Pharmacology Flashcards
3 types of immunosuppression
calcinurin inhibitors (cyclosporin), purine synthesis blockers (azathioprine), steroids
how do calcineurin inhibitors work
act by inhibiting T helper cells (hence NK cells and cytotoxic T cell activation, dec cytokine release)
purine synthesis blockers work how?
block purine synthesis which leads to suppression of B-cell proliferation
which drug cannot be mixed with azathioprine
azathioprine + allopurinol
steroids act ___ ______ to suppress activity to T and B cells
non-selectively
what are 5 diuretics
CAi, loop diuretics, thiazide, K-sparing, osmotic
what is an example of CAi
acetazolamide
how CAi work
in proximal convoluted tubule- Na+ is exchanged for H+ via CA. this is inhibited so inc excretion of HCO3-, Na+, K+, H2O
what are CAi used for
following eye surgery, prophylaxis of altitude sickness
side effects of CAi
alkaline diuresis hence metabolic acidosis
examples and method of effect of loop diuretics
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
what are loop diuretics used for
reduce NaCl, H2O overload, acute pulmonary oedema, kidney failure, ascites, nephrotic syndrome
risks of loops
hypokalaemia, hypocalcaemia, hypomagnaseamia
hyperuricaemia
inc digoxin toxicity
metabolic alkalosis, hypovolaemia, hypotension
example of thiazide diuretics and how they work
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
thiazides are used for…
hypertension, mild heart failure, severe resistant oedema, renal stones, diabetes insipidus
side effects of thiazides
hypokalaemia*, hypoMg
metabolic alkalosis, hypovolaemia & hypotension
hyperuricaemia
male sexual dysfunction**
K-sparing diuretics examples and mode of action
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
when to give K-sparing diuretics
HF*, 1y hyperaldosteronism, resistant renal HT, 2y hyperaldosteronism
main comp of K-sparing diuretics
hyperkalaemia
example of osmotic diuretics and how they work
mannitol- enter nephron via glom.filt but not reabsorbed- act to prevent reabsorption of water and dec Na reabsorption too (from filtrate to plasma)
when are osmotic diuretics given
prevention of acute hypovolaemic renal failure**, acutely raised ICP/ IOP
vasopressin agonist is…
desmopressin- synthetic analogue of VP with V2r selectivity inc reabsorption of H2O
what is vasopressin agonist used for
neurogenic diabetes insipidus (no VP secretion from pituitary)
Vaptans examples and mode of action
conviptan, competitive antagonist of VP receptors aka. block V2 causing excretion of H2O w/o accompanying Na (inc plasma Na+)
vaptans used for…
HF, hypervolaemia, hyponatraemia, SIADH
SGLT2 inhibitors…
canagliflozin- blocks Na/glucose co-transporter so glucose eliminated via urine
used for: T2D
SE: thrush
uricosuric agents…
probenecid- blocks urate réabsorption in proximal tubule- GOUT
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
diuretics all work at the ____ membrane
apical
how do diuretics enter cell
via
- glomerular filtrate
- secretion via transport process in proximal tubule
what are the transport processes used by diuretics
- organic anion transporters: acidic drugs (thiazides/loop)- by diffusion or by exchange with a-KG
- organic cation transporters: basic drugs- basolateral membrane enter cell via diffusion, apical enter cell via MRP1 or OC+/H+ anti-transporters
what produces prostaglandins
COX1 & COX2
what is the action of prostaglandins (PGE2 and PGI2) in the kidneys
affect renal blood flow (local vasodilators) hence affect GFR
how do NSAIDs affect prostaglandins
inhibit COXs hence may precipitate renal failure in pt dependent on prostaglandin vasodilatory effect
what is the triple whammy effect
ACEi/ARBs + diuretics + NSAIDs
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
which drug reaction type is the most dangerous
Type B- drug rashes, bone marrow aplasia, hepatic necrosis
