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MRCP Revision > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

Clostridioides difficiles pathophysiology and features

A

G +ve, spore-forming, toxin-producing bacillus

RF: PPIs, clindamycin, second-third gen cephalosporins leading cause

Faeco-oral transmission via spores
Exotoxin A and B acts on epithelial cells and inflammatory cells –> colitis

Diarrhoea, abdo pain, raised WCC

Risk of toxic megacolon

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2
Q

C Diff severity scale

A

Public Health England severity scale:

Mild: normal WCC

Mod:
- WCC<15
- 3-5 loose stools/day

Severe:
- WCC>15 or
- raised creat (>50% baseline)
- Temperature >38.5
- or Evidence of severe colitis

Life-threatening:
- Hypotension
- Partial/complete ileus
- Toxic megacolon
- Radiological evidence of severe disease

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3
Q

How to diagnose C Diff

A

C Diff toxin (CDT) in stool
C Diff antigen only shows exposure

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4
Q

C Diff treatment

A

Isolation until 48hrs post last diarrhoea, gloves + apron + hand washing

1st episode:
1. oral vanc 10 days
2. oral fidaxomicin
3. oral vanc +/- IV metron

Recurrent: (in 20% of patients, rises to 50% after 2nd episode)
within 12 weeks of symptom resolution: oral fidaxomicin
after 12 weeks of resolution: oral vanc or fidaxomicin

Life threatening:
oral vanc + IV metro + specialist advice ?surgical

Others:
- bezlotoxumab (targets exotoxin B, not cost-effective according to NICE)
- faecal microbiota transplant (for 2 or more episodes)

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5
Q

What is Eosinophilic oesophagitis?

A

Allergic inflamation of oesophagus likely secondary to allergic reaction to ingested food

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6
Q

How does eosinophilic oesophagitis present?

A

-pain, dysphagia
-strictures/fibrosis (56%)
-food impaction (55%)
-regurgitation/vomiting
-anorexia, weight loss
- failure to thrive in children

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7
Q

Risk factors for eosinophilic oesophagitis

A

atopy/allergies/asthma, males (3:1), FHx of atopy, Caucasians, ages 30-50, coexisting autoimmune PMH

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8
Q

How do you investigate and diagnose eosinophilic oesophagitis

A

Endoscopy with biopsy - eosinophils>15 per high power microscopy field

PPI trial - no improvement, persistence of eosinophilia

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9
Q

Biopsy findings for eosinophilic oesophagitis

A
  • dense eosinophilic epithelial infiltration
  • > 15 eosinophils per high power microscopy field for diagnosis

Others:
- reduced vasculature, thick mucosa, mucosal furrows, strictures, laryngeal oedema
- epithelial desquamation, eosinophilic microabscesses, abnormally long papillae

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10
Q

How to manage eosinophilic oesophagitis

A
  • Refer to Gastro

Diet: (3 methods)
- elemental diet involving amino acid mixture 6 weeks
- exclusion of 6 food groups associated with allergy
- targetted elimination diet (exclude foods identified as allergy-triggering using allergy testing)
(involve dietician)

Meds:
- topical oral steroids - fluticasone, budesonide 8 weeks then reassessment

Radical:
-oesophageal dilatation: 56% require this at some point to reduce burden from strictures

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11
Q

Complications and prognosis of eosinophilic oesophagitis

A
  • Strictures (56%)
  • Impaction (55%), 38% require endoscopic removal of impaction
  • Mallory-Weiss tears

px: chroic, comes back if treatment stopped

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12
Q

What is Gilbert’s syndrome

A

autosomal recessive deficiency of UDP glucuronosyltransferase resulting in defective bilirubin conjugation

unconjugated bilirubinaemia, exacerbated by illness/infection, exercise, fasting

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13
Q

How to investigate and manage Gilbert’s syndrome

A

rise in bilirubin after fasting
- IV nicotinic acid test with exaggerated rise in unconjugated bilirubin

no treatment required

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14
Q

What is SBBOS

A

Small bowel bacterial overgrowth syndrome, resulting in GI symptoms, with lots of overlap with IBS symptoms incl diarrhoea, bloating, flatulence, abdo pain

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15
Q

Risk factors for SBBOS

A
  • congenital, neonatal GI abnormalities
  • scleroderma
  • diabetes mellitus
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16
Q

Diagnosing SBBOS

A

Hydrogen breath test
small bowel aspiration, culture (invasive, difficult)
?abx trial

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17
Q

Managing SBBOS

A
  • correct underlying cause
  • Rifaximin trial (co-amox/metro can also be used in majority)
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18
Q

PBC

A

primary biliary cholangitis/cirrhosis

(M rule - IgM, aMa M2 subtype, Middle aged females)

  • chronic inflammation dmaaging interlobular bile ducts –> cholestasis –> cirrhosis

Itching in middle aged females (9:1), fatigue, cholestatic jaundice, raised ALP
- Hyperpigmentation on pressure points
- RUQ pain in 10%
- xanthelasma/xanthomata
- clubbing, hepatosplenomegaly
- can lead to liver failure

Assx: Sjogren’s (80%), RhArth, Systemic sclerosis, thyroid disorders

Ix:
- AMA M2 subtype (98%)
- sm antibodies 30%
- raised IgM
- Exclude extrehaptic obstruction with imaging (USS/MRCP)

Mx:
- ursodeoxycholic acid (slows progression, symptoms)
- cholestyramine for pruritis
- fat-soluble vitamins
- liver transplant if bili>100

Complications:
- cirrhosis –> portal HTN –> ascites, varices
- osteomalacia, osteoporosis
- HCC 20-fold risk

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19
Q

Barrett’s

A

lower oesophageal metaplasia (squamous –> columnar), risk of adenocarcinoma 50-100 fold

Short (<3cm) or long (>3cm)

Prev 1/20

RF: GORD, Males (7:1), smoking, obesity
- ETOH not independent RF

Mx:
- high dose PPIs
- endoscopic surveillance (every 3-5 yrs for metaplastic patients)
- endoscopic intervention for dysplasia including radiofrequency ablation (1st line, esp for low-grade) or mucosal resection

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20
Q

Gastrin source, stimuli, actions

A

Source: G cells in antrum (lowermost part) of stomach

stimuli:
- gastric distension
- vagal stimulation by Gastrin-releasing peptide
- luminal peptides/amino acids

Inhibited by:
- low pH, somatostatin

Actions:
- acid and intrinsic factor secretion by parietal cells
- pepsinogen secretion by chief cells
- increases gastric motility
- stimulates parietal cell maturation

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21
Q

CCK source, stimuli, actions

A

Source: I cells in upper small intestines

Stimuli: patially digested proteins, triglycerides

Actions:
- secretion of enzyme-rich fluid from pancreas
- gallbladder contraction
- relaxation of sphincter of Oddi
- reduces gastric emptying
- trophic effect on pancreatic acinar cells
- induces satiety

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22
Q

Secretin source, stimuli, actions

A

Source: S cells in upper small intestine

Stimuli: acidic chyme, fatty acids

Actions:
- bicarb-rich fluid secretion from pancreas and hepatic duct cells
- reduces gastric acid secretion
- trophic effect on pancreatic acinar cells

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23
Q

VIP source, stimuli, actions

A

Source: small intestine, pancreas

stimuli: neural

actions:
- stimulates pancreatic and intestinal secretion
- inhibits acid secretion

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24
Q

Somatostatin source, stimuli, actions

A

Source: pancreatic and gastric D cells

Stimuli:
- fat, bile salts, glucose in intestinal lumen

Actions:
- reduces acid, pepsin, gastrin, pancreatic enzyme, insulin, glucagon secretion
- inhibits trophic effects of gastrin
- stimulates gastric mucus production

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25
Q

What foods can Coeliac disease patients have and what to avoid

A

Gluten - including wheat, barley, rye, oats (some can tolerate)

Can have rice, potatoes, maize/corn

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26
Q

How to check Coeliac gluten-free compliance

A

TTG abs

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27
Q

Why are coeliacs immunocompromised and what is necessary for this?

A

Functional hyposplenism

pneumococcal vaccine + booster every 5 eyears

flu vaccines (on individual basis)

28
Q

Commonest site for pancreatic cancer

A

head of pancreas (80%)

29
Q

Associations for pancreatic cancer

A

-age
-smoking
-DM
-chronic pancreatitis
-HNPCC
-MEN association
-BRCA2
-KRAS

ETOH not independent risk factor

30
Q

1st line imaging for ?pancreatic cancer

A

High-Res CT –> double duct sign (simultaneous dilatation of CBD, pancreatic ducts)

(USS has 60-90% sensitivity, MRCP for further visualiation)

31
Q

Management of pancreatic cancer

A

<20% get surgery - Whipple’s resection (pancreaticoduodenectomy) for head of pancreas resectable lesions with adjuvant chemo

ERCP with stenting for palliation

32
Q

Side effects of Whipple’s

A

Dumping syndrome
Peptic ulcers

33
Q

UC flare severity classification

A

Truelove and Witts
mild: <4, small blood
mod: 4-6, more blood, no systemic upset
severe: >6, systemic upset (pyrexia, tachycardia, anaemia, raised CRP)

34
Q

UC flare acute management

A

Proctitis:
topical/rectal 5-ASA –> after 4wks, oral 5-ASA –> oral steroids

Proctosigmoiditis/left sided:
topical/rectal 5-ASA –> after 4 wks, HIGH DOSE oral 5-ASA +/- topical steroids –> oral 5-ASA + oral steroid

Extensive:
topical/rectal 5-ASA –> after 4 wks, HIGH DOSE oral 5-ASA + steroid

Severe colitis:
- Admission
- IV steroids
- IV ciclosporin 2nd line
- consider surgery

35
Q

Maintaining remission of UC after flare

A

Proctitis/proctosigmoiditis:
- topical/rectal 5-ASA alone or with oral or just oral

Left-sided/extensive:
- low dose oral 5-ASA

Severe or 2 or more exacerbations in 1 year:
- oral azathioprine or oral mercaptopurine

36
Q

What can cause false negative Coeliac serology test with anti-TTG?

A

Selective IgA deficiency - so test IgA with TTG always

37
Q

Haemochromatosis genetics

A

Autosomal recessive, mutations in HFE gene in chromosome 6

38
Q

Best marker for Haemochromatosis screening

A

In general poopulation, Transferrin saturations (higher than 45% should be investigated further)

In family members with HH, HFE genetic mutation testing for C282Y, H63D mutations

39
Q

Iron studies in Haemochromatosis

A

Transferrin sats>55% in men, >50% in women
Raised ferritin >500, iron
low TIBC

40
Q

Managing haemochromatosis

A

venesection with transferin sats kept below 50%, ferritin below 50

desferrioxamine second line

41
Q

Managing anal fissures

A

Acute (<6 wks):
- soften stool (diet, bulk-forming laxatives, lactulose)
- lubricants (petroleum jelly)
- topical anaesthetics
- analgesia

Chronic (>6wks):
- topical GTN for 8 wks
- consider sphincterotomy or botulinum toxin in secondary care if ineffective

42
Q

What happens to calcium in pancreatitis and why

A

Hypocalcaemia (hypercalcaemia can cause pancreatitis though) - would indicate for severe pancreatitis

Leaking lipase from pancreas breaks fat into triglycerides and fatty acids, which combine with calcium (saponification) to form soap

43
Q

Rare opthalmic complication of acute pancreatitis

A

Ischaemic (Purtscher) retinopathy - can cause blindness

44
Q

Non-pancreatitis causes of raised amylase (may be related)

A
  • pseudocyst
  • mesenteric infarct
  • perforated viscus
  • acute cholecystitis
  • diabetic ketoacidosis
45
Q

What is Peutz-Jeghers?

A

Autosomal dominant syndrome with numerous hamartomatous polyps in GIT (esp SB), due to gene encoding serine threonine kinase LKB1 or STK11

Freckles on lips, face, palms, soles

Complications:
- intussusception, SBO
- GI bleeding

46
Q

Which IBD associates with PSC

A

UC

47
Q

Which IBD has higher risk of Colorectal Ca

A

UC

48
Q

UC histology

A
  • No inflammation beyond submucosa (unless fulminant)
  • inflammatory cell infiltrate in lamina propria
  • crypt abscesses (neutrophils migrate through walls of glands)
  • goblet cell depletion
49
Q

Crohns histology

A
  • Full thickness inflammation involving all layers from mucosa to serosa
  • Increased goblet cells
  • Granulomas
50
Q

UC endoscopy appearance

A
  • Widespread ulceration
  • Pseudopolyps (preservation of adjacent mucosa, appearing like polyps)
51
Q

Crohns endoscopy appearance

A
  • Deep ulcers
  • Skip lesions
  • Cobblestone appearance
52
Q

Crohns small bowel enema signs

A
  • Kantor’s string sign for strictures
  • Proximal bowel dilatation
  • Rose thorn ulcers
  • fistulae
53
Q

UC barium enema signs

A
  • loss of haustra
  • pseudopolyps with superficial ulcers
  • drainpipe colon in long-standing disease
54
Q

Commonest SBP organisms

A

G-ve enteric most common
1. E Coli
2. Klebsiella

amongst G +ves, S Pneumoniae then S viridans and Staph

55
Q

Diagnosis of SBP

A

Neutrophils >250 cells/ml on ascitic tap

56
Q

When should antibiotic prophylaxis be offered in ascites?

A
  • past history/episode of SBP
  • fluid protein <15g/l
  • Child-Pugh >9
  • hepatorenal syndrome
57
Q

1st line Abx in SBP

A

IV cefotaxime

58
Q

Plummer-Vinson syndrome

A

(Also known as Paterson-Brown-Kelly syndrome)
Triad of dysphagia, glossitis, iron-deficiency anaemia

59
Q

Which vein clots in Budd Chiari

A

Hepatic vein thrombosis

60
Q

Causes of Budd-Chiari

A
  • Polycythaemia rubra vera
  • Thrombophilia (Activated Protein C resistance, antithrombin III deficiency, protein C and S deficiencies)
  • Pregnancy
  • COCP use (20% of cases)
61
Q

1st line investigation for Budd Chiari

A

USS Doppler hepatic veins

62
Q

Smoking’s association with IBD

A

RF for Crohns, worsened severity and complications, reduced response to treatment

Actually opposite for UC

63
Q

Crohn’s management to induce remission

A
  • Stop smoking
  • Elemental diet
  • Steroids
  • 5-ASA 2nd line, less effective than in UC
  • Azathioprine or mercaptopurine as add-ons for remission, not as monotherapy - can consider methotrexate instead
  • Infliximab in refractory or fistulating Crohns
  • metronidazole for isolated peri-anal disease
64
Q

Crohn’s management for maintaning remission

A
  • Stop smoking
  • Azathioprine or mercaptopurine 1st line
  • Methotrexate 2nd line
65
Q

What needs to be monitored before starting azathioprine or mercaptopurine?

A

TPMT activity - this breaks azathioprne into active form

66
Q

complications of Crohn’s

A

small bowel cancer 40 fold
Colorectal cancer 2 fold
Osteoporosis

67
Q
A

MRCP Revision (1 decks)

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