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CV Block > Autonomic Drugs/Receptors > Flashcards

Autonomic Drugs/Receptors Flashcards

1
Q

Mechanism of Alpha 1 receptors:

A

Gq coupled receptor. Gq pathways activate IP3 and DAG from membrane phospholipids. IP3 released intracellular calcium stores, which causes SMOOTH MUSCLE CONTRACTION

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2
Q

Mechanism of Alpha 2 receptors:

A

Gi coupled receptor. Gi pathways inhibit adenylyl cyclase, which is responsible for the formation of cAMP under normal circumstances.

When blocked, there is a DECREASE in cellular cAMP.

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3
Q

What type of G protein is coupled with B1, B2, and B3 receptors? What is its mechanism?

A

Beta receptors are Gs coupled receptors. They stimulate Adenyate Cyclase to cause INCREASE in cellular cAMP levels.

This increase in cAMP levels causes different outcomes in different target cells, however. If B2 receptors in the heart are stimulates, it causes increased HR/contractility. If B2 receptors in skeletal muscle are stimulated, there is smooth muscle relaxation and vasodilation.

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4
Q

Dopamine 1 receptors are paired with which type of G protein?

A

Gs (increase cellular cAMP via adenylate cyclase stimulation)

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5
Q

You’re having a bronchospasm. What class of drug would you give to make it stop?

A

B-agonist

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6
Q

Drug of choice for anaphylactic shock

A

Epinephrine

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7
Q

Norepinephrine has an effect on which sympathetic receptors? Which one is left out?

A

Norepinephrine effects a 1&2, and B1.

No action on B2

MOSTLY EFFECTS ALPHA RECEPTORS (vasoconstriction, increase BP), with a slight B1 effect (increase in HR/contractility)

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8
Q

Alpha receptor antagonist drug names end in what?

A

a1 “specifics” end in “azosin.”

Teferazosin
Prazocin
Doxazocin

A1=A2 end in “amine”.

Phenoxybenzamine
Phentolamine

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9
Q

Which alpha antagonists are dose specific? explain.

A

Phenoxybenzamine and PHENTOLAMINE

LOW DOSE: specificity for a2 receptors on the presynaptic membranes of sympathetic neurons. Blocking alpha 2 receptors blocks their normal negative feedback of Norepinephrine, so there are inotropic (cardiac stimulatory) effects.
- increases BP because NE is not inhibited.

HIGH DOSE: greater Alpha 1 specificity. Blocking alpha 1 receptors causes vasodilation and a decrease in BP

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10
Q

Drugs with more alpha 2 blocking ability will have what effects on the heart?

A

Drugs with more a2 blocking ability will lead to INOTROPIC effects:

Tachycardia
Greater CO
Increased BP

This is due to the increased release of Norepinephrine. There is no negative feedback of NE due to loss of a2 receptors.

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11
Q

Drugs with more alpha 1 blocking ability will have what effects on the heart? Vasculature?

A

Blocking Alpha 1 receptors relates to smooth muscle contraction. This won’t have too much effect on the heart except for smooth muscle relaxation of the peripheral vasculature, which LOWERS THE BP. There may be a compensatory increase in HR.

The drugs block the already-circulating E and NE from binding alpha receptors and inducing vasoconstriction.

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12
Q

Adverse Effects of Alpha Blocker Therapy:

A

Initial dose can cause Orthostatic Hypotension. So take it before bed and with food.

Can cause sinus tachycardia, angina (chest pain with exertion), and heart palpitations.

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13
Q

Which Alpha Blocker should only be used in emergency HTN situations?

A

Phentolamines

(Remember: blocks a1 at high doses for a decrease in TPR and BP, and at low doses, blocks a2 for a cardiac stimulatory effect)

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14
Q

Why aren’t alpha blockers used frequently anymore?

A

They have an increased risk of heart attack, compared to the use of diuretics for HTN therapy.

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15
Q

Which alpha blocker covalently binds to block its target receptor?

A

Phenoxybenzamine – LONG duration of action because the

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16
Q

Orthostatic Hypotension is the biggest problem in which Alpha Blocker?

A

Prazocin

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17
Q

What is the general rule of B1 or 2 specificity when it comes to the naming of B-blockers?

A

If the letter starts with A-N = B1 specific

If it’s anywhere from P on, it’s B1=B2.

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18
Q

What is the B-blocker with the shortest duration of action?
What is it used for?
How is it administered?

A

Esmolol
15 minute diration
IV administered for hour by hour BP control.

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19
Q

Which B-blockers are membrane stabilizers and how do they do this?

Because they stabilize the membrane, what other condition can they be used for?

A

Mnemonic: PRO rACE CAR driver

Propranolol
Acebutolol
Carvedilol

They block the fast Na+ channels of myocytes and slow down the action potential.

The MOA of these drugs means they can also be used as ANTIARRHYTHMICS.

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20
Q

By what route are most B-blockers administered? What’s the exception?

A

Orally, except for Esmolol , which is IV admin.

It’s T/2 is so short you can use it for hour by hour control of HTN.

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21
Q

Which B-blockers have Intrinsic Sympathomimetic Activity? (AKA, are partial agonists for B-receptors)

What type of drug reactivity does this help eliminate?

A

Pindolol
Acebutolol
Carteolol

These drugs physically block Epinephrine from binding B-receptors, while slightly activating them, themselves. They prevent EXCESSIVE activation of B-receptors, while maintaining a little of their physiological activity.

This slight activation prevents the adverse effects of completely blocking B-receptors:

  • Bradychardia
  • Negative Inotropy (decreased contractility)
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22
Q

What 2 extended actions does Carteolol have?

A

Slight B-agonism

NO production = vasodilatory effects

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23
Q

Which 2 B-blockers are also partial A-receptor agonists? What does this extended action help prevent?

A

Carvedilol
Labetalol

When first starting a B blocker, vessels can try to compensate for the resulting slowed heart rate and vasodilation by reflex compensation mechanisms.
This is accomplished normally by a-receptor activation, which constricts the peripheral blood vessels, and negates the effect of the B-blocker.

Carvedilol and Labetolol eliminate this compensatory mechanism.

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24
Q

What B-blocker has antioxidant activity?

A

Carvedilol

Carvedilol has 3 extended actions:

  1. Antioxidant generation
  2. Membrane stabilization - via fast Na+ channel blockade
  3. Partial alpha agonist - prevents the compensatory increase in TPR after B-blockade
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25
Q

Why should you step-down doses and restrict exercise when coming off a B-blocker?

A

Sudden systemic elimination of B-blocker effects will cause a sympathetic surge. Your body has responded to the B-receptor blockade by up regulating B-receptors. This causes tachycardia, angina, and sometimes sudden death when sympathetic stimulation is no longer inhibited.

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26
Q

Patients with ___________________ should not take B-blockers. (multiple conditions)

A
  1. Congestive Heart Failure. –> These people need all the sympathetic stimulation they can get to maintain their cardiac output.
  2. People with Conduction Defects/ or are on anti-arrhythmics –> B-blocker use causes bradycardia and bradyarrhythmia

(Verapamil is the anti-arrhythmic he gave us in the ppt. If you’re on it, avoid B-blockers)

  1. Athsmatics –> B-2 receptor blockade can kill them if they are already bronchoconstricted. It won’t allow them to get air!
  2. Diabetics: B-blockers take away the means to control blood glucose level (gluconeogenesis/glycogenolysis) and the means to detect low sugar levels (tachycardia).
    THIS IS ONLY SEEN IN NONSPECIFIC B-BLOCKERS –> you can use a B1 specific.
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27
Q

Which of the following B-blockers possesses a cardiac-specific effect?

A. Atenolol
B. Pindolol
C. Propranolol
D. Timolol

A

Atenolol

Remember: Any B blocker that starts with P, on, has equal B1 and B2 effects.

B1 specifics start with A-N.

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28
Q

Which of the following is least likely in a patient who suddenly stops long term use of B-blockers?

A. Angina
B. MI
C. Tachycardia
D. Orthostatic Hypotension
E. Sudden death
A

D. Orthostatic Hypotension.

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29
Q 
Which one of these drugs would also be applicable to a man who suffers from Benign Prostatic Hyperplasia? 
A. Atenolol
B. Prazocin
C. Clonidine
D. Trimethaphan

WHY??

A

B. Prazocin (Alpha blocker)

Most of the autonomic receptors in the prostate are A1 receptors. Blocking them causes relaxation of the bladder and prostate muscles, relieving the pain.

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30
Q

Do beta blockers cause Na+ and water retention?

A

NOPE. They work simultaneously in the heart (reduce HR, contractility, and thus, CO) AND KIDNEYS (prevent Renin release).

B1 receptors are in kidneys.

You don’t have to administer a diuretic with them, but their effect of decreasing HTN are additive if you do.

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31
Q

When is a diuretic indicated?

A

Diuretics are indicated in low to normal renin HTN cases. In high-renin HTN cases, you just need to give a B-blocker, because it will stop renin release via B1 receptor blockade in the Kidneys

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32
Q

What is (according to Dr. Bahouth) one of the most effective drug combo for HTN?

A

B-blocker and a diuretic

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33
Q

Which B-blocker is available as an eye drop?

A

Timolol - treats glaucoma

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34
Q

Name the 3rd generation B-blockers and their extra activities.

A

Labetalol - Nonselective B and A1 receptor antagonist
(Given in HTN emergencies)

Carvedilol - Nonselective B and A1 receptor antagonist,
AND antioxidant effects

Nebivolol - highly B1 selective, with NO-mediated vasodilation

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35
Q

Which of the 3rd generation B-blockers is used in diabetics with metabolic syndrome? Why is it used?

A

Nebivalol

HIGHLY B1 specific, with an added effect of NO induction. (vasodilatory effect lowers BP even more)

There are only B2 receptors in the liver, so there is no inhibition of gluconeogenesis/glycogenolysis.

Mnemonic: The drug that starts with “N” releases “NO”

36
Q

Which anti-hypertensive drug is the first-line treatment for CHF?

A

ACE inhibitors, followed by 3rd generation B-blocker, Carvedilol

37
Q

What is the most potent vasoconstrictor we have in our bodies?

A

Angiotensin II

38
Q

What is an ACE inhibitor?

A

A drug that blocks the effects of Angiotensin Converting Enzyme. ACE (located in the lungs) converts Angiotensin 1 to Angiotensin II (active form), which then binds to Angiotensin Receptor Type 1, causing vasoconstriction. (among other things….)

It increases renal blood flow (via increase in blood volume) without in increase in GFR (no extra peeing… fluid stays in the body)

39
Q

Name the 6 things that increase levels of Angiotensin II cause.

A
  1. Na+ retention in the proximal tubule of Kidney.
  2. Makes pituitary release more VASOPRESSIN (molecule most responsible for H20 retention)
  3. Aldosterone secretion from the renal cortex –> increased Na+ /H2O retention in kidneys
    (Aldosterone is a mineralocorticoid responsible for K+ levels) … It causes increased K+ resorption in the kidneys.
  4. Thirst - hypothalamus effect
  5. Vasoconstriction –> systemic
  6. Cardiac and vascular hypertrophy –> acts on cell transcription mechanisms to cause thickening of vessel walls and heart. PROMOTES HEART FAILURE
40
Q

Why do ACE inhibitors cause a chronic dry cough?

A

Bradykinin levels rise because ACE is responsible for the breakdown of this molecule. We have receptors for this in our trachea, and it causes cough.

41
Q

Can you use ACE inhibitors in Pregnancy?

A

Yes in the 1st trimester, but cause fetal defects if used in the 2nd and 3rd trimesters.

42
Q

If coughing becomes too much of a problem with a patient on ACE inhibitors, what drug type do you give them to maintain their current pharmacological benefit, but get rid of the cough?

A

ARBS (Angiotensin Receptor Blockers)

They have no effect on Bradykinin, but don’t allow Angiotensin II to work because the receptor is unavailable for binding!

43
Q

ACE inhibitors all end in what suffix?

A

“pril” ex: Captopril

44
Q

ARBs (Angiotensin Receptor Blockers) end in what suffix?

A

“sartan”

Example: Valsartan

45
Q

What ARB would you give a hypertensive patient with Gout? Why?

A

Losartan.

It’s Urosuric:

It’s the only drug known to increase uric acid secretion in the urine AND lower BP.

46
Q

Can you give an ACEI/ARB in pregnancy?

A

NOPE –> all have fetotoxicity

47
Q

MOA of Calcium channel blockers.

A 
For HTN (dihydropyridines): Decrease BP by relaxing arteriolar smooth muscle and decreasing peripheral vascular resistance. (Decrease TPR causes a decrease in MAP)
Not much effect on venous smith muscle.

For Arrhythmias (Non-dihydropyridines): Increases the threshold membrane potential of L-type Ca2+ channels in the SA node. It takes longer for the funny current to depolarize the membrane enough to reach it!

(Phase 4 elongation of pacemaker cells) —> but these are used more in arrhythmias.

48
Q

Why do patients with Coronary Artery Disease benefit from Ca2+ channel blockers?

A

Dihydropyridine Ca2+ channel blockers (Nefidipine) prevent smooth muscle contraction, esp. in the coronary arteries, allowing greater bloodflow to the area.

49
Q

The main Ca2+ channel blocker for controlling HTN is…

WHat about for controlling arrhythmias?

A

Dyhidropyridines = Nefidipine
Used for HTN.

Non-dyhydropyridines = Verapamil and Diltiazem
Used for Arrhythmia control. Cause Phase 4 elongation (longer generation time) of SA nodal cells via blockage of L-type Ca2+ channels. Reduce inotropy/chronotropy of heart too.

50
Q

An athlete comes to you with HTN, but doesn’t want his/her performance to be affected. What do you give them?

A

CALCIUM CHANNEL BLOCKERS!

No sympathetic inhibition, so their response to exercise is ok!

No B blocker because there will be no exercise induced increase in heart rate (despite increased metabolic demand)

51
Q

What are the only HTN drugs that cause an increase in survival rate of patients that take it?

A

ACE inhibitors

Bisoprolol (3rd generation B-blocker)

Diuretics

Btw…. this is the best regimen for HTN treatment. Trifecta!

52
Q

Name a drug that is a sympathetic AGONIST but still lowers blood pressure.

A

Clonidine/Methyldopa/Guanfacine

Alpha2-receptor agonists. Activated Alpha 2 receptors prevent the release of stored NE. Decrease sympathetic output causes a decrease in peripheral resistance and a decrease in HR, therefore a decrease in BP.

53
Q

Main side effect of Alpha2 agonists.

A

SEDATION, drowsiness, fatigue.

Alpha2 agonists act in the Rostral Ventrolateral Medulla of the brain, and since they are centrally acting agents, they have neural side effects.

These drugs won’t work if they’re not lipophillic, cause their MOA is on the presynaptic neurons in the CNS!

(He said REMEMBER THIS)

54
Q

If you come off of an Alpha2 agonist suddenly, what happens?

A

You get HTN because you can now release all the stores of NE you have. There was no stimulation in the periphery, so your body upregulated NE receptors, and now they have something to bind to.

55
Q

When is clonidine indicated?

A

Only after Diuretic and Ace inhibitors already don’t work. STUBBORN HTN.

They’re called TERTIARY agents cause it’s the 3rd one you add on to the regimen if diuretics and ACE inhibitors (together) don’t work.

56
Q

Why are NSAIDs contraindicated when a person takes ACE inhibitors or ARBs?

A

NSAIDs work by inhibiting the synthesis of Prostaglandins. (COX inhibitors)

But PGs are responsible for the micro-control of renal perfusion. Inhibiting these leads to the worsening of HTN through decreased kidney function, which causes increased fluid retention. (increases BP)

57
Q

What B-blocker causes nightmares? Why

A

Propranolol –> lipophilic drugs penetrate the CNS

58
Q

What effects do B-blockers have on your lipid profile?

A

B3 receptors are in adipocytes. (mediate lipolysis)

Blocking these receptors with nonspecific B-blockers INCREASES TG LEVELS in the blood and DECREASES HDL levels.

B1 specific blockers or those with partial B agonism (Pindolol, Acebutolol, Carteolol) don’t have this effect.

59
Q

Why do diabetics have to be careful on B-blockers? (maybe even NOT take them at all)

A

There are B receptors in the liver that mediate glycogenolysis and gluconeogenesis. Blocking these will stop these processes, and can WORSEN HYPOGLYCEMIA.

In diabetics, tachycardia is a sign of low blood sugar. B-blockers mask this tachycardia, and diabetics lose the intrinsic indication they’re low.

60
Q

The arterioles, veins, and heart are consistently under what kind of tone?

What happens to this tone when you apply a ganglionic blocker?

A

Arterioles: Sympathetic

Veins: Sympathetic

Heart: Parasympathetic

Apply a ganglionic blocker and you lose your predominant tone.

ARTERIOLES: Vasodilation = increased peripheral bloodflow = hypotension

VEINS = Dilation; pooling of peripheral blood; decreased venous return

HEART: Tachycardia (loss of parasympathetic regulation)

61
Q

MOA of ganglionic blockers. Can you affect just one ganglion?

A

Compete with Ach for binding the nicotinic receptor, or block the ion channel, PREVENTING DEPOLARIZATION.
The EPSP is blocked, and IPSP is increased.

Nicotinic receptors are responsible for causing depolarization (opening of Na+ and K+ channels)

Remember: Ach is the primary neurotransmitter in BOTH sympathetic and parasympathetic neurons. (the effector neurons in the sympathetic system use Catecholamines, but these are first activated by Ach in a ganglion)

Can’t effect just one ganglion!

62
Q

What are the intended side effects of a ganglionic blocker?

Can these also be side effects?

A

Loss of sympathetic tone to vasculature = Decrease BP

Loss of parasympathetic tone to the heart = tachycardia

CAN ALSO CAUSE SIDE EFFECTS as a result of their intended effect:

Postural HTN
Extreme Tachycardia
Arrhythmia

63
Q

WTF is the Hexamethonium man?

A

He’s the example of what happens when you lose all of your homeostatic autonomic tone.

  1. PInk complexion: peripheral vasdilation
  2. Faints when he stands (hypotension)
  3. Dry mouth
  4. Urinary retention/constipation
64
Q

MOA of A2 - agonists.

A

Presynaptic membrane –> autoreceptor activation causes decreased synthesis and storage of NE. The withdrawal of sympathetic tone produces a balanced fall in TPR and systolic/diastolic BP.

Post-synaptic membrane –> Heteroreceptor activation increases parasympathetic stimulation (bradycardia and hypotension)

65
Q

Which produces more of a beneficial effect: An A2-agonist’s action on presynaptic auto receptors or post-synaptic heteroreceptors?

A

POST-SYNAPTIC HETERORECEPTOR ACTIVATION

Induces bradycardia and hypotensive effects.

The overall activity is an increase in parasympathetic stimulation via heteroreceptor activation (vagal activation) and inhibition of sympathetic stimulation via auto receptors.

66
Q

Do a2 agonists penetrate the BBB?

A

YES! Their primary effect is on neurons and the CNS, so they have to.

If they did not, they would have no BP lowering effect.

67
Q

Do you prescribe a diuretic with A2 agonists?

A

Yep.

68
Q

WHich a2 agonists can be used in pregnancy?

Which one is also a prodrug that must be metabolized to it’s active form?

A

Methyldopa and Guanfacine can be taken during pregnancy.

Methyldopa is a prodrug. Bioactivated to 2-methylnorepinephrine.

69
Q

Which A2 agonist has the longest 1/2 life?

A

Guanfacine

70
Q

You’re taking iron supplements and the doc wants to prescribe you an A2 agonist. Which one can you not take? Of the 2 left, you want the one that is IV available, not oral. Which one do you end up taking?

A

You can’t take Methyldopa because it is chelated by iron supplements.

The other 2 drugs left are Guanfacine and Clonidine. Guanfacine is only available orally.

You take Clonidine (IV admin)

71
Q

You can’t take an A2 agonist when you’re pregnant cause you’re allergic. What’s the second line treatment? (Hint: it’s a mixed action B-blocker)

A

Labetalol

Combined A and B receptor blocker.

72
Q

A retarded doctor prescribes an ACE inhibitor (or an ARB) to a pregnant woman. What happens to the baby?

A

Neonatal renal failure/ birth defects

73
Q

MOA of Reserpine

A

Binds to VMAT2 on adrenergic storage vesicles (NE/E) in central and peripheral adrenergic neurons. Prevents the uptake and storage of NE and Epi into vesicles.

Recovery requires synthesis of new vesicles, so drug effect lasts DAYS to WEEKS.

74
Q

What is the most common side effect/toxicity of any sympathetic antagonist that penetrates the BBB?

A

Sedation!

75
Q

What extra neural side effect does Reserpine have?

A

Sedation and suicidal thoughts.

76
Q

Back to B-blockers….

Which one of the following B-blockers would be less likely to initiate an attack in an asthmatic patient? 
-Pindolol
Propranolol
Carvediolol
Betaxolol
A

Betaxolol, since it’s a B-1 specific. Remember the trick.

A-N = B1 specific

P-Z B1=B2

77
Q

Why don’t you let a patient take Verapamil and a B-blocker at the same time?

A

They are both negative inotropes. (Verapamil is a Ca2+ channel blocker)

They have the risk of collectively reducing heart activity to the point of asystole.

78
Q

What does sympatholytic mean and which drugs fall under that category?

A

Sympatholytic means it blocks the effects of the sympathetic nervous system.

Reserpine
Methyldopa
Clinidone
Guanifacine

The A2 agonists/ storage depleter (reserpine)

79
Q

What B-blocker penetrates the BBB? (the main one mentioned)

A

Propranolol is very lipophillic (remember…. lipophillic drugs have neuronal consequences… like bad dreams)

80
Q

You have a patient with High Renin HTN. What do you give them?

A

B-blocker

Ace Inhibitor

Diuretic

81
Q

Your patient has low renin HTN. What do you give them?

A

CCB (Nefidipine)

Low renin HTN more common in black and old people.

82
Q

The suffix “azocin” indicates what drug class?

A

A blockers

83
Q

“pril”

A

ACE inhibitor (Captopril)

84
Q

“sartan”

A

ARB (Losartan)

85
Q

“dipine”

A

Dyhydropyridine CCB (Nifedipine)

CV Block (13 decks)

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