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Cardio Exam 1 > Ca Channel Antagonists HTN > Flashcards

Ca Channel Antagonists HTN Flashcards

1
Q

Ca is key is what processes?

A

Contractility of skeletal, cardiac and SM

Release of neurotransmitters from vesicles by exocytosis

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2
Q

In resting conditions intracellular calcium is? Extracellular?

A

Low

High

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3
Q

These calcium levels are achieved by?

A

Active efflux pumps

Active reuptake of calcium into sarcoplasmic reticulum

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4
Q

Voltage-gated Ca channels

A

Open in response to depolarization of cell membrane

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5
Q

Three types of Voltage-gated Ca channels

A 
L type
T type (transient, tiny)
N type (neuronal)
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6
Q

L type

A

Long lasting large channels
Cardiac, SM, SA and AV nodal cells
-Located on the plasma membrane

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7
Q

Agonists-mediated Ca release

A

results from activation of IP3 by an agonist to release intracellular Ca from storage sites (SR)

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8
Q

Receptor-operated Ca channels

A

Receptor forms a channel and the channel opens when the receptor is occupied by a ligand
- NMDA receptor

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9
Q

What initiates a contraction?

A

Entry of calcium into the smooth muscle cell or myocardial cells

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10
Q

So calcium enters the SM cell, now what?

A

Ca complexes with calmodulin to activate MLCK

MLCK phosphorylates myosin causing an interaction between myosin and actin

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11
Q

Myosin and actin are?

A

The main cells involved in contraction of a cell

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12
Q

What is different between cardiac and SM cells?

A

SA and AV do not contract, they generate impulses that spread throughout the heart
Calcium helps generate the impulses

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13
Q

Calcium Channel Blockers Dihydropyridines

A
  • End in dipine
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14
Q

Calcium Channel Blockers Non- Dihydropyridines

A

Diltiazem

Verapamil

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15
Q

CCB MOA

A

Inhibit L type calcium channels leading to decreased peripheral resistance and reduced BP

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16
Q

Resting State

A

Closed by ready to open

Waiting for potential change in the membrane

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17
Q

Open State

A

Open channel and calcium is entering the cell

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18
Q

Inactivated (Closed) state

A

Closed and not ready to open
Even if there is a change in potential, the channel will not open
Channel is trying to recover

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19
Q

Dihydropyridines MOA

A

Prefer the closed channel – they bind and stabilize it so the recovery process takes much longer

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20
Q

Where are the most closed channels?

A

Vasculature- Arterial muscle cells

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21
Q

Non-dihydropyridines MOA

A

Prefer the open channels – bind and force them to close with a slow recovery period

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22
Q

Where are the most open channels?

A

Myocardium

Work mainly on SA and AV

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23
Q

CCB Cardiovascular effect

A

Inhibit L type channels and reduce contraction of SM cells → vasodilation , contraction of cardiac myocites (inotropic effect), and pacemaker rate in SA and conduction velocity in AV node (chronotropic effect)

24
Q

What exactly occurs in the vasodilatory effect?

A

Decrease peripheral resistance and vascular resistance

Increased blood flow

25
Q

Non-dihydropyridine decrease?

A

Vessel tone
Heart rate
AV conduction

26
Q

Non-dihydropyridine increase?

A

Blood flow

Peripheral vasodilation

27
Q

Dihydropyridine decrease?

A

Vessel tone

28
Q

Dihydropyridine increase?

A

Blood flow
Peripheral vasodilation
Heart rate
heart contractility

29
Q

CCB uses?

A

HTN
Angina pectoris
Superventricular arrhthmia
Migraine

30
Q

Verapamil and Diltiazem Adverse Effects

A

Major: Cardiodepression
Mod: HYPOtension, AV node blockade, peripheral edema, liver enzyme elevation
Minor: headaches, facial flushing dizziness, constipation

31
Q

DHP Amlodipine Adverse Effects

A

Edema, dizziness, flushing, gingivial hyperplasia, CV, CNS, GI
CYP3A4 inhibitors: HYPOtension, kidney failure
- Long term = increased risk of breast cancer

32
Q

Alpha 1 Adrenergic Receptor Blocker

A

End in -zosin
Doxazosin (Cardura)
Terazosin (Hytrin)
Prazosin (Minipress)

33
Q

Alpha 1 Adrenergic Receptor Blocker MOA

A

Blocks in arteries and veins

Probable blockage of adrenoreceptors

34
Q

Alpha 1 Adrenergic Receptor Blocker Effects

A

Decreased peripheral resistance
Decrease cardiac preload (venous return)
Supress sympathetic outflow in CNS
Decrease LDL, TG and increased HDL

35
Q

Alpha 1 Adrenergic Receptor Blocker Adverse Effects

A

First dose effect – postural/orthostatic HYPOtension

36
Q

Define First dose effect – postural/orthostatic HYPOtension

A

When you change positions, you experience a drop in BP which makes you feel dizzy, unconscious, and not get enough blood to the brain so you might faint

37
Q

How does the body prevent all the blood going to your legs when you stand up?

A

Vasoconstriction

38
Q

Central Alpha 2 Adrenergic Receptors Agonists

A

Clinidine (Catapres)
Guanfacine (Tenex)
Guanebenz (Wytensin)
Methyldopa (Aldomet)

39
Q

Central Alpha 2 Adrenergic Receptors Agonists MOA

A

Activation of central alpha2 receptors (CV control centers) –> suppression of sympathetic outflow from the brain
Possible stimulation of presynaptic alpha 2 receptors and decrease NE release

40
Q

Clonidine/Guanfacine Caution

A

50% excreted unchange in the urine so watch in renal insuf.

41
Q

Clonidine Effects

A

Decrease BP
Decrease HR
Decrease intraocular pressure

42
Q

Clonidine Adverse Effects

A

Sedation and dry mounth
Sexual dysfunction (hyperprolactinemia)
Bradycardia
Withdrawal rxns

43
Q

Methyldopa

A

PRO-DRUG

Delayed peak effects for 6-8 hours –> duration = 24 hours

44
Q

Methyldopa adverse effects

A 
Sedation and dry mounth
Sexual dysfunction (hyperprolactinemia)
Bradycardia
Withdrawal rxns
Hepatoxicity 
Hemolytic anemia
45
Q

Methyldopa is beneficial in?

A

Pre-eclampsia

46
Q

Reserpine Sympatholytic Drug

A

Interferes with function of SNS
Normally there is recycling of NE and Epi
VMAT2 picks up NE/Epi and takes it back to be reused
Reserpine BLOCKS VMAT2 via irreversible binding

47
Q

Reserpine Adverse Effects

A

Increase sodium and water retention
Sedation and inability to concentrate
Depression and suicidal thoughts (depletion of Epi)

48
Q

Reserpine Effects

A

Lowers BP via cardiac output and peripheral resistance

49
Q

Direct vasodilator

A

Hydralazine (Apresoline)

Minoxidil (Loniten)

50
Q

Hydralazine Effects

A

Decrease in peripheral resistance

Minimal effect on veins (no postural hypotension)

51
Q

Hydralazine Adverse Effects

A

Drug-induced lupus syndrome
Increased sodium and water rentention
Headache, HYPOtension, tachycardia, angina pectoris

52
Q

Hydralazine Caution

A

Aggravation of myocardial ischemia –> steals blood from dying regions

53
Q

Minoxidil MOA

A

PRO-DRUG

Activates ATP dependent potassium channels in SM and causes an efflux of K from cells leading to relaxation of the SM

54
Q

Minoxidil Effects

A

Dilation of arterioles and decreased peripheral resistance

55
Q

Minoxidil Adverse Effects

A

Increased retention of sodium and water
Tachycardia, angina pectoris, myocardial ischemia
Hypertrichosis (stim hair growth)

Cardio Exam 1 (7 decks)

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