Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI > GI UWorld: Path and Pharm > Flashcards

GI UWorld: Path and Pharm Flashcards

1
Q

Crohn’s disease: gross appearance and histology

A

Linear ulcers and normal mucosa interspersed –> cobblestone appearance. Creeping fat.Histo: non-caseating granulomas, lymphoid inflammatory infiltrate (Th1 mediated)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What cell type mediates Crohn’s disease?

A

Th1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe squamous cell carcinoma histology. What is the importance of keratin?

A

Nests of neoplastic squamous cells with abundant eosinophilic cytoplasm and distinct bordersKeratinization means that the tumor is poorly differentiated –> poor prognosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What 3 organisms are most common causes of esophagitis? What patients is this found in?

A

Found in immunocompromised. Candida albicans, HSV-1, and CMV.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Gross and histologic features: Candida esophagitis

A

Gross: white pseudomembranesHisto: yeast cells and pseudohyphae that invade mucosal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Gross and histologic features: HSV esophagitis

A

Gross: “punched out” ulcersHisto: eosinophilic intranuclear inclusions in multinuclear squamous cells at margins of ulcers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Gross and histologic features: CMV esophagitis

A

Gross: linear ulcerations

Histo: intranuclear and cytoplasmic inclusions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where is H. pylori found in greatest concentration in the GI tract?

A

Prepyloric area of the gastric antrum (even if it is a duodenal ulcer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Presentation of carcinoid syndrome

A

Dyspnea, wheezing, cutaneous flushing, diarrhea. Maybe right sided valvular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Tx of carcinoid syndrome

A

Resection and somatostatin analogue, aka octreotide (inhibits secretion of many hormones)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Where should you biopsy for Hirshprung’s?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Abetalipoproteinemia presentation

A

Presents in early childhood. Failure to thrive, steatorrhea, malabsorption, acanthocytosis, ataxia, night blindness.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Abetalipoproteinemia: labs and biopsy

A

Low plasma triglycerides, low cholesterol, no chylomicrons, VLDLs, apoBs. Poor absorption of ADEK.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Classification of adenomatous polyps

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Difference between erosions and ulcers

A

Erosions do not fully extend through the muscularis mucosa (but they can reach it)

Ulcers penetrate through the mucosa into submucosa.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the first event in the pathogenesis of acute appendicitis?

A

lumen obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Histology of Crohn’s disease

A

Non-caseating granulomas, lymphoid aggregates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Multiple hemorrhagic polypoidal lesions, spindle cells with surrounding blood vessel proliferation in the setting of untreated HIV. Dx?

A

Kaposi’s sarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Kaposi’s sarcoma: colonoscopy findings, biopsy findings, other organ system involvement

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

CMV colonoscopy and biopsy findings

A

Colonoscopy: multiple ulcers, mucosal erosions
Biopsy: cytomegalic cells with inclusion bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Cryptosporidium colonoscopy and biopsy findings

A

C: nonulcerative inflammation
B: Basophilic clusters on surface of intestinal mucosal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Characteristics of colitis-associated colorectal carcinoma

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Congenital pyloric stenosis: “olive sized” mass is from:

A

smooth muscle hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Systemic mastocytosis: cause and effects

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which gastritis is associated with the antrum?

A

Type B - H. pylori

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Differentiate between acute and chronic gastritis

A

Inflammation
Acute = neutrophil dominant
Chronic = lymphocyte and plasma cell predominant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Presentation of chronic gastritis

A

epigastric abdominal pain, occasional nausea, not related to food intake, inflammatory infiltrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Presentation of Crohn’s

A

Fever, right lower quadrant pain (terminal ileitis), diarrhea, involves GI tract not stomach!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Damage seen in pernicious anemia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What stimulus causes parietal cell proliferation?

A

Gastrin: facilitates HCl secretion, AND has a trophic effect causing proliferation and hyperplasia

Seen in Zollinger-Ellison syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Definitive dx for celiac

A

Small intestine biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

CREST syndrome contains esophageal dysmotility. What is the cause, and what are symptoms?

A

Fibrous replacement of muscularis –> esophageal dysmotility

Heartburn, dysphagia, regurgitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Which polyps are likely to undergo malignant transformation

A

Adenomatous polyps, increased risk with size, villous pattern, and sessile growth.

Others like hyperplastic, lymphoid, harartomatous, lymphoid are not at risk.

34
Q

What is toxic megacolon? What disease is it associated with? What is typical presentation, and how do you diagnose?

A

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.

35
Q

What is a Cushing Ulcer?

A

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.

36
Q

Adenoma-carincoma sequence

A

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!

37
Q

Insidious development of non-bloody diarrhea, fever, malaise, fistula. Dx?

A

Crohn’s

38
Q

How does h. pylori cause gastritis?

A

Infection leads to decrease number of somatostatin producing cells, which results in higher gastrin levels. Occurs in antrum, can cause duodenal ulcers.

39
Q

Why do people with Crohn’s get gallstones?

A

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

40
Q

Histologic findings: GERD

A

Basal zone hyperplasia, elongation of lamina propria papillae, inflammatory cells

41
Q

Jejunal biopsy shows flattening of mucosa, atrophy of villi, chronic inflammation of lamina propria. Dx?

A

Celiac sprue

42
Q

Lab values in alcoholic hepatitis

A

AST&raquo_space; ALT (ratio greater than 1.5)

43
Q

Microscopic appearance of carcinoid tumor

A

Uniform cells in nests or sheets. Minimal to no variation in size or shape. Eosinophilic cytoplasm, oval/round stippled nuclei

44
Q

What is the central enzyme activation in acute pancreatitis that causes all the other stuff?

A

Trypsin –> trypsinogen

45
Q

Most pronounced changes in CF

A

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)

46
Q

Where are ulcers not likely to cause malignancy?

A

Duodenum

47
Q

Tx of duodenal ulcers

A

Usually caused by H.pylori –> triple therapy (2 abx and a ppi)

48
Q

Cause of zenker diverticulum

A

Cricopharyngeal muscle dysfunction from diminished relaxation of pharyngeal muscle during swallowing. Increased intraluminal pressure causes herniation, forming the diverticulum. Usually elderly pts

49
Q

Diffuse esophageal spasm

A

periodic, non-peristaltic contractions of esophagus. Corkscrew esophagus seen on barium swallow. Symptoms are intermittent dysphagia and chest pain, may mimic unstable angina.

50
Q

Mechanism of polyethylene glycol, similar drugs

A

Osmotic laxitive. Similar to magnesium hydroxide, magnesium citrate, lactulose.

51
Q

Diarrhea in Crohn’s

A

Secretory diarrhea with high electrolyte content

52
Q

Drug that inhibits gastric acid secretion to ACh, histamine, and gastrin

A

Proton pump inhibitors (-prazole)

53
Q

Adenoma carinoma sequence mutations

A

1) APC
2) K-ras
3) p53

54
Q

Crohn’s associated with increased activity of which molecule?

A

NF-kB, which is responsible for cytokine production

55
Q

Where does iron absorption take place?

A

Duodenum, proximal jejunum

56
Q

Treatment for CF

A

N-acetylcysteine is a mucolytic agent

Supplement pancreatic lipase to improve malabsorption

57
Q

GI side effect of mu opioids

A

Contraction of smooth muscle leads to sphincter of Oddi constriction, increases common bile duct pressures, can lead to biliary colic.

58
Q

Inflammation pattern: Crohn’s vs ulcerative colitis

A

Crohn’s: transmural inflammation, fistulas, skip lesions

UC: mucosal and submucosal, continuous

59
Q

Manifestations of adult lead poisoning

A

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)

60
Q

Lactase deficiency: stool osmotic gap, breath hydrogen content, stool pH, D-xylose absorption

A

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)

61
Q

Tx for arsenic poisoning

A

Demercaprol. Displaces arsenic fro sulfhydryl groups of enzymes

62
Q

Where is colon cancer most often found?

A

Rectosigmoid colon. Leads to obstruction symptoms.

63
Q

Intestinal hypoperfusion/ chronic mesenteric ischemia

A

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

64
Q

Anal fissures: where do they occur, and what are they associated with?

A

Posterior midline distal to the dentate line

Associated with low fiber diets and constipation

65
Q

Diarrhea, weight loss, epigastric-region calcifications in chronic alcoholic: dx? Cause of symptoms?

A

Chronic pancreatitis with pancreatic exocrine insufficiency and malabsorption. Secondary to alcohol-induced protein precipitation in pancreatic ducts.

66
Q

Most important risk factors for esophageal squamous and adenocarcinoma

A

Squamous: EtOH, smoking, N-nitroso foods. Irritation from other things less important

Adeno: Barrett’s, GERD, obesity, tobacco.

67
Q

First step in assessing malabsorption syndromes

A

Stool stain to look for fat in stool

68
Q

Diphenoxylate

A

Opiate anti-diarrhia. Binds to mu-opiate receptors and slows motility. Useful in low doses, combined with atropine to discourage abuse

69
Q

Tx for secretory diarrhea

A

Octreotide (somatostatin analog)

Bismuth also works

70
Q

Most common location for intussusception

A

ileocecal junction

71
Q

Presentation of intussusception

A

colicky, intermittent abdominal pain, nausea, vomiting, currant jelly stools, mass in RL quadrant

72
Q

Decreased visual acuity and tunnel vision in low light ddx

A

Toxic retinopathy due to phenothiazines or chloroquine
vitamin a deficiency
Congenital rubella or syphilis
Diabetic retinopathy

73
Q

How do urinary stones form in Crohn’s?

A

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

74
Q

Dermatitis herpetiformis: associated with what GI disease

A

Autoimmune disorder associated with celiac. papulovesicular skin rash, small vesicles on extensor surfces. symmetric and pruritic. IgA deposition at tips of dermal papillae

75
Q

How does Shigella get taken up?

A

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

76
Q

Lactase deficiency histology

A

Normal intestinal mucosa

77
Q

How do right and left colon cancer present?

A

R: systemic symptoms, anemia
L: obstruction symptoms

78
Q

Recurrent, grossly-bloody stool associated with abdominal discomfort and low grade fever dx?

A

ulcerative colitis

79
Q

Tenesmus and thin stool dx

A

Space-occupying lesion of rectum, often presentation of rectal adenocarcinoma

80
Q

Duodenal ulcer found in distal duodenum (or other atypical location)

A

Zollinger-Ellison syndrome, caused by gastrin-secreting tumors of pancreas or duodenum

81
Q

What is PAS staining useful for?

A

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.

82
Q

Transmural inflammation in Crohn’s causes

A

Strictures: chronic inflammation causes edema, fibrosis –> narrowing of lumen

Fistula: inflammation and necrosis of wall cause ulcer formation, which penetrate wall to form fistulae

GI (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions