pharm new version Flashcards
(69 cards)
what are the side effetcs of calcium channel blockers
- hypotension ,
2, constipation - headaches
- peripheral oedema
ccb’s: amlodipine (vasoselective), verapamil and diltiazem (cardio-selective)
what is baxdrostat
selective inhibitor of aldosterone synthase
what is aprocitentan
endothelin antagonist (PRECISION trial)
what drugs can be used in pregnancy (for hypertension)
labetalol (combined non selective B receptor antagonist + a1 blocker)
nifedipine (dihydropyridine - calcium channel blocker) but shorter half life than amlodipine
what are the significant absolute contradincations when considering anti-hypertensives?
- ACEi and ARB: hyperK (> 5.5) and pregnancy
- bilateral severe renal artery stenosis - diuretics: active gout (hyperuricaemia)
- beta-blockers: acute asthma excerbation
- beta-blockers and calcium channel blockers: bradycardia, heart block.
which alpha blocker cna produce parkinsonism
methydopa
May produce Parkinsonism
Hyperprolactinaemia, gynaecomastia and rarely, galactorrhea
Hepatotoxicity uncommon (5% of patients have abnormal LFTs)
Haemolytic anaemia
why are beta blockers useful in hypertension
Inhibits renin release from juxtaglomerular apparatus (stimulated by the sympathetic nervous system via B1 receptors)
what is sacubitril
Nephrilysin inhibitors, e.g. Sacubitril act by inhibiting Neprilysin, which is responsible for the breakdown of natriutic peptide into its inactive forms. Sacubitril acts by increasing levels of natriuretic peptide, increasing its effect, which is natriuesis (increasing Na+ and water excretion), vasodilation (decreasing TPR and afterload) and inhibiton of the RAAS system.
what are the 4 classes in the vaughan-williams classification
- sodium channel blocers
- beta blockers
- potassium channel blockers
- calcium channel blocers
what class is quinidine
class Ia
Blocks Na+ conductance
Blocks multiple K+ channels
Prolongs AP, vagal inhibition (increasing HR)
Recurrent ventricular arrhythmias
what class is lignocaine
IB
Blocks cardiac Na+ channels
Ventricular arrhythmias post-MI
C/I: AV block
SE: CNS side effects *
what class is flecainide
Flecainide is Ic
Blocks Na+ channels
Shortens AP
Supraventricular arrhythmia including AFib.
C/I: LV dysfunction, heart failure
what is the ABC approach to Afib
AFib approach: ABC
1. Anticoagulation and Avoid stroke
2. Better symptom control (rate and rhythm control)
3. CVS risk factors and concomitant disease management.
what drugs can cause brady cardia
Pharmacodynamic:
Beta Blockers + Digoxin + Verapamil = Heart Block
Beta Blockers + Verapamil - negative chronotropes (reduce heart rate) and negative inotropes (decrease myocardial contractility). When used together, they can lead to excessive suppression of heart rate and cardiac contractility, causing bradycardia, heart block, or even heart failure in susceptible patients.
Pharmacokinetics:
Verapamil + Digoxin - Verapamil inhibits the P-glycoprotein (P-gp) transporter, a protein that plays a crucial role in the elimination of digoxin from the body. When verapamil is administered, it can reduce digoxin clearance, leading to increased digoxin plasma levels and a higher risk of digoxin toxicity (manifesting as gastrointestinal symptoms, arrhythmias, or CNS disturbances).
side effects of amiordarone
CROHN-DE
CVS - brady, hypotension, qtc prolongations and arrhythmias (torsades)
Resp - pulmonary fibrosis
Ocular - corneal microdeposits
Hepatic - enzyme inhibition, abnormal LFTs
Neuromuscular - peripheral neuropath
Derm - photosensitivity
Endocrine - hypo or hyperthyroidism
what drug interaactions does amiordaone have
CYP enzyme inhibitor: could increase warfarin (CYP 2C9) concentration
P-glycoprotein inhibitor: increase digoxin (PgP) uptake and concentration
Hence interaction with digoxin may be PK and PD. (Amiordarone produces bradycardia, so does digoxin)
what CYP can amiodarone inhibit
2C9
what are the 2 most impt side effects of all statins
- hepatotoxicity
- most likely in the first few months
- monitor LFTs, basline and while on treatment
- if AST and ALT > x3 of ULN, stop/avoid the statin - myopathy which can progress to rhabdomyolyisis
- presenting as muscle pain or weakness
- muscle specific CK levels rise, can be up to x5-10 ULN, so monitor
- AKI possible
- if symptoms resolve, consider rechallengign with lower dose or alternate statin
what enzyme does statins inhibit
hmg-coa reductase
Inhibits HMG-coA reductase (cholesterol synthesis), causes
1. Activation of SREBP, upregulation of LDL receptors
2. Depletion of cholesterol supply, reduction of VLDL synthesis
what statin is not metabolised by CYP450
pravastatinwh
which is the preferred stattin of choice
atorvastatin
what receptor does Ezetimibe act on
NPC1L1 (enterocyte absorption of cholesterol)
what receptors does cholestyramine inhibit
trick question
it binds to bile acids and salts in the small intestine, and the resin/bile acid complex is excreted in the poop, lowering bile acid concentraton.
1. liver uptakes more cholesterol containing LDL particles to make more bile, hence decrease blood LDL levels
2. upregulation of LDL receptors
which lipid therapy agent itnerferes with absorptio of fat soluble vitamins
cholestyramine
Interferes with absorption of fat-soluble vitamins, thyroxine, thiazide diuretics, digoxin, warfarin, beta blocks, therefore taken at least 1h before or after 4-6h after taking the resin
