Core Flashcards
1
Q
Crohn’s:
- What is it?
- What is the presentation?
- What are the main signs O/E? (4) What are the extraintestinal signs related (4) and unrelated to disease activity? (3)
- What are the main Ix that are done and what is seen on each? (4) How is the diagnosis made?
- What is the most important aspect of Mx?
- How do you Mx a mild flare up and inducing remission? (2)
- How do you Mx a severe flare up? (3)
- What is the drug treatment for maintaining remission? (2)
- What are the indications for surgery? (2)
- What are the main complications? (5)
A
- A chronic inflammatory condition of the digestive tract from the mouth to the anus - but mainly the terminal ileum and colon
- Presents in late adolescence/early adulthood with weight-loss and diarrhoea, abdominal pain and lethargy (failure to thrive in children)
- Abdominal tenderness, right iliac fossa mass and perianal abscesses and fistulae
Related to disease activity = Arthritis (pauciarticular (2-4 joints affected) and asymmetric), Episcleritis, Erythema nodosum and osteoporosis
Unrelated to disease activity = Arthitis (polyarticular 5+joints and symmetrical), pyoderma gangrenosum, clubbing
- Diagnosis is made via a combination of endoscopy and histology.
Bloods = raised CRP
Endoscopy (Ix of choice) = deep ulcers and skip lesions
Histology = Inflammation for all layers from mucosa to serosa, increased goblet cells and granuloma formation
Small bowel enema (for terminal ileum examination) =
Strictures (Kantor’s string sign), proximal bowel dilation, ‘rose thorn’ ulcers and fistulae
- Stop smoking
- 1st = Oral Pred 30mg
2nd = 5-ASA drugs e.g. sulfasalazine or mesalazine (less effective) - IV hydrocortisone, IV fluids and nil by mouth
- 1st = Azathioprine
2nd = Methotrexate - Failure to respond to drugs or intestinal obstruction from : stricturing terminal ileal disease (very common), perforation or abscess.
- Bowel obstruction via stricturing terminal ileal disease, intestinal fistulae, abscess formation, small bowel and colorectal cancer and osteoporosis
2
Q
Ulcerative Colitis:
- What is the pattern on inflammation?
- When is the peak age of incidence? (2)
- What are the main symptoms? (4) What are the signs of an acute severe flare up? (4)
- What tests might you order? (5) What is the purpose of the tests?
- What might you see on AXR which is suggestive of UC? (4)
- Which criteria assesses the severity of UC?
- What are the complications of UC? (5)
- What factors can trigger a UC flare up? (4)
- What classifies a flare up as mild/moderate/severe?
A
- Continuous inflammation which begins in the rectum (proctitis = 50%) which can ascend proximally (left sided colitis = 30%) or the entire colon (pancolitis - 20%)
- 15-25 and 55-65
- Symptoms = progressive bloody diarrhoea, abdominal cramping (particularly LLQ), tenesmus, frequency
Signs = non-specific in remission, acute severe flare up = pyrexia, abdominal distension, anaemia, hypoalbuminaemia - Bloods/ FBC (anaemic), LFTs (low albumin), CRP/ESR (raised), cultures (rule out infection)
Stool/ Faecal calprotectin, CDT/MC + S to rule out gastroenteritis (C. Diff can mimic UC)
CXR/ to assess for perforation
AXR/ Good initial investigation
Colonoscopy = typically diagnostic
5. Lead piping (lack of haustra) Thumb printing (wall thickening) Colonic dilatation (>6cm) Pseudopolyps
- Truelove and Witts criteria
- Bowel perforation, bleeding, toxic megacolon, venous thrombosis and colon cancer
- Stress, NSAIDs, smoking cessation and Abx
- Mild = <4 stools per day with no blood or systemic signs
Moderate = 4-6 stools per day with no systemic signs
Severe = 6+ stools per day with systemic signs (pyrexia, anaemia, distension or tenderness)
3
Q
Ulcerative Colitis Management:
- How is a mild-moderate flare up remission induced? (Proctitis, left sided colitis and pancolitis)
- How is a severe colitis flare up remission induced? (2)
- How is remission maintained in mild/moderate (proctitis and L sided colitis) and severe disease?
- How is an acute flare up managed? (4)
- When is emergency surgery indicated? (2)
- When is elective surgery indicated? (2)
A
- Proctitis:
1st = topical aminosalicyclate
2nd (no improvement after 4 weeks) = + oral aminosalicyclate
3rd (still no improvement) = + topical/oral steroid
LSC
1st = topical aminosalicyclate
2nd (4wk) = + high dose oral aminosalicyclate OR switch to high dose oral aminosalicyclate and topical corticosteroid
3rd = STOP topical - oral aminosalicyclate and oral corticosteroid
Pancolitis
1st = topical aminosalicyclate + high dose oral aminosalicyclate
2nd = STOP topical - high dose oral aminosalicyclate and corticosteroid
- 1st = IV steroids (or IV ciclosporin if steroid CI)
2nd = IV steroid + ciclosporin OR consider surgery - Proctitis = one of: topical aminosalicyclate, oral + topical aminosalicyclate or just oral aminosalicyclate (worst)
L sided colitis = low maintenance dose of oral aminosalicyclate
Severe or >=2 exacerbations/year = oral azothioprine or mercaptopurine
- Resuscitate
- IV 100mg hydrocortisone
- LMWH (thromboprophylaxis)
- Monitor
- If any of the complications occur or failure to respond to Rx
- Chronic symptoms despite Rx or carcinoma/high grade dysplasia
4
Q
Viral Hepatitis:
- Describe Hep A in terms of mode of spread and signs and symptoms (4)How is it managed?
- Describe Hep B in terms of method of spread, signs and symptoms(2) and management
- When are the following Hep B serologies seen: HBsAg, Anti-HBs, Anti-HBc, HBeAg?
- Describe Hep C in terms of method of spread, How is it managed? (2)
- How is Hep D spread?
- What will be the signs on LFTs of chronic hepatitis? (3)
- What are the extra hepatic signs of Hep B?(3)
- Which condition increases the risk of Hep C?
A
- Faeco-Oral
Initially signs of fever, N+V, malaise then jaundice
Supportive Mx - Cause of chronic hepatitis - blood products (IVDU, haemodialysis etc.)
Similar signs to Hep A + extra hepatic signs
Supportive Mx - HBsAg 1-6mth = acute infection (infective)
HBsAg >6mth = chronic disease (infective)
Anti-HBs = immunity via exposure or immunisation (-ve in chronic disease)
Anti-HBc = previous or current infection (present for 6mth)
HBeAg = currently infected - Cause of chronic hepatitis - blood products
Mx = PEGinterferon a-2a/2b + ribivarin - With Hep B - can get Hep B infection then Hep D or together at the same time. But Hep B infection is required.
- ALT >1000, raised ALP and bilirubin
- Result of immune complex deposition:
- Urticaria or vasculitic rash
- GN
- Arthritis - Cirrhosis
5
Q
Liver Failure:
- What are the acute causes? (Infection, toxins, vasc, other)
- What is the chronic cause of acute liver failure?
- What are the signs of liver failure? (3)
- What might be seen on LFTs which point to the cause of liver failure? (2) How can you differentiate between acute and chronic liver failure on LFTs?
- What is hepatorenal syndrome? When would you suspect it? What is the pathophysiology? What are the two main types? (2)
- How do you manage hepatorenal syndrome? (3)
- How do you Mx liver failure?
- What are the main complications and how are they managed? (7)
- Which drugs should you avoid in liver failure? (3)
- Which drugs are hepatotoxic? (6)
- What are the poor prognostic factors for liver failure? (5)
- What is Budd-Chiari syndrome? How does it present? (3) How is it diagnosed?
A
- Infection (Hep A/B)
Toxins (alcohol/paracetamol/drugs)
Vascular (Budd Chiari)
Other (Wilson’s) - Cirrhosis - decompensated liver failure
- Jaundice, Oedema/Ascites, encephalopathy
- AST:ALT >2 = Alcohol
AST:ALT <1 = Viral
Low Alb = chronic *
PT = increased in acute *
- best
5. Renal failure in patients with advanced CLF - if there’s liver failure and signs of pre-renal RF but not improving with volume correction.
Path: cirrhosis = splanchnic arterial vasodilation results in reduced effective circulatory volume which activates RAS and causes arterial vasoconstriction. This results in persistent underfilling of renal circulation leading to RF.
Type 1 = rapid progressive deterioration (survival <2 weeks)
Type 2 = steady deterioration (survival 6mth)
- IV albumin + terlipressin (splanchnic vasoconstrictor)
Haemodialysis (supportive Rx)
Liver transplant is the optimal treatment - Manage in ITU and treat the underlying cause:
- Maintain good nutrition via NG
- Prophylactic PPI
- Thiamine supplementation - Bleeding: Vit K, blood, FFP
- Sepsis: tazocin
- Ascites: fluid and Na+ restriction, diuretic (K+ sparing)
- Hypoglycaemia: regular BM and IV dextrose <2mmol
- Encephalopathy: avoid sedatives
- Seizures: lorazepam
- Cerebral oedema: mannitol
- Opiates, oral hypoglycaemics, Na+ containing IVI
- Paracetamol, methotrexate, 5-ASA, TB drugs, tetracycline and gentamycin
- Grade 3/4 encephalopathy, Age >40, Alb <30g/L, Raised INR, drug induced
13. Hepatic vein thrombosis due to underlying coagulopathy Triad: - Sudden onset severe abd. pain - Ascites - tender hepatomegaly
Mx: doppler US (best)
6
Q
Cirrhosis:
- What a the most common causes? (7)
- What are the autoimmune causes? (4)
- How is a diagnosis of cirrhosis made?
- What are the complications of cirrhosis? (4)
- What conservative advice would you give? (3)
- How do you manage the following causes of cirrhosis?
- What are the triggers for decompensation?
A
- Alcohol, NAFLD, Hep B/C, haemachromatosis, autoimmune, Wilson’s and a1-antitrypsin
- Autoimmune hepatitis, primary sclerosing cholangitis, primary biliary cirrhosis
- Fibroscan - transient elastography. Uses US to detect the extent of fibrosis.
- Decompensation, SBP, portal hypertension, increased risk of HCC
- Good nutrition, alcohol abstinence, HCC and oesophageal varices screening
- HCV = PEGinterferon
PBC = ursodeoxycholic acid
Wilson’s = penecillamine - Anything really: alcohol, infection, constipation, dehydration
8.
