Pharmacology Exam 2

Front 1

Describe the role of APC'S?

Back 1

Antigen presenting cells.
Displays foreign antigens complexes with MHC on its surface.
Process antigens and present them to T CELLS.
Phagocytose bacterium of parasite.
APC- MHC11-CD4- T CELL (BACTERIA)
Nucleated cells MHC1-CD8-T CELLS (VIRUSES)
activation of adaptive immune system.

Front 2

Cytoxic T CELLS?

Back 2

CD8, CELL DEATH

Front 3

Helper T cells?

Back 3

CD4 T CELLS,
Interact w macrophages, b cells, cytokines

Front 4

Eicosanoids?

Back 4

Involved in inflammatory and cellular signaling.
ex: prostaglandins, prostacyclins, thromboxanes, leukotrienes.
*Common precursor to eicosanoids is arachidonic acid*
Pathways of arachidonic acid metabolism are the cyclooxygenase pathway and the lipooxygenase pathway.
NSAID'S inhibit this pathway.
NSAID's inhibit COX 1 AND COX 2.

Front 5

HISTAMINES?

Back 5

Helper T Cells recruit B Cells to produce an immune response.
IgE antibody spec. to that allergen.
IgE causes degranulation of mast cells and basophils.
SYNTHESIS: mast cells and basophils, gastric mucosal cells, neurons in CNS,
ACTIVITY: inflammatory mediator, reg. gastric acid secretion, reg. neurotransmission.
*TYPE H1*= (sm. muscle, vasc. endothelium, brain)
lungs- bronchoconstriction, asthma
vasc. sm mucle-postcapillary venule dilation/erythema
peripheral nerves sensitisation-
itching/pain
*TYPE H2*
(gastric parietal cells, cardiac muscles, mast cells, brain)
heart- minor Inc. HR and contx
stomach-gastric acid secretion, PUD/GERD

Front 6

H1 ANTIHISTAMINES?

Back 6

*Inverse agonists*
Stabilize the inactive H1 receptor conformation. ( seven transmembrane g coupled receptors)
excellent absorption
CMAX 2-3 hrs
Hep. metabolized by CYP 450
1st generation and 2nd generation

Front 7

FIRST GENERATION H1 ANTIHISTAMINES?
SECOND GENERATION H1 ANTI-HISTAMINES?

Back 7

1ST= lipophilic, neutral at physiologic pH, dipenhydramine, promethazine, doxepin,
X THE BBB EASILY!!!
2nd= Albumin binding, does NOT cross the BBB, not dist. widely bc of alb. binding,
ionized @ physiologic ph, loratadines, desloratadine, cetirizine, fexofenadine

Front 8

EFFECTS OF H1 ANTI-HISTAMINES?

Back 8

effective for:
rhinitis, conjunctivitis, urticaria, pruritis. NOT EFFECTIVE FOR ANAPHYLAXIS OR ASTHMA.
good for motion sickness, chemo related N/V, insomnia.
AE: cns toxicity. sedative effects. cardiac tox, prolonged QT interval. Anticholinergic efffects-pupil dilation , dry mouth, urinary hesitancy

Front 9

Leukotrienes?

Back 9

fatty signaling molecules.
found in leukocytes.
role is to trigger contractions of sm. muscle lining the trachea.
therefore, to treat asthma:
leukotriene antagonists

Front 10

Differences between chronic asthmatic rxn and acute asthamtic rxn? Treat with?

Back 10

chronic= bronchoconstriction, vasogenic efema, mucus hypersecretion, AIRWAY REMODELING
acute= bronchoconstriction, airway edema, mucus
treat with:
B AGONISTS
ANTI-CHOLINERGICS
METHYLXANTHINES

Front 11

Beta agonists used to treat asthma?

Back 11

Epinephrine- agonizes B2 (bronchodilation), B1 (tremors, tachy, palp,) ALPHA (periph. vc)
not used bc of effects on B1.
Isoproterenol, metaproterenol - agonize B2 AND B1
Terbutaline, Albuterol. agonize B2.
levaalbuterol- is an isolated stereoisomer) AGONIZES B2
BETA AGONISTS:
rapid onset, 15-30 min
fast peak effect 30-60 min
short duration of action 4-6 hrs
rescue inhalers during acute attacks.
can be used prophylactically before a known trigger (exercize)

Front 12

Long acting beta agonists?
(LABA)?

Back 12

Salmeterol, formoterol.
Contain lipophlic side chains that resist degradation.
12-24hr dur. of action
good 4 prev. of bronchoconstriction
not good for monotherapy, dont treat underlying inflamm.
pot. cardiac tox.
should be used w corticosteroid.

Front 13

Anticholinergics for asthma?

Back 13

Atropine- highly absorbed across resp. epithelium.AE: tachy, dry mouth, GI upset
Ipatromium bromide- Quarternary ammonium salt derivative of atrophine. not sig. absorbed. depos. in mouth and inadv. oral absorption.
Tiotopium- sim to ipratropium but longer acting. slow dissociation from receptors.
MOA: competetive antagonists at muscarinic Ach receptor sites. M3 receptor most IMP bc it mediates sm musc relaxation and mucus gland secretion in the airway. trmt of COPD.

Front 14

Methylxanthines?

Back 14

Theophylline, aminophylline
moa: inhibition of PDE (phosphodiesterase)
airway sm muscle-bronchodilation
inflamm. cells-anti-inflamm
Adenosine receptor antagonism (secondary effect)
Inc. ventilation dur. hypoxia
Inc. endurance of diaph. muscles
dec. mast cell release
narrow therapeutic index
CYP450 1A2 METAB.
CIG. SMOKING induces cyp1a2.
AE: n/v, ha. irritability, insomnia, seizures, brain damage, hyperglycemia, hypokalemia, hypotension, cardiac arrhythmias, death
-Work in conjunction w cAMP,
Inc. prod. of cAMP, more cAMP->pka->bronchodilation.
Theophylline inhibits the breakdown of cAMP.

Front 15

Anti-inflammatory agents to treat asthma?

Back 15

corticosteroids, cromolyns, leukotriene inhibitors, anti-IgE antibodies.
CORTICOSTEROIDS- Inc. B2 REC, dec. pro inflamm proteins, induces apoptosis in inflamm cells, suppresive but not cure.
Inhaled- 25% reaches airways
give PO. first pass metab.
AE: osteopenia, osteoporosis, delayed growth in children, hyperglycemia, oropharyngeal candidiasis.
CROMOLYNS-stablilze mast cells. inhibits rel of inflamm mediators from eosinophils, neutrophils, monocytes, macrophages, lymphocytes.
Does not relieve an allerg. response after initiation.
PROPHYLACTIC THERAPY.
less sys. absorption.
LEUKOTRIENE INHIBITORS-
Zileuton stops brkdown on arachidonic acid.
Montelukast and zefirkulast inhibit binding of leukotrines in airway. less effective than corticosteroids.
all are hepat. metabolized.
ANTI-IGE ANTIBODY-
binds to IgE, dec. circ. IgE,
prev. binding of IgE to mast cells, downregulation of receptors, rare ae: triggers immune response. given sq q 2-4 wks.

Front 16

Anti-gout drugs?

Back 16

goal to relieve pain and inflammation. reduction and severity of attacks.
probenecid, allopurinol, prednisone.
allopurinol: moa, inhibits uric acid production. prodrug. conv. by xanthine oxidase. drug interactions: azathioprine, trt RA, Inc. levels of 6 mercaptapurine
ACUTE GOUT TRT WITH NSAIDS, COLCHICINE, GLUCOCORTICOIDS.
CHRONIC GOUT TRT W ALLOPURINOL, PROBENECID, SULFINPYRAZONE.
Probenecid- prophylaxis only. se: GI dist. hypersensitivity.
Moa: dec. urate reabsorp. in prox. tubule, urate stays in kidney and gets elim,
drug int: pcn, naproxen
to minimize kidney stones: high lfuid intake, alkalanize the urine.

Front 17

Some factors about non-opioid analgesics?

Back 17

First line agents for mild to mod. pain.
Cieling effect of ASA and APAP between 650 and 1300mg.
NSAID'S other than ASA-analgesic cieling may be higher.
tolerance does not develop.

Front 18

Acetaminophen?

Back 18

Sim. efficacy and potency as ASA.
no anti-inflamm effect
overdose can cause fatal hepatic injury.
Caution in pt's : isoniazid, heavy ETOH
otc max dose 3 g per day
4g per day max safe dose.

Front 19

Salicylates?

Back 19

ASA effective for mild to mod. pain.
unlike other NSAID'S, irreversible inhibition of COX.
Single dose can precipitate asthma.
Can cause GI bleeding, PUD.
salicylate overdose: metab. acidosis, tinnitus.
avoid use in kids w viral syndromes (reye's)

Front 20

Non-acetylated salicylates?

Back 20

More favorable tox. profile.
dont interfere w plt. aggregation.
rarely assoc. w GI bleed.
well tolerated by asthmatic pt.

Front 21

traditional NSAID'S?

Back 21

analgesic efficacy.
anti-inflammatory.
moa: inhibit COX.
Block conversion of arachidonic acid to prostaglandins.
dec. prod and rel. of PG's.
weak acids, well absorbed.
ae: gastric ulceration ( cox1)
inhibit plt function (cox 2)
inhibit renal fun (cox 1 and 2)
hypersens. rxn (cox 1)
more effects w COX1 inhibition.
NSAID'S CAN PRECIPITATE ASTHMA AND ANAPHYLACTOID RXN'S IN ASA SENSITIVE PT.'S
- Reversible inhibition of plt aggregation.
preg- avoid in 3rd trimester

Front 22

Gi adverse effects of nsaid's?
Renal adv. effects "?

Back 22

DYSPEPSIA, GI BLEEDINGS, PUD.
Inhibition of the prostaglandins that maintain normal gastric mucosa. Inc. acid production.
dec. mucus prod/gastric bld. flow.
lipid-soluble at a low ph., enters gastric mucosal cells and becomes trapped.
Renal- dec. renal bld. flow, fluid and Na retention.
risk factors: old age, chf, htn, renal insufficiency, vol. depletion, diuretic therapy.
NSAID'S CAN DISPLACE HIGHLY PROTEIN BOUND AGENTS. Inc. levels of warfarin, phenytoin, sulfonamides, digoxin.
Reduces effects of diuretics., B Blockers, ace, via supression of renal prostaglandins.

Front 23

Celebrex?

Back 23

Inhibit COX 2.
Non- selective inhibition of cox1 and cox 2. no more effective at red. pain/inflamm.
COX1- gastric protection and prod. of TXA2.
COX2- prod. prostacyclin (vasodilator, plt. inhibitor)
consider risk for cardiac and GI events.
risk vs benefit.
take w food.
PO.
CI FOR PAIN IN POST OP CABG SURGERY.
Inc. risk of cv thrombosis.
Inc. risk for GI bld/ulceration.

Front 24

OPIOID RECEPTORS?

Back 24

mu1- when agonized= supraspinal anesthesia, bradycardia, sedation.
mu2=Resp. depression, euphoria, physical dependence.
delta= spinal analgesia, resp. depression
kappa=spinal analgesia, resp. depression, sedation, dysphoria
sigma=dysphoria, delirium, hallucinations

Front 25

OPIOID CHARACTERISTICS?

Back 25

Moderate to severe pain.
agonists, partial agonists and antagonists.
no max dose vs ceiling effect (partial agonist)
all hepatically metab.
non cyp450 pathways.

Front 26

FULL AGONIST OPIOIDS?

Back 26

Morphine, oxycodone, hydropmorphone, methadone, meperidine, fentanyl.

Front 27

PARTIAL OPIOID AGONISTS?

Back 27

Pentazocine, stadol, nubain, buprenex.

Front 28

FULL OPIOID AGONISTS?

Back 28

Codeine, hydrocodone, propxyphene.

Front 29

true or false
The NT that modulate mood, sleep-wake cycle, motivation, and pain perception are Serotonin (5HT) and Norepinephrine.

Back 29

TRUE

Front 30

Explain why long term therapy for depression is key?

Back 30

Because even though you are still blocking the reuptake over time down regulation of the auto-receptors occurs so less neg. fb=>less reuptake=>greater therapeutic effect.

Front 31

What happens when you agonize 5HT?

Back 31

Increased appetite, improved sleep, improved mood.
And specifically the receptor 5ht1a= improved MOOD.
Side effects if agonized=
Inc. anxiety, jitters, sex. dysfunction, sleep disturbances
and if 5HT3=Nausea, diarrhea

Front 32

If agonize norepi? Side effects?

Back 32

Increased interest, energy, concentration, cognition, mood.
SE= Inc. HR, Inc. BP, anxiety.

Front 33

TRUE OR FALSE
Tryptophan is the basic building block of serotonin and tyrosine is the building block of dopamine (norepi)

Back 33

TRUE

Front 34

HOW DO MAOI'S WORK?
SE? AE? PK?

Back 34

Inhibition of MAO inhibits degradation of monoamines which increase available 5HT AND NOREPI.
MAO-A inhibits deg of serotonin, norepi and epi, more effective for depression.
MAO-B inhibits deg of dopamine. more effective for parkinsons.

AE: tyramine toxicity, excess tyramine displaces catecholamines, can cause hypertensive crisis.
tyramine restrictive diet.
PK: very high absorbed, lipophilic, enter cns to work, hepat. metab to active metabolites then renally excreted.
CYP450 drug interactions, also tca's, ssri's, pseuephedrine, dextromethorphan.
Transdermal patch safer bc avoids first pass, dec. sensitivity to tyramine.

Front 35

HOW DO TCA'S WORK?
TYPE'S?
SE? AE?

Back 35

Work @ reuptake portion of Na Ion channel. Prevents reuptake of norepi back in to neuron= more norepi in synaptic cleft.
- Secondary amines are active metabolites of other agents. More effects on NE than 5HT. (nortriptyline, desipramine)
-Tertiary amine- more effects
on 5HT than NE.
(amitryptalline, imipramine, doxepin, clomipramine.
ANTAGONIZING 5HT AND NE reuptake so inc. levels in synaptic cleft.
NO EFFECT ON DOPAMINE REUPTAKE!!!
Can be used to trt neurogenic pain.
AE: first degree AV block, bundle branch block
antagonizing of musc./cholinergic rec which cause n.v, anorexia, tachy, blurred vision.
antag adrenergic receptors orthostatic hypotension, reflex
tachy, drowsiness.
antag histamines can cause sedation, wt gain, confusion.
PK: substrate of CYP450, esp. 2D6. Drug interactions, dont administer drugs that inhibit cyp450, bc inc. levels of tca's.
low dose can be used for sleep and pain.
WIDE DOSING RANGE.

Front 36

HOW DO SSRI'S WORK?
TYPES? AE? PK?

Back 36

Selective for serotonin.
Prozac, celexa, zoloft, lexapro.
treat depression AND anxiety.
Ist choice bc higher selectivity and less side effects.
AE: *Sexual dysfunction, (5hd2), serotonin syndrome hyperthermia, muscle rigidity, myoclonus.
fluoxetine and paroxetine subs and inhib of cyp2d6.
celexa and lexapro less drug interactions.

Front 37

SNRI'S?

Back 37

Block reuptake of serotonin and norepi.
concentration dependent (Effexor)
AE: Increased BP
cymbalta: trt for neuropathic pain. metab. cyp2d6 and 1a2.

Front 38

ATYPICAL ANTIDEPRESSANTS?

Back 38

Wellbutrin.
Inhibits dopamine and NE reuptake.
least sexual side effects (bc doesn't effect serotonin)
CI: seizure disorder, eating disorder
MERTAZAPINE:
antag. 5HT2/3 AND alpha 2 adr. receptors
moa unknown.
antag histamine receptors
less sex. dysfunction
ae: inc. appetite, sedation
PK: hepat. metab. by CYP2B6.

Front 39

Most effective treatment for parkinson's?

Back 39

Levodopa
readily transported across BBB via protein.
given with carbidopa which doesnt cross bbb.
continued use results in desensitization
AE: dyskinesia

Front 40

true or false
Stimulation of D1 receptor is EXCITATORY.
and stimulation of D2 is inhibitory.

Back 40

TRUE

Front 41

Describe the "typical anti-psychotics"?

Back 41

-Antagonize D2 receptors in all CNS dopaminergic pathways.
-Antagonism in mesolimbic pathway causes decrease of positive symptoms.
*very effective for delusions*
AE: ontarget= EPS, parkinsonian, tardive dyskinesia, NMS (life threatening), Inc. prolactin.
off target effects= anticholinergic effects, orthostatic hypotension, failure to ejaculate.
Higher potency has d2 related effects. Lower potency has more off target than d2 related effects.
EX: high potency- fluphenazine and haloperidol
more eps effects, anti-chol.
low potency- chlorpromazine
fewer eps effects but h1, a1 and muscarining blocking effects
DECREASE POSITIVE SYMPTOMS

Front 42

ATYPICAL ANTI-PSYCHOTICS?

Back 42

Better for side effects profile.
better for NEGATIVE SYMPTOMS, less EPS BC faster dissociation.
MOA: 5HT AND D2 ANTAG.

Front 43

ANTI-MIGRAINE DRUGS?
MOA? AE? CI?

Back 43

"TRIPTANS"
moa: 5HT 1B/1D agonists in vasculature, potent VC of intracranial blood vessels, inhibit vasoactive peptides, interruption of pain signal transmission.
EX: Imitrex, axert ,frova, zomig.
fastest onset-rizatriptan
various formulations for all.
CI: Ischemic heart dz, htn, ischemic stroke, pregnancy
risk of serotonin syndrome if given with ssri's, snri's.
"ERGOTS"- MOA: 5HT 1B/1D AGONISTS.
Poorly tolerated, n/v.
DHE45- fewer side effects.
use w anti-emetic. no rebound HA.
to prevent migraines= beta blockers, ca channel blockers, tca's, ergot derivatives, anti-convulsants.

Front 44

Classes of anti-emetics?
MOA?

Back 44

4 CLASSIFICATIONS:
Dopamine D2 Receptors, muscarinic cholinergic receptors, histaminic receptors, 5HT3 receptors.
-High binding affinity for a spec. type of receptor= benzamides, butryrophenes, phenothiazines.
CORTICOSTEROIDS- often given to prevent chemo induced N/V.
ANTIHISTAMINES- Work directly on the vomiting center and vestibular pathway.

Front 45

ANTI-CONVULSANTS PART 1
(Na channel Inhibitors) ?

Back 45

Na Channel Inhibitors= slows rate of recovery from inactivated state to closed state. By slowing recovery, reduces firing.
90-95%albumin bound.
EX: Phenytoin, Fosphenytoin.
Zero-order kinetics.
AE: CNS depression, n/v/c.
hirsutism, acne, sjs, alt of vit d metabolism.
metab by CYP3A4.
-Narrow therapeutic range, keep between 10-20 mcg for total drug availability.
TEGRETOL- 75-90%protein bound. autoinducer. hepat. metab. to active metabolite.
first-order kinetics.
AE: cns depression, hyponatremia, rash, leukopenia.
TDM=6-12MCG/ML. (Narrow index)
LAMICTAL-similar moa of phenytoin.55% protein bound.
AE: CNS depression, n/v. rash, serious rash assoc w rapid titration.

Front 46

ANTI-CONVULSANTS PART 2?
(Ca channel Inhibitors)

Back 46

Ethosuximide- no substantial protein binding, long half life
GOOD FOR ABSENCE SEIZURES.
AE: GI upset, anorexia, sleep terrors, psychosis.
VALPROIC ACID=80-90% protein bound. Also slows rate of Na channel recovery after inactivation and INCREASED GABA activation.
(Increased gaba acitivity, Inc. inhibition of firing)
AE: CNS depression, tremor, GI upset, LFT elev.
TDM: 50-120mcg/ml
GABAPENTIN= enhances GABA mediated inhibition.
100% renally excreted.
AE: cns depression, wt gain.
Used more for peripheral neuropathy.

Front 47

ANTI-CONVULSANTS PART 3
(Glutamate receptor inhibitor)

Back 47

Felbamate=Enhances gaba transmission and limits Na firing.
22-25%protein binding.
Inducer of CYP3A4, Inhibitor of CYP2C19.
AE: BLACK BOX WARNING FOR ACUTE HEPATIC FAILURE AND APLASTIC ANEMIA.
-Other giutamate receptor inhibitors: GABITIRL, TOPAMAX, KEPPRA.
*Keppra has little to no drug interactions, and is 66% renally excreted.

Front 48

Which anticonvulsants used for BROAD SEIZURE TYPES?
for NARROW SEIZURE TYPES?
ABSENCE SEIZURE?

Back 48

BROAD= Felbamate, Lamotrigine, Rufinamide, Topiramate, Valproate, Zonisamide.
NARROW= Carbamazepine, Gabapentin, Phenobarbitol, Phenytoin, Vigabatrin, Oxycarbazapine.
ABSENCE= Ethosuximide

Front 49

Useful drugs for opiate addiction?

Back 49

Methadone and Buprenorphone.

Front 50

Acute treatment for Alcohol abuse vs chronic treatment?

Back 50

acute- benzodiazepines
can be used for alcohol w/drawal.
Potential for abuse and dependency.
Diazepam- long half life 100 hrs. Self-tapering effects.
Chronic- ANTABUSE-
inhibits enzyme that metabolizes alcohol (aldehyde dehydrogenase) only works if pt is taking alcohol.
AE: facial flushing, HA, orthostatic hypotension.Causes alcohol aversion.
nonadherence=failure
CAMPRAL- maintenance of alc. abstinence, works on gaba/glutamate, no aversion.
TREAT WITHDRAWAL S/S, BENZO'S VERY EFFECTIVE.

Front 51

TOBACCO CESSATION?

Back 51

Nicotine directly activates nicotinic Ach receptors. Centrally produces strong dependency.
When plasma levels low, craving is high.
TREAT: gum, inhalers, patch
GUM- shouldn't be chewed, can cause tingling/jaw pain.
lozenge to be kept in mouth, SE: HA, FLATULENCE.
PATCH= dosed based on how many cig smoking. Can cause skin rash/sleep disturbances.
(remove at night)
INHALER=SE: Cough/scratchy throat.
avoid in asthma.
ZYBAN= moa unknown, possible noradrenergic effects.
one yr quit rate 22-32%, AE: difficulty sleeping, GI upset.
CHANTIX= works at agonist on subtype of nicotinic Ach receptor. blocks the feeling of "Reward". No known drug interactions. AE: Nausea, HA, insomnia, abnormal dreams.
BUPROPRION HAS BLACK BOX WARNINGS: Depression, suicidal ideation, suicide attempts, aggression, hostility.
Weigh risks vs benefits, asses psych status.

Front 52

TRUE OR FALSE
NSAID'S can precipitate asthma and anaphylactoid reactions in aspirin sensitive patients.

Back 52

TRUE

Front 53

TRUE OR FALSE
Salicylate build up can lead to tinnitus/hearing loss?

Back 53

TRUE

Front 54

PREGNANCY WARNINGS REGARDING NSAID'S?

Back 54

Avoid in 3rd trimester, Category D Premature closure of Ductus Arteriosus.

Front 55

TRUE OR FALSE
NSAID'S can displace highly protein bound agents (Warfarin, phenytoin, sulfonamides, digoxin)

Back 55

TRUE
Can also decrease effects of diuretics, beta blockers, ace's via suppression of renal prostaglandins.

Front 56

Which anti-gout med increases the levels of NSAID'S?

Back 56

Probenecid- Because it blocks the excretion of acids.

Front 57

How does ibuprofen decrease pain?

Back 57

By inhibiting COX and prostaglandins.

Front 58

Methotrexate?

Back 58

Used to treat RA, inhibits t cell activation.
AE: include stomatitis, leukopenia, fatigue, fever.
PCN can inc. risk of toxicity.
Monitor CBC, liver function tests, creatinine.

Front 59

Acetaminophen?

Back 59

-Similar efficacy and potency as ASA.
-No anti-inflammatory effect
-Overdose can cause fatal hepatic injury
-Max safe dose 4g per day
-Caution in pt on isoniazid, heavy ETOH

Front 60

What is the black box warning for NSAID'S?

Back 60

Can have lethal effects for CV and GI Risks (bc inhibition of cox 2 means increased risk of clotting)
Severe GI BLEEDING, PUD.

Front 61

Characteristics of full opioid agonists?

Back 61

Indicated for moderate to severe pain.
No ceiling effect.
Tolerance can develop.
ex: codeine, hydrocodone

Front 62

WHICH TCA is also used for headache, migraine, nerve pain, PTSD, eating disorders, and has anti-cholinergic side effects?

Back 62

Amytriptalline

Front 63

Trial period for anti-depressants?

Back 63

8 weeks

Front 64

Treatment for acute GOUT?

Back 64

NSAID'S, COLCHICINE, GLUCOCORTICOIDS.

Front 65

TREATMENT FOR CHRONIC GOUT?

Back 65

ALLOPURINOL, PROBENECID, SULFIPYRAZONE.

Front 66

Steroids should be tapered off over 2 weeks to avoid what?

Back 66

Addisonian crisis

Front 67

FIRST LINE THERAPY FOR ASTHMATICS?

Back 67

LEVALBUTEROL

Front 68

TRUE OR FALSE
INHALED DOSES OF STEROIDS ARE SMALLER BC THEY AVOID FIRST PASS METABOLISM?

Back 68

TRUE

Front 69

Probenecid?

Back 69

Prophylactic treatment of gout.
No effect on acute!!
SE: Hypersensitvity, GI distress
MOA: Decreases urate reabsorption in proximal tubules
*Blocks secretion of PCN

Front 70

Acute gout tx?

Back 70

NSAID'S, COLCHICINE, GLUCOCORTICOIDS

Front 71

TX of chronic gout?

Back 71

Allopurinol, Probenecid, Sulfinpyrazone

Front 72

Salicylates? Indications? DIfference from NSAID'S? SE?

Back 72

More commonly used to prevent plt aggregation, good for mild to mod. pain.
*can precipitate asthma in ASA sensitive pt*
SE: GI bleeding, PUD
Overdose can cause tinnitus and metab. acidosis.
Avoid w viral cond. in kids: Reye's syndrome

Front 73

true or false
Non-acetylated salicylates have a better tox profile Bc they don't interefere w plt. aggregation and don' t cause GI bleeding. Also they are tolerated by asthmatic patients

Back 73

TRUE

Front 74

WHAT IS SIGNIFICANT ABOUT CELEBREX?

Back 74

Selectively inhibits COX 2.
(COX2 works as a vasodilator and platelet inhibitor)
So therefore, dangerous to give to pt. w hx of uncontrolled HTN, OR ischemic heart dz, bc of risk of excessive plt aggregation and vasoconstriction.
Weigh benefits vs risks

Front 75

Which opioids agonize at mu receptors?

Back 75

Morphine, codeine, fentanyl, heroin

Front 76

Which opioids agonist at k receptors?

Back 76

Pentazocine

Front 77

Treatment for RA?

Back 77

For symptoms:
NSAID'S, CORTICOSTEROIDS (intra-articular, systemic)
for prevention or to slow dz progression: DMARD'S

Front 78

Some long term effects of corticosteroids?

Back 78

Hyperglycemia, Cataracts, Glaucoma, Osteoporosis, Cushings, Addrenal suppresion, Na and water retention.

Front 79

What are the pathways that ETOH affects and treatment for ETOH addiction and withdrawal?

Back 79

GABA, NMDA, cannabinoid receptors.
GABA- Mediates anxiolytic and sedative effects, motor coordination, tolerance and dependance.
TRMT: Benzos, antabuse, campral, naltrexone

Front 80

Which three benzo's have the least likely drug interactions, have a short duration, and don't have active metabolites?

Back 80

LOT=
LORAZEPAM
OXAZEPAM
TEMAZEPAM

Front 81

Which three benzo's are long acting and less likely to cause withdrawl symptoms bc of longer half life?

Back 81

CDC=
CLONAZEPAM
DIAZEPAM
CHLORDIAZEPOXIDE

Front 82

How does naloxone work?

Back 82

Pure competitive opioid antagonist.
(Displaces the agonist at the site of the receptor)
Parenteral only.
Reversal of opioid OD.

Front 83

REVIA?

Back 83

Pure competitive opioid antagonist.
Given PO in reg release and extended release
Longer half life
trmt for alcoholism.If on opioids, could have withdrawal.

Front 84

Two anticholinergics used for asthma and COPD?

Back 84

Ipatromium bromide and Tiotropium