Chap 17- GI Tract Flashcards

1
Q

upper division of GIT

A
  • oral cavity
  • pharynx
  • esophagus
  • stomach
  • responsible for food consumption and chemical digestion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

lower division of GI tract

A
  • small intestine
  • large intestines
  • anus
  • where absorption of nutrients takes place
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the accessory system to the GIT?

A
  • hepatobiliary system
  • liver
  • gall bladder
  • pancreas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the function of the hepatobiliary system?

A

secrete digestive enzymes required for food metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the layers of the GI tract?

A
  • mucosa
  • submucosa
  • muscle
  • serosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the peritoneum?

A

large serous outer membrane that lines abdominal cavity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the divisions of the peritoneum?

A
  • parietal
  • visceral
  • peritoneal cavity= space between the two
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

mesentary

A
  • double layer peritoneum

- has BV and nerves that supply intestinal wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A

mucosa layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the portions of the mucosa layer?

A
  • epithelium
  • lamina propria
  • muscularis mucosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what do goblet cells secrete?

A

mucus that protects epithelium from digestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

paneth cells

A
  • secrete antimicrobial peptides

- found in epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the lamina propia?

A

layer of CT tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the role of the muscularis mucosal layer?

A
  • contracts to make closer contact with food particles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is found in the submucosa?

A
  • blood vessels
  • lymphatic vessels
  • submucosal plexus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the function of the submucosal plexus?

A
  • regulate secretions of GIT
  • regulate blood supply
  • aka meissner’s plexus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what makes up the muscularis externa layer?

A
  • circular muscle fibers
  • longitudinal muscle fibers
  • myenteric plexus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the role of the myenteric plexus?

A
  • regulate peristalsis
  • help move digested material out of gut
  • aka Auerbach’s plexus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what controls swallowing?

A
  • swallowing center in medulla

- CN 5, 9, 10 and 12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

digestive juices of salivary glands

A
  • bicarbonate- moisten food

- salivary lipase- digest fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

digestive juices of stomach

A
  • hydrochloric acid
  • pepsin
  • gastric lipase
  • intrinsic factor
  • mucus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

hydrochloric acid

A

kill bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

pepsin

A

digest protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
gastric lipase
digest fat
26
intrinsic factor
aids in B12 absorption
27
mucus
protects stomach lining
28
agenesis
- absence of part of GIT | - extremely rare
29
atresia
- development of part of GIT is incomplete - common - most commonly occurs at tracheal bifurcation and associated with a fistula - associated with other congenital malformations
30
what is the result of atresia and fistula at the tracheal bifurcation
- aspiration - suffocation - pneumonia - severe flid and electrolyte imbalances
31
acquired stenosis causes
- inflammatory scarring - GERD - irradiation - systemic sclerosis - caustic injury
32
diaphragmatic hernia
- incomplete formation of diaphragm | - abdominal viscera herniate into thoracic cavity
33
omphalocele
- closure of abdominal musculature is incomplete | - abdominal viscera herniate into ventral membranous sac
34
meckel's diverticulum
- true diverticulum - outpouching of all four layers of GI wall - due to failed involution of vitelline duct
35
what is the vitelline duct?
connects yolk sac to developing embryos digestive system
36
characteristics of meckel's diverticulum
- 2% of population - present within 2 ft of ileocecal valve - 2X as common in males - if have symptoms, symptomatic by age 2
37
what can also happen with meckel's diverticulum?
- ectopic pancreatic tissue - ectopic gastric tissue - secretions from these can lead to peptic ulceration
38
symptoms of meckel's diverticulum
- painless bright red blood per rectum (BRBPR) - abdominal pain resembling apendicitis - obstruction
39
pyloric stenosis
- 3/5 times more common in males - present between 3-6 weeks of life - hyperplasia of pyloric muscularis externa which obstructs gastric outflow
40
pyloric stenosis symptoms
- projectile non-bilious vomiting after feeding - frequent demands of refeeding - edema and inflammatory changes in mucosa/ submucosa which can aggravate narrowing
41
who is at an increased risk for developing pyloric stenosis?
- monozygotic twins - dizygotic twins - siblings - turner syndrome - trisomy 18 - erythromycin or azithromycin exposure
42
causes of acquired pyloric stenosis
- antral gastritis - peptic ulcers close to pyloris - stomach cancer
43
hirschsprung disease
- aka congenital aganglionic megacolon - associated with down syndrome - no migration of neural crest cells leads to aganglionosis
44
clinical features of hirschsprung disease
- failure to pass meconium in immediate postnatal period - obstruction/ constipation - ineffective peristalsis - abdominal distension - bilious vomiting
45
what are major consequences of hirschsprung disease?
- enterocolitis - fluid and electrolyte disturbances - perforation - peritonitis
46
achalasia
- occurs due to increased tone of lower esophageal sphincter - low levels of NO and VIP - high levels of ACh
47
triad of achalasia
- aperistalsis - increased tone of lower esophageal sphincter - incomplete relaxation of lower esophageal sphincter
48
primary cause of achalasia
ganglion cell degeneration
49
secondary causes of achalasia
- chagas disease - diabetic neuropathy - infiltrative disorders - down syndrome - alacrima - adrenal insufficiency
50
symptoms of achalasia
- dysphagia for solids and liquids - difficulty in belching - regurgitation - chest pain - weight loss
51
reflux esophagitis
- aka GERD - due to loose lower esophageal sphincter and increased abdominal pressure - sensitive to acid
52
causes of GERD
- alcohol and tobacco - obesity - CNS depressants - pregnancy - hiatal hernia - decreased gastric emptying
53
clinical features of GERD
- heart burn - dysphagia - regurgitation of gastric contents
54
complications of GERD
- ulceration - hematemesis - melena - structure development - barrett esophagus
55
what type of cells line the mouth to esophagus
stratified squamous epithelium
56
what type of cells line the stomach to terminal anus
ciliated columnar epithelium
57
esophageal varices
- 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
varices
dilation of vein
59
how does portal HTN cause esophageal varices?
- increased pressure causes blood to flow from portal system to systemic system - puts pressures on walls of veins (thin walls) - increased pressure -> varices
60
barrett esophagus
- due to chronic GERD - intestinal metaplasia - replacement of normal stratified squamous epithelium with simple columnar epithelium - increased risk of esophageal adenocarcinoma
61
how do you identify barrett esophagus
- endoscopy | - prompted by GERD sx
62
esophageal tumors
- 7th leading cause of cancer deaths | - mostly in elderly
63
what is the most common type of esophageal tumor world wide?
- squamous cell carcinoma | - mainly associated with alcohol and tobacco use
64
what is the most common type of esophageal tumor in the US?
- adenocarcinoma | - due to association with GERD, barrett esophagus, and obesity
65
clinical features of esophageal tumors
- dysphagia - odynophagia (painful swallowing) - progressively increasing obstruction - weight loss - hemorrhage - lymph node metastasis= poor prognosis
66
anatomical regions of stomach
- cardia- continues with esophagus - fundus - body - antrum
67
cells of cardia and antrum
- mucin secreting foveolar cells - form small glands - antral glands also have G cells that release gastrin
68
what is the role of gastrin
- stimulate acid secretion by parietal cells in fundus and body
69
chief cells
- found in body and fundus | - produce and secrete digestive enzymes like pepsin
70
acute gastritis causes
- NSAIDs - alcohol - bile - stress - mucosal erosion or hemorrhage
71
sx of acute gastritis
- variable - epigastric pain, N/V - mucosal erosion/ ulceration/ hemorrhage - hematemesis - melena
72
protective factors in stomach
- mucus secretion - bicarbonate secretion - mucosal BF - epithelial barrier - epithelial regeneration - prostaglandins
73
pathogenesis of acute gastritis
- 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
what is the most common cause of chronic gastritis?
- h. pylori infection | - 2nd most common= autoimmune
75
how does chronic gastritis normally present
antral gastritis
76
pathophys of chronic gastritis infection
- 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
what does urease do
- neutralize gastric acid | - mechanism of h. pylori
78
peptic ulcer diease
- complication of chronic gastritis | - mucosal ulceration in duodenum or stomach
79
what is peptic ulcer disease associated with
- h pylori infection - NSAIDs - cigarette smoking
80
why is h. pylori associated with peptic ulcer disease?
- 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
clinical features of peptic ulcer disease
- epigastric burning - iron deficiency anemia - hemorrhage - perforation - N/V, bloating - weight loss - complications= bleeding, perforation, obstruction
82
gastric polyps
- 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
fundic gland polyps
- in individuals with adenomatous polyposis - increased prevalence due to PPIs - asymp or have N/V and epigastric pain
84
why are PPIs associated with fundic gland polyps
- reduces acid secretion | - stimulates oxyntic gland growth (acid secreting glands)
85
gastric adenocarcinoma
- most common malignancy of stomach - have intestinal or diffuse type - early sx similar to chronic gastritis and PUD
86
intestinal type gastric adenocarcinoma
bulky mass
87
diffuse type gastric adenocarcinoma
spreads and invades walls of GIT early
88
precursors for gastric adenocarcinoma
- gastric dysplasia - adenomas - overall incidence has decreased due to decreased h pylori infections and decreased consumption of carcinogens
89
what is the most common cause of intestinal obstruction
adhesions
90
hernia
- weakness or defect in abdominal wall | - permits protrusion of serosa lined pouch of peritoneum
91
volvulus
twisting of bowel
92
intussusception
- segment of intestine is constricted by wave of peristalsis - telescopes into immediately distal segment - common in kids < 2
93
what are main arteries of GI T
- celiac a - superior mesenteric a - inferior mesenteric a
94
hyper coagulable states that can lead to ischemic bowel disease
- severe atherosclerosis - aortic aneurysm - oral contraceptives - embolism - hypoperfusion
95
result of ischemic bowel disease
- mucosal infarction - mural infarction - transmural infarction- across all four layers
96
pathogenesis of ischemic bowel disease
- phase 1= hypoxic injury - phase 2= reperfusion injury - most damage done in phase 2 due to ROS
97
clinical features of ischemic bowel disease
- common in elderly - sudden cramping, lower left abdominal pain - blood diarrhea - can lead to shock
98
infectious enterocolitis
- major cause of death world wide especially in kids <5 | - e. coli is major cause
99
symptoms of infectious enterocolitis
- diarrhea - abdominal pain - urgency - perianal discomfort - incontinence - hemorrhage
100
cholera and enterocolitis
- spreads through contaminated drinking water - causes rice water stools at a rate of 1 L/hour - vomitting - dehydration, hypotension, shock, death
101
pathophys of cholera infection
- 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
camylobacter enterocolitis
- most common bacterial enteric pathogen in developed countries - impt cause of travelers diarrhea - associated with undercooked chicken, unpasteurized milk
103
virulence factors of campylobacter
- motility - adherence - toxin production CDT - invasion into lamina propia and lymph nodes
104
result of camylobacter infection
- watery diarrhea - dysentery - reactive arthritis - GBS
105
shigellosis
- 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
clinical features of shigellosis
- most infections and deaths occur in kids <5 - 1 week incubation period - diarrhea - fever - abdominal pain
107
pathophys of shigellosis
- invade m cells - reaches basolateral side and enters macrophages - macrophages release cytokines IL1 and IL8 - attracts PMN -> decreased absorption, increases permeability
108
how does shigella spread once in GIT
spreads horizontally from cell to cell
109
salmonella
- causes typhoid fever and salmonellosis - over 1m cases each year in US - peak incidence in summer and fall
110
type III secretion system
- found in salmonella | - transfers bacterial proteins into M cells and enterocytes
111
clinical features of salmonella
- 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
subtypes of typhoid fever
- typhi | - paratyphi
113
typhoid fever
- infects blood vessels and lymphatics - can travel to other parts of body - leads to typhoid nodules and typhoid ulcers
114
clinical features of typhoid fever
- N/V/D (bloody) - anorexia - abdominal pain - rose spots
115
extraintestinal complications of typhoid fever
- encephalopathy - meningitis - seizures - endocarditis - myocarditis - pneumonia - cholecystitis
116
e. coli
- colonize healthy GIT - most nonpathogenic - some can cause diseases
117
classifications of e. coli
- enterohemorrhagic - enterotoxigenic - enteroinvasive - enteropathogenic
118
enterohemorrhagic e. coli
- 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
enterotoxigenic e. coli
- non-penetrating - travelers diarrhea - heat stable and heat labile toxin - increase adenylate cyclase -> increase cAMP -> increased secretions - secretory diarrhea, dehydration, shock
120
enterinvasive e. coli
- penetrating - transm via food, water, person to person - doesnt produce toxin - invade epithelial cells -> dysentery
121
enteropathogenic e. coli
- non-penetrating - impt cause of endemic diarrhea in kids <2 - attach to epithelium -> loss of microvilli -> mucus diarrhea
122
pseudomembranous colitis
- caused by c. diff - highly related to antibiotic use - recurrent infection - forms a white membrane
123
risk factors for pseudomembranous colitis
- advanced age - hospitalization - antibiotic tx
124
clinical features of pseudomembranous colitis
- fever - leukocytosis - abdominal pain - cramps - watery diarrhea - dehydration - protein loss leading to hypoalbuminema
125
pathogenesis of pseudomembranous colitis
- disruption of bacterial flora - colonization with c diff - toxins released - mucosal damage and inflammation
126
viral gastroenteritis
- most common causes are rotavirus and norovirus - rotavirus most common in kids - infections spread easily - usually self limiting - infective inoculum= 10 particles
127
pathophys of viral gastroenteritis
- 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
inflammatory bowel disease
- crohn's and/or ulcerative colitis - inappropriate mucosal immune acvtivation - 2 diseases often coexist
129
crohn's disease
- skip lesions in any part of GIT - transmural inflammation - hypoalbuminemia - fibrosing strictures - fistulae between bowel loops and can involve other areas
130
ulcerative colitis
- involves colon and rectum - continuous involvement - causes superficial ulcers and pseudopolyps - bloody diarrhea - 30% require colectomy