Pharmacology Exam 2

Front 1

How is adrenergic stimulation dissipated in the synapse? how is this different from cholenergic stimulation?

Back 1

Norepinephrine is removed from the synapse via reuptake, whereas acetylcholine is broken down in the synapse.

Front 2

What is the role of MAO? Where is it found in the synapse?

Back 2

It breaks down NE after re-uptake. It is found in the presynaptic neuron.

Front 3

What affect does adrenergic stimulation have on urination? on pupils? on insulin release?

Back 3

increases urinary retention, pupillary dilation (mydriasis), decreased insulin release

Front 4

What two drugs are general alpha and beta agonists?

Back 4

Epinephrine, norepinephrine

Front 5

What two drugs are non-selective alpha antagonists? What therapeutic effects do these drugs have?

Back 5

phentolamine, phenoxybenzamine.
cause vasodilation.
Phentolamine = nonspecific competitive antagonist. Used to DX pheochromocytoma. Frost bite and erectile dysfunction. Active ingredient in ORAVERSE.
Phenoxybenzamine = nonspecific noncompetitive antagonist. Used to TX pheochromocytoma, BPH.

Front 6

what two drugs are specifically alpha-1 agonists? what conditions do these drugs treat

Back 6

phenylephrine and methoxamine.
phenylephrine (nasal decongestant, pupillary dilation)
methoxamine (tx for hypotension)

Front 7

what two drugs are alpha-1 antagonists?
what conditions do these drugs treat?

Back 7

Prazosin - osins, and Tamulosin (Flomax).

tx for hypertension, benign prostate hyperplasia

Tamulosin - used to aid in urinary release

Front 8

What 3 drugs are alpha-2 agonists? what conditions do these drugs treat?

Back 8

clonidine, methyldopa, guanfacine

Tx for ADHD and htn

Front 9

What drug is specifically an alpha-2 agonist? what are the therapeutic effects of this drug?

Back 9

yohimbine - aphrodisiac

Front 10

What drug, besides epi and NE, is a non-selective beta agonist? what conditions is this used to treat?

Back 10

Isoproterenol.

tx: shock, asthma attack, bradycardia

Front 11

what 2 drugs are non-selective beta antagonists? what conditions do these drugs treat?

Back 11

propranolol, timolol.

propranolol - (Htn, migraines, hyperthyroid, MI, anxiety) by reducing cardiac contractility

timolol - tx glaucoma, htn, prevent heart attack

timolol-

Front 12

what drug is a beta-1 agonist? what conditions does it treat?

Back 12

Dobutamine, tx: CHF, shock, hypotension

Front 13

What 2 drugs are beta-1 antagonists? what are they used to treat?

Back 13

atenolol, metaprolol (htn, MI, angina)

Front 14

What 2 drugs are beta-2 agonists? what are they used to treat? what are some important side effects?

Back 14

albuterol, ritrodine

albuterol - asthma, COPD
ritrodine - delay premature labor

side effects: skeletal muscle tremor, tachycardia

Front 15

Name a drug that is specifically a beta-2 antagonist.

Back 15

There are none, there would be no therapeutic effect to causing bronchoconstriction

Front 16

What is the active ingredient in Oraverse? what kind of drug is this?

Back 16

Phentolamine, non-selective alpha blocker.

Front 17

What is the major effect of alpha-1 stimulation?

Back 17

Vasoconstriction, mydriasis

Front 18

What is the major effect of alpha-2 stimulation?

Back 18

inhibition of neurotransmitter (NE) release

Front 19

where are beta-1 receptors mainly found? beta-2 receptors?

Back 19

beta-1 receptors in the heart. stimulation causes increased cardiac contractility

beta-2 - in skeletal blood vessels, bronchial walls. causes vasodilation and bronchodilation

Front 20

Epi is _____ selective at low doses.

Back 20

beta

Front 21

What class of drugs will cause Epi reversal?

Back 21

alpha-1 antagonists, ex. prazosin. Epi will only have beta (vasodilation) effects.

Front 22

what are examples of indirect sympathomimetics?

Back 22

cocaine, imipramine - blocks re-uptake
amphetamine, tyramine - increase NE release
ephedrine, mephenteramine - nasal decongestion and bronchodilation.

Front 23

what category of agonists are actually indirect sympatholytics?

Back 23

alpha-2 agonists:
ex. clonidine, methyldopa, guanethidine
tx: used to treat drug withdrawal, AHDH, htn

Front 24

why does bupivacaine have the slowest onset but the longest duration of action?

Back 24

longest duration of action? high protein binding ability

slowest onset: low ph, low ratio of unionized form to ionized form

Front 25

What are the structural differences in articaine vs. lidocaine that relate to more rapid onset and shorter systemic half-life?

Back 25

articaine contains a thiophene ring making it more lipid soluble, allowing more rapid onset. has a shorter half-life than lido because it contains an ester, so is partially metabolized in the bloodstream by plasma cholenesterases.

Front 26

What are the advantages and disadvantages of articaine vs. lidocaine?

Back 26

advantages: profound infiltration anesthesia, Rapid metabolism makes reinjection safer since less systemic accumulation

disadvantages: higher incidence of parasthesia

Front 27

What are the advantages and disadvantages of having epinephrine in the local anesthetic cartridge

Back 27

advantages: hemostasis, decreased systemic absorption, longer duration of action.

disadvantages: medical conditions that make it unsafe (MI, htn, angina, hyperthyroid, diabetes, ASA III, cocaine or amphetamine abuse)

Front 28

Differences between NSAIDS and opioids

Back 28

• NSAIDs:
o Inhibit prostaglandin synthesis, peripherally and centrally
o Most have good anti-inflammatory action
o All have analgesic ceiling
o More favorable side effect profile than opioids
o Available OTC
• Opioids:
o Act on CNS pain mechanisms
o Lack anti-inflammatory effects
o No ceiling dose
o More problematic side effects
o Subject to Controlled Substances Act limitations

Front 29

Oxford league table – most effective analgesic for dental pain?

Back 29

• NSAIDs

Front 30

What is the point of a preoperative dose?

Back 30

• Provides analgesia before the procedure, pain stimulus begins
• Provides some anti-inflammatory action before inflammation from treatment kicks in
• Minimizes the need for after-procedure need for medications

Front 31

. Why is PRN dosing of pain medications not the best strategy?

Back 31

• Because if the patient waits til they are already experiencing pain, the sensory neurons are sensitized to pain mediators, requiring more drug and a longer period of time to eleviate pain.
• Non-painful stimuli will create pain if sensory neurons are sensitized to pain stimuli (allodynia)
• Note: hyperalgesia is when pain stimuli create an exaggerated response

Front 32

hyperalgesia definition

Back 32

when pain stimuli create an exaggerated response

Front 33

allodynia definition

Back 33

non-painful stimuli create pain because sensory neurons are sensitized

Front 34

what causes pain?

Back 34

histamine, seratonin, bradykinins. Prostaglandins DON’T CAUSE PAIN directly. Prostaglandins sensitize nerve endings to pain producing chemicals:

Front 35

role of cox-1

Back 35

synthesizes prostaglandins that regulate normal body functions
o Homeostatic functions
o GI tract cytoprotection
o Renal tract
o Platelet functions (thromboxane production, increased platelet aggregation)
o Macrophage differentiation

Front 36

role of cox-2

Back 36

o Sensitization of neurons to pain causing chemicals:
 Histamine, seratonin, bradykinin

Front 37

. Major clinical use of aspirin?

Back 37

antithrombosis

Front 38

Side effects of aspirin

Back 38

• Increased bleeding time due to inhibition of platelet aggregation
• Can cause GI ulceration and bleeding

Front 39

MOA of aspirin effects on GI tract

Back 39

• Cause GI ulcers and bleeding because of prostaglandin synthesis inhibitors
o Prostaglandins regulate acid secretion in the GI tract
o They also regulate mucus secretion

Front 40

MOA of aspirin vs. vioxx on platelets – how do they differ?

Back 40

• Aspirin is a Cox 1 and Cox 2 inhibitor
o Cox 1 has prothrombotic effect promoting thromboxane, promoting platelet aggregations
o Cox 2 has antithrombotic effect promoting prostacyclin, blocking platelet aggregation
o Aspirin causes IRREVERSIBLE effects on thromboxane and REVERSIBLE effects prostacyclin (increases bleeding time!)

• Vioxx is a Cox 2 inhibitor only
o Thromboxane is left UNINHIBITED, leaving people to die of thrombosis

Front 41

11. How does ibuprofen differ from aspirin in terms of its effects on platelet function?

Back 41

o NSAIDs just cause reversible effects on both thromboxane and prostacycline

Front 42

. Analgesic dose of ibuprofen vs. Tylenol; ceiling doses?

Back 42

• Ibuprophen dose: 200mg-800mg q4-6 hr. max 3200 (recently changed to 2600mg. Analgesic Ceiling: 400-600mg
o Anti-inflammatory action keeps increasing with dose
• Tylenol dose: 325-650 mg q4-6h max 4000. 2000 in liver disease Ceiling: 1000mg

Front 43

Difference between naproxen and ibuprofen

Back 43

• Naproxen has slower onset but longer duration of action

Front 44

Interaction between ibuprofen and aspirin and advise to avoid

Back 44

• Ibuprofen taken before ASA blocks access for binding and decreases ASA’s anti-platelet effect. Patients should take ASA 0.5-2hrs before ibuprofen, or else ibuprofen 8 hours before ASA.

Front 45

. Dolobid – how does it differ from ibuprofen and aspirin and acetaminophen?

Back 45

• NO ANTIPYRETIC EFFECT
• Doesn’t increase bleeding time

Front 46

. Toradol – how does it differ from other NSAIDS – 3 ways

Back 46

• Available in PO and IV forms
• Also available as “Sprix” for intranasal delivery.
• For short term use only (<5 days) – GI ulcerations. Worst GI effects of all the NSAIDs

Front 47

DDIs with NSAIDs

Back 47

a. Ibuprofen and lithium
 NSAIDS decrease renal lithium excretion, leading to toxicity
b. Ibuprofen and aspirin
• Ibuprofen taken before ASA blocks access for binding and decreases ASA’s anti-platelet effect. Patients should take ASA 0.5-2hrs before ibuprofen, or else ibuprofen 8 hours before ASA.
c. NSAIDS and alcohol
* increased GI bleeding
d. NSAIDS and antihypertensives
NSAID use beyond 5 days may decrease anti-htn action and raise BP.
e. NSAIDS and herbals
many have antiplatelet activity that is additive with NSAIDS/ASA.
f. NSAIDS and SSRIs
cause internal GI bleeding. Anti-depressant effects are attenuated
g. NSAIDS and PPIs
PPIs exacerbate NSAID-induced intestinal damage

Front 48

a. Advantages/differences of acetaminophen vs NSAIDS and aspirin

Back 48

no GI upset, no effect on bleeding, doesn’t increase blood pressure, no allergic reaction.

Front 49

Why was VIOXX taken from market?

Back 49

Cause hypercoagulable state because it inhibits prostacyclin and leaves thromboxane uninhibited

Front 50

How does VIOXX differ from ibuprofen in terms of its effects on platelets?

Back 50

vioxx only inhibits prostacyclin, whereas ibuprofen inhibits both thromboxane and prostacycline

Front 51

Which cox-2 inhibitor drug is still available?

Back 51

Celebrex

Front 52

which NSAID should not be given to patient with sulfa-allergies?

Back 52

Celebrex

Front 53

DDIS with Celebrex?

Back 53

Anything requiring 2d6: lithium, codeine, hydrocodone, oxycodone, metaprolol, antacids, coumadin

Front 54

. What is meant by tolerance and physical dependence to opioid analgesics?

Back 54

Physical dependence is a state of adaptation that is manifested by a drug class specific withdrawal syndrome that can be produced by abrupt cessation, rapid dose reduction, decreasing blood level of the drug, and/or administration of an antagonist.
*Tolerance: Tolerance is a state of adaptation in which exposure to a drug induces changes that result in a diminution of one or more of the drug’s effects over time.

Front 55

what drug is used for overdose of opiods?

Back 55

naloxone

Front 56

what is the long acting opioid antagonist?

Back 56

naltrexone