Abdominal Flashcards

1
Q

What are the causes of cirrhosis?

A

Alcohol
Viral (hepatitis B, hepatitis C)
Autoimmune (primary biliary cirrhosis, primary sclerosing cholangitis, autoimmune hepatitis)
Metabolic (NAFLD, haemochromatosis, cystic fibrosis)
Drugs (methotrexate, isoniazid, amiodarone, phenytoin)

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2
Q

What are the complications of cirrhosis?

A
Portal hypertension (varices, ascites, hypersplenism)
Liver dysfunction (coagulopathy, encephelopathy, jaundice, hypoalbuminaemia)
Hepatocellular carcinoma
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3
Q

What are the causes of decompensation in cirrhosis?

A
Infection
Spontaneous bacterial peritonitis
Hypokalaemia
GI bleeding
Sedatives
Hepatocellular carcinoma
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4
Q

How do you classify the severity of hepatic encephalopathy?

A

Reversible neurological dysfunction or coma related to decompensated liver disease
Graded from 1 to 4 depending on degree of impairment
Asterixis may be present at any stage

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5
Q

How do you assess the severity of cirrhosis?

A

The Childs-Pugh score
Prognostic score based on bilirubin, albumin, INR, ascites and encephalopathy
Graded from A-C (A best prognosis)

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6
Q

How would you manage a patient with cirrhosis?

A

Slow or reverse liver disease (alcohol abstinence, antiviral therapy)
Preventing further liver damage (immunisations, abstinence)
Preventing complications (hepatoma surveillance, endoscopy, prophylaxis against variceal bleeds with propranolol)
Liver transplantation

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7
Q

What are the most common causes of ascites?

A

Cirrhosis
Malignancy
Heart failure

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8
Q

What initial investigations would you use to determine the cause of the ascites?

A
Paracentesis (albumin and protein, white cell count, gram stain, culture, cytology)
Abdominal ultrasound (mass, splenomegaly, portal hypertension, thrombosis)
Blood tests (liver function, clotting, full blood count)
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9
Q

How do you classify transudative and exudative ascites?

A

Comparing the ascitic fluid albumin to the patient’s serum albumin
The serum ascites/albumin gradient (serum albumin - ascitic albumin)

A result of >11 suggests transudative, <11 suggests exudative

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10
Q

What is the pathophysiology of ascites in cirrhosis?

A

Only occurs following the development of portal hypertension

Disruption of portal blood flow due to liver fibrosis, resulting in accumulation of fluid in the peritoneal cavity

The cirrhotic liver releases vasodilatory compounds, which cause sphlanchnic vasodilation. This decreases systemic vascular resistance > lower circulating volume and blood pressure > activates the renin-angiotensin-aldosterone system, which results in sodium and water retention

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11
Q

What is the initial treatment of ascites in cirrhosis?

A

Sodium restriction
Fluid restriction
Diuretic therapy, initially with aldosterone antagonists, with loop diuretics added once naturesis is achieved
Liver transplantation

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12
Q

What are the causes of isolated hepatomegaly?

A
Cirrhosis
Carcinoma
CCF
Infection (HBV, HCV)
Auto-immune (PBC, PSC, AIH)
Infiltration (amyloid, myeloproliferative disorders)
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13
Q

Which tumours commonly spread to the liver?

A
Colorectal (most common)
Upper GI
Lung 
Breast
Renal
Endometrial
Bone
Sarcomas
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14
Q

What are the infective causes of acute hepatitis?

A
Hepatitis A
Hepatitis B
Hepatitis C
Hepatitis E
Epstein-barr virus
Cytomegalovirus 
Toxoplasmosis 
Herpes simplex virus
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15
Q

What are the causes of splenomegaly?

A
Portal hypertension 
Haematological malignancy 
Infection (HIV, endocarditis, epstein-barr)
Congestion (cardiac failure)
Primary splenic disease (splenic vein thrombosis)
Haemolysis
Thalassaemia
Glycogen storage disorders
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16
Q

How would you evaluate a patient with splenomegaly?

A

History - constitutional symptoms, risk factors for HIV, features pancytopenia, travel history, autoimmune disease, liver disease

Investigations - full blood count, blood film, liver function, LDH, autoimmune screen, imaging (ultrasound and full CT imaging if looking for disseminated malignancy), lymph node or bone marrow biopsy

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17
Q

What are the significance of b-symptoms on Hodgkin’s lymphoma?

A

Fever >38, weight loss >10% body weight in 6 months, drenching night sweats

Presence of these alters the patient’s clinical staging

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18
Q

What are the cytogenetics of chronic myeloid leukaemia?

A
The philadelphia chromosome is present in 90-95% of patients with CML
Chromosomal translocation (fusion of c-abl oncogene of chromosome 9 with bcr on chromosome 22.

This fusion leads to increased oncogene activity through tyrosine kinase signalling

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19
Q

What are the causes of hyposplenism?

A
Splenic infarction 
Splenic artery thrombosis
Infiltrative conditions (amyloidosis, sarcoidosis)
Coeliac disease
Autoimmune disease
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20
Q

What advice should patients with hyposplenism/post-splenectomy be given?

A

Vaccinations (pneumococcal, haemophillus influzena B and meningococcal group C
Prophylactic antibiotics
Malaria prophylaxis and travel advice
Medic alert card or bracelet

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21
Q

What is Felty’s syndrome?

A

Triad of seropositive arthritis with neutropaenia and splenomegaly

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22
Q

What is the mode of inheritance of hereditary haemochromatosis?

A

Autosomal recessive
HFE gene is located on the short arm of chromosome 6
Most caucasian patients are homozygous for the cysteine to tyrosine substitution at position 282

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23
Q

How is haemochromatosis diagnosed?

A

Iron overload suggested by iron studies
Transferrin saturation >60% in males and >50% in females
Liver biopsy to show parenchymal iron deposition

Genetic testing for C282Y and H63D
First degree relatives should undergo genetic testing

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24
Q

What is the treatment of haemochromatosis?

A

Vensection (initially twice weekly until transferrin saturation below 50%, and then maintenance every three months)
Hepatocellular carcinoma surveillance

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25
Q

What are the clinical features of primary biliary cirrhosis?

A

Fatigue
Pruritis
Hypercholesterolaemia
Liver disease occurs late

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26
Q

How is primary biliary cirrhosis diagnosed?

A

Serum anti-mitochondrial antibodies are present in >95%
The histological lesion is a portal tract granuloma
Imaging may be done to exclude extra-hepatic cholestasis

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27
Q

Which drugs can cause cholestasis?

A
Phenothiazines
Sulphonamides
Penicillins
Rifampicin
Macrolides
Carbamazepine 
Androgenic steroids
Diclofenac
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28
Q

What is the management of primary biliary cirrhosis?

A

Supplementation of fat soluble vitamins
Treatment of bone disease (vitamin D, calcium, bisphosphonates)
Treatment of hypercholesterolaemia
Treatment of liver disease (ursodeoxycholic acid improves liver biochemistry and slows disease progression)
Management of pruritis (colestyramine, rifampicin, naltrexone)
Anti-histamines do not work and may worsen encephalopathy
Management of fatigue (exclude co-existent anaemia and hypothyroidism)
Referral for transplantation (bilirubin >50, refractory fatigue or pruritis)

29
Q

What are the major causes of chronic renal disease in developed countries?

A
Diabetes 
Glomerulonephritis
Hypertension 
Drugs
Polycystic kidney disease
Obstructive uropathy
30
Q

What are the principles of the management of chronic renal disease?

A

Treatment of reversible causes (cessastion of drugs, treatment of vasculitis, exclusion of obstruction)
Slowing disease progression (treatment of hypertension, treatment of cardiovascular risk factors, managing diabetes)
Treatment of the complications of chronic renal disease (volume overload, high phosphate, metabolic acidosis, anaemia, renal bone disease)

31
Q

What are the indications for renal replacement therapy?

A
Pericarditis or pleuritis due to uraemia
Uraemic bleeding diathesis (platelet dysfunction)
Volume overload refractory to diuretics
Refractory hypertension 
Refractory acidosis
Encephalopathy 
Removal of toxins (lithium, salicylates)
32
Q

What are the complications of haemodialysis?

A

Removal of too much circulating fluid
Bacteraemia
Bleeding secondary to heparin use
Dialysis related amyloidosis

33
Q

What are the complications of peritoneal dialysis?

A

Bacterial peritonitis
Solute clearance or ultrafiltration failure
Diabetes (glucose in filtration fluid)
Local complications (hernias, catheter site infection)

34
Q

What are the manifestations of renal osteodystrophy?

A

Increased bone turnover due to secondary hyperparathyroidism, which may cause bone pain and bone cysts

Osteomalacia

35
Q

What is the definition of nephrotic syndrome?

A

Proteinuria >3g in 24 hours
Hypoalbuminaemia
Oedema

36
Q

What are the causes of nephrotic syndrome?

A

In adults, approximately 30% have a systemic disorder (diabetes, SLE)
The remainder are due to intrinsic renal disease

Minimal change disease - idiopathic, diabetes, NSAIDs, Hodgkin’s lymphoma
Focal segmental glomerulosclerosis - idiopathic, HIV, NSAIDs, obesity
Membranous glomerulonephritis - infection, autoimmune disease, solid organ malignancy
Mesangiocapillary glomerulonephritis - infection, autoimmune disease, cryoglobulinaemia

37
Q

What are the complications of nephrotic syndrome?

A
Oedema
Hypertension
Hypercholesterolaemia
Thrombosis 
Infection
38
Q

What are the differentials of bilateral renal cysts?

A

Polycystic kidney disease
Multiple simple cysts
Tuberous sclerosis
Trisomies 13 (Patau) 18 (Edward) and 21 (Down’s)

39
Q

What is the differential diagnosis of a single palpable kidney?

A

Polycystic kidney disease
Hydronephrosis
Hypertrophy of a single functioning kidney
Renal cell carcinoma

40
Q

What is the differential diagnosis for bilateral palpable kidneys?

A

Polycystic kidney disease
Bilateral hydronephrosis
Amyloidosis
Bilateral renal cell carcinoma (von Hippel lindau syndrome)

41
Q

What are the genetics of adult Polycystic kidney disease?

A

Typically autosomal dominant
ADPKD1 accounts for 90%, chromosome 16
Most of the remainder are ADPKD2, chromosome 4, less severe phenotype

42
Q

What are the features of autosomal dominant Polycystic kidney disease?

A

Flank and abdominal pain
Acute pain suggests haemorrhage, infection or torsion
Nocturia due to impaired ability to concentrate urine
Hypertension
Recurrent UTI
Haematuria

43
Q

What are the extra renal manifestations of autosomal dominant Polycystic kidney disease?

A

Cerebral aneurysm
Liver cysts
Pancreatic cysts
Valvular heart disease - mitral valve prolapse and aortic regurgitation

44
Q

What are the principles of management of autosomal dominant Polycystic kidney Disease?

A

Nephrectomy for recurrent bleeds, infection, increase in size
Management of renal failure (control hypertension, adequate nutrition, treat anaemia, phosphate binders, vitsmin D)
Dialysis
Renal transplantation
Screening of relatives
Genetic counselling

45
Q

What is von Hippel lindau syndrome?

A

Autosomal dominant condition
Chromosome 3
Cerebellar, retinal and spinal haemangioblastomas
Cysts occur in the kidneys, liver, spleen and epidydymis
Increased risk of renal cell carcinoma and phaeochromocytoma

46
Q

What are the causes of a right upper quadrant mass?

A

Liver
Right kidney
Gallbladder
Colon

47
Q

What are the causes of a left upper quadrant mass?

A

Spleen
Left kidney
Pancreas
Colon

48
Q

What are the causes of a right lower quadrant mass?

A

Colon
Small intestine
Appendix
Pelvic mass

49
Q

What are the causes of a left lower quadrant mass?

A

Sigmoid colon

Pelvic mass

50
Q

What inherited conditions predispose to colorectal cancer?

A

Hereditary non-polyposis colorectal cancer (lynch syndrome) - autosomal dominant
Familial adenomatous polyposis - autosomal dominant
Peutz-Jeghers syndrome - associated with pigmented lesions in the buccal mucosa and lips, autosomal dominant

51
Q

What are the indications for kidney transplant?

A

Most common are glomerulonephritis, diabetic nephropathy, Polycystic kidney disease

52
Q

What complications may occur following renal transplantation?

A
Rejection (acute or chronic)
Infection secondary to immunosuppression
Skin malignancy, lymphoproliferative disease, hypertension, hyperlipidaemi
Recurrence of original disease
Chronic graft dysfunction
53
Q

What are the indications for liver transplantation?

A

Cirrhosis
Acute hepatic failure (paracetamol overdose, hepatitis)
Primary biliary cirrhosis
Haemochromatosis

54
Q

What are the side effects of organ transplantation medications?

A
Fine tremor (tacrolimus)
Steroid side effects
Gum hypertrophy (ciclosporin)
Hypertension (ciclosporin, tacrolimus)
Skin damage and malignancy
55
Q

What are the indications for splenectomy?

A

Rupture

Haematological (ITP, hereditary shperocytosis)

56
Q

What are the causes of massive splenomegaly?

A
Myeloproliferative disorders (CML, myelofibrosis)
Tropical infection (malaria)
57
Q

What are the causes of moderate splenomegaly?

A

Myelo/lymphoproliferative disorders

Infiltration (Gaucher’s, amyloidosis)

58
Q

What are the causes of mild splenomegaly?

A

Myelo/lymphoproliferative disorders
Portal hypertension
Infection (EBV, infective endocarditis, infective hepatitis)
Haemolytic anaemia

59
Q

What are the complications of haemochromatosis?

A

Diabetes, hypogonadism, testicular atrophy
Cardiac failure
Pseudo-gout

60
Q

What autoantibodies are implicated in liver disease?

A

Primary biliary cirrhosis - anti-mitochondrial antibodies
Primary scelrosing cholangitis - Anti-nuclear antibodies, anti-smooth muscle antibodies
Autoimmune hepatitis - anti-smooth muscle, anti-liver/kidney microsomal type 1

61
Q

What are the clinical signs of decompensated liver disease?

A

Ascites
Asterixis
Encephelopathy

62
Q

What complications may occur secondary to cirrhosis?

A

Variceal haemorrhage
Hepatic encephalopathy
Spontaneous bacterial peritonitis

63
Q

How would you investigate a patient with suspected cirrhosis?

A

Liver screen - autoantibodies and immunoglobulins, hepatitis serology, ferritin, caeruloplasmin, alpha 1 antitrypsin, alphafetoprotein

Hepatic function - albumin, INR

Liver biopsy
ERCP to exclude or diagnose primary sclerosing cholangitis

64
Q

How would you investigate a patient with suspected IBD?

A
Stool MC&S
FBC and inflammatory markers
Sigmoidoscopy or colonoscopy and biopsies
Bowel contrast study (look for fistulae)
CT scanning
65
Q

What is the treatment of Chron’s disease?

A

Mild/moderate: oral steroid, 5-ASA
Severe: IV steroids, infliximab
Maintenance: oral steroids, azathioprine, methotrexate, TNF-inhibitors (infliximab)

Nutritional support
Psychological support
Surgery

66
Q

What is the medical treatment of ulcerative colitis?

A

Mild/moderate: topical steroids, oral steroids, 5-ASA
Severe: IV steroids, IV ciclosporin
Maintenance: oral steroids, 5-ASA, azathioprine

Nutritional support
Psychological support
Surgery

67
Q

What are the indications for surgery in Chron’s?

A

Obstruction
Complications from fistulae
Failure to respond to medical therapy

68
Q

What are the indications for surgery in ulcerative colitis?

A

Chronic symptomatic relief
Emergency surgery for refractory colitis
Colonic dysplasia/carcinoma

69
Q

What are the causes of gynaecomastia?

A
Puberty and senility
Genetic: Kleinfelter’s
GI: Cirrhosis
Drugs: Spironolactone, Digoxin
Endocrine: Thyroid disease, Addison
Testicular tumour