Pharmacology Exam 1 Study Guide

  1. What med route has the best absorption rates?
  2. ___ is the transmission of meds from the locaation of administration (GI, muscle, skin, subQ) to bloodstream.
  3. Enteral means...
    thru the GI tract
  4. Parenteral means...
    by injection
  5. There is no significant barrier to absorption of subQ and IM meds. Why?
    Capillary wall has large spaces between cells
  6. Rate of absorption for subQ and IM meds is determined by what 2 things?
    • solubility of the med in water
    • blood perfusion at site of injection
  7. List the 3 major factors for distribution of drugs in the body.
    • blood flow to tissues
    • ability to exit vascular system
    • ability to enter cells
  8. ___ refers to the ability of a drug to reach the systemic circulation from its site of administration.
  9. Differences in bioavailability occur primarily with ___ preparations, not with ___ preparations.
    oral; parenteral
  10. Differences in bioavailability are of greatest concern for which drugs?
    those w/ narrow therapeutic range
  11. ___ refers to the rapid hepatic inactivation of certain oral drugs.
    1st pass effect
  12. Explain the 1st pass effect.
    When oral drugs are absorbed from the GI tract, they are carried directly to the liver via the hepatic portal vein. If the capacity of the liver to metabolize a drug is extremely high, that drug can be completely inactivated on its first pass through the liver. As a result, no therapeutic effects can occur.
  13. How can you circumvent the 1st pass effect with drugs that undergo rapid hepatic metabolism?
    Administer parenterally, which permits the drug to temporarily bypass the liver and reach therpeutic levels in the systemic blood
  14. When plateau must be achieved more quickly, a large initial dose - or ___ - can be administered.
    loading dose
  15. The highest drug level is referred to as the ___, and the lowest drug level is referred to as the ___.
    peak concentration; trough concentration
  16. ___ concentration levels are drawn just before administering the next dose; ___ concentration levels are drawn after administering the medication (depending on route, etc.)
    Trough; peak
  17. What is the time required for the amount of a drug to be reduced by 50%?
  18. T/F Half-life is a factor in determining dosing interval.
  19. A ___ is a nearly unavoidable secondary drug effect produced at therapeutic doses.
    side effect
  20. List 2 main characteristics of side effects.
    • predictable
    • dose-dependent
  21. T/F An adverse drug rxn is a side effect.
    F; side effects are considered adverse rxns
  22. List 6 adverse rxns besides side effects and allergic rxns.
    • toxicity
    • idiosyncratic effect
    • iatrogenic disease
    • physical dependence
    • carcinogenic effect
    • teratogenic effect
  23. ___ is an adverse drug rxn caused by excessive dosing.
  24. T/F Toxicity includes only those severe rxns that occur when dosage is excessive.
    F; Although the formal definition of toxicity includes only those severe rxns that occur when dosage is excessive, in everday parlance the term toxicity has com eto mean any severe ADR, regardless of the dose that caused it
  25. An allergic rxn is an ___ response.
  26. T/F For an allergic drug rxn to occur, there must be prior sensitization of the immune system
  27. T/F The intensity of an allergic drug rxn is determined primarily by drug dosage.
    F; determined primarily by degree of sensitization of the immune system, not by drug dosage
  28. Most serious allergic drug rxns are caused by which drug family?
  29. An ___ is an uncommmon drug response resulting from a genetic predisposition.
    idiosyncratic effect
  30. An ___ is a disease produced by a physician or drugs.
    iatrogenic disease
  31. Iatrogenic diseases are nearly identical to ___ (naturally occurring) diseases.
  32. ___ develops during long-term use of certain drugs, such as opioids, alcohol, barbiturates, and amphetamines.
    Physical dependence
  33. ___ is a state in which the body has adapted to drug exposure in such a way that an abstinence syndrome will result if drug use is d/c.
    Physical dependence
  34. ___ refers to the ability of certain medications and environmental chemicals to cause cancers.
    Carcinogenic effect
  35. A ___ can be defined as a drug-induced birth defect.
    teratogenic effect
  36. What populations are at greatest risk for med reactions, toxicity, and ADRs?
    • old
    • young
    • severe illness
    • polypharmacy
    • HTN
    • epilepsy
    • heart disease
    • psychoses
  37. ___ is that component of a drug response that is caused by psychologic factors and not by the biochemical or physiologic properties of the drug.
    Placebo effect
  38. A ___ is a preparation that is devoid of intrinsic pharmacologic activity.
  39. T/F The placebo effect is believed to be a large fraction of the total response of any given drug.
    F; a small fraction
  40. T/F The placebo effect is always positive.
    F; can be positive and negative
  41. T/F Enough research has been done to indicate that significant gender-related differences exist in drug responses.
    T (even though for many drugs, we don't know much about gender related differences b/c until recently, essentially all drug research was done on men)
  42. When used to treat heart failure, digoxin may (increase/decrease) mortality in women while having no effect on mortality in men.
  43. Alcohol is metabolized more (slowly/quickly) by women than by men. As a result, a woman who drinks the same amount as a man (on a wt. adjusted basis) will become (more/less) intoxicated.
    slowly; more
  44. Certain opioid analgesics are much more effective in (men/women) than in (men/women). As a result, pain relief can be achieved at lower doses in (men/women).
    • women; men
    • women
  45. Quinidine causes greater QT interval prolongation in (men/women) than in (men/women). As a result, (men/women) given the drug are more likely to develop torsades de pointes, a potentially fatal cardiac dysrhythmia.
    • women; men
    • women
  46. In what year did the FDA pressure drug companies to include women in clinical drug trials?
  47. What are the major organs effected by alcohol?
    • CNS
    • cardiovascular system
    • respiratory system
    • liver
    • stomach
    • kidneys
    • pancreas
  48. What 2 acute effects does alcohol have on the brain?
    • general depression of CNS function
    • activation of reward circuit
  49. What are 2 neuropsychiatric syndromes common in alcoholics?
    • Wernicke's encephalopathy
    • Korsakoff's psychosis
  50. Both Wernicke's and Korsakoff's are caused by ___ deficiency, which results from poor diet and alcohol-induced suppression of ___ absorption.
  51. A neuropsychiatric syndrome common in acoholics characterized by confusion, nystagmus, and abnormal ocular movements; readily reversible with thiamin
    Wernicke's encephalopathy
  52. A neuropsychiatric syndrom common in alcoholics characterized bypolyneuropathy, inability to convert short-term memory into long-term, and confabulation; not reversible.
    Korsakoff's psychosis
  53. T/F Low to moderate drinking helps preserve cognitive function in older people and may protect against development of dementia.
  54. T/F Alcohol is a great sleep aid.
    F; it actually disrupts sleep
  55. What is the most prominent cardiovascular effect when alcohol is consumed in moderation?
    Dilation of cutaneous blood vessles, which increases blood flow to the skin imparting a sensaiton of warmth, while promoting heat loss
  56. What are two cardivascular effects of chronic and excessive alcohol consumption?
    • direct damage to myocardium (increasing risk of HF)
    • dose-dependent elevation of BP
  57. T/F There is clear evidence that people who drink moderately experience less ischemic stroke, CAD, MI, and HF. With heavy drinking the risk of heart disease and stroke is increased.
  58. Moderate alcohol consumption includes ___ drinks/day or less for men and ___ drink/day or less for women.
    2; 1
  59. Heavy alcohol consumption includes ___ or more drinks/day.
  60. Like all other CNS depressants, alcohol depresses ___.
  61. Alcohol-induced liver damage can progress from ___ to ___ to ___, depending on amount consumed.
    fatty liver; hepatitis; cirrhosis
  62. T/F Alcohol abuse is unquestionably the major cause of fatal cirrhosis.
  63. ___ is a condition characterized by proliferation of fibrous tissue and destruction of liver parenchymal cells.
  64. Immoderate use of alcohol can cause ___ by (1) stimulating secretion of gastric acid, and (2) in high concentrations, injuring gastric mucosa directly.
    erosive gastritis
  65. Alcohol is a ___. It promotes urine formation by inhibiting the release of ADH from the pituitary.
  66. How does ADH work?
    Acts on kidneys to promote water reabsorption, thereby decreasing urine formation.
  67. About 35% of cases of acute pancreatitis can be attributed to alcohol, making alcohol the ___ most common cause of the disorder. Only ___% of alcoholics develop pancreatitis.
    second; 5
  68. What are the common social factors of drug abuse?
    • desire for social status and approval
    • peer pressure
  69. List factors that contribute to drug abuse.
    • reinforcing properties of drugs
    • physical dependence
    • psychologic dependence
    • social factors
    • drug availability
    • individual vulnerability
  70. ___ is an intense subjective need for a drug.
    Psychologic dependence
  71. What are the drug schedules for addictive substances?
    • Schedule 1: high tendency for abuse, no accepted medical use; marijuana, ecstasy, LSD, GHB; not sold by pharmacies, not available w/ physician prescription
    • Schedule 2: high tendency for abuse, may have accepted medical use, can produce dependency/addiction; cocaine, opium, morphine, fentanyl, amphetamines, methamphetamines; may be available w/ physician prescription
    • Schedule 3: less abuse/addiction potential, accepted medical use; anabolic steroids, codeine, ketamine, hydrocodone w/ aspirin, hydrocodone w/ acetaminophen; may be available w/ prescription
    • Schedule 4: low abuse potential, accepted medical use, limited addictive properties; valium, xanax, phenobarbital, rohypnol; may be available w/ prescription
    • Schedule 5: lowest chance of abuse, accepted medical use in US, lowest chance of dependence; cough suppressants w/ codeine; regulated but don't generally require prescription
  72. What medications interact with alcohol?
    • CNS depressants: intensifies psychologic and physiologic manifestations of CNS depression, and greatly increases risk of death from respiratory depression
    • NSAIDs: significant gastric bleeding
    • Acetaminophen: poses risk of potentially fatal liver injury
    • Disulfiram: variety of potentially dangerous adverse effects
    • Antihypertensives: alcohol counteracts (since it raises BP when consumption is high); in moderation, may aid antihypertensives
  73. What are the underlying causes of malnutrition in the chronic alcoholic?
    • poor diet
    • malabsorption of nutrients and vitamins
  74. Malabsorption in the chronic alcoholic results from...
    alcohol induced damage to the GI mucosa
  75. Why does poor diet occur in the chronic acoholic?
    Meet up to 50% of caloric needs w/ alcohol, and therefore consume subnormal amounts of foods w/ high nutritional value
  76. B/c of their poor diet, alcoholics are in need of ___, ___ and ___.
    fat; protein; vitamins
  77. The ___ vitamins are especially needed in alcoholics.
  78. T/F Alcoholics frequently require fluid replacement therapy and antibiotics.
  79. What drugs are used in the rehab of alcoholism?
    • benzodiazepines
    • disulfiram
    • naltrexone
    • acamprosate
    • topiramate
  80. In theory, any drug that has cross-dependence with alcohol (any CNS depressant) should be effective in facilitating withdrawal, however in actual practice, ___ are the drugs of choice.
  81. T/F Benzodiazepines are most effective at facilitating alcohol withdrawal, but are not always safe.
    F; are safe
  82. How do benzodiazepines facilitate alcohol withdrawal?
    Decrease withdrawal symptoms, stabilize vitals, prevent seizures and delirium tremens
  83. What benzodiazepines are used most often to facilitate alcohol withdrawal?
    • chlordiazepoxide (Librium)
    • diazepam (Valium)
    • oxazepam (Serax)
    • lorazepam (Ativan)
  84. T/F To facilitate alcohol withdrawa, benzodiazepines are only administered around around the clock on a fixed schedule.
    F; PRN administration is just as effective and permits speedier withdrawal
  85. What are some other drugs that may be combined with a benzodiazepine to improve alcohol withdrawal outcome?
    • carbamazepine (antiepileptic)
    • clonidine (alpha adrenergic agonist)
    • atenolol, propranolol (beta adrenergic blockers)
  86. In the US, what 3 drugs are approved for maintaining alcohol abstinence?
    • disulfiram (Antabuse)
    • naltrexone (ReVia, Vivitrol)
    • acamprosate (Campral)
  87. ___ works by causeing an unpleasant rxn if alcohol is consumed; disrupts alcohol metabolism.
  88. ___ blocks the pleasurable effects of alcohol and decreases craving.
  89. ___ reduces some of the unpleasant feelings (tension, dysphoria, anxiety) brought on by alcohol abstinence.
  90. Of the 3 alcohol abstinence drugs, which appears to be the most effective?
  91. This alcohol abstinence drug has no applications outside the treatment of alcoholism.
  92. The constellation of effects caused by alcohol plus disulfiram is referred to as ___ syndrome, a potentially dangerous event. In its mild form manifestations include: n/v, flushing, palpitations, headache, sweating, thirst, chest pain, weakness, blurred vision, hypotension; the rxn can be brought on by as little as ___ mL of alcohol. Severe manifestations are life threatening and include: respiratory depression, cardiovascular collapse/dysrhythmias, MI, acute CHF, convulsions, death.
    acetaldehyde; 7
  93. T/F Alcoholics who lack the determination to stop drinking should not receive disulfiram.
  94. What are some key points in disulfiram patient education?
    • Avoid ALL forms of alcohol
    • Effects will persist about 2 weeks after last dose
    • Carry identification indicating status
  95. Naltrexone falls under what drug class?
    Pure opioid antagonist
  96. What happens if naltrexone is given to an opioid dependent individual?
    Since it's an opioid antagonist, it precipitates withdrawal
  97. T/F Unlike disulfiram, patients are not required to stop drinking before starting naltrexone.
    F; like disulfiram, patients must stop
  98. Which alcohol abstinence drug should be used only as part of a comprehensive management program that includes psychosocial support?
  99. T/F Combining acamprosate with naltrexone is more effective than acamprosate alone, but no better than naltrexone alone.
  100. Which 2 alcohol abstinence drugs are oral, and which is oral and IM?
    • disulfiram, acamprosate
    • naltrexone
  101. What are 2 drugs that are less commonly used for alcohol abstinence, and what are they currently approved for?
    • topiramate (Topamax); epilepsy and migraine
    • ondansetron (Zofran); n/v in cancer patients
  102. ___ is the principle methylxanthine employed in asthma.
    Theophylline (Uniphyl)
  103. What are the 2 most prominent actions of the methylxanthines?
    • CNS excitation
    • bronchodilation
  104. This drug has a narrow therapeutic range, is usually administered by mouth, and is not administered by inhalation b/c it is not active by this route.
  105. In the past, this drug was a first line med for asthma and nearly all patients with chronic asthma took it. However, use of this drug has declined sharply. Why?
    theophylline; we now have safer, more effective meds (inhaled glucocorticoids, inhaled beta2 agonists)
  106. Benefits of theophylline derive primarily from ___.
  107. Oral theophylline is used for maintenance therapy of...
    chronic stable asthma
  108. Although (more/less) effective than beta2 agonists, theophylline has a (longer/shorter) duration of action.
    less; longer
  109. Becasue its effects are prolonged, theophylline may be most appropriate for patients who experience what?
    nocturnal attacks
  110. T/F Theophylline is metabolized in the liver, and rates of metabolism are fairly consistent.
    F; rates of metabolism vary widely
  111. What is the therapeutic drug level range for theophylline?
    5-15 mcg/mL
  112. ___ is a methylxanthine with pharmacologic properties like those of theophylline, and should thus be avoided.
  113. What drugs reduce theophylline levels?
    • phenobarbital
    • phenytoin
    • rifampin
  114. What drugs increase theophylline levels?
    • cimetidine
    • fluoroquinolone antibiotics (ciprofloxacin)
  115. ___ (formerly available as Truphylline) is a theophylline salt that is considerably more soluble than theophylline itself.
  116. T/F Pharm properties of aminophylline and theophylline are identical.
  117. Which route is most often used for aminophylline?
  118. Because of its relatively high solubility, ___ is the preferred from of theophylline for IV use.
  119. The usual loading dose for aminophylline is ___; the maintenance therapeutice range is ___.
    • 6mg/kg
    • 10-20 mcg/mL
  120. This asthma inhalation device is small, hand-held, pressurized and delivers a measured dose of drug with each actuation. Hand-lung coordinaiton is required. Only 10% of the dose reaches the lungs; about 80% impacts the oropharynx and is swallowed, and the remaining 10% is left in the device or exhaled.
    MDI (metered dose inhaler)
  121. This asthma inhalation device delivers drugs in the form of a dry, micronized powder directly to the lungs. No propellant is employed and they are breath activated (don't require lung-hand coordination). About 20% of dose reaches the lungs.
    DPI (dry powder inhaler)
  122. This asthma inhalation device is a small machine used to convert a drug solution into amist. Takes several minutes to deliver, but may be most effective.
  123. What are the 2 major classifications of asthma drugs?
    • anti-inflammatories
    • bronchodilators
  124. What are 4 anti-inflammatory drug classifications for asthma?
    • glucocorticoids
    • leukotriene modifiers
    • cromolyn, nedocromil
    • omalizumab
  125. What are 3 brochodilator drug classifications for asthma?
    • beta2 adrenergic agonists
    • methylxanthines
    • anticholinergics
  126. beclomethasone dipropionate (QVAR)
    budesonide (Pulmicort)
    ciclesonide (Alvesco)
    flunisolide (Aerobid)
    fluticasone propionate (Flovent)
    mometasone furoate (Asmanex)
    triamcinolone acetonide (Axmacort)
    What are these?
    anti-inflammatories, inhaled glucocorticoids
  127. prednisone
    What are these?
    anti-inflammatories, oral glucocorticoids
  128. montelukast (Singulair)
    zafirlukast (Accolate)
    zileuton (Zyflo)
    What are these?
    anti-inflammatories, leukotriene modifiers
  129. cromolyn (Intal)
    nedocromil (Tilade)
    What are these?
  130. omalizumab (Xolair)
    What is this?
    anti-inflammatory, IgE antagonist
  131. albuterol (AccuNeb, ProAir, Proventil, Ventolin)
    bitolterol (Tornalate)
    levalbuterol (Xopenex)
    pirbuterol (Maxair)
    What are these?
    bronchodilators, inhaled short acting beta2 adrenergic agonists (SABAs)
  132. arformoterol (Brovana)
    formoterol (Foradil, Perforomist)
    salmeterol (Serevent)
    What are these?
    bronchodilators, inhaled long acting beta2 adrenergic agonists (LABAs)
  133. albuterol (VoSpire)
    terbutaline (Brethine)
    What are these?
    bronchodilators, oral beta2 adrenergic agonists
  134. theophylline (Theo24, Theochron, Uniphyl, Elixophyllin)
    What is this?
    bronchodilator, methylxanthine
  135. ipratropium (Atrovent)
    tiotropium (Spiriva)
    What are these?
    bronchodilators, anticholinergics
  136. This med class is the foundation of asthma therapy, is taken daily for long-term control, and addresses the underlying disease process (inflammation).
  137. What are the principle prophylactic anti-inflammatories used for asthma?
  138. These are 1st line drugs used for asthma, are considered very safe, are not administered PRN, and have adverse effects of oropharyngeal candidiasis and dysphonia.
    Inhaled glucocorticoids
  139. When are oral glucocorticoids indicated for asthma?
    When severe; only when symptoms can't be controlled w/ safer meds (inhaled glucocorticoids, beta2s)
  140. Toxicity of oral glucocorticoids (increases/decreases/stays the same) with duration of use.
  141. Although alone these are less effective than glucocorticoids, they are very effective when combined with glucocorticoids.
    Leukotriene modifiers
  142. Although used for prophylaxis of chronic asthma, this class of anti-inflammatories should not be used as 1st line therapy.
    Leukotriene modifiers
  143. This class of anti-inflammatories for asthma is only administered orally.
    Leukotriene modifiers
  144. This is the safest of all antiasthma meds; used for prophylaxis of chronic asthma, EIB, allergic rhinitis; must be administered on a fixed schedule.
  145. This anti-inflammatory asthma med is no longer available in the US.
  146. Cromolyn is AKA a ___
    mast cell stabilizer
  147. This anti-inflammatory med is a 2nd line agent indicated only for patients whose asthma is caused by specific allergen, and when preferred options have failed. It's very expensive, viscous, and is only administered subQ. It's long-term safety is unknown.
  148. This major class of asthma meds provides symptomatic relief but does not alter the underlying disease process (inflammation).
  149. T/F Unless attacks are mild/infrequent, patients taking a bronchodilator should also be taking inhaled glucocorticoids for long-term suppression of inflammation.
  150. There is evidence that this class of bronchodilators can increase risk of asthma related death when used alone.
    Beta2 adrenergic agonists
  151. Beta2 adrenergic agonists are most effective for...
    relieving acute bronchospasm and preventing EIB
  152. What are the 3 subclasses of beta2 adrenergic agonists?
    • SABAs
    • LABAs
    • oral
  153. These beta2 adrenergic agonists are used to abort an ongoing attack, are adnministered PRN or before exercise.
  154. These beta2 adrenergic agonists are used to abort an ongoing attack and for prolonged prophylaxis (though not 1st choice), are administered on a fixed schedule, and should never be used alone.
  155. These beta2 adrenergic agonists are used for long-term control of asthma (though not 1st choice) and should never be used alone.
  156. This class of bronchodilators is only approved for COPD, but is used for asthma. They block muscarinic receptors in bronchi, and are only administered by inhalation. Contraindicated in those with peanut allergy.
  157. Combination asthma meds combine what two classes of drugs? What are 2 examples?
    • glucocorticoids (anti-inflammatories) + LABAs (bronchodilators)
    • Advair, Symbicort
  158. These are reserved for asthma not adequately controlled with an inhaled glucocorticoid alone.
    Glucocorticoid/LABA combo
  159. Allergic rhinits can be either ___ or ___.
    seasonal; perennial/non-seasonal
  160. What causes seasonal allergic rhinitis?
    Outdoor allergens (hay fever; occurs Spring, Fall)
  161. What causes perennial allergic rhinitis?
    Indoor allergens (dust mites, pet dander)
  162. What are side effects of antihistamines?
    • sedation
    • dry mouth
    • dry eyes
    • constipation
    • bitter taste
  163. In what ways are antibiotics misused?
    • untreatable infection
    • fever of unknown origin
    • absence of adequate bacteriologic info
    • omission of surgical drainage
    • when surgery should be employed
  164. What is the only situation in which fever, by itself, constitutes a legitimate indication for antibiotic use?
    In severely immunocompromised host
  165. T/F Except in life-threatening situations, antibiotic therapy should not be undertaken in the absence of bacteriologic info.
  166. What are the major side effects of antibiotics?
    • Aminoglycosides: hearing loss, dizziness, kidney damage
    • Cephalosporins: n/d, allergic rxns
    • Fluoroquinolones: nervousness, tremors, seizures, inflammation/rupture of tendons, arrhythmias, diarrhea and colitis, sometimes fatal liver damage
    • Macrolides: n/v/d, arrhythmias, jaundice
    • Monobactam: allergic rxns
    • Penicillins: n/v/d, allergy w/ serious anaphylaxis
    • Polypeptides: kidney and nerve damage
    • Sulfonamides: n/v/d, allergy, decrease in white blood cell and platelet counts, sensitivity to sunlight, possibly increased tendency to bleed if used with warfarin
    • Tetracyclines: GI upset, sensitivity to sunlight, staining of teeth in the fetus if used late in pregnancy or in children under 8 years of age
  167. Without this - consisting of immune system and phagocytic cells - successful antimicrobial therapy would be rare.
    Host defenses
  168. T/F In most cases, the drugs we use do not cure infection alone. Rather, they work in concert with host defense systems to subdue infection.
  169. When treating immunocompromised, the only hope of treating infection lies w/ drugs that are rapidly ___, and even those may prove inadequate.
  170. What class does gentamycin belong to?
  171. Gentamicin treats serious infections caused by what kind of bacteria?
    Gran-negative bacilli (Pseudomonas aeruginosa, E. coli)
  172. In hospitals where resistance isn't a problem, ___ is often the preferred aminoglycoside for use agains E. coli. Why?
    • gentamycin
    • Cheaper
  173. Gentamicin is cross-resistant to ___.
  174. For infections that are resistant to gentamicin and tobramycin, ___ is usually effective.
  175. What med can be combined with vancomycin, a cephalosporin, or a peniccilin to treat serious infections caused by certain gram-positive cocci (Enterococcus, streptococci, Staph)?
  176. Like all other aminoglycosides, gentamicin is toxic to what 2 things?
    • kidney
    • ear
  177. Gentamicin is inactivated by ___ and should not be mixed with these drugs in the same IV.
  178. Drug or chemical damage to the inner ear.
  179. T/F Only some aminoglycosides can accumulate w/in the inner ear, causing cellular injury that can impair both hearing and balance.
    F; all
  180. How do aminoglycosides cause impairment of hearing?
    By damaging sensory hair cells in the cochlea
  181. How do aminoglycosides cause disruption of balance?
    By damaging sensory hair cells of the vestibular apparatus
  182. The risk of ototoxicity is r/t primarily excessive ___ levels of drug.
  183. Is cellular injury from ototoxicity d/t prolonged exposure or brief exposure at high levels?
    Prolonged exposure
  184. In addition to high trough levels, the risk of ototoxicity is increased by wht 3 things?
    • renal impairment
    • concurrent use of ethacrynic acid
    • aminoglycosides in excessive doses or form more than 10 days
  185. What is the first sign of impending cochlear damage?
    High-pitched tinnitus
  186. What's the first sign of impending vestibular damage?
  187. What are later signs of damage from ototoxicity?
    • nausea
    • unsteadiness
    • dizziness
    • vertigo
  188. Ototoxicity is largely (reversible/irreversible).
  189. What's the most serious adverse effect of vancomycin?
  190. Renin Angiotensin Aldosterone System
    Image Upload 1
  191. What 4 drug classes are associated w/ RAAS?
    • ACE (angiotensin converting enzyme) inhibitors
    • ARBs (angiotensin II receptor blockers)
    • DRIs (direct renin inhibitors)
    • aldosterone antagonists
  192. For many of the RAAS related meds, aldosterone release is inhibited, which may result in ___, especially when combined with potassium supplements, salt substitutes, potassium-sparing diuretics, or other RAAS meds. Why?
    • hyperkalemia
    • With inhibition of aldosterone, instead of reabsorbing sodium/water and excreting potassium, the body reabsorbs potassium and excretes sodium/water.
  193. What is the major vasoconstricort of the RAAS, and how does volume increase to increase BP?
    • angiotensin II
    • With stimulated production of aldosterone, kidneys then retain sodium/water and excrete potassium, increasing fluid volume.
  194. What meds cause vasodilation and a decrease in afterload? How do they work?
    • *Calcium channel blockers (diltiazem, verapamil, nifedipine), alpha adrenergic blockers (phentolamine, prazosin, terazosin), ACE inhibitors (captopril, enalapril), ARBs (losartan), DRIs (aliskiren), others (*hydralazine, *minoxidil, nitroprusside, *diazoxide)
    • All of these drugs dilate resistance vessels (arterioles), causing a decrease in cardiac afterload (the force the heart works against to pump blood). By decreasing afterload, arteriolar dilators reduce cardiac work while causeing cardiac output and tissue perfusion to increase.
  195. These block beta adrenergic receptors.
    Beta adrenergic antagonists (beta blockers)
  196. What makes the difference between a beta blocker being therapeutic vs nontherapeutic?
    Selectivity...therapeutic effects result from blockade of beta1 receptors of the heart only; nontherapeutic effects result from blockade of both beta1 and beta2 receptors
  197. What are the 3 major consequences of blocking beta1 receptors in the heart?
    • reduced HR
    • reduced force of contraction
    • reduced velocity of impulse conduction through the AV node
  198. What are beta blockers used for?
    • angina pectoris
    • HTN
    • cardiac dysrhythmias
    • MI
    • HF
    • hyperthyroidism
    • migraine
    • stage fright
    • pheochromocytoma
    • glaucoma
  199. What are the 2 "c's" associated with beta blockers?
    • conduction
    • contraction
  200. What's the most important factor of success of thrombolytic drugs?
    Time b/w onset of symptoms and delivery of the med
  201. How long do you have to administer a thrombolytic med for it to be effective following a stroke?
    3 hours
  202. What's the chief use for low-molecular wt heparins?
    prevention and treatment of DVT
  203. The most significant adverse effects of alpha adrenergic antagonists result from blockade of (alpha1/alpha2) receptors.
  204. What are the main side effects of pts on alpha blockers?
    • orthostatic hypotension
    • reflex tachycardia
    • nasal congestion
    • inhibition of ejaculation
    • sodium retention, increased fluid volume
  205. What are the main side effects of pts on beta blockers?
    • Beta1: bradycardi, reduced CO, precipitation of HF, AV heart block, rebound cardiac excitation
    • Beta2: bronchoconstriction, inhibition of glycogenolysis
  206. What med would you give if the pt's fluid volume increased after giving an alpha blocker?
  207. Why is heparin not administered orally? What is used instead?
    • It's too large and too polar to permit intestinal absorption
    • Warfarin
Card Set
Pharmacology Exam 1 Study Guide