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Pharmacology Exam 1 > Autonomic Pharmacology > Flashcards

Autonomic Pharmacology Flashcards

1
Q

What drugs are part of the Direct-Acting Cholinoceptor Agonists: Choline Esters class?

A

Acetylcholine

Methacholine

Carbachol

Bethanechol

Mnemonic: Ace Met Beth in his Car and Ester on a date

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2
Q

Characteristics of Choline Esters

A

All have cationic quaternary ammonium –> makes them insoluble in lipids

(Poor GI absorption/Poor CNS distribution)

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3
Q

Which two Choline Esters are insusceptible to Cholinesterase?

A

Carbachol

Bethanechol

Mnemonic: Beth avoids AchE in her Car

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4
Q

What is the action of Choline Esters similar to?

A

M2 or M3 Activation

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5
Q

Acetylcholine

  1. Class
  2. Muscarinic Effects
  3. Nicotinic Effects
A

Class: ***Prototype*** Choline Ester (Direct-Acting Cholinoceptor Agonist)

Muscarinic:

Cardiovascular-

Low Doses: Vasodilation –> reflex tachycardia

High Doses (M2 Effects): Bradycardia ; Decreased A-V conduction; (-) Inotropy

Bronchial constriction, increased bronchial secretion

Salivary excretion, tears, sweat

Urinary bladder contraction

Eye short-lasting miosis

Nicotinic: NOT COMMONLY SEEN, since Ach does not penetrate the fat surrounding skeletal muscle and autonomic ganglia

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6
Q

Acetylcholine

  1. Clinical Uses (2)
A

Use:

Eye Surgery (short-lasting MIOSIS)

PROVOCATION TEST in Coronary Angiography (Dx: Coronary Vasospasm)

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7
Q

Methacholine (Provocholine)

  1. Class/About
  2. Clinical Uses
A

Class: Choline Ester (Direct-Acting Cholinoceptor Agonist)

Similar to Ach in action, but has longer half life

Use:

  1. Methacholine Challenge (inhaled) –> Bronchiolar Hypersensitivity (excessive BronchoCONSTRICTION)
  2. Belladonna alkaloid poisoning (SubQ) –> Dose would NOT elicit normal MUSCARINIC effects in someone with this
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8
Q

Carbachol

  1. Class
  2. Effects
  3. Clinical Uses
A

Class: Choline Ester (Direct-Acting Cholinoceptor Agonist)

Effects:

Therapeutic Doses: Activate both NICOTINIC and MUSCARINIC cholinoceptors (Nicotinic effects - Autonomic Ganglia, Adrenal Medulla, Skeletal muscle)

High Doses: Muscarinic effects - May include CARDIAC ARREST

Use:

Glaucoma (contracts Ciliary muscle, enlarges canal of Schlemm, increases drainage of Aq. Hum., Decreases Intraocular Pressure)

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9
Q

Bethanechol (Urecholine)

  1. Class
  2. Effects
  3. Clinical Uses
A

Class: Quaternary Choline Ester (Direct-Acting Cholinoceptor Agonist)

Effects: Acts Predominantly on M3 (NO nicotinic effects)

Genitourinary: increased detrusor tone, decreases outlet resistance of internal sphincter

Gastrointestinal: increased motility and secretion

Weak effects on M2 - minimal cardiac effects

Clinical Uses:

Gastric Atony after vagotomy to reduce reflux (INCREASES lower esophageal sphincter tone)

Gastric Emptying Abnormalities

Urinary RETENTION (in the ABSENCE of obstruction)

Mnemonic: Beth think Bladder

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10
Q

What drugs are part of the Direct-Acting Cholinoceptor Agonists: Muscarinic Alkaloids class?

A

Muscarine

Pilocarpaine

Mnemonic: Al has a Pile of Muscles

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11
Q

Muscarine

  1. Class
  2. Properties
A

Class: Muscarinic Alkaloid (Direct-Acting Cholinoceptor Agonist) Quaternary Ammonium Compound

Properties: No Nicotinic Activity; 100x more potent than Ach and has a longer duration of action than Ach, as it is not broken down by AchE because it is not a choline ester)

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12
Q

Muscarine Poisoning

  1. Cause
  2. Symptoms
A

Cause: Mushrooms (e.g. Amanita Muscaria)

Sx: A very WET PICTURE

  • Salivation, sweat, tear flow
  • Abdominal pain, nausea, diarrhea, blurred vision, dyspnea
  • Severe Cases: cardiac/respiratory failure and Death

***Symptoms normally subside within 2 hours***

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13
Q

Pilocarpine (Isopto Carpine, Salagen)

  1. Class
  2. Effects
  3. Clinical Use
A

Class: Muscarinic Alkaloid (Direct-Acting Cholinoceptor Agonist) Tertiary Amine

Effects: Produces Ophthalmic (M3) Effects similar to Ach (applied Topically)

Contracts iris sphincter muscles –> Miosis

Frees entrance to Canal of Schlemm –> Narrow-angle Glaucoma

Enhances tone of trabecular network –> Wide-angle Glaucoma

Contracts the ciliary muscle (Lens becomes more spherical) –> Accomodation__/LOSS of FAR vision

Uses:

GLAUCOMA (***Drug of choice***), Xerostomia (dry mouth - given orally), tests the AUTONOMIC STATE (similar to Methacholine Challenge)

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14
Q

What drugs are part of the Direct-Acting Cholinoceptor Agonists: Nicotinic Alkaloids class?

A

Nicotine

Succinylcholine

Mnemonic: Nicotine Succs

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15
Q

Nicotine

  1. Class
  2. Action on NM
A

Class: ***Prototype***Nicotinic Alkaloid (Direct-Acting Cholinoceptor Agonist)

NM Action:

Skeletal Muscle Contraction

Fasciculations, spasm

Depolarizing Blockade –> Paralysis (Similar to Succinylcholine under neuromuscular blocking drugs)

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16
Q

Nicotine

  1. Action on NN
A

NN Action: Stimulate both sympathetic and parasympathetic post-ganglion neurons

Cardiac: increased heart rate (sympathetic > parasymp)

Vascular: mostly sympathetic innervation –> peripheral vasoconstriction

GI: increased gut motility/secretion

Carotid Bodies: increased respiratory rate

Medullary Emetic Chemoreceptors: nausea and vomiting

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17
Q

Nicotine

  1. Clinical Indications
A

Smoking cessation

-Stimulates the hypothalamus to secrete more cortisol

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18
Q

What are some Contraindications (3) and Drug Interactions (3) to consider when administering Direct-Acting Cholinoceptor Agonists?

A

Contraindications:

Peptic Ulcers (Increased Gastric Acid secretion)

GI Tract Disorders

Asthma (Bronchoconstriction)

Drug Interactions: Drugs having antimuscarinic properties can block the effects of muscarinic agonists

(e.g. Quinidine (antiarrhythmics), Procainamide (antiarrhythmics), Tricyclic Antidepressants

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19
Q

What drugs are part of the Indirect-Acting Cholinesterase Inhibitors/Cholinomimetics: Reversible class?

A

Edrophonium

Neostigmine

Physostigmine

Donepezil

Tacrine

Mnemonic: Ed and Don Physically Tackled Neo

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20
Q

Edrophonium

  1. Class
  2. Characteristics
  3. Clinical Uses
A

Class: Indirect-Acting Cholinesterase Inhibitors/Cholinomimetic: Reversible

Characteristics: Short-acting

Uses: Diagnosis of MYASTHENIA GRAVIS (MG) ; If Edrophonium IMPROVES the symptoms, then it confirms diagnosis of MG vs. Cholinergic crisis, neurasthenic/infectious/endocrine/congenital/neoplastic/degenerative neuromuscular disorders

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21
Q

Neostigmine, Pyridostigmine

  1. Class
  2. Characteristics
  3. Clinical Uses
A

Class: Indirect-Acting Cholinesterase Inhibitors/Cholinomimetic: Reversible

Chracteristics: Quaternary amines (NO CNS ENTRY), Intermediate Acting

Uses: Ileus (Abdominal Distension), Urinary Retention (Non-obstructive), Myasthenia, Reversal of non-depolarizing NM Blockers

Mnemonic: Neostigmine has Neo (No) CNS action

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22
Q

Physostigmine

  1. Class
  2. Characteristics
  3. Clinical Uses
A

Class: Indirect-Acting Cholinesterase Inhibitors/Cholinomimetics: Reversible

Characteristics: Tertiary Amine (ENTERS CNS), Intermediate Acting

Uses: Glaucoma (2nd line due to blocked accomodation and causation of myopia); antidote to Atropine Overdose

Mnemonic: Physostigmine physically enters the CNS

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23
Q

Donepezil, Tacrine

  1. Class
  2. Characteristics
  3. Clinical Uses
A

Class: Indirect-Acting Cholinesterase Inhibitors/Cholinomimetics: Reversible

Characteristics: Lipid-soluble (ENTERS CNS)

Use: Treats Alzheimer Disease (increases cholinergic neurotransmitters in the CNS)

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24
Q

Organophosphates

  1. Class
  2. Characteristics
  3. Clinical Uses
A

Class: Indirect-Acting Cholinesterase Inhibitors/Cholinomimetics: IRr__eversible

Characteristics: Lipid-soluble (CNS ENTRY), Long-acting IRREVERSIBLE inhibitors of AchE

Uses: Glaucoma (echothiophosphate), Insecticides (malathion, parathion), Nerve Gas (sarin)

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25
Q

Symptoms of AchE Inhibitor/Cholinomimetic Toxicity

A

D - Diarrhea

U - Uncontrolled urination (contraction of detrusor)

M - Miosis (constriction of sphincter)

B - Bronchiolar constriction

B - Bradycardia (decreased contractility)

E - Excitement, convulsion, coma

L - Lacrimation (tears)

S - Sweating

S - Salivation

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26
Q

How is AchE Inhibitor/Cholinomimetic Toxicity managed clinically?

A

Symptomatic

Airway control/oxygen delivery

Cardiovascular support

Antidote: Atropine (muscarinic receptor antagonist)

-Relieves tracheobronchial/salivary secretion, bronchoconstriction, bradycardia, peripheral ganglionic and central actions of anti-AchE

Regeration of AchE: Praladoxim (2-PAM)

  • Reverses phosphorylation of AchE (by AchE inhibitors)
  • Does not work for neostigmine, physostigmine, or rapidly-aged phosphorylated AchEs
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27
Q

What drugs are part of the Cholinoceptor-Blocking Drugs: Muscarinic Receptor Antagonist (Antimuscarinic) class?

A

Atropine

Ipratropium

Benztropine

Mnemonic: Ipray for a Benz and Atrophy

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28
Q

Atropine

  1. Class
  2. Characteristics
A

Class: ***Prototype*** Muscarinic Receptor Antagonists (Antimuscarinic)

Characteristics: Tertiary Amine (ENTERS CNS), Competes with Ach & M at receptors ; DOES NOT DISTINGUISH between M1, M2, M3 receptors

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29
Q

Atropine

  1. Pharacologic Effects (in order of increasing dose)
A

Decreased secretions (salivary, bronchiolar, sweat)

Mydriasis and Cycloplegia

Hyperthermia

Tachycardia

Sedation

Urinary retention and constipation

Behavioral excitation and hallucinations

***Note: completely counteracts vasodilation caused by choline esters

DOES NOT affect blood pressure when given ALONE

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30
Q

Atropine

  1. Clinical Uses
A

Uses:

Antispasmodic (relaxes)

Antisecretory (dries)

Management of AchE inhibitor overdose

Antidiarrheal (dries)

Ophthalmology

Prevents vagal reaction (pericardiocentesis) by increasing heart rate

Treatment of acute intoxication: Symptomatic, Physostigmine

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31
Q

Ipratropium (Atrovent)

  1. Class
  2. Characteristics
  3. Clinical Uses
A

Class: Non-selective Muscarinic Receptor Antagonist (Antimuscarinic)

Characteristics: Mainly acts on M3 in Bronchial smooth muscle/glands when inhaled ; Quaternary amine (NO CNS ENTRY)

  • Decreases bronchoconstriction
  • Decreases bronchial constriction

Uses: ***1ST LINE THERAPY*** for COPD ; also used for asthma (2nd line therapy)

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32
Q

Benztropine (Cogentin)

  1. Class
  2. Characteristics
  3. Clinical Uses
A

Class: Muscarinic Receptor Antagonists (Antimuscarinic)

Characteristics: Tertiary Amine (CNS ENTRY) ; Acts on Muscarinic receptors in the BRAIN and PARASYMPATHETIC EFFECTOR SITES

  • Re-establishes Dopaminergic-Cholinergic Balance** in patients with **Parkinson’s Disease (PD: decreased dopaminergic –> cholinergic goes unchecked)
  • Decreases GI/GU secretions (Dries) and motility
  • Increases heart rate

Uses: Parkinson’s Disease (2nd or 3rd line therapy to antipsychotic)

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33
Q

What drugs are part of the Cholinoceptor-Blocking Drugs: Nicotinic Receptor Antagonists (NN & NM)/GANGLION BLOCKING AGENTS class?

A

Hexamethonium

Mecamylamine

Mnemonic: Mecca Hex

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34
Q

Hexamethonium and Mecamylamine

  1. Class
  2. Characteristics
  3. Clinical Uses
A

Class: ***GANGLION BLOCKING AGENTS*** Nicotinic Receptor Antagonists (Antinicotinic NN & NM)

Characteristics: Reduce predominant autonimic tone

-Prevent baroreceptor reflex changes in Heart Rate

***Most are no longer available due to TOXICITIES***

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35
Q

What are the effects of Ganglion Blocking Agents on Arterioles, Veins, Heart, Iris, Ciliary Muscle, GI Tract, Bladder, Salivary Glands, Sweat Glands?

A

Arterioles (SANS) –> Vasodilation, hypotension

Veins (SANS) –> Dilation, decreased venous return, decreased CO

Heart (PANS) –> Tachycardia

Iris (PANS) –> Mydriasis

Ciliary Muscle (PANS) –> Cycloplegia (paralysis –> loss of accomodation)

GI Tract (PANS) –> Decreased tone/motility - constipation

Bladder (PANS) –> Urinary retention

Salivary Glands (PANS) –> Xerostomia

Sweat Glands (SANS) –> Anhidrosis

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36
Q

What drugs are in the Cholinoceptor-Blocking: Neuromuscular Blocking Drugs (Antinicotinic NM) class?

A

D-tubocurarine (Non-depolarizing)

Succinylcholine (Depolarizing)

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37
Q

What are some important properties of Neuromuscular Blocking Drugs? Clinical Uses?

A
  • They all structurally resemble Ach
  • Interfere with transmission at the neuromuscular endplate
  • Interefere by preventing channel opening** (Non-depolarizing) or channel **closing (Depolarizing)
  • Highly ionized, Quaternary Amines (NO CNS ENTRY)

Clinical Uses: Facilitation of Tracheal Intubation ; optimize surgical conditions while ensuring adequate ventilation

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38
Q

D-Tubocurarine

  1. Class
  2. Mechniasm of Action
A

Class: Non-Depolarizing Neuromuscular (NM) Blocking Drug

MoA:

Small Doses: Prevent opening of Na+ channel by binding to receptor and competing with Ach

Large Doses: enter channel pores

-Block pre-junctional Na+ channels –> Decreased Ach release

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39
Q

Succinylcholine (Anectine)

  1. Class
  2. Mechanism of Action
A

Class: Depolarizing Neuromuscular (NM) Blocking Drug

MoA:

Phase 1 Blockade: Binding to NM receptors –> persistant depolarization –> paralysis

-Augmented by AchE inhibitors

Phase 2 Blockade: End plate is finally repolarized, however, is DESENSITIZED and will not depolarize easily again

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40
Q

What are some clinical uses of Neuromuscular Blockers (i.e. D-tubocurarine and Succinylcholine)?

A
  1. Decrease neuromuscular transmission during anesthsia
    - Larger muscles are more resistant than smaller muscles
    - Diaphragm responds last (recovery is in reverse order)
  2. Tracheal Intubation
  3. Control of Ventilation
  4. Treatment of Convulsions
    - Decreased manifestations of seizures
    - No effect on central processes that occur during convulsion
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41
Q

What are some side effects of Neuromuscular Blockers?

A
  1. Cardiovascular: Hypotension (Histamine release due to Tubocurarine) –> prevented with ANTIHISTAMINES
    - High doses –> Ganglion blockade –> severe HYPOtension
  2. Hyperkalemia (response to Succinylcholine from patients with burns, nerve damage, or neuromuscular disease)
  3. Increased Intraocular Pressure (due to Succinylcholine ; only contraindicated if anterior chamber is OPEN due to trauma)
  4. Increased Gastric Pressure (can cause aspiration/regurgitation in heavily-muscled patients)
  5. Muscle Pain (heavily-muscled and largely-dosed patients)
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42
Q

What drugs are part of the Selective Direct Acting Adrenergic Agonist class?

A

Phenylephrine (a1)

Clonidine (a2)

Terbutaline (B2)

Fenoldopam (D1)

Mnemonic: You can Find Old Pam playing the Pine TPC

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43
Q

Phenylephrine (Neo-Synephrine)

  1. Class
  2. Mechanism of Action
  3. Clinical Uses
A

Class: alpha 1 - Selective Adrenergic Receptor Agonist

MoA:

  • Activate alpha adrenergic receptors on vascular smooth muscle –> increased blood pressure and increased TPR
  • Activate Beta receptors only at HIGH concentrations

Use:

  • Antihypotensive
  • Paroxysmal Atrial Tachycardia
  • Nasal Decongestant
  • Mydriatic
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44
Q

Clonidine (Catapres)

  1. Class
  2. Mechanism of Action
  3. Clinical Uses
A

Class: alpha 2 - Selective Adrenergic Receptor Agonist

MoA: Activate Central alpha 2 receptors –> Decreased Central sympathetic outflow –> Decreased Blood Pressure

Uses: Systemic Hypertension

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45
Q

a-methyldopa (Aldomet)

  1. Class
  2. Mechanism of Action
  3. Clinical Uses
A

Class: alpha 2 - Selective Adrenergic Receptor Agonist

MoA: Activate Central alpha 2 receptors –> Decreased Central sympathetic outflow –> Decreased Blood Pressure

Uses: Systemic Hypertension

46
Q

Apraclonidine (Lodipine)

  1. Class
  2. Mechanism of Action
  3. Clinical Uses
A

Class: alpha 2 - Selective Adrengergic Receptor Agonist

MoA: Decreased aqueous humor production –> Decreased Intraocular pressure

Use: GLAUCOMA

47
Q

Brimonidine (Alphagan)

  1. Class
  2. Mechanism of Action
  3. Clinical Uses
A

Class: alpha 2 - Selective Adrengergic Receptor Agonist

MoA: Decreased aqueous humor production –> Decreased Intraocular pressure

Use: GLAUCOMA

48
Q

What are some adverse effects of alpha 2 - Selective Adrenergic Receptor Agonists?

A

Dry Mouth

Sedation

Hypotension

49
Q

Metaproterenol (Metaprel)

  1. Class
  2. Mechanism of Action
  3. Clinical Uses
A

Class: Beta 2 - Selective Adrenergic Receptor Agonists

MoA:

***Resistant to methylation by COMT***

-Beta 2-Selective (LESS selective than Albuterol or Terbutaline)

Uses: Long-term treatment of obstructive airway diseases - ASTHMA** ; treats **Acute Bronchospasm

50
Q

Terbutaline (Bricanyl)

  1. Class
  2. Mechanism of Action
  3. Clinical Uses
A

Class: Beta 2 - Selective Adrenergic Receptor Agonists

MoA: ***NOT a substrate for COMT methylation***

-Beta 2-Selective

Uses:

  • Long-term treatment of obstructive airway diseases
  • Acute Bronchospasm
  • Emergency treatment of Status Asthmaticus (IV use)
51
Q

Albuterol (Ventolin, Salbutamol)

  1. Class
  2. Mechanism of Action
  3. Clinical Uses
A

Class: Beta 2 - Selective Adrenergic Recptor Agonist

MoA:

  • Beta 2 - Selective (Same as Terbutaline)
  • Treats Acute Bronchospasm

Uses:

(Same as Terbutaline)

-Delays PRETERM LABOR

52
Q

Ritodrine (Yutopar)

  1. Class
  2. Mechanism of Action
  3. Clinical Uses
A

Class: Beta 2 - Selective Adrenergic Receptor Agonist

MoA:

-Beta 2 - Selective Agonist

Uses:

  • Designed specificall for use as a _***UTERINE RELAXANT***_
  • Arrests Premature Labor
  • Prolongs Pregnancy
53
Q

What are some adverse effects of Beta 2 - Selective Adrenergic Receptor Agonists?

A

Caused by a result of excessive activation of Beta receptors

  1. Tachycardia (especially those with CAD or arrhythmia)
    - Risk for adverse CV events INCREASED with use of MAO inhibitors, as they allow buildup of Beta 2 agonists in plasma ; wait 2 weeks between MAO use and Beta 2 administration)
  2. Increased glucose, lactate, and free fatty acids
  3. Decreased plasma K+ (potassium) (especially in patients with cardiac disease –> taking Digoxin and diuretics)
54
Q

How can Beta 2 - Selective Adrenergic Receptor Agonist adverse effects be reduced?

A

By using INHALATION THERAPY rather than parenteral or oral

55
Q

Fenoldopam (Corlopam)

  1. Class
  2. Mechanism of Action
  3. Clinical Uses
  4. Side Effects
A

Class: D1 - Selective Adrenergic Receptor Agonist

MoA:

  • Mainl a D1 Receptor Agonist
  • Some stimulation of alpha 2 (a2) adrenoceptors –> feedback inhibition of Norepinephrine release
  • Leads to renal, peripheral, and coronary vasoDILATION

Use:

_***HYPERTENSIVE CRISIS***_ (Given IV)

Side Effect: Hypotension

56
Q

What drugs are in the Non-Selective Direct Acting Adrenergic Agonist class?

A

Isoproterenol (B1 B2)

Dobutamine (B1 a1 B2)

Epinephrine (B1 B2 a1)

Norepinephrine (a1 B1)

Dopamine (D1 D2 a)

57
Q

Isoproterenol (Isuprel)

  1. Class
  2. Effects
  3. Clinical Uses
A

Class: B1 B2 Agonists

***No effect on alpha (a) receptors***

Effects:

-Cardiovascular: Decreased TPR, Increased Heart Rate (arrhythmias), Increased Myocardial Contractility

-Bronchodilation (STRONG)

Uses:

  • Bradycardia (Treated via Reflex Tachycardia from B1 receptors)
  • A-V block

-TORSADES de POINTES (Ventricular Fib)

-Pacemaker Placement

58
Q

Dobutamine (Dobutrex)

  1. Class
  2. Effects
A

Class: B1, a1, B2 Receptor Agonist

***Mainly acts on Beta 1 (B1) at Therapeutic Doses (considered Selective)

-Directly interacts with a and B receptors; DOES NOT release NE from sympathetic nerve endings

Effects:

Cardiovascular: Positive inotropic effect on heart ( >Isoproterenol)

  • Positive Chronotropic effect (Increased SA node automaticity and A-V conduction)
  • TPR is NOT AFFECTED (Due to a1-B2 Balance)
59
Q

Dobutamine (Dobutrex)

  1. Adverse Effects
  2. Clinical Uses
A

AE:

  • Excessive increases in blood pressure and heart rate
  • Increased ventricular response rate in patients with A-Fib
  • Ventricular ectopic activity
  • May increase the size of Myocardial Infarct
  • Tolerance

Uses:

  • Short-term treatment of Cardiac Failure (post cardiac surgery, CHF, MI) –> ***Increases Contraction WITHOUT increasing the Heart Rate
  • Longer-term efficacy is uncertain
  • Stress Tests (pts with CAD)
60
Q

Epinephrine (Adrenaline)

  1. Class
  2. Effects
  3. Clinical Uses
A

Class: a and B receptor Agonist

***Beta (B) has higher affinity** for **Epinephrine so B goes First dosewise

Effects (IV):

-Small Doses: B1 –> Increased Pulse Pressure, Heart Rate, Stroke Volume, and Cardiac Output

B2 –> Decreased Total Peripheral Resistance

-Moderate Doses: B1 –> (Same as above)

B2 –> (Same as above) + Decreased Diastolic Blood Pressure

a1 –> Increased TPR and Blood Pressure ***Counteracts B2***

-High Doses: a1, B1, and B2 are all same as above, except that alpha 1 (a1) predominates** which –> **REFLEX BRADYCARDIA (Potentially)

Uses: Subcutaneously causes slow absorption, vasoCONSTRICTION for SUTURING

61
Q

What is the Epinephrine Reversal Phenomenon and How does it work?

A

If you block a or B receptors prior to administration of Epinephrine, the response will be much more pronounced

a receptor antagonism (e.g. Phentolamine) –> Increased vasoDILATION –> Decreased TPR –> Decreased Mean Arterial Pressure

***Opposite with B receptor antagonism

62
Q

What are the Vascular Effects of Epinephrine** and where are the **main sites of action?

A

Main Sites of Action: Smaller ARTERIOLES and Precapillary SPHINCTERS

Leads to a General redistribution of blood flow

  • Cutaneous Flow Decreases
  • Skeletal Muscle Flow Increases
  • Cerebral Circulation shows little or no vasoconstriction (@ thereapeutic doses)
  • Renal Blood Flow Decreases, GFR <->, Filtration Fraction Increases, Renin Secretion Increases (Beta 1 (B1))
  • Pulmonary Blood Flow: both PAP and PVP Increase
  • Coronary Blood Flow Increases (Increased relative diastole, aortic pressure, and metabolic stimulation)
63
Q

What are the Cardiac Effects of Epinephrine?

A

Powerful Cardiac Stimulant: B1

  • Increased Heart Rate, Shortened Systole, Diastole <->
  • Increased Inotropy (Contraction), Lusitropy (Relaxation; active process),and chronotropy (Heart Rate) –> Increased Myocardial Oxygen Consumption
  • Increased Automaticity –> Arrhythmias (potentially)
  • ECG Changes
64
Q

What are the Smooth Muscle effects of Epinephrine?

A

***Vascular smooth muscle is most affected

-Most important during Cardiac Arrest

GI Smooth Muscle: Relaxation

65
Q

What are the Toxic/Adverse Effects of Epinephrine? Contraindications?

A

AE:

  • Throbbing headache, tremor, palpitations
  • Cerebral Hemorrhage (LARGE doses, rapid IV)
  • Arrhythmias
  • Angina (in pts with CAD)

***Contraindications: Patients using NON-SELECTIVE BETA BLOCKERS***

66
Q

What are the Therapeutic Uses of Epinephrine?

A
  • Hypersensitivity Reactions (including Anaphylaxis)
  • Cardiac Arrest
  • Local Anesthetics
  • Post-extubation croup, viral croup (Dilates Bronchiole Smooth Muscle)
67
Q

Norepinephrine

  1. Class
  2. Properties
A

Class: a1 >> B1 >>>>>> B2 Receptor Agonist

***Potent alpha (a) agonist ( <epinephrine><u>LITTLE ACTION</u> on <strong>B2 receptors</strong></epinephrine>

68
Q

Norepinephrine

  1. Cardiovascular Effects
A
  • Increase Systolic and Diastolic Blood Pressure, as well as Pulse Pressure
  • Increase Coronary Flow (Coronary dilation/elevated BP)
  • <-> / Decrease Cardiac Output
  • ***Increase Total Peripheral Resistnace (TPR)***
  • Decrease Renal Blood Flow
  • Decrease Splanchnic and Hepatic Blood Flow
69
Q

Norepinephrine

  1. Toxicity/Adverse Effects
  2. Therapeutic Uses
A

AE: Similar to those of Epinephrine (e.g. Restlessness, Throbbing Headache, Tremor, Palpitations, Cerebral Hemorrhage (large doses/Rapid IV), Cardiac Arrhythmias, Angina (pts with CAD))

***Greater elevation of Blood Pressure (Treats HYPOtension)***

Leads to Reflex BRADYcardia

Uses:

-Treatment of Hypotension (dose titration needed)

70
Q

Dopamine

  1. Class
  2. Properties
A

Class: D1, D2, B1, a1 Receptor Agonist

Properties:

  • Immediate metabolic precursor of Norepinephrine and Epinephrine
  • In CNS: Neurotransmitter important in regulation of movement
  • In Periphery: Synthesized in the epithelial cells of the proximal tubule –> ***Local Diuretic/Natriuretic Effects***
  • Substrate for both MAO and COMT (ineffective if given orally)
71
Q

How do low doses (< 2 ug/kg/min) of Dopamine lead to Increased Urine Output via Presynaptic D2 Receptors?

A

Dopamine (low dose) –> Presynaptic D2 receptors (on peripheral circulation nerves) –> Decreased NE release and Decreased stimulation of VSMCs –> Vasodilation –> Increased GFR and Increased RBF –> Increased Na+ Filtered –> ***Na+ Diuresis***

72
Q

How do low doses (< 2 ug/kg/min) of Dopamine Increase Urine Output via Vascular D1 Receptors?

A

Dopamine (low dose) –> Vascular D1 receptors (renal, mesenteric, coronary) –> Vasodilation –> Increased GFR, RBF (Renal Blood Flow) –> Increased Na+ Filtered –> ***Na+ Diuresis***

73
Q

How does low dose (< 2 ug/kg/min) Dopamine cause Increaed Urine Output via Renal Tubular Cell D1 receptors?

A

Dopamine (low dose) –> Renal Tubular Cell D1 receptors –> Increased Proximal, Henle Loop [cAMP] –> Decreased Na+-K+-ATPase –> Decreased Na+ Reabsorption –> ***Na+ Diuresis***

74
Q

Dopamine

  1. Cardiovascular Effects of Moderate Doses (2-5 ug/kg/min)
A
  • Increased Inotropic Effect (B1) (Increased cardiac contractility, Tachycardia, Increases Systolic Blood Pressure/Pulse Pressure ; NO EFFECT on Diastolic Blood Pressure)
  • Release of Norepinephrine from nerve terminals
  • Little Effect on Total Peripheral Resistance
75
Q

Dopamine

  1. Precautions, Adverse Reactions, Contraindications
A
  • Hypovolemia should be corrected before use of Dopamine
  • Tachycardia, Angina, Arrhythmias, Headache, Hypertension
  • Extravasation –> Ischemic Necrosis and Sloughing
  • MAO Inhibitor or Tricyclic Antidepressant –> AVOID Dopamine (or use with EXTREME CAUTION)

***Inhibit Degradation***

76
Q

Dopamine

  1. Therapeutic Uses
A

Uses:

  • Severe CHF, particularly in patients with oliguria (abnormally small amount of urine) and low/normal peripheral vascular resistance
  • Cardiogenic/Septic Shock
  • May acutely improve Cardiac and Renal Function in severely ill patients with chronic Heart Disease or Renal Failure
77
Q

Ephedrine (Ephedrine, Ephedra)

  1. Class
  2. Characteristics
A

Class: ***The ONLY Mix-Acting Adrenergic Agonist***

Acts on a1, a2, B1, B2, and releasing agent

Characteristics:

  • First orally active sympathomimetic drug
  • Found in ma-huang
  • High bioavailability and a relatively long duration of action
  • A Mild CNS stimulant
  • Pseudoephedrine** (ephedrine enantiomer) is a **Decongestant
78
Q

What drugs are part Indirect-Acting Releasing Agents?

A

Amphetamine

Tyramine

79
Q

Amphetamine

  1. Class
  2. Characteristics
A

Class: Indirectly Acting Sympathomimetic Amine Releasing Agent

Characteristics:

  • Structurally related to Norepinephrine –> Transported into the terminal by NET1
  • Displaces Norepinephrine –> Norepinephrine is then released Independent of Exocytosis and does NOT require the presence of Ca++
  • Partially active by inhibiting NET 1 (decreasing reuptake of NE) and partially by inhibiting MAO (decreasing metabolization of NE)
80
Q

Amphetamine

  1. Effects on the CNS
A
  • ***Releases Biogenic Amines from storage sites in nerve terminals
  • Stimulates the medullary respiratory center
  • Stimulates cortex and reticular activating system –> this prevents Fatigue and delays the need for sleep
  • Treats obesity (Decreased food intake)
81
Q

Amphetamine

  1. Cardiovascular Responses
A
  • Activates peripheral alpha (a) and beta (B) (like Norepinephrine)
  • Increases Systolic/Diastolic Blood Pressure
  • Increases Heart Rate
  • Cardiac arrhythmias (may occur)
82
Q

Amphetamine

  1. Effect on the Bladder Sphincter
A

Increased Bladder Sphincter Contraction

Treats: Enuresis and Incontinence

83
Q

Tyramine

  1. Class
  2. Characteristics
  3. Adverse Effects
A

Class: Indirectly Acting Sympathomimetic Amine Releasing Agent

Characteristics:

  • Used to synthesize Norepinephrine and Epinephrine via the alternate pathway
  • Destroyed by MAO in the gut wall and liver

AE:

-Action is Increased by MAO inhibition –> Ingestion of Tyramine-rich foods ***FERMENTED CHEESE*** –> Sudden and Dangerous rise in Blood Pressure

84
Q

What is the main drug in the alpha (a) Adrenoceptor Antagonist: a1 >>> a2 class?

A

Prazosin

Also, Terazosin and Doxazosin

85
Q

What is the main drug in the alpha (a) Adrenoceptor Antagonist a1 > a2 class?

A

Phenoxybenzamine

86
Q

Which drug(s) are part of the alpha (a) Adrenoceptor Antagonist a1 = a2 class?

A

Phentolamine

87
Q

Which drug(s) are part of the alpha (a) Adrenoceptor Antagonist a2 > a1 class?

A

Yohimbine

Rauwoscine

Torazoline

88
Q

What determines the effecs of Reversible alpha receptor antagonists? Irreversible?

A

Reversible: effects are determined by the half-life of the inhibitor/antagonist

Irreversible: effects are determined by the rate of production of new receptors

89
Q

What are the effects of alpha receptor antagonists?

A
  • Decrease blood pressure –> orthostatic hypotension
  • Tachycardia (Transient, Reflex Tachycardia)
  • Reverse the pressor effects of a and B agonists
  • Miosis (M3 is unopposed, conracts sphincter)
  • Nasal Stuffiness
  • Decreased resistance to urine flow
90
Q

What are the therapeutic uses of alpha receptor antagonists?

A
  • Pheochromocytoma (Rare –> Releases Norepinephrine)
  • Hypertensive emergency
  • Chronic hypertension
  • Peripheral vascular disease (Small doses)
  • Urinary obstruction
  • Erectile dysfunction (promotes ejaculation)
91
Q

Phenoxybenzamine (Dibenzyline)

  1. Class
  2. Mechanism
  3. Effects
A

Class: alpha (a) receptor antagonist

MoA: Irreversibly blocks a1 and a2 (LONG duration of action)

  • Also blocks H1, Acetylcholine, and Serotonin (5-HT) receptors
  • Indirect Baroreflex activation

Effects:

-Decreases Blood Pressure but Heart Rate Rises due to Baroreflex Activation

92
Q

Phenoxybenzamine (Dibenzyline)

  1. Clinical Uses
  2. Toxicity
A

Uses:

  • Treats Pheochromocytoma
  • Treats High Catecholamine states

Toxicity:

Half life is >1 day

-Orthostatic hypotension, Tachycardia, Myocardial Ischemia (increased heart rate can exacerbate this), Problems with ejaculation (due to alpha 1a blockade)

93
Q

Prazosin (Minipress)

  1. Class
  2. Mechanism
  3. Effects
  4. Clinical Uses
  5. Toxicity
  6. Similar drugs
A

Class: alpha (a) adrenoceptor antagonist

MoA: Blocks alpha 1 (a1) but NOT alpha 2 (a2)

-Relaxes arterial, venous, and prostate smooth muscle

Effects:

-Decreases blood pressure

Uses:

-Treats Hypertension and Benign Prostatic Hyperplasia

Toxicity:

-Larger depressor effect with first dose may cause Orthostatic Hypotension (watch for Tachycardia)

Similar Drugs: Doxazosin and Terazosin

94
Q

Tamsulosin (Flomax)

  1. Class
  2. Mechanism
  3. Effects
  4. Clinical Uses
  5. Toxicity
A

Class: alpha (a) adrenoceptor antagonist

MoA: slightly selective for alpha 1A (PROSTATE)

Effects:

-alpha 1a (a1A) blockade may relax prostatic smooth muscle more than vascular smooth muscle

Uses:

-Treats _***BENIGN PROSTATIC HYPERPLASIA***_

Toxicity: Orthostatic Hypostension is less common with this subtype

95
Q

Yohimbine

  1. Class
  2. Mechanism
  3. Effects
  4. Use
  5. Toxicity
A

Class: alpha (a) adrenoceptor antagonist

MoA: Blocks alpha 2 (a2) (has CNS activity) and increases norepinephrine release

Effects: INCREASES Blood Pressure and Heart Rate

Uses: Treats ***Erectile Dysfunction***

-Hypotension, as well, but not as much

Toxicity:

  • Anxiety
  • Excess pressor effect if NET1 is blocked
96
Q

Labetalol

  1. Class
  2. Mechanism
  3. Effects
  4. Use
  5. Toxicity
A

Class: Beta (B) and alpha 1 (a1) adrenoceptor antagonist

Moa: ***Blocks BOTH (B > a1)***

Effects:

Decreases Blood Pressure w/ limited heart rate increase

Uses:

***Used in High Sympathetic States*** (e.g. Hypertensive Crisis, Hypertension, Pheochromocytoma)

-Good because it will not/very limited reflex Tachycardia

Toxicity:

***LESS Tachycardia***

97
Q

What are the drugs in the B1 = B2 Non-Selective 1st Generation Beta (B) Adrenoceptor Antagonists class?

A

Propranolol

Nadolol

Timolol

Pindolol* (ISA)

Mnemonic: These drugs are Not Sharp like a PiNTiP

98
Q

What are the drugs in the B1 >>> B2 Selective 2nd Generation Beta (B) Adrenoceptor Antagonist class?

A

Atenolol

Metoprolol

Esmolol

Betaxolol

Acebutolol* (ISA)

Mnemonic: Slimey AMEBA

***Selectivity is lost at HIGH DOSES***

99
Q

What are the drugs in the B1 = B2 >or= a1 > a2 Vasodilatory 3rd Generation Mixed a-B Antagonist class?

A

Labetalol

Carvedilol

100
Q

What are the Cardiovascular Effects of Beta Receptor Antagonists? Clincal uses?

A

Effects:

  • Decreased inotropic/chronotropic effect –> Decreased Blood Pressure in hypertensive (***no effect on normotensive individual; thefore used for GLAUCOMA)
  • Decreased myocardial oxygen consumption
  • Decreased renin release

Uses:

  • Treats Hypertension
  • Glaucoma (blocks B1 and B2 in Ciliary Epithelium
  • Arrhythmias
  • Ischemic Heart Disease
101
Q

What are the Respiratory Effects of Beta Receptor Antagonists?

A

-Beta 2 (B2) Blockade –> Increased airway resistance –> undesiable in asthma and COPD

***No Beta Blocker is completely free of B2-blocking effect***

102
Q

What are the effects of Beta Receptor Antagonists in the Eye?

A

Decreased aqueous humor production –> Decreased intraocular pressure

103
Q

What are the Metabolic Effects of Beta Recptor Antagonists?

A

Inhibits lipolysis

May decrease glucagon release

Increases VLDL

Decreases HDL

_***BAD EFFECTS ON CHOLESTEROL***_

104
Q

What are the Therapeutic Uses of Beta Receptor Antagonists?

A

Treat:

  • Hypertension
  • Ischemic Heart Disease
  • Arrhythmias
  • Heart Failure - especially 3rd Degree and onward (caused by reduction in myocardial contraction –> reflex INCREASE in circulating catecholamines (e.g. Norepinephrine/Epinephrine) and INCREASED plasma renin activity –> OVERACTIVATION of B1 receptors in Heart and subsequent downregulation of adrenergic receptors)

***Treated with really low doses of B1-selective antagonists

  • Glaucoma
  • Hyperthyroidism (Symptomatic; treats increased heart rate)
  • Neurologic Diseases (e.g. migraines, anxiety, etc.)
105
Q

What are the 3 important Clinical Considerations for choosing Beta Blockers? (List them in order of clinical consideration)

A

1. Cardioselectivity (e.g. AMEBA group) - DO NOT use Non-Selective in pts with Asthma/COPD (due to B2 blocking effect –> Bronchiole CONSTRICTION); Use Selective** and keep the **Dose Low

2. Intrinsic Sympathomimetic Activity (ISA)

-e.g. Pindolol and Acebutolol (allows use of Beta blocker without dropping the Heart Rate)

3. Lipid Solubility

106
Q

What are the four factors to consider related to lipid solubility when using Beta blockers?

A

1. Plasma Levels and Duration of Action (fat tissue)

  • Lipophilic Beta-Blockers: (e.g. propranolol/metoprolol) produce lower plasma concentration and have less predictable plasma concentration because they are metabolized by the liver
  • Hydrophilic Beta Blockers: longer biological action (allow once-a-day dosing)

2. CNS

-Hydrophilic Beta-Blockers enter the brain much less than Lipophilic

3. Kidney

-Hydrophilic are effected by kidney functions; Lipophilic are not

4. Age

-Older = lower liver function –> higher plasma concentrations of lipophilic Beta Blockers –> higher incidence of side effects

107
Q

What are the Adverse Effects of Beta Receptor Antagonists?

A
  • Fatigue
  • Worsening PVD (Due to B2 blockade –> Vasoconstriction in microvasculature)
  • Worsening Bronchospasm
  • Decreased Sexual Functions (Common)
  • Increased Diabetes incidence
  • _***Masked Symptoms of HYPOGLYCEMIA***_

Pay attention to this, especiall in patients with advanced diabetes, due to downregulation of neuro contorls of glycemia

Signs = drop in blood sugar with faster heart rate, agitation, palpitations, ***SWEATING***

***If you block beta receptors, these go away, except Sweating***

108
Q

What are the effects of Choline Esters (Direct-Acting Cholinoceptor Agonists)?

A

Cardiovascular –> Hypotension, Bradycardia, SLOWED conduction/PROLONGED refractory period

GI–> INCREASED motility, acid secretion, NVD

GU –> INCONTINENCE

Eye –> Miosis (pupillary CONSTRICTION via sphincter muscle)

Respiratory –> BronchoCONSTRICTION

Glands –> INCREASED SECRETION

109
Q

What drugs are not effected by prior treatment with Reserpine** or **Guanethidine and actually potentiated by these drugs, as well as Cocaine?

A

DIRECT-ACTING ADRENERGIC AGONISTS

Both Selective (e.g. Phenylephrine, Clonidine, Terbutaline, Fenoldopam)

and Non-Selective (e.g. Isoproterenol, Dobutamine, Epinephrine, Norepinephrine, Dopamine)

110
Q

What drugs are reduced by prior treatment with Reserpine** or **Guanethidine?

A

Ephedrine (a mix-acting Adrenergic Agonist)

111
Q

What drugs are abolished by prior treatment with Reserpine** or **Guanethidine?

A

INDIRECT-ACTING

Including Releasing Agents (e.g. Amphetamine and Tyramine)

Uptake Inhibitors (e.g. Cocaine)

and MAO/COMT Inhibitors (e.g. Pargyline and Entacapone)

Pharmacology Exam 1 (3 decks)

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