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CMP > AKI prescribing > Flashcards

AKI prescribing Flashcards

1
Q

What are the 3 principles of AKI prescribing?

A
  1. Don’t give the drug in first place
  2. Adjust dose, if you do
  3. Stop the lot
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2
Q

What are the main categories of drugs that are nephrotoxic?

A 
ACEi/ARBs
NSAIDs
Diuretics
HMG-CoA Reductase inhibitors (‘statins’)
Metformin (not directly but causes lactic acidosis)
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3
Q

What percentage of medical admissions is AKI a feature of?

A

> 30%

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4
Q

What are the risk factors for AKI?

A

Patient-related factors:Age, sex, race, Pre-existent renal disease (CKD)
Specific disease (diabetes mellitus, multiple myeloma, proteinuric patients)
Sodium-retaining states (cirrhosis, heart failure, nephrosis)
Hypovolaemia (’dry’) and Sepsis (esp both)
Acidosis, potassium and magnesium depletion
Hyperuricemia, hyperuricosuria (acute neoplasia (esp haem) and Rx)
Renal transplantation

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5
Q

What are the pre renal drug-induced causes of AKI?

A

Haemodynamically mediated AKI (ACE/ARB and NSAIDs)

Hypovolaemia (Diuretics), including osmotic nephrosis (Mannitol)

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6
Q

What are the renal drug-induced causes of AKI?

A

Acute tubular necrosis (consequence of pre-renal)
Uncertain (Aminoglycoside)
Acute allergic interstitial nephritis (eg Penicillins, NSAIDs)
Rhabdomyolysis (HMG CoA Reductase Inhibitors)
Glomerulonephritis (Endocarditis)
Vasculitis (Hydralazine)

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7
Q

What are the renovascular drug-induced causes of AKI?

A 
Thrombosis (HUS/TTP; eg Ciclosporin and Tacrolimus)
Cholesterol emboli (Warfarin)
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8
Q

What are the post renal drug-induced causes of AKI?

A 
Intratubular obstruction (Tumour Lysis Syndrome)
Nephrolithiasis (Acute Urate Nephropathy)
Papillary necrosis (NSAIDs)
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9
Q

What are the pre-renal causses of AKI?

A

Excessive GI loss, eg laxatives (diarrhoea) or vomiting

Excessive renal loss, eg diuretics

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10
Q

How do NSAIDs cause AKI?

A

Haemodynamic - interfere with prostaglandin production

Acute interstitial nephritis

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11
Q

How do NSAIDS cause CKD?

A

From habitual use

Exacerbated by other drugs (anti-hypertensives, esp ACE inhibitors)
May have typical radiological features when advanced (papillary necrosis)

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12
Q

How do ACE inhibitors and ARBs cause AKI?

A

can cause a deterioration in renal function, via renal underperfusion (haemodynamic mechanism)

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13
Q

What is the electrolyte imbalance associated with spironolactone?

A

hyperkalaemia

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14
Q

What is acute tubular necrosis?

A

medical condition involving the death of tubular epithelial cells that form the renal tubules of the kidneys

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15
Q

When would you biopsy a patient with acute tubular necrosis?

A

if still on dialysis at 3 months

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16
Q

What antibiotic is associated with AKI?

A

Aminoglycosides: gentamicin

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17
Q

How do Aminoglycosides cause AKI?

A

Interferes with intracellular transport in lysosomes

Release of lysosomal enzymes

18
Q

What patients are at risk of AKI from IV contrast?

A

diabetic nephropathy,
CCF
hypovolaemia

19
Q

What are the indications for amphotericin?

A

IV administration for systemic invasive fungal infections

Oral for GI mycosis

20
Q

What are the SE of amphotericin?

A

Local/systemic effects with infusion (fever)
AKI or CKD
Tubular dysfunction (membrane permeability)
Hypokalaemia, RTA, diabetes insipidus, hypomagnesaemia
Pre hydration/saline loading may avoid problems

21
Q

How do we minimise toxicity from amphotericin?

A

liposomal packing of Amphotericin

22
Q

What are the drugs indicated in acute interstitial nephritis?

A

AB (30-50%) (Penicillins/Cephalosporins, Rifampicin, Sulphonamides
PPIs
NSAIDS
Other (Allopurinol, Phenytoin,
Quinolones, Cimetidine, Chinese herbs)

23
Q

What is the clinical presentation of acute interstitial nephritis?

A

Fever - 30% (‘drug fever’)
Eosinophilia – 20%
Rash – 15%
Triad of rash, fever, and eosinophilia = 10%
Or ..asymptomatic (AKI, subacute AKI etc)

24
Q

What are the none drug causes of acute interstitial nephritis?

A

Autoimmune disorders or other systemic disease (eg, SLE, Sjögren’s, sarcoidosis)
Infections remote to the kidney (eg, Legionella, leptospirosis, and streptococcal organisms),
Tubulointerstitial nephritis with uveitis (TINU)

25
Q

What is rhabdomyolysis?

A

breakdown of skeletal muscle

26
Q

What is “crush syndrome”

A

the systemic manifestation of muscle cell damage (usually from a crush injury)

27
Q

Causes of rhabdomyolysis?

A

Muscle injury: trauma, burns, electrocution, immobilisation, DKA, ischemia, compression, vascular inury, compartment syndrome

medications/toxins: alcohol, cocaine, amphetmines, statins, major tranquilizers, tentanus, venom

increased muscular activity: sport, seizures, status asthmaticus, inflammatory/inherites myopathies

28
Q

Clinical features of rhabdomyolysis?

A

Breakdown of skeletal muscle fibres
Specifically sarcolemma resulting in release of myoglobin
Tea or coca cola like urine
Oliguria

29
Q

How is rhabdomyolysis diagnosed?

A

Δ clinical, AKI, CK↑, +ve urinary myoglobin

30
Q

What drugs can cause antineutrophil cytoplasmic autoantibodies vasculitis

A 
Hydralazine
Ciprofloxacin, Sulphonamides
Phenytoin
Allopurinol
Some PPIs
Other (Propylthiouracil, Minocycline, Penicillamine)
31
Q

Causes of mesangiocapillary glomerulonephritis?

A

Endocarditis ± drugs (aminoglycosides, vancomycin, penicillins)

32
Q

Causes of membranous glomerulonephritis?

A

gold/penicillamine

33
Q

What are the clinical signs of HUS/TTP?

A

AKI
Haemolytic anaemia
Thrombocytopenia
± CF dependent on other features

34
Q

What are the causes of HUS/TTP?

A

Many
Including drugs
Eg. Ciclosporin/Tacrolimus)

35
Q

How do NSAIDS cause post renal AKI?

A

Cause analgesic nephropathy via papillary necrosis

36
Q

How do high-doses of sulphonamides (acetazolamide/methotrexate) cause AKI?

A

cause crystalluria and can therefore cause obstruction

37
Q

What is papillary necrosis?

A

characterized by coagulative necrosis of the renal medullary pyramids and papillae brought on by several associated conditions and toxins that exhibit synergism toward the development of ischemia

38
Q

What are the causes of papillary necrosis?

A

POSTCARDS

Pyelonephritis

Obstruction of the urinary tract

Sickle cell hemoglobinopathies, including sickle cell trait

Tuberculosis

Cirrhosis of the liver, chronic alcoholism

Analgesic abuse

Renal transplant rejection, radiation

Diabetes mellitus

Systemic vasculitis

39
Q

What should be considered before prescribing to a patient with AKI?

A
  1. Use drugs only when there is a definite indication
  2. Choose a drug that has no or minimal nephrotoxicity
  3. Use recommended dosage regimens for renal failure
  4. Look at previous levels
  5. Use surrogates, eg heart rate in betablocker
  6. Monitor the patient carefully for evidence of clinical effectiveness and toxicity of drugs
40
Q

How is digoxin toxicity treated?

A

supportive: correct electrolyte imbalances, atropine for bradycaardia, avoid cardiac stimulantes

limit absorption: charcoal effective within 8hrs

specific measures: DIGIBIND, binds plasma digoxin and complex eliminated by kidneys

enhanced elimination: dialysis is ineffective!

41
Q

What needs to be on a TTO for someone with AKI?

A

stage of AKI
Evidence of medicine reveiw
Type of blood tests required on discharge
Frequency of blood tests on discharge

42
Q

What is the target BP range in CKD?

A

without proteinuria: 120-139/<90mmHg

with proteinuria or DM: 120-129/<80mmHg

CMP (4 decks)

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