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Finals Revision > Renal > Flashcards

Renal Flashcards

1
Q

What rise in creatinine for criteria for AKI?

A

> 25 micromol/L in 48 hours
50% in 7 days

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2
Q

What urine output for criteria for AKI?

A

<0.5ml/kg/hr for > 6 hours

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3
Q

What are some pre-renal causes for AKI?

A

Inadequate blood supply
- Dehydration
- Hypotension
- Heart failure

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4
Q

What are some renal causes of AKI?

A

Glomerulonephritis
Interstitial nephritis
Acute tubular necrosis

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5
Q

What are some post-renal causes of AKI?

A

Obstruction causing back pressure and reduced kidney function
- Kidney stones
- Masses such as cancer in the abdomen or pelvis
- Ureter or ureteral stictures
- Enlarged prostate or prostate cancer

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6
Q

What is the management of an AKI?

A
  1. Treat underlying cause: fluid rehydration, stop nephrotoxic medications, relieve obstruction
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7
Q

What are some complications of an AKI?

A

Hyperkalaemia
Fluid overload, heart failure and pulmonary oedema
Metabolic acidosis
Uraemia - can lead to encephalopathy or pericarditis

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8
Q

What result on a urine albumin:creatinine ratio is significant?

A

> 3mg/mmol

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9
Q

What complications can you get in CKD?

A

Anaemia
Renal bone disease
Cardiovascular disease
Peripheral neuropathy
Dialysis related problems

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10
Q

What is first line to treat hypertension in patients with CKD?

A

ACE inhibitors - but serum potassium needs to be monitored!

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11
Q

What do you get in bloods in renal bone disease?

A

High serum phosphate (reduced phosphate excretion)
Low active vit D and so low calcium
Secondary hyperparathyroidism

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12
Q

What is osteosclerosis?

A

Osteoblasts respond by increasing their activity to match the osteoclasts but this new tissue is not properly mineralised due to the low calcium.

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13
Q

What causes acute interstitial nephritis?

A

Drugs (e.g. NSAIDs or antibiotics)
Infection
(hypersensitive reaction)
Often accompanied by rash, fever, eosinophilia

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14
Q

What are the main complications of hyperkalaemia?

A

Cardiac arrhythmias
Ventricular fibrillation

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15
Q

What can cause hyperkalaemia?

A

AKI
CKD
Rhabdomyolysis
Adrenal insufficiency
Tumour lysis syndrome
Aldosterone antagonists (spironolactone)
ACEi
ARBs
NSAIDs
Potassium supplements

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16
Q

What are the ECG changes in hyperkalaemia?

A

Tall peaked T waves
Flattening or absence of P waves
Broad QRS complexes

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17
Q

What is the management for hyperkalaemia?

A

Calcium gluconate - stabilises the cardiac muscle cells
Insulin and dextrose (act rapid 10 units and 50ml of 50% dextrose) - drives carbohydrates into cells and takes potassium with it
Also: nebulised salbutamol, IV fluids, calcium resonium, sodium bicarbonate, dialysis

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18
Q

What is acute tubular necrosis?

A

Necrosis of the epithelial cells of the renal tubules - usually due to AKI. These cells can regenerate so it is reversible after 7-21 days.
Caused by ischaemia or toxins (e.g. radiology contrast dye, gentamicin, NSAIDS)

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19
Q

What do you see on urinalysis in acute tubular necrosis?

A

Muddy brown casts

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20
Q

What is Type 1 Renal tubular acidosis?

A

The distal tubule is unable to excrete hydrogen ions

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21
Q

What can cause Type 1 Renal tubular acidosis?

A

Genetic
SLE
Sjogren’s syndrome
Primary biliary cirrhosis
Hyperthyroidism
Sickle cell anaemia
Marfan’s

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22
Q

How does Type 1 Tubular acidosis present?

A

Failure to thrive
hyperventilation
CKD
Bone disease
Hypokalaemia
Metabolic acidosis
High urinary pH
TREAT: oral bicarbonate

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23
Q

What is Type 2 Renal tubular acidosis?

A

Proximal tubule is unable to reabsorb bicarbonate
Usually caused by Fanconi’s syndrome
Same Ix and Mx as Type 1

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24
Q

What is Type 3 Renal tubular acidosis?

A

Mixture of type 1 and type 2

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25
Q

What is Type 4 Renal tubular acidosis?

A

Reduced aldosterone - most common cause
Due to adrenal insufficiency, ACEi, Spironolactone, SLE, Diabetes, HIV

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26
Q

What is different in the U&Es of Type 1 and 2, and Type 4?

A

Type 1 and 2 - hypokalaemia
Type 4. - Hyperkalaemia, high chloride, low urinary pH.
Both are metabolic acidosis

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27
Q

What is the management for Type 4 Renal Tubular Acidosis?

A

Fludrocortisone
Sodium bicarbonate and treatment of hyperkalaemia may be needed too

28
Q

Is the autosomal dominant or autosomal recessive type of PKD more common?

A

Autosomal dominant

29
Q

What are the autosomal dominant genes in PKD?

A

PKD-1: chromosome 16 (85%)
PKD-2: chromosome 4

30
Q

What are the extra-renal manifestations of PKD?

A

Cerebral aneurysms
Hepatic, splenic, pancreatic, ovarian, prostatic cysts
Cardiac valve disease (mitral regurgitation)
Colonic diverticula
Aortic root dilatation

31
Q

What are the complications of PKD?

A

Chronic loin pain
Hypertension
Cardiovascular disease
Gross haematuria
Renal stones
End-stage renal failure

32
Q

How does autosomal recessive type PKD present?

A

Oligohydramnios in pregnancy (foetus doesn’t produce enough urine), leading to the underdevelopment of the lungs.
Rarer and more severe

33
Q

What is the management of PKD?

A

Tolvaptan (a vasopressin receptor antagonist) - slows the development of cysts and progression of renal failure

34
Q

What is the criteria for a Stage 2 AKI?

A

Creatinine rise x2 from baseline or
Reduced urine output of less than 0.5ml/kg/hr for 12 hours or more

35
Q

What is the criteria for Stage 3 AKI?

A

Creatinine rise x3 from baseline within 7 days or
Creatinine rise to >354 micro mol/L with either acute rise (>26) in past 48 hrs or 50% rise from baseline in 7 days
Urine output of less than 0.3ml/kg/hr for 24 hrs
Anuria for 12 hrs
Any requirement for renal replacement therapy

36
Q

What are the nephrotoxic drugs?

A

Aminoglycosides
Amphotericin
Cytotoxic drugs such as cisplatin
Diuretics
Immunosuppressants (E.g. ciclosporin and tacrolimus cause renal vasoconstriction
Radiocontrast
NSAIDs (renal hypo perfusion)
Lithium salts

37
Q

How does the heart rate change from sitting to standing in hypovolaemia?

A

Rises by 30 or more

38
Q

What is the equation for creatinine clearance?

A

(Urine creatinine x urine volume)/plasma creatinine

39
Q

What % of cardiac output do kidneys get?

A

20%

40
Q

What are the major endocrine functions of the kidney?

A

Secretion of EPO
Alpha1- hydroxylation of vit D
Production of Renin

41
Q

What is creatinine

A

An ed product of skeletal muscle metabolism

42
Q

When should creatinine clearance be used instead of plasma creatinine and GFR?

A

When the are highly significant falls of GFR (this can happen before serum creatinine rises)

43
Q

What are the common causes of hypokalaemia

A

Diuretic therapy
Acute illness
GI losses

44
Q

What are the features of hypokalaemia?

A

Weakness
Intestinal ileus
Decreased renal-concentrating ability
ECG changes: T-wave flattening, U waves, increased tachyarrhythmias

45
Q

What are the three types of hyponatraemia?

A

Hypovolaemia
Normovolaemia
Hypervolaemia

46
Q

What are common causes of hyponatraemia?

A

SIADH
Heart failure
Inappropriate IV dextrose in post op patients
Iatrogenic Addison’s disease (over-rapid corticosteroid withdrawal)

47
Q

What are the signs of hypovolaemia?

A

Thirst
Tachycardia
Hypotension
Postural fall in BP
Reduced skin turgor

48
Q

Why do you have to correct sodium carefully?

A

To avoid central pontine myelinolysis

49
Q

What is central pontine myelinolysis?

A

Encephalopathy
Cranial nerve palsies
Quadriplegia

50
Q

What are the most common causes of SIADH?

A

Idiopathic
Post op pain/infection/drugs
CNS: infection/stoke/neoplasia
Lung infection/tumour
Prostate/GI/haem malignancy
Drugs: Vasopressin, Carbemazepine, cyclophosphamide, aspirin

51
Q

What are the features of nephritis?

A

haematuria, oliguria, proteinuria (moderate), fluid retention

52
Q

What is the most common cause of nephritis?

A

IgA glomerulonephritis (Berger’s disease)

53
Q

What age group does IgA glomerulonephritis particularly affect?

A

People in their 20s, often within 48hrs of an infection (e.g. URTI)

54
Q

What is seen on histology in IgA glomerulonephritis?

A

IgA deposits
Mesangial proliferation

55
Q

What is membranous nephropathy?

A

A type of glomerulonephritis where immune complexes deposit in the glomerular basement membrane, causing thickening and proteinuria (can also cause nephrotic syndrome)

56
Q

What is seen on histology in membranous nephropathy?

A

IgG and complement deposits on the basement membrane

57
Q

What are the causes of membranous nephropathy?

A

Idiopathic (70%)
Drugs such as: NSAIDs
Malignancy
SLE

58
Q

What is membranoproliferative glomerulonephritis?

A

Immune complex deposits
Mesangial proliferation
Classically in people in under thirties

59
Q

How soon after infection does post-streptococcal glomerulonephritis start?

A

Usually 1-6 weeks after streptococcal infection (e.g. tonsillitis or impetigo)

60
Q

What is seen in histology in rapidly progressive glomerulonephritis?

A

Glomerular crescents

61
Q

What is Goodpasture syndrome?

A

Anti-glomerular basement membrane syndrome

62
Q

What antibodies are seen in Goodpasture syndrome?

A

Anti-glomerular basement membrane antibodies (a-GBM antibodies

63
Q

What are the features of Goodpasture syndrome?

A

Haematuria
Pulmonary haemorrhage (antibodies also attack the basement membrane in the lungs): this can look like a ground glass appearance on CXR

64
Q

What are the autoantibodies in microscopic polyangiitis?

A

p-ANCA

65
Q

What are the autoantibodies in granulomatosis with polyangiitis?

A

c-ANCA

66
Q

What investigation is used to find out the cause of the glomerulonephritis?

A

Renal biopsy is sometimes used - histology

67
Q
A

Finals Revision (20 decks)

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