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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
Presentation of coeliac disease
``` Young - failure to thrive Diarhhoea / steatorrhoea - mucus Bloating Abdominal pain / discomfort Anaemia Dermatitis herpetiformis Weight loss Malnutrition ```
26
Investigations of coeliac
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
Management of coeliac disease
``` Patient education Lifelong gluten free diet Consultation with a dietician Dietary councilling Calcium/ vitamin D supplementation Pneumococcal vaccine (functional hyposplenism) ``` Annual review Dexa
28
What foods contain gluten?
Wheat (bread, pasta) Barley Oats Rye
29
What is primary biliary cholangitis and its presentation?
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
Investigations of PBC
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
Management of PBC
Bile acid analogue - urodeoycholic acid Immunomodulation therapy - prednisolone with azathioprine Anti-pruritis - colestyramine Liver transplant for end-stage
32
What is primary sclerosing cholangitis?
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
Investigstions for PSC
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
Management of PSC
``` 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
What is used to prevent oesophagus varices?
Proanolol (non-selective B blocker) ``` Terlipressin = treat Propranolol = prevent ```
36
Who meets referral criteria for urgent dyspepsia?
All with dysphagia All with upper GI mass >55 with alarm or persistant symptoms
37
If stable, what test should be done on patients with upper GI bleed?
Endsocopy within 24h
38
Harmartomatous polyps in the GI tract and facial freckles is associated with what condition? What type of genetic condition? Complications?
Peutz-Jeghers syndrome Autosomal dominant BO - intersucseption GI bleeding
39
UC presentation
``` Rectal bleeding (proctitis) Diarrhoea Bloody stool Abdo pain Skin changes Eye problems Arthritis Malnutrition ```
40
What are risk factors for UC?
Family history | HLA-B27 association (ankylosing spond)
41
Extra-abdominal manifestations of IBD
Skin - erythema nordosum, pyoderma gangrenosum Eyes - anterior uveitis, episcleritis Joints - arthritis, ank. Spondylitis (UC) Renal stones PSC (UC)
42
Investigations for IBD
``` 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
What is a serological marker likely to be positive in UC?
pANCA
44
What is a mild flare of UC?
<4 motions a day Small bleeding No systemic upset
45
What is a moderate flare of UC?
4-6 motions a day Moderate bleeding Minimal systemic signs
46
What is a severe flare of UC?
>6 motions a day Severe bleeding Systemic signs
47
Complications of IBD
Toxic dilatation (UC more common) VTE Colon cancer PSC SBO (crohns) Abscess formation Perforatiin Malnutrition
48
Differences in presentation between UC/crohns
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
Differences in pathology of UC/crohns
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
Management of UC
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
Managemenr of crohn's disease
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
Differentials for bloody diarrhoea
``` Drugs - PPIs, NSAIDs, Abx IBS IBD Gastroenteritis - e. Coli, c. Diff., shigella, campylobacter Cancer Ischaemic colitis Mesenteric ischaemia ```
53
What is wilsons disease?
Autosomal recessive condition characterised by error in copper metabolism and accumulation
54
Pathophysiology of wilsons disease
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
Presentation of wilsons disease
``` 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
Tests for wilsons disease
``` 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
Management of wilsons disease
``` Diet - avoid foods with high copper (liver, chocolate, nuts) Check water sources for copper Drugs - lifelong penicillamine Liver transplantation Screen siblings ```
58
What is hereditary haemochromatosis
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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