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Pharmacology COPY > EXAM #1: AUTONOMIC PHARMACOLOGY > Flashcards

EXAM #1: AUTONOMIC PHARMACOLOGY Flashcards

1
Q

What is a selective direct acting adrenergic agonist?

A
  • Direct acting= drug that directly agonizes an adrenergic receptor
  • Selective= the drug is specific for a single type of adrenergic receptor e.g.alpha-1
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2
Q

What is a non-selective directing acting adrenergic agonist?

A
  • Direct acting= drug that directly agonizes an adrenergic receptor
  • Non-selective= drug is NOT specific for a single type of adrenergic receptor and can act on MULTIPLE types of adrenergic receptors
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3
Q

How will reserpine or guanethidine affect administration of a direct acting adrenergic agonist? What about cocaine?

A
  • NO effect with reserpine or guanethidine

- Cocaine may potentiate the effects

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4
Q

What is a mix-acting adrenergic agonist?

A

Drugs that BOTH:

1) Increase the release of NE
2) Bind and activate adrenergic receptors

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5
Q

What drug is a mix-acting adrenergic agonist?

A

Ephedrine

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6
Q

How the the response of mixed-acting adrenergic agonists impacted by prior treatment by reserprine or guanethidine?

A

The response to the mixed agonist will be reduced compared to if it was given alone

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7
Q

What is an indirect acting adrenergic agonist? How will the response of an indirect-acting adrenergic agonist be impacted by prior treatment by reserprine or guanethidine?

A

Indirect agonist= drug that increases the AVAILABILITY of NE or Epi by a variety of methods

There will NOT be a response if there is pre-treatment with reserpine or guanethidine.

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8
Q

What are the three types of indirect-acting adrenergic agonists?

A

1) Releasing agents
2) Uptake inhibitors
3) MAO/COMT inhibitors

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9
Q

What class of drug is Phenylephrine?

A

Alpha-1 selective adrenergic receptor agonist

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10
Q

What are the clinical indications for Phenylephrine?

A
  • Hypotension
  • Rhinitis
  • Paroxysmal atrial tachycardia
  • As a Mydriatic
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11
Q

Why is Phenylephrine used for paroxysmal atrial tachycardia?

A

1) Causes an increase in mean BP

2) Reflex bradycardia will slow the atrial focus causing tachycardia

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12
Q

What are the alpha effects of Phenylephrine?

A

Activation of vascular smooth muscle increases BP and increase TPR

Note that there will be beta effects are high doses

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13
Q

List the alpha-2 selective adrenergic receptor agonists.

A

1) Clonidine
2) a-methyldopa
3) Apraclonidine
4) Brimonidine

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14
Q

What is the clinical indication for Clonidine and a-methyldopa?

A

Systemic hypertension

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15
Q

What is the clinical indication of apraclonidine and brimonidine?

A

Glaucoma

Note that despite being alpha-2 agonists, these drugs do NOT have a hypotensive effect

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16
Q

What is the mechanism of action of the alpha-2 selective adrenergic receptor agonists?

A

There are two mechanisms:

1) Activation of central alpha-2 receptors to decreases SNS outflow and blood pressure
2) Active alpha-2 receptors to decrease aqueous humor production and decrease intraocular pressure

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17
Q

What are the adverse effects of the alpha-2 selective adrenergic receptor agonists?

A
  • Dry mouth (xerostomia)
  • Sedation
  • Hypotension
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18
Q

List the Beta-2 selective adrenergic receptor agonists.

A

Metaproterenol
Terbutaline
Albuterol
Ritodrine

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19
Q

What is the therapeutic use of metaproterenol?

A

1) Long-term treatment of obstructive airway disease, asthma
2) Acute bronchospasm

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20
Q

What are the characteristics specific to metaproterenol?

A
  • Resistant to methylation by COMT

- B2 selective, but less than albuterol or terbutaline

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21
Q

What is the therapeutic use of Terbutaline?

A

1) Long-term treatment of obstructive airway disease
2) Acute bronchospasm
3) Emergency treatment of status asthmaticus (IV)

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22
Q

What are the characteristics specific to Terbutaline?

A
  • Beta-2 selective

- NOT a substrate for COMT methylation

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23
Q

What is the therapeutic use of Albuterol?

A

1) Acute bronchospasm

2) Delay pre-term labor

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24
Q

What is the therapeutic indication for Ritodrine?

A

Uterine relaxation to:

1) Arrest premature labor
2) Prolong pregnancy

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25
Q

What are the adverse effects of B2 receptor agonists?

A
  • Tachycardia
  • Increased plasma glucose, lactate, and FFA
  • Decreased plasma K+
  • Tremors, restlessness, and anxiety
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26
Q

What increases the risk of tachycardia with B2 selective agoists?

A
  • Pre-existing CAD or arrhythmia

- MAO inhibitor

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27
Q

What route of administration diminishes the risk of adverse effects of B-2 selective agonists?

A

Inhalation

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28
Q

What is the D1 selective receptor agonist?

A

Fendolopam

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29
Q

What is the clinical indication for Fendolopam?

A

Hypertensive crisis

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30
Q

What are the physiologic effects of Fendolopam?

A

Renal, mesenteric, periperal, and coronary vasodilation

Note that RBF is maintained and natriuresis is promoted

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31
Q

What is the side effect of Fendolopam?

A

Hypotension

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32
Q

List the non-selective adrenergic receptor agonists.

A 
Isoproterenol 
Dobutamine 
Epinephrine 
Norepinephrine 
Dopamine
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33
Q

What receptors does Isoproterenol primarily interact with?

A

Beta 1 and 2

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34
Q

What are the clinical indications for Isoproterenol?

A
  • Brady-arrhythmias
    1) Bradycardia
    2) Complete A-V block
  • Torsdes de pointes
  • CHF as a positive ionotrope
  • MI

Note that use during MI can lead to myocardial necrosis

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35
Q

What are the physiologic effects of Isoproterenol?

A
  • Increased HR
  • Increased myocardial contractility
  • Decreased TPR
  • Bronchodilation
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36
Q

What receptor does Dobutamine act on? What is the predominate receptor interaction at therapeutic doses?

A

Alpha-1
Beta-1
Beta-2

**Beta-1 is primary at therapeutic doses*

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37
Q

What are the clinical indications for Dobutamine?

A

1) Short-term treatment of cardiac failure

2) Stress test for CAD–drug induced

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38
Q

What are the cardiovascular effects of Dobutamine?

A
  • Positive ionotorpe
  • Positive chronotrope

Note that TPR is NOT affected*

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39
Q

What are the adverse effects of Dobutamine?

A
  • HTN and tachycardia
  • Increased ventricular response in a-fib
  • Ventricular ectopy
  • May increase size of MI
  • Tolerance develops
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40
Q

What is the effect of epinephrine at low IV doses? Specifically, what receptors are implicated, and what are the receptor specific effects?

A

B1=

  • Increased pulse pressure
  • Increased HR
  • Increased SV
  • Increased CO

B2= vasodilation–>decreased TPR

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41
Q

What is the effect of epinephrine at intermediate IV doses? Specifically, what receptors are implicated, and what are the receptor specific effects?

A

Same beta 1 and 2 effects, PLUS:

Alpha-1= increased TPR and increased BP

*****Note that at moderate doses, beta-2 effects are counter acted by alpha-1 stimulation.

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42
Q

What is the effect of epinephrine at high IV doses?

A
  • Mostly alpha-1 effects instead of beta i.e. increased TPR and BP
  • Potential REFLEX BRADYCARDIA
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43
Q

Why does epinephrine initially have strong beta effects and then alpha effects at higher doses?

A

Beta receptors have a higher affinity for epinephrine; thus, they are saturated first

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44
Q

What is the purpose of subcutaneous epinephrine?

A

Epi is often a component of local anesthetics; it is included to:

  • Cause vasoconstriction
  • Vasoconstriction limits diffusion of the anesthetic
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45
Q

What is the epinephrine reversal phenomenon?

A
  • Epinephrine activates both alpha and beta receptors
  • Pretreatment with an alpha or beta antagonist will potentiate the effects of epinephrine via the alternate receptor type
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46
Q

What is the outcome of the epinephrine reversal phenomenon with alpha receptor antagonism?

A

Beta effects are enhanced:

  • Vasodilation
  • Decreased TPR
  • Decreased MAP
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47
Q

What is the outcome of the epinephrine reversal phenomenon with beta receptor antagonism?

A

Alpha effects are enhanced:

  • Vasoconstriction that is “unmasked”
  • Dramatically increased MAP
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48
Q

What are the main sites of action of epinephrine in the vasculature?

A

Smaller arterioles and precapillary sphincters

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49
Q

What are the vascular effects of epinephrine?

A

Epinephrine causes the redistribution of blood flow

  • Cutaneous blood flow is reduced
  • Skeletal blood flow is increased
  • Coronary blood flow is increased
  • Little to no change in cerebral blood flow
  • RBF is decreased
  • GFR is unchanged
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50
Q

What happens to the filtration fraction with epinephrine administration? Why?

A

Increased

FF= GFR/RPF
GFR is unchanged but RPF decreases

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51
Q

What are the cardiac effects of epinephrine?

A

Epinephrine is a POWERFUL cardiac stimulant (B1)

  • Increased HR
  • Shortened systole (Diastole unchanged)
  • Positive ionotrope
  • Positive lusitropy
  • Positive chronotrope
  • Increased automaticity

The net effect is increased myocardial oxygen consumption

Note that increased automaticity can lead to arrhythmia

52
Q

What is lusitropy?

A

Relaxation of cardiac muscle; this is INCREASED by epinephrine i.e. despite B1 mediate ionotrope effects, the heart also relaxes more in disatole

53
Q

What are the smooth muscle effects of epinephrine?

A
  • Vascular smooth muscle most affected

- GI smooth muscle relaxation

54
Q

Which effect of Epi is MOST IMPORTANT in treating shock, vascular or cardiac?

A

Vascular

55
Q

What are the contraindications for epinephrine? Why?

A

Patient on nonselective B-blockers

  • This will cause epinephrine reversal phenomenon
  • Unmasked increase in BP can lead to hypertensive crisis
56
Q

What are the therapeutic uses of epinephrine?

A

1) Anaphylaxis/ hypersensitivity
2) Cardiac arrest
3) Part of local anesthetic cocktail
4) Post-extubation or viral croup
5) Severe respiratory distress from bronchospasm (asthma)

57
Q

What are the toxicities and adverse effects of epinephrine?

A
  • Restlessness, tremors, palpitations
  • Headache
  • Cerebral hemorrhage
  • Cardial arrhythmia
  • Angina in patients with CAD
58
Q

How does norepinephrine differ in receptor stimulation compared to epinephrine?

A
  • Potent alpha-1
  • Little B2
  • Same B1

Recall that epinephrine is not a potent alpha-1 agonist until it is given in high doses

59
Q

What are the cardiovascular effects of norepinephrine?

A
  • Increased systolic/diastolic BP and pulse pressure
  • Increased coronary blood flow
  • Unchanged or decreased CO
  • Increased TPR
  • Decreased RBF
  • Decreased splanchnic and hepatic blood flow
60
Q

What is the theraputic indication for NE?

A

Hypotension

61
Q

What are the effects of low dose DA administration? Draw the effects of low dose DA administration.

A
  • Activation of D1 receptors on RENAL BLOOD VESSELS causing VASODILATION
  • Activation of D1 receptors on TUBULAR CELLS causes decrease Na+ reabsorption
  • D2 in peripheral circulation= decreased NE release and vasodilation
62
Q

What is low dose DA used for clinically?

A

D1 effects:

  • Diuretic
  • Naturesis/ Na+ diuresis

*****Little cardiac activity at this dose

63
Q

What are the effects of moderate DA administration?

A

B1

  • Positive ionotrope
  • Positive chronotrope
  • Increased systolic blood pressure/ pulse pressure
  • No effect on diastolic blood pressure

Release of NE from nerve terminals (increases blood pressure)

64
Q

What are the effects of high DA administration?

A

A1

- Vasoconstriction and increased blood pressure

65
Q

What are the indications for DA?

A
  • CHF
  • Cardiogenic shock
  • Septic shock
  • Short-term enhancement of cardiac and renal function
66
Q

What are the precautions for DA administration?

A

1) Hypovolemia should be corrected before DA use
2) Tachycardia, angina, arrhythmia, headache and HTN
3) Extravasation may cause ischemic necrosis and sloughing
4) Avoid with MAOI or tricyclic antidepressants

67
Q

What is ephedrine?

A

Mixed-acting adrenoceptor agonist

68
Q

What is unique about ephedrine?

A
  • First orally active sympathomimetic

- Banned b/c of safety concerns

69
Q

What is the clinical use for PSEUDOephedrine?

A

Nasal decongestant

70
Q

What are the two indirect acting releasing agents?

A

Amphetamine

Tyramine

71
Q

What is amphetamine’s mechanism of action?

A
  • Transported into the nerve terminal by NET1
  • Taken up into pre-synaptic vesicles
  • Displaces NE from the vesicle
  • NE escapes via NET1

Exocytosis is NOT involved in the release of NE

72
Q

What are the effects of amphetamine on the CNS?

A
  • Mainly releases biogenic amines from storage sties in nerve terminals*
  • Stimulates medullary respiratory center
  • Stimulates cortex and reticular activating center
  • Decreases food intake
73
Q

What are the cardiovascular response to amphetamine?

A
  • Activates peripheral alpha and beta receptors
  • Increased blood pressure (systolic and diastolic)
  • Increased heart rate

Arrhythmias may occur as well*

74
Q

What are the clinical indications for amphetamines?

A

1) Narcolepsy
2) Obesity
3) Enuresis and incontinence; increases bladder sphincter contraction

Firecracker: ADHD

75
Q

What is Tyramine?

A

Natural monoamine derived from tyrosine

76
Q

What can Tyramine be used to synthesize?

A

NE and epinephrine

77
Q

What is the “cheese effect?”

A

Tyramine can cause a sudden and dangerous increase in BP in the presence of MAO inhibition
- Fermented cheese is rich in tyramine

Ingestion of cheese/ tyramine and blood pressure change is called the cheese effect.

78
Q

What determines the duration of effects via reversible vs. irreversible alpha receptor antagnoists?

A

Reversible= half-life

Irreversible= production of new receptors

79
Q

What are the general effects of alpha receptor antagonists?

A

1) Decreased blood pressure and orthostatic hypotension
2) Tachycardia (reflexive)
3) Reverse pressor effects of alpha and beta agonists
4) Miosis (radial m.)
5) Nasal stuffiness
6) Decreased resistance to urine flow

80
Q

What are the indications for alpha receptor antagonists?

A

1) Pheochromocytoma
2) HTN emergency
3) Chronic HTN
4) PVD
5) Urinary obstruction
6) ED

The alpha receptor antagonist will dilate the ureteral sphincter.

81
Q

What is the mechanism of Phenoxybenzamine?

A
  • Irreversible alpha-1 and alpha-2 blocker

- Indirect baroreflex activation

82
Q

What are the effects of Phenoxybenzamine?

A
  • Lowers blood pressure

- Increases HR due to baroreflex activation

83
Q

What are the indications for Phenoxybenzamine?

A

1) Pheochromocytoma

2) High catecholamine states

84
Q

What is the mechanism of action for Prazosin, Doxazosin, and Terazosin?

A
  • Specific alpha-1 blockade

- Do NOT block alpha-2

85
Q

What are the physiologic effect of Prazosin, Doxazosin, and Terazosin?

A

Lower BP

86
Q

What are the therapeutic uses of Prazosin, Doxazosin, and Terazosin?

A

1) HTN

2) BPH

87
Q

What is the adverse effect associated with Prazosin, Doxazosin, and Terazosin?

A

Large depressor effect with first dose may cause orthostatic hypotension

88
Q

What is Tamsulosin’s mechanism of action? What is the brand name?

A

Highly selective alpha-1a receptor antagonist

Note that this is also called “Flomax”

89
Q

What are the physiologic effects of Tamsulosin?

A

Selective alpha-1a blockade relaxes prostatic smooth muscle more than vascular

90
Q

What is the clinical indication for Tamsulosin?

A

BPH

91
Q

What is an adverse effect associated with Tamsulosin?

A

Orthostatic hypotension, though less common b/c of alpha-1a specificity

92
Q

What is Yhoimbine’s mechanism of action?

A

Blocks alpha-2 receptors, which:

  • Increases central SNS activity
  • Increases NE release
93
Q

What are the physiologic effects of Yhoimbine?

A
  • Raise blood pressure
  • Raise HR

Note that these effects are NOT why this drug is used clinically.

94
Q

What are the clinical indications for Yhoimbine?

A

ED

95
Q

What are the adverse effects associated with Yhoimbine?

A
  • Anxiety

- Excess pressor effect if NET1 is blocked

96
Q

What is Labetalol’s mechanism of action?

A
  • Inhibits BOTH alpha and beta receptors

This is useful for high SNS states

97
Q

What are the physiologic effects of Labetalol administration?

A

Lowers BP with limited increase in HR

98
Q

What are the clinical indications for Labetalol?

A

HTN

99
Q

Why is Labetalol a preferred anti-hypertensive?

A

Less tachycardia, which can be v. good to prevent myocardial ischemia

100
Q

What is a first generation beta blocker? What is the prototypical compound?

A

Non-selective beta receptor antagonist

- E.g. propranolol

101
Q

What is a second generation beta blocker?

A

Relative selective beta-1 receptor antagonist

**Note that this is only at low doses; high doses will activate beta-2 receptor*

102
Q

What are the third generation beta-blockers?

A

Vasodilatory

103
Q

What is the receptor specificity for the 3rd generation beta blockers?

A

B1= B2>a1>a2

104
Q

List the first generation beta blockers.

A

Propranolol
Nadolol
Timolol
Pindolol

105
Q

List the second generation beta blockers.

A 
Atenolol 
Metoprolol 
Esmolol 
Beliprolol 
Acebutolol
106
Q

List the 3rd generation beta blockers.

A

Labetalol

Carvedilol

107
Q

What are the cardiovascular effects of beta receptor antagonists?

A
  • Negative ionotrope
  • Negative chronotope
  • Decrease BP in patients with HTN (not normotensive individuals)
  • Decrease myocardial oxygen consumption
  • Decrease renin release

Great for patients with ischemic heart disease coming from HTN

108
Q

What are the respiratory effects of beta receptor antagonists?

A

B2= bronchoconstriction and increased airway resistance

109
Q

What are the ocular effects of beta receptor antagonists?

A
  • Decreased aqueous humor production

- Decreased intraocular pressure

110
Q

What are the metabolic effects of beta receptor antagonists?

A
  • Lipolysis inhibition
  • Decreased glucagon release
  • Increased VLDL
  • Decreased HDL
111
Q

List the therapeutic indications for beta blockers.

A

1) HTN
2) CAD
3) Arrhythmia
4) Heart failure
5) Glaucoma
6) Hyperthyroidism
7) Neurologic disease (anxiety)

112
Q

What are the important properties to consider when selecting a beta blocker?

A
  • Cardioselectivity–asthma, COPD, chronic lung disease
  • Intrinsic Sympathomimetic Activity (ISA)
  • Lipid solubility
113
Q

What are the adverse effects of beta blockers?

A
  • Worsened bronchospasm
  • Worsened PVD (B2= vasoconstriction in microvasculature)
  • Fatigue
  • Decreased sexual function
  • Increased incidence of DM
  • Masking hypoglycemic symptoms
114
Q

In regards to “cardioselectivity,” what type of beta-blocker is preferred for HTN, CAD, and CHF?

A

Beta-1 specific

115
Q

What is Intrinsic Sympathomimetic Activity?

A

Drugs that agonize beta receptors but simultaneously block the greater effects of endogenous catecholamine agonism

116
Q

Why is ISA desirable in a beta blocker?

A

Less potential for bradycardia

117
Q

What is the desired feature of a beta-blocker in regards to lipid solubility? Why?

A

NOT lipid soluble i.e. hydrophillic b/c:

1) Higher plasma concentrations
2) Longer biological action
3) Greater predictability
4) Less CNS effects

118
Q

What are the four factors related to lipid solubility that need to be considered prescribing a beta blocker?

A

1) Plasma levels/ duration of action
2) CNS
3) Kidney
4) Age/ liver

119
Q

What two drugs have ISA? What class are they?

A 
Pindolol= 1st gen
Acebutolol= 2nd gen.
120
Q

What should you do in a HTN patient with asthma that is not responding to selective beta-blockade with Metoprolol?

A
  • Add another selective beta blocker

- DON’T increase dose

121
Q

Why are beta blockers given in CHF? Aren’t beta-blockers going to further decrease CO?

A

Despite being a negative ionotrope, beta blockers are given b/c there is an increase in circulating catecholamines to compensate for poor CO. Beta-1 receptors are over-activated chronically and downregulate. Low does Beta-1 “protects” receptors from overactivation without diminishing contractility.

122
Q

What is the mnemonic to remember the cardio-selective beta-blockers?

A

AMEBA

Atenolol
Metoprolol
Esmolol 
Beliprolol 
Acebutolol
123
Q

What type of beta blockers are affected by kidney and liver function?

A

Lipophillic

124
Q

How do beta-blockers mask the symptoms hypoglycemia?

A

1) DM patient develops hypoglycemia
2) Physical signs of hypoglycemia include:
- Increased HR
- Palpitations
- Agitation
3) Without these symptoms, patient does NOT know that they are beginning to become hypoglycemic

125
Q

What symptoms of hypoglycemia is NOT masked by beta-blockers that patient can be weary of?

A

Sweating–tell patients to be aware of this!

Pharmacology COPY (64 decks)

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