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renal > pharmacology > Flashcards

pharmacology Flashcards

1
Q

what is natriuresis?

A

the process of excretion of sodium in the urine via action of the kidneys. ↓ the concentration of NA+ in the blood.

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2
Q

what promotes natriuresis?

A

promoted (more sodium is excreted) by ventricular and atrial natriuretic peptides as well as calcitonin

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3
Q

what inhibits natriuresis?

A

inhibited (sodium is conserved) by chemicals such as aldosterone

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4
Q

what is required to compensate for the body’s tendency to decrease pH due to metabolic production of CO2 (glycolysis)?

A

formation of acidic urine

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5
Q

how do diuretics work?

A

↑ the volume of urine produced by promoting the excretion of Na+, Cl-, HCO3 and water from the kidneys

NET result is ↑ urine flow, altered pH and altered ionic composition of blood and urine

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6
Q

what are the different classes of diuretics?

A

Osmotic diuretics
Carbonic anhydrase inhibitors
Loop diuretics
Thiazide diuretics
Potassium sparing diuretics

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7
Q

where do carbonic anhydrase inhibitors act and what do they do?

A

proximal tubules
inhibit bicarbonate reabsorption

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8
Q

where do osmotic diuretics act and what do they do?

A

proximal tubules, loop of henle and collecting duct

inhibit water and Na+ reabsorption

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9
Q

where do loop diuretics act and what do they do?

A

thick ascending limb of loop of henle

inhibition of Na+, K+ and Cl-

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10
Q

where do thiazides act and what do they do?

A

early distal tubule

inhibit Na+, Cl- co-transport

loss of Na+, increase of Ca2+

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11
Q

where do potassium sparing diuretics act and what do they do?

A

late distal tubule and collecting duct

inhibit Na+ reabsorption and K+ secretion

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12
Q

what are examples of osmotic diuretics?

A

mannitol, isosorbide, glycerine and urea

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13
Q

what is the result of osmotic diuresis?

A

blood volume decreased
large volume of dilute urine produced

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14
Q

why is mannitol the osmotic diuretic of choice?

A

1) it is inherently non-toxic
2) it is freely filtered
3) it is non-reabsorbable
4) it is not metabolised
5) the other agents may pass into cells to a limited extent

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15
Q

what are the adverse effects of osmotic diuretics?

A

cardiovascular toxicity immediately after injection - increases workload of the heart

don’t use on patients with congestive heart failure

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16
Q

what are some examples of carbonic anhydrase inhibitors?

A

Acetazolamide, Methazolamide

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17
Q

what are indications to give carbonic anhydrase inhibitors?

A

Raised intra-ocular pressure in open-angle glaucoma
Ocular hypertension when monotherapy is inadequate

18
Q

what are the side effects of carbonic anhydrase inhibitors?

A

Metabolic acidosis
Renal stones (Calcium and phosphate)
Renal potassium wasting (enhanced K+ secretion due to NaHCO3)

19
Q

what are examples of loop diuretics and what do they do?

A

furosamide, torasamide - act on the chloride-binding site and directly inhibit the carrier

20
Q

when would you prescribe a loop diuretic?

A

to treat water imbalances associated with congestive heart failure and kidney failure and pulmonary oedema

21
Q

what are the contraindications of loop diuretic?

A

Loop diuretics can interact negatively with other medications - NSAIDs reduce their effect & aminoglycoside antibiotics used with them can increase risk of hearing loss and kidney damage

Low potassium levels associated (hypokalemia) with loop diuretics increase the risk of digoxin toxicity, a medicine prescribed for congestive heart failure

22
Q

what are some examples of thiazide diuretics?

A

Hydrochlorothiazide, clorothiazide, bendroflumethiazide

23
Q

when would you prescribe a thiazide diuretic?

A

to treat high blood pressure and congestive heart failure, oedema arising due to heart failure, cirrhosis, chronic kidney failure and nephrotic syndrome

24
Q

when should you not give a thiazide?

A

if the patient has:
Hypotension
Gout
Renal failure
Lithium therapy
Hypokalemia
May worsen diabetes so a consideration but often still prescribed due to the benefits

chronic administration can also cause hyperglycaemia

25
Q

why do thiazides cause gout?

A

they reduce the clearance of uric acid since they compete for the same transporter, and therefore raise the levels of uric acid in the blood

26
Q

what is lost in use of thiazides?

A

Na, K and Cl

27
Q

what are the 2 types of K+ sparing diuretics?

A

aldosterone antagonists
Na+ channel inhibitors

28
Q

when would you use a K+ sparing diuretic?

A

usally in combination with thiazides and loops to reduce K+ loss when hypokalaemia is a concern

29
Q

what are examples of aldosterone antagonist diuretics?

A

spironolactone, eplerenone

these are K+ sparing diuretics

30
Q

what are examples of Na+ channel inhibitors?

A

amiloride, triamterene

these are K+ sparing diuretics

31
Q

what are the adverse affects of K+ sparing diuretics?

A

hyperkalaemia- can cause cardiac arrhythmias

shouldn’t give / take care alongside drugs that increase K+ levels e.g. ACEis

32
Q

what is the therapeutic index (TI)?

A

50% of toxic dose / 50% effective dose

33
Q

describe phase 1 of drug metabolism

A

usually through Cyp P450
- Oxidation, Reduction and Hydrolysis

this is where the majority of adverse drug reactions occur

34
Q

describe phase 2 of drug metabolism

A

conjugation (water soluble)
enables excretion in urine / bile

35
Q

what is a type A ADR?

A

Augmented pharmacologic effects
- dose dependent and predictable

e.g. ACEI / ARB causing D&V in pre-renal failure

36
Q

what is a type B ADR?

A

Bizarre effects (or idiosyncratic)
- dose independent and unpredictable

e.g. drug rashes, chloramphenicol causing bone marrow aplasia, halothane causing hepatic necrosis

37
Q

what are the 3 types of type A ADRs?

A

Drug-drug interactions

Drug-disease interactions

Drug-food interactions

38
Q

what is a type C ADR?

A

chronic effects- due to prolonged use of a drug

e.g. steroids causing cushing’s or osteoporosis, beta-blockers causing diabetes, NSAIDs causing hypertension

39
Q

what is a type D ADR?

A

delayed- can be many years after treatment

e.g. secondary malignancy post chemotherapy, craniofacial abnormalities in children in those taking isotretinoin who get pregnant (up to 1 month post treatment)

40
Q

what is a type E ADR?

A

end of treatment- rebound effects due to abrupt withdrawal of treatment

e.g. beta-blocker withdrawal causing angina, steroid withdrawal causing addisonian crisis

renal (23 decks)

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