Test 1 Flashcards

(65 cards)

1
Q

What ace inhibitors have long 1/2 life, which is not a pro drug like all others

A

Fosinopril and ramipril have long 1/2 lives

Captopril is not a pro rug

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2
Q

ARB receptor blockers dosing

A

1 day orally.

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3
Q

Renin inhib. What other drug reduces it’s efficiency?

A

NSAIDs

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4
Q

Therapeutic uses for BB

A

HTN patients with arrhythmia, prev heart attack, agnina, chronic heart failure, migraine, anxiety, glaucoma.

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5
Q

Longest half life of calcium channel blockers

A

Amlodipine

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6
Q

Adverse effects/contra for calcium channel blockers

A

Most AE due to hypotension- dizzy, peripheral edema, reflex tachycardia, headache, fatigue.

Contra in HF patient

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7
Q

Hydrazaline usually take what with it

A

Vasodilator. Usually take BB to help with reflex tachycardia (prevent adverse effects of arrhythmia and angina) and a diuretic to help with reflex water retention.

Monotherapy in pregnancy ok

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8
Q

How does minoxidil work

A

Hyperpolarizes K+ channels. Oral admin for severe, non responsive HTN.

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9
Q

How to treat diabetes insidious symptoms of polyuria and polydipsia?

A

Thiazide

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10
Q

Most common diuretic

Most efficacious

A

Common- Thiazide

Loop works best- use in HF

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11
Q

CAI location of action and what are they used for

Avoid in pts with

A

PCT.
used to tx glaucoma, mountain sickness and pseudotumor cerebri.

Acetazolamide- 2 250 tablets for glaucoma.

Avoid in pts with liver problems.

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12
Q

What drug may reduce effects of loop diuretics

A

NSAIDS

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13
Q

Loop diuretic DOC

Adverse effects

A

Used to reduce acute pulmonary edema due to HF.
Also treats hyperglycemia and hyperkalemia.

Adverse effects: ototoxicity and hyperuricemia, hypovolemia (shock)

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14
Q

Thiazide diuretics are derived from

A

Sulfa.

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15
Q

How long does it take thiazide diuretics to work? Adverse effects

A

1-3 weeks.

Hyperuricemia= gout

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16
Q

Aldosterone antag Potassium Sparing diuretics adverse effects

A

Gi upset, peptic ulcer, chemical resembles sex hormones.

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17
Q

Resistance is influenced by what 2 things

A

Diameter (Direct)
____
Blood vol (indirect)

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18
Q

most common cardiovascular disease

A

HTN

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19
Q

How do baroreceptors control CO and peripheral resistance

A

Fall in BP causes baroreceptors to send fewer impulses to cardiovascular centers in the spinal cord. Reflex response of increase sympathetic and decrease parasympathetic. Vasoconstriction and inc erase CO

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20
Q

2 systems that control CO and peripheral resistance

A

Baroreceptors (quick)

RAAS (Slow)

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21
Q

Conversion of angiotensinogen to angiogtension II

A

Angiotensinogen converted by renin to angiotensin 1. Then converted by ace to angiotensin II

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22
Q

Role of angiotensin II

A

Vasoconstrictor
Increases levels of aldosterone, which causes reabsorption of sodium and water= increasing blood volume.
Induces cardiac hypertrophy. Causes myocardial stiffness and fibrosis and apoptosis

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23
Q

How do baroreceptors increase sympathetic activity

A

When they sense a decrease in blood pressure, they stimulate B1 to increase heart rate and force of contraction.

They also stimulate alpha 1 to cause vasoconstriction.

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24
Q

4 tips to manage HF

A

Decrease activity
Decrease Na intake
Treat co-morbid conditions
Avoid NSAIDS, alcohol, calcium channel blockers

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25
Pharmacokinetics of digoxin
Little metab- leads body the same | Long 1/2 life bc accumulates in muscle. High Vd.
26
Digoxin adverse effects
Toxicity- arrhythmia, Gi probs, HA, confusion, fatigue **blurred vision, halos, color distortion. Flashes, yellow vision. Drug/drug interactions with other drugs that also decrease K+ levels in blood: erythromycin, tetracycline, verapamil, quinidine
27
Milrinone MOA and admin
PDE 5 inhibitor- cannot break down cAMP, which results in an increased level of calcium inside cell. IV
28
Aldosterone antagonists. Why are these good to use in HF and which one has less side effects
Good to use in HF because HF patients have increased levels of aldosterone. Sprironolactone has more side effects due to sex hormones. Epelerone has less.
29
Vasodilators
Hydrazaline Minoxidil Isosorbide dinitrate and isosorbide mononitrate release NO (also organic nitrates)
30
2 BB approved for chronic HF
carvedilol and metoprolol. Only use in chronic
31
What drugs to use for high risk/no symptoms to lots of symptoms of HF patients
High risk/no symptoms Risk factor reduction and inform patient ACE or ARB ACE + BB Digoxin + diuretic + diet restriction Lots of symptoms
32
Quinidine adverse effects
Na channel blocker Type IA Increase concentration of digoxin GI blurred vision due to anticholinergic activity
33
Procainide adverse effects
``` Lupus, CNS side effects Metabolites show class III activity ```
34
Disopyramide adverse effects
Dry mouth, urine retention, blurred vision, constipation. Similar to anticholinergic.
35
Flecainide and propafenone (1C) adverse effects
Metallic taste, constipation, induce arrhythmia
36
``` How does each class affect the heart contraction? Class I thru 4 ```
1: Na blocker. Slows phase 0, also affects phase 3 2: BB. Slows AV node. Slows phase 4. 3: K+. Prolongs phase 3 and QT interval (4) 4. Refractory period prolonged (phase 4) AV and SA node prolonged. Slows depol (phase 0) 0 and 3 4 3 and 4 0 and 4
37
Potassium channel blocker drugs
Amiodarone long half life, lots of side effects, Whorl keratopathy, NAION. Dronedarone- short half life, less side effects Ibutalide- Dofetilide Sotalol- BB but high Class III activity
38
Amiodarone
``` Complex- has class 1-4 actions DOC for atrial fib and anti anginas ``` ``` Long half life and lots of side effects -pulmonary fibrosis -GI -CNS: dizzy, tremor -Blue skin NAION Whorl keratopathy ```
39
4 other anti-arrhythmic drugs
Adenosine- caffeine decreases effectivity Digoxin- Positive inotropic? ocular toxicity! Magnesium- unknown MOA Potassium- balance
40
Arrhythmias have disfunction of
1. Impulse generation 2. Impulse conduction Both cause CO to decrease Worsened by ischemia, acidosis, electrolyte imbalances tricky to treat!
41
phases of heart contraction
phase 0: depol. Na+ flows into cell. Phase 1: K+ channels open, then quickly close. Na+ channels inactivated. Phase 2: Ca++ channels open and Ca++ enters cell, K+ leaks out. Plateau Phase 3: Ca++ channels cost. K+ opens and K+ exits cell causing repol. Phase 4: gradual increase in Na+ permeability. Na+ can start entering cell, causing depol.
42
Force of contraction is directly related to unbound intracellular calcium levels. Sources of intracellular calcium.
1. Voltage sensitive channels that cause calcium to move into cell 2. Exchange with sodium 3. Release from SR and mitochondria
43
Abnormal automaticity causing arrhythmia
When sites other than SA show enhanced automaticity. Ex: Damaged myocardial cells may remain partially depolarized, allowing them to reach threshold sooner. Tx with drugs that decrease calcium or sodium
44
Abnormal impulse conduciton
Blocked nerve impulse may cause short circuit= premature contraction and re-entry defect. Tx: Slow conduction or increase refractory period. Converts unidirectional block that may cause flutter into bidirectional block.
45
How to treat angina
Decrease myocardial O2 requirements by decreasing cardiac work or increase 02 delivery with vasodilators.
46
Determinants of cardiac O2 demand
Wall stress HR Contractility Any increase = increase 02 demand. Often during physical activity
47
Determinants of coronary blood flow
Perfusion pressure (diastolic) Duration of diastole Coronary vascular resistance
48
Determinants of vascular tone
Arteriole tone (controls peripheral vascular resistance, systolic wall stress) Venous tone (controls amount of blood returning to heart. Diastolic wall stress)
49
3 types of angina
1. Stable/classic/typical. usually due to blockage of coronary artery. Short lasting, happens during activity. Treat with rest or nitroglycerin. 2. Variant/vasospastic. Occurs at rest. Unrelated to activity or HR. Respond well to vasodilators and calcium channel blockers. 3. Unstable. (maybe due to plaque rupture) Classic angina getting worse- attacks with less exertion. Rest and nitroglycerin do not work.
50
Organic nitrates - 3 types - Admin
Nitroglycerin Isosorbide di- and mono nitrate Admin sublingual or patch (first pass inactivates) Tolerance develops quickly- do 12 hours on/12 off.
51
DOC for acute angina
nitroglycerin.
52
Nitroglycerine adverse effects
HA, tachycardia due to vasodilation, orthostatic hypotension, 12 hours on/12 off to avoid tolerance. Do to combine with PDE type 5 inhibitor.
53
Preferred BB for angina
Atenolol, metoprolol
54
What type of angina is BB not helpful for
Vasospastic angina because BB is not a vasodilator.
55
DOC for chronic angina
BB or Ranolzaine (Sodium channel blocker)
56
MOA of ranolzaine
Sodium channel blocker. Tx chronic angina. Inhibits late phase of Na+ current during depol. Improves diastolic function and increases O2 supply
57
3 type 5 PDE inhibitors
Sildenafil Tadalafil - more selective to PDE 5, not 6. Vardenafil
58
MOA and side effects of PDE 5 inhibitors
MOA: Prevents inactivation of cGMP. No increases cGMP inside the cell, which leads to vasodilation. Type 5 usually breaks it down. Ocular side effects bc similar to PDE 6 inside the eye, a phototransductor. Causes mild impairment of color vision- blue/yellow/pink tinge. Last mins to hours. Also causes blurred vision. Do not take with organic nitrates= severe vasodilation.
59
ADP receptor blockers have what side effects
Severe bruising, life threatening TTP | PP bound, 450 met
60
What anti-thrombin med is excreted by the liver
Argatroban.
61
DOC for dabigitran
prevent stroke because atrial fib
62
administration for Xa inhibiting drugs
Apixiban and rivaroxaban are oral | Fondaparinux is Sub Q
63
What thrombolytic drug is only approved for pulmonary emboli and is produced naturally by the liver
Urokinase.
64
What thrombolytic agent is fibrin selective and a DNA recombinate
Alteplase
65
What additional meds should you take with thrombolytic agents?
Aspirin. As it breaks down clot, may induce more clotting.