Abdomen Flashcards
Name some clinical signs of chronic liver disease
- General: cachexia, icterus (also in acute), excoriation and bruising
- Hands: leuconychia, clubbing, Dupuytren’s contractures and palmar erythema
- Face: xanthelasma, parotid swelling and fetor hepaticus
- Chest and abdomen: spider naevi and caput medusa, reduced body hair, gynaecomastia and testicular atrophy (in males)
What are the signs of hepatomegaly?
Palpation and percussion:
- Mass in RUQ that moves with respiration, that you are not able to get above and is dull to percussion
- Estimate size (finger breadths below the diaphragm)
- Smooth or craggy/nodular (malignancy/cirrhosis)
- Pulsatile (TR in CCF)
Auscultation:
- Bruit over liver (hepatocellular carcinoma)
What features in examination may suggest an underlying cause of hepatomegaly?
- Tattoos and needle marks - infectious hepatitis
- Slate-grey pigmentation - haemochromatosis
- Cachexia - Malignancy
- Mid-line sternotomy scar - CCF
What are the signs of acute decompensation of liver disease?
- Ascites: shifting dullness
- Asterixis: ‘liver flap’
- Altered consciousness: encephalopathy
What are the causes of hepatomegaly?
Cirrhosis (alcoholic)
Carcinoma (secondaries)
Congestive Cardiac Failure
Infectious (HBV and HCV)
Immune (PBC, PSC and AIH)
Infiltrative (amyloid and myeloproliferative disorders)
What investigations would you want in a patient with suspected hepatomegaly?
- Bloods: FBC, U&S, LFTs, glucose, Coag
- AUSS
- Tap ascites (if present)
What investigations would you want in a patient with suspected cirrhosis?
Liver screen bloods including:
- Autoantibodies and immunoglobulins (PBC, PSC and AIH)
- Hep B and C serology
- Ferritin (haemochromatosis)
- Caeruloplasmin (Wilson’s Disease)
- Alpha-1 anti-trypsin
- AFP (HCC)
Hepatic synthetic function:
- INR (acute)
- Albumin (chronic)
Liver Biopsy (diagnosis and staging)
ERCP (diagnose/exclude PSC)
What investigations would you carry out if you were suspecting a malignancy in liver?
- Imaging: CXR and CT abdomen/chest
- Colonoscopy/Gastroscopy
-Biopsy
What complications can arise as a result of cirrhosis?
- Variceal haemorrhage due to portal hypertension
- Hepatic encephalopathy
- Spontaneous bacterial peritonitis
Describe Childs-Pugh classification of cirrhosis.
Prognostic score based on bilirubin/albumin/INR/ascites/encephalopathy
Score 5-6 - 100% 1 year survival
Score 7-9 - 81% 1 year survival
Score 10-15 45% 1 year survival
What are the causes of ascites?
Cirrhosis (80%)
Carcinomatosis
CCF
How is ascites treated in cirrhosis?
- Abstinence from alcohol
- Salt restriction
- Diuretics (aim 1kg weight loss/day)
- Liver transplantation
Name the causes of palmar erythema
- Cirrhosis
- Hyperthyroidism
- Rheumatoid arthritis
- Pregnancy
- Polycythaemia
What are the causes of gynaecomastia?
- Physiological: puberty and senility
- Kleinfelter’s syndrome
- Cirrhosis
- Drugs e.g. spironolactone and digoxin
- Testicular tumour/orchiectomy
- Endocrinopathy e.g. hyper/hypothyroidism and Addison’s
What autoantibodies are involved in Liver Disease?
- PBC: anti-mitochrondrial antibody (M2 subtype) in 98%, increased IgM
- PSC: ANA, anti-smooth muscle antibody may be positive
- AIH: anti-smooth muscle, anti-liver/kidney microsomal type 1 (LKM1) and occasionally ANA may be positive.
What are the clinical signs of haemochromatosis?
- Increased skin pigmentation (slate-grey colour)
- Stigmata of chronic liver disease
- Hepatomegaly
What scars could be seen in a patient with haemochromatosis?
- Venesection
- Liver biopsy
- Joint replacement
- Abdominal rooftop incision (hemihepatectomy for HCC)
What can be found on examination to suggest complications as a result of Haemochromatosis?
- Endocrine: ‘bronze diabetes’ (e.g. injection sites), hypogonadism and testicular atrophy
- Cardiac: congestive cardiac failure
- Joints: arthropathy (pseudo-gout)
What is the mode of inheritance of haemochromatosis?
- Autosomal recessive on chromosome 6
- HFE gene mutation: regulator of gut iron absorption
- Homozygous prevalence 1:300, carrier rate 1:10
- Males affected at an earlier age than females - protected by menstrual cycle iron losses
How would a patient with haemochromatosis present?
- Fatigue and arthritis
- Chronic liver disease
- Incidental diagnosis or family screening
What investigation findings would be in-keeping with haemochromatosis?
- Raised serum ferritin
- Raised transferrin saturations
- Liver biopsy in keeping
- Genotyping
Aside from ferritin, transferrin sats, liver biopsy and genotyping, what other investigations would you request in a patient with suspected haemochromatosis?
- Blood glucose: to check for coinciding diabetes
- ECG, CXR, Echo: to check for evidence of cardiac failure
- Liver ultrasound and alpha-fetoprotein: to check for evidence of HCC
How would you treat a patient with suspected Haemochromatosis?
- Regular venesection (1 unit/week) until iron deficient, then venesect 1 unit, 3-4 times/year
- Avoid alcohol
- Surveillance for HCC
How would you screen family members for Haemochromatosis?
- Iron studies (ferritin and TSAT)
If positive:
- Liver biopsy
- Genotype analysis
What is the prognosis of someone with haemochromatosis?
- 200x increased risk of HCC if cirrhotic
- Reduced life expectancy if cirrhotic
- Normal life expectancy without cirrhosis and effective treatment
What are the clinical signs of splenomegaly?
- General: anaemia, lymphadenopathy (axillae, cervical and inguinal areas), purpura
- Abdominal: LUQ mass that moves inferomedially with respiration, has a notch, is dull to percussion and you cannot get above nor ballot, estimate size and check for hepatomegaly.
What signs may suggest an underlying cause of splenomegaly?
- Lymphadenopathy: haematological and infective
- Stigmata of chronic liver disease: cirrhosis with portal hypertension
- Splinter haemorrhages, murmur etc: bacterial endocarditis
- Rheumatoid hands: Felty’s syndrome
What are the causes of splenomegaly?
Massive splenomegaly (>8cm)
- Myeloproliferative disorders (CML and myelofibrosis)
- Tropical infections (malaria, visceral leishmaniasis, kala-azar)
Moderate splenomegaly (4-8cm):
- Myelo/lymphoproliferative disorders
- Infiltration (Gaucher’s and amyloidosis)
Tip (<4cm):
- Myelo/lymphoproliferative disorders
- Portal hypertension
- Infections (EBV, infective endocarditis and infective hepatitis)
- Haemolytic anaemia
What investigations would you request in a patient with suspected splenomegaly?
- AUSS
Then if haematological:
- FBC and Blood film
- CT chest and abdo
- Bone marrow aspirate and trephine
- Lymphnode biopsy
If infectious:
- Thick and thin films (malaria)
- Viral serology
What are the indications for splenectomy?
- Rupture (trauma)
- Haematological (ITP and hereditary spherocytosis)
What is required post-splenectomy?
- Vaccination (ideally 2/52 prior to protect against encapsulated bacteria): pneumococcus, meningococcus and haemophilus influenzae (Hib)
- Prophylactic penicillin (lifelong)
- Medic alert bracelet
What are the clinical signs of renal enlargement?
- HTN
- AV fistulae (thrill and bruit), tunnelled dialysis line
- Immunosuppressant ‘stigmata’ e.g. Cushingoid habitus due to steroids, gum hypertrophy with ciclosporin
- Palpable kidney: ballotable, can get above it and moves with respiration
- Polycystic kidneys: both may/should be palpable, and can be grossly enlarged (will feel cystic or nodular)
- Iliac fossae: scar with (or without!) transplanted kidney
- Ask to dip urine: proteinuria and haematuria
- Ask to examine external genitalia (varicocele in males)
What conditions are associated with enlarged kidneys?
- Hepatomegaly: PKD
- Indwelling catheter: Obstructive nephropathy with hydronephrosis
- Peritoneal dialysis catheter/scars
What are the causes of unilateral kidney enlargement?
- PKD (other kidney not palpable or contralateral nephrectomy - flank scar)
- Renal Cell Carcinoma
- Simple cysts
- Hydronephrosis due to ureteric obstruction
What are the causes of bilateral kidney enlargement?
- PKD
- Bilateral renal cell carcinoma (5%)
- Bilateral hydronephrosis
- Tuberous sclerosis (renal angiomyolipomata and cysts)
- Amyloidosis
What investigations would you request in a patient with an enlarged kidney?
- U&Es
- Urine cytology
- AUSS +/- biopsy
- Intravenous urography
- CT if carcinoma is suspected
- Genetic studies (ADPKD)
What is autosomal dominant kidney disease?
- Progressive replacement of normal kidney tissue by cysts leading to renal enlargement and renal failure (5% of ESRF in UK)
- 85% ADPKD1 (chromosome 16) and 15% ADPKD2 (chromosome 4)
- ESRF by age 40-60 years (earlier in ADPKD1 than 2)
How does ADPKD present?
- HTN
- Recurrent UTIs
- Abdominal pain (bleeding into cyst and cyst infection)
- Haematuria
- Hepatic cysts and hepatomegaly (rarely liver failure)
- Intracranial berry aneurysms (neurological sequelae/craniotomy scar)
- Mitral valve prolapse
How is ADPKD treated?
- Need genetic counselling of family and family screening; 10% represent new mutations
- Nephrectomy for recurrent bleeds/infection/size
- Dialysis
- Renal transplant
What are the clinical signs of Liver trasplant?
- Mercedez-Benz or rooftop scar
- Evidence of chronic liver disease
What system is used to classify the malignant risk of renal cysts based on imaging on CT?
The Bosniak system - Bosniak I cyst is simple, category IV is malignant. Category II and III cysts are ‘indeterminate’ and may require prolonged follow up.
What conditions cause cystic renal disease?
- PKD
- VHL Syndrome
- Tuberous Sclerosis
What inherited conditions cause glomerular disease?
- Alport syndrome
- Congenital nephrotic syndrome
- Nail-patella syndrome
- Familial GN (e.g. some forms of focal segmental glomerulosclerosis or IgA nephropathy)
- Charcot Marie Tooth disease
What metabolic disorders have renal involvement?
- Fabry’s disease (XL)
- Primary amyloidosis (AD)
- Familial Mediterranean fever (AR)
- Cystinosis (AR)
- Primary oxalosis (AR)
Name some inherited tubular disorders
- Cystinuria (AR)
- Schwachman syndrome (AR)
- Marble brain disease (AR)
- Hypophosphatasia (AR)
- Benign familial haematuria (AD)
- Reflux nephropathy (AR)
How does Alport syndrome present?
- Deafness (bilateral and sensorineural is characteristic)
- Persistent non-visible haematuria
- Proteinuria and CKD (hereditary congenital haemorrhagic nephritis)
- 30% develop nephrotic syndrome
- Ocular abnormalities in 40% (lenticonus - conical or spherical protrusion of the lens into anterior chamber, retinal flecks and cataracts)
- Macrothrombocytopenia
- Leiomyomas
What are the diagnostic criteria for ADPKD?
In patients with FHx:
- 2 cysts, either unilateral or bilateral if aged <30 years
- 2 cysts in each kidney in patients aged 30-59 years
- 4 cysts in each kidney in patients >60 years
- Diagnosis is supported by hepatic or pancreatic cysts
Sporadic cases:
- Bilateral renal enlargement and cysts, or the presence of multiple bilateral renal and hepatic cysts
- No manifestations suggesting an alternative renal cystic disease
How do you treat PKD?
- HTN control and RAAS blockade (ie ACEi)
- Tolvaptan (ADH receptor antagonist) limits cyst development
- Nephrectomy (partial or full) to remove problematic cysts and reduce mass effects
- Renal transplant and dialysis
Describe PBC
- Autoimmune condition of the liver
- More common in women
- Causes small bile duct obliteration and build up of toxins which can no longer be excreted efficiently
- Alk Phos is raised - released by biliary tree and bile ducts
- Anti-mitrochondrial antibody postive and raised IgM
- Strongly associated with other autoimmune diseases such as RA, Sjogren’s and CREST syndrome
How do patients with PBC present?
- May be asymptomatic - might be diagnosed after an incidental finding of raised ALP
- Pruritus
- Cholestatic jaundice
- Diarrhoea
- Lethargy
- Xanthelasmata due to hypercholesterolaemia
- Skin pigmentation
- Clubbing
- Hepatosplenomegaly
- Portal HTN
- Varices
- Osteoporosis and osteomalacia
How do you manage a patient with PBC?
- Regular monitoring with liver function tests and ultrasound scans
- Cholestyramine relieves pruritus
- Ursodeoxycholic acid
- Obeticholic acid - either as monotherapy or in combination with ursodeoxycholic acid if this is not tolerated or no response. Acts to reduce circulating bile acid
- Liver transplantation - indications are intractable pruritus ad end stage disease. Relapse following transplant is relatively uncommon and the prognosis post-transplant is generally very good.
What are the causes of chronic renal failure?
- Diabetic nephropathy
- HTN
- Glomerulonephritis
- PKD
- Chronic pyelonephritis
- Obstructive/reflux nephropathy
What are the advantages of renal transplantation over continued dialysis?
- Improved Quality of Life
- Increase in patient survival rate compared with dialysis (although selection of fitter patients for surgery may improve bias)
- Cost-effective in long-term
Which conditions have a high risk of recurrence following renal transplant?
- Focal segmental glomerular sclerosis
- Amyloidosis
- IgA nephropathy
- Haemolytic uraemic syndrome
Which patients are more at risk of rejection of kidney transplant?
- Those who have received previous transplants
- Those who have received multiple blood transfusions
- Those who have had previous rejection reactions
- Afro-Caribbean patients
- Children
What are the different mechanisms of transplant rejection?
Hyperacute rejection:
- due to presence of recipient antibodies against the donor kidney
- occurs within minutes of revascularisation
- kidney swells and becomes discoloured
- there is clumping of RBCs and platelets, fibrin is deposited and interstitial haemorrhage occurs
- rarely seen because of antibody cross-reactivity testin
- transplant nephrectomy is needed
Acute rejection:
- acute deterioration in allograft function that is associated with specific pathological changes in the graft
- 2 forms of rejection - acute cell mediated rejection and acute antibody mediated rejection
- common in first 2 weeks but can occur up to 6 months post-transplant
- treated with high dose steroids (often reversible)
- difficult to distinguish from ATN or drug nephrotoxicity
Antibody mediated rejection (needs 3 out of 4 criteria):
- Graft dysfunction
- Histological evidence of tissue injury
- Positive staining for C4d
- Presence of donor specific antibody
Chronic renal transplant rejection:
- gradual decrease in kidney function that starts to become evident 3 months after the transplantation surgery
- HTN and proteinuria are the most important features of declining renal function. Transplant vasculopathy is the single most important feature of chronic renal transplant rejection
What is involved in donor work-up for transplant?
- Recipient cross-match, screening for transmissible disease
- MR angiography and isotope renography (the donor keeps the kidney with a greater functional percentage)
- ABO and HLA typing
- Virology (Hep B, Hep C, CMV which may require tx pre-transplantation)
- Urinalysis and culture
- Consider effects of co-morbidities
- Cardiovascular assessment
- Psychological assessment
What is the mechanism of action and side effects of Ciclosporin?
Inhibits production of IL-2 and TNF-alpha by binding to cyclophilin protein and inhibiting calcineurin
SEs: Nephrotoxicity, Hyperkalaemia, Hypomagnesaemia, gingival hyperplasia, hyperlipidaemia, glucose intolerance, HTN
What is the mechanism of action and side effects of Tacrolimus?
Inhibits the production of IL-2 by helper T cells by binding calcineurin to tacrolimus binding protein
SEs: Nephrotoxicity, Neurotoxicity, glucose intolerance, prolonged QT (rare)
What is the mechanism of action and side effects of Mycophenolate mofetil?
A prodrug, The active compound is mycophenolic acid which inhibits the enzyme inosine monophosphate dehydrogenase (required for guanosine synthesis). Impairs B- and T-cell proliferation selectively because of the presence of guanosine salvage pathways in other rapidly dividing cells.
SEs: Nausea, Diarrhoea, Leucopenia, Anaemia and thrombocytopenia
What is the mechanism of action and side effects of Azathioprine?
A derivative of 6-mercaptopurine. It functions as an anti-metabolite to inhibit DNA and RNA synthesis.
SEs: Leucopenia, thrombocytopenia, GI disturbance, cholestasis, alopecia
What is the mechanism of action and side effects of Steroids in transplant?
Reduce IL1-3, IL-6 and TNF-alpha production and inhibit T-cell activation. There is impairment of dendritic cell function.
SEs: glucose intolerance, bone disease (osteoporosis, avascular necrosis), cataracts, Cushingoid appearance, infections, poor wound healing
What is the mechanism of action and side effects of Sirolimus/Everolimus (mTOR inhibitors)?
TOR is a regulatory kinase. Inhibition reduces cytokine-dependent cellular proliferation at the G1-S phase of the cell cycle.
SEs: Hyperkalaemia, Hypomagnesaemia, Hyperlipidaemia, Leucopenia, Anaemia, Impaired wound healing, joint pain
What complications can arise as a result of immunosuppression?
- New onset diabetes after transplantation
- HTN
- Hyperlipidaemia
- Non-skin malignancies
- Squamous cell carcinoma of skin
- Some malignancies are thought to be related to viral infections e.g. cervical cancer (HPV), lymphoma (EBV) and Kaposi sarcoma (HHV-8)
- Opportunistic infections
- Polyomavirus BK infection
- CMV infection
- Problems associated with steroids: high BMs, HTN, thin skin, obesity and characteristic fat distribution, confusion, peptic ulcers, poor wound healing
What causes an increased SAAG?
- Cirrhosis
- Alcoholic hepatitis
- Schistosomiasis
- Fulminant hepatic failure
- Budd-Chiari Syndrome
- Acute or chronic portal vein obstruction
- Cardiac diseases
- SBP
What are the contraindications for renal transplantation?
- Active malignancy (cancer-free for at least 2 years)
- Active infection: exclude dental sepsis and gallstones (risk of cholecystitis)
- Advanced atheromatous disease (relative contraindication)
What are the causes of low or normal SAAG?
- Nephrotic syndrome
- Protein-losing enteropathy
- Peritoneal carcinomatosis
- TB Peritonitis
- Pancreatic duct leak
- Biliary ascites
How does hereditary spherocytosis present?
- Pallor
- Jaundice
- Splenomegaly
- Fatigue
What are the DDx for hereditary spherocytosis?
- Non-haemolytic anaemia e.g. iron deficiency
- Other causes of haemolytic anaemia eg G6PD deficiency
- Other causes of jaundice e.g. hepatitis
What investigations would you like in a patient with suspected hereditary spherocytosis?
- FBC - Hb may be reduced or normal, mean corpuscular Hb concentration may be elevated, mean corpuscular volume may be normal or reduced
- Reticulocyte count - elevated
- Blood smear - spherocytes present
- Serum bilirubin - elevated unconjugated bilirubin
- Serum aminotransferases - normal
- Direct anti-globulin test - negative
- Peripheral blood smear in hereditary spherocytosis
How are patients with hereditary spherocytosis managed?
- Supportive care
- Red blood cell transfusions
- Folic acid supplementation
- Splenectomy with pre-op vaccination regimen and/or cholecystectom or cholecystotomy (due to increased incidence of gallstones)
- Post-splenectomy antibiotic pneumococcal prophylaxis - phenoxymethylpenicillin or amoxicillin
What complications can arise as a result of hereditary spherocytosis?
- Aplastic crisis
- Gallstones
- Bone marrow expansion
- Extramedullary haematopoiesis
- Post-splenectomy sepsis
- Post-splenectomy vascular complications
What are the DDx of coeliac disease?
- Crohn’s Disease
- UC
- Malignancy e.g. GI and haematological cancers
- PUD
- Giardiasis
- Tropical sprue
- Small intestinal bacterial overgrowth
- IBS
- Cow’s milk protein intolerance
- Non-coelic gluten sensitivity
- Infections e.g. HIV, TB
How does coeliac’s disease present?
- Diarrhoea: either chronic or intermittent
- Bloating
- Abdo pain/discomfort: recurrent abdo pain, distention or cramping
- Failure to thrive (children)
- Weight loss
- Fatigue
- IDA resulting in microcytic anaemia
- Vit B12/folate deficiency causing a macrocytic anaemia
- Osteopenia/osteoporosis
What conditions are associated with coeliac’s disease?
- Dermatitis herpetiformis
- Down’s Syndrome
- Selective IgA deficiency
- Autoimmune conditions e.g. T1DM, Thyroid disease, Liver disease
How is coeliac’s disease investigated?
- Need to have gluten over previous 6 weeks
- FBC/Iron/Vit B12/folate/calcium
- IgA-tTG levels
- Endomysial antibody (EMA) - can be used if IgA-tTG is unavailable or weakly positive
- Skin biopsy if rash suggestive of dermatitis herpetiformis
- Small intestine endoscopy if serological tests positive for confirmation - histology shows intra-epithelial lymphocytes, villous atrophy and crypt hyperplasia
How are patients with coeliac’s disease managed?
- Gluten free diet and dietician referral
- If refractory - dietician and Gastroenterologist review. May require steroids
- Calcium and Vit D supplementation in all patients.
- Iron should only be given if IDA
What is coeliac crisis?
- A rare, life threatening syndrome where coeliac patients present with hypovolaemia, severe watery diarrhoea, hypocalcaemia and hypoalbuminaemia
- Management includes rehydration and electrolyte abnormalities correction
- Would consider a short course of corticosteroids
What complications arise as a result of coeliac disease?
- Osteoporosis/Osteopenia
- Osteomalacia
- Abnormal LFTs
- Hyposplenism
- Dermatitis herpetiformis
- Malignancies e.g. T-cell lymphoma, carcinomas of the upper digestive tract
- Increased risk of vaccine failure (may require multiple doses to invoke immunity)
- Infertility
Name some causes of Jaundice?
Jaundice can be pre-hepatic, hepatic or post-hepatic
Pre-hepatic causes (raised unconjugated bilirubin and raised urinary urobilinogen):
- Increased haemolysis such as in Haemolytic anaemia
- Gilbert’s
Hepatic Causes (raised conjugated and unconjugated bilirubin, some urobilinogen and conjugated bilirubin in urine):
- Alcoholic Liver disease
- MASLD
- Viral hepatitis
- Autoimmune hepatitis
- Certain medications
Obstructive Jaundice (Steatorrhoea, dark urine):
Extra Heptatic:
- Gallstones
- Cholangiocarcinoma
- Biliary strictures (PSC, iatrogenic)
- Pancreatic head tumour
- Enlarged porta hepatis lymphnodes
- Mirizzi’s syndrome (stones in gallbladder or cystic duct)
Intra-hepatic
- PBC
- PSC
- Drugs
- Obstetric cholestasis
What bloods give an indication of the synthetic function of the liver:
- Raised INR (early sign)
- Low albumin
- Low glucose (reduced gluconeogenesis)
What are the indications for Liver Biopsy?
- To determine degree of disease (e.g. steatosis or cirrhosis).
- Post-transplant to look for signs of rejection
- To investigate focal lesions if nature is unclear from imaging
What scoring systems can be used to predict prognosis in Cirrhosis?
- MELD score - based on Bilirubin, INR, Creatinine, Sodium - slightly more accurate than Childs-Pugh score
- Childs Pugh Score
What are the causes of pancreatitis?
Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps and Malignancy
Autoimmune
Scorpion sting
Hyperlipidaemia and Hypercalcaemia
ERCP
Drugs e.g. valproate, azathioprine, thiazides
What is the Glasgow prognostic score for pancreatits?
PaO2<8kPa
Age >55 years
Neutrophilia WCC >15
Ca2+ <2mmol/L
Renal impairment (urea >16mmol/L)
Enzymes (raised LDH and AST)
Albumin <32
Sugar (Glucose >10mmol/L)
If scores 3 or more then severe
What are the complications of pancreatitis?
Acute:
- SIRS
- Sepsis
- ARDS
Chronic:
- Portal vein thrombosis
- Pancreatitic Pseudocyst
- Splenic vein thrombosis
- Pseudocyst. compression of duodenal obstruction, biliary obstruction or pancreatic obstruction
