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Block 9 Week 1 Meg > Leblanc: Alpha-Beta Blockers > Flashcards

Leblanc: Alpha-Beta Blockers Flashcards

1
Q

What are the actions of catecholamines?

A

peripheral excitatory or inhibitory activity on certain vascular smooth muscles

peripheral inhibitory activity on some smooth muscles (gut, bronchials)

cardiac excitation (increased HR and contractile force, increased conduction velocity)

increased glycogenolysis in liver and skeletal muscle

increased release of FFAs from adipose tissue

modulates secretion of insulin, renin, pituitary hormones

CNS: wakefulness, appetite

also inhibits or increases neurotransmitter release

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2
Q

What do alpha-1 receptors do?

A

smooth muscle - contraction

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3
Q

What do alpha-2 receptors do?

A

nerve terminals - decrease neurotransmitter release

smooth muscle - contraction

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4
Q

What do beta-1 receptors do?

A

cardiac muscle - + chronotropic (heart rate), ionotropic (contractility), and dromotropic (conduction velocity)
smooth muscle relaxation
glycogenolysis

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5
Q

What do beta-2 receptors do?

A

smooth muscle - relaxation

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6
Q

What is the order of the affinity of catecholamines for alpha receptors?

A

Epi > NE&raquo_space; Iso

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7
Q

What is the order of the affinity of catecholamines for beta receptors?

A

B1: Iso > Epi = NE
B2: Iso > Epi&raquo_space; NE

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8
Q

Which G proteins do the following receptors act on?

alpha-1
alpha-2
beta

A

alpha 1: Gq
alpha 2: Gi/o
beta: Gs

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9
Q

Describe the pathway following alpha 1 activation

A

alpha 1 –> Gq –> PLC –> PIP2 –> IP3 (increases Ca++) and DAG (PKC) –> smooth muscle contraction

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10
Q

Describe the pathway following alpha 2 activation

A

alpha 2 –> Gi/o –> blocks Ca++ –> inhibits neurotransmitter release

alpha 2 –> Gi/o –> inhibits AC –> no cAMP –> increases Ca++ –> smooth muscle contraction

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11
Q

Describe the pathway following beta receptor activation

A

beta –> Gs –> stimulates AC –> increased cAMP –> increased cardiac contractility, smooth muscle relaxation, glycogenolysis

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12
Q

These two receptors have opposing effects on adenylate cyclase and cAMP production

A

alpha 2 (inhibits cAMP) and beta (increases cAMP)

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13
Q

Explain what norepinephrine does to pulse rate, blood pressure, and peripheral resistance

A

α1 effect: ↑ TPR, ↑ systolic pressure, ↑ diastolic pressure

β1 effect: ↑ SV ↑ pulse pressure, but decreased pulse rate

**decreases in pulse rate is reflex response (NE activates alpha 1 causing constriction of blood vessels and increased blood pressure and TPR, so HR decreases in order to compensate)

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14
Q

Explain what epinephrine does to pulse rate, blood pressure, and peripheral resistance

A

epi increases pulse rate (Beta 1)

increases systolic pressure (Alpha 1), but decreases diastolic pressure (decreases TPR) so BP stays the same

decreases TPR

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15
Q

Explain what isoproterenol does to pulse rate, blood pressure, and peripheral resistance

A

Works on beta receptors (unopposed)

increases pulse rate

increases systolic, decreases diastolic BP

decreases peripheral resistance

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16
Q

Except for Phenoxybenzamine (PBZ) and related compounds, all α receptor antagonists are (blank)

A

competitive antagonists

**this means they are reversible and can be competed off to reverse effects

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17
Q

alpha antagonists work primarily through effects on (blank) receptors in smooth muscle cells

A

alpha 1

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18
Q

What do alpha 2 receptors primarily act on?

A

CNS

**limit sympathetic outflow, and increase parasympathetic outflow

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19
Q

How are alpha 2 receptors involved in metabolic activity?

A

decrease insulin release (insulin promotes fat storage)

decrease lipolysis

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20
Q

What effects do alpha-1 antagonists have on the cardiovascular system?

A

decrease BP, esp in the upright position

**when BP drops low enough, it is compensated for by a baroreflex response

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21
Q

T/F: α1-Adrenergic receptor antagonists will also inhibit the effects of sympathomimetic drugs administered externally (e.g. to reverse an adverse effect)

A

True

**ex: can block the effects of phenylephrine (alpha1 agonist) completely!

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22
Q

What do alpha 2 antagonists do?

A

In the periphery, they increase the release of NE from nerve endings

CNS – Pontomedullary Region:
Increase Σ outflow by augmenting the release of NE which will increase by stimulation both α1 and β1 receptors in the periphery → ↑ BP

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23
Q

Blocks α1 and α2 “irreversably” by a covalent modification of the receptors

A

Phenoxybenzamine

24
Q

What are the major effects of phenoxybenzamine (alpha 1 and 2 blocker)?

A

blocks alpha receptors in smooth muscles, leads to decrease in peripheral resistance

enhanced baroreflex response increases HR
**blockage of alpha 2 also may increase HR further by increasing sympathetic outflow

25
Q

What are the therapeutic used for phenoxybenzamine?

A

pheochromocytoma: tumors of adrenal medulla which cause secretion of enormous quantities of catecholamines –> severe hypertension **can be used to counteract this

can be used in prep for surgery for pheochromocytoma removal

first drug prescribed to treat benign prosthatic hypertrophy in men!

26
Q

What are the adverse effects of phenoxybenzamine?

A

postural hypotension **can be bad in patients that are hypovolemic or already taking a vasodilator, also can induce arrhythmias due to reflex tachycardia

27
Q

Blocks α1 and α2 with a similar affinity; the interaction is competitive and reversible
Cardiovascular effects are similar to PBZ
Stimulates GI smooth muscles and enhances gastric acid secretion

A

Phentolamine

28
Q

What are the therapeutic uses for phentolamine?

A

used in pheochromocytoma patients for short term control of hypertension, can also relieve pseudo-obstruction of the bowel by suppressing inhibitory effects of catecholamines on GI smooth muscle

can be rapidly infused to alleviate a sever hypertensive episode

can be used to limit dental necrosis after given an alpha agonist to prevent loss of local anesthetic (in some pts, will completely inhibit blood supply to the mouth and lead to necrosis)

can be used in Raynaud’s disease

can be used after rapid withdrawal of clonidine or following the ingestion of tyramine-rich food during use of MAOIs

impaired erection in men

29
Q

Prototype of a growing family of α1-selective antagonists with greater clinical utility
Affinity for α1 over α2 is ~ 1000 –fold
Displays similar affinities for the different subtypes of α1 receptors: α1A ≈ α1B ≈ α1D
Also a potent inhibitor of cyclic nucleotide phosphodiesterases (PDE)
Block of α1 receptors in arterioles and veins → ↓ peripheral vascular resistance → ↓ BP → ↓ venous return to the heart
Does not generally increase heart rate
Although much weaker, may also decrease ↓ Σ outflow in the CNS

A

Prazosin

30
Q

Prazosin blocks α1 receptors in arterioles and veins. What does this do?

A

decreases TPR and BP and decreases venous return to the heart

**blocks the baroreflex mechanism (doesn’t increase HR) - can be good for pts with HTN

31
Q

Prazosin has favorable effects on (blank)

A

lipids!

↓ LDL, ↓ triglycerides and ↑ HDL levels

32
Q

What is prazosin used for therapeutically?

A

Essential Hypertension (mild to moderate)
Vasodilator used in Congestive Heart Failure
Benign Prosthatic Hypertrophy (BPH):
↓ Smooth muscle tone
↓ Growth of smooth muscle cells
Marked interest in these compounds due to their hypolipidemic effects

33
Q

Adverse effects of prazosin?

A

First dose effect: marked postural hypotension and syncope can be seen 30 to 90 min after the initial dose
Important to check both supine and standing BP

34
Q

Newer well absorbed α1 antagonist with some subtype selectivity: α1A ≈ α1D > α1B
Useful in BPH due to favorable blockade of α1A receptors with little undesirable effect on BP
Side effect: abnormal ejaculation

A

Tamsulosin

35
Q

Selective α2 receptor antagonist that is structurally similar to reserpine
Readily enters the CNS: ↑ BP and ↑ heart rate
↑ motor activity and produces tremors
Historically: extensively used to treat male sexual dysfunction; efficacy by far surpassed by the development of PDE5 inhibitors

A

yohimbine

**no real clinical use

36
Q

What are beta blockers used for?

A

HTN
CHF
ischemic heart diseases
certain arrhythmias

37
Q

What is the prototype beta-blocker?

A

isoproterenol

38
Q

Recall the effects of Beta adrenergic stimulation

A

low tonic stimulation –> modest positive chronotropic and inotropic effects
more prominent effects during intense stimulation (stress and exercise)

39
Q

What effect does short-term administration of beta blockers have?

A

decreased cardiac output
decreased peripheral resistance

**effects increase in proportion to the potency of inhibition and compensatory reflex mechanisms

40
Q

What effect does long-term administration of beta-blockers have?

A

pulse rate returns to normal levels or decreases in HTN patients

can decrease pulse rate, while maintaining cardiac output

41
Q

What effects do beta blockers have on cardiac chronotropy and dromotropy?

A

↓ Automaticity in the SA and AV nodes, as well as in the Purkinje system by decreasing the slope of Phase 4 depolarization
↓ Conduction velocity in atria and the conduction system
↑ refractory period of the AV node

**basically decrease conduction velocity

42
Q

Beta blockers are also (blank), because they decrease cardiac contractility, O2 consumption of the heart, and incidence of supraventricular and ventricular deleterious arrhythmias

A

antiarrhythmic

**β blockers are considered Class II antiarrhythmic agents

43
Q

Some β blockers display (blank) activity that may contribute to their antiarrhythmic activity:

A

stabilizing

**Local anesthetic effects by blocking voltage-dependent Na+ channels (e.g. propranolol)

44
Q

How are beta blockers thought to work as antihypertensive agents?

A

↓ CO
↓ β1-mediated renin

  • *these are postulated mechanisms
  • *generally, no effect in normal patients

some beta blockers are vasodilators

↑ NO
Activation of β2 receptors
Block of α1 receptors
Block of Ca2+ channels in VSMCs
Stimulation of K+ channels in VSMCs
Antioxidant activity
45
Q

How are beta blockers thought to work as antianginal agents?

A

↓ Sympathetic influence on the heart → ↓ cardiac contractility → ↓ O2 consumption of the heart → improves the cardiac reserve for a better match between the metabolic demands of the heart and its ability to generate work in patients with Coronary Artery Diseases (CAD)
β blockers with vasodilating properties can reduce the incidence of vasospastic episodes in patients with CAD

46
Q

What effect can B2 blockers have on the pulmonary system?

A

can produce life threatening bronchoconstriction in COPD and asthma patients

47
Q

What are the metabolic effects of beta blockers? For this reason, beta blockers should be used with caution in what patient population?

A

blunt the responses of glucose mobilization during hypoglycemia and glycogenolysis in Type 1 DM
decrease insulin sensitivity
decrease lipid mobilization and release of FFA from adipose tissue

**should be used with caution in diabetics

48
Q

What role do beta blockers have on insulin sensitivity?

A

↓ by “Classical” β blockers

Worsen the glycemic index of normal as well as insulin-resistant patients

49
Q

What role do beta blockers have on lipid metabolism?

A

β blockers ↓ hormone-mediated lipase activation and ↓ release of free fatty acids from adipose tissue
Non-selective β blockers → ↓ HDL, ↑ LDL and ↑ Triglyceride levels whereas β1-selective antagonists produce the opposite

50
Q

What are the most common uses for beta blockers?

A 
Essential Hypertension
Angina Pectoris
Arrhythmias
Glaucoma
Post-MI Therapy
Congestive Heart Failure (all grades)
51
Q

In what patient populations are beta blockers contraindicated?

A

patients with COPD or asthma
patients with cardiac conduction disturbances
patients with hypoglycemia (can block B2 glycogenolysis effects)
rapid withdrawal can cause adverse effects (angina attacks)

52
Q

Side effects of beta blockers?

A 
Tiredness
Dizziness
Vivid Dreams
Insomnia
Hallucinations
Depression
53
Q

How are beta blockers administered?

A

orally
IV (in critical ER settings)
ophthalmic solutions (glaucoma)

54
Q

Many beta blockers display prominent 1st passage metabolism through the portal system. Why is this important to consider?

A

this may decrease their bioavailability

**ex: only 25% of propranolol reaches the systemic circulation even though its absorption is nearly complete

55
Q

If you OD on beta blockers, what can occur and what can be used to treat these conditions?

A

hypotension: isoproterenol (or an alpha agonist)
bradycardia: atropine, pacemaker
prolonged conduction times (increased PR interval)
widened QRS
seizures, depression

Block 9 Week 1 Meg (9 decks)

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