Dental Drugs

Front 1

A drug is

Back 1

exogenous chemical agent to modify physiology

Front 2

Toxicology is

Back 2

adverse effect of drug

Front 3

What are the 4 descriptors of drug action?

Back 3

symptomatic, physiological, cellular, molecular

Front 4

3 types of drug permeation?

Back 4

1. Aqueous and 2. Lipid diffusion
3. Special carriers

Front 5

What must a drub be to pass through a membrane?

Back 5

uncharged

Front 6

What determines charge of a drug?

Back 6

1. Acid: pH is above pKa for charge (-)
2. Base: pH is below pKa for charge (+).

Front 7

what are the types of receptors 4?

Back 7

1. Regulatory
2. Enzymes
3. Transport proteins
4. Structural proteins

Front 8

signaling mechanisms 6?

Back 8

1. intracellular, 2. Integral membrane proteins with INTRINSIC enzyme activity and 3. those with ASSOCIATED enzyme activity
4. Ligand gated
5. G-protein
6. Second messengers

Front 9

If the signal goes intracellular, it must be?

Back 9

lipid soluble drug

Front 10

EC50 is

Back 10

concentration fo drug needed to achieve 50% of maximal effect

Front 11

E max is?

Back 11

maximal drug response

Front 12

B max is

Back 12

maximum number of BINDING sites/receptors

Front 13

Kd is

Back 13

concentration of drug to get 50% of binding sites occupied

Front 14

T or F
Every receptor needs to be occupied in order to achieve maximal effect of drug.

Back 14

false. (why else would there be an E max?)

Front 15

how do competitive antagonists differ from irreversible antagonists?

Back 15

1. Reversible vs. irreversible binding.
2. Increasing [agonists] will produce same response, but irreversible will not

Front 16

a partial agonist is

Back 16

one that does not produce to maximal response thus decreasing effect (like an antagonist).

Front 17

Potency vs. efficacy

Back 17

P: is if drug requires less concentration to produce 50% of maximal response.
E: dose does not matter. it is which will produce the greater response/Effect.

Front 18

median effective dose (ED50) is

Back 18

when 50% of pts get desired response

Front 19

Median toxic dose (TD50)

Back 19

concentration that is toxic to 50% of pts

Front 20

Median Lethal dose (LD50)

Back 20

concentration to kill 50% of pts.

Front 21

The therapeutic index aka? Is?

Back 21

therapeutic window. range between ED50 and TD50

Front 22

Idiosyncratic means

Back 22

individual, unusual response to drug

Front 23

Tolerance vos tachyphylaxis

Back 23

tol: decreased response to drug with repeated use
Tach: rapid diminishment of responsiveness to drug

Front 24

Fasted route of drug administration?

Back 24

Intravenous

Front 25

Bioavailability is?
Determined by?

Back 25

fraction of unchanged drug that gets into circulation

Extent of absorption, first pass elimination, first pass effect (liver)

Front 26

Clearance is the

Back 26

rate of elimination / by the concentration of the drug

Front 27

A first order elimination vs zero order

Back 27

1. when rate depends on concentration of drug (half life)
0. constant rate of elimination to 0.

Front 28

Biotransformation is

Back 28

conversion of compounds from lipophilic to polar

Front 29

Phases of drug metabolism are

Back 29

1. untroduce/unmask functional group
2. Conjugation of a polar group

Front 30

3 types of phase 1 drug metabolisms include

Back 30

1. cytochrome p450-dependent
2. Oxidations
3. Cytochrome p45- independent.

Front 31

what are the phase 2 metabolism exs given?

Back 31

anything that ends in conjugation.
acetylation, glucoronidation, methylation

Front 32

Which are oxidations?

Back 32

hydroxylations, oxidative dealkylation, oxidation, deamination

Front 33

which are cytochome p450 independent?

Back 33

dehydration, reductions, hydrolysis

Front 34

what are some ex. of endogenous compounds taht can affect drug biotransformation?

Back 34

glutathione, glucuronic acid, sulfate

Front 35

Other factors that affect biotransformation?

Back 35

genetics, disease, age/sex, drug interactions, diet, environment

Front 36

Parasympathetic vs. sympathetic length?

Back 36

PS long then short
S: short then long

Front 37

What is the Neurotransmitter for the ganglia?

Back 37

Nicotinic

Front 38

What is the neurotransmitter for Skeletal muscle?

Back 38

Muscarinic

Front 39

Nicotinic antagonist is? for Muscarine?

Back 39

Hexamethonium.

Curarine (skeletal muscle) and atropine

Front 40

Alpha adrenergic agonist is? Antagonist?

Back 40

Epi
phenoxybenzamine

Front 41

Beta adrenergic agonist is? antagonist is?

Back 41

epi

propranol

Front 42

Choline esters (enhance cholinergic function.) and the naturally occurring cholinergic stimulants?

Back 42

Acetylcholine, methacholine,
carbachol, Bethanechol
Nicotine, muscarine, pilocarpine

Front 43

Anticholinesterace agents that are reversible?

Back 43

Physo_,Neo_, Pyrido_stigmines
edrophonium, donepezil and tacrine.

Front 44

Irreversible anticholinesterases

Back 44

Parathion, malathion
Sarin and soman

Front 45

Cholinesterase reactivator?

Back 45

pralidoxime (2-PAM)

Front 46

Muscarinic blocking drugs ?

Back 46

I-STABO
Ipratropium, Scopolamine, tropicamide, atropine, benztropine, oxybutynin

Front 47

Ganglionic transmission is by? what blocks it

Back 47

nicotine
Hexamethonium

Front 48

Examples of structures with cholinergic synapses

Back 48

neuroeffector junctions, autonomic ganglia, neuromuscular junction, symp to medulla, sweat glands, CNS

Front 49

Which type are the non-innervated Ach receptors?

Back 49

muscarinic

Front 50

Rate of synthesis of ACh depends on?

Back 50

Pump action to transport it

Front 51

Botulinum toxin does?

Back 51

prevents release of ACh from nerve terminal

Front 52

Latrotoxin does?

Back 52

causes excessive fusing of the granules with nerve membrane (all the ACh gets released into the cleft).

Front 53

where are the Muscarinic receptor types each found?

Back 53

M1: Autonomic ganglia
M2: heart
M3: peripheral autonomic organs and glands, blood vessels
others are in gi. and all are in the CNS

Front 54

Hemicholinium does?

Back 54

blocks transport of choline (thus decreasing choline function

Front 55

what does Muscarinic receptor activation do the heart?

Back 55

Slow heart rate by increasing K permeability-->increase phase 4 depolarization. (does not affect ventricular contraction

Front 56

what does Muscarinic receptor activation do to the Vascular smooth muscle?

Back 56

Vasodilation and decrease blood pressure (via non-innervated muscarinic receptors)-->release EDRF (NO)

Front 57

EDRF is?

Back 57

Endothelium derived relaxing factor

Front 58

what does Muscarinic receptor activation do to the eye?

Back 58

sphincte muscle of iris and ciliary body-->miosis (constriction) and cyclotonia (spasm of accommodation).

Front 59

what does Muscarinic receptor activation do to the GI?

Back 59

increase tone and motility (lower esophageal sphincter is stimulated)

Front 60

what does Muscarinic receptor activation do to the bronchiolar smooth muscle?

Back 60

constriction

Front 61

what does Muscarinic receptor activation do to the Secretory glands?

Back 61

all glands seem to secrete.

Front 62

what does Muscarinic receptor activation do to the CNS?

Back 62

Undetermined

Front 63

Where do ACh receptors get affected by Nicotine?

Back 63

NMJ
Autonomic ganglia
Adrenal medulla: (chromaffin cells)
CNS

Front 64

what affects do choline esters have on salivation?

Back 64

increase: also SLUD (include also Miosis, decrease BP and cause vomiting) so not used much

Front 65

ACh as a drug?

Back 65

not very effective, does not last long. low doses affect Muscarinic receptors, high also get nicotinic receptors

Front 66

Methacholine affect differs from ACh by?

Back 66

longer lasting, muscarinic selective (not used because generalized effects

Front 67

Carbachol structure is?

effects? uses?

Back 67

ACh with an NH2

Nicotinic selective miosis in eye

Front 68

Bethanechol strucute is?

effects receptors?

Back 68

ACh with methyl and NH2 groups.

Muscarinic effect

Front 69

Bethanechol uses?

Back 69

treat post-operative urinary retention and atony of GI tract, and to treat esophageal reflux

Front 70

What are teh 3 naturally occuring Cholinergic stimulants?

Back 70

All alkaloids: Nocotine, muscarine, and pilocarpine

Front 71

Muscarine antidote is?

Back 71

atropine

Front 72

Pilocarpine used for?

Back 72

Glaucoma tx

Front 73

ACHASE inhibitors main use is?

Back 73

tx of myasthenia gravis and glaucoma
for antidote to curare

Front 74

Physostigmine is useful for?

Back 74

tx of atropine poisoning.

Front 75

Which ACHASE inhibitors can cross blood brain barrier?

Back 75

Physostigmine, donepezil and tacrine

Do not: Neostigmine,

Front 76

Neostigmine is used for

Back 76

tx myasthenia gravis (used with atropine)

Front 77

Pyridostigmine is for?

Back 77

Myasthenia gravis

Front 78

Edrophonium is used for?

Back 78

to determine dose of other drugs to be used for M.G. (because it only works for a few minutes) this helps avoid ACHASE inhibition too much (cholinergic crisis) and insufficient ACHASE inhibition (myasthenic crisis)

Front 79

Donepezil and tacrine used for?

Back 79

tx of alzheimer's disease

Front 80

Pralidoxime is used for?

Back 80

ACHASE reactivation (tx. of overdose of anti ACHASEs

Front 81

how does atropine differ from scopolamine?

Back 81

Atropine: CNS excitation. low doses (in CNS) cause a paradoxical bradycardia through vagal stimulation
Scopo: depression

Front 82

how does tropicamide differ from atropine and scopolamine?

Back 82

shorter lasting effect so it is better for use with ophthalmic exams.

Front 83

ipratropium is used for?

Back 83

bronchodilator. second line drug for tx. beneficial when used with other drugs.

Front 84

Benztropine is used for

Back 84

CNS intimuscarinic drug (parkisons tx)

Front 85

Oxybutynin is for?

Back 85

tx spasms of bladder

Front 86

Hexxamethonium is for

Back 86

ganglionic blockade (only use experimentally right now)

Front 87

if a person is given nicotine, it does?

Back 87

block autonomic ganglia (b/c it sustains post ganglionic depolarization)

Front 88

which systems have predominant sympathetic tone?

Back 88

Arterioles, veins, and sweat glands

Front 89

which have predominant parasympathetic tone

Back 89

heart, iris, ciliary muscle, GI (and Urinary), salivary

Front 90

how does curare differ from succinylcholine?

Back 90

Curare is competative inhibitor to stop movement at NMJ
Succinylcholine is sustained depolarization (thus stopping movement)

Front 91

Tetrodotoxin is for?

Back 91

stop nerve action potential (stops Na+ transport)

Front 92

Batrachotoxin is for?

Back 92

stop nerve action potential by opening K+ channels

Front 93

Hemicholinium does?

Back 93

blocks reuptake of choline

Front 94

Botulinus toxin does?

Back 94

blocks ACh release

Front 95

Antibiotics can do to ACh?

Back 95

stop its release

Front 96

How to enhance ACh release?

Back 96

Latrotoxin, catecholamines (epi/NE)

Front 97

Snake alpha-bungarotoxins do?

Back 97

irreversibly inhibit binding of ACh to receptor

Front 98

competitive NMJ blocking drugs affect first?

Back 98

smaller muscles then larger. recovery is in the reverse order

Front 99

what % of receptors must be blocked to lose fuction of NMJ?

Back 99

75%

Front 100

NMJ blocker from indians? its main side effect is ?

Back 100

curare (d-tubocurarine)

hypotension:blockade of autonomic gangla and releaes of histamine

Front 101

Doxacurium is?

(excreted by?)

Back 101

long acting curare-like drug that does not block autonomic ganglia (but does block NMJ)

(2/3 by liver)

Front 102

Pancuronium does?

(excrete by)

Back 102

same as curare without side affects of hypotension and bronchoconstriction (kidney)

Front 103

Atracurium is

Back 103

competetive NMJ blocking drug and releases histamine

Front 104

vecuronium differs from pancuronium by?

Back 104

effect is half as long but more potent and is highly metabolized

Front 105

Mivacurium is good because?

(metabolized by?)

Back 105

shortest duration and is competitive

(plasma cholinesterase)

Front 106

only way to sustain block of muscle function is?

Back 106

sustained depolarization?

Front 107

what is the only clinically used drug for sustained depolarization of muscles?

Back 107

succinylcholine

Front 108

succinylcholine lasts?

Back 108

5 min because of plasma and liver pseudocholinesterases

Front 109

succinylcholine side affects?

Back 109

histamine, stimulates autonomic ganglia, increaes BP and bradycardia
in rare cases: malignant hyperthermia. increases pressure in eye, CSF, and GI

Front 110

when is succinylcholine contraindicated?

Back 110

glaucoma, brain tuors, and after meals

Front 111

Spasmolytics are

Back 111

drugs used to tx muscular spasm associated with stroke, multiple sclerosis and cerebral palsy
to decrease activity of motorneuron flow

Front 112

Diazepam aka? it is for?

side effect is?

Back 112

valium Gaba inhibition (CNS)

at levels needed can cause sedation

Front 113

Baclofen aka? unique because

Back 113

Lioresal. is only effective orally taken agonist for presynaptic CNS GABAb receptor

Front 114

Tizanidine aka? Does?

Back 114

Zanaflex: clonidine-like: alpha stimulant-->decrease spasticity by CNS inhibition. it has less hypotension

Front 115

Cyclobenzaprine aka? used for?

Back 115

flexeril: short term tx of spasms

Front 116

Dantrolene aka? does? side effects?

Back 116

Dantrium: interfere with excitation-contraction coupling in muscles (blocks Ca release)

causes muscle weekness and sedation

Front 117

Dantrolene is for tx of?

Back 117

malignant hyperthermia

Front 118

Botulinum is for?

Back 118

tx more generalized spastic disorders (cerebral palsy)

Front 119

competitive NMJ blocking drugs?

Back 119

D-tubocurarine, doxacurium (Neuromax), Pancuronium (pavulon), Atracurium (tracrium), Cisatracurium (Nimbex), Vecuronium (Norcuron), Mivacurium (Mivacron)

Front 120

Depolarizing NMJ blocking drugs?

Back 120

succinylcholine (anectine)

Front 121

Spasmolytic drugs?

Back 121

diazepam (valium),
Baclofen (lioresal),
Tizanidine (anaflex)
Cyclobenzaprine (flexeril)
Dantrolene (dantrium)
Botox

Front 122

Catecholamines are

Back 122

Epi, NE, Isoproterenol, dopamine

Front 123

Non-chatecholamine alpha sympathomimetics include (6)?

Back 123

1. tyramine, 2. amphetamine, 3 methamphetamine, 4. methylphenidate, 5. ephedrine, 6. phenylephrine

Front 124

Beta agonsts?

Back 124

terbutline, albuteral, salmeterol, ritrodrine, dobutamine

Front 125

Sympathomimetics that inhibit reuptake?

Back 125

Cocaine, tricyclic antidepressants,

Front 126

CNS acting sympatho-inhibitory agents?

Back 126

clonadine, and alpha methyl dopa

Front 127

Alpha antagonists?

Back 127

phentolamine, phenoxybenzamine, pra_,Doxa_, and tera_zosins

Front 128

Beta blockers?

Back 128

propranolol, metoprolol, atenolol, pindolol, timolol, esmolol.
Please make all pindexes timely and esthetic

Front 129

alpha and beta blockers?

Back 129

labetalol and carvedilol

Front 130

how is epi made?

Back 130

tyrosine-->DOPA-->Dopamine-->NE-->epi

Front 131

how does epi differ form NE?

Back 131

Epi: hormonal control
NE: neuronal

Front 132

rate limiting step in epi formation

Back 132

tyrosine to dopa (all other steps can be inhibited by 90% plus without altering rate of synthesis)

Front 133

When NE is released into a synaptic cleft, what else is released?

Back 133

ATP, chromogranin, and dopamine beta-hydroxylase

Front 134

COMT vs. MAO?

Back 134

COMT: post synaptic cell (uptake 2)
MAO: pre synaptic cell (uptake 1)
both in liver and used for NE breakdown. (but 90% goes back into presynapctic cell to be used again)

Front 135

how test for Pheochromocytoma?

Back 135

look for VMA in urine

Front 136

Beta 1 receptors are located?

why are they unique?

Back 136

heart and JG apparatus

only ones innervated!

Front 137

which drugs are direct action on receptors?

Back 137

TARDS, and epi, Ne, dopamine and isoprterenol.
Phenylephrine, and methoxamine

Front 138

Indirect action on sympathemomimetics/

Back 138

tyramine, amphetamine, methamphetamine, methylphenidate, ephedrine

Front 139

Isoproterenol is used for?

Back 139

increase dilation of bronchioles (because is selective for Beta receptors)

Front 140

Dopamine is for? can be used to tx?

Back 140

1. sythesis of epi and NE in peripheral 2. Pyramidal motor system (its defect leads to parkinsons)

renal insufficiency

Front 141

What does tyramine need in order to function?

Back 141

causes release of NE (it is indirect method) so it requires NE.

Front 142

amphetamines can only be used for?

sideaffects?

Back 142

Narcolepsy and ADHD

CNS excitation and convulsions (large doses)

Front 143

Methylphenidate is aka?

Back 143

Ritalin

Front 144

Ephedrine is unique because?

used for?

Back 144

Direct and indirect action

asthma, decongestion of nose and ears
Short lasting mydriasis without cycloplegia

Front 145

Phenylephrine aka?

uses?

Back 145

neo-synephrine.
nasal spray for Alpha receptors causing nasal constriction (decrease runny nose)

Front 146

Terbutaline is like?

uses?

Back 146

metaproterenol but has higher cardiac side effects

prevent premature birth

Front 147

Ritodrine is used for?

Back 147

delay premature labor (taken orally)

Front 148

Dobutamine does?

Back 148

Beta 1 receptors (not dopamine receptors)
increases cardiac output without vasoconstriction

Front 149

uses of dobutamine?

Back 149

short term tx of cardiac insufficiency (organic heart diseaes or cardiac surgery)

Front 150

what 2 drugs prevent reupake of NE?

Back 150

Cocaine and tricyclic antidepressants

Front 151

what are teh adrenergic blockers?

used for tx of?

Back 151

Clonidine and alpha methyl dopa

High BP (decrease sympathetic tone)