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Abdo Paces Flashcards

1
Q

Causes of enlarged kidneys

A

ADPKD
Recessive form of PKD
Von Hippel Lindau
Tuberous Sclerosis
Hydronephrosis
Renal cell carcinoma (5%)

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2
Q

Genetics of PKD

A

Autosomal dominant:
PKD1: chromosome 16 in 80%- mean age to ESKD = 54
PKD2: chromosome 4 in 15% - mean age to ESKD = 74
Autosomal recessive:
Chromosome 6 - ESKD in early childhood

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3
Q

Clinical presentation on PKD

A

Abdominal mass or pain
Hypertension
UTI
Renal calculus
Haematuria
Intracranial bleed

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4
Q

Diagnostic criteria for ADPKD

A

In a patient known to be at 50% risk because of FHx, dx is suggested by:
- 2 cysts, either unilateral or bilateral at <30 yrs
- 2 cysts in each kidney in patients aged 30-59yrs
- 4 cysts in each kidney in patients >60yrs
- dx supported by hepatic or pancreatic cysts

In 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

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5
Q

Management of PKD

A
  • management of cardiovascular risk factors
    -BP control and RAAS blockade
  • tolvaptan (ADH receptor antagonist) limits cyst development
  • may require nephrectomy to remove problematic cysts and reduce mass effects
  • renal transplant and dialysis
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6
Q

Extra renal manifestations of PKD

A
  • hypertension
  • liver cysts (70%)
  • pancreatic cysts (10%)
  • berry aneurysms (5%)
  • diverticular disease
  • mitral valve prolapse
  • aortic incompetence
  • hepatic fibrosis
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7
Q

Pathophysiology of PBC

A

Autoimmune condition
Progressive inflammation and destruction of small intrahepatic ducts.
Antimitochondrial antibodies (AMA) is hallmark feature
Strongly associated with RA, sjorgens, CREST

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8
Q

Presentation of PBC

A

Incidental finding of raised ALP
Pruritus
Cholestatic jaundice
Diarrhoea
Lethargy
Xanthelasmata
Skin pigmentation
Clubbing
Hepatosplenomegaly
GI bleed
Osteoporosis

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9
Q

Diagnosis of PBC

A

AMA antibodies present in 95% of cases
Raised ALP
Raised IgM
May require liver biopsy for confirmation

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10
Q

Management of PBC

A

Cholestyramine for pruritis
Ursodeoxycholic acid
Obeyicholic acid either as mono therapy or combination with urso if not tolerated or response (reduces circulating bile acid)
Liver transplant

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11
Q

Complications of PBC

A

Hepatic cancer
Cirrhosis
Liver failure
Osteoporosis
Vitamin deficiency

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12
Q

Causes of hepatomegaly

A

Cirrhosis
Carcinoma
Congestive cardiac failure
Hepatitis B or C
PBC, PSC, AIH
Amyloid
Myeloproliferative disorder

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13
Q

Causes of cirrhosis

A

Alcohol
NAFLD
Hepatitis C and B
Autoimmune hepatitis
PBC
PSC
Wilson’s
Haemachromatosis
a1 antitripsin disease
HHT
Medications

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14
Q

Liver screen bloods

A

Autoimmune antibodies (ANA, AMA, SMA, LKM)
Immunoglobulins
Hepatitis b and c serology
Ferritin
Caeruloplasmin
a1 antitrypsin
AFP

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15
Q

Presenting a chronic liver disease patient

A
  1. Peripheral stigmata of liver disease
  2. Hepatomegaly
  3. Evidence of portal hypertension
  4. Evidence of decompensation
  5. Evidence of cause of liver disease
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16
Q

Classification of cirrhosis

A

Bilirubin, albumin, INR, ascites, encephalopathy
A= 5-6
B= 7-9
C= 10-15

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17
Q

Causes of palmer erythema

A

Cirrhosis
Hyperthyroidism
RA
Pregnancy
Polycythaemia

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18
Q

Causes of gynaecomastia

A

Puberty, old age
Kleinfelters syndrome
Cirrhosis
Drugs - spironolactone or digoxin
Testicular tumour/orchidectomy
Hyper/hypothyroidism
Addisons

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19
Q

Autoantibodies in PSC

A

ANA
anti- smooth muscle may be positive

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20
Q

Autoantibodies in autoimmune hepatitis

A

Anti smooth muscle
Anti LKM1
ANA

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21
Q

Causes of chronic renal failure

A

Diabetic nephropathy (34%)
Hypertension (29%)
Glomerulonephritis (14%)
PKD (14%)
Chronic pyelonephritis (10%)
Obstructive/reflux nephropathy

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22
Q

Advantages of transplant over continued dialysis

A

Improved quality of life
Increase patient survival rate
Cost effective in the long term

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23
Q

Renal diseases where there are a high risk of reoccurrence in transplanted kidney

A

Focal segmental glomerular sclerosis
Amyloidosiss
IgA nephropathy
HUS

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24
Q

Technical considerations for renal transplant

A

Atheromatous iliac vessels
Bladder dysfunction
Bleeding or infection on PKD cysts
Large and bulky kidneys
Uncontrolled hypertension
Renal calculi
Persistent anti- glomerular antibodies

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25
Q

Methods of transplant rejection

A

Hyper acute
- due to presence of recipient antibodies against the donor kidney
- requires removal of transplant kidney
Acute cell mediated rejection
- mononuclear cell infiltration occurs in the interstitial and subsequently in vessel walls
- treated with high dose steroids
Acute antibody mediated rejection
- at least 3/4 of graft dysfunction, histological evidence of tissue injury, positive staining for C4d, presence of donor specific antibodies
- poor prognosis, treated with plasmapheresis and IVIg
Chronic rejection

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26
Q

Kidney donor work up

A

-Cross match and screening of transmissible disease
- MRA and isotope renography

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27
Q

MOA and side effects of ciclosporin

A

Calcineurin inhibitor
Inhibits production of IL-2 and TNF-a by binding to ciclophilin protein and inhibiting calcineurin
SE: nephrotoxic, hyperkalaemia, hypomagnesaemia, gingival hypertrophy, hyperlipidaemia, glucose intolerance, hypertension

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28
Q

MOA and side effects of tacrolimus

A

Calcineurin inhibitor
Inhibits production of IL-2 by helper T cells, by binding Calcineurin to tacrolimus binding protein
SE: nephrotoxicity, neurotoxicity ( tremor), glucose intolerance, prolonged QT

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29
Q

MOA and SE of mycophenolate mofetil

A

A prodrug. The active compound is mycophenolic acid which inhibits the enzyme required for guanosine synthesis which results in impaired b and T cell proliferation.
SE: nausea, diarrhoea, leukopenia, anaemia, thrombocytopenia

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30
Q

MOA and side effects of azathioprine

A

Anti-metabolite to inhibit DNA and RNA synthesis
SE: leukopenia, thrombocytopenia, GI disturbance, cholestasis, alopecia

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31
Q

MOA and SE of steroids

A

Reduce IL-3, IL-6 and TNF-a production and inhibit T cell activation.
SE: glucose intolerance, oseoporosis, AVN, cataracts, cushiongoid appearance, infections, poor wound healing

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32
Q

MOA and SE of sirolimus

A

Inhibition of TOR (a regulatory kinase)
SE: hyperkalaemia, hypomagnesaemia, hyperlipidaemia, leukopenia, anaemia, impaired wound healing, joint pain

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33
Q

Complications of immunosuppression

A
  • New onset diabetes after transplantation
  • Hypertension
  • Hyperlipidaemia
  • SCC of the skin
  • malignancy related to viral infection eg. HPV and cervical cancer, lymphoma and EBV, or Kaposi sarcoma and HHV-8
  • CMV due to reactivation of endogenous disease or transmission from a donor
  • BK infection
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34
Q

Prognostic factors of renal transplant

A
  • primary diagnosis
  • previous graft failure
  • episodes of rejection
  • kidney total ischaemic time
  • donor factors eg. Age
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35
Q

CI to renal transplant

A

Active malignancy ( must be cancer free for 2 years)
Active infection
Advanced atheromatous disease is a relative contraindication

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36
Q

Calculating SAAG

A

Serum albumin - ascitic fluid albumin

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37
Q

Causes of increased SAAG

A

Cirrhosis
Alcoholic hepatitis
Schistosomiasis
Fulminant hepatic failure
Budd Chiari
Portal vein obstruction
Cardiac disease
SBP

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38
Q

Causes of normal or low SAAG

A

Nephrotic syndrome
Protein losing enteropathy
Peritoneal carcinomatosis
Tuberculous peritonitis
Pancreatic duct leak
Biliary ascites

39
Q

Treatment of ascites

A
  • fluid restriction
  • low salt intake
  • diuretic therapy
  • paracentesis
  • prophylactic abx
40
Q

Indications for dialysis in CKD

A

Uraemic symptoms
Uncontrollable fluid overload
EGFR of 5-7

41
Q

Indications for dialysis in AKI

A

Severe metabolic acidosis pH <7.1
Hyperkalaemia refractory to treatment
Refractory fluid overload
Signs of uraemia
Certain toxins

42
Q

Complications of peritoneal dialysis

A

Bacterial peritonitis
Ultrafiltration failure
Encapsulating peritoneal sclerosis
Hernias
Fluid leak, eg through diaphragm causing pleural effusion
Malnutrition

43
Q

Complications of haemodialysis

A

Hypotension
Infection, at access point or bacteraemia
Venous stenosis or occlusion
Air embolus
Anaphylactic reaction to sterilising agent

44
Q

Long term complications of dialysis

A

Vascular disease
Cardiac valve calcification - particularly aortic
Dialysis related amyloid due to a build up of beta2 microglobulin
Pseudogout and gout

45
Q

Causes of splenomegaly

A
  1. Infiltration
    - lymphoma, amyloidosis, sarcoidosis, Gaucher’s disease, thyrotoxicosis
  2. Increased function
    - spherocytosis, thalassaemia, sickle cell anaemia, infections (chronic malaria, visceral leishmaniasis, glandular fever, brucellosis, RA with feltys, SLE, sarcoidosis
  3. Abnormal blood flow
    - cirrhosis with portal hypertension, hepatic or portal vein obstruction
46
Q

Causes of massive splenomegaly

A

CML
Myelofibrosis
Gauchers storage disease
Chronic malaria
Kala- azar (visceral leishmaniasis)

47
Q

Causes of moderate splenomegaly

A

Myelo/lymphoproliferative disorders
Infiltration eg. Amyloidosis

48
Q

Causes of mild splenomegaly

A

Myelo/lymphoproliferative disorders
Portal hypertension
Infections eg. EBV, IE, infective hepatitis
Haemolytic anaemia

49
Q

Investigations in patients with splenomegaly

A

US abdo
FBC + film
CT CAP
Bone marrow aspirate and trephine
Lymph node biopsy
Thick and thin films x 3 for malaria
Viral serology

50
Q

Indications for splenectomy

A

Rupture (trauma)
Haematological (ITP or hereditary spherocytosis)

51
Q

Splenectomy work up

A

Vaccination (ideally 2 weeks prior to protect against encapsulated bacteria)
- pneumococcus
- meningococcus
- haemophilus influenza
Prophylactic penicillin life long
Medic alert bracelet

52
Q

Reasons for liver transplant

A

Cirrhosis
- alcohol, NAFLD, Haemachromatosis, Wilson’s
Acute hepatic failure
- hepatitis A and B, paracetamol overdose
Hepatocellular carcinoma

53
Q

What scoring system is used for deciding to list chronic liver disease patients for transplant

A

Model for End Stage Liver Disease (MELD)
Comprised of INR, creatinine, bilirubin, sodium
Score > or = 49

54
Q

Complications of liver transplant

A

Initially:
- haemorrhage, graft failure, infection, vascular and biliary complications, rejection
Delayed complications:
- immunosuppression side effects, disease relapse, chronic graft rejection

55
Q

Clinical signs of haemochromatosis

A

Increased skin pigmentation (slate grey colour)
Stigmata of chronic liver disease
Hepatomegaly
Venesection scars
Liver biopsy scar
Swelling and squaring off of MCP joints
Joint replacement scars
CCF
Evidence of diabetes monitoring (Bronze diabetes)
Hypogonadism and testicular atrophy

56
Q

Inheritance of haemochromatosis

A

Autosomal recessive on chromosome 6
Variable penetrance
HFE gene mutation: regulator of gut iron absorption
Males affected earlier then females due to menstrual iron losses

57
Q

How May Haemachromatosis present

A

Fatigue
Arthritis
Chronic liver disease
Screening

58
Q

Investigations for Haemachromatosis

A

Dx:
Increased serum ferritin
Increased transferrin saturation
Liver biopsy used to assess severity of cirrhosis
Genotyping

Additional:
BM/ HbA1c
ECG, CXR, Echo
Us liver, afp
Joint X-rays: chondrocalcinosos

59
Q

Treatment of haemochromatosis

A

Regular venesection (1unit/week) until ferritin 20-30mg/L and transferritin saturation <50%
Then maintenance venesection 1 unit 3-4 times/ year based on ferritin and transferritin levels

Avoid alcohol
Surveillance for HCC

60
Q

Screening for haemochromatosis

A

1st degree relative >20 yrs old:
Ferritin > 300 in men and >200 in women
Transferrin saturation > 50% in males and > 40% in females
If positive:
genotyping

61
Q

Prognosis of haemochromatosis

A

200x increased risk of HCC if cirrhotic
Reduced life expectancy if cirrhotic
Normal life expectancy without cirrhosis + effective treatment

62
Q

Pathogenesis of Haemachromatosis

A

Mutation in the HFE gene which causes increased intestinal iron absorption, leading to iron deposition in joints, liver, heart, pancreas, pituitary, adrenals and skin

63
Q

Pathophysiology of hereditary spherocytosis

A

An inherited defect in the structural proteins of red blood cell membranes (usually dominant inheritance). Mutation in 1 of 5 genes. Abnormalities result in changes in red cell shape due to defects in skeletal proteins (alpha spectrin, beta spectrin, ankyrin, band 3 protein and protein 4.2).
These red cells are more fragile and so go through haemolysis predominantly in the spleen

64
Q

Clinical presentation of hereditary spherocytosis

A

Pallor, jaundice, splenomegaly, fatigue, RUQ pain (gall stones)

65
Q

Inv/diagnosis in suspected hereditary spherocytosis

A

Low Hb, increased mean corpuscular Hb concentration, MCV low
Reticulocyte count elevated
Blood smear showing spherocytes
Elevated unconjugated bilirubin
DAT -ve
EMA binding or Osmotic fragility test

66
Q

Management of hereditary spherocytosis

A

Folic acid supplementation
Splenectomy +/- cholecystectomy
Pre op vaccination regime + post op prophylactic abx

67
Q

Complications of hereditary spherocytosis

A

Aplastic crisis usually secondary to infection
Anaemia
Gall stones
Bone marrow expansion
Extramedullary haematopoeisis
Post splenectomy sepsis
Post splenectomy thrombosis

68
Q

Aetiology of coeliac disease

A

Gluten peptides are found in barley, wheat and rye.
There is an increased immunological response to ingested gluten.
Predisposing factors include: association to HLA antigens, presence of HLA-DQ2 in 95%, the rest are DQ8, other autoimmune conditions.

69
Q

Pathophysiology of coeliac disease

A

Gluten peptides are resistant to human proteases allowing them to persist in the small intestinal lumen. These peptides trigger immune activation in the intestinal submucosa mediated by T helper cells.
Epithelium of small intestine is damaged causing loss of brush border, villous atrophy, crypt hyperplasia.

70
Q

Associated conditions with coeliac disease

A

Dermatitis herpetiformis
Down syndrome
Selective immunoglobulin A deficiency
Auto immune conditions

71
Q

Diagnosis and inv of coeliac disease

A

FBC, iron studies, b12, folate, calcium
IgA tTg levels
EMA
Small intestinal biopsy showing intraepithelial lymphocytes, villous atrophy, crypt hyperplasia

72
Q

Where would you expect to palpate combined pancreatic and kidney transplant?

A

Pancreas: right iliac fossa
Kidney: left illiac fossa

73
Q

Prognosis of SPK transplantation vs. Isolated renal transplant

A

10 year prognosis similar
>10 years spk has greater survival

74
Q

Benefits of pancreatic transplant

A

Improved quality of life
Improved glycaemic control
Does not reverse established CVD but does slow progression
Improved neuropathy
Improved nephropathy
The effects on retinopathy are unclear

75
Q

Pathophysiology of alcohol dependency

A

Long term alcohol consumption down-regulates inhibitory neuronal GABA receptors, up regulates excitatory glutamate receptors and increases norepinephrine activity.
Cessation of alcohol leaves the excitatory state unopposed.

76
Q

Pathogenesis of alcohol liver disease

A

Alcohol metabolism requires alcohol dehydrogenase, this process reduces NAD to NADH. Excessive NADH increases fatty acid synthesis, promoting fatty infiltration.

77
Q

Pathogenesis of alcoholic hepatitis

A

Acetaldehyde binds to macromolecules in hepatocytes eg. Enzymes and proteins. The immune system detects these complexes and neutrophil infiltration occurs. Hepatocyte necrosis and inflammation occurs.

78
Q

Pathogenesis of cirrhosis

A

Alcohol directly affects stellate cells which transform into collagen- producing myofibroblast cells. There is loss of normal hepatic architecture with modular regeneration and fibrosis.

79
Q

Causes of chronic pancreatitis

A

Alcohol
Cystic fibrosis
Smoking
Hypercalcaemia/hyperlipidaemia
Autoimmune disease
Drugs eg. Azathioprine

80
Q

Clinical presentation of chronic pancreatitis

A

Malabsorption and steatorrhoea
Abdomen pain radiating to the back
Pain may be relieved by leaving forward
DM
Erythema ab igne

81
Q

Clinical presentation of acute pancreatitis

A

Severe epigastric pain radiating to back
Worse after meals, improved on leaning forward
N&V
Tachycardia/hypotension/oliguria
Cullens sign
Grey-turners sign

82
Q

Investigation of acute pancreatitis

A

AXR: sentinel loop of adynamic bowel adjacent to pancreas
Raised amylase and lipase
CT

83
Q

Investigating chronic pancreatitis

A

Pancreatic calcification on AXR or CT
ERCP: irregular dilatation and stricturing of the pancreatic ducts
MRCP
EUS
Faecal elastase
Oral glucose tolerance test

84
Q

Management of chronic pancreatitis

A

Abstain from alcohol and smoking
Creon + PPI
Dietitian assessment
Analgesia
Diabetes monitoring
Vit D replacement

85
Q

Kings college criteria for transplant in paracetamol overdose

A

pH < 7.3
Or all of the following:
- PT > 100
- creatinine > 300
- grade 3 or 4 encephalopathy

86
Q

Kings college criteria for liver transplant in acute liver failure

A

PT > 100
Or any 3 of the following;
Age <10 or > 40
Bili > 300
Coag- INR > 3.5
Duration (jaundice to HE > 7 days)
Etiology- absence of hep A or B or presence of a drug reaction

87
Q

What is the cause of Wilson’s disease?

A

Autosomal recessive defect in ATP7B on chromosome 13, resulting in reduced excretion of copper into the bile and subsequent accumulation in other organs including the liver and brain

88
Q

Investigations for Wilson’s disease

A

Low caeruloplasmin levels
High urinary copper levels

89
Q

How is Wilson’s managed

A

Avoidance of high copper containing foods (shellfish, avocados)
Alcohol cessation
Copper chelation with penicillamine and zinc acetate

90
Q

How can Wilson’s present

A

Acute or chronic liver failure
Haemolysis
Neurological involvement inc. movement disorders
Psychiatric manifestations
Cardiomyopathy
Fanconi’s syndrome

91
Q

What are the commonest causes of HCC

A

CLD particularly hepatitis b and c, alcoholism, hereditary haemochromatosis and PBC. In some countries there is a link with aflatoxins.

92
Q

What primary sites metastasise to the liver?

A

Stomach, pancreas, colon, lung, breast, ovarian, melanoma

93
Q

Evidence of pancreatic exocrine insufficiency

A

Fatty stools
Weight loss
Vit D deficiency
Hypomagnesia
Low faecal elastase

Paces (6 decks)

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