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Flashcards in Intestinal Disorders Deck (69):
1

HLA associated with coeliac

HLA-DQ2

2

Describe Marsh criteria for Coeliac disease

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

3

Complications of coeliac disease

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

4

Where is bile stored

Gallbladder

5

Describe what happens when bile acids reach the colon

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

6

Possible pathology of bile acid malabsorption

Overproduction of bile acids

7

Causes of bile acid malabsorption

TI disease (Crohn's) or resection
Cholecystectomy
Idiopathic

8

How can we assess for BAM?

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

9

Treatment of BAM

Cholestyramine
Colesevelam

10

1st line medical treatment of anal fissure

Topical diltiazem

Can give Botox

Surgery - literal sphincterotomy

11

How acquire strongyloidiasis?

Walking barefoot on soil

Asymptomatic in acute phase

12

Treatment of strongyloidiasis

Ivermectin

13

Symptoms associated with strongyloidiasis

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

14

Complications of strongyloidiasis

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

15

Rome 3 criteria in IBS

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

16

What test should be performed before diagnosing a patient with IBS

FBC, ESR, CRP, TTG

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

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

17

How can you reduce the risk of radiation enteritis

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

18

Treatment of radiation enteritis

Sucralfate enemas
Hyperbaric O2
Loperamide

19

Describe the different types of radiation enteritis

Acute = within 6 weeks - direct mucosal damage

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

20

What are the different causes of proctitis

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

21

Type of bacteria in c diff

Gram +Ve bacillus

22

Describe different toxins in c diff

Toxin A - enterotoxin
Toxin B - cytotoxin

They produce inflammation = diarrhoea and possibly paeudomembranous colitis

23

Which toxin do some c diff strain NOT produce

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

24

Describe different types of cytotoxin testing in c diff

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

25

What is the gold standard cytotoxic test in c diff

Cell culture cytotoxic assay

26

Gold standard diagnostic test in SBBO

Duodenal aspirates with cultures

These can identify asymptomatic patients

27

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

Ileocaecal valve
Acidity
Peristalsis

28

Risk factors for SBBO

Billroth 2 procedure as anatomy involves blind-end loop
Dysmotility (DM), strictures

29

Which antibiotics can cause and false negative result and why

Staph, strep viridins, enterococcus, pseudomonas

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

30

Diagnosis of SBBO

Hydrogen breath test

31

Describe the role of hydrogen breath test

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

Which hormone stimulate sensory neurones

Serotonin.

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

33

How can we improve continence in DM

Biofeedback therapy
Clonidine for gastroparesis (but lots of SE)

34

Life cycle of giardia

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

Symptoms of giardia

Diarrhoea
Bloating
Flatulence
Abdominal pain
Malabsorption
Weight loss

36

Treatment of giardia

Tinidazole

37

How is giardia spread

Faecal-oral route

38

Diagnosis of collagenous colitis

Increase in collagen layer

Collagen band > 10micro-grams thick

Usually type 1 or 3 collagen

39

Diagnosis of lymphocytic colitis

Increase intraepithelial lymphocytes

>20 lymphocytes per 100 epithelial cells

40

Treatment of microscopic colitis

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

41

Is microscopic colitis associated with malignancy?

No

Associated with coeliac disease

42

Describe the screening involved for CRC in patients with acromegaly

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

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

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

Mode of inheritance in HNPCC

AD

45

Describe the gene mutations in HNPCC

MSH2, MLH1, MSH6, PMS2

46

When to start screening in HNPCC

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

Repeat every 18/12 until age 70

47

Mutation in FAP

AD

APC mutation on 5q21

Endoscopy at 20 years and then every 5 years

48

Describe the types of polyposis syndrome

Juvenile polyposis syndrome
Peats-Jeghers syndrome
PTEN

49

Mutation in PJS

AD

serine threnonine kinase 11 (STK11) on chromosome 19

50

Diagnosis of PJS

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

51

Surveillance in PJS

OGD at 8 years, then 3 yearly if polyps found

52

Mechanism of action of prucalopride

5HT4 receptor agonist

For chronic constipation

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

53

What is the weakest independent risk factor for faecal incontinence

Forceps delivery

54

What is the pigment found in melanosis coli

What is the cause

Lipofuscin - brownish discolouration of colonic wall

Laxative abuse


Brown bowel syndrome - lipofuscin deposits at tunica muscularis

55

How can we measure colonic transit

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

How can we diagnose slow bowel transit

>6 radio-opaque markers left throughout the colon

57

Diagnose dyssynergic defecation

>6 markers in rectosigmoid region

58

Describe the causes of primary constipation

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

59

Secondary causes of constipation

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

60

Diagnosis and treatment of dyssnergic defecation

Anorectal manometry

Rx -biofeedback therapy

61

Describe B12 absorption

- 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

Does nicorandil cause colonic ulceration?

Yes

63

Infective colitis histology

Normal crypt architecture
Neutrophils
Crypt abscesses

64

Signs in VIPoma

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

65

Why do patients get diversion colitis

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

Y enterocolitica:

- cause
- mimics
-symptoms
- endoscopy findings

Gram negative bacilli/rod from contaminated pigs

Resembles Crohn's - terminal ileitis

Diarrhoea, abdo pain, fever

Normal endoscopy findings

67

Typhoid fever:

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

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

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

68

When should chemoprophylaxis for diarrhoea be offered?

IBD pt
Liver/kidney/heart disease pt
Immunosuppressive

Can give rifampicin

69

Treatment of giardia

Tinidazole

Metronidazole