pharmacology of CKD Flashcards
what is the MOA for statins?
selective, competitive inhibitor for hydroxymethylglutaryl-CoA reductase
(converts HMG-CoA to mevalonate in cholesterol synthesis)
reducing hepatic cholesterol synthesis causes an upregulation of LDL-receptors and increased hepatic uptake of LDL-cholesterol from the circulation
what is the drug target for statins?
hydroxymethylglutaryl-CoA reductase (HMG-CoA reductase)
what are the main side effects of statins?
muscle toxicity risk
constipation/diarrhoea/general GI effects
what should patients on statins be followed up for?
hyperkalaemia
acute renal failure
MOA of aspirin
irreversible inactivation of COX
prevents arachnidonic acid oxidation to prostaglandins
reduction of thromboxane A2 in platelets reduces aggregation
PGE2 reduction reduces sensation of pain (at sensory neurones) and decreases fever (in brain)
aspirin drug target
cycloxygenase enzyme
side effects of aspirin
dyspepsia
haemorrhage
what precautions should be taken into account when prescribing aspirin?
avoid greater than 160mg in elderly
coadminister PPI if peptic ulcer PMH
MOA trimethoprim
direct competitor of dihydrofolate reductase in bacteria
inhibits reduction of dihydrofolic acid - tetrahydrofolic acid (active) which is required for synthesising purines for DNA/protein production
drug target for trimethoprim
dihydrofolate reductase in bacteria
side effects of trimethoprim?
diarrhoea
skin reactions
what should be monitored when administrating trimethoprim?
folate levels
serum electrolytes - hyperkalaemia
MOA of gentamicin
binds to bacterial 30s ribosomal subunit
disturbs translation of mRNA leading to formation of dysfunctional proteins
drug target gentamicin
30s ribosomal subunit
side effects gentamicin
ototoxicity
nephrotoxicity
why is gentamicin ineffective against anaerobic bacteria?
can pass through gram -ve cell membrane in an oxygen dependent manner
things to take into account when prescribing for patient with reduced renal function
may the drug damage the kidney - e.g ibuprofen
is the drug properly eliminated by the kidney - e.g morphine metformin warfarin
what treatment should always be initiated for CKD regardless of cause
BP control to slow CKD progression
proteinuria in CKD
marker of glomerular dysfunction
and is damaging itself
interventions for proteinuria
ACEi/ARB
SGLT-2 inhibitors
salt restriction
stop other BP meds if ACEi reduces bp too low
trimethoprim messes with what calculation and why
GFR
inhibits active secretion of creatinine so breaks the link between GFR and serum creatinine
