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PT1 B3 > Lecture 82-83: diseases and pathology of the large intestine > Flashcards

Lecture 82-83: diseases and pathology of the large intestine Flashcards

1
Q

what diseases comprise Inflammatory Bowel Disease

A

UC
CD
(Microscopic colitis)

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2
Q

Etiology of IBD?

A

idiopathic:
○ Not just one etiology
§ Environmental: NSAIDs, Tobacco
§ Luminal Antigens: triggering immune system (nonpathogenic and pathogenic bacteria)
§ Genetics – the strongest evidence (chromosome 5, 10 )

hygiene hypothesis

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3
Q

• Ulcerative Colitis:

– where does this disease manifest?

A

Colonic involvement
continous
can have rectal involvement

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4
Q

Intestinal manifestatins of UC?

A

Blood diarrhea

Tenesmus

Acute toxic Presentation – fevers, abd pain, sepsis like

toxic Megacolon

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5
Q

what is seen on endoscopy of Ulcerative Colitis ?

A

§ Loss of vascular markings

§ Friable, edematous, inflamed mucosa

§ White Patches – ulcers and mucus

§ Pseudo-polyps: lesions due to constant cell turn over in the setting of constant colitis; not a sign of active disease
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6
Q

Micropathology of UC?

  • what is indicative colitis?
    what is indicative of IBD?
    what is indicative of UC?
A

limited to mucosal involvement

Indicative of Colitis: Active Inflammation – Neutrophils involving the crypts (Crypitis); Crypt Abscesses -

Indicative of IBD: Architectural abnormality
Feature of chronic injury; regenerative; weird crypt shapes

Indicative of UC: – continuous lesions confined to the mucosa

No Granulomas

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7
Q

what is the risk of CRC in UC patients?

A

8% by 20 years;

increased risk the longer you have UC

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8
Q

• Crohn’s Disease

– where does this disease manifest?

  • what is spared?
A
  • may be multi focal but can involve the entire GI tract

classically the terminal ileum and colon

Rectal sparing

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9
Q

Gross morphology of Crohn’s

some buzzwords

A

Skip lesions – (non continuous involvement)
Longitudinal ulcers,
“cobblestoning”

Transmural Invlvement: Strictures and fistulas

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10
Q

micropathologyof crohn’s

    • what’s indicative of colitis?
  • -what’s indicative of IBD?
    • what’s specific to Crohn’s ?
A

□ Skip lesions – areas of sparing and areas of involvement — macro and micro
□ Granulomas

Transmural Inflammation

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11
Q

Complications (colonic) of IBD

A

§ Malabsorption, weight loss, etc.

Transmural inflammation (CD) — scarring, stricture, perforation, fistula

Crohn’s – Perianal involvement

CRC – due to chronic inflammatory processes

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12
Q

extra manifestations of IBD

A
  • peripheral arthritis
  • Erythema Nodosom (CD)
  • Pyoderma Gangrenosum (UC)
  • Eye: Uveitis; Episcleritis
  • PSC (UC)
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13
Q

Treatment of IBD

A

Drugs:
CD: Corticosteroids, abx, infliximab, adalimumab

UC: Amino-ASA; 6 MP; Infliximab

Surgery for management of complications;

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14
Q

IBD

induce remission?

Maintain remission ?

A

○ Induce remission: steroids; aminosalicylates, abx, immunomodulators

Maintain Remission: immunomodulators, aminosalicylates, abx

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15
Q

Microscopic Colitis -

what is it? 
what is a possible etiology? 
how does it present? 
endoscopy findings? 
what are the two types? 
prognosis 
Treatment?
A

Idiopathic inflammation of the colon

possible etiology: NSAIDs

watery non bloody diarrhea; normal endoscopy

Collaenous vs Lymphocytic Collitis

Benign course
Treat: Symptomatic; reassurance

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16
Q

Collaenous Microscopic Colitis - male to female ratio?

- histo features?

A

females > males)
□ Increased intra-epithelial lymphocytes

Sub epithelial collagen table Markedly increased in thickness

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17
Q

Lymphocytic Colitis

male to female ratio?
- histo features?

A

(Females = Males)

Increased Intraepithelial lymphocytes

Preserved architecture

18
Q

Infectious Colitis: C. Diff

  • microbio
  • best assay for dectecion
  • risk factors;
A

anearobic, gram postive, spore forming bacillus

Assay of Choice : PCR

Risk: #1 Nosicomial GI Infection — usually older patients who have finished an course of anitbiotics

19
Q

C. Diff Colitis

  • presentation?

Micropathology?

A

Non bloody, watery diarrhea, fever, leukocytosis, abd cramping

path: Pseudo-membranes; volcanoe lesions

20
Q

C. Diff Colitis

treatment

A

○ Metronidazole
○ Vancomycin

If relapse – retreat or change meds

2nd replase: probiotics; Fecal Transplant

Severe - colectomy;

21
Q

HIV/AIDs Colitis

  • what is to be assumed when an HIV patient has diarrhea?
A

§ Diarrhea in 1/3 –> 2/3s of patients with HIV

§ Sometimes secondary infection can be indentified (syphilis, crypto, spirocheosis)

§ Assume HIV patinet with diarrhea is an opportunisitic infection until proven otherwise

§ HIV Enteropathy when no secondary infection is identified

22
Q

Ischemic Colitis

    • what is it?
    • classically involves what side and why?
    • presentation?

– gross pathology?

A

reduction of blood flow and insufficient to meet the demands of discrete regions of the colon — leading to necrosis

classically involving the left side of the colon, due to vulnerable vascular supply (less redundancy)

• Gross: Infarcts, Ulcers, pseudomembranes, Colonic edema
23
Q

Ischemic Colitis

Acute vs Chronic — micropathology

A

• Acute: necosis and inflammation
• Chronic: Fibrosis, atrophic crypts, cellular atypia
§ “whithered” glands in the setting of atrophy and diminished supply

24
Q

Ischemic Colitis

acute vs chronic – causes

A

Acute – thombosis, trauma, patients at risk for MI

Chronic – § PVD, CVD, “gut angina” — older patients

§ Young patients who are avid runners
25
Q

Risk factors for ischemic colitis ?

Presenation ?

A

Embolic disease, Previous Cardiopulmonary bypass, MI, Drugs, Hemodialyiss, thrombotic condtions, venous thrombosis, exercise and long distance running

left sided abd pain; hematochezia

26
Q

what are the two types of premalignant polyps of colo-rectal cancer ?

– gross morphological differences

Microscopic differences

A

Adenoma Polyp – usually portruding out of the mucosa;
Picket Fence nuclei

Serrated Polyp – usually flat/sessile
Mucin rich
serrated appearance
No picket fence nuclei

27
Q

Adenoma Polyp vs Serrated genetic differences?

A

Adenoma — Chromosomal instability pathway (KRAS, APC, BRAF)

SErrated – CPG island methylator phenotype (gene silencing mutations); Microsatellite instability (MMR genes)

28
Q

what are the two colon cancer “polyposis” syndromes (malignant)?

what is the genetic mutaiton of each

what is the risk of cancer progression

A

FAP – Familial Adenomatous Polyposis

APC mutation –
100% risk of CRC
Treat with prophylactic colectomy

Hereditary Non Polyposis Colon Cancer (HNPCC) -- Lynch Syndrome
MMR gene (Microsatellite instability)

80% risk of CRC
also risk of endometrial and ovarian cancers

29
Q

name two colonic polyposis syndromes which are mostly benign?

A

Peutz Jeghers: Mostly benign Polyps
Colorectal cancer risk
present with intussception

Juvenile Polyposis: Mostly Benign Poylps
Increased cancer risk: GI and Pancreatic cancers

Polyps may auto-amputate

30
Q

Molecular aspects of Colon cancer: describe three pathways of carcinogenesis

A

1) Chromosomal Instability (80%) (APC, KRAS, BRAF, p53)
seen in sporadic cancers and FAP

2) Microsatellite Instability Pathway (15%)
mutations in MMR genes
seen in Lynch and Sporadically

3) CpG islands: Gene silencing via methylation

31
Q

why is testing molecular phenotypes of CRCs important?

A

may direct treatment options

example – KRAS and BRAF mutations are negatively predictive of anti-EGFR therapies

32
Q

what is the most common CRC?

what are some risk factors for CRC?

A

Adenocarcinoma

Risk factors: Adematous and Serrated Polyps, family hx, IBD, Tobacco use, diet of high meat and low fiber

33
Q

Adenoma-Carcinoma Progression:

order of gene events?

A

APC
KRAS
P53, DCC

Low grade dysplasia –> High grade dysplasia –> invasive carcinoma

34
Q

In terms of IBD diseases, which has a greater risk for colon cancer ?

A

UC > CD

35
Q

Irritable Bowel Syndrome – what is it?

what is the Rome III criteria?

A

Abn stool frequency and abnormal stool passage (straining, urgnecncy, incomplete evaculation)

ROME: at least two of the following

1) Discomfort improved with defecation
2) Onset associated with change in frequency of stool
3) onset associated with change in form of stool

36
Q

Diagnosis?

Etiology?

Treatment ?

A

Dx – more of a diagnosis of exclusion. Do bx to r/o other disease

Etiology – unclear (increased motiligy, CNS/ENS dysregulation)

Treatment – Fiber, anti-diarrheals, antispasmodics, laxatives

37
Q

what is the differnce betwen a false and true diverticulum?

A

False (majority) – only mucosa and submucosa ooutpouch

true – all 3 walls of the gut outpouch (meckel’s)

38
Q

Diverticulitis
risk factors:
- classic symptoms:

complication

A

Risk factors; Age, western diet

LLQ pain, fever, leukocytosis

fistula

39
Q

Appendicitis

  • pathogenesis

presentation –

Treat –

A

Obstruction of lumen (fecalith, lymphoid hyperplasia)
Resulting ischemia and perforation of appendix

Classic symptoms: migratory abd pain (umbilicus, mcburney’s point), N/V

IVF, electrolytes, abx, percutaneous drainage, Surgery

40
Q

Hirschsprung’s Disease

-- what is it?
who presents? 
--  Symptoms? 
-- Radiology tests 
pathology? histology? 
Treatment?
A

Motility Disorder – congenital loss of ganglia; leading to loss of peristalsis

Symptoms: in infants (neonates); delayed meconium passage; Constipation - but very severe

• Radiology: barium enema shows transition zone from normal to abnormal bowel

Pathology – absence of ganglion cells. Hetertrophic nerves with no ganglion cells

Treatment: resection of the aganglionic segment

PT1 B3 (16 decks)

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