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Pharm > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

1-antihistamines

2-histamine distribution

3-histamine release

4-histamine receptor subtypes

A

1-H1 blockers—-used for mild allergy, rhinitis, cold symptoms, & controllign nausea

  • usually in acid-related disorders of the stomach
  • in dentistry—antihistamines w/ CNS activity= used for sedative & anti-nausea effects
  • –they inhibit salivary & airway secretions

2-amine signaling molecule from AA histidine

  • in the body but high in tissues w/ mast cells
  • skin, mucosal of lung & GI
  • basophils have histamines—imp neurotrans
  • in gastric= secrete histamine= stimulus for acid production by parietal

3-via antibody/antigen release of histamine from mast cells—component of type 1 IgE allergic reactions

  • also released as part of IgM
  • also via chemical/anaphylactoid release, not immuno

4-H1-H4 = GPCRs—linked to diff intracellular 2nd messenger pathways
H1= operates via Gq and PLC-IP3-Ca2 & cAMP
all histamine antagonsists block H1 & H2 receptors
***in this presentation all block H1 receptor subtype

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2
Q

1-integument

2-cardio

3-airways

4-GI

5-nervous

A

1-histamine in skin= triple response of lewis

  • few seconds= red spot few mm in diameter around injection= product of local NO to H1 activation
  • delayed & slow bright red flare around spot= discharge around nerve terminals
  • w/in min a wheal appears in red spot= edema= inc vascular perm

2-H1 & H2 receptor activation= vasodilation of arteriole
-H1= rapidi & transient NO vasodilation
H2= cAMP= longer vasodilation
-dec BP= bc of dec in volume ===histamine shock

3-H1= dominant subtype in human bronchiolar SM= bronchoconstriction
-asthmatics sensitive to bronchospastic effects of exogenous histamine

4-histamine released from ECL of stomach epi in response to ACh by vagal discharge and by hormone gastrin

  • released histamine then activates H2 receptors on parietal cells= synthesis & secretion of HCL
  • peptic acid production & selective H2 blockers (tx for stomach acids)

5-regulation of thermoreg, circadian rhythm, sleep, appetite, learning & memory
H1= nerve endings produce pain, burning & itching

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3
Q

1-scromboid food poisoning

2-cutaneous mastocytosis

3-carcinoid tumors

A

1-eating tuna or histidine rich fish—inadequately refrigerated

  • bacteria convert histidine to histamine—not destroyed via cooking
  • causes flushing, rash diarrhea & headache
  • quick after ingestion—need H1 or H2 antag to tx

2-rare w/ overprolif of mast cells in upper layers of skin

  • urticaria pigmentosa= common subtype & seen by small macule or raised papules= freckles
  • –itching= histamine release

3-rare neuroendocrine tumors in digestive tract & lungs

  • *-secrete histamine & serotonin/bradykinins/prostaglandins**
  • pruritis (histamine) , diarrhea (seratonin), & flushing
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4
Q

1-therapeutic antihistamines

2-antihistamines reduce severity

A

1-divided into 1st & 2nd generation agents

  • distinctions between them= CNS penetration & anticholinergic effects
  • –1st generation- cross BB barrier & cause sedation (children & elderly) &&& block cholinergic receptors= dry mouth & urinary retention
  • -1st generation can be more strong w/ sedation*
  • –2nd generation= in periphery & are free of CNS effects & lack cholinergic activity—function as inverse agonists but not antagonists (functional antag of histamine)

2-pain, itch, flare, vasodilation, inc vascular permeability & nasal congestion

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5
Q

1-histamine antag

2-allergy

3-cold

4-nausea

5-sedatives

6-other

A

1-dont block histamine release from mast cells but block effects of histamine at target cells—dont reverse anaphylaxis & arent imp in asthma therapy

2-antihistamines used for allergy symptoms= rhinitis, relief of sneezing, wheezing, itching of ENT

3-antihistamines alleviate burning, itching, & runny nose
-common in OTC cold remedies

4-antihistamines are useful antiemetics in tx & prevention of motion sickness & vertigo
-can treat nasua & vomiting during preggo

5-H1 antag= sedation—-in night time cold remedies= nyquil & OTC sleep aids

6-due to anticholinergic effects, antihistamines used in context
-mgt of parkinson & pulm medicines

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6
Q

1-ADME

2-adverse effects

A

1-antihistamines available in prep= oral, injection, topical, & opthamologic

  • rapidly absorbed , produce a peak effect w/in 1-2 hrs
  • –w/ duration of 4-6 hrs
  • some metabolized by liver

2-w/ antihistamines that cross BB barrier…sedation= common— 1st generation—
patients develop tolerance to sedation—effects inc w/ alc, barbiturates, benzodiazepines & opiods

  • 1st generation antihistamines—w/ anticholinergic= dy mouth, hot skin, constipation, retention, etc—pentrate CNS= severe sedation
  • acute antihistamine poisoning resembles atropine poisoning= excitation, hallucination, tremor, mydriasis, fever

-terfenadine & astemizole—withdrawn bc of arrhythmias in patients that inhibited conversion of antihistamines into active form
prodrugs block cardiac K channels

-no antihistamines in late preggo

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7
Q

1-very sedating 1st generation antihistamines

2-sedating 1st generation antihistamines

3-2nd generation H1 antag (non sedating)

A

1-Promethazine hydrochloride (phenergan)
-hydroxyzine (visatril)

2-diphenhyramine (benadryl)

  • dimenhydrinate (dramamine)
  • meclizine (antivert)

3-loratadine (claritin/alavert)

  • desloratidine (clarinex)
  • certirizine (zyrtex)
  • levocertirizine (xyzal
  • fexofenadine (allegra)
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8
Q

1-epinephrine

2-levonordefrin

3-adrenergic receptors at smooth muscle end organs

4-Norepinephrine

A

1-sympathomimetic—vasoconstrictor w/ LA
stimulates all alpha & beta receptors
-tx of shock & asthma bronchoconstriction

2-vasoconstrictor—combine w/ mepivacaine—structure w/ adrenergic receptor are close to NE

3- ABCD
Alphas Constrict
Betas Dilate

4-stimualtes a1 & b1 receptors but not B2

  • vasoconstriction= inc BP
  • discontinued as alternate to epi to mix w/ LA
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9
Q

1-selective B2 agonists

2-selective B3 agonists

3-selective a1 agonists

4-alpha recetors

A

1- has “ter” in it
-inhaled= tx of bronchoconstriction in asthma & COPD

2- has “begron” in it
-orally for over-active bladder—relaxes SM via B3

3-“rin”
-tx of nasal congestion & ortho hypotensive symptoms

4-“sin” in it, stimulate alpha recepors “rin”

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10
Q

1-indirect acting sympathomimetic agent

2-cardio condition DANGERS

3-symp nerve activity

3-blocking b2 in epi

A

1-cocaine—good anesthetic - inhibits reuptake of NE at symp nerve terminal= leaving NE available to receptors present—inhibits uptake of E too
by that inhibition= constriction of BV at site of Local injection—mucuous membranes & via nose

2-cardio condition= exacerbated via epi if in sysetmic
OR if px is taking drug that blocks beta 2 adrenergic = inc in systemic arterial pressure bc alpha receptor vasoconstriction isi left unopposed by beta 2 vasodilation

3-high symp nerve activity= stimulate saliva secretion
but much less volume than parasymp nerves & has more proteins/mucus
=constriciton of BF to salivary glands= drying cavity & anxious px

4-block b2 in epi it is basically like NE

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11
Q

1-beta blocker

2-beta blockers

A

1-nonselective b blocker can inhibit beta 2 receptor mediated vasodilation= inc in systemic arterial p after admin of epi by dentist bc alpha receptor mediated vasoconstrictor of epi will be unopposed by b2 vasodilation

2-“olol”
acebutolol
atenolol
Esmolol
Metoprolol
Nadolol
Pinadolol
Propranolol
Timolol

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12
Q

1-acebutolol

2-Atenolol

3-Esmolol

4-Metoprolol

5-Nadolol

6-Pindolol

7-Propranolol

8-Timolol

9-labetalol

A

1-Receptor= B1
Partial Agonist
Membrane Stabilizing

2-Receptor= B1
Low Lipid Solubility

3-Receptor = B1
Low Lipid Solubility

4-Receptor= B1
Moderate Lipid Solubility

5-Receptor= B1 & B2
Low Lipid Solubility

6-Receptor= B1 & B2
Partial Agonist
Moderate Lipid Solubility

7-Receptor= B1 & B2
Membrane Stabilizing
High Lipid Solubility

8-Receptor= B1 & B2
eye

9-combination of nonselective B-blocker plus a selective a1-blocker
-tx of moderate to severe primary hypertension & emergency tx of hypertensive crisis

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13
Q

1-1-inhibition of B1 receptors

2-inhibition of B2 receptors

3-partial agonists

A

1-inhibit cardiac B1 receptors…all b-blockers dec symp cardiac functions (HR, contractility, conduction)
by dec HR & contractility= dec myocardial O2 deficity= angina sooo= antianginal
-dec rate & contractility= dec CO= dec arterial pressure in hypertensive= dec in renin secretion=antihypertensive
-dec automaticity= prevent arrhythmias= slowing conduction velocity= tx of supraventircular arrhytmias

2-inhibiting B2 receptor mediation of aqueous humor in eye—lowering intraocular pressure to tx glaucoma
-timolol- used bc it has no membrane stabilizing action

3-w/ ISA dont interfere as much w/ B2 mediated relaxation of vessels in Skeletal muscle—enhance relaxation to dec total peripheral arterial resistance
===antihypertensive mechanism

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14
Q

1-mechanism of action for a adrenergic blockers

2-side effects

A

1-inhibition of vascular & peripheral a adrenergic receptors= most important

  • noncomp inhibition (phenoxybenzamine)= action slows in onset but irreversible
  • comp inhibition= fast in onset & can be reversed
  • dec in BP= dec in vascular resistance bc of inhibition of a1 mediated arterial vasoconstriction

2-too much lost of a-receptor functions in body= nasal congestion, dec ejac, tachycardia, fluid retention & orthostatic hypotensive symptoms

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15
Q

1-noneselective a1 a2 blockers

2-selective a1 blockers

A

1- phenoxybenzamine
phentolamine

2-prazosin
terasozin
doxazosin
tamsulosin
alfuzosin
silodosin

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16
Q

1-phenoxybenzamine

2-phentolamine

A

1-prevents epi from binding

  • long acting irreversible inhibitor of a1 & a2
  • prevents severe catecholamine hypertensive episode during preop period prior to surgery
  • in px’s to treat hypertension in pheochromocytoma

2-reversibly inhibits a1 & a2 receptors

  • *short** acting
  • dx of phenochromocytoma
  • oraverse = reverse oral soft-tissue anesthesia
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17
Q

1-prazosin

2-side effects of alpha blockers

3-doxazosin & terazosin

4-tamsulosin & silodosin

5-alfuzosin

A

1-selective a 1 blocker—tx of mild-mod hypertension

  • relaxes SM of bladder & urethra= relieving obstructive urinary symptoms of BPH
  • used for raynauds & PTSD

2-orthostatic hypotension w/ syncope=1st dose phenomenon

3-newer= like prazosin but have longer 1/2 lives

4-blocking subtype A alpha 1 receptor

  • in SM of bladder & prostate
  • treat BPH = more specific w/ less side effects

5-used for BPH= uroselectivity
-accumulates in prostatic tissue

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18
Q

1-standing upright

A

1-suddent standing upright after reclining = orthostatic hypotensive if taking phenoxybenzamine & prazosin, doxazosin & terazosin
—maybe in tamsulosin, silodosin & alfuzosin

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19
Q

1-peripherally acting symp neuronal blockers

2-centrally acting symp neuronal blockers

A

1-dec availability of symp transmitter NE to receptors
-reserpine

2-stimulates CNS a2 adrenergic receptors= indirectly reduce nerve traffic from central symp vasomotor centers to periph organs

  • *methyldopa
  • clonidine*
  • guanabenz
  • guanfacine
20
Q

1-reserpine

2-centrally acting adrenergic neuronal inhibitors

A

1-dec uptake of DA & NE into storage vesicles w/in symp nerve endings===depleting stored level of NE
in CV= reduces BP by dec CO & peripheral arterial resistance
—tx of hypertension
side effects= sedation & mental depression bc transmitter depletion
—postural hypotension, bradycardia & fluid retention bc of periph sympathetic depleting mechanism
-severe diarrhea & ulcers bc of unopposed parasymp in GI tract

2-a2 receptor agonists—act more at CNS than at a2 sites

  • act on vasomotor centers= dec symp outflow from peripheral organs like heart, kidney, vessels
  • no interference w/ normal reflex mediated changes in symp outflow
21
Q

1-alpha methyldopa

2-clonidine

A

1-enzymes that convert dopa to DA to NE also convert to alpha methylNE= a2 adrenergic **agonist

  • central vasomotor= dec outflow of symp to peripheral**===dec HR & CO & renin
  • tx of hypertension during preggo
  • side effects= dry mouth & sedation & can cause autoimmune disorders

2-direct alpha 2 adrenergic agonist, dec symp flow from CNS vasomotor centers

  • tx of hypertension (like methyldopa) & for tx of withdrawal of addictive drugs & ADHD/hotflashes/PTSD
  • orally & dermal path for smoother BP control
  • in spine= analgesic
22
Q

1-guanaben

2-guanfacine

3-long term use of reserpine

4-centrally acting agents

A

1-alpha 2 antihypertensive use & side effects like clonidine
-lowers cholesterol & fluid retention= less than for clonidine

2-tx of ADHD in kids
-alpha 2 hypertensive use= like clonidine but less sedation

3-may cause supersensitivity to action of catecholamines= CV problems

4-known to cause dry mouth= inc incidence of oral candidiasis/ dental caries

23
Q

1-ganglionic stimulant & inhibitor

2-tx of adverse nicotine effects

3-smoking cessation

4-dental related

A

1-nicotine—act on nicotinic receptors in autonomic ganglia

  • agonist at low doses= stimulates receptor & cell
  • antagonist at high doses= inhibits receptors & cell
  • affects all nicotinic receptors
  • –CNS, CV, GI, & Skeletal Muscle

2-symptom directed

  • GI symptoms like diarrhea
  • CV symptoms= hypotensive fainting
  • skeletal muscle symptoms= resp paralysis

3-fums, pathces, sprays, inhalers
-gradually dec doses to wean pt. off addiction

4-tobacco use= perio disease & delayed would healing

24
Q

1-b2 agonist bronchodilators

2-muscarinic antagonist bronchodilators

3-methylxanthines

4-corticosteroids

5-omalizumab

A

1-albuterol
formoterol
epinephrine

2-ipratropium
tiotropium
aclidinium

3-theophylline

4-prednisone
budesonide
fluticasone
beclomethasone

5-anti-IgE ab

25
Q

1-leukotriene pathway inhibitors

2-mast cell stabilizer

3-coformulations

A

1-zileuton
montelukast

2-cromolyn

3-advair diskus
combivent
symbicort

26
Q

1-asthma

2-explanation of asthma

A

1-chronic disease in kids

  • prevalance rate: 5-17 yrs old
  • blacks are more likely to get it & die from it
  • asthma affects 7% of preggo women
  • strong genetic component—many responsible genes
  • allergenic rhinitis in 80% & also eczema
  • atopy= risk factor and predisposition to allergenic hypersensitivity reactions w/ high IgE levels

2-IgE mediated immune reaction

  • allergens provoke IgE production
  • IgE bind to mast cells, release histamine/leukotrienes/prostaglandins
  • bronchoconstriction, vascular leakage= early response
  • several hours later= late asthma response= infiltration of immune mediators & bronchiole constriction
  • most astham attacks arent triggered by allergens but by viral infection
27
Q

1-asthma triggers

2-airway histo

3-in dentistry

A

1-resp infection, rhinovirus & influenza

  • household allergens: dust/bugs
  • environmental: cold, fog, smoke
  • emotions: anxiety, stress, laughter
  • chemicals: aspirin, NSAIDS, nonselective B blockers

2-airway obstruction—bronchospasm, edema, & mucus hypersecretion
bronchial hyper-responsiveness
airways inflammation—mast, Th2, eosino, lympho

3-stress of exam
aspirin/NSAIDS
opioids
Dec Resp Drive
Pts. not able to recline for long periods
Xerostomia bc of mouth breathing
inhaled steroids= delay healing time—predispose to oral candidiasis

28
Q

1-asthma pharmacotherapy

2-preferred mode of delivery

3-oral dose

A

1-focuses on airway dilation & anti inflam activity

  • *—B2 agonists & corticosteroids**
  • –muscarinic antag
  • –methylxanthines
  • –mast cell stabilizers

2-inhaled

  • *-reduces side effects of beta agonists & inhaled corticosteroids**
  • required for anticholinergic & cromolyn
  • >80% of dose swallowed into GI even when admin

3-oral dose for same drug is 20x’s larger than inahled dose
-more systemic side effects

29
Q

1-b2 receptors

2-b2 agonists

3-b2 agonists adverse effects

A

1-inhibitory= relax SM—bronchioles, arterioles, uterus, GI, iris, ciliary
excitatory= SkM= inc contractility/glycogenolysis
-heart= inc tropic properties
-liver= inc genolysis & neogenesis
-islets= inc insulin secretion
——-but mainly SM relaxation via gAMP—activates a signaling cascade that inhibits contractile mechanisms & reduces cell excitability
*B2 agonists reverse bronchoconstriction—activation of B2 on airway cell types contribute to therapeutic effect

2-relieve bronchoconstriction and get max bronchodilation in 15-30 min

3-are extrapulomnary

  • uncommons w/ inhalers—muscle tremor bc of skeletal muscle B2 & tachycardia bc of arterial B2
  • hypoxemia bc of inc V/Q mismatch
  • hypokalemia bc of stimulation of muscle K uptake
30
Q

1-epi

2-antimuscarinics

3-caffeine

A

1-bronchodilator —activates a, B1, & B2 receptors
-inc vasoconstriction, inc peripheral vascular resistance, and dec mucosal edema (including in the upper airway)
-B1= inc heart inotropy & chronotropy
-B2= bronchodilation
side effects= tachycardia, arrhythmias, worsening of angina

2-2ndary agents…not as effective as B2 agonists
in COPD—antimuscarinics are bronchodilators of choice
-reduce air trapping & improve exercise tolerance

-block excitatory muscarinic receptors on SM

3-in severe asthma, pts who dont response to B2 agonists and in COPD
-side effects= nausea, vomiting & headache

31
Q

1-Theophylline

2-inhaled corticosteroids

A

1-PDE inhibition

  • blocks adenosine receptors, inc IL-10 release
  • prevent proinflamm gene regulation
  • promote apoptosis of eosinophils
  • quickly & completely absorbed from GI
  • –side effects= nausea, vomiting & headache

2-1st line therapy for all but mildest asthmatics
useful in other inflamm lung diseases—sarcoidosis, interstitial lung diseases, pulm eosinophilic
-ICS are much less effective in COPD
-activate glucocorticoid receptors—GR receptors= transcription factors
-antiinflamm arises from transcriptional repression
–prevents vascular perm & inhibits effect on mucus glycoprotein secretion, no direct effects on contractile SM

32
Q

1-addition of acetyl groups to histone relaxes DNA

2-adverse corticosteroids

3-numerous ICS

A

1-histones are rich in lysine residues that can acetylate

  • relaxation allows for easier reading
  • removal of acetyls carried out by HDAC (histone deacetylases)—inc HDAC= gene repression

2-local ICS effects include hoarseness,weakness of voice, & oropharyngeal candidiasis

3-are available—budesonide, fluticasone have lower oral bioavailability bc of 1st pass metabolism

  • –fewer side effects
  • early therapy give greater improvement
  • search for dissociated steroids= SEGRAs (selective glucocorticoid receptor agonist), retaining gene repression but minimizing pro transcription
33
Q

1-antag of inflamm mediators

2-immunosuppressive

A

1-anti histamines= little benfit in asthma
anti leukotrienes= add on for asthmatics poorly controlled by ICS

2-omalizumab= anti IgE Ab—blocks binding to IgE on mast cells

  • expensive
  • used in severe asthma
  • not in ectopic dermatitis
34
Q

1-b2 agonists

2-corticosteroids

A

1-functional antagonists of airway contraction

  • inhibit bronchonstriction & cause bronchodilation on airway SM
  • prevents mast cell release of histamine/bronchoconstrictors
  • reduces microleakage & inc ciliary escalator
  • –short= albuterol (SABAs)
  • –long=formoterol & salmeterol (LABAs)
  • –use epi in a life threatening situation—A1= vasoconstriction B1= inotropy

2-no direct bronchodiliating but turn off proinflam genes= protect airways from damage
-lipid soluble that bind to glucocorticoid receptors
& goes to DNA
-budesonide & fluticasone= 1st pass metabolism
-dysphonia (hoarseness of voice) common side effect of ICS

35
Q

1-muscarinic antagonists

2-methylxanthines

3-leukotriene pathway inhibitors

4-Advair

5-combivent

6-symbicort

A

1-bronchiolar Sm popuated w/ cholinergic muscarinic receptors of M3 subtypes

  • activation causes SM contraction via Ip3-Ca pathway
  • muscarinic antagonism promotores bronchodilation
  • tiotropium, ipratropium & aclidinium

2-theophylline

  • direct bronchodilators to relax SM—additional anti-inflam actions
  • cheap
  • broncodilation from inhibition of SM PDE that break down cAMP & are antiinflam

3-interrupt leukotriene synthesis /receptors
-aspirin exacerbated asthma —AERD

4-fluticasone & salmeterol—ICS & B2 agonist

5-ipratropium & salbutamol—M antagonist & B2 agonist

6-umeclidium & vilanterol—m antagonist & B2 agonist

36
Q

1-strong analgesis (u agonists)

2-partial agonists & mixed agonist/antagonists analgesics

3-opiod antagonists

A

1-morphine
codeine
fentanyl
heroin
Hydrocodone
hydromorphone
meperidine
methadone
oxycodone

2-pentazocine
-buprenorphine
butorphanol
tramadol
tapentadol

3-naloxone
naltrexone

37
Q

1-opiate

2-opioid

3-narcotic

4-analgesic reaction

A

1-derived from opium

2-similar to drugs derived from opium

3-sleep inducing but can be seen to mean opioid

4-morphine is more effective for dull constant pain than sharp somatic pain
-at cellular & molecular levels—morphone= agonist at receptors for endogenous opioid peptides & modifies processing of pain

38
Q

1-Mu opioid receptors

2-K opioid receptors

3-D opioid recetors

4-morphine

5-pentazocine

6-naloxone

A

1-in brainstem, spinal cord & limbic
-supraspinal analgesia, sedation & euphoria

2-in brainstem, spinal cord, limbic system
-mediate spinal analgesia, sedation & dysphoria

3-brainstem & limbic system
mediate dysphoria & hallucinations

4-opioid analgesics…strong at mu, moderate at k and weak at D

5-related drugs act as strong agonists at k receptors, partial agonists/antag at mu

6-antagonists at all types of opioid receptors

39
Q

1-morphine

A

1-sedation & mental clouding—floating dream like state

  • relief of anxiety & apprehension
  • euphoria or dysphoria
  • nausea
  • depressiong of respiration( toxicity)
  • constriction of pupils—pin point
  • antitussive= depression of cough control
  • seizures
  • endocrine disturbances
  • inc circular SM dec propulsive of longitudinal= dec GI motility, inc retention, bronchoconstriction
  • orthostatic hypotension
  • cutaneous vasodilation
  • inc CSF pressure
  • immunosuppression
  • —route of admin via—IV, IM or SC
  • less potent bc of 1st pass effect
  • metabolism in the liver & excretion in urine
  • can cross placenta
40
Q

1-opioid poisoning

2-morphine*

3-codeine

4-hydromorphone

5-oxycodone

6-hydrocodone

A

1-CNS depression (stupor/coma)
depressed depth & rate of respiration
pin point pupils
—tx= support respiration & narcotic antag

2-sulfate salt—Route of admin- absorbed from GI not effect orally bc of 1st pass metabolism
-10 mg dose —used for more severe pain

3-phosphate or sulfate salt—weak

  • route of admin = orally
  • dose 1/12 potency of morphine—30-60 mg
  • mild/mod pain & antitussive

4-like morphine but more potent

5-morphine/codeine mix..orally for mod-severe pain
-sustained release oral prep for mgt of severe chronic pain

6-like codeine & oxycodone
orally w/ acetaminophen for mild-mod pain
-antitussive currently one of the most widely prescribed opioids
-most common

41
Q

1-meperidine

2-heroin

3-methadone

4-fentanyl

5-opiod combo prep

A

1-synthetic
-route of admin= oral /paraenteral
1/10 potency of morphine
-weaker effects on SM than morphine–less constipation & urine retention
-mod to severe pain
-not appropriate for chronic pain bc of buildup of an active metabolite that can cause seizures

2-more potent & euphoric than morphine—duration of action about 4-6 hrs

  • not in US bc of abuse
  • injection, snorting or smokine

3-less euphoric & longer duration than heroin or morphine

  • analgesic in tx opioid addiction
  • dosing= tricky and needs to be done carefully w/ monitoring

4-very potent mu agonist

  • given parenterally to supplement surgical anesthesia
  • available to manage chronic pain
  • tx of breakthrough pain
  • combo prep containing fentanyl plus droperidol can induce neuroleptic analgesia—surgery
  • admin Nitrous oxide= neuroleptic anestesia

5-hydrocodone/acetaminophin

42
Q

1-pure antagonists

2-mixed agonist-antagonists

3-pentazocine

4-butorphanol

5-buprenorphine

A

1-block all types of opioid receptors

2-block some types of opioid receptors but act as agonists

3-agonists effects are dom—at K receptors but partial at Mu receptors & antagonists at mu receptors in high doses

  • less effective than morphine
  • sedation
  • CNS stimulation w/ hallucinations are more common than w/ morphine

4-like pentazocine

5-partial agonist at mu, vert high= mu antag

  • analgesic effects may be less than morphine= abuse= lower
  • reduces drug craving in heroin addicts
  • suboxone= combo product containing bupre & naloxone
  • injection, sublingually or intranasally
  • primary agent used for office based tx of opioid addiction outside of methadone clinics
43
Q

1-tramadol

2-tapentadol

3-pure opioid antag

4-naloxone

5-naltrexone

A

1-mild- mod pain

  • weak mu agonist
  • inhibits reuptake of NE & serotonin
  • good analgesis w/ only mild side effects in general—side effecst= opioids

2-like tramadol, but has greater activity at mu receptors
-mod to severe pain

3-block most opioid effects & can precip a withdrawal syndrome in addicts

4-drug of choice of opioid posiining can reverse respiratory depressant

  • not effective orally bc of 1st pass metabolism
  • included in combo w/ oral narcotic analgesics to prevent abuse—precips withdrawals in addicts
  • short duration

5-orally effective, long acting antag

  • used in immunizing addicts
  • risk of hepatotoxicity is a drawback
  • effectiveness in long term tx of opioid dependence isnt clear
  • patient compliance = problem
  • opioid addic must first be detoxified before naltrexone initiated
  • dec craving for alc in alcoholics & approved for use in tx of alcholism
44
Q

1-therapeutic of opioid antag

2-opiod dependence & addiction

3-characteristic of acute withdrawal syndrome

4-duration & intensity of acute withdrawal

A

1-tx opioid induced overdose toxicity= resp depression in adults as well as in neonates

  • dx opioid physical dependence
  • tx of compuslive opioid abusers
  • reduce craving for alc in recovering alc

2-physical dependence—tolerance= high degree of tolerance to the analgesic, euphoric sedative & resp depressant effects of opioids= little tolerance to opioid induced miosis of constipation

3-craving
anxiety, hostility, insomina
dilation of pupils
GI hypermotility
goose flesh, chills, sweating
hyperalgesia

4-short acting= heroin= intense symptoms, short duration
long acting= mod symptoms, long duration

45
Q

1-biochem basis of dependence

2-tx of dependence

3-hospital dependence vs street dependence

A

1-physical dependence to opioids is currently thought to result from compensatory changes in opiod receptors

  • one mechanism= depletion of endogenous stores of enkephalins in response to chronic exposure to opiod agonists—specialized neurons release enkelaphins & endorphins that act on opiod receptors on target cells so you feel good
  • agonists bind to and stimulate synaptic opioid to produce the high
  • chronic= opiod agonist that will down regulate the synthesis & become depleted of transmitter

2-cold turkey vs weaning pt off

  • methadone= substitution= wean off or maintenance= maintant pt on drug
  • buphenorphine= alt to methadone
  • naltrexone= long acting opioid antag
  • clonidine= reduce severity of withdrawal symptoms = dec craving for drug

3-opioid dependence in medical= medically valid
known and strictly controlled doses & then weaned off
in street= mild altering effects
= unknown doses w/ insanitary condition

  • –HEP, Misc infections, AIDS
  • –OD

Pharm (3 decks)

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