GI UWorld: Path and Pharm Flashcards
Crohn’s disease: gross appearance and histology
Linear ulcers and normal mucosa interspersed –> cobblestone appearance. Creeping fat.Histo: non-caseating granulomas, lymphoid inflammatory infiltrate (Th1 mediated)
What cell type mediates Crohn’s disease?
Th1
Describe squamous cell carcinoma histology. What is the importance of keratin?
Nests of neoplastic squamous cells with abundant eosinophilic cytoplasm and distinct bordersKeratinization means that the tumor is poorly differentiated –> poor prognosis.
What 3 organisms are most common causes of esophagitis? What patients is this found in?
Found in immunocompromised. Candida albicans, HSV-1, and CMV.
Gross and histologic features: Candida esophagitis
Gross: white pseudomembranesHisto: yeast cells and pseudohyphae that invade mucosal cells
Gross and histologic features: HSV esophagitis
Gross: “punched out” ulcersHisto: eosinophilic intranuclear inclusions in multinuclear squamous cells at margins of ulcers.
Gross and histologic features: CMV esophagitis
Gross: linear ulcerations
Histo: intranuclear and cytoplasmic inclusions
Where is H. pylori found in greatest concentration in the GI tract?
Prepyloric area of the gastric antrum (even if it is a duodenal ulcer)
Presentation of carcinoid syndrome
Dyspnea, wheezing, cutaneous flushing, diarrhea. Maybe right sided valvular disease
Tx of carcinoid syndrome
Resection and somatostatin analogue, aka octreotide (inhibits secretion of many hormones)
Where should you biopsy for Hirshprung’s?
Must go down to the submucosa to see the lack of ganglion cells - mucosa alone is not enough.
Also this is for the constricted portion, not dilated.
Abetalipoproteinemia presentation
Presents in early childhood. Failure to thrive, steatorrhea, malabsorption, acanthocytosis, ataxia, night blindness.
Abetalipoproteinemia: labs and biopsy
Low plasma triglycerides, low cholesterol, no chylomicrons, VLDLs, apoBs. Poor absorption of ADEK.
Classification of adenomatous polyps
Tubular: smaller, pedunculated, dysplastic mucosal cells form tubular-shaped glands.
Villous: larger, sessile, dysplastic epithelial cells form villi-like projections. Velvety or cauliflower like masses. Increased risk of adenocarcinoma.
Difference between erosions and ulcers
Erosions do not fully extend through the muscularis mucosa (but they can reach it)
Ulcers penetrate through the mucosa into submucosa.
What is the first event in the pathogenesis of acute appendicitis?
lumen obstruction
Histology of Crohn’s disease
Non-caseating granulomas, lymphoid aggregates
Multiple hemorrhagic polypoidal lesions, spindle cells with surrounding blood vessel proliferation in the setting of untreated HIV. Dx?
Kaposi’s sarcoma
Kaposi’s sarcoma: colonoscopy findings, biopsy findings, other organ system involvement
Colonoscopy: red/violet, flat maculopapular lesions or hemorrhagic nodules
Biopsy: spindle-shaped tumor cells with small vessel proliferation.
Endothelial malignancy in skin, mouth, GI tract, respiratory tract, associated with HHV-8 and HIV
CMV colonoscopy and biopsy findings
Colonoscopy: multiple ulcers, mucosal erosions
Biopsy: cytomegalic cells with inclusion bodies
Cryptosporidium colonoscopy and biopsy findings
C: nonulcerative inflammation
B: Basophilic clusters on surface of intestinal mucosal cells
Characteristics of colitis-associated colorectal carcinoma
Affects younger patients, multifocal, progresses from flat non-polypoid lesions, mucinous or signet ring histology, early p53 and late APC mutations, disease is dependent on length of colitis (>10 years)
Congenital pyloric stenosis: “olive sized” mass is from:
smooth muscle hypertrophy
Systemic mastocytosis: cause and effects
Mast cell proliferation in marrow and organs.
Syncope, flushing, hypotension, tachycardia, bronchospasm, pruritis.
GI symptoms from increased gastric acid secretion: diarrhea (inactivated pancreatic enzymes), nausea, vomiting, cramps.
Which gastritis is associated with the antrum?
Type B - H. pylori
Differentiate between acute and chronic gastritis
Inflammation
Acute = neutrophil dominant
Chronic = lymphocyte and plasma cell predominant
Presentation of chronic gastritis
epigastric abdominal pain, occasional nausea, not related to food intake, inflammatory infiltrate
Presentation of Crohn’s
Fever, right lower quadrant pain (terminal ileitis), diarrhea, involves GI tract not stomach!
Damage seen in pernicious anemia
Immune mediated destruction of gastric mucosa –> Chronic atrophic gastritis. Loss if IF-secreting cells (B12 deficiency, megaloblastic anemia), lymphocytic and plasma cell infiltration, megaloblastic changes
What stimulus causes parietal cell proliferation?
Gastrin: facilitates HCl secretion, AND has a trophic effect causing proliferation and hyperplasia
Seen in Zollinger-Ellison syndrome
Definitive dx for celiac
Small intestine biopsy
CREST syndrome contains esophageal dysmotility. What is the cause, and what are symptoms?
Fibrous replacement of muscularis –> esophageal dysmotility
Heartburn, dysphagia, regurgitation
Which polyps are likely to undergo malignant transformation
Adenomatous polyps, increased risk with size, villous pattern, and sessile growth.
Others like hyperplastic, lymphoid, harartomatous, lymphoid are not at risk.
What is toxic megacolon? What disease is it associated with? What is typical presentation, and how do you diagnose?
Complete cessation of neuromuscular activity leads to distension and thinning of the walls. Colonoscopy and barium studies are contraindicated because of the risk of perforation - plain X-ray is done instead. Complication of ulcerative colitis. Presents with acute abdomen and shock.
What is a Cushing Ulcer?
Seen in brain injury. Increased intracranial pressure –> Increased vagal stimulation causes increased HCl production, causing acute gastritis. Can occur in duodenum, stomach, or esophagus. Prone to perforation.
Adenoma-carincoma sequence
Normal, APC mutation (increased risk for polyps), K-ras mutation (formation of polyp), p53 mutation, COX-2 overexpresssion, DCC inactiation, methylation abnormalities all lead to cancer.
Aspirin (cox inhibitor) helps fight this!
Insidious development of non-bloody diarrhea, fever, malaise, fistula. Dx?
Crohn’s
How does h. pylori cause gastritis?
Infection leads to decrease number of somatostatin producing cells, which results in higher gastrin levels. Occurs in antrum, can cause duodenal ulcers.
Why do people with Crohn’s get gallstones?
Increased biliary acid wasting. Normally bile acids are recycled in the ileum. Less bile acid in bile –> cholesterol precipitates in gall bladder bile and forms stones
Histologic findings: GERD
Basal zone hyperplasia, elongation of lamina propria papillae, inflammatory cells
Jejunal biopsy shows flattening of mucosa, atrophy of villi, chronic inflammation of lamina propria. Dx?
Celiac sprue
Lab values in alcoholic hepatitis
AST»_space; ALT (ratio greater than 1.5)
Microscopic appearance of carcinoid tumor
Uniform cells in nests or sheets. Minimal to no variation in size or shape. Eosinophilic cytoplasm, oval/round stippled nuclei
What is the central enzyme activation in acute pancreatitis that causes all the other stuff?
Trypsin –> trypsinogen
Most pronounced changes in CF
Respiratory tract (increased viscosity of bronchial secretions, impaired clearance, repeated pulmonary infections). Pancreas (viscous secretions accumulate in duct –> malabsorption and steatorrhea, evenually fibrosis of pancreatic tissue). Intestinal obstruction (meconium ileus)
Where are ulcers not likely to cause malignancy?
Duodenum
Tx of duodenal ulcers
Usually caused by H.pylori –> triple therapy (2 abx and a ppi)
Cause of zenker diverticulum
Cricopharyngeal muscle dysfunction from diminished relaxation of pharyngeal muscle during swallowing. Increased intraluminal pressure causes herniation, forming the diverticulum. Usually elderly pts
Diffuse esophageal spasm
periodic, non-peristaltic contractions of esophagus. Corkscrew esophagus seen on barium swallow. Symptoms are intermittent dysphagia and chest pain, may mimic unstable angina.
Mechanism of polyethylene glycol, similar drugs
Osmotic laxitive. Similar to magnesium hydroxide, magnesium citrate, lactulose.
Diarrhea in Crohn’s
Secretory diarrhea with high electrolyte content
Drug that inhibits gastric acid secretion to ACh, histamine, and gastrin
Proton pump inhibitors (-prazole)
Adenoma carinoma sequence mutations
1) APC
2) K-ras
3) p53
Crohn’s associated with increased activity of which molecule?
NF-kB, which is responsible for cytokine production
Where does iron absorption take place?
Duodenum, proximal jejunum
Treatment for CF
N-acetylcysteine is a mucolytic agent
Supplement pancreatic lipase to improve malabsorption
GI side effect of mu opioids
Contraction of smooth muscle leads to sphincter of Oddi constriction, increases common bile duct pressures, can lead to biliary colic.
Inflammation pattern: Crohn’s vs ulcerative colitis
Crohn’s: transmural inflammation, fistulas, skip lesions
UC: mucosal and submucosal, continuous
Manifestations of adult lead poisoning
Colicky abdominal pain, constipation, headache, blue-ish pigment at gum-tooth line, wrist or foot drop (peripheral neuropathy), microcytic hypochromic anemia (inhibits enzymes needed for heme synthesis)
Lactase deficiency: stool osmotic gap, breath hydrogen content, stool pH, D-xylose absorption
Stool osmotic gap increased, stool pH decreased (bacteria produce H+ when digesting lactose), breath hydrogen increased, D-xylose unchanged (decreased with others i.e. Celiac)
Tx for arsenic poisoning
Demercaprol. Displaces arsenic fro sulfhydryl groups of enzymes
Where is colon cancer most often found?
Rectosigmoid colon. Leads to obstruction symptoms.
Intestinal hypoperfusion/ chronic mesenteric ischemia
With atherosclerosis involving intestinal arteries. Painful, especially after eating when blood needed for digestion. Weight loss common
Hypoperfused areas show mucosal atrophy and loss of villi
Anal fissures: where do they occur, and what are they associated with?
Posterior midline distal to the dentate line
Associated with low fiber diets and constipation
Diarrhea, weight loss, epigastric-region calcifications in chronic alcoholic: dx? Cause of symptoms?
Chronic pancreatitis with pancreatic exocrine insufficiency and malabsorption. Secondary to alcohol-induced protein precipitation in pancreatic ducts.
Most important risk factors for esophageal squamous and adenocarcinoma
Squamous: EtOH, smoking, N-nitroso foods. Irritation from other things less important
Adeno: Barrett’s, GERD, obesity, tobacco.
First step in assessing malabsorption syndromes
Stool stain to look for fat in stool
Diphenoxylate
Opiate anti-diarrhia. Binds to mu-opiate receptors and slows motility. Useful in low doses, combined with atropine to discourage abuse
Tx for secretory diarrhea
Octreotide (somatostatin analog)
Bismuth also works
Most common location for intussusception
ileocecal junction
Presentation of intussusception
colicky, intermittent abdominal pain, nausea, vomiting, currant jelly stools, mass in RL quadrant
Decreased visual acuity and tunnel vision in low light ddx
Toxic retinopathy due to phenothiazines or chloroquine
vitamin a deficiency
Congenital rubella or syphilis
Diabetic retinopathy
How do urinary stones form in Crohn’s?
Disease in terminal ileum –> decreased bile acid recycling –> fat malabsorption –> Ca binds to fat in bowel –> oxalate loses its normal binding partner and is more free to be absorbed –> oxalate stones
Dermatitis herpetiformis: associated with what GI disease
Autoimmune disorder associated with celiac. papulovesicular skin rash, small vesicles on extensor surfces. symmetric and pruritic. IgA deposition at tips of dermal papillae
How does Shigella get taken up?
Specific for M-cells at base of villi within Peyer’s patch of ileum. M-cells are antigen-sampling cells. Shigella lyses endosome, multiplies, and spreads to other epithelial cells causing cell death and ulceration with hemorrhage and diarrhea
Lactase deficiency histology
Normal intestinal mucosa
How do right and left colon cancer present?
R: systemic symptoms, anemia
L: obstruction symptoms
Recurrent, grossly-bloody stool associated with abdominal discomfort and low grade fever dx?
ulcerative colitis
Tenesmus and thin stool dx
Space-occupying lesion of rectum, often presentation of rectal adenocarcinoma
Duodenal ulcer found in distal duodenum (or other atypical location)
Zollinger-Ellison syndrome, caused by gastrin-secreting tumors of pancreas or duodenum
What is PAS staining useful for?
Highlighting polysaccharaides of fungal cell wall, mucosubstances secreted by epithelia, basement membranes.
When used with diastase, it highlights glycoprotein in cell walls that are diastaste resistant like Whipple disease.
Transmural inflammation in Crohn’s causes
Strictures: chronic inflammation causes edema, fibrosis –> narrowing of lumen
Fistula: inflammation and necrosis of wall cause ulcer formation, which penetrate wall to form fistulae
