Term
|
Definition
-inhalation
-suppresses inflammation and decreases bronchial hyperresponsiveness (asthma)
-oral candidiasis, hoarsness, altered bone metabolisma, growth suppression |
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Term
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Definition
-supresses inflammation and decerases bronchial hyperresponsiveness (asthma)
-interact with steroid receptors in cyto--> steroid complex moves to nuc, activates glucco response element, influences protein syn. Annexins: inhib; PLA2, phospholipid to AA, PGs and leukotrienes. Reduce eosin, baso, amst + inhib their mediators, reduce edema + VD, decerase exudation, reduce sens to irritant, block late phase rxn
-oral
-effect virtually every organ in body: suppression of HPA and growth, osteoporosis, increased IOP and cataracts
-most effective antiasthmatic for severe/acute. onset of action takes hours. allergic rhitnits
-control rheumatoid arthritis in patients who do not have generalized disease
-rapidly relieve symptoms slow appearance of new bone erosions. Bridging (while classic DMARDS take effect), contin low dose therapy, short term high dose for flares, locally (intraarticular injection: flares of only a few joints)
-Inhibit recruitment of leukocytes and monocyte macropha (ihibi MIF, inhib antigen display,inhib syn IL-1, decerase activation of T cells), inhib syn/secr of chemotactic substances, arac ac metab (by stim produc of annexins which inhib PLA2) and cytokines, maintain capilalry integrity, maintain vascular tone. inhib syn IL-2 ( T cell lymphocytopenia, little B cell effect on Ab)
-withdrawl (flare up underlying disease, adrenal insufficiency) systemic (CV/renal **mineralo** (edema, hypokalemia, retention, hyperten) CNS (euphoria, depress, psychosis) endocrine (growth failure, suprresion HPA) GI (peptic ulder, hemorrhage) Immuno (sucept to infec) Metab (hyperglyc, hyperlip, neg N2 nalance) muscoskeltal (osteoporosis/ necrosis/ myopathy) ophthalmological (glaucom, cataracts)
-drugs that alter hepatic metabolism (p450 inducers increase steroid metab, inhibitos decerase steroid metab)
-allergic, cerebral or colalgen disorders, malignancies, hepatic diseases, renal disease, respiratory disorders, shock, arthritis, rheumatic carditis, dermatologic, GI
-***middle potency, less mineralocorticoid effects than hydrocort |
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Term
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Definition
-inhalation (asthma), intranasal, ocular
-inhibits mast cell degranualtion, decreases # inflammatory cells infilitrating and bronchia hyperresponsiveness
-bronchonstriction, cough, wheezing (due to irritation) nasal mucosa or eye irritation
-Alternative treatment for mild persistent asthma, exercise induced, or exposure to allergens. Prophylactic, must be administered well before patient exposed to an allergen(2-6 wks). nasal: allergic rhinit. is, eye: conjunctivitis. Not effective alone for anaphyalxis or asthm |
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Term
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Definition
-intravenously, subcut every 2-4 wks
-Ab directed against IgE. Blocks binding of IgE to mast cells and basophils. Decreases circulating free IgE (prevents mast cell degranulation)
-headache and injection site rxns (uticaria)
-allergic asthma, (allergic rhinitis- not approved but effective)
-intravenous or subcut every 2-4 wks |
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Term
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Definition
-oral
-*not a BD* inhibits PDE4, increasing intracellular levels of cAMP and reducing inflammation. Metab in liver, to N-oxide active metabolite. Good Bioavail
-GI: N, D, weight loss
-inhibitors of p450 enxymes increase blood levels. Inducers, decerase blood levels (drug interactions)
-asthma, reduction of inflammation |
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Term
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Definition
-leukotriene modifiers (long term)
-competitive antagonist at cysLT1, blocks LTC4, LTD4, and LTE4. Prevent BC from increased inflamm cell number
-Headache, GI upset, myalgia
-drug interactions: inducers/inhibitors of p450 enzymes
-anti-asthmatic prevents BC
-oral only
-allergic rhinitis (decerase nasal congestion, itching, sneezing), asthma (prevent bronchoconst) |
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Term
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Definition
-give 4 times/day
-Blocks 5-lipoxygenase, so blocks LT formation and decerases inflammation/BC
-causes: Hepatitis (monitor liver function), upset stomach
-drug interactions: inhibits P450so increased warfarin, propranolol and theophylline concentrations
-contrain for: patients w/ liver disease or increased liver enzymes
-not used as often as montelukast for anti-asthmatic |
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Term
| Albuterol (also terbutaline) |
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Definition
-activation fo beta2 recptors, increase AC--> increase intracell cAMP--> BD
-inhaled and oral
-anxiety, tremor, restlessness, tachycardia, hypokalemia (more commone with oral and parenteral administration)drug tolerance with reg use, increased exacerbations
-corticosteroids enhance response to beta agonists
-Emergency treatment with glucocorticoids. BD in asthma or COPD, prevent exersice asthma. onset 5-15 min, inhaled for acute relief, lasts up to 6 hours |
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Term
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Definition
--activation fo beta2 recptors, increase AC--> increase intracell cAMP--> BD
-inhaled
-anxiety, tremor, restlessness, tachycardia, hypokalemia (more commone with oral and parenteral administration)drug tolerance with reg use, increased exacerbations
-corticosteroids enhance response to beta agonists
-BD in asthma or COPD, prevent exersice asthma. preventatvive not for acute bronchospasm, 30-50 min onset, >12 hrs duration |
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Term
| Aminophylline (theophylline ethylenediamine) |
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Definition
-contians 85% theophylline- more sol. . take into account when dosing
-rapid infusion --> cardiac arrest and death
-increased t1/2 w/: cimetidine, macrolide antibiotics, hepatic cirrhosis, premies, oral contracept. Decerase t1/2 w/: cig smoke, phenytoin, barbiturates
-Use with caution: Hepatic or cardiac dysfunction, seizure disorders, peptic ulcer disease (increases acid secretion)
-reversible airway obstruction due to asthma or chronic lung disease |
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Term
| Theophylline (a methylxanthine: others = caffeine + theobromine) |
|
Definition
-SM relaxation (important bronchi) --> BD. Phosphodiesterase inhib --> increase cAMP, adeosine receptor blockade. Rapidly and 100% absorbed orally, sust release prep decerase flunc btwn doses and increased compliance. 1st order elim, zero order at high conc. Hepatic metab (90% elim)
-oral (not dose dependent with effects)
-CNS stim (decerase drowsiness (low doses) convuslsions (high)) increased sens of medulalry resp centers to CO2, N and V mediated by CNS action. CV: tachycardia/ PVCs (high conc), decerased peripheral vasuclar resistance (aka hypten), diuretic. Can cause seizures, aryth and death (monitor serum levels at first) Most severe can occur 1st
-increased t1/2 w/: cimetidine, macrolide antibiotics, hepatic cirrhosis, premies, oral contracept. Decerase t1/2 w/: cig smoke, phenytoin, barbiturates
-Use with caution: Hepatic or cardiac dysfunction, seizure disorders, peptic ulcer disease (increases acid secretion)
-reversible airway obstruction due to asthma or chronic lung disease-increased t1/2 w/: cimetidine, macrolide antibiotics, hepatic cirrhosis, premies, oral contracept. Decerase t1/2 w/: cig smoke, phenytoin, barbiturates
-Use with caution: Hepatic or cardiac dysfunction, seizure disorders, peptic ulcer disease (increases acid secretion)
-reversible airway obstruction due to asthma or chronic lung disease |
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Term
| Tiotropium and Ipratropium |
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Definition
-Competitive muscarinic receptor antagonists. Block BC and increased secretions
-inhaled
-not well absorbed --> no Ses. Possible dry mouth (does not cross BBB)
-COPD |
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Term
|
Definition
-interact with steroid receptors in cyto--> steroid complex moves to nuc, activates glucco response element, influences protein syn. Annexins: inhib; PLA2, phospholipid to AA, PGs and leukotrienes. Reduce eosin, baso, amst + inhib their mediators, reduce edema + VD, decerase exudation, reduce sens to irritant, block late phase rxn
-intranasal
-dry/irri/burning of nasal mucosa, sore throat, epistaxis, headache
-most effective drug to prevent and relieve allergic rhinitis symptoms. onset of action takes hours |
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Term
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Definition
-stim alpha-1 adrenergic receptors on venous sinusoids --> VC --> decerased vol nasal sinuses
-intranasal
-rebound VD and congestion w/ prolonged use, nasal irritation
-relief of congestion only |
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Term
|
Definition
-stim alpha-1 adrenergic receptors on venous sinusoids --> VC --> decerased vol nasal sinuses
-oral
-CNS excitation (insom, excit, headache, nervous), CV stim (palpi, tachy, HTN) GI (N, V), Urinary retention (males)
-contrain: CAD, HTN, enlarged prostate
-relief of congestion only |
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Term
|
Definition
-compet muscarinic receptor antag. Blocks nasal discharge
-intranasal
-dry nose/mouth, pharyngeal irri, urniary teten, increased intraoc P (inadvertent in eye)
-contrain: gluacoma, prostatic hypertrophy
-reduce watery nasal secretions (not for sneeze, itch, congest) |
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Term
|
Definition
-alpha 1R activation: Vc --> increased vaso resist, and BP. Beta R activatio: bronchodilation, increased cardiac rate and contractility. Inhib release of emdiators from mast and baso
-subcutaneously (EpiPen), every 5 mib
-toxcity or inadequate response to epi injections (need to add other therapeutic modalities)
-Anaphylaxis, hypotension and or bronchoconstriction |
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Term
| Chlorpheniramine and Diphenhydramine |
|
Definition
-1st gen antihistamines
-H1 receptor competitive antagonists of histamine. CV: part inhibi VD, block cap perm, flare + itch inhib. Airway SM: hit induc bronchocon asthmatics. Neural tissue: inibib pruritis
-oral, topical, parenteral
-CNS: decreased alertness, slow rxn, somnolence. (CNS stim certain ppl/ children, also feature of poisoning) GI: anorexia, N V D, constipation
-CNS effects worse w/ concurrent ingestion of alcohol or CNS depressents
-acute allergy (hay fever, pollinosis) w/ rhinitis, urticaria, conjunctivitis. Prevention of motion scikness, sedation. Not effective alone for anaphyalxis or asthma |
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Term
Certizine
Fexofenadine
Loratadine |
|
Definition
**Certizine: CNS: decreased alertness, slow rxn, somnolence. (CNS stim certain ppl/ children, also feature of poisoning)
-H1 receptor competitive antagonists of histamine. CV: part inhibi VD, block cap perm, flare + itch inhib. Airway SM: hit induc bronchocon asthmatics. Neural tissue: inibib pruritis Metabolites active, bind with high affin to H1 Rs.
-oral only
-acute allergy (hay fever, pollinosis) w/ rhinitis, urticaria, conjunctivitis. prolonged duration of action (days) |
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Term
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Definition
-analgesic + antipyretic sim to asprin, weak antiinflammatory, can't inhibit COX in presence of high conc of peroxidases (aka sites of inflammation), COX inhibitiom more pronouced in brain (antipyretic)
-oral or rectal. Metab in liver + small fraction by P450 to reactive metabolite NAPQ1
-low risk at low dose daily. Higher dose = NSAID effect profile
-alcohol increases liver damage risk patients w/ alcoholic lvier disease
-first line for fever/pain in children. mild/mod pain. Combine with NSAID for pain (replace opioid) |
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Term
|
Definition
-esterases (plasma) convert to salicylic acid --> covalently modify COX-1/2 (irrevers) inhib = no effect leukotri syn. Duration related to turnover rate of COX in diff tissues. Antipyretic, analgesic, antiinflam (inhib prostag produc)
-oral + rectal. Metab liver, excrete urine. Plasma 1/2 life 20 min, 2-3hrs salicylate and 30 + at toxic. Zero order, dispropor increase plasma conc w/ dose increase, saturated liver enzy increased unchanged drug urien (low dose still 1st order)
-GI (naus, vom, bleed, ulcer), renal fail, impair platelet func (inhib COX in platelets) Hypersens rxns, Reye's syn (children w/ viral infec, noninflam encephalopathy, epatic dysfunc, metabolic derange)
-increased bleeding risk with other NSAIDs or Warfarin, other drugs that cause GI ulceration
-children w/ viral infection, hypersens to NSAIDS, salicyalte poisoning (nau, vom, tinnitus, CNS effects, hyperthermia, uncoup oxida phosphor (acidosis), resp+ renal acidosis (low blood pH reduc plasma bicarc)
-mild/mod pain
-anti-inflam + analg by inhib PG produc, inhib COX. Do not prevent/slow joint destruction
-rapid analg + anti-inflam . Not for monotherapy |
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Term
|
Definition
-more selective for COX-2*. Compet inhibi active sites COX-1/2 (inhib prostag produc) no effect leukotri syn. Antipyretic, analgesic + antiinflam
-metab liver excre urine.
-Small risk w/ short term. Less severe GI tox** Long term: GI (anorex, nau, dyspep, abdom pain, ulcer), renal fail/ edema, impair platelet func, hypsersens (poten fatal) **does not increase CV events
-increase risk GI ulcer w/ glucocorticoids, low-dose asprin. Increase bleeding risk w/ Warfarin (inhib Warfarin metab/ platelet func)
-hypersens to asprin or other NSAIDs
-More effective than acetaminophen, combine with acteminophen for opoid replace or with...mild/mod pain
-anti-inflam + analg by inhib PG produc, inhib COX. Do not prevent/slow joint destruction
-rapid analg + anti-inflam . Not for monotherapy |
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Term
|
Definition
-oral or I.V.
-repletes gluthaione stores and conjugates directly with NAPQ1
-overdose of acetaminophen can be used to replenish gluthalione stores |
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Term
|
Definition
-Compet inhibi active sites COX-1/2 (inhib prostag produc) no effect leukotri syn. Antipyretic, analgesic + antiinflam
-metab liver excre urine.
- Small risk w/ short term. Less severe GI tox** Long term: GI (anorex, nau, dyspep, abdom pain, ulcer), renal fail/ edema, impair platelet func, hypsersens (poten fatal) **does not increase CV events increase risk GI ulcer w/ glucocorticoids, low-dose asprin. Increase bleeding risk w/ Warfarin (inhib Warfarin metab/ platelet func)
-hypersens to asprin or other NSAIDs
-alt to acteminophen for children ncuz adverse effects lim when used for antipyresis. More effective than acetaminophen, combine with acteminophen for opoid replace or with..mild/mod pain
-anti-inflam + analg by inhib PG produc, inhib COX. Do not prevent/slow joint destruction
-rapid analg + anti-inflam . Not for monotherapy |
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Term
|
Definition
-longest half-life (once or twice daily dose poss)* Compet inhibi active sites COX-1/2 (inhib prostag produc) no effect leukotri syn. Antipyretic, analgesic + antiinflam
-metab liver excre urine.
- Small risk w/ short term. Less severe GI tox** Long term: GI (anorex, nau, dyspep, abdom pain, ulcer), renal fail/ edema, impair platelet func, hypsersens (poten fatal) **does not increase CV events increase risk GI ulcer w/ glucocorticoids, low-dose asprin. Increase bleeding risk w/ Warfarin (inhib Warfarin metab/ platelet func)
-hypersens to asprin or other NSAIDs
-More effective than acetaminophen, combine with acteminophen for opoid replace or with..mild/mod pain
--anti-inflam + analg by inhib PG produc, inhib COX. Do not prevent/slow joint destruction
-rapid analg + anti-inflam . Not for monotherapy |
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Term
|
Definition
-Inhibit recruitment of leukocytes and monocyte macropha (ihibi MIF, inhib antigen display,inhib syn IL-1, decerase activation of T cells), inhib syn/secr of chemotactic substances, arac ac metab (by stim produc of annexins which inhib PLA2) and cytokines, maintain capilalry integrity, maintain vascular tone. inhib syn IL-2 ( T cell lymphocytopenia, little B cell effect on Ab)
-withdrawl (flare up underlying disease, adrenal insufficiency) systemic (CV/renal **mineralo** (edema, hypokalemia, retention, hyperten) CNS (euphoria, depress, psychosis) endocrine (growth failure, suprresion HPA) GI (peptic ulder, hemorrhage) Immuno (sucept to infec) Metab (hyperglyc, hyperlip, neg N2 nalance) muscoskeltal (osteoporosis/ necrosis/ myopathy) ophthalmological (glaucom, cataracts)
-drugs that alter hepatic metabolism (p450 inducers increase steroid metab, inhibitos decerase steroid metab)
-allergic, cerebral or colalgen disorders, malignancies, hepatic diseases, renal disease, respiratory disorders, shock, arthritis, rheumatic carditis, dermatologic, GI
-least potent, greatest minalocoritcoid effects **** |
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Term
|
Definition
-Inhibit recruitment of leukocytes and monocyte macropha (ihibi MIF, inhib antigen display,inhib syn IL-1, decerase activation of T cells), inhib syn/secr of chemotactic substances, arac ac metab (by stim produc of annexins which inhib PLA2) and cytokines, maintain capilalry integrity, maintain vascular tone. inhib syn IL-2 ( T cell lymphocytopenia, little B cell effect on Ab)
-withdrawl (flare up underlying disease, adrenal insufficiency) systemic (CV/renal **mineralo** (edema, hypokalemia, retention, hyperten) CNS (euphoria, depress, psychosis) endocrine (growth failure, suprresion HPA) GI (peptic ulder, hemorrhage) Immuno (sucept to infec) Metab (hyperglyc, hyperlip, neg N2 nalance) muscoskeltal (osteoporosis/ necrosis/ myopathy) ophthalmological (glaucom, cataracts)
-drugs that alter hepatic metabolism (p450 inducers increase steroid metab, inhibitos decerase steroid metab)
-allergic, cerebral or colalgen disorders, malignancies, hepatic diseases, renal disease, respiratory disorders, shock, arthritis, rheumatic carditis, dermatologic, GI
-*** most potent, no mineralcoritcoid effects |
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Term
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Definition
-adenosine acts on cell surface R, inhib produc of inflam cytok (TNF alha and gamma) + inhib other cell func. Induces increase in adenosine release from injured cells, inhibs inflam
-GI (mucositis, vom, diar) Thrombocytopenia, Nephrotocicity, if long term hepatox + pneumonitis, teratogenic. (can manage with leucovorin or folic acid*)
-DMARD of choice. Combo with TNF inhib= effective
-prego (teratogenic), renal disease, lung disease, chronic liver disease
-immunosuppressive + antiinflam. Slow acting wks to months |
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Term
|
Definition
-prodrug convert by colon bacteria to sulfapyridine and 5-aminosalicylic acid (prob increases adenosine levels, decre IL-1 and TNF-alpha release, inhibi NF-kappaB)
-GI( N,V, abd pain, dia, anorexia), hypersense to sulfapy (fever, exfoliative dermatitis, other)
-safer, for milder cases
-patients allergic to sulfa drugs
-immunosuppressive + antiinflam. Slow acting wks to months |
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Term
|
Definition
-human IgG Ab to TNF-alpha, binds it so can't binds its R
-increased risk infeciton, latent TB can activate. Injection rxns. Subcut (can cause erythema, pain pruritus)
-combo of TNF-alpha inhib with anakinra increased risk serious infections
-more effective than methotrexate and other DMARd for halting joint destruction, long term safety unclear |
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Term
|
Definition
-IL-1 R antagonist, compet antag of IL-1 R
-subcut (erythema, pain, pruitus) increased risk infection
-combo of TNF-alpha inhib with anakinra increased risk serious infections
-patients w/ infection, history recurring infection or medical condition predisposing to infection |
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Term
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Definition
-fusion protein (ligand-binding portion p75 TNF R linked to Fc portion human IgG) binds TNF alpha and beta* forms inactive complexes prevents interaction with TNF R on cell surface, activates cells
-increased risk infeciton, latent TB can activate. Injection rxns. Subcut (can cause erythema, pain pruritus)
-combo of TNF-alpha inhib with anakinra increased risk serious infections
-more effective than methotrexate and other DMARd for halting joint destruction, long term safety unclear |
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Term
|
Definition
-chimeric monoclonal Ab (mouse and human IgG portions) Binds TNF-alpha so can't bind R
-increased risk infeciton, latent TB can activate. Injection rxn. I.V. (poss infusion rxn: fever+ chills)
-combo of TNF-alpha inhib with anakinra increased risk serious infections
-more effective than methotrexate and other DMARd for halting joint destruction, long term safety unclear |
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Term
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Definition
-mu, delta, kappa GPCRs, G0 inhibib Ca, Gi activates K+, decerase NT release and neural activation, inhib pain transmission. Alter emotional pain cerebrocortex, increase euphoria and sleep, depress cough medulla
-metab to morphine. reduce pain: 1) NSAID inhiib PG, 2) opoids decerase pain transmission, antitussive effects
-used with non opiods, used for antitussive effects
-Medullary (decerase resp, increase pCO2, vomiting (trigger CTZ), tolerance), Miosis (disinhib Edinger-Westphal nuc, increase parasym, tolerance does not develop), Constipation (sphinctertone, tolerance does not develop), Biliary colic (epigastric ditress), Histamine release (itching, hypoten, broncocon (asthmatcis)*)physical dependence (abstinence syndrome: chills, fever, sweat, yawn, diarr, naus/vom, dizz, HTTN)
-other sedatives, alc/barbiturates … increase sedaiton/ decrease resp
-hepatic disease (increased oral bioavail), renal disease (accum or metab--> CNS agitation, confus, delirum), pulmonary disase (emphysema), patients with head trauma (block pupillary reflex, increase intracranial pressure)
-severe pain |
|
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Term
|
Definition
-mu, delta, kappa GPCRs, G0 inhibib Ca, Gi activates K+, decerase NT release and neural activation, inhib pain transmission. Alter emotional pain cerebrocortex, increase euphoria and sleep, depress cough medulla
-Medullary (decerase resp, increase pCO2, vomiting (trigger CTZ), tolerance), Miosis (disinhib Edinger-Westphal nuc, increase parasym, tolerance does not develop), Constipation (sphinctertone, tolerance does not develop), Biliary colic (epigastric ditress), Histamine release (itching, hypoten, broncocon (asthmatcis)*)physical dependence (abstinence syndrome: chills, fever, sweat, yawn, diarr, naus/vom, dizz, HTTN)
-other sedatives, alc/barbiturates … increase sedaiton/ decrease resp
-hepatic disease (increased oral bioavail), renal disease (accum or metab--> CNS agitation, confus, delirum), pulmonary disase (emphysema), patients with head trauma (block pupillary reflex, increase intracranial pressure)
-**greater intensity (80-100x morph) more potent, shorter duration of action, prego= tertagnic, caridac pateints --> bradycardia and hypoten
-transdermal patch
-severe pain |
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Term
|
Definition
-mu, delta, kappa GPCRs, G0 inhibib Ca, Gi activates K+, decerase NT release and neural activation, inhib pain transmission. Alter emotional pain cerebrocortex, increase euphoria and sleep, depress cough medulla
-Medullary (decerase resp, increase pCO2, vomiting (trigger CTZ), tolerance), Miosis (disinhib Edinger-Westphal nuc, increase parasym, tolerance does not develop), Constipation (sphinctertone, tolerance does not develop), Biliary colic (epigastric ditress), Histamine release (itching, hypoten, broncocon (asthmatcis)*)physical dependence (abstinence syndrome: chills, fever, sweat, yawn, diarr, naus/vom, dizz, HTTN)
-other sedatives, alc/barbiturates … increase sedaiton/ decrease resp
-hepatic disease (increased oral bioavail), renal disease (accum or metab--> CNS agitation, confus, delirum), pulmonary disase (emphysema), patients with head trauma (block pupillary reflex, increase intracranial pressure)
-**parenterally, orally, rectally. Metab liver extenssice 1st pass (oral)
-severe pain |
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Term
|
Definition
-mu, delta, kappa GPCRs, G0 inhibib Ca, Gi activates K+, decerase NT release and neural activation, inhib pain transmission. Alter emotional pain cerebrocortex, increase euphoria and sleep, depress cough medulla
-Medullary (decerase resp, increase pCO2, vomiting (trigger CTZ), tolerance), Miosis (disinhib Edinger-Westphal nuc, increase parasym, tolerance does not develop), Constipation (sphinctertone, tolerance does not develop), Biliary colic (epigastric ditress), Histamine release (itching, hypoten, broncocon (asthmatcis)*)physical dependence (abstinence syndrome: chills, fever, sweat, yawn, diarr, naus/vom, dizz, HTTN)
-other sedatives, alc/barbiturates … increase sedaiton/ decrease resp
-hepatic disease (increased oral bioavail), renal disease (accum or metab--> CNS agitation, confus, delirum), pulmonary disase (emphysema), patients with head trauma (block pupillary reflex, increase intracranial pressure)
-**less antitussive + constipating for pulm disease patients. Metab to normeperidine= proconvulsant + hallucigenic.
-good for patients with pulmonary dissease (less antitussive and constip) normeperidine accumaltes in kidney if decerased renal function, liver disease meperidine accum, normerperidine can cause seizsures so not for ppl w/ them
-severe pain |
|
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Term
|
Definition
-mu, delta, kappa GPCRs, G0 inhibib Ca, Gi activates K+, decerase NT release and neural activation, inhib pain transmission. Alter emotional pain cerebrocortex, increase euphoria and sleep, depress cough medulla
-Medullary (decerase resp, increase pCO2, vomiting (trigger CTZ), tolerance), Miosis (disinhib Edinger-Westphal nuc, increase parasym, tolerance does not develop), Constipation (sphinctertone, tolerance does not develop), Biliary colic (epigastric ditress), Histamine release (itching, hypoten, broncocon (asthmatcis)*)physical dependence (abstinence syndrome: chills, fever, sweat, yawn, diarr, naus/vom, dizz, HTTN)
-other sedatives, alc/barbiturates … increase sedaiton/ decrease resp
-hepatic disease (increased oral bioavail), renal disease (accum or metab--> CNS agitation, confus, delirum), pulmonary disase (emphysema), patients with head trauma (block pupillary reflex, increase intracranial pressure)
-**longer duration of action and better oral bioavail
-severe pain
-potent in naive patients, percip withdrawal in physically dependent patients |
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Term
|
Definition
-mixed agonist (k)/ antag (mu).
-orally w/ naloxone to prevent abuse (naloxone inactivated orally but blocks effects of drug when administered I.V
-Psychotomimetic (e.g. hallucinations) hypertension and tachycardia |
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Term
|
Definition
pure antagonist, blocks opiod effects at all receptor subtypes (competitive), percipitates withdrawal (if addicted) reverse mu agonists
-(fast onset but also fast offset) small doses 0.4 to 0.8 mh give intramuscualrly or IV
-antagonist, opioids
-used for overdose, administer until opioid elim. Reverses resp depress in neonates (mothers used opioid). increased resp rate in 1 to 2 min, reversed sedative effects, BP back to norm |
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