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JL Renal and Urology > Week 4 (2) > Flashcards

Week 4 (2) Flashcards

1
Q

What is the definition of CKD?

A

Reduced GFR and/or evidence of kidney damage - has to be more measurements

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2
Q

Do muscular people produce more creatinine?

A

Yes

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3
Q

When can eGFR over estimate?

A

If muscle mass is low - only valid if serum creatinine is stable

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4
Q

What stages of kidney disease are based purely on GFR?

A

3-5

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5
Q

What does CKD increase risk of?

A

Cardiovascuklar disease

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6
Q

What increases the progression of CKD?

A

Proteinuria

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7
Q

What can diabetes, hypertension, vascular disease, chronic glomerulonephritis, reflux nephropathy and PCK all cuse?

A

CKD

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8
Q

When do symtpoms of CKD due to reduced GFR occur?

A

Less than 20 GFR

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9
Q

Name some non-soecific symptoms of CKD?

A
  1. Tiredness
  2. Poor appetite
  3. Itch
  4. Sleep disturbance
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10
Q

How is proteinuria reduced in CKD?

A
  1. Control BP
  2. ACEI and ARB
  3. Spironolactone
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11
Q

How is CVS disease risk reduced in CKD?

A
  1. Srtop smoking
  2. Statins
  3. BP and proteinuria
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12
Q

What are complications of CKD?

A

Anaemia - erythropoietin produiction declines

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13
Q

Where is vitamin D hydroxylated?

A

In the kidney

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14
Q

In CKD, impaired Vitamin d hydroxylation leads to reduced calcium absorptin - leading to?

A

Secondary hyperparathyroidism

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15
Q

In CKD what causes high phosphate and high calcium?

A

Vascular calcification

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16
Q

How is bone disease mkanaged in CKD?

A

Alfacalcidol - hydroxylated vit D so doesnt need kidneys

Phosphate

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17
Q

wHEN IS dialysis recommended?

A

Wjen GFR about 20

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18
Q

What does a rising creatinine mean for mortality with AKI?

A

Increases

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19
Q

What is AKI defined as?

A

An abrupt reduction in kidne function defined as

  1. Absolute increase in serum creatinine by >26.4
  2. OR increase in creatinine by >50%
  3. Or a reduction in urine output
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20
Q

What can hypovolaemia (haemorrhage, burns), hypotension (shock, sepsis) and renal hypoperfusion (NSAIDS, COX, ACEI, ARB, hepatorenal syndrome) all cause?

A

AKI - pre renal causes

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21
Q

What is reversible volume depletion leading to oliguria and increased creatinine?

A

Pre-renal AKI

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22
Q

What do ACI do to GFR?

A

Small fall in it

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23
Q

How much cardiac output do the kidneys recieve?

A

20%

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24
Q

What does untreated pre renal AKI lead to?

A

Acute tubular necrosis

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25
Q

Give two common causes of acute tubular necrosis?

A

Dehydration, sepsis, rhabdomyolysis and drug toxicity

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26
Q

What do you give in fluid challenge for hypovolaemia in treatment of pre renal AKI?

A

Crystalloid 0.9% NaCl

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27
Q

Name a vascular cause of renal AKI?

A

GPA

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28
Q

Name a glomerular cause of AKI?

A

Glomerulonephritis

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29
Q

Name three causes of interstitial nephritis leading to AKI?

A
  1. Drugs
  2. Infection TB
  3. Systemic Sarcoid
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30
Q

Name 4 causes of tubular injury which lead to AKI?

A
  1. Ischaemia - prolonged renal hypoperfusion
  2. Drugs - gentamicin
  3. Contrast
  4. Rhabdomyolysis
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31
Q

What does fluid overload, PO, uraemia including itch, pericarditis and oliguria all suggest?

A

AKI

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32
Q

What are two urgent indications for renal biopsy?

A
  1. Suspected rapidly progressive GN

2. Positive immunology and AKI

33
Q

What is renal biopsy contraindicated in?

A

Hydronephrosis

34
Q

Name some life threatening complications of AKI?

A
  1. Hyperkalaemia
  2. Fluid overload PO
  3. Sever eacidosis
  4. Uraemic pericardial effusion
  5. Severe uraemia
35
Q

What do stones, cancers, stricutres and extrinsic pressure all potentially cause?

A

Post renal AKI

36
Q

How do you treat hydronephrosis causing post renal AKI?

A

Nephrostomy

37
Q

What are some ECG hyperkalaemia changes?

A

Tented T waves, flattened p waves, prolonged PR interval, depressed ST segment

38
Q

How is hyperkalaemia initially treated?

A

Protect myocardium - 10mls 10% calcium gluconate (2-3 mins)
Insulin (actrapid) with 50mls 50% dextrose (30 mins)
Salbutamol nebs (90mins)

39
Q

How is hyperkalaemia treated not in the acute setting?

A

Prevent absorption from GI tract - calcium resonium

40
Q

What part of the kidney are the glomeruli part of?

A

Renal parenchyma

41
Q

Is acute GN treatable?

A

Yes

42
Q

Name a size and charge selective barrier?

A

Glomerular capillary wall

43
Q

In GN - what does disruption of the barrier lead to?

A

Haematuria and/or proteinuria

44
Q

What kind of lesion does damage to endothelial or mesangial cells lead to?

A

Proliferative lesion and red cells in urine

45
Q

What does damage to podocytes lead to and what comes in the urine?

A

Non-proliferative lesion and protein in the urine

46
Q

Name three things to look for on urinalysis for GN?

A

RBC (dysmorphic), RBC and granular casts, lipiduria

47
Q

What type of process is nephritic syndrome indicative of?

A

Proliferative process

48
Q

What does nephritic syndrome involve?

A
  1. Acute renal failure
  2. Oliguria
  3. Oedema
  4. Hypertension
  5. Active urinary sediment - RBC, granular casts
49
Q

What is nephrotic syndrome indicative of?

A

Non-proliferative process

50
Q

Name some complications of nephrotic syndrome?

A
  1. Infections
  2. Renal vein thrombosis
  3. Pulmonary emboli
  4. Volume depletion (aggtressive use of diuretics)
  5. Vit D deficiency and subclinical hypothyroidism
51
Q

When looking at histology to classify GM - what four things are looked at?

A
  1. Proliferative or non-proliferative
  2. Focal/diffuse (greater than 50% glomeruli affected)
  3. Global/segmental
  4. Crescentic (RPGN in vasculitis)
52
Q

What is the target for hypertension when treating GN?

A

Less than 130/80

53
Q

Other than anti-hypertensives how else is GN treated?

A

ACEI, diuretics and statins, fish oil

54
Q

What is a treatment for GN involving TPE-therapeutic plasma exchange

A

Plasmapharesis

55
Q

What immunosuppressive drugs can treat GN?

A
  1. Corticosteroids
  2. Azathioprine
  3. Alkylating agents (cyclophosphamide)
  4. Calcineurin inhibitors (cyclosporin and tacrolimus)
  5. Mycophenolate Mofetil MMF
56
Q

What is the general management for nephrotic patients?

A
  1. Fluid restriction
  2. Salt restriction
  3. Diuretics
  4. ACEI/ARBS
  5. IV ablumin (if volume deplete)
57
Q

What is the commonest cause of nephrotic syndrome in children?

A

Minimal change nephropathy

58
Q

What is found on EM in minimal change nephropathy?

A

Foot process fusion on EM

59
Q

Do you get complete remission with oral steroids in minimal change nephropathy?

A

Yes 94% do

60
Q

What is the commonest cause of nephrotic sybndrome in adults?

A

fsgs - Focal Segmental Glomerulosclerosis

61
Q

What can cause secondary FSGS?

A

HIV/heroin use/obesity/reflux nephropathy

62
Q

What is seen on renal biopsy in FSGS?

A

LM with minimal Ig

IF with complement deposition

63
Q

What is the prognosis for FSGS?

A

50% progress to end stage renal failure after 10 years

64
Q

What is the second commonest cause of nephrotic syndrome in adults?

A

Membranous nephropathy

65
Q

What are some important secondary causes of membranous nephropathy?

A

Infections - hep B and parasites
CTDs - lupus
Malignancy - carcinomas/lymphoma
Drugs - penicillamine/gold

66
Q

What does renal biopsy show on membranous nephropathy?

A

Subepithelial immune complex deposition in the basement membrane
Thickened basement membrane - silver stain

67
Q

What three things can treat membranous nephropathy?

A
  1. Steroids
  2. Alkylating agents
  3. B cell monoclonal Ab
68
Q

What antibody is present in 70% of primary membranous nephropathy?

A

Anti PLA2r

69
Q

What is the commonest nephropathy in the world?

A

IgA nephropathy

70
Q

What type of haematuria preseents after a resp/GI infection in IgA nephropathy?

A

Macroscopic

71
Q

What nephropathy is associated with HSP?

A

IgA nephropathy

72
Q

What is seen on renal biopsy in IgA nephropathy?

A

LM - mesangial cell proliferation and expansion

IF - IgA deposits in mesangium

73
Q

How is IgA nephropathy treated?

A

BP control
ACEI/ARB
Fish oil

74
Q

What active urinary sediment is seen in RPGN?

A

RBCs, RBC and granular casts

75
Q

What is seen on biopsy in RPGN?

A

Glomerular crescents

76
Q

What two ANCA-positives cause RPGN?

A

Wegener’s granulomatosis

Microscopic polyangitis

77
Q

What three ANCA negatives cause RPGN?

A
  1. Goodpastures
  2. HSP
  3. SLE
78
Q

Give three drug treatments for RPGN?

A

Steroids (IV methylprednisolone)
Cytotoxics (cyclophosphamide)
Monoclonal antibodies against CD20 b cells (rituximab)

JL Renal and Urology (9 decks)

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