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09/09/2011

Additional Medical Flashcards

 


 

Cards

Term

ALPHA-2A AGONISTS

 CLONIDINE,GUANFACINE, METHYLDOPA

 

Definition

inhibit sympathetic outflow from cardiovascular control centers of thebrain (the NTS and RVLM) by:

 

            a) inhibiting presynaptic Ca2+ channels -> ↓ NE release

               b) opening postsynaptic K+ channels -> K+ efflux -> hyperpolarization

 

                        Net effect: ↓ peripheral resistance, HR and CO with ↑ vagal tone.  The ↑ vagal tone can cause marked bradycardia in some patients.

Term

CLONIDINE (Catapres) ALPHA-2A AGONISTS

 

Definition

Higher doses stimulate vascular α2B receptors -> vasoconstriction.  This might explain the loss of therapeutic effect with higher doses and the initial ↑ in BP when clonidine is given IV.  Given orally, drug levels do not rise as rapidly and the central effects override any vasoconstrictionfollowing oral administration.

USES:            - Antihypertensive

                        - Treat autonomic withdrawal symptoms from opiates, EtOH & nicotine

                        -  Epidural (Duraclon) for severe pain in cancer patients who do not respond to opioids.

                        - Tourette's syndrome                                                                        - Anxiety & panic attacks

                        - Attention deficit hyperactivity disorder (ADHD)                       

- Menopausal flushing

CAUTION Discontinue slowly to avoid rebound sympathetic activity that can lead to a  hypertensive crisis, tachycardia or an arrhythmia

MOST COMMON SIDE EFFECTS:                       

a) dry mouth

b) sedation

c) Constipation is common.  Clonidine ↓s Ach release by stimulating α2A heteroreceptors on myenteric and submucosal cholinergic neurons -> ¯ peristalsis by relaxing intestinal smooth muscles -> ↑ time for Na+/H2O reabsorption.  It also ¯s GI secretions.  This can cause weight gain.  A diuretic can be added to combat any significant Na+/H2O retention.

d) sexual dysfunction in males. 

Term
 GUANFACINE (Tenex) ALPHA-2A AGONISTS
Definition

- more selective than clonidine -> fewer side effects.  Long t ½ permits once  a day dosing.  Give at bedtime to minimize effects of sedation.

 

            USES: Antihypertensive & to manage withdrawal symptoms from heroin et al.  Extended release form is approved for threating ADHD.

Term
METHYLDOPA (generic) ALPHA-2A AGONISTS
Definition

PRODRUG.

            Metabolized to α-methyl-norepinephrine, an α2 agonist that displaces NE in nerve terminals and is released in its stead.

            In  ̴ 20% of patients, chronic use can cause a (+) Coomb’s test for autoantibodies vs the Rhlocus on RBCs.  1-5% of these patients develop hemolytic anemia.

            Methyldopa has been proven safe to use during pregnancy and is a first line drug in this situation.

Term

.  ALPHA ANTAGONISTS

-ZOSIN

PRAZOSIN (Minipress),TERAZOSIN (Hytrin),DOXAZOSIN (Cardura)

Definition

↓ BP by inhibiting vasoconstriction, not by causing vasodilation.  The endpoint is the same but the magnitude of effect and how you got there is different.




Term

PRAZOSIN (Minipress)

ALPHA ANTAGONISTS

Definition

selectively blocks a1 in arterioles & veins thus decreasing peripheral resistance & venous return. 


It does not cause reflex tachycardia or INCREASE ­ CO.

           

  LOW BP might cause Na+/H2O retention.  A diuretic can be added.  Short t ½ – dosed 2-3x/day

 

Term
TERAZOSIN (Hytrin)
Definition

a1 selective - T ½ = 9-12 hrs.  Dosed 1-2 x/day.  Generally, no reflex    tachycardia

USES:           

- Antihypertensive

- Benign prostatic hypertrophy (BPH) – might have actions within the prostate as well as on urethral smooth muscle.

Term

.  DOXAZOSIN (Cardura)

ALPHA ANTAGONISTS

Definition

- a1 selective.  T ½ = 22 hrs – 1x/day.  Causes slight reflex tachycardia

 

            USES:            - Antihypertensive            - BPH

 

** All 3 of these Rxs cause a “1st Dose Effect” characterized by postural hypotension & syncope.

 

It occurs:            a) 30-90 minutes after the 1st dose

                        b) after a rapid ↑ in dose

                        c) after adding another antihypertensive medication to the regimen

 

            MECHANISM: It has been postulated that this results from delayed baroreflex compensation for the ↓ BP leading to an exaggerated postural hypotension effect & some tachycardia.

 

                        To minimize the risk of injury from hypotension, it is recommended that the 1st dose betaken at bedtime.

Term

BETA BLOCKERS

-OLOL

PROPRANOLOL,NADOLOL (Corgard),TIMOLOL (generic), PINDOLOL (generic),LABETALOL (Trandate),PENBUTOLOL (Levatol),CARVEDILOL (Coreg)

Definition

Blocking β2 receptors in vasculature can -> unopposed α1-mediated                                     vasoconstriction and ↑ vascular resistance.  However, the net effect is a ↓ in BP from combined                                                             (-) inotropic effects and inhibition of renin release.

 

            WHAT IS THE EFFECT ON HR, CONTRACTILITY, CO & MYOCARDIAL O2 DEMAND?

 

            CAUTION if asthma / COPD / bronchospasms -            WHY?

 

 

            CAUTION if DIABETIC –            WHY?  Remember your autonomics!

 

                        In the sympathetic fight or flight response, glucose is needed for energy.  Sympathetic signals are sent to the adrenal medulla to release catecholamines, namely EPI.

 

                        One role of EPI is to stimulate glycogenolysis partly through a β2 mechanism.  By blocking β receptors, you inhibit glycogenolysis -> ↓ blood sugar.

 

                        In diabetics on β blockers, when the next dose of insulin or oral hypoglycemic is due, blood sugar will ↓ even further and the patient can become hypoglycemic.

 

                        WHAT IS A CARDINAL CARDIOVASCULAR SIGN OF HYPOGLYCEMIA?

 

                        WHY DOES THIS OCCUR?

 

 

                        WILL YOU SEE IT?                                    WHY?  (Think this through!)

 

 

 

                                                MONITOR BLOOD GLUCOSE CAREFULLY!

 

            ¯ BP/CO can ¯ renal blood flow causing Na+/H2O retention.  If so, add a diuretic.

 

            Discontinue slowly to avoid precipitating an arrhythmia, angina attack or sudden death.

1.  BRADYCARDIA

2.  FATIGUE – This is related to a ↓ in muscle K+.  β2 stimulation normally drives K+ into tissues.              Therefore, β block can be expected to do the opposite.  However, they generally do not cause                                                                         frank hyperkalemia.

3.  INCREASE­ PLASMA LIPIDS

Term

PROPRANOLOL (Inderal)

BETA BLOCKERS

Definition

nonselective, blocks β1 and β2 equally.  Therapeutic effects based on blocking β1.  Higher doses have a "quinidine-like" local anesthetic effect.

 

            USES: hypertension, supraventricular arrhythmias, MI, angina, migraine, block symptoms                                                             associated with hyperthyroidism & pheochromocytoma

Term

NADOLOL (Corgard)

BETA BLOCKERS

Definition
T ½ = 20-24 hrs thus once a day.              USES: hypertension, angina
Term

TIMOLOL (generic)

BETA BLOCKERS

 

Definition

hypertension, migraine

 

Term

PINDOLOL (generic)

BETA BLOCKERS

Definition

has high intrinsic sympathomimetic activity (ISA).  It therefore does not ¯ BP & HR as much as other β blockers.  This can be useful in hypertensive patients with bradycardia.

 

            WHAT DOES HAVING ISA MEAN?

Term

LABETALOL (Trandate)

 BETA BLOCKERS

 

Definition

has 4 different isomers each with different activity.

 

            Some                        a) block α1 -> vasodilation -> ↓ BP

            Others              b) block β1 -> ↓ HR & BP

            Still another            c) stimulates β2 -> vasodilation -> ↓ BP

            Effect c) enhances effect a) whereas effect b) prevents reflex stimulation of HR caused byeffects a) and c).  By blocking α1, there is no ↑ in peripheral vascular resistance inresponse to ↓ BP.  This is good for the elderly and African-Americans hypertensives who generally do not respond well to β blockers.

 

            Expect some orthostatic hypotension from the vasodilation.

 

            NET EFFECT:  ↓ BP with little or no significant ­ in HR

Term

PENBUTOLOL (Levatol)

BETA BLOCKERS

Definition
for hypertension
Term

CARVEDILOL (Coreg)

BETA BLOCKERS

Definition

– for hypertension.  Racemic mixture – nonselective α & β block

 

            Approved for CHF - WHAT IS THE RATIONALE?  In CHF, with the ↓ in CO, there is ↓perfusion of carotid baroreceptors that sense a ↓ in BP.  They send reflex sympathetic signals to ↑ HR and vasoconstrict.  This ↑s afterload which further ↓s CO and can furtherdamage the heart.  β block is used to block this ↑ in sympathetic activity from thebaroreceptors.

 

            Rx Interactions:            - ¯ digoxin clearance -> digoxin toxicity.  ¯ Dose of digoxin.

                                                - Inhibitors of CYP2C9 (amiodarone, fluconazole et al.) ↑carvedilol levels                                                                                     -> ↑ β block & slowing of HR and conduction.

 

            CAUTION: Rare, but serious, hypersensitivity reactions (anaphylaxis, angioedema, urticaria)                                                 have occurred.  Do not use if there is a history of Stevens-Johnson syndrome,angioedema or any other serious allergic reaction that can be life-threatening

Term

SELECTIVE b1 BLOCKERS (best for patients with compromised respiratory function)

 

Definition

1.  ATENOLOL (Tenormin)

2.  METOPROLOL (Lopressor)

3.  BETAXOLOL (generic)

4.  ACEBUTOLOL (Sectral)

5.  BISOPROLOL

6.  NEBIVOLOL (Bystolic) 

Term

 ATENOLOL (Tenormin) 

 

SELECTIVE b1 BLOCKERS

Definition
– hypertension, angina, MI
Term

METOPROLOL (Lopressor)

SELECTIVE b1 BLOCKERS

Definition
– hypertension, angina, MI
Term

BETAXOLOL (generic)

SELECTIVE b1 BLOCKERS

Definition
– hypertension.  CAUTION if pregnant.  Can ¯ placental perfusion (a riskw/ all β blockers) -> fetal death, premature delivery, fetal bradycardia, hypoglycemia.
Term

ACEBUTOLOL (Sectral)

SELECTIVE b1 BLOCKERS

Definition
hypertension, ventricular arrhythmias.  Parent & metabolite diacetolol                         are active.  Diacetolol has ISA.            WHAT IS A RX W/ ISA GOOD FOR
Term

BISOPROLOL (Zebeta)

SELECTIVE b1 BLOCKER

Definition
for hypertension
Term

NEBIVOLOL (Bystolic)

SELECTIVE b1 BLOCKER

Definition

for hypertension

 

Term

Ca2+ CHANNEL BLOCKERS (CCBs)

-ipine

VERAPAMIL (Calan), DILTIAZEM (Cardizem), NIFEDIPINe (Procardia),NIMODIPINE (generic), ISRADIPINE (DynacirCR), NICARDIPINE (Cardene),FELODIPINE (generic), NISOLDIPINE (Sular),AMLODIPINE (Norvasc),  CLEVIDIPINE (Cleviprex)

Definition

 

            3 Chemical classes:            a) phenylalkylamines                        Prototype: verapamil

                                                b) benzothiazepines                        Prototype: diltiazem

                                                c) dihydropyridines                        Prototype: nifedipine

 

            MECHANISM: block L-type Ca2+ channels.  On T tubules, this site is sometimes called the DHP                                                                                     receptor (DHP = dihydropyridine)

 

            Dihydropyridines preferentially interact with vascular smooth muscles b/c vascular smooth                                     muscle remains depolarized longer than the nodes permitting access to the Ca2+ channel.

 

            They all preferentially bind to open or inactivated channels, i.e. those in a depolarized state.

 

            Those acting mainly on vascular smooth muscle relax arterial, not most venous, smooth muscle.

 

            WILL THIS DECREASE PRELOAD OR AFTERLOAD?

 

            WHY ISN’T SKELETAL MUSCLE AFFECTED?


Avoid short acting forms.  They can cause reflex tachycardia & activation of the RAAS which is             associated with ↑ morbidity & mortality in patients with chronic hypertension.  Most of these             products are now available in a long acting, controlled release form that circumvents activation                         of the RAAS.

CAUTIONS FOR Ca2+ CHANNEL BLOCKERS:

 

1. They are extensively metabolized by the liver so any ↓ in hepatic function -> significant ↑ Rx levels

            -> hypotensive episodes from excessive vasodilation or cardiodepressant effects.

 

2. CCBs are (-) inotropes.  In patients with CHF, the effect is additive.  If you add a vasodilator, the             heart could go into decompensation. Although dihydropyridines have minimal effects on the             heart, the potential is there so be careful!

 

3. Do not take with grapefruit juice.  This juice contains furanocoumarins that inhibit the metabolism of                                                             CCBs -> ↑ Rx levels and side effects.

 

RX INTERACTIONS:  b Blockers used with verapamil or diltiazem cause additive (-) inotropy ->                        cardiac decompensation (fatigue, shortness of breath, edema, paroxysmal nocturnal dyspnea)

 

NON-LABELED USES: Raynaud’s phenomenon

SIDE EFFECTS (mostly dihydropyridines): headache, facial flushing, dizziness & pedal edema

 

CCBs are often used with a nitrovasodilator to lower BP – WHY?

Term

VERAPAMIL (Calan)


CCB

Definition

CCBs WITH PROMINENT EFFECTS ON THE NODES

– acts on nodes & vascular smooth muscle but used mainly for angina and various arrhythmias. 

Term

 

DILTIAZEM (Cardizem)

CCB

Definition

CCBs WITH PROMINENT EFFECTS ON THE NODES

also acts on nodes & vascular smooth muscle but is generally used for angina & various arrhythmias.  

Term
CCBs THAT ACT MAINLY ON VASCULAR SMOOTH MUSCLE (dihydropyridines)
Definition

 NIFEDIPINE (Procardia) can cause excessive vasodilation which can ↑ HR & O2 demand.

 

            WHAT CAN YOU DO ABOUT IT?

 

  NIMODIPINE (generic), ISRADIPINE (Dynacirc CR), NICARDIPINE (Cardene),  FELODIPINE (generic), NISOLDIPINE (Sular), AMLODIPINE (Norvasc),  CLEVIDIPINE (Cleviprex) – an IV product for use when oral therapy is not feasible.

Term

ACE INHIBITORS (ACEIs)

-APRIL

 CAPTOPRIL (Capoten),  LISINOPRIL (Prinivil) – excreted unchanged, TRANDOLAPRIL (Mavik), QUINAPRIL (Accupril),  RAMIPRIL (Altace),FOSINOPRIL (Monopril)

MOEXIPRIL (Univasc),  BENAZEPRIL (Lotensin),ENALAPRIL (Vasotec), PERINDOPRIL (Aceon)

 

Definition

RENIN:            WHERE IS IT SYNTHESIZED?

 

                                    WHAT STIMULATES ITS RELEASE?

 

                                    WHAT DOES IT DO?

 

            WHAT CONVERTS ANG I TO ANG II?                       

 

            EFFECTS OF ANG II:

            a) ↑s total peripheral resistance by constricting arterioles and to some extent venules.

            b) ↑ aldosterone release from the zona glomerulosa of the adrenal cortex.

 

                        WHAT DOES ALDOSTERONE DO?

 

 

            c) releases ADH.            WHAT DOES ADH DO?

 

            d) releases NE from sympathetic nerve endings -> potentiation of vasoconstriction by Ang II.

            e) ↑s sympathetic outflow from CNS through effects on circumventricular organs (SFO, OVLT).

            f) causes remodeling (proliferation and hypertrophy of vascular smooth muscle and cardiacmyocytes)

All are used for hypertension.  Some are also used for heart failure / MI / left ventricular dysfunction /                                                                                                 diabetic neuropathy

SIDE EFFECTS common to all:

 

1.  1st DOSE EFFECT: similar to that seen with the α1 blockers (see above)

 

2.  DRY COUGH – incidence 25+%.  More common in women.  Referred to as the bradykinin cough             b/c ACE also metabolizes bradykinin.  Thus, ACEIs ↑ bradykinin levels.  Bradykinin is a             vasodilator and releases histamine -> fluid accumulation in the lungs.  It has been suggested that                                                                         this contributes to the cough.

 

3.  HYPERKALEMIA – This is predictable.            WHY?  (Think about what Ang II does!)

 

 

 

            Factors that ­ the risk of hyperkalemia:

 

            a) renal insufficiency, particularly if CHF

            b) adding a K+-sparing diuretic

            c) K+ supplements

 

            d) NSAIDS – This should also be predictable – WHY?

 

                        NSAIDS inhibit synthesis of PGs that normally dilate renal arteries thus causing             constriction of renal arteries & ↓ renal blood flow -> Na+/H2O retention.  By retaining Na+, less             Na+ is presented to the distal tubules where it is normally reabsorbed in exchange for K+.  By not             reabsorbing as much Na+, you are not excreting as much K+ -> hyperkalemia.

 

            e) β blockers – WHY?  Stimulating β2 receptors normally drives K+ into tissues.  Blocking these                                                                         receptors would have the opposite effect -> hyperkalemia.

All are used for hypertension.  Some are also used for heart failure / MI / left ventricular dysfunction /diabetic neuropathy

4.  ANGIOEDEMA – Infrequent but potentially fatal.  Rapid swelling in the nose, throat,             mouth, glottis,             larynx, lips & tongue.  AFRICAN-AMERICANS are at greater risk than Caucasians and Asians.

 

5.  FETAL TOXICITY – Pregnancy category D: (+) evidence of human fetal risk but benefits might                                     outweigh risks in life-threatening situations or diseases for which safer Rxs cannot beused or are ineffective

 

            Continuous administration during the 2nd-3rd trimesters can -> oligohydramnios, fetal calvarial &                                                 pulmonary hypoplasia, growth retardation & death.

 

            Several ACEIs have been detected in breast milk.  Be careful if nursing.  These Rxs can causeanuria and death in the neonate.

 

Rx INTERACTION: NSAIDS -> Na+/H2O retention.  Certain PGs inhibit ADH.  Inhibiting synthesis of             these PGs -> ↑ ADH -> H2O retention.  This interferes with the actions of             antihypertensive Rxs                                                 & can -> weight gain.  See 3d) above to explain Na+ retention.

 

** ACEIs tend to be less effective in African-Americans than they are in other races.

 


Term

ACEIs

 


ACTIVE (not proRxs):

Definition

1.  CAPTOPRIL (Capoten) – food ¯s absorption – give 1 hr before meals.


2.  LISINOPRIL (Prinivil) – excreted unchanged


used for hypertension.  Some are also used for heart failure / MI / left ventricular dysfunction /diabetic neuropathy

Term

ACEIs

PRO-RXS

Definition

 TRANDOLAPRIL (Mavik),  QUINAPRIL (Accupril),RAMIPRIL (Altace), FOSINOPRIL (Monopril), MOEXIPRIL (Univasc),BENAZEPRIL (Lotensin),ENALAPRIL (Vasotec),PERINDOPRIL (Aceon)

 

            The suffix "lat" denotes the active form of the Rx.  Ex: ramiprilat, enalaprilat, fosinoprilat

 

All are used for hypertension.  Some are also used for heart failure / MI / left ventricular dysfunction /diabetic neuropathy

Term

ANGIOTENSIN II RECEPTOR BLOCKERS (ARBs)

-ARTAN


CANDESARTAN (Atacand), EPROSARTAN (Teveten),

IRBESARTAN (Avapro), LOSARTAN (Cozaar), OLMESARTAN (Benicar), VALSARTAN (Diovan), TELMISARTAN (Micardis), AZILSARTAN (Edarbi)

Definition

Blocking AT-1 receptors will have similarbenefits as the ACEIs.


Theoretically, they should be more effective that ACEIs b/c Ang II can be synthesized from                                     angiotensinogen by other enzymes such as chymase in connective tissues and mast cells and by trypsin. These other enzymes are not inhibited by ACEIs.

 

            They are in pregnancy category D but they do not cause angioedema and the incidence of coughis less b/c they do not interfere with the metabolism of bradykinin.

 

            Hyperkalemia is common if decreased renal function or if taking K+ sparing diuretics.

Term

CANDESARTAN (Atacand)

ANGIOTENSIN II RECEPTOR BLOCKER (ARB)

Definition

is a prodrug activated by ester hydrolysis on absorption.

 

            OTHER USE:  prophylaxis against migraine RX INTERACTION:  ­s Li+ levels

Term

IRBESARTAN (Avapro)


ANGIOTENSIN II RECEPTOR BLOCKER (ARB)

Definition
 approved to treat diabetic nephropathy
Term

 LOSARTAN (Cozaar)


ANGIOTENSIN II RECEPTOR BLOCKER (ARB)

Definition

Parent & metabolite are active giving it a long t ½ thus 1x/day dosing.  It is less effective in African-Americans but this does not apply to all ARBs. 

Also approved for  diabetic nephropathy.

 

            FOOD INTERACTION: Avoid grapefruit juice - delays conversion to its active metabolite.

Term

TELMISARTAN (Micardis)

ANGIOTENSIN II RECEPTOR BLOCKERS (ARBs)

Definition
T ½ = 24 hrs
Term

HYDRALAZINE (generic)

MISCELLANEOUS VASODILATORS

Definition

Relaxes arteriolar smooth muscle by

 

            a) ↓ IP3-mediated release of Ca2+ from the SR

            b) opens ATP-dependent K+ channels (K+ATP) -> hyperpolarization

 

            This causes a dramatic ­ in sympathetic activity resulting in:

 

            a) ↑ HR & contractility                        WHAT CAN YOU DO ABOUT IT?

 

            b) ↑ plasma renin                                    WHAT CAN YOU DO ABOUT IT?

 

            c) fluid retention from ↑ renin                        WHAT CAN YOU DO ABOUT IT?

 

 

            Hydralazine is metabolized by acetylation.  WHAT IS THE SIGNIFICANCE OF THIS?

 

 

            Most common side effects:  Hypotension, tachycardia, headache.  Strong baroreflex can cause                                                                         myocardial ischemia which could precipitate an angina attack.

            Most serious side effects:

 

                        a) Lupus syndrome – 4x more often in women & more common in Caucasians.                                                              Generally with chronic use.  Incidence related to dose and acetylator phenotype.

 

                        b) Symptoms resembling serum sickness

 

            BIDIL – hydralazine + isosorbide: Promoted for African-Americans who don’t respond well to                                                                                                 β blockers, ACEIs or ARBs.

 

Term

NITROPRUSSIDE (Nitropress)


MISCELLANEOUS VASODILATORS

Definition

metabolized to nitric oxide in vascular smooth muscle or liberates             nitric oxide through a non-enzymatic mechanism.  Dilates arteries and veins.  Given by IV                                                 infusion.  Light sensitive - the IV bag and line must be wrapped in foil.

 

            Onset within 30 seconds.  Hypotensive effects disappear within 3 minutes of discontinuation.

 

            Nitric oxide is metabolized to cyanide which in turn is metabolized to thiocyanate for excretion. Chronic infusion or ↓ renal function can cause accumulation of cyanide or thiocyanate ->  toxicity (thiocyanate: nausea, disorientation, spasms, convulsions, psychosis).

 

            USES: hypertensive emergencies / controlled hypotension to ¯ bleeding during surgery / acute   CHF to elicit a reflex ­ CO

Term

FENOLDOPAM (Corlopam)


MISCELLANEOUS VASODILATORS

Definition

IV for hypertensive emergencies.  MECHANISM:  Stimulates DA D1    receptors in coronary, renal & mesenteric arteries

 

            CAUTION if:    a) using with a b blocker -> ­­ hypotension

                                                b) glaucoma -> ­ intraocular pressure

                                                c) allergic to sulfas.  Contains sulfite

Term

MINOXIDIL (generic)


MISCELLANEOUS VASODILATORS

Definition

ProRx.  Activates K+ channels -> K+ efflux -> hyperpolarization ->             relaxation of vascular smooth muscle.  It dilates arteriolar resistance vessels with no significant             effect on venous capacitance.  It elicits a strong baroreflex ­ in CO, stimulates renin release &             causes fluid retention.            WHAT CAN YOU DO ABOUT THIS?

 

 

            It can flatten & invert T-waves & cause pericardial effusions -> tamponade.  It is generally used                                     with a diuretic for severe hypertension that is unresponsive to diuretics alone.

 

            Chronic use can cause hypertrichosis.             WHAT ELSE IS THIS RX IS USED FOR?

Term

RX TREATMENT FOR PULMONARY ARTERIAL HYPERTENSION (PAH)

 

Definition

Pulmonary arterial constriction, hypertrophy & fibrosis -> right ventricular overload & failure.


EPOPROSTENOL (Flolan), TREPROSTINIL (Remodulin), ILOPROST (Ventavis), BOSENTAN (Tracleer),AMBRISENTAN (Letairis)

Term

EPOPROSTENOL (Flolan)


PAH Rx

Definition
– a PGI2 for IV use in patients refractory to other therapy.  Dilates             pulmonary & systemic arterial beds -> ↓ afterload & ↑ CO.  It also inhibits platelet aggregation
Term

TREPROSTINIL (Remodulin)


PAH Rx

Definition

– a PGI2 analog with actions similar to epoprostenol.

 

Term

ILOPROST (Ventavis)


PAH Rx

Definition
– a  PGI2 analog that dilates pulmonary and systemic arteries.
Term

BOSENTAN (Tracleer)


PAH Rx

Definition

- MECHANISM:  Antagonist at endothelin-1 (ET-1) receptors ETA & ETB.

            ET-1 is a powerful vasoconstrictor whose levels in the pulmonary artery are elevated in PAH.

 

            ETA mediates vasoconstriction & cell proliferation.  ETB mediates vasodilation, anti-proliferation                                                                         & clearance of ET-1

 

            CAUTION:            a) potential liver toxicity. Liver transaminases may be elevated 3x the upper limit                                                                                                 of normal.

                                    b) teratogenic in animals so be careful if pregnant.

                                    c) potential to ↓ sperm count.

            Metabolized by & induces CYP3A4 & CYP2C9.  It can induce its own metabolism.

 

            Bosentan must be obtained from the manufacturer through a limited access program.

Term

AMBRISENTAN (Letairis)


PAH Rx

Definition
selective ETA antagonist.  Same cautions as with bosentan except             monthly liver enzyme tests are not required.  Available only through the access program.
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