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27 Cards in this Set

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Dihydropyridines (Amlodipine and Nifedipine)
Block Ca in vascular peripheral arterioles: Decrease PVR
Do not affect nodal conduction
*Good for angina
Verapamil Contraindication
LV Dysfunction- can cause heart failure in patients with low cardiac reserve
CCB Side Effects
Hypotension
Cardiac depression
Headache
Flushing
Constipation
*Nifedipine: Tachycardia and Edema
CCB Drug Interactions
Verapamil/Diltiazem and B Blocker: Marked bradycardia and conduction blockade
Verapamil/Diltiazem and Digoxin: conduction blockade
Amlodipine and ACE-I reduced CV events- good combo!
CCB Indications
Low renin hypertension (AA and elderly)
Isolated systolic hypertension (elderly)
B Blocker MOA- Heart, Vessels, Kidney
Heart: Prevent NE from binding receptor and increasing cAMP so ultimately Ca can't come in and myosin can't form crossbridges
Vessels: cAMP has opposite effects leading to dilation so the blockade actually vasoconstricts
Kidney: Blocks receptor leading to decreased renin production
Propranolol
Nonselective antagonist of B1 and B2
SEs: Bronchial constriction, acute withdrawl syndrome, increased lipids, glucose intolerance
*Caution in patients with diabetes or hyperlipidemia
B Blocker Indications
Mild and moderate hypertension
Patients on vasodilators to prevent reflex tachycardia
Patients with underlying heart disease (CHF, Ischemia, MI)
ACE-I
Inhibits the formation of AngII so there is no Aldo activation and Na retention, vasodilation of vessels and blocked Bradykinin degradation
ACE-Is
Enalapril- renal excretion
Ramipril- Quick
Lisinopril- give once daily
Captopril- taste changes
ACE-I SEs and CIs
SEs: Hypotension, hyperkalemia, angioedema (AA) due to bradykinin, cough, rash, taste change
CIs: K sparing diuretics, many AAs, Pregnancy (slows cell prolif.)
ARB: Losartan
AT1 receptor: vasoconstriction, SNS activation, Na/H2O retention, cell proliferation
SEs: some angioedema, dizziness
CI: pregnancy
ACE/ARB Indications
Heart failure, renal disease, *diabetes
A-1 Blockers: -zosins
Peripheral A1 blockers
Bind NE released from nerve terminals
Decrease vascular tone and PVR
Prazosin- SEs of dizziness, HA, drowsiness, first dose phenom. of orthostatic htn
Doxazosin and Terazosin- Longer T1/2 and used for BPH due to relaxing of vascular SM
Guanethidine
Enters nerve terminals via NE transporter and depletes NE stores in vessicles
Acts as a false NT
Reserpine
Blocks transport of dopamine into storage granules
Acts centrally and peripherally
SEs of Guanethidine and Reserpine
Orthostatic hypotension, depression, congestion, bradycardia, impotence, diarrhea, salt and water retention
Guanethidine and Reserpine Drug Interactions
Drugs that alter the amine pump: MOAIs, Tricyclic antidepressants, Ephedrine, Amphetamines, Phenothiazines
*These agents could also cause htn after chronic use of guanethidine due to receptor hypersensitivity
**Both are LAST RESORT drugs for refractory htn
Central A2 Agonists
A2 acts to stimulate PNS and decrease SNS
Agonists are methyldopa and clonidine
Peripheral a2 cause vasoconstriction (give high IV dose to get this effect)
Clonidine
Central A2 agonist
Transdermal patch administration
SEs: dry mouth, drowsiness, dizziness
Useful in diagnosis of pheochromocytoma (<500pg/ml if tumor free)
Tricyclic antidepressants can reverse its anti-htn effects
Methyldopa
SEs: Sedation, dry mouth, dizziness, sodium retention, orthostatic htn, and hemolytic anemia (if long use)
First choice for htn of pregancy
Clonidine and Methyldopa Drug Interactions
Tricyclic antidepressants prevent the anti-htn effect
Barbiturates reduce efficacy through hepatic enzyme induction
MOAIs when co-administered produce htn and CNS stimulation
Hydralazine
Vasodilator
Direct action on arterioles via Ca
Stored in arterial wall so prolonged action
SEs: Reflex tach, Na/H20 retention, headache, nausea, dizziness, Lupus syndrome
Minoxidil
Vasodilator
Activates K channels: hyperpolarizes and relaxes cell
Must be metabolized by liver into active form
SEs: is hydralazine w/o lupus syndrome, hypertrichosis
*treats severe htn and must be given with sympatholytic and diuretic
Sodium Nitroprusside
For Htn Crisis
NO dilates vascular SM
Given IV- effects stop when IV stops
Toxic metabolite cleared by kidneys
SEs: rebound htn, tolerance
Diazoxide
Vasodilator of arterial muscle only, no effect on venous system
Activates K channels
Labetalol/Carvedilol
Mix of A/B receptor antagonists
Labetolol 1:3 selectivity A:B
Carvedilol 1:10 selectivity A:B
*Decrease TPR without reflex tach
Useful for pts with pheochromocytoma