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GIR: Test 3 > Inflammatory Bowel Disease > Flashcards

Inflammatory Bowel Disease Flashcards

1
Q

what Dx do the following symptoms indicate?

s/s: loose stools (10/d), blood in stool, LLQ abd cramping that improves with defecation, diarrhea at night!

A

Ulcerative colitis

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2
Q

PE: fever, orthostatic hypotension, tachy, LLQ tenderness (no rebound or peritoneal signs)

Rectal exam: BRB (bright red blood per rectum)

exam indicates what DDx?

A

infectious diarrhea, IBS, IBD –> Ulcerative colitis

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3
Q

orthostatic hypotension indicative of…?

A

dehydration

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4
Q

Red flags that indicate ulcerative colitis?

A

blood in stool, nocturnal diarrhea, young age

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5
Q

Lab results indicate what Dx?

elevated WBC (mostly neutrophils), low Hgb, elevated ESR

stool: leukocytosis, -ve bacterial cultures

CT abdomen: thickening of sigmoid and descending colon (no abscess or diverticula)

A

ulcerative colitis

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6
Q

what are the proper steps in Dx of UC?

A

HPI, PE, stool sample, CBC, CT abdomen, colonoscopy

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7
Q

what is colitis?

A

damage to the mucosa of the colon

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8
Q

diffuse mucosal granularity, erythema, exudate

A

colonoscopy of UC description = colitis

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9
Q

distortion of crypt architecture (long term problem) crypt abscesses (full of inflammatory cells)

A

UC biopsy

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10
Q

diagnosis?

  • young female on HRT (oral contraceptives)
  • watershed areas of colon affected
  • sparing of rectum
A

ischemic colitis (the whole colon is not affected)

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11
Q

watershed areas of colon

A

splenic flexure and rectosigmoid junction (limited blood supply here)

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12
Q

blood supply to the large intestine

A

SMA from aorta supplies terminal ileum IMA supplies left side of colon

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13
Q

diagnosis?

mimics UC but biopsy shows virus for differentiation

A

CMV colitis

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14
Q

three classifications of UC

A

proctitis, left sided colitis, pancolitis

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15
Q

what is the diagnosis?

s/s: bloody diarrhea, abd pain, fecal urgency, disease limited to colon (does NOT spread to SI)

rectum is involved & inflammation is limited to mucosa and submucosa

A

Ulcerative colitis

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16
Q

complex immunological disorder w/ complex pathogenesis

chronic idiopathic intestinal inflammation

A

IBD

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17
Q

idiopathic disease: combo of genetics, bacteria, and immunological response

A

IBD

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18
Q

two main subtypes of IBD

A

UC and Crohn’s disease

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19
Q

UC vs Crohn’s disease

A

Crohn’s is any part of the GI tract (including SI)

UC starts at anus and is uninterrupted

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20
Q

IBD epidemiology

A

bimodal peak: 15-25 y/o and 50-70 y/o

more common in Ashkenazi Jews

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21
Q

what is a risk factor for Crohn’s disease but NOT a risk factor for UC?

A

appendectomy

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22
Q

smoking and IBD

A

UC: better prognosis if you smoke

Crohn’s: worse prognosis if you smoke

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23
Q

IBD seen in what climates/countries?

A

colder climates and developed countries

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24
Q

hygiene hypothesis

A

increased frequency to Abx, less exposure to bacteria…extreme sanitation leading to higher incidence of IBD

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25
Q

water absorption in GI tract

A

> 200 cc of stool = diarrhea

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26
Q

normal intestinal electrolyte absorption

A

Na: electrogenic Na abs and electroneutral NaCl abs

K: secretion & absorption

Cl: secretion

short chain FA abs

H2O: doesn’t need transporters

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27
Q

IBD causes ________ diarrhea

A

inflammatory

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28
Q

secretory diarrhea

A

excess electrolytes (NaCl) w/ water following

AKA massive volume of plasma-like fluid

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29
Q

inflammatory diarrhea

A

inflammatory mediators affect apical membrane transporters:

  • so Na abs is diminished (leading to more water in the lumen as well now)
  • so Cl secretion is therefore increased as well
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30
Q

what does IBD do exactly to cause defective Na absorption?

A

1) colonocyte properites change when inflammed
2) there is reduced Na pump activity
3) high [inflammatory cytokines] result in gene depression of enterocyte cellular transport function

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31
Q

name one inflammatory cytokine involved in IBD leading to disturbed colonocyte function

A

TNF

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32
Q

List of other possible causes of diarrea in IBD

A

bile induced, fatty diarrhea, short bowel syndrome, concurrent C diff colitis, CMV, SI bacterial overgrowth, celiac sprue, untreated lactose intolerance, NSAID associated enteropathy, IBS

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33
Q

inflammatory diarrhea can be caused by either _______ or ________

A

infectious diarrhea or immunological diarrhea

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34
Q

infectious diarrhea (left) and immunological diarrhea (right)

A

IBD is immunological. this is when activation of immune system causes severe inflammation, damage of enterocyte, and malabs.

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35
Q

pathogenesis of IBD (two factors that play a role)

A
  • host (genetics + immune system)
  • microbes in the lumen
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36
Q

pathogenesis of IBD (specific immunological reasons)

A

excessive immune reactivity OR inadequate immune responses to intestinal microbiota

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37
Q

microbiome bs microbiota

A

microbiome: ecological community of pathogenic microorganisms (bacteria, fungus, yeast) and humans themselves
microbiota: ONLY microorganisms
* There are 10x more bacterial cells than human cells*

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38
Q

gut flora has the largest # of bacteria/greatest # of species compared to any other area of the body

when is this gut flora established in the human body?

A

1-2 years after birth

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39
Q

what dominates the micronbiota?

A

bacteriodetes and Firmicutes

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40
Q

+ve role of microbes

A

nutrition, energy metabolism, proper “conditioning of intestinal & peripheral immune systems

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41
Q

-ve role of microbes

A

microbial-derived factors promote IBD in the context of underlying genetic immune defect

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42
Q

what leads to changes in the communities of intestinal bacteria?

A

dietary factors, helminth exposure, Abx exposure

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43
Q

What four ways does the mucosal layer above enterocytes protect us?

A
  • intact intestinal epithelium
  • secretion of protective factors
  • innate immune system
  • acquired immune system
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44
Q

How does dysregulation at the epithelial barrier occur?

A
  • alterations in intestinal mucus
  • high # of bacteria w/in mucus
  • increased intestinal permeability (aka LEAKY GUT)
  • abnormalities in Paneth cells
45
Q
A

Bacteria enters the endothelium and stimualtes an Ag presenting cell. This stimulates T cells and make cytokines. Leads to inflammation

46
Q

homing

A

recruitment of neutrophils from BV to the mucosa

47
Q

diapedesis

A

once leukocytes are adherent, they traverse the endothelium

48
Q

how does a neutrophil get from BV to the cell that is signaling inflammation?

A

leukocytes roll along the endothelium due to chemokine secretion. chemokines secreted from the tissues activate adhesion molecules (causing firm adhesion).

49
Q

increased expression of adhesion molecules on leukocytes & endothelial cells + increased chemokines + increased leukocyte binding to vascular endothelial cells is seen in what diagnosis?

A

IBD

50
Q

what heterodimer is important for mediating lymphocyte trafficking to the lamina propria in the gut?

A

alpha-4-beta-7 integrin

51
Q

CD4 T cells secrete what two main inflammatory mediators?

A

IFN gamma and TNF

52
Q

Tx for Crohn’s disease targeting inflammatory mediator?

A

anti-TNF alpha

53
Q

IBD pathogenesis

A

alterations in intestinal microbiota + dysregulated immune responses + genetic susceptibility

54
Q

what protein/gene is mainly associated with IBD?

A

nucleotide-binding oligomerization domain (NOD2)

(70% of gene susceptiblity shared between Crohn and UC)

55
Q

NOD2 gene is associated with severe Crohn’s disease:__________

A

ileal and fibrostenosing Crohn disease

56
Q

autophagy

A

process that mediates resistance to intracellular pathogens

57
Q

mutation of ATG16L1 a/w Crohn’s disease leads to?

A
  • changes in Paneth cells & goblet cells
  • decreased ability to clear bacteria
  • increased secretion of cytokines
58
Q

s/s: non-bloody diarrhea, right sided abd pain, weight loss, fever

PE: ulcers in mouth, RLQ tendereness, anal fissure

labs: anemia, elevated CRP, elevated ASCA, low vit B12, low vit D

Diganosis?

A

Crohn’s disease

59
Q

s/s: diarrhea, RLQ abd pain, sore throat, reactive arthritis

A

Yersinia enterocolitica (IBD mimic)

Dx made via stool culture

60
Q

s/s: apthous mouth uclers, RLQ pain, diarrhea, and genital ulcers

Diagnosis?

A

Behcet’s disease (IBD mimic)

this is a systemic vasculitis (Asian descent often)

61
Q

deep ulcers, skip lesions

A

Crohn’s disease

(skip lesions –> some areas of colon look normal and some have ulcers)

62
Q

terminal ileum w/ severe stricture, inflammation, and ulcers. skipped lesions present

diagnosis?

A

Crohn’s disease

63
Q

three main areas of Crohn’s distribution

A
  • most are ileocolic (usually right side of colon involved)
  • then ileal
  • least are colic
64
Q

what is the terminal ileum attached to?

A

the cecum (And appendix is right next to it)

65
Q

diagnosis?

A

Crohn’s disease

CT shows TI involvement (thickening of wall)

66
Q

diagnosis?

A

Crohn’s disease

Small bowel shows string where there is narrowing of the TI (RLQ).

There are normal dilated loops of bowel elsewhere

(b) and (c) show thickened bowel

67
Q

diagnosis?

A

Crohn’s disease

This has deeper inflammation than UC. Granulomas exist in the mucosa

68
Q

CDAI (Crohn’s disease activity index)

A

>150 (active disease)

>450 (severe disease)

It is a combo of obj + subj measurements

69
Q
A

Crohn’s: inflammation throughout mucosa, thickening of wall, granuloma, cobblestoning appearance of mucosa

UC: superficial inflammation, lots of ulcers (thru polyps sometimes), & bulging areas

70
Q

what are the 5 possible complications of Crohn’s?

A

transmural inflammation, strictures, fistulas, abscess, and anal fissure

71
Q

s/s: abd pain, diarrhea, weight loss, transmural inflammation, ulcers in mouth possible

colonoscopy: skipped lesions
histology: granuloma

diagnosis?

A

Crohn’s disease

symptoms depend on location of disease

72
Q

two possible skin manifestation in IBD?

A

erythema nodosum and pyoderma gangrenosum

73
Q

erythema nodosum

A
  • painful nodular lesions on the trunk and anterior shins
  • improves w/ disease Tx
74
Q

pyoderma gangrenosum

A
  • necrotizing, painful lesion
  • can be anywhere
  • pathergy (touching it makes it worse)
75
Q

in regards to ulcers in IBD….ulcer progression is __________ of disease progression

A

independent

76
Q

other possible extraintestinal manifestations of IBD?

A

w/ active IBD: peripheral arthropathy (swelling of joints)

indepdent of IBD activity: bamboo spine, PSC

77
Q

primary sclerosing cholangitis

A
  • elevated alk phos
  • ERCP shows “beads on a string” or “chain of lakes”
  • risk factor for colon cancer (screen hearly)

-

78
Q

IBD can also cause pancreatitis…

A
  • this can be medication related (mesalamine)
  • this can be IgG related autoimmune pancreatitis
  • this can be duodenal Crohn’s affecting pancreatic duct
79
Q

______________________ risk in IBD is HIGH!!!!

A

thromboembolic

80
Q

two main reasons IBD pt die:

A

clots or cancer

81
Q

how do nutritional issues arise in Crohn’s?

A

TI is where multuple nutrients are abs…

small bowel disease or diminsihed abs due to surgeries (ileal resection)

82
Q

ileal resection results in what nutritional deficiencies?

A

Vit B12, bile acid, Vit D, and Zinc

83
Q

s/s: sebhorrheic rash on legs/face, scaling around nose & mouth, diarrhea

A

zinc deficiency

84
Q

short bowel syndrome?

A

less than 200 cm of small bowel remain after resection

85
Q
A

Crohn’s: transmural that may cause fistula or penetration

UC: superficial involving mucosa

86
Q
A
87
Q

Treatment of IBD

interpretation: refractory may need surgery or biologic Tx

A

UC Tx normally begins with mild category

88
Q

list of drug classes for IBD Tx

A

biologics, immunomodulators, corticosteroids, Abx, and aminosalicylates

89
Q

aminosalicylates (ASA)

A

These are drugs used for UC only (work on the large intestine)

5 main release sites

-give folates as well for Tx!!!!

90
Q

ASA adverse effects

A
  • headache, fatigue, rash
  • inhibits intestinal folate absorption
91
Q

Mesalamine

A

-this is an ASA that causes interstitial nephritis

92
Q

corticosteroids

A
  • blocks production of PG
  • side effects: HTN, hypokalemia, Cushing’s syndrome, osteoporosis, DM, muscle wasting
93
Q

biologics (anti-TNF alpha) –> Infliximab, adalimumab

A
  • serum sickness is possible side effect, T cell lymphoma, opportunistic infections
  • adalimumab better
  • can treat UC and Crohn’s
94
Q

PML

A
  • demyelinating disease (leads to severe death or disability)
  • due to reactivation of JC virus
  • can be caused by natalizumab (Ab against alpha-4 integrin)
95
Q

goals of surgery as Tx in UC

A

cure the disease & prevent cancer

(this si done if pt fails medical therapy)

96
Q

indications for sugery in UC

A

toxic megacolon, hemorrhage, medical intractability, or malignant degeneration (dysplasia)

97
Q

three possible surgeries for UC

A

1) colectomy: this cures the disease [disease is limited to colon] & prevents cancer
2) ileal pouch
3) anal anastomosis
* ileostomy = bag*

98
Q
A

toxic distenstion of the colon with UC (hemorrhage, tachy, abd tender/distended, dialted colon on xray)

99
Q

when is surgery indicated in Crohn’s disease?

A

fistula or strictures (most pt will need surgery)

-the longer you’ve had the disease, the more likely you’ll need surgery

100
Q

IBD pt live as long as normal pt UNLESS one of these two things happen

A

thromboembolic event or cancer

101
Q

risk factors for colon cancer in IBD

A
  • age of colitis onset < 15 y/o
  • disease extent
  • duration (>8 yr of pancolitis or left sided colitis)
  • severity (colonic strictures)
  • inflammatory complications
  • PSC or FH of CRC
102
Q

why do IBD pt develop colitis associated neoplasm?

A

Genes! KRAS, c-src, p53, APC, chromosomal instability (CIN) & microsatellite instability (MSI)

aneuoploidy refelcts a difference in chromosome # in neoplastic lesions and in flat, nondysplasitc colonic mucosa

103
Q

chain of events: how normal cells get dysplasia/malignant cells

A

cancer development in IBD is a little different than sporadic progression (which has adenoma stages).

IBD: areas of dysplasia develop along areas of inflammation. finding these dysplastic lesions may be difficult

104
Q
A

colitis w/o dysplasia –> indefinite dysplasia –> high grade dysplasia –> cancer

105
Q

what are the special charactersitics of colitis associated neoplasm?

A

inflammation –> multifocal dysplasia –> cancer

106
Q

colonoscopy & chromendoscopy (standard of care for surveillance)

A

colonoscopy: looks for areas of abnormal lesions in inflammed colon
* biopsy anything that looks unusual*
chromendoscopy: spread dye along the wall to identify unusual areas
* high grade dysplasia = colectomy for Tx*

107
Q

consequences of ileal resection in Crohn’s disease

A
  • fat malabsorption (treat with low fat diet and medium chain TG)…if >100 cm of TI removed
  • bile malabsorption (treat with bile absorbing agent like cholestyramine powder)…if <100 cm of TI removed
108
Q

how does nephrolithias occur in pt with Crohn’s?

A
  1. free Ca binds to FA instead of oxalate (oxolate now can form stones)
    1. Ca supplements will decrease formation of oxalate kidney stones
  2. severe diarrhea can lead to severe dehyration & uric acid stones can form
109
Q

IBD drugs and pregnancy

A
  • methotrexate CONTRAINDICATED
  • azathioprine: it is okay
  • aminosalicylates: def good!!!
  • fertility may be affected after surgery (ileal pouch anal anastomosis - IPAA)

GIR: Test 3 (4 decks)

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