Pharmacology Flashcards

1
Q

3 types of immunosuppression

A

calcinurin inhibitors (cyclosporin), purine synthesis blockers (azathioprine), steroids

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2
Q

how do calcineurin inhibitors work

A

act by inhibiting T helper cells (hence NK cells and cytotoxic T cell activation, dec cytokine release)

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3
Q

purine synthesis blockers work how?

A

block purine synthesis which leads to suppression of B-cell proliferation

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4
Q

which drug cannot be mixed with azathioprine

A

azathioprine + allopurinol

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5
Q

steroids act ___ ______ to suppress activity to T and B cells

A

non-selectively

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6
Q

what are 5 diuretics

A

CAi, loop diuretics, thiazide, K-sparing, osmotic

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7
Q

what is an example of CAi

A

acetazolamide

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8
Q

how CAi work

A

in proximal convoluted tubule- Na+ is exchanged for H+ via CA. this is inhibited so inc excretion of HCO3-, Na+, K+, H2O

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9
Q

what are CAi used for

A

following eye surgery, prophylaxis of altitude sickness

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10
Q

side effects of CAi

A

alkaline diuresis hence metabolic acidosis

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11
Q

examples and method of effect of loop diuretics

A

furosemide- thick ascending loop of henle. blocks Na/K/Cl co-transporter via Cl- site preventing dilution (loss of sediment) of tubular fluid preventing dilution of filtrate. Hence more Na+ reaches the distal nephron- less ADH secreted so more H2O stays in the filtrate and is secreted as urine

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12
Q

what are loop diuretics used for

A

reduce NaCl, H2O overload, acute pulmonary oedema, kidney failure, ascites, nephrotic syndrome

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13
Q

risks of loops

A

hypokalaemia, hypocalcaemia, hypomagnaseamia

hyperuricaemia

inc digoxin toxicity

metabolic alkalosis, hypovolaemia, hypotension

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14
Q

example of thiazide diuretics and how they work

A

bendroflumethazide- milder diuresis that block Na/Cl co-transporter in distal convoluted tubule by binding to Cl- site preventing dilution of filtrate, ^ load of Na+ reaching collecting tubules (less ADH), inc Ca2+ reabsorption

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15
Q

thiazides are used for…

A

hypertension, mild heart failure, severe resistant oedema, renal stones, diabetes insipidus

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16
Q

side effects of thiazides

A

hypokalaemia*, hypoMg
metabolic alkalosis, hypovolaemia & hypotension

hyperuricaemia

male sexual dysfunction**

17
Q

K-sparing diuretics examples and mode of action

A

amiloridine, spironolocatone- aldosterone antagonists (Na/K exchange in collecting tubules blocked). sprionolactone competes with aldosterone for intracellular receptors causing dec gene expression/ synthesis of proteins that activate Na+ channels

18
Q

when to give K-sparing diuretics

A

HF*, 1y hyperaldosteronism, resistant renal HT, 2y hyperaldosteronism

19
Q

main comp of K-sparing diuretics

A

hyperkalaemia

20
Q

example of osmotic diuretics and how they work

A

mannitol- enter nephron via glom.filt but not reabsorbed- act to prevent reabsorption of water and dec Na reabsorption too (from filtrate to plasma)

21
Q

when are osmotic diuretics given

A

prevention of acute hypovolaemic renal failure**, acutely raised ICP/ IOP

22
Q

vasopressin agonist is…

A

desmopressin- synthetic analogue of VP with V2r selectivity inc reabsorption of H2O

23
Q

what is vasopressin agonist used for

A

neurogenic diabetes insipidus (no VP secretion from pituitary)

24
Q

Vaptans examples and mode of action

A

conviptan, competitive antagonist of VP receptors aka. block V2 causing excretion of H2O w/o accompanying Na (inc plasma Na+)

25
vaptans used for...
HF, hypervolaemia, hyponatraemia, SIADH
26
SGLT2 inhibitors...
canagliflozin- blocks Na/glucose co-transporter so glucose eliminated via urine used for: T2D SE: thrush
27
uricosuric agents...
probenecid- blocks urate réabsorption in proximal tubule- GOUT
28
oedema is...
the imbalance between rate of formation and absorption of IF- usually caused by any disease that inc capillary pressure or dec oncotic pressure
29
diuretics all work at the ____ membrane
apical
30
how do diuretics enter cell
via 1. glomerular filtrate 2. secretion via transport process in proximal tubule
31
what are the transport processes used by diuretics
1. organic anion transporters: acidic drugs (thiazides/loop)- by diffusion or by exchange with a-KG 2. organic cation transporters: basic drugs- basolateral membrane enter cell via diffusion, apical enter cell via MRP1 or OC+/H+ anti-transporters
32
what produces prostaglandins
COX1 & COX2
33
what is the action of prostaglandins (PGE2 and PGI2) in the kidneys
affect renal blood flow (local vasodilators) hence affect GFR
34
how do NSAIDs affect prostaglandins
inhibit COXs hence may precipitate renal failure in pt dependent on prostaglandin vasodilatory effect
35
what is the triple whammy effect
ACEi/ARBs + diuretics + NSAIDs
36
what are the different drug reaction types
``` A: augmented pharmacological effect B: bizarre- dose dependent and unprecedented C: chronic effects D: delayed E: end of tx effects F: failure of therapy ```
37
which drug reaction type is the most dangerous
Type B- drug rashes, bone marrow aplasia, hepatic necrosis