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
Q

vaptans used for…

A

HF, hypervolaemia, hyponatraemia, SIADH

26
Q

SGLT2 inhibitors…

A

canagliflozin- blocks Na/glucose co-transporter so glucose eliminated via urine
used for: T2D
SE: thrush

27
Q

uricosuric agents…

A

probenecid- blocks urate réabsorption in proximal tubule- GOUT

28
Q

oedema is…

A

the imbalance between rate of formation and absorption of IF- usually caused by any disease that inc capillary pressure or dec oncotic pressure

29
Q

diuretics all work at the ____ membrane

A

apical

30
Q

how do diuretics enter cell

A

via

  1. glomerular filtrate
  2. secretion via transport process in proximal tubule
31
Q

what are the transport processes used by diuretics

A
  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
Q

what produces prostaglandins

A

COX1 & COX2

33
Q

what is the action of prostaglandins (PGE2 and PGI2) in the kidneys

A

affect renal blood flow (local vasodilators) hence affect GFR

34
Q

how do NSAIDs affect prostaglandins

A

inhibit COXs hence may precipitate renal failure in pt dependent on prostaglandin vasodilatory effect

35
Q

what is the triple whammy effect

A

ACEi/ARBs + diuretics + NSAIDs

36
Q

what are the different drug reaction types

A
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
Q

which drug reaction type is the most dangerous

A

Type B- drug rashes, bone marrow aplasia, hepatic necrosis