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CRRAB I Mike Rose > Treatments Quiz 3 > Flashcards

Treatments Quiz 3 Flashcards

1
Q

Tyramine

A

MOA: Reverse the direction of the axoplasmic catecholamine pump.

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2
Q

Amphetamine

A

Reverses the direction of the axoplasmic catecholamine transporter. Increases NE and thus BP.

Toxicity: CNS stimulation, mydriasis, hypertension, tachycardia, hyperthermia.

Therapeutic uses: Narcolepsy, hyperkinetic syndrome (ADHD), obesity

Oral activity and distributes to the brain. Excretion in urine (not degraded by COMT.

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3
Q

Imipramine

A

MOA: Inhibit action of the axoplasmic catecholamine transporter (Tricyclic antidepressant)

Uses: refractory depression and enuresis

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4
Q

Cocaine

A

Inhibit action of the axoplasmic catecholamine transporter

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5
Q

Reserpine

A

Inhibits the granular pump accumulating catecholamines in vesicles (results in depletion of catecholamines)

Serious side effects.

First ever antihypertensive

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6
Q

Guanethidine

A

MOA: 1.induce release from vesicle, probably via displacement

  1. slow acting (norepinephrine gets degraded by Monoamine oxidase)
  2. depletes norepinephrine stores
  3. reduces responses to sympathetic stimulation
  4. inactive in the presence of inhibitors of the axoplasmic transporter or monoamine oxidase inhibitors, such as pargyline or phenelzine
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7
Q

Tolcapone

A

COMT inhibitor. Increases synaptic/circulating catecholamines

Used as adjunct in Parkinson’s.

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8
Q

Pargyline

A

MOA: Type b (present in various organs) MAOI. Potentiates action of catecholamines.

Must avoid foods high in tyramine

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9
Q

Isoproternol

A

Beta 1 and 2 Adrenergic Agonist (very little alpha).

Net cause is decreased blood pressure due to radius being to the fourth power vs. HR and SO being to the first.

Causes increase HR and decreased BP.

Administration - parenteral or aerosol

Metabolism by COMT not MAO

Therapeutic use- cardiac stimulant (ß1)

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10
Q

Dobutamine

A

MOA: Selective ß1 agonist (actually has vascular activity but net effect is ß1 agonist). Positive inotrope.

Contraindications: a fib

Therapeutic use: CHF or MI w/ heart failure

Administered IV

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11
Q

Phenylephrine

A

MOA: alpha 1 agonist

Used to reverse hypotension and paroxysmal atrial tachycardia. Also used as a decongestant, topical vasoconstrictor, and mydriatic.

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12
Q

Midodrine

A

MOA: alpha 1 agonist

Used to treat orthostatic hypotenison.

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13
Q

Metaproterenol

A

MOA: Beta-2 selective agonist

Use: Bronchodilator- ashtma,

Side effects: tachycardia, palpitations, tremor, headache.

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14
Q

Terbutaline

A

MOA: Beta-2 selective agonist

Use: Bronchodilator- ashtma, , delay labor

Side effects: tachycardia, palpitations, tremor, headache.

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15
Q

Albuterol

A

MOA: Beta-2 selective agonist

Use: Bronchodilator- ashtma

Side effects: tachycardia, palpitations, tremor, headache.

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16
Q

Ritrodine

A

MOA: Beta-2 selective agonist

Use: Delay labor

Side effects: tachycardia, palpitations, tremor, headache.

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17
Q

Epinepherine

A

MOA cardiovascular - therapeutically usually vasoconstricts ( 1), can vasodilate (ß2); directly increases heart rate and force but reflexes to the elevation in blood pressure can suppress heart rate (vagal stimulation)

Administration - (1:1000 SC 0.01mg/kg), intraocular or inhaled

Metabolism - MAO and COMT

Contraindications - hyperthyroidism, hypertension, halogen-hydrocarbon anesthetics

Therapeutic uses

  1. hypersensitivity reactions-low BP and bronchospasm ( 1 and ß2) (More Beta-2 involvement than NE)
  2. with anesthetics ( 1)- vasoconstriction prevents diffusion of anesthetic
  3. topical hemostatic ( 1)
  4. restore heart beat (ß1)
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18
Q

Norepinepherine

A

MOA cardiovascular - vasoconstriction (1); increased heart rate & force (ß1); reflex reduction in heart rate (mediated by vagus nerve)

Administration - i.v.

iii. Contraindications - hyperthyroidism, anesthesia, pregnancy
iv. Therapeutic use-hypotension

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19
Q

Dopamine

A

MOA:
cardiovascular – positive inotrope (ß1); vasodilator in renal and mesenteric vasculature at low doses (dopaminergic); vasoconstrictor (1) at higher doses

neural - releases norepinephrine from nerves

Administration - i.v.

Therapeutic use- shock - maintains renal perfusion (

20
Q

Ephedrine

A

MOA: Releases NE by reversing axoplasmic pump and has direct effects. Cardio - increase BP. CNS - smaller than amphetamine

Administration - oral

Toxicity: similar to a combination of epinephrine and amphetamine

Therapeutic uses: bronchospasm, in medications for colds- releases norepinephrine to vasoconstrict, reducing mucosal congestion via 1; also bronchodilates (ß2) by a direct effect

21
Q

Pseudoephedrine

A

MOA: Stereoisomer of ephedrine (release norepinephrine from nerves by reversing the catecholamine axoplamic uptake pump) commonly used to treat nasal congestion.

Administration: Oral

22
Q

Eplerone

A

MOA: Aldosterone antagonist (more selective for the mineralcorticoid receptor than spironalactone). Potassium sparing diuretic.

Adverse effects: hyperkalemia, hypotension, dizziness, altered renal function, and increased creatinine. (Fewer sexual side effects than spironolactone)

23
Q

Spironolactone

A

MOA: Aldosterone receptor antagonist (also to a lesser extent, an antiandrogen, progestin, and antigonadotropin.) Potassium sparing diuretic.

Adverse effects: hyperkalemia, hypotension, dizziness, altered renal function, and increased creatinine. (Also sexual side effects such as gynecomastia)

Used topically as androgenic alopecia in men and woment and hirsutism, acne, and seborrhea in women

24
Q

Lisinopril (also ramipril and enalipril)

A

Class ACE Inhibitor

MOA: Block Angiotensin Converting Enzyme (ACE) which normally converst angiotensin I to angiotensin II. This in turn blocks angiotensin’s vasoconstriction and signaling to the adrenal gland to produce aldosterone and to the pituitary gland to produce ADH. Blocking these hormones decreases renal fluid retention.

25
Q

Losartan (and other artan’s)

A

Class ARB

MOA: Blocks Angiotensin II receptors which.in turn blocks angiotensin’s vasoconstriction and signaling to the adrenal gland to produce aldosterone and to the pituitary gland to produce ADH. Blocking these hormones decreases renal fluid retention.

26
Q

Furosemide (Lasix)

A

MOA: Blocks NKCC in ascending limb of loop of Henle. This prevents the resorbtion of 1 Na, 1 K, and 2 Cl- and their accompanying units of water causing diuresis.

Diuretic of choice in heart failure.

27
Q

Hydrochlorthiazide (HCTZ)

A

MOA: blocks Na/Cl transport in the DCT causing a decrease in Na resorption and subsequent diuresis.

Not used in acute situations.

28
Q

Acetazolamide

A

MOA: Blocks carbonic anhydrase. The mechanism of diuresis involves the proximal tubule of the kidney. The enzyme carbonic anhydrase is found here, allowing the reabsorption of bicarbonate, sodium, and chloride.

By excreting bicarbonate, the blood becomes acidic, causing compensatory hyperventilation, increasing levels of oxygen and decreasing levels of carbon dioxide in the blood

29
Q

Bidil

A

Isosorbide Dinitrate/ Hydralazine

Hydralazine - is a direct-acting smooth muscle relaxant used to treat hypertension by acting as a vasodilator primarily in arteries and arterioles. MOA is unknown.

Isosorbide Dinitrate- Same mech as NO. Increased cGMP –> decreases IC Ca++ –> increases MLC phospatase –> vasodilation (especially venous) –> decreased cardiac preload.

This pill is specifically for African Americans w/ CHF. (Hydralizine doesn’t improve m&m for whites)

30
Q

Isosorbide Dinitrate

A

MOA: Same as NO. Increased cGMP –> decreases IC Ca++ –> increases MLC phospatase –> vasodilation (especially venous) –> decreased cardiac preload.

Longer half life than NO –> worse in acute treatment, better longterm.

Uses: CHF

31
Q

Hydralazine

A

MOA: Direct-acting smooth muscle relaxant used to treat hypertension by acting as a vasodilator primarily in arteries and arterioles. MOA is unknown.

Not used in CHF. (except in African Americans in conjunction w/ Isosorbide Dinitrate)

32
Q

Procainamide

A

Class IA Antiarrhthmic

Cardiac Effects:
Slows upstroke of AP, slows conduction, prolongs QRS on ECG, prolongs APD by non-specific blockade of K+ channels.

Extracardiac Effects: Ganglion-blocking properties  reduces peripheral vascular resistance and can cause hypotension.

Toxicity: Excessive AP prolongation, QT-interval prolongation, induction of torsades de pointes arrhythmia and syncope, and excessive slowing of conduction. Long-term can cause syndrome resembling lupus erythematosus.

PK: Drug metabolite (N-acetylprocainamide, NAPA) has class III activity and is associated with torsades.
Eliminated by hepatic metabolism to NAPA, the NAPA via renal elimination.  T1/2 of NAPA is longer than procainamide!  Plasma protein binding 15 – 20%.

Uses: Most atrial and ventricular arrhythmias. Avoid long-term therapy  frequent dosing and lupus-related events. 2nd or 3rd choice drug for treatment of sustained ventricular arrhythmias associated with acute MI.

33
Q

Quinidine

A

Class IA Antiarrhytmic

Cardiac effects:Slows upstroke of AP, slows conduction, prolongs QRS on ECG, prolongs APD by non-specific blockade of K+ channels, antimuscarinic effects.

Toxicity: Adverse GI effects of diarrhea, nausea, and vomiting observed in ⅓ to ½ of patients. Cinchonism (headache, dizziness, tinnitus) observed at toxic concentrations.

PK: Readily absorbed from the GI tract and eliminated by hepatic metabolism, renal excretion.

Uses: Rarely used because of cardiac and extracardiac adverse effects and the availability of better tolerated drugs.

34
Q

Disopyramide

A

Class IA Antiarrhythmic

Cardiac Effects: Slows upstroke of AP, slows conduction, prolongs QRS on ECG, prolongs APD by non-specific blockade of K+ channels, antimuscarinic effects.

Extracardiac Effects: Atropine-like activity  urinary retention, dry mouth, blurred vision, constipation.

Toxicity: Same as quinidine. May precipitate heart failure de novo or in patients with preexisting depression of left ventricular function. Not to be used as first line drug in USA or in patients with heart failure.

PK: Loading doses not reccommended. because of risk of precipitating heart failure. Hepatic metabolism, renal excretion. Protein binding 50 – 65%.

Therapeutic Use: Ventricular arrhythmias.

35
Q

Lidocaine

A

Class IB Antiarrhythmic

Cardicac Effects: Selective depression of conduction in depolarized cells. Little effect seen on ECG in normal sinus rhythm.

Toxicity: One of the least cardiotoxic Class I antiarrhythmics. Most common adverse effects: paresthesias, tremor, nausea of central origin, lightheadedness, hearing disturbances, slurred speech, convulsions. These effects occur most commonly in elderly or vulnerable patients.

PK: Extensive first-pass hepatic metabolism. Must give parenterally. T1/2 1 – 2 hours.

Uses: Agent of choice for termination of ventricular tachycardia and prevention of ventricular fibrillation after cardioversion in the setting of acute ischemia. Prophylactic use may actually increase total mortality –> not advised!

36
Q

Mexiletine

A

Class IB Antiarrhythmic

Cardiac Effects: This is an orally active congener of lidocaine. Selective depression of conduction in depolarized cells. Little effect seen on ECG in normal sinus rhythm.

Extracardiac Effects: Significant efficacy in relieving chronic pain, especially due to diabetic neuropathy and nerve injury (off-label use.)

37
Q

Flecainide

A

Class IC Antiarrhythmic

Cardiac Effects: Slows upstroke of AP, slows conduction. Potent blocker of Na+ and K+ channels with slow unblocking kinetics (but does not prolong the AP or QT-interval.)

38
Q

Propafenone

A

Class IC Antiarrhythmic

Slows upstroke of AP, slows conduction. Weak β-blocking activity. Spectrum of action similar to quinidine, but does not prolong AP.

39
Q

Propanolol

A

Non-selective Beta Blocker

MOA: Slow heart rate, decrease the AV node conduction velocity (increase PR interval), Increase AV node refractory period

Has some class I activity. Adverse effects include bronchospasm, bradycardia, fatigue.

40
Q

Sotalol

A

Non-selective Beta Blocker.

MOA: Slow heart rate, decrease the AV node conduction velocity (increase PR interval), Increase AV node refractory period

Prolongs the action potential (delays the slow outward current of K+)

41
Q

Esmolol

A

Beta-1 selective blocker

MOA: Slow heart rate, decrease the AV node conduction velocity (increase PR interval), Increase AV node refractory period

Very short acting. Used primarily for intraoperative and acute arrhythmias.

42
Q

Acebutol

A

Beta-1 selective blocker.

MOA: Slow heart rate, decrease the AV node conduction velocity (increase PR interval), Increase AV node refractory period

Best choice for patients w/ asthma

43
Q

Metoprolol

A

Beta-1 selective blocker

MOA: Slow heart rate, decrease the AV node conduction velocity (increase PR interval), Increase AV node refractory period

First choice post MI.

44
Q

Terazosin

A

Alpha 1 blocker

45
Q

Clonidine

A

o α2 agonist, antihypertensive, major site of action medulla oblongata
o Decreases sympathetic activity w/o interfering w/ reflexes
o Oral/transdermal
o Also tx for ADHD w/ Ritalin or Adderall
o Side Effects: depression, sexual dysfx, dry mouth, bradycardia

46
Q

α-methyldopa

A

o α2 agonist, antihypertensive, major site of action medulla oblongata
o Decreases sympathetic activity w/o interfering w/ reflexes
o Oral antihypertensive safe to use in pregnancy
o Converted to methyl-NE by dopamine β-hydroxylase
o Side Effects: depression, sexual dysfx, dry mouth, bradycardia

47
Q

Guanabenz

A

o α2 agonist, antihypertensive, major site of action medulla oblongata
o Decreases sympathetic activity w/o interfering w/ reflexes
o Side Effects: depression, sexual dysfx, dry mouth, bradycardia

CRRAB I Mike Rose (13 decks)

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