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Pathophys Exam I > GI Mod 1 > Flashcards

GI Mod 1 Flashcards

1
Q

accessory organs of digestive system

A

liver, gallbladder, exocrine

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2
Q

4 layers of the GI tract

A
  1. mucosea
  2. submucosa
  3. muscularis
  4. adventitious (serosa)
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3
Q

3 parts of the mucosa layer of the GI tract

A
  1. mucosa epithelium
  2. lamina propria
  3. muscularis mucosae
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4
Q

what is the submucosa made up of in the GI tract

A

glands and associated ducts

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5
Q

what is the muscularis layer of the GI tract made up of

A
  1. circular layer

2. longitudinal layer

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6
Q

what is the adventitious (Serosa) layer of GI tract made up of

A

connective tissue

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7
Q

the enteric nervous system is considered part of which nervous system

A

ANS

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8
Q

the enteric nervous system functions ________ and influenced extrinsically via what nervous systems

A
  • autonomously

- parasympathetic/sympathetic nervous systems

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9
Q

3 enteric plexuses

A
  1. submucosal plexus (Meissner plexus)
    - located in submucosa
  2. myenteric plexus (Auerbach plexus)
    - located bw circular and longitudinal layers of muscularis
  3. subserosal plexus
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10
Q

three general functional components of enteric plexuses

A
  1. sensory neurons monitor: distension and the chemical status of GI tract
  2. motor neurons control: motility of the gut wall, smooth muscle of GI vasculature, secretions of the mucosa/submucosa
  3. interneurons communication bw sensory and motor
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11
Q

definition of appetite

A

hunger

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12
Q

definition of satiety

A

sensation of fullness/satisfied

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13
Q

two centers that control appetite and satiety

A

lateral center and medial center

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14
Q

where are the two centers that control appetite and satiety located

A

hypothalamus

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15
Q

function of lateral center

A

(appetite center)
stimulate appetite
excitatory to hunger contractions in stomach

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16
Q

stimulus of lateral center

A
  • smell (CN 1), visual, taste (CN 7&9), hearing (CN8)
  • physiological depletion of nutrient/energy stores
  • memory/fantasy - limbic/insular lobes
  • gastric hormones
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17
Q

what gastric hormone stimulates appetite

A

ghrelin - hunger hormone - released from stomach

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18
Q

what is the function of the medial center

A

(satiety center)
suppress appetite
inhibitory to hunger contractions in stomach

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19
Q

stimuli of medial center

A

hormones:

  1. GI hormones - released during food ingestion (CCK,GLP) - short term
  2. Letpin - released by fat cells and chief cells
  3. PYY - released by SI after meal
  4. INsulin - released by pancreas after increase in blood glucose after meal
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20
Q

extrinsic regulation of the GI tract

A

sympathetic regulation and parasympathetic regulation

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21
Q

sympathetic regulation of the GI tract

  1. pathway
  2. function
A 
pathway - nerves of sympathetic tract in thoracic and upper lumbar regions
function - inhibitory to GI tract - decrease peristalsis and secretions, inhibit blood flow to GI tract
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22
Q

parasympathetic regulation of GI tract

A 
pathway - vagus nerve (esophagus to transverse colon) and pelvic nerves of sacral plexus 
function - excitatory to GI tract - increase peristalsis and secretions, relax involuntary sphincters of GI tract, facilitate blood flow to GI tract
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23
Q

peristalsis require what two movements? how does the vagus nerve play into it?

A

requires contraction and relaxation

-vagus nerve has dual role on the smooth muscle of GI

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24
Q

structures of the GI tract

A

mouth, esophagus, stomach, SI, LI, rectum, anus

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25
Q

intrinsic regulation of the GI tract by?

A

enteric nervous system

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26
Q

how does the GI function autonomously

A

intrinsic system can feedback on itself - “brain in the gut”

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27
Q

two plexuses that are responsible for in the intrinsic regulation

A
  1. myenteric plexus (Auerbach’s) - controls motility

2. submucosal plexus (Meissner’s) - controls secretions and absorption

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28
Q

7 specific functions of the enteric nervous system

A
  1. controls motility - peristalsis/sphincter control
  2. regulation of fluid exchange and local GI blood flow
  3. regulation of gastric and pancreatic secretion
  4. regulations of gastrointestinal endocrine cells
  5. defense reactions
  6. entero-enteric reflexes
  7. ENS and CNS interaction
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29
Q

how does the enteric nervous system regulat fluid exchange and local GI blood flow

A
  1. regulates permeability to ions thus influencing fluid
  2. influences vasodilation of BC
  3. influences fluid secretion
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30
Q

how does the enteric nervous system regulate GI endocrine cells

A

can signal release of GI hormones

ex. excessive serotonin released from GI walls = nausea/vomit

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31
Q

examples of defense reactions of the enteric nervous system

A

vomit, diarrhea, exaggerated propulsive motility reflexes

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32
Q

what are the entero-enteric reflexes of the enteric nervous system

A

signaling system bw regions of the GI tract

  1. ex. gastric activity stimulates SI motility and relaxation of ileocecal valve
  2. ex. small intestine activity signals release of enzymes from pancreas
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33
Q

how many neurotransmitters exist in intrinsic nervous system of GI

2 functions and examples of each

A

20+

  • ex’s: excite smooth muscle (contract): ACh and substance P
  • ex’s: inhibit smooth muscle: nitric oxide & VIP (vasoactive intestinal peptide)
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34
Q

general function of extrinsic GI regulation

A

directly influences intrinsic system (parasympathetic - excitatory to GI motility and secretions; sympathetic - inhibitory to GI motility and secretions)

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35
Q

general function of intrinsic nervous system of GI

A
  1. myenteric plexus - located in muscular layers = controls motility
  2. submucosal plexus - located within/beneath mucosal layers so controls secretions
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36
Q

function of mouth

A

salivation

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37
Q

3 salivary glands of the mouth

A

submandibular
sublingual
parotid

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38
Q

autonomic control of saliva

A

both parasympathetic and sympathetic systems stimulate salivary glands - secretion of saliva IS NOT controlled by hormones

39
Q

what does saliva contain? (3)

A
  1. water - with mucus, sodium, bicarb, chloride, and potassium (bicarbs maintain pH in mouth to neutralize bacteria = tooth decay)
  2. salivary amylase - digestion initiated in mouth, begins first steps of break down of carbs
  3. immunoglobulin A - prevents infection (animals lick their wounds)
40
Q

hormones in obseity

A

Leptin: increased (resistance) - effectiveness may be blunted
ghrelin: decreased - body trying to tell brain its not hungry

*role of each not fully understood in obesity - pharmaceutical target

41
Q

role of hormones in hunger

A

ghrelin - fast acting

  • levels rise just before meals
  • most circulating levels produced by stomach
  • other roles: memory & sleep
42
Q

roles of leptin in satiety

A
  1. long term role in energy balance and suppressing food intake
  2. released from fat cells
43
Q

role of PYY in satiety

A

fast acting, counteracting role to ghrelin post feeding

-released from SI

44
Q

3 portions of the esophagus

A
  1. upper third - striated (voluntary)
  2. middle third - mixed muscle
  3. lower third - smooth (involuntary) muscle
45
Q

location of UES

A

junction of lower pharynx and esophagus

approx at level of cricoid cartilage

46
Q

function of UES

A

prevent air from entering esophagus during ventilation

47
Q

location of LES

A

narrowing of the esophagus proximal to the junction of esophagus and stomach

48
Q

function of LES

A

barrier to reflux of the acidic content of the stomach

49
Q

LES is maintained by what

A

increased smooth muscle tone

50
Q

what is resting tone of LES

A
  1. LES smooth muscle tone increased to 20 mmHg

- belching: air pressure in stomach exceeds LES pressure

51
Q

how does swallowing tie in with LES

A

LES smooth muscle to tone is relaxed

peristaltic wave relaxes smooth muscle of LES

52
Q

where are the control centers for swallowing

A

located in brainstem (reticular formation)

-complex function requiring coordination bw digestive tract and respiratory system

53
Q

phases of swallowing

A
  1. voluntary (oropharyngeal) phase chewing and pushed past uvula; soft palatte contracts to close nasopharynx
  2. pharyngeal phase - epiglottis closes off larynx/trachea 1-2 seconds
  3. esophageal phase - bolus enters esophagus and ends as bolus enteres stomach - 5-10sec
54
Q

how is the bolus of food moved

A

peristalsis

55
Q

role of insulin in satiety

A

fast acting, post feeding

released from pancreas

56
Q

how is peristalis coordinated

A

contraction/relaxation of longitudinal/crcular muscles

57
Q

what is the esophageal muscular pressure range

A

35 to 80 mmHg

58
Q

differences in esophageal pressures by the three portions

A
  1. upper portion & lower - tend to be higher (60-80)

2. middle portion - lower pressure (30-45 mmHg)

59
Q

what happens if esophageal pressure is

A

may leave food residue within esophagus

60
Q

what is the effect of tension on esophageal movement?

what happens with intense contractions?

A

(distention of esophagus)
increases force of contractions
–intense contractions = substernal pain similar to angina/heartburn

61
Q

control of peristalsis

A

requires complex coordinated signaling

  • -parallel vagal inhibitory and excitatory pathways to coordinated
  • -vagus nerve has both excitatory and inhibitory pathways to coordinate contraction/relaxation of esophageal peristalsis
62
Q

what is primary peristalsis

A

normal peristaltic wave as bolus descends in esophagus
coordinated muscular activity of all phases of swallowing
-oral phase, pharyngeal peristalsis, UES relaxation, esophageal peristalsis, and LES relaxation

63
Q

what is secondary peristalsis

A

food residue from ineffective primary peristalsis or a bolus that is stuck will cause addition or second peristaltic wave
-esophageal peristaltic wave only - DOES NOT incldue swallowing reflex

64
Q

what does bolus/food residue distenetion cause

A

intrinsic feedback to:

  1. constrict esophagus above the distention
  2. relax esophagus below distention
  3. which pushes residue/bolus along
65
Q

what happens when swallowing food

A
  1. a single swallow will initiate esophageal peristaltic contraction that lasts about 5-10 seconds short refractory period also follows peristaltic contraction (inhibits ability to swallow a second bite of food)
  2. in general: attempting to swallow food more frequently than 10-15 seconds is difficult because of inhibitory mechanisms
66
Q

what happens when swallowing liquid

A
  1. normal drinking - swallow every 1-2 seconds
  2. the quick subsequent swallows create and inhibitory reflex that prevents the esophagus from ongoing contraction
    - -this inhibitory reflex cause esophagus to stay relaxed to allow more liquid to descend
  3. this will continue until the last swallow in a series of swallows - after which a full peristaltic contraction will occur
67
Q

basal tone of LES is a net result of 3 factors

A
  1. myogenic tone that is independent of any neural input
  2. excitatory vagal tone (cholinergic)
  3. inhibitory vagal tone (nitrergic - NO)
68
Q

what is deglutitive inhibition

A

inhibitory reflex triggered by quick subsequent swallows that prevent the esophagus from ongoing contraction

69
Q

normal tone of UES

A

50 mmHg

70
Q

factors that increase LES pressure

A
  1. vagus nerve influence - excitatory pathways of vagus nerve, cholinergic post gagnlionic neurons release ACh
  2. gastrin - in stomach promtoes acid secretion/motility so need to keepy LES closed
71
Q

factors that decrease LES pressure

A
  1. vagus nerve influence
  2. hormones
  3. common foods/substances suggested to relax LES
72
Q

how does vagus nerve decrease LES pressure

A

non cholinergic post gagnlionic neurons (stimulate NO and VIP release)

73
Q

how do hormones decrease LES pressure

A

progesterone, secretin, glucagon

-progesterone levels elevated during pregnancy and second half of menstrual cycle - transient reflux may occur

74
Q

what common foods decrease LES pressure

A

(relax LES)

-fried fatty foods, tomatoes, citrus, high protein diet, chocolate, peppermint, tobacco, alcohol, caffeine

75
Q

what is GERD

A

gastroesophageal reflux dz

  • decreased LES pressure and ineffective clearance mechanism of secondary peristaltic waves
  • chronic acid reflux results in inflammation/pain and eventrual destruction of esophageal wall (esophagitis)
76
Q

meds for GERD

A
  1. antacids - neutralize stomach acids
  2. histamine receptor blockers - decrease acid secretion histamine receptors
  3. proton pump inhibitors - stop acid secretion
  4. parasympathetic drugs - increase LES tone
77
Q

what is Achalasia

A

(opposite of GERD)

  • failure to relax = peristalsis of esophageal musculature + failure of LES to relax
  • rare, causes pain with eating and drinking
  • looks like cardiospasm, so rule out cardiac issues first
  • unknown etiology thought to be defect of intrinsic esophagus plexus (loss of inhibitory neurons in esophageal layers)
78
Q

treatment for achalasia

A 
pneumatic dilation (stretch LES to relax)
meds
79
Q

what is esophageal varices

A

severely dilated sub mucosal veins in the esophagus
most often a consequence of portal HTN (common with cirrhosis)
pts have tendency to develop bleeding (chronic GI bleed can progress to severe systemic consequences)

80
Q

what is barretts’s esophagus

A

where normal mature cells lining esophagus are replaced with abnormal cells due to exposure to stomach acids
-normal esophageal squamous epithelium is replaced by a spectrum of metaplastic columnar mucosa

81
Q

what is metaplasia

A

one mature adult cell type is replaced by another type of mature cells

82
Q

symptoms of barrett’s esophagus

A

metaplasia itself does not cause physical heartburn sytmpoms but is histological reflection of the chronic exposure to acid
–the stomach acid is the physical stimulus for heartburm symptoms

83
Q

do all pts with GERD develop Barrett’s?

A

NO

84
Q

what kind of cancer can develop with Barrett’s esophagus

A

adenocarcinoma

85
Q

will all pts with Barrett’s esophagus develop cancer?

A

no

86
Q

risk of cancer with Barrett’s esophagus

A

1:300

87
Q

amunt of what in Barrett’s esophagus will increase risk of cancer

A

dysplasia

88
Q

what is dysplasia

A
  1. abnormal development/matruation of cells
  2. delay/abnormal differentiation of cells results in number of immature cells
  3. often an indication of early neoplastic process
89
Q

how does esophageal cancer rank among other cancers

A

8th most common

90
Q

what % of esophageal cancers are adenocarcinmoa

A

50%

91
Q

what population does adenocarcinoma affect

A

caucasian male

92
Q

what % of population is afflicted with GERD

A

20% - in US and western Europe

93
Q

what % of pts with Barrett’s esophagus deevlop adenocarcinoma each year

A

0.5-1%

94
Q

pts with Barrett’s esophagus whould be monitored how often and with what procedure?

A

yearly with endoscopy and biopsy of the esophagus

Pathophys Exam I (9 decks)

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