renal 5 Flashcards

1
Q

what is nephrotoxic drug

A

a drug that has potential to damage the kidney

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2
Q

when a patient has CKD/AKI what do you need to consider - the medication review

A
  • stop the drug?
  • withhold the drug?
  • amend the dose?
  • continue the drug?
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3
Q

how can kidney failure affect absorption

A

Patients with renal failure typically have oedema as their kidneys are less efficient at removing water and salt
Oedema can affect the wall of the bowel
This may lead to reduced absorption of drugs

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4
Q

how can kidney failure affect distribution

A

Drug distribution may also be affected by water balance
Oedema increased/dehydration will affect drugs that are more hydrophilic
Nephrotic syndrome leads to decreased protein levels in the blood. Many drugs are bound to proteins when in the blood. Lack of proteins will mean higher levels of free drug in the blood leading to toxicity e.g. phenytoin

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5
Q

how can kidney failure affect metabolism

A

Kidneys have a role in the metabolism of many drugs
Kidney failure means that these drugs will no longer be metabolised by the kidneys e.g. vitamin D
Uraemia can also reduce liver function leading to decreased metabolism of drugs

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6
Q

how can kidney failure affect excretion

A

Reduced renal clearance means increased levels of drugs or their metabolites in the blood
MDRD or Cockroft and Gault equations can be used to estimated kidney function
This value can be used to decide whether a drug should be suspended or a dose reduced
Useful resources = BNF/BNFC, SPC or Renal Drug Handbook

Cockroft & Gault = F x (140-age) x weight (kg) / serum creatinine
F = 1.04 for females and 1.23 for males

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7
Q

what are the nephrotoxic drugs?

A
CANDA
Contrast media
ACE Inhibitors
NSAIDs
Diuretics
ARB’s
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8
Q

what makes contrast media nephrotoxic?

A

Contract induced nephropathy
Can occur in any patient with intra venous or intra-arterial contrast
Known renal dysfunction or CrCl = <60ml/min consider non-central imaging
Avoid in patients with renal failure!!

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9
Q

what makes ACE inhibitors nephrotoxic?

A

Used to treat hypertension, heart failure, nephropathy
Works on RAAS system  inhibits conversion of angiotensin I to angiotensin II (lecture 1!)
Renal failure = reduced renal perfusion
ACEIs reduce blood pressure = worsening of renal failure (lecture 2!)
Hold in renal failure!!
NB. Renoprotective in CKD
If initiating in patients with CKD  risk Vs benefit

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10
Q

what makes NSAIDs nephrotoxic?

A

Analgesic, antipyretic and anti-inflammatory
Non-selective COX inhibitors e.g. aspirin, ibuprofen, diclofenac, naproxen
Selective COX II inhibitors e.g. celecoxib
Inhibit prostaglandins = inhibits vasodilation of afferent arteriole = reduces kidney perfusion (lecture 2!)
PLUS promote sodium retention and therefore fluid retention
Hold in renal failure!!

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11
Q

where does ace inhibitor prevent constriction

A

afferent arteriole

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12
Q

aim of diruetics?

A
Diuretics cause diuresis
“water tablets”  take in the morning
Primary aim to increase NaCl excretion and hence water excretion
This can be achieved:
	- directly: by acting on the nephron
	- indirectly: by modifying the content of the filtrate
The are various classes of diuretics (PLATO)
	- Potassium-sparing diuretics
	- Loop diuretics
	- Aldosterone antagonists
	- Thiazide or thiazide-like diuretics
	- Osmotic diuretics
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13
Q

what makes ARB nephrotoxic?

A

Blocks angiotensin ii
Renal failure = reduced renal perfusion
ACEIs reduce blood pressure = worsening of renal failure (lecture 2!)
Hold in renal failure!!

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14
Q

how can analgesic cause nephrotoxicity

A

Analgesics

- Opiates: reduced excretion = risk of accumulation = increased 	risk of side effects. Review dose!
- Fentanyl and oxycodone = usually used in AKI/CKD
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15
Q

antibiotics - nephrotoxicity

avoid?

A

Antibiotics

- Aminoglycosides: gentamicin = avoid/reduce dose and follow 	guidelines 
- Glycopeptides: vancomycin = avoid/reduce dose and follow 	guidelines
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16
Q

how can hypertensives cause nephrotoxicity

A

Antihypertensives

- May exacerbate poor renal perfusion = hold if BP low

17
Q

how can anticholinergics cause nephrotoxicity

A

Anticholinergics

- Can cause urinary retention e.g. antihistamines, 	anticholinergics, antispasmodics
- Review and reduce dose
18
Q

The are various classes of diuretics

A

The are various classes of diuretics (PLATO)

- Potassium-sparing diuretics
- Loop diuretics - do not. offer in renal impairment 
- Aldosterone antagonists
- Thiazide or thiazide-like diuretics
- Osmotic diuretics
19
Q

what are examples of loop diuretics

A

Furosemide and bumetanide

20
Q

what is the indications for loop diuretics

A

Indications:

Acute pulmonary oedema
Congestive heart failure
Fluid overload in renal/liver disease
Hypertension

21
Q

what is the mechanism of action of loop diuretics

A

Act on the thick ascending limb of the loop of Henle
Inhibit Na+ reabsorption = less water uptake = increased urine production
Inhibit K+ and Cl- re-absorption into the body
Inhibit Ca2+, Mg2+ re-absorption
Inhibit urate excretion

22
Q

what is the adverse reactions of loop diuretics

A

Cause water excretion = dehydration = hypotension
Inhibit Na reabsorption = hyponatraemia
Inhibit K reabsorption = hypokalaemia
Inhibit Ca2+ reabsorption = hypocalcaemia
Inhibit Mg2+ re-absorption = hypomagnesia
Inhibit urate excretion = gout

23
Q

what are examples of thiazide

A
  • hydrochlorothiazide

- bendroflumethiaziade

24
Q

what are thiazide like diuretic examples

A

indapamide, chlortalidone, metolazone

25
Q

where doed the mechanism of action of Thiazide and thiazide-like diuretics take place

A

Act on the distal convoluted tubule of the nephron

26
Q

what are therapeutic indication of Thiazide and thiazide-like diuretics

A

Oedema of cardiac, renal or hepatic origin

Hypertension: monotherapy or as an adjunct

27
Q

what is the mechanism of action of thiazide or thiazide like drugs

A

Inhibit Na+ reabsorption = increases water excretion
Inhibit Cl- reabsorption
Inhibit K+ and Mg re-absorption
Increase Ca2+ re-absorption into the body

28
Q

what are the adverse reactions of thiazide or thiazide like drugs

A

Adverse effects: hypokalaemia, hyponatraemia, hyperuricaemia & hypercalcaemia, vasodilation (could be used as a positive), hyperglycaemia

29
Q

which gland signals to the release of aldosterone

A

adrenal

30
Q

what is the mechanism of action for aldestrone antagonist

A

Adrenal gland: signal to release aldosterone = Na + reabsorption = more H20 reabsorption

Aldosterone increases water and sodium re-absorption in the collecting tubule
Inhibiting aldosterone means that less water and Na will be reabsorbed
Increases reabsorption of K+ so known as “potassium sparing” (see below!)
Can be used alongside diuretics that increase K+ excretion
Spironolactone and eplerenone

31
Q

what are example potassium sparing diuretics

A

Sprinolactone/eplerenone (see above) & amiloride and triamterene Co-amilofruse/co-amilozide

32
Q

what is the mechanism of potassium-sparing diuretics

A

Inhibit Na reabsorption = increases water excretion
Reduces excretion of K = potassium sparing (sometimes leads to hyperkalaemia)
Diuretics that do not promote the secretion of potassium into the urine i.e. conserve potassium
Usually used in conjunction with other diuretics that cause hypokalaemia e.g. loop or thiazide diuretics
Promote excretion of uric acid
Limited diuretic effect

33
Q

what is the example of osmotic diuretics

A

-mannitol solution for infusion

A carbohydrate; not a drug
Freely filtered through glomerulus but is not re-absorbed
Within kidney tubules it has an osmotic effect, preventing water re-absorption and producing diuresis

34
Q

what is the therapeutic indications for osmotic diuretics

A

Prevention and/or treatment AKI
Reduction of intracranial pressure & cerebral oedema
Reduction of intraocular pressure
Promotion of elimination of renally excreted toxic substances in poisoning