Abdominal Flashcards
Management of coeliac disease?
Patient education
Primary management is the avoidance of gluten (wheat, rye and barley-containing foods)
Dietician input
Gluten-free food prescriptions
Vitamin supplements if needed
NB: around 30% of patients with coeliac disease have hyposplenism, consider influenza, meningococcal and pneumococcal vaccines
How do we diagnose coeliac disease?
Must enquire if the patient is on a diet containing gluten or not.
Gluten-free diet can make TTG normal.
If patient is on a gluten-containing diet and coeliac disease is suspected, the gold standard diagnostic test is an OGD with biopsies from the D2 region.
Looking for subtotal or total villous atrophy.
Investigations for coeliac disease?
Bedside: obs, history, urine dip and MC+S
Bloods: FBC (anaemia), haematinics (cause of anaemia), WCC, CRP (infection), UE, LFTs
Specific to coeliac: anti-TTG antibody test and screen for other AI conditions (TFTs)
Imaging: OGD and biopsies
Differential diagnosis of coeliac disease?
Inflammatory bowel disease
Infective cause
Other autoimmune diseases such as thyroid disease
What clinical findings would you expect in a patient with coeliac disease?
Often a normal abdominal examination.
Important negatives include:
- lack of signs of anaemia
- no lymphadenopathy
- no signs of cachexia
Investigations for suspected IBD?
Bedside: obs, stool culture for microscopy, culture and c. diff toxin, faecal calprotectin
Bloods: FBC, B12 and folate (malabsorption), UEs, CRP, LFTs (liver abnormalities as an extra-intestinal manifestation of iBD or PBC / PSC / AIH)
Imaging: AXR (rule out toxic megacolon), sigmoidoscopy / colonoscopy + biopsy for histological confirmation, MRI entercolysis if Crohn’s is suspected (to detect small bowel strictures)
What are the differences between Crohn’s and UC?
Crohn’s has skip lesions, UC is continous
Crohn’s is transmural, UC is superficial
Crohn’s affects the whole GI tract, whereas UC affects the large bowel (predilection for rectum)
Smoking increases your Crohn’s risk, whereas it decreases your UC risk
In Crohn’s, fistulae and stenosis is common, whereas it is rare in UC
What are some emergency indications for surgery in IBD?
Toxic megacolon
Haemorrhage
Perforation
What screening tests should be considered prior to starting biologic therapy for IBD?
History and exam (previous TB)
Hepatitis serology
HIV test
CXR (TB)
T-spot test for TB
Name some biologics used in IBD.
UC: infliximab and golimumab
Crohn’s: infliximab and adalimumab
(Vedolizumab is used for both CD and UC in patients who fail first-line treatment)
What extra-intestinal manifestations of IBD can occur?
Skin: erythema nodosum, pyoderma gangrenosum, aphthous ulceration
Joints: seronegative arthritides
Eye: uveitis, scleritis / episcleritis
HPB: PSC in UC, cholangiocarcinoma
Renal: oxalate stones
Name some surgeries that are commonly performed in cases of IBD.
Subtotal colectomy with end ileostomy
End ileostomy with mucous fistula (usually emergency)
Proctocolectomy and end ileostomy
Proctocolectomy with ileo-anal pouch reconstruction
What stomas might be seen in a patient with IBD?
Stoma in RIF: likely ileostomy, contents are semi-liquid and stoma is spouted
Stoma in LIF: likely a colostomy, solid contents, flush to skin
Also look for other scars associated with prior abdominal surgery (e.g. mucous fistula scar)
Ask patient to cough to assess for a parastomal hernia
Management of IBD?
Medical:
Steroids (in acute-severe disease, IV hydrocortisone)
5-ASA (standard of care to maintain remission)
Disease-modifying agents: azathioprine, MTX, mercaptopurine
Biological agents: for patients who have 2 or more flares on 5-ASA requiring steroids
Surgical:
For fistulae, strictures, failure to respond to medical therapy, haemorrhage, perforation, toxic megacolon
Other:
Nutritional support (elemental and low-residue diet)
Psychological support
Tell me about the drainage of a transplanted pancreas.
Traditionally, they were drained into the bladder so lipase could be measured in patient’s urine to assess for rejection, however increased incidence of UTIs.
More recently, transplanted pancreases are attached to the small bowel and drained via the bowel.
What different types of renal transplant are available?
Live donors: altrustic or related to the patient
Cadaveric donors: after circulatory or neurological death
What is the benefit of a simultaneous kidney pancreas transplant (SPK)?
A combined kidney and pancreas transplant intends to cure both the patient’s ESRF and diabetes.
This means the patient can be free of haemodialysis and insulin therapy.
Reduces risk of vascular complications of diabetes too.
Type 1 diabetics typically receive combined transplantation, but more recently have been offering them to T2 diabetics who meet criteria and are insulin-dependent.
What are the different causes of jaundice?
Can be divided into:
Pre-hepatic: haemolytic anaemia, drugs, Gilbert’s syndrome
Hepatic: viral hepatitis, alcohol, NAFLD, autoimmune hepatitis, biliary malignancy
Post-hepatic: gallstones, CBD stricture, extra-hepatic malignancy, pancreatitis
Management of ascites?
Diagnostic or therapeutic ascitic tap - calculate SAAG, send for cytology and culture
Limit salt intake to 5 - 6.5 g/day
Spironolactone
Give albumin
Consider TIPSS in refractory ascites
Treat SBP with IV antibiotics (ciprofloxacin)
Acute management of upper GI bleed?
Use BSG’s acute upper GI bleeding bundle:
A to E assessment, stabilise patient, IV crystalloid
Transfuse if Hb <70 g/L
Calculate Glasgow-Blatchford score (consider discharge if 0 - 1)
If suspected variceal bleed, give terlipressin + antibiotics
OGD within 24h
If haemodynamically unstable, major haemorrhage protocol +/- critical care review
Define ‘acute liver failure’
Loss of liver function in days or weeks (<6 mo)
In a patient WITHOUT pre-existing liver disease
Acute liver injury, encephalopathy and raised INR
Investigations in a patient with chronic liver disease?
Bedside: full history including PMH, drug / alcohol / FH / travel history
Bloods: FBC, UEs, LFTs including GGT, coagulation screen, BBV screen, ferritin, immunoglobulins, caeruloplasmin, autoantibody screen
Imaging: USS abdomen, CT +/- biopsy. Test for fibrosis with fibroscan (usually as OP)
Which autoantibodies are tested for on an autoantibody screen in the context of CLD?
ANA
AMA
Smooth muscle
LKM antibody
Tumour markers (AFP for HCC)
What autoantibodies are associated with PBC?
Positive anti-mitochondrial antibody.
Raised IgM level.
What are the causes of CLD?
Most common 3 causes are:
1. Alcohol
2. NAFLD
3. Viral hepatitis
Other important causes are:
- Autoimmune: AI hepatitis, PBC, PSC
- Haemochromatosis, Wilson’s, A1AT deficiency
- HHT
- Drug causes
Why do we calculate the SAAG in ascites and what does it tell us?
The SAAG (serum ascites albumin gradient) allows us to differentiate between portal hypertensive and non-portal hypertensive causes of ascites.
Portal hypertensive causes have a SAAG >11 g/L:
- CCF
- Portal vein thrombosis / Budd-Chiari
- Cirrhosis
Non-portal hypertensive causes have a SAAG <11 g/L:
- TB
- Malignancy
- Pancreatitis
- Nephrotic syndrome
How is PBC managed?
Treatment of choice - ursodeoxycholic acid
Smoking cessation
Liver transplantation
How do patients with PBC present?
Fatigue and pruritus are most common
Can progress to CLD + cirrhosis
There is a link with HCC
What are the features of hepatic decompensation?
‘JAVEC’
Jaundice
Ascites
Variceal haemorrhage
Encephalopathy
Coagulopathy
Name some absolute contraindications to liver transplantation?
Severe irreversible pulmonary disease
Severe extrahepatic disease with high mortality
Ongoing alcohol / drug use
Active or previous extra-hepatic malignancy
Indications for liver transplant
Acute liver failure: paracetamol, hepatitis (viral or ischaemic)
Chronic liver failure:
- Alcoholic liver disease
- NAFLD
- Chronic viral hepatitis
- Autoimmune: PSC, PBC, AIH
- Genetic: Wilson’s, haemochromatosis, A1AT deficiency
Why is the use of haemodialysis preferable to PD in a patient with polycystic kidney disease?
The bulk of PKD and the fluid required in the peritoneal cavity can cause discomfort to patients.
Having PD increases the risk of cyst infection, which can lead to a number of complications.
What are the potential complications of dialysis?
HD: dialysis washout, infection, bleeding, B2 microglobulin amyloidosis, psychological
PD: peritonitis, diabetes, local complications (catheter site infections, hernias)
Why might a patient have a tunneled line rather than an AV fistula?
Tunnelled (Tesio) lines are usually a temporising measure whilst waiting for an AV fistula to mature.
Can also be created as emergency access for haemodialysis.
Tunnelled lines are prone to infection, have a shorter lifespan and lower blood flow rates, so dialysis takes longer.
What are the differences between haemodialysis and peritoneal dialysis?
HD:
- Takes place via a fistula / tunneled line
- 3x a week, for 4 hours each time
PD:
- Takes place via a catheter leading into the abdominal cavity
- Toxins diffuse across the peritoneum into the diasylate fluid
- Fluid is either removed as the patient sleeps (automatic PD) or at various points through the day (continuous ambulatory PD)
What are the most common causes of ESRD?
Diabetes
Hypertension
ADPKD
Glomerulonephritis
TIP: try to work out WHY the patient has developed ESRD
What investigations would you request for a patient with AKI / CKD of unknown cause?
Bedside: urine dip (blood / protein)
Bloods: FBC / LFT / UE / clotting / WCC and CRP, PSA (obstructive uropathy), ANA, ANCA, anti-GBM, complement, myeloma screen, immunoglobulins, blood cultures
Imaging: CXR (infection, pulmonary haemorrhage), renal USS (obstruction / size / cysts), biopsy if cause remains unclear
Management of CKD / ESRF
MDT approach
Address underlying cause / reversible causes (diabetes, GN, HTN)
BP control with ACEi / ARB
Treatment of complications: renal osteodystrophy, anaemia, secondary / tertiary hyperparathyroidism
Early dialysis / transplant planning - ‘predialysis clinic’ with doctors / nurses / dieticians / psychologists to start working patient up for transplant
What are some barriers / contraindications to renal transplant?
Donor matching
Active / recent malignancy
Ongoing deep-seated infection
Active vasculitis
Severe obesity due to technical difficulty
In terms of renal function, define ESRF?
A patient who has an eGFR of less than 15ml per minute.
When would you start working a patient up for renal transplantation?
As they approach ESRF, but before they require dialysis.
When they receive transplantation is based on the availability of donors.
Transplanting patients before they end up on dialysis carries a better prognosis.
What clinical signs would you expect if your patient has had an SPK?
Lower midline abdominal incision, with palpable kidney in iliac fossa but no overlying scar.
Evidence of previous diabetes.
Patients often younger, transplanted in their 30s-40s.
What problems can follow renal transplantation?
Rejection: acute / chronic
Infection: pneumocystis / CMV / BK virus
Skin malignancies
Graft dysfunction
Hypertension and high lipids - CVD
Immunosuppression side effects / toxicity
Recurrence of disease
List some side effects of long-term immunosuppression.
Infection / malignancy
Steroids: skin thinning, easy bruising, Cushing’s syndrome
Ciclosporin: gingival hyperplasia, hirsuitism, renal impairment
Tacrolimus: tremor and diabetes
What are the signs of a failing renal transplant?
Declining renal function
Proteinuria
Tenderness over graft site
Fluid overload
When presenting a renal transplant patient, which 3 things are important to state?
- Underlying reason for renal failure
- Current RRT modality
- Complications of past / current treatment
If you suspect haemochromatosis, which investigations would you like to perform?
Ferritin levels (raised)
Transferrin saturation (raised)
To make diagnosis, need HFE gene testing
List some causes of gum hypertrophy.
Drugs: ciclosporin, phenytoin, nifedipine
Scurvy
Acute myelomonocytic leukaemia
Pregnancy
Familial
If you saw jaundice in the context of a liver transplant patient, what would you be thinking of?
This raises the question of graft dysfunction or extrahepatic causes
Need to do a conjugated and unconjugated bilirubin
How are patients selected for liver transplant?
MDT approach
Patient needs to have significant liver dysfunction
Certain criteria and guidelines which are used to predict liver prognosis (UK End Stage Liver Disease Model)
What are the top 3 reasons for needing liver transplantation?
Cirrhosis (haemochromatosis, NAFLD, AI liver disease, viral hepatitis)
Acute hepatic failure (hep A, B, paracetamol)
Hepatic malignancy (HCC)
What are the survival rates of patients with a liver transplant?
80% 1-year survival
70% 5-year survival
What signs / symptoms may a patient with ADPKD present with?
Hypertension
Signs of renal failure
Proteinuria / haematuria
Extrarenal manifestations of ADPKD such as liver cysts, pancreas, spleen, epididymis, thyroid
Loin pain: due to renal haemorrhage, calculi or infection
What is the inheritance modality of ADPKD?
Autosomal dominant condition with 2 main associated genetic mutations.
80% of patients - mutation on chromosome 16
15% of patients - mutation on chromosome 4
The remaining 5% have no detectable genetic abnormality
PKD 2 is associated with less severe disease with later onset. Fewer cysts and later progression to renal failure.
Important positive and negative signs when presenting a patient with suspected ADPKD?
Positive signs: bilateral ballotable masses in the flanks, which I can get above.
Negative signs: no evidence of kidney disease. The patient is euvolaemic and has no evidence of previous or current RRT.
What are the extrarenal manifestations of ADPKD?
Hypertension
Cysts in liver, pancreas, epididymis
Colonic diverticulae
Cardiac valve disease
Abdominal / inguinal herniae
Most significant = IC Berry aneurysms which may present with intracranial or subarachnoid haemorrhage. Rupture is associated with uncontrolled HTN
What are the indications for nephrectomy in a patient with ADPKD?
In general, should be avoided and the old kidney is usually left in situ.
However, may be required in cases of:
- To make room for a transplanted kidney (volume in abdomen)
- RCC
- Chronic pain
- Chronic infection
- Significant haematuria
What is the management of ADPKD?
Management is multi-modal, and implemented by the MDT
- BP control with ACEi’s
- Control of hyperlipidaemia (as CKD = major risk of IHD)
- Tolvaptan may be of use earlier in the disease
- May eventually require RRT or transplant
- High fluid, low-salt diet
Differentials for unilateral kidney enlargement?
PKD
Renal cell carcinoma
Renal cysts
Hydronephrosis
Differentials for bilateral kidney enlargement?
PKD
Bilateral RCC
Bilateral hydronephrosis
Tuberous sclerosis
Amyloidosis
Indications for splenectomy?
Rupture (trauma)
Haematological (ITP and hereditary spherocytosis)
What forms part of the splenectomy workup?
Vaccination: 2 weeks prior against encapsulated bacteria - pneumococcal, flu, meningococcal
Lifelong penicillin
Medic alert bracelet
Causes of massive splenomegaly?
Massive = >8cm ‘MMM’
CML
Myelofibrosis
Malaria / visceral leishmaniasis
Causes of moderate splenomegaly? (4 - 8 cm)
Myelo / lymphoproliferative disorder
Gaucher’s disease
Amyloidosis
What prognostication scores are used to determine the benefit of steroids in alcoholic hepatitis?
Patient admitted with alcoholic hepatitis:
- Assessment of disease severity with Maddrey’s Discriminant Function score. If >=32, trial of prednisolone 40mg / day.
- Assess treatment response at day 7 with Lille score. If <0.45, continue treatment for 28 days. If Lille score >=0.45, stop treatment and assess for early liver transplantation in highly selected patients.
