Gastrointestinal Tract Flashcards
1
Q
Upper Division of GI System
A
Oral cavity, pharynx, esophagus and stomach
2
Q
Lower Division of GI system
A
small intestine, large intestine, and anus
3
Q
Hepatobilary system
A
liver, gallbladder, and pancreas
- Helps to further digest food from GI tract
4
Q
Four layers in the GI system
A
mucosa, submucosa, muscle, and serosa
5
Q
What is the Peritoneum ?
What are the layers within the membrane?
A
large serous membrane that lines the abdominal cavity
Parietal peritoneum
Paritoneal cavity- space inbetween the layers
Visceral peritoneum
6
Q
what is the mesentery
A
double layer peritoneum containing blood vessels and nerves that supplies the intestinal wall
7
Q
What are the components that make up the gastriontestinal wall in each of the four layers, mucosa, submucosa, muscular, serosa? What are each of those components responsible for?
A
-Epithelium-most exposed part of the mucosa
>Composed of simple columnar epithelium or stratified squamous epithelium
>also present are goblet (secrete mucus that protects epithelium from digestion) and endocrine cells (secrete hormones into the blood)
-Lamina propia (still in mucosa)
>contains myofibroblasts, blood vessels, nerves and several different immune cells and the muscularis mucosa (layer of smooth muscle that aids in peristalsis along the gut)
- Submucosa contains the submucosa nerve plexus (meissner’s plexus) along with blood vessels and elastic fibers to allow for stretch with increased capacity, but maintains the shape of the instestine
- In the muscle layer (aids in persistalsis) you have the circular smooth muscle first, then there is the myenteric plexus (Auerbach’s plexus) then there is the longitudal muscle layer
- Serosa is a serous membrane that covers the muscalaris externa of the digestive tract in the peritoneal cavity
8
Q
What occurs in the upper GI tract?
A
- Food enters mouth to begin mechanical and chemical digestion
- Swallowing is coordinated by CN 5, 9, 10, 12
9
Q
Hydrochloric acid function
A
kills bacteria
10
Q
pepsin function
A
digest proteins
11
Q
gastric lipase function?
A
digest fat
12
Q
intrinsic factor function
A
aids in vit B12 absorption
13
Q
Mucus function
A
protects the stomach lining
14
Q
bicarbonate function
A
moistens food
15
Q
What is agenesis and is it common?
A
absence of the esophagus and no its rare
16
Q
what is atresia and is it common
A
incomplete development of the esophagus and its more common
17
Q
Where does atresia occur?
When is it usally discovered
A
-Occurs near the bifurcation of the trachea
-discovered shortly after birth when the new born starts regurgitating his mothers breast milk - can lead to aspiration, suffication, pneumonia and severe electrolyte imbalances
18
Q
What is the pathology of atresia ?
A
Stenosis ⇒ Decreased lumen –> partial/complete obstruction
19
Q
Fistulas can be accquired due to ?
A
tumors
20
Q
acquired stenosis
A
inflammatory scarring
Ex: GERD, irradiation
21
Q
What is a diaphragmatic hernia?
How can this affect the fetus?
A
incomplete formation of the diaphragm allows abdominal content to seep out into the thoracic cavity- affects development of pulmonary system
22
Q
What is omphalocele ?
A
Occurs when closure of the abdominal musculature is incomplete and the abdomindal organs seep into a ventral sac outside the body
23
Q
Meckels diverticulum occurs because of
A
failed involution of the vitelline duct
24
Q
Meckels Diverticulum
- Occurs in what % of the population?
- the diverticulum is present within how many feet of the ileocecal valve?
- How long is the diverticulum?
- How common is it in males vs. females?
- At what age do people start experiencing symptoms ?
A
- 2%
- 2 feet
- 2 inches
- twice as common in males
- most symptomatic by age 2(only 4% are ever symptomatic
25
What causes the symptoms in meckels diverticulm
ectopic pancreatic or gastric tissue that are present and still functional
26
What is the pathogenesis of meckels diverticulm?
What symptoms are present?
Tissues secrete acid --\> peptic ulceration of adjacent smal intestinal mucosa
## Footnote
**painless BRBPR-bright red bleeding per rectum**
27
What is the most common site of congential diverticulum
ileium of small intestine
28
Cogenital: Pyloric Stenosis presents when?
Presents between the 3-6 weeks of life as new onset regurgitation, **projectile, _non-bilous vomiting after feeding,_** and frequent demands of refeeding
29
Pyloric stenosis is caused by?
Hyperplasia of the plyloric muscularis externa (where digested food sits), obstructs the gastric outflow tract
30
Acquired pyloric stenosis are?
antral gastritis or peptic ulcers close to the pylorus ((the opening from the stomach into the duodenum (small intestine))
31
Pyloric Stenosis how often in live births and typically more so in what gender?
3-5 times more common in males and occurs in 1 in 300-900 live births
32
**There is an increased risk of pyloric stenosis occuring in ?**
Twins, siblings, turner syndrome and trisomy 18, exposure to macrolides
33
**Hirschsprung disease pathogenesis**
There is no nerve supply because neural crest cells didnt migrate so the descending colon wont have submucosal and mesenteric nerve plexus. This means parastalsis wont occur and there will start to be abdominal distention and can lead to perforation
34
Clinical features of hirschsprung disease
* Failure to pass **meconium** (first poop)
* Constipation leads to abdominal distention **(congenital aganglionic megacolon)**
35
**Pathogenesis of Achalasia**
* decrease NO, VIP
* Increase ACh
* Increase tone of lower esophageal sphincter
-this leads to incomplete relaxation of the LES and leads to aperistalsis (this can cause the esophagus to get backed up with food)
36
Symptoms of Achalasia
* **dysphagia for solids and liquids**
* **difficulty burping**
* **regurgitation**
* **chest pain**
* **weight loss**
37
Primary alchalasia is due to
**ganglion cell degeneration**
38
**Secondary alchalasia is due to**
* Chagas disease
* diabetic neurorapathy
* lesions in the vagus nerve
39
Esophageal cause of hematemesis (vomiting blood)?
* **Lacerations (mallory wise syndrome)**
* **esophageal perf. (cancer)**
* **Varices (cirrhosis)**
* **reflux esophagitis**
* **esophageal ulcers**
* **barrett esophagus**
* **adeno/squamous cell carcinoma**
* **chemical and pill esophagitits**
40
What is Reflux esophagitis aka GERD ?
How does the body protect the esophagus cells from the acid?
- reflux of gastric contents into the lower esophagus
- submucosal glands protect the **squamous cell epithelium (because its sensitive to acid)** by secreting mucin and HCO3
41
What is the pathogenesis of reflux esophagitis?
decrease gastric emptying + decrease tone of lower esophageal sphincter + increase in abdominal pressure
42
What are the clinical features of reflux esophagitis?
* **Most frequent is heartburn, dysphagia, and regurgitation of sour-tasting gastric contents**
43
what are the complications that can occur due to reflux esophagitis?
* **ulceration**
* **hematemesis**
* **melena**
* **stricture development**
* **barrett esophagus**
44
What are esophageal varices?
**dilation of veins due to increase pressure at the junction between the portal and systemic venous system**
45
Clinical features of esophageal tumors
**-presents with dysphagia (90%)**
- pain with swallowing (odynophagia)
- prominent weight loss and debilitation due to impaired nutrition and the effects of the tumor itself
46
What causes a poor prognosis with esophageal tumors ?
If the esophgeal tumor is diagnosed early what is the survival rate?
presence of lymph node metastases
5 year survival rate for 80% of patients but if its diagnosis later then there is a less than 25% chance that the patient will make it to 5 years
47
The stomach is divided into four major anatomic regions ?
* **the cardia (where esophagus meets stomach)**
* **fundus (dome shaped)**
* **body and**
* **antrum (gastric outlet so digested contents can go from stomach to duodenum**
48
The antral galnds contain what cells and what is the function of those cells?
* G cells-release gastrin to stimulate luminal acid secretion by parietal cells within the gastric fundus and body
49
Cardia and antrum are lined with what cells that form what?
mucin-secreting foveolar cells that form small glands
50
The well-developed glands of the body and fundus also contain what type of cells that secrete what?
**chief cells that produce and secrete digestive enzymes such as pepsin and chiamosin**
51
Acute Gastiritis is marked by?
**mucosal injury or dysfunction**
52
What are the causes of acute gastritis?
* **NSAIDs**
* **Alcohol**
* stress induced injury
* curling ulcers (occurs after burns)
* portal hypertension
53
What are the symptoms of acute gastritis?
What symptoms can occur in severe cases?
* it can be asymptomatic or it can be variable degrees of epigastric pain, nausea and vomiting
* mucosal erosion, ulceration, hemorrhage, hematemesis, melena, or rarely massive blood loss
54
Acute gastris occurs due to an imbalance of protecting and damaging factors, what are they?
**-Damaging factors**
\>gastric acidity
\>peptic enzymes
**-injury**
\>H. pyloric infection
\>NSAID
\>tobacco
-protective factors
\>surface mucus secretion
\>bicarbonate
55
What is the pathogenesis of acute gastritis?
* Loss of protective mechanism
* NSAID--\> decreased cox--\> degreased PGE2/I2--\> decreased mucosal protection
* H.pylori --\> decrease of bicarbonate
* Hypoexemia and decreased oxygen because of high altitudes can cause it
56
What is the most common cause of chronic gastritis?
What disease can it lead to ?
Most common -H. Pylori (90%), autoimmune gastritis (\<10%), chronic NSAID USE (but its more with acute gastritis)
peptic ulcer disease
57
Pathogenesis of chronic gastritis becuase H. pylori infection?
* H. Pylori uses flagella like tail to burrow into stomach lining --\> inflammation
* **H. pylori can survive harsh acidic environment** (unlike other bacteria) because they can produce **urease** that can neutralize stomach acid
* Urease reacts with urea to form ammonia, which is toxic to human cells
* H. pylori can also cause **overproduction of stomach acid**
58
Virulence factors of H. Pylori
* flagella
* urease
* LPS and outer proteins-adhere to host cells and inflammation
* Exotoxins (vacA)- gastric mucosal injury
* Secretory enzymes -mucinase, protease, lipase (mucosal injury)
* Effectors-host cell growth and apoptosis inhibition
* Type IV secretion system -injection of effectors
59
Peptic ulcer disease is a complication of what disease?
Peptic ulcer disease is associated with ?
- Complication of chronic gastritis
- H.pylori infection, NSAIDs, Cigarette smoking
60
What are the clinical features of peptic ulcer disease?
What complication can occur from this disease?
* epigastric burning
* **Pain tends to occur 1 to 3 hours after meals during the day, is worse at night and is relieved by alkali or food (helps you differiente from colcisitis pain**
* **N**ausea, vomiting, bloating, belching, significant weight loss
-Bleeding, perforation, obstruction
61
What are the most common type of Gastric Polyps?
-Inflammatory and hyperplastic polyps (75%)
62
What is the pathogenesis of Gastric polyps ?
What should be done once the polyp is discovered?
What causes increase in fundus polyps ?why?
H. pylori--\> Chronic gastritis --\> reactive hyperplasia --\> polyps
- If it is greater than 1.5 it should be resected and examined histologically
- ;use of proton pump inhibitor therapy (prilosec, omeperazole, prevacid)
\>b/c it will increase gastrin which will lead to oxynitic gland growth(gastrin secreting gland wont be have to produce more HCL so it will just become bigger)
63
What is the most common maligancy of the stomach ?
-gastric adenocarcinoma (90% of gastric cancers are adenocarcinomas)
\>intestinal type: associedt with environemtn and food factors
\>diffuse type: associated with mutations
64
advanced symptoms of gastric adenocarcinoma
* weight loss
* anorexia
* early satiety (primarily in diffuse cancers)
65
What is the most common cause of intestinal obstruction ?
adhesions
66
What is a hernia?
any weakness or defect in the abdominal wall-permit protrusion of a serosa-lined pouch of peritoneum called hernia sac
67
What is a volvulus?
twisting of bowel
68
What does intussusception mean?
when is it most common?
segment of the intestine constricted by a wave of peristalsis, telescopes into the immediately distal segment
-Most common in children less than 2 years
69
Pathogenesis of Ischemic bowl disease
Hypoperfusion (but basically anything that could block blood flow aka decreasing it )--\> Ischemia --\> hypoxic injury (phase I)--\> reperfusion injury (phase II-damage via ROS)
you can have infarction:
* of mucosal layer
* mural (mucosal + submucosal)
* transmural (all layers are involved)
this starts off the process
70
Ischemic bowel disease is most common around what age?
## Footnote
What are some common symptoms, what can these lead to?
- 70 years of age
- sudden onset of cramping, left lower abdominal pain, a desire to defecate, and bloody diarrhea --\> shock and vascular collaspe
71
What is responsible for causing Infectious enterocolitis?
Pathogenesis?
enterotoxigenic E. Coli
-vibrio cholerae becomes contaminates drinking water and food --\> interferes with the absorptive function of enterocytes, but its **non-invasive** (intestinal cells)--\> leads to cholera
72
Infectious enterocolitis is responsible for?
\>2000 deaths/day among children in developing countries and greater than 10% of all deaths before age 5 world wide
73
what are the symptoms of cholera ?
What is the pathogenesis of the diarrhea caused by cholera?
* **watery diarrhea** (rice water stools; rate- 1 l/hr)
* dehydration
-cholera toxin causes increase in cAMP which causes ion channels to activate causing electrolytes and water to rush outside the cells
74
Campylobacter Enterocolitis is caused by? what is significant about this bacteria?
What can this disease end up resulting in?
* Campylobacter jejuni most common bacterial enteric pathogen in developed countries
* Important cause of travelers diarrhea
- reactive arthritis erythema nodosum and Guillain barré syndrome
75
What are the four major virulence properties of this campylobacter enterocolitis ?
* motility -flagella
* adherence -flagella
* colonization-flagella
* toxin production- cytotoxins
76
What is the most common cause of bloody diarrhea?Why?
* Shigellosis- shigella, secretes shiga toxin which decreases protein synthesis and causes invasion and inflammation
77
Salmonella is caused by?
salmonella can cause?
It posses virulence genes that can ?
* S. typhi - typhoid fever
* S. enteritidis, typherium-non typhoid fever
- food poisoning
- encode a type III secretion system capable of transferring bacterial proteins into M cells and enterocytes
78
Salmonella clinical features
Fever often resolves within 2 days but inflammatory diarrhea can persist for a week
79
Typhoid fever has what two subtypes?
Pathogenesis
Clinical features
- typhi and paratyphi
- s. typhi migrates to blood vessels and lymphatics and cause typhoid nodules and ulcers
**-Rose spots**
**-Extraintestinal complications**
80
Inflammatory bowel disease leads to what two disease
* crohns disease
* ulcerative colitis
81
Crohns disease causes what to develop?
30% of patients with ulcerative colitis end up requiring
- fistulae between loops of bowel
- colectomy because of uncontrolable symptoms
82
Ascaris lumbricoides
girant round worm (1 to 2 feet)
83
Strongyloides
threadworm
84
necator duodenale and ancylostoma duodenale
hook worms
85
enterobius vermicularis
pin worms
86
trichuris trichura
whip worm
87
Viral gastroenteritis is caused by what in adults and what in kids
* adults-norovirus
* kids-rotavirus
88
What is a major problem of pseudomembranous colitis and what is caused by?
* major challenge-recurrent infections
* caused by C. diff
89
Enteropathogenic E. Coli
* important cause of endemic diarheaa particulary in children less than 2 years of age
* P for PEDIACTRIC
90
Enteroinvasive E.Coli do not produce?
toxins they instead invade epithelial cells --\> dysentry
91
Enterotoxigenic E. coli
Its non penetrating instead it produces a heat-stable and labile toxin that leads to --\> Travelers diarrhea
92
Enterohemorrhagic E.coli
secretes shigella like toxin
associated with the consumption of inadequately cooked ground beef
