GI physiology Flashcards

1
Q

Steps in smooth muscle contraction

A

voltage-gated Ca entry, SR Ca release –> increased intracellular Ca –> binds calmodulin –> activates MLCK –> myosin phosphorylation by ATP –> crossbridge cycling –> contraction

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2
Q

resting membrane potential of circular smooth muscle cells

A

-60 mV

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3
Q

slow waves/ basic electric rhythm

A

spontaneous rhythmic waves of depolarization. magnitude = 10-15 mV

Does not cause contraction

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4
Q

Effect of Ach on smooth muscle

A

causes action potentials to fire at each slow wave peak –> voltage-gated channel opening –> contraction at the frequency of BER (12/min)

more action potentials –> greater force of contraction

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5
Q

predominant motor activity in the intestines

A

segmentation = isolated, uncoordinated smooth muscle contraction/relaxation –> mixing without net propulsion –> ensures proper digestion and absorption

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6
Q

coordinated (via vagal input) contractions of adjacent segments in a proximal to distal manner

A

peristalsis

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7
Q

intestinal relaxation distal to food bolus, produced by pressure of the proximal bolus

A

receptive relaxation

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8
Q

effect of cutting the vagus nerve

A

BERs remain, but are disorganized –> abolished peristalsis

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9
Q

phases of swallowing

A

voluntary = tongue moves food back to pharynx –> soft palate pushed upward, closed nasopharynx via upper constrictor muscle contraction

pharyngeal = respiration inhibited for 1-2 seconds, larynx raises and glottis closes

esophageal = UES relaxation, peristalsis –> food descends esophagus –> LES relaxation

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10
Q

Phases of gastric motility

A

after eating, contractions start in mid-stomach at frequency of 3/min –> stronger, faster contractions in antrum –> transient opening of pylorus –> smaller particles and chyme leave the stomach, most content reflected back (retropulsion)

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11
Q

what increases rate of gastric emptying?

A

combination of gastric distension and gastrin

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12
Q

control of gastric emptying

A

duodenal distention and irritation (acidity and high osmolarity) –> reflex inhibition of gastric peristalsis, increased pyloric tone

fats in duodenum –> CCK secreted by enteric endocrine cells –> decreased gastric motility

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13
Q

transit time of chyme in intestines

A

3-5h

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14
Q

Purpose of myoelectric motor complexes

A

every 90 minutes –> removes bacteria and indigestible material

only occurs during fasting

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15
Q

Normal fecal fluid loss

A

100-200ml

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16
Q

mass movements

A

colonic forward propulsion. giant migrating contractions

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17
Q

primary stimulator of colonic contractions

A

distention

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18
Q

gastrocolic reflex

A

stimulates mass movements, pushing feces into the rectum

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19
Q

defecation reflex

A

spinal reflex, mediated by the pelvic nerves –> relaxation of internal anal sphincter

sufficient to empty lower bowel in babies and pts with damaged spinal cords

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20
Q

Parietal cells

A

secrete HCl via ATP consumption –> luminal pH of 2

secrete intrinsic factor –> B12 absorption

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21
Q

Mechanism of acid secretion by parietal cells

A

CO2 diffuses into the cell from blood –> combines with OH- from H2O (produces H+, which is pumped to lumen via H/K ATPase) –> HCO3-, via carbonic anhydrase –> exchanged for Cl- in blood via Cl/HCO3 exchanger –> Cl to lumen via luminal Cl channel

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22
Q

Stimulation of acid secretion

A

Direct path: Ach from vagus nerve –> M3 receptors –> parietal cell acid secretion

Gastrin –> increased intracellular Ca –> direct and/or indirect path –> H+ secretion

Indirect path: Ach from vagus nerve –> ECL M3 receptors –> Histamine release –> parietal cell H2 receptor binding –> Gs –> adenylate cyclase –> Ca and cAMP –> kinase activation –> phosphorylation of H/K ATPase

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23
Q

4 phases of gastric acid secretion

A

basal (inter-digestive) phase,

3 phases associated with eating: cephalic phase, gastric phase, intestinal phase

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24
Q

Circadian rhythm –> rate of acid secretion in lowest in the morning before awakening and highest in the evening. resting pH = 3-7

A

basal (inter-digestive) phase

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25
Q

initiated by smell, sight, taste and swallowing of food

A

cephalic phase

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26
Q

Vagal mediation of cephalic phase

A

stimulation of vagus –> release of Ach, triggering of histamine release from ECL cells, release of gastrin-releasing peptide (GRP) from the vagal and enteric neurons, and inhibition of somatostatin release from delta cells in the stomach

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27
Q

How much acid secretion is accounted for by the cephalic phase?

A

30% of total acid secretion

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28
Q

initiated by entry of food into the stomach

A

gastric phase

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29
Q

components of the gastric phase

A

food distends the gastric mucosa –> vagovagal and ENS reflexes

partially digested proteins –> antral gastrin (G) cell stimulation –> gastrin secretion

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30
Q

How much acid secretion is accounted for by the gastric phase?

A

50-60%

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31
Q

stimulation of the intestinal phase

A

presence of amino acid and partially digested peptides in the proximal portion of the small intestine –> duodenal gastrin (G) cell stimulation –> gastrin secretion –> acid secretion in stomach

32
Q

Function of mucosal barrier

A

protect mucosa from acid, prevent diffusional dissipation of the pH gradient

33
Q

fat absorption

A

fat digestive products –> lacteal –> –> thoracic duct –> blood stream

34
Q

total absorptive area of the intestinal surface

A

200-400 square meters

35
Q

secreted by the salivary glands, digests starch, in the mouth

product = polysaccharides

A

Amylase

36
Q

secreted by serous glands of the tongue, digests fat, in mouth and stomach

Products: monoglycerides, fatty acids

A

lingual lipase

37
Q

secreted by the stomach, digests protein

product: polypeptides

A

pepsin

38
Q

secreted by the pancreas, digests proteins and polypeptides, located in the duodenum and jejunum

Product: small peptides and amino acids

A

trypsin, chymotrypsin, elastase, carboxypeptidases

39
Q

secreted by the pancreas, digests starch, located in the duodenum and jejunum

Product = maltose, maltotriose, and alpha-limit dextran

A

amylase

40
Q

Secreted by the pancreas, digests fat, located in the duodenum and jejunum

products = monoglycerides, fatty acids, cholesterol

A

lipase and colipase, phospholipase A2, cholesterol ester hydrolase (non-specific lipase)

41
Q

Secreted by the liver, emulsify and dissolve fats, located in the duodenum and jejunum

A

bile salts

42
Q

secreted by the stomach, kills bacteria and denatures proteins, located in the stomach

A

HCl

43
Q

Ubiquitous secretion, buffers pH

A

NaHCO3

44
Q

Ubiquitous secretion, lubricates and protects mucosal surfaces

A

mucus

45
Q

Specificity of amylase digestion

A

catalyzes the hydrolysis of a-1,4 linkages (amylopectins)

will never digest cellulose (dietary fiber, a-1,6 linkages), will NEVER PRODUCE free glucose (products converted to glucose by brush-border enzymes)

46
Q

transports glucose and galactose from intestinal lumen into the cytosol

A

Na-dependent glucose transporter (SGLT1) in the brush border or apical membrane of enterocytes

47
Q

transports fructose from the lumen into the cytosol

A

GLUT5 (Na-independent fructose transporter)

48
Q

transports fructose, glucose and galactose from cytosol to the blood

A

GLUT2 (Na-independent fructose transporter)

49
Q

causes lactose intolerance

A

absence of lactase (brush-border enzyme)

50
Q

lactose intolerance

A

unabsorbed lactose –> osmotic diarrhea; gut bacteria metabolize lactose –> gas

51
Q

causes glucose-galactose intolerance

A

genetic absence of SGLT1 (Na/glucose cotransporter) –> potentially fatal in neonates

lack of Na and glucose absorption, –> lack of fluid absorption, osmotic fluid secretion –> diarrhea

52
Q

treatment associated with glucose-galactose malabsorption

A

replace dietary glucose with fructose (uses different transporter)

53
Q

two classes of peptidases

A

endopeptidases (hydrolyze interior peptide bonds) and exopeptidases (hydrolyze one amino acid at a time from the C terminus of proteins and peptides)

54
Q

Pepsin, trypsin, chymotrypsin, elastase

A

endopeptidases

55
Q

Carboxypeptidases A and B

A

exopeptidases

56
Q

converts dipeptides to amino acids

A

Dipeptidase

57
Q

removes dipeptides from the N terminus

A

Dipeptidyl aminopeptidase

58
Q

removes one amino acid at a time from the N terminus

A

Aminopeptidase

59
Q

What is the status of pepsinogen at pH 1-3

A

activated to pepsin

60
Q

What is the status of pepsinogen at a pH above 5

A

inactive; remains pepsinogen

61
Q

Patients with their stomach removed can’t secrete HCl or pepsin. Does this mean that they can’t digest protein?

A

No! neither pepsin, nor HCl are essential for protein digestion

62
Q

Steps of small intestinal protein digestion

A

activation of trypsinogen to trypsin by enterokinase (brush border) –> activation of all other precursors by trypsin –> hydrolysis of proteins to amino acids and di-, tri-, oligopeptides via trypsin, chymotrypsin, elastase, carboxypeptidase A and B –> brush border proteases hydrolyze oligopeptides to amino acids –> pancreatic proteases digest themselves and each other

63
Q

Which two amino acids require a specialized carrier for efficient absorption?

A

proline and glycine

64
Q

patients lack the Na-amino acid transporters (genetic) –> lack capacity for renal or intestinal absorption of cysteine, lysine, arginine and ornithine

excretion of amino acid in the feces/urine

A

Cysteinuria

65
Q

genetic absence/defect of the neutral amino acid transporter

A

Hartnup disease

66
Q

genetic absence/defect in the Cl channel CFTR

A

Cystic fibrosis

67
Q

digests triglycerides –> 2-monoglyceride and two free fatty acids, which can be absorbed

A

pancreatic lipase

68
Q

solubilizes 2’-monoglycerides and fatty acids

A

bile-salt micelles

69
Q

process of triglyceride absorption

A

pancreatic lipase digestion –> bile salt micelle solubilization –> entry into enterocyte –> triglycerides resynthesized –> packaged into chylomicrons with cholesterol and apolipoproteins –> golgi –> incorporated into secretory vesicles –> exocytosis to interstitial space –> lacteals (too large for capillaries)

70
Q

What other nutrients are absorbed via the same route as fats and cholesterol?

A

Vitamin A, D, E, and K. All are fat-soluble

71
Q

fat malabsorption disorders

A

Liver disease c bile salt deficiency

Pancreatic insufficiency (lack pancreatic lipase)

Weight loss medication use –| lipase activity –> anal leakage

72
Q

Two important principles for water absorption

A

water readily moves across the intestinal epithelium –> chyme in duodenum rapidly brought to isotonic equilibrium with the blood

water absorption follows the absorption of solutes (absorbed isotonically)

73
Q

important mechanism for colonic absorption of Na

A

epithelial sodium channels (ENaC)

74
Q

Significance of K secretion in colon

A

increased Na absorption –> increased K secretion

net K secretion when lumenal [Na] drops below 25 mM

severe diarrhea –> significant fluid loss –> hypokalemia

75
Q

How is B12 absorbed?

A

in complex with intrinsic factor in the distal ileum

76
Q

Result of impaired absorption of B12

A

pernicious anemia