Flashcards in Module 2: GI: Intestinal Obstruction, Hirsch Disease, Diverticulosis, Pseudo, Amoebic and Ischemic Bowel Deck (35):
Starting off intestinal obstruction is more common in small or large bowel?
There are numerous causes for small bowel obstruction. What are the extramural/mechanical causes (most common)?
--Peritoneal disease/adhesions from surgery -- bands of adhesive tissue
--Intussusception --telescoping of proximal bowel segment into distal
--Volvulus: twisting of the bowel loop
What are the luminal causes for small bowel obstructions?
Muconium ileus in infants with CF
Gallstone ileus: stone lodges in the terminal ileum often forms a cholecystoduodenal fistula
What are the intramural (inside the wall) causes for small bowel obstruction?
--Polypoid or infiltrative neoplasms
Finally what are the pseudo-obstruction causes for small bowel obstruction?
Failure of propulsion
Paralytic ileus following peritoneal irritation (surgery)
--bowel not moving but nothing is really blocking it, something is wrong with the SM
Now moving on to the large intestine. The first pathology to be discussed is Hirschsprung's Disease. What is the presentation and what population is it found in?
Most common cause of congenital intestinal obstruction
--delayed passage of meconium in newborn, constipation, abdominal distention
--more common in males with down syndrome
What is the pathogenesis for Hirschsprung's Disease?
Defect in migration and survival of neuroblasts -- congenital absence of ganglion cells in submucosal and myenteric plexus --- functional obstruction --- dilatation and hypertrophy proximal to affected segment (congenital megacolon)
--rectum is always affected
What is the investigation for Hirschsprungs Disease and Complications?
Investigation: rectal biopsy with Calretinin stain
Complications; enterocolitis, perforation --- peritonitis
Moving on to another important topic in regards to large intestine pathology is Diverticulosis. What is diverticulosis, etiology and what part of the population do we see it in?
Population: common in Western World (50% of individuals over 60 years old) men
Diverticulosis: Acquired pseudo-diverticulum: involves mucosa and a small amount of submucosa (not the entire bowel wall)
Etiology: is idopathic but predisposing factors: elderly on a low fiber diet or long standing history of constipation
--associated with AD polycystic kidney disease!!!!
What is the pathogenesis for Diverticulosis?
Decreased dietary fiber --- sustained bowel contractions and increased intraluminal pressure --- herniation of the colonic wall at sites of focal defects
What is the presentation for a patient with Diverticulosis?
--incidental finding of colonoscopy
What is the most common location for Diverticulosis?
Sigmoid colon (flask like structures)
--hence why when it turns into diverticulitis there is LLQ pain.
What are the complications of Diverticulosis?
1. Bleed -- bright red blood in stool (hematochesia)
2. Fistula formation
--enterocolonic fistula (small bowel and colon)
--colovesicle fistula (colon and bladder), patinet will have gas bubbles in urine called pneumoaturia and fecal matter in the urine, fecaluria, and this is why patients will get recurrent UTIs (E.coli)
3. Fecal impaction leads to acute diverticulitis
--LLQ pain , fever, WBCs elevated (neutrophils)
4. Diverticulitis abscess: collection of pus with SPIKING fevers
5. Never turns into cancer
6. Chronic diverticulitis: stricture formation and obstruction
What are the complications associated with recurrent acute diverticulitis?
Turns into chronic inflammation forming fibrosis
--stricture formation which leads to intestinal obstruction to perforation to peritonitis to E. coil sepsis to DIC
Moving on to the next large intestine pathology is pseudomembrane colitis. What is the etiology for this?
Gram Positive Clostridium Difficile (part of normal flora) after long standing broad spectrum abx use
--seen in hospitalized patients
What is the pathogenesis for pseudomembrane colitis?
--denuded (Stripped) surface epithelium and superficially damaged crypts distended by macrophages exudate erupt forming a mushrooming cloud
--they coalesce to produce pseudomembrane (fibrin, PMNs and necrotic debris)
What is the most common location for pseudomembrane colitis?
How do patients present with pseudomembrane colitis?
Massive Bloody Diarrhea
Mucoid (Secretory) diarrhea: lose potassium and albumin anytime you have this kind of diarrhea
Describe the images of slide 12.
Gross: Yellow pseudomembrane on the colon
Histology: Huge pseudomembrane as the top layer of the mucosa (Which destroyed the surface epithelium and superficial crypts)
What is the best investigations for pseudomembrane colitis?
Stool assay for exotoxin (gram positive)
CBC: high neutrophilia
Hypokalemia: mucoid diarrhea
Hypoalbuminemia: mucoid diarrhea
What are the complications associated with pseudomembrane colitis?
1. Toxic Megacolon: damaged mucosa ---- exposes the submucosa plexus called Meisner's Plexus --- leads to a lack of peristalsis --- leads to back up of intestinal contents ---- colon becomes toxic and big --- and this can perforate ---- peritonitis --- sepsis ---DIC
2. Bleeding can lead to hypovolemic shock ---- leads to acute tubular necrosis (tubules are most sensitive to ischemia) --- renal failure
3. Subendocardial MI from the hypovolemic shock
4. Hypokalemia ---- cardiac arrhythmia's
5. Hypokalemia ---- nerve condition problems
6. Hypoalbuminemia --- leads to peripheral edema due to losing oncotic pressure
What is the treatment for pseudomembrane colitis?
Why is a colonoscopy not the best investigation for pseudomembrane colitis?
You should never do a colonoscopy on a patient with colitis they can perforate
The next colitis to mention is Amoebic Colitis. What is the etiology for this?
Parasitic infection with Entamoeba Histolytica acquired via fecal-oral route (ingesting the cyst)
--stem will say that patient has travel history to the tropics
What is the pathogenesis for Amoebic Colitis?
Infection with cyst (4 nuclei) --- transform to trophozoite (1 nucleus + RBC via erythrophagocytosis)
--trophozoite form is damaging
--cyst form in infective
What do you see on histopathology in patients with Amoebic Colitis? (PIC13)
Flask Shaped Ulcer in the colon
-goes into the submucosa causing colitis
Pic to right shows the erythrophagocytosis (Trophozoites and RBC)
How do patients with Amoebic Colitis present?
--very similar symptoms as pseudomembrane colitis except with this condition the stem will say travel
What investigations are done for Amoebic Colitis?
Stool Assay for cyst/trophozoite: best investigation
4 nuclei in the cyst, 1 nucleus in the trophozoite (Erythrophagocytosis)
What are the complications in Amoebic Colitis?
1. Perforation ---- peritonitis ---- sepsis ---DIC
2. Organism travels from GI to the liver via the portal vein because the liver drains GI then to lung and brain all forming abscesses in the liver, lung and brain (know order)
----organism is atypical so we get PMNs and eosinophils
Now moving onto Ischemic Bowel Disease. What is the etiology for this ?
Volvulus, intussusception in children
Atherosclerotic plaques with superimposed thrombosis
Systemic Embolus from left mural thrombosis
--2months after an MI
PAN vasculitis (4th most common site): transmural
Hypercoaguable states (factor V laden, protein C and S deficiencies) --nephrotic syndromes
PNH (platelet dysfunction)
Hypovolemic shock (mucosa is infected because it is the last place to get blood): most common cause
What is the presentation for ischemic bowel disease?
Decrease bowel sounds
Lower Abdominal Pain
--pain after eating due to decreased blood flow due to atherosclerosis
High WBCs (PNMS are elevated --- neutrophilia)
What investigations are done for ischemic bowel disease/
Angiogram --- confirm ---- surgical emergency for laparotomy
Biopsy: coagulative necrosis
What are the complications for ischemic bowel disease?
Perforation --- peritonitis --- sepsis ---DIC
Finally lets touch on Chronic Ischemic Colitis. What is the pathogenesis?
Chronic Inflammation and fibrosis ---- stricture formation or perforation