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Pharmacology > Blood Pressure Lowering Drugs > Flashcards

Blood Pressure Lowering Drugs Flashcards

1
Q

RAAS antagonist
class: ACE inhibitors
MOA

A
  • Inhibition of ACE reduces the synthesis of angiotensin II and prevents bradykinin breakdown.
  • The bradykinin»>angiotensin II leads to vasodilation
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2
Q

RAAS antagonist
class: ACE inhibitors
Adverse Effects

A
  • Dry cough (due to bradykinin), hyperkalemia, ARF, angioedema
  • Contraindicated in pregnancy and in pts w/ bilateral renal artery stenosis
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3
Q

RAAS antagonist
class: Angiotensin-II receptor blockers (ARBs)
MOA

A
  • ARBs block type 1 angiotensin II receptors on blood vessels and other tissues, like heart
  • leads to preventing angiotensin induced vasoconstriction
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4
Q

RAAS antagonist
class: Angiotensin-II receptor blockers (ARBs)
Adverse Effects

A

-hyperkalemia, ARF
no increase in bradykinin, so no dry cough or angioedema
-Contraindicated in pregnancy and in pts w/ bilateral renal artery stenosis

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5
Q

RAAS antagonist
class: Neprilysin Inhibitor plus angiotensin-II receptor blocker
MOA

A
  • Neprilysin is a enzyme that degrades bradykinin and other peptides, inhibition of this enzyme increases bradykinin leading to vasodilation
  • Used only in combo w/ ARBs
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6
Q

RAAS antagonist
class: Neprilysin Inhibitor plus angiotensin-II receptor blocker
Adverse Effects

A
  • Hyperkalemia, angioedema, renal function deterioration, hypotension
  • Overlap or use w/in 36hrs of ACE inhibitors can increase risk of angioedema=contraindicated
  • Contraindicated in pregnancy and in pts w/ bilateral renal artery stenosis
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7
Q

RAAS antagonist
class: Aldosterone Antagonists
MOA

A

Block the aldosterone receptor in the renal collecting tubule, increasing the Na+ and water excretion while conserving the K+ and H+

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8
Q

RAAS antagonist
class: Aldosterone Antagonists
Adverse Effects

A
  • Hyperkalemia, renal function deterioration, gynecomastia

- Risk of hyperkalemia is increased w/ declining renal function and w/ the concurrent use of ARBs or ACE

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9
Q

RAAS antagonist
class: Direct Renin Inhibitor
MOA

A

Produce vasodilation by inhibiting the activity of renin, which is responsible for stimulating angiotensin II formation

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10
Q

RAAS antagonist
class: Direct Renin Inhibitor
Adverse Effects

A

Diarrhea, hyperkalemia, angioedema

Contraindicated in pregnancy

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11
Q

Sympatholytics
class: Alpha-1 blockers
MOA

A

Drugs block the binding of Epi and NE to alpha-1 adrenoreceptors in the vascular smooth muscle causing vasodilation

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12
Q

Sympatholytics
class: Alpha-1 blockers
Adverse Effects

A 
headache and dizziness
orthostatic hypotension
nasal congestion
reflex tachycardia
fluid retention
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13
Q

Sympatholytics
class: Beta-1 selective blocker
MOA

A

Bind and block Epi and NE on beta-1 predominately in the heart and kidney
Causes decrease in HR, CO, BP, and renin release

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14
Q

Sympatholytics
class: Nonselective beta blocker
MOA

A

Block beta 1 and 2 equally
Beta-1: decrease in HR,CO, BP, and renin release
Beta-2: bronchospasm and vasoconstriction

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15
Q

Sympatholytics
class: Vasodilating beta blockers
MOA

A

Have additional vasodilating properties via the alpha-1 blockade on top of the beta inhibition

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16
Q

Sympatholytics
class: Beta Blockers
Adverse Effects

A 
Exaggeration of decrease in HR, CO, BP
Smooth muscle spasm
CNS penetration-insomnia, depression
Shitty quality of life
Adverse metabolic effects 
Withdrawal phenomenon
17
Q

Sympatholytics
class: Central alpha-2 agonists
MOA

A

Suppress NE release by binding to and activating alpha 2 adrenoreceptors causing:

  • reduced sympathetic outflow of the heart=decrease CO,HR, and contractility
  • reduced sympathetic output of vasculature=vasodilation, reduced SVR, decreased art pressure
18
Q

Sympatholytics
class: Central alpha-2 agonists
Adverse Effects

A
  • sedation, dry mouth, nasal mucosa, bradycardia, orthostatic hypotension, and impotence
  • contipation, nausea, GI upset
  • sudden stop can lead to rebound HTN from the excessive sympathetic activity
19
Q

Vasodilators
class: Non-Dihyropyridine CCB
MOA

A

Bind and block L-type Ca+ channels located on the vascular smooth muscle, cardiac myocytes, and cardiac nodal tissue( SA and AV nodes)

20
Q

Vasodilators
class: Non-Dihyropyridine CCB
Effects

A
  • vascular smooth muscle relaxation=vasodilation
  • decreased myocardial force generation=neg inotropy
  • decreased HR, particularly at the AV node
21
Q

Vasodilators
class: Non-Dihyropyridine CCB
Adverse Effects

A
  • flushing, headache, peripheral edema, excessive hypotension and bradycardia, impaired electrical conduction( AV node block), depressed contractility
  • Contraindicated: current bradycardia, heart conduction defects, and heart failure by systolic dysfunction
22
Q

Vasodilators
class: Dihydropyridine CCB
MOA

A
  • prevent the flow of Ca+ through L-type Ca+ channels specifically on the vascular smooth muscle
  • results in vasodilation, reduced SVR and BP
23
Q

Vasodilators
class: Dihydropyridine CCB
Adverse Effects

A

Peripheral edema, flushing, headache, excessive hypotension, reflex tachycardia

24
Q

Direct Vasodilators

MOA

A
  • Directly relaxing the arteriolar smooth muscle
  • little effect on veins=decreasing SVR
  • lowers after load= great for HF
25
Q

Direct Vasodilators
Hydralazine
Adverse Effects

A
  • headaches, flushing, baroreceptor-mediated reflex tachycardia, Na+ and water retention
  • Lupus like syndrome
26
Q

Direct Vasodilators
Minoxidil
Adverse Effects

A
  • headaches, flushing, baroreceptor-mediated reflex tachycardia, Na+ and water retention
  • Hypertrichosis and pericardial effusion
27
Q

Vasodilators
class: Nitrates
MOA

A

increase activation and release of NO

venous dilation reduces preload=reduces stress and O2 demand of the heart

28
Q

Vasodilators
class: Nitrates
Adverse Effects

A

headache, reflex tachycardia, nitrate tolerance, risk of cyanide
-great potentiate w/ phosphodiesterase inhibitors=can lead to hypotension and paired coronary perfusion

29
Q

Diuretics
class: Loop diuretics
MOA

A
  • inhibit NA+-K+-Cl- cotransporter in thick ascending limb=increased water and Na+ loss
  • very effective place to loss water=powerful diuretic
30
Q

Diuretics
class: Loop diuretics
Adverse Effects

A
  • hypotension, renal insufficiency, low lytes, ototoxicity,

- chronic therapy=hyperuricemia ( gout)

31
Q

Diuretics
class: Thiazide diuretics
MOA

A
  • inhibit the Na+-Cl- transporter in distal tubule of nephron=increased release of Na+ and water
  • stops reabsorbtion=less effective
32
Q

Diuretics
class: Thiazide diuretics
Adverse Effects

A

Hypovolemia, low lytes, gout, metabolic alkalosis

33
Q

K+ Sparing Diuretics

2 types

A

Na+ Channel Blockers

Aldosterone Receptor Antagonists

34
Q

ACE inhibitor

drug name suffix

A

Most end in w/ a

-pril

35
Q

Angiotensin II

drug name suffix

A

Most end w/ a

-tan

36
Q

Beta Blockers

drug name suffix

A

Most end w/ a

-lol

37
Q

Non-DHP CCBs

2 drug names

A

Verapamil

Diltiazem

38
Q

Dihydropyridine CCBs

drug name suffix

A

Most end w/ a

-pine

39
Q

Combination recommended for black HF pts who remain symptomatic despite optimal med therapy

A

2 direct vasodilators:
Isosorbide dinitrate
Hydralazine

Pharmacology (5 decks)

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