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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
Give two common causes of acute tubular necrosis?
Dehydration, sepsis, rhabdomyolysis and drug toxicity
26
What do you give in fluid challenge for hypovolaemia in treatment of pre renal AKI?
Crystalloid 0.9% NaCl
27
Name a vascular cause of renal AKI?
GPA
28
Name a glomerular cause of AKI?
Glomerulonephritis
29
Name three causes of interstitial nephritis leading to AKI?
1. Drugs 2. Infection TB 3. Systemic Sarcoid
30
Name 4 causes of tubular injury which lead to AKI?
1. Ischaemia - prolonged renal hypoperfusion 2. Drugs - gentamicin 3. Contrast 4. Rhabdomyolysis
31
What does fluid overload, PO, uraemia including itch, pericarditis and oliguria all suggest?
AKI
32
What are two urgent indications for renal biopsy?
1. Suspected rapidly progressive GN | 2. Positive immunology and AKI
33
What is renal biopsy contraindicated in?
Hydronephrosis
34
Name some life threatening complications of AKI?
1. Hyperkalaemia 2. Fluid overload PO 3. Sever eacidosis 4. Uraemic pericardial effusion 5. Severe uraemia
35
What do stones, cancers, stricutres and extrinsic pressure all potentially cause?
Post renal AKI
36
How do you treat hydronephrosis causing post renal AKI?
Nephrostomy
37
What are some ECG hyperkalaemia changes?
Tented T waves, flattened p waves, prolonged PR interval, depressed ST segment
38
How is hyperkalaemia initially treated?
Protect myocardium - 10mls 10% calcium gluconate (2-3 mins) Insulin (actrapid) with 50mls 50% dextrose (30 mins) Salbutamol nebs (90mins)
39
How is hyperkalaemia treated not in the acute setting?
Prevent absorption from GI tract - calcium resonium
40
What part of the kidney are the glomeruli part of?
Renal parenchyma
41
Is acute GN treatable?
Yes
42
Name a size and charge selective barrier?
Glomerular capillary wall
43
In GN - what does disruption of the barrier lead to?
Haematuria and/or proteinuria
44
What kind of lesion does damage to endothelial or mesangial cells lead to?
Proliferative lesion and red cells in urine
45
What does damage to podocytes lead to and what comes in the urine?
Non-proliferative lesion and protein in the urine
46
Name three things to look for on urinalysis for GN?
RBC (dysmorphic), RBC and granular casts, lipiduria
47
What type of process is nephritic syndrome indicative of?
Proliferative process
48
What does nephritic syndrome involve?
1. Acute renal failure 2. Oliguria 3. Oedema 4. Hypertension 5. Active urinary sediment - RBC, granular casts
49
What is nephrotic syndrome indicative of?
Non-proliferative process
50
Name some complications of nephrotic syndrome?
1. Infections 2. Renal vein thrombosis 3. Pulmonary emboli 4. Volume depletion (aggtressive use of diuretics) 5. Vit D deficiency and subclinical hypothyroidism
51
When looking at histology to classify GM - what four things are looked at?
1. Proliferative or non-proliferative 2. Focal/diffuse (greater than 50% glomeruli affected) 3. Global/segmental 4. Crescentic (RPGN in vasculitis)
52
What is the target for hypertension when treating GN?
Less than 130/80
53
Other than anti-hypertensives how else is GN treated?
ACEI, diuretics and statins, fish oil
54
What is a treatment for GN involving TPE-therapeutic plasma exchange
Plasmapharesis
55
What immunosuppressive drugs can treat GN?
1. Corticosteroids 2. Azathioprine 3. Alkylating agents (cyclophosphamide) 4. Calcineurin inhibitors (cyclosporin and tacrolimus) 5. Mycophenolate Mofetil MMF
56
What is the general management for nephrotic patients?
1. Fluid restriction 2. Salt restriction 3. Diuretics 4. ACEI/ARBS 5. IV ablumin (if volume deplete)
57
What is the commonest cause of nephrotic syndrome in children?
Minimal change nephropathy
58
What is found on EM in minimal change nephropathy?
Foot process fusion on EM
59
Do you get complete remission with oral steroids in minimal change nephropathy?
Yes 94% do
60
What is the commonest cause of nephrotic sybndrome in adults?
fsgs - Focal Segmental Glomerulosclerosis
61
What can cause secondary FSGS?
HIV/heroin use/obesity/reflux nephropathy
62
What is seen on renal biopsy in FSGS?
LM with minimal Ig | IF with complement deposition
63
What is the prognosis for FSGS?
50% progress to end stage renal failure after 10 years
64
What is the second commonest cause of nephrotic syndrome in adults?
Membranous nephropathy
65
What are some important secondary causes of membranous nephropathy?
Infections - hep B and parasites CTDs - lupus Malignancy - carcinomas/lymphoma Drugs - penicillamine/gold
66
What does renal biopsy show on membranous nephropathy?
Subepithelial immune complex deposition in the basement membrane Thickened basement membrane - silver stain
67
What three things can treat membranous nephropathy?
1. Steroids 2. Alkylating agents 3. B cell monoclonal Ab
68
What antibody is present in 70% of primary membranous nephropathy?
Anti PLA2r
69
What is the commonest nephropathy in the world?
IgA nephropathy
70
What type of haematuria preseents after a resp/GI infection in IgA nephropathy?
Macroscopic
71
What nephropathy is associated with HSP?
IgA nephropathy
72
What is seen on renal biopsy in IgA nephropathy?
LM - mesangial cell proliferation and expansion | IF - IgA deposits in mesangium
73
How is IgA nephropathy treated?
BP control ACEI/ARB Fish oil
74
What active urinary sediment is seen in RPGN?
RBCs, RBC and granular casts
75
What is seen on biopsy in RPGN?
Glomerular crescents
76
What two ANCA-positives cause RPGN?
Wegener's granulomatosis | Microscopic polyangitis
77
What three ANCA negatives cause RPGN?
1. Goodpastures 2. HSP 3. SLE
78
Give three drug treatments for RPGN?
Steroids (IV methylprednisolone) Cytotoxics (cyclophosphamide) Monoclonal antibodies against CD20 b cells (rituximab)

JL Renal and Urology (9 decks)

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