Anti-hypertensives I Flashcards
Which anti-hypertensive drugs work in the indiciated areas of the body below?
Sympatholytics (i.e. alpha receptor agonists): clonidine
Drugs that:
- Decrease cardiac output: Beta blockers (propanolol, metaprolol etc); Non-dihydropyridine CCBs
- Vascular smooth ms dilation: (a lot, see below)
- Na+/water elimination: RAAS inhibitors, diuretics
Study this slide
What is the effect of pre-synaptic adrenergic agonists on NE release?
Presynaptic adrenergic agonists: referring to alpha 2 agonists >> cause decreased NE release
What is the effect of post-synaptic antagonists on hypertension regulation?
Post synaptic antagonists: alpha and beta blockers >> decrease HTN (various effects)
___ is a sympatholytic (alpha 2 agonist) drug that acts on A2 receptors in the CNS to reduce HR and BP
Clonidine is a sympatholytic (alpha 2 agonist) drug that acts on A2 receptors in the CNS to reduce HR and BP
**also used in neuropsychiatric disorders, and can cause drowsiness and sedation**
Once started, clonidine should not be abruptly discontinued. Why is that?
Abrupt discontinuation results in withdrawal syndrome: rebound hypertension and tachycardia (can be life-threatening)
___, ___ and ___ are anti-HTNs used in pregnancy
Methyldopa, nifedipine and labetalol are anti-HTNs used in pregnancy
How do Beta blockers work?
Beta blockers: basically block increased intracellular Ca2+ and subsequent contractility by blocking the beta receptors
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Why are the effects of beta blockers not long term?
What is unique about the beta blocker Nebivolol?
Effects aren’t long term b/c there are compensatory responses in peripheral vasculature
Nebivolol promotes NO release (which you will recall is a potent vasodilator)
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**know that non selective beta blockers aren’t first line for HTN because they also beta 2 effects**
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What are the side effects of beta blockers in pts with: restrictive airway disease (COPD,asthma), peripheral vascular disease, Type 2 diabetes mellitus?
Restrictive airway disease: asthma or COPD exacerbation
PVD: unopposed alpha 1 vasoconstriction (can worsen symptoms)
Diabetes mellitus: Hypoglycemia
Beta blockers are contraindicated in which conditions? (5)
(Symptomatic) Bradycardia
(Symptomatic) Hypotension
(Severe) restrictive airway disease
Cardiogenic shock (remember, volume ok but pump is broken)
2nd or 3rd degree heart block
Describe the mechanism of action of calcium channel blockers
CCBs block L type calcium channels on vasc sm muscle, cardiac myocytes or SA/AV nodal cells
What are the effects of CCBs in the cells indicated below?
**see below**
Which CCBs would you use for the scenarios below?
**see below**
What are the classes of calcium channel blockers?
Dihyropyridines - ipine- drugs
Non-dihydropyridines
What are the 2 main Dihydropyridine CCBs?
**Fill in the blanks**
Amlodipine and Nifedipine (remember the big knife in sketchy. Can be used in pregaz)
What are the 2 main non-dihydropyridines?
Diltiazem and Verapamil (has the most cardio-depressive effects)
What are the adverse effects of dihydropyridines (3)?
What are the adverse effects of non-dihydropyridines (3)?
**see below**
Describe the mechanism of action of nitrovasodilators
**remember that NO is a vasodilator thru decreased calcium for muscle contraction >> vasodilation**
What is a potent nitrovasodilator used for HTN treatment?
Na+ nitroprusside
What are the effects low vs high NO concentrations/i.e which vessels (large/small/veins/arteries) get dilated at these concentrations?
- Low NO concentrations vasodilate veins and coronary arteries
- High NO concentrations are required for vasodilation of large arteries
How does nitroglycerin work as a vasodilator?
Nitroglycerin is broken down by Aldehyde dehydrogenase-2 first and then it forms NO (so indirectly contributes NO, compared to Na+-nitropusside which directly gives NO)
Why wouldn’t you use a PDE inhibitor concurrently with a nitrovasodilator?
Phosphodiesterase normally breaks down cGMP. If you use a drug that inhibits PDE at the same time as using a nitrovasodilator, that’ll cause severe hyPOtension
What are the clinical indications for nitrates?
Chest pain/angina
Acute coronary syndromes
Acute decompensated heart failure
(mainly nitroglycerin + long acting nitrates are indicated in BP)
A challenge with using nitrates for BP is the development of nitrate tolerance. What are 4 mechanisms thru which tolerance develops?
**see below**
What are 3 strategies to combat nitrate tolerance?
Nitrate-free interval (6-8 hours “off” each day)
Concomitant use of an antioxidant (e.g., hydralazine)
Concomitant use of neurohormonal antagonists
**think about how tolerance develops. your interventions should be addressing that**
What is the mechanism by which sodium nitroprusside has adverse effects?
Major adverse effect on Na+-nitropusside is mediated by accumulation of toxic metabolites
Sodium nitroprusside is broken down to cyanide (toxic) which is conjugated by the liver to form thiocynate (also toxic) which is then renally excreted. Pts with liver or kidney disease should not be on nitrates for extended periods for this reason.
**can be fixed with Hydroxycobalamin/Na-thiosulfate/nitrites**
