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Year 5 path SW > Chempath 19: Assessment Of Renal Function 2 > Flashcards

Chempath 19: Assessment Of Renal Function 2 Flashcards

1
Q

Define acute kidney injury ?

A

Rapid abrupt reduction in kidney function leading to inability to maintain electrolytes, acid-base and fluid haemostasis

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2
Q

A patient on the ward has an increase of creatinine clearance of 30 µmol/L. Is this patient having an AKI ?

A

Yes

AKI stage 1: increase of serum creatinine by >= 26µmol/L or >1.5 x reference serum creatinine

AKI stage 2: >2x reference serum creatinine

AKI stage 3: >3x reference serum creatinine or increase >= 354µmol/L

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3
Q

Outline 2 physiological mechanisms that work to maintain GFR and renal blood flow at a constant rate ?

A

Myogenic stretch- If the afferent arteriole is stretched due to high pressure, it will constrict in order to keep blood pressure entering Glomerulus constant (and GFR)

Tubuloglomerular feedback- High chloride ions (sign of high GFR) are detected in the afferent arteriole, this triggers it to constrict to reduce GFR and chloride ions in the distal tubule

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4
Q

List 4 pre-renal causers of AKI (excluding drugs) ?

A

Haemorrhage
Hypotension (shock, sepsis, anaphylaxis)
Oedema (HF, Cirrhosis, nephrotic syndrome)
renal artery stenosis

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5
Q

List 4 drugs that can cause pre-renal AKI ?

A

ACE inhibitors- reduce efferent arteriole vasoconstriction
NSAIDs - decreases afferent arteriole dilation
Calcineurin inhibitors- decrease afferent arteriole dilation
Diuretics- reduce preload, affect tubular function

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6
Q

What is the difference between AKI and ATN (acute tubular necrosis) ?

A

AKI has no structural damage and responds immediately to restoration of the circulation volume.

ATN is caused by Ischaemic damage and will not respond to correction of the circulating volume.

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7
Q

In ATN what feature may be seen in the urine on microscopy?

A

Epithelial cell casts

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8
Q

List 4 post renal causes of AKI?

A 
Renal calculi (stones)
BPH
Blocked urinary catheter 
Urethral strictures 
Cervical cancer

Anything that blocks the outflow of urine from the kidneys. This causes increased pressure in the tubules, which reduces the pressure gradient across the Bowman’s capsule and hence causes GFR to decline.

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9
Q

List 4 renal causes AKI?

A

Glomerular disease E.g Glomerulonephritis
Tubular disease E.g. ATN
Vascular disease E.g. Small vessel vasculitis- (HSP, Churg-Strauss syndrome, microscopic polyangitis, granulomatosis with polyangitis)
Interstitial disease E.g. Interstitial nephritis

Direct tubular injury
Usually ischaemic
Endogenous toxins - myoglobin, immunoglobulins
Exogenous toxins - aminoglycisides, amphoteracin, Aciclovir

Immune dysfunction

Infiltration/abnormal protein deposition
Amyloidosis
Lymphoma
Myeloma related renal disease

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10
Q

What measure is used to stage Chronic kidney disease (CKD)

A

GFR

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11
Q

Which stage of CKD is considered end-stage kidney failure?

What GFR indicates this ?

A

Stage 5

GFR <15 or dialysis dependent

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12
Q

Which one of these is not considered a common risk factor for CKD ?

A) Diabetes mellitus 
B) Obesity 
C) hypertension 
D) drinking 5 glasses of water per day 
E) Renal stones
F) Polycystic kidney disease
A

D) drinking 5 glasses of water per day

This is a healthy amount of water

All the others are risk factors for CKD

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13
Q

Which 3 endocrine functions of the kidneys may be disturbed during CKD ?

A

EPO- required for haemopoiesis
RAS- renin release for ADH secretion
Vitamin D- The kidney activates vitamin D to calcitriol

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14
Q

What kind of acid base dysfunction would you expect in CKD ?

A

Metabolic Acidosis

You can no longer make HCO3- ions to mop up excess H+

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15
Q

List some signs/symptoms of Uraemia ?

A 
Nausea and vomiting 
Progressive weakness
Shallow respiration 
coma 
Tremor
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16
Q

Which electrolyte is most markedly abnormal in CKD ?

A

K+

There is a hyperkalaemia because the kidney exchanges the excess H+ ions in the blood with intracellular pottasium

17
Q

What treatments are there for hyperkalaemia ?

A 
Calcium gluconate (cardioprotective) 
Insulin with glucose (Insulin causes uptake of K+ into cells)
Salbutamol (NA-K ATP pump on liver and muscles causes K+ uptake)
Sodium bicarbonate (corrects metabolic acidosis but slower)
18
Q

How does CKD cause Osteopenia ?

A
  • Excess H+ ions are not mopped up by HCO3-

- H+ can be exchanged for calcium in the bone

19
Q

What type of anaemia is associated with CKD ?

A

Anaemia of chronic disease

Normocytic normochromic

20
Q

Are the levels low or high in CKD ?

Phosphate
Calcium
PTH
Calcitriol

A

Phosphate: High
Calcium: Low/ normal
PTH: high
Calcitriol: Low

Calcium is very confusing in CKD. It is low because of low activated vitamin D (calcitriol). But this causes high PTH which releases more calcium from the bone so can make the level normal. In long standing CKD there may be tertiary hyperparathyroidism which causes high calcium

21
Q

Give an example of a potassium sparing diuretic ?

A

Spironolactone

22
Q

What is renal osteodystrophy ?

What signs would you expect ?

A

A constellation of bone diseass associated with CKD in which phosphate is high and calcium is low causing increased PTH release. This causes bone resorption.

Signs: osteopenia, Osteomalacia, salt and pepper skull (osteoschlerosis), brown tumours, “rugger jersey spine”.

23
Q

What is the normal response to reduced circulating volume

A

Activation of central baroreceptors
Activation of RAS
Release of vasopressin
Activation of sympathetic system

24
Q

Pathophysiology of post renal AKI

A

GFR is dependent on the hydraulic pressure gradient
Obstruction results in increased tubular pressure
Causes an immediate decline in GFR

Prolonged obstruction:
Glomerular ischaemia
Tubular damage
Long term interstitial scarring

25
Q

Consequences of CKD

A

Failure of homeostatic function

  • acidosis
  • hyperkalaemia

Failure of hormonal function

  • anaemia
  • renal bone disease

Cardiovascular disease

  • vascular calcification
  • uraemic cardiomyopathy
26
Q

What can be used to treat renal acidosis

A

Oral sodium bicarbonate

27
Q

List 4 renal bone diseases

A

Osteitis fibrosis cystica
Osteomalacia
Adynamic bone disease
Mixed osteodystrophy

Can’t excrete phosphate from kidneys
Also can’t make activates vitamin D
Body makes PtH to try remove phosphate
Phosphate complexes with calcium, lowering the amount of calcium in blood
In response to high PTH bone becomes resistant to PTH

28
Q

What is osteitis fibrosa cystica

A

Caused by osteoclasts resorption of calcified bone and replacement b fibrous tissue

29
Q

How can renal bone disease be treated

A

Phosphate control (reduce)

  • diet
  • phosphate binders

Vit D receptor advocators

  • 1 alpha calcidol
  • paracalcitol

Direct PTH suppression
- Cinacalet

Year 5 path SW (106 decks)

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