Pharmacology Test 1

Front 1

Henderson-Hasselbach equation

Back 1

pH = pKa + log[A-]/[HA]

pH = pKa + log[B]/[BH+]

Front 2

Which form of the drug can cross membranes and thus equilibrate?

Back 2

Uncharged form

Front 3

Fick's Law

Back 3

The rate of absorption is dependent on the surface area of the barrier

Greater SA = Greater absorption

Front 4

pH and absorption with weak acids/bases

Back 4

Weak acids absorbed more in stomach (because environment is lower in pH)

Weak bases absorb more in small intestines (higher in pH)

Front 5

Break down of body water compartments and average levels

Back 5

Total body water- 60% or 42L
Intracellular - 40-44% or 29 L
Extracellular (Interstitial + Plasma) - 16-20% or 14 L
Interstitial - 12-16% or 11L
Plasma - 4% or 3L

Front 6

Whole blood volume (including water in RBCs)

Back 6

2 times plasma volume

Front 7

Calculate plasma concentration of a drug

Back 7

Tc = ((1-hematocrit) * 1 * Cp) + (hematocrit * 0.7 * Ci)

Total concentration in blood = (fraction of blood that is serum * serum water content * concentration of drug in plasma) + (fraction of blood that is cells * cell water content * concentration of drug in cells)

Front 8

% of cell content that is water

Back 8

70%

Front 9

Significance of plasma concentration

Back 9

Plasma concentration is the amount distributing and leaving the capillaries

Front 10

What must a drug have to cross the blood-brain barrier/

Back 10

High lipid partition coefficients (ie how soluble is it in lipids)

Front 11

What limits the accumulation of drugs in body fat?

Back 11

1. Most drugs have a low lipid partition coefficient

2. Low blood supply to fat tissue (>2% CO)

Front 12

Enteral routes of drug administration

Back 12

Oral
Sublingual
Rectal

Front 13

Parenteral

Back 13

I.V.
Subcutaneous
Intramuscular
Spinal
Topical
Inhalation

Front 14

Oral administration

Back 14

-undergoes first pass metab
-convenient, self-administered, safe, economical
-absorption depends on many factors, relatively slow
-usually absorbed in mucosa of sm. intestine

Front 15

Sublingual administration

Back 15

-no first pass
-avoid exposure to gastric environment
-more difficult, many drugs not taken up by oral mucosa
-absorbed by oral mucosa

Front 16

Rectal administration

Back 16

-no first pass
-avoids exposure to gastric environment
-most drugs not well absorbed
-absorbed by rectal mucosa

Front 17

IV administration

Back 17

-no first pass
-rapid response, highly regulated by infusion rate, large doses can be given over time, easy to discontinue
-drugs cannot be withdrawn once administered, no oily solutions, infections, venous thrombosis
-injected directly into circulation

Front 18

Subcutaneous administration

Back 18

-no first pass
-rate of absorption dependent on blood flow, small doses used for local effect
-tissue damage and distention, leakage into subQ tissue, slow uptake if poor peripheral circulation
-injected under the skin

Front 19

Intramuscular administration

Back 19

-no first pass
-rate of absorption dependent on blood flow and water solubility
-injected into skeletal muscle

Front 20

Inhalation administration

Back 20

-no first pass
-convenient, can be self-administered
-greatly dependent on molecular size and lipid solubility
-Gases or aerosols

Front 21

Muscarinic Receptor Agonists

Back 21

Bethanechol
Pilocarpine

Front 22

Muscarinic Antagonists

Back 22

Atropine
Scopolamine
Ipratropium
Tolterodine
Oxybutynin

Front 23

Bethanechol (prominent action)

Back 23

-increase GI tone
-increase urinary bladder tone

-miosis
-spasm of accomodation

Front 24

Bethanechol (therapeutic application)

Back 24

Ileus for post-op or neurogenic
Urinary tract motility post-op or neurogenic

Front 25

Bethanechol (side effects)

Back 25

Heart block
Syncope
Cardiac arrest

*Contraindicated - asthma, hyperthyroidism, and coronary insufficiency

Front 26

Bethanechol (comments)

Back 26

Choline ester
Resistant to AChE
PO and SC

Front 27

Bethanechol (class)

Back 27

muscarinic receptor agonist

Front 28

Pilocarpine (class)

Back 28

muscarinic receptor agonist

Front 29

Pilocarpine (prominent action)

Back 29

Miosis
Spasm of accomodation

Front 30

Pilocarpine (therapeutic application)

Back 30

Mitotic agent
Glaucoma
Xerostomia (dry mouth)

Front 31

Pilocarpine (side effects)

Back 31

Excessive parasymp. activity

*Contraindicated - asthma, COPD, peptic ulcer disease

Front 32

Pilocarpine (comments)

Back 32

Alkoloid
PO or eye drops

Front 33

Atropine (class)

Back 33

muscarinic antagonist

Front 34

Atropine (prominent action)

Back 34

Competitive muscarinic blockade
Mydriasis
Cycloplegia
Tachycardia
Smooth muscle relaxation
Inhibition of secretions
CNS stimulation

Front 35

Atropine (therapeutic applications)

Back 35

Counteract muscarinic toxicity
Mydriatic for eye exams
Reversal of sinus bradycardia
Cardiac arrest

Front 36

Atropine (side effects)

Back 36

*Dry as a bone, blind as a bat, hot as a hare, red as a beet, mad as a hatter*

-Glaucoma
-Tachycardia (secondary to cardiac insufficiency or thyrotoxicosis)
-Dry mouth
-Urinary retention
-Hot, flushed skin
-Constipation
-Airway dilation
-Mydriasis
-CNS stimulation

Front 37

Atropine (comments)

Back 37

Competitive antagonist
Given by all routes

Front 38

Scopolamine (class)

Back 38

muscarinic antagonist

Front 39

Scopolamine (prominent action)

Back 39

*Same as atropine, but CNS sedation)

Mydriasis
Cycloplegia
Tachycardia
Smooth muscle relaxation
Inhibition of secretions
CNS sedation

Front 40

Scopolamine (therapeutic application)

Back 40

Treatment and prevention of motion sickness

Front 41

Scopolamine (side effects)

Back 41

*Same as atropine except CNS depression*

*Dry as a bone, blind as a bat, hot as a hare, red as a beet, mad as a hatter*

-Glaucoma
-Tachycardia (secondary to cardiac insufficiency or thyrotoxicosis)
-Dry mouth
-Urinary retention
-Hot, flushed skin
-Constipation
-Airway dilation
-Mydriasis
-CNS depression

Front 42

Ipratropium (class)

Back 42

muscarinic antagonist

Front 43

Ipratropium (prominent actions)

Back 43

Airway dilation
Relaxes smooth muscle in airway

Front 44

Ipratropium (therapeutic application)

Back 44

Bronchodilator in asthma and COPD
Acute bronchospasm

Front 45

Ipratropium (side effects)

Back 45

*Similar to Scopolamine, but less because of poor penetration*

*Dry as a bone, blind as a bat, hot as a hare, red as a beet, mad as a hatter*

-Glaucoma
-Tachycardia (secondary to cardiac insufficiency or thyrotoxicosis)
-Dry mouth
-Urinary retention
-Hot, flushed skin
-Constipation
-Airway dilation
-Mydriasis
-CNS depression

Front 46

Ipratropium (comments)

Back 46

Doesn't cross blood-brain barrier
Inhaled

Front 47

Tolterodine/Oxybutynin (class)

Back 47

muscarinic antagonist

Front 48

Tolterodine/Oxybutynin (prominent actions)

Back 48

*Same as atropine*

-Competitive muscarinic blockade
-Mydriasis
-Cyclopegia
-Tachycardia
-Smooth muscle relaxation
-Inhibition of secretions
-CNS depression

Front 49

Tolterodine/Oxybutynin (therapeutic)

Back 49

Relieve bladder spasms
Reducing involuntary voiding

Front 50

Tolterodine/Oxybutynin (side effects)

Back 50

*Similar to Scopolamine, but less because of poor penetration*

*Dry as a bone, blind as a bat, hot as a hare, red as a beet, mad as a hatter*

-Glaucoma
-Tachycardia (secondary to cardiac insufficiency or thyrotoxicosis)
-Dry mouth
-Urinary retention
-Hot, flushed skin
-Constipation
-Airway dilation
-Mydriasis
-CNS depression

Front 51

Organophosphate Poisoning (Muscarinic effects)

Back 51

Ciliary spasm
Marked miosis
Bronchoconstriction
Inc. bronchial secretions
Sweating
Salivation
Bradycardia
Hypotension
Involuntary defecation/urination

Front 52

Organophosphate Poisoning (Nicotinic effects)

Back 52

Weakness
Muscle fasciculation (twitching)
Muscular paralysis

Front 53

Organophosphate Poisoning (CNS effects)

Back 53

Confusion
Ataxia
Convulsions
Coma
Respiratory depression
Cardiovascular

Front 54

Edrophonium (class)

Back 54

cholinesterase inhibitor

Front 55

Edrophonium (comments)

Back 55

IM or IV
No CNS effects
Excreted in urine

Front 56

Edrophonium (mechanism)

Back 56

reversible binding to AChE

Front 57

Edrophonium (therapeutic)

Back 57

Diagnosis of myasthenia gravis

Front 58

Tacrine (class)

Back 58

cholinesterase inhibitor

Front 59

Tacrine (comments)

Back 59

PO
Enters CNS
p450

Front 60

Tacrine (mechanism)

Back 60

reversible binding to AChE

Front 61

Tacrine (therapeutic)

Back 61

Treatment of Alzheimers

Front 62

Donepezil (class)

Back 62

cholinesterase inhibitor

Front 63

Donepezil (comments)

Back 63

PO
p450
Parent and metabolites excreted

Front 64

Donepezil (mechanism)

Back 64

reversible binding to AChE

Front 65

Donepezil (therapeutic)

Back 65

Treatment of Alzheimer

Front 66

Physostigmine, Neostigmine, and Pyridostigmine (class)

Back 66

cholinesterase inhibitor

Front 67

Physostigmine, Neostigmine, and Pyridostigmine (comments)

Back 67

Physo - IM, IV, Eye drop
Neo - IM, IV, SC, PO
Pyrido - IM, IV, PO

*All hydrolyzed by ChE

Front 68

Physostigmine, Neostigmine, and Pyridostigmine (mechanism)

Back 68

reversibly bind to AChE

Front 69

Neostigmine (therapeutic)

Back 69

-Paralytic ileus and atony of bladder from surgery (**preferred)
-Treatment and diagnosis of myasthenia gravis
-Reversal of NM blockade

Front 70

Physostimine (therapeutic)

Back 70

Wide angle glaucoma
Treatment for CNS toxicity - anticholinergic poisoning

Front 71

Pyridostigmine (therapeutic)

Back 71

-Treatment of myasthenia gravis
-Reversal of NM blockade
-Pretreatment to reduce risk of mortality to nerve gases

Front 72

Demecarium (class, comments, mechanism, therapeutic)

Back 72

ChE inhibitor

Eye drop

Reversibly binds to AChE

Treats glaucoma

Front 73

Echothiophate (class, comments, mechanism, therapeutic)

Back 73

Organophosphate

Well absorbed through skin, lung, gut and conjunctiva

Irreversibly binds to AChE

Glaucoma

Front 74

Parathion (class, comments, mechanism, therapeutic)

Back 74

Organophosphate

Well absorbed through skin, lung, gut and conjunctiva

Irreversibly binds to AChE

Insecticide

Front 75

Sarin and Soman (class, comments, mechanism, therapeutic)

Back 75

Organophosphate

Well absorbed in skin, lung, gut and conjunctiva

Irreversibly binds to AChE

Nerve gas

Front 76

Epinephrine (class)

Back 76

Direct acting sympathomimetic agent

Front 77

Epinephrine (receptors)

Back 77

alpha 1
alpha 2
beta 1
beta 2 (less so)

Front 78

Epinephrine (action)

Back 78

-Vasodilation in skeletal and coronary blood vessels (through beta receptors)
-Vasoconstriction of cutaneous vessels (through alpha 1)

Front 79

Epinephrine (comments)

Back 79

MAO phase 1
COMT phase 2 breakdown

Front 80

Epinephrine (therapeutic)

Back 80

Used in anaphylaxis
Glaucoma (open angle)
Asthma
Hypotension

Front 81

Norepinephrine (class)

Back 81

Direct acting sympathomimetic agent

Front 82

Norepinephrine (receptors)

Back 82

alpha 1
alpha 2
beta 1 (less so)

Front 83

Norepinephrine (action)

Back 83

-Vasoconstriction (alpha 1)
-Pupillary dilator muscle contraction (mydriasis)
-Intestinal and bladder sphincter muscle contraction

Front 84

How does norepinephrine affect heart rate and blood pressure with respect to homeostatic reflexes?

Back 84

Reflex bradycardia via the homeostatic baroreflex is overcome by a compensatory reflex preventing an otherwise inevitable drop in heart rate to maintain blood pressure

Front 85

Norephinephrine (therapeutic)

Back 85

Hypotension (vasopressor)

Front 86

Phenylephrine (class)

Back 86

Direct acting sympathomimetic

Front 87

Phenylephrine (receptors)

Back 87

alpha 1
alpha 2 (less so)

Front 88

Phenylephrine (action)

Back 88

-Gq receptor
-Vasoconstriction (alpha 1)
-Pupillary constriction (mydriasis)

Front 89

Phenylephrine (therapeutic)

Back 89

Nasal decongestion

Front 90

Clonidine (class)

Back 90

Direct acting sympathomimetic

Front 91

Clonidine (receptors)

Back 91

Alpha 2

Front 92

Clonidine (action)

Back 92

-Gi receptors
-Vasodilation through the inhibition of NE in CNS (decreases release of Ca++ in presynaptic neurons)
-Inhibits secretions

Front 93

Clonidine (therapeutic)

Back 93

Treats hypertension
Decrease sympathetic tone

Front 94

Clonidine (side effects)

Back 94

Salt and water retention
Dry mouth
Withdrawal

Front 95

Oxymetazoline (class, receptors)

Back 95

Direct acting sympathomimetic
Alpha 1 & 2

Front 96

Isoproterenol (class)

Back 96

Direct acting sympathomimetic

Front 97

Isoproterenol (receptors)

Back 97

Beta 1
Beta 2

Front 98

Isoproterenol (action)

Back 98

-Vasodilation
-Decreases blood pressure
-Increase heart rate (chronotropic)
-Increase heart contractility (inotropic)
-Bronchodilation

Front 99

Isoproterenol (therapeutic)

Back 99

Asthma
COPD
Cardiac stimulant

Front 100

Isoproterenol (comments)

Back 100

Not sensitive to MAO
Sensitive to COMT

Front 101

Dobutamine (class)

Back 101

direct acting sympathomimetic

Front 102

Dobutamine (receptors)

Back 102

Beta 1

Much less so:
Alpha 1
Alpha 2
Beta 2

Front 103

Dobutamine (action)

Back 103

-Gs receptor
-Dopamine derivative
-Increases heart contractility (inotropic)
-Little effect on heart rate
-Increase renin in JG cells

Front 104

Dobutamine (comments)

Back 104

Short half life
Not sensitive to MAO
Sensitive to COMT

Front 105

Dobutamine (therapeutic)

Back 105

Acute heart failure
Cardiac stress testing

Front 106

Metaproterenol
Albuterol
Salmeterol
Terbutaline (class)

Back 106

direct acting sympathomimetic

Front 107

Metaproterenol
Albuterol
Salmeterol
Terbutaline (receptors)

Back 107

Beta 2

Beta 1 (much less so)

Front 108

Metaproterenol
Albuterol
Salmeterol
Terbutaline (action)

Back 108

-Gs receptor
-Relaxation/inhibition
-Vasodilation in blood vessels
-Bronchodilation
-Excitatory effects in heart (high doses)
-Stimulates insulin release (Beta 2 receptors on islets of langerhans cells)

Front 109

Metaproterenol
Albuterol
Salmeterol
Terbutaline (comments)

Back 109

Not sensitive to MAO or COMT
Cardiac effects only at high doses

Front 110

Metaproterenol
Albuterol (therapeutic)

Back 110

Acute asthma
COPD

Front 111

Salmeterol (therapeutic)

Back 111

Long term asthma treatment
COPD

Front 112

Terbutaline (therapeutic)

Back 112

Reduce premature uterine contractions

Front 113

Ephedrine (class)

Back 113

Mixed action sympathomimetic

Front 114

Ephedrine (receptors)

Back 114

Alpha 1
Some Beta

Front 115

Ephedrine (action)

Back 115

-releases NE
-Stimulates heart (beta receptors and NE) -- tachycardia, arrthymia
-Vasoconstriction--> increase BP
-Increases mood and elation
-CNS effects

Front 116

Ephedrine (therapeutic)

Back 116

Asthma
Nasal decongestant
Performance enhancing drug
Vasopressor

Front 117

Dopamine (class)

Back 117

Mixed action sympathomimetic

Front 118

Dopamine (receptors)

Back 118

D1 (low dose)
Alpha 1 (high doses)
Alpha 2 (high doses)
Beta 1 (medium dose)
Beta 2 (medium dose)

**D1>B>A**

Front 119

Dopamine (action)

Back 119

-directly activates receptors
-indirect action-> releases NE
-Vasodilation in some vascular beds (renal, mesenteric, and coronary) -->increases renal perfusion
-Stimulates heart (beta receptors and NE)
-Inotropic and chronotropic

Front 120

Dopamine (therapeutic)

Back 120

-Shock (due to loss of renal perfusion)
-Heart failure

Front 121

Amphetamine (class)

Back 121

Indirect sympathomimetic

Front 122

Amphetamine (action)

Back 122

-Releases stored catecholamines (Primarily dopamine; also NE and Epi)
-Stimulate heart
-Increase BP
-CNS effects (paranoid schizophrenia)

Front 123

Amphetamine (receptors)

Back 123

Alpha 1
Beta 2

Front 124

Amphetamine (therapeutic)

Back 124

Vasopressor
ADHD
Narcolepsy
Weight loss

Front 125

Tyramine (class and action)

Back 125

Indirect sympathomimetic
Releasing agent

Front 126

Cocaine (class)

Back 126

Indirect sympathomimetic

Front 127

Cocaine (action)

Back 127

-Inhibits uptake into presynaptic vesicle (Uptake 1)
-Vasoconstriction
-Local anesthesia

Front 128

Pargyline (class and action)

Back 128

Indirect sympathomimetic
MAO/COMT inhibitor

Front 129

Entacapone (class and action)

Back 129

Indirect sympathomimetic
MAO/COMT inhibitor

Front 130

Enzyme kinetics:

Km in relation to affinity

Back 130

Smaller Km = Higher affinity

Front 131

Enzyme kinetics:

Y-intercept in relation to V-max

Back 131

Larger Yi = Lower V-max

Front 132

Enzyme kinetics:

Competitive vs. Noncompetitive inhibitors

Back 132

Competitive:
-resemble substrate
-overcome by inc. in substrate
-bind to active site
-no effect on V-max
-increase Km
-decrease potency

Noncompetitive:
-do not resemble substrate
-unaffected by inc. in substrate
-do not bind to active site
-decrease Vmax
-no effect on Km
-decrease efficacy

Front 133

Volume of distribution (definition and equation)

Back 133

Relates the amount of drug in the body to the plasma concentration

Vd = amount of drug in body/plasma drug concentration

Vd= dose/Cp(0)

Front 134

Volume of distribution (significance)

Back 134

Low Vd (4-8L) - distribute in blood, are large charged molecules

Medium Vd -distribute in extracellular space or body water, are small hydrophilic molecules

Large Vd (>body weight) - distribute into all tissues, are small lipophilic molecules that bind strongly to EXTRAvascular proteins

*Vd of plasma protein bound drugs is altered by liver/renal disease (Dec. protein binding, Inc. Vd)

Front 135

Clearance

Back 135

Relates the rate of elimination to the plasma concentration

Cl = rate of elimination of the drug / plasma drug concentration

Cl= Vd * Ke

Front 136

Elimination constant

Back 136

Ke = 0.7/ half-life

Ke= Cl / Vd

Front 137

Half-life

Back 137

The time required to change the amount of drug in the body by 1/2 during elimination --> first order property

t(1/2) = 0.7*Vd / Cl

**Takes 5 half lives for a drug to reach steady state (Css)

Front 138

Bioavailability

Back 138

Fraction of administered drug that reaches circulation

IV: F= 100%
Orally: F = % that survives first pass in liver or gut

Front 139

Loading dose

Back 139

Dl = target plasma concentration * volume of distribution / bioavailability

Dl = Cp * Vd / F

Front 140

Maintenance dose

Back 140

Dm = target plasma concentration * clearance / bioavailability

Dm = Cp * Cl / F

Front 141

Zero order elimination

Back 141

Rate of elimination is constant regardless of Cp

Cp linearly dec. with time

Ex. Phenytoin, Ethanol, Aspirin

Front 142

First order elimination

Back 142

Rate of elimination proportional to the drug concentration

Cp dec. exponentially with time

Front 143

Phase 1 metabolism

Back 143

-Usually yields slightly polar, water-soluble metabolites that are often still active

-Cytochrom P-450

-Reduction, oxidation, hydrolysis

-Geriatric patients lose phase 1 first

Front 144

Phase 2 metabolism

Back 144

-Usually yields very polar, inactive metabolites (renally excreted)

-Conjugation

-Glucuronidation, acetylation, sulfation

-Slow acetylators have greater side effects from certain drugs because of dec. rate of metabolism

Front 145

Efficacy

Back 145

Maximal effect a drug can produce

Front 146

Potency

Back 146

Amount of drug needed for a given effect

Inc. potency = Inc. affinity for receptor

Front 147

Therapeutic Index

Back 147

Safer drugs have higher TI values

TI = median lethal dose / median effective dose

TI = LD50 / ED50

Front 148

Phenoxybenzamine (class)

Back 148

Alpha blocker

Front 149

Phenoxybenzamine (receptor)

Back 149

Alpha 1
Alpha 2

**Non-selective**

Front 150

Phenoxybenzamine (action)

Back 150

-Acts on same receptor site as agonist
-Forms a covalent bond and alkylates receptor (IRREVERSIBLE)
-Dynamically like a noncompetitve antagonist
-Also blocks ACh, histamine, and serotonin receptors
-Blocks uptake 1

Front 151

Phenoxybenzamine (therapeutic)

Back 151

Pheochromocytoma

Front 152

Phenoxybenzamine (side effects)

Back 152

Orthostatic hypotension
Reflex tachycardia

Front 153

Phentolamine (class)

Back 153

alpha blocker

Front 154

Phentolamine (receptor)

Back 154

Alpha 1
Alpha 2

**Non-selective**

Front 155

Phentolamine (action)

Back 155

-Competitive blocker (reversible)
-Potent vasodilator
-Blocks uptake 1

Front 156

Phentolamine (side effects)

Back 156

Reflex tachycardia

Front 157

Prazosin (class)

Back 157

Alpha blocker

Front 158

Prazosin (receptors)

Back 158

Alpha 1

Front 159

Prazosin (therapeutic)

Back 159

-Hypertension
-Urinary retention in benign prostatic hypertrophy

Front 160

Prazosin (side effects)

Back 160

1st dose orthostatic hypotension
Inhibition of ejaculation
Nasal congestion
Tachycardia

Front 161

Yohimbine and Tolazoline (class and receptors)

Back 161

Alpha blocker
Alpha 2

Front 162

List the beta blockers

Back 162

Propranolol
Timolol
Pindolol
Nadolol
Metoprolol
Atenolol
Alprenolol
Labetalol

Front 163

Beta 1 selective antagonists

Back 163

Atenolol
Metoprolol
Alprenolol

*For patients with comorbid pulmonary disease

Front 164

Non-selective beta antagonists

Back 164

Propranolol
Timolol
Pindolol
Nadolol

Front 165

Non-selective alpha and beta antagonist

Back 165

Labetalol

Front 166

Anti-adrenergic agents

Back 166

Guanethidine
Reserpine
Alpha methyldopa
Alpha methyl-p-tyrosine

*Alpha 2 agonists - decrease central adrenergic outflow

Front 167

Pre-synaptic parasympathetic nerves release ________?

Back 167

ACh to Nicotinic receptors

Front 168

Post-synaptic parasympathetic nerves release ________?

Back 168

ACh to Muscarinic receptors

Front 169

Pre-synaptic sympathetic nerves release ________?

Back 169

ACh to Nicotinic receptors

Front 170

Post-synaptic sympathetic nerves release ________?

Back 170

NE to alpha/beta receptors

EXCEPT:
-Dopamine to dopamine receptors in renal vascular smooth muscle

-ACh to Muscarinic receptors in sweat glands

-Epi and NE in adrenal medulla to systemic blood circulation

Front 171

Types and properties of ACh receptors

Back 171

Nicotinic:
-ligand gated Na+/K+ channels
-Nn (autonomic ganglia)
-Nm (neuromuscular junctions)

Muscarinic:
-G protein coupled receptors
- M1, M2, M3, M4, M5
-M1, M3 (Gq-->PLC-->DAG, IP3)
-M2 (Gi--> inhibit cAMP)

Front 172

Alpha 1 receptors (class and general function)

Back 172

-Gq
-increase vascular smooth muscle contraction
-increase pupillary dilator muscle contraction (mydriasis)
-increase intestinal and bladder sphincter muscle contraction

Front 173

Alpha 2 receptors (class and general function)

Back 173

Gi

-decrease sympathetic outflow
-decrease insulin release

Front 174

Beta 1 receptors (class and general function)

Back 174

Gs

-Increase heart rate (chronotropic)
-Increase heart contractility (inotropic)
-Increase renin release
-Increase lipolysis

Front 175

Beta 2 receptors (class and general function)

Back 175

Gs

-Vasodilation
-Bronchodilation
-Increase heart rate (chronotropic)
-Increase heart contracility (inotropic)
-Increase lipolysis
-Increase insulin release
-Decrease uterine tone

Front 176

M1 receptors (class and general function)

Back 176

Gq

-CNS
-Enteric nervous system

Front 177

M2 receptors (class and general function)

Back 177

Gi

-decrease heart rate
-decrease atria contractility

Front 178

M3 receptors (class and general function)

Back 178

Gq

-increase endocrine gland secretions (sweat, gastric acid)
-increase gut peristalsis
-increase bladder contraction
-bronchoconstriction
-increase pupillary sphincter muscle contraction (miosis)
-ciliary muscle contraction (accomodation)

Front 179

Hemicholinium

Back 179

Blocks uptake of choline into presynaptic neuron

Front 180

Vesamicol

Back 180

Blocks packaging of ACh into vesicle

Front 181

Ca++ in presynaptic neuron has what effect?

Back 181

Triggers release of ACh or NE

Front 182

Botulinum toxin

Back 182

Inhibits release of ACh into synapse

Front 183

Metyrosine

Back 183

Blocks conversion of tyrosine into DOPA

Front 184

Reserpine

Back 184

Blocks packaging of dopamine into vesicles to become NE

Front 185

Guanethidine

Back 185

Blocks release of NE

Front 186

Cocaine, TCAs, amphetamine

Back 186

Blocks reuptake of NE into presynaptic neuron

Front 187

Amphetamine

Back 187

Promotes release of NE into synapse

Front 188

What is the function of presynaptic alpha 2 autoreceptors on sympathetic nerve endings?

Back 188

Negative feedback on NE release

Front 189

What is the function of presynaptic angiotensin II receptors on sympathetic nerve endings?

Back 189

Promote release of NE into synapse

Front 190

What is the function of presynaptic M2 receptors on sympathetic nerve endings?

Back 190

Inhibit release of NE into synapse

Front 191

Ganglionic Antagonists
(drugs and action)

Back 191

Mecamylamine
Trimethaphan

-Tachycardia
-Decrease GI tone/motility
-Urinary retention
-Mydriasis
-Decrease heart contractility
-Vasodilation
-Decrease CO

Front 192

D-tubocurarine

Back 192

Neuromuscular blocker (competitive)

-Lowers AP below threshold
-Long lasting
-Blocks autonomic ganglia
-Moderately releases histamine
-Antagonized by neostigmine

Front 193

Neuromuscular blockers (competitive)

Back 193

Botulinium
d-tubocurarine
gallamine
pancuronium
atracurium
vecuronium
cistracurium
miracurium

Front 194

Neuromuscular blockers (depolarizing)

Back 194

Decamethonium
Succinycholine

Front 195

Succinylcholine

Back 195

Depolarizing neuromuscular blocker

-Stimulates autonomic ganglia and cardiac muscarinic receptors
-Slightly releases histamine
-Augmented by neostigmine
-Short acting (4-8 min)
-Causes muscle soreness
-Prolonged apnea
-Not sensitive to AChE

Front 196

Neuromuscular blockers (therapeutic use)

Back 196

Muscle relaxation
Endotracheal intubation
Maintaining controlled ventilation

Front 197

Neuromuscular blockers (side effects)

Back 197

Malignant hypothermia (Ca++ excreted without reuptake-->sustained muscle contraction-->acidosis and inc. body temperature)