GI Physiology I Flashcards

(70 cards)

1
Q

salivary glands

A

submandibular
sublingual
parotid
buccal glands

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2
Q

saliva

A

hypotonic, protein, ucus, amylase, lysozyme

taste, lubricate, protect, digest, speech

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3
Q

amylase

A

saliva - alpha-amylase
-carb digestion

cleaves alpha-1,4 glycosidic bonds in starch

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4
Q

lingual lipase

A

saliva - fat digestion

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5
Q

IgA

A

in saliva

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6
Q

bicarbonate

A

in saliva

minimize tooth decay and neutralize reflux gastric acid

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7
Q

taste

A

carbs and fats

not protein**

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8
Q

parotid

A

serous gland

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9
Q

submandibular and sublingual

A

mixed gland

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10
Q

ductal cells

A

water impermeable

  • water not absorbed along with solute
  • remains in lumen - results in hypotonic saliva
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11
Q

acinar cells

A

produce saliva

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12
Q

saliva composition

A

NaCl low

K and HCO3 high

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13
Q

high saliva flow

A

saliva resembles plasma

high NaCl
low K

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14
Q

low saliva flow

A

saliva dissimilar to plasma

low NaCl
high K

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15
Q

salivary secretion control

A

ANS - mainly PS

+ smell, taste, sound, sight, chewing, spicy and sour, smoking

  • sleep, fear, anti-cholinergic, anti-depresants, dehydration, fatigue
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16
Q

xerostomia

A

dry mouth - absent saliva

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17
Q

sjogrens syndrome

A

autoimmune against salivary and lacrimal glands

xerostomia and keratoconjunctivitis sicca (dry eyes)

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18
Q

drooling

A

excess saliva - increased nervous stimulation

tx - anticholinergics and remove glands

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19
Q

parkinsons

A

increased saliva production

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20
Q

cystic fibrosis

A

high Na, Ca, and protein in saliva, sweat

lack CFTR

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21
Q

addisons

A

increased Na in saliva

decreased reabsorption**

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22
Q

primary aldosteronism

A

cushings

  • decreased Na in saliva
  • more reabsorbed**

salivary NaCl zero
increased K levels

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23
Q

digoxin therapy

A

increase Ca and K in saliva

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24
Q

upper esophagus

A

skeletal m - voluntary

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25
lower esophagus
smooth m - involuntary
26
primary peristalsis of esophagus
local reflex with opening of UES
27
secondary peristalsis of esophagus
distension of esophagus
28
LES
tonically closed due to sphincter pressure by diaphragm relaxes with distension of esophagus and swallowing vagal stimulation
29
dysphagia
difficulty swallowing
30
achalasia
failure of LES to relax
31
diffuse esophageal spasms
uncoordinated esophageal contraction
32
hiatal hernia
moves LES into thoracic cavity - increased GE reflux
33
GERD
when LES doesn't work properly
34
barrets esophagus
long term GERD -columnar cells replace squamous mucosa adapt to acid exposure predispose to esophageal cancer
35
dysphagia
common in elderly | -structural, functional, disease - neuro dx, stroke, parkinsons, myasthenia gravis, xerostomia
36
achalasia
lack of peristalsis in esophagus LES does not relax food at level of LES chagas disease - trypanosoma cruzi
37
trypanosoma cruzi
chagas disease | -achalasia
38
birds beak on barium radio
achalasia
39
LES closed except
primary peristalsis - 2 sec after swallow - NO and VIP release secondary peristalsis - distension after esophagus
40
NO, VIP
LES relaxation
41
DES
diffuse esophageal spasm -contraction of esophagus uncoordinated prevent food reaching stomach dysphagia, regurg, chest pain unknown cause trigger - hot/cold food
42
hiatal hernia
protrusion of upper stomach into thorax through diaphragm -burning feeling in throat and chest like GERD
43
stomach secretion
2L/day isotonic fluid proximal - pepsinogen, HCl, IF, mucus, bicarb, water distal - gastrin, mucus, somatostatin
44
parietal cells
release HCl and IF
45
chief cells
release pepsinogen and renin
46
mucous neck cells
release mucus and bicarb
47
endocrine cell
ECL - enterochromaffin like - histamine G cells - gastrin D cells - somatostatin
48
oxyntic glands
fundus and body of stomach - parietal cells - chief cells - mucous cells
49
pyloric glands
antrum and pyloric region - G cells - gastrin - mucous cells
50
stomach mucosa
replaced every 3 days
51
mucus secretion
surface epithelial cells - thick viscous alkaline mucous neck cells - thin watery
52
parietal stimulation
ACh gastrin histamine
53
D cell stimulation
acid in stomach | -release of somatostatin
54
somatostatin
inhibit gastric acid release
55
G cell stimulation
ACh, peptides, AAs release gastrin
56
gastrin
stimulate gastric acid secretion
57
non-parietal cells
basal secretion between meals high in Na and Cl low in H and K
58
parietal cells
stimulated secretion after meal -stimulated by gastrin and histamine high in H and Cl low in Na and K
59
rate of gastric secretion
inverse relationship between lumen concentration of H and Na as function of gastric secretion low rate - high Na, low H high rate - high H, low Na
60
acid secretion
H from H2CO3 -HCO3 exchanged for secreted Cl requires lots of energy - H/K ATPase
61
parietal cell agonist
ACh, gastrin, histamine -more acid ACh - M3 receptors gastrin - CCK8 receptor - gastrin 1500x more potent than histamine -histamine - H2 receptor
62
parietal cell antagonist
somatostatin and PGs | -less acid
63
gastrin secreting tumor
zollinger-ellison | -too much acid secreted
64
atrophic gastric
pernicious anemia - destruction of IF secreting parietal cells - macrocytic anemia
65
NSAIDs
cause decreased mucous production - because decreased PGs
66
direct vs. indirect parietal cell activation
direct - ACh, gastrin, histamine act on parietal indirect - ACh and gastrin stimulate ECL - more histamine
67
synergistic stimulation and potentiation of acid secretion from parietal cells
direct stimulation
68
vagotmomy
cutting vagus nerve -inhibits gastric acid secretion to tx peptic ulcers selective - cut nerves supplying parietal cells only
69
phases of gastric acid secretion
cephalic - 30% total - reflex to medulla - sight, smell, taste gastric - 50-60% -food distends gastric mucosa intestinal - 10% - peptides in duodenum - 3 hormones that inhibit acid secretion - secretin, GIP, CCK
70
secretin, CIP, CCK
three hormones that inhibit gastric acid secretion