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Flashcards in Pathology Deck (65)
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What are the criteria for determining the malignant potential of adenomatous polyps?

1. degree of dysplasia
2. villous adenomas more likely to be malignant than tubular
3. larger size more likely to be malignant
(4. PATHOMA: sessile/grows against wall more likely to be malignant than pedunculated/grows on a stalk)


Describe these types of non-neoplastic polyps:
- hyperplastic
- hamartomatous
- inflammatory
- lymphoid

Hyperplastic - hyperplasia of glands, most common
classically show a serrated/saw-tooth appearance, usually left-sided

Hamartomatous - sporadic or in Peutz-Jeghers syndrome or juvenile polyposis

Inflammatory - ulcerative colitis and Crohn disease; composed of regenerating intestinal mucosa

Lymphoid - found in children; intestinal mucosa infiltrated with lymphocytes


Nephrolithiasis in Crohn disease - what type of stones? Mechanism?

Calcium oxalate stones

Impaired bile acid absorption in the terminal ileum leads to loss of bile acids in the feces and subsequent fat malabsorption. Excess lipids in the lumen bind calcium ions and these soap complexes are then also excreted in feces. Oxalate normally binds calcium ions to form an unabsorbable complex for excretion, but with calcium bound to lipids, free oxalate is absorbed to form stones.

Thus oxalate normally is NOT absorbed much, but the inflammation associated with Crohn's increases the uptake of oxalate, leading to stone formation.


IBD with:
- crypt abscesses filled with neutrophils?
- lymphoid aggregates with granulomas?

Location of each?
Extent of inflammation?
Which is associated with P-ANCA?

Ulcerative colitis = crypt abscesses filled with neutrophils
- begins in rectum and extends proximally up to cecum, continuous
- mucosal and submucosal ulcers
- associated with P-ANCA positivity

Crohn's disease = lymphoid aggregates with granulomas
- most commonly in terminal ileum (anywhere from mouth to anus), skip lesions
- fill-thickness/wall inflammation with knife-like fissures


What are the layers of the intestinal wall? Where is the myenteric plexus? The submucosal plexus?

Muscularis propria (inner circular and outer longitudinal muscle layers)

Myenteric/Auerbach's plexus is between the inner circular and outer longitudinal muscle layers of the muscularis propria (regulates motility).

Submucosal/Meissner's plexus is located in the submucosa (regulates blood flow, secretions, and absorption).


How to diagnose Hirschprung's disease?

Absence of both myenteric and submucosal autonomic plexi.

Rectal suction biopsy (not just standard mucosal biopsy) needed to get a piece of the submucosa, the most superficial layer in which an absence of ganglion cells can be seen.

Want a biopsy from the narrowed area (where absence of ganglion cells will be found) rather than dilated/normal regions.


Alternating constipation and non-bloody diarrhea with fistula?

Crohn's disease
lesions affect the entire thickness of the bowel wall, creating risk of fistula development (due to wall rupture)

Irritable bowel syndrome (IBS) is NOT associated with fistulas.


Longitudinal GE junction tears in an alcoholic vomiting?

Mallory-Weiss syndrome
due to increased intraabdominal and intraluminal gastric pressure due to abdominal straining (retching or vomiting).


What is a hiatal hernia and what are its associations?

herniation of the upper part of the stomach into the thorax

increased risk for GERD and for Mallory-Weiss syndrome


Celiac disease - what are the lab findings and how is it diagnosed?

Autoantibodies (very sensitive and specific):
- IgA against tissue transglutaminase
- IgA against endomysium
- IgA against gliadin
- IgG: in pts with IgA deficiency (associated with celiac disease), IgG levels useful

Confirmatory diagnosis:
Small intestinal biopsy
- flattening of the mucosa with loss of villi
- chronic inflammatory infiltration of the lamina propria
Most pronounced changes in duodenum and proximal jejunum because higher concentration of gluten in these regions.


What stain is used to identify Tropheryma whippelii in the lamina propria of the small bowel? What does this stain detect?

Period acid-Schiff (PAS) stain
detects polysaccharides (glycogen) and mucosubstances (glycoproteins, glycolipids, mucins)

Glycoprotein in the cell walls of T. whippelii colors magenta with PAS.


Epigastric pain that worsens after meals leading to weight loss in pt with HTN, hyperlipidemia, and history or coronary artery disease?

Chronic mesenteric ischemia - generalized atherosclerosis that involves the intestinal arteries

Bowel suffers from diminished blood supply, particularly after meals when there is more demand.


Papulovesicular skin rash and periodic abdominal discomfort/diarrhea? Mechanism?

Dermatitis herpatiformis (small vesicles that occur symmetrically on extensor surfaces that are very pruritic)
associated with celiac disease

Immunofluorescence reveals IgA deposits at the tips of the dermal papillae.


Features of colorectal carcinoma associated with ulcerative colitis? What factors increase risk in these pts?

unlike sporadic colorectal cancer, colitis-associated carcinomas:
- more likely to arise from NON-polypoid dysplastic lesions
- multifocal in nature
- develop early p53 mutations and late APC mutations
- higher histological grade

Increased risk with pt history of >10 years and greater extent of colonic involvement (pancolitis)


Carcinoid tumor diagnosis? Treatment?

Increased level of 5-HIAA in urine is diagnostic

- surgical excision of tumor
- for disseminated disease, octreotide (somatostatin analog)

Octreotide acts on somatostatin receptors and inhibits secretion of many hormones and hormone-like substances.


Where is the most common site in the GI for a carcinoid tumor? What tumor marker is used?
When do symptoms of serotonin syndrome begin to manifest?
What are the effects on the heart and why?

small bowel
chromogranin positive (neurosecretory granules of tumor cells)

Metastasis of carcinoid tumor to the liver allows serotonin syndrome to manifest by bypassing liver metabolism. In GI, serotonin goes through portal circulation and MAO in liver degrades serotonin to 5-HIAA before getting systemic.

Right-heart valvular fibrosis (increased collagen) leading to tricuspid regurgitation and pulmonary valve stenosis.
Left-sided lesions not seen because MAO in the lung metabolizes serotonin before it reaches that side.


What does squamous cell carcinoma of the esophagus consist of? Where in the esophagus is it located? Major risk factors?

solid nests of neoplastic squamous cells with abundant eosinophilic cytoplasm and distinct borders (areas of keratinization may be seen = white blobs = well-differentiated)

Upper 2/3 of esophagus most common

most common causes/risk factors = alcohol and tobacco
but any irritation to the esophagus increases risk


Mechanism of H.pylori-induced duodenal ulcers vs. gastric ulcers?

duodenal ulcers:
decrease in somatostatin-secreting cells in gastric mucosa leading to unchecked gastrin production

gastric ulcers:
destruction of local mucosal layer from bacteria presence and inflammatory response (increased acid not required)


Describe Virchow's node, Sister Mary Joseph nodule, and Krukenberg tumor. Associated with?

Virchow's node: left supraclavicular node (drains stomach)

Sister Mary Joseph nodule: sucutaneous mass in the periumbilical region

Krukenberg tumor: mucin-producing, signet-ring neoplastic cells in ovarian stroma

All indicate metastasis of gastric cancer.


How does Shigella gain access to the GI mucosa?

invades the M cells in Peyer's patches of the ileum through endocytosis
then lyses endosome, multiplies, and spreads laterally into epithelial cells


How do right-sided colon cancers present? Left-sided?

Right-sided: grows as exophytic/raised masses leading to blood loss; larger caliber than left so no obstruction
- iron deficiency anemia (fatigue and pallor) from blood loss
- anorexia, malaise, weight loss

Left-sided: infiltrate intestinal wall and encircle lumen; present with symptoms of partial obstruction
- decreased stool caliber, constipation
- cramping abdominal pain and distention
- nausea and vomiting


Curling ulcer? Cushing ulcer?

Curling ulcers - arise in proximal duodenum in association with severe trauma or burns

Cushing ulcers - arise in the esophagus, stomach, or duodenum in pts with high intracranial pressure
Increased intracranial pressure directly stimulates vagus nerve leading to hypersecretion of gastric acid.

Both are stress-induced acute gastric mucosal defects.


Obstructive jaundice with enlarged but nontender gallbladder? Risk factors?

Courvoisier sign
indicates adenocarcinoma at head of pancreas compressing bile duct
(tumors at body and tail do not obstruct common bile duct and do not produce symptoms until they invade the splanchnic plexus)

Pancreatic cancer risk factors:
- smoking (most important environmental)
- age
- diabetes
- chronic pancreatitis
- genetic predisposition (hereditary pancreatitis, MEN syndromes, FAP, HNCC, etc.)


Obstructive jaundice signs?

dark urine, pale stools, pruritis


Abdominal pain with white chalky lesions in mesentery (fat cell destruction and calcium deposition)? What is the process responsible for these findings?

Acute pancreatitis
pancreas is edematous with focal areas of fat necrosis, calcium deposition, and interstitial edema

- duct obstruction leads to stasis of pancreatic secretions
- lipase (does not need activation) digests adipose cells
- free fatty acids bind calcium ions to precipitates as insoluble calcium salts (white, chalky deposits)
- focal necrosis and Ca2+ precipitation induce inflammatory rxn
(acute interstitial pancreatitis)

- if inflammatory process continues, blood flow will be compromised by edema leading to ischemic damage of acinar cells and trypsin release leads to activation of other proteolytic enzymes and autodigestion of pancreatic tissue (acute necrotic pancreatitis)
- destruction of blood vessels can cause hemorrhage into necrotic areas


Where are parietal cells found in the gastric glands? Where are chief cells found?

Parietal cells (HCl, IF)
superficial region of gastric glands (oxyniti/pale pink)

Chief cells (pepsinogen)
deeper region of the gastric glands (small, basophlic, granular)


Describe chronic gastritis type A vs. type B.
Location? Mechanism? Associations?

Type A:
- located in fundus/body (first part of stomach)
- Autoimmune disorder with Autoantibodies against parietal cells, leading to loss of HCl and IF production (Achlorhydria, Anemia)
- Associated with other Autoimmune disorders

Type B:
- located in antrum (second part of stomach after fundus/body)
- due to H.pylori infection
- associated with increased risk of gastric adenocarcinoma and MALT lymphoma

Both are NONerosive (vs. acute gastritis, which is erosive)


Problems night driving with generalized pruritis and dry skin?

Vitamin A deficiency
from biliary obstruction leading to chronic cholestasis and fat soluble vitamin malabsorption


What does urease convert urea into? What is used to conduct a rapid urease test?

carbon dioxide and ammonia (causes a pH increase)

rapid urease test: sample from gastric mucosa of pt is added to solution containing urea and pH indicator


Pt with antacid-resistant heartburn has fingertip ulceration and telangiectasias? Mechanism of heartburn development?

CREST syndrome
Raynaud syndrome
Esophageal dysmotility

Mech unk, but CD4 accumulation and stimulation of fibroblasts, which produce collagen leading to excessive tissue fibrosis.

Esophageal dysmotility due to atrophy and fibrous replacement of esophageal muscles -- esophageal body and LES become atonic and dilated, resulting in severe reflux.