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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what promotes natriuresis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what inhibits natriuresis?

A

inhibited (sodium is conserved) by chemicals such as aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the different classes of diuretics?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A

proximal tubules
inhibit bicarbonate reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are examples of osmotic diuretics?

A

mannitol, isosorbide, glycerine and urea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the result of osmotic diuresis?

A

blood volume decreased
large volume of dilute urine produced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are some examples of carbonic anhydrase inhibitors?

A

Acetazolamide, Methazolamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
why do thiazides cause gout?
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
what is lost in use of thiazides?
Na, K and Cl
27
what are the 2 types of K+ sparing diuretics?
aldosterone antagonists Na+ channel inhibitors
28
when would you use a K+ sparing diuretic?
usally in combination with thiazides and loops to reduce K+ loss when hypokalaemia is a concern
29
what are examples of aldosterone antagonist diuretics?
spironolactone, eplerenone these are K+ sparing diuretics
30
what are examples of Na+ channel inhibitors?
amiloride, triamterene these are K+ sparing diuretics
31
what are the adverse affects of K+ sparing diuretics?
hyperkalaemia- can cause cardiac arrhythmias shouldn't give / take care alongside drugs that increase K+ levels e.g. ACEis
32
what is the therapeutic index (TI)?
50% of toxic dose / 50% effective dose
33
describe phase 1 of drug metabolism
usually through Cyp P450 - Oxidation, Reduction and Hydrolysis this is where the majority of adverse drug reactions occur
34
describe phase 2 of drug metabolism
conjugation (water soluble) enables excretion in urine / bile
35
what is a type A ADR?
Augmented pharmacologic effects - dose dependent and predictable e.g. ACEI / ARB causing D&V in pre-renal failure
36
what is a type B ADR?
Bizarre effects (or idiosyncratic) - dose independent and unpredictable e.g. drug rashes, chloramphenicol causing bone marrow aplasia, halothane causing hepatic necrosis
37
what are the 3 types of type A ADRs?
Drug-drug interactions Drug-disease interactions Drug-food interactions
38
what is a type C ADR?
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
what is a type D ADR?
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
what is a type E ADR?
end of treatment- rebound effects due to abrupt withdrawal of treatment e.g. beta-blocker withdrawal causing angina, steroid withdrawal causing addisonian crisis