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PNS/Cardiology > Antihypertensives I and II > Flashcards

Antihypertensives I and II Flashcards

1
Q

What are the two direct vasodilators?

A

Hydralazine

Minoxidil

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2
Q

Are the direct vasodilators working on veins or arterioles?

A

Arterioles

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3
Q

What is the major effect of arteriolar vasodilation?

A

Decreased afterload

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4
Q

What other effects result from the arteriolar vasodilation?

A

Nonpostural fall in BP
LV filling pressure high
Reflex increase in cardiac work and HR
Reflex increased plasma renin

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5
Q

The reflex increase in cardiac work & HR and reflex increase in plasma renin caused by direct vasodilators can ultimately result in ______

A

Increased BP (not the goal of vasodilators)

Must block these two reflexes from occurring using a beta blocker and a diuretic
(Therefore direct vasodilators are 3rd or 4th line antihypertensives)

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6
Q

Which is the more potent direct vasodilator?

A

Minoxidil

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7
Q

What is a potential side effect of minoxidil?

A

Hypertrichosis (hair growth, rogaine)

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8
Q

What is a potential side effect of hydralazine?

A

Lupus-like syndrome (malaise, arthralgia, vasculitis)

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9
Q

How is minoxidil activated?

A

Gets sulfated in liver

Therefore cannot be given by injection

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10
Q

What are the channels opened by minoxidil?

A

ATP-sensitive K+ chanels (K-ATP)

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11
Q

What causes K-ATP channels to open and what does the opening do to the membrane potential?

A

Decreased ATP, increased ADP causes channel opening (decreased metabolic state)

K+ leaves the cell, membrane hyperpolarizes, reduces energy demand of the cell

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12
Q

What happens to the K-ATP channels in cardiac myocyte that is hypoxic/ischemic?

A

Hypoxia/ischemia –> ATP decreases, ADP increases –> K-ATP channels open –> AP duration decreases, contractility decreases –> energy demand decreases

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13
Q

What happens to smooth muscle cell that is hypoxic?

A

Hypoxia –> ATP decreases, ADP increases –> K-ATP channels open –> muscle hyperpolarizes –> Ca2+ channels close –> relaxation of vascular smooth muscle
–> increased blood flow

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14
Q

What causes the production of adenosine?

A

Decrease in ATP, increase in ADP

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15
Q

What is the mechanism of action of adenosine?

A

Opens K-ATP channels causing vasodilation

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16
Q

What happens to K-ATP channels in pancreatic beta cells when there is an increase in blood glucose?

A

Increased blood glucose –> Increased ATP, Decreased ADP –> K-ATP channels close –> Ca2+ channels open
–> insulin release increases

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17
Q

What is the mechanism of action of sulfonylureas?

A

Inhibit K-ATP channels, causing insulin release

Thereby acts as a glucose lowering agent

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18
Q

What is the mechanism of action of diazoxide?

A

Opens K-ATP channels, causing decreased insulin release

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19
Q

What are the two subunits of the pancreatic Beta cell K-ATP channel?

A

SUR1

Kir 6.2

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20
Q

What inhibits the SUR1 subunit of K-ATP channel?

A

Sulfonylureas

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21
Q

What activates the SUR1 subunit of K-ATP channel?

A

Diazoxide

ADP

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22
Q

What inhibits the Kir 6.2 subunit of K-ATP channel?

A

ATP

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23
Q

What type of K-ATP channels (VSM, cardiac, pancreatic) is minoxidil selective for?

A

VSM

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24
Q

What type of K-ATP channels (VSM, cardiac, pancreatic) is adenosine selective for?

A

Cardiac

VSM

25
Q

What type of K-ATP channels (VSM, cardiac, pancreatic) is diazoxide selective for?

A

Pancreatic

VSM

26
Q

What is unique about the K-ATP channels involved in the cardioprotectant mechanisms of diazoxide and adenosine?

A

They are mitochondrial K-ATP channels

27
Q

Describe the concept of ischemic preconditioning

A

A previous short period of ischemia protects the heart when a longer period of ischemia occurs

28
Q

What occurs in the early phase (<3 hrs) of ischemia to be protective?

A

Mitochondrial K-ATP channels open –> closure of mitochondrial permeability transition pore –> sustained mitochondrial function

29
Q

What occurs in the late phase (24-48 hrs) of ischemia to be protective?

A

Reperfusion injury salvage kinases (RISK) –> gene transcription –> increased expression of protective proteins like heat shock proteins and superoxide dismutase

30
Q

What is the role of adenosine in ischemic preconditioning?

A

Binds Adenosine receptors in the heart, causing opening of both sarcolemmal and mitochondrial K-ATP channels

31
Q

What is the role of adenosine in the nuclear stress test?

A

Dilates arterioles in normoxic myocardium, diverting flow from the hypoxic region and enhancing contrast between hypoxic and normoxic areas

32
Q

What drugs should be avoided during ischemic pre/post conditioning?

A

Sulfonylureas - inhibit K-ATP channels
Methylxanthines (caffeine, theophylline) - adenosine receptor antagonists, can prevent adenosine from opening mitochondrial K-ATP channels

33
Q

What is the mechanism of reserpine?

A

Irreversibly blocks VMAT

Causes depletion of NE in storage vesicles

34
Q

When used in a large dose, what does reserpine do?

A

Sedative, tranquilizer

35
Q

When used in a lower dose, what does reserpine do?

A

Peripheral sympatholytic, causes vasodilation

36
Q

What are some of the adverse CNS effects of reserpine?

A

Increased risk of clinical depression

Exacerbation of parkinsonism

37
Q

What is the mechanism of clonidine and methyldopa?

A

Central alpha-2 agonists
Decrease sympathetic outflow to cardiovascular system (inhibit NE release)
Baroreceptor reflexes remain intact

38
Q

What patient population is methyldopa a first line antihypertensive?

A

Pregnant patients

39
Q

What are adverse effects of central alpha-2 agonists?

A

Drowsiness, somnolence
Dry mouth
Sudden withdrawal causes excess of sympathetic outflow, resulting in exacerbation of hypertension

40
Q

What is the mechanism of action of metyrosine?

A

Competitive inhibitor of tyrosine hydroxylase

Inhibits formation of NE at rate limiting step

41
Q

What is a major clinical use of metyrosine?

A

Used in management of inoperable pheochromocytomas

42
Q

What are the two categories of calcium channel blockers?

A

Dihydropyridines (DHPs)

Non-DHPs

43
Q

What drugs are the DHPs?

A

Nifedipine

Amlodipine

44
Q

What drugs are the non-DHPs?

A

Verapamil

Diltiazem

45
Q

Are the calcium channel blockers primarily arteriolar or venous vasodilators?

A

Arteriolar

46
Q

What is the action of calcium channel blockers on coronary arteries?

A

Dilates coronary arteries

Useful in coronary vasospasm

47
Q

Do DHPs or nonDHPs have cardiodepressant action?

A

NonDHPs

48
Q

At what type of L-type Calcium channels do calcium channel blockers act?

A

1.2 and 1.3
No effect on skeletal muscle or retina
Main effects on cardiac muscle and vascular smooth muscle (vasodilator)

49
Q

What are the different gating modes of the L-type calcium channel?

A

2 - long-opening
1 - brief-opening
0 - rare-opening

50
Q

Which mode of the calcium channel is stabilized by calcium channel blockers?

A

0 - rare opening

51
Q

What are the different conformations of the L-type calcium channel?

A

Closed
Open
Inactivated

52
Q

What conformation of the calcium channel do nonDHPs bind tighter to?

A

Open
Bind more tightly when channel is phasic between open and closed conformations (i.e. in cadiac muscle)
Hence, better cardiodepressant effect for nonDHPs

53
Q

What conformation of the calcium channel do DHPs bind tighter to?

A

Inactive

Find more inactive state in tonically depolarized cells (always some calcium mediated contraction and tone maintained

54
Q

What happens to heart rate when cardiac L-type channels are blocked?

A

Decreases
Because SA node automaticity is decreased
Slows rate of upstroke of action potential

55
Q

What happens to conduction velocity when cardiac L-type channels are blocked?

A

Decreased conduction velocity
Because AV node conduction is slowed
Slows rate of upstroke of action potential

56
Q

What happens to cardiac contractility when cardiac L-type channels are blocked?

A

Decreased contractility

Reduced inward Ca current during plateau phase

57
Q

What are adverse effects for DHPs?

A

Hypotension, flushing, headache
Reflex sympathetic activation
Swollen ankles

58
Q

What are adverse effects for nonDHPs?

A 
LV dysfunction (decreased contractility)
AV block (slowed conduction)
Avoid combination with beta-blockers (similar cardiodepressant effect)
GI (constipation)
59
Q

How are calcium channel blockers metabolized?

A

By CYP450 enzyme CYP3A4 in the liver

Avoid combination with competitive substrates/inhibitors of CYP3A4 (like statins, grapefruit juice)

PNS/Cardiology (33 decks)

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