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Patho 2 > Chap 17- GI Tract > Flashcards

Chap 17- GI Tract Flashcards

1
Q

upper division of GIT

A
  • oral cavity
  • pharynx
  • esophagus
  • stomach
  • responsible for food consumption and chemical digestion
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2
Q

lower division of GI tract

A
  • small intestine
  • large intestines
  • anus
  • where absorption of nutrients takes place
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3
Q

what is the accessory system to the GIT?

A
  • hepatobiliary system
  • liver
  • gall bladder
  • pancreas
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4
Q

what is the function of the hepatobiliary system?

A

secrete digestive enzymes required for food metabolism

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5
Q

what are the layers of the GI tract?

A
  • mucosa
  • submucosa
  • muscle
  • serosa
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6
Q

what is the peritoneum?

A

large serous outer membrane that lines abdominal cavity

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7
Q

what are the divisions of the peritoneum?

A
  • parietal
  • visceral
  • peritoneal cavity= space between the two
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8
Q

mesentary

A
  • double layer peritoneum

- has BV and nerves that supply intestinal wall

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9
Q

what layer of the GI wall comes in contact with food?

A

mucosa layer

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10
Q

what are the portions of the mucosa layer?

A
  • epithelium
  • lamina propria
  • muscularis mucosa
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11
Q

epithelium in GI wall

A
  • made of simple columnar or stratified squamous cells
  • contains goblet cells and endocrine cells
  • had depressions that store stem cells and immune cells
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12
Q

what do goblet cells secrete?

A

mucus that protects epithelium from digestion

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13
Q

paneth cells

A
  • secrete antimicrobial peptides

- found in epithelium

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14
Q

what is the lamina propia?

A

layer of CT tissue

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15
Q

what is the role of the muscularis mucosal layer?

A
  • contracts to make closer contact with food particles
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16
Q

what is found in the submucosa?

A
  • blood vessels
  • lymphatic vessels
  • submucosal plexus
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17
Q

what is the function of the submucosal plexus?

A
  • regulate secretions of GIT
  • regulate blood supply
  • aka meissner’s plexus
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18
Q

what makes up the muscularis externa layer?

A
  • circular muscle fibers
  • longitudinal muscle fibers
  • myenteric plexus
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19
Q

what is the role of the myenteric plexus?

A
  • regulate peristalsis
  • help move digested material out of gut
  • aka Auerbach’s plexus
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20
Q

what controls swallowing?

A
  • swallowing center in medulla

- CN 5, 9, 10 and 12

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21
Q

digestive juices of salivary glands

A
  • bicarbonate- moisten food

- salivary lipase- digest fat

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22
Q

digestive juices of stomach

A
  • hydrochloric acid
  • pepsin
  • gastric lipase
  • intrinsic factor
  • mucus
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23
Q

hydrochloric acid

A

kill bacteria

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24
Q

pepsin

A

digest protein

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25
Q

gastric lipase

A

digest fat

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26
Q

intrinsic factor

A

aids in B12 absorption

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27
Q

mucus

A

protects stomach lining

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28
Q

agenesis

A
  • absence of part of GIT

- extremely rare

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29
Q

atresia

A
  • development of part of GIT is incomplete
  • common
  • most commonly occurs at tracheal bifurcation and associated with a fistula
  • associated with other congenital malformations
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30
Q

what is the result of atresia and fistula at the tracheal bifurcation

A
  • aspiration
  • suffocation
  • pneumonia
  • severe flid and electrolyte imbalances
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31
Q

acquired stenosis causes

A
  • inflammatory scarring
  • GERD
  • irradiation
  • systemic sclerosis
  • caustic injury
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32
Q

diaphragmatic hernia

A
  • incomplete formation of diaphragm

- abdominal viscera herniate into thoracic cavity

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33
Q

omphalocele

A
  • closure of abdominal musculature is incomplete

- abdominal viscera herniate into ventral membranous sac

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34
Q

meckel’s diverticulum

A
  • true diverticulum
  • outpouching of all four layers of GI wall
  • due to failed involution of vitelline duct
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35
Q

what is the vitelline duct?

A

connects yolk sac to developing embryos digestive system

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36
Q

characteristics of meckel’s diverticulum

A
  • 2% of population
  • present within 2 ft of ileocecal valve
  • 2X as common in males
  • if have symptoms, symptomatic by age 2
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37
Q

what can also happen with meckel’s diverticulum?

A
  • ectopic pancreatic tissue
  • ectopic gastric tissue
  • secretions from these can lead to peptic ulceration
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38
Q

symptoms of meckel’s diverticulum

A
  • painless bright red blood per rectum (BRBPR)
  • abdominal pain resembling apendicitis
  • obstruction
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39
Q

pyloric stenosis

A
  • 3/5 times more common in males
  • present between 3-6 weeks of life
  • hyperplasia of pyloric muscularis externa which obstructs gastric outflow
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40
Q

pyloric stenosis symptoms

A
  • projectile non-bilious vomiting after feeding
  • frequent demands of refeeding
  • edema and inflammatory changes in mucosa/ submucosa which can aggravate narrowing
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41
Q

who is at an increased risk for developing pyloric stenosis?

A
  • monozygotic twins
  • dizygotic twins
  • siblings
  • turner syndrome
  • trisomy 18
  • erythromycin or azithromycin exposure
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42
Q

causes of acquired pyloric stenosis

A
  • antral gastritis
  • peptic ulcers close to pyloris
  • stomach cancer
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43
Q

hirschsprung disease

A
  • aka congenital aganglionic megacolon
  • associated with down syndrome
  • no migration of neural crest cells leads to aganglionosis
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44
Q

clinical features of hirschsprung disease

A
  • failure to pass meconium in immediate postnatal period
  • obstruction/ constipation
  • ineffective peristalsis
  • abdominal distension
  • bilious vomiting
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45
Q

what are major consequences of hirschsprung disease?

A
  • enterocolitis
  • fluid and electrolyte disturbances
  • perforation
  • peritonitis
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46
Q

achalasia

A
  • occurs due to increased tone of lower esophageal sphincter
  • low levels of NO and VIP
  • high levels of ACh
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47
Q

triad of achalasia

A
  • aperistalsis
  • increased tone of lower esophageal sphincter
  • incomplete relaxation of lower esophageal sphincter
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48
Q

primary cause of achalasia

A

ganglion cell degeneration

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49
Q

secondary causes of achalasia

A
  • chagas disease
  • diabetic neuropathy
  • infiltrative disorders
  • down syndrome
  • alacrima
  • adrenal insufficiency
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50
Q

symptoms of achalasia

A
  • dysphagia for solids and liquids
  • difficulty in belching
  • regurgitation
  • chest pain
  • weight loss
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51
Q

reflux esophagitis

A
  • aka GERD
  • due to loose lower esophageal sphincter and increased abdominal pressure
  • sensitive to acid
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52
Q

causes of GERD

A
  • alcohol and tobacco
  • obesity
  • CNS depressants
  • pregnancy
  • hiatal hernia
  • decreased gastric emptying
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53
Q

clinical features of GERD

A
  • heart burn
  • dysphagia
  • regurgitation of gastric contents
54
Q

complications of GERD

A
  • ulceration
  • hematemesis
  • melena
  • structure development
  • barrett esophagus
55
Q

what type of cells line the mouth to esophagus

A

stratified squamous epithelium

56
Q

what type of cells line the stomach to terminal anus

A

ciliated columnar epithelium

57
Q

esophageal varices

A
  • abnormal dilation of veins at junction between portal vein and systemic venous system
  • present in half of pts with cirrhosis
  • is a medical emergency, can lead to severe bleeding and shock
58
Q

varices

A

dilation of vein

59
Q

how does portal HTN cause esophageal varices?

A
  • increased pressure causes blood to flow from portal system to systemic system
  • puts pressures on walls of veins (thin walls)
  • increased pressure -> varices
60
Q

barrett esophagus

A
  • due to chronic GERD
  • intestinal metaplasia
  • replacement of normal stratified squamous epithelium with simple columnar epithelium
  • increased risk of esophageal adenocarcinoma
61
Q

how do you identify barrett esophagus

A
  • endoscopy

- prompted by GERD sx

62
Q

esophageal tumors

A
  • 7th leading cause of cancer deaths

- mostly in elderly

63
Q

what is the most common type of esophageal tumor world wide?

A
  • squamous cell carcinoma

- mainly associated with alcohol and tobacco use

64
Q

what is the most common type of esophageal tumor in the US?

A
  • adenocarcinoma

- due to association with GERD, barrett esophagus, and obesity

65
Q

clinical features of esophageal tumors

A
  • dysphagia
  • odynophagia (painful swallowing)
  • progressively increasing obstruction
  • weight loss
  • hemorrhage
  • lymph node metastasis= poor prognosis
66
Q

anatomical regions of stomach

A
  • cardia- continues with esophagus
  • fundus
  • body
  • antrum
67
Q

cells of cardia and antrum

A
  • mucin secreting foveolar cells
  • form small glands
  • antral glands also have G cells that release gastrin
68
Q

what is the role of gastrin

A
  • stimulate acid secretion by parietal cells in fundus and body
69
Q

chief cells

A
  • found in body and fundus

- produce and secrete digestive enzymes like pepsin

70
Q

acute gastritis causes

A
  • NSAIDs
  • alcohol
  • bile
  • stress
  • mucosal erosion or hemorrhage
71
Q

sx of acute gastritis

A
  • variable
  • epigastric pain, N/V
  • mucosal erosion/ ulceration/ hemorrhage
  • hematemesis
  • melena
72
Q

protective factors in stomach

A
  • mucus secretion
  • bicarbonate secretion
  • mucosal BF
  • epithelial barrier
  • epithelial regeneration
  • prostaglandins
73
Q

pathogenesis of acute gastritis

A
  • loss of protective mechanisms
  • NSAIDS are cox inhibitors -> decreased PGE2/I2
  • h. pylori -> decreased bicarb
  • some chemicals/ alcohol can cause direct epithelial damage
  • chemo decreases epithelial regeneration
74
Q

what is the most common cause of chronic gastritis?

A
  • h. pylori infection

- 2nd most common= autoimmune

75
Q

how does chronic gastritis normally present

A

antral gastritis

76
Q

pathophys of chronic gastritis infection

A
  • h. pylori swims via flagella
  • attaches to epithelium via proteins
  • secretes urease and neutralizes acid
  • injects exotoxin into host which causes epithelial death
  • mucinase degrades mucus layer
  • can extend from antrum to fundus
77
Q

what does urease do

A
  • neutralize gastric acid

- mechanism of h. pylori

78
Q

peptic ulcer diease

A
  • complication of chronic gastritis

- mucosal ulceration in duodenum or stomach

79
Q

what is peptic ulcer disease associated with

A
  • h pylori infection
  • NSAIDs
  • cigarette smoking
80
Q

why is h. pylori associated with peptic ulcer disease?

A
  • causes more gastrin to be secreted -> increased acid and decreased bicarb -> antral and duodenal uclers
  • can progress to fundus and cause gastric atrophy increasing risk of stomach cancer
81
Q

clinical features of peptic ulcer disease

A
  • epigastric burning
  • iron deficiency anemia
  • hemorrhage
  • perforation
  • N/V, bloating
  • weight loss
  • complications= bleeding, perforation, obstruction
82
Q

gastric polyps

A
  • usually due to inflammatory and hyperplastic polyps
  • generally are small
  • if greater than 1.5 cm must be biopsied
  • can be due to inflammatory response from h. pylori
83
Q

fundic gland polyps

A
  • in individuals with adenomatous polyposis
  • increased prevalence due to PPIs
  • asymp or have N/V and epigastric pain
84
Q

why are PPIs associated with fundic gland polyps

A
  • reduces acid secretion

- stimulates oxyntic gland growth (acid secreting glands)

85
Q

gastric adenocarcinoma

A
  • most common malignancy of stomach
  • have intestinal or diffuse type
  • early sx similar to chronic gastritis and PUD
86
Q

intestinal type gastric adenocarcinoma

A

bulky mass

87
Q

diffuse type gastric adenocarcinoma

A

spreads and invades walls of GIT early

88
Q

precursors for gastric adenocarcinoma

A
  • gastric dysplasia
  • adenomas
  • overall incidence has decreased due to decreased h pylori infections and decreased consumption of carcinogens
89
Q

what is the most common cause of intestinal obstruction

A

adhesions

90
Q

hernia

A
  • weakness or defect in abdominal wall

- permits protrusion of serosa lined pouch of peritoneum

91
Q

volvulus

A

twisting of bowel

92
Q

intussusception

A
  • segment of intestine is constricted by wave of peristalsis
  • telescopes into immediately distal segment
  • common in kids < 2
93
Q

what are main arteries of GI T

A
  • celiac a
  • superior mesenteric a
  • inferior mesenteric a
94
Q

hyper coagulable states that can lead to ischemic bowel disease

A
  • severe atherosclerosis
  • aortic aneurysm
  • oral contraceptives
  • embolism
  • hypoperfusion
95
Q

result of ischemic bowel disease

A
  • mucosal infarction
  • mural infarction
  • transmural infarction- across all four layers
96
Q

pathogenesis of ischemic bowel disease

A
  • phase 1= hypoxic injury
  • phase 2= reperfusion injury
  • most damage done in phase 2 due to ROS
97
Q

clinical features of ischemic bowel disease

A
  • common in elderly
  • sudden cramping, lower left abdominal pain
  • blood diarrhea
  • can lead to shock
98
Q

infectious enterocolitis

A
  • major cause of death world wide especially in kids <5

- e. coli is major cause

99
Q

symptoms of infectious enterocolitis

A
  • diarrhea
  • abdominal pain
  • urgency
  • perianal discomfort
  • incontinence
  • hemorrhage
100
Q

cholera and enterocolitis

A
  • spreads through contaminated drinking water
  • causes rice water stools at a rate of 1 L/hour
  • vomitting
  • dehydration, hypotension, shock, death
101
Q

pathophys of cholera infection

A
  • enters in cell
  • increases adenylate cyclase
  • leads to increase in cAMP
  • cAMP opens ion channel CTFR
  • loss of chloride, water, Na
  • results in severe secretory diarrhea
102
Q

camylobacter enterocolitis

A
  • most common bacterial enteric pathogen in developed countries
  • impt cause of travelers diarrhea
  • associated with undercooked chicken, unpasteurized milk
103
Q

virulence factors of campylobacter

A
  • motility
  • adherence
  • toxin production CDT
  • invasion into lamina propia and lymph nodes
104
Q

result of camylobacter infection

A
  • watery diarrhea
  • dysentery
  • reactive arthritis
  • GBS
105
Q

shigellosis

A
  • due to shigella flexneri
  • secretes shiga toxin which decreases protein synthesis
  • one of most common causes of dysentery
  • fecal-oral or conatminated water transmission
106
Q

clinical features of shigellosis

A
  • most infections and deaths occur in kids <5
  • 1 week incubation period
  • diarrhea
  • fever
  • abdominal pain
107
Q

pathophys of shigellosis

A
  • invade m cells
  • reaches basolateral side and enters macrophages
  • macrophages release cytokines IL1 and IL8
  • attracts PMN -> decreased absorption, increases permeability
108
Q

how does shigella spread once in GIT

A

spreads horizontally from cell to cell

109
Q

salmonella

A
  • causes typhoid fever and salmonellosis
  • over 1m cases each year in US
  • peak incidence in summer and fall
110
Q

type III secretion system

A
  • found in salmonella

- transfers bacterial proteins into M cells and enterocytes

111
Q

clinical features of salmonella

A
  • indistinguishable from other enteric pathogens
  • inflammatory diarrhea
  • fever resolves in 2 days but diarrhea persists for a week
  • organism can be shed in stool for several weeks
112
Q

subtypes of typhoid fever

A
  • typhi

- paratyphi

113
Q

typhoid fever

A
  • infects blood vessels and lymphatics
  • can travel to other parts of body
  • leads to typhoid nodules and typhoid ulcers
114
Q

clinical features of typhoid fever

A
  • N/V/D (bloody)
  • anorexia
  • abdominal pain
  • rose spots
115
Q

extraintestinal complications of typhoid fever

A
  • encephalopathy
  • meningitis
  • seizures
  • endocarditis
  • myocarditis
  • pneumonia
  • cholecystitis
116
Q

e. coli

A
  • colonize healthy GIT
  • most nonpathogenic
  • some can cause diseases
117
Q

classifications of e. coli

A
  • enterohemorrhagic
  • enterotoxigenic
  • enteroinvasive
  • enteropathogenic
118
Q

enterohemorrhagic e. coli

A
  • non-penetrating
  • secretes shigella-like toxin which inactivates ribosomes
  • assoc with inadequately cooked ground beef
  • hemolytic uremic syndrome -> cytokine release -> RBC lysis, renal failure, thrombocytopenia
119
Q

enterotoxigenic e. coli

A
  • non-penetrating
  • travelers diarrhea
  • heat stable and heat labile toxin
  • increase adenylate cyclase -> increase cAMP -> increased secretions
  • secretory diarrhea, dehydration, shock
120
Q

enterinvasive e. coli

A
  • penetrating
  • transm via food, water, person to person
  • doesnt produce toxin
  • invade epithelial cells -> dysentery
121
Q

enteropathogenic e. coli

A
  • non-penetrating
  • impt cause of endemic diarrhea in kids <2
  • attach to epithelium -> loss of microvilli -> mucus diarrhea
122
Q

pseudomembranous colitis

A
  • caused by c. diff
  • highly related to antibiotic use
  • recurrent infection
  • forms a white membrane
123
Q

risk factors for pseudomembranous colitis

A
  • advanced age
  • hospitalization
  • antibiotic tx
124
Q

clinical features of pseudomembranous colitis

A
  • fever
  • leukocytosis
  • abdominal pain
  • cramps
  • watery diarrhea
  • dehydration
  • protein loss leading to hypoalbuminema
125
Q

pathogenesis of pseudomembranous colitis

A
  • disruption of bacterial flora
  • colonization with c diff
  • toxins released
  • mucosal damage and inflammation
126
Q

viral gastroenteritis

A
  • most common causes are rotavirus and norovirus
  • rotavirus most common in kids
  • infections spread easily
  • usually self limiting
  • infective inoculum= 10 particles
127
Q

pathophys of viral gastroenteritis

A
  • release NSP4 -> increased Ca concentration and permeability
  • release of peptide amines -> stimulate enteric NS -> secretary diarrhea
  • when virus multiples cells die -> less nutrient absorption -> osmotic diarrhea
128
Q

inflammatory bowel disease

A
  • crohn’s and/or ulcerative colitis
  • inappropriate mucosal immune acvtivation
  • 2 diseases often coexist
129
Q

crohn’s disease

A
  • skip lesions in any part of GIT
  • transmural inflammation
  • hypoalbuminemia
  • fibrosing strictures
  • fistulae between bowel loops and can involve other areas
130
Q

ulcerative colitis

A
  • involves colon and rectum
  • continuous involvement
  • causes superficial ulcers and pseudopolyps
  • bloody diarrhea
  • 30% require colectomy

Patho 2 (15 decks)

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