P- Small and Large Intestines Flashcards
What are the layers of the small bowel from the lumen out?
- mucosa
- lamina propria
- muscularis mucosa
- submucosa
- muscularis propria
- serosa
Describe the mucosa of the small bowel.
It consists of crypts and villi line by simple columnar epithelium.
the villi is: enterocytes(absorptive), Goblet cells (mucus), and enteroedocrine
the crypts are Paneth cells (secrete lysozomal enzymes and factors) and stem cells
What are the 3 sections of the small intestine and what are the distinguishing features of each part?
- Duodenum - Brunner’s glands (submucousal glands that secrete bicarb, pepsinogen, glycoproteins)
- Jejunum (no special features. longest part)
- Ileum - Peyer’s patches - increased mucosal lymphoid tissue which clusters into nodules
What are the layers of the colon and rectum from lumen out?
Mucosa Lamina Propria Muscularis mucosa submucosa muscularis propria serosa
Describe the mucosa of the colon and rectum.
The absorptive simple columnar epithelium has crypts and glands arranged in parallel in the lamina propria. There are no VILLI.
The cells of epithelium are :endocrine, Goblet cells, undifferentiated stem cells and columnar cells
Describe the proliferative zone of the colon mucosa.
It is located in the bottom of the crypts and scattered mitotic figures go 1/3 to 1/2 up the crypt.
As the cells move up the crypt they:
- increase cytoplasm
- decrease N/C ratio
- maintain proper polarity (nucleus at the base of the cell)
Ischemic injury can occur anywhere in the GI tract, but what are the 2 places it occurs most frequently?
It occurs most frequently at watershed areas where the collaterals are small and narrow.
- rectosigmoid junction - terminal branches of IMA
- ** splenic flexure - terminal branches of SMA
Why is the small intestine much more vulnerable to ischemia than the colon?
Because the colon can get some accessory supply and drainage from the retroperitoneal portions (ascending/descending)
What typically causes acute enterocolitis? What kind of infarct would occur?
What typically causes chronic enterocolitis?
Acute- thrombus/embolism in the celiac, SMA or IMA which can cause hemorrhagic infarct {hemorrhagic infarct is seen in organs with dual blood supply}
Chronic- gradual build up of atherosclerosis in vessels supplying the bowel
What patient population is most likely to be affected by ischemic enterocolitis?
Incidence increases with:
- age
- cardiovascular disease
- DM
What are the 3 major variables in ischemic bowel disease?
- severity of the vascular compromise
- period over which the compromise developed
- vessel involved
Why are the splenic flexure and rectosigmoid junction considered “watershed areas”?
Splenic flexure- termination of SMA, IMA
Rectosigmoid- termination of IMA, pudendal, iliac
Because the blood supply terminates here, these areas are most suceptible to injury by hypotension or hypoxemia
In addition to the major arteries to the intestines, what other blood supply is involved in intestinal circulation?
Intestinal capillaries run from the crypts alongside the glands to the surface and empty into postcapillary venules.
This protects the stem cells of the crypt so they can repopulate the surface.
The epithelium is more susceptible to ischemic injury because they are last to receive blood supply
What is a morphological signature of ischemic intestinal disease?
- surface epithelium atropy
- sloughing/necrosis of epithelium
- normal or hyperproliferative crypts
What are predisposing conditions to bowel infarcts due to arterial thrombus?
- atherosclerosis
- vasculitis
- dissecting aneurysm
- hypercoagulable states
- angiography procedures/surgery accidents
What are predisposing conditions to bowel infarcts due to arterial embolism?
- cardiac vegetations
- angiographic procedures
- aortic atheroembolism
What are predisposing conditions to bowel infarcts related to venous thrombosis?
- hypercoagulable state
- sepsis
- post-op
- vascular-invasive cancer (hepatocellular carcinoma)
- cirrhosis
- abdominal trauma
What are predisposing factors to bowel infarct related to NON-occlusive ischemia?
Anything that gives low flow
- cardiac failure
- shock
- dehydration
- vasoconstrictive drugs (cocaine)
What is the difference between a mucosal, mural and transmural infarct?
Mucosal - does not go below the muscularis mucosa (due to acute/chronic hypoperfusion)
Mural- mucosa AND submucosa (due to acute/chronic hypoperfusion)
Transmural- all layers of the wall (due to occlusion of major mesenteric artery)
Describe what you would see with transmural infarct due to an acute arterial obstruction.
What is occuring in the mucosal layer? Muscularis propria? Serosa?
- sharp demarcation between normal/ ischemic bowel
- infected bowel is intensely congested, purple/red and hemorrhagic
- wall becomes thick, edematous, rubbery
- Coag necrosis of muscularis propria in 1-4 days with the potential for perforation
- serositis- purulent exudate and fibrin deposition
A patient presents with sudden, severe abdominal pain and tenderness. They have nausea, vomiting, melena. They are progressing to shock/vascular collapse. Peristaltic sounds have diminished and they have rigidity of the abdomen. What are 4 potential things this could be?
- acute transmural infarction
- acute appendicitis
- perforated ulcer
- acute cholecystitis
Describe the difference in margins between arterial occlusion and venous occlusion causing transmural infarction of the bowel.
Arterial - sharply defined borders of ischemic area
Venous- margins are less distinct
Describe the lesions associated with mucosal and mural infarcts. What layers are involved? What parts of the bowel? What forms at the edges of the segments?
They can affect anywhere from the stomach to the anus.
The lesions can be continuous but are most often patchy and segmental.
Mucosa- hemorrhagic and ulcerated
Bowel wall is thickened with edema and can involve just the mucosa or extend down into the submucosa.
Serosa hemorrhage and serositis are ABSENT.
At the edges of the affected segments, pseudomembranes form. They are necro-inflammatory exudates overlying the mucosa.
As long as the ______________ is spared, mucosal and mural infarct lesions are completely reversible.
Muscularis propria
What is the difference between congenital and acquired diverticulosis? What are examples of each?
- Congenital -involves all three layers of bowel INCLUDING the muscle
- Meckel diverticulum
- normal appendix - Acquired- lack or have attenuated muscularis propria due to focal weakness or increased intraluminal pressure (80% in the sigmoid colon)
- Zenker diverticulum
- colonic diverticulum
What are the 2 influences that lead to the genesis of a diverticula?
- exaggerated peristaltic contractions (elevated intraluminal pressure)
- inherent anatomy - incomplete longitudinal muscle layer gathered in tenia coli and neurovascular bundles penetrating the inner circular muscle alongside tenia coli
Western diets lead to diverticula because the low fiber diet increased transit time, thus increasing #1)
Describe the gross morphology of diverticulosis.
- multiple small, flask-like envaginations along the tenia coli filled with mucus or stool
- bulging into the serosa or omental appendices
- thickened circular muscle of the colon with “accordion” mucosal folds
Describe diverticulosis microscopically?
there will be an absence of muscle except for some random bundles of muscularis mucosa.
Inflammation may be present if there is obstruction or perforation. This can extend into the pericolic fat and give the appearance of colon carcinoma
A patient presents with cramping, discomfort, sensation of the inability to completely empty rectum. They have alternating constipation and diarrhea. What are you suspicious of and what are some of the complications associated?
Diverticulosis.
Complications:
- diverticulitis - inflammation/infection
- peritonitis
- hemorrhage
- perforation with abscess resembling a mass or forming a sinus tract
- adhesions
- obstruction
- fistula to bowel/bladder
What is treatment for diverticula?
- High fiber diet
- if diverticulitis–> antibiotics
- if peritonitis/perforation–> resection
What are 80% of SBO due to?
Mechanical obstructions due to:
- adhesions
- hernia
- volvulus
- itussusception
What is the leading cause of SBO in industrialized nations? What is most closely associated with the formation?
Post-op adhesions- fibrous bridges between bowel loops when peritonitis (due to surgery, infection, endometriosis) heals.
Surgeries most closely related with formation are:
- appendectomy
- colorectal surgery
- gynocologic procedures
- GI precedures
What is the most common form of SBO associated with post-op adhesions? How does it occur?
It is most associated with strangulated SBO and it occurs when distended loops of bowel twist on the mesenteric pedicle causing arterial occlusion–> bowel ischemia/necrosis.
What are hernias? What are the locations where they are most likely to occur? When do they become medical emergencies?
A hernia is when the contents of a body cavity bulge out of the area where they should be contained. Usually it is bowel or abdominal fatty tissue.
Usually they are asymptomatic, but can cause emergency if they get “incarcerated” and strangulated.
Usual sites:
- inguinal
- femoral
- umbilicus
- surgical scars (incisional)
In children, intussusception is a common cause of abdominal pain. In adults, what does it point to?
Intraluminal tumor
What is a volvulus?
It is when the bowel twists completely on its mesenteric attachment site
What is the pathological process for SBO?
1. venous drainage is impaired if the process continues 2. arterial inflow is cut off 3. infarction ensues 4. mucosa gets ischemic first and sloughs off leading to currant jelly stool (blood, mucus, mucosa)
If untreated
5. transmural gangrene and perforation
When must surgery be done for a strangulated bowel to drastically reduce the mortality rate?
36 hours or less
A patient presents with abdominal pain and nausea. Two days ago he was having diarrhea, but now he is constipated. He is developing fever and tachychardia.
When ascertaining his history you discover he has had prior appendectomy. What are you concerned about?
A small bowel obstruction- and you should be exceptionally concerned because fever/tachycardia is an indication of possible strangulation
What is Hirschprung disease?
Who does it affect? What is treatment?
It is congenital aganglionic megacolon.
A segment of the colon (short segment disease) or the entire colon (long segment disease) is missing the myenteric (aucher) and submucousal (meissners) plexuses.
The portion of the colon missing innervation is narrowed and the proximal portion is dilated .
Because it is congenital it is frequently seen in infants and children.
Infants- alternating diarrhea/constipation
Children- constipation
Treatment is surgery to remove the aganglionic portion of the colon
What genes are though to be mutated in Hirschprung disease? What is the penetrance?
It is thought to be a mutation in the RET gene that inactivates RET receptor kinase activity.
RET promotes survival of neurites and provides directions to migrating neural crest cells.
The penetrance is variable and dependent on environmental factors.
What is the epidemiology of Hirshprung?
Are male or female children more affected?
1/5000 live births
4 to 1 male to female predominance but females more freq get long segment disease
What is the official definition of diarrhea?
Increased stool weight of 250-300 g/day but a good working definition is:
3 or more watery stools/day Or a definite decrease in consistency of increase in frequency
Who is most negatively affected by diarrheal disease?
It is the leading cause of death in children in developing countries and is greatest in children under 1
This is because diarrhea can lead to dehydration and hypokalemia
What is the basic pathogenesis of all forms of diarrhea?
There is a reversal of normal net absorptive processes of water and electrolytes to secretion.
- osmotic force to drive water into the gut
- active secretory state induced by enterocytes
What is the difference between acute diarrhea and chronic diarrhea in terms of time frame? causes?
Acute -lasts days to a week.
Infectious causes - virus, parasite, bacterial
Non-infectious- IBS, drugs, food, thyrotoxicosis, carcinoid
Chronic- lasts atleast 3 weeks
IBS, IBD (Crohn’s, ulcerative colitis), intestinal bacterial overgrowth, chronic bacteria (Giardia), colon cancer, fat/carb malabsorption, lax abuse, endocrine (addison’s )
A patient presents with abdominal bloating/cramps. There is increased borborygmi (rumbling) and abdominal pain. The stool is loose and watery. They have increased sense of urgency for the restroom and nausea/vomiting. Is this likely to be uncomplicated or complicated diarrhea?
uncomplicated
A patient presents with blood, mucus and undigested food in the stool. They have weight loss, fever, electrolyte loss, dehydration and vascular collapse. Is this uncomplicated or complicated diarrhea?
complicated
What is the mechanism by which secretory diarrhea occurs?
Does it abate with fasting?
What are common causes?
In secretory diarrhea, there is prolonged increase in enterocyte levels of cAMP which secretes Cl and water follows. This occurs by increased activation of adenyl cyclase.
This form of diarrhea persists with fasting!!
Causes:
vibrio cholerae, E. coli heat labile toxin, laxatives, hormone-producing tumors, drugs, metals
What is the mechanism by which osmotic diarrhea occurs?
Does it abate by fasting?
What are the 2 usual causes?
If there is excessive solute retained in the intestinal lumen water will not be absorbed–> osmotic diarrhea.
This will abate by fasting.
It usually occurs by:
- ingestion of a poorly absorbed substrate (carbs-mannitol, sorbitol), epson salts, MgOH2
- malabsorption - ex. lactose intolerance
What is the mechanism of exudative diarrhea?
How does it have components of secretory and osmotic diarrhea?
Does it abate with fasting?
What are the usual causes?
Bacterial or viral infection:
1. increase serum/blood exudation into the lumen with WBC inciting cytokines to increase secretion (secretory) and leukocytes using ROS to destroy cells and grow new ones that are deficient in brush border enzymes/transporters (malabsorption/osmotic)
- destroy enterocytes so there is reduce absorption of water and solutes
It does NOT abate with fasting
Describe the pathology of malabsorption diarrhea.
It can be just one nutrient (lactase deficiency–> lactose diarrhea)
Or it can be diffuse disorder (celiac sprue) where there is a general malabsorption which increases stool output and causes high volume diarrhea.
It will abate with fasting
What are the functions of the small bowel? How does this contribute to the symptoms of diarrheal disease?
It absorbs nutrients and secretes enzymes and fluid. Dysregulation due to infection can lead to:
large volume diarrhea/ NO fever/NO blood or inflammatory cells
abdominal cramping
bloating, gas, weight loss
What are the functions of the colon? How does this contribute to the symptoms of diarrheal disease?
It absorbs water and electrolytes (Na) and secretes K and Cl. Dysregulation leads to:
Frequent, small volume diarrhea/FEVER/blood and inflammatory cells
Viruses are usually the cause of acute infectious gastroenteritis in the US, however, what are the top 5 bacterial/protozoa causes?
- salmonella
- camylobacter
- shigella
- E. coli O157:H7
- cryptosporidium
