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Abdomen Flashcards

1
Q

Name some clinical signs of chronic liver disease

A
  • 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)
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2
Q

What are the signs of hepatomegaly?

A

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)

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3
Q

What features in examination may suggest an underlying cause of hepatomegaly?

A
  • Tattoos and needle marks - infectious hepatitis
  • Slate-grey pigmentation - haemochromatosis
  • Cachexia - Malignancy
  • Mid-line sternotomy scar - CCF
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4
Q

What are the signs of acute decompensation of liver disease?

A
  • Ascites: shifting dullness
  • Asterixis: ‘liver flap’
  • Altered consciousness: encephalopathy
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5
Q

What are the causes of hepatomegaly?

A

Cirrhosis (alcoholic)
Carcinoma (secondaries)
Congestive Cardiac Failure
Infectious (HBV and HCV)
Immune (PBC, PSC and AIH)
Infiltrative (amyloid and myeloproliferative disorders)

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6
Q

What investigations would you want in a patient with suspected hepatomegaly?

A
  • Bloods: FBC, U&S, LFTs, glucose, Coag
  • AUSS
  • Tap ascites (if present)
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7
Q

What investigations would you want in a patient with suspected cirrhosis?

A

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)

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8
Q

What investigations would you carry out if you were suspecting a malignancy in liver?

A
  • Imaging: CXR and CT abdomen/chest
  • Colonoscopy/Gastroscopy
    -Biopsy
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9
Q

What complications can arise as a result of cirrhosis?

A
  • Variceal haemorrhage due to portal hypertension
  • Hepatic encephalopathy
  • Spontaneous bacterial peritonitis
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10
Q

Describe Childs-Pugh classification of cirrhosis.

A

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

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11
Q

What are the causes of ascites?

A

Cirrhosis (80%)
Carcinomatosis
CCF

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12
Q

How is ascites treated in cirrhosis?

A
  • Abstinence from alcohol
  • Salt restriction
  • Diuretics (aim 1kg weight loss/day)
  • Liver transplantation
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13
Q

Name the causes of palmar erythema

A
  • Cirrhosis
  • Hyperthyroidism
  • Rheumatoid arthritis
  • Pregnancy
  • Polycythaemia
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14
Q

What are the causes of gynaecomastia?

A
  • 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
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15
Q

What autoantibodies are involved in Liver Disease?

A
  • 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.
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16
Q

What are the clinical signs of haemochromatosis?

A
  • Increased skin pigmentation (slate-grey colour)
  • Stigmata of chronic liver disease
  • Hepatomegaly
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17
Q

What scars could be seen in a patient with haemochromatosis?

A
  • Venesection
  • Liver biopsy
  • Joint replacement
  • Abdominal rooftop incision (hemihepatectomy for HCC)
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18
Q

What can be found on examination to suggest complications as a result of Haemochromatosis?

A
  • Endocrine: ‘bronze diabetes’ (e.g. injection sites), hypogonadism and testicular atrophy
  • Cardiac: congestive cardiac failure
  • Joints: arthropathy (pseudo-gout)
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19
Q

What is the mode of inheritance of haemochromatosis?

A
  • 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
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20
Q

How would a patient with haemochromatosis present?

A
  • Fatigue and arthritis
  • Chronic liver disease
  • Incidental diagnosis or family screening
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21
Q

What investigation findings would be in-keeping with haemochromatosis?

A
  • Raised serum ferritin
  • Raised transferrin saturations
  • Liver biopsy in keeping
  • Genotyping
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21
Q

Aside from ferritin, transferrin sats, liver biopsy and genotyping, what other investigations would you request in a patient with suspected haemochromatosis?

A
  • 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
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22
Q

How would you treat a patient with suspected Haemochromatosis?

A
  • Regular venesection (1 unit/week) until iron deficient, then venesect 1 unit, 3-4 times/year
  • Avoid alcohol
  • Surveillance for HCC
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22
Q

How would you screen family members for Haemochromatosis?

A
  • Iron studies (ferritin and TSAT)

If positive:
- Liver biopsy
- Genotype analysis

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23
Q

What is the prognosis of someone with haemochromatosis?

A
  • 200x increased risk of HCC if cirrhotic
  • Reduced life expectancy if cirrhotic
  • Normal life expectancy without cirrhosis and effective treatment
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24
Q

What are the clinical signs of splenomegaly?

A
  • 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.
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25
Q

What signs may suggest an underlying cause of splenomegaly?

A
  • Lymphadenopathy: haematological and infective
  • Stigmata of chronic liver disease: cirrhosis with portal hypertension
  • Splinter haemorrhages, murmur etc: bacterial endocarditis
  • Rheumatoid hands: Felty’s syndrome
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26
Q

What are the causes of splenomegaly?

A

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

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27
Q

What investigations would you request in a patient with suspected splenomegaly?

A
  • 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

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28
Q

What are the indications for splenectomy?

A
  • Rupture (trauma)
  • Haematological (ITP and hereditary spherocytosis)
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29
Q

What is required post-splenectomy?

A
  • Vaccination (ideally 2/52 prior to protect against encapsulated bacteria): pneumococcus, meningococcus and haemophilus influenzae (Hib)
  • Prophylactic penicillin (lifelong)
  • Medic alert bracelet
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30
Q

What are the clinical signs of renal enlargement?

A
  • 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)
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31
Q

What conditions are associated with enlarged kidneys?

A
  • Hepatomegaly: PKD
  • Indwelling catheter: Obstructive nephropathy with hydronephrosis
  • Peritoneal dialysis catheter/scars
32
Q

What are the causes of unilateral kidney enlargement?

A
  • PKD (other kidney not palpable or contralateral nephrectomy - flank scar)
  • Renal Cell Carcinoma
  • Simple cysts
  • Hydronephrosis due to ureteric obstruction
33
Q

What are the causes of bilateral kidney enlargement?

A
  • PKD
  • Bilateral renal cell carcinoma (5%)
  • Bilateral hydronephrosis
  • Tuberous sclerosis (renal angiomyolipomata and cysts)
  • Amyloidosis
34
Q

What investigations would you request in a patient with an enlarged kidney?

A
  • U&Es
  • Urine cytology
  • AUSS +/- biopsy
  • Intravenous urography
  • CT if carcinoma is suspected
  • Genetic studies (ADPKD)
35
Q

What is autosomal dominant kidney disease?

A
  • 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)
36
Q

How does ADPKD present?

A
  • 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
37
Q

How is ADPKD treated?

A
  • Need genetic counselling of family and family screening; 10% represent new mutations
  • Nephrectomy for recurrent bleeds/infection/size
  • Dialysis
  • Renal transplant
38
Q

What are the clinical signs of Liver trasplant?

A
  • Mercedez-Benz or rooftop scar
  • Evidence of chronic liver disease
39
Q

What system is used to classify the malignant risk of renal cysts based on imaging on CT?

A

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.

40
Q

What conditions cause cystic renal disease?

A
  • PKD
  • VHL Syndrome
  • Tuberous Sclerosis
41
Q

What inherited conditions cause glomerular disease?

A
  • 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
42
Q

What metabolic disorders have renal involvement?

A
  • Fabry’s disease (XL)
  • Primary amyloidosis (AD)
  • Familial Mediterranean fever (AR)
  • Cystinosis (AR)
  • Primary oxalosis (AR)
43
Q

Name some inherited tubular disorders

A
  • Cystinuria (AR)
  • Schwachman syndrome (AR)
  • Marble brain disease (AR)
  • Hypophosphatasia (AR)
  • Benign familial haematuria (AD)
  • Reflux nephropathy (AR)
44
Q

How does Alport syndrome present?

A
  • 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
45
Q

What are the diagnostic criteria for ADPKD?

A

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

46
Q

How do you treat PKD?

A
  • 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
47
Q

Describe PBC

A
  • 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
48
Q

How do patients with PBC present?

A
  • 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
49
Q

How do you manage a patient with PBC?

A
  • 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.
50
Q

What are the causes of chronic renal failure?

A
  • Diabetic nephropathy
  • HTN
  • Glomerulonephritis
  • PKD
  • Chronic pyelonephritis
  • Obstructive/reflux nephropathy
51
Q

What are the advantages of renal transplantation over continued dialysis?

A
  • 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
52
Q

Which conditions have a high risk of recurrence following renal transplant?

A
  • Focal segmental glomerular sclerosis
  • Amyloidosis
  • IgA nephropathy
  • Haemolytic uraemic syndrome
53
Q

Which patients are more at risk of rejection of kidney transplant?

A
  • Those who have received previous transplants
  • Those who have received multiple blood transfusions
  • Those who have had previous rejection reactions
  • Afro-Caribbean patients
  • Children
54
Q

What are the different mechanisms of transplant rejection?

A

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

55
Q

What is involved in donor work-up for transplant?

A
  • 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
56
Q

What is the mechanism of action and side effects of Ciclosporin?

A

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

57
Q

What is the mechanism of action and side effects of Tacrolimus?

A

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)

58
Q

What is the mechanism of action and side effects of Mycophenolate mofetil?

A

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

59
Q

What is the mechanism of action and side effects of Azathioprine?

A

A derivative of 6-mercaptopurine. It functions as an anti-metabolite to inhibit DNA and RNA synthesis.

SEs: Leucopenia, thrombocytopenia, GI disturbance, cholestasis, alopecia

60
Q

What is the mechanism of action and side effects of Steroids in transplant?

A

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

61
Q

What is the mechanism of action and side effects of Sirolimus/Everolimus (mTOR inhibitors)?

A

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

62
Q

What complications can arise as a result of immunosuppression?

A
  • 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
63
Q

What causes an increased SAAG?

A
  • Cirrhosis
  • Alcoholic hepatitis
  • Schistosomiasis
  • Fulminant hepatic failure
  • Budd-Chiari Syndrome
  • Acute or chronic portal vein obstruction
  • Cardiac diseases
  • SBP
63
Q

What are the contraindications for renal transplantation?

A
  • Active malignancy (cancer-free for at least 2 years)
  • Active infection: exclude dental sepsis and gallstones (risk of cholecystitis)
  • Advanced atheromatous disease (relative contraindication)
64
Q

What are the causes of low or normal SAAG?

A
  • Nephrotic syndrome
  • Protein-losing enteropathy
  • Peritoneal carcinomatosis
  • TB Peritonitis
  • Pancreatic duct leak
  • Biliary ascites
65
Q

How does hereditary spherocytosis present?

A
  • Pallor
  • Jaundice
  • Splenomegaly
  • Fatigue
66
Q

What are the DDx for hereditary spherocytosis?

A
  • Non-haemolytic anaemia e.g. iron deficiency
  • Other causes of haemolytic anaemia eg G6PD deficiency
  • Other causes of jaundice e.g. hepatitis
67
Q

What investigations would you like in a patient with suspected hereditary spherocytosis?

A
  • 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
68
Q

How are patients with hereditary spherocytosis managed?

A
  • 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
69
Q

What complications can arise as a result of hereditary spherocytosis?

A
  • Aplastic crisis
  • Gallstones
  • Bone marrow expansion
  • Extramedullary haematopoiesis
  • Post-splenectomy sepsis
  • Post-splenectomy vascular complications
70
Q

What are the DDx of coeliac disease?

A
  • 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
71
Q

How does coeliac’s disease present?

A
  • 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
72
Q

What conditions are associated with coeliac’s disease?

A
  • Dermatitis herpetiformis
  • Down’s Syndrome
  • Selective IgA deficiency
  • Autoimmune conditions e.g. T1DM, Thyroid disease, Liver disease
73
Q

How is coeliac’s disease investigated?

A
  • 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
74
Q

How are patients with coeliac’s disease managed?

A
  • 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
75
Q

What is coeliac crisis?

A
  • 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
76
Q

What complications arise as a result of coeliac disease?

A
  • 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
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