GI Flashcards Preview

Pathology > GI > Flashcards

Flashcards in GI Deck (57)
Loading flashcards...
31

Describe diverticula of the large intestine and their complications.

outpouching of intestinal wall

(solitary/multiple, congenital acquired)

 

In the colon = protrusion of the mucosa/submucosa

complications >> perforation >> pericolonic abscess, fistulas, fibrosis, bleeding

32

Compare hemorrhoids and intestinal angiodysplasia.

Hemorrhoids = varicosities of anal/perianal region

External = below anorectal line

Internal = above anorectal line

 

Angiodysplasia = localized vascular lesion (colon)

dilated thin-walled BV that anastamose between arteries/veins in mucosa/submucosa

33

Compare occlusive and nonocclusive ischemic bowel disease.

occlusive = caused by thrombi/emboli

thrombus often found in superior mesenteric artery. Can lead transmural infarction of intestine >> high mortality

 

nonocclusive = atherosclerotic narrowing of arteries

scattered multiple infarcts >> hemorrhagic patches (ulcerate and become fibrotic)

34

How common is inflammatory bowel disease?

Ulcerative colitis 3x more common than Crohn's

- more common in whites, Jews

- peaks 20-30 yrs/o

- family predisposition

 

35

Compare Crohn's and ulcerative colitis.

Crohn's = chronic inflammation of the terminal ileum/colon

- begins with "apthous ulcers" over peyer's patches

- shallow mucosal defects >> transmural inflammation *often assoc. with granulomas

- fibrosis of muscularis and serosa = cobblestone appearance

>> strictures, adhesions >> fistulas

36

What is pseudomembranous colitis?

When balance between host and intestinal flora has been lost. 

e.g. c difficile after broad-spectrum antibiotics

- predominantly involves colon

- exotoxin of c diff acts on epithelial cells of the intestine >> ulcers (superficial) and focal necrosis

- ulcers covered wth layer of exudative fibrin, inflammatory cells, mucin = pseudomembranes

37

Compare diarrhea caused by small intestinal disease with diarrhea caused by large intestinal disease.

SI: large, watery, rarely have blood

LI: small, mucoid, commonly have blood, may have leukocytes

38

What are the clinical and pathologic features of acute appendicitis?

= usually caused by enterogenic bacteria that become pathogenic after obstruction of the lumen of the appendix

Bacteria become trapped >> multiply become noxious and cause ulceration

Sudden fever, leukocytosis, abdominal pain

39

Compare infectious and sterile peritonitis.

INFECTIOUS

= bacterial invasion of abdominal cavity

- rupture of stomach, abscess

- preexisting ascites

- infection from fallopian tubes

 

STERILE

= chemical irritation

- pancreatitis

- rupture of gallbladder

- postsurgical

40

Describe the pathogenesis and pathology of acute peritonitis.

serosal surface (intestines) and parietal peritoneum are congested and edematous

** exudate contains PMNs and fibrin >> fibrous adhesions

Symptoms: sharp abd pain, rebound tenderness, guarding. Intestines become paralzyed (high mortality)

41

List the most common causes of intestinal obstruction.

Paralytic ileus

or

Mechanical obstruction

- atresia
- stenosis
-strictures
- intussusception
- volvulus
- hernia
- adhesions
- neoplasms

42

What are the most common types of hernia?

Inguinal = most common

Inguinal: protrudes through inguinal canal or into scrotum

Femoral: occurs through femoral canal (groin)

Periumbilical: around umbilicus, ant abd wall

Diaphragmatic: through hiatus and exctends into thoracic cavity

 

43

Compare intussusception and volvulus.

intussusception = invagination of one segment of the intestine into another

compromised blood flow >> necrosis

 

volvulus = rotation around its mesenteric attachment site

twisting of arteries/veins >> infarction

44

Classify malabsorption syndromes according to their pathogenesis.

Inadequate intraluminal digestion

Primary mucosal absorptive defects

Impeded transport of nutrients

Pathologic

1. those that have characteristic findings

2. those that have non-specific findings
3. Those that have no pathologic findings

45

Compare celiac sprue and tropical sprue.

Celiac = hypersensitivity to gliadin in dietary grains

- SI shows mucosal atrophy with flattening of villi

- may develop T cell lymphoma

- affects proximal > distal intestine

 

Tropical = caused by bacteria

SI looks the same as Celiacs

- affects distal > proximal

- no allergy to gliadin

- responds to ABs

46

What are the clinical features of malabsorption syndrome?

Most prominent deficiencies = protein and lipids

protein (+ iron malabs) >> anemia

hypoalbuminemia >> edema

amenorrhea, impotence, muscle weakness

steatorrhea >> decreased vit ADKE

>> bleeding disorders

>> osteomalacia

47

How common are intestinal neoplasms and where are they most often located?

48

Classify intestinal neoplasms.

Non-neoplastic polyps

Neoplastic polyps

Malignant neoplasms

49

What are the risk factors for intestinal neoplasms?

Genetics: polyposis syndroms (FAB or Gardners, autosomal dominant), non-polyposis colorectal cancer

Diet: red meat, fat, refined carbs, lo vegetables

Oncogenes/TSG: TP53, KRAS; dysregulation of epithelial mucosal cells

 

50

What are polyps, and how are these intestinal lesions classified?

Polyps occur as the result of accumulation of irregular cells. They protrude into the lumen of the intestine
villous or tubular

 

 

51

Compare neoplastic and non-neoplastic polyps.

Non-neoplastic

Hyperplastic: most common, rectosigmoid area

Hamartoma: children < 5, retention polyps, peutz-jeghers (autosomal dominant)

Inflammatory: IBD, pseudopolyps

Neoplastic

Tubular: pedunculated polyps, cuboidal epithelium

Tubulovillous: predominantly tubular that appear villous 25%

Villous: sessile, fingerlike villi, lined with single nonclassifiable cell type

52

What are the clinical features of large intestinal cancer?

adenocarcinomas 50x more common in the LI

Early = no symptoms

Late = chronic blood loss, constpation, pencil-like feces, hematochezia, bleeding

53

Compare adenocarcinomas of the right and left colon.

right = intraluminal fungating or ulcerating masses

left = napkin ring stenotic lesions

54

What is CEA, and what is the clinical value of this tumor marker?

CEA is normally produced by embryonic intestine. In adult not found, except for special circumstances like regenerating epithelium of ulcerative colitis. 

CEA can be measured in serum . . . but is NOT useful for early detection or screening. Useful for recurrence.

55

How do carcinoids differ from adenocarcinoma of the large intestine?

Carcinoids = neuroendocrine tumors of low malignancy

- located in submucosa where they form small modules elevating the overlying mucosa)

- mostly small < 2cm

56

What is carcinoid syndrome?

When carcinoids metastasize to the liver, they release their secretory product into venous blood >>

symptoms: serotonin, bradykinin, histamine, bronchial wheezing, flushing, colic, diarrhea

57

Ulcerative colitis

Ulcerative colitis = intestinal inflammation (colon)

- starts with initial rectal lesions, spreads proximally

- mucosa with "sandpaper" appearance, prone to bleeding and infection

- atrophy of crypts + aggregate of leukocytes = crypt abcesses

- confluent ulcerations = serpiginous

- formation of pseudopolyps (residual, heavily inflamed mucosa)