Pharm Exam II

  1. Mechanisms of Adrenergic Receptor
    Activation by Agonist Drugs (4)
    • Direct Receptor Binding
    • Promotion of Norepinephrine (NE) Release
    • Inhibition of NE Reuptake
    • Inhibition of NE Inactivation-
  2. Catecholamines and noncatecholamines differ in three respects:
    • Oral usability
    • Duration of action
    • Ability to act in the CNS
  3. Catecholamine's: (Epineherine, Norepinepherine)
    3 properties in common
    • Cannot be used orally
    • Brief duration of action
    • Cannot cross the blood-brain barrier
  4. Norepinephrine, dopamine, & dobutamine only work if
    given by continuous infusion
  5. Catecholamine’s are ____ _____, cannot cross the blood-brain barrier
    polar molecules
  6. Catecholamine's: IV solutions can turn pink or brown over time;
    Discard if discolored
  7. Adrenergic Agonists affect: (4)
    • alpha 1,
    • alpha 2,
    • beta 1 &
    • beta 2 adrenergic receptors
  8. Noncatecholamines (4)
    • can be given orally &
    • have longer half-lives
    • less polar,
    • can cross the blood brain barrier
  9. Alpha 1 Receptors :cause two responses
    • vasoconstriction (in blood vessels of skin, viscera, and mucous membranes) &
    • mydriasis (dilation of the pupil)
  10. Alpha 1 Activation
    Stop bleeding primarily in skin & mucous membranes (Epinephrine)
  11. Alpha 1 Activation
    Nasal Decongestion
    Relieve congestion by vasoconstriction of mucous membranes (phenylephrine & pseudoephedrine)
  12. Alpha 1 Activation
    Adjunct to Local Anesthesia-
    Combined with anesthetics to delay anesthetic absorption, vasoconstriction at the site.(Epinephrine)
  13. Alpha 1 Activation
    Elevation of BP-
    Vasoconstriction can elevate BP, ONLY usedwhen other therapies have failed
  14. Alpha 1 Activation
    facilitates eye exams & ocular surgery
  15. Alpha 1 Adverse Effects (3)
    • Hypertension
    • Necrosis
    • Bradycardia
  16. Alpha 1 Adverse Effects 
    • Widespread vasoconstriction can cause HTN, particularly parenteral administration IV:
    • Must monitor CV status continuously
  17. Alpha 1 Adverse Effects
    Extravasation & necrosis with IV infiltrate,(intense vasoconstriction), alpha 1 blocker (antagonist) to minimize damage (phentolamine)
  18. Alpha 1 Adverse Effects
    Reflex response to increase in BP, cancause cardiac collapse & impaired tissue perfusion
  19. Alpha 2 Activation
    Peripherally inhibit NE release (but little clinical relevance)
  20. Alpha 2 Activation
    In CNS receptors cause
    • Reduction of sympathetic outflow to heart & blood vessels
    • Relief of severe pain
  21. Beta 1 Activation
    • Heart Failure
    • Shock
    • Atrioventricular (AV) Heart Block
    • Cardiac Arrest from Asystole
  22. Beta 1 Activation
    Heart Failure-
    Beta 1 receptors increase force of contraction (inotropic effect),improves cardiac Fxn
  23. Beta 1 Activation
    - (Shock=profound hypotension) Beta 1’s increase heart rate (HR), force of contraction=increased cardiac output (CO), & improves tissue perfusion
  24. Beta 1 Activation
    Atrioventricular (AV) Heart Block-
    Beta 1’s enhance conduction through AV node (temporarily, until pacemaker )
  25. Beta 1 Activation
    Cardiac Arrest from Asystole-
    Beta 1’s can initiate acontraction in a heart that has stopped, (CPR & TXrequired, Epinephrine)
  26. Beta 1 Adverse Effects (2)
    • Altered Heart Rate or Rhythm
    • Angina Pectoris
  27. Beta 1 Adverse Effects
    Altered Heart Rate or Rhythm
    Overstimulation of beta 1’s can produce tachycardia & dysrhythmias
  28. Beta 1 Adverse Effects
    Angina Pectoris-
    Angina Pectoris- Beta 1’s increase cardiac oxygen demand, which can cause angina in pts with impaired coronary circulation
  29. Beta 2 Activation (3)
    • Limited to lungs and uterus
    • Asthma- Beta 2 receptors promote bronchodilation, Selective beta 2 receptors(albuterol) preferred, (Drugs that activate beta 1 receptors can stimulate tachycardia & angina).Most via inhalation to minimize adverse systemic effects, systemic toxicity with overdosing
    • Can Delay Preterm Labor- Relaxes uterine smoothmuscles
  30. Beta 2 Adverse Effects (2)
    • Hyperglycemia
    • Tremor
  31. Beta 2 Adverse Effects Hyperglycemia
    • (highest risk: diabetic pts)
    • beta 2 receptors stimulate breakdown of glycogen into glucose
  32. Beta 2 Adverse Effects
    Most common, beta 2;s in muscles cause enhanced contractions, fades over time, minimized by starting at low dose
  33. Dopamine Receptor
    • Activation of peripheral dopamine receptor causes dilation of renal vasculature
    • *Dopamine (the drug) used in shock to dilaterenal blood vessels & reduce risk of renal failure
    • Dopamine also enhances cardiac performance
    • Assess Urinary output (UOP), increases when kidneys are functioning, shock=no/low perfusion to kidenya and low UOP
  34. Epinephrine
    Receptor specificity:
    alpha 1, alpha 2, beta 1 and beta 2
  35. Epinephrine
    Therapeutic Uses:
    • Alpha 1-mediated vasoconstriction
    • Beta 1’s - to overcome AV heart block,
    • Beta 2’s: promotes bronchodilation
    • **Epinephrine is the Tx of choice for anaphylactic shock*
  36. Epinephrine Therapeutic Uses: Alpha 1-mediated
    vasoconstriction, used to delayabsorption of anesthetics, control superficial bleeding, &elevate BP. (Was used for nasal decongestion) Alsomydriasis.
  37. Epinephrine Therapeutic Uses: Beta 1’s -
    to overcome AV heart block, & restore cardiac function in pts experiencing cardiac arrest.
  38. Epinephrine Therapeutic Uses:Beta 2’s:
    promotes bronchodilation
  39. Epinephrine ROUTE:
    Topical, injection or IV administration only.
  40. Epinephrine  half-life
    Short (due to MAO and COMT)
  41. Epinephrine Adverse Effects:
    • Can cause Hypertensive Crisis-
    • Can cause Dysrhythmias-
    • Angina Pectoris-
    • Necrosis Following IV Extravasation-
    • Hyperglycemia
  42. Epinephrine Adverse Effects:Hypertensive Crisis
    Can cause Hypertensive Crisis- Alpha 1 stimulation,vasoconstriction, dramatic increase in BP (IV infusion)
  43. Epinephrine Adverse Effects: Dysrhythmias
    Can cause Dysrhythmias- Beta 1 stimulation
  44. Epinephrine Adverse Effects: Angina Pectoris
    Angina Pectoris- Beta 1 increases cardiac work & oxygendemand
  45. Epinephrine Adverse Effects: Necrosis
    Necrosis Following IV Extravasation-alpha-adrenergic antagonist can minimize (phentolamine)
  46. Epinephrine Adverse Effects:Hyperglycemia
    Hyperglycemia- beta 2’s, typically in diabetic pts only
  47. Epinephrine Drug Interactions: (5)
    • MAO Inhibitors
    • Tricyclic Antidepressants-
    • General Anesthetics-
    • Alpha-adrenergic Blocking Agents
    • Beta-adrenergic Blocking Agents-
  48. Epinephrine Drug Interactions:MAO Inhibitors-
    Prolong and intensify the effects ofepinephrine & other catecholamines
  49. Epinephrine Drug Interactions: Tricyclic Antidepressants-
    Block the uptake ofcatecholamines, so can intensify & prolong epinephrineeffects.
  50. Epinephrine Drug Interactions: General Anesthetics-
    Can cause tachydysrhythmias when used together
  51. Epinephrine Drug Interactions:
    Alpha-adrenergic Blocking Agents
    (antagonists) Can prevent receptor activation by epinephrine(*Phentolamine: antidote used to treat toxicity)
  52. Epinephrine Drug Interactions: Beta-adrenergic Blocking Agents-
    Can prevent receptoractivation by epinephrine, reduce adverse effectscaused by epinephrine
  53. Epinephrine
    Catecholamine or Noncatecholamine
  54. Norepinephrine (6)
    • Receptor specificity: Alpha 1, Alpha 2, Beta 1
    • Catecholamine
    • *Same as Epi, except no Beta 2 stimulation
    • Does not promote hyperglycemia
    • Typically only used in hypotensive states & cardiacarrest
    • IV infusion only
  55. Isoproterenol (3)
    • Receptor Specificity: Beta 1 and Beta 2
    • Catecholamine
    • *First beta selective medication
  56. Isoproterenol Therapeutic Uses:
    • Cardiovascular-overcome AV heart block, restart heart following cardiac arrest, increase cardiac output in shock 
    • Bronchospasm- Not used to treat asthma ONLY bronchospasm, (more selective medications treat asthma)
  57. Isoproterenol
    Adverse Effects:
    • Beta 1 activation- tachy-dysrhythmias & angina
    • Beta 2 activation- hyperglycemia
  58. Isoproterenol Drug Interactions:
    • Effects are enhanced by MAO Inhibitors andtricyclic antidepressants; Reduced by beta-blockers
    • Can cause dysrhythmias when given with inhaled anesthetics
  59. Inotropic drugs influence the
    • strength or contractilty of muscle tissue.
    • Increase the force of the heart's contractions
  60. Two types of Inotropic drugs
    Cardiac Gylcosides and phophodiesterase (PDE) inhibitors
  61. -Slow heart rate and slow electrical impulse conduction through the AV node.
    -Useful for pts who have artrial fibrillations.
    -Can help control HR and prevent it from becoming too fast
    - Incrs. perfusion of tissues improves function/help decrease edema (interstitial fld)
    Cardiac Glycosides
  62. Cardiac Glycosides Prototype
  63. Digoxin Actions
    • Inhibits sodium-potassium- activated adenosine triphosphas: reg. amt. of Na and K+ inside the cell resulting in increased intracellular levels of Na and K.
    • Promotes the movement of Ca from extra cellular to intracellular cytoplasm and strengthens myocardial contraction
    • Acts on the CNS to enhance vagal tone, slowing contractions through the SA and AV nodes- provides an antiarrhythmic effect.
  64. Digoxin Indications (3)
    • heart failure
    • Atrial Fib. and flutter
    • Supraventricular tachycardia
  65. Digoxin Nursing Considerations
    • Monitor pt for adverse effects
    • W/hold if apical pulse is less than 60 bpm and notify prescriber
    • monitor serum K and digoxin levels
    • assess renal function
  66. Digoxin Pharmacokinetics
    • intestinal asbsorption varies greatly
    • cap. most efficent, then elixr then tabs
    • absorp. hightest concen. in heart musc., liver, and kideny
    • poorly bound to plasma protiens
    • Most is excrete from kid. unchanged
  67. Digoxin Pharmacodynamics
    • boost intracellular Ca at the cell membrane
    • enable stronger heart contractions
    • may enhance movement of Ca into myocardial cells and stimulate the release for block re-uptake of noreponephrine at the adrenergic nerve terminal
    • Works on CNS to slow HR
    • Increases refractory period
  68. Digoxin PK
    heart failure
  69. Digoxin ______ Cardiac Output:
    • Increased:
    • -Increases contractilityby restoring cardiac muscle fibers to near health,increases the stroke volume of failing heart =cardiac output rises
  70. Digoxin Three major secondary responses due to increased cardiac output:
    • – Decreased sympathetic tone
    • – Urine production increases
    • – Renin release declines
    • – These responses can reverse virtually all signs and symptoms of heart failure.
  71. Digoxin (Cardiac Glycoside)Adverse Effects 1:
    Cardiac Dysrhythmias
  72. Digoxin (Cardiac Glycoside) Adverse Effects 1: Cardiac Dysrhythmias:
    Digoxin: used in therapeutic doses to slow fastheart rates, but causes dysrhythmias if given inhigh doses or in the presence of hypokalemia
  73. Elevated digoxin levels- Narrow therapeutic window/Range:
    (0.5-0.8 ng/mL; variance among range, most state no higher than 1.5 ng/ml) levels slightly higher than therapeutic produce toxicity
  74. Managing Digoxin-Induced Dysrhythmias:–
    • Withdraw digoxin & potassium-wasting diuretics
    • – Monitor serum potassium
    • – Anti-dysrhythmic drug is sometimes needed (Lidocaine & phenytoin most effective for ventricular dysrhythmias, atropine for bradycardias)
    • – Can give reversal agent: Digibind or Digifab, Cost$2,000-$3,000, only use when severe (also can cause arrhythmias as it binds digoxin)
  75. Digoxin (Cardiac Glycoside) Adverse Effects 2: Non-cardiac Adverse Effects
    • **GI- anorexia, nausea, and vomiting
    • **CNS- Fatigue & visual disturbances (blurred vision, yellow tinge to vision, halos around dark objects)
  76. Digoxin (Cardiac Glycoside) Drug Interactions:
    • *Diuretics- Thiazide and Loop Diuretics promoteloss of potassium (increases risk of dysrhythmias)
    • ACE Inhibitors and ARBs- Can increase potassiumlevels (decreases digoxin levels)
    • Sympathomimetics- Can add to the inotropiceffects of digoxin
  77. Plasma Digoxin Levels:
    • Therapeutic Range: 0.5-0.8 ng/mL.
    • Anything over 1 ng/mL offers no additional benefit and increases the risk of toxicity.
  78. Herbs and Digoxin
    St. John's wort and ginseng can ^ levels of digoxin and  ^ risk of toxicity
  79. S/S of Digoxin toxicity:
    • slow to rapid ventricular rhythms
    • nausea and vomiting
    • blurred vision
    • anorexia
    • abdomin. discomfort
    • mental changes
  80. Classification of Antidysrhythmic Drugs
    • Class I: Sodium Channel Blockers
    • Class II: Beta Bloacker
    • Class III: Potassium Channel Blockers
    • Class IV: Calcium Channel Blockers
    • Other: Adenosine and Digoxin
  81. Most Antidysrhythmic Drugs most:
    • Slow conduction or part of the cardiac cycle/HR
    • Improve Contractility
    • Correct Dysrhythmia
  82. Sodium Channel Blockers
    Slow impulse conduction in the atria, ventricles, and HIS Purkinje system- Largest group
  83. Beta Blockers
    • Reduce Ca entry & depress phase 4 depolarization
    • reduce automaticity in SA node
    • Slow Slow conduction velocity in AV node
    • Reduce force of contraction
  84. Beta-Adrenergic Blockers
    Nonselective agents
    • Carteolol,
    • Nadolol,
    • Penbutolol,
    • Pindolol,
    • Propanolol,
    • Sotalol,
    • Timolol
    • Carvedilol,
    • Labetalol
  85. Carteolol, Nadolol,Penbutolol, Pindolol,Propanolol, Sotalol, Timolol
    Receptors Blocked
    Beta 1, Beta 2
  86. Carvedilol, Labetalol
    Receptors Blocked
    Beta1, Beta 2, Alpha 1
  87. Beta 1-Selective Agents
    • Acebutolol,
    • Atenolol,
    • Betaxolol,
    • Bisoprolol,
    • Esmolol,
    • Metoprolol,
    • Nebivolol
  88. Lidocaine (Xylocaine) PT
    • limited to short-term
    • therapy for ventricular dysrhythmias. Not
    • effective against supraventricular dysrhythmias
  89. Lidocaine (Xylocaine) PK
    If given orally, most of the drug would be inactivated in the first pass.
  90. Lidocaine (Xylocaine)Adverse
    • CNS effects- drowsiness, confusion, paresthesias, tremor
    • Toxic doses- (severe CNS effects), convulsions & respiratory arrest
  91. Lidocaine (Xylocaine)Therapeutic range;
    1.5-5 mcg/ml
  92. Lidocaine (Xylocaine) dose
    50-100 mg (1mg/kg) followed by infusion rate of 1-4mg per min
  93. Lidocaine (Xylocaine) special instructions
    Only the IV form is used , never the lidocain eused as a local anesthetic
  94. Propanolol (Inderal, Inderal LA)
    • Class II: Beta Blockers for Dysrhythmia
    • *nonselective beta adrenergic antagonist
  95. Propanolol (Inderal, Inderal LA) Effects on the Heart & ECG-
    • Decreased automaticity of SA node,
    • Decrease velocity of AV node, &
    • Decreased myocardial contractility (force of contraction),
  96. **Only four of all beta blockers are approved for treating dysrhythmias:
    • propranolol,
    • acebutolol,
    • esmolol, and
    • sotalol
    • (All others just for HTN)**
  97. Beta Blockers for Dysrhythmia PD:
    • *Competitively Blocks catecholamine's at non-CNS beta adrenergic receptor sites,
    • particularly the heart to decrease CO,
    • central effect decreases sympathetic outflow to periphery,
    • prevents release of renin from kidneys.*
  98. (Beta Blockers) *Overall Therapeutic Effects*:
    • – Reduced Heart Rate
    • – Reduced Force of Contraction
    • – Reduced Velocity of Conduction through the AV node.
  99. (Beta Blockers) for *Heart Failure- Only drugs:
    • carvedilol (Coreg),
    • bisoprolol (Zebeta), &
    • metoprolol (Lopressor).*
  100. Propranolol (Inderal/Inderal LA) Therapeutic Uses:
    • Hypertension,
    • angina pectoris,
    • cardiac dysrhythmias, and
    • myocardial infarction.
  101. metoprolol (Lopressor,Toprol XL) is a
    • Beta Blocker
    • 2nd-Generation, selective cardiac (beta 1) blockade
  102. Beta Blockers: Metoprolol (Lopressor,Toprol XL)• Therapeutic Uses:
    • Primarily HTN,
    • also angina pectoris,
    • heart failure, &
    • myocardial infarction.
  103. Class III: Potassium Channel Blockers work by
    Delay repolarization of fast action potentials
  104. Potassium Channel Blockers prototype
    Amiodarone (Cordarone),
  105. Amiodarone is highly effective for ____ ___& is widely used for this purpose (BUT IT IS NOT APPROVED FOR THIS USE)
    atrial fibrillation
  106. Amiodarone is Effective against
    both atrial & ventricular dysrhythmias
  107. Amiodarone (Cordarone, Pacerone)ORAL half life
    Extremely long half-life (25-110 days), continuesto act long after it is discontinued
  108. Amiodarone (Cordarone, Pacerone) ORAL THERAPY• Adverse Effects:
    • **Pulmonary Toxicity- lung damage**,
    • Cardiotoxicity
    • Thyroid Toxicity-  
    • Liver Toxicity-
    • Opthalmic Effects-
    • Toxicity in Pregnancy & Breast-feeding
    • Dermatological Toxicity-
    • CNS reactions- ataxia, dizziness, tremor,mood alteration, & hallucinations (Safety). GIreactions- anorexia, N/V
  109. Amiodarone ORAL is ineractions
    • *increased by grapefruit juice* and CYP3A4(toxicity can result)•
    • cholestyramine & agents thatinduce CYP3A4 (St. John’s Wart, rifampin)•
    • *Risk of severe dysrhythmias is increased by diuretics(reduced levels of potassium and magnesium) & by drugs thatprolong QT interval• *Combining amiodarone with beta blockers,verapamil or diltiazemcan excessive slowing of heart rate
  110. Amiodarone (Cordarone, Pacerone) IV THERAPY• Therapeutic Use-
    Approved only for initia ltreatment & prophylaxis of recurrent ventricular fibrillation & hemodynamically unstable ventricular tachycardia in pts refractory to safer drugs.
  111. Amiodarone (Cordarone, Pacerone) IV THERAPY• NOT approved uses*
    • Also used to treat atrial fibrillation,
    • AV nodal reentrant tachycardia and
    • shock-resistant ventricular fibrillation (NOT approved uses)
  112. CALCIUM CHANNEL BLOCKERS action on muscle
    • *Calcium channels regulate muscle contraction in vascular smooth muscle.•
    • *If calcium channels are blocked, contraction will be prevented; vasodilation will result•
    • *Calcium Channels Blockers act selectively on peripheral arterioles and arteries & arterioles of the heart.•
    • *No significant effect on veins.
  113. CALCIUM CHANNEL BLOCKERS action on heart:
    • In heart, calcium channels help regulate the myocardium,
    • sinoatrial (SA) node,
    • & atrioventicular (AV) node•
  114. If calcium channels are blocked:,
    • contractile force will diminish
    • heart rate is reduced
  115. Calcium Channel Blockers• Three families
    • The largest family is dihydropyridines
    • Phenylakylamine is next family: Verapamil is the only drug in this family•
    • Benzothiazepine is the final family: Diltiazemis the only drug in this family
  116. Dihydropyridines act primarily on
  117. Calcium Channel Blockers• Verapamil and Diltiazem act on
    arterioles & the heart
  118. Calcium Channel Blockers: Verapamil Used for
    • angina pectoris,
    • essential hypertension&
    • cardiac dysrhythmias*.
  119. **Overall effect of verapamil is
    simply vasodilation, reduced arterial pressure, &increased coronary perfusion**
  120. Calcium Channel Blockers: Verapamil administration
    Given IV or orally.
  121. Calcium Channel Blockers: Verapamil• Therapeutic Uses
    • **Angina Pectoris-
    • **Essential HTN-
    • **Cardiac Dysrhythmias-
  122. Calcium Channel Blockers: Verapamil• Adverse Effects:
    • Common effects- *Constipation most common
    • **Other common effects – dizziness, facial flushing,headache, & edema of the ankles & feet (all from vasodilation)•
    • Cardiac Adverse Effects- *Bradycardia, Sick Sinus Syndrome, and 2nd or 3rd degree blocks (slowed conduction)
  123. Calcium Channel Blockers: Verapamil• Drug and Food Interactions:
    • Digoxin- 
    • Beta-Adrenergic Blocking Agents-
    • Grapefruit Juice- il
  124. Diltiazem
    • Similar to verapamil except:
    • • Bigger first-pass effect, starts working in minutes,peaks in 30 minutes
    • • Diltiazem is less likely to cause constipation
  125. Calcium Channel Blockers:
    • Dihydropyridines•
    • Nifedipine (Adalat CC, Nifedical XL, Nifediac CC,Procardia, Procardia XL)
  126. Calcium Channel Blockers: Nifedipine Net Effects–
    Lowers BP, increases heart rate, & increases contractileforce
  127. Calcium Channel Blockers: Nifedipine• Therapeutic Uses:
    • • Angina Pectoris-
    • HTN- Essential HTN, *Only sustained release should beused.
  128. Calcium Channel Blockers: Nifedipine Adverse Effects–
    • Flushing, dizziness, headache, peripheral edema, & gingivalhyperplasia
    • – Reflex tachycardia (avoided if with Beta-blocker)
    • Rapid-acting nifedipine is associated with increased mortality and therefore is used with EXTREME CAUTION.
  129. Calcium Channel Blockers• Drugs:
    • (many end in dipine, but not all)
    • amlodipine (Norvasc),
    • bepridil (Vascor),
    • diltiazem(Cardizem),
    • felodipine (Plendil) SR,
    • isradipine(DynaCirc) SR,
    • nicardipine (Cardene) SR,
    • nifedipine(Procardia) SR,
    • nimodipine (Nimotop),
    • nisoldipine(Sular),
    • verapamil (Isoptin, Calan)
  130. Digoxin (Lanoxin)•_____ inotrop action:
    Positive inotrop action, increases force ofventricular contraction
  131. Digoxin (Cardiac Glycoside)• Plasma Digoxin Levels:• Therapeutic Range:
    0.5-0.8 ng/mL.
  132. Hormones of the Posterior Pituitary– 2
    • Oxytocin- facilitates uterine contraction during labor.–
    • Antidiuretic Hormone (ADH)- promotes renalconservation of water.
  133. Anterior pituitary gland dysfunction:
    – Growth hormone (GH) deficiency (short stature) & excess (gigantism)
  134. Posterior pituitary gland dysfunction (major disorders):–
    • Diabetes Insipidus (DI)
    • – Syndrome of Inappropriate Antidiuretic Hormone (SIADH).
  135. Thyroid gland dysfunction:–
    • Hyperfunction (hyperthyroidism) or
    • hypofunction (hypothyroidism)
    • – Dysfunction can be congenital defect or by a problem later in life.
  136. Parathyroid gland dysfunction:
    • – PTH a major regulator of serum calcium and phosphate.
    • – Decrease in serum calcium concentration main stimulus/regulator of PTH, response rate in seconds
    • – Decrease in serum phosphate causes an indirect effect on PTH by combining with calcium and decreasing serum calcium concentrations
  137. Growth Hormones• GH deficiency, causing short stature, was initially treated with:
    GH injections extracted from the pituitary glands of cadavers.
  138. Growth Hormones• GH deficiency, causing short stature, Now treated
    synthetic human GH (rhGH), produced fromrecombinant DNA
  139. Growth Hormones Prototype drug:
    • somatropin (several brand names).
    • In pediatric patients: VERY EXPENSIVE $20,000-$50,000 yr
  140. Somatropin (Human Growth Hormone)• Implementation: Daily administration• Routes:
    SubQ (preferred) or IM
  141. Somatropin (Human GrowthHormone)•
    Minimizing Adverse Effects and Interactions:
    • *Hyperglycemia- GH can elevate plasma glucose levels in diabetics.Increase insulin dose as needed.•
    • *Hypothyroidism- GH may suppress thyroid function. Assessthyroid function before treatment and periodically thereafter. Iflevels of thyroid hormone fall, institute replacement therapy.•
    • Interaction with Glucocorticoids- Glucocorticoids can opposegrowth-stimulating effects of GH.
  142. GH therapy may induce ____ _____
    insulin resistance.
  143. Growth Hormone Agonists• GH excess leads to:
    • Gigantism-
    • Acromegaly
  144. Growth Hormone Agonists• GH excess 

    Prototype drug:
    Octreotide acetate (Sandostatin)
  145. posterior pituitary stores two hormonesproduced in the hypothalamus:
    • Vasopressin
    • and Oxytocin.
  146. ____ & _____ are syntheticanalogues of the naturally occurring posteriorpituitary hormone.
    Desmopressin & vasopressin
  147. Posterior Pituitary Hormone Regulators Prototype drug:
    Desmopressin (DDAVP,Stimate, Minirin). [vasopressin (Pitressin)]
  148. ____a drug identical to natural ADH, can cause _____ _____
    Vasopressin, profound vasoconstriction.
  149. Desmopressin Routes–
    Intranasal, PO, SubQ, and IV–
  150. Vasopressin routes
    - IM, SubQ
  151. ADH (Vasopressin orDesmopressin)• Ongoing Evaluation and Interventions:• Evaluating Therapeutic Effects:– Teach the patient to
    monitor and record dailyintake and output of fluid
  152. Oxytocins• Interventions:
    Baseline and ongoing maternal HR and BP, uterine activity: timing and length of contractions, and fetal heart rate.
  153. Oxytocins Drugs-
    • *ergonovine (Ergotrate);
    • *methylergonovine (Methergine);
    • oxytocin(Pitocin, Syntocinon)
    • *used post delivery to decrease risk of hemorrage
  154. PITOCIN
    • P- Pressure is elevated•
    • I – Intoxication with water•
    • T- Tetanic contractions•
    • O- Oxygen decrease in fetus•
    • C- Cardiac arrhythmia•
    • I- Irregularity in fetal heart rate•
    • N- Nausea and vomiting
  155. Estrogen• Action-
    Development and maintenance for adequate functioning of female reproductive system; affects release of pituitary gonadotropins; promotes adequate use in bone structures.•
  156. Estrogen• Indications
    - Moderate to severe vasomotor symptoms associated with menopause;postpartal breast engorgement, hormonal replacement therapy; prevention of osteoporosis and cardiovascular disease.
  157. (Estratab, Estratest, Menest);
    estradiol (Climara, Estrace, Estrace Vaginal Cream,Estraderm, Vivelle);
    estradiol cypionate (depGynogen,Depo-Estradiol, Dura-Estrin, etc.) estradiol valerate.–
    Esterified estrogens:
  158. Premarin, Premarin Intravenous, Premphase, Prempro)
    Conjugated estrogens:
  159. Progestins Often used with estrogen to:
    – stimulate endogenous hormones– Restore hormonal balance– Treat hormone-sensitive tumors (suppress tumor growth)– Contraception
  160. Types of Anti-hypertensives
    • Calcium Channel Blockers
    • • Angiotensin II Receptor Blockers (ARBs)
    • • losartan (Cozaar)
    • • Beta Blockers• propranolol (Inderal), atenolol (Tenormin)
    • • Angiotensin – Converting Enzyme (ACE) inhibitors• captropril (Capoten)
    • • Alpha – Beta Blockers• labetalol (Normodyne, Trandate)
  161. Angiotensin II Receptor Blockers (ARBs)• Prototype:
    Losartan (Cozaar)
  162. Losartan (Cozaar) Mechanism of action
    Blocks binding of Angiotensin II at receptors, so blocks the actions of Angiotensin II (vasoconstriction & aldosterone secreting effects)
  163. Losartan (Cozaar) Adverse effects•
    *Most common - Hypotension, diarrhea,*dizziness, Most serious (but rare) *Angioedema
  164. ARB’s: Nursing Interventions•
    • Do not use for pregnant/Breast feeding patients, (risk of birthdefects and fetal injury)
    • those with severe CHF•
    • Frequently used for DM patients with kidney damage•
    • Assist patients when getting OOB or with position changes, teachabout orthostatic hypotension•
    • Assess/Avoid use of prescription potassium/OTC potassiumsupplements, like salt substitutes•
    • Lifestyle changes along with pharmacotherapy•
    • Avoid giving with grapefruit juice•
    • Monitor BUN, Creatnine, BP level* may need combo therapy
  165. Angiotensin – Converting Enzyme (ACE)inhibitors• Prototype:
    captopril (Capoten) oral
  166. Angiotensin – Converting Enzyme (ACE)inhibitors
    • HTN,
    • *CHF,
    • diabetic Nephropathy,
    • LV dysfuncion post MI, & off label uses *( in combination with others)
  167. Angiotensin – Converting Enzyme (ACE) inhibitors Preg.
    • Class C (1st Tri)
    • Class D (2nd & 3rd) *Black box warning forfetal injury and birth defects
  168. Angiotensin – Converting Enzyme (ACE)inhibitors Contra:
    Hx Angioedema or Hypersensitivity
  169. Angiotensin – Converting Enzyme (ACE)inhibitors PD:
    prevents conversion of angiotensin I to angiotensin II,decreasing secretion of aldosterone which prevents Na &H2O retention, decreases PVR & BP
  170. Adverse effects of captopril (Capoten)
    • Persistent nonproductive *cough,
    • (*inhibits degradation of Bradykinin) rash
    • *first dose hypotension/& hypotension, HyperKALEMIA,
    • angioedema,
    • neutropenia,
    • & dyspnea,
    • dysgeusia, others less common
  171. captopril (Capoten) Drug/agent Interactions:
    • Drugs that raise K level,
    • other BP lowering agents such as diuretics & other BP lowerin =increased risk of hypotension,
    • lithium,
    • NSAIDS
  172. captopril (Capoten) Nursing Considerations•
    • Administer captopril 1 hour before meals, other ACE inhib’s can be given with food•
    • Monitor the patient for at *least 2-3 hours after the initial dose and until blood pressure stabilizes, and intermittently during use•
    • Assess blood reports for WBC,
    • *Hyperkalemia, Hyponatremia,neutropenia, & assess urine for proteinuria, UOP, BUN & Creatnine(renal insuffic./DM)•
    • Body Position changes/safety, *watch closely when used in combo with diuretics, (also watch BP, electrolyte levels, s/s hypovolemia)
  173. Other ACE Inhibitors:•
    • Lisinipril (Prinivil, Zestril),
    • Benazepril (Lotensin),
    • *enalapril (Vasotec)
    • *asIV form,
    • ramipril (Altace),
    • quinapril (Accupril),
    • moexipril (Univasc),
    • moexipril (Monopril),
    • perindopril (Aceon).
  174. Alpha – Beta Blockers Adverse effects•
    Diarrhea, N/V IV dosing, dizziness, weakness, orthostatic hypotension,elevations in BUN and serum creatinine levels, tingling of scalp, andfatigue
  175. Alpha-beta blockers• Contras:
    • • Patients with bradycardia, 2 or 3rd degree heart block, bronchial asthma, uncompensated CHF, cardiogenic shock (can exacerbate disease)
    • • Cautions: preg. Class C no studies, other: (see table 47-8 p 545) CHF,emphysema, bronchitus, DM
  176. Alpha-beta blockers
  177. Alpha-beta blockers Drug interaction
    • : beta-adernergic agonists,
    • cimtieidine,
    • nitroglycerine,
    • halothane,
    • oral antidiabetic agents, others…
  178. Alpha-beta blockers Nursing Interventions•
    • Administer oral labetalol with food•
    • Do not stop drug abruptly•
    • Prepare IV infusions of labetalol carefully•
    • Patient safety, assist OOB/position changes•
    • Observe the patient closely for signs of heart failure.•
    • Monitor BP closely of patients receiving IV infusions of labetalol, particularlypost CVA (titrate carefully)
  179. Centrally acting Alpha-2 Agonists• Prototype:
    Clonidine (Catapress)
  180. Clonidine (Catapress) Approved for:
    HTN & Severe pain
  181. Centrally acting Alpha-2 Agonists PD:
    • Stimulates the alpha 2 receptors in the medulla oblongata,
    • Inhibits neuron firing,
    • suppresses release of NE from sympathetic NS,(so decreased activation of alpha & Beta A. receptors in periphery)
    • inhibits sympathetic NS response•
    • Reduced sympathetic outflow of NE= decreased HR, BP, decreasedvasoconstriction, decreased renal vascular resistance, but renal blood flowand GFR remain the same•
    • Initial mild vasoconstriction when alpha receptors in periphery arestimulated, then sympathetic outflow is reduced (sympatholytic) and result isvasodilation•
    • Reduces Renin activity, excretion of aldosterone and catecholamines•
    • Little to no orthostatic hypotension, b/c equal positional BP lowering•
    • Stimulates growth hormone release
  182. Centrally acting Alpha-2 Agonists Transdermal drug: is released at a constant rate for 7 days, reapplyweekly to maintain therapeutic plasma levels (reach therapeutic at at2-3 days), lower level in plasma level from transdermal than oraldosing, half life 19 hours, if patch not replaced plasma level dropsafter 8 hours
    Transdermal drug: is released at a constant rate for 7 days, reapply weekly to maintain therapeutic plasma levels (reach therapeutic at at 2-3 days), lower level in plasma level from transdermal than oral dosing, half life 19 hours, if patch not replaced plasma level drops after 8 hours
  183. Centrally acting Alpha-2 Agonists PK:
    • Well absorbed GI & skin, 40-60%,
    • oral onset 30-60 min,
    • peak 3-5hours,
    • eliminated unchanged in urine,
    • metabolized in liver
  184. Centrally acting Alpha-2 Agonists PT:
    • often a secondary or supplemental medication to lower BP(usually not a monotherapy)•
    • Oral, parenteral, transdermal patch•
    • Varied off label usage: sympathetic inhibition, *prevention of s/s of alcohol, methadone, or opiate withdraw during detox, constitutional growth delay in children, diabetic diarrhea, menopausal flushing, dxpheochromocytoma, allergen induced extrinsic asthma, others…
  185. Centrally acting Alpha-2 Agonists: Clonidine Contras:
    • Preg. Class C,
    • caution with severe CAD,
    • recent MI,
    • CVA,
    • chronic renal failure,
    • very careful dilution of parenteral form (500mcg/ml),
    • not recommendedfor epidural/obstetrical use
  186. Centrally acting Alpha-2 Agonists: Clonidine Adverse Effects:
    *dry mouth, *drowsiness, dizziness, sedation, constipation,*erythema. *Rebound HTN if withdrawn abruptly. (*transdermal) Many othersthat are less common, see textOver dosage: bradycardia, hypotension, CNS & Resp. depression, apnea,seizures, hypothermia, aggitaion, irritability, N/V/D, hypo-ventilationarrythmia….
  187. Clonidine Nursing Interventions:
    • Nursing Interventions:•
    • Assess for cardiac or vascular disease•
    • Teach how to monitor BP & pulse rate•
    • Apply patch over a hairless area on upper torso/arm, rotate applicationsites when time to change (7 day), if loosens apply adhesive tape/dsg•
    • Instruct dosage reduced gradually to prevent rebound hypertension•
    • Discard patches safely•
    • Ice chips/hard candy for dry mouth•
    • Fluids/exercise to avoid constipation•
    • Caution with work that requires alertness until effect of drug on person is known (drowsiness)
  188. Peripheral Alphas Major differences from central alphas (clonidine)
    • is unique therapeutic use:
    • terazosin & doxazosin are used to treat benign prosthetic hyperplasia (BPH, relax smooth muscle in bladder neck and prostate gland due to alpha blockade, which increases urine flow)
  189. Antihypertensives: General Nursing Care
    • Monitor blood pressure and pulse during therapy•
    • Some require BP and P before administering and at sometime interval after•
    • Observe for orthostatic hypotension (take precautions)•
    • Most require periodic monitoring of lab (very with drug)•
    • If IV most have additional special precautions•
    • Food decreases absorption to some extent
  190. Specific Nursing Care• Angiotensin II Receptor Blockers (ARBs)
    • • Avoid giving losartan with grapefruit juice, ok with food.
    • • Monitor creatinine, BUN, hemoglobin, and hematocrit levels.
    • • If taking a potassium supplement, contact prescribingprovider.
  191. Specific Nursing Care Beta Blockers
    • • Take pulse before each dose•
    • Do not stop abruptly•
    • Orthostatic hypotension precautions•
    • Monitor I & O and daily weight
  192. Vasodilator: Nitroprusside(Nitropress)• Mechanism of action
    Directly & Rapidly relaxes vascular smooth muscle, allowing dilation of peripheral arteries and veins.
  193. Vasodilator: Nitroprusside(Nitropress) Adverse reactions
    • Severe hypotension•
    • Cyanide toxicity; Particularly if infused too rapidly,•
    • Not for patients with liver disease, or low thiosulfate stores in body (thecofactor needed to detoxify cyanide)•
    • Can cause sodium retention, may need to administer a loop diuretic suchas Furosemide (Lasix) to excrete sodium
  194. Vasodilator: Nitroprusside(Nitropress) Nursing Interventions•
    • Must use infusion pump•
    • Infusion must be titrated to reduce blood pressure withoutcompromising organ perfusion
    • Start nitroprusside at a low infusion rate (0.3 mcg/kg per minute)and increase gradually until the desired effect has been achieved orthe maximum infusion rate (8-10 mcg/kg per minute) is attained.
    • *Maximum infusion time 10 minutes
    • Monitor BP continuously during therapy
    •  Monitor for cyanide toxicity and excessive hypotension
    • IV solutions have a *faint brown color if brightly colored (blue,green, dark red, DISCARD)

    *SOLUTION is degrade by light, opaqueIV bag needed, never mix with other drugs
  195. Nitrates•
    • Nitrates improve the circulation to the heart itself by redistributing bloodflow to the collateral vessels
    • Nitrates dilate vascular smooth muscle and both venous and arterial vessels (although more relaxation occurs on the venous side).•
    • Venous dilation decreases the returning flow of blood to the heart (preload).•
    • Arterial dilation reduces systemic vascular resistance and arterial pressure (afterload).•
    • These effects decrease the workload on the heart andits oxygen needs.
  196. Nitrates Prototype drug:
    nitroglycerin (Nitrostat)
  197. nitroglycerin (Nitrostat) Admin.
    • Topical Linguial spray,
    • SL & IV,onset 1-3 min,
    • transdermal 30-60 min.
    • Duration IV 3-5 min,
    • SL: 30-60 min,
    • topical/transdermal: up to 24 hours.
    • nIV only if all other medications not effective, continuous drip, continuous heart & BP monitoring, glass bottle &special tubing only
  198. Treatment and prevention of anginapectoris, NOT used for HTN.
    Given SL, 2.5-5mg; oral tablets (chewable orswallow) or capsules, *immediate and *sustained release. Oral 5-40mg,onset 20-40 min, longer duration than nitroglycerin, SL 1-2 hers, Oral 4-6hours. Less rapid relief of chest pain, limited to use of acute angina inpatient’s that are intolerant of SL nitroglycerine
    Isosorbide dinitrate (Isordil)
  199. Amyl Nitrate:
    capsule that is crushed and vapors inhaled, onset 30-60seconds, duration 3-5 min, no effect on coronary arteries, highly flammable
  200. Nitrates PD:
    • Relaxes vascular smooth muscle and dilates both arterial and venousvessels.
  201. Nitrates Patient and family education•
    • Explain the purpose and adverse effects of nitroglycerin.•
    • Instruct patients to sit or lie down when experiencing angina.•
    • Explain that postural hypotension may occur, change positions slowly,sit for dose, refill and store appropriately: light sensitive•
    • Explain how to administer SL form for angina attack: Sit/lie down &rest, place one tab under tongue, no eat/drink till after fullydissolved and absorbed, if chest pain not relieved in 5 min call 911and take another SL tab per above, up to three SL tabs in 15 minutes
  202. Nitrates Nitrates Patient and family education• Explain how to administer SL form for angina attack
    • : Sit/lie down &rest,
    • place one tab under tongue,
    • no eat/drink till after fully dissolved and absorbed,
    • if chest pain not relieved in 5 min call 911 and take another SL tab per above,
    • up to three SL tabs in 15 minutes
  203. Amyl Nitrate: * Antidote for
    Cyanide poisoning.
  204. HDL Cholesterol LevelCategory
    High HDL cholesterol. An HDL of 60 mg/dL and above is considered protective against heart disease
  205. HDL Cholesterol
    Good Cholesterol
  206. IDLs become
    • low density lipoproteins
    • (“bad cholesterol”)
    • These can deliverfat to the liverand by other tissues
  207. LDL receptors:
    • are necessary for th eliver to take them up
    • Some LDLs are taken up by scavenger cells like macrophages
  208. High-density lipoproteins -HDL
    • (“good cholesterol”)
    • are made in the liver
    • They go out to the peripheral tissues and pickup lipid
    • Then they carry itback to the liver
  209. Statins Actions:
    •  Lower blood cholesterol levels and thus decrease the uptake of modified lipoproteins by vascular cells.
    •  Can lower LDL cholesterol by 20-60% when given at their maximum recommended dose.
    •  Raise HDL levels between 5 and 10% and lowertriglycerides between 10 and 33%.
    •  Evidence exists that statins work in other ways beside lowering cholesterol levels to decrease the occurrence of cardiovascular events
    •  Often first drug of choice b/c research backs decrease in cardiac related mortality
  210. Statins Prototype drug:
    lovastatin (Mevacor)
  211. Statins Pharmacokinetics (PK)
    •  High first-pass effect.
    • Highly protein bound.
    • Excreted primarily through the gastrointestinal tract.
  212. Statins Contraindications and precautions (Contras)
     Active liver disease and pregnancy
  213. Statins Pharmacodynamics (PD)
     Competitively inhibits HMG-CoA reductase, which is the enzyme that catalyzes the early rate-limiting step in cholesterol biosynthesis.
  214. Statins Pharmacotherapeutics (PT)
    Used for primary hypercholesterolemia and combined hyperlipidemia.
  215. Statins Adverse effects (AE)
     Muscle & joint aches, weakness, cramps, muscle damage, liver damage, and rhabdomyolysis
  216. Statins Drug interactions (DI)
    •  Itraconazole,
    • erythromycin, and
    • grapefruit juice
  217. statins Health status
     Assess cholesterol levels & past medical history
  218. Statins Life span and gender
     Pregnancy category X; assess age of patient.
  219. Statins Lifestyle, diet, and habits
     Treat elevated
  220. Statins Minimizing adverse effects
    • Liver function test (AST and ALT) results should be monitored before starting therapy 
    • Evaluate the patient carefully for muscle soreness,tenderness, or pain and CK levels
  221. Statins Maximizing therapeutic effects
    • **Most effective when administered in the evening
    • *Immediate-release administered after evening meal
    • *Extended-release administered at bedtime
  222. Statins Ongoing assessment and evaluation
     The patient should have liver function tests and CK measurement performed periodically throughout drug therapy.
  223. Statins Patient and family education
    • Stress the importance of following a lowc holesterol and low-saturated-fat diet.
    • **Instruct patients to report any unexplained muscle pain, tenderness, or weakness.
    • Photosensitivity may occur.
  224. Closely Related to Lovastatin
    • Atorvastatin (Lipitor), f
    • luvastatin (Lescol),
    • pravastatin (Pravachol),
    • rosuvastatin
    • (Crestor),
    • and simvastatin (Zocor).
    • All work similarly to lower LDL cholesterol andhave similar adverse effects.
  225. Fibric Acid Derivatives: Two frequently used:
    • Fenofibrate (Tricor, Lipofen),
    • Gemfibrizol (Lopid, Gemcor)
  226. Fenofibrate (Tricor, Lipofen),Gemfibrizol (Lopid, Gemcor)
    Similar drugs, pharmacodynamics not clearly understood, Fenofibrate: believed to lower plasma triglycerides by inhibiting the synthesis of triglycerides & amount of VLDL released in blood,and helps catabolize VLDL. Gemfibrozilmay inhibitperipheral lipolysis & reduce hepatic triglycerideproduction.
  227. Cholesterol Absorption Inhibitors
    • Ezetimibe (Zetia) – anti-lipid drug used for hypercholesterolemia
    • Pediatric use - restricted to children older than 10years of age with familial homozygous hypercholesterolemia
    • Given orally once daily either as mono-therapy or in combination therapy with a statin
    • It localizes and appears to act at the brush border of the small intestine, where it inhibits the absorption of cholesterol.
    • Decreases LDL about 17% but has no effect on HDL or triglyceride
  228. Nicotinic Acid
    • Nicotinic acid (niacin or vitamin B3) is used to treathyperlipidemia.
    • Reduces levels of triglycerides and LDL cholesterol levelsand raises levels of HDL cholesterol.
    • Triglycerides and VLDL levels are reduced by 25% to 30% in1 to 4 days. LDL level reductions may be seen in 5 to 7 days,with the maximal effect seen in 3 to 5 weeks
  229. Nicotinic Acid Adverse effects
    • The newer sustained-release forms of nicotinic acid have fewer adverse effects
    • Larger doses produce peripheral vasodilation, mostly in the cutaneous vessels of the face, neck, and chest(*Teach to take Ibuprofen or an NSAID 30-60 min prior to said prevent this adverse effect*)
  230. Nicotinic Acid Contraindications:
    • hepatic dysfunction,
    • active peptic ulcer,
    • severe hypotension,
    • and hemorrhaging.
  231. Bile Acid Sequestrants
    • cholestyramine(LoCholest, Questran, Prevalite) and colestipol (Colestid)
    • are used to reduce elevated serum cholesterol levels in patients with primary hypercholesterolemia who have not responded to other drug therapy
    • Not absorbed orally but work in the lower GI tract.
    • Reduction in LDLs is apparent in 4 to 7 days andranges between 15% and 30%
    • promote the oxidation of cholesterol to bile acids
    • Constipation is a side effect
  232. Unfractionated Heparin•
    • Rapid-acting anticoagulant:
    • only parenteral
  233. Unfractionated Heparin PD:
    • suppresses coagulation by helping anti-thrombin inactivate clotting factors, primarily thrombin &factor Xa; which ultimately suppresses formation of fibrin•
    • fibrin forms clots in veins, so heparin is useful in preventing & treating venous thrombi
  234. Unfractionated Heparin PK:
    • • Absorption and Distribution- Unable to cross membranes, (i.e. placental or breastmilk)
    • cannot be absorbed orally•
    • Protein/Tissue Binding- Binds
    • nonspecifically to many cells, to free heparin it highly variable•
    • Metab./Excretion- Half-life is short(about 1 ½ hrs) in normal liver/renalfunction; Longer in liver/renal impairment•
    • Time Course- IV bolus is given followedby infusion, or given via Subcutaneous
    • Adjunct to other thrombolytic therapy in acut emyocardial infarction (MI)
  235. Unfractionated Heparin Therapeutic Uses:
    • Preferred anticoag. in pregnancy, & in situations requiring rapid onset of anticoagulant effects
    • :pulmonary embolism (PE), evolving stroke,and massive deep vein thrombosis (DVT).•
    • Used in open heart surgery and renal dialysis to prevent coagulation in heart-lung & dialysis machines•
    • Low-dose therapy to prevent post operative venous thrombosis (often SC injection).•
    • Can be used to treat disseminated intravascular coagulation (DIC)
  236. Unfractionated Heparin Adverse Effects:
    •  Hemorrhage- bleeding develops in 10% of pt’s, main complication, can occur anywhwere in body, can be fatal.
    • If bleeding develops, stop heparin!
    • Spinal/Epidural Hematoma-pressure on the spinal cord caused by bleeding, results in paralysis (can be permanent)•
    • Risk is increased by: use of indwelling epidural catheter, use of other anticoagulants, use of antiplatelet drugs,Hx of traumatic or repeated epidural or spinal puncture, spinal deformity orinjury/surgery
    • Heparin-Induced Thrombocytopenia(HIT)- potentially fatal immune-mediated disorder characterized by reduced platelet count & paradoxal increase in thrombotic events. Thrombus formation=risk of DVT, PE, CVA, & MI.
    • STOP heparin & give non-heparinanticoagulant, Watch platelet counts,<100,000 should stop heparin.
  237. Unfractionated Heparin Precautions/Contras:
    • • Use with extreme caution in pts with high likelihood of bleeding(hemophilia, increased capillary permeability, dissecting aneurysm, peptic ulcer disease, severe hypertension or threatened abortion)
    • *Caution in severe liver/renal disease•
    • Contraindications- NOT for use in pts with thrombocytopenia & uncontrolled bleeding. Avoid during & immediately after eye, brain, or spinal cord surgery,also lumbar puncture & use of regional anesthetics
  238. Unfractionated Heparin Drug Interactions
    • Caution with in antiplatelet medications
  239. Unfractionated Heparin Laboratory Monitoring:
    • Activated Partial Thromboplastin time (aPTT,also abbreviated PTT
    • normal range 24- 40seconds)
    • Therapeutic usually 1.5- 2.5 X the control (normal)
    • Heparin increases aPTT to 60-80 seconds
    • MUST MONITOR aPTT contant, daily ormore
  240. Low-Molecular Weight Heparin(LMW)
    • LMWH preparations composed of molecules that are shorter than in unfractionated heparin•
    • As effective as unfractionated heparin & easier to use•
    • Now considered first-line therapy for prevention and treatment of DVT•
  241. Low-Molecular Weight Heparin(LMW)Four products available
    • : *enoxaparin(Lovenox),
    • *fondaparinux, (Arixtra),
    • dalteparin (Fragmin),
    • and tinzaparin(Innohep)
  242. Low-Molecular Weight Heparin(LMWH)• Therapeutic Use- (Approved)
    • • Prevention of DVT following surgery(abdominal, hip & knee replacement)•
    • Treatment of established DVT, with or without PE•
    • Prevention of ischemic complication inpts with unstable angina, non Q-wave MI and ST-elevation MI.
  243. Low-Molecular Weight Heparin admin.
    • All LMW heparins are administered subcutaneously
    • Dosage is weight-based & adjusted according to aPTT measurements (but doNOT need to follow aPTT daily)
    • Typically given once or twice a day
  244. Low-Molecular Weight Heparin• Adverse Effects and Interactions:
    • *Bleeding (less than unfractionated heparin)• Thrombocytopenia•
    • Severe neurologic injury- including permanent paralysis when given to pts undergoing spinal puncture or spinal or epidural anesthesia.
    • –Risk is higher in pts with concurrent use of antiplatelet drugs
  245. Warfarin (Coumadin, Jantoven)
    • Vitamin K antagonist,
    • oldest oral anticoagulant
    • Used to prevent thrombosis,
    • but has delayed onset (about 2-3 days for peak effects)
    • Often used for long-term prophylaxis
  246. Warfarin (Coumadin, Jantoven) PD:
    • Suppresses coagulation by decreasing production of four clotting factors VII, IX,X & prothrombin
    • (Vitamin K dependent clotting factors)
  247. Warfarin (Coumadin, Jantoven)• Time Course:•
    • Half-life 6 hrs-2.5 days,
    • initial response may not be evident until 8-12 hrs after first dose•
    • Peak effect takes several days•
    • When stopped it takes 2-5 days for new clotting factors to develop adequately.
  248. Warfarin (Coumadin, Jantoven) Therapeutic Uses:
    • Prevention of venous thrombosis &associated PE
    • Prevention of thrombo-embolism in pts with prosthetic heart valves
    • Prevent of thrombosis in pts with atrialfibrillation
    • Reduce the risk of recurrent transientischemic attacks (TIA) & recurrent MI
    • Atrial Fibrillation-high risk of CVA 2nd to clot formation in atrium.
    • Warfarin is still widely used, two new drugs: dabigatran (Pradaxa)and rivaroxaban (Xarelto) are easier to use,
  249. Warfarin (Coumadin, Jantoven) Monitoring Treatment:
    • • Prothrombin Time (PT) the coagulation test sensitive to alterations in vitamin K-dependent clotting factors
    • –Average pretreatment clotting time: 12 seconds(average range 10-15 seconds)
    • – PT control 12 – 15 sec; Therapeutic 1.5 -2.5 Xcontrol• International normalized ratio (INR) is now the test of choice, but monitor BOTH
    • Normal INR – 0.75-1.25; Therapeutic is 2-4.
    • Goal of INR 2-3 sec for most pts.
    • – Goal of INR 3-4 is sometimes recommended forprosthetic heart valves and a few other conditions•
    • INR daily first 5 days of treatment, adjust dose accordingly, then twice a week for the next 1-2 weeks,then once a week for 1-2 months, finally once every
  250. Warfarin (Coumadin, Jantoven) Adverse Effects:
    •  Hemorrhage-Bleeding is the major complication, can occur at any site
    • Monitor closely for signs of bleeding(reduced BP, increased heart rate,bruises, petechiae, hematomas, red or black stools, cloudy or discolored urine,pelvic pain, headache, and lumbar pain).
    •  Fetal Hemorrhage and Teratogen; Do NOT use in pregnancy, Category X
    •  Breast-Feeding- Warfarin enters breastmilk, should NOT breast feed
  251. Warfarin (Coumadin, Jantoven) Drug Interactions:
    • Drugs that increase the effects of warfarin:– ex: Aspirin
    • Drugs that promote bleeding:
    • Drugs that decrease the effects of warfarin:– Carbamazepine, phenobarbital, phenytoin, rifampin, oral contraceptives, vitamin K, cholestyramine, colestipol.
  252. Warfarin (Coumadin, Jantoven) Nursing Interventions:
    • o Educate well
    • o Take coumadin same time every day (5-6pm)
    • o Can be crushed if needed & can take with food
  253. Direct Thrombin Inhibitors• Dabigatran Etexilate (Pradaxa) Therapeutic Uses:
    • Atrial Fibrillation- Prevention of stroke or systemic embolism in pts with nonvalvular vatrial fibrillation.(Dose 150 mg BID)
    • Knee or Hip Replacement- Prevention of venous thrombo embolism (220 mg Daily)
  254. Aspirin  PD:
    Suppresses platelet aggregation by causing irreversible inhibition of cyclooxygenase (an enzyme needed by platelets to synthesize thromboxane A2)
  255. Aspirin Indications for antiplatelet therapy:
    • Ischemic stroke (reduce risk of death & nonfatalCVA)
    • Transient ischemic stroke (TIA, to reduce the riskof nonfatal/fatal CVA)
    • Chronic stable angina(reduce risk MI & suddendeath)
    • Unstable angina (reduce combined risk of death/MI)
    • Coronary stenting (to prevent re-occlusion)
    • Acute MI (reduce the risk of vascular mortality)
    • Previous MI(to reduce the combined risk ofMI/death)
  256. Aspirin is used for primary prevention, is typically dosed at
    81 mg/day
  257. Aspirin Adverse Effects:
    • Risk of GI bleed◦
    • Proton pump inhibitors reduce the risk of GI bleeds, & Peptic ulcer disease
    • Risk of hemorrhagic stroke
  258. P2Y12 Adenosine Diphosphate Receptor Antagonists
     Block the P2Y 12 ADP receptor on platelets and reduce ADP stimulate daggregation
  259. P2Y12 Adenosine Diphosphate Receptor Antagonists Four are available:
    • Clopidogrel (Plavix),
    • prasugrel (Effient),
    • ticlopidine (Ticlid),
    • and ticagrelor (Brilinta)
    • The first three cause IRREVERSIBLE receptor blockage. The last has reversible receptor blockade.
  260. P2Y12 Adenosine DiphosphateReceptor Antagonists Clopidogrel (Plavix) Adverse Effects:
    • mild GI: dyspepsia (can take with food), abd. pain, diarrhea, rash
    • Bleeding- Risk of serious bleeding, but causes less GI bleeding and less intracranial hemorrhage than aspirin.
  261. Teach s/s of bleeding Plavix
    and to call MD; Do NOT stopp lavix unless MD says to stop (often stopped 5 days before surgeries)
  262. Hemorheologic Drugs PD:
    • Act on the RBC to increase the flexibilityof RBC and reduce blood viscosity;
    • thereby prevent thrombus formation & increase oxygenation of cells through microvasculature
  263. Hemorheologic Drugs PT:
    PAD, to manage intermittent claudication(many off label uses)
  264. Hemorheologic Drugs Prototype:
    Pentoxifylline (Trental)
  265. Hemorheologic Drugs Metab:
    RBC & Liver, 4-8 weeks till full effect
  266. Hemorheologic Drugs Adverse:
    • CNS, CV &GI: HA, dizziness,tremor, dyspepsia, N/V, (Give with food) others less common; pg.614, No Alcohol(CNS),
    • No smoking, (causesvasoconstriction)
    • Baseline assessment of
  267. Thrombolytic (Fibrinolytic)Drugs
    Given to remove (dissolve) thrombi that have already formed. (Anticoagulants are for PREVENTION of thrombi)
  268. Thrombolytic (Fibrinolytic)Drugs Three drugs:
    alteplase (tPA), reteplase(Retavase), and tenecteplase (TNKase)
  269. Absolute Contraindications for Thrombolytics:◦
    • Any prior intracranial hemorrhage◦
    • Known structural cerebral vascular lesion◦
    • Ischemic stroke within last 3 months(except ischemic stroke within 4.5 hrs)◦
    • Known internal bleeding◦
    • Active internal bleeding (other than menses)◦ Suspected aortic dissection
  270. Kidney, 3 functions:
    • – Cleansing of extracellular fluid and maintenance of ECF volume and composition
    • – Maintenance of acid-base balance
    • – Excretion of metabolic wastes and foreign substances.
  271. PD:**Diuretics work
    by interfering with reabsorption
  272. Diuretics PD
    • Most diuretics share same mechanism of action: blockade of sodium and chloride reabsorption–
    • Creates osmotic pressure inside nephron that blocks passive reabsorption of water
    • – If water and solutes are not reabsorbed, they are excretedfrom the body•
    • The increase in urine flow is directly related to the amount of sodium & chloride reabsorption blocked•
    • Diuretics that act early in nephron block the greatest amount of solute reabsorption (greatest results)•
    • Diuretics increase urine output (UOP) by 1.8 L forevery 1% of solute reabsorption that is blocked; if give TOO much, = dehydration
  273. Adverse Effect: Impact on ECF• Diuretics can cause:
    • – Hypovolemia (from excessive fluid loss)
    • – Acid-base imbalance
    • – Altered electrolyte levels.
    • – Short-acting diuretics minimize these effects.
  274. Classification of Diuretics
    • High ceiling (Loop) diuretics- Furosemide (Lasix) 
    • Thiazide diuretics – hydroclorothiazide (HCTZ)
    • Osmotic diuretics – mannitol (Osmitrol)
    • Potassium-sparing diuretics:
    •       – Aldosterone antagonists – spironolactone (Aldactone)
    •       – Nonaldosterone antagonists- triamterene (Dyrenium)
  275. High-Ceiling (Loop) Diuretics
    • Most effective diuretics available
    • Produce more loss of fluid & electrolytes than any other diuretic
    •  Furosemide (Lasix) is most frequently prescribed loop diuretic
  276. Loop Diuretics: Furosemide
    • Sulfa based drug* assess hypersensitivity
    • Acts in ascending limb, Loop of Henle; blocks reabsorption of sodium & chloride
    • Can produce profound diuresis
    • Can be given orally (diuresis starts within 60 minutes, lasts 8 hrs), IV (diuresis in 5 minutes,lasts 2 hrs) and IM.
    • • *IV therapy is used in critical situations (pulmonary edema)•
    • *Typically used when less powerful diuretics no longer (*but not always)
  277. Loop Diuretics: Furosemide• Therapeutic Uses:•
    • Pulmonary edema associated with congestive heart failure•
    • Edema of hepatic, cardiac or renal origin that is unresponsive to less efficacious diuretics•
    • Hypertension that cannot be controlled with other diuretics
    • Especially useful in pts with severe renal impairment, can promote diuresis even when renal blood flow and glomerular filtration rate are low
  278. Loop Diuretics: Furosemide• Adverse Effects:
    • Hyponatremia, Hypochloremia & Dehydration b/c can produce excessive loss of sodium, chloride, & water
    • Orthostatic Hypotension – Due to loss of volume and relaxation of venous smooth muscle (reduces venous return to the heart).
    • Hypokalemia- Potassium loss due to increased secretion in distal nephron
    • Ototoxicity- Rarely causes permanent deafness/hearing impairment, most hearing impairment is transient, (Usually in high dose, IV,renal impaired)
    • Hyperglycemia- Can result from inhibition of insulinrelease. Watch closely in diabetic pts. (uncommon)•
    • Hyperuricemia- Frequent, most pts area symptomatic, but for pts predisposed to gout can cause a gout attack
    • Pregnancy- Class C,
    • Lipids, Calcium & Magnesium- Furosemidedecreases HDL, raises LDL cholesterol &triglycerides. Increases risk of magnesium deficiency, increased excretion of calcium (*elders with Osteoporosis are at risk for fractures)
  279. Loop Diuretics: Furosemide• Drug Interactions:
    • Digoxin- If potassium is low, serious risk of druginduced toxicity (ventricular dysrhythmias)
    • Ototoxic drugs- (Especially gentamycin) can causepermanent hearing loss. Avoid combined use ofthese drugs.
    • Potassium-Sparing Diuretics- Can reduce the riskof hypokalemia
    • Lithium- Can allow lithium levels to accumulate totoxic levels
  280. Other Loop Diuretics:
    • • Ethacrynic acid (Edecrin) Not sulfa based, safe foruse in sulfa allergy, not for use in children, for edema only, not HTN
    • Torsemide (Demadex) metab. to active & inactive metabolites
    • Bumetanide (Bumex) for edema only, more potent,*black box warning: More profound diuresis (H2O &electrolytes), not for children, *careful dosing
  281. Loop Diuretics: Furosemide• Drug Interactions:•
    • Anithypertensive Agents- Furosemide can cause hypotension, potentiated by antihypertensive drugs•
    • Nonsteroidal Aspirin, Anti-inflammatory Drugs(NSAIDS)-
    • Decrease the effects of diuretics, ACEinhibitors (1st dose hypotension) others… see table
  282. Loop Diuretics: Furosemide Contra’s:
    Sulfa allergy/hypersensitivity, Precautions:*poor renal function, SLE (lupus) Assess
  283. Thiazide Diuretics• PD:
    • Increase renal excretion of sodium, chloride,potassium, & water•
    • Elevates plasma levels of uric acid & glucose•
    • Greatest difference between thiazides & loop diuretics: maximum diuresis of thiazides is considerably lower than in loop diuretics
    • Thiazides are not effective when urine flow isscant (anuria, severe renal failure)•
    • Sulfa based drug
  284. Thiazide Diuretics drug
    Hydrochlorothiazide (HydroDIURIL, HCTZ) most widely used thiazide diuretic
  285. Thiazides: Hydrochlorothiazide• Therapeutic Uses:•
    • Essential Hypertension- Primary use is for HTN, and is often FIRST DRUG OF CHOICE.•
    • Edema- Mild to moderate, heart failure•
    • Diabetes Insipidus- Causes fluid retention instead(unsure why)•
    • Postmenopausal Osteoporosis Protection, Promotestubular reabsorption of calcium
  286. Thiazides: Hydrochlorothiazide• Adverse Effects:
    • • Hyponatremia, Hypochloremia & Dehydration-Milder than loop diuretics•
    • Hypokalemia- Eat potassium rich foods,
    • *careful if taking digoxin.•
    • Pregnancy and Lactation: Direct and Indirect effects on developing fetus, and impair fetal blood flow– Should not be used routinely during pregnancy,caution
  287. Thiazides: Hydrochlorothiazide• Adverse Reaction:
    • Hyperglycemia- Can elevate glucose in diabetic pts•
    • Hyperuricemia- Retention of uric acid, can causegout.•
    • Lipid and Magnesium- Increase LDL, total cholesterol and triglycerides. Can cause magnesium deficiency.
  288. Thiazides: Hydrochlorothiazide• Drug Interactions:
    Same as loop diuretics, Slightly different chemical structure, indications for use, PK’s
  289. Potassium-Sparing Diuretics
    • • Produce increased urine production, but limited,so not often used for diuresis•
    • Produce substantial decrease in potassium excretion, so these drugs are often used to counteract potassium loss caused by thiazide & loop diuretics.
  290. Potassium-Sparing Diuretics Two subcategories
    • :– Aldosterone Antagonists
    •        - spironolactone (Aldactone)
    • – Non-aldosterone antagonists
    •      - triamterene(Dyrenium) and amiloride (Midamor)
  291. Potassium-Sparing Diuretics:Spironolactone• PD:
    • Blocks the actions of aldosterone in distal tubule, (blocks all aldosterone receptors:glucocorticoid, mineral corticoid, androgen, &progesterone)•
    • Aldosterone promotes sodium uptake in exchange for potassium secretion
  292. Potassium-Sparing Diuretics:Spironolactone• PD:
    Spironolactone causes retention of potassiumand increased excretion of sodium
  293. Potassium-Sparing Diuretics:Spironolactone (Aldactone)• Therapeutic Uses:
    • HTN & Edema- Most commonly used in combination with a loop or thiazide diuretic to counteract the potassium-wasting effects of the more powerful diuretics•
    • Heart Failure (CHF) Proven to reduce mortality andhospital admissions•
    • Other Uses- Primary hyper-aldosteronism, Offlabel: premenstrual syndrome, polycystic ovarysyndrome, acne * assess what drug is used for
  294. Potassium-Sparing Diuretics:Spironolactone• Adverse Effects:•
    Hyperkalemia- Most likely when spironolactone isused alone, stop use if hyperkalemia develops
  295. Potassium-Sparing Diuretics:Spironolactone• Drug Interactions
    • Thiazide & Loop diuretics- given to counteract the potassium-wasting effects.•
    • Agents that raise potassium levels should never be given with potassium supplements, salt substitutes or another potassium-sparing diuretic
  296. Osmotic Diuretic: Mannitol•
    • Mannitol is the only osmotic diuretic on the market•
    • Simple, six-carbon sugar
  297. Osmotic Diuretic: Mannitol•PD:
    • Mechanism of Diuretic Action
    • :– Freely filtered at the glomerulus
    • – Undergoes minimal tubular reabsorption
    • – Undergoes minimal metabolism
    • – Is pharmacologically inert (no direct effects on biochemistry or physiology of cells)
    • – Pulls off fluid by increased osmotic force/pressure
  298. Osmotic Diuretic: Mannitol• Administered
    IV, most of the drug makes it past the glomerulus, creates increased osmotic force that inhibits passive reabsorption of water (Urine flow increases).
  299. Osmotic Diuretic: Mannitol• Therapeutic Uses:
    • Prophylaxis of Renal Failure- (dehydration,severe hypotension, hypovolemic shock) cause slow blood flow to the kidney, causing reduction in filtrate volume. Ceases urine production,=kidney failure•
    • Mannitol pulls water into the nephron (even when blood flow is low), preserves urine output & may prevent kidney failure
    • Reduction of Increased Intracranial Pressure
    • Reduction of Increased Intra-occular Pressure
  300. Osmotic Diuretic: Mannitol• Adverse Effects:
    Sudden increase of ECF / Edema- can leave the vascular space at all capillary beds except the brain. It will draw water with it which causesedema. Watch for *CHF & *pulmonary congestion (most succeptible: pt’s with history of these).
  301. Osmotic Diuretic: Mannitol• Nursing Interventions
    • Administer only on a pump, low test dose on all patients with renal impairment, patient on heart monitor, monitor ECG tracings•
    • Monitor UOP constantly & carefully•
    • Assess vitals,*BP, pulse•
    • Assess lung sounds•
    • High risk for major F/E changes, *safety, orthostatic hypotension
  302. Osmotic Diuretic: Mannitol Contra’s/Prec:
    children, CHF pts, Preg class C, elderly with caution, renal failure, electrolyte imbalance, others…
  303. hypoglycemia is and the CM *BS frequently
    • less than 70mg/dl,
    • 50-60 start feeling symptoms but varies in each person.
  304. Regular Insulin Pharmacotherapeutics
     All types of diabetes mellitus
  305. Regular Insulin:Pharmacokinetics
    • Administered: SC or IV.
    • *Only insulin that can be given IV
  306. Regular Insulin: Pharmacodynamics
    Injected insulin mimics the effect of endogenous insulin
  307. Regular Insulin: Contraindications and precautions
    Hypoglycemia (BG <50)
  308. Regular Insulin:Adverse effects
    Hypoglycemia and lipoatrophy
  309. Regular Insulin: Drug interactions
    •  *Alcohol,
    • *beta blockers: mask hypoglycemia, dobutamine,
    • niacin,
    • MAOIs,
    • thiazide diuretics, and
    • tetracycline,
    • *These and other hypoglycemic agents increase risk of hypoglycemia;Hyperglycemic agents (steroids) counteract effects of insulin
  310. Regular Insulin: Planning & Interventions Maximizing therapeutic effects
    •  Store opened vials of regular insulin at room temperature.
    • Administer regular insulin with an insulin syringe into an appropriate subcutaneous site.
  311. Regular Insulin: Planning & Interventions Minimizing adverse effects
    •  Injection-site rotation also helps prevent lipodystrophy.
    • Assess blood glucose level prior to administration.
  312. Three rapid-acting insulins;
    • aspart (NovoLog)
    • lispro (Humalog)
    • glulisine (Apidra).
    • Administer within 15 minutes of start of the meal.
  313. Intermediate Insulin: NPH
    • Onset: 1–2 hours.
    • Peak: 6–14 hours.
    • Duration: up to 24hours
  314. Glargine (Insulin) Duration:
    Onset: 1 hr , 24 hours. No peak.
  315. Two classes are Oral Antidiabetic agents:
    • 1. Sulfonaureas: Glyburide (Diabeta); Glipizide (Glucotrol)
    • 2. Meglitinides Repaglinide (Prandin) Nateglinie (Starlix)
  316. Four classes Antihyperglycemic agents or insulin sensitizers:
    • 1.*Biguanides, *Metformin, (Glucophage),
    • 2.Thiazolinediones, Rosiglitazone (Avandia) & Pioglitizone (Actos)
    • 3. Alpha-glucosidase inhibitors : Acrabose (Precose); Miglitol(Glyset)
    • 4. Gliptins: (DPP-4 inhibitors) Sitagliptin (Januvia), linagliptin,Saxagliptin
  317. Oral Antidiabetic Medications Prototype drug:
    Glyburide (DiaBeta), also Glipizide (Glucotrol)
  318. Glyburide: Core Drug Knowledge PT:
    Adjunct TX to lower blood glucose levels in DM type 2.
  319. Glyburide: Core Drug Knowledge PK: Administered:
  320. Glyburide: Core Drug Knowledge 
    Metabolism: liver.

    Excreted: urine and feces.
  321. Glyburide: Core Drug Knowledge Onset:
    2 hours. Protein bound.
  322. Glyburide: Core Drug Knowledge Onset:PD:
    • Hypoglycemic action of glyburide results from the stimulation of pancreatic beta cells.
    • * Not effective intype 1 DM,
  323. Glyburide: Core Drug Knowledge Contraindications and precautions◦
    • Hypersensitivity,
    • & Hypersensitivity to Sulfa drugs,
    • not foruse in pregnancy/lactation
  324. Glyburide: Core Drug Knowledge Adverse effects◦
    Hypoglycemia, anorexia, nausea, vomiting, heartburn, metallictaste/mouth, rare: research about possible CV toxicity
  325. Glyburide: Core Drug Knowledge Drug interactions◦
    • Drug interactions are possible because these drugs are metabolized by the CYP3A3/4 system, *Alcohol,
    • beta blockers
    • 9block insulin release, mask hypoglycemia), & drugs that can intensify Hypoglycemia:
    • *, sulfa antibiotics,
    • NSAIDS
  326. Glyburide: Planning & Interventions Maximizing therapeutic effects
    • Administer glyburide before breakfast or the first main meal of the day
    • A second dose may be given before dinner if needed
  327. Glyburide: Planning & Interventions Minimizing adverse effects
    • Monitor the patient’s blood glucose levelsvperiodically throughout therapy to detecthypoglycemia, why?
    • Monitor patients with renal and hepatic impairment for signs of adverse effects
  328. Glyburide: Teaching, Assessment &Evaluation Patient and family education
    • Teach about patient/family diabetes management
    • Teach the S/S of hypoglycemia
  329. Glyburide: Teaching, Assessment &Evaluation Ongoing assessment and evaluation
    Interview the patient and family and observe for therapeutic and adverse responses to glyburide and adherence to TX(s)
  330. Meglitinides Repaglinide (Prandin):PT:
     Adjunct TX to lower blood glucose levels in DM type 2.
  331. Meglitinides Repaglinide (Prandin): PK:
     Admin.: oral before each meal. Metab.: liver. Excreted:primarily in feces., therefore preferred in patients whoare elderly or w/decreased renal function. Onset: 30minutes. Protein bound.
  332. Meglitinides Repaglinide (Prandin): PD:
    (similar to sulfonylureas, differ chemically) Hypoglycemic action similar, stimulates beta cells, but more rapid absorption & shorter duration, than glyburide, advantage: rapid excretion prevents beta cells from being overly stimulated=Less like to cause hypoglycemia. Only taken if food is eaten
  333. Nonsulfonylureas/Antihyperglycemics Prototype drug,
    1. Biguanide: *Metformin:(Glucophage
  334. Metformin:PK:◦
    Administered: oral. Metabolism: liver. Excreted: kidneys.
  335. Metformin:Pharmacodynamics◦
    Decreases hepatic glucose production, decreases intestinal absorption of glucose, and improves insulin sensitivity by increasing peripheral glucose uptake in skeletal muscle and adipose tissue cells
  336. Metformin:Contraindications and precautions
    • Hepatic disease,
    • *Renal disease,
    • *Uncompensated Heartfailure,
    • *Lactic acidosis (most often in renal disease, CHF )
  337. Metformin: Adverse effects
    • Anorexia,
    • nausea and vomiting,
    • weight loss,
    • abdominal discomfort,
    • dyspepsia,
    • flatulence,
    • diarrhea,
    • and a metallic taste sensation
  338. Metformin:PT:
    • Adjunct to lower blood glucose in type 2 DM.
    • Also lowers Triglyceride and LDL Levels, promotes weight loss.◦
    • Other (off label)uses: trials promising for Gestational Diabetes,Polycystic ovarian disease, (lowers androgen levels) others…
  339. Metformin:Drug interactions
    • May react with contrast media used for radiographicprocedures
    • *held for at least 48 hours, Alcohol*
  340. Metformin: Core Patient Variables
    • Assess medical hx/current medical status,
    • Pregnancy category B.
    • Lifestyle, diet, and habits
    • Assess diet, exercise and alcohol intake
  341. Metformin: Planning & Interventions Minimizing adverse effects◦
    Taking the drug at mealtimes and using gradual dosage increments minimize these effects.
  342. Metformin: Planning & Interventions Maximizing therapeutic effects◦
    • Administer metformin twice a day with the morning and evening meal.◦
    • Adherence with the recommended diabetic diet and daily exercise help in the control of type 2 DM
  343. Metformin: Teaching, Assessment &Evaluation
    • Patient and family education
    •  Teach patients to take metformin with meals, morning and evening.
    • Emphasize that patients should not use alcohol while taking metformin.
    • Ongoing assessment and evaluation
    • Monitor blood glucose levels (fasting and hemoglobin A1C)throughout metformin therapy.
  344. Nonsulfonylurea # 2 ThiazolidinedionesPK /Mode of action:
    •  Improves insulin sensitivity in muscle & adipose
    • suppresses glucose production in liver
    • Decreases intestinal absorption of glucose
  345. Nonsulfonylurea # 2 Thiazolidinediones Prototype drug:
    Rosiglitazone (Avandia)& Pioglitazone (Actos)
  346. Rosiglitazone (Avandia):PT:
    • Adjunct TX to diet and exercise lower BG in type 2 DM.◦
    • Does not promote weight loss◦
    • Used alone, with sulfonylurea, metformin, or insulin
  347. Rosiglitazone (Avandia): PK:
    Adm oral. Metab.: liver through the P-450 system—2C8& 2C9 (not major pathways). Protein bound. Excreted:kidneys and GI tract
  348. Rosiglitazone (Avandia):PD:
    • ◦ Activates receptor PPAT gamma in nucleus which turnson insulin responsive genes to regulate carb & lipidmetabolism to:
    • Decrease hepatic glucose production,and improves insulin sensitivity by increasingperipheral glucose uptake in muscle & adipose tissues
  349. Rosiglitazone (Avandia):Contra’s
     Heart failure, Hepatic disease, may increase LDL,triglyceride levels and elevate HDL
  350. Rosiglitazone (Avandia):Adverse effects
    • URI, HA, Moderate weight gain, *edema/fluid retention (rare but can exacerbate Heart Failure) mild anemia, hepatic toxicity,women—increased risk of falls & fractures; lactic acidosis,
    • *Hypoglycemia,
    • *women may resume ovulation and will need alternate birth contro
  351. Rosiglitazone (Avandia):Drug interactions
    Rifampin & Cimetidine decrease blood level o frosiglitazone; Gemfibrizol, Atorvastatin & ketoconazoleincrease levels & risk of hypoglycemia, insulin alsopromotes fluid , caution when used together
  352. Alpha-glucosidase Inhibitors.
  353. Alpha-glucosidase Inhibitors.Prototype drug: Acarbose (Precose) also Miglitol (Glyset)
    Acarbose (Precose) also

    Miglitol (Glyset)
  354. Alpha-glucosidase Inhibitors.Mode of action:
    • Improves insulin action
    • Delays the digestion of carbohydrates
  355. Acarbose (Precose), & Miglitol (Glyset) PT
    : Adjunct to type 2 DM Tx, results in substantial reduction inpost prandial glucose levels, can be used alone incombination with sulfonylurea, metformin or insulin.
  356. Acarbose (Precose), & Miglitol (Glyset)PK:
    Administered: oral with first bite of food. Slows downenzymes that digest CHO in the small intestine, inhibitspancreatic alpha amylase—reducing rate of digestion ofcomplex CHO = less glucose absorption. Metabolism: GItract Excreted: kidneys and GI tract.
  357. Acarbose (Precose), & Miglitol (Glyset)PD:
    Inhibits alpha glucosidase, enzyme on the brush borderof small intestine needed to break down sugars andcomplex carbs into monosacharides that can beabsorbed, slows digestion of CHO=*Lowers postprandialserum glucose
  358. Acarbose (Precose), & Miglitol (Glyset) Contra’s:
     Diseases of the bowel, hiatal hernia or conditions exacerbated by increased formation of gas, chronic liver disease, renal impairment. Treat hypoglycemia with oral glucose tablets, not table sugar WHY?
  359. Acarbose (Precose), & Miglitol (Glyset) Adverse effects
    Flatulence, diarrhea, abdominal pain; does not causehypoglycemia, hyperinsulinemia or weight gain; lacticacidosis.
  360. Acarbose (Precose), & Miglitol (Glyset) Drug interactions
    Increase blood glucose levels with steroids; effects decreased with intestinal absorbents—activated charcoal, pancreatic enzymes.
  361. Glucose-Elevating Agents
    • Glucagon is a hyperglycemic polypeptide hormone produced by the alpha cells of the pancreatic islets of Langerhans.
    • Its physiologic effect is generally the opposite ofthat of insulin.
    • Glucagon is the body’s first line of defense against hypoglycemia.
    • Main stimulus to glucagon secretion: decrease inintracellular glucose concentrations when adrop in serum blood sugar.
  362. Glucagon: PT:
  363. Glucagon: PK:
    T½: 3 to 10 minutes.
  364. Glucagon:PD:
    Increases blood glucose levels by stimulating glycogenolysis in the peripheral tissues
  365. Glucagon:Adverse effects
    • Hypotension,
    • respiratory distress,
    • nausea and vomiting
  366. Glucagon:Drug interactions:
    Oral anticoagulants
  367. Glucagon:Nursing Diagnosis:
    • • Risk for Injury related to hypotension from the adverse effects of glucagon•
    • Desired outcome: substantial hypotension will not resultfrom glucagon treatment.
  368. Glucagon: Planning & InterventionsMaximizing therapeutic effects
    • Use reconstituted glucagon immediately
    • A dose of 0.5 to 1 mg is usually effective
  369. Glucagon: Minimizing adverse effects
    Administer supplemental carbohydrates as soon as possible once consciousness has been achieved,followed by protein, Why?
  370. Glucagon: Teaching, Assessment &Evaluation
    • Education (Pt. & Family)
    • Emphasize measures to prevent hypoglycemicreactions from insulin
    • Instruct on proper technique for emergency administration of glucagon
    • Ongoing assessment and evaluation
    • Monitor blood glucose levels before, during, & after glucagon administration
Card Set
Pharm Exam II