Only The Drugs

Front 1

Succinylcholine

Back 1

neuromuscular blocking agentused for surgery and tofacilitate tracheal intubation.

Slow contintuous IV push

Bindingof succinylcholine to the nicotinic acetylcholine receptor results in opening of thereceptor's cationchannel. A disorganized depolarizationof the motor end plate occurs and calcium isreleased.

Front 2

Butyrylcholinesterase(BChE)

Back 2

wasfound to be responsible for the prolongation of action of the muscle relaxantsuccinylcholine.

Mutantalleles at the BCHE locus are responsible for succinylcholine sensitivity.

Front 3

Cocaine

Back 3

a pyschostimulant drug of abuse

induces local anesthesia and vasoconstriction so that it diminishes bleeding

metabolizedby hepatic esterasesand plasmabutyrylcholinesterase.

Front 4

N-acetyltransferase(NAT)

Back 4

The first recognized drug toxicity associated with slow acetylator status

Front 5

Isoniazid

Back 5

Pharmacogeneticsof Isoniazid. Variation in the N-acetyltransferase genedivides people into “slowacetylators” and “fast acetylators”.

Front 6

Primaquine

Back 6

Mechanism of Action

Generation of active oxidation products.

Toxicityand Side Effects

Prototype example of drug thatcauses hemolytic anemia in patients with glucose-6-phosphate dehydrogenase deficiency

Front 7

Glucose-6-Phosphate DehydrogenaseDeficiency

Back 7

is agroup of hereditary abnormalities in which the activity of the erythrocyte enzymeG-6-PD is markedly diminished. Such a deficiency may result in hemolyticanemia, particularlyafter the administration of drugs, during infections, possibly during diabeticacidosis, and in the neonatal period.

Primaquineinduces hemolytic anemia. Favism (hemolytic anemia caused by favabean) Neonatal icterus (jaundice) Effects cells other than erythrocytes

Front 8

Azathioprine

Back 8

TPMT metabolizes 6-mercaptopurine and azathioprine, drugs

Front 9

Methotrexate

Back 9

Treats several kinds of cancer, including cancer of the blood, bone, lung, breast, head, or neck. Also treats rheumatoid arthritis and psoriasis (a skin disease).

Front 10

Thiopurine Methyl Transferase (TPMT)

Back 10

metabolizes6-mercaptopurine and azathioprine, drugs that are used for the treatment of childhoodleukemia autoimmune diseases.

Front 11

Deficiency in TPMT

Back 11

Inpeople with a deficiency in TPMT, In 85-90% of affected people, this deficiencyresults from one of three variant alleles. One in 300 people have twovariant alleles. These people need only 6-10%of the standard dose of the drug.

Front 12

Mephenytoin

Back 12

1.Anti-epileptic drug mephenytoin: There are marked differences betweenpopulations with respect to the frequency of poor metabolizers. In East Asian populations (Japanese, Chinese,and Koreans) 18.5% are poor metabolizers.

Front 13

alpha1-antagonists

Back 13

antihypertensive drug

Front 14

insulin

Back 14

diabetes

Front 15

aspirin

Back 15

analgesic

Front 16

opiates

Back 16

analgesic physical dependence

Front 17

Statins

Back 17

reducecholesterol muscle aches/inflammation

Front 18

Toxic Reactive Oxygen Species

Back 18

1.ionizingradiationwith biological molecules as a by-product of cellularrespiration

2.Synthesizedby enzymes in phagocytic cells like neutrophils and macrophages, such as NADPHoxidase

Free radicals react with the fatty acid side chains of lipids in the cell membrane

Front 19

Glutathione

Back 19

Glutathione(GSH) is a tripeptideconsisting ofcysteine-glycine and glutamate (detoxifyingagent) .

GSH is an antioxidantnucleophilic scavenger

Depletion of Glutathione during Oxidative Stress

Front 20

Acetaminophen

Back 20

Acetaminophenis the active ingredient on Tylenol.Tylenolis a commonly used an over-the-counter drug. Acetaminophen lowersfevers and diminishes headache pain, but it is NOT an anti-inflammatory substance.

also safer forhemophiliacs and children than aspirin.

Front 21

Adverse Acetaminophen

Back 21

Acetaminophen has a narrow therapeutic index. The common dose is close to the overdose, making it arelatively dangerous substance.

Acetaminophenoverdosescan lead to liver failure and death withindays. Because of the wide over-the-counter availability of the drug,it is sometimes used in suicide attempts.

Front 22

N-acetyl-p-benzoquinoneimine (NAPQI)

Back 22

NAPQI depletesthe liver's glutathione, leading to liver failure, Lipid oxidation, Oxidation of Ca++-ATPase proteins

Leading to hepatic cell death

Risk factors for toxicity include excessive chronic alcohol intake, fasting anorexia

Front 23

Thalidomide

Back 23

Thalidomide was developed in Germany in the 1950’s. It was prescribed as a sedative,tranquilizer and antiemetic drug for morning sickness.

Phocomelia

Front 24

Diethylstilbestrol (DES)

Back 24

DES is a synthetic nonsteroidalestrogen synthesized in 1938 and classifiedas an endocrinedisruptor. From 1940-1970, DES was given to pregnant women in the mistakenbelief it wouldreduce the riskof pregnancy complications and miscarriage.

In 1971, DESwas shown to causea rare vaginal tumor in females who had beenexposed to this drug in utero.

Front 25

Mercury

Back 25

Mercury isconsidered by many to be even more toxic than lead.

Although mercury ispoorly absorbed from the gastrointestinal tract, mercury vapor is easily takenin through the lungs and readily passes into the brain, liver, and especially thekidneys.

Front 26

Metallothionine

Back 26

Metallothionineis a cysteine-rich protein produced by the liver to bind heavy metals andprotect other proteins in the body

Front 27

ELIXIRSULFANILAMIDE

Back 27

commoncomponent of antifreezeand a known toxin.

Over 100people diedafter takingthis medication and many werechildren. The public outcry reshaped the drug provisions of a law to prevent such an event from recurring. In 1938 President FDRoosevelt signed the Food,DrugandCosmetic Act.

Front 28

Methadone

Back 28

–oncedaily oral dose—no injection needed

–suppresseswithdrawal and reduces craving

–patientscheat to get faster, higher rush

–communitycomplaints about traffic around centers

Front 29

LAAM

Back 29

–oraldose 3 times per week

–suppresseswithdrawal and reduces craving

–cardiovasculareffects—removed from use in Europe•

Front 30

Antagonisttherapy

Back 30

–Usedto prevent relapse—cannot cheat•naltrexone & antibodies

Front 31

Naltrexone

Back 31

–competitivelyblocks agonist effects

–precipitateswithdrawal

–notoften used for opioid abuse—same problems as for alcohol: general anhedonia

Front 32

Antibodies

Back 32

–body’simmune system destroys compound

–cancheat by using drug from different structural class

Front 33

Catacholamines

Back 33

Epinephrine α1+ β2+β1

Norepinephrine α1 + β1

Isoproterenol β2+ β1

Dopamine β1

Dobutamine β1

Front 34

Non-Catecholamines

Back 34

ARE Direct-ActingAgonists

Albuterol, LABAs, Apraclonidine , Clonidine ,Midodrine, Oxymetazoline,, Phenylephrine, Ritodrine

Imidazaline actions: Apraclonidine and clonidineDominantAlpha 2 actions: clonidine, apraclonidineDominantBeta 2 actions: Albuterol (asthma), ritrodrine (labor)Dominantalpha 1 actions:oxymetazoline, phenylephrine, midodrine

Front 35

a1

Back 35

Phospholipase C activation; increased IP3; Ca2+ release

Contract smooth muscles; exocrine gland secretion; neuronal excitation

smooth muscle, iris dilator muscle, smooth muscle of urinary bladder

Front 36

a2

Back 36

a2 Inhibition of adenylyl cyclase; decreased cAMP

Inhibition of norepinephrine release; decreases secretion of aqueous humor; decreased insulin secretion; platelet aggregation; CNS effects

cause feedback inhibition of NorEpi release, on platelets, activation mediatesaggregation, in pancreas, mediate inhibition ofinsulin secretion

Occurs when sympathetic nervoussystem is activated

Front 37

b1

Back 37

b1 Adenylyl cyclase activation; increased cAMP; protein kinase activation

Increased heart rate, contractility, and conduction. Increased secretion of renin

oPositive chronotrophic effect (Ý heart rate), oPositive ionotropic effect (Ý contractility), oPositive dromotropic effect (Ý cardiac impulse conductionvelocity),

Front 38

b2

Back 38

b2 Adenylyl cyclase activation; increased cAMP; protein kinase activation

Glycogenolysis; relaxation of smooth muscles; uptake of potassium by skeletal muscles

relaxation of certain smooth muscles: bronchial, uterine, vascular

Front 39

b3

Back 39

b3 Adenylyl cyclase activation; increased cAMP; protein kinase activation

b3 lipolysisof triglycerides in adipose tissue

Front 40

NorEpi

Back 40

activatesa1-receptors vasoconstriction Ý peripheral resistance Ý systolic AND diastolic bloodpressure

Front 41

Epi

Back 41

activatesa1- AND b2-receptors

Ý systolic blood pressure (Ýheart rate & Ý cardiac output) may EITHER increase OR decrease diastolicpressure

low doses ß due to vasodilation (b2-mediated) high doses Ý due to vasoconstriction (a1-mediated)

Front 42

Isoproterenol

Back 42

activatesb1 AND b2 Ýcardiac stimulation WITHvasodilation

Front 43

Amphetamine

Back 43

Indirect-actingadrenergic agonists

–Highlylipophilic–

Ýsynaptic NorEpiin both CNS & PNS

•Vasoconstriction,cardiac stimulation & Ýbloodpressure

Front 44

Tyramine

Back 44

Indirect-actingadrenergic agonists

–foodsources, normally degraded by MAO in gut

–Onlya problem if MAO inhibitors are used•Ýbloodpressure

Front 45

Ephedrine

Back 45

Mixed-actingadrenergic agonists

–Absorbedwell in gut–Lipophilic(enters the CNS), & is MAO resistant–Durationof action is several hours

Front 46

Pseudoephedrine

Back 46

Mixed-actingadrenergic agonists

•(isomerof ephedrine)

–Nasaldecongestant (via a1vasoconstriction)

Front 47

•Adverse (both ephedrine & pseudoephedrine)

Back 47

–Tachycardia(via b1)

–Ýblood pressure

–Urinaryretention

Front 48

Doxazosin

Back 48

(likeprazosin) selective alpha1 blocker forhypertension

Front 49

Tamsulosin

Back 49

uroselective alpha 1 blocker for BPH

Front 50

Alfuzosin

Back 50

uroselective alpha 1 blocker for BPH

Front 51

Antagonist Therapeutic& Adverse Effects

Back 51

Therapeuticeffects of adrenergic antagonists involve blocking a1- and/or b1- receptors

a1-blockade: relaxes smooth muscle

b1-blockade: reduces sympathetic

stimulation of the heart

Adverseeffects of adrenergic antagonists involve blocking a2- and/or b2-receptors

Front 52

Doxazosin

Back 52

a selective alpha1-blocker, does notblock alpha2-adrenoceptor-mediated inhibition of norepinephrine release.Therefore, doxazosincauses less tachycardia than does phentolamine.

Front 53

DOPAMINERECEPTOR AGONISTS

Back 53

L-DOPA (3,4-dihydroxyphenylalanine) –dopamine precursor; highly effective; absorption is protein meal dependent

Bromocriptine (PARLODEL) - ergot alkaloid, some selectivityfor the D2 subtype

Ropinirole (REQUIP) – some selectivity for D2subtype. Can induce sudden sleep.

Pramipexole (MIRAPEX) – some selectivity for the D3subtype. Has other actions.

Rotigotine (NEUROPRO) – non-ergot. Transdermal patchused to treat restless leg syndrome.

Apomorphine (APOKYN) – a D2-like (D2, D3, D4) fullagonist

Front 54

AROMATIC AMINO ACID DECABOXYLASE(AAAD) INHIBITORS

Back 54

Carbidopa (called SINEMET when combined with L-DOPA) – peripheral AAAD inhibitor

Front 55

CATECHOLAMINE-O-METHYLTRANSFERASE(COMT) INHIBITORS (relates to L-DOPA treatment)

Back 55

Tolcapone (TASMAR) Entacapone (COMTAN)

Front 56

MONOAMINEOXIDASE B (MAO-B) INHIBITORS (relates to L-DOPA treatment)

Back 56

Selegiline (DEPRENYL OR ELDEPRYL) – only selective for MAO-B atlower concentrations.

Rasagiline (AZILECT) – very potent and selective

NOTE: Risk of hypertensive crisis when given with large doses of L-DOPA

Front 57

ANTI-GLUTAMERGICS(maybe a dopamine releaser too)

Back 57

Amantadine (SYMMETREL) - weak NMDA receptor antagonist (also a dopamine releaser)

NOTE: contraindicated in those at risk for seizures or congestive heart failure

Front 58

ANTI-CHOLINERGICS(muscarinic receptor antagonists)

Back 58

Trihexyphenidyl (ARTANE) Benztropine (COGENTIN)

NOTE: contraindicated in co-morbid AD, open angle glaucoma,gastrointestinal disease and prostatic hyperplasia

Front 59

Parkinson’s diseaseTreatments

Back 59

Thedopamine precursor L-DOPA activelytransported across gut and brain barriers by aromatic amino acid transporter. Theenzyme aromatic amino acid decarboxylase (AAAD) converts the dopamineprecursor, L-DOPA, to dopamine and AAAD is localized in both the periphery andin the central nervous system toprevent peripheral conversion L-DOPA is administered in combination with an AAADinhibitor that cannot cross the BBBleading to proportionally higher concentrations of dopamine in the brain. Carbidopa isan example of a peripheral AAAD inhibitor.

Front 60

Catechol-O-methyltransferase(COMT)

Back 60

1.AAADinhibition results in up regulation of the enzyme Catechol-O-methyltransferase(COMT)which increases levels of 3-methyoxydopa (3-MODA). Increased 3-MODA results in competition for L-dopa active transport acrossintestine and brain barriers, but it does not activate dopamine receptors.

Front 61

COMTinhibitors

Back 61

tolcapone and entacapone

Front 62

MAO-Binhibitors

Back 62

MAOB inhibitors slow the metabolisms of dopamine

Front 63

Selegiline

Back 63

isa selective MAO B inhibitor only at lower doses

Front 64

Rasagiline

Back 64

1.is a more selective MAO-B inhibitors than Selegiline and is more potent.

Front 65

MAO-inhibitors Adverse

Back 65

A.Givinga non-selective MAOI with L-DOPA can lead to a hypertensive crisis.

B.Acutetoxic interactions with tricyclic antidepressants, meperidine or 5-HT reuptakeinhibitors since can cause serotonin syndrome.

Front 66

Anticholinergics

Back 66

Drug treatments for PD

(useful in early stages of PD)

tonicinhibitory dopaminergic control of cholinergic interneurons in striatum is lostin PD and blocking muscarinic receptors prevents the overactivity of the cholinergic interneurons

Front 67

Levodopa

Back 67

Drug treatments for PD

(L-DOPA) – a dopamine precursor that restores thelost dopamine. Given in combination with carbidopa.

Front 68

Amantadine

Back 68

Drug treatments for PD

– an antiviral agent that also actsas a weak antiglutamatergic (reduces glutamatergic excitation).

Front 69

. MAO-B inhibitors

Back 69

Drugtreatments for PD

prolong the actions of dopamine, bypreventing is degradation.

Front 70

Tacrine and Donepezil

Back 70

Alzheimer’s Disease Treatment

arereversible AChEinhibitors, whichis in contrast to irreversible AChE inhibitors that are toxicinsecticides or chemical warfare agents

Front 71

DOPAMINERECEPTOR ANTAGONISTS

Back 71

Anti-Huntington’sDisease Drugs

Haloperidol (HALDOL)

– D2 receptor antagonists (andacts on other D2-like receptors and Sigma-1 receptors); suppresses dyskinesia but may enhance rigidity; also usedto treatpsychosis if present.

Front 72

GABARECEPTOR POTENTIATOR

Back 72

Anti-Huntington’sDisease Drugs

Diazepam(VALIUM)

– GABA-A receptor allosteric potentiator of GABA responses; alleviatesdyskinesias; also used to treatanxiety but abuse and addiction potential

Front 73

MONOAMINESTORAGE DEPLETER

Back 73

Anti-Huntington’sDisease Drugs

Tetrabenazine (XENAZINE)

– a vesicular mononamine transport (VMAT) inhibitor; suppressesdyskinesia;potential to increase risk of depression.

Front 74

REVERSIBLEACETYLCHOLINE ESTERASE INHIBITORS (rAChEI)

Back 74

Anti-Alzheimer’sDisease Drugs

Tacrine (COGNEX) – may also facilitate AChrelease. Potential heptotoxicity.

Donepezil (ARICEPT) – long half life, highlyselective for CNS AChE

Rivastigmine (EXELON) – long lasting, CNS selective Galantamine (RAZADYNE) – natural product; derived fromthe bulbs of daffodils

Front 75

ANTI-GLUTAMATERGIC

Back 75

Anti-Alzheimer’sDisease Drugs

Front 76

Amyotropic Lateral Sclerosis (ALS)

Back 76

amotor disorder due to death of spinal alpha motor neurons (in anterior horn)and cortical neurons in the motor cortex and the tracts they form (corticospinal and corticobulbar).Senses and mental function are typically intact.

Front 77

Multiple Sclerosis (MS)

Back 77

an inflammatory autoimmune centralnervous system disorder affecting myelinated nerve fibers with a variablecourse and severity and phase presentation (often periods of remission andrelapse).

Front 78

Sclerosis

Back 78

means scaring and in these cases the meaning is specificallyglia scaring. In other words, glia replace the lost motor neurons in the caseof ALS and replace the myelinatedsheath in the case of MS

Front 79

GABAUPTAKE BLOCKER

Back 79

Anti-AmyotropicLateral Sclerosis

Riluzole (RILUTEK)

– multiple and complex mechanismsof action: blockGABA uptake; increase glutamate uptake and inhibits (presynaptic) glutamate release;block voltage-dependent sodium channels.

Front 80

GABA-BRECEPTOR AGONIST

Back 80

Anti-AmyotropicLateral Sclerosis

SPASMOLYTIC DRUGS

Baclofen (LIORESAL)

– metabotropic GABA-B receptoragonist; spasmolytic with low sedation potential; p-chlorophenyl-GABA; off label use for reducingcravings for alcohol.

Front 81

PRESYNAPTICCALCIUM CHANNEL BLOCKER

Back 81

Anti-AmyotropicLateral Sclerosis

SPASMOLYTIC DRUGS

Gabapentin(NEURONTIN)

– multiple complex mechanisms ofaction: facilitationof GABA release; reduction of glutamate release. Both effectslikely mediated via antagonism of predominately presynaptic N-typevoltage-dependent calcium channels. Itdoes not act directly in GABA receptors despite it being a GABA analogue.

Front 82

GABA-BRECEPTOR AGONIST

Back 82

Anti-Multiple Sclerosis Disease DrugsSPASMOLYTIC DRUGS

Baclofen (LIORESAL)

– metabotropic GABA-B receptoragonist; spasmolytic with low sedation potential; p-chlorophenyl-GABA; off label use for reducingcravings for alcohol.

Front 83

ALPHA-2AGONIST

Back 83

Anti-Multiple Sclerosis Disease DrugsSPASMOLYTIC DRUGS

Tizanidine (ZANAFLEX)

– α2adrenergic receptor agonist; antinocioceptive when used as an epidural

Front 84

STEROIDS

Back 84

Anti-Multiple Sclerosis Disease Drugs

ANTI-INFLAMMATORY / IMMUNOSUPRESSANT DRUGS

Prednisone(PREDNISONE INTENSOL) – Glucocorticoid receptor agonist

Front 85

CYTOKINES

Back 85

Anti-Multiple Sclerosis Disease Drugs ANTI-INFLAMMATORY / IMMUNOSUPRESSANT DRUGS

Interferon Beta-1b (BETASERONE, EXTAVIA) – Type I interferon receptoragonist

Front 86

Schizophrenia

Back 86

psychiatric disorder presentingbroadly as a disrupted ability to accurately interpret the world around oneself,which results in impaired logical reasoning, impaired organizational, communication andsocial skills, and a loss of motivation. Severity and duration of symptomsusually progressive.

Front 87

NeurolepticMalignant Syndrome

Back 87

Alife-threating disorder! Can be considered an extreme form ofextrapyramidal side effect in those that are hypersensitive. Symptoms include intense muscle rigidity initially, high fever, and altered blood pressure and pulse rate(autonomic instability). It is thought to be due to rapid blockade ofpost-synaptic dopamine receptors. Treat with anti-parkinsonian drugs (e.g., bromocriptine)

Front 88

D2 dopamine

Back 88

Biogenicamine GPCR systems associated with common drug side effects

antagonism

Extrapyramidal Neuroendocrine

Parkinsonism, tardive dyskinesia Male gynecomastia & Amenorrhea

Front 89

Alpha-1 adrenergic

Back 89

Biogenicamine GPCR systems associated with common drug side effects

antagonism

Autonomic

Sexual Orthostatic hypotension, reflex tachycardia Anorgasmia, delayed ejaculation

Front 90

M1 muscarinic

Back 90

Biogenicamine GPCR systems associated with common drug side effects

antagonism

Autonomic CNS

Dry mouth, fecal/urinary retention, blurry vision Mental slowing (confusion)

Front 91

H1 histaminergic

Back 91

Biogenicamine GPCR systems associated with common drug side effects

antagonism

CNS

Sedation

Front 92

Serotonergic(some 5HT1A, more 5HT2A/C)

Back 92

Biogenicamine GPCR systems associated with common drug side effects

agonism

Sexual

Decreased libido, delayed ejaculation

Front 93

Alpha-2 adrenergic

Back 93

Biogenicamine GPCR systems associated with common drug side effects

agonist

CNS

Sedation, muscle relaxant, sexual dysfunction

Front 94

Typical Antipsychotics

Back 94

(D2 receptor antagonist – treats positive symptoms; extrapyramidal& neuroendocrine side effects, risk of tardive dyskinesia)

Front 95

Haloperidol (HALDOL)

Back 95

Typical Antipsychotics

– D2 receptor antagonists (andacts on other D2-like receptors and Sigma-1 receptors), very potent

Front 96

Chlorpromazine (THORAZINE)

Back 96

Typical Antipsychotics

– not that selective over D1-likereceptors or other biogenic amine GPCRs like H1 histamine receptors or alpha-1adrenergic receptors; used in emergency room setting to calm patients withdrug-induced psychosis

Front 97

Thioridazine (MELLARIL)

Back 97

Typical Antipsychotics

– side effects include cardio-and retinotoxicity; substantial anticholinergiceffect; mesoridazine is active metabolite (causesorthostatic hypotension)

Front 98

Atypical Antipsychotics

Back 98

(relatively weaker D2 receptor antagonist – treats positive symptoms;Also 5HT2A/5HT2C antagonist and 5HT1A agonist – treats negative symptoms;metabolic side effects)

Front 99

Clozapine (CLOZARIL)

Back 99

Atypical Antipsychotics

– Side effects include sedationand risk for potentially life-threatening agranulocytosis and seizures

Front 100

Olanzapine (ZYPREXA)

Back 100

Atypical Antipsychotics

– Side effects include sedationand weight gain

Front 101

Molindone (MOBAN)

Back 101

Atypical Antipsychotics

– has many active metaboliteswith long half-lives some with MAO-A inhibitory activity

Front 102

Risperidone (RISPERAL)

Back 102

Atypical Antipsychotics

– side effects includeorthostatic hypotension and extrapyramidal signs at higher doses;contraindicated in those with cardiovascular disease as can cause arrhythmias; Paliperidone is primary active metabolite

Front 103

Aripiprazole (ABILIFY)

Back 103

Atypical Antipsychotics

– A weak partial agonist

Front 104

Tricyclic Antidepressants (TCA):

Back 104

MixedSERT and NET reuptake inhibitors (SNRI)

mixedNET and SERT blockers; side-effects often due to interactions with specificGPCRs (histamine and/or muscarinic and/or adrenergic receptors); TCA refers toa specific type of tricyclic pharmacophore.

Front 105

Amitriptyline (ELAVIL)

Back 105

Tricyclic Antidepressants (TCA):

MixedSERT and NET reuptake inhibitors (SNRI)

has a significant H1 histaminereceptor component (sedation); also used to treat PMS.

Front 106

Clomipramine (ANAFRANIL)

Back 106

Tricyclic Antidepressants (TCA):

Mixed SERT and NET reuptake inhibitors (SNRI)

– also interacts with Sigma-1receptors; also used to treat OCD

Front 107

Venlafaxine (EFFEXOR)

Back 107

Non-Tricyclic Antidepressants

Mixed SERT and NET reuptake inhibitors (SNRI)

– also used to treat generalized anxiety disorder, social phobia and panicdisorder; can increase intraocular pressure so may be contraindicated in thosewith glaucoma; selective for SERT only at lower doses

Front 108

Buproprion (WELLBUTRIN)

Back 108

Non-Tricyclic Antidepressants Mixed SERT and NET reuptake inhibitors (SNRI)

– also used to as a cessation treatment for cigarette smokers; it7-hydroxy metabolite inhibits NET; does not cause sexual dysfunction but doeslower seizure threshold. So may be contraindicated in those with seizuredisorders

Front 109

Duloxetine (CYMBALTA)

Back 109

Non-Tricyclic Antidepressants Mixed SERT and NET reuptake inhibitors (SNRI)

– also used to controlfibromyalgia and diabetic neuropathy

Front 110

Fluoxetine (PROZAC)

Back 110

Selective Serotonin Reuptake Inhibitor (SSRI)

– also used to treat bulimia andOCD

Front 111

Fluvoxamine (LUVOX)

Back 111

Selective Serotonin Reuptake Inhibitor (SSRI)

– also used to treat OCD and PTSD

Front 112

Paroxetine (PAXIL)

Back 112

Selective Serotonin Reuptake Inhibitor (SSRI)

– also used to treat OCD and PTSD

Front 113

Sertaline (ZOLOFT)

Back 113

Selective Serotonin Reuptake Inhibitor (SSRI)

– also interacts with Sigma-1receptors; also used to treat OCD

Front 114

Mirtazapine (REMERON)

Back 114

ATYPICAL ANTIDEPRESSANTS (5HT2A AND 5HT2C RECEPTOR ANTAGONISTS)

– also an alpha-2 antagonist (thus can increase blood pressure)

Front 115

Nefazodone (NEFADAR)

Back 115

ATYPICAL ANTIDEPRESSANTS (5HT2A AND 5HT2C RECEPTOR ANTAGONISTS)

– Structurally similar to trazadone (has a triazopiperizine pharmacophore)

Front 116

Phenelzine (NARDIL)

Back 116

MONOAMINEOXIDASE A INHIBITORS (METABOLIZER OF 5HT, NE AND TYRAMINE)

– irreversible, effects persistfor 2-3 weeks; has a hydrazide pharmacophore; risk of hypertensive crisis; acetylase sensitive metabolism

Front 117

Tranylcypromine (PARNATE)

Back 117

MONOAMINEOXIDASE A INHIBITORS (METABOLIZER OF 5HT, NE AND TYRAMINE)

– reversible but binds verytightly so effects persist for up to 1 week; risk of hypertensive crisis

Front 118

Moclobemide (AURORIX)

Back 118

MONOAMINEOXIDASE A INHIBITORS (METABOLIZER OF 5HT, NE AND TYRAMINE)

– reversible and a short-acting (thus no significant risk of ahypertensive crisis).

Front 119

Lithium(LITHOTAB)

Back 119

ANTI-MANIADRUGS (FOR TREATING THE MANIC PHASE OF BIPOLAR DISORDER OTHERWISE KNOWN ASMANIC-DEPRESSION)

– also a mood-stabilizer; narrow therapeutic window (cardiotoxicity and neurotoxicity); side-effects include folliculitis

Front 120

Carbamazepine (TEGRETOL)

Back 120

ANTI-MANIADRUGS (FOR TREATING THE MANIC PHASE OF BIPOLAR DISORDER OTHERWISE KNOWN ASMANIC-DEPRESSION)

– also a mood-stabilizer

Front 121

Valproate (DEPAKOTE)

Back 121

ANTI-MANIADRUGS (FOR TREATING THE MANIC PHASE OF BIPOLAR DISORDER OTHERWISE KNOWN ASMANIC-DEPRESSION)

– a lipid

Front 122

Amphetamine (ADDERALL)

Back 122

CENTRALNERVOUS SYSTEM STIMULANTS – all the psychostimulantshave potential cardiovascular toxicity

Blocks & reverses DAT/NET also a VMAT2 blocker.

Front 123

Methylphenidate (RITALIN)

Back 123

CENTRALNERVOUS SYSTEM STIMULANTS – all the psychostimulantshave potential cardiovascular toxicity

– A DAT/NET inhibitor

Front 124

Atomoxetine (STRATTERA)

Back 124

CENTRALNERVOUS SYSTEM STIMULANTS – all the psychostimulantshave potential cardiovascular toxicity

– A selective NET inhibitor

Front 125

Benzodiazepines(BZD)

Back 125

were developed to minimize depth ofCNS depression

•someBZDs good sedatives, others anti-epileptic, sedativeamnestic

•maybe able toseparateout addictionliability too.

Anxiety, Sleep disorders, Seizure disorders, Anesthesia adjunct, Withdrawal

Front 126

diazepam(Valium)

Back 126

Benzodiazepines

Agonists

wide range of BZD actions, long-acting

Front 127

chlordiazepoxide(Librium)

Back 127

Benzodiazepines

Agonists

water soluble

Front 128

flumazenil(Romazicon)

Back 128

Benzodiazepines

Antagonists

blocks the effects of BZDs§will precipitate withdrawal inBZD-dependent subjects

Front 129

Barbiturates

Back 129

These drugs see little use due to narrowtherapeutic window and abuse liability

more predictable dose-responseeffects than BZDs , but retained the CNS depression

Front 130

phenobarbital

Back 130

Barbiturates

sleep

Front 131

pentobarbital

Back 131

Barbiturates

seizure disorders

Front 132

zolpidem(Ambien)

Back 132

Non-BZD,Non-barbiturates

used for sleep, acts at W-1subtype

Insomnia

Front 133

zaleplon(Sonata)

Back 133

Non-BZD,Non-barbiturates

used for sleep, acts at α1subunit, short-acting

Insomnia

Front 134

eszopiclone(Lunesta)

Back 134

Non-BZD,Non-barbiturates

Front 135

Serotonergics

Back 135

Use of serotonin receptors

Front 136

buspirone(BuSpar)

Back 136

Serotonergics

mildto moderate GAD and smoking cessation

notuseful for panic or OCD

agonistat 5-HT1Areceptors, which are presynaptic autoreceptors

Front 137

fluoxetine(Prozac)

Back 137

Serotonergics

panicdisorder and obsessive-compulsive disorder

Front 138

clomipramine(Anafranil)

Back 138

Serotonergics

obsessive-compulsivedisorder

Front 139

Melatonin

Back 139

Pineal gland releases melatonin 2 hrsbefore bedtime

–Melatoninuseful for prevention of jet lag, changing shifts

•long-termuse alters fertility (which is diurnal cycle dependent) and worsens movementdisorders

•causesbirth defects if taken during pregnancy

Front 140

ramelteon(Rozerem)

Back 140

Melatonin

•melatoninreceptor agonist

•reducedlatency to sleep without rebound insomnia

•noteffective for long-term use

Insomnia

Front 141

Antihistamines

Back 141

•some cause drowsiness

–newgeneration anti-allergy compounds do not cross blood-brain barrier, so muchless sedation/hypnosis

Front 142

diphenhydramine(Benadryl)

Back 142

Antihistamines

Front 143

hydroxyzine

Back 143

Antihistamines

Front 144

Panicdisorder

Back 144

Recurrent, non-reactive

Terror, doom

fluoxetine

Front 145

GABAa

Back 145

Inhibitory, post-synaptic

powerful and rapid suppression ofexcitation greatly enhances precision of excitatory synaptic transmission

Cl-channel

–GABAagonists decrease anxiety

–GABAantagonists induce anxiety and panic

Front 146

Serotonin

Back 146

–↑ levels related to ↑ increased anxiety

–↓ levels related to ↓ anxiety

Front 147

JMis a 29 year old male who reports he feels stressed and exhausted all the time.He reports persistent worries about potential layoffs at work and eventsoutside work and has taken sick days off work due to these worries.

Back 147

A.generalizedanxiety disorder.

B.panicattacks.

C.obsessive-compulsivedisorder.

D.phobias.

E.post-traumaticstress disorder.

Front 148

Jeanette, a married 52-year-old whitefemale with 2 children, visits her primary careclinician (PCC) for a regularly scheduled checkup. She is perimenopausal,has a BMI of 27, is diabetic, and was diagnosed with an anxiety disorder whilein her mid-20s. She is currently stable and continues to take paroxetine foranxiety. Jeanette states that lately she has been very tired during the day andshe has had increasing trouble trying to sleep. She usually doesn’thave much trouble falling asleep, but awakens several times every night, andoften has difficulty getting back to sleep. Jeanette agrees to take a medication to treat sleep maintenance symptomsof insomnia.

Back 148

A.Zolpidem.

B.Flumazenil.

C.Pentobarbital.

D.Fluoxetine.

E.Buspirone.

Front 149

Whydoes Benadryl knock me out, but Claritin and Allegra don’t?

Back 149

A.diphenhydramine (Benadryl) acts at H1 receptors and loratadine(Claritin) acts at H2.

B.diphenhydramine acts at H3 receptors and loratadineacts at H1.

C.diphenhydramine acts at H2 receptors and loratadineacts at H4.

D.diphenhydramine and loratadinehave different affinities for mast cells.

E.diphenhydramine penetrates into the brain, but loratadinepenetrates poorly.

Front 150

Non-steroidalanti-inflammatory drugs (NSAIDs)

Back 150

Counterthe action of the cyclooxygenase (COX) enzymes which synthesize prostanoids(prostaglandins, prostacyclin, & thromboxane), that cause inflammation

Front 151

Corticosteroids(specificiallyglucocorticoids)

Back 151

Activateglucocorticoid receptors which block expression of inflammatory proteins

Front 152

Aspirin

Back 152

NSAID

analgesic,antipyretic, anti-inflammatory

–aspirincovalently (irreversibly)inhibits COX 1&2

–recoveryof COX in most tissues is by synthesis of new enzyme.

–Plateletscannot synthesize new COX, so inhibition is irreversible.

–otherNSAIDs produce reversibleinhibition of COX.

adverse: GI, Bleeding, Reye's Syndrome swelling of liver and heart

Front 153

Ibuprofen

Back 153

NSAID

Front 154

Naproxen

Back 154

NSAID

Front 155

Ketoprofen

Back 155

NSAID

Front 156

Celecoxib

Back 156

–selectiveCOX-2 inhibitor

–Significantlyfewer GI ulcers

–Donot effect platelets and bleeding time

–Expensive

–Associatedwith an increased risk of serious adverse Cardio Vascular event

Front 157

Acetaminophen

Back 157

–Non-NSAID•Non-narcoticanalgesic & antipyretic

•Welltolerated, lacks GI and platelet side effects, NO Reyes Syndrome

•Usefulanalgesic, antipyretic for children and those with contraindications to aspirin

–preferredto NSAIDs as cheaper, and fewer adverse effects

Front 158

Cyclooxygenase

Back 158

•AllNSAIDS inhibit the enzyme cyclooxygenase(COX).

•Cyclooxygenaseis a key enzyme responsible for the synthesis of prostaglandins.

•Prostaglandinscontribute to a number of inflammatory processes.

Front 159

COX-1inhibitors

Back 159

reducefever and inflammation

produceulcers and cardiac side effects

aspirin,naproxen, and ibuprofen COX-1 > COX-2

Front 160

COX-2inhibitors

Back 160

reducefever and inflammation

reducedulcers BUT produce cardiac side-effects

celecoxib, rofecoxib, andvaldecoxib COX-2 >> COX-1

Front 161

Opioids

Back 161

–respiratorydepression.

–developmentof physical tolerance/dependence.

Front 162

Prednisone

Back 162

–syntheticcorticosteroid (highly lipophilic)

–greaterpotency than cortisol

–powerfulbroad-spectrum immunosuppressant–prodrug forprednisolone (the active form) •convertedto prednisolone in liver

AdverseEffects suppression, dependence, withdraw

Front 163

beta-lactams

Back 163

inhibittranspepidation thatresults in cross-linking.

Front 164

erythromycin

Back 164

causesan inhibition of translocation.

Front 165

penicillins

Back 165

inhibittranspepidation thatresults in cross-linking.

Front 166

streptomycin

Back 166

causesa misreading of mRNA

Front 167

tetracycline

Back 167

competitionwith tRNA forA site on ribosome.

Front 168

cephalosporin

Back 168

inhibittranspepidation thatresults in cross-linking.

Front 169

methotrexate

Back 169

An antimetabolite that inhibits the conversion of folicacid to tetrahydrofolic acid by binding to the enzyme dihydrofolatereductase.

The result is an inhibition of thymidine synthesis

Acute lymphocytic leukemia in children

Front 170

puromycin

Back 170

causes a premature termination of thepeptide chain.

Front 171

sulfonamides

Back 171

inhibit the synthesis of folate in bacteria. Sulfonamides are bacteriostatic

Front 172

trimethoprin

Back 172

afolateantagonist.

Front 173

delavirdine

Back 173

Mechanism

1. Binds to the lipohilic pocket of RT to allosterically distort the polymerase active site. 2. Acts synergistically with NRTIs

3. Inhibits the P-450 system, so decreases the metabolism of protease inhibitors.

Side Effects:Rash (not as sever as with Nevirapine) Resistance:Rapid if given alone Decreased rate of resistance if givenwith NRTIs

Front 174

indinavir

Back 174

Side Effects (ProteaseInhibitors)

increase bilirubin without other hepaticabnormalities and nephrolithiasis due to crystallizationof drug in urine

Front 175

saquinavir

Back 175

Side Effects (ProteaseInhibitors)

mild diarrhea,abdominal discomfort and nausea

low bioavailability (4-5%)/metabolized by P-450 co-administration with rifamycinor cabamazepine can further decrease plasma concentrations.

Front 176

zidovudine(AZT)

Back 176

analogue of the pyrimidine thymidine

inhibitor of reverse transcriptase.

Treatment of AIDSand AIDS related symptoms,

reducesthe risk of transmission

Front 177

interferona2b

Back 177

areinducible proteins synthesized by mammaliancells.

Interferons areinvolved in cell growth, regulation and modulation of the immuneresponse.

Classifiedas immunomodulators

Front 178

nevirapine

Back 178

Treatmentof AIDS and AIDS related symptoms

Prevention of transmission of HIV virus from infected mothers to newborns

Front 179

ritonavir

Back 179

Side Effects (ProteaseInhibitors)

nausea,vomiting and diarrhea

elevated hepatic aminotransferase andtriglyceride levels

inhibits CYP3A4, leading to decreasedmetabolism of other drugs

Front 180

nelfinavir

Back 180

Side Effects (ProteaseInhibitors)

diarrhea,asthenia, headache and moderate hypertension

Front 181

ribavirin

Back 181

adenosine/guanosineanalogue.

Usedto treat viral respiratory infections including influenza, respiratory syncytialvirus (RNA paramyxovirus)

Used to treat early stages of Lassa fever, an arenovirus infection.

Front 182

cyclophosphamide

Back 182

Alkylating agents

Cyclophosphamide is a most widely used nitrogen mustard. broad spectrum

neuroblastomas, lung cancer, ovarian, cervical, and testicular cancer

Front 183

methotrexate

Back 183

Antimetabolites

Acute lymphocytic leukemia in children

immunosuppressive agent inbone marrow and organ transplantation procedures

treatnon-Hodgkin's lymphomas and breast cancer

embryological effects; also used to treat severepsoriasis

Front 184

vincristine and vinblastine

Back 184

Vinca Alkaloids

Mitotic Spindle Poisons

childhood acute leukemias & Hodgkin's and Non-Hodgkin’slymphomas

Toxicity:neuropathy, severe constipation, leukopeniaand GI disturbances

Front 185

prednisone

Back 185

Corticosteroids

Usedin the treatment of migraine and cluster headaches severe cankersore ofthe mouth ulcer Lymphoidtumors

Toxicity; Cushingsyndrome/weight gain osteoporosis, glaucoma, cataracts, Type II diabetes

Front 186

tamoxifen

Back 186

Antiestrogens

Tamoxifen binds to estrogen receptors (ER) causing them to bind tightly totheir DNA target sites but doesnot elicit the normal gene expression response. At high concentration thiseffectively blocks any estrogenmediated responses. breast cancer

Toxicity; ovariandysfunction, premature osteoporosis and cardiovascular disease.