8 - Pharmacology of AntiHT's Flashcards

1
Q

What drug based on MOA?

Selectively block a1-adrenoreceptors
@arterioles & venules

Arterial pressure
by dilation of resistance/capacitance BVs

Vasodilation –> HypoTensive effect

A
  • *a1-adrenoceptor Antagonists**
  • *Prazosin / Terazosin / Doxazosin**

orthostatic hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What drug based on MOA?

**Inhibit NaCl Reabsorption in the DCT**
in luminal (urine-side) epithelium

Direct effect:
Block Na+/Cl- Transporter

Enhances Ca2+ Reabsorption

A

THIAZIDES
Chlorthiazide / HCTZ / Methylclothiazide

Non-thiazide Sulfonamide:
Chlorthalidone / Indapamide / Metolazone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Fenoldopam

Class / MoA / ADR

A

Parenteral Vasodilator

  • *Dilates Arterioles**
  • not veins*

D1 Agonist –> also produces natriuresis

Intraocular pressure = do NOT use in GLAUCOMA pts

ADRs:
TachyCardia & Provokes ANGINA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What drug based on MoA?

  • *Dilates Arterioles**
  • no vein effect*

TachyPhalaxis
develops rapidly, limits use in MONOtherapy

Usually used for:
Combination Therapy for Severe HTN

A

HYDRALAZINE
Oral Vasodilator

may provoke ANGINA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Which Beta Blockers have

Intrinsic Sympathomimetic Activity = ISA

Partial AGONIST @ B2-Ne Receptors
but is overidden by:
B1-NE blockade

A

ISA BB’s = PAP

Pindolol / Acebutolol / Penbutolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What drug based on MoA?

  • *Dilates Arterioles**
  • no vein effect*

Metabolite: opens K+ channels in smooth muscle
of arterioles

Topical

A
  • *MINOXIDIL**
  • *Vasodilator**

Used for HAIR GROWTH = Rogaine

  • may provoke ANGINA*
  • *Headache / Sweating / Hirsutism**
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What drug based on MoA?

  • *Blocks AT2 Effects**
  • antagonism of* AT2 type 1 receptor
A
  • *ARBS**
  • artans

NO COUGH, NO EFFECT ON BRADYKININ

clinically similar effects to ACE-i’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  • *ADR’s of BETA BLOCKERS**
  • olols
A

BradyCardia / ↓cardiac contractility & excitibility

CNS = sedation / depression / sleep disturbance

REBOUND SYMPATHETIC STIMULATION
upon abrupt withdrawal = nervousness / tachycardia / HTN

HYPOGLYCEMIA
may exacerbate hypoglycemic episodes in insulin dependent diabetics
BetaBlockers may MASK hypoglycemia in diabetic pts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

CCB ADR’s

A
  • *CARDIAC DEPRESSION**
  • *Greater in Non-DHP’s (Verapamil/Diltiazem)** > DHP’s (amlodipine)
  • *BradyCardia / AV block / HF**

Short Acting Nifedipine = ↑risk of MI –> use LONG ACTING

Dizziness / Constipation / Peripheral Edema

FLushing / Nausea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Diazoxide

Class / MoA / ADR

A

Parenteral Vasodilator

  • *Dilates Arterioles**
  • not veins*

Opens K+ channels = stabilize smooth muscle membranes of arterioles

ADRs:
TachyCardia & Provokes ANGINA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which Beta Blockers have

a-NE-blocking Activity

Stereoisomers have BOTH:
B-NE & a-NE antagonist activity

A

LABETOLOL

CARVEDILOL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What drug based on MOA?

Inhibits synthesis of AT2
vasoconstrictor activity
↓aldosterone release –> Na+ & H2O Retension

Blocks breakdown of BRADYKININ
↑bradykinin = vasoDilation

↓PVR

A

ACE INHIBITORS

BP by ↓PVR

CO & HR are UNCHANGED

no reflex tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

ADRs of ARBS

A
  • *similar to ACE-inhibitors**
  • EXCEPT FOR:*
  • *COUGH_ & _ANGIOEDEMA**
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What drug based on MOA?

Direct agonist of a-adrenoreceptors @medulla:
sympathetic outflow / ↓BP / ↓Bradycardia
ParaSympathetic Tone

Initially, ↑BP

  • > due to stimulation of peripheral a-receptors on arterioles
  • when given IV = transient vasoconstriction*
A
  • *CLONIDINE**
  • *Guanzbenz** & Guanfacine

CNS-Acting Sympathoplegics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Special Uses for
BETA BLOCKERS w/ ISA

ISA BB’s = PAP

Pindolol / Acebutolol / Penbutolol

A

PVR –> ↓BP

LESS depression of CO & HR
due to greater B2 agonist > B2 antagonist activity

Useful in pts with:
Bradyarrhythmias & Peripheral Vascular Disease

do NOT use in patients with ANGINA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What drug based on MOA?

In brain:
a-methyl-NE –> stimulates post-synaptic a-adrenoreceptors
PVR ~↓CO

Sympathetic Outflow

  • in periphery:*
  • *a-methyl-NE replaces NE stores** as false transmitter
  • not responsible for antiHTN action*
A

METHYLDOPA
CNS-acting Sympathoplegics

17
Q

What drug based on MOA?

Taken up into pre-synaptic NE vesicles –> REPLACES NE

_*Inhibits release of* NE_
@ postganglionic sympathetic effector site on BV

= VASODILATION

A
  • *Guanethidine**
  • *Adrenergic Neuron Blocker**

more potent vs Reserpine

  • *SEVERE HTN**
  • many drug interations*

Impairs baroreceptor reflex –> orthostatic hypotension

18
Q

ADR’s

THIAZIDES
Chlorthiazide / HCTZ / Methylclothiazide

Non-thiazide Sulfonamide:
Chlorthalidone / Indapamide / Metolazone

A

HypoKALEMIA

HyperUricemia
gout

HyperGlycemia & HyperLipidemia
<15% increase in serum cholesterol & LDL

19
Q

ADR’s

CNS-Acting Sympathoplegics
Methyldopa / Clonidine

Guanfacine / Guanabenz

A

Dry Mouth + Sedation

SUDDEN WITHDRAWAL –> SEVERE HTN CRISIS
if after chronic use
Due to: Rebound sympathetic activity
dose should be TAPERED OFF

20
Q

Compelling Indications for

ACE INHIBITORS

A

HF** / **Recent Strole
use with DIURETICS

Post - MI

Diabetes

CKD

21
Q

What drug based on MOA?

INHIBITION of CA++ Influx
into smooth muscle of arterioles

PVR

More Cardiac Depressant activity vs counterpart

Conduction thru AV Node

↓HR –> Cardiac Output

Negative Inotropic Effect

A
  • *Non-DHP Calcium Channel Blockers**
  • *Verapamil > Diltiazem**

Vasodilator

More cardiac deppressant vs DHP’s

22
Q

Sodium Nitroprusside

Class / MoA / ADR

A

Parenteral Vasodilator

Dilates Arterioles & VEINS

Potent –> used for HYPERTENSIVE EMERGENCIES

ADRs:
Accumulation of CYANIDE

TachyCardia & Provokes ANGINA

23
Q

What drug based on MOA?

Blocks uptake of: NE / DA / 5-HT into pre-synaptic vasicles

depletion of NE stores –> inhibit release of NE
@ post ganglionic sympathetic effector site on BVs

= VASODILATION

A
  • *RESERPINE**
  • *Adrenergic Neuron Blocker**

Mild-Moderate HTN

may cause PARKINSONISM = DA depletion

Impairs baroreceptor reflex –> orthostatic hypotension

24
Q

Ace Inhibitor ADRs

A

Acute RENAL failure

HYPERkalemia
more likely w/ renal insufficiency / diabetes
due to inhibitory action on aldosterone secretion

AngioEdema

DRY COUGH

  • *ASPIRIN + NSAIDS**
  • may diminish HypoTensive response*
  • *PREGNANCY WARNING**
  • contraindicated during 2nd & 3rd trimesters*
25
Q

What drug based on MOA?

Primarily: ↓CO

Kidneys:
antagonize renin production

Peripheral sympathetic neurons on BVs:
antagonize pre-synaptic B-adrenoceptors = vasodilation

unlikely brain effects:

A
  • *BETA BLOCKERS**
  • *-OLOLS**

Non Selective = NPC
Propranolol / Naldolol / Carteolol

Selective B1 = BBEAM
Bisoprolol / Betaxolol / Esmolol (IV) / Atenolol / Metoprolol

26
Q

What drug based on MOA?

Inhibition of Na+ influx through ion channels
@late DCT & collecting tubule
(luminal = urine-side)

A

K+-Sparing Diuretic
inhibit Na+ influx in distal & collecting tubules

Triamterene + Amiloride

avoids K+ depletion, of Thiazides

ENHANCES natriuretic effect of other diuretics

27
Q

CNS-Acting Sympathoplegics
USES

Methyldopa / Clonidine

Guanfacine / Guanabenz

A

Sympathetic nervous system OUTFLOW from brain

Moderate HTN

Intact barorecetor reflex
advantage = low orthostatic HTN

28
Q

What drug based on MOA?

INHIBITION of CA++ Influx
into smooth muscle of arterioles

PVR

Reflex sympathetic Activation –> TachyCardia

HR –> ↑CO

A
  • *DHP Calcium Channel Blockers**
  • *Amlodipine / Nifedipine / Felodipine**

Vasodilator

less cardiac depression vs NON-DHP’s

29
Q

What drug based on MOA?

Block Aldosterone receptors
@ late DCT

A
  • *K+-Sparing Diuretic**
  • *ALDOSTERONE ANTAGONIST**

Spironolactone + Eplernone

avoids K+ depletion, of Thiazides

ENHANCES natriuretic effect of other diuretics

30
Q

Thiazide Uses

Chlorthiazide / HCTZ / Methylclothiazide

Non-thiazide Sulfonamide:
Chlorthalidone / Indapamide / Metolazone

A

Most Frequently prescribed diuretic class

Mild-Moderate Essential HTN
w/ normal cardiac & renal fxn

Lower Doses = similar antiHT action vs higher doses

Higher doses = MORE NATRIURETIC effect

31
Q

Which drug have a COMPELLING INDICATION for:

POST MI

HIGH CORONARY RISK

HEART FAILURE

A
  • *BETA BLOCKERS**
  • olols
32
Q

What Drug based on MOA?

Inhibits action of RENIN
Angiotensinogen –/–> Angiotensin 1

AT1

AT2

↓Aldosterone

A

Direct RENIN Inhibitors

ALISKIREN / REMIKIREN

33
Q

Diuretics as AntiHypertensives
Clinical Effects

Thiazide + K-sparing Diuretics

A
  • *BP = CO** x PVRCO = HR x SV
  • *P**eripheral Vascular Resitance

Initially diuretics (ACUTE):
Blood VolumeCO , while ↓Na+ stores,
PVR may increase

After 6-8 weeks:
Na+ depletion –> ↓PVR
and CO returns to NORMAL

34
Q

Compelling Indications for ARBS

A

CKD

DIABETES