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Pharmacology Exam Review

Pharmacology Exam Review. Ch. 1. Chemical name : chemical structure Code name : experiential drug Generic name: Assigned by United States Adopted Name Council, drug shows therapeutic use and the manufacturer wishes to market the drug Trade name: brand name or proprietary name

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Pharmacology Exam Review

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  1. Pharmacology Exam Review

  2. Ch. 1 • Chemical name: chemical structure • Code name: experiential drug • Generic name: Assigned by United States Adopted Name Council, drug shows therapeutic use and the manufacturer wishes to market the drug • Trade name: brand name or proprietary name • Official name: experiential drug becomes approved, generic name becomes official name

  3. Ch. 1 • FDA: approval of drugs, lengthy, costly, research phases • Orphan drugs: rare disease drug, fewer than 200,000 people • Prescription: includes: • Name/address/date • Rx, superscription • Inscription • Subscription • Sig, signature • Name of prescriber

  4. Ch. 1 • OTC: without prescription • Know abbreviations: QID, BID, TID, Q4…

  5. Ch. 2 • Agonist: drug binds to a receptor creates an effect • Antagonist: blocks receptor effect • Bioavailibility: amount of drug available for action in systemic system • Drug administration routes: • Enteral (GI), Parenteral (IV), Transdermal, inhalation, topical

  6. Ch. 2 • First pass effect: initial metabolism in the liver of a drug taken orally before the drug reaches the systemic system • Hypersensitivity: allergic/immune mediated reaction to a drug, can be serious requiring mechanical ventilation • Idiosyncratic effect: unexpected reaction to drug, other than a allergic reaction

  7. Ch. 2 • Pharmacodynamics: mechanism of drug action by which drug molecule causes effect; after kinetic phase • Pharmacokinetics: time course and disposition based on absorption, distribution, metabolism, eliminitaion • Pharmacogentics: genetic factors, influence drug response

  8. Ch. 2 • Synergism: combined effect greater than individual • Tachyphylaxis: rapid decrease in response to a drug • Tolerance: decreased intensity of a drug • Pinocytosis: substance goes into a cell by process of membrane engulfment and transport of the substance into the cell

  9. Ch. 2 • Metabolism: liver primary site of metabolism and biotransformation • Excretion: Kidney primary site • Receptors: linked to G proteins, cause both constriction and dilation from epinphrine or Ach stimulation

  10. Ch. 3 • Aerodynamic diameter of a particle: determines deposition in airway • Dead volume: amount of solution that remains in a SVN after sputtering • HFA: hydrofluoroalkane, propellant for MDIs • Spacer, reservoir and holding chambers

  11. Ch. 3 • Aerosol delivery: • Advantages: • Smaller doses, rapid onset, targeted delivery, fewer side effects, painless, lung provides portal to body • Disadvantages: • Many variables, dose reproducibility, difficult coordination, lack of knowledge, lack of standardized info, varying devices

  12. Ch. 3 • Mass Median Aerodynamic Diameter (MMAD) • Indicates where the mass of drug is centered in a distribution of particle sizes • >10 nasopharngeal and oropharyngeal regions • 5-10 microns: central airways • 2-5 microns: lower airway (bronchodilator range) • 0.8-3 microns: small airways, alveoli

  13. Ch. 3 • Mechanisms of Deposition • Inertial impaction: function of particle size and velocity and increases with larger size and higher velocities • Gravitational settling: sedimentation, particle size and time • Diffusion (Brownian motion): affects particles less than 1 micron

  14. Ch. 3 • Devices: DPI, MDI, SVN, USN, SPAG • USN: electric powered, piezoelectric principle, • SPAG: Ribavirn • SVN: gas powered, uses a baffle to disperse particles to form aerosol from liquid • Time: 10-15 minutes, decreases with higher flows, flow set at 6-8 liters, volume 3-5 ml. • Advantages of SVN: can nebulize many drugs, mixtures, minimal coordination, useful in old/young, low inspiratory flows, modifiable doses • Disadvantages: expensive/cumbersome, Tx time lengthy, variability in performance, contamination

  15. Ch. 3 • BAN: Aeroclipse, undiluted meds, shorter tx times • MDI: drug, propellent, canister, valve, and mouth piece. HFA, portable/compact, short tx time, hard to coordinate, difficult to assess depletion, large oral impaction w/o holding chamber. Shake canister if not used frequently, may prime device, recommend spacer/holding chamber over open mouth • Breath actuated inhalers: Maxair

  16. Ch. 3 • Holding chamber: one way valve/spacer, holds the aerosol cloud until inspiration occurs, decreases waste and oral impaction, reduce electrostatic charge, do not wipe inside. • DPI: requires inspiratory flow of 30-90 L/min, old/young may not be able to use • IPPB, Endotracheal tube administration, mask, mouth piece.

  17. Ch. 5 • Ach: transmission stimulates bronchoconstriction, muscle contraction. Responds to cholingergic/nicotinic receptors. Destroyed by cholinesterase. Blocked by anti-cholinergics, parasympatholytics • Adrenergic: stimulates receptors for norepinephrine/epinephrine. Beta agonist, receptors alpha/betas, causes bronchodilation, increased HR, alpha constriction

  18. Ch. 5 • Peripheral nervous system: outside the CNS, includes sensory/sympathetic and parasympathetic nerves, Autonomic nervous system (parasympathetic and sympathetic branch) • Sympatholytic, sympathomimetic, cholinergic, anticholinergic, antiadrenergic, adrenergic, parasympatholytic

  19. Ch. 5 • Efferent: from brain to body • Afferent: from body to brain • Cholinergic: stimulated by Ach, contraction…cholinesterase destroys AcH • M1-3 in lungs, M3 when stimulated by Ach causes constriction. M2 cholinesterase decreases AcH. Anticholinergics block all M receptors; all are G linked

  20. Ch. 5 • Anticholingerics: • Atropine: blocks salivary glands, increases HR, bronchodlation, pupil construction • Atrovent • Tiotropium Adrenergics: Alpha and Beta receptor stimulators (know what each does)

  21. Ch 6 • Adrenergics: beta agonist, bronchodilators • Asthma paradox: increased asthma mortality despite knowledge and tachnology • cAMP: produced by Beta receptor stimulation, from conversion of ATP by adenlycyclase • cGMP: opposite effect of cAMP, causes bronchoconstriction • Downregulation: long term desensitization of Beta receptors to beta agonists

  22. Ch. 6 • Fast acting vs long acting • Ultra short: Racemic, stridor/airway swelling • Adrenergics are stereoisomers, Levalbuterol does not have the S-isomer • Albuterol/Proventil/ProAir/Ventoline • Beta receptors • SVN 0.5% soln, 0.5 ml, 2.5 mg, 0.63 mg, 1.25 mg, TID/QID. • MDI (proAIR) 90 ug/puff x 2 puffs • Onset 15 min, peak 30-60 min, duration 5-8 hours

  23. Ch. 6 • Beta 2 agonists cause: • Bronchial smooth muscle relaxation • Inhibition of histamine release • Stimulation of mucociliaryclearence • Are called sympathomimimic as they mimic epinephrine, also called adrenergics, or beta agonists • Adrenergic stimulation causes: Beta 1, Beta 2 and Alpha responses

  24. Ch. 6 • Racemic Epinephrine/microNefrin/Nephron • Alpha 1 and Beta receptors • Vasoconstriction for stridor • SVN 2.25% solution, 0.25-0.5 ml • Onset: 3-5 min, peak 5-20 min, duration: 0.5-2 hr • Increases HR, bronchodilates and vasoconstricts • Side effects: HR increases, tremors, shakiness

  25. Ch. 6 • Levalbuterol/Xopenex • SVN: 0.31, 0.63, 1.25 mg TID • MDI: 45 ug/puff x 2, q4-6 • Same onset/peak/duration as albuterol • One less isomer than albuterol (no S-isomer) • Pure R-isomer of racemicalbuterol • Side effects: tremor, less HR changes

  26. Ch 6 • Long acting (prophylactic) • Not for acute bronchospasm • Brovana/arfometerol, SVN only • Formoterol/Foradil • Mixed with Pulmicort to make symbicort • Dose 12 ugBID • Salmeterol/Serevent • Mixed with Flovent to make Advair • Dose DPI 50 ug/BID • Onset 20 min, peak 5-6, duration 12 hrs

  27. Ch. 6 • Saligenin agents: albuterol, beta 2 preferential drug • Short/long acting bronchodilators: Have antiinflammatory effects, however not enough to replace antiinflammatory drugs • Used in treatment of COPD, asthma • LABA prophylactic use, BID, stays attached to beta receptor longer

  28. Ch. 6 Mode of Action of Adrenergics: Once attached to a β2 receptor in bronchial smooth muscle the drug then attaches to the intracellular Gs protien which stimulates adenlycyclase to form cAMP from ATP which then decreases Ca2+↓ and Myosin resulting in SM relaxation . Also activate β receptors on mast cell mb. , thus used in prophylaxis of allergic asthma .

  29. Ch. 6 • Side effects: • Tremor, palpitations, headache, insomnia, nervousness, dizziness, nausea, tolerance, loss of bronchoprotection, hypokalemia; downregulation • Routes of administration with adrenergics: • Continuous SVN: severe asthma, 10-15 mg an hour of albuterol • SVN route the best route

  30. Ch. 6 • Respiratory assessment with adrenergics: • Assess effectiveness; peak flows • Breath sound change • Vital signs • A 20% change in HR from baseline may warrant a change in therapy • Check glucose, potassium levels • Device education

  31. Ch. 7 • Anticholinergics: only two used for the inhalation route: • Atrovent(Ipatropium Bromide), 0.5 mg SVN, MDI dose • Spiriva (Tiotropium Bromide), handihaler dry powder • Both have little systemic side effects • Use one or the other. Used for COPD and also during asthmatic attacks

  32. Ch. 7 • Combivent: Combo of Atrovent and Albuterol in a MDI • Duoneb: Combo of Albuterol and Atrovent in a SVN • Give combos for synergetic effect • Atropine: No longer aerosolized, used to increase HR, dry mouth. Tertiary compound, means it crosses BBB has systemic effects

  33. Ch. 7 • Spiriva • DPI, 18 ug/inhalation, given QD • Onset 30 min, peak 3hr, duration 24 hrs • Atrovent: • MDI (HFA)17 ug/puff x 2 puffs, QID • Onset 15 min, peak 1-2 hr, duration 4-6 hrs • SVN 0.02% solution, 0.5 mg TID

  34. Ch. 7 • Mode of action of anticholinergics • cGMP inhibits constriction and mucus production • cGMP acts as a secondary messenger much like cAMP but instead of converting ATP, cGMP prevents neurotransmitters from entering the bronchial smooth muscle cell • Unlike sympathometic bronchodilators, Atrovent/Spiriva do not cross the blood brain barrier and thus have essentially no systemic side effects (both are derivatives of Atropine, but are quaternary amines) • Slower bronchodilator effects and less intense than adrenergics

  35. Ch. 7 • Atrovent is non selective M blocker • Quaternary compund, does not cross the BBB • Spiriva: dissociates more slowly from M1 and M3 receptors. More selective than Atrovent • M2: inhibits further AcH release • Cholinergic effects: decrease HR, miosis, contraction of lens, salivation, urination, secretion of mucus, bronchoconstriction • AcH destroyed by cholinesterase

  36. Ch. 7 • Anticholinergic effects: increased HR, pupil dilation, flattened lens (USE CAUTION WITH ATROVENT WITH patients with Glaucoma), drying of upper airway, urinary retention, antidiarrheal, mucociliary slowing • Adverse effects: dry mouth, cough, avoid spraying in eye

  37. Ch. 8 • Methylxanthines: derived from Xanthines, consist of Caffeine, theophylline, and theobromine • Phosphodiesterase: enzyme that inhibits cAMP. Xanthine believed to inhibit this enzyme, thus increasing bronchodilation • Uses: Apnea/bradycardias; most common use of Xanthine, in form of Caffiene for neonates

  38. Ch. 8 • Uses: COPD as a weak bronchodilator, increasing respiratory muscle strength, increases contractility for patients on long term mechanical ventilation (helps with diaphragm wasting); respiratory muscle endurance, central ventilatory drive, cardiovascular effects by increasing CO, and antiinflammatory effects

  39. Ch. 8 • Theophylline: lots of side effects, must keep in narrow therapeutic range, headache, anxiety, restlessness, nausea, anorexia, vomiting, abdomial pain, hematemesis, tachypnea, palpitations, SVT, ventricular arrhythmias, hypotension, diruresis

  40. Ch. 9 • Abhesives: coating of film that preventsor reduces adhesion • Elasticity: rheologic property characteristic of solids it is represented by the storage of modulus G • Expectorant: medication meant to increase the volume or hydration of airway secretions • Gel: macromolecular description of pseudo-plastic material viscosity and elasticity

  41. Ch. 9 • Mucin: principle airway gel forming mucins • Mucoactive agent: effect on mucus secretion • Mucokinetic agent: increases ciliary clearance or respiratory mucus • Mucolytic agent: degrades polymers in secretions • Mucoregulatory agent: reduces volume of airway mucus secretion and appears to be especially effective in hypersecretory states

  42. Ch. 9 • Know layers of mucosa (gel, sol layer, epithelial cells, cilia, goblet cells, bronchial glands- produce most mucus) • Produce 100 ml of mucus daily • Acetylcysteine (NAC): Mucomyst, 10%/20%, SVN 3-5 ml • Causes bronchospasm, give with bronchodilator • Rotten egg smell, nausea • Directly instilled, or aerosolized • Breaks down sulfhydryl groups for disulfide bonds of mucus • Given to COPD, pneumonia, congestion, acetaminophen overdose • Incompatible with anti-biotics (do not mix mucomyst)

  43. Ch. 9 • Factors affecting mucus transport: • COPD/CF • Airway drying • Narcotics • Artificial airways/suctioning • Cigarette smoke • Pollution • Hyperoxia/hypoxia

  44. Ch. 9 • Food intake (milk) in particular does not increase mucus • Adrenergics: increase cilia beat and mucus production • Cholinergics: increase ciliary beat and mucus • Anticholinergics: decrease cilia beat and decrease mucus production • Xanthines: increase cilia beat and production • Steroids: no effects on cilia, decrease mucus production

  45. Ch. 9 • Sputum: mucus plus oral secretions • Bronchorrhea: watery sputum • Asthma: inflammation/increased mucus production • CF: impaired proteins, get frequent infections such as pseudomonas, require Dornase Alfa. Most congestion is not mucin, instead puss from neutrophil degradation

  46. Ch. 9 • Physical properties of mucus include viscosity, elasticity, cohesion, and adhesity. • Dornase Alfa: • Pulmozyme dose 2.5 mg • Given during infections with CF • Reduces extracellular DNA and F-actin polymers, reduces viscosity and adhesiveness of mucus • Does not cause bronchospasm, may cause pharyngitis, laryngitis, rash, chest pain, conjunctivitis

  47. Ch. 9 • Expectorants: • Sodium Bicarb: increases pH of mucus weakening bonds lowering viscosity and elasticity, used directly or aerosolized. Weak • Guaifesnsin: cilitoxic when applied directly • Hypertonic Saline: >0.9%, for induction of cough • Use adjunct therapy for mucus control • PEP, CPT, IPPB, Heated humidity, postural drainage, Bronchodilators, Vest • Bland aerosols (without medications)

  48. Ch. 10 • Surfactant agents regulate surface tension in films at gas-liquid interfaces, described by LaPlace’s Law • Surfactants are used are prophylactic or rescue treatment for RDS • Used exogenous surfactants include: • Beractant (Survanta), Calfactant (infasurf), Poractantalfa (Curosurf)

  49. Ch. 10 • Surfactant is directly instilled into the airway via endotracheal tube and adaptor, must closely monitor patient for compliance changes in order to prevent pneumothorax • Surfactants used are all natural based • Surfactant is composed of: • 85-90% lipids and 10% Proteins • Exogenous surfactant enter into the alveolar pool and replace deficient natural surfactant

  50. Ch. 11 • Adrenal cortical hormone: chemicals secreted by the adrenal cortex (steroids) • Endogenous: made within body • Exogenous: outside body • IgE: immune antibody, increased with allergen • Prostglandin: hormone type substances circulating in body • Steroids: Glucocorticoids or corticosteroids, antiinflammatory effect

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