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Pharmacology > Adrenergics and cholinergics > Flashcards

Adrenergics and cholinergics Flashcards

1
Q

Epinephrine Therapeutics

A

Therapeutic uses: hypersensitivity reaction (effect on beta 2)
Increase duration of action of local anesthetics (vasoconstriction so not washed out of tissue)
Bradyarrhythmias, opthalmic use on alpha 1 (mydriatic, decrease hemorrhage, conjunctival congestion

Low dose infusion: overall decrease in PVR and diastolic because B2 (dilation of some vascular beds) dilation in skeletal muscle
High dose infusion : then alpha 1 constriction of blood vessels in skeletal muscle
Skeletal muscle has both alpha 1 and beta 2

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2
Q

Norepinephrine

A 
Receptor selectivity: alpha 1, alpha 2, beta 1 
CV effects (alpha 1 mainly): increases PVR, mean BP, reflex bradycardia (baroreceptors sense and withdraw symp tone to heart)
Absorption, fate, excretion: not orally effective, short t1/2, parenterally admonished 
Therapeutics: Vasoconstrictor under intensive care situations (shock, hypotension in reduced sympathetic tone), spinal anesthesia/block which blocks tone to blood vessels so NE compensates
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3
Q

Dopamine Dosing

A 
CV actions (dose-dependent): 
Low dose (0.5 micrograms/kg/min)- "renal dose"; dilation of renal and mesenteric arteries which decreases PVR and diuresis and urine production (D1 receptor) 
Intermediate dose (5-10 microgram/kg/min)- "cardiac dose"; increases HR, contractile force and cardiac output (D1 + B1 receptor)
High Dose (10-20 ug/kg/min)- "pressor dose"; vasoconstriction and increase PVR (D1 + A1+ B1)
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4
Q

Dopamine

A

Absorption, fate, excretion: similar to Epi; low F so administered IV (parenterally); dose titration to achieve desired effect

Therapeutic uses: severe decompensated heart failure, shock (cardiogenic, septic) and use pressor dose with low BP

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5
Q

Isoproterenol

A

Receptor selectivity- beta 1, beta 2 (group on amine)
CV effects- decreased PVR , increased HR, contractile force, CO, Decreased mean blood pressure (systolic increase and diastolic decrease)
Respiratory effect: bronchodilation
Absorption, fate, excretion: metabolized by COMT, brief duration of action, parenterally administered
Therapeutic uses: emergency use to stimulate heart rate during bradycardia or heart block

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6
Q

Dobutamine Structure

A

Asymmetric carbon-> (-) is alpha 1 and beta agonist, (+) is alpha 1 antagonist and beta agonist
Overall effect of racemic mixture function as beta 1 agonist
Catecholamines and large substitution on amino group so beta selective

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7
Q

Dobutamine

A

CV effects: increased HR, contractility, CO, minimal change in PVR and BP
Absorption, fate, excretion: metabolized rapidly and brief duration of activity, parenterally administered
Therapeutic uses: short term treatment of cardiac decompensation (cardiac surgery, CHF, infarction), cardiac stress testing (if too weak to exercise then this mimics effects of exercise)
Heart failure causes volume overload with high BP so increase CO without affect on blood pressure

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8
Q

Albuterol

A

B2 adrenergic receptor agonist (methyl hydroxyl on ring so not metabolized by COMT)
Administer by inhalation or orally
Short acting and rapid onset (gone 2-4 hours after inhalation)
Therapeutic use: rapid onset bronchi constriction
Adverse effects: tremor, anxiety, tachycardia (into systemic circulation and activate other beta 1 receptors)

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9
Q

Salmeterol

A

B2 adrenergic receptor agonist (inhalation)
Long duration of action (>12 hours)–> lipophilic and deposits in tissue so stay in lungs for long time
Therapeutic Use: Chronic obstructive pulmonary disease, moderate to severe persistent asthma; slow onset so not suitable as mono therapy for acute bronchospasm

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10
Q

Phenyleprine

A

Alpha 1 adrenergic receptor agonist
Increases systolic and diastolic BP
Reflex decrease in heart rate–> baroreceptors activity
Decrease blood flow in most vascular beds
Therapeutic uses:
Opthalmic (radial muscle)- midratic, decrease hemorrhage, congestion
Nasal decongestant (constrict vessels in nasal cavity)- oral or nasal spray
Use with local anesthetic to increase duration of action
Treatment of hypotension

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11
Q

Clonidine

A

Alpha 2 adrenergic receptor agonist (directly stimulates reduction of sympathetic outflow from central alpha 2 receptors)
Orally active
Therapeutic use: anti-hypertensive (blocks tone from central receptors to heart and vessels–> central not peripheral)
Major adverse effects: sedation (CNS function), dry mouth, sexual dysfunction, bradycardia, edema, rebound hypertension with sudden discontinuation

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12
Q

Methyldopa

A

Alpha 2 adrenergic receptor agonist
Orally active pro-drug–> stored in nerve terminals as alpha-methyl dopamine and alpha-methyl norepinephrine and released with nerve stimulation
Both are alpha-2 receptor agonists which stimulate central receptors to reduce sympathetic outflow
Major therapeutic use: anti-hypertensive
Side effects: similar to clonidine

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13
Q

Epinephrine

A

Receptor selectivity–> alpha 1, alpha 2, beta 1, beta 2
CV effects: potent vasopressor (alpha 1) but can dilate some vascular beds (beta 2), cardio stimulatory (beta 1)
Respiratory effects: bronchodilation (Beta 2)
Metabolic effects: increase blood glucose and fatty acids
Absorption, fate, excretion: not orally effective with rapid t1/2
Low dose: increase systolic and decrease diastolic

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14
Q

Tyramine

A

Indirect acting on alpha and beta receptors
Normal: Tyramine is AA compound in food and absorbed and degraded by MAO in liver (foods= cheese, beer, sausage)
MAO inhibitor with tyramine rich food: tyramine absorbed but not degraded so then activate alpha and beta receptors to release NE and sympathetic surge
Complication of surge: alpha 1 receptor activated–> hypertension

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15
Q

Amphetamine

A

Indirect release of NE
Orally bioavailability- long half life because no MAO degradation
Powerful CNS stimulation (adrenergic)–> Wakefulness, depress appetite, stimulate respiratory center (increase respiration)
Therapeutic Uses: Narcolepsy, attention deficit/ hyperactive disorder
Release NE and other biogenic amines (dopamine) from granules

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16
Q

Pseudoephedrine

A

Direct alpha 1 and beta 2 agonist activity
Orally effective but minimal CNS stimulation
Therapeutic use:: Nasal decongestant
Absorbed orally and longer half life than catecholamines
Availability is restricted

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17
Q

Guanethidine and Guanadrel

A

Inhibit NE release and deplete neuronal amine stores
Orally active, long lasting
Do NOT penetrate CNS
Taken into adrenergic nerves via NET and deplete stores of NE slowly (eventually inhibit adrenergic effects)
Drug requires NET so any other substance/drug that inhibits NET will affect activity (tricyclics antidepressants, coccaine)
Therapeutic use: essential hypertension
Side effects: Orthostatic hypotension, male sexual dysfunction, diarrhea (no opposition to parasympathetic tone), muscle weakness, edema

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18
Q

Reserpine

A

Diffuse into adrenergic neurons (lipophilic no NET needed)
Deplete nerves of NT by inhibiting VMAT
Orally active
Therapeutic: Treatment of hypertension
Enter brain and adverse CNS effects including depression (suicidal tendencies) and sedation
Adverse effects: diarrhea, Orthostatic hypotension, increased gastric acid secretion (no opposition for parasympathetic tone)

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19
Q

Phenoxybenzamine

A

Alpha 1 and alpha 2 adrenergic receptor
Irreversible antagonist –> binds to receptor with covalent bond so permanently binds and no receptor function till new receptors are made (Emax decrease but change in EC50)
Long duration of action
Therapeutic uses: pheochromocytoma (tumor produces lots of catecholamines so block alpha receptors to block blood pressure changes)
Side effects: limit usefulness of treating HTN
Hypotension
Reflex cardio stimulation ( tachycardia, ionotropy)

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20
Q

Phentolamine

A

Alpha 1 and alpha 2 adrenergic receptor antagonist
Competitive, reversible antagonist–> overcome by increasing level of agonist
Orally active
Shorter duration of action (2-4 hours)
Therapeutic uses: Pheochromocytoma
Side Effects: limit usefulness for treating HTN
Hypotension
Reflex cardio stimulation (tachycardia and ionotropy)

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21
Q

Prazosin

A

Selective competitive antagonist of alpha 1 receptors
Short duration of action
Minimal tachycardia because little blockade of presynaptic alpha 2 receptors
Decrease vascular tone in resistance (arteries) and capacitance (veins) beds
Produce favorable effect on lipid profile
Clinical use: hypertension, short term treatment of heart failure
Side effects:
first dose phenomena–>Orthostatic hypotension

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22
Q

Tamsulosin

A

Orally active for alpha 1 adrenergic receptor antagonist (alpha 1a vs. alpha 1B)
Favors blockade of alpha 1a on prostate
Treatment: Benign prostatic hyperplasia (BPH) with little effect on blood pressure
Not approved for treatment of hypertension

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23
Q

Distinguishing feature someone B adrenergic receptor antagonist

A

Relative affinity for B1 and B2
Intrinsic sympathomimetic activity (acts as partial agonist)
Capacity to induce vasodilation
Pharmacokinetic properties

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24
Q

B adrenergic receptor antagonists Pharmacological properties

A

CV: slow heart rate and decrease contractility, reduce sinus rate and activity of ectopic pacemakers (slow AV and atrial node conduction), anti-hypertensive (block renin release),
Pulmonary: bronchoconstriction
Metabolic: block sympathetic mediated mobilization of glucose and free fatty acids in the circulation

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25
Q

B Adrenergic Receptor Antagonist Adverse Effects

A

CV: induce heart failure in susceptible patients, bradycardia, worsen peripheral vascular disease
Pulmonary: increase airway resistance in those with asthma/COPD
CNS: fatigue,sleep disturbances, depression
Metabolism: blunt recognition of hypoglycemia and may delay recovery from insulin0induced hypoglycemia

26
Q

B adrenergic receptor antagonist: therapeutic uses

A

Cardiovascular diseases: hypertension, angina, acute coronary syndromes (MI), congestive heart failure
Glaucoma: chronic open-angle glaucoma
Other Use: migraine prophylaxis, anxiety provoking stimulus, essential tumors

27
Q

Propranolol

A

Non-selective (1st generation)–> B1 and B2 receptor antagonist
Orally bio available but short half life and significant first pass metabolism
Clinical uses:
Hypertension, angina, cardiac arrhythmia, MI, pheochromocytoma, migraine prophylaxis, essential tremors

28
Q

Timolol

A

Orally bioavailability antagonist B1 and B2
First generation Beta blocker
Therapeutics: hypertension, angina, cardiac arrhythmias, MI, Pheochromocytoma, migraine prophylaxis, essential tremors
ALSO wide angle glaucoma

29
Q

Metoprolol

A

2nd generation –> Orally bioavailable B1 selective antagonist
uses: Hypertension, angina, MI, cardiac arrhythmia, pheochromocytoma, migraine prophylaxis, essential tremor
ALSO heart failure
Adverse effects: less bronchoconstriction at lower doses

30
Q

Atenolol

A 
2nd generation (B1 selective antagonist)
Orally bioavailable--> longer duration of action allowing once per day dosing and less penetration to CNS 
Therapeutic uses: MI, arrhythmia, hypertension, angina, essential tremors, pheochromocytoma, migraine prophylaxis 
Adverse effects: less bronchoconstriction at lower doses
31
Q

Labetolol

A

3rd generation–> alpha 1, beta 1 and 2 antagonist
Orally bioavailable
Therapeutic uses: essential hypertension (chronic), hypertensive emergencies

32
Q

Carvedilol

A

Second generation–> alpha 1, beta 1, beta 2
Anti-oxidant properties
Blocks L-type calcium channels at higher doses
Therapeutic uses: hypertension, Heart failure, MI

33
Q

Effects of Muscarinic Receptor Activation

A

CV: vasodilation (M3), decreased heart rate and AV nodal conduction (M2)
Pulmonary: Bronchoconstriction (M3), Increased bronchial secretion (M3)
Urinary Tract: detrusor muscle contraction, increase voiding pressure, ureter peristalsis (M3)
GI tract: increase tone/amplitude of contractions and increased secretory activity (M3)
Miscellaneous Peripheral effects: increase secretion from glands (M3) and miosis and accommodation for near vision (m3)
CNS: cortical arousal

34
Q

Bethanechol

A

Muscarinic receptor agonist
Choline esters (similar structure to Ach)
Oral or subcutaneous (low bioavailability)
Treat: urinary retention (post- op urinary retention, urinary retention with diabetic neuropathy, bladder disorders)

35
Q

Pilocarpine

A 
Muscarinic receptor agonist 
Choline esters 
Effects: 
xerostomia (dry mouth)
Topically in ophthalmology for treatment of glaucoma and as a mitotic agent
36
Q

Common adverse effects of Muscarinic receptor agonist

A

SLUDGE (salivation, lacrimation, urination, defecation, GI upset, emesis)
Diaphoresis (sweating)
Diarrhea, abdominal cramps, nausea
Difficulty with visual accommodation
Hypotension
Contraindications: asthma, COPD, urinary/GI obstruction, acid-peptic disease, CV disease with bradycardia or hypotension

37
Q

Muscarinic Receptor Antagonists Pharmacological Effects

A

CV (M2): tachycardia and facilitate AV nodal conduction, block reflex slowing of HR and AV nodal conduction, No direct effect on vascular tone and blood pressure
Respiratory (M3): bronchodilation and decrease in secretions
Eye (M3): dilation pupil, paralysis of accommodation
GI tract (M3): decreased secretions and motility
Other smooth muscle (M3): decrease contractions of ureter and bladder
Sweat glands- temperature: decrease sweating
CNS: CNS depression and drowsiness

38
Q

Atropine

A

Muscarinic antagonist (alkaloid class)
Non-subtype selective
Orally bioavailable
Uses: Bradyarrhythmias, opthalmic uses (produce mydriasis and cycloplegia), uses during anesthesia (prevent reflexes in GI and bronchial secretions), anti-cholinesterase or muscarinic toxicity

39
Q

Scopolamine

A

Muscarinic Antagonist non subtype selective (alkaloid)
Orally bioavailable
More prominent CNS effects than atropine
Uses: motion sickness and vestibular disease

40
Q

Ipratropium

A

Muscarinic antagonist non-subtype selective (semi-synthetic)
Little penetration into CNS due to positive charge (Quat. Ammonium)
Uses: Helps with COPD and night asthma because decreases secretion and causes bronchodilation –> long life

41
Q

Tropicamide

A

Muscarinic Receptor antagonist (Synthetic antagonist)
Fast onset (20-40 min) and short duration of action (4-6 hours)
Therapeutic use: Mydriatic and cycloplegic (dilation and paralyze muscle control of the eye)

42
Q

Oxybutynin

A

Muscarinic receptor antagonist (synthetic antagonist)
Therapeutic use: overactive bladder, incontinence
High incidence of anti-muscarinic side effects: xerostomia (mainly), blurred vision, constipation, drowsiness/confusion

43
Q

Darifenacin

A

Muscarinic receptor antagonist (synthetic)
Therapeutic use: overactive bladder, incontinence
Some selectivity for M3 receptor subtype results in less CNS side effects

44
Q

Glycopyrrolate

A

Therapeutic use: block parasympathomimetic effects during reversal of neuromuscular blockade with anticholinesterase agents
Quaternary amine- no CNS penetration

45
Q

Muscarinic Receptor Antagonists Adverse effects

A

Xerostomia
Blurred vision
Dyspepsia, constipation, urinary retention
Tachycardia
Hyperthermia
Cognitive impairment (drowsiness, confusion)
Use with Caution: glaucoma, benign prostatic hyperplasia, angina, arrhythmias

46
Q

Muscarinic Antagonist Toxicity

A 
Hot as a Hare
Dry as a Bone 
Red as a Beet 
Blind as a bat 
Mad as a hatter
47
Q

Acetylcholinesterase Inhibitors

A

Therapeutic uses:
Antony of smooth muscle of the intestinal tract and urinary bladder
Glaucoma
Myasthenia Gravis
Reversal of paralysis by competitive neuromuscular junction blocking agents
Pharmacological uses:
Stimulation of muscarinic receptor response at autonomic effector organs
Stimulation followed by depression and paralysis of all autonomic ganglia and skeletal muslce (nicotinic)

48
Q

Edrophonium

A 
Acetylcholineserase inhibitors (Non-covalent) 
Limited to periphery because of charge 
Rapid onset and short duration of action 
Therapeutic use: diagnosis of myasthenia Gravis, reversal of paralysis by competitive neuromuscular blocking agents
49
Q

Physostigmine

A

Achesterase inhibitor (reversible carbamate inhibitors)
Alkaloid from Calabar bean
Slowly reversible
Tertiary amine (lipophilic)- CNS effects
Therapeutic use: treatment of chronic wide-angle glaucoma and toxicity by anti muscarinic drug poisoning

50
Q

Neostigmine

A

Acetylcholinesterase inhibitor (reversible carbamate inhibitors)
Synthetic
Slowly reversible
Quaternary amine so no CNS penetration
Treatment: Myasthenia Gravis treatment , prevention and treatment of post-operative Antony of gut and bladder, reverse of paralysis by competitive neuromuscular blocking agent

51
Q

Organophosphorus Compounds

A

Phosphorylate serine in substrate binding domain of acetylcholinesterase
Regeneration of enzyme is very slow and significant regeneration is not observed
Return of activity depends on synthesis of new enzyme
Nerve gas: sarin, tabun, soman
Insecticides: Malathion (rapidly detoxified in higher organisms)

52
Q

Organophosphorus Compounds Toxicity and Treatment

A

Toxicity: symptoms manifest as nicotinic and muscarinic symptoms; most compounds lipophilic and penetrate CNS
Symptoms include SLUDGE, hypotension, bradycardia, difficulty with visual accommodation, medullary respiratory depression, muscle paralysis because of depolarizing neuromuscular junction blockade, death due to respiratory failure

Treatment: Remove poisoning, maintain open airway, treat convulsions and shock, atropine (block peripheral and central muscarinic effects and Pralidoxime )

53
Q

Pralidoxime

A

Antidote for Organophosphorus compound toxicity
Reactivates acetylcholinesterase peripherally
Takes phosphate off to regenerate the enzyme
Use within 2-3 hours

54
Q

Competitive Neuromuscular Blocking Agent

A

Based on duration of procedure and minimizing cardiovascular compromise or other adverse effects with attention to modes of elimination in patients with hepatic or renal failure

Antagonist of nicotinic receptors at Nm junction

55
Q

Rocuronium

A

Competitive Neuromuscular Blocking Agent
Intermediate duration of action (30-60 minutes)
Rapid onset (1-2 minutes)
Elimination: hepatic
Minimal CV effects
No histamine release

56
Q

Atracurium

A

Competitive Neuromuscular Blocking Agent
Duration of action: Intermediate (45 minutes)
Onset 3 minutes
Spontaneously degrades in plasma; metabolism by plasma esterase a
Minimal CV effects
Slight histamine release

57
Q

Vercuronium

A 
Competitive Neuromuscular Blocking Agent
Intermediate duration of action (40-45 minutes)
Onset 2-3 minutes 
Hepatic and Renal elimination 
Minimal CV effects 
Histamine release: none
58
Q

Pancuronium

A 
Duration of action: long (85-100 min)
Onset: 3-4 min
Renal and hepatic elimination 
Slight increase in HR 
No histamine release
59
Q

Depolarizing Neuromuscular Blockers

A

Activate nicotinic receptors at the neuromuscular junction (Nm) maintaining motor end plate depolarization and preventing transmission of another AP

60
Q

Succinylcholine

A

Depolarizing neuromuscular blocker
Quaternary ammonium–> no CNS penetration not orally absorbed
Very rapid onset and ultra short duration of action because rapidly metabolized by plasma pseudocholinesterase
Onset 1-2 min, duration 5-8 min
Used frequently for tracheal intubation
Genetic variation ins pseucholinesterase activity

61
Q

Adverse effects of Neuromuscular Junction Blocking Agents

A

Prolonged apnea, CV collapse, effects due to histamine release like anaphylaxis
Malignant hyperthermia –> contracture, rigidity, heat production from skeletal muscle resulting in severe hyperthermia, metabolic acidosis, tachycardia (genetics from mutation of ryanodine receptor of L-Ca channel)
Hyperkalemia

Pharmacology (12 decks)

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