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Cardiology > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Drug that can cause facial flushing and pleuritis

A

Niacin (adenosine can also cause flushing)

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1
Q

Statins inhibit

A

HMG CoA Reductase

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1
Q

What is the name of the one ganglionic blocker that we need to know for the CV system?

A

Trimethaphan

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1
Q

Which artery supplies the SA and AV nodes?

A

RCA

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2
Q

Drug that can cause myalgia, myopathy, and hepatotoxicity

A

Statins

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2
Q

What is Mecamylamine (Inversine) used for clinically?

A

Mecamylamine (Inversine) is an orhpan drug that is FDA approved for Tourette’s syndrome, a nicotinic-responsive psychiatric disorder.

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2
Q

When do coronary arteries fill?

A

During diastole

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3
Q

Prevents absorption of Cho in gut

A

Ezetimibe

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3
Q

On what type of receptors do ganglionic blockers act as antagonists?

A

Ganglionic blockers are antagonists of the cholinergic nicotinic (Nn) receptors (henceforth knows as nAchR).

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3
Q

What inhibits the Na/K ATPase creating less extracellular Ca and more intracellular thus increasing contractility?

A

Digoxin/digitalis

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4
Q

Example of IA anti arrhythmic drugs.

A

procainamide

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4
Q

What neurotransmitter do ganglionic blockers antagonize?

A

acetylcholine (Ach)

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4
Q

How to calculate EF?

A

What heart can pump out over what can hold. SV/EDV.

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5
Q

Mech and result of IA arrhythmic drugs.

A

block of Na channel (as well as K). This prolongs AP.

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5
Q

What is the mechanism of action for ganglionic blockers?

A

They compete with Ach for receptor binding. When they bind, they prevent the opening of Na+ and K+ channels (preventing depolarization of the postsynaptic membrane by the initial ESPS)

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5
Q

2 Equations for CO

A

CO = SV X HR. CO= rate of O2 consumption / (arterial O2 - Venous O2)

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6
Q

Drugs that can disrupt digoxin?

A

Quinidine and Verapamil

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6
Q

How are nAchR different in structure/function than muscarinic Ach receptors (mAchR)?

A

The nAchR are ligand-gated ion channels whereas the mAchR are G protein receptors

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6
Q

Equation for SV

A

EDV-ESV

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7
Q

What is the reversing agent for Digoxin?

A

Antibody for Digoxin

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7
Q

Where are nAchR located (pre- or postganglionic as well as where in the body)?

A

nAchR are present on the post-ganglionic membrane in the somatic nerves, skeletal muscle, sympathetic chain ganglia (autonomic ganglia), the adrenal medulla, and certain areas in the brain.

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7
Q

Do polycythemia, hyper proteinemic states, hereditary spherocytosis increase or decrease resistance in vessel?

A

Increase resistance because increase viscosity.

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8
Q

What is dobutamine and what does it do?

A

Beta 1 agonist. Increases HR and Contractility

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8
Q

Why aren’t ganglionic blockers used much clinically?

A

Lots of side effect. The inhibition of nAchRs cause global effects (as seen by all the places nAchR are present). It’s hard to address the action against one ganglia and not the others.

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8
Q

S3 heart sound

A

rapid ventricular filling. Dilated cardiomyopathy(ventricles) CHF, Mitral regurg, Left to right shunt.

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9
Q

Adenosine is drug of choice for

A

Supraventricular Tachycardia (Such as AV Nodal)

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9
Q

What do the electrical events subsequent to the initial EPSP (excitatory postsynaptic potential) modulate?

A

The electrical events subsequent to the initial EPSP are thought to modulate the probability that a subsequent EPSP will reach the threshold potential (they modulate how soon the postsynaptic ganglion can receive its next signal).

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9
Q

S4 heart sound (right before S1)

A

High atrial pressure. LVH with atrial kick. Hypertrophic cardimyopathy, aortic stenosis, chronic HTN with LVH, after MI.

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10
Q

Example of IB anti-arrhythmic drugs.

A

Lidocaine

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10
Q

What is the predominate tone of arterioles and what is the effect of ganglionic blockage?

A

The predominate tone of arterioles is sympathetic (adrenergic) and the effects of ganglionic blockage are vasodilation, increased peripheral blood flow, hypotension.

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10
Q

At Carter’s Xing Vehicles Yield

A

JVP Pulse order.

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11
Q

Mech and result of IB anti-arrhythmic drugs.

A

Blocks Na. AP shortened.

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11
Q

What is the predominate tone of veins and what is the effect of ganglionic blockage?

A

The predominate tone of veins is sympathetic (adrenergic) and the effects of ganglionic blockage are dilation, peripheral pooling of blood, decreased venous return, and decreased cardiac output.

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11
Q

Normal S2 splitting happens with….

A

inspiration because it causes more venous return to right ventricle (negative pressure in chest due to diaphragm lowering) so pulmonic valve takes longer to close than aortic

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12
Q

IB useful in what condition

A

Acute ischemic ventricular arrythmia

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12
Q

What is the predominate tone of the heart and what is the effect of ganglionic blockage?

A

The predominate tone of the heart is parasympathetic (cholinergic) and the effect of ganglionic blockage is tachycardia.

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12
Q

Phase zero of cardiac action potential

A

Upstroke, voltage gated Na+ channels open. Sodium channel blockers would affect this.

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13
Q

What is an example of IC anti-arrhythmic drugs.

A

Flecainide (Encainide and Propafenone)

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13
Q

Do ganglionic blockers block the sympathetic nervous system, the parasympathetic nervous system, or both?

A

Both.

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13
Q

Phase one of cardiac action potential

A

inactivation of sodium channels, K+ channels begin to open.

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14
Q

When are IC anti arrhythmic drugs.usually used?

A

When others have not worked. These are potentially dangerious. Contraindicated post MI.

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14
Q

What are the specific adverse effects of using ganglionic blockers?

A

Loss of cholinergic function of the sympathetic nervous system (orthostatic hypotension, tachycardia, and arrythmias) as well as loss of cholinergic function of the parasympathetic nervous system (blurred vision, double vision, asthma secondary to histamine release, dry mouth, constipation, paralytic ileus, nausea/vomiting, urinary retention, impotence, drowsiness, seizures, hallucinations, tremor, confusion, and neuromuscular blockade).

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14
Q

Phase 2 of cardiac action potential

A

Calcium influx through voltage gated calcium channels. Plateau.

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15
Q

What must happen to stop angina? (2 things)

A

Raise Oxygen delivery or Lower oxygen demand

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15
Q

Phase 3 of cardiac action potential

A

Rapid repolarization with massive efflux of K+ with opening of voltage gated slow K+ channels and closing of Ca2+ channels. Potassium channel blockes would affect this.

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16
Q

What are some alpha-2 agonists? (2)

A

clonidine and methyldopa

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16
Q

Phase 4 of cardiac action potential

A

RMP with K+ permeability.

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17
Q

What is mech of alpha-2?

A

Decreases sympathetic outflow in CNS.

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17
Q

Pacemaker action potential

A

Phase 4- RMP (K+ permeable). Na+ channels gradually open until threshold causes opening of voltage gated Ca2+ channels and phase 0 happens (upstroke). No plateua and now Potassium brings it back doen in phase 3.

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18
Q

What are some ganglion blocking drugs?

A

Hexamethonium and Trimethaphan

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18
Q

What inhibits phase zero of pacemaker action potential?

A

Calcium channel blockers.

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19
Q

What is a drug that depletes nerve terminals of NE stores?

A

Reserpine

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19
Q

What suppresses the slope of phase 4 in pacemaker action potential.

A

Beta blockers.

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20
Q

Mech of hydralazine and nitroprusside

A

Vasoldilate by NO release

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20
Q

4 classes of antiarrhythmics

A

No Bad Boy Keeps Clean. 1- Na+, 2- Beta Blockers. 3-K+. 4- Calcium channel blockers.

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21
Q

Mech of minoxidil and diazoxide

A

Vasodilate by Hyperpolarizing vasc smooth muscle cells by opening K channels

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21
Q

Sodium channel blockers

A

Class 1 antiarrhythmics. Increase slope of phase 0 for cardiac action potential (sodium depolarization) so increase refractory period thus decreasing heart rate

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22
Q

Mech of Verapamil, Dilitiazem, and nifedipine

A

Vasodilate by reducing Ca influx.

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22
Q

Sodium channel blocker used for Wolf Parkinson White

A

Procainamide. Can cause SLE (antihistone antibodies).

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23
Q

What is the mechanism and result of Digoxin?

A

Ionotrope. Blocks Na/K Atpase. W/o gradient, Ca stays in cell. Increase contractility. Also can increase Vagal activity.

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23
Q

Quinidine toxicity

A

Cinchonism (headache and tinnitus), thrombocytopenia, torsades (arrhythmia).

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24
Q

What other kind of drug can negatively interact with digoxin use?

A

Diuretics. Verapamil and Quinidine

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24
Q

Beta blockers

A

Class 2 antiarrhythics. Suppress abnormal pacemakers by decreasing slope of phase 4 (Calcium influx).

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25
Q

Nitroprusside, Diazoxide, and Labetalol are useful in

A

acute events (fast and short acting). Nitroprusside has very fast duration.

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25
Q

Sotalol and amiodarone

A

Class 3 antiarrhythmics. Potassium channel blockers. Used for atrial fib. Amiodarone for WPW.

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26
Q

Example of ACE inhibitor

A

captopril (Enalapril, fosinopril)

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26
Q

Pulmonary fibrosis, hepatotoxicity, hypo/hyperthryoidism are side effects of……

A

Amiodarone. Check PFTs, LFTs, TFTs

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27
Q

Example of ARB

A

Losartan (Valsartan)

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27
Q

Class 3 antiarrhythmics

A

K+ channel blockers. Class 3 phase 3…. (repolarization due to K+)

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28
Q

Example of renin inhibitor

A

Aliskiren

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28
Q

Verapamil and diltiazem

A

Class 4 antiarrhythmics, Calcium channel blockers. Non-Dihydropyridine CCB’s. Prolong phase 0 of pacemaker cells (depolarization due to calcium).

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29
Q

Which drug can cause excessive hair?

A

Minoxidil (hairy like an Ox)

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29
Q

Adenosine

A

Pushes K+ out of cells hyperpolarizing the cell and preventing depolarization causing flat line. Diagnose and abolish supraventricular tachycardia.

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30
Q

Which drugs can cause lupus-like syndrome? (2)

A

Hydralazine and Procainamide

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30
Q

Conduction delay through AV node on ECG

A

PR interval

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31
Q

Which drugs should definitely not be used with asthmatics?

A

Beta blockers (can constriction of airways)

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31
Q

Mechanical contraction of ventricles on ECG

A

QT interval

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32
Q

Which drug can cause a + Coombs test?

A

Methyldopa

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32
Q

T wave inversion on ECG

A

Indicative of MI

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33
Q

What set of drugs have highest risk for postural hypotension? (orthostatic)

A

Because this is due to venous pooling, alpha blockers can cause this. (alpha-1 selective)

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33
Q

QRS complex

A

Depolarization of ventricles. Less than 3 little boxes (120 msec).

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34
Q

Chronic cough most often occurs from which HTN drug?

A

ACE inhibitor (Captopril)

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34
Q

Drugs which can prolong QT interval (possibly leading to torsades)

A

Macrolides (erithromycin), haloperidol and risperidone, methadone, protease inhibitors, chloroquine and primaquine, antiarrhythmics.

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35
Q

Which HTN drug can cause hyperglycemia?

A

Diazoxide. (hyperpolarizer due to open K channels)

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35
Q

How to treat torsades

A

magnesium

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36
Q

What HTN drugs can cause constipation?

A

Verapamil and Nifedipine

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36
Q

Electrical signal not going through AV node

A

Wolf Parkinson White

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37
Q

Which two kinds of HTN drugs can cause renal damage in patients with prexisting renal vasc disease or in fetus?

A

ACE inhibitors and ARBs

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37
Q

Early ventricular depolarization with a delta wave on ECG

A

Wolf Parkinson White can lead to reentry current and supraventricular tachycardia.

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38
Q

Nitrates release what powerful vasodilator

A

NO

38
Q

How to treat WPW

A

Procainamide (NA channel blocker), Amiodarone (calcium channel blocker)

39
Q

Nitrites can cause what effect that can counteract cyanide poisoning?

A

Methemglobinemia

39
Q

Irregularly irregular ECG with no discrete P waves how do you treat?

A

Atrial fibrillation and treat with Digoxin with beta blocker or CCB

40
Q

Verapamil and dilitiazem cause vasoldilation as well as what other effect in the heart?

A

Reduction of rate and contractility of heart. Useful in AV node arrhythmias as well.

40
Q

Sawtooth appearance on ECG how do you treat?

A

Atrial flutter so use Na+ channel blocker or K+ channel blocker (Sotalol and amiodarone).

41
Q

Ca blockers are useful in which types of angina?

A

Effort and vasospastic (usually as prophyactics)

41
Q

Completely erratic rhythm with no identifiable waves

A

Ventricular fibrillation. Leads to death.

42
Q

Are beta blockers used as prophylactics or in acute attacks for angina?

A

prophylactic. More effective in effort angina, not vasospastic.

42
Q

Which baroreceptor (and which nerve is it on) responds to only increase in BP

A

Aortic arch (vagus nerve)

43
Q

Using beta blockers can help with nitrate therapy by?

A

Blocking compensatory effects from the vasodilation of nitrates.

43
Q

Which baroreceptor (and which nerve is it on) responds to both increase or decrease in BP

A

Carotid sinus (glossopharyngeal nerve)

44
Q

What drugs can cause a throbbing headache?

A

Nitrates (hypotension and meningeal vasodilation).

44
Q

HTN, bradycardia, respiratory depression. Also what kind of receptors are this sensed by.

A

Cushing triad due to Increased ICP sensed by CHEMORECEPTORS.

45
Q

What is the major common determinant of oxygen consumption in myocardium?

A

Myocardial fiber tension

45
Q

What releases NO which can lead to vasodilation?

A

Endothelial Cells.

46
Q

Which Beta blocker has a very short action?

A

Esmolol

46
Q

What stimulates endothelial cells to release NO leading to vasodilation?

A

Bradykinin, Ach, alpha 2 agonist, histamine, serotonin, shear stress

47
Q

Toursade de pointes can be caused by drugs that do what?

A

Prolong the QT interval

47
Q

Inhibits cGMP phosphodiesterase

A

Sildenafil. Leading to more cGMP and thus more vasodilation.

48
Q

Which part of the conduction systems is especially sensitive to Beta Blockers

A

AV Node

48
Q

Which drug do you give for HTN but patient has renal stones?

A

Thiazide diuretics because thiazides retain Ca. Loops lose calcium so don’t give with renal stones.

49
Q

What are some examples of class III anti-arrhythmic drugs?

A

Sotalol, Ibutilide, Dofetilide, Amiodarone (kind of)

49
Q

Which drug increases cGMP (decreasing afterload because it works on arterioles>veins) for use for HTN in pregnancy

A

Hydralazine

50
Q

What is the effect of Class III drugs and how is it accomplished?

A

Prolongation of the AP by blocking K channels that would be be repolarizing the cell. This also raises the refractory period to help inhibit rapid tachycardias.

50
Q

What drug is a K+ channel opener relaxing hyperpolarizing and relaxing vascular smooth vessels for use in HTN?

A

minoxidil (hypertrichosis side effect)

51
Q

Which class III drug can cause Toursade de Pointes and signs of Beta blockade?

A

Sotalol (Procainamide IA also can)

51
Q

Calcium channel blocker for use in HTN (reduces vascular smooth muscle contraction)

A

Nifedipine (verapamil and diltiazem are antiarrhythmics at the heart).

52
Q

What is considered to be the most effective antiarrhythmic drug and why?

A

Amiodarone. It has a variety of mechanisms (blocks K, Na, Ca, and Beta receptors). This broad spectrum also make it very dangerous to be used.

52
Q

With smooth muscle spasm (prinzmetal’s angina, raynaud’s) what kinds of drug do you use?

A

Dihydropyridine Ca Channel Blocker (-dipines)

53
Q

What are some toxicities of Amiodarone?(4)

A

Microcrystalline deposits in cornea and skin, thyroid dysfunction (hyper or hypo), paresthesias, tremor, and pulmonary fibrosis.

53
Q

Releases NO in endothelial cells of smooth muscles (increasing cGMP) dilating veins more than arteries and decreasing preload.

A

Nitroglycerin

54
Q

What kind of levels of K can cause Procainamide toxicity?

A

Hyperkalemia

54
Q

What drug can cause cyanide toxicity and vasodilates both arterioles and veins for use in malignant HTN?

A

Nitroprusside. (labetolol also used in malignant HTN)

55
Q

Administration of what can help with procainamide toxicity?

A

Sodium lactate

55
Q

What antihypertensive drug has a first dose orthostatic hypotension?

A

Alpha Blockers (-zosins)

56
Q

If a patient has a supraventricular tachycardia (AV Nodal) what might your drug and second drug of choice be?

A

Adenosine (less toxic) or Ca channel blockers.

56
Q

What anti-HTN drugs are ototoxic (especially with aminoglycosides)?

A

Loop Diuretics. And loops lose calcium.

57
Q

What drug can cause Cinchonism?

A

Quinidine (made from chinchona tree)

57
Q

What class of anti-HTN drugs can cause angioedema (swollen lips, eyes, face)?

A

ACE inhibitors

58
Q

What class of drugs can reduce Na channels and decrease APs in ischemic tissue?

A

IB drugs. Mexiletine can be given orally.

58
Q

Anti HTN drugs that can result in hypercalcemia, hypokalemia?

A

Thiazide diuretics. Thiazides DON’t lose CA2+.

59
Q

Which anti-arrhythmic drug has the longest half life?

A

Amiodarone.

59
Q

First line treatment for aortic dissection?

A

Beta blockers.

60
Q

Which hyperlipids drugs are contraindicated in pregnancies?

A

HMG CoA Reductase Inhibitors (statins) can be teratogens.

60
Q

Tearing chest pain radiating to the back (or scapula), CXR shows mediastinum widening?

A

Aortic Dissection

61
Q

What does gemfibrozil do to lipoprotein lipase?

A

Increases is by interacting with the PPAR-alpha. This drops VLDL synthesis (lowers triglycerides).

61
Q

Main risk factor for AAA?

A

Atherosclerosis of descending aorta (most common site)

62
Q

What can chronic OH use do to lipid panels?

A

Increase VLDL and TGs. (risk of pancreatitis). Strangely, it also can raise HDL.

62
Q

To have angina must have narrowing of at least…..

A

75% of Coronary Artery

63
Q

Which hyper lipids drug can exacerbate gout and glucose intolerance?

A

niacin

63
Q

What drugs lower LDL the most?

A

HMG-CoA Reductase inhibitors (statins)

64
Q

If a patient has normal Cholesterol levels and high Triglycerides, what might be a good drug choice?

A

Gemfibrozil (fibric acid derivatives)

64
Q

Side effects of statins?

A

Rhabdomyolysis (muscle breakdown), hepatotoxicity (increased LFT’s), myositis (muscle inflammation), myalgia (muscle pain)

65
Q

What is preferred HTN drug for someone with diabetes?

A

ACE Inh. provided kidney is functioning.

65
Q

What drug raises HDL the most?

A

Niacin

66
Q

Which drugs can not only lower systemic BP but also minimize occurrence of vasospasm?

A

nondihydropyridine class of Ca blockers: Verapamil and Diltiazem. Dihydrppyridines (nifedipine) will lower BP by vasoldilation, but are more likely to cause compensatory mechanisms that will negate the desired change.

66
Q

Red, flushed face, hyperglycemia, hyperuricemia side effects

A

Niacin

67
Q

What compensatory effects might come from hydralazine use and what could correct them?

A
  1. Heart symp activation - Beta blockers 2. Renin Angiotensis system- Diuretic
67
Q

Drug that tastes really bad and lowers LDL

A

Bile acid resines(cholestyramine)

68
Q

What types of K levels can have adverse effects with digoxin?

A

hypokalemic

68
Q

What drug causes liver to use more cholesterol?

A

Bile acid resins (block intestinal reabsorption of bile acids so liver must use cholesterol to make more)

69
Q

What drug is potentially dangerous to use in a patient with vasospasms?

A

Beta blockers. This can remove the ability of the body to dialate using B receptors.

69
Q

What drug can cause cholesterol gallstones?

A

Bile acid resins

70
Q

What potentially dangerous metabolite can come from nitroprusside?

A

cyanide

70
Q

Which drug blocks cholesterol absorption? (Blocks at small intestine brush border.)

A

Ezetimibe.

71
Q

Discontinuation of what drug can cause a “rebound” rise in BP?

A

Clonidine

71
Q

Which drugs decrease triglycerides most?

A

Fibrates

72
Q

Vasoconstriction of blood vessels

A

Alpha-1 Agonist, Alpha-2 Agonist

72
Q

Which drug upregulates LPL?

A

Fibrates

73
Q

Hypotension RVLM

A

Alpha-2 Agonist

73
Q

What can lead to pancreatitis?

A

Increased TG’s.

74
Q

Cardiac Stimulation (Increased HR/contractility)

A

Beta-1 Agonist

74
Q

Which lipid lowering drug binds to C. Dificile?

A

Cholestyramine (bile acid resin)

75
Q

How can you prevent the flushing reaction of Niacin?

A

Aspirin

76
Q

Dilation of blood vessels

A

Beta-2 Agonist

76
Q

Which anti-HTN drug can cause hyperkalemia?

A

ACE inhibitors. Don’t have us much aldosterone which helps excrete potassium.

77
Q

Inhibition of NE release (adrenergic nerve)

A

Alpha-2, Beta-2 Agonist

77
Q

Chest pain at rest (secondary to coronary artery spasm) with ST elevation on ECG?

A

Prinzmetal’s angina

78
Q

Decreased GI motility & tone

A

Alpha-1 Agonist

78
Q

How to treat prinzmetal’s angina?

A

Nifedipine (dihydropyridine ca channel blockers.

79
Q

Stimulation of glycogenolysis (Liver)

A

Alpha-1 Agonist

79
Q

What most commonly leads to aortic dissection?

A

HTN

80
Q

Contraction of sphincter muscle (GI, Bladder, Radial muscle in eye)

A

Alpha-1 Agonist

80
Q

What can lead to sharp chest pain that is relieved by sitting forward?

A

Pericarditis which can be caused by Rheumatic fever among other conditions. Also fibrinous pericarditis from an MI (presents with friction rub).

81
Q

Best treatment for angina?

A

Nitrates + Beta blockers

82
Q

Decreased GI motility & tone

A

Alpha-1, Alpha-2, Beta-1, Beta-2 Agonist

82
Q

Contraction bands seen…….

A

at least 2 hours since MI.

83
Q

Inhibition of insulin release (pancreas)

A

Alpha-2 Agonist

83
Q

What are the cells of acute inflammation in an MI (2-4 days)

A

Neutrophils

84
Q

Inhibition of lipolysis (fat cell)

A

Alpha-2 Agonist

84
Q

What kind of necrosis occurs in an MI?

A

Coagulative necrosis

85
Q

Platelet Aggregation

A

Alpha-2 Agonist

85
Q

Compression of heart by blood leaking into pericardium

A

Cardiac Tamponade.

86
Q

Fatty acid mobilization (adipose tissue)

A

Beta-1 Agonist

86
Q

Cells of inflammation in an MI 5-10 days after?

A

Macrophages come in and degrade things.

87
Q

Increased Renin release (kidney)

A

Beta-1 Agonist

87
Q

After 10 days from an MI at risk for……..

A

Ventricular aneurysm at bulging scar.

88
Q

Increased Insulin secretion (pancreas)

A

Beta-2 Agonist

88
Q

When does toponin I rise after an MI?

A

After 4 hours and elevated 7-10 days.

89
Q

Glycongenolysis/Gluconeogenesis (Liver/Muscle)

A

Beta-2 Agonist

89
Q

ECG changes of ST elevation can indicate what type of MI?

A

Transmural infarct

90
Q

Increased Glucagon secretion

A

Beta-2 Agonist

90
Q

ECG changes of ST depression can indicate what type of MI?

A

Subendocardial infarct/

91
Q

Relaxation of bronchial sm. muscle, bladder detrussor muscle, pregnant uterus

A

Beta-2 Agonist

91
Q

ECG changes of t wave inversion can indicate what type of MI?

A

Transmural infarct

92
Q

Inhibition of ACh release (parasympathetic nerve)

A

Alpha-2 Agonist

92
Q

What persists on ECG weeks after MI?

A

Q wave

93
Q

Most specific marker of an MI (gold standard).

A

Troponin I

94
Q

Inhibition of 5-HT release (serotonergic nerve)

A

Alpha-2 Agonist

94
Q

Severe MI then five days later have mitral regurg what happened?

A

Macrophages came and degraded things and we had rupture of the papillary muscle.

95
Q

Conducting Tissue and EKG

A

Direct action on B1 receptors

95
Q

What drugs directly aid conversion of plasminogen to plasmin (which degrades fibrin)?

A

Thrombolytics. Streptokinase, Urokinase, tPA.

96
Q

Epinephrine

A

Decrease threshold of depolarization of SA node

96
Q

When do you use thrombolytics?

A

STEMI MI.

97
Q

Increase in HR (B1 action)

A

Isoproteronol >>> Epinephrine

97
Q

What do you treat thrombolytic toxicity?

A

Aminocaproic acid

98
Q

Isoproterenol

A

increased excitability and automaticity shortens refractory period elevation, flattening, or inversion of T wave

98
Q

What does aspirin do?

A

Irreverisbly inhibits COX-1 and COX-2 to prevent conversion of arachidonic acid to thromboxane A2 (clotting).

99
Q

NE

A

sinus bradycardia A-V dissociation Ventricular tachycardia

99
Q

How do you treat aspirin toxicity?

A

NaHCO3

100
Q

NE Reflex

A

Decrease in HR due to marked increase in BP Most prominent with A1 agonists

100
Q

What do Clopidogrel and Ticlopidine do?

A

ADP receptor blockers which inhibits platelet aggregation. Inhibits figrinogen binding by preventing glycoprotein IIb/IIIa expression

101
Q

Phase 0 (EKG)

A

Sharp depolarization due to Na+ influx

101
Q

Which drugs inhibit platelet aggregation by preventing glycoprotein IIb/IIIa expression? (what other drug also does this)

A

Clopidogrel and Ticlopidine. Abciximab is the other drug (monoclonal ab binds glycoprotein Iib/IIIa receptor).

102
Q

Phase 1 (EKG)

A

Sharp hyperpolarization, then flattening Ca++ influx

102
Q

Which drug inhibits platelet aggregation by binging to the glycoprotein IIb/IIIa receptor on activated platelets?

A

Abciximab

103
Q

Balloon appearance on x ray of heart (big and circular)?

A

Dilated Cardiomyopathy.

104
Q

Most common cause of US of myocarditis?

A

Coxsackie Virus. (also eckovirus and influenza virus)

105
Q

Lymphocytes with myocyte necrosis?

A

Myocarditis (viral infection).

106
Q

Cause of sudden death in young athletes?

A

Hypertrophic cardiomyopathy

107
Q

Disoriented, tangled, hypertrophied myocardial fibers?

A

Hypertrophic cardiomyopathy

108
Q

What can you hear with hypertrophic cardiomyopathy?

A

S4 heart sound.

109
Q

Endomyocardial fibrosis with eosinophilic infiltrate?

A

Loffler’s Syndrome

110
Q

How to increase contractility and cardiac output?

A

Digoxin/digitalis

Cardiology (10 decks)

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