esophageal physiology and swallowing disorder Flashcards

0
Q

odynophagia

A

painful swallowing

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1
Q

dysphagia

A

difficulty swallowing

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2
Q

globus

A

sensation of fullness in upper throat (feels better with swallowing) –marble

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3
Q

pyrosis

A

heart burn, substernal lcoation-ascneding up chest

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4
Q

regurgitation

A

return of sour gastric contents

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5
Q

water brash

A

spontaneous salivation from reflux

triggered frm vagus

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6
Q

rumination

A

chewing one’s cud

can get dental erosion

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7
Q

primitive gut forms during

A

week 4 gestation

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8
Q

trachoesophageal septum splits primitive gut into

A

ventral trachea and dorsal esophagus

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9
Q

developmental abnormalities of esophagus include

A
short esophagus
esophageal stenosis (usually in distal third due to incomplete recanalization during 8th week dev)
esophageal atresia (typically occurs with a tracheoesophageal fistula)
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10
Q

upper 5% of esoph

A

skeletal/striated

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11
Q

middle 35%

A

mixed skeletal and striated with circular muscles and long muscles

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12
Q

lower 60%

A

smooth muscle w/ circular msucles and long. muscles

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13
Q

c6

A

beginning at upper eso spinchter

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14
Q

t3

A

aortic arch presses on eso

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15
Q

t10

A

passes through diaphragmatic hiatus to reach stomach

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16
Q

job of inner circular layer of muscles

A

prox connected to cricopharyngeous

forms upper eso spinchter (UES) and (LES)

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17
Q

UES formed by

A

cricopharyngeus muscles

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18
Q

at rest, UES is

A

closed to avoid swallowing air

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19
Q

N supply UES

A

pharyngeal branch of vagus

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20
Q

LES at rest

A

closed to prevent reflux

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21
Q

what keeps LES closed

A

normal muscle tone + fibers of right diaphragmatic crus and phrenoesophageal ligament

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22
Q

nerve supply to LES

A

parasymp, symp, enteric fibers

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23
Q

neurotransmitters at LES

A

inhib: NO>VIP
excite: Ach>substance P

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24
Q

microscopic anatomy (4 layers) of esophagus

A

mucosa
submucousa
muscularis propia (inner and outer layers)
*no serosal layers

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25
Q

arteries of esophagus

A

upper-inferior thyroid artery
middle- R & L bronchial arterioles
mid-distal/distal- branch from thoracic aorta and esophagial branch of L gastric artery

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26
Q

veins of esophagus

A

upper: submucosal plexus–>inferior thyroid vein
middle: azygous and hemizygous
mid-distal.distal- gastric vein

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27
Q

intrinsic motor system nerves

A

ens–>myenteric plexus between muscle layers

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28
Q

extrinsic motor/secretory

A

post gang fibers (symp)-inhibit motility

vagus (parasymp)- stim motility/secretory

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29
Q

sensory nerves

A

vagus–>nucleus tractus solitaris–>CNS

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30
Q

sensory issues present as

A

chest pain
heart burn
dusphagia

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31
Q

sensory chemo R

A

located in mucosa and submucosa–>sense chemical irritants

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32
Q

sensory mechano-nociceptors

A

submucosa–>adventitia–>respond to lumen distention NOT teraing (why endoscopy doesnt hurt)

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33
Q

normal swallowing relies upon

A

intact neuromuscular fx of the tongue, pharynx, and esophagus

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34
Q

swallowing is controlled by this brainr egion

A

medulla

35
Q

sensory input from pharynx via

A

CN 5, 10, 11

36
Q

motor output via CN

A

5,7,9,10,12

37
Q

3 regions of stomach

A

LES and cardia
fundus/body
antrum/pyloris

38
Q

LES and cardia

A

mucous, hco3-

prevents reflux, entry of food, regluates burps

39
Q

fundus and body

A

H+, intrinsic factor, mucous, hco3-

reservoir, tonic force during emptying

40
Q

antrum and pyloris

A

mucous, hco3-

mixing, grinding, seviing, regulate emptying

41
Q

surface and neck cells

A

mucous, hco3-, peptides

lubricate, protect/repair

42
Q

parietal cells

A

H+, intrinsic factor

protein degradation, binding B12, protection from bacteria

43
Q

chief cells

A

pepsinogen, gastric lipase

p: protein digestion
gl: triglyc digestion

44
Q

endocrine cells

A

gastric (gcell), histamine (ECL cell), somatostatin (d cell)

regulate acid secretion

45
Q

parietal cells have lots of mito

A

becuse runnign their h pumps takes lots of energy

46
Q

resting state has

A

short microvilli with a cystoplasmic tubulovesicular system

47
Q

secretory state has

A

long microvilli and canalicular system

48
Q

resting state mech

A

gastric acid pump (HK ATPase) in tubulovesicle and inactive
cannicully collapsed
low flow of acid

49
Q

secretroy state

A

stimulation by Ach, gastrin, histamine–>g pump incorporated into canaliculus–>expands canaliculus and activates it–>excahnges H for K–>releases HCL

50
Q

2 component model

A

inr esting state, juice is mostly NaCl, with little H and K so PH >4 and non-parietal predominates

while n secretory state, mostly Hcl, little Na and K so PH<4, parietal predominates

51
Q

why is it important HCO3- is recycled

A

alkaline tide– Hco3 drains into capillaries of parietals cells then drains to venous surrounding surface cells to help make surface mucosa

104
Q

what protects the gastric mucosa?

A

mycous and bicarb

105
Q

mucous neck cells secrete and are stim by

A

stim by vagus (ach)

secrete soluble mucous

106
Q

surface neck cells are stim by and secrete

A

stim by alcohol/chemicals nad physical friction of food–> release insoluble mucous

107
Q

agents known to disrupt the barrier and cause ulceration

A

weak acids
alcohol
nsaids
detergents (bile salts)

108
Q

three responses to a meal

A

endocrine/paracrine/neurocrine

109
Q

cephalic phase

A

thinking about food via vagally mediated pathway

110
Q

gastric phase

A

foo enters and buffers gastric juice

111
Q

when ph gets to six

A

more gastrin secreted

112
Q

fundal distention does

A

2 things- vagal arch and mechanoreceptor stim (to increase parietal cell H+ secretioin)

113
Q

what shuts everything off

A

somatostatin

114
Q

intestinal phase

A

mediated by chyme entering duodenum 1st hour post meal

115
Q

what does chyme do

A

slows gastric emptying

decreases acid secretion actively by producing inhibitors and passively by decreasing distention

116
Q

stimulatory factors

A

amino acids ins mall intestine stim relase of gastrin

117
Q

inhibitory factors

A

chyme in upper intesting inhibit gastric acid scertion– maybe via secretin and GIP

118
Q

swallowing sensory input to pharynx via

A

CN 5, 10, 11

119
Q

motor output of swallowing via

A

CN 5,7,9,10,12

120
Q

globus

A

feeling of lump or tickle int hroat that’s constant in nature, does not interfere with swallowing

121
Q

main cause globus

A

UES problem-spasm, incomplete relaxation, or hypertensive UES

122
Q

other ddx globus

A

GERD

visceral hypersenstivity

123
Q

odynophagia

A

pain swallowing cause by injurt to mucoa=sal lining by viral infection, medications, gerd

124
Q

tx odynophagia in known hiv

A

2 PPI+ antifungal agent until sx reslve

125
Q

tx odoynophagia in non HIV or refractory HIV

A

upper endo to figure out whats going on

126
Q

oropharyngeal dysphagia

A

transfer dysphagia; difficulty initiating a swallow or transferring food from mouth to esophagus; food “sticks int hroat”

127
Q

three types of abnormalities by oropharyngeal dysphagia

A

neuro
structural
muscoloskeleton

128
Q

dx of oropharyngeal dysphagia

A

Hx Pe

cineradio is the best

129
Q

tx OD

A

speech path, tx underlying disorder, avoid thin fluids, maybe entubation

130
Q

esophageal dysphagia

A

food sticks in chest

–intralumninal obstruction

131
Q

functional esophageal dysphagia

A

spasm; motor failure

132
Q

anatomical esophageal dysphagia

A

extrinsic compression by vessesls or mass

structural lesions- diverticula, esoph rings, webs, esophagitis, strictures, tumors

133
Q

red flag symptoms

A
weight loss
anemia
chronic GERD
melena
hemataemesis
134
Q

studies to asscess esophgeal fxq

A

barium swallow FIRSt
cineesophragram
upper endoscopy (EGD)- if positive red flag or barium swallow is abnormal
esophageal manometry- to assess LES fux and eso body peristalsis
ph studies
impedence

135
Q

hypercontractle manometric states

A

achlasia- failure relax LES

spastic disorders- diffuse esophageal spasm

136
Q

hypocontractile states manometric fingeings

A
ineffective motility (achalsia, scleroderma/crest)
hypotensive LES, transient LES relaxations