Chronic Kidney Disease Flashcards

1
Q

What are the stages of chronic kidney disease?

A
1 - 90ml/min 1.73m2 or greater eGFR
2 - 60-89
3A - 45-59
3B - 30-44
4 - 15-29
5 - less than 15 or on dialysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the cardiovascular risks associated with CKD?

A

CV risk worsens with stage of CKD
- especially if proteinuria is present
Should be addressed in the early stages
Increased calcium and phosphate in the blood combine to form an insoluble compound that is deposited in artery walls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How can the porgression of CKD be slowed?

A

BP control
- 130/80 target for those with proteinuria
Inhibition of the renin-angiotensin system confers greater benefit that lowering BP alone
- ACEI/ARB
- only in patients with proteinuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the anti-proteinuric action of ACE inhibitors in CKD.

A

Reduction of the systemic blood pressure
Relaxation of the efferent arteriole from the glomerulus
- additional reduction of intraglomerular pressure
Gradual reduction in glomerular permeability to protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How can being on ACEI/ARBs be problematic in CKD?

A

If the systemic pressure drops for any reason (e.g. blood loss), the patient can’t constrict the efferent arteriole.
This means the perfusion pressure within the glomerulus drops, and not enough blood gets filtered

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How are the consequences of stage 4 CKD treated?

A

Adjust drug doses - e.g. insulin
Anaemia - erythropoietin (EPO injections)
Acidosis - sodium bicarbonate
Hyperkalemia - correct acidosis (potassium attracted out the cell by acidic blood), restrict diet and stop relevant drugs (e.g. K sparing diuretics and ACEI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How can chronic kidney disease cause secondary hyperparathyroidism?

A

Kidney damage means there is a decrease in hydroxylated vitamin D, and an increase in phosphate (not being peed out)
Both of these factors contribute to a decrease in serum calcium
This is detected by the parathyroid gland, which increases PTH secretion
Increased PTH leads to calcium being taken from bone (accompanied by phosphate)
So a person is likely to have low/normal calcium and high phosphate
PTH can’t exert its normal effect on the kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What biochemistry results would you expect in CKD?

A
Sodium - normal/low
Potassium - raised 
Bicarbonate - low
Albumin - low
Calcium - low/normal
Phosphate - high
PTH - high (increases as renal function decreases)
Anaemia - normochromic normocytic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How is secondary hyperparathyroidism prevented?

A

Phosphate binder consumed with meals
- leaches phosphate from food and moves phosphate into the bowels
Alfacalcidol - vitamin D analogue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How is secondary hyperparathyroidism treated?

A

Cinacalcet - blocks calcium receptors on the PT gland

Parathyroidectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the intraceable symptoms of stage 5 CKD?

A
Tiredness
Oedmea - peripheral/pulmonary 
Thirst
Nausea 
Metallic taste (uraemic syndrome)
Coldness
Itch
Restless legs
Irregular menstrual cycles 
Chest pain (beware pericarditis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is someone managed in stage 5 CKD?

A

Dialysis

Palliative care plan if they chose not to dialyse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly