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Pathology > Lower GI Histopath > Flashcards

Lower GI Histopath Flashcards

1
Q

What is Hirschsprung’s disease?

A

Absence of ganglion cells in myenteric plexus (80% males)

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2
Q

Presentation of Hirschsprung’s (1)

A

Signs & symptoms of obstructions in babies (mostly males)

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3
Q

Hirschsprung’s association (1), Genetics (1), biopsy (1), treatment (1)

A

Associated with Down’s

Genetics - RET proto-oncogene Cr10

Biopsy - hypertrophied nerve fibres, no ganglia

Treatment - resection of affected segment

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4
Q

5 congenital lower GI diseases

A

Atresia

Stenosis

Duplication

Imperforate anus

Hirschsprung’s disease

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5
Q

Mechanical causes of obstruction: (6)

A

Constipation

Diverticular disease

Adhesions

Hernia

Volvulus - complete twisting of bowel loop at mesenteric base around vascular pedicle (in infants its mostly sigmoid, in elderly its caecal)

Intussuception

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6
Q

Causes of acute colitis (3)

A

Infection

chemo/radiotherapy

Drugs

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7
Q

Causes of chronic colitis (2)

A

IBD TB

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8
Q

Ischaemic colitis causes (3)

A

Arterial/ venous occlusion

small vessel disease

low flow state

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9
Q

Where is it most common for ischaemic colitis to occur?

A

Watershed areas (weak points at the borders supplied by the IMA & SMA)- splenic flexure, rectosigmoid

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10
Q

C. Diff - cause (1), exotoxin results in (1), Investigation (1), treatment (1)

A

Abx - kill off commensals exotoxin causes pseudomembranous colitis

Ix - stool culture

Rx- metronidiazole or vancomycin (2nd line)

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11
Q

Diverticular disease - what is it (1), where does it occur mostly (1), symptoms (1),

A

High intraluminal pressure results in outpouchings in weak points of bowel wall (low fibre diet)

PR bleed sometimes (mostly asymp)

Occurs 90% of time in left colon

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12
Q

Complications of diverticular disease (3)

A

Diverticulitis - fever & peritonism

Perforation fistula obstruction

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13
Q

Epidemiology of IBD - age of onset, race,

A

Both peak age in 20’s White ppl > non-white

Crohn’s symptoms worsened by smoking

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14
Q

MZ twin concordance IBD

A

UC - 15%

Crohn’s - 50% aetiologies unknown

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15
Q

Pathophysiology of Crohn’s (6)

Distribution, lesion characeristics, inflammation

A

Whole GIT affected - most common in terminal ileum & caecum

Patchy distribution - SKIP lesions COBBLESTONE appearance - areas of healthy mucosa lie above diseased mucosa

1st lesion = APTHOUS ULCER; deep ROSETHORN ulcers (which can join to form serpentine ulcers)

NON-CASEATING GRANULOMAS seen TRANSMURAL inflammation

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16
Q

Pathophysiology of UC (6)

A

Extends proximally from rectum

Continuous involvment of mucosa

Small bowel not affected

Superficial inflammation (confined to mucosa) - superficial ulcers Islands of regenerating mucosa bulge into lumen > pseudopolyps

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17
Q

Clinical features of Crohn’s (3)

A

intermittent diarrhoea

pain

fever

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18
Q

Clinical features of UC (3)

A

Diarrhoea - more BLOODY & mucus

Crampy abdo pain relieved by defecation

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19
Q

Non-GI manifestations of IBD - eyes (1) skin (4), joints (4), Liver (3)

A

Stomatitis - due to malabsroption & fe def

Eyes - uveitis

skin - eryethema nodosum, pyoderma gangrenosum, erythema multiforme, clubbing

Joints - _asymmetrical migrating polyarthropath_y of large joints, sacroiliitis, myositis, ankylosing spondylitis

Liver - PSC (UC > CD), pericholangitis, steatosis

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20
Q

Complications of CD (4)

A

Strictures - require resection

Fistulae

abscess formation

perforation

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21
Q

Complications of UC (4)

A

severe haemorrhage

toxic megacolon ( damage to muscularis propria with disruption of neuromuscular function > colonic dilatation)

adenocarcinoma (20-30 times increased risk)

22
Q

Investigations CD (3)

A

markers of inflammation e.g. ESR, CRP

Barium contrast

Endoscopy

23
Q

Investigations UC (3)

A

rectal biopsy

colonoscopy

stool culture

24
Q

Management of CD: mild, severe, additional therapies

A

Mild - prednisolone

Severe - IV hydrocortisone, metronidazole

Additional - Azathioprine, methotrexate, infliximab

25
Q

Management of UC: mild (2), moderate (3), severe (3)

A

prednisolone + mesalazine

moderate - pred, 5-ASA, steroid enema

Severe: admit, NBM IV fluids, rectal steroids 5 ASA for remission

26
Q

What is carcinoid syndrome?

A

Tumours of enterochromaffin cells, secrete serotonin (5-HT). (mostly bowel, but can be lung/ovaries/testis)

27
Q

Carcinoid syndrome features (3)

A

Bronchoconstriction

Diarrhoea

Flusing

28
Q

Carcinoid crisis features (5)

A

lifethreatening vasodilation

Hypotension

Tachycardia

Bronchoconstriction

Hyperglycaemia

29
Q

Ix of carcinoid syndrome (1)

A

24 hour urine 5-HIAA (main metabolite of serotonin)

30
Q

Rx of carcinoid (1)

A

Octreotide (SS analogue)

31
Q

Colonic adenoma (neoplastic polyp), what is it? symptoms if any?

A

Benign dysplastic lesions (precursor to adenocarcinoma)

mostly asymp, regular surveillance if over 3.4 cm

45% malignant change

32
Q

Classification of colonic adenomas (3)

A

Tubular

Tubulovillous

Villous

33
Q

What does a villous adenoma cause?

A

Hypoproteniaemic hypokalemia

(leak large amounts of protein & K+)

34
Q

Risk factors for malginancy in colonic adenomas (3)

A

Large size - most imp rf

increased villous component

degree of dysplasia

35
Q

Describe the progression of colonic adenoma to carcinoma

A

Normal colon > at risk mucosa after ‘first hit’ mutation in 1st copy of APC gene (FAP pts born with this mutation) from at risk > adenoma after 2nd hit mutation to remaining APC gene Adenoma > carcinoma following activaftion o KRAS, LOF mutations of p53

36
Q

What is hamartomatous polyp?

A

A benign focal malformation that represents a neoplasm in the tissue of its origin

Juvenile polyps

37
Q

How is Peutz-Jegher’s syndrome inherited?

A

Autosomal dominant - mutation of LKB1 gene (suspected TS gene)

38
Q

Presentation of Peutz-Jegher’s syndrome? (3)

A

multiple polyps,

mucocutaneous hyperpigmentation,

freckles around mouth, palms & soles

39
Q

What are pts with Peutz-Jegher’s at risk of? (2)

A

intussusception

malignancy

40
Q

Epidemiology of colorectal cancer - age group, ethinicity, type, most common site of cancer

A

2nd most common cause of cancer related deaths in UK

Age 60-79 commoner in western population

98% are adenocarcinoma 45% occur in rectum

41
Q

Aetiology of Colorectal cancer (6)

A

Obesity

Diet - low fibre, high fat

Chrnoic IBD

Genetic - HNPCC, FAP

NSAIDs are protective (NSAIDs inhibit COX-2 which is overexpressed in 90% of cancers)

42
Q

Clinical features of right sided bowel cancer (2)

A

fe-def anaemia

weight loss

43
Q

Clinical features of left sided bowel cancer (3)

A

PR bleeding

Crampy LLQ pain

change in bowel habit

44
Q

Ix (4) of bowel cancer

A

protcoscopy colonoscopy barium enema CT/MRI

CEA - only for monitoring progress of therapy

45
Q

Dukes staging of colorectal cancer

A

A - confined to mucosa (5 yr survival > 95%)

B1 - extending into muscularis propria no LNs

B2 - transmural invasion no LNs

C1 - extenting to muscularis propria + LNs

C2 - transmural + LN

D - distant mets (5 yr survival

46
Q

Management of Rectal/ low sigmoid cancer

A

If < 1-2 cm above anal sphinc (lower third of rectum) abdomino-perineal resection

If > 1-2 cm above anal sphincter > anterior resection

Sigmoid cancer > sigmoid colectomy

47
Q

Management of other colon cancers: desecending colon & distal transverse

Ascending colon & proximal transverse

transverse colon

A

Left hemicolectomy if descending/ distal transverse

Right hemicolectomy if ascending/ proximal transverse

Extended right hemicolectomy if transverse colon

radiotherapy post op to decrease recurrence chemotherapy if palliative - 5-FU

48
Q

FAP mutations (2)

A

70% AD mutation in APC gene

30% AR mutation in DNA mismatch repair genes

49
Q

Presentation (1) & management of FAP (1)

A

Present between 10-15 yrs > 100 adenomatous polyps required for diagnosis, (usually see 1000s)

At birth hypertrophy of retinal pigment epithelium

ALL will get carcinoma if untreated by 30! so do prophylactic colectomy

50
Q

Gardners

A

Like FAP with extra interstinal features e.g. osteomas & dental caries

51
Q

HNPCC/ lynch syndrome mutations (1),

A

AD mutations in DNA mismatch repair genes

Carcinomas usually in right colon, few polups but fast progression to malignancy (present <50 yrs)

Assc with other cancers - endometrial ovarian, small bowel. stomach

52
Q

What other cancers is HNPCC associated with (5)

A

endometrial, ovarian, small bowel, transitional cell, & gastric carcinoma

Pathology (20 decks)

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