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Patho - GIT > Intestines > Flashcards

Intestines Flashcards

1
Q

Conditions of the small & large intestines

A

Congenital

  1. Meckel diverticulum
  2. Hirschsprung disease

Acquired

  1. Ischemic bowel disease
  2. Intestinal obstruction
  3. Infectious enterocolitis
  4. Acute appendicitis
  5. Pseudomembranous colitis
  6. Intestinal tuberculosis
  7. Amebiasis
  8. Inflammatory bowel disease (CD, UC)
  9. Diverticular disease
  10. Neoplasms
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2
Q

Features of Meckel diverticulum

A
  • blind outpouching of GIT on anti-mesenteric border of ileum
  • mimics acute appendicitis
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3
Q

Features of Hirschsprung disease

A
  • congenital aganglionic megacolon
  • absence of neural crest derived ganglion cells within the colon - lacking Meissner submucosal & Auerbach myenteric plexus
  • absence of co-ordinated peristalsis - functional obstruction of affected bowel & proximal dilation
  • constipation, abdominal distension, bilious vomiting
  • enterocolitis, megacolon, fluid & electrolyte disturbances, perforation, peritonitis, sepsis
  • surgical removal of aganglionic segment
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4
Q

Conditions predisposing to ischemic bowel disease (5)

A
  1. Arterial thrombosis - atherosclerosis, vasculitis, hypercoagulability
  2. Arterial embolism - vegetations, aortic atheroembolism
  3. Venous thrombosis - hypercoagulability, oral contraceptives, sepsis
  4. Non-occlusive ischemia - congestive cardiac failure, shock, dehydration, drugs
  5. Others - radiation, volvulus, herniation, adhesions
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5
Q

Causes of intestinal obstruction (4)

A

Mechanical

  1. Herniation
  2. Adhesions
  3. Volvulus
  4. Intussusception - intussusceptum (proximal), intussuscipiens (distal)
  5. Others - strictures, atresias, stones, tumour

Functional
- bowel infarction, ileus, loss of ganglion cells

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6
Q

Effects of intestinal obstruction

A
  • mesentery (and vessels running through) is affected
  • arterial, venous & lymphatic obstruction
  • ischemia, congestion, edema
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7
Q

Causes of infectious enterocolitis

A
  1. Bacteria - E. coli, Salmonella, Shigella, Vibrio cholerae, Campylobacter jejuni, Mycobacteria
  2. Viruses - rotavirus, enteric adenovirus, in immunosuppressed patients - HSV, CMV
  3. Fungi - candida, aspergillus, mucormycosis, histoplasma
  4. Protozoa & parasites - Entameba histolytica, Giarda, Ascaris etc
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8
Q

Causes of acute appendicitis

A
  • obstruction of lumen by fecolith, foreign matter, lymphoid hyperplasia
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9
Q

Pathogenesis of acute appendicitis (5)

A
  1. Obstruction of lumen
    - increased luminal pressure, ischemia, stasis - bacterial infection
  2. Multiplication of luminal bacteria
  3. Invasion of mucosa & wall
  4. Acute inflammatory response - neutrophils
  5. Necrosis & ulceration
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10
Q

Morphology of acute appendicitis

A
  • mucosal ulceration, necrosis
  • acute suppurative inflammation in the wall (transmural)
  • fibrinopurulent serosal exudate (neutrophilic infiltrate)
  • edema & turgidity
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11
Q

Effects & complications of acute appendicitis (3)

A
  1. Abdominal pain - umbilical to R iliac fossa
  2. Nausea, vomiting, low grade fever, mildly elevated peripheral white cell count
  3. Perforation - generalised peritonitis, pelvic/subphrenic abscesses
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12
Q

Features of pseudomembranous colitis

A
  • antibiotic-associated - disruption of normal colonic microbial flora - C. diff overgrowth
  • formation of pseudomembranes - adherent layer of inflammatory cells & debris at sites of mucosal injury - damaged crypts spew out mucopurulent exudates
  • fever, leukocytosis, abdo pain/cramps, watery diarrhea
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13
Q

Diagnosis of pseudomembranous colitis

A
  • detect C. difficile toxin

- histopathology

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14
Q

Features of intestinal tuberculosis

A
  • most commonly ileocecal region
  • circumferential ulcers, thickening of wall, strictures
  • regional lymphadenopathy
  • miliary spread
  • caseating granulomas - epithelioid histiocytes, Langhan giant cells, central caseous necrosis
  • Ziehl-Neelsen stain for AFB
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15
Q

Features of amebiasis

A
  • Entameba histolytica
  • colorectum esp cecum, asc colon
  • bloody diarrhea w mucus, intestinal pain, fever (amebic colitis)
  • ingested cysts release trophozoites - invade colonic epithelium
  • amoeba proteins aid tissue invasion: proteinases break down, lectin bind, amebapore makes holes
  • diffuse colitis, flask shaped ulcers w shaggy edges, napkin-like constrictive mass (gran tissue)
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16
Q

Features of inflammatory bowel disease

A
  • idiopathic chronic conditions resulting from inappropriate mucosal immune activation
  • involves altered host interaction w intestinal microbiota, epithelial dysfunction, altered composition of gut microbiome, abnormal host immunoreactivity
  • genetic predispositions, infectious agents
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17
Q

Features of Crohn Disease

A
  • recurrent granulomatous fibrosing inflammatory disorder
  • affecting terminal ileum/colon +/- other systemic manifestations
  • segmental, skip lesions, but full thickness
  • transmural chronic inflam w lymphoid follicles
  • non caseating granulomas
  • discrete ulcers, deep
  • fibrosis
18
Q

Complications of Crohn Disease (7)

A
  1. Lymph node involvement
  2. Strictures, narrowed lumen (string sign)
  3. Fissures, fistulas
  4. Pericolic abscesses
  5. Perforation, peritonitis, pain
  6. Nutritional deficiencies - malabsorption (term ileum - B12)
  7. Risk of malignancy in GIT
19
Q

Morphology of Crohn Disease

A

G:

  • cobblestone appearance
  • deep ulcers & fissures

M:

  • transmural inflammation - chronic inflam cells in all layers of gut wall
  • non-caseating granulomas
  • distortion of mucosal architecture
  • crypt abscesses
20
Q

Features of Ulcerative Colitis

A
  • recurrent, acute-on-chronic, ulcero-inflammatory
  • affects mainly rectum & distal colon
  • extensive, diffuse, superficial
  • higher association/risk than CD for CRC
  • systemic manifestations: erythema nodosum, migratory polyarthritis, sacroilitis, ankylosing spondylitis, uveitis, conjunctivities, primary sclerosing cholangitis
21
Q

Active vs chronic phases of Ulcerative Colitis

A

Active phase

  • irregular mucosal surface with luminal pus
  • shallow ulceration
  • colicky aching pain
  • chronic inflam cells in lamina propria
  • neutrophil infiltration w cyst abscesses
  • congestion & edema
  • mucin depletion of goblet cells
  • occasional acute hemorrhage, diarrhea

Chronic phase

  • ulceration w healing
  • mucosal atrophy
  • inflammatory pseudopolyps - extensive epithelial regeneration - risk of dysplasia
22
Q

Complications of Ulcerative Colitis (3)

A
  1. Malignancy
  2. Nutritional deficiencies
  3. Toxic megacolon - severe acute dilation - rupture - peritonitis
23
Q

Morphology of Ulcerative Colitis

A

G:

  • shallow ulcers
  • pseudopolyps & mucosal bridges (regenerating)

M:

  • inflammatory pseudopolyps
  • inflammation limited to mucosal layer
  • crypt abscesses
  • mucosal atrophy w loss of folds
24
Q

Features of diverticular disease

A
  • mucosal outpouching through areas of weakness in gut wall due to increased intraluminal pressure
  • most commonly in the sigmoid colon
25
Q

Effects & complications of diverticular disease (2)

A
  1. Acute inflammation - diverticulitis
    - pericolic abscesses, fibrosis, adhesions
    - perforation, peritonitis
    - colovesical fistula formation
    - strictures & intestinal obstruction
  2. Erosion of blood vessesls
    - bleeding
    - iron def anemia
26
Q

Neoplasms/pre-cancerous conditions of the bowel

A
  1. Hamartomatous polyps, Peutz-Jeghers Syndrome
  2. Adenoma
  3. Colorectal Carcinoma
27
Q

Features of adenomas of the bowel

A

Growth patterns

  • tubular - narrow base with stalk, tubular invaginations
  • tubulovillous
  • villous - broad base, finger like projections
28
Q

Malignant potential of adenomas of the bowel

A
  • early detection - 70-80% survive ≥5y
  • degree of dysplasia
  • type of polyps - malignant risk of villous > tubulovillous > tubular
  • sessile vs pedunculated - sessile most likely to have submucosal invasion
  • size & number of polyps
29
Q

Risk factors of colorectal carcinoma

A
  • 60-79y
  • familial syndromes (FAP, HNPCC)
  • pre-existing colorectal pathologies (CD, UC)
  • obesity, inactivity, dietary factors (high calorie, low fibre, high carb, red meat)
30
Q

Gross morphology of colorectal carcinoma

A
  • polypoidal, fungating or ulceratied
  • proximal colon: larger tumours, tend to grow as polypoid, exophytic masses - obstruction, anemia
  • distal colon: circumferential growth/apple core lesions, annular, encircling lesions - produce napkin ring constrictions of the bowel - obstruction - occult bleeding, pain, change in bowel habits
31
Q

Microscopy of colorectal carcinoma

A
  • well, moderate (90%) or poorly differentiated
  • prominent desmoplastic response
  • abundant intraluminal eosinophilic necrotic debris
  • extracellular mucin pools in mucinous subtype
32
Q

Features of FAP

A
  • familial adenomatous polyposis, hereditary AD disorder
  • mutations in APC gene chromosome 5q21
  • numerous colorectal adenomas + extra colonic manifestations eg congenital hypertrophy of retinal pigment epithelium
  • associated neoplastic syndromes - Gardner’s, Turcot
33
Q

Features of HNPCC

A
  • hereditary non-polyposis colorectal cancer, AD disorder
  • genetic defect involving at least 4 mismatch repair genes
  • predominantly R colonic involvement with the development of sessile serrated adenomas
  • Amsterdam criteria - 3 family members w cancer, 2 gen apart, 1 w early onset cancer bef 50y
34
Q

Pathways of molecular pathogenesis of CRC

A
  1. Chromosomal Instability Pathway

2. Microsatellite Instability Pathway

35
Q

Features of the chromosomal instability pathway

A
  • associated with FAP
  • APC (tumour suppressor) loss of function
  • allows increased Wnt/ß-catenin pathway signalling
  • drives cell cycle
  • increased proliferative activity
  • accumulation of further mutations: K-RAS, SMAD2, SMAD4, p53, telomerase
  • poorer prognosis
36
Q

Features of the microsatellite instability pathway

A
  • associated with HNPCC
  • MSH2, MSH6, MLH1 (DNA mismatch repair genes) loss of function
  • allows accumulation of mutations in microsatellites (generally silent)
  • mutations within coding/promoter regions - further mutations
37
Q

Staging of colorectal cancer

A
  • invasive carcinoma - beyond muscularis mucosa (rather than BM)
  • T1/2/3/4 - submucosa/muscularis propria/pericolorectal tissues/visceral peritoneum & adheres to other organs/structures
  • N1/2 - cancer cells found in/near 1-3/≥4 nearby lymph nodes
  • M1a/b - spread to 1/>1 distant organ/set of lymph nodes
38
Q

Clinical features of CRC

A
  • altered bowel habits
  • signs of chronic blood loss - iron def anemia, melena
  • mets commonly to liver
39
Q

Prognostic factors of CRC (5)

A
  1. Staging
  2. Presence of familial syndromes (worse)
  3. Molecular pathway implicated (chromosomal poorer)
  4. Concomitant inflammatory bowel disease (increased recurrence risk)
  5. Presence of K-RAS mutations (less likely to respond to treatment)
40
Q

Causes of upper GI bleeding (8)

A
  1. Erosive duodenitis
  2. Duodenal ulcer
  3. Gastric erosions
  4. Gastric ulcer
  5. Esophageal varices
  6. Mallory-Weiss tear
  7. Esophagitis
  8. Neoplasm
41
Q

Causes of lower GI bleeding (8)

A
  1. Hemorrhoids
  2. Solitary rectal ulcer
  3. Diverticulosis
  4. Meckel diverticulum
  5. Colitis - ischemic, radiation, ulcerative, infective
  6. Intussusception
  7. Angiodysplasia
  8. Neoplasm

Patho - GIT (5 decks)

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