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Medicine > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

Dysphagia- difficulty swallowing liquids and solids from start. Rule out what?

A

Motility disorder - achalasia or CND or pharyngeal cause

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2
Q

Painful swallowing differentials?

A

Ulcer

Malignancy, oesophagitis, candida in immune suppressed

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3
Q

Intermittent dysphagia

A

Oesophageal spasm

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4
Q

Neck bulge or gurgle on drinking

A

Pharyngeal pouch

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5
Q

What is alchalasia and how does it present?

A

Loss of coordinated peristalsis and lower oesophageal sphincter fails to relax

Dyshapgia, regurgitation and decreased weight

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6
Q

Investigations and management of achalasia

A

Manometry or contrast swallow - dilated tapering oesophagus

Treatment - surgical myotomy, endoscopic balloon dilatation. Botulinum toxin injection. Calcium channel blockers may also relax the sphincter
High dose PPI

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7
Q

Dyspepsia Alarm symptoms

A

Alarm

Anaemia 
Loss of weight
Anorexia 
Recent onset / progressive 
Milena/haematemesis 
Swallowing difficulty
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8
Q

Investigations for dyspepsia

A

If 55 years old or less - test and treat for H. Pylori - using urea breath test of stool antigen
Positive = PPI and 2 Abx (amoxicillin and clarithromycin)
Negative = PPI and lifestyle modifications

Consider - FBC (anaemia) u/E, CRP
Endoscopy for biopsies or ulcers and rule out malignancy
With repeat endoscopy to see if ulcer healed

ALARM symptoms - urgent referral for endoscopy

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9
Q

Pain a couple of hours after a meal + dyspepsia diagnosis?

A

Duodenal ulcer

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10
Q

Pain with meal, + dyspepsia. Diagnosis?

A

Peptic ulcer

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11
Q

What is zollinger Ellison syndrome and its features?

A

Gastrin-secreting tumour (gastrinoma) usually of pancreatic origin
Results in hypersecretion of gastric acid causing peptic ulceration

Epigastric pain as a result of ulceration and GOTD
Diarrhoea (acid damages pancreatic enzymes)

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12
Q

Causes of upper GI bleed

A 
PUD
Inflammation - oesophagitis, gastritis, duodenitis
Oesophageal or gastric varices
Mallory-weiss tear from sever vomiting 
Upper GI cancer
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13
Q

Investigations of upper GI bleed

A

FBC - anaemia
Cross match and coag
Increased urea - absorption and metabolism of blood
LFTs

Erect CXR
Consider CT abdo-chest

Risk assessment - blatchford score, rockall full score

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14
Q

Management of an acute GI bleed

A 
ABCDE 
Oxygen if hypoxic and able 
Contact senior staff (surgeon on call)
Nill by mouth 
Insert 2 wide bore cannula 
IV fluids - o negative blood if appropriate 
Urinary catheter 
Transfuse if Hb < 70 g/L
Cross match and coag

Urgent endoscopy
If that fails - surgery
PPIs after endoscopy

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15
Q

Management of varicle bleeding

A

ABCDE
Fluids (treat as GI bleed)
Terlipressin IV 1-2 mg while waiting band ligation
Broad spectrum abx
Endoscopic banding
Sengstaken-blakemore tube to compress varices
Alcoholics - B1 (thiamine)

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16
Q

What causes unconjugated hyperbilirubinaemia?

A

Over production - haemostasis, ineffective erythropoiesis

Impaired hepatic uptake- drugs (paracetamol), ischaemia hepatitis

Water insoluble so does not enter urine.

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17
Q

What causes conjugated hyperbilirubinaemia?

A

Post-hepatic causes

Excreted in urine as its water soluble. Urobilinogen is absent in obstructive disease as it doesn’t enter the GI tract, instead leaks into the blood where it cannot be broken down into urobilinogen. Faeces dark (less bile into GI tract)

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18
Q

Causes of cholestasis

A 
PBC, PSC
drugs - co-amoxiclav 
Common bile duct gall stones
Pancreatic cancer 
Compression of the bile duct - cholangiocarcinoma
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19
Q

What can co-amoxiclav cause?

A

Jaundice - cholestasis / post-hepatic jaundice

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20
Q

Tests in jaundice

A

Urine - bilirubin, urobilinogen
Bloods - FBF, clotting, reticulocyte count, coombs test, malaria parasites
Chemistry- U+Es (urea up in haemolysis), albumin
US - look at bile ducts, pancreatic mass
ERCP - if bile ducts open
MRCP, LIVER BIOPSY, CT/MRI (MALIGNANCY)

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21
Q

Will you see bilirubin in the urine of pre-hepatic jaundice?

A

No, as it is un-conjugated and therefore not water-soluble

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22
Q

Bloody diarrhoea differentials

A

IBD
campylobacter / shigella / colorectal Cancer / colitis
Colonic polyps

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23
Q

Management of diarrhoea

A

Treat the cause
Oral rehydration unless severe - IV rehydration and electrolyte replacement
Codeine phosphate or loperamide
Avoid Abx unless infection is cause

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24
Q

What is the cause of coeliac disease?

A

Gladin which is a part of gluten is modified during digestion by the enzyme tissue transglutaminase (tTG)
Autoimmune response to the complex that forms
Anti-tTG antibodies damage intestine and connective tissue in muscles

25
Q

Presentation of coeliac disease

A 
Young - failure to thrive 
Diarhhoea / steatorrhoea - mucus 
Bloating 
Abdominal pain / discomfort 
Anaemia
Dermatitis herpetiformis
Weight loss
Malnutrition
26
Q

Investigations of coeliac

A

IgA-tTG
Total IgA - are they deficient as an enitrety?
Endomysial antibody
Small bowel histology - gold standard

Consider- FBC, blood smear (iron deficiency)
Vitamin D / calcium / B12 / folate

27
Q

Management of coeliac disease

A 
Patient education 
Lifelong gluten free diet 
Consultation with a dietician 
Dietary councilling 
Calcium/ vitamin D supplementation 
Pneumococcal vaccine (functional hyposplenism)

Annual review
Dexa

28
Q

What foods contain gluten?

A

Wheat (bread, pasta)
Barley
Oats
Rye

29
Q

What is primary biliary cholangitis and its presentation?

A

Chronic autoimmune disease - progressive destruction of small intrahepatic bile ducts, causing cirrhosis

Female predominance.
Usually 4th-5th decade of life

Fatigue and pruritus - earliest symptoms
Jaundice later
Hepatosplenomegaly
Facial hyperpigmentation and xanthelasmas

Leads to cholestasis as fibrosis of biliary tracts prevents excretion
Cholesterol that is normally metabolised by liver and excreted as bile salts not deposits in eyes and tendons

30
Q

Investigations of PBC

A

Obs
Lfts - cholestatic picture
Autoimmune profile - AMA positive in 95%
High levels of IgM are indicative

Imaging - USS of MRCP
Exclude biliary obstruction
Liver biopsy

31
Q

Management of PBC

A

Bile acid analogue - urodeoycholic acid
Immunomodulation therapy - prednisolone with azathioprine
Anti-pruritis - colestyramine
Liver transplant for end-stage

32
Q

What is primary sclerosing cholangitis?

A

Intrahepatic or extra hepatic ducts become strictured and fibrotic - causes obstruction to bile flow
Causes - combination of genetic and environmental factors

Any age can be affected
60% men
80% of patients have inflammatory bowel disease (UC)

Jaundice
Chronic RUQ pain
Pruritus
Fatigue

33
Q

Investigstions for PSC

A

General bloods
LFTs - cholestatic picture
Autoantibodies - non are specific
P-ANCA
ANA
(Not necessarily an autoimmune disease - doesn’t respond to immunomodulation)
MRCP - lesions and strictures to bile ducts

34
Q

Management of PSC

A 
Observation and lifestyle changes - healthy diet and limit alcohol 
DEXA
Pruritus relief - chloestyramine
Urodeocholic acid - slows disease progression 
Monitor for complications 
ERCP - dilate and stent strictures
Liver transplant 
Immunomodulation
35
Q

What is used to prevent oesophagus varices?

A

Proanolol (non-selective B blocker)

Terlipressin = treat
Propranolol = prevent
36
Q

Who meets referral criteria for urgent dyspepsia?

A

All with dysphagia
All with upper GI mass
>55 with alarm or persistant symptoms

37
Q

If stable, what test should be done on patients with upper GI bleed?

A

Endsocopy within 24h

38
Q

Harmartomatous polyps in the GI tract and facial freckles is associated with what condition?

What type of genetic condition?

Complications?

A

Peutz-Jeghers syndrome
Autosomal dominant

BO - intersucseption
GI bleeding

39
Q

UC presentation

A 
Rectal bleeding (proctitis)
Diarrhoea
Bloody stool
Abdo pain 
Skin changes 
Eye problems
Arthritis 
Malnutrition
40
Q

What are risk factors for UC?

A

Family history

HLA-B27 association (ankylosing spond)

41
Q

Extra-abdominal manifestations of IBD

A

Skin - erythema nordosum, pyoderma gangrenosum
Eyes - anterior uveitis, episcleritis
Joints - arthritis, ank. Spondylitis (UC)
Renal stones
PSC (UC)

42
Q

Investigations for IBD

A 
Fbc - anaemia, infection 
U+E - dehydration 
LFF - low albumin as a marker of severity, PSC
CRP
ESR

stool mc&s - exclude infection
Faecal calprotectin

AXR - thumb printing, lead pipe, dilatation

Lower GI endoscopy

Serological markers- pANCA (UC)

43
Q

What is a serological marker likely to be positive in UC?

A

pANCA

44
Q

What is a mild flare of UC?

A

<4 motions a day
Small bleeding
No systemic upset

45
Q

What is a moderate flare of UC?

A

4-6 motions a day
Moderate bleeding
Minimal systemic signs

46
Q

What is a severe flare of UC?

A

> 6 motions a day
Severe bleeding
Systemic signs

47
Q

Complications of IBD

A

Toxic dilatation (UC more common)
VTE
Colon cancer
PSC

SBO (crohns)
Abscess formation
Perforatiin
Malnutrition

48
Q

Differences in presentation between UC/crohns

A

Crohns - diarrhoea usually non-bloody. Weight loss more prominent, upper GI symptoms - mouth ulcers, perianal disease. Abdominal mass palpable in RIF

UC - bloody diarrhoea mor common. Abdo pain in Left lower quadrant

49
Q

Differences in pathology of UC/crohns

A

Distribution- continous in UC, skip lesions in Crohns
Site - anywhere in crohns, rectal and proximal coclon in UC
Inflammation- confined to mucosa in UC as well as crypt abscesses and goblet cell dysplasia in crohns, transmural involvement, extensive fibrosis and fissures. Granuloma formation

50
Q

Management of UC

A

Mild - mesalazine - give PR for distal disease. Topical steroids have a role

Moderate- induce remission with oral pred. Then taper. Maintain on mesalazine.

Severe - admit for IV rehydration, electrolyte replacement, IV steroids

Monitor, assess severity, rehydrate for all

Other therapies- azathioprine if continuous flares also consider biological therapies - inflixamab, adalimumab

Surgery if medical management fails

51
Q

Managemenr of crohn’s disease

A

Assess severity. Consider psych input, optimise nutrition

Mild/moderate - prednisolone for 1 week then taper

Sever - admit for hydration/ electrolyte replacement. Iv steroids
VTE prophylaxis
Monitor - if improving, switch to oral pred
If no improvement - biologics have a role

Anti-diarrhoeals
Anti-spasmodics
Osteoperosis
Colonoscopg surveillance

Lifestyle - smoking cessation

52
Q

Differentials for bloody diarrhoea

A 
Drugs - PPIs, NSAIDs, Abx
IBS
IBD
Gastroenteritis - e. Coli, c. Diff., shigella, campylobacter
Cancer 
Ischaemic colitis 
Mesenteric ischaemia
53
Q

What is wilsons disease?

A

Autosomal recessive condition characterised by error in copper metabolism and accumulation

54
Q

Pathophysiology of wilsons disease

A

In Liver, copper is incorporated into caeruloplasmin
In hepatocytes
In wilsons, this process is impaired as well as excretion
Copper accumulates in liver and other organs

55
Q

Presentation of wilsons disease

A 
Behavioral problems - depression, reduced libido, memory loss 
Tremor
Dysarthria - slurred speech 
Dystonia 
Kayser-fleischer rings
Children may present with liver disease 
Young adults - CNS signs
56
Q

Tests for wilsons disease

A 
Urine 24h copper excretion is high 
Increased LFTs
Serum copper - low
Serum caeruloplasmin - low 
Molecular genetics testing 
Slit lamp for eye signs 
Liver biopsy - increased hepatic copper, cirrhosis 
MRI - degeneration of key areas of brain
57
Q

Management of wilsons disease

A 
Diet - avoid foods with high copper (liver, chocolate, nuts) 
Check water sources for copper 
Drugs - lifelong penicillamine
Liver transplantation 
Screen siblings
58
Q

What is hereditary haemochromatosis

A

Autosomal recessive condition that causes the body to absorb too much iron from the diet

Cause - mutation in HFE (protein that regulates iron entry to cells)
Leads to decreased hepcidin synthesis - leads to increased iron absorption
Damage to liver, joints, anterior pituitary, pancreas, heart, thyroid

Medicine (25 decks)

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