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Pharmacology II > Anti-Hypertensives part 1 > Flashcards

Anti-Hypertensives part 1 Flashcards

1
Q

What is the main action of ACE inhibitors?

A

○ Competitively inhibits angiotensin-converting enzyme (ACE)

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2
Q

What are the physiologic results of action by an ACE inhibitor?

A
  1. Prevents conversion of angiotensin I to angiotensin II
  2. Results in lower levels of angiotensin II
  3. Results in increased plasma renin activity
  4. Results in a reduction of aldosterone secretion.
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3
Q

Why would a drug targeting the inhibition of Angiotensin II formation be used to lower hypertension or BP?

A

Angiotensin II is a “potent” vasoconstrictor

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4
Q

Why would it be beneficial for an ACE inhibitor to lower aldosterone secretion? Remember, this is in a patient with hypertension

A

This decreases sodium and water retention by the kidneys, which in turn lowers blood pressure

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5
Q

ACE inhibitors are given drug names that end in what suffix?

A

“-pril”

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6
Q

Name the 9 ACE inhibitors

A
  1. benzepril (Lotensin)
  2. captopril (Capoten)
  3. enalapril (Vasotec)
  4. foxinopril (Monopril)
  5. lisinopril (Prinivil, Zestril)
  6. moexipril (Univasc)
  7. quinapril (Accupril)
  8. ramipril (Altace)
  9. trandolopril (Mavik)
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7
Q

Name the original ACE inhibitor

A

enalapril (Vasotec)

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8
Q

Which of the group of ACE inhibitor drugs is the biggest market seller in the US?

A

lisinopril (Prinivil, Zestril)

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9
Q

If a patient is taking an ACE inhibitor and presents with a large amount of caries and enamel demineralization, what might you suggest is occurring in this patient?

A

One of the side effects of ACE inhibitors is a chronic dry cough. Some patients attempt using cough syrups/lozenges for relief which may lead to caries and demineralization.

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10
Q

Name the side effects of ACE inhibitors

A
  • Chronic dry cough

- Angioneurotic edema with first dose (aka: angioedema)

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11
Q

What is the physiology behind chronic dry cough caused by ACE inhibitors?

A

ACE (enzyme that catalyzes conversion of Angiotensin I to Angiotensin II) is also the enzyme that INACTIVATES bradykinin. When this enzyme is inhibited, bradykinin is active. The cough is then mediated by bradykinin release in the bronchial tree.

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12
Q

Prinivil, Zestril (ACE inhibitors) are considered the drug of choice for what type of patients?

A

For hypertension in patients with diabetes.

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13
Q

Name the 3 oral complications of ACE inhibitors

A
  1. Xerostomia
  2. Dry cough
  3. Angioedema
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14
Q

What is the target of action for ARBs (Angiotensin Receptor Blockers)?

A

○ Attach to angiotensin II receptor = block effect of angiotensin II

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15
Q

The result of action for ARBs results in what effects?

A
  1. Initially –> blocks vasoconstrictor and aldosterone-secreting effects of angiotensin II
  2. The increase in plasma Renin (negative feedback loop) causes:
    • vasodilation
    • decreased sodium
    • water retention
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16
Q

ACE inhibitors and ARBs target the same pathway but different players in that pathway. Is there a preference between the two clinically when prescribing?

A

Yes, ARBs are often preferred over ACE inhibitors because their action is more specific, at the receptor. This results in fewer side effects which means it is better tolerated by patients.

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17
Q

What drug may have an adverse effect with ARBs?

A

NSAIDS, they may decrease the effectiveness of ARBs

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18
Q

6 adverse effects of ARBs

A
  1. CNS (dizziness, fatigue..)
  2. Upper respiratory infections
  3. GI effects - diarrhea
  4. Pain - muscle cramps, leg pain
  5. Angioedema (rare)
  6. Teratogenicity
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19
Q

The Angiotensin Receptor Blocker drugs generally have names that end in what suffix?

A

“-artan”

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20
Q

Name the 7 common ARB drugs

A 
candesartan (Atacand)
eprosartan (Teveten)
irbesartan (Avapro)
losartan (Cozaar)
olmesartan (Benicar)
telmisartan (Micardis)
valsartan (Diovan)
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21
Q

Other than its target of action, what differentiates Renin Inhibitors from ACE inhibitors and ARBs?

A

Renin inhibitors don’t allow for an increase in Renin which have been known to have an effect causing some vasodilation

22
Q

Name the lone drug considered a Renin Inhibitor

A

aliskiren (Tekturna)

23
Q

What is the mechanism of action for calcium channel blockers?

A

○ Inhibits calcium ion from entering the “slow channels” or select voltage-sensitive areas of vascular smooth muscle and myocardium during depolarization

24
Q

What is the result of the action for calcium channel blockers?

A
  • This produces relaxation of coronary vascular smooth muscle and coronary vasodilation
  • Increases myocardial oxygen delivery
25
Q

Ca Channel blockers are used for what cardiovascular disorders?

A
  1. Hypertension
  2. Angina
  3. Arrhythmias
26
Q

REVIEW: How does calcium function in muscle contraction?

A

Ca+ activates calmodulin, which turns on myosin kinase, which phosphorylates myosin so that it can better bind actin and produce muscle contraction

27
Q

Describe the differences in the targets between verapamil (Calan) and nifedipine (Procardia) which are both calcium channel blockers

A 
verapamil = major effects are on the heart
nifedipine = more effects on the blood vessels
28
Q

Gingival hyperplasia is a known side effect in Ca channel blockers. Which of the many Ca Channel blocker drugs are associated with the greatest number of cases of gingival hyperplasia?

A

nifedipine (Procardia)

29
Q

Which of the Ca Channel blocker drugs is the #1 seller in US market?

A

amlodipine (Norvasc) (newest drug)

30
Q

Name the Ca Channel Blocker drugs

A
  • Amlodipine (Norvasc)
  • Bepridil (Vascor)
  • Diltiazem (Icardizem, Dilacor)
  • Felodipine (Plendil)
  • Isradipine (DynaCirc)
  • Nicardipine (Cardene)
  • Nifedipine (Adalat, Procardia)
  • Nisoldipine (Sular)
  • Verapamil (Calan)
31
Q

Observance of a Ca channel blocker drug causing gingival hyperplasia after how many months is indicative of how severe condition will become

A

After 3 months

32
Q

Is there any way to limit the drug-induced gingival hyperplasia

A

Good oral hygiene limits extent and severity of lesion.

33
Q

By percentages, which Ca Channel Blocker drugs are most involved with gingival hyperplasia

A

nifedipine (30%)
verapamil (8%)
diltiazem (2%)
amlodipine (

34
Q

What is the mechanism of action for clonidine (Catapres)

A
  • Alpha-2 agonist
    • Stimulates alpha-2 on brainstem
    • Activates inhibitory neuron
  • *Decreases sympathetic outflow from CNS
35
Q

How is clonidine administered?

A

Orally or via transdermal patch

36
Q

Adverse effects of clonidine (Catapres)

A
  • Dizziness and sedation
  • Rapid elevation of BP if sudden discontinuation
  • *Xerostomia
  • *Parotid gland swelling and pain
  • *Dysgeusia (unpleasant taste)
37
Q

Name the alpha-2 agonist drugs

A

clonidine (Catapres)

guanfacine (Intuniv, Tenex)

38
Q

Describe the Catecholamine Release Blockers mechanism of action

A
  • Block granular uptake and storage (depeletion) of norepinephrine = decrease sympathetic activity due to lack of neurotransmitter supply
39
Q

Name the two Catecholamine release blocker drugs

A
  • reserpine
  • guanethidine (no longer used in US)

** Not used very much anymore but may show up on the Board Exam

40
Q

Describe the specific mechanism of action for the drug reserpine

A

Decreased BP via depletion of NE and dopamine

41
Q

reserpine can also be used in treating what other cases?

A

Agitated psychoses/schizophrenia

- It crosses the Blood Brain Barrier

42
Q

Adverse effects of reserpine

A

Causes mental depression and risk for suicide

43
Q

Describe the specific mechanism of action of guanethidine

A

Uncouples action potential from exocytotic release of transmitter (blocks AP)

44
Q

Catecholamine Release blockers are contraindicated in what patients?

A

Patients with peptic ulcers (causes increased HCl secretion)

45
Q

Side effects of Catecholamine Release blockers

A
  • Lethargy

- Nasal congestion

46
Q

Name the 6 dental drug interactions with Antihypertensive medications

A
  1. Enhanced hypotension with general anesthetics and CNS depressants
  2. Prolonged action of analgesics, sedatives and tranquilizers (central acting drugs)
  3. Potentiated response to vasoconstricting drugs
  4. OTC sympathomimetics (Cold, asthma tablets) may counteract antihypertensive therapy
  5. Use of NSAIDS longer than 3 weeks decreases effectiveness of diuretics, beta blockers and ACE inhibitors
  6. Nicotine in cigars and cigarettes constricts blood vessels and increases blood pressure
47
Q

Which NSAID is the worst offender in decreasing the effectiveness of diuretics, beta blockers and ACE inhibitors on hypertension

A

indomethacin

48
Q

Name 4 dental considerations when dealing with patients with hypertension

A
  1. Prevent sudden changes in posture
  2. Decrease stress
  3. Tissue retraction with vasopressors is contraindicated (gingival retraction cord with epinephrine)
  4. Rebound hypertension may develop if antihypertensive agents are abruptly withdrawn
49
Q

Which type of patients may abruptly stop taking hypertension and experience rebound hypertension

A

Men who experience impotence while on beta blockers may abruptly stop taking the medication = severe, rebound hypertension

50
Q

Define the effects the following drugs have on potassium

  • Diuretics
  • ACE Inhibitors
  • ARBs
A

Diuretics = make you LOSE potassium
ACE Inhibitors = Increase potassium
ARBs = Increase potassium

Pharmacology II (24 decks)

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