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Year 5 > Nephrology > Flashcards

Nephrology Flashcards

1
Q

AKI Staging

A

Stage 1 - creatinine 1.5-2x increase (urine <0.5 for >6 hours)
Stage 2 - creatinine 2-3x increase (urine <0.5 for >12 hours)
Stage 3 - creatinine >3x increase (urine <0.3 for >24 hours OR anuric for 12 hours)

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2
Q

Main causes of pre renal AKI

A

Hypovolemia - secondary to dehydration, sepsis, diarrhoea and vomiting

Renal artery stenosis

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3
Q

Main causes of post renal AKI

A

Kidney stones
BPH
External compression of urethra

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4
Q

Investigations when suspecting AKI

A

Blood pressure - hypovolemia may present with low BP
Renal USS - to rule out obstructive cause
Urinalysis - look for blood/protein which may point to cause
Bloods - FBC, U&E etc need to know K+ levels

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5
Q

Which medications would you stop in the presence of an AKI?

A

NSAIDs
ACEi or ARBs
Diuretics
Gentamicin

Consider stopping - metformin, lithium, digoxin

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6
Q

Main points for management of AKI

A 
If pre renal cause - give fluids 
Stop nephrotoxic drugs 
Manage hyperkalamia if present 
Refer to nephrology if deemed to be renal cause 
Refer to urology if post renal cause
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7
Q

Staging of CKD

A

Stage 1 - eGFR >90 (with signs of kidney damage on other tests)
Stage 2 - eGFR 60-90 (with signs of kidney damage on others)
Stage 3 - eGFR 30-60
Stage 4 - eGFR 15-30
Stage 5 - eGFR <15

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8
Q

When would you use a ACEi in a patient with CKD

A

Evidence of proteinuria
If ACR >70
If patient has coexistent HTN or diabetes

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9
Q

What type of anaemia is seen in patients with CKD

A

Normochromic, normocytic anaemia

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10
Q

At what stage of CKD would you expect to see anaemia due to reduced production of EPO

A

Stage 4

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11
Q

What is the cardiac risk factor associated with anaemia in CKD

A

Left ventricular hypertrophy

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12
Q

Management of anaemia in CKD

A

Erythropoietin and darbepoetin (EPO)

- need to assess iron status before EPO administration as it can cause iron deficiency

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13
Q

What type of hyperparathyroidism is typically seen in patients with CKD?

A

Secondary - high PTH, low calcium, high phosphate

Tertiary (in chronic renal failure) - very high PTH, high calcium, high phosphate

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14
Q

What is the relationship between phosphate and calcium in the body

A

Inverse relationship

As phosphate rises, calcium levels fall - this is because phosphorous binds to calcium reducing the available free calcium in the blood

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15
Q

Management of mineral bone disease in CKD

A

Reduce dietary phosphate
Phosphate binders e.g, sevelamer
Vitamin D replacement - alfacalcidol

Parathyroidectomy - in extreme cases

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16
Q

Features of autosomal dominant polycystic kidney disease (ADPKD)

A 
Hypertension 
Recurrent UTIs 
Abdominal pain 
Early satiety - as kidneys occupy large volume of abdomen 
Renal stones 
Haematuria 
CKD
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17
Q

Extra-renal manifestations of ADPKD

A

Liver cysts - can cause hepatomegaly
Berry aneurysms - can cause subarachnoid haemorrhage
Cardiovascular manifestations - mitral valve prolapse, aortic dissection

Rarely presents with cysts in pancreas, spleen, thyroid, oesophagus, ovaries

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18
Q

Nephrotic Syndrome Triad

A

Proteinuria
Hypoalbuminaemia
Oedema - due to hypoalbuminaemia

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19
Q

Complications of nephrotic syndrome

A

Increased infection risk - due to urinary IgG loss
Increased thromboembolism risk - due to urinary antithrombin III loss
Hyperlipidemia
Hypocalcaemia- due to urinary Vit D loss

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20
Q

Types of Nephrotic Syndrome

A 
Minimal change disease 
Membranous glomerulonephritis 
Focal segmental glomerulosclerosis 
Amyloidosis 
Diabetic nephropathy
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21
Q

Most common area prone to thrombosis in nephrotic syndrome

A

Renal vein thrombosis

22
Q

Most common type of nephrotic syndrome in children

A

Minimal change disease

23
Q

Type of nephrotic syndrome typically presenting in young adults

A

Focal segmental glomerulosclerosis (FSGS)

24
Q

Type of nephrotic syndrome typically associated with lupus

A

Membranous glomerulonephritis

25
Q

Features of nephritic syndrome

A

Haematuria with red cell casts
Proteinuria
Hypertension

26
Q

Types of Nephritic Syndrome

A

Rapidly progressive glomerulonephritis
IgA nephropathy
Post streptococcal glomerulonephritis
Alport’s syndrome

27
Q

Most common type of nephritic syndrome

A

IgA nephropathy

28
Q

Difference between IgA nephropathy and post streptococcal glomerulonephritis

A

IgA nephropathy - typically occurs 1-2 days post URTI
Post streptococcal - typically occurs 1-2 weeks

IgA nephropathy - main symptom is macroscopic haematuria
Post streptococcal - main symptom is proteinuria

Post streptococcal - associated with low complement levels

29
Q

Markers of poor prognosis in IgA nephropathy

A 
Male gender 
Proteinuria 
Hypertension 
Smoking 
Hyperlipidemia
30
Q

What type of vasculitis is associated with IgA nephropathy

A

Henoch Scholein Purpura

31
Q

What are the causes of rapidly progressive glomerulonephritis

A

Goodpastures syndrome
Wegener’s granulomatosis
SLE
Microscopic polyarteritis

32
Q

What is Alport’s syndrome and what is the triad of symptoms

A

X-linked dominant condition, results in defect in GBM

Presents with
Kidneys - Microscopic haematuria / kidney failure
Ears - bilateral sensorineural hearing loss
Eyes - lenticonus, retinitis pigmentosa

33
Q

What is goodpastures syndrome?

A

Anti-glomerular basement (GBM) disease
Type of small vessel vasculitis
Presents with both pulmonary haemorrhage and rapidly progressive glomerulonephritis

34
Q

Features of rhabdomyolysis

A

AKI - with extremely raised creatinine
Elevated creatinine kinase (CK)
Myoglobinuria - presence of myoglobinuria in urine (brown urine)

35
Q

Management of rhabdomyolysis

A

Rapid IV fluids - to maintain good urine output

36
Q

Causes of rhabdomyolysis

A

Prolonged seizure

Fall and prolonged lie

37
Q

What is haemolytic uraemic syndrome (HUS)

A

AKI typically seen following bout of gastroenteritis or bloody diarrhoea in young children

38
Q

Most common cause of HUS

A

Caused by E.Coli 0157

Producing Shiga toxin

39
Q

Features of HUS

A

AKI
Microgiopathic haemolytic anaemia
Thrombocytopenia

40
Q

Management of HUS

A

Supportive treatment - fluids, blood transfusion and dialysis if necessary

Plasma exchange - reserved for severe cases of HUS not associated with diarrhoea

41
Q

How long does an AV fistula take to mature

A

6-8 weeks

42
Q

Complications of fistulas

A

Infection
Thrombosis - may be detected in a sense of a bruit
Stenosis - may present with limb pain
Steal syndrome - ischaemia to the hand/arm following fistula formation

43
Q

Difference between acute and chronic graft failure in transplanted kidney

A

Acute < 6 months

Chronic >6 months

44
Q

Causes of acute graft failure in transplanted kidney

A

Mismatched HLA

Cytomegalovirus infection

45
Q

Causes of chronic graft failure

A

Antibody and cell mediated mechanism causing fibrosis to transplanted kidney (chronic allograft nephropathy)

Recurrance of original disease in transplanted kidney

46
Q

What is a normal anion gap

A

Anion gap: (Na + K) - (Bicarbonate + chloride)

Normal gap = 8-14

47
Q

Causes of normal anion gap in metabolic acidosis

A

GI bicarbonate loss e.g, diarrhoea, fistula
Renal tubular acid is
Drugs
Addison’s disease

48
Q

Causes of raised anion gap in metabolic acidosis

A 
Lactic acidosis 
Ketoacidosis 
Urea - renal failure 
Acid poisoning e.g, salicylates, methanol 
Antifreeze, ethylene glycol
49
Q

Reasons for acute dialysis

A 
A - acidosis (metabolic)
E - electrolytes (hyperkalemia)
I - intoxication e.g, ethylene glycol 
O - oedema 
U - uremia
50
Q

What should you consider in patients with sterile pyuria (raised wcc in urine) with negative urine culture

A

Tuberculosis

Year 5 (17 decks)

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