Gastro

Question 1

Inflammatory bowel disease- son of a bitch!

Clinical signs

Answer 1

General malnourished/thin appearance
Cushingoid features suggesting steroid therapy (E.G brusing, buffalo hump, striae)

Hands- Clubbing, small joint arthropathy (As well as alrge joint arthropathy and spondyloarthropaties

Face- Cushing features
Uveitis
Mouth ulcers

Abdomen- Likely have large number of operative scars

May include evidence of laparotomy and smaller incisions for colectomy, bowel resections and hemicolectomy

May have stomas in place, RIF and LIF for ileo and colostomy respectivly

Skin on legs may have erythema nodosum or pyoderma gangrenosum.
Also peripheral oedema from low albumin

Also may have signs of immunosuppression.

Question 2

UC vs Crohn’s

Answer 2

CD affects any part of GI tract from mouth to anus with skip lesions.
UC only affects the colon, can cause terminal ileum disease due to backwash ileitis

Histology- CD transmural inflammation with granulomas
UC is mucosal inflammation with crypt abscesses

Pathology- More likely to have fat malapsorption and vitamin deficiencies in CD due to small bowel being affected

But may be cases where it is ahrd to differentiate between the two.

Question 3

Truelove and witts criteria

Answer 3

Mild <4 stools a day, no systemic symptoms and normal esr
Moderate- >4 stools with minimal systemic disturbance
Severe- >6 stools a day with blood, evidence of systemic disturbance as evidenced by fever, tahcycardia, anaemia or raised ESR >30

Question 4

Managment of Crohn’s -chronic

Answer 4

Chronic disease- trial treatments to see which helps
Initially ASA (such as mesalazine)
Then oral or IV steroids if more severe
Can use steroid sparing agents such as azathioprine and step up to monoclonal antibodies such as infliximab

Advise to stop smoking

Question 5

Management of acute colitis

Answer 5

If mild or moderate can give oral steroids

In severe need hospital admission and IV steorids
If no improvement after 3 days can use IV ciclosporin
If still no improvement can trial an IV anti-TNF alpha agent

High risk of progressing or requiring a colectomy

Question 6

When to operate in IBD

Answer 6

If toxic megacolon
If despite 3/7 of intense treatment continues to have high stool frequency and raised CRP
If no response to intensive treatment at 10/7
Need to monitor closly for perforation

Question 7

Chronic liver disease- clinical signs

Answer 7

May generally appear malnourished or jaundiced

Hands- Clubbing, leukonychia
Palmar erythema, dupytrens contracture
Asterixis

Arms- bruising, excoriations, tatoos
Face- Scleral icterus
Chest- spidernaevi, gynaecomastia
Abdomen- Ascites, Hepatomegaly and splenomegaly
Scars from liver transplant, from liver biopsy and from drain insertion

Pitting oedema due to hypoalbuminaemia

Question 8

Signs of portal hypertension

Answer 8

Splenomegaly
Caput medusa
Oesophageal varices
Ascites

Question 9

Causes of CLD

Answer 9

Alcohol
NAFLD
Viral- Hep B and C
AI- AI hepatitis, PBC, PSC
Metabolic- Wilson's Haemachromatosis
Drug induced- Isoniazid, methotrexate

Question 10

Complications of CLD

Answer 10

Portal hypotension
GI haemorrhage- from variceal bleeds
Anaemia and thrombocytopenia
Ascites
SBP
Hepatic encephalopathy 
Hepatorenal syndrome
Hepatopulmonary syndrome

Question 11

Child Pugh score

Answer 11

Uses- Acites, encephalopathy, albumin, bilirubin and INR to assess
1, 2 or 3 points for each marker.

Grade A= 5-6 points 100% 1 year survival
Grade B 7-9 points 80% 1 year survival
Grade C >9 points 50% 1 year survival

Question 12

Ascites causes

Answer 12

Cirrhosis wiht portal hypertension
Malignancy- e.g GI, liver, ovarian, peritoneum
Congestive cardiac failure
Nephrotic syndrome

Uncommon cuases- Budd chiari, portal vein thrombosis, constrictive pericardidis
TB peritonitis
Ovarian conditions, e.g Meig’s disease with fibroma causing asictes

Question 13

SAAG

Answer 13

Calculate by taking serum albumin from ascitic alubmin
If >11 then is a transudate as a high gradient of protein
If <11 is an exudate as low gradient of protein.

Question 14

Physiology of ascites in CLD

Answer 14

Renal hypoperfusion increases renin from JG aparatus
Renin activates aldosterone
Poor hepatic function reduces aldosterone and ADH breakdown
These increase water and salt absorption
Hypoalbminaemia also reduces oncotic pressure

Have reduced oncotic pressure, increased water and salt retention and high portal pressures.
This get ultrafiltration of fluid into abdominal cavity.