from stomach

❌ reflex from small intestine

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8
Q

What’s the excitatory reflex?

A

food causes distention–> excitatory reflex–>food ➩ distal stomach–>antral pump switched ON + intensified to prolong relaxation..

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9
Q

What’s the ❌ reflex?

A

from antrum descending❌ reflex causes pyloric relaxation- NO/VIP–> antral contraction –> food➩pylorus–> food is the duodenal stimuli–> sends ascending excitatory reflex causing pyloric contractions so closed until chyme neutralised

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10
Q

What’s reciprocal vagal control?

A

accomodation ⇶Ach–>contractions + NANC ⇶⇑VIP/NO–> relax

emptying ↑cholingeric + ↓NANC

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11
Q

What’s gastric emptying dependent on?

A

Propulsive force by tonic contractions

Stomach’s ability to differentiate food + their components- liq/solid

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12
Q

Liq emptying?

A

đŸƒâ€â™‚ïždisperse, no lag time, pass in spurts, if ↑nutrient then retained longer

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13
Q

Solid emptying?

A

2 phases: lag time+ linear phase
Liq part emptied + solid retained in proximal stomach
Trituration of larger particles →small 2mm
60min

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14
Q

What does lag time depend on?

A

particle size

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15
Q

Fatty foods emptying?

A

Liq at body temp∎float on top of liquid layer∎SLOW

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16
Q

Indigestible solids emptying?

A

Not emptied in immediate post-prandial period

MMC activity

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17
Q

Determinants of motility rate?

A

Food : carb>🐟>fat>indigestible
Osmotic p of duodenal contents : hyperosmolar chyme ↓ gastric emptying
Vagal innervation > over-distension : ↓motility
Hormones(somatostatin, secretin, CCK, GIP): ❌ emptying
Injury + infections : ↓ motility

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18
Q

What controls gastric motility myogenically?

A

Intestinal Cajal Cells

Basic Electrical Rhythm

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19
Q

What’s ICC?

A

Specialised pacemaker cells located in the wall of stomach, small+large intestine
Membranes undergo rhythmic depolarisation + repolariation which creates BER

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20
Q

What’s BER?

A

determines the ƒ of the contractions in the GI, when at max it produces smooth muscle cell contraction so depolarises + contracts rhythmically when exposed to hormonal signals

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21
Q

Process of myogenic control of motility?

A

ICC in fundus produce depolarisation from RMP–> ripples move to antrum - BER 3 waves/min

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22
Q

What ↓BER?

A

Sympathetic - NA/A on the GI smooth muscle
Depolarisation of GI smooth muscle by Ca/Na influx
Repolarisation of GI smooth muscle by K+ efflux

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23
Q

What ↓ fundic motor activity?

A 
GRP
Cholecystokinin (CCK)
Secretin
VIP
Somatostatin
Glucagon
Duodenal distension, duodenal acid
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24
Q

What ↑ fundic motor activity?

A

Motilin

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25
Q

What ↑ intestinal motility?

A

CCK, gastrin, motilin

serotonin, insulin

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26
Q

What ↓ intestinal motility?

A

Secretin

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27
Q

What are the -ve feedback systems of gastric emptying?

A

Antral over-distension: Vago-vagal reflex

Duodenal over-distension + chemical stimulation: Vago-vagal reflex + hormones

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28
Q

Types of motility control along alimentary tract?

A

Segmentation
Peristalsis
Migrating Motor Complex MMC
Mass movements

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29
Q

Phases of motor activity?

A

I: quiescence/quiet period <12hrs
II: irregular propulsive contractions
III: burst of uninterrupted phasic contractions (peristaltic rush)

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30
Q

What’s segmentation + process?

A

Contractions churn + propel food ➩ anus
Originates in ICC–>Ă· –>subĂ· of chyme w contents∎ contact w intestinal walls for absorption–> slow migration of chyme ➩ ileum
Duodenum/jejunum: 10-12 contractions/min
Ileum: 8-9 contractions/min

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31
Q

What’s peristalsis + process?

A

Spreads food allowing đ”Œ to mix + global movement

Propagating contractions of sucessive sections of circular muscle–> relaxation where bolus moving-VIP/NO

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32
Q

How to regulate peristalsis?

A

neural reflexes

  • Sensory neurones detect stimulation of the bolus via cholinergic interneurones –>❌ motor neurones ⇶ VIP/NO–>relax circular in front of bolus
  • Excitatory motor neurones ⇶ Ach/Substance P–>contracts behind bolus
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33
Q

What’s MMC?

A

Highly organised motor activity,cyclically recurring seq of events between meals when ‘empty’ -phase III

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34
Q

Process of phase III?

A

From lower stomach–>burst of high ƒ, large amplitude contractions migrating along intestine then die out
90-120min intervals

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35
Q

Functions of MMC?

A

“Intestinal housekeeper”
Removes indigestible out stomach ∔ contractions + wide sphincter
Removes dead epithelial cells by abrasion
Prevents 🐛 overgrowth
Prevents colonic 🐛entering small intestine

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36
Q

Control of MMC?

A

?-Stomach cells produce “slow 🌊” –> contractions are coordinated by ICC–> initiated by the vagus in upper GI
-Cyclical secretion of MOTILIN from stomach + duodenum

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37
Q

What’s the motor activity when fed?

A 
Segmentation
Peristaltic contractions (slow waves)
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38
Q

What does large intestine do?

A

Absorption of H2O+ions–>🐛–>storage of waste–>elimination

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39
Q

What are ‘fermenting chambers’?

A

allow the hydrolysis of fibre + indigestible

40
Q

Features of motility in the large intestine?

A

Intensive missing
Fermentation
Slow propagating- slow aboral flow

41
Q

Function of taenia coli longitudinal muscle?

A

Segmental/haustral contractions-mix contents

42
Q

Peristalsis in large intestine?

A

slow, moves contents ➩anus, distension initiates contraction

43
Q

How is mass movement in large intestine?

A

powerful contraction of mid-transverse colon that sweeps colon contents ➩ rectum-for colonic evacuation

44
Q

What’s diarrhoea?

A

frequent (>3x/day) liq faeces

45
Q

What’s constipation?

A

difficulty opening + emptying bowels hard faeces

46
Q

Functions of alimentary?

A

Absorption of nutrients, salts and water
Absorption of fluid ⇶small intestine back➩blood
Absorption by transport of ions
Colon absorbs 90% of the H2O from the contents –>semi-solid material ~200ml

47
Q

Diff between Marasmus vs Kwashiorkor

A
  • Undernourishment –>sig low weight for child’s age

- Insufficient 🐟-E malnutrition –>oedema, irritability, enlarged liver w fatty infiltrates

48
Q

What are villus cells?

A

Involved with ABSORPTION +⇶HCl for gastric use

49
Q

What are crypt cells?

A

Base of villus, involved in SECRETION,defence,signalling,replenish epithelial cells up the villi by stem cells

50
Q

What mediates intestinal digestion + absorption?

A

Enterocytes-villus + crypt

51
Q

🚌 methods across enterocytes?

A 
Transcellular= transport of solutes by a cell via cell eg glucose from lumen to extracellular fluid via epithelial cells
Paracellular= passage of Na+,Cl-,H2O between cells via tight junctions, passive, variable, regulated
52
Q

What’s carb digestion + absorption?

A

Only monosaccharides absorbed
Complex carbs→disaccharides by amlyases
Specific brush border enzymes convert di→ mono (eg glucose +galactose

53
Q

E value of carb?

A

17.5 kJ/g

54
Q

Where does carb digestion occur?

A

intestinal lumen + brush border

55
Q

Types of brush border đ”Œ for carb?

A

Sucrase: sucrose→glucose + fructose
Glucoamylase : glucose oligomers → glucose
Lactase : lactose→ galactose + glucose

56
Q

Types of intestinal lumen đ”Œ for carb?

A

salivary + pancreatic amylase

57
Q

What are glucose oligomers?

A

molecular complex that has few monomer units eg maltotriose (trisaccharide)

58
Q

What’s maltotriose?

A

has 3 glucose linked w α-1,4 glycosidic bonds + produced by α-amylase on amylose in starch

59
Q

How’s glucose + galactose absorbed via enterocytes?

A

đŸƒâ€â™‚ïž by luminal glucose carrier system actively

60
Q

How’s fructose + mannose absorbed via enterocytes?

A

slowly by GLUT 5 on basolateral membrane

61
Q

Process of glucose + galactose absorption?

A

Cytoplasmic Na+ pumped out via basolateral membrane (close to the blood)–>intracellular electrochemical gradient–>Na+ enters enterocytes w glucose via glucose/Na+ co transporter SGLT1–>Glucose enters blood via GLUT-2

62
Q

What’s a competitive ❌ of glucose 🚌?

A

Galactose

63
Q

Process of fructose absorption?

A

GLUT5 + GLUT2 on enterocyte–>GLUT 5 on basolateral membrane

64
Q

What’s mannose?

A

Sugar monomer of the aldohexose series of carbs

65
Q

What digests 🐟?

A

pepsin: →polypeptides

66
Q

What digests polypeptides?

A

pancreatic proteases: →di-/tri-peptides

67
Q

What digests di-peptides?

A

di-peptidases: →AA

68
Q

Why is diffusion is more vital for the basolateral transport of AA?

A

basolateral membrane more permeable to AA than brush border membrane

69
Q

What do cytoplasmic peptidases do?

A

cleave the di-peptides →AA

70
Q

Where does 🐟 digestion occur + how?

A

-Intestinal lumen–pepsins +pancreatic proteases :proteins →oligopeptides+AA
-Brush border–specific peptidases : oligopeptides→
di/tripeptides + AA (absorbed → enterocytes)
-Enterocytes–cytoplasmic peptidases : di/tripeptides → AA –> pass→ blood

71
Q

What are the mechanisms of 🐟 absorption?

A
  • AA 🚌on a Na+/AA carrier like glucose,(separate carriers for diff AAs) –> AT from enterocyte→blood –> 🚌liver via portal vein
  • Some di-/tri-peptides 🚌using H+ grad
72
Q

What are diff types of dietary lipids?

A

TG 90%, phospholipids, cholesterol, fat soluble vitamins A,D,E,K

73
Q

Where’s lipid digestion?

A

Mouth: salivary lipase

SMALL INTESTINE

74
Q

Why’s TG dissolved in aq before digestion?

A

Lipases are soluble so TG emulsified by chyme

75
Q

Optimal lipid in diet?

A

20% - fish + olive oil

76
Q

What digests lipids?

A

Gastric lipase 10-30% of fats

pancreatic lipase rest

77
Q

What facilitates digestion + absorption of lipids?

A

Emulsification

Micelle formation

78
Q

Where does emulsification happen?

A

In duodenum by bile salts

79
Q

Process of emulsification?

A

Bile emulsification –> emulsion droplets–> pancreatic lipase binds to the hydrophilic+emulsion droplets bind to the hydrophobic region of the colipase–>digestion of emulsion droplets

80
Q

Function of sphincter of oddi?

A

Controls the flow of bile + pancreatic juice via ampulla of Vater

81
Q

Where do bile salts come from?

A

Bile salts produced in liver, stored in gallbladder, comes down common bile duct, joins w pancreatic duct which ⇶pancreatic lipase + colipase

82
Q

Function of colipase?

A

dissolves lipid in aq ∔ amphipathic-hydrophilic + hydrophobic regions

83
Q

How fat droplets broken down?

A

muscular actions–>bile salts (prevents combining)

84
Q

How micelles formed?

A

bile salts form a layer of phospholipids around digested lipids

85
Q

Why micelles?

A

200x smaller than emulsion droplets so small enough to fuse w enterocytes via pinocytosis

86
Q

What’s a micelle?

A

lipid∞arranged in spherical form in aq

Bile salts, monoglycerides,free FA, cholesterol, vit A,D,K

87
Q

What happens after micelle fuses w enterocyte?

A
  • Short chain free FA enter portal vein, combine w bile in the liver to form more micelles via lipases
  • FA + monoglycerides = TGC, packaged w cholesterol, phospholipids, apolipoproteins ➩ chylomicrons–>🚌 to lymph
88
Q

How chylomicrons enter the lymph?

A

via lacteals–> 🚌via lymph vessels➩blood(via thoracic duct near the neck connect w left subclavian vein)→ wall of capillaries →FA → liver + fat cells

89
Q

Function of lipoprotein?

A

allow fats to move through the H2O inside+outside cells

90
Q

Types of lipoprotein?

A 
LDL = has ↑fat, 🚌 fats → adipose tissue, clogs
HDL = carries fats to liver for recycling + excretion
91
Q

Role of albumin?

A

FA 🚌to target cells

92
Q

What happens if there’s absorption of many chylomicrons?

A

lymph draining from the small intestine looks milky

93
Q

What leads to fat malabsorption

A

gallstones, pancreatitis, Crohn’s,liver disease

94
Q

Where are triacylglycerols of chylomicrons + VLDL hydrolysed?

A

Golgi by lipase

95
Q

What’s Steatorrhoea?

A

fatty stools which smell and float
Intestinal discomfort
Body is deprived of fat-soluble nutrients, e.g. Vits A, D, E, K

GI (15 decks)

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