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Alice's finals cards > Renal medicine > Flashcards

Renal medicine Flashcards

1
Q

How is AKI diagnosed?

A

By measuring the serum creatinine

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2
Q

What are the NICE criteria for AKI?

A

Rise in creatinine >25micromol/L in 48 hours

Rise in creatinine >50% in 7 days

Urine output of <0.5ml/kg/hour for >6 hours

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3
Q

Give examples of 2 iatrogenic causes of AKI

A

Nephrotoxic medications such as NSAIDs and ACE-i

Use of contrast medium in CT scans

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4
Q

Give 3 pre-renal causes of AKI

A

Dehydration
Hypotension
Heart failure

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5
Q

Give 3 renal causes of AKI

A

Glomerulonephritis
Interstitial neprhitis
Acute tubular necrosis

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6
Q

Give 4 post-renal causes of AKI?

A

Kidney stones
Masses in abdomen or pelvis
Ureter or urethral strictures
Enlarged prostate

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7
Q

What are the investigations for AKI?

A

Urinalysis
Ultrasound
Blood

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8
Q

What is the management of AKI?

A

Correct underlying cause
Stop nephrotoxic drugs
Relieve obstruction

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9
Q

What are some possible complications of AKI?

A

Hyperkalaemia
Fluid overload
Metabolic acidosis
Uraemia (leads to encephalopathy or pericarditis)

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10
Q

What are potential symptoms of CKD?

A 
Usually asymptomatic
Prurituis
Loss of appetite
nausea
Oedema
Muscle cramps
Peripheral neuropathy
Pallor
HTN
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11
Q

What are the investigations and results for CKD?

A

Bloods (decreased eGFR)
Urine albumin:creatinine ratio >3mg/mmol
Haematuria
Renal ultrasound

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12
Q

How is CKD diagnosed?

A

Decreased eGFR 3 months apart

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13
Q

How is CKD staged?

A

Using the G (eGFR) and A (ACR) scores.

G1 = eGFR >90
G2 = eGFR 60-89
G3a = eGFR 45-59
G3b = eGFR 30-44
G4 = eGFR 15-29
G5 = eGFR <15 (known as “end-stage renal failure”)
A1 = < 3mg/mmol
A2 = 3 – 30mg/mmol
A3 = > 30mg/mmol
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14
Q

If someone, being investigated for CKD, has a score of G1 A1, what severity is their CKD?

A

They have perfectly healthy kidneys

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15
Q

How can metabolic acidosis in CKD be managed?

A

Oral sodium bicarbonate

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16
Q

How can anaemia in CKD be managed?

A

Iron and erythropoietin

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17
Q

Which antihypertensive is first line in patients with CKD?

A

ACE-i

Serum potassium must be monitored because ACE-i and CKD both cause hyperkalaemia

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18
Q

What are the features of renal bone disease?

A

Osteomalacia
Osteoporosis
Osteoclerosis

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19
Q

What are the X ray changes seen in renal bone disease?

A

Sclerosis at both ends of the vertebra and oestomalacia in the middle. This is known as “rugger jersey” because it is stripey and the radiologist who named it must have been a Tory

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20
Q

What are the indications for acute dialysis?

A 
AEIOU
A-acidosis
E-electrolyte abnormalities
I-intoxication
O-oedema
U-uraemia
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21
Q

Which kind of catheter is used in peritoneal dialysis?

A

Tenckhoff catheter

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22
Q

What are the potential complications of peritoneal dialysis?

A

Bacterial peritonitis
Peritoneal sclerosis
Ultrafiltration failure
weight gain

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23
Q

What are the two access options for haemodialysis?

A

Tunnelled cuffed catheter

AV fistula

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24
Q

What is heard on auscultation of A-V fistula?

A

Machinery murmur

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25
Q

What is STEAL syndrome?

A

Develops when there is an AV fistula whihc “steals” blood from the distal limb. It causes distal ischaemia

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26
Q

Which scar is given in renal transplant?

A

Hockey stick

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27
Q

What is the usual immunosuppressant regime for renal transplant?

A

Tacrolimus
Mycophenolate
Prednisolone

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28
Q

What are the 3 complications of transplant?

A

Rejection
Failure
Electrolytes imbalances

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29
Q

What are the features of nephritic syndrome?

A

Haematuria
Oliguria
Proteinuria (<3g/24hrs if more then nephrotic)
Fluid retention

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30
Q

What are the features of nephrotic syndrome?

A

Peripheral oedema
Proteinuria (>3g/24hrs)
Serum albumin less than 25g/L
Hypercholesterolaemia

31
Q

What is interstitial nephritis?

A

There is inflammation of the space between the cells and tubules

32
Q

What can cause glomerulosclerosis?

A

Glomerulonephritis, obstructive uropathy, focal segmental glomerulosclerosis

33
Q

How is glomerulonephritis treated?

A

Immunosuppression (steroids)

Blood pressure control

34
Q

What is the most common cause of primary glomerulonephritis?

A

IgA nephropathy (Berger’s disease)

35
Q

What is seen on histology of IgA nephropathy (Berger’s disease?

A

IgA deposits and glomerular mesangial proliferation

36
Q

What is the presentation of Goodpasture’s syndrome?

A

AKI and haemoptysis

37
Q

What causes Goodpasture’s syndrome?

A

Anti-GBM antibodies attck the glomerulus and pulmonary basement membranes. This causes glomerulonephritis and pulmonary haemorrhage

38
Q

What is the anti-hypertensive class of choice in diabetes?

A

ACE-i. Protects against diabetic nephropathy

39
Q

What are the 2 types of interstitial nephritis?

A

Acute interstitial nephritis and chronic tubulointerstitial nephritis

40
Q

What causes acute interstitial nephritis?

A

It is usually a hypersensitivity reaction to drugs or infection

41
Q

What are the features of acute interstitial nephritis?

A

Rash
Fever
Eosinophilia

42
Q

What causes acute tubular necrosis?

A

Ischaemia or toxins

43
Q

How long does it take to recover from acute tubular necrosis?

A

7-21 days

44
Q

What is found in the urine in acute tubular necrosis

A

Muddy brown casts

45
Q

What is the management of acute tubular necrosis?

A

Supportive management
IV fluids
Stop nephrotoxic medications
Treat complications

46
Q

What is renal tubular acidosis?

A

There is metabolic acidosis due to pathology in the tubules of the kidney

47
Q

What is type 1 renal tubular acidosis?

A

There is pathology in the distal tubule which means it is unable to excrete hydrogen ions

48
Q

What is the management of type 1 renal tubular acidosis?

A

oral bicarbonate

49
Q

What is the main cause of type 2 renal tubular acidosis?

A

Fanconi’s sydrome

50
Q

What causes type 4 renal tubular acidosis?

A

Reduced aldosterone

51
Q

How is type 4 renal tubular acidosis managed?

A

Fludrocortisone

52
Q

What causes Haemolytic uraemic syndrome?

A

When there is thrombosis in small blood vessels throughout the body. Usually triggered by shiga toxin

53
Q

What is the shiga toxin produced by?

A

e.coli

54
Q

How does HUS present

A 
e.coli causes bloody diarrhoea. About 5 days after this HUS occurs
Reduced urine output
Haematuria
Abdo pain
Lethargy
Confusion
Bruising
HTN
55
Q

How is HUS managed?

A

It is a medical emergency. It is self limiting and requires supportive management

56
Q

What is rhabdomyolisis?

A

A condition when skeletal muscle breaks down and releases breakdown products into the blood

57
Q

Which breakdown product of rhabdomyolyosis is the most dangerous?

A

potassium. Causes hyperkalaemia which can lead to cardiac arrest

58
Q

Why can rhabdomyolysis lead to AKI?

A

Myoglobin is a breakdown product which is toxic to the kidneys in high concentrations

59
Q

What can cause rhabdomyolysis?

A

Prolonged immobility
Extremely rigorous exercise
Crush injuries
seizures

60
Q

What are the signs and symptoms of rhabdomyolysis?

A 
Muscle aches and pains
Oedema
Fatigue
Confusion
red-brown urine
61
Q

What are the investigations for rhabdomyolysis?

A

Blood tests: high CK, U&Es chaotic

ECG for hyperkalaemia (long QRS, peaked T)

62
Q

What is the management of rhabdomyolysis?

A

IV fluids
IV sodium bicarbonate
IV mannitol to increase GFR

63
Q

What is the main complication of hyperkalaemia?

A

Cardiac arrhythmia, particularly VF

64
Q

What are the main conditions which can cause hyperkalaemia?

A

AKI/ CKD
Rhabdomyolysis
Adrenal insufficiency
Tumour lysis sundrome

65
Q

Which medications can cause hyperkalaemia?

A 
Aldosterone antagonists
ACE-i
Angiotensin II receptor blockers
NSAIDs
Potassium supplements
66
Q

What can result in a falsely raised potassium?

A

Haemolysis of the sample

67
Q

What are the ECG findings in hyperkalaemia?

A

Tall peaked T waves
Flattening or absence of p waves
Broad QRS

68
Q

What is the mainstay of treatment in hyperkalaemia?

A

Insulin and dextrose infusion (drived K+ into cells) and IV calcium gluconate (stabilise heart muscle)

69
Q

What is the level of potassium which needs treating?

A

> 6.5mmol/L

If >6.mmol/L do ECG and treat as well if it has changes

70
Q

What are the associated findings of polycystic kidney disease found outside of the kidney?

A

Hepatic cyst

Cerebral aneurysms

71
Q

What is the inheritance pattern of PKD?

A

There is an autosomal dominant and autosomal recessive type. The dominant type is more prevalent

72
Q

How is PKD diagnosed?

A

Ultrasound scan and genetic testing

73
Q

What are the genes associated with PKD?

A

PKD-1 and PKD-2

74
Q

How is PKD managed?

A

Tolvaptan (vasopressin receptor antagonist)

Alice's finals cards (21 decks)

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