D2 - Pharm Exam #2

Front 1

Methacholine

Back 1

• Choline ester Specific ONLY for muscarinic receptors

Front 2

Carbachol

Back 2

Direct Acting Cholinergic Agonist
• Resistant to AChE (longer duration)

Front 3

Bethanechol

Back 3

• Resistant to AChE (longer duration) AND
• Specific ONLY for muscarinic receptors

Front 4

Pilocarpine (Cevilemine)

Back 4

• Stimulation of M3 receptors causes contraction of iris sphincter muscle (miosis)

• Contraction of ciliary muscle causes lens thickening

• Combination allows lowering of ocular pressure and outflow of aqueous humor through Canal of Schlemm

Front 5

Isoflurophate

Back 5

- POISON - IRREVERSIBLE Indirect Acting Agonist (AChE inhibitor)

- Can lead to poisoning: excess ACh activity in CNS, PNS

- Reversal by antidote: PRALIDOXIME

Front 6

Echothiophate

Back 6

- Poison - IRREVERSIBLE Indirect Acting Agonist (AChE inhibitor)

• Used for biological warfare

• Can lead to poisoning: excess ACh activity in CNS, PNS

- Reversal by antidote: PRALIDOXIME** (+ atropine to reverse CNS effects)

Front 7

PRALIDOXIME

Back 7

antidote for irreversible AChE inhibitors

Front 8

Edrophonium

Back 8

REVERSIBLE AChE inhibitor

Used as a diagnostic test for myasthenia gravis

Front 9

Pyridostigmine

Back 9

REVERSIBLE AChE inhibitor

Used to maintain therapeutic effects during treatment of myasthenia gravis

Front 10

Neostigmine and Ambenonium

Back 10

REVERSIBLE AChE inhibitor


Treatment of:
• Postoperative ileus
• Congenital megacolon
• Urinary retention due to surgery, spinal injury, disease
• Reflux esophagitis

Front 11

Physostigmine

Back 11

REVERSIBLE AChE inhibitor

Treatment of:
• Glaucoma
• Atropine poisoning

Front 12

Carbaryl

Back 12

REVERSIBLE AChE inhibitor

• Insecticide

Front 13

Atropine

Back 13

Muscarinic (M) Receptor Antagonist

• Effective in blocking exogenously administered cholinergic agonists

• TOXIC in high doses
"atropine fever"

• Eye: dilation = mydriasis, paralyze ciliary muscle = Cycloplegia

Front 14

"Atropine fever”

Back 14

loss of sweating (cholinergic sympathetics to sweat glands) leading to dangerously elevated temperature

Front 15

Ipratropium

Back 15

Muscarinic (M) Receptor Antagonist

Like atropine

Front 16

Scopolamine

Back 16

Muscarinic (M) Receptor Antagonist


• More sedative effects than atropine
• Patch for motion sickness

Front 17

Tubocararine

Back 17

NON-DEPOLARIZING BLOCKER
Neuromuscular Junction (NM) Receptor Antagonist

• Produce a competitive blockade via binding at nicotinic receptor site to compete with the natural transmitter ACh

• Adjuncts in surgery that require general anesthesia

• Enable muscle relaxation without the need to produce dangerously deep anesthesia

Front 18

Metocurine

Back 18

NON-DEPOLARIZING BLOCKER
Neuromuscular Junction (NM) Receptor Antagonist

• Produce a competitive blockade via binding at nicotinic receptor site to compete with the natural transmitter ACh

• Adjuncts in surgery that require general anesthesia

• Enable muscle relaxation without the need to produce dangerously deep anesthesia

Front 19

Pancuronium

Back 19

NON-DEPOLARIZING BLOCKER
Neuromuscular Junction (NM) Receptor Antagonist

• Produce a competitive blockade via binding at nicotinic receptor site to compete with the natural transmitter ACh

• Adjuncts in surgery that require general anesthesia

• Enable muscle relaxation without the need to produce dangerously deep anesthesia

Front 20

Gallamine

Back 20

NON-DEPOLARIZING BLOCKER
Neuromuscular Junction (NM) Receptor Antagonist

• Produce a competitive blockade via binding at nicotinic receptor site to compete with the natural transmitter ACh

• Adjuncts in surgery that require general anesthesia

• Enable muscle relaxation without the need to produce dangerously deep anesthesia

Front 21

Vecuronium

Back 21

NON-DEPOLARIZING BLOCKER
Neuromuscular Junction (NM) Receptor Antagonist

• Produce a competitive blockade via binding at nicotinic receptor site to compete with the natural transmitter ACh

• Adjuncts in surgery that require general anesthesia

• Enable muscle relaxation without the need to produce dangerously deep anesthesia

Front 22

Succinylcholine

Back 22

DEPOLARIZING BLOCKER Neuromuscular Junction (NM) Receptor Antagonist

non-competitive

• Adjuncts in surgery that require general anesthesia
• Enable muscle relaxation
• Genetic variations of Pseudocholinesterase may result in longer duration of action of succinylcholine

Front 23

Phase I block

Back 23

produced by persistent ACh-like action of succinylcholine at NM receptor site – open channel, leading to persistent end-plate depolarization and initial desynchronized muscle contractions

• Because of persistent depolarization of end-plate, subsequent contracts CANNOT occur

Front 24

Phase II block

Back 24

- end-plate repolarizes despite presence of succinylcholine. But, end-plate has become “DESENSITIZED” and channel remains in prolonged closed state
• Terminated by hydrolysis by AChE & Pseudocholinesterase

Front 25

Mecamylamine

Back 25

DEPOLARIZING BLOCKER
Nicotinic Ganglionic (Nn) Blocking Agent

• Block actions of ACh at preganglionic nicotinic receptor of autonomic ganglia within the SYMP and PARA nervous systems

limited only to emergency room management of hypertensive crisis and used for controlled hypotension during surgery

Front 26

Trimethaphan

Back 26

DEPOLARIZING BLOCKER
Nicotinic Ganglionic (Nn) Blocking Agent

• Block actions of ACh at preganglionic nicotinic receptor of autonomic ganglia within the SYMP and PARA nervous systems

limited only to emergency room management of hypertensive crisis and used for controlled hypotension during surgery

Front 27

Hexamethonium

Back 27

DEPOLARIZING BLOCKER
Nicotinic Ganglionic (Nn) Blocking Agent

• Block actions of ACh at preganglionic nicotinic receptor of autonomic ganglia within the SYMP and PARA nervous systems

limited only to emergency room management of hypertensive crisis and used for controlled hypotension during surgery

Front 28

Epinephrine

Back 28

MIXED (a1 = a2; B1 = B2)


• CV: positive ionotropic action (B1) – increase force of contraction (CO)
• CV: positive chronotropic action (B1) – increase rate of contraction (HR)

• B1 - CO↑, HR↑, Systolic BP ↑
• B2 – increase vasodilation = TPR↓: Diastolic BP ↓*

Front 29

Norepinephrine

Back 29

MIXED (a1 = a2; B1 >>> B2)


• B1 - CO↑, HR↓ (reflex bradycardia)**
• B1 - Systolic BP ↑*
• B2 no effect = no vasodilation = Diastolic BP ↑**

Front 30

Isoproterenol

Back 30

BETA AGONIST
(B1 = B2 >>>> a)

• Increase HR, increase SBP
• Decrease TPR, decreased DBP
• Similar effects as epinephrine

Front 31

Dobutamine

Back 31

BETA 1 AGONIST
(B1 > B2 >>>>> a)

• Increases HR and CO, SV
• Short-term treatment of cardiac decompensation (after surgery, MI)

Front 32

Terbutaline

Back 32

BETA 2 AGONIST
(B2 >> B1 >>>>>a)

Front 33

Metaproterenol

Back 33

BETA 2 AGONIST
(B2 >> B1 >>>>>a)

Front 34

Albuterol

Back 34

BETA 2 AGONIST
(B2 >> B1 >>>>>a)

- Tolerance can develop by receptor down-regulation
• Relieve bronchodilation
• Treatment of asthma

Front 35

Ritodrine

Back 35

BETA 2 AGONIST
(B2 >> B1 >>>>>a)

• Uterine relaxant – prevention of premature labor & prolongs pregnancy

Front 36

Salmeterol and Formoterol

Back 36

BETA 2 AGONIST
(B2 >> B1 >>>>>a)

• LONGEST LASTING: 12 hour duration, but slower acting

o Advair = salmeterol + fluticasone
o Symbicort = formoterol + budesonide

Front 37

Bitolterol

Back 37

PRODRUG
B2 AGONIST

• Esterases in lung metabolize drug to active form: Colterol

Front 38

Phenyleprine and Methoxamine

Back 38

ALPHA 1 AGONIST
(a1 > a2 >>>> B)

• Nasal decongestant (less fluid through nasal passages due to vasoconstriction)
• Opthalmic use: mydriatic – dilation of pupils
• Can terminate episodes of supraventricular tachycardia
• May cause hypertension

Front 39

Pseudoephedrine (Sudafed)

Back 39

ALPHA 1 AGONIST
(a1 > a2 >>>> B)

• Used in preparation of meth
• Decongestant

Front 40

Clonidine

Back 40

ALPHA 2 AGONIST


• Alpha 2 activation leads to presynaptic inhibition of NE release – inhibition of Sympathetic NS
• Lowers blood pressure
• Patch delivers constant rate for 1 week

Front 41

Amphetamine

Back 41

MIXED EFFECTS; INDIRECT-ACTING DRUG
• Strong CNS stimulant
• Reuptake into terminals and displace NE from vesicles leads to release of NE (indirect)

Front 42

Prazosin

Back 42

ALPHA 1 ANTAGONIST

• Inhibitory feedback mechanism for NE
• Less effect on baroreceptor reflex
• Antihypertensive, without tachycardia or orthostatic hypotension

Front 43

Terazosin

Back 43

ALPHA 1 ANTAGONIST
• Longer action than Prazosin
• Antihypertensives
• Relax muscle in prostate

Front 44

Tamsulosin

Back 44

ALPHA 1 ANTAGONIST
- useful in BPH with little effect on BP

Front 45

Propranolol

Back 45

NON-SELECTIVE BETA BLOCKER (no ISA)
• Effects (B1):
o Blunt expected rise in HR (negative chronotropy)
o Decrease force of contraction (negative inotropy)
o Decreased conduction velocity in AV node
o Decreased CO
o Decreased cardiac work
o Decreased BP (beta 2 activity)
o Decreased O2 consumption
o BENEFICIAL EFFECTS FOR ANGINA
o inhibition of renin release
o decreased intraocular pressure

• Effects (B2):
o Problems in asthmatics: bronchoconstriction
o Problems in diabetics
o Beneficial: antagonism of catecholamine-induced tremor

Front 46

Nadalol

Back 46

NON-SELECTIVE BETA BLOCKER
• Long-acting (duration up to 24 hours)

Front 47

Timolol

Back 47

NON-SELECTIVE BETA BLOCKER
• Useful in ophthalmic prep – open-angle glaucoma

Front 48

Pindolol

Back 48

NON-SELECTIVE BETA BLOCKER (has ISA)

Front 49

Acebutolol

Back 49

SELECTIVE B1 BLOCKER (has ISA)

Front 50

Atenolol

Back 50

SELECTIVE B1 BLOCKER

Front 51

Metoprolol

Back 51

SELECTIVE B1 BLOCKER

• 1st pass metabolism by CYP2D6 – susceptible to pharmacogenetic modification

Front 52

Nebivolol

Back 52

MOST SELECTIVE B1 BLOCKER

Front 53

Labetolol

Back 53

NON-SELECTIVE BETA BLOCKER + ALPHA 1 BLOCKER

Front 54

Carvedilol

Back 54

NON-SELECTIVE BETA BLOCKER + ALPHA 1 BLOCKER + Ca CHANNEL BLOCK

Front 55

Esmolol

Back 55

SELECTIVE B1 BLOCKER

• SHORTEST ACTING
- Metabolized by esterases in blood, t½ is 10 mins

Front 56

List four antivirals used to treat influenza

Back 56

1. Amantadine, 2. Rimantadine - mechanism: block uncoating of influenza A viruspreventing
penetration of virus into host

3. Relenza
4. Tamiflu - neuraminidase inhibitors

Front 57

List two neuraminidase inhibitors

Back 57

Relenza
Tamiflu

Inhibit influenza virus neuraminidase, an enzyme known to cleave the budding
viral progeny from its cellular envelope attachment point

Front 58

List the interferon used to treat hepatitis B

Back 58

Interferon alpha-2b

Front 59

Acyclovir (Zovirax)

Back 59

Mechanism: Inhibits DNA synthesis and
viral replication by being incorporated into viral DNA

• Dental use: tx of recurrent mucosal and cutaneous herpes simplex infections in immunocompromised patients

Front 60

Valacyclovir (Valtrex)

Back 60

• Mechanism: converted to acyclovir by hepatic enzymes then goes through mechanism
above

• Dental use: tx of herpes labialis (cold sores)

Front 61

Famciclovir (Famvir)

Back 61

Mechanism: converted to penciclovir to inhibit viral DNA synthesis

• Dental use: management of acute herpes zoster (shingles); tx of herpes labialis

Front 62

Penciclovir (Denavir)

Back 62

Mechanism: inhibits viral DNA synthesis and replication

• Dental use: tx of herpes labialis; apply locally as cream to lesion

Front 63

List the four subclasses of HIV drugs

Back 63

1. Nucleoside Reverse Transcriptase Inhibitors - (Retrovir)

2. Protease Inhibitors - Indinavir

3. Nonnucleoside Reverse Transcriptase Inhibitors - (Rescriptor)

4. Fusion Protein Inhibitors - (Fuzeon)

Front 64

How do Nucleoside Reverse Transcriptase Inhibitors work against the HIV virus?

Back 64

Work by inhibiting the viral enzyme reverse transcriptase. Without reverse transcriptase, the viral RNA cannot be made into a DNA segment and DNA integration (chain elongation) does not take place.

Front 65

How do Protease Inhibitors work against the HIV virus?

Back 65

Inhibit protease, the enzyme responsible for cleaving viral precursor peptides into infective virions.

Front 66

How do the Nonnucleoside reverse transcriptase inhibitors work against the HIV virus?

Back 66

Inhibits the catalytic reaction of reverse transcriptase that is independent of nucleotide binding.

Front 67

How do Fusion Protein Inhibitors work against the HIV virus?

Back 67

Inhibits the fusion of HIV-1 virus with CD4 cells by blocking the conformational change in viral envelope fusion protein required for membrane fusion and entry into the CD4 cells.

Front 68

Using Zidovudine (Retrovir) as the example of a Nucleoside Reverse Transcriptase Inhibitors describe the use and unlabeled use from DIHD.

Back 68

Use: Treatment of HIV infection in combination with at least two other antiretroviral agents; prevention of maternal/fetal HIV transmission as monotherapy

Unlabeled Use: Postexposure prophylaxis for HIV exposure as part of a multidrug regimen.

Front 69

Using Indinavir (Crixivan) as the example of a Protease Inhibitor describe the use from DIHD

Back 69

Treatment of HIV infection; should always be used as part of a multidrug regimen (at least three antiretroviral agents)

Front 70

7. Using Delavirdine (Rescriptor) as the example of a Nonnucleoside Reverse Transcriptase Inhibitor describe the use from DIHD.

Back 70

Treatment of HIV-1 infection in combination with at least two additional antiretroviral agents

Front 71

Using Enfuvirtide (Fuzeon) as the example of a Fusion Protein Inhibitor.describe the use from DIHD.

Back 71

Treatment of HIV-1 infection in combination with other antiretroviral agents in treatment-experienced patients with evidence of HIV-1 replication despite ongoing antiretroviral therapy

Front 72

Cancer drugs
"-bines"

Back 72

Antimetabolites

Front 73

Cancer drugs
"-icins" or "-mycins"

Back 73

Antibiotics

Front 74

Cancer drugs
"-axel" or "Vin-"

Back 74

Microtubulue inhibitors

Front 75

Cancer drugs
"-mab"

Back 75

Monoclonal antibodies

Front 76

Methotrexate

Back 76

Antimetabolite

Inhibition of DHF reductase leads to an inhibition of purine ring and dTMP synthesis

Front 77

MECAMYLAMINE

Back 77

blocks nicotinic effects

Front 78

VARENICLINE

Back 78

partial agonist of a2b4 receptor

nicotine replacement and receptor antagonist. Considered the most effective drug for addiction. May lead to suicide.

Front 79

BUPROPION

Back 79

Leads to 40% smoking cessation

Front 80

NALOXONE

Back 80

antagonist which blocks opiate effects

Front 81

METHADONE

Back 81

slow-acting Full agonist of opiate receptors. Blunt opiate withdrawal – patient remains in normal range without fluctuations between sick / high

Front 82

BUPRENORPHINE

Back 82

substitute opiate addiction

o Partial agonist – mild agonist activity but prevents opiod from binding – limited euphoric effect, but enough to stop withdrawal symptoms.

o Safe medication with fewer side effects. Can be prescribed by physician and used in young people. Reduces negative attitudes associated with Methadone.

o Has a “floor effect” on respiratory rate -- does not decrease to ZERO like other opiods

Front 83

DISULFIRAM

Back 83

Treatment for alcoholics

Inhibition of Aldehyde dehydrogenase – buildup of acetoaldehyde = unpleasant

Front 84

Protirelin

Back 84

Hypothalamic Preparation Used as a Diagnostic Agent in patients with pituitary or hypothalmic dysfunction