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Flashcards in Exam 2 Deck (45):
1

1-antihistamines

2-histamine distribution

3-histamine release

4-histamine receptor subtypes

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

2

1-integument 

2-cardio

3-airways

4-GI

5-nervous

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 
 

3

1-scromboid food poisoning

2-cutaneous mastocytosis

3-carcinoid tumors

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

4

1-therapeutic antihistamines 
 

2-antihistamines reduce severity 

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

5

1-histamine antag 

2-allergy

3-cold

4-nausea

5-sedatives

6-other

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 

6

1-ADME

2-adverse effects

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 

7

1-very sedating 1st generation antihistamines

2-sedating 1st generation antihistamines

3-2nd generation H1 antag (non sedating)

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)

8

1-epinephrine


2-levonordefrin
 

3-adrenergic receptors at smooth muscle end organs

4-Norepinephrine

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 

9

1-selective B2 agonists

2-selective B3 agonists

3-selective a1 agonists

4-alpha recetors

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"

10

1-indirect acting sympathomimetic agent

2-cardio condition DANGERS

3-symp nerve activity

3-blocking b2 in epi

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

11

1-beta blocker

2-beta blockers

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

12

1-acebutolol

2-Atenolol

3-Esmolol

4-Metoprolol

5-Nadolol

6-Pindolol

7-Propranolol

8-Timolol

9-labetalol

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

13

1-1-inhibition of B1 receptors

2-inhibition of B2 receptors

3-partial agonists

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 

14

1-mechanism of action for a adrenergic blockers

2-side effects

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

15

1-noneselective a1 a2 blockers

2-selective a1 blockers

1- phenoxybenzamine
phentolamine

2-prazosin
terasozin
doxazosin
tamsulosin
alfuzosin
silodosin

16

1-phenoxybenzamine

2-phentolamine

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 

17

1-prazosin

2-side effects of alpha blockers

3-doxazosin & terazosin

4-tamsulosin & silodosin

5-alfuzosin

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
 

18

1-standing upright

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

19

1-peripherally acting symp neuronal blockers

2-centrally acting symp neuronal blockers

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

1-reserpine

2-centrally acting adrenergic neuronal inhibitors

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

1-alpha methyldopa

2-clonidine

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

1-guanaben

2-guanfacine

3-long term use of reserpine

4-centrally acting agents 

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

1-ganglionic stimulant & inhibitor

2-tx of adverse nicotine effects

3-smoking cessation

4-dental related

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

1-b2 agonist bronchodilators

2-muscarinic antagonist bronchodilators

3-methylxanthines 

4-corticosteroids

5-omalizumab

1-albuterol
formoterol
epinephrine

2-ipratropium
tiotropium
aclidinium

3-theophylline

4-prednisone
budesonide
fluticasone
beclomethasone

5-anti-IgE ab
 

25

1-leukotriene pathway inhibitors

2-mast cell stabilizer

3-coformulations

1-zileuton
montelukast

2-cromolyn

3-advair diskus 
combivent
symbicort

26

1-asthma

2-explanation of asthma

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

1-asthma triggers

2-airway histo

3-in dentistry

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

1-asthma pharmacotherapy

2-preferred mode of delivery

3-oral dose

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

1-b2 receptors

2-b2 agonists

3-b2 agonists adverse effects

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

1-epi

2-antimuscarinics

3-caffeine

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

1-Theophylline

2-inhaled corticosteroids
 

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

1-addition of acetyl groups to histone relaxes DNA

2-adverse corticosteroids

3-numerous ICS

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

1-antag of inflamm mediators

2-immunosuppressive

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

1-b2 agonists

2-corticosteroids

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

1-muscarinic antagonists

2-methylxanthines

3-leukotriene pathway inhibitors

4-Advair

5-combivent

6-symbicort

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

1-strong analgesis (u agonists)

2-partial agonists & mixed agonist/antagonists analgesics

3-opiod antagonists

1-morphine
codeine
fentanyl
heroin
Hydrocodone
hydromorphone
meperidine
methadone
oxycodone

2-pentazocine
-buprenorphine
butorphanol
tramadol
tapentadol

3-naloxone
naltrexone

37

1-opiate

2-opioid

3-narcotic

4-analgesic reaction

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

1-Mu opioid receptors

2-K opioid receptors

3-D opioid recetors

4-morphine

5-pentazocine

6-naloxone

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

1-morphine

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

1-opioid poisoning

2-morphine*

3-codeine

4-hydromorphone

5-oxycodone

6-hydrocodone

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

1-meperidine 
 

2-heroin

3-methadone

4-fentanyl

5-opiod combo prep

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

1-pure antagonists
 

2-mixed agonist-antagonists

3-pentazocine

4-butorphanol

5-buprenorphine

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

1-tramadol

2-tapentadol

3-pure opioid antag

4-naloxone

5-naltrexone

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

1-therapeutic of opioid antag

2-opiod dependence & addiction
 

3-characteristic of acute withdrawal syndrome

4-duration & intensity of acute withdrawal

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

1-biochem basis of dependence

2-tx of dependence

3-hospital dependence vs street dependence

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