Anti-Hypertensive Agents

Front 1

What is the concept behind using a diuretic to treat HTN? What happens initially after use? What happens later?

Back 1

Initially, plasma volume decreases, which decreases EDV and increases TPR, but after several weeks, there is an increase in plasma volume and a decrease in TPR

Front 2

What happens to plasma renin levels with chronic diuretic use?

Back 2

they are elevated

Front 3

When are diuretics most effective?

Back 3

When there is a low rening dependent HTN

Front 4

Adverse effects of diuretics?

Back 4

Volume depletion
Hypokalemia
hypercuricemia(gout)
hypercalcemia
Hypercholesterolemia
Hyperkalemia (in K sparing)

Front 5

Other than HTN, what can diuretics be used to treat?

Back 5

CHF/edema
CNS edema
Nephrolithiasis
Electrolyte d/o

Front 6

MOA of thiazides?

Back 6

Block NaCl resorption from DCT

Front 7

MOA Furosemide?

Back 7

LOH drug, blocks NKCC transporter

Front 8

Use of furosemide?

Back 8

HTN and resistant edema

Front 9

MOA of K sparing diuretics?

Back 9

Antagonize aldosterone

Front 10

Which durg can be esp useful in chronic cardiac failure?

Back 10

Spironolactone

Front 11

Adverse effects of Spironolactone?

Back 11

Gynecomastia
Sexual dysfxn

Front 12

What hemodynamic effect do vasodiltors have?

Back 12

Decrease TPR and increase HR
Decrese in renal perfusion pressure and increase in SNS --> renin release

Front 13

Adverse effects of vasodilators?

Back 13

Can precipitate angina
Causes vascular HA

Front 14

Which vasodilator is safe in pregnancy?

Back 14

Hydralazine

Front 15

Adverse effects of hydralazine?

Back 15

Potential for lupus syndrome (pericarditis)

Front 16

MOA of minoxidil?

Back 16

K channel opener, very potent
Vasodilation

Front 17

ADverse effects of minoxidil?

Back 17

Hypertricosis
Na-volume retention/weight gain prominent
Pericardial effusions

Front 18

What must be co-administered with minoxadil?

Back 18

LOH diuretic and B-blocker

Front 19

MOA of Na-Nitroprusside (SNP)

Back 19

NO activates guanylate cyclase --> formation of cyclic GMP and vasodilation
Dilates arterioles and venules, lowering preload and afterload

Front 20

Main fxn of SNP?

Back 20

Treats HTN emergencies and pulmonary edema
Has a very rapid onset and offset

Front 21

What receptors does NE have strong affinity for?

Back 21

A1=A2 >>>> B

Front 22

Phentolamine administration? MOA?

Back 22

IV
non-selective a-antagonist

Front 23

Phenoxybenzamine administration? MOA?

Back 23

Oral
non-selective a-antagonist

Front 24

Examples of alpha1 antagonists?

Back 24

Prazosin
Erazosin
Doxazosin

Front 25

Hemodynamic effecs of a-1 antagonists?

Back 25

Vasodilation --> increased VR/CO, decreased TPR, decreased HR
No reflex SNS b/c a2 receptors are not blocked

Front 26

Which drug class can treat HTN and BPH?

Back 26

a1 antagonists

Front 27

Which drug in addition to treating HTN also increases HDL and deceases LDL?

Back 27

a1 antagonists

Front 28

Why are a2 antagonists effective?

Back 28

suppresses SNS sympathetic outflow
No serious adverse effects

Front 29

Alpha methyldopa?

Back 29

a prodrug
inhibits CNS NE release

Front 30

Adverse effects of alpha-methyldopa?

Back 30

Postural HTN
Hepatic toxicity
hemolytic anemia

Front 31

Clonidine

Back 31

Lowers BP by agonizing a2 receptors

Front 32

Where are B1 receptors located?

Back 32

SA node, ventricles, JG cells (mediate renin release)

Front 33

Where are B2 receptors?

Back 33

vascular smooth muscle, mediates vasodilation and decreses TPR

Front 34

What are the immediate hemodynamic effects of beta blockers?

Back 34

decrease in CO and increase in TPR, raising BP slightly
Several days/weeks later TPR declines b/c there is a beta-adrenergic inhibition of renin release

Front 35

Propranolol

Back 35

nonselective beta blocker
high lipid solubility (can enter CNS)

Front 36

Metrolprolol

Back 36

beta1 blocker
Less lipid soluble

Front 37

Atenolol

Back 37

beta1 blocker
less lipid soluble

Front 38

Pindolol

Back 38

ISA (intrinsic sympathetic agonist)
has less bradycardia at rest

Front 39

Acebutolol

Back 39

ISA (intrinsic sympathetic agonist)
less bradycardia at rest

Front 40

Labetolol

Back 40

alpha-beta receptor antagonist
alpha antagonism speeds onset, but ultimately is b-blocker

Front 41

Carvedilol

Back 41

alpha-beta receptor antagonist
alpha antagonism speeds onset, but ultimately is b-blocker

Front 42

Use of alpha-beta receptor antagonists?

Back 42

(labetolol and carvedilol)
tx of HTN emergency

Front 43

random roles of ACE

Back 43

degrades bradykinin, substance P, and other neuropeptides

Front 44

what is the primary sie effect seen in ACE-I? What causes it?

Back 44

Cough and edema
increases levels of bradykinin, substance P

Front 45

Net hemodynamic change in ACE-I?

Back 45

Decrease in TPR and CO, w/o increase in HR

Front 46

Which drug class is useful in decreasing the amt of LV remodeling?

Back 46

ACE-I

Front 47

Adverse effects of ACE-I?

Back 47

Hypotension in high renin or v-depleted states
hyperkalemi a
renal fialure in bilateral renovascular dz
cough
edema

Front 48

In addition to HTN, what else can ACE-I treat?

Back 48

CHF
Nephropathy from DM-I

Front 49

Types of ca channel blockers?

Back 49

DHP
Phenylalkylamine CCB
Benzothiazapine CCB

Front 50

How do the -dipines work?

Back 50

they are DHP CCBs
Inhibit L channels in peripheral arteriole sm and cardiac muscle (cardiac to lesser extent)

Front 51

Adverse effects of DHP?

Back 51

can precipitate angina or MI

Front 52

Verapamil?

Back 52

Phenylalkylamin CCB
Inhibits L channel in myocardium, SA and AV node, NON-vascular sm muscle

Front 53

Net hemodynamic effect of verapamil?

Back 53

Decreased CO d/t negative inotropic and chronotropic effects

Front 54

Adverse effects of verapamil?

Back 54

Constipation
Can systolic cardiac dysfunction and worsen CHF
Can produce/worsen heart block

Front 55

Diltiazem

Back 55

Benzothiazapine CCB
Inhibits Ca influx through L channels in cardiac and peripheral vascular sm muscle

Front 56

Which CCB has the most benefits?

Back 56

Diltiazem
SAFE in CAD, less risk in CHF

Front 57

MOA of sartans

Back 57

AT1 receptor antagonist
Secondary rise in plasma renin

Front 58

Metabolism of candesartan cilexetil

Back 58

gets coverted to cadesartan in intestinal wall

Front 59

which HTN med is used to also slow progression of nephropathy in DMII

Back 59

irbesartan
losartan

Front 60

Aliskiren

Back 60

direct renin inhibitor (still in clinical trials)
[renin] increased, but diminished renin activity
AI, AII, aldosterone levels decreased

Front 61

what drugs can be used to treat HTN with low renin levels

Back 61

diuretic
CCB
a-blocker

Front 62

what drugs can be used to treat HTN with high renin

Back 62

ACI-I
ARB
b-blocker

Front 63

what class of drugs do AA respond best to? worst to?

Back 63

Diuretics, CCB, a-blockers

less response to ACE-I and b-blockers when used alone

Front 64

What are the renin levels in elderly??

Back 64

low

Front 65

what drug combo used to treat LVH

Back 65

b-blocker and ACE-I

Front 66

Drug combo to treat cardiac failure

Back 66

diuretics + ACE-I

Front 67

What should not be used in PVD?

Back 67

non-selective B-blocker- can worsen sx
B2 causes vasodilation!!!

Front 68

Which HTN drugs worsen hyperlipemia

Back 68

diuretics
b-blockesr

Front 69

which drugs can exacerbate asthma

Back 69

b-blockers and a-b-blockers
(b2 receptors dilate bronchiles)

Front 70

what do OTC cold medication interact with? what can result?

Back 70

ACE-I --> accel HTN

Front 71

what drugs are contra-indicated in pregnancy?

Back 71

ACE-I
ARBs
(both are teratogenic)