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Flashcards in CKD Deck (27)
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1
Q

what would you expect to happen to creatinine and eGFR in CKD?

A

decreased eGFR <60

increased creatinine- need to measure Cr twice 90 days apart to assess baseline

2
Q

is CKD reversible?

A

no it is irreversible

3
Q

Kidney function declines with age naturally, how is CKD different?

A

the decline in kidney function is accelerated by an active problem

4
Q

what would you expect the kidneys in CKD to look like on an US scan?

A

small shiny kidneys

5
Q

what are the 5 commonest causes of CKD?

A
  1. Diabetes
  2. HTN
  3. chronic glomerulonephritis,
  4. reflux nephropathy
  5. PCKD
6
Q

what are the functions of the kidney?

A
A WET BED
A- acid base balance
W- water homeostasis
E- erythropoiesis (EPO from juxtaglomerular apparatus)
T- toxin removal
B- BP control (through Renin release)
E- Electrolyte balance 
D- Vit D activation (PTH acts on the kidney to activate VitD)

when the kidney fails the above functions become impaired

7
Q

When the kidneys fail what happens to kidney function ?

A

kidney function declines.

patients have an increased risk of CVD

8
Q

outline how you would manage CKD patients? (mild mod and severe)

A

Mild- manage CV risk, treating risk factors such as BP, fluid and environment
Mod- renal specific effects need to me managed e.g. EPO, bone and CV risk
Severe- this is when there is low clearance and eGFR is very low- discussions need to be had about treatment and outcomes- prognosis poor) they may be in ESRD requiring dialysis and or transplant

9
Q

what are the 2 types of transplant donors?

A

live or deceased

10
Q

what are the 2 types of dialysis?

A

Haemodialysis and peritoneal dialysis

11
Q

True or false: with CKD there is an increased risk of CVD equivalent to the risk of having had a previous MI

A

True

12
Q

what happens to acid base balance in CKD?

A

decreased renal H+ excretion results in a metabolic acidosis (reduced pH, low HCO3, base deficit, possibly some respiratory compensation)

13
Q

what happens to the water homeostasis in CKD?

A

urine output is usually preserved until late
Nocturia- due to loss of phyisiological nocturnal anti-diuresis
Polyuria and thirst- occurs mainly due to loss of urine concentrating ability
HTN mainly due to volume expansion

patients cam become oliguric (<0.5ml/kg/hr)in acute on chronic disease

14
Q

what happens when the kidneys fail to regulate fluid and electrolyte balance?

A

hyperkalaemia and hyperphosphataemia

15
Q

what happens when the kidneys fail to excrete metabolic waste products?

A

results in uraemia syndrome
usually occurs late when eGFR <15ml/min
clinical features: N, anorexia, lethargy, itch, restless legs
very late features: pericarditis, neuropathy

16
Q

why does HTN occur in CKD?

A

due to volume expansion

17
Q

what happens when the kidney fails to produce EPO?

A

results in a normochromic anaemia of renal failure

18
Q

what happens when the kidney fails to hydroxylate (activate) vit D?

A

deficiency in activated Vit D results in hypocalcaemia, osteomalacia, secondary hyperparathyroidism
combined picture of renal osteodystrophy when calcium is resorbed from bone.

19
Q

In the management of CKD how would you manage the failure to excrete waste products and among acid base balance?

A

RRT
dialysis (haemodyalysis or peritoneal dialysis)
renal transplantation

20
Q

In the management of CKD how would you manage the failure to regulate fluid and electrolyte balance?

A

fluid restrict
restrict dietary potassium, phosphate
give phosphate binders such as calcichew
treat hyperkalaemia

21
Q

In the management of CKD how would you manage the failure to synthesis erythropoeitin?

A

give recombinant EPO ingestion 1-3x/week

22
Q

In the management of CKD how would you manage the failure to activate vitamin D?

A

give activated Vit D e.g. calcitriol

aim to normalise serum calcium and suppress parathyroid hormone levels tp 2-3x normal

23
Q

how would you manage the CV risk in CKD patients?

A

manage HTN aiming for BP<140/90 (or <130/80 if DM) use ACEi
statins (irrespective of lipids)
low dose aspirin

24
Q

what is sevelamer?

A

Sevelamer is a non-calcium based phosphate binder that treats hyperphosphataemia in patients with CKD mineral bone disease
It is licensed for the treatment of hyperphosphataemia in patients on haemodialysis or peritoneal dialysis.

25
Q

name a non-calcium based phosphate binder that treats hyperphosphataemia in patients with CKD mineral bone disease?

A

Sevelamer

It is licensed for the treatment of hyperphosphataemia in patients on haemodialysis or peritoneal dialysis.

26
Q

what is a contraindication for sevelamer?

A

bowel obstruction

27
Q

what is a contraindication for the use of the non-calcium based phosphate binder sevelamer?

A

bowel obstruction