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Pharm > Antihypertensives > Flashcards

Antihypertensives Flashcards

1
Q

Hydraulic equation

A

BP=CO (HRxSV) x PVR

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2
Q

Regulates parasympathetic activity

A

Vagus nerve

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3
Q

Preload is the result of what vessel characteristic

A

Venous capacitance

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4
Q

If Peripheral resistance increases

A

More pressure needed to keep blood moving

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5
Q

Autonomic feedback loop involves (components)

A

Baroreceptors, sympathetic and parasympathetic nervous systems

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6
Q

Sympathetic response to low BP

A

Vasoconstriction, increased heart rate, increased PVR and increased contractility

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7
Q

Parasympathetic response to high BP

A

Decreased heart rate.

*BP= CO (HRxSV) x PVR

Lowering one factor in the equation lowers BP.

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8
Q

Hormonal loop involves what organ? What specific area of said organ?

A

The hormonal loop involves the kidneys. The juxtaglomerular apparatus of the kidneys detects changes in renal blood flow and oxygen delivery.

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9
Q

Centrally acting sympathoplegics

A

Methyldopa, clonidine, dexmedetomidine

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10
Q

Adrenoceptor Antagonists

A

Propranolol, metoprolol, Prozasin, terasozin, doxazosin

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11
Q

Clonidine and methyldopa antihypertensive activity

A

Primarily due to alpha agonist activity in brain stem which leads to decreased sympathetic stimulation. Bind more tightly with Alpha 2 than Alpha 1.

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12
Q

Centrally acting alpha 2 agonist

A

Dexmedetomidine

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13
Q

Primary use of methyldopa

A

Pregnancy induced HTN

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14
Q

Explain why clonidine causes brief rise in BP before exhibiting anti-HTN effects

A

Binds to alpha 1 in periphery prior to getting to CNS and binding to alpha 2

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15
Q

Limitations of propranolol as treatment for HTN

A

Not cardioselective

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16
Q

Alternative beta blocker that is a used for HTN rather than propranolol

A

Metoprolol. Beta 1 selective, decreased HR and Contractility.

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17
Q

Short acting Beta 1 uses for transient elevations in heart rate

A

Esmolol

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18
Q

Action of Alpha 1 blockers and their role in anti HTN

A

Block alpha 1 at arterioles and venules. Dilates resistance (arteries) and capacitance vessels (veins).

Increased capacitance volume results in decreased circulating blood volume (lower BP)

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19
Q

Oral vasodilators

A

Hydralazine and minoxidil

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20
Q

Parenteral vasodilators

A

Nitroprusside and fenoldopam

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21
Q

Combination vasodilators

A

Calcium ch blockers

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22
Q

Why vasodilators are best used in combination with other drugs

A

The reduction of PVR and MAP leads elicits compensatory responses. Alternative drugs that combat these mechanisms improve outcome.

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23
Q

Vasodilator drugs MOA (from compensatory diagram)

A

Decreased SVR, Decreased MAP.

24
Q

Hormonal loop response to vasodilators

A

Decreased MAP sensed, increased Renin which increases angiotensin II, increased Aldosterone. Increased sodium retention and thereby increased water and volume. Which all leads to increased MAP

25
Q

Sympathetic Response to low MAP associated with vasodilator use.

A

Increased venous tone, increased contractility, increased heart rate, decreased capacitance, increased SVR, increased CO. All leads to increased MAP.

26
Q

Often first drug choice for HTN. Blocks portion of compensatory mechanism seen with vasodilator use

A

Diuretics. Block action of hormonal loop.

27
Q

PO vasodilator that induces NO release in endothelium

A

Hyrdalazine.

28
Q

PO vasodilator that opens K+ channels in smooth muscles

A

Minoxidil

29
Q

Vasodilator that releases NO directly into bloodstream

A

Nitroprusside. Used for HTN emergencies and heart failure

30
Q

Vasodilator that metabolizes into cyanide

A

Nitroprusside

31
Q

Vasodilator that targets Dopamine 1

A

Fenoldopam

32
Q

Target for calcium channel blockers

A

L type calcium channel

33
Q

Calcium Ch Blocker Drugs

A

Verapamil
Diltiazem
Dihydropyridine “-pine”

34
Q

Calcium Channel Blockers target different areas to lower blood pressure. Which one effects the heart, peripheral vasculature and which is mixed.

A

Verapamil- heart
Diltiazem- both
Dihydropyridines- peripheral vasculature. (Less cardiac effects)

35
Q

List the two classes of Angiotensin inhibitors

A

ACE inhibitors and ARBs

36
Q

What stimulates release of Renin in the kidney

A

Decreased arterial pressure
Reduced sodium delivery
Sympathetic stimulation

37
Q

Only Renin blocker

A

Aliskiren

38
Q

How is angiotensin II unique from angiotensin I?

A

Angiotensin II can cause vasoconstriction by itself. Whereas angiotensin cannot.

39
Q

Explain the relationship between ACE and Bradykinin

A

ACE breaks down Bradykinin into inactive metabolites.

40
Q

Explain why ACE inhibitors blocking breakdown of bradykinin is significant

A

Bradykinin will increase prostaglandin synthesis. Bradykinin is a vasodilator as are prostaglandins. This will help with lowering blood pressure.

However, 10% of patients on ACEI will develop chronic cough. This cough can be debilitating and require change in medication.

41
Q

What suffix is associated with ACEI

A

-pril

42
Q

Contraindications for ACEI

A

Hypovolemic pts and first trimester pregnancy (teratogenesis)

43
Q

Suffix associated with ARBs

A

-sartan

44
Q

How are ARBs more beneficial than ACEI

A

ARBs have no effect on bradykinin therefore no cough is seen with ARBs.

45
Q

Pulmonary Hypertension treatments

A

Prostaglandins (prostacyclin) and endothelin receptor antagonists Bosentan (Tracleer), Tezosentan
Also help (sildenafil, milrinone)

46
Q

Endothelin is produced in response to

A

Low shear stress

47
Q

Endothelin function

A

Vasoconstriction in the lung.

48
Q

Why are ET (endothelin) blockers more effective for pulmonary HTN?

A

Endothelin causes vasoconstriction on the lungs. Therefore blocking this will help decrease pressure in the lungs.

49
Q

Outpatient therapy for HTN initial, non pharmacological

A

Decrease sodium intake. Increase exercise. Lose weight.

50
Q

First line antihypertensives outpatient.

A

Low dose diuretic
Beta blocker
Calcium channel
Dual therapy

51
Q

Hypertensive Crisis divided into what two categories

A

Hypertensive urgency
Hypertensive emergency

52
Q

How does Hypertensive Urgency differ from hypertensive emergency

A

Urgency is same parameters for blood pressure as emergency (>180/110). The difference is there is no end organ damage with urgency. BP can be lowered in hours or days

53
Q

Hypertensive emergency

A

BP >180/110
Acute end organ damage. BP must be lowered immediately

54
Q

Most common drugs utilized during hypertensive emergencies

A

Nitroprusside and Fenoldopam

55
Q

Most common drugs utilized during hypertensive emergencies

A

Nitroprusside and Fenoldopam (increases renal perfusion)

56
Q

What two areas in the brain stem control sympathetic and parasympathetic outflow

A

(RLVM) Rostral Ventrolateral Medulla
(NTS) Nucleus of the Tract Solitarius

Pharm (8 decks)

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