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GIS > GIS11 Pathology Of Small And Large Bowel > Flashcards

GIS11 Pathology Of Small And Large Bowel Flashcards

1
Q

Common diseases of small and large intestines

A
  1. Intestinal obstruction (anywhere in intestine —> digested food, faeces, mucus unable to pass through obstructed part —> intestine swells up —> ischaemic +/- perforate —> life-threatening)
  • Mechanical
    —> Physical blockage (e.g. tumour, external compression, solid objects)
    —> Extramural / Mural / Luminal
  • Functional (pseudo-obstruction)
    —> no mechanical blockage
    —> Paralytic ileus (intestine stop peristalsis)
    —> very ill patient (sepsis) / after abdominal surgery
  1. Ischaemic bowel disease
  2. Diverticular disease of colon
  3. Inflammatory bowel disease (Crohn’s disease + ulcerative colitis) (idiopathic)
  4. Neoplasms of intestine
    - Intestinal polyps
    - Colorectal carcinoma
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2
Q

Intestinal obstruction causes

A
  1. Extramural:
    - *Adhesion (previous surgery create adhesion bands —> interfere with peristalsis)
    - *Hernia (protrusion of abdominal organs into orifice e.g. inguinal / femoral canal)
    - *Volvulus (intestine twist around itself —> obstruction and strangulation)
    - External compression
  2. Mural:
    - *Tumour
    - *Intussusception (一段腸道套入另一段腸道, intestinal wall gets caught in peristaltic wave and gets carried along —> 縮窄腸道)
    - Strictures from previous inflammation
  3. Luminal:
    - Foreign object
    - Parasite
    - Bezoar
  4. Functional obstruction
    - *Paralytic ileus

*common

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3
Q

Intestinal obstruction signs and symptoms

A
  1. ***Absolute constipation
    - no defecation / passage of flatus (gas)
  2. ***Abdominal distension
    - peristalsis may be visible on abdominal wall
  3. ***Colicky pain
    - caused by intense peristalsis
    - pain comes and goes in waves
  4. Vomiting
    - more common in proximal small intestinal obstructions
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4
Q

Intestinal obstruction complications

A

Increasingly distended by fluids and gases
1. **fluids and electrolytes excreted into distended intestine
—> **shock, electrolyte imbalance

  1. increased luminal pressure compresses blood vessels in intestinal wall (esp in closed loop obstruction)
    —> intestinal **ischaemia
    —> **    perforation
    —> acute peritonitis
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5
Q

Intestinal obstruction diagnosis

A

Physical examination:

  1. ***Abdominal distension, visible peristalsis waves
  2. ***Hyperactive bowel sounds (except Paralytic ileus: Hypoactive)
  3. Visible hernia

X-ray:

  1. ***Dilated bowel loops on supine abdominal X-ray
  2. ***Multiple fluid levels on erect abdominal X-ray
  3. Sigmoid volvulus (visible)
  4. ***Contrast follow-through (delineate level of obstruction)
  5. CT scans (look for masses)
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6
Q

Ischaemic bowel disease - blood supply
—> ischaemic enteritis (small intestine)
—> ischaemic colitis (large intestine)

A

Ischaemic enteritis —> small intestine
Ischaemic colitis —> large intestine

  1. Superior mesenteric artery
    - Jejunum (jejunal artery)
    - Ileum (ileal artery)
    - Cecum (ileocolic artery)
    - Ascending colon (right colic artery)
    - Transverse colon (middle colic artery)
  2. Inferior mesenteric artery
    - Descending colon (left colic artery)
    - Sigmoid colon (sigmoid artery)
    - Proximal rectum (superior rectal artery)
  3. Left and right internal iliac arteries
    - Distal rectum (middle and inferior rectal artery)
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7
Q

Causes of ischaemic bowel disease

A
  1. Acute occlusion of arterial supply
    - blood supply to a segment of intestine cut off
    - Thrombosis, embolism, ruptured atherosclerotic plaque, vasculitis etc.
    - ***Dusky serosa of gangrenous part —> transition zone between viable part and gangrenous part
  2. Chronic ischaemia
    - Decreased blood supply over a long period of time (months)
    - Usually due to Atherosclerosis
    - Mucosa of chronically ischaemic part of intestine —> ***fibrotic
  3. Generalised hypotension
    - decreased blood supply to entire GI tract
    - Shock, severe blood loss
    - bowel at **“watershed areas” most susceptible to damage (e.g. **splenic flexure: watershed zone between SMA and IMA)
  4. Bowel strangulation
    - Severe external compression of intestinal wall (intestinal obstruction)
    - Sigmoid volvulus, strangulated hernia
    - blood unable to flow to strangulated part of intestine —> ischaemia + gangrene
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8
Q

Acute bowel ischaemia signs and symptoms

A
  1. ***Sudden onset of abdominal pain
  2. ***Bloody diarrhoea
  3. ***Shock
  4. Fever and signs of peritonitis if perforation
  5. ***Metabolic acidosis on arterial blood gas (electrolyte imbalance, HCO3↓)
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9
Q

Acute bowel ischaemia diagnosis

A
  1. CT scan with IV contrast

2. Laparoscopy / Laparotomy

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10
Q

Diverticular disease

A

Diverticulum: outpouching of intestinal wall

True diverticulum:

  • contains ***all layers of intestinal wall (mucosa, submucosa, muscularis propria, serosa)
  • usually ***congenital

False diverticulum:

  • only contains mucosa, some submucosal tissue, serosa, ***NO muscularis propria
  • ***acquired
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11
Q

False Diverticular disease Pathogenesis

A

Low fibre diet, chronic constipation, hard stool
—> **increased intraluminal pressure from peristalsis
—> mucosa pushed through **defects in the muscularis propria (where blood vessels and nerves travel through the muscularis propria)
—> formation of diverticula

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12
Q

Diverticular disease signs and symptoms

A
  1. Usually asymptomatic
  2. Most common around sigmoid colon, but can appear anywhere along colon (rarely in small intestine)
  3. ***Acute diverticulitis (diverticulum becomes inflamed)
  4. ***Diverticular abscess (forms around the inflamed diverticulum)
  5. ***Acute peritonitis (diverticular abscess ruptures into peritoneum)
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13
Q

Idiopathic inflammatory bowel disease

A

Chronic inflammatory disorder of small / large intestine of unknown etiology

Major features:

  • **Inflammation + **Ulceration of bowel mucosa
  • Relapsing clinical course over many years

2 entities:

  1. Crohn’s disease
  2. Ulcerative colitis
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14
Q

***Crohn’s disease vs Ulcerative colitis

A

Crohn’s disease:

  • affect ***entire GI tract (mouth to anus)
  • ***skip lesions: normal bowel between 2 or more segments of inflamed bowel
  • inflammation involves ***full thickness of bowel wall (transmural)

Ulcerative colitis:

  • ***large intestine only
  • ***continuous involvement from rectum to proximal colon, no skip lesions
  • inflammation involves ***mucosa and submucosa only
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15
Q

IBD proposed pathogenesis

A
  1. Abnormal gut ***microbiota?
  2. Defects in **tight junctions between epithelial cells (genetic causes?)
    —> increased intestinal permeability
    —> influx of bacterial components
    —> Activated T helper cells
    —> **    hyperactive mucosal immune response
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16
Q

***IBD morphology

A

Crohn’s disease

  1. Skip lesions
  2. Elongated ***serpentine (snake-like) ulcers
  3. Deep fissures between islands of relatively normal mucosa (cobblestone)
  4. Strictures, Thickened **rigid bowel wall (*lead-pipe)
  5. Fat wrapping around serosa (creeping fat)

Ulcerative colitis

  1. Continuous lesions beginning from Rectum
  2. ***Broad shallow ulcers
  3. Inflammatory ***pseudo-polyps (islands of regenerating mucosa between ulcers)
  4. Normal bowel wall
  5. Normal serosal surface
17
Q

IBD clinical features

A 
Crohn’s disease:
- abdominal pain
- diarrhoea
- weight loss
- malaise, anorexia, fever
- extra-intestinal manifestations
—> uveitis (eye)
—> arthritis (joint)
—> ankylosing spondylitis (spine)
—> sclerosing cholangitis (liver and bile duct)

Ulcerative colitis:

  • ***Bloody diarrhoea with mucus
  • ***Lower abdominal pain
  • malaise, anorexia (less severe)
  • extra-intestinal (similar to Crohn’s)
18
Q

IBD complications

A 
Crohn’s disease
1. Intestinal ***obstruction (strictures)
2. Intestinal ***perforation (fissure)
3. ***Fistula formation (fissures)
—> between bowel loops
—> between bowel and urinary bladder
—> between bowel and vagina
—> between bowel and abdominal skin
—> anal fistula
4. Increased risk of colorectal carcinoma

Ulcerative colitis

  1. ***Toxic megacolon
    - severely dilated colon filled with gas
    - impending perforation
    - high mortality
  2. Increased risk of colorectal carcinoma
19
Q

Colon polyps

A
  • proliferation of colonic epithelium into a raised or mushroom-shaped structure
  • associated with increased risk becoming carcinoma (neoplastic polyps)
  • major types:
    1. Hyperplastic polyps
    1. Adenomas
      1. Inflammatory polyps
      2. Harmatomatous polyps (proliferation of both epithelial and stromal cells, can be hereditary)
20
Q

Hyperplastic polyps

A
  • ***Benign proliferation of colonic epithelium
  • very common after 50-60 years
  • gross morphology: ***mushroom-shaped mucosal protrusion
  • microscopic morphology: elongated gland with serrated (saw teeth-like) surface
21
Q

Adenoma

A
  • **Neoplastic proliferation of colonic epithelium —> **potential to become carcinoma
  • gross morphology: ***Pedunculated (elongated stalk) polyp
  • microscopic morphology: Tubular, Villous, Tubulo-villous (not much clinical significance)
  • ***Epithelial dysplasia present
    —> degree of epithelial dysplasia (low grade / high grade) correlate with risk of becoming carcinoma
    —> low grade: elongated nuclei
    —> high grade: complex architecture, multiple branching gland, fusion of glands
22
Q

Colorectal carcinoma

A
  • Carcinoma from epithelium of large intestine
  • Most common in HK by incidence
  • age of onset: usually 60-70

Risk factors:

  • Diet / Lifestyle: ***smoking, low intake of fibre, obesity, red meat and refined carbohydrate
  • GI diseases: Crohn’s disease, Ulcerative colitis
  • Genetics: positive family history, hereditary colorectal carcinoma syndrome
23
Q

***Colorectal carcinoma morphology

A

Gross appearance:

  1. ***Polypoid mass (with central ulceration)
  2. ***Everted edges
  3. Constricting annular mass around colonic circumference (sometimes)

Microscopic appearance:

  1. Cuboidal to columnar cells forming irregular gland-like structures
  2. High N/C ratio, enlarged nuclei, severe variation in nuclear diameter
  3. Invasion beyond muscularis mucosae
24
Q

Colorectal carcinoma Grading and Staging

A

Grading:

  • Well / Moderately / Poorly differentiated
  • Tumour graded on how much it resembles normal colonic epithelial cells
  • Grade determine how much ***gland formation the tumour has

Staging:

  • T: Depth of tumour invasion (into submucosa, into / beyond muscularis propria, perforate visceral peritoneum, invasion into adjacent organs)
  • N: Number of regional lymph nodes with metastatic carcinoma
  • M: Distant metastasis
25
Q

***Colorectal carcinoma Signs and symptoms

A 
Right colon (caecum, ascending)
1. Anaemia
2. Malaise
3. Weight loss
(Stool still fluid in right colon —> can pass through tumour constriction —> not much change in bowel habit)

Left colon (left transverse, descending, sigmoid)

  1. Altered bowel habit
  2. ***Haematochezia (passage of fresh blood with stool)
  3. ***Tenesmus (feeling of incomplete defecation; if tumour in rectum)
  4. ***Intestinal obstruction
26
Q

Adenoma-Carcinoma sequence in FAP

A
  1. Normal colon:
    - Inherited / acquired mutations of Tumour suppressor gene (1st hit) (APC)
  2. Mucosa at risk:
    - methylation abnormalities/ inactivation of normal alleles (2nd hit) (***APC)
  3. Adenomas:
    - protooncogene mutations (KRAS)
    - homozygous loss of additional Tumour suppressor genes / overexpression of COX-2 (    p53, LOH, SMAD2, SMAD4)
  4. Carcinoma:
    - additional mutations, gross chromosomal alteration (telomerase, many genes)
27
Q

Familial colorectal cancer syndrome

A

Familial adenomatous polyposis (FAP)

  • autosomal dominant
  • hundreds of adenomatous polyps in colon (pan-colonic)
  • > 90% chance of developing into colorectal cancer by 50 years old
  • skin and bone tumours (variant of FAP)
  • brain tumours (variant of FAP)
  • **- APC gene (tumour suppressor gene)
  • **- APC/WNT pathway —> chromosomal instability
  • **- diagnosis: Endoscopy: at least 100 polyps in the colon

Hereditary non-polyposis colorectal cancer (HNPCC, Lynch syndrome)
- autosomal dominant
- colon cancer (esp. proximal colon, little to no polyps)
- gastric carcinoma
- endometrial / ovarian carcinoma
- ureter and renal pelvis carcinoma
- biliary tract carcinoma
**- MSH2, MLH1
**- mutation in DNA mismatch repair pathway —> microsatellite instability
***- diagnosis: Amsterdam criteria II
—> 3 people in a family got colorectal cancer / non-GI tumours
—> 2 successive generations affected
—> 1 person is 1st degree relative
—> 1 person diagnosed before 50 years old
—> + NOT FAP (must satisfied)

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