1. Home
  2. Flashcards
  3. Preview

Pharm Test 1.txt

  1. Movement of drug from administration site into bloodstream
    Absorption
  2. Movement of drug through the bloodstream to tissues and cells
    Distribution
  3. Conversion of the drug into another substances
    Metabolism
  4. Removal of the drug or substance it became from the body
    Excretion
  5. The rate at which drug molecules disappear from the circulatory system, primarily through hepatic (liver) metabolism and renal excretion
    Clearance (or clearance rate)
  6. Process during distribution in which a
    portion of drug is attracted to and binds to protein, such as albumin in blood,
    preventing it from passing through capillary walls; therefore this portion is
    inactive and cannot achieve therapeutic effect.
    Protein binding
  7. The portion of being distributed in the body that is not bound to protein & therefore is active & can achieve therapeutic effect
    Free drug
  8. Drug molecules that attach to receptors on cells to stimulate the cell to act; they promote function
    Agonist
  9. Drug molecules that attach to receptors & prevent something else from attaching ( block the receptor) and causing an effect
    Antagonists or blockers
  10. The amount of time that is required to remove half or 50% of blood concentration of a drug
    Half-life
  11. The point at which the amount of drug that is administered and the amount that is being eliminated from the body balance off. The balance creates a stable level of drug in the blood
    Steady-state
  12. The rate at which drug molecule disappear from the circulatory system, primarily through hepatic metabolism and renal excretion
    Clearance
  13. Another term for metabolism of drugs. When drugs are changed from their original form to a new form in the body
    Biotransformation
  14. Product of metabolism, a drug that is metabolize is generally changed into an inactive form on its way to excretion . Occasionally a drug be metabolized in active metabolites substance that can achieve an independent effect that can be either therapeutic
    Metabolites
  15. The rate of metabolism of a drug varies as it is circulated through the bloodstream, to the portal circulation, and through the liver. The percentage of the drug metabolites on the first circulation or pass through the liver is high then the drug loses effectiveness during this first pass before reaches the general circulation. Loss of effectiveness in the first pass
    First pass effect
  16. A system of liver enzyme families three of which are involved in drug metabolism. drugs can either induce or inhibit P-450 system altering metabolism of other drugs
    P-450 System
  17. A drug's relative pharmacologic activity. The amount of drug that must be given in order to produce a particular response. Highly potent drugs often have a higher affinity for the receptor site on the cell so little is needed to produce its effects
    Potency
  18. How well a drug produces its desired effect. Is relative to the intrinsic activity. The higher the activity the greater the efficacy
    Efficacy
  19. The dose of a drug that is required to produce a therapeutic effect in 50% of the population. Often considered the standard or typical dose and is chosen when the drug therapy is initiated
    ED50 Effect dose 50.
  20. The point at which the dose of a drug would be fatal in 50% of the population
    LD50 Lethal dose 50
  21. a drug dose that is administered consistently over time, such as every day. Often achieved after 4-5 half-lives.
    Maintenance dose
  22. A higher dose of a drug given initially at the start of drug therapy when the drug has a longer half-life and needs to achieve steady-state in the shortened time frame due to the patient's medical condition requiring immediate steady-state for effective treatment
    Loading dose
  23. Ratio comparison used to determine the safety of a drug. The ED 50 is divided by the LD50 in ratio form and if there is little difference between the two the drug has a narrow therapeutic index and is therefore not very safe due to difficulty in dosing the drive safely
    Therapeutic index
  24. An immune system antigens/antibody response after drug is taken again it involves the release of histamine, which leads to allergic signs and symptoms and possibly anaphylaxis; the most serious allergic response
    Allergic response
  25. An unusual adverse effect of a drug, can be opposite response from what is anticipated. An individual's unique response to a drug, also called paradoxical effect
    Idiosyncratic response
  26. When two or more drugs that are alike in therapeutic Effect are combined, and the resulting response is the sum of the drug effects. Can be an intentionally more therapeutic, or unintentionally cause harm
    Additive effect
  27. When two or more unlike drugs, in terms of therapeutic effect or mechanism of action, are used together to produce a combined effect. Outcome response is greater then if either was used alone
    Synergistic effect
  28. An interaction between drugs in which one of the two drugs is increased. I.e. A drug that has mild effect may enhance the effects of a second drug
    Potentiated effect
  29. Drug
    A chemical that can affect living processes
  30. Pharmacology
    The study of drugs in their interactions with living systems
  31. The study of drugs in humans
    Clinical pharmacology
  32. The use of drugs to diagnose prevent or treat disease or to prevent pregnancy
    Therapeutics/Pharmacotherapeutics
  33. Nursing responsibility six rights
    • Right drug,
    • right patient,
    • right dose,
    • right Route,
    • right time,
    • right documentation
  34. In order to anticipate problems the nurse must understand... (3)
    • 1.The patient and the disorder being treated
    • 2. What drugs are contraindicated
    • 3. Probable consequences of the interactions between drugs and patient
  35. Antitussives
    Suppress cough reflex
  36. Antitussives prototype
    Dextromethorphan (DMX)
  37. Dextromethorphan (DMX) Pharm. therapeutic
    Used to treat constant nonproductive cough
  38. Dextromethorphan (DMX) pharmacodynamic
    Directly affects the cough Center in the Medulla
  39. Dextromethorphan (DMX). Contraindications
    Chronic cough associated with emphysema and asthma
  40. Dextromethorphan (DMX) adverse effects
    Nausea, vomiting, drowsiness, dizziness, irritability, restlessness. Possible poisoning/overdose for euphoric effects
  41. Dextromethorphan (DMX). Drug interactions
    • MAOIs
    • fluoxetine
    • quinidine
    • sibutramine
  42. Dextromethorphan (DMX) asses
    • Contraindications (emphysema and asthma)
    • Pregnancy/class-c
    • May cause drowsiness assess for operation of heavy equipment
    • May impair motor/orientation – help ambulated- safety
  43. Dextromethorphan (DMX) important to asses
    • Frequently assess respiratory status
    • Ck for clear airwAy
  44. Other antitussives
    • Codeine, hydrocodone
    • Diphenhydramin Benadryl
    • Benzonatate
  45. Codeine, hydrocodone
    Oral, at CNS depressant. Works on medullary center
  46. Codeine, hydrocodone contraindications
    Post op patients who need to cough and deep breathe and those with chronic cough
  47. Benzonatate
    • Tessalon/ Tessalon perles
    • Non-narcotic, anesthetizes stretch receptors in respiratory system to reduce cough reflex
    • Used in endoscopy
  48. Decongestants taken to
    decrease nasalcongestion r/t infections/inflammatoryresponse in the upper respiratory tract
  49. Decongestants Work by
    constricting nasal arterioles,thereby decreasing the swelling of thenasal membrane & decrease mucus
  50. Oral Decongestants
    absorbed in thebody, increasing the chance of adverseeffects
  51. Topical decongestants
    same therapeutic effects as oral; riskadverse effects diminished
  52. Decongestants Prototype drug:
    pseudoephedrine
  53. pseudoephedrine PT
    • Reduction of volume of nasal mucus, temporary relief of nasal congestion
    • decrease inflamination
  54. pseudoephedrine PK
    • oral onset 30 min,
    • topical 5-10 (sympathomimetic*)
  55. pseudoephedrine PD
    Vasoconstriction of nasal arterioles/mucus membranes
  56. Pseudophedrine Contra:
    Caution with preg./lact. Preg C
  57. Pseudophedrine Adverse:
    Tension, anxiety, restlessness, tremor, insomnia, &weakness (can cause sensory/visual effects in CNS,hallucination, & CV effects
  58. Pseudophedrine Drug interactions
    MAOIs, guanethidine, methyldopa, or furazolidone
  59. Pseudophedrine Drug interactions assess
    Medical Hx: Heart disease/CAD, HTN, DM,Hyperthyroid, BPH, ^ intra-occular pressure, depression
  60. Pseudophedrine Teach/Monitor:
    • ^fluid intake, humidification, avoid smoke filled places,
    • *Rebound congestion, dizziness, weakness,tremor, urinary retention, caution: OTC meds:
  61. phenylephrine
    • (Sudafed PE,
    • Powerful Alpha adenergic stimulant, decreasesnasal congestion, oral, spray, drops, avoid inabraded nasal mucosa + severe CNS/CV/Urinaryadverse effects
  62. Antihistamines:
    • relieve symptoms of allergies
    • Block the action of histamine released duringinflammatory response to an antigen
    • Restores normal airflow through the upperrespiratory system
  63. Antihistamines Prototype drug:
    fexofenadine (Allegra).
  64. fexofenadine PT
    Relieves seasonal & perennial allergysymptoms
  65. fexofenadine PK
    oral, Peak: 2–6 hours
  66. fexofenadine PD
    Selectively blocks the effects of histamine at H1-receptor sites.
  67. fexofenadine Adverse
    ^viral infections, nausea, vomiting,dysmenorrhea, dyspepsia, *CNS: drowsinessfatigue, but less anticholinergic/CNS effects b/c2nd generation; *elders, all antihistamines maycause thickened resp. secretions
  68. fexofenadine Interact:
    Rifampin & juices reduce absorption
  69. fexofenadine Assess: For
    Hx of Cardio-Vascular (CV) diseasepreg./lact, (class C)& renal status, how often drinksapple, grapefruit, or orange juice
  70. fexofenadine Teach/Monitor:
    Use as prescribed & caution OTC,Why?, take with full glass H2O/^ fluids, humidifier,avoid juices at adm., caution with OTC, safety forCNS effects, adverse effects decrease after a fewdays, no alcohol, Why?
  71. Cetirizine
    Antihistamines (Zyrtec) Once a day, a little more sedation
  72. Loratadine
    Claritin Antihistamines Once a day, less CNS effects thanfexofenadine.
  73. Desloratidine
    Antihistamines Clarinex) Longer acting form ofloratadine/claritin, more potent, less CNS effects due to lessaffinity for the H1 receptors in CNS
  74. First Generation Antihistamines
    Chlorpheniramine (Chlor-Trimenton, Clemastine(Tavist, twice a day), Dipenhydramine (Benadryl). Most not aslong acting, must take 4+ times a day, sedating, Benadryl oftenused as a sleep aide
  75. Expectorant Drugs
    • Expectorants liquefy lower respiratory tract secretions
    • Decreases the viscosity of secretions, improves airflow
  76. Expectorant Drugs
    guaifenesin
  77. guaifenesin PT
    Relieves dry, nonproductive cough, loosenssecretions so they can be expectorated
  78. guaifenesin PK
    oral, Onset: 30 minutes, Duration: 4–6 hrs
  79. guaifenesin PD
    Enhances output of respiratory tract secretions byreducing adhesiveness & surface tension
  80. guaifenesin Adverse effects
    GI symptoms, headache, and dizziness, (possible CNSeffects)
  81. guaifenesin Contras/Interact:
    Hypers???, preg class C, Assess smoking. No important drug interactions, no alcohol
  82. Guaifenesin Teach/Monitor:
    • Good pulmonary hygiene, (coughing,deep breathing, drinking plenty of fluids, humidifier,cough etiquette
    • eat small, frequent meals to alleviate GI upset,
    • Explain drug helps makes it easier to cough upsecretions,  
    • Do not use guaifenesin for longer than 1 week forpersistent cough (unless cleared with HC provider)
    • not for smokers cough, no alcohol, caution OTC,
    • Assess effectiveness, response, report fever
  83. Terpin Hydrate,
    Expectorants:^ fluid secreted in resp tract, 42%Alcohol, not used much, Contra. preg
  84. Iodine Preparations (SSKI, Potassium iodide)
    Expectorants:Used forCOPD, CF, used less, thyroid effects, Preg. Class X
  85. Mucolytics
    • break down mucus
    • Administered by a nebulizer or by direct instillationinto the trachea.
    • Reserved for patients who have major difficultymobilizing and coughing up secretions
  86. Mucolytics
    Acetylcysteine (Mucomyst).
  87. Acetylcysteine PT:
    to liquefy the thick, tenacious secretions
  88. Acetylcysteine PK:
    inhalation, Onset: 1 min.
  89. Acetylcysteine PD:
    splits disulfide bonds that are responsible forholding the mucous together
  90. Acetylcysteine Adverse effects:
    Bronchospasm, bronchoconstriction,chest tightness, burning sensation in upper airway,rhinorrhea

    Administer an inhaled beta agonist beforeadministering acetylcysteine
  91. Pregnancy Basic Considerations
    • Any treatment during pregnancy requirescareful consideration.
    • • The treatment benefits must be balanced withthe risks of treatment.
    • • Risk also applies to the fetus.
    • • Most drugs have NOT been tested duringpregnancy.
    • • Therefore the risks for most drugs areunknown.
  92. 1st priority (legally) baby or mother?
    • mother
    • Conditions that threaten the mother’s healthmust be addressed, as the health of the fetusdepends upon the health of the mother.
  93. 3rd trimester of pregnancy renal blood flow is doubled:
    This can result in accelerated clearance of the drugs.(The dose should be increased to compensate for thisincreased clearance).
  94. Hepatic metabolism also increases during pregnancy.
    (Doses need to be adjusted)
  95. Tone and motility of bowels decreases in pregnancy.
    This allows for more drug to be absorbed. It alsoallows more time for reabsorption of drugs thatundergo enterohepatic recirculation (drug effects couldbe prolonged).
  96. Essentially ____drugs can cross the placenta...
    • all 
    • although some cross more readily than others.
  97. Drugs that are _____  soluble cross the placenta easily.
    lipid
  98. Drugs that are ____, ____ _____, or ____ ____ cross with difficulty.
    • ionized,
    • highly polar,
    • or protein bound
  99. teratogenesis
    production ofbirth defects
  100. Incidence of Congenital Anomalies______
    • RARE
    • Incidence of major structural abnormalities (lifethreatening or require surgical correction) is between 1-3%
    • .– ½ are obvious and reported at birth.
    • – ½ involve internal organs and are not discovered untillater in life or upon autopsy
  101. Cause of Congenital Anomalies include
    • Genetic predisposition (25% of all defects)
    • • Environmental chemicals
    • • Drugs (<1% of all defects)
    • • The majority of congenital anomalies are fromunknown causes.
  102. Teratogenesis Preimplantation/ presomite period – (Conception throughweek 2)
    Teratogensact in an “all-or-nothing” fashion. Ifthe dose is high, death often results. If the dose issublethal, likely to have full recovery.
  103. Teratogenesis Embryonic period (week 3 – 8/ first trimester)
    Exposure toteratogensat this stage often produce gross malformations.Mothers must be very careful in the first trimester.
  104. Teratogenesis Fetal period (week 9 to term)-
    Exposure often disruptsfunction rather than gross anatomy. Growth anddevelopment of the brain are especially important in thisstage (can cause learning disabilities and behavioralabnormalities).
  105. Only a few drugs are considered ________teratogens.
    PROVEN

    Lack of proof of teratogenicity does NOT mean that a drug is safe (only that available data is insufficient to make a decision).
  106. To prove that a drug is a teratogen, three criteria must be met:
    • Drug must cause a characteristic set of malformations
    • • Must act only during a specific window of vulnerability (weeks 4-7 of gestation)
    • .• The incidence of malformations should increase with increasing dosage and duration of exposure.
  107. teratogen
    Drugs are put into one of five risk categories:
    A,B, C, D, and X.
  108. Category ___ is the least dangerous, with the risk _______ as you progress through the alphabet.
    A; increasing
  109. Category __ are drugs known to cause fetal harm,and their risk to the fetus outweighs any possible therapeutic benefit.
    X
  110. FDA Pregnancy Risk Category A
    Remote risk of fetal harm. Controlled studies in women have been done andhave failed to demonstrate a risk of fetal harm during the first trimester, andthere is no evidence of risk in later trimester.
  111. FDA Pregnancy Risk Category B
    Slightly more risk than A. Animal studies show no fetal risk but controlled studieshave not been done in women.

    OR

    Animal studies do show a risk of fetal harm but controlled studies in women have failed to demonstrate a risk during the first trimester and there is no evidence of risk in later trimesters.
  112. FDA Pregnancy Risk Category C
    Greater risk than B: Animal studies show a risk of fetal harm, but no controlled studies have been done in women. OR No studies have been done in women or animals.
  113. FDA Pregnancy Risk Category D
    Proven risk of fetal harm. Studies in women show proof of fetal damage, but the potential benefits of use during pregnancy may be acceptable despite the risk (treatment of life-threatening disease for which safer drugs are ineffective).WARNING will appear on drug label.
  114. FDA Pregnancy Risk Category X
    Proven risk of fetal harm. Studies in women or animals show definite risk of fetal abnormality. OR Adverse reaction reports indicate evidence of fetal risk.The risks clearly outweigh the benefit. CONTRADICTION will appear on drug label.
  115. The first step Responding to Teratogen Exposure
    after exposure is to determine when the pt became pregnant and when the drug was taken.

    If exposure was not during weeks 3-8, the pt should be reassured that the risk is minimal.
  116. Drugs that are ____ ____ enter breast milk more readily.
    lipid soluble
  117. Drugs that____, ____ ____ or ____ ____ are tend to be excluded. from passing into breast milk
    ionized, highly polar, or protein bound
  118. Dosing immediately____ breast-feeding to minimize drug concentrations in milk at the next feedin
    AFTER
  119. Pharmacokinetics
    • The study of drug movement throughout thebody.•
    • Also involves drug metabolism and excretion.
  120. Combination of metabolism plus excretion is called:
    elimination.
  121. Three ways to cross cell membranes:
    • -Passage through channels or pores - rare (too small)
    • -Passage with aid of a transport system
    • -Direct Penetration of the membrane
  122. Direct Penetration of the membrane
    • – Most common because most drugs are too big to pass through channels/pores.
    • – Most drugs lack transport systems.
  123. Drugs MUST be ____ ____ (____)to penetrate cell membranes
    lipid soluble (lipophilic)
  124. Polar Molecules  “Like dissolves like”
    Polar molecules will dissolvein Polar solvents (water) but not in nonpolarsolvents (oil).– Cannot get through the lipid (oil/ fat) membranethat surrounds cells
  125. Factors affecting drug absorption:
    • Rate of dissolution
    • Surface area
    • Blood flow
    • Lipid solubility
    • pH Partioning
  126. Rate of dissolution
    Faster a drug can dissolve, the quickerit can be absorbed
  127. Surface area
    Area available for absorption, more area =faster absorption
  128. Blood flow
    More blood flow = more absorption.
  129. Lipid solubility:
    Highly lipid-soluble drugs are absorbed faster. (penetrate membranes)
  130. pH Partioning
    Absorption is enhanced when thedifference in pH is more favorable in the blood plasmathan site of administration. (Acidic oral medications tendto be absorbed faster because the blood is more basic thanthe stomach).
  131. Generic medications have the same ____ _____,  but not always the same
    chemical equivalency, bioavailability.
  132. Chemical Equivalents-
    Contain the same AMOUNT of the identical drug.
  133. Bioavailability
    – Drug is ABSORBED at the same rate and extent.
  134. Enteric-coated–
    Drug is covered with materialdesigned to dissolve in intestines NOT stomach.
  135. Distribution Determined by three major factors:
    • – Blood flow to tissues
    • – Ability of drug to exit the vascular system
    • – Ability of drug to enter cells.
  136. The capillaries in the brain have tight junctions that prevent drugs passing between the capillary cells. (Unique to the brain).
    Blood-Brain Barrier (BBB)
  137. Only ____ _____ (____) drugs or drugs with a ____ ____ can cross the BBB. (______drugs do not crosswell.)
    Lipid Soluble (lipophillic); Transport System: Hydrophyllic
  138. ____do not have a fully developed BBB, so they are highly sensitive to meds that act on the brain and CNS poisons.
    Newborns
  139. Lipid-soluble, nonionized compounds ____ ____to the fetus.
    readily pass
  140. The importance of protein binding is that
    • drug distribution will be restricted.
    • Bound drug molecules cannot leave thebloodstream and therefore cannot be used.
  141. Drug metabolism has six possible consequences of therapeutic significance:
    • – Accelerated renal excretion of drugs
    • – Drug inactivation
    • – Increased therapeutic action
    • – Activation of “prodrugs”
    • – Increased toxicity
    • – Decreased toxicity
  142. The most important consequence of drug metabolism is
    promotion of renal drug excretion.
  143. Metabolism can convert active drug compounds into inactive forms.
    Drug inactivation
  144. Metabolism can increase the effectiveness of some drugs.
    Increased Therapeutic Action
  145. A prodrug is a compound that is pharmacologically inactive when administered and then is converted to its active form within the body.
    Activation of Prodrugs
  146. Converting drugs to inactive forms can decrease toxicity. Metabolism can alsoincrease the toxicity by converting safe compounds into toxicforms. (Tylenol)
    Increased or Decreased Toxicity
  147. First-Pass Effect
    Rapid hepatic inactivation of certain oral drugs.
  148. Minimum Effective Concentration (MEC)
    • The plasma drug level below which therapeuticeffects will NOT occur.
    • – Drug level must be above the MEC to providebenefit.
  149. Toxic Concentration
    • – The plasma drug level at which toxic effects begin.
    • – Drug levels must be below toxic concentration to prevent harm.
  150. Dose-response relationship has three phases:
    • Phase 1 – Occurs at low doses, the curve is flat because doses are too low to elict a measured response. (sub therapeutic) 
    • Phase 2 – An increase in dose elicts a correspondingincrease in response. This phase during which the dose-response relationship is graded.
    • Phase 3 – As the dose goes higher, we eventually reach a point where an increase in dose is unable to elicit a further increase in response. The curve flattens.
  151. The largest effect that a drug can produce.
    Maximal Efficacy
  152. The intensity of the responseto a drug is proportional to the number of receptorsoccupied by that drug and that a maximal response willoccur when all available receptors have been occupied.(Does not explain why one drug is more potent thananother or have higher efficacy than another).
    Simple Occupancy Theory:
  153. Ascribes affinity and intrinsicactivity that describe the ability of a drug to bind to thereceptor and the ability to influence receptor function
    Modified Occupancy Theory
  154. The strength of attraction between a drug and its receptor.
    Affinity
  155. Drugs with ____ affinity are ____ attracted to their receptors.
    high; strongly
  156. Drugs with ___ affinity are ____potent.
    high; very
  157. Refers to the ability of a drug to activate the receptor following binding.
    Intrinsic Activity
  158. Drugs with ____ intrinsic activity cause ______receptor activation.This relates to the ____ efficacy.
    high; intense: maximal
  159. Two drugs can occupy the same number of receptors but the drug with the _____ intrinsic activity will produce more intense responses.
    greater;
  160. MIMIC the body’s own regulatory molecules.
    Agonists –
  161. BLOCK the body’s own regulatory molecule.
    Antagonists –
  162. _____ have Affinity for a receptor but no intrinsic activity.
    Antagonists
  163. Has both affinity and high intrinsic activity.
    Agonists
  164. Most _____ are competitive
    antagonists
  165. Noncompetitve antagonists bind _____ to receptors.
    IRREVERSIBLLY
  166. ________ (Surmountable) Antagonists• Bind reversibly to receptors.
    Competitive
  167. Neonates and Infants:Because organ systems that regulate drug levels are not fully developed, these patients are at risk of more____ & ____effects.
    intense and prolonged
  168. Drug-metabolizing capacity of newborns is ____
    low
  169. Lower Resp. Drugs two main types:
    Anti-inflammatory agents and bronchodilators
  170. The principal anti-inflammatory agents are
    glucocorticoids.
  171. The principal bronchodilators are
    beta 2 agonists.
  172. Three advantages of inhalation:
    • Therapeutic effects are enhanced, delivered directly tosite of action–local
    • Systemic effects minimized–
    • Rapid relief of acute attacks
  173. Three types of inhalation devices:
    • Metered-dose inhalers–
    • Dry-power inhalers–
    • Nebulizers
  174. Metered-Dose Inhalers (MDI)•When 2 puffs are ordered, an interval of at least ____should separate the puffs
    1 minute
  175. *If used for exercise-induced asthma, must use ____ exercise
    BEFORE
  176. MDI Administration:Wait ____before a second dose of the same medication
    1 minute
  177. MDI Administration:Wait ____ before inhalation of a different medication
    2-5 minutes
  178. Adverse effects are few with Glucocorticoid inhalers
    • Oropharyngeal candidiasis*
    • • Dysphonia (hoarseness, speaking difficulty)
    • • *Bone loss in premenopausal women
    • • *Rinse mouth/Gargle after each use, use a spacer
    • • Take lowest dose possible
    • • *Take calcium and vitamin D
    • • *Perform weight bearing exercises
  179. **Inhaled Glucocorticoids:
    • – Beclomethasone propionate (QVAR)
    • – Budesonide (Pulmicort, Asthmacort)
    • – Fluticasone propionate (Flovent)
    • – Ciclesonide (Alvesco)
    • – Flunisolide (Aerospan)
    • –Mometasone furoate (Asmanex)
  180. Glucocorticoids/Corticosteroids• Physiologic Effects: Metabolic
    • carbs-Hyperglycemia
    • Proteins- Reduces muscle mass, decreases protein matrix of bone, and causes thinning of skin.
    • Fats- Fat redistribution- Pot belly, “moon face” and“buffalo hump”
  181. Glucocorticoids/Corticosteroids• Physiologic Effects: Cardiovascular
    If endogenous glucocorticoids are LOW, capillariesbecome more permeable (third spacing of fluid),vasoconstriction is suppressed, & BP drops(hypotension)
  182. Glucocorticoids/Corticosteroids• Pharmacodynamics (PD):
    • Glucocorticoid receptors are located inside the cell,rather than on the cell surface
    • – Glucocorticoids modulate the production of regulatoryproteins, rather than the activity of signaling pathways
  183. Glucocorticoids/Corticosteroids• Pharmacotherapeutics (PT): Anti-inflammatory &Immunosuppressant Effects:
    • – Inhibit synthesis of chemical mediators (prostaglandins,leukotriene's, histamine), to reduce swelling, warmth,redness, & pain
    • • Suppress infiltration of phagocytes
    • • Suppress proliferation of lymphocytes to reducethe immune component of inflammation
  184. Glucocorticoids/Corticosteroids• Adverse Effects
    • Typically ONLY occur when doses are high and durationis longer than a few days
    • – Adrenal Insufficiency- glucocorticoid drugscan suppressproduction of glucocorticoids by the adrenal glands
    • – Osteoporosis- & resulting fractures, frequent & serious complication of prolonged therapy
    • – Infection- Suppression of the immune system increases risk of infection• *Pts should avoid close contact with people who have communicable diseases
    • Glucose Intolerance- Pts with diabetes may need to reduce caloric intake or increase the dosage of hypoglycemic medication
    • Skin: Thin skin, ecchymosis, skin tears, muscle wasting, decreased SC tissue
    • Myopathy- Can cause myopathy (muscle injury),
    • Growth Retardation- suppresses growth in children.– Can be minimized with alternate-day therapy
    • Fluid and Electrolytes: *Hypernatremia, *Edema & *Hypokalemia
    • Psychological Disturbances: 60% have mild reaction: insomnia,anxiety, agitation or irritability; 6% severe reaction: delirium,hallucinations, depression, euphoria, or mania
    • Cataracts & Glaucoma:
    • Peptic Ulcer Disease:
    • Iatrogenic Cushing’s Syndrome:
  185. Glucocorticoids/Corticosteroids• Drug Interactions
    • Interactions related to potassium loss-*Used withcaution when combined with digoxin, thiazide orloop diuretics.•
    • NSAIDS- increases risk of PUD.•
    • Insulin/oral hypoglycemics- May need to increasedoses to combat hyperglycemia• Vaccines- Can decrease antibody response ofvaccines & if live virus vaccine is used, increasedrisk of developing the viral disease
  186. Glucocorticoids/Corticosteroids• Contraindications
    Pts with systemic fungal infections or receiving live virusvaccines
  187. Sys. Glucocorticoids/CorticosteroidsPrecautions, Use with caution in pts:
    • – pediatric, pregnant or breast feeding
    • – Hypertension, heart failure, renal impairment,esophagitis, gastritis, peptic ulcer disease, myastheniagravis, diabetes mellitus, osteoporosis, & infectionsresistant to treatment
    • – concurrent therapy with potassium-depleting diuretics,digoxin, insulin, oral hypoglycemics & NSAIDS
  188. Leukotriene Modifiers• PD:
    • Suppress effects of endogenous leukotriene's (chemicalmediators that promote vasodilation; eosinophilinfiltration, mucus production, & airway edema.)
    • • Decrease inflammation, bronchoconstriction, edema,mucus secretion, & recruitment of eosinophils &otherinflammatory cells
  189. Three leukotriene modifiers:
    • zileuton (Zyflo),
    • zafirlukast(Accolate),
    • and montelukast (Singulair).
  190. Leukotriene Modifiers PT:
    Recommended as second-line therapy forasthma/bronchospasm; add-on therapy when an inhaledglucocorticoid alone is inadequate
  191. Leukotriene Modifiers Adverse E:
    All can cause adverse neuropsychiatric effects,including depression, suicidal thinking, & suicidal behavior
  192. Leukotriene Receptor Antagonists
    Leukotrienes: inflammatory mediators that arepowerful broncho-constrictors and vasodilators• Leukotrienes identified as important mediators inthe pathology and symptomatology of asthma• Result in airway hyper-reactivity,bronchoconstriction, and hyper-secretion
  193. Leukotriene Receptor Antagonists Prototype drug:
    zafirlukast (Accolate)
  194. Zafirlukast (Accolate)-PK:
    Food reduces absorption (give 1hr before or 2 hrs after meals)
  195. Zafirlukast (Accolate) Adverse E:-
    Possible liverinjury, (monitor serum liver function tests: “LFTs”particularly Alanine aminotransferase “ALT” )
  196. Montelukast (Singulair)-
    Leukotriene Modifiers Does NOT cause liver injury.
  197. Cromolyn Sodium:
    • Mast Cell Stabilizer drugs
    • A preventative drug that decreases episodes of asthma/bronchospasm (nasal: rhinitis)induced by different antigens (exercise, pollutants, allergans)
  198. Cromolyn Sodium: 2 types–
    • Nasal inhaler: trade Nasal crom
    • – Respiratory Inhalation: trade: Intal
  199. Cromolyn Sodium PD:
    • Mast Cell Stabilizer drugs
    • An anti-inflammatory agent, shields mast cells and prevents them from rupture & degradation after contactwith antigen, prevents release of histamine, possibly leukotriene's, & other chemical mediators by an unclearmechanism, possibly due to influx of calcium
    • **Does NOT cause bronchodilation**
  200. Cromolyn Sodium Adverse effects:
    Safest of all anti-asthma meds,occasionally cough or *bronchospasm
  201. Bronchodilators Prototype drug:
    albuterol
  202. albuterol PT:
    Symptomatic relief ofbronchospasm & bronchoconstriction, does notalter underlying disease process (inflammation
  203. Bronchodilators: Beta 2-Adrenergic Agonists PD
    Selective Activation of beta 2-adrenergic receptors insmooth muscle of the lung, promotes bronchodilation– Suppress histamine release in the lung & increasescilliary motility
  204. Bronchodilators: Beta 2-Adrenergic Agonists Route and Time Course:
    • All oral preparations are long acting
    • – Short-acting inhaled preparations, effects begin almost immediately, peaks in 30-60 min. Used to end anattack, NOT for prophylaxis
    • – Long-acting inhaled preparations, onset depends onthe drug, used on a fixed-schedule
  205. Short-Acting Inhaled Beta2 Agonists (SABA)-
    • – Taken prn to relieve ongoing attack
    • – Take before exercise to prevent an attack
    • – For a severe acute attack, a nebulized SABA is thetreatment of choice, but MDI may be equally effective
  206. Long-Acting Inhaled Beta2 Agonists-
    • – Frequent attacks can inhale a LABA for long-term control
    • – Fixed schedule, not PRN
    • – Should be combined with a glucocorticoid,contraindicated for use alone. Many times both drugsare delivered in the same inhaler (Combo inhaler)
  207. Bronchodilators: Beta 2-AdrenergicAgonistsAdverse Effects:
    SABA inhaled-
    well tolerated, systemic effects include tachycardia, palpitations, angina and tremor. Possibleanxiety, restlessness/nervousness, irritability
  208. Bronchodilators: Beta 2-AdrenergicAgonistsAdverse Effects:
    LABA inhaled-
    Increased risk of severe asthma &asthma related death but only when used as a monotherapy (used alone)
  209. Bronchodilators: Beta 2-Adrenergic Agonists Adverse Effects:
    Oral-
    Relative selectivity (can produce beta 1 receptoractivation in the heart which results in angina pectoris,palpitations, and tachydysrythmias)• Can also cause tremor by activating beta 2 receptors in skeletal muscle. (tremor is reduced by lowering the dosage)
  210. LABA/Glucocorticoid Combinations
    • • Fluticasone/salmeterol (Advair)• Budesonide/formoterol (Symbicort)• Mometasone/formoterol (Dulera)
    • *All carry black box warnings: possible increasedrisk of asthma severity or asthma-related death
  211. Methylxanthines or XanthineDerivatives PD
    prominent CNS excitation, & bronchodilation–May also cause cardiac stimulation, vasodilation& diuresis.• Theophylline (Theo-24, Theochron, Elixophyllin) isthe principle methylxanthine used in asthma• Caffeine is also a methylxanthine
  212. Xanthine Derivatives
    excellent bronchodilators but do notwork as rapidly as beta-adrenergic agonist drugs
  213. Xanthine Derivatives
    Prototype drug: theophylline (Slo-phyllin)
  214. Methylxanthines: Theophylline
    **Very narrow therapeutic window or range– **Must monitor blood concentration of drug
  215. Methylxanthines: Theophylline PD
    Produces bronchodilation by relaxing smooth muscle of the bronchi.
  216. Methylxanthines: Theophylline PT
    Asthma, CAL, COPD– Oral: used for maintenance therapy for chronic stable asthma.
  217. Methylxanthines: Theophylline• **THERAPEUTIC DRUG LEVELS:
    10-20 mcg/mL.
  218. Methylxanthines: Theophylline Drug Interactions:
    Caffeine- Intensifies the effects of theophylline(adverse effects on CNS & heart).– **NO CAFFEINE IF TAKING THEOPHYLLINE• Drugs That Reduce Theophylline Levels:– Phenobarbital, phenytoin, and rifampin• Drugs that Increase Theophylline Levels:– Cimetidine and fluoroquinolone antibiotics(ciprofloxacin)
  219. ANTICHOLINERGIC DRUGS  PD:
    Improve lung function by blocking muscarinicreceptors in bronchi, causes bronchial dilation• Two agents available: ipratropium (Atrovent) &tiotropium (Spiriva).
  220. ANTICHOLINERGIC DRUGS PT
    Approved only for chronic obstructivepulmonary disease (COPD), but often used forasthma.• Spiriva has a longer duration of action
  221. Respiratory Anticholinergic Agents
    Inhaled anticholinergic drugs are considered firstlinetreatment for patients with CAL.
  222. Respiratory Anticholinergic Agents
    Prototype drug: ipratropium bromide (Atrovent)
  223. Anticholinergic: Ipratropium (Atrovent)Adverse Effects:
    • Systemic effects minimal, Quaternary ammoniumcompound, carries a positive charge, therefore notreadily absorbed from lungs or GI tract (local action)
    • • Most common- dry mouth and irritation of pharynx
    • • If systemic absorption occurs can raise intraocularpressure in pts with glaucoma• Associated with adverse cardiovascular events (MI,CVA, and death).
    • • Combivent (ipratropium/albuterol) contains soyalecithin and individuals with peanut allergy can react
  224. Anticholinergic: Tiotropium (Spiriva)
    • Tiotropium: a long-acting inhaled anticholinergic
    • Therapeutic effects begin about 30 minutes afterinhalation, peaks in 3 hrs, and persists for 24 hrs
    • Will not help with acute attack•
    • Do NOT swallow capsules,(
  225. Anticholinergic: Tiotropium (Spiriva) Adverse Effects:
    • Most common: dry mouth, (sugarless candy canhelp)diminishes over time
    • • Systemic anticholinergic effects (constipation,urinary retention, tachycardia, blurred vision) areminimal due to poor systemic absorption
Author
eshea
ID
259113
Card Set
Pharm Test 1.txt
Description
Intro pharm terms and resp. drugs
Updated

  1. Home
  2. Flashcards
  3. Preview