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GASTROENTEROLOGY SCE > Intestinal Disorders > Flashcards

Intestinal Disorders Flashcards

1
Q

HLA associated with coeliac

A

HLA-DQ2

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2
Q

Describe Marsh criteria for Coeliac disease

A
  1. Lymphocytic infiltration
  2. Crypt hyperplasia
  3. Villous atrophy (C is the worst category)
  4. Flat strophic mucosa (may develop T-cell lymphoma)

Mucosa architecture is normal

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3
Q

Complications of coeliac disease

A

Osteoporosis (do DXA scans)
Autoimmune disease
NHL (T-cell)
Pneumococcus sepsis (hyposplenism)

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4
Q

Where is bile stored

A

Gallbladder

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5
Q

Describe what happens when bile acids reach the colon

A

Colonic bacteria dehydroxylates bile acids to secondary bile acids that stimulates water and electrolyte release = diarrhoea

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6
Q

Possible pathology of bile acid malabsorption

A

Overproduction of bile acids

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7
Q

Causes of bile acid malabsorption

A

TI disease (Crohn’s) or resection
Cholecystectomy
Idiopathic

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8
Q

How can we assess for BAM?

A

Measure turnover of radiolabelled bile acids

Measure serum metabolites

Quantification of excreted bile by seHCAT - retained fraction assessed with gamma cameras 7 days after po administration.
- <15% = BAM

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9
Q

Treatment of BAM

A

Cholestyramine

Colesevelam

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10
Q

1st line medical treatment of anal fissure

A

Topical diltiazem

Can give Botox

Surgery - literal sphincterotomy

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11
Q

How acquire strongyloidiasis?

A

Walking barefoot on soil

Asymptomatic in acute phase

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12
Q

Treatment of strongyloidiasis

A

Ivermectin

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13
Q

Symptoms associated with strongyloidiasis

A

Area of pruritis at site (migration of larvae) of entry
Diarrhoea
Abdominal pain
Weight loss

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14
Q

Complications of strongyloidiasis

A

Hyper infection syndrome = widespread dissemination of larvae into tissues = bloody diarrhoea, bowel perforation, gram -Ve sepsis

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15
Q

Rome 3 criteria in IBS

A

Symptoms improve with defecation
Onset associated with change in frequency of stool
Onset associated with change in form (appearance) of stool

Other supportive symptoms = abnormal stool frequency, defecation straining, urgency, bloating

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16
Q

What test should be performed before diagnosing a patient with IBS

A

FBC, ESR, CRP, TTG

NOT necessary to perform USS, flexi, TFTs, FOB, breath tests

Women >50 do Ca-125 (if >35 do USS)

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17
Q

How can you reduce the risk of radiation enteritis

A

Insert tissue expander to push loops of bowel out of radiotherapy field

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18
Q

Treatment of radiation enteritis

A

Sucralfate enemas
Hyperbaric O2
Loperamide

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19
Q

Describe the different types of radiation enteritis

A

Acute = within 6 weeks - direct mucosal damage

Chronic = years after - atrophy and fibrosis of epithelium due to obliterative arteritis = chronically ischaemic segment of bowel

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20
Q

What are the different causes of proctitis

A 
HIV
LGV - histology can resemble Crohn's 
Gonorrhoea
Syphilius
HSV
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21
Q

Type of bacteria in c diff

A

Gram +Ve bacillus

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22
Q

Describe different toxins in c diff

A

Toxin A - enterotoxin
Toxin B - cytotoxin

They produce inflammation = diarrhoea and possibly paeudomembranous colitis

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23
Q

Which toxin do some c diff strain NOT produce

A

Toxin A - so may get false negative if just test for toxin A

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24
Q

Describe different types of cytotoxin testing in c diff

A
  1. Cell culture cytotoxic assay - gold standard. If +Ve no further confirmatory tests are needed. Expensive
  2. Enzyme immune assay (EIA) - use reagents to detect toxin A and B. Quicker but more false negatives
  3. PCR - rapid. High sensitivity and specificity
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25
Q

What is the gold standard cytotoxic test in c diff

A

Cell culture cytotoxic assay

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26
Q

Gold standard diagnostic test in SBBO

A

Duodenal aspirates with cultures

These can identify asymptomatic patients

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27
Q

Normally, why is there very few bacteria in the small bowel

A

Ileocaecal valve
Acidity
Peristalsis

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28
Q

Risk factors for SBBO

A

Billroth 2 procedure as anatomy involves blind-end loop

Dysmotility (DM), strictures

29
Q

Which antibiotics can cause and false negative result and why

A

Staph, strep viridins, enterococcus, pseudomonas

These bugs don’t produce hydrogen so get false negative result

30
Q

Diagnosis of SBBO

A

Hydrogen breath test

31
Q

Describe the role of hydrogen breath test

A

Some bacteria ferment carbohydrates and produce H+

Get double peak pattern:

  1. Metabolism by small bowel bacteria
  2. Colonic bacteria metabolism - more prolonged peak
32
Q

Which hormone stimulate sensory neurones

A

Serotonin.

This activates myenteric plexus and then cholinergic neurones release substance P + acetylcholine = contraction of smooth muscle behind area of stretch = peristalsis

33
Q

How can we improve continence in DM

A

Biofeedback therapy

Clonidine for gastroparesis (but lots of SE)

34
Q

Life cycle of giardia

A

Cyst ingested - excystation of trophozoites - organism released - sexual reproduction in gut - colonise in small bowel by adhering to mucosa - cytokine release - water and electrolyte loss - trophozoites encyst and pass in faeces

35
Q

Symptoms of giardia

A 
Diarrhoea
Bloating
Flatulence
Abdominal pain
Malabsorption
Weight loss
36
Q

Treatment of giardia

A

Tinidazole

37
Q

How is giardia spread

A

Faecal-oral route

38
Q

Diagnosis of collagenous colitis

A

Increase in collagen layer

Collagen band > 10micro-grams thick

Usually type 1 or 3 collagen

39
Q

Diagnosis of lymphocytic colitis

A

Increase intraepithelial lymphocytes

> 20 lymphocytes per 100 epithelial cells

40
Q

Treatment of microscopic colitis

A 
Stop offending meds (NSAIDS, SSRIs, PPI)
Loperamide
Cholestyramine
Aminosalicylates
Budesonide - if severe
41
Q

Is microscopic colitis associated with malignancy?

A

No

Associated with coeliac disease

42
Q

Describe the screening involved for CRC in patients with acromegaly

A

Start screening age 40 or if raised ILGF-1
3 yearly screening - adenoma, raised ILGF-1
5 yearly if original colon negative

Hyperplastic polyp or normal ILGF-1 = 5-10year screening intervals

43
Q

Which hereditary condition associated with bowel cancer is inherited in an AR fashion

A

MUTYH ASSOCIATED EITH POLYPOSIS (MAP)

100% will have colon cancer by age 60

Start screen age 25 years and perform every 2-3 years with dye spray

44
Q

Mode of inheritance in HNPCC

A

AD

45
Q

Describe the gene mutations in HNPCC

A

MSH2, MLH1, MSH6, PMS2

46
Q

When to start screening in HNPCC

A

Age 25 or 5years less than 1st case of 1st degree relative

Repeat every 18/12 until age 70

47
Q

Mutation in FAP

A

AD

APC mutation on 5q21

Endoscopy at 20 years and then every 5 years

48
Q

Describe the types of polyposis syndrome

A

Juvenile polyposis syndrome
Peats-Jeghers syndrome
PTEN

49
Q

Mutation in PJS

A

AD

serine threnonine kinase 11 (STK11) on chromosome 19

50
Q

Diagnosis of PJS

A

> 2 polyps histologically or single polyp and a first degree relative with condition

51
Q

Surveillance in PJS

A

OGD at 8 years, then 3 yearly if polyps found

52
Q

Mechanism of action of prucalopride

A

5HT4 receptor agonist

For chronic constipation

Give when tried 2 classes of laxatives at highest tolerated doses for 6/12

53
Q

What is the weakest independent risk factor for faecal incontinence

A

Forceps delivery

54
Q

What is the pigment found in melanosis coli

What is the cause

A

Lipofuscin - brownish discolouration of colonic wall

Laxative abuse

Brown bowel syndrome - lipofuscin deposits at tunica muscularis

55
Q

How can we measure colonic transit

A

Ingest radiopaque marker and perform AXR. 24 plastic markers, AXR on day 6. Normal transit time is <5 markers left

Radioisotopes and scintigraphy
Ingest of pressure and pH capsule and tracking its movement

56
Q

How can we diagnose slow bowel transit

A

> 6 radio-opaque markers left throughout the colon

57
Q

Diagnose dyssynergic defecation

A

> 6 markers in rectosigmoid region

58
Q

Describe the causes of primary constipation

A
  • slow transit - prolonged delay of transit time of stool
  • dyssnergic defecation - difficulty expelling stool from rectum
  • IBS-C = constipation and abdominal pain
59
Q

Secondary causes of constipation

A 
Drugs - opioids, anti-cholinergics
Hypercalcaemia
Cancer
Stricture
Fissure
Hypothyroidism
Parkinson's
MS
Psychiatric
60
Q

Diagnosis and treatment of dyssnergic defecation

A

Anorectal manometry

Rx -biofeedback therapy

61
Q

Describe B12 absorption

A
  • cobalamin released from food by action of Pepsins in acid in stomach
  • salivary R protein binds to free cobalamin protecting it from acid degradation
  • in duodenum, pancreatic enzymes hydrolyse the R-protein, releasing cobalamin which binds to IF (secreted from parietal cells)
  • complex taken up by cells in TI

LACK OF PANCREATIC ENZYMES CAN RESULT IN DEFECTIVE RELEASE OF COBALAMIN FROM R PROTEIN FOR IF BINDING

62
Q

Does nicorandil cause colonic ulceration?

A

Yes

63
Q

Infective colitis histology

A

Normal crypt architecture
Neutrophils
Crypt abscesses

64
Q

Signs in VIPoma

A

Diarrhoea
Hypokalaemia
High stool weight and no reduction in stool weight on day 4 (the fasting day)

65
Q

Why do patients get diversion colitis

A

Deficiency of short chain fatty acids which normally provide nutrients to the colonocytes

This causes reduced acetate, butyrate resulting in less absorption of Na and fluids

66
Q

Y enterocolitica:

  • cause
  • mimics
  • symptoms
  • endoscopy findings
A

Gram negative bacilli/rod from contaminated pigs

Resembles Crohn’s - terminal ileitis

Diarrhoea, abdo pain, fever

Normal endoscopy findings

67
Q

Typhoid fever:

  1. Cause
  2. Symptoms
  3. What is Faget’s sign?
    4.
A

Salmonella typhi - more common in females (‘typhoid Mary)

Fever, headache, RIF pain, splenomegaly and rose spot on chest

68
Q

When should chemoprophylaxis for diarrhoea be offered?

A

IBD pt
Liver/kidney/heart disease pt
Immunosuppressive

Can give rifampicin

69
Q

Treatment of giardia

A

Tinidazole

Metronidazole

GASTROENTEROLOGY SCE (11 decks)

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