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Pharmacology Test 3 > CHAPTER 11 ANTIHYPERTENSIVES > Flashcards

CHAPTER 11 ANTIHYPERTENSIVES Flashcards

1
Q

What is the Hydraulic Equation?

A

BP = CO x PVR

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2
Q

Blood Pressure is maintain by regulating _________(systolic) and _______(diastolic).
Short term effect of BP is directly affected by these two components.

What is long term effect affected by?

A

CO (systolic)
PVR (diastolic)

Long term effect: Kidneys

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3
Q

Describe the mechanism of response when there is a decrease in BP.

A
  1. Decrease BP will be sensed in the baroreceptors and send signal to the VMC.
  2. VMC will decrease parasympathetic activity and increase sympathetic activity.
  3. Sympathetic activity will speed up HR. Adrenal medulla will release epinephrine. Dropping ESV. More blood entering artery system. Increase SV.
  4. Other factors that epinephrine will play: increasing activity of resp pump, increase skel musc pump, increase sympathetic venoconstriction, increasing venous return and increasing EDV.
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4
Q

How many percent of our blood is stored in the veins?

A

75%

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5
Q

What are the 4 anatomical sites of blood pressure control?

A
  1. Resistance Arterioles (use alpha1 blockers)
  2. Capacitane Venules (use NO)
  3. Heart (Beta blockers)
  4. Kidneys (Aldosterone or RAAS system can affect kidney volume)
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6
Q

What are three main sources of PVR?

A

Blood vessel diameter
Blood viscosity (dehydration)
Total vessel length (obesity)

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7
Q

If blood vessel diameter is doubled how does it affect resistance?

A

Decrease resistance 16 times. Alpha blocker effect.

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8
Q

What are the four groups of antihypertensive agents?

A

Diuretics - deplete sodium
Sympathoplegics- decrease PVR/CO
Vasodilaors: Relax vascular SM
Anti-ANG: Block activity and production

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9
Q

Name targets and drugs for sympathoplegics for HTN?

A

VMC central acting (methyldopa/clonidie/dex)
Alpha receptors of the vessels (prazosin, phentolamine)
Beta1 receptors of the heart (propranolol)
Beta1 receptor of the JG cells (propranolol)

Sympathetic nerve terminals
sympathetic ganglia

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10
Q

Name targets for diuretics for HTN?

A

Kidney Tubules (Thiazides)

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11
Q

Name targets for Direct Vasodilators for HTN?

A

Vascular Smooth Muscles (Hydralazine, CCB, Fenoldopam, Minoxidil)

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12
Q

What are usually first line therapy for antihypertension?

A

Diuretics

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13
Q

What receptors do clonidine and methyldopa act on?

A

Alpha-2 agonist activity in brainstem to decrease sympathetic stimulation. Remember Alpha-2 decreases cAMP.

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14
Q

How does methyldopa and clonidine work as a centrally acting sympathoplegic drug?

A

Methyldopa
1. Analog of L-dopa, methyldopa is coverted a-methylNE and cross the BBB to the alpha2 (nucleus of tractus solitarius) in the brainstem.
2. NTS will send a signal to the Rostral Ventrolateral Medulla to inhibit sympathetic outflow.
3. NTS will also stimulate the VN and increase parasympathetic activity.

Clonidine will cross the BBB and affect both NTS and RVLM.

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15
Q

Methyldopa isn’t usually used as a first line agent d/t to many SE. When is it used as a treatment fallback?

What is the primary side effect of Methyldopa?

A

Pregnancy, no effect on the fetus.
Sedation is the primary SE

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16
Q

How come clonidine does not have as big of an effect as methyldopa?

Side Effects of clonidine?

What are other uses of clonidine?

A

It is a partial alpha 2 agonist can cross the BBB and used as a backup antihypertensive

Side Effect: sedation, dry mouth

ADHD, Tourettes, W/d, Anxiety, PTSD

17
Q

What adrenoreceptor antagonist are uses to treat hypertension?

A

Beta blockers: propanolol (nonselective)
Beta-1 selective blocker: Metoprolol, atenolol, esmolol (short acting)

Alpha-1 blockers (phentolamine, prazosin)

18
Q

List 4 mechanism of vasodilators?
What is the overall effect from all 4 mechanism?

A
  1. Release of Nitric Oxide from endothelium (hydralazine)
  2. Reduction of calcium influx (verapamil, dilt, cardene)
  3. Hyperpolarization of SM through K+ channels (minoxidil)
  4. Activation of D1 receptors (Fenoldopam)

Overall effect: relax smooth muscle, reduction of PVR, MAP

19
Q

What are the compensatory responses in the body if you just give vasodilators by itself? How do you combat this?

A

Decrease in arterial pressure will trigger renin release from the kidneys for sodium retention to increase plasma volume resulting in increase arterial pressure.

Decrease in arterial pressure will increase sympathetic outflow causing an increase in HR, Contractility, and a decrease in venous capacitance to increase CO that will increase arterial pressure.

Polypharmacy to combat compensatory response.
Diuretic will increase renal Na+ excretion and block the aldosterone effect.
Beta blocker can stop the sympathetic outflow of the heat and systemic vascular resistance.

20
Q

How does hydralazine work as a vasodilator?
Toxicity?

A

Dilates arterioles through NO production in the endothelium.

NO will migrate to smooth muscle cells and increase activity of guanylyl cyclase where GTP will covert to cGMP.

cGMP will block Ca2+ on the cell surface prevent trigger Ca2+ from coming in to cause a contraction.

Toxicity: HA, Nausea, flushing, worse in slow acetylators (phase2 metabolism)

21
Q

How does Minoxidil work as a vasodilator?

What can be used for topically?

A

Opens K+ channels in the smooth muscle, stabilizing the membrane potential, less likely to contract. Dilating the arterioles.

Well absorbed topically: Rogaine (hypertrichosis, hair growth)

22
Q

How does Sodium Nitroprusside work as a vasodilator?
When is this used?
Fast?

A

Only drug to have nitric oxide in it that breaks down in the blood to release NO and increase intracellular cGMP to relax cGMP that will block Ca2+ channels.

Use in HTN emergencies and cardiac failure, dilates both arterial and venous vessels.

Very Fast 10 mins

For Continuous IV infusion: protect from light

23
Q

Toxicity for sodium Nitroprusside?
Treatment?

A

There is cyanide in this drug. CN is slowing eliminated by the kidneys.

CN accumulation >48 hours can lead to acidosis, arrhythmias, death. Worse in patient w/ renal failure.

Treatment: Sodium Thiosulfate (Hypo) can facilitate metabolism of cyanide

24
Q

How does Fenoldapam work as a vasodilator?

A

Agonist of D1 receptors - increase kidney perfusion, sodium, water excretion decreasing BP.

Usually used for post-op hypertension or HTN emergencies
Peripheral arteriolar dilator

25
Q

What are the three main groups of CCB?
How do they work differently to achieve the same effect?

A

Verapamil - block Ca2+ channels in the heart
Diltiazem - has equal effects on both heart and periphery
Dihydropyridine (Nicardipine) - block Ca2+ channels in the peripheral vasculature

26
Q

What is the only drug that is a renin inhibitor?

A

Aliskiren
Inhibit the conversion of angiotensinogen to angiotensin I

Don’t use with DM (kidney damage) or with ACE Inhibitors or ARBs

27
Q

Where does ANGI get converted to ANGII ?

What enzyme is responsible for the conversion that can be a target hypertension?

A

Lungs
Angiotensin Converting Enzyme (ACE)

ACE Inhibitors (Captopril)

28
Q

Major SE for ACE Inhibitors?

A

Severe, dry cough in 10% of the population d/t inflammation in lungs. Nonproductive and irritating.

When you take an ACE inhibitor Bradykinin is around for a longer period of time since ACE usually breaks down bradykinin.

Bradykinin is associated with inflammation, it will increase prostaglandin synthesis will increase dilation, decrease peripheral vascular resistance and decreasing BP.

29
Q

What sites does ANG II bind to?
What does it do?
How can we block this?

A

ANG II binds to the Adrenal Cortex will secrete aldosterone, increase sodium and water retention, increasing BP.

ANG II binds to the arterioles and cause vasoconstriction increase peripheral resistance, increasing BP.

ARB (Losartan and Valsartan) can block this.

30
Q

What is pulmonary hypertension?

A

Increased pressure in the pulmonary arteries.

The musculature of the pulmonary artery is increased, limiting the size of the artery and the heart has to pump harder against it.

Reft ventricle pump less blood into the pulmonary artery, less blood will become oxygenated causing more systemic problem from deoxygenation.

31
Q

What are diagnostic test for pulmonary HTN?
Causes?
Prognosis?
Treatment?

A

Dx: Echocardiogram, Cardia Cath
Causes: HBP, congenital, emphysema, clots, HF
Prognosis: Poor
Tx: Prostaglandins (Epoprostanol)- continuous IV infusion
Endothelin Receptor Antagonist (Bosentan)

32
Q

What is the primary effect of Endothelin?

A
  1. Endothelin is produced by vascular endothelium cells (line blood vessels).
  2. When endothelin is release it binds to ETA and ETB on the vascular smooth muscles.
  3. This will cause vasoconstriction: increase BP and proliferation of SM cells (long term effect), this is what causes the pulmonary hypertension thickening.
33
Q

What causes the production of Endothelin?

A

Low shear stress
ANG II
Cytokines
Thrombin

L.A.C.T.

34
Q

In a normal response, what can inhibit the pathway of Endothelin?

A

High shear stress
ANP
PGI2
NO

H.A.P.N.

In a pathologic response, we have a chronic increase in endothelin.

35
Q

What is the secondary effect of Endothelin?

A
  1. Endothelin binds to the surface of ET receptors of the vascular endothelium.
  2. Endothelium will stimulate the production of NO.
  3. Gas NO will diffuse across and cause vasodilation (negative feedback) PGI2 also diffuse across and cause vasodilation.
36
Q

What does an Endothelin Receptor Antagonist Do?

A

Endothelin Receptor Antagonist block ETA and ETB of the vascular smooth muscle

Bosentan, increase lifespan of people with pulmonary hypertension

37
Q

What are initial outpatient therapy for hypertension?

A

Initial: Behavior cut back on Na+ and weight loss

Evaluate use of drugs that increase BP: Decongestants, NSAIDs, contraceptives, herbal medication.

38
Q

What are therapies for mild HTN?

A

Single drug use
First line drugs: Best guess, play the odds
Beta blockers or low dose diuretics

39
Q

Nitroglycerin’s effect on
Venous Capacitance
Preload
Afterload

A

Nitroglycerin will increase venous capacitance, decrease preload, decrease afterload

Pharmacology Test 3 (6 decks)

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