GI histology and pathophys Flashcards

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1
Q

major functions of the GI tract

A
ingestion
fragmentation
digestion
absorption
elimination of waste
defense - big one
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2
Q

4 major layers of GI tract

A

mucosa
submucosa
muscular propria
adventitia

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3
Q

layers of mucosa in GI tract

A
epithelium
lamina propria (defense)
muscularis mucosae (smooth muscle)
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4
Q

things found in submucosa

A
collagenous tissue
blood vessels
glands
lymphatics
nerves
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5
Q

role of submucosa

A
  • binds mucosa to muscular wall
  • secretion
  • supply
  • control
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6
Q

layers of muscularis propria

A

inner circular muscle layer

outer longitudinal muscle layer

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7
Q

role of muscularis propria

A

provide peristaltic contraction

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8
Q

4 types of mucosa in GI

A

protective
secretory
absorptive
lubricative

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9
Q

protective mucosa feature/location

A
  • epithelium is squamous cells

- oral cavity, pharynx, esophagus, anus

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10
Q

secretory mucosa feature/location

A
  • closely packed tubular glands

- stomach

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11
Q

absorptive mucosa feature/location

A
  • finger-like projections

- small intestine

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12
Q

lubricative mucosa feature/location

A
  • closely packed straight tubular glands (elongated)

- large intestine

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13
Q

air pressure level in esophogus

A

low (-5mmHg)

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14
Q

anti reflux barriers

A
  • lower esophageal sphincter
  • diaphragmatic sphincter
  • acute angle of stomach and esophagus connection
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15
Q

functions of stomach

A

fragmentation

digestion

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16
Q

parts of stomach

A

fundus
body
pylorus

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17
Q

cell types found in stomach

A

mucus
parietal
chief

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18
Q

mucus cell function

A

mucus secretion in stomach

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19
Q

parietal cell function

A

acid secretion

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20
Q

chief cell function

A

pepsin secretion

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21
Q

3 segments of small intestine

A

duodenum
jejunum
ileum

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22
Q

length of small intestine

A

23 feet

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23
Q

ways small intestine increases surface area

A
  • plicae circulares are folds of mucosa/submucosa
  • numerous villi and crypts on the mucosal surface
  • microvilli on the villi
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24
Q

amylase role

A

convert poly-, di- or mono-saccharides to glucose and maltose

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25
Q

role of disaccharidase and oigosaccaridase

A

convert maltose to monosaccharides

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26
Q

carbohydrate digestion sequence

A
  • poly, di, and mono saccharides broken down to glucose/maltose
  • maltose broken down to monosaccharidrd that are then absorbed
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27
Q

pepsin role

A

protease - breaks proteins down to poly peptides

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28
Q

where do amino acids go after the breakdown of peptides

A

liver

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29
Q

what needs to happen to digest fats

A

emulsification and then lipases can break them down

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30
Q

stomach absorbs what

A

water
alcohol
aspirin

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31
Q

duodenum absorbs what

A
iron, calcium, magnesium, sodium
fats
monosaccharides
water
AA's
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32
Q

jejunum absorbs what

A

monosaccharides

AA’s

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33
Q

Ileum absorbs what

A

bile salts
Vit B12
chloride

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34
Q

colon absorbs what

A

water

electrolytes

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35
Q

functions of colon

A

absorb water
store stool
propel stool

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36
Q

primary reservoir for stool

A

ascending colon

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37
Q

cellular components of large intestine

A
large glands
goblet cells - secretion
absorptive cells
blood vessels
lymphatic
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38
Q

mucosa-associated lymphoid tissues (MALT)

A
  • defense mechanism
  • T and B cells
  • most active during childhood
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39
Q

GERD

A

symptoms/complications due to reflux of gastric contents into esophagus or beyond
-may or may not have erosions

40
Q

GERD prevalence

A

10-20%
no difference between males/females
males may have more erosive esophagits

41
Q

potential causes of GERD

A
  • decreased lower esophageal sphincter pressure
  • decreased mucosal resistance to acid
  • decreased esophageal or gastric motility
  • decreased salivary buffering of acid
42
Q

drugs that may reduce LES pressure

A

anticholinergics
barbiturates
amlodipine
estrogen/progesterone

43
Q

drugs that irritate esophageal mucosa

A

nsaids
aspirin
bisphophonates
potassium

44
Q

main symptoms of GERD

A

heartburn
regurgitation
chest pain
dysphagia

45
Q

ALARMD symptoms

A
  • anemia
  • loss of weight
  • anorexia
  • recent onset
  • melena or hematemesis
  • dysphagia
46
Q

GERD diagnosis

A

-if heartburn/regurgitation you may presume GERD and treat with PPI

47
Q

when to do endoscopy in GERD patients

A

if they have ALARMD symptoms

48
Q

H.pylori screening in GERD

A

not recommended

49
Q

ambulatory reflux monitor

A

catheter that goes through the nose and down the esophagus to monitor pH

50
Q

complications of GERD

A

erosive esophagitis
esophageal strictures
Barrett’s esophagus (>50 y/o)
esophageal adenocarcinoma

51
Q

peptic ulcer disease

A
  • injury to digestive tract resulting in mucosal break

- usually in stomach or proximal duodenum

52
Q

aggressive factors in PUD development

A

gastric acid

pepsin

53
Q

protective factors against PUD

A

mucus secretion
bicarbonate secretion
prostaglandins

54
Q

causes of PUD

A

H.pylori
NSAID induced
stress-related (ICU patients)

55
Q

H.pylori PUD is usually where

A

duodenum

56
Q

NSAID induced PUD is usually where

A

stomach

57
Q

symptoms of H.pylori PUD

A

epigastric pain

58
Q

symptoms of NSAID induced PUD

A

usually asymptomatic

59
Q

PUD that is acute

A

stress-related

60
Q

symptoms of PUD

A

non-specific*
abdominal burning
fullness
cramping

61
Q

symptoms of duodenal ulcers

A

pain 1-3 hours after meals or at night and is relieved by eating

62
Q

symptoms of gastric ulcer

A

postprandial pain, n/v

weight loss

63
Q

PUD symptoms in elderly

A

usually asymptomatic

64
Q

complications of PUD

A

bleeding - due to erosion into an artery
perforation - sudden sharp pain
gastric outlet obstruction

65
Q

h.pylori transmission

A

usually fecal-oral

66
Q

h.pylori risk factors

A

low socioeconomic status
many siblings
infected parent
contaminated water

67
Q

where does h.pylori infect

A

between gastric mucus layer and surface epithelial cells

68
Q

how does h.pylori protect itself

A

produces urease which converts urea in gastric juice to ammonia and CO2 to alkalinize the environment

69
Q

complications of h.pylori

A

chronic gastritis
gastric and duodenal ulcers
malignancy

70
Q

indications for h.pylori testing

A
  • active or past PUD with no reported cure
  • initiation of chronic NSAID
  • unexplained iron deficiency anemia
  • idopathic thrombocytopenic purpura
  • low grade gastric MALT lymphoma
  • Hx of endoscopic resection of early gastric cancer
71
Q

when to consider non-endoscopic testing of h.pylori

A

< 60 with uninvestigated dyspepsia and no alarm symptoms

72
Q

when is testing for h.pylori unnecessary

A

typical symptoms of GERD

no PUD history

73
Q

endoscopic tests for h.pylori

A

histology
culture of biopsy
biopsy rapid urease test

74
Q

non-invasive h.pylori tests

A

antibody detection in serum (ELISA)
urea breath test
fecal antigen

75
Q

h.pylori test of choice during active bleed or EGD

A

biopsy rapid urease test

76
Q

most convenient h.pylori test

A

urea breath test

77
Q

risk factors for NSAID induced ulcers or upper GI bleed

A
>65
hx of PUD
high does of NSAID
alcohol
cigarettes
bisphosphonates, SSRIs, corticosteroids, anticoags, antiplatelets
78
Q

inflammatory bowel disease

A

chronic inflammatory disease of GI tract with alternating remission and recurrence

79
Q

features of Crohns disease

A
  • all segments can be affected (ileum and colon most common)
  • transmural inflammation
  • discontinuous distribution
80
Q

features of ulcerative colitis

A
  • limited to colon and rectum
  • inflammation is mucosal only
  • continuous distribution
81
Q

crohns disease onset

A

usually 20-40s

82
Q

ulcerative colitis onset

A

usually 30s

83
Q

inflammatory bowel disease greatest incidence poplulation

A

developed countries and urban areas

Jewish

84
Q

risk factors for inflammatory bowel disease

A
  • altered GI bacteria composition
  • genetics
  • cytokine dysregulation
  • smoking (for crohns disease)
  • nsaid and OC use
85
Q

inflammatory bowel disease symptoms

A
abdominal pain
diarrhea
blood in stools
weight loss
fever
extraintestinal manifestations
86
Q

gold standard for inflammatory bowel disease diagnosis

A

endoscopy with biopsies

87
Q

labs to do when diagnosing IBD

A
cmp
cbc
crp
esr
fecal calprotectin
c.diff
stool culture
88
Q

complications of crohn’s disease

A

small bowel stricture and obstruction
fistulas
abscesses
intestinal cancer

89
Q

complications of ulcerative colitis

A
  • hemorrhoids, anal fissures
  • perirectal abscesses
  • toxic megacolon
  • colonic stricture
  • colorectal cancer
90
Q

most commonly diagnosed GI condition

A

irritable bowel syndrome

91
Q

Rome IV criteria for IBS

A

-recurrently abdominal pain (at least once weekly) with two or more of following
o related to defecation
o associated with change in stool frequency
o associated with change in stool appearance

92
Q

typical symptoms of IBS

A
  • diarrhea or constipation*
  • bloating
  • straining during defecation
  • feelings of incomplete evacuation
93
Q

IBS diagnosis

A

Rome IV criteria started at least 6 months prior and been present in last 3 months

94
Q

IBS may be triggered by

A
  • gastroenteritis
  • food intolerances
  • chronic stress
  • diverticulitis
  • surgery
95
Q

IBS and serotonin

A

associated with an increase after meals in IBS with diarrhea