GI Flashcards
1
Q
Malabsorption syndromes (5)
A
- Celiace dz
- villous atrophy/flat-blunting of villi
- crypt hyperplasia
- intraepithelial lymphocyte infiltration
- dermatitis herpetiformis
- disaccharidase deficiency
- NML villi
- osmotic diarrhea
- pancreatic insufficiency
- d-xylose absorption test: nml
- d/t CF, obstructing ca, chronic pancreatitis
- tropical sprue
- responds to AB
- visitor to the tropics!!!
- whipple dz
- PAS +
- CAN:
- cardiac symptoms
- arthralgias
- neuro s/s
2
Q
three phases of the stimulation of acid secretion in tummy
A
- cephalic-cholinergic and vagal
- gastric-
- intestinal
3
Q
Physio of acute viral hepatitis
A
- acute viral hep causes hepatocyte APOPTOSIS and NECROSIS
- APOPTOTIC hepatocytes do the following:
- shrink
- undergo nuclear fragmentation
- become intensely EOS-inophilic
- APOPTOTIC hepatocytes…bodybodybody rockin everywhere
- aka ACIDOPHILIC BODIES
- aka COUNCILMAN BODIES
- aka APOPTOTIC BODIES
4
Q
Tropheryma whippelii classic histo
A
- small intestine mucosa w/ enlarged, foamy macrophages
- mac packed with BOTH:
- rod-shaped bacilli
- PAS (+), diastase-resistant granules
- (granules consist of lysosomes and partially digested bacteria)
5
Q
Whats up with amino-salicylic acid derivs?
A
use them to treat UC!!!
6
Q
ZES CP
A
- distal duodenal ulcer
- high-nml gastrin levels that rise in resp to secretin admin
- also: multuple ulcers and ulcers refractory to therapy
- also also: diarrhea, b/c pancreatic/intestinal enzymes are inactivated by gastric acid=cant digest nutrients properly
- cause: gastrin-secreting tumors (gastrinomas)
- often malig
- location: small intestine or pancreas
- gastrin:
- causes parietal cell hyperplasia
- stim gastric acid secretion=peptic ulcers + heartburn
7
Q
proximal duodenal ulcers vs. ulcers beyond the duodenal bulb
A
- most prox caused by H pylori or NSAID
- most beyond bulb: ZES
8
Q
acute appendicitis termed
A
- periumbilical (visceral) pain that migrates to the RLQ
- NVDF
- first event in pathogenesis: OBSTRUCTION OF LUMEN of the appendix
- caused by: fecaliths (mc), hyperplastic lymphoid follicles, foreign bodies, tumors, nematodies
- retained mucus causes appendicular wall to distend–>impairs venous outflow=hypoxia=ischemia=bacterial invasion
- bad stuff: necrosis of the wall with rupture…inflamm fluid and bacteral contents spill into the peritoneal cavity=peitonnitis
- peak incidence: kids 6-10, but happen in ALL age grous
9
Q
pigmented stones: brown vs. black (both assoc with acute calculous cholecystitis)
A
- brown: d/t biliary tract infections (microbes producing beta-glucuronidases)
- black: in the setting of:
- chronic hemolytic anemia (sickle cell dz)
- INC enterohepatic cycling of bilirubin (Crohn dz)
10
Q
acute acalculous cholecystitis
A
- acute inflamm of GB. SANS gall-stones
- who? CRITICALLY ILL pts (sepsis, severe burns, trauma, IC)
- prog: HIGH mortality
- PP: secondary to GB stasis and ISCHEMIA…cause inflamm of and injury to the GB wall
11
Q
acute acalculous cholecystitis CP
A
- fever, RUQ pain, Murphys (+), leukocytosis, mild LFT elevations
- PE: jaundice and plpable RUQ mass
- diagnostic study: US
12
Q
chronic cholecystitis termed
A
- PP: repeated mild attacks of acute cholecystitis
- gross: thikening of GB wall
- US: shrunken, fibrosed GB
- chronic may lead to porcelain GB, with INC r.o GB carcinoma
13
Q
Hi, my name is proximal colon…
A
water and electrolyte absorption
14
Q
Hi, my name is distal colon…
A
i store feces
15
Q
Hi, my name is ileum..
A
i absorb bile salts and Vit B12
