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MS1 Unit 7 > Physio > Flashcards

Physio Flashcards

1
Q

major functions of GI tract

A

motility, secretion, digestion, absorption, excretion

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2
Q

upper esophageal sphincter

A

maintains highest resting pressure of all sphincters, and forward passage of material

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3
Q

lower esophageal sphincter

A

separates esophagus and stomach. consists of smooth muscle that relaxes during swallowing. coordinates passage of food into stomach and prevents reflux

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4
Q

pyloric sphincter

A

separates the stomach from duodenum. resting pressure contributes to regulation of gastric emptying and prevention of duodenal gastric reflux

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5
Q

ileocecal sphincter

A

separates ileum and cecum, prevents backflow of colonic contents into the ileum

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6
Q

internal and external anal sphincters

A

internal (smooth muscle) and external (skeletal muscle) control elimination of waste products

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7
Q

enteric nervous system

A

branch of the ANS with plexuses (myenteric and submucosal)

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8
Q

myenteric plexus

A

between the longitudinal and circular muscle layers of the GI tract, goes from end of esophagus to rectum. stim increases tonic contraction of the gut, intensity of rhythmic contractions, and velocity of conduction of excitatory waves which enhances peristalsis

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9
Q

submucosal plexus

A

between the circular muscle and submucosa in the small and large intestines. controls local intestinal secretions, absorption, and contraction of the muscle

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10
Q

types of receptors in the ENS

A

mechano, chemo, osmo, along with parasympathetic fibers

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11
Q

segmental/mixing contractions

A

chyme distends the walls which causes local contractions mixing chyme with secretions. 2/3 per minute

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12
Q

peristaltic contractions (myenteric reflex)

A

move material form mouth to colon, relatively weak contractions. 3-5 hours needed to go from pylorus to ileocecal valve

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13
Q

gastroileal reflex

A

triggers opening of the ileocecal valve to allow chyme through

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14
Q

enterogastric reflex

A

decreases gastric motility and secretions and contracts pyloric sphincter

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15
Q

pathological ileus

A

state where normal periods of quiescence are much longer. inhibitory neurons are abnormally active

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16
Q

migrating motor complex

A

contractions that pass down the stomach and small intestine

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17
Q

motilin

A

made in duodenal mo cells, released into circulation and stimulates contractions during active phase

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18
Q

deglutition

A

swallowing. voluntary and involuntary events.

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19
Q

pharyngeal phase

A

areas near the pharyngeal opening transmit impulses through CN v and IX which initiates swallowing

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20
Q

GERD

A

gastroesophageal reflux disease. failure of the ability to maintain the lower esophageal sphincter

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21
Q

achalasia

A

when lower esophageal sphincter fails to relax during swallowing

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22
Q

sections of the stomach

A

proximal gastric reservoir, distal antral pump

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23
Q

paracrines

A

released by endocrine cells of GI tract. act locally in same tissue that secretes them

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24
Q

neurocrines

A

made in neurons in GI tract and released following an action potential. diffuse across cleft and act on target cell

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25
Q

saliva functions

A

secreted by acinar cells, lubricates, protects, and has amylase in it

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26
Q

sjogren syndrome

A

autoimmune disease that distroys salivary and lacrimal glands.

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27
Q

xerostomia

A

dry mouth

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28
Q

kallikrein

A

activation of salivary glands releases this, resulting in production of bradykinin a vasodilator

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29
Q

oxyntic glands

A

inside surfaces of the body and fundus of the stomach. secrete mucus (mucous neck cells), pepsinogen/lipase (peptic cells), and HCl/intrinsic factor (parietal cells)

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30
Q

achlorhydria

A

lack of stomach acid secretion due to destruction of parietal cells

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31
Q

pyloric glands

A

secrete mucus for protection of pyloric mucosa from stomach acid. also secrete gastrin and somatostatin

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32
Q

pepsinogen to pepsin activation

A

at ph from 3-5, pepsinogen activates spontaneously to pepsin

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33
Q

alkaline mucous layer

A

protects gastric mucosa. erosive gastritis can result from NSAID use because it inhibits prostaglandin synthesis in stomach

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34
Q

stimulators of acid secretion

A

histamine, vagus, gastrin, insulin, caffeine, stress

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35
Q

inhibitors of acid secretion

A

somatostatin, glucose insulinotropic peptide, gastric inhibitory peptide, secretin

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36
Q

H2 receptor antagonists

A

effective as antacid agents because they block binding of ACh, gastrin, and histamine

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37
Q

cephalic phase

A

smelling, tasting, and conditioned reflexes stimulate HCl secretion through direct stim of vagus

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38
Q

gastric phase

A

Secretes HCl due to distension of stomach and presence of breakdown products of protein

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39
Q

intestinal phase

A

mediated by products of protein degradation, secretes HCl

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40
Q

pancreas

A

exocrine secretions into ducts then to the lumen (aqueous juice high in HCO3 from duct/centro-acinar cells and enzyme juice from acinar cells)

endocrine secretions into blood from islet of langerhans regulate blood sugar

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41
Q

pancreatic aqueous secretions

A

bicarb neutralizes stomach acid and allows enzymes to work at optimal neutral pH. pepsin inactivated at neutral. prevents dmg to duodenal and intestinal mucosa. dilutes enzyme juice (prevents it from becoming sticky)

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42
Q

pancreatitis

A

enzymes are released into the cell instead of being packaged into granules

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43
Q

secretion of chloride by acinar cells

A

NaCl secretion leads to influx of water and sodium into cell. ACh and CCK stim NaCl secretion

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44
Q

cystic fibrosis

A

defective CFTR channel, causing thick and viscous pancreatic secretions. messes with digestion. Pulmonary mucous is thick causing dyspnea and death

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45
Q

phases of pancreatic secretion

A

cephalic: more acini activation than ductal aqueous secretion.
gastric: distenstion of stomach induces vaso vagal reflex, gastrin stims acinar cells to make enzymes and parietal cells to make HCl

intestinal phase: secretin and CCK are made

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46
Q

secretin

A

released into blood from duodenal mucosa in response to acid in duodenum. causes duct cells to make aqueous secretion. “nature’s antacid” lots of bicarb

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47
Q

Cholecystokinin (CCK)

A

hormone released in response to protein digestion products or fatty acids. stims enzyme secretion by acinar cells. low volume, high enzyme content. causes gall bladder contraction to release bile. slows gastric emptying

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48
Q

rate limiting step in bile acid formation

A

addition of hydroxyl group by cholesterol 7 alpha hydroxylase. inactivated by bile acid, activated by cholesterol

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49
Q

choleretic

A

agent that stims the liver to increase output of bile

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50
Q

bile salts

A

amphipathic. can emulsify and solubilize fats and steroids. water soluble. conjugated with glycine or taurine in liver. bacteria deconjugate bile salts back to bile acids

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51
Q

formation of gallstones

A

supersaturation of cholesterol, nucleation and precipitation, then growth of microstones to form macrostones

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52
Q

cholecystitis

A

inflammation of gall bladder usually caused by blockage of the cystic duct by a gallstone.

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53
Q

insulin

A

made by beta cells which are located at the center of the islets of langerhans in the pancreas. it is an anabolic hormone secreted in times of excess nutrient availability. calls for storage of energy

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54
Q

glucagon

A

catabolic hormone, secreted during food deprivation. allows utilization of stored nutrient reserves by mobilizing glycogen, fat, and protein

55
Q

somatostatin

A

paracrine hormone that inhibits release of insulin and glucagon as well as gastrin, gastric acid secretion, and all gut hormones

56
Q

islet of langerhans

A

in pancreas. beta cells in center secrete insulin, proinsulin, and c-peptide. alpha cells at periphery secrete glucagon. delta cells in periphery secrete somatostatin. blood flow is from center to periphery.

57
Q

pancreatic polypeptide

A

made by F cells in periphery of islet of langerhans. inhibits gall bladder contraction and inhibits pancreatic exocrine secretion during strenuous exercise, after ingestion of a protein rich meal, or during hypoglycemia

58
Q

glucagon synth and degradation

A

made as 160 AA pre-proglucagon. processing yields glucagon, glicentin, glicentin like peptide, glucagon like peptides 1 and 2. glucagon is degraded in liver and kidney, very little excreted.

59
Q

stimulators of glucagon secretion

A

hypoglycemia, increase in arginine and alanine (indicative of protein degradation), exercise, stress

60
Q

inhibitors of glucagon secretion

A

somatostatin, insulin, hyperglycemia

61
Q

effect of glucagon on liver

A

antagonizes action of insulin by stimulating glucose output via gluconeogenesis and glycogenolysis and increased lipolysis. activates protein kinase A, which phosphorylates enzymes.

62
Q

insulin synth and degradation

A

synthed in preproinsulin form. packaged in golgi and processed. secreted in granules with zinc which form 6 insulin molecules into hexamers. cleaved to insulin and c-peptide. c-peptide gets secreted in urine and is used to detect insulin levels

63
Q

insulin secretion by beta cells

A

glucose picked up by b cells, used to make ATP. elevated ATP inhibits potassium channel and depolarizes cell. voltage gated Ca channels open, and Ca comes in. this causes release of insulin granules. AA levels increased also lead to elevated ATP.

64
Q

glucagon stimulation of insulin secretion

A

glucagon binds G alpha B receptor and activates protein kinase A, which raises Ca concentration and inreases exocytosis. somatostatin binds G alpha I and inhibits protein kinase A

65
Q

incretins

A

CCK and GIP, glucagon-like peptide 1

provide advance notice of feeding and stimulate insulin secretion: oral glucose yields more insulin than IV glucose

66
Q

catecholamines and insulin during exercise

A

insulin secretion up due to epinephrine. local innervation through norepinephrine acts through alpha receptor and predominates. net result is to suppress insulin secretion and prevent excess glucose uptake. allows liver to supply glucose and fatty acids to muscle

67
Q

action of insulin on liver

A

stimulates glucose uptake and decreases glucose output. stims formation of glycogen and inhibits glycogenolysis. promotes glycolysis and lipogenesis.

68
Q

action of insulin on muscle

A

stims glucose uptake by increasing GLUT-4 and promotes glycogenesis while inhibiting glycogenolysis. supplies acetyl CoA for fatty acid synth

69
Q

action of insulin on adipocyte

A

stims glucose uptake via GLUT-4 and increases glycolysis, leading to upped alpha glycerophosphate which leads to increased esterification of fats. decreases lipolysis. makes fattty acids but inhibits them to be used as an energy source

70
Q

glucose tolerance test

A

can diagnose diabetes. diabetes if plasma glucose is higher than 200 mg/dL at the second hour

71
Q

type 1 diabetes

A

insulin deficiency

72
Q

insulinemia

A

high insulin in blood

73
Q

glucagon deficiency

A

rare

74
Q

glucagonoma

A

high levels of glucagon in blood, causes hyperglycemia

75
Q

orixigenic factors

A

neurotransmitters that stim feeding (neuropeptide Y)

76
Q

anorexigenic factors

A

inhibit feeding. corticotropin releasing hormone, GLP-1, alpha MSH, CART

77
Q

CCK

A

(I cells) diffuses locally in a paracrine fashion. sends message that ingested fat/protein is being processed and will soon be absorbed

78
Q

ghrelin

A

secreted from oxyntic glands of stomach. stimulates food intake.

79
Q

leptin

A

derived from white adipocytes. influences energy homeostasis. stimulate receptors to reduce food intake, inhibit AgRP and NPY (which stim food intake)

leptin and leptin receptor mutations cause obesity

80
Q

MC4R receptor mutation

A

cause obesity. receptor for alpha melanocyte stimulating factor from POMC neurons

81
Q

folds of kerckring

A

finger like projections that stick into the lumen

82
Q

celiac disease

A

decrease in absorptive surface area due to a reduction in the number and size of microvilli

83
Q

enterocytes

A

absorptive cells that make up villi. they are columnar epithelial cells in a single layer

84
Q

goblet cells

A

secrete mucous in response to Ach released from parasymp cholinergic nerve fibers.

85
Q

crypt

A

undifferentiated cells of the crypt secrete NaCl into lumen and water follows osmotically. crypt cells move up the villi and eventually become absorptive cells

86
Q

transcellular pathway

A

transfer of materials across the brush border, through the cytoplasm, and then across the basolateral membrane

87
Q

shunt pathway

A

aka paracellular pathway. through tight junctions and the extracellular space

88
Q

brush border

A

aka apical membrane. has glycoprotein matrix and is major membrane for absorption of nutrients. contains etoenzymes that complete digestive process

89
Q

basement membrane

A

aka lamina propria, contains capillaries and lacteals

90
Q

water absorption

A

drudoenum and upper jejunum, completely absorbed by end of jejunum

91
Q

what does ileum absorb?

A

fluid and electrolytes, along with B12 and ionized bile salts. if jejunum is removed, ileum can adapt and take over its role

92
Q

what does duodenum absorb?

A

calcium and iron

93
Q

what does jejunum absorb?

A

jejunal enterocytes absorb Na+ and HCO3-, along with glucose and amino acids.

94
Q

how does Na+ enter jejunal enterocyte?

A

Na/glucose and Na/amino acid cotransport.

Na/H antiport, keeps internal pH of enterocyte near neutral

95
Q

NaCl absorption by ileal absorptive cell

A

enter via Na/H antiport in parallel with Cl/HCO3 exchange. Cyclic AMP inhibits NaCl absorption by ileum.

96
Q

vipoma tumors

A

secrete a lot of VIP, resulting in greatly decreased NaCl absorption leading to increased osmolarity in lumen and diarrhea

97
Q

cholera

A

toxin increases cAMP, inhibits NaCl absorption, increases NaCl secretion by jejunal crypt cells.

98
Q

absorption of iron

A

heme iron. iron is absorbed as heme, then the iron is freed within the cell.

non-heme iron. Fe++ forms insoluble complexes with food, but is released by gastric acid. Some Fe++ goes to Fe+++ and is secreted. Fe++ absorbed via cotransport with a proton

99
Q

calcium absorption in duodenum

A

passive paracellular absorption occurs throughout small intestine. Active transcellular absorption occurs only in duodenum. Ca enters thru channel, and is taken in by organelles. the enterocyte extrudes Ca across basolateral membrane thru Ca pump and Na/Ca exchanger. Vitamin D stimulates all three steps of absorption.

100
Q

long term regulation of calcium

A

increased absorption of Ca inreases plasma concentration of Ca, which decreases parathyroid hormone secretion which inhibits formation of active vitamin D, which decreases synth of calbindin, which decreases absorption of Ca

101
Q

enterokinase

A

trigger for intestinal protein digestion. converts trypsinogen to trypsin. trypsin then activates endo and exopeptidases yielding chymotrypsin, elastase, and carboxypeptidase A and B

102
Q

exopeptidases

A

carboxypeptidase A and B

103
Q

endopeptidases

A

trypsin and chymotrypsin

104
Q

absorption of amino acids

A

most AAs are mediated by Na coupled AA transporters. transport against concentration gradient. Na out, AA in.

105
Q

absorption of oligopeptides

A

done by PepT1, an H+/oligopeptide cotransporter. moves oligos across apical membrane

106
Q

hartnup disease

A

system B apical membrane AA transporter. this reduces absorption of neutral AAs. a lot of tryptophan is excreted in the urine

107
Q

cystinuria

A

system B 0 AA transporter is defective. absorption of cystine and basic AA is reduced. cystine makes kidney stones

108
Q

ptyalin

A

salivary amylase, begins conversion of starch to sugars. inactivated in the stomach, works best at pH 6.7

109
Q

digestion and absorption of sugars

A

glucose and galactose compete for the same Na-coupled carrier.

110
Q

glucose-galactose malabsorption

A

rare genetic disease in which Glc/Gal carriers (SGLT1) are missing/bad. accumulation of Glc in intestine causes diarrhea, dehydration, and death. restricted to fructose diet since that can be absorbed

111
Q

cholecystokinin

A

CCK. released in duodenum due to presence of fats. slows gastric motility, stimulates pancrease to make enzymes, stims intestinal fluid secretion and gall bladder contration, relaxes sphincter of oddi

112
Q

micelles

A

include long chain fatty acids, cholesterol, monoglycerides, phospholipids, bile salts, fat soluble vitamins

113
Q

NPC1L1

A

niemann-pick C1 like 1. used to absorb cholesterol.

114
Q

ApoB48

A

key component of chylomicrons. chylomicrons also depend on microsomal triglyceride transfer protein, MTP. Transports newly formed apoproteins to the chylomicrons

115
Q

abetalipoproteinemia

A

visible fat laden enteroctes duee to MTP mutation. decreased plasma triglyceride and cholesterol levels, and deficiencies in fat soluble vitamins

116
Q

micturition

A

the process by which the urinary bladder empties when full

117
Q

detrusor

A

smooth muscle of the bladder. contraction helps with emptying the bladder

118
Q

pontine micturition center

A

controls the detrusor muscle and the urinary sphincters

119
Q

suprapontine center

A

exert tonic inhibition over the pontine micturition center providing voluntary control

120
Q

autonomous neurogenic bladder

A

sacral spinal centers damaged. lower motor neuron

121
Q

benign prostatic hyperplasia/hypertrophy

A

enlargement of prostate gland, squeezes the urethra. lead to more frequent urination, dribbling/leakage, weak stream, urgency

122
Q

constipation

A

results from poor motility which leads to greater absorption of liquids and hard feces

123
Q

diarrhea

A

rapid movement of fecal matter through the large intestine causing little absorption

124
Q

osmotic diarrhea

A

results from non-absorbable solutes in the lumen (lactase deficiency/lactose not broken down)

125
Q

secretory diarrhea

A

results from excessive secretion of fluids by crypt cells due to bacterial overgrowth

126
Q

ileocecal valve

A

separates the small and large intestine. prevents backflow of fecal matter from colon to small intestine

127
Q

gastroilieal reflex

A

activated when food enters the empty stomach. intensifies peristalsis of the small intestine and relaxes the ileocecal sphincter allowing passage from ileum to colon

128
Q

what does colon absorb?

A

absorbs Na, Cl, and H20 and secretes K and HCO3

129
Q

mode of active Na absorption by large intestine

A

Na-H and Cl-HCO3 exchange is coupled by a change in intracellular pH that results in electroneutral NaCl absorption. creates an osmotic gradient across intestinal mucosa, promoting absorption of water. Na channels are also used in the entire colon allowing H20 and Cl to follow passively through intracellular tight junctions

130
Q

haustrations

A

specialized for slow segmental propulsion and mixing, allowing time for electrolyte and fluid absorption, solidifying the chyme

131
Q

taenia coli

A

3 flat bands of longitudinal muscle

132
Q

gastrocolic reflex

A

increased incidence of mass movements, which force the chyme/feces towards the rectum

133
Q

hirschsprung’s disease

A

present at birth. lack of ENS in the distal part of the GI tract. obstructive syndrome in infants or constipation

134
Q

defecation reflex

A

triggered by distension of rectum. sensed by mechanoreceptors which activate myenteric nerves. fortified by parasymp defecation reflex

MS1 Unit 7 (3 decks)

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