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Synoptic Revision > Renal > Flashcards

Renal Flashcards

1
Q

Define Acute Kidney Injury (AKI)

A

An abrupt decline in kidney function i.e. glomerular filtration rate (can be hours or days)

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2
Q

What are the 3 classifications of AKI?

A
  • Pre-renal
  • Post-renal
  • Intrinsic
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3
Q

Define Pre-renal AKI

What is is caused by? (6)

A
  • Blood flow to kidneys reduced, can cause ischaemic injury if not managed
  • Reduced BP, hypovolaemia (blood loss), dehydration, GI bleed, sepsis and liver failure
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4
Q

Define Post-renal AKI

What can it be caused by?

A
  • Obstruction to the outflow from kidneys
  • Benign prostatic hypertrophy (BPH), prostate cancer, renal calculi, retroperitoneal fibrosis (scar tissue at back of abdomen)
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5
Q

Define Intrinsic AKI

A
  • Damage to the function tissues of the kidney
  • Acute interstitial nephritis (inflammation of renal interstitium), hypersensitivity reaction (often drug induced), myeloma (type of blood cancer), vasculitis (immunological renal disease
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6
Q

How can glomerular filtration rate measured?

A
  • eGFR (ml/min/1.73m2)

- Creatinine clearance (ml/min)

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7
Q

What is the formulae used to calculate creatinine clearance

A

CrCl = F(140 - age) x weight / Serum Creatinine

F = 1.04 female F = 1.23 male

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8
Q

In what patients MUST creatinine clearance be calculated?

A
  • Patients taking: Direct Oral Anticoagulants (DOACs) e.g. Dabigatran
    Nephrotoxic drugs e.g. Cisplatin, Methotrexate, ACE
    inhibs, Cyclosporine, NSAIDs, Tacrolimus
    Drugs excreted renally e.g. antibiotics, beta-blockers,
    diuretics, lithium, digoxin
  • > 75 years
  • Extremes of muscle mass
  • Narrow therapeutic index drugs e.g. Digoxin
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9
Q

What are the steps taken after a patient is found to have a low CrCl?

A
  • Establish AKI or CKD
  • Review all medications and assess adjustments e.g. always stop ACE inhibs in AKI, BUT not CKD as it is renal protective
  • Check dosing based on eGFR

-

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10
Q

Define Chronic Kidney Injury (CKD)

A

Abnormalities of kidney function or structure present, for > 3 months, with health implications

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11
Q

What is ACR?

A
  • Albumin : Creatinine ratio
  • Normally proteins are not filtered into tubules of nephron, they remain in blood due to size
  • As CKD progresses, structure breaks down causing ‘leaks’ allowing protein to be filtered and into the urine where it can be detected
  • Greater amount of albumin in urine = more severe CKD
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12
Q

What are the risk factors for CKD? (6)

A
  • Hypertension (more strain on tubules)
  • UTIs, especially recurrent ones
  • Medication e.g. Lithium, NSAIDs
  • CVD
  • Age
  • Malignancy
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13
Q

How is CKD testing prompted?

A
  • Albumin, proteins or blood in urine

- Ultrasound or biopsy results

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14
Q

What are the clinical complications of CKD? (8)

A
  • Acidosis
  • Anaemia
  • Dyslipidaemia
  • Fluid overload
  • Hyperkalaemia
  • Hypertension
  • Mineral & bone disorder
  • Uraemia
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15
Q

What is acidosis?

How is it managed?

What are the SE of treatment?

A
  • Result of blood becoming more acidic due to kidneys inability to excrete H+ and reabsorb HCO3-
  • Long term sodium bicarbonate (1g TDS)
  • Increase in Na = water retention (Na and water diffuse together)
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16
Q

What is renal anaemia?

What causes it?

How do you manage it?

A
  • When quality or quantity of RBC are below normal
  • Lack of circulating iron: by blood loss, dietary inadequacy, poor absorption of Fe due to uraemia or use of phosphate binders, impaired erythropoiesis due to lack of erythropoietin, long term use of immunosuppressants
  • Pre-dialysis management: oral iron, 3 months MAX
  • Dialysis patients: IV iron, given after dialysis
17
Q

What is erythropoietin?

A
  • A naturally occurring hormone produce by the kidneys
  • Stimulates bone marrow to produce red blood cells (erythrocytes)
  • CKD patients have little to no circulating EPO
18
Q

How can you manage a lack of erythropoietin?

A

Erythropoietin stimulating agents (ESA)

  • Eprex: recombinant human EPO, given SC once weekly
  • Aransep: Given IV to dialysis patients, once weekly
19
Q

What is dyslipidaemia?

How do you manage?

A
  • Abnormal lipid metabolism in CKD
  • Causes high rate of CVD in CKD
  • Atorvastatin 20mg OD
20
Q

How does fluid overload occur in CKD?

A

Due to kidneys inability to maintain Na and fluid balance

21
Q

How would you manage fluid overload in CKD?

A
  • Restrict Na diet (salt), and fluid intake
  • Diuretic therapy: Loop diuretic e.g. furosemide in high dose
  • If medication ineffective = dialysis
  • AVOID meds with high Na e.g. effervescent medication
22
Q

What can be the consequence of hyperkalaemia (high potassium)?

A
  • Damaging to hear muscles and cause abnormal rhythms
23
Q

How would you manage hyperkalaemia in CKD? (4)

A

Non-pharmacological: restrict dietary potassium

Pharmacological:

  • Calcium resonium orally TDS
  • IV Calcium gluconate
  • Actrapid insulin (pushed K+ into cells, avoiding heart)
  • Dialysis as last option

BEWARE drugs exacerbating hypokalaemia e.g. potassium sparing diuretics e.g. Spironolactone) Digoxin and NSAIDs

24
Q

How would you manage hypertension in CKD?

A
  • ACE inhibitor e.g. Ramipril
  • Angiotensin Receptor Blockers (ARBs) e.g. _____sartan

RENOPROTECTIVE IN CKD

25
Q

Why are mineral and bone disorders such an issue in CKD?

A
  • Kidneys responsible for balancing potassium and calcium in blood
  • These are essential for bone development and regrowth
26
Q

How do the kidneys balance calcium in the blood? (4)

A
  • Healthy kidneys activate Vitamin D into calcitriol
  • Calcitriol maintains blood calcium levels
  • Healthy kidneys also remove excess phosphorus
27
Q

What happens to mineral levels in CKD?

A
  • Production of calcitriol stops
  • Causes reduction in calcium in blood (hypocalcaemia)
  • Phosphorus levels in blood rise
28
Q

How is calcitriol deficiency managed in CKD?

A
  • Alfacalcidol (activated Vit D)
29
Q

How is high phosphorus in blood (Hyperphosphatemia) managed in CKD?

A
  • Phosphate binders e.g. Sevelemar or Lanthanum carbonate TDS
  • Restricted phosphate diet
30
Q

What is Hyperparathyroidism?

A
  • Parathyroid hormone is continually stimulated to release parathyroid hormone (PTH)
  • Parathyroid gland becomes enlarged as a result
  • Result is hypercalcaemia
31
Q

how is Hyperparathyroidism managed?

A
  • Cinacalcet

- Parathyroidectomy (removal of gland)

32
Q

What is uraemia?

A
  • Build up of urea in blood
  • Serious and result in emergencies e.g. encephalopathy and pericarditis (irritation or infection to heart muscle tissue)
33
Q

How is uraemia managed?

A

Dialysis to remove waste products

34
Q

What medications are given to diabetes patients with CKD?

A
  • Metformin 1st line IF CrCl > 30 ml/min
  • CAUTION: Sulphonylureas in renal failure, increased risk of hypoglycaemia –> risk in elderly (falls)
  • Pioglitazone fine in renal failure BUT contra-indicated in heart failure

Synoptic Revision (7 decks)

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