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Flashcards in GI Mod 1 Deck (94):
1

accessory organs of digestive system

liver, gallbladder, exocrine

2

4 layers of the GI tract

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

3

3 parts of the mucosa layer of the GI tract

1. mucosa epithelium
2. lamina propria
3. muscularis mucosae

4

what is the submucosa made up of in the GI tract

glands and associated ducts

5

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

1. circular layer
2. longitudinal layer

6

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

connective tissue

7

the enteric nervous system is considered part of which nervous system

ANS

8

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

-autonomously
-parasympathetic/sympathetic nervous systems

9

3 enteric plexuses

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

10

three general functional components of enteric plexuses

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

11

definition of appetite

hunger

12

definition of satiety

sensation of fullness/satisfied

13

two centers that control appetite and satiety

lateral center and medial center

14

where are the two centers that control appetite and satiety located

hypothalamus

15

function of lateral center

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

16

stimulus of lateral center

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

17

what gastric hormone stimulates appetite

ghrelin - hunger hormone - released from stomach

18

what is the function of the medial center

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

19

stimuli of medial center

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

20

extrinsic regulation of the GI tract

sympathetic regulation and parasympathetic regulation

21

sympathetic regulation of the GI tract
1. pathway
2. function

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

22

parasympathetic regulation of GI tract

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

23

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

requires contraction and relaxation
-vagus nerve has dual role on the smooth muscle of GI

24

structures of the GI tract

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

25

intrinsic regulation of the GI tract by?

enteric nervous system

26

how does the GI function autonomously

intrinsic system can feedback on itself - "brain in the gut"

27

two plexuses that are responsible for in the intrinsic regulation

1. myenteric plexus (Auerbach's) - controls motility
2. submucosal plexus (Meissner's) - controls secretions and absorption

28

7 specific functions of the enteric nervous system

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

29

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

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

30

how does the enteric nervous system regulate GI endocrine cells

can signal release of GI hormones

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

31

examples of defense reactions of the enteric nervous system

vomit, diarrhea, exaggerated propulsive motility reflexes

32

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

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

33

how many neurotransmitters exist in intrinsic nervous system of GI

2 functions and examples of each

20+
-ex's: excite smooth muscle (contract): ACh and substance P
-ex's: inhibit smooth muscle: nitric oxide & VIP (vasoactive intestinal peptide)

34

general function of extrinsic GI regulation

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

35

general function of intrinsic nervous system of GI

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

36

function of mouth

salivation

37

3 salivary glands of the mouth

submandibular
sublingual
parotid

38

autonomic control of saliva

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

39

what does saliva contain? (3)

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

hormones in obseity

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

role of hormones in hunger

ghrelin - fast acting
-levels rise just before meals
-most circulating levels produced by stomach
-other roles: memory & sleep

42

roles of leptin in satiety

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

43

role of PYY in satiety

fast acting, counteracting role to ghrelin post feeding
-released from SI

44

3 portions of the esophagus

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

45

location of UES

junction of lower pharynx and esophagus
approx at level of cricoid cartilage

46

function of UES

prevent air from entering esophagus during ventilation

47

location of LES

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

48

function of LES

barrier to reflux of the acidic content of the stomach

49

LES is maintained by what

increased smooth muscle tone

50

what is resting tone of LES

1. LES smooth muscle tone increased to 20 mmHg
-belching: air pressure in stomach exceeds LES pressure

51

how does swallowing tie in with LES

LES smooth muscle to tone is relaxed
peristaltic wave relaxes smooth muscle of LES

52

where are the control centers for swallowing

located in brainstem (reticular formation)
-complex function requiring coordination bw digestive tract and respiratory system

53

phases of swallowing

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

how is the bolus of food moved

peristalsis

55

role of insulin in satiety

fast acting, post feeding
released from pancreas

56

how is peristalis coordinated

contraction/relaxation of longitudinal/crcular muscles

57

what is the esophageal muscular pressure range

35 to 80 mmHg

58

differences in esophageal pressures by the three portions

1. upper portion & lower - tend to be higher (60-80)
2. middle portion - lower pressure (30-45 mmHg)

59

what happens if esophageal pressure is

may leave food residue within esophagus

60

what is the effect of tension on esophageal movement?
what happens with intense contractions?

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

61

control of peristalsis

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

what is primary peristalsis

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

what is secondary peristalsis

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

what does bolus/food residue distenetion cause

intrinsic feedback to:
1. constrict esophagus above the distention
2. relax esophagus below distention
3. which pushes residue/bolus along

65

what happens when swallowing food

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

what happens when swallowing liquid

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

basal tone of LES is a net result of 3 factors

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

68

what is deglutitive inhibition

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

69

normal tone of UES

50 mmHg

70

factors that increase LES pressure

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

factors that decrease LES pressure

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

72

how does vagus nerve decrease LES pressure

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

73

how do hormones decrease LES pressure

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

74

what common foods decrease LES pressure

(relax LES)
-fried fatty foods, tomatoes, citrus, high protein diet, chocolate, peppermint, tobacco, alcohol, caffeine

75

what is GERD

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

meds for GERD

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

what is Achalasia

(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

treatment for achalasia

pneumatic dilation (stretch LES to relax)
meds

79

what is esophageal varices

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

what is barretts's esophagus

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

what is metaplasia

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

82

symptoms of barrett's esophagus

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

do all pts with GERD develop Barrett's?

NO

84

what kind of cancer can develop with Barrett's esophagus

adenocarcinoma

85

will all pts with Barrett's esophagus develop cancer?

no

86

risk of cancer with Barrett's esophagus

1:300

87

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

dysplasia

88

what is dysplasia

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

how does esophageal cancer rank among other cancers

8th most common

90

what % of esophageal cancers are adenocarcinmoa

50%

91

what population does adenocarcinoma affect

caucasian male

92

what % of population is afflicted with GERD

20% - in US and western Europe

93

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

0.5-1%

94

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

yearly with endoscopy and biopsy of the esophagus