Diuretics and Antihypertensives Flashcards

1
Q

Beta Blockers decrease blood pressure by

A

decrease cardiac output and inhibits the release of renin which decreases production of angiotensin II and aldosterone secretion

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2
Q

Example of selective BB

A

Metoprolol, atenolol

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3
Q

Which type of BB can NOT be used for asthma

A

nonselective BB

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4
Q

BB on DOC for?

A

previous MI, supraventricular tachyarrythmias, stable ischemic heart disease, chronic HF

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5
Q

Never give BB to?

A

those with asthma, 2nd degree heart block, 3rd degree heart block, diabetes or severe PAOD

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6
Q

ADEs of BB

A

 Common SE—lower BP and bradycardia [the person
 Lipid Altercations—non-cardioselective BB will decrease HDL [good cholesterol] and increase the trigs
 Fatigue, insomnia and sexual dysfunction can be seen in non-cardioselective BB

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7
Q

What happens if you abruptly stop a BB?

A

cause severe HTN, and even angina, acute MI and even sudden death [in those with ischemic heart disease]; taper these drugs over a few weeks when stopping them—even if they are being given for headache

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8
Q

ACE inhibitors MOA

A

reduce PVR without increasing CO, HR or contractibility; ACEI block ACE—which converts angiotensin I to angiotensin II

 ACEIs also prevents the breakdown of bradykinin, which increases NO and prostacyclin from the vessels
 NO and prostacyclin are potent vasodilators of the arterioles and veins
 By reducing levels of angiotensin II, aldosterone levels are decreased, as is Na+
 ACEI reduce cardiac preload and afterload—important reason we use these drugs in folks with CAD

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9
Q

ACE inhibitors recommended for?

A

high BP in those with DM, CKD, MI, HF, high risk of CAD and those with proteinuria

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10
Q

Examples of ACE

A

captopril
enalapril
lisinopril

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11
Q

What does chronic use of ACEIs do?

A

keep BP low, cause LVH to regress and prevent ventricular remodeling in those who have had and MI or those with HF

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12
Q

ACEI are first line in?

A

HF, high BP, CKD and those at risk for CAD

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13
Q

Pharmacokinetics of ACEI

A

 Oral bioavailable as drug or
 All but Captopril and Lisinopril undergo hepatic conversion to active metabolites—so these 2 are preferred in those with live compromise
 Fisinopril is only ACEI not renally eliminated—so no dose adjustments with this drug in those with CKD
 Enalapril is available IV

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14
Q

ADES and serious ADEs of ACEI

A

ADEs:
Cough [more frequent in women]
 Seen in 10%, thought to be from increased bradykinin and substance P
Elevation of serum creatinine up 30% from baseline [this is acceptable]
Low BP Dysguesia

Serious ADEs:
 Skin rash
 Angioedema—thought to be from elevated bradykinin levels
 Monitor serum creatinine
 These drugs cause body to hold K+, so monitor K+ and about K+ supplements, potassium sparing diuretics and salt substitutes
 ACEI induce fetal malformations—cannot be used by pregnant woman

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15
Q

Angiotensin II Receptor Blockers (ARBs)

A

 Prototype drug is Losartan
 These drugs block the AT1 receptor, decreasing activation of AT1 receptors by
angiotensin II
 Their effects are much like the ACEIs
 ARBs do not increase bradykinin levels—so can be used in those who cough on an ACEI or those who have developed angioedema on an ACEI
 1st line agents for DM, HF, CKD
 ADEs are similar to ACEIs [except the cough and angioedema]
 CANNOT be used with an ACEI
 Teratogenic in pregnant women

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16
Q

Renin Inhibitors

A

 Prototype drug is Aliskeren—Tekturna
 This drug inhibits renin and acts earlier in the RAAS system than ACEIs or ARBs
 Aliskeren cannot be given with an ACEI or an ARB
 Can cause diarrhea in high doses—can cause cough and angioedema, but less often than ACEIs
Contraindicated in pregnancy
Metabolized by CYP34A—many drug-drug interactions