General Flashcards

Question

Epinephrine [E]

Answer 1

Vasoconstrictor locally Increases HR and CO Mainly Beta receptors Increases: - -HR - -SV - -CO - -arrhythmias - -Coronary Blood flow - -Systolic arteriole pressure - -Mean arterial pressure - -Mean pulmonary blood pressure Widens Pulse pressure!! (ESPECIALLY low dose given subcutaneously) *at low doses, may DECREASE BP (so on time curve, pressure goes up initially, but as drug concentration declines the pressure goes below normal!) SA node and AV node (not really ventricular tissue) Vasodilation: --skeletal muscle Vasoconstriction: - -cutaneous - -renal (so incr renin secretion & dec BF) Increases: - -pulmonary pressures (arteries and veins) - -Coronary BF IV, inhaled, IM, subcutaneous (allergies) NOT oral ``` side effects: Cerebral hemorrhage (esp w/ non-selective BB) ``` Ventricular arrhythmias Angina Indications: emergency relief of anaphylaxis vasoconstrictor w/ local anasthetics Restoring cardiac rhythm in pts w/ cardiac arrest

Answer 2

renal clearance

Answer 3

Class Ic antiarrhythmic potent and long-acting CAST trial DELAYED pro-arrhythmic side effects Only life-threatening arrhythmias typically treated Contraindicated in STRUCTURAL HEART DISEASE!!!

Answer 4

Pure Class III antiarrhythmic IV only acute termination of a fib or atrail flutter side effects: torsades/transient assystole

Answer 5

non-selective beta + a1 antagonist given IV for HTN emergencies

Answer 6

Class Ib antiarrhythmic Na channel blocker binds to open and inactivated Na channels RAPID! especially good b/c no effect on normal HR, but good for tach NOT effective for atrial arrhythmias IV (b/c hepatic metab.)

Answer 7

a lysine derivative of enalaprilat; renoprotective

Answer 8

prodrug --One metabolite, EXP 3174, has increased potency as an AT1 receptor antagonist. • Competitive antagonist of thromboxane A2 receptor; attenuates platelet aggregation. * Unique in that it increases uric acid urinary excretion (Uricosuric). HTN gout treatment!! * Inhibits CYP activity. Short half-life ARB that increases excretion of uric acid ARB metabolized by CYP3A4 Side effects: Hypotension • In hypovolemic and/or Na-depleted patients. Hyperkalemia • Especially in renal insufficiency, or in patients using K-sparing diuretics or K supplements. Hepatic dysfunction • Reported with Losartan and Valsartan. Fetotoxicity • Like ACE inhibitors should not be given to pregnant women.

Answer 9

.Centrally acting alpha-2a adrenergic agonist agonists of postsynaptic a2-adrenoreceptors in rostral ventrolateral medulla (RVLM) decreases sympathetic outflow from RVLM to heart and vessels decrease in PVR and HR converted into alpha-methyl NE (dopamine-->NE, but w/ methyl group, it is a false transmitter) a2a agonist in RVLM decreases sympathetic tone, reduction in BP due to decrease in TPR obsolete pre-eclampsia Side effects: sedation, sleep disturbances, erectile sexual dysfunction Na/H2O retention lactation due to increased prolactin secretion Side effects: - -sedation - -Positive coombs test - -prodrug converted to a-methyl-NE

Answer 10

thiazide-like diuretic CHF

Answer 11

CHF treatment 50-100-fold more selective in blocking β1-adrenergic receptors “Cardioselective agents” some MSA, cardioselective, lipid soluble

Answer 12

oral open K channels-->hyperpolarization of VSM Relaxes ARTERIOLE smooth muscle by opening K+-ATPase channels (dilates arteries, NOT veins) Causes reflex tachycardia and strong renin release!! (so take w/ BB and diuretics long-term) Causes Hirsutism (increases hair...) Rogaine!...male-pattern baldness

Answer 13

First generation BB

Answer 14

drugs w/ NO mediated vasodilation Highly β1 selective; devoid of ISA, membrane stabilizing activities, and α1 blocking activities. * Has antioxidant activity/neutral to favorable effects on both carb and lipid metabolism. * decreased BP by decreasing HR and peripheral vascular resistance. * Significantly increases stroke volume, maintains CO and systemic blood flow. Used in HTN but NOT CHF • Drug of choice for HTN with metabolic syndrome!!!

Answer 15

arterial vasodilation! ``` Coronary vasodilation Reduced afterload (arterial) ``` short acting!! great for relaxing coronaries not used for HTN b/c reflexively activate SNS, increasing HR

Answer 16

organic nitrate ester reductase -->NO-->GC-->cGMP-->PKG-->SM relaxation Decreases demand and increases supply! increase NO --vasodilates--> decreases afterload --venodilates--> decreases preload (so decreases contractility via Frank-Starling) decreased preload coronary vasodilation (prevents or reverses vasospasm) BP: unchanged/slight decrease HR: unchanged or slight increase Pulmonary vascular resistance: decreased CO: reduced (slightly) ``` mucosal --sublingual --nasal sprays oral transdermal paste IV ``` ``` High doses... --extreme vasodilation ....hypotension ....reflexive increase in HR and contractility (worsens angina!!!) ``` transient headache (meningeal arteries dilated until tolerance) rash ***Drug interaction*** --Sildenafil (Viagra) [Type 5 PDE inhibitors] (increases cGMP by decreasing metabolism) Rapidly metabolized (short-lived) ok and beneficial for exertional angina --can take it when they need it challenge for otherstolerance (avoided by "nitrate free" interval each day... i.e. remove patch at night) anginal rebound Do Not suddenly interrupt IV nitroglycerin in unstable angina...overlap w/ oral or patch form (coronary vasospasm has been observed after abrupt stop) ``` coronary vasodilation reduced preload (venous) reduced afterload (arterial) ```

Answer 17

Pro-drug that's broken down into NO -->increase in cGMP--> muscle relaxation active in arterioles AND mainly veins!!! Awesome for HF treatment! Decreases CO in normal pts Increases CO in pts w/ Left ventricular HF b/c decreases afterload (along w/ preload) Very short half-life, given w/ pump

Answer 18

Increases BP Mainly alpha receptors Increases: - -SV - -arrhythmias - -coronary blood flow - -Systolic arteriole pressure - -diastolic arteriole pressure - -mean arteriole pressure - -Mean pulmonary pressure

Answer 19

First generation BB

Answer 20

a1>a2 noncompetitive (covalent) LONG-LASTING alpha1 and alpha 2 antagonist a2 antagonism can inc. presynaptic NE release...increase CO...tempering BP lowering action indications: sympathetic excess secondary to pheochromocytoma, Raynaud's phenomenon, frostbite, acrocyanosis ``` slow onset (several hours) long duration (3-4 days) ``` ``` side effects: sinus-tach nasal congestion drowsiness, fatigue, weakness... tachycardia...cardiac arrhythmias ```

Answer 21

a1=a2 short-acting competitive antagonist alpha1 and alpha 2 receptors DOSE DEPENDENCY!!!! small dose...greater effect on a2 receptors--> increase in CV force b/c increase release of NE (positive inotropic effect dominates...inc BP Large dose...greater effect on a1 receptors--> vasodilation and reduction BP Indications: pheochromocytoma and hypertensive emergency **postural hypotension reflex tachycardia that precipitates cardiac arrhythmias (these efffects severely limit use for essential HTN)

Answer 22

a1>>>>>>>>>a2 direct acting agonist Increases BP Alpha receptors systemic arteriole vasoconstriction--> - -increased systolic and diastolic pressures - -REFLEXIVE decrease in HR and CO IV, IM, SC control of hypotension, especially associated w/ regional or spinal anesthesia ``` adverse effects: angina anxiety hallucinations/psychosis HTN... ```

Answer 23

does not inhibit decrease renin release High ISA, some MSA, no cardioselectivity, lipid soluble Non-selective drugs with partial agonist activity. Decrease CO and HR less than other

Answer 24

``` a-1>>>>>>>>a-2 Most prominent (of A-blockers) first dose hypotension ``` antihypertensive (Monotherapy not recommended w/ any a1 blockers)

Answer 25

Class Ia antiarrhythmic Na channel blockers drug-induced lupus!!! hepatic acetylation and renal excretion IV acute control of atrial and vent arrhythmias/ short term treatment

Answer 26

Class Ic antiarrhythmic BB activity

Answer 27

decrease HR and contractility--> Decrease CO inhibit renin release (EXCEPT Pindolol) Decrease central sympathetic outflow (except for those w/ low lipid solubility) Decrease release of peripheral NE by inhibiting presynaptic beta adrenergic Especially useful in pts w/ high renin level HTN w/ chronic use... decrease CO and peripheral resistance and arterial pressure 1st and 2nd generation BBs: High renin HTN (young and caucasian) Non-selective BB that produces resting bradycardia and decrease HR during exercise --> hypotension membrane stabilizing activity: antiarrhythmic produces bronchospasm; contraindicated in asthmatics slow withdrawal of drug to prevent reflex tachycardia MSA, lipid soluble

Answer 28

prodrug, activated by deesterification Long half-life given once daily

Answer 29

novel metabolic modulator MOA: unknown partial fatty acid oxidase inhibitor--> increases glucose oxidation--> increased O2 utilization efficiency in heart No effect on HR or BP Indications: chronic stable angina in combination w/: - -amlodapine, - -BBs, or - -Nitrates will not relieve acute anginal attacks Pregnancy category C Expensive w/ only marginal benefit Contraindication: use w/ cyp3A inhibitors hepatic impairment

Answer 30

``` Inhibits VMAT (uptake 2) Depletes NE and 5-HT from neurons ``` Decreased sympathetic tone reduces TPR, CO, renin release, BP oral mild to moderate HTN Side effects: CNS effects (sedation and mental depression) gastric and duodenal ulcers Shouldn't be used in pts w/ Hx of depression

Answer 31

Class III K channel blocker w/ nonselective BB activity ``` contraindications: long QT renal insufficiency asthma/copd ... ```

Answer 32

a-1>>>>>>>a-2 treatment of symptoms of BPH, urinating and bladder emptying problems, etc. Also lower BP Treatment of choice for older men w/ HTN and prostate problems

Answer 33

competition w/ ACh ``` Side effects: Postural hypotension tachycardia arrhythmias Blurred/double vision asthma (secondary to histamine release) Dry mouth, constipation, paralytic ileus, N/V urinary retention impotence drowsiness, seizures, hallucinations, ```

Answer 34

minimal arterial vasodilation Negative chronotropic and inotropic effects (especialy verapamil!) More selective for heart, less selective for vessels --not as effective vasodilating Used as antiarrhythmic and antianginal rather than anti-HTN ***coronary artery dilators!!!! so help w/ angina!

Answer 35

first dose orthostatic hypotension sinus-tach (angina, palpitations), syncope, vertigo (b.c a2 receptors blocked...inc NE release) In HTN: advantages: - -improve lipid profile and insulin resistance - -good in physically active pts - -relieve urinary symptoms in BPH pts * *Prototypical pts: - -elderly pts w/ BPH and normal CV function - -young physically active pts - -African American pts w/ no success w/ other drugs disadvantages: - -not good as monotherapy - -increased incidence of HF Caution: --First dose Orthostatic HTN decreased TPR and BP relieve symptoms of BPH by relaxing muscles of bladder and prostate Increase HDL Lower LDL beneficial effect on insulin resistance First dose orthostatic hypotension common w/ short-acting drug **i.e. prazosin dizziness, vertigo, drowziness, palpitations

Answer 36

``` Best class for treatment of angina Decreases: --HR (in exercise) --contractility (in exercise) --afterload ``` Does NOT decrease: - -preload - -coronary vasospasm ``` Rationale for combining w/ nitrates: Reduces: --LVEDP --LV volume --dilates coronary arteries ``` BBs prevent reflex tachycardia and positive inotropic effect rationale for combining w/ DHPs - -prevent coronary vasospasm - -reduce systemic vascular resistance BBs prevent reflex tachycardia and positive inotropic effect Reduced HR Decreased contractility Reduced afterload (arterial) --indirect effect due to decreased renin release and some blockage of sympathetic outflow ``` In HTN: Advantages: --secondary protection in CAD --useful in HTN pts w/.... .......tachycardia .......high CO .......high renin .......hyperthyroidism .......migraine .......glaucoma .......stage fright --Bisoprolol=standard treatment w/ ACEI and diuretics (34% mortality benefit) ``` Disadvantages: - -less effective in elderly and AA - -multiple side effects and contraindications (especially 1st and 2nd generation BBs) - -Should not be discontinued abruptly BBs do not cause H20 and salt retention --so can be administered w/out diuretic But has additive antihypertensive effect when administered w/ diuretic ``` preferred in HTN of pts w/: MI ischemic heart disease HF hyperthyroidism migraines ``` treatment for: Sinus and AV arrhythmias open angle glaucoma anxiety Side effects: Cold extremities Bradycardia Bronchospasm (avoid ALL drugs w/ asthma; permitted w/ COPD) CNS side effects Metabolic Drug withdrawal syndrome fatigue, decreased exercise tolerance, impotence In diabetes... Hypoglycemia --b2 adrenoceptors stimulate glycogenolysis and gluconeogenesis and glucagon release --b-blockers may mask tachycardia which is warning sign for insulin induced ``` BB toxicity: Symptoms: --bradycardia --hypotension --arrhythmias --hypothermia --hypoglycemia --seizures ```

Answer 37

antagonists of NICOTINIC cholinergic receptors (ionotropic receptors) compete w/ ACh for ganglionic nicotinic receptor sites OR block ion channel initial EPSP is blocked, ganglionic transmission inhibited

Answer 38

In HTN: Advantages: --Good for all degrees of HTN --especially good in pts w/ high renin levels (young people and caucasians) --increase efficacy of diuretics --thiazide + ACEI good even in low-renin HTN --initial drug used for HTN in DIABETICS (followed by CCB added on) --may preserve renal function in non-DN --initial anti-HTN in pts prone to HF Disadvantages: --hyperkalemia block ACE conversion of Ang I to Ang II block ACE degredation of bradykinins, ect. Hypotensive effects result from inhibiting the action of angiotensin II (AII) and stimulating action on the Kallikerin-kinin system. decrease aldosterone secretion some Production of renin and AI is increased – Accumulating AI is directed down alternative metabolic routes, resulting in increased production of vasodilator peptides as to Ang1-7, which are believed to be protective (in HF?) ACEI increases renal blood flow via vasodilation of afferent and efferent arterioles increase RBF occurs w/out increase in GFR: thus filtration fraction is decreasedDecrease TPR and BP in HTN states dilates arteries and veins baroreceptors remain in tact postural Hypotension not a problem AntiHTN when: Na retention OR high renin HF! SIDE EFFECTS 1. Hypotension in hypovolemic and/or Na+ -depleted patients – Precipitous first-dose hypotension unless dose is gradually increased. 2. Hyperkalemia (especially with renal insufficiency, or in pts receiving K-sparing diuretics or K supplements). 3. Dry cough (most common),angioneurotic edema or angiodema; both related to bradykinin actions. – Bradykinin activates stretch receptors in the trachea, which might causes dry cough in ~10-15% of patients receiving ACEI. 4. Angioedema: (fluid and red blotches in face) infrequent but potentially fatal. – Reported with all ACEIs. 5. Fetotoxicity: contraindicated in the 2nd and 3rd trimesters of pregnancy.

Answer 39

MOA 1. Selectively block AT II type 1 receptors, which are responsible for all of the vascular, renal and central effects of AII. 2. Cause vasodilation and increase Na and H20 excretion. Thus, they decrease TPR, plasma volume, CO, and BP. 3. Have no effect on bradykinin, therefore they are THE substitute when ACEI cause cough. 4. Do not block the action of AII on AT2 receptors, which are thought to be protective.

Answer 40

direct effects predominate decrease: - -HR - -contractility - -AV conduction rate --> reduces demand and prevents/ reverses vasospasm Don't combine with Beta Blockers!! bradycardia asystole AV block **contraindicated in HF! pregnancy category C Coronary vasodilation Reduced HR Decreased Contractile force Reduced afterload (arterial)

Answer 41

more potent vasodilators-->reflex cardiac stimulation direct and indirect effects balanced Reduces demand by reducing afterload increases supply by coronary vasodilation Combine w/ Beta Blockers!!! excessive vasodilation... peripheral edema (b/c increased precapillary dilation) paradoxical exacerbation of angina (dilated skeletal muscle vessels stealing all supply from coronary vessels...decreased supply) In HTN: Advantages: --HTN and CAD treatment --more powerful and preferred for treatment of HTN than non-dyhydropyridines (unless short-acting) --Very effective in elderly and AA w/ low-renin HTN --safe for diabetics Disadvantages: - -not as trusted as ACEIs, diuretics, and BBs - -may increase risk of CAD or HF Decrease BP and SVR in arterioles AND venules) Do NOT cause large baroreceptor-mediated sympathetic discharge, so very little change in HR!!! (EXCEPT short-acting DHP (i.e. nifedipine) do reflexively increase HR by sympathetic activation) --Low renin HTN!!! (elderly and AA) --older pts w/ systolic HTN --Many studies show no survival benefit ``` Side effects: Peripheral ankle edema Hypotension Constipation Reflex tachycardia (shorter-acting drugs) ```

Answer 42

Highly effective agents for relief in exertional and vasospastic angina In CAD...fail to prevent reinfarctions or CHD death Impaired LV function...increases mortality BBs are better In HTN...higher rates of MI, HF (immediate release) less CV events (slow-release)