C: Anti-Htn Drugs

Front 1

How do diuretics work in the short term? In the longer term?

How much can they lower BP?

In more severe HTN, what drug classes require Diuretics as a combo? Why?

Back 1

reduce BP by reducing BV and CO... later CO is returned to normal by a drop in SVR.

10-15mmHg

sympathoplegic and vasodilator drugs, which can cause Na retention

Front 2

Indapamide
- class/primary effect?
- additional effect?

Back 2

diuretic, decreases Na stores
direct vasodilating effect

Front 3

Amiloride
- class/primary effect?
- additional effect?

Back 3

diuretic, decreases Na stores

inhib SMC response to contractile stimuli by effecting Ca++ ion movement.

Front 4

Sympathoplegic drugs come in 3 classes, name 'em.

Back 4

CNS, Adrenergic neuron blocking agents, adrenoreceptor antagonists.

Front 5

Describe the action of the CNS subclass of Sympathoplegic drugs.

Back 5

Act on the vasomotor area of the medulla
- interact w/ a-adrenergic receptors on neurons that modulate the baroreceptor reflex
+ inhibit symp. influence --> allow parasympathetics to predominate.

--> lower of BP

Front 6

Why aren't ganglion-blocking agents used to treat HTN anymore?

Back 6

too many side effects.

Front 7

What is the site of action for adrenergic neuron blocking agents?

Back 7

sympathetic nerve endings

Front 8

Guanethidine
- class/subclass?
- mechanism?

Back 8

- sympathoplegic, adrenergic blocker
- gets take up by NE reuptake, and replaces NE in storage vesicles.
+ also blocks electrical conduction at terminal by blocking Na+ channels.

Front 9

Reserpine
- class/subclass?
- mechanism?

Back 9

- sympathoplegic, adrenergic blocker
- blocks storage vesicle NE transporter --> depletes NE stores in the vesicles

Front 10

Where do a1-blockers b/?

How do they mediate their effects?

Back 10

a1-receptors on post-synaptic sympathetic terminals

decrease IP3 lvls in arterioles and venules --> promote vasodilation

Front 11

How do vasodilators work?

What are the subclasses?
- which are used for emergent treatment? long term?

Why are vasodilators used in combo w/ other drugs?

Back 11

relax vascular smooth muscle, leading to resistance vessel dilation and increased capacitance

oral vasodilators - long
parenteral vasodilators - emergent
Ca++ channel blockers - both

b/c they induce compensatory mechanisms.

Front 12

Hydralazine
- class/subclass
- characteristics
- mechanism
- effective alone? why or why not?

Back 12

- vasodilator, oral
- dilates arterioles, NOT veins
- not well understood
- no, resistance develops

Front 13

Minoxidil
- class/subclass
- characteristics
- mechanism
- **major side effects**

Back 13

- vasodilator, oral
- dilates arterioles, NOT veins
- acts as an opener of smooth muscle K+ channels --> hyperpolarizes cells --> makes it hard for Ca++ channels to open --> makes harder for it to contract
- tachycardia via the baroreceptor reflex; hirsutism
+ one trade name is Rogaine

Front 14

Sodium nitroprusside
- class/subclass
- characteristics
- mechanism

Back 14

- vasodilator, parenteral
- dilates BOTH venous and arterial vessels
- works like nitrates and nitrites by stim of the soluble guanylyl cyclase --> increased cGMP and vascular smooth muscle relaxation

Front 15

What is the primary effect of the anti-Ang drugs?

Back 15

reduction in peripheral vascular resistance --> reduces BP

Front 16

What are the two things that ACE does that ACE inhibitors stop, w/ resultant therapeutic effect?

What is the combined therapeutic effect?

What are some other effects of ACE inhibitors?

Examples of ACE inhibitors? (3)

Side effects?

Back 16

Ang I --> Ang II
inactivates the (vasodilator) product of kallikrein-mediated kininogen cleavage: bradykinin

Reduction of SVR w/o elevation of HR

promote sodium excretion and water loss

Captopril, enalapril, benazapril

***Severe hypotension in pts w/ low fluids***
renal failure
dry cough
angioedema
HYPERkalemia

Front 17

Does chronic admin of ACE inhibitors completely block Ang I --> Ang II? Why or why not?

Back 17

No, other enzymes can convert ang I to Ang II

Front 18

What do AT1 blockers do?

Effects of Ang II b/ to receptor? (3)

ARB (AT1 blocker) drug examples?

Side effects?

Do ARBs affect Bradykinin metabolism like ACE inhibitors?

Back 18

block b/ of Ang II to it's receptor

1. promotes IP3 --> increased Ca lvls in postsynaptic membrane --> increased contraction
2. b/ presynaptically and increase NE vesicle storage & release
3. interferes w/ NE reuptake, prolonging it's effect

losartan and valsartan

***Severe hypotension in pts w/ low fluids***
HYPERkalemia
renal failure
**NO dry cough & angioedema

No.

Front 19

If a pt is low on fluids, should they be given ACE inhibitors w/o proper rehydration?

Back 19

No, can lead to severe hypotension.

Front 20

Which drug class has the potential for more complete blocking of Ang II effects? ARB or ACEinhib

Back 20

ARBs, b/c other enzymes other than ACE can convert Ang I --> Ang II

Front 21

Name the class/subclass:
- methyldopa
- doxazosin
- tetrazosin
- fenoldopam
- diazoxide
- nitroprusside
- minoxidil
- hydralazine
- captopril
- losartans
- prazosin
- propranolol
- metoprolol
- nadolol
- clonidine
- reserpine
- guanethidine

Back 21

CNS
methyldopa
clonidine
Adrenergic neuron blocking agents
guanethidine
reserpine
Adrenoreceptor antagonists
propranolol (b
metoprolol (b
nadolol (b
prazosin (a
tetrazosin (a
doxazosin (a

c. Vasodilators
hydralazine
minoxidil
nitroprusside
diazoxide
fenoldopam
Ca2+-channel blockers
d. Antiangiotensin drugs
captopril (ACE inhibitor)
losartan and other sartans (ARBs)

Front 22

Do ARBs cause hyperkalemia? ACE-inhibitors?

Renal insufficiency?
Dry cough?
hypotension?
Angioedema?

Back 22

Yes, both do.

Both.
Primarily ACE inhibitors.
Both.
Primarily ACE inhibitors.