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GI > Intestines > Flashcards

Intestines Flashcards

1
Q

causes of intestinal obstruction

A

hernia

intussusception

volvulus

adhesions

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2
Q

what does intestinal obstruction look like

A

abd pain

distension

N/V

constipation

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3
Q

features of intussusception

A

currant jelly stools

bilious vomiting

knees to chest if in pain

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4
Q

what causes intussusception

A

idiopathic

viral infection

rotavirus vaccines

hyperplasia of peyer patches and other mucosa-associated lymphoid tissue

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5
Q

what causes intussusception in adults

A

tumors

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6
Q

complications of intussusception

A

obstruction

infarction

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7
Q

what causes necrotizing enterocolitis

A

enteral feeding leads to introduction of bacteria which causes tissue destruction via inflammatory mediators

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8
Q

how does PAF increase mucosal permeability

A

enterocyte apoptosis

loosening of tight intercellular junctions

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9
Q

clinical presentation of necrotizing enterocolitis

A

premature infant

bloody stool

abd distension

circulatory collapse

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10
Q

diagnostics of necrotizing enterocolitis

A

high PAF levels in stool and serum

pneumatosis intestinalis

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11
Q

Morphology of necrotizing enterocolitis

A

friable, congested, gangrenous segments of terminal ileum, cecum or right colon

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12
Q

what is diverticulosis

A

acquired pseudo outpouching of the colonic mucosa and submucosa through the muscularis propria

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13
Q

most common site of diverticulosis

A

sigmoid colon

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14
Q

pathophysiology of diverticulosis

A

increased intraluminal pressure leads to increased peristaltic contractions

At weak points where the nerve and vasa recta penetrate the muscularis propria, the mucosa and submucosa outpouch

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15
Q

clinical features of diverticulosis

A

often asymptomatic

most common cause of rectal bleeding

intermittent cramping and lower abd discomfort

alternating bowel habits

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16
Q

complications of diverticulosis

A

diverticulitis

fistulas

perforation

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17
Q

clinical presentation of ischemic bowel

A

sudden severe crampy LLQ abd pain

loose bloody stools

bloating

signs of septic shock

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18
Q

what causes ischemic bowel

A

compromised blood flow leads to hypoxia and inflammation/ necrosis of mucosa

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19
Q

diagnostics of ischemic bowel

A

increased inflammatory markers

pnematosis intestinalis

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20
Q

Morphology of ischemic bowel

A

edema

cyanosis

necrosis

ulceration

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21
Q

associations of ischemic bowel

A

ischemia

vasoactive drugs

colonic obstruction

emboli

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22
Q

complications of ischemic bowel

A

strictures

sepsis

multiorgan failure

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23
Q

how is irritable bowel typically diagnosed

A

clinical presentation

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24
Q

pathogenesis of irritable bowel

A

altered GI motility

visceral hypersensitivity

altered permeation of the mucosa

psychological onset

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25
Q

presentation of irritable bowel

A

chronic abd pain usually alleviated by bowel movements

change in bowel habits

early satiety

mucus in feces

bloating reflux

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26
Q

compare and contrast the presentation of UC vs Crohns

A

UC: LLQ abd pain usually before or during defecation with bloody diarrhea

Crohns: RLQ abd pain with watery diarrhea

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27
Q

compare and contrast the pathogenesis of UC vs Crohns

A

UC: Increased Permeability for luminal bacteria stimulates activation of macrophage and dendritic cells, causing TH2 CD4 cells to produce proinflammatory cytokines

Crohns:

TH1 mediated inflammation of the bowel

Loss of function mutation to NOD2

28
Q

compare/ contrast the site of origin of UV vs Crohns

A

UC: starts at the rectum

Crohns: can start anywhere in the GI tract

29
Q

compare/ contrast diagnostics specific to UC vs Crohns

A

UC: elevated pANCA, lead pipe appearance of haustra, continuous lesions

Crohns: elevated ASCA, string sign, creeping fat, cobblestone sign

30
Q

compare/ contrast the Macromorphology of UC vs Crohns

A

UC: crypt abscesses, pseudopolyps

broad-based ulcers

Crohns: fistulas, linear ulcers, aphthous ulcers

31
Q

compare/ contrast the Micromorphology of UC vs Crohns

A

UC: inflammation of only the mucosa and submucosa

Crohns: transmural inflammation with noncaseating granulomas

32
Q

compare/ contrast the Associations of UC vs Crohns

A

UC: smoking relieves symptoms, prior inflammatory bowel disease, PSC, HLA-B27

Crohns: nicotine makes it worse, emotional/ physical stress, HLA-B27

33
Q

Complications of UC

A

Toxic megacolon

perforation

peritonitis

increased risk of colorectal carcinoma

34
Q

Complications of Crohns

A

Malabsorption- osteoporosis

Kidney Stones

Gallstones

Peritoneal/Perianal Abscesses

Increased risk of carcinoma if there is colonic involvement

35
Q

presentation of celiac disease

A

chronic recurring diarrhea

abd pain/ distension

steatorrhea

flatulence

bloating

N/V

malabsorption

dermatitis herpetiformis

arthritis

aphthous ulcers, delayed puberty

short stature

36
Q

Pathogenesis of Celiac Disease

A

tissue transglutaminases are released upon consumption of gluten, causing modifications of gliadin

modified gliadin activates T cells, causing intestinal inflammation

37
Q

Diagnostics of Celiac Disease

A

anti-gliadin antibodies

anti-tissue transglutaminase antibodies

anti-endomysial antibodies

38
Q

Morphology of Celiac disease

A

villous atrophy

crypt hyperplasia

39
Q

Associations of Celiac disease

A

HLA-DQ2

HLA-DQ8

gluten consumption

Autoimmune thyroid disease

Turners

Downs

Dermatitis herpetiformis

40
Q

Complications of Celiac Disease

A

iron deficiency/ malabsorption anemia

enteropathy associated T cell lymphoma

small intestinal adenocarcinoma

41
Q

Clinical presentation of Whipple Disease

A

abd pain

malabsorptive diarrhea

enteropathic arthritis

weight loss

sacroiliitis

LAD

cardiac symptoms

Myoclonus

ataxia

impaired ocular function

42
Q

What causes Whipple’s Disease

A

T. whipplei infiltrates and obstructs lymphatics

43
Q

Morphology of Whipples Disease

A

Micro: PAS + macrophages

Macro: shaggy appearance of mucosa with white/ yellow mucosal plaques

44
Q

What is another name for environmental enteropathy

A

tropical sprue

45
Q

where is lactase located

A

apical brush border membrane of the villous absorptive epithelial cells

46
Q

histology of Lactase deficiency

A

Unremarkable

47
Q

What is abetalioproteinemia

A

inability to secrete triglyceride-rich lipoproteins

48
Q

Pathogenesis of Abetalipoproteinemia

A

Autosomal Recessive mutation of the microsomal triglyceride transfer protein (MTP) results in failure of intraepithelial processing and transport

49
Q

Morphology of Abetalipoproteinemia

A

vacuolization of small intestinal epithelial cells

appears on oil red O stain

presence of burr cells

50
Q

clinical presentation of abetalipoproteinemia

A

failure to thrive

diarrhea

steatosis

All in infancy

51
Q

Risk factors of Intestinal Adenocarcinoma

A

Low fiber

high fat/ carbs

Ulcerative colitis

HNPCC/ Lynch Syndrome

FAP

Villous neoplastic polyps in intestines

52
Q

What is Lynch Syndrome

A

Autosomal dominant familial clustering of cancers in the colorectum, endometrium, stomach, ovary, brain, small bowel and hepatobiliary tract

SHE COBB

53
Q

What causes Lynch Syndrome

A

DNA mismatch repair genes (MSH2 and MLH1) lead to microsatellite instability

54
Q

What is FAP

A

Familial Adenomatous Polyposis

Autosomal dominant condition characterized by APC gene mutations on chromosome 5q21

55
Q

Extraintestinal manifestations of FAP

A

congenital hypertrophy of the retinal pigment epithelium

56
Q

What is Gardner Syndrome

A

FAP

Osteoma

Desmoid Tumors

57
Q

What is Turcot Syndrome

A

FAP

Medulloblastoma

Glioblastoma

58
Q

most common type of polyp and what does it look like

A

hyperplastic type

epithelial proliferation with serrated architecture

59
Q

Where are inflammatory polyps seen

A

Ulcerative colitis due to frequent regeneration of mucosa

60
Q

2 types of hamartomatous polyps

A

Peutz Jeger Syndrome

Juvenile Polyp

61
Q

Risk of FAP

A

100% chance of adenocarcinoma if not resected

62
Q

Describe Juvenile Polyps

A

retention polyp

mostly in rectum

presents in children< 5 y/o with rectal bleeding

No increased chance of carcinoma unless there are multiple juvenile polyps in the stomach and colon

63
Q

What is Peutz-Jeger Syndrome

A

Autosomal Dominant condition in which there are multiple hamartomatous polyps and mucocutaneous hyperpigmentation

Increased risk of breast, colon, pancreatic, lung and thyroid cancer

64
Q

Compare and contrast the morphology of Colon adenocarcinoma

R sided vs L sided

A
65
Q

Diagnostics of Colonic Adenocarcinoma

most common site for metastasis

A

CEA+

liver (portal drainage)

66
Q

Pathogenesis of colonic Adenocarcinoma

A
  1. APC mutation
  2. inhibition of beta catenin synthesis
  3. unregulated Wnt pathway
  4. Upregulated cell proliferation

GI (7 decks)

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