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Pathology Term 2 > Week 6 - LOWER GIT > Flashcards

Week 6 - LOWER GIT Flashcards

IBD, Polyps, Colon Cancer, Malabsorption, Haemorrhoids

1
Q

What are the 3 supposed etiological factors for IBD?

A

*unkown etiology

  1. genetic susceptibility –> HLA-DR1/DR7
  2. environmental factor –> gut flora
  3. immune dysfunction –> autoimmunity
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2
Q

True or False?

IBD increased risk in western countries

A

True

-hygiene theory?

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3
Q

True or False?

Smoking decreases risk and severity of chron’s disease but increases risk/severity of ulcerative colitis

A

False

-other way around

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4
Q

What 2 inflammatory mediators play a role in the development of IBD?

A
  1. TNF-alpha
    - T cell over activation (increased inflamm.)
  2. IL-10
    - mutations of IL-10 and its receptor genes –> severe/early onset IBD –> decreased anti-inflammatory effect
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5
Q

What is the new drug of promise for IBD?

A

Anti-TNF alpha antibody

e.g. remicade/infliximab

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6
Q

What is the pathogenesis of IBD?

A
  1. excess TNF-alpha
  2. decreased IL-10 (IL-10 normally STOPS inflamm.)
  3. UNCONTROLLED INFLAMMATION
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7
Q

Compare CD and UC, and what % is Inderterminate Colitis?

A

CD:

  • whole GIT
  • patchy “skip lesions”
  • thick, narrow, deep ulcers - transmural
  • chronic granuloma
  • ulcerations/fissures
  • fibrous

UC:

  • colon mucosa ONLY (not serosa)
  • continuous, thin, dilated
  • acute inflammation
  • ulcers/pseudopolyps
  • broad, shallow ulcers
  • NO thickening, fibrosis, narrowing or granulomas

*10% cases = indeterminate colitis (mixed pattern)

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8
Q

Where can CD affect and where does it most commonly affect?

A
  • ANYWHERE in the GIT (mouth –> anus)

- commonly affects cecum + terminal ileum (RLQ)

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9
Q

What are the gross features of CD?

A
  1. mucosa –> “cobblestone” (narrow deep ulcer)
  2. wall –> thick + fibrotic
  3. skip lesions (patchy)
  4. creeping mesenteric fat (as inflammation spreads to the serosa)
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10
Q

What is ‘string sign’?

A

radiographical sign on CD whereby narrow crohn’s segments DO NOT take up the contrast/dye

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11
Q

What are microscopic features of CD?

A
  • narrow deep ulcers
  • transmural inflammation
  • lymphocytes
  • granuloma ( lymphocytes, macrophages, giant cells, NO caseation)
  • crypt abscess (also in UC) –> WBCs accumulate within crypts
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12
Q

True or False?

Skip lesions present in both CD and UC

A

False

- only in CD

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13
Q

What are the features + complications of CD?

A
  • spreading, granulomatous inflammation
  • fibrosis
  • thickening
  • narrowing
  • obstruction
  • adhesions
  • fistula/sinus –> watering pot perineum
  • abscess
  • anemia (iron/B12)
  • adenocarcinoma
  • malabsorption synd.
  • polyarthritis
  • erythema nodosum/pyoderma granulosum
  • apthous ulcers
  • scleritis
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14
Q

When does UC affect the ileum?

A

“backwash ileitis”

-when whole of colon is affected, inflammatory mediators can enter ileum causing ileitis (inflamm.) –> but NO ulcer formation

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15
Q

True or False?

inflamm. in UC is limited to mucosa

A

True

-serosa is normal (unlike in CD)

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16
Q

What is toxic megacolon?

A
  • total paralysis and loss of peristalsis of colon due to toxic damage to muscular layer
  • dilated, stasis, gangrene
  • complication of UC
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17
Q

Why is the active disease of UC in the right side of the colon?

A
  • UC begins in the rectum and gradually spreads from L –> R colon
  • therefore L side becomes atrophic with atrophic mucosa and smooth sides (inactive UC phase) and R side becomes active (red/granular)
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18
Q

What is a pseudopolyp?

A
  • complication of UC

- oedematous, intact area of mucosa between broad/shallow ulcers

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19
Q

What are the gross and microscopic features of UC?

A

Gross:

  • ulcers (broad/shallow)
  • pseudopolyps

Micro:

  • acute inflammation limited to mucosa
  • crypt abcsess (WBCs inside glands)
  • pseudopolyps
  • NO granuloma
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20
Q

What 2 key complications can occur in UC but not in CD?

A
  1. toxic megacolon
  2. perforation

N.B. Haemorrhage risk markedly increased in UC compared to CD

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21
Q

Which IBD is colonic cancer more likely to occur in?

A

UC - pancolitis

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22
Q

Which IBD has an increased risk of developing malabsorption syndrome and why?

A

CD

  • involves ileum –> impaired fat metabolism/B12 absorption –> malabsorption
  • UC only affects colon
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23
Q

Which macrophage activation pathway is seen in UC and CD?

A

UC –> M1 (increased inflamm. + NO fibrosis)

CD –> M2 (significant fibrosis + granulomatous inflamm.)

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24
Q

What are the types of polyps?

A
  1. non-neoplastic (90%)
    - low/no malignancy
    - hyperplastic –> most common
    - inflammatory/pseudopolyps –> IBD
    - hamartoma/congenital/juvenile polyps
  2. neoplastic (10%) adenoma
    - high malignancy (oncogene activation)
    - tubular (90%), tubulovillous (10%), villous (1%)
    - sporadic/familial (FAP, HNPCC)
    - adenocarcinoma
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25
Q

What are the features of hyperplastic polyps?

A
  • commonest –> non-neoplastic
  • small (<5mm)
  • distal/L side - sigmoid colon
  • sessile, multiple, normal colour

Micro:

  • increase large glands
  • hyperplasia
  • NO dysplasia (normal function)
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26
Q

What neoplastic polyp is similar in appearance to hyperplastic polyps?

A

Sessile Serrated Adenoma

  • neoplastic
  • R side (cecum)
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27
Q

Clinically, what is the commonest polyp seen?

A

hyperplastic polyp

28
Q

What type of congenital polyps are present in children <3yrs and in adults?

A

<3yrs
-juvenile polyps (rectum)

adults
-retention polyps

*congenital hamartomas

29
Q

What are the 2 types of juvenile polyposis syndromes?

A
  1. Peutz-Jeghers Syndrome
    - STK11 (tum. spp. gene)
    - SI, stomach, colon
    - oral pigment macules –> brown/black ulcers in mouth
  2. Cowden Syndrome
    - PTEN (tum. spp. gene)
    - GI polyps with lipomas, neuromas, etc
    - GI malignancy
30
Q

How many polyps are seen in familial adenomatous polyposis (FAP) and what gene mutation causes it?

A
  • 100 - 2500
  • APC gene mutation (autosomal dominant)
  • 100% pts. will get adenocarcinoma <50yrs
31
Q

What is HNPCC also referred to as?

A

Lynch syndrome

32
Q

How many polyps are present in HNPCC and what genes are mutated?

A
  • none or <100 polyps
  • MSH2 or MLH1 (DNA repair genes)
  • malignancy later age than FAP (still younger than sporadic colon cancer)
33
Q

What is the commonest neoplastic polyp type?

A

tubular adenoma (90%)

34
Q

Describe gross appearance of tubular vs. villous adenomas?

A

Tubular
-like a ‘fruit’ hanging from a stalk (pedunculated)

Villous
-like a ‘carpet’ of multiple villous structures

35
Q

What is the commonest carcinoma of the colon?

A

adenocarcinoma

36
Q

What % of colon cancer is sporadic and what is the peak age group? What % is familial?

A
  • 80% sporadic (peak 60-70yrs)

- 20% familial (<50yrs)

37
Q

What is the most popular population screening method for colon cancer?

A

Stool Occult Blood

-in >50y.o.

38
Q

What are the 2 types of colon cancer?

A
  1. Right/Proximal/Familial

2. Left/Distal/Sporadic

39
Q

Why is it supposed aspirin has a protective effect on colon cancer?

A
  • aspirin inhibits COX2

- colon cancer expresses increased levels of COX2

40
Q

What are the 2 main etiological factors for colon cancer?

A
  1. Environmental
    - decreased dietary fibre + increased refined fat/carbohydrates –> increased anaerobic bacteria –> increased cholesterol –> increased risk
    - aspirin, calcium, folates –> PROTECTIVE
  2. Genetic
    - APC/B-catenin –> tumour spp. genes (80%)
    - MLH1/MSH2 –> DNA repair + TGF-B genes (20%)
    - other genes: - BAX, KRAS, TP53, etc.
41
Q

What are the 2 pathogenetic pathways for colon carcinoma?

A
  1. More common 80%
    - germline/somatic mutations of tum. spp. gene (APC) –> first hit
    - inactivation of normal allele (risk factors) –> second hit
    - overexpression of COX2 –> adenomas (dysplasia) –> carcinomas
  2. DNA mismatch repair pathway 20%
    - MLH1/MSH2 –> HNPCC
    - microsatellite instability –> microadenomas –> carcinomas (NO polyps)
42
Q

What is the commonest clinical feature of colon cancer?

A

ASYMPTOMATIC

  • fatigue (IDA)
  • wt. loss, etc. (normal malig. features)
43
Q

What are the clinical features of L + R sided colon cancer?

A

Left:

  • distal/rectal tumours may be palpable on P/E
  • colicky lower abdo. pain –> constricting/early obstruction
  • diarrhoea, bleeding –> fresh blood
  • sporadic increased

Right:

  • anemia/wt. loss
  • polypoid
  • NO obstruction
  • occult bleeding –> requires lab tests
  • familial increased
44
Q

What are some rare complications of colon cancer?

A
  • perforation
  • peritonitis
  • abscess
  • fistula
45
Q

Which side colon cancer is referred to as ‘napkin ring’/apple core?

A

Left-sided:

  • constricting –> obstruction
  • fresh blood in stools
  • distal colon
  • sporadic common
  • CONSTIPATION
46
Q

What are the microscopic features of adenocarcinoma of the colon?

A

irregular, pleomorphic cells forming irregular glands (with necrosis)

47
Q

Outline Dukes staging for colon cancer? and clinically, when is the Dx. most likely to be made at?

A

A –> tumour confined within bowel wall
B –> extension through bowel wall (no LN involvement)
C –> tumour involving LN’s
D –> distant metastasis

*B/C –> 65% of diagnoses made here

48
Q

True or False?

familial cancers commonly located on L side

A

False

- right side

49
Q

Why can you get mixture carcinomas in anal canal?

A
  • comprised of 3 different types of epithelium
  • deep –> superficial:
    1. columnar - adeno.
    2. transitional - mixed (basaloid squamous carcinoma)
    3. squamous - squamous
50
Q

Where do basaloid squamous carcinomas occur and describe features?

A
  • rectum/anal canal (transitional epithelium)
  • basal cell carcinoma (i.e. skin)
  • basaloid cells around tumour (palisading “fence-like”)
  • keratin pearls + mucin may be present
  • locally invasive (no metastasis)
51
Q

What is the definition of diarrhoea and what are the causes/

A
  • increase in stool mass (>200g/day), frequency or fluidity volumes (>200mL/day)
    causes: - infection, inflammation, ischaemia, malabsorption + nutrition
52
Q

What are the types of diarrhoea?

A
  1. secretory
    - excess intestinal secretion
    - isotonic stool persists during fasting
    - bile/pancreatic disorders
  2. osmotic
    - unabsorbed luminal solutes
    - lactase deficiency
  3. malabsorptive
    - fat, pale, greasy stools –> relieved by fasting
  4. exudative
    - inflamm/infection
    - purulent, bloody –> continues during fasting
    - IBD
53
Q

What are the 3 main causes of malabsorption disorders?

A
  1. Secretory defects –> bile, pancrease
  2. Motility/bacteria –> DM, infections
  3. Mucosal damage –> sprue, whipple
54
Q

What are the clinical features of malabsorption disorders?

A
  • chronic diarrhoea (decreased absorption)
  • wt. loss, anorexia, bloating –> due to fermentation of nutrients causing increased CO2
  • steatorrhoea –> pale, greasy stools
  • Vit D (hypocalcemia) + Vit K (bleeding) deficiencies
  • ADEK –> fat-soluble vitamins decreased due to decreased FAT absorption
55
Q

What vitamins are deficient in malabsorption disorders and why?

A

ADEK –> fat-soluble vitamins

-due to decreased fat absorption in malabsorption syndromes

56
Q

What % of bile acids are actively reabsorbed and where does this occur?

A

95% in terminal ileum and recycled through enterohepatic cycle 6-8x/day

57
Q

What alleles are affected in celiac disease and what autoantibodies do celiacs possess?

A
  • HLA-DQ2 or DQ8

- IgA antigliadin Ab/IgA transglutaminase Ab –> JEJUNUM

58
Q

What is the pathogenesis of celiac disease?

A
  • immune enteropathy to protein gluten (gliadin fraction)
  • genetic predisposition –> HLA DQ2/DQ8 + IgA antigliadin Ab –> cross-reacts with jejunal mucosa brush border –> inflammatory/immune-mediated damage of jejunal mucosa –> decreased SA –> decreased absorption (VILLOUS ATROPHY = DECREASED ABSORPTIVE CAPACITY)
59
Q

What is the pathogenesis of tropical sprue/ environmental enteropathy?

A
  1. poor hygiene/sanitation
  2. feco-oral infections
  3. intestinal inflammation
  4. immune activation
  5. environmental enteropathy
  6. malabsorption
  7. malnutration –> back to 1.
60
Q

What is autoimmune enteropathy?

A

IPEX

  • Immune dysregulation Poly-Endocrinpathy + X-linkage
  • severe diarrhoea in young children
61
Q

What is the pathogenesis of lactose intolerance?

A

lactase deficiency –> increased lactose –> osmotic diarrhoea –> lactose fermented by bacteria (increased CO2 –> gas + cramps)

62
Q

What is seen on microscopy of Whipple’s disease?

A
  • plenty of foamy macrophages in mucosa, full of partly digested rod-shaped bacilli –> Tropheryma whippelii (gram + actinomycete)
  • PAS stain +, little/no inflamm.
63
Q

True or False?

Malabsorption in Whipple’s is due to lymphatic block

A

True

64
Q

What are haemorrhoids and what are typical causes?

A
  • dilatation of veins due to increased haemorrhoidal venous pressure
    causes: - straining, constipation, pregnancy, portal HTN
65
Q

What are the 2 types of haemorrhoids?

A
  1. External
    - inferior plexus
    - below anorectal line
  2. Internal
    - superior plexus
    - above anorectal line
66
Q

What are the clinical features and Tx. of haemorrhoids?

A

CF’s:

  • > 30yrs
  • pain, mass, bleeding
  • bright red blood on toilet paper

Tx.

  • scleropathy
  • band ligation
  • IR coag.
  • surgery

Pathology Term 2 (6 decks)

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