Exam Two.txt

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Exam Two.txt
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Lecture One
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Exam Two - Lecture One
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  1. A SBP <120 and a DBP <80 is considered what BP Classification?
    1. Normal
  2. A SBP 120-135 and a DBP 80-89 is considered what BP Classification?
    1. Prehypertension
  3. A SBP 140-159 and a DBP 90-99 is considered what BP Classification?
    1. Stage I Hypertension
  4. A SBP >160 and a DBP >100 is considered what BP Classification?
    1. Stage II Hypertension
  5. A SBP greater than or equal to 140 and a DBP greater than or equal to 90 is classified as what?
    1. Hypertension
  6. Normal BP is what?
    1. A SBP <120 and a DBP <80
  7. Prehypertension is what?
    1. A SBP 120-135 and a DBP 80-89
  8. Stage I Hypertension is what?
    1. A SBP 140-159 and a DBP 90-99
  9. Hypertension is what?
  10. 1. A SBP greater than or equal to 140 and a DBP greater than or equal to 90
  11. Heart Rate x Stroke Volume equals what?
    1. Cardiac Output
  12. Cardiac Output is equal to what?
    1. Heart Rate x Stroke Volume
  13. End Diastolic Volume - End Systolic Volume equals what?
    1. Stroke Volume
  14. What is stroke volume influenced by?
    • 1. Preload
    • 2. Contractility
    • 3. Afterload
  15. Cardiac Output x Stroke Volume is equal to what?
    1. Blood Pressure
  16. What is determined by viscosity and vessel length an diameter?
    1. Resistance
  17. BP is maintained in a moment-to-moment fashion. As these moments add up, the risk of what can occur?
    1. End organ damage increases exponentially
  18. What percentage of patients can a specific cause of hypertension be established in?
    1. 10-15 %
  19. Patients in whom no specific cause of hypertension can be found are said to have what?
    1. Essential or primary hypertension (The majority of patients are this)
  20. Patients with a specific etiology are said to have what?
    1. Primary Hypertension
  21. Carbonic Anhydrase Inhibitors, Loop, Thiazide, K+ Sparing are all considered what?
    1. Diuretics
  22. Examples of Diuretics are (list them)?
    • 1. Carbonic Anhydrase Inhibitors
    • 2 Loop
    • 3. Thiazide
    • 4. K+ Sparing
  23. Examples of Sympathoplegics are what (list them)?
    • 1. Centrally Acting
    • 2. Ganglion-blocking,
    • 3. Alpha and Beta Adrenoreceptor Antagonists
  24. Centrally Acting, Ganglion-Blocking, α and β Adrenoreceptor Antagonists are considered what?
    1. Sympathoplegics
  25. Examples of Vasodilators are what (list them)?
    1. Direct and Ca++ Channel Blockers
  26. Direct and Ca++ Channel Blockers are considered what?
    1. Vasodiators
  27. Angiotensin Production / Action Blocking Agents
    • 1. ACE
    • 2. ARBs
  28. What will lower blood pressure by depleting the body of sodium and reducing blood volume and perhaps by other mechanisms.
    1. Diuretics
  29. Diuretics will do what?
    1. Lower blood pressure by depleting the body of sodium and reducing blood volume and perhaps by other mechanisms.
  30. What will lower blood pressure by reducing peripheral vascular resistance, inhibiting cardiac function, and increasing venous pooling in capacitance vessels. These agents are further subdivided according to their putative sites of action in the sympathetic reflex arc.
    1. Sympathoplegic Agents.
  31. Sympathoplegic Agents will do what?
    • 1. lower blood pressure by reducing peripheral vascular resistance,
    • 2. which will nhibiting cardiac function, (This effect may reduce cardiac output)
    • 3. and increasing venous pooling in capacitance vessel (This effect may reduce cardiac output)
  32. Direct Vasodilators will do what?
    1. reduce pressure by relaxing vascular smooth muscle, thus dilating resistance and-to varying degrees - increasing capacitance as well
  33. What will reduce pressure by relaxing vascular smooth muscle, thus dilating resistance and-to varying degrees - increasing capacitance as well?
    1. Direct Vasodilators
  34. Agents that block production of action of angiotensin will do what?
    1. Reduce peripheral vascular resistance and (potentially) blood volume
  35. Sites of Action of the major classes of Anti-Hypertensive Drugs; What acts on the Sympathetic nerve terminals?
    • 1. Guanethidine
    • 2. Guanadrel
    • 3. Reserpine
  36. Sites of Action of the major classes of Anti-Hypertensive Drugs; What acts on the Beta Receptors of the Heart?
    • 1. Propranolol and other
    • 2. Beta Blockers
  37. Sites of Action of the major classes of Anti-Hypertensive Drugs; What acts on the Angiotensin receptors of vessels?
    • 1. Losartan and other
    • 2. Angiotensin Receptor Blockers
  38. Sites of Action of the major classes of Anti-Hypertensive Drugs; What acts on the Alpha Receptor of Vessels?
    • 1. Praxosin and other
    • 2. Alpha 1 blockers
  39. Sites of Action of the major classes of Anti-Hypertensive Drugs; What acts on the Kidney tubules?
    1. Thiazides, etc
  40. Sites of Action of the major classes of Anti-Hypertensive Drugs; What acts on the Beta Receptors of juxtaglomerular cells that release renin?
    • 1. Proparanolol and other
    • 2. Beta Blockers
  41. Sites of Action of the major classes of Anti-Hypertensive Drugs; What acts on the Vascular smooth muscle?
    • 1. Hydralazine
    • 2. Minoxidil
    • 3. Nitroprusside
    • 4. Diazoxide
    • 5. Verapamil and other Calcium channel Blockers
    • 6. Fenoldopam
  42. Sites of Action of the major classes of Anti-Hypertensive Drugs; What acts on the Sympathetic Ganglia?
    1. Trimethaphan
  43. Sites of Action of the major classes of Anti-Hypertensive Drugs; What acts on the Vasomotor center?
    • 1. Methyldopa
    • 2. Clonidine
    • 3. Guanabenz
    • 4. Guanfacine
  44. Sites of Action of the major classes of Anti-Hypertensive Drugs; What acts on the area after Angiotension I and before Angiotension II?
    • 1. Captopril and other
    • 2. ACE Inhibitors
  45. When treating elevated arterial blood pressure what is manipulated?
    • 1. Cardiac Output
    • 2. Heart Rate
    • 3. Circulating fluid Volume
    • 4. Peripheral vascular resistance
    • 5. and Renin Activity
  46. Without Compelling Indication what are the considerations for initial pharmacological therapy for category Normal?
    1. No Antihypertensive drug indicated for Category Normal
  47. Without Compelling Indication what are the considerations for initial pharmacological therapy for category Pre-Hypertension?
    1. No Antihypertensive drug indicated for Category Pre-hypertension
  48. Without Compelling Indication what are the considerations for initial pharmacological therapy for category Stage 1 Hypertension?
    • 1. Thiazide-type diuretic for most
    • 2. May consider ACE Inhibitor,
    • 3. ARB,
    • 4. BB,
    • 5. CCB or
    • 6. combination of above
  49. Without Compelling Indication what are the considerations for initial pharmacological therapy for category Stage 2 Hypertension?
    • 1. 2-drug combination for most
    • 2. Usually thiazide-type diuretic OR
    • 3. ACE Inhibitor, ARB, BB OR
    • 4. CCB
  50. WITH Compelling Indication what are the considerations for initial pharmacological therapy for category Normal?
    1. Drugs for Compelling indications
  51. WITH Compelling Indication what are the considerations for initial pharmacological therapy for category Pre-Hypertension?
    1. Drugs for Compelling Indications
  52. WITH Compelling Indication what are the considerations for initial pharmacological therapy for category Stage 1 Hypertension?
    1.Drugs for Compelling Indications, Other antihypertensive drugs (diuretic, ACE inhibitor, ARB, BB, CCB) as needed
  53. WITH Compelling Indication what are the considerations for initial pharmacological therapy for category Stage 2 Hypertension?
    1. Drugs for Compelling Indications, Other antihypertensive drugs (diuretic, ACE inhibitor, ARB, BB, CCB) as needed
  54. Pharmacologic treatments for hypertension include what?
    • 1. Diuretic
    • 2. Sympathoplegics - Central Acting
    • 3. Sympathathetic Nerve Terminal Blockers
    • 4. Alpha Blockers
    • 5. Beta Blockers
    • 6. Calcium Channel Blockers
    • 7. Parenteral Vasodilators
    • 8. RAAS - ACE, ARB, Renin Inhibitors
  55. The purpose for using Diuretics to treat Hypertension is what?
    1. Increase volume of urine
  56. What is the difference between a Diuretic and Natriuretic?
    • 1. Diuretic - Increases urine Volume
    • 2. Natriuretic - Increases renal Na+ excretion
  57. Name the sub classes of Diuretics.
    • 1. Carbonic Anhydrase Inhibitors
    • 2. Loop
    • 3. Thiazides
    • 4. K+ Sparing
    • 5. Osmotics?
  58. When using Diuretics to treat hypertension what are the effects?
    • 1. A Decrease of Blood Pressure by 10 - 15 mm Hg
    • 2. Thiazide - do NOT see greater results with higher doses
    • 3. Loop - DO see greater results with higher doses
  59. When using Diuretics to treat hypertension what are the Side Effects?
    • 1. K+ loss (except for potassium sparing)
    • 2. Mg+ loss
    • 3. Increase lipid concentrations
    • 4. Impaired glucose tolerance
  60. When using Diuretics to treat hypertension what are the CONTRAINDICATIONS?
    • 1. Use Caution with Diabetes due to impaired glucose tolerance
    • 2. Hyperlipidemia due to the increase lipid concentrations
    • 3. Gout
    • 4. Renal Insuficiency
    • 5. Beware of Drug interactions: Digitalis, ACE
  61. Functions of the segment of the nephron Glomerulus are:
    • 1. Formation of glomerular filtrate
    • 2. water permeability in the Glomerulus is Extremely High
  62. Functions of the segment of the nephron Proximal convoluted tubule (PCT) are:
    • 1. Reabsorption of 65% of filtered Na+/K+/CA2+ and Mg+
    • 2. 85% of NaHCO3, and
    • 3. Nearly 100% of glucose and amino acids.
    • 4. Isosmotic reabsorption of water
    • 5. Water permeability in the Proximal convoluted tubule (PCT) is very high
  63. Functions of the segment of the nephron Proximal tubule, straight segment are:
    • 1. Secretion and reabsorption of organic acids and bases
    • 2. including uric acid and most diuretics
    • 3. Water permeability in the Proximal tubule, straight segment is very high
  64. Functions of the segment of the nephron Thin descending limb of Henle's Loop are:
    • 1. Passive reabsorption of water
    • 2. Water permeability in the Descending limb of Henle's loop is High
  65. Functions of the segment of the nephron Thick ascending limb of Henle's Loop (TAL) are:
    • 1. Active reabsorption of 15-25% of filtered Na+/K+/Cl-
    • 2. Secondary reabsorption of Ca2+ and Mg+
    • 3. Water permeability in the Thick ascending limb of Henle's Loop (TAL) is Very Low
  66. Functions of the segment of the nephron Distal Convoluted Tubule (DCT) are;
    • 1. Active reabsorption of 4-8% of filtered Na+ and Cl-
    • 2. Ca2+ reabsorption under parathyroid hormone control
    • 3. Water permeability in the Distal Convoluted Tubule (DCT) is very low
  67. Functions of the segment of the nephron Cortical Collecting tubule (CCT) are:
    • 1. Na+ reabsorption (2-5%) coupled to K+ and H+ secreation
    • 2. Water permeability in the Cortical Collecting tubule (CCT) is variable
  68. Functions of the segment of the nephron Medullary collecting duct are;
    • 1. Water reabsorption under vasopressin control
    • 2. Water permeability in the Medullary collecting duct is variable
  69. Name the Diuretic (s) that have a major action at the segment of the nephron Glomerulus:
    1. None - Glomerulus
  70. Name the Diuretic (s) that have a major action at the segment of the nephron Proximal Convoluted Tubule (PCT):
    • 1. Carbonic Anhydrase Inhibitors
    • 2. Adenosine Antagonists (under investigation)
    • 3. Proximal Convoluted Tubule (PCT)
  71. Name the Diuretic (s) that have a major action at the segment of the nephron Proximal Tubule, straight segments;
    1. None - Proximal Tubule, straight segments
  72. Name the Diuretic (s) that have a major action at the segment of the nephron Thin Descending limb of Henle's loop:
    1. None - Thin Descending limb of Henle's loop
  73. Name the Diuretic (s) that have a major action at the segment of the nephron Thick ascending limb of Henle's Loop (TAL):
    1. Loop Diuretics - Thick ascending limb of Henle's Loop (TAL)
  74. Name the Diuretic (s) that have a major action at the segment of the nephron Distal Convoluted Tubule (DCT)
    1. Thiazides - Distal Convoluted Tubule (DCT)
  75. Name the Diuretic (s) that have a major action at the segment of the nephron Cortical Collecting Tubule (CCT):
    • 1. K+ sparing Diuretics
    • 2. Adenosine Antagonists (Under Investigation)
    • 3. Cortical Collecting Tubule (CCT)
  76. Name the Diuretic (s) that have a major action at the segment of the nephron Medullary Collecting Duct:
    1. Vasopressin Antagonists - Medullary Collecting Duct
  77. What segment of the nephron is the site for formation of glomerular filtrate, is highly permeable to water, has no transporters and no clinical site of action for diuretics?
    1. Glomerulus
  78. What is the Renal Tubule Transport Mechanisms for the Proximal Convoluted Tubule (PCT):
    • 1. NaHCO3, NaCl, glucose, AAs reabsorbed via specific transport systems in proximal convoluted tubule (PCT).
    • 2. K+ reabsorbed via paracellular pathway
    • 3. Water reabsorbed passively
  79. Proximal Convoluted Tubule (PCT) Reabsorption is:
    • 1. Na+ 66%
    • 2. NaHCO3 85%
    • 3. K+ 65%
    • 4. H2O 60%
    • 5. Glucose 100%
    • 6. Amino Acids 100%
  80. In the Proximal Convoluted Tubule (PCT) the Na+H+ exchanger (NHE3) initiates what?
    1. NaHCo3 reabsorption
  81. In the Proximal Convoluted Tubule (PCT) Carbonic Anhydrase activity drives what?
    • 1. HCO3 reabsorption
    • 2. If blocked, no exchange of Na+ for H+, thus lose NA+ and thus more urine is produced
    • 3. Site of action for CAIs (acetazolamide)
  82. What is located in the outer medulla and composed of Thin Descending (dl), Thin Ascending (al), and the Thick ascending limbs (TAL)
    1. Loop of Henle
  83. The Thin Descending limb of Henle's loop has
    1. Water extracted from Thin descending (dl) by osmosis d/t hypertonic medullary intertitium
  84. Which segment of Loop of Henle is impermeable to water?
    1. Thin ascending limb of Henles loop
  85. Thick ascending limb of Henle's Loop (TAL):
    • 1. Actively reabsorbs c. 25% of filtered NaCl from lumen, but nearly impermeable to water.
    • 2. Na+K+2Cl- cotransporter (NKCC2)
  86. The site of action for Loop diuretics is what?
    1. Thick ascending limb of Henle's Loop (TAL):
  87. What is selectively blocked by loop diuretics at the Thick ascending limb of Henle's Loop (TAL):
    1. NKCC2
  88. About 10% of filtered NaCl is reabsorbed where?
    1. Distal Convoluted Tubule (DCT)
  89. Distal Convoluted Tubule (DCT) is relatively impermeable to water, thus the reabsorption of NaCl will do what?
    1. Further dilutes the tubular fluid
  90. Distal Convoluted Tubule (DCT) is the site of action for what?
    • 1. Thiazide Diuretics
    • 2. NaCl transporter: Na+ and Cl- cotransporter (NCC)
    • 3. NCC Blocked by thiazide diuretics
  91. Collecting Tubule System does connects what and is composed of what?
    • 1. Connects DCT to the renal pelvis and ureter.
    • 2. Composed of connecting tubule, collecting tubule, and collecting duct (formed from connection of 2 collecting tubules).
  92. Only 2-5% of NaCl reabsorption occurs here:
    1. Collecting tubule system
  93. The 2 cell types responsible for ion transport in the Collecting Tubule System
    • 1. Principal cells: Na+, K+ and Water
    • 2. Intercalated cells; H+ and HCO3- secretion
  94. Collecting tubule System Transport Mechanisms:
    • 1. Principal cells = epithelial Na+ channel (ENaC).
    • 2. Intercalated cells = H+ATPase and Cl/HCO3- exchanger
  95. Site of action for K+ sparing Diuretics is what?
    1. Cortical Collecting Tubule (CCT)
  96. What is Carbonic Anhydrase Inhibitor's mechanism of Action?
    1. Blocks dehydrogenation of carbonic acid in PCT >  Sodium Bicarb secretion > diuresis
  97. What are the indications for carbonic Anhydrase Inhibitor?
    • 1. Urinary Alkalinization - weak acid OD, Pure uric acid stones, hemoglobinuria (heat stroke)
    • 2. Glaucoma
    • 3. Acute Mountain sickness
    • 4. Metabolic Alkalosis
  98. Urinary Alkalinization, Glaucoma, Acute Mountain Sickness and Metabolic alkalosis are all indications for what?
    1. Carbonic Anhydrase Inhibitor
  99. What is a Carbonic Anhydrase Inhibitor Drug Name?
    1. Acetazolamide (Diamox)
  100. Pharmacokinetics of Carbonic Anhydrase Inhibitor include what?
    • 1. Onset diuresis 30 min
    • 2. Peaks in 2 hours
    • 3. Half life 10-15 hours
  101. Side Effects of Carbonic Anhydrase Inhibitor are what?
    • 1. Drowsiness
    • 2. Anorexia
    • 3. Paresthesias
  102. Cautions / contraindications for carbonic Anhydrase Inhibitor include what?
    • 1. Calcium Calculi
    • 2. Acidosis
    • 3. Renal Potassium wasting
    • 4. Cirrhosis (decreased NH4 excretion)
  103. The mechanism of action for Loop Diuretics is what?
    • 1. Blocks reabsorption of NaCl in the Thick ascending limb of Henle's Loop (TAL) by interfering with Na/K/CL transporter
    • - 25% of Na reabsorption occurs in TAL
    • - Interfering with K+ recycling >  Ca++ and Mg++ excretion
    • - Encourages prostaglandin synthesis > PGE2 inhibits salt transport > diuresis >
  104. Clinical Indications for Loop diuretics include?
    • 1. Edema
    • 2. Hypercalcemia
    • 3. acute renal failure
    • 4 Hyperkalemia
    • 5. Anion Over Dose
  105. Bumetanide, Furosemide, torsemide, ethacrynic acid are drug names for what?
    1. Loop diuretics
  106. What are some drug names for loop diuretics?
    • 1. Bumetanide
    • 2. Furosemide
    • 3. torsemide
    • 4. ethacrynic acid
  107. Pharmacokinetics of Loop Diuretics include what?
    • 1. Onset and clearance depend on delivery method and renal function
    • 2. Rapidly absorbed and not inhibited by acidosis
  108. Cautions / Contraindications for Loop Diuretics include What?
    • 1. slight chance of hypersensitivity with sulfa allergy
    • 2. Hyperuricemia
    • 3. Ototoxicity (concurrent use of aminoglycosides)
    • 4. Hypomagnesemia / Hypokalemic Metabolic Alkalosis
  109. Usual dosing for Loop Diuretics are dependent upon what?
    1. delivery method and renal function
  110. What are the Side effects for Loop diuretics?
    • 1. Dizziness
    • 2. Photosensitivity
    • 3. Orthostatic Hypotension
  111. The mechanism of action for Thiazides include what?
    • 1. Block Reabsorption of NaCl in DCT
    • 2. Enhance Ca2+
    • 3. Compete with uric acid secretion in PCT
  112. What are the clinical indications for Thiazides?
    • 1. Hypertension
    • 2. Heart Failure
    • 3. Calculi - Hypercalciuria
    • 4. Nephrogenic diabetes insipidus
  113. Hypertension, Heart Failure, Calculi - Hypercalciuria, and Nephrogenic diabetes insipidus are all indications for what diuretic?
    1. Thiazides
  114. What are some drug names for Thiazides?
    • 1. HCTZ
    • 2. Chlorothiazide
    • 3. Chlorthalidone et al
  115. What is the usual dosing for Thiazides?
    1. The usual dosing for Thiazides is oral HCTZ 12.5mg - 100mg PO
  116. What are the side effects of Thiazides?
    • 1. Orthostatic Hypotension
    • 2. Photosensitivity
    • 3. Electrolyte imbalance
  117. Orthostatic Hypotension, Photosensitity, electrolyte imbalance are all side effects for what drug?
    1. Thiazides
  118. What is the Pharmacokinetics for Thiazides?
    • 1. HCTZ - Onset 2 hours Peak 4-6 Duration 6-12 hours
    • May take up to 3 weeks to see full effect with initial treatment
    • 2. Chlorthalidone - Onset 2 hours duration up to 72 hours
  119. Cautions / Contrindications for Thiazides are what?
    • 1. Hypomagnesemia / Hypokalemic Metabolic Alkalosis
    • 2. Slight chance of hypersensitivity with Sulfa Allergy
    • 3. Hyperuricemia
    • 4. Hyperglycemia / hyperlipidemia
  120. The mechanism of action for Potassium Sparing Diuretics include what?
    • 1. Prevent K+ secretion by opposing aldosterone in DCT
    • Antagonism of mineralcorticoid receptors or block Na influx
  121. What are the clinical indications for Potassium Sparing Diuretics?
    • 1. Hypertension
    • 2. Hyperaldosteronism primary or secondary
    • 3. Edema
  122. Hypertension, Hyperaldosteronism, and edema are all clinical indications for what diuretic drug?
    1. Potassium Sparing Diuretics
  123. What are some drug names for Potassium Sparing Diuretics?
    • 1. Spironolactone
    • 2. Triamterene
    • 3. Amiloride
    • 4. Eplerenone
  124. What are the usual dosing for Potassium Sparing Diuretics?
    • 1. Can use in combination with Thiazide
    • 2. Spironolactone, Amiloride and triamterene have black box warnings
  125. What are some side effects for Potassium Sparing Diuretics?
    • 1. Hyperkalemia
    • 2. gynecomastia
    • 3. N / D
    • 4. Sexual Dysfunction
    • 5. rénal calculi (triamterene)
  126. Hyperkalemia, gynecomastia, N / D, Sexual Dysfunction and rénal calculi (triamterene) are side effects of what diuretic?
    1. Potassium Sparing Diuretics
  127. What is the Pharmacokinetics of Potassium Sparing Diuretics?
    1. Mechanism of action dependent
  128. What are some contraindications / cautions for Potassium Sparing Diuretics?
    • 1. Concomitant use of Beta Blockers, ACE
    • 2. Hepatic Impairment
    • 3. NO K+ supplementaiton
  129. What is the mechanism of action for Osmotic Diuretics?
    • 1. Proximal and descending Loop of Henle
    • 2. Osmotic flow after filtration in the glomerulus
  130. What are the clinical indications for Osmotic Diuretics?
    • 1. Water > Na excretion
    • Hemolysis, rhabdomyolysis
    • 2. Decrease Intracellular volume
  131. What is a drug name for Osmotic Diuretics?
    1. Mannitol (parental only)
  132. What is the usual dosing for Osmotic Diuretics?
    1. 12.5-25g IV
  133. Side effects for osmotic diuretics are what?
    • 1. Headache
    • 2. N/V
    • 3. Dizziness
  134. What are the Pharmacokinetics for Osmotic Diuretics?
    1. Poor GI Absorption - osmotic diarrhea
  135. What are some cautions / contraindications for Osmotic diuretics?
    • 1. Initial  Extracellular Volume Expansion
    • 2. Dehydration,
    • 3. hyperkalemia,
    • 4. hyper/hyponatremia
  136. What are some considerations with diuretics?
    • 1. Most renal diseases cause retention of Na and water
    • 2. Cirrhotic conditions are not greatly impacted by loop diuretics but are responsive to Spironolactone and Eplerenone
    • 3. 80% of renal calculi contain calcium
    • 4. Heart failure treatment is a balance between stimulating cardiac output with adequate filling pressure and decreasing the fluid volume load
  137. Diuretic Toxicity (slide 41)
    • 1. Diuretic toxicity is related to the differing mechanisms of action and clinical indications.
    • 2. Hint: Pay attention to the ion exchange, tranport, and cotransport mechanisms (Figures 15-2, 3, 4, 5, p. 253-254)
  138. Discuss some of the Diuretic uses for Carbonic Anhydrase Inhibitors:
    • 1. Glaucoma (reduces aqueous humor formation)
    • 2. Urinary Alkalinazation for cystinuria (Increases urinary pH from 7.0 to 7.5 and increases cystine reabsorption)
    • 3. Metabolic Alkalosis, esp. in CHF pts (due to excessive diuresis, volume replacement contraindicated, aczetaloamide used to correct alkalosis and add additional diuresis
    • 4. Acute Mtn Sickness (Mild S&S- weakness, dizziness, insomnia, HA. Serious S&S- pulm or cerebral edema. CAIs decrease CSF formation and pH, thus causing increase ventilation, diminish symptoms of sickness.
  139. When a Carbonic Anhydrase Inhibitor is used to treat Glaucoma what are the expected results
    1. Reduces aqueous humor formation
  140. When a Carbonic Anhydrase Inhibitor is used to treat Urinary Alkalinazation for cystinuria what are the expected results
    1. Increases urinary pH from 7.0 to 7.5 and increases cystine reabsorption
  141. When a Carbonic Anhydrase Inhibitor is used to treat Metabolic Alkalosis, esp. in CHF pts, what are the expected results
    1. due to excessive diuresis, volume replacement contraindicated, aczetaloamide used to correct alkalosis and add additional diuresis
  142. When a Carbonic Anhydrase Inhibitor is used to treat Acute Mtn Sickness what are the expected results
    1. Mild S&S- weakness, dizziness, insomnia, HA. Serious S&S- pulm or cerebral edema. CAIs decrease CSF formation and pH, thus causing increase ventilation, diminish symptoms of sickness.
  143. Discuss Diuretic Toxicity for Carbonic Anhydrase Inhibitors for the following conditions: Hyperchloremic Metabolic Acidosis, Renal stones and renal K+ wasting:
    • 1. Hyperchloremic Metabolic Acidosis: Results from chronic loss of HCO3-
    • 2. Renal Stones: Calcium salts insoluble with relatively alkaline pH, thus increased risk of renal stones
    • 3. Renal K+ wasting: occurs secondary to increased Na+ and HCO3- delivered to collecting tubule- Na+ reabsorbed and K+ secreted
  144. Discuss the diuretic uses for Loop:
    • 1. Primary- Acute Pulmonary Edema, other edema, Hypercalcemia.
    • 2. Hyperkalemia (increase urinary excretion of K+)
    • 3. Acute Renal Failure (increase rate of urine flow and K+ excretion)
    • 4. Anion Overdose (tx toxic ingestion of substances reabsorbed in TAL- bromide, fluoride, iodide, etc. Must be used with Saline to offset Na+ loss)
  145. Discuss slide 45 Diuretic Toxicity: Loop
    • 1. Hypokalemic Metabolic Alkalosis: Inhibits NaCl reabsorption leads to increased NaCl delivered to collecting duct, thus increased secretion of K+ and H+.
    • 2. Ototoxicty: Dose-related hearing loss, usually reversible. Worsened with other ototoxic agents (aminoglycosides, etc.)
    • 3. Hyperuricemia: Hypovolemia induced gout from increased uric acid reabsorption in proximal tubule. Prevent by using low dose loop diuretics to avoid hypovolemia.
    • 4. Hypomagnesemia: Results from chronic use of loop diuretics. Tx with oral magnesium supplements.
    • 5. Loop diuretics except ethacrynic acid are sulfonamides. Therefore, reactions can involve Sulfa allergy S&S: skin rash, eosinophilia, interstitial nephritis.
    • 6. Severe dehydration, hyponatremia, hypocalcemia and secondary parathyroidism.
  146. Diuretic use for Thiazides include what?
    • 1. HTN
    • 2. Heart Failure
    • 3. Nephrolithiasis from idiopathic hypercalcuria
    • 4. Nephrogenic diabetes insipidus
  147. Discuss slide 47 Diuretic Toxicity: Thiazides:
    • 1. Hypokalemic Metabolic Alkalosis & Hyperuricemia (similar to loop)
    • 2. Impaired CHO Tolerance d/t impaired pancreatic release of insulin and diminished tissue utilization of glucose
    • 3. Hyperlipidemia: Increase of 5-15% in total serum cholesterol and LDLs.
    • 4. Hyponatremia: Occurs from combination of hypovolemia-induced increase in ADH, reduced renal diluting capacity, and increased thirst.
    • 5. Thiazides also sulfonamides, thus cross-reactivity. Rare- photosensitivity, dermatitis. Extremely rare- hemolyitic anemia, thrombocytopenia, and acute necrotizing pancreatitis.
  148. Discuss the diuretic use of Potassium Sparing
    • 1. Useful in mineralocorticoid excess or hyperaldosteronism whether primary (Conn’s syndrome, ectopic adrenocorticotropic hormone production) or secondary (heart failure, cirrhosis, nephrotic syndrome, or other conditions from decreased intravascular volume).
    • 2. Used when other diuretic classes, loop and thiazide, may exacerbate secondary mineralocorticoid excess from volume contraction. Blunt the K+ secretion response.
  149. Discuss diuretic Toxicity for Potassium Sparing
    • 1. Hyperkalemia: Exacerbated in renal disease or by concomitant use of drugs that reduce renin (B Blockers, NSAIDS, etc.) or angiotensin II activity (ACE, ARB).
    • 2. Hyperchloremic Metabolic Acidosis: Inhibited H+ secretions in parallel with K+ secretion- mimics type IV renal tubular acidosis.
    • 3. Gynecomastia (impotence, BPH): Caused by spironolactone exerting steroidal effects on other receptors. Has not been reported with with eplerenone (more selective for mineralocorticoid receptors and inactive on androgen/progesterone receptors).
    • 4. Acute Renal Failure: Triamterene combined with indomethacin has been reported to precipitate ARF.
    • 5. Kidney Stones: Triamterene slightly soluble and precipitates in urine, leading to stones.
  150. What is the purpose of Sympathoplegics - central acting?
    1. Block Vasoconstriction
  151. What medications are considered Sympathoplegics - central acting?
    1. Primarily Methyldopa and Clonidine
  152. What are the mechanism of action for Sympathoplegics - central acting?
    1. Impair Baroreceptor reflexes
  153. What is the half life of Sympathoplegics - central acting?
    • 1. Varies by drug
    • 2. Methyldopa - 2 hours
    • 3. Clonidine - 8-12 hours
  154. What are some side effects for Sympathoplegics - central acting?
    • 1. Sedation
    • 2. postural hypotension
    • 3. mental fog
    • 4. dry mouth
  155. Sympathoplegics - central acting? Slide 51
    • 1. Specific MoA of Clonidine:
    • 2. Lowers BP by reduction of cardiac output due to heart rate decrease, relaxation of capacitance vessels, and decrease in PVR.
    • - d/t direct stimulation of α adrenoreceptors in arterioles and in the medulla of the brain and inhibits other pressor effects of αlpha agonists as a partial agonist at αlpha receptors.
    • - In animals, hypotensive effect blocked by centrally acting α antagonists. Clonidine reduces sympathetic and increases parasympathetic tone- decreased BP and bradycardia.
    • - Higher affinity for presynaptic α2 adrenergic receptors, thought to reduce norepinephrine release in the brain.
  156. What are some contraindications / cautions for Sympathoplegics - central acting?
    • 1. Depression
    • 2. SLOW taper off Clonidine!
  157. What are some toxicity for the use of Central Acting Sympathoplegics? CAS
    • 1. Most common undesirable effect of CAS is pronounced sedation
    • 2. Long term tx with CAS has been linked to the following:
    • 1. Persistent mental lassitude
    • 2. Impaired concentration
    • 3. Nightmares, depression, vertigo.
    • 4. EPS can occur, but infrequent.
    • 5. Lactation in men and women from increased prolactin (associated with hypothalamic dopaminergic inhibition associated with methyldopa-
    • + Coombs test for 10-20% of pts tx’d for >12 mos. Can make blood cross-matching difficult, associated with hemolytic anemia, and fever.
  158. The purpose of Sympathetic Nerve Terminal Blockers is what?
    1. Block vasoconstriction
  159. List some examples of Sympathetic Nerve Terminal Blockers:
    • 1. Guanadrel
    • 2. Reserpine
  160. What is the mechanism of action for Sympathetic Nerve Terminal Blockers?
    1. Block nicotinic acetylcholine channels on sympathetic and parasympathetic ganglia
  161. What are some side effects / Toxicity for Sympathetic Nerve Terminal Blockers?
    • 1. Profound orthostatic hypotension
    • 2. Sexual dysfunction
    • 3. depression
    • 4. nightmares
    • 5. diarrhea
    • 6. Parkinsonian extrapyramidal effects
  162. What are some contraindications for Sympathetic Nerve Terminal Blockers?
    1. This drug is rarely used
  163. What is the purpose of Beta Blockers?
    • 1. Block beta receptor activity
    • 2. Reduce mortality post MI, in CHF
  164. What are some subclasses of Beta Blockers?
    • 1. Nonselective – Propranolol
    • 2. Cardioselective (non β2)– Metoprolol, Atenonlol, Esmolol
    • 3. Nonselective with ISA (-TPR, mod – HR/CO)- Pindolol Acebutolol
    • 4. Mixed α and β – labetalol, carvedilol and nebivolol
  165. Which beta blocker is nonselective?
    1. Propranolol
  166. Which beta blocker is cardioselective (non beta 2)?
    • 1. Metoprolol
    • 2. Atenonlol
    • 3. Esmolol
  167. What beta blocker is nonselective with ISA?
    1. Pindolol Acebutolol
  168. What beta blocker is mixed alpha and beta?
    • 1. Labetalol
    • 2. carvedilol
    • 3. nebivolol
  169. What is the mechanism of action for Beta Blockers?
    • 1. Negative Ionotropic effect
    • 2. Negative chronotropic effect
    • 3. block renin production
  170. What is the half life of Beta Blockers?
    1. 3-30 hours depending
  171. What are some side effects of Beta Blockers?
    • 1. Headach
    • 2. rash
    • 3. Dizziness
  172. What are some contraindications / Cautions for Beta Blockers?
    • 1. Arrhythmias
    • 2. Nonselective beta Blocker - Asthma / COPD
    • 3. Bradycardia
    • 4. Severe CHF
  173. What is the purpose of Alpha Blockers?
    1. Vasodilation
  174. What is the Benefit of Alpha Blockers?
    • 1. BPH
    • 2. Bladder obstruction
  175. What is the mechanism of action for Alpha Blockers?
    1. Block Alpha Receptor at arterioles and venues
  176. What is the half life of Alpha Blockers?
    1. 3-22 hours
  177. What are the side effects of Alpha Blockers?
    • 1. NaCl and water Retention
    • 2. Orthostatic hypotension (dosing)
    • 3. Dizziness
    • 4. headache
  178. What are some contraindications / cautions for Alpha Blockers?
    1. Primarily used as adjunctive therapy (use with Beta blocker, diuretic)
  179. What is the purpose of Vasodilators: Calcium Channel Blockers?
    • 1. Decrease SVR
    • 2. May Decrease HR, Cardiac Output
    • 3. decrease Cardiac muscle oxygen demand
    • 4. Works best in combination
  180. What are some subclasses of Vasodilators: Calcium Channel Blockers?
    • 1. Dihdropyridine - smooth muscle
    • 2. Non-dihydropyridine (cardiac) Verapamil and Diltiazem
  181. What is the mechanism of acton for Vasodilators: Calcium Channel Blockers?
    • 1. Decrease Ca++ influx
    • 2. Decrease conduction and contractility
    • 3. Relaxation of arteriole smooth muscle
    • 4. Sympathetic and RAAS reflexive systems intact
  182. What are the side effects from Vasodilators: Calcium Channel Blockers?
    • 1. Slight reflex tachycardia (with dihydropyridines)
    • 2. Edema
    • 3. Increase generally as dose increases
  183. What are the contraindications for Vasodilators: Calcium Channel Blockers?
    • 1. NO short acting
    • 2. Not as single treatment
  184. What is the mechanism of action for the Calcium Channel Blockers: Diltiazem?
    • 1. Voltage gated L-type calcium channels in cardiac and smooth muscle
    • - Composed of several subunits, chiefly a1 and a2
    • - 4 variants of a1: Diltiazem and verapamil don’t occupy same receptors as dihydropyridines, but on same a1-subunit.
    • - Act similarly to Na+ channel blockade by local anesthetics- Drugs act from inner side of membrane and bind more effectively to open channels and inactivated channels.
    • - Drug binding reduces frequency of opening in response to depolarization.
    • -Results in marked decrease in transmembrane calcium current and long-lasting relaxation in smooth muscle and decreased contractility and SA & AV nodal conduction velocity in cardiac muscle.
  185. What is the purpose of Vasodilator Hydrazaline?
    1. Decease PVR
  186. What is the mechanism of action for the Vasodilator Hydrazaline?
    1. Arteriole Dilation only
  187. What are some uses for the Vasodilator Hydrazaline?
    • 1. Adjunctive use with Severe HTN/CHF particularly in AA
    • 2. Dose ranges from 40 mg/d to 200 mg/d, 2-3xs daily
    • 3. Higher the dose – greater effect
  188. What are some side effects for Vasodilator Hydrazaline?
    1. SLE like syndrome with high doses (400 mg/d)
  189. What are some cautions with Vasodilator Hydrazaline?
    • 1. Ischemic CAD - provoke angina from reflex
    • 2. Tachycardia and sympathetic stimulation
  190. What is the purpose of Parental Vasodilators?
    • 1. Decrease PVR
    • 2. Work best in combination (Beta Blocker and Diuretics)
    • 3. hypertensive emergencies
  191. Name some Parental Vasodilators Drugs:
    • 1. Diazoxide
    • 2. Fenoldopam
    • 3. Nitroprusside
  192. What is the mechanism of action for Parental Vasodilators?
    • 1. Relaxation of arteriole smooth muscle
    • 2. Sympathetic and RAAS reflexive systems intact (Figure 11-4, page p. 174)
  193. What are some cautions for Parental Vasodilators?
    • 1. Reflexive tachycardia
    • 2. Rapid toxicity
  194. Discuss the Parental Vasodilators Sodium Nitroprusside: slide 62
    • 1. Sodium Nitroprusside
    • - Used for HTN emergencies and heart failure.
    • -Dilates both arterial and venous vessels= reduced PVR.
    • -Activates guanylyl cyclase by nitric oxide release and direct enzymatic stimulation. Increases cGMP which relaxes vascular smooth muscle.
    • -Doses: 0.5 mcg/kg/min to 10 mcg/kg/min.
    • -High doses can lead to cyanide toxicity.
    • -Complex of iron, cyanide groups, and nitroso moiety.
    • -Rapidly metabolized by RBC uptake, cyanide metabolized by rhodanase to thiocyanate, to ecf, kidneys. -High doses overwhelm this, lead to increased cyanide levels.
    • -Must protect from light.
  195. What is the purpose of ACE Inhibitors?
    • 1. Decrease TPR
    • 2. Does not stimulate reflexive tachycardia
  196. Name some ACE Inhibitors: "pril"
    • 1. captopril
    • 2. enalapril
    • 3. lisinopril
    • 4. benazepril
  197. What are the mechanism of action for ACE Inhibitors?
    • 1. Blocks conversion of Angiotensin I into Angiotension II
    • 2. Inactivates bradykinin
    • 3. improves glomerular flow by decreasing resistance and pressure
  198. What is the Pharmacokinetics for the ACE Inhibitor: Captopril?
    • 1. (h) - 2.2 hours
    • 2. Bioavailability: 65%
    • 3. Initial dose: 50-75 mg/d
    • 4. usual Maintenance Range: 75-150 mg/d
    • 5. Reduce dose in moderate renal insuficiencey (Cr Cl < 30 ml/min)
  199. What is the half life for ACE Inhibitors?
    • 1. Generally about 12 hours
    • 2. Excreted via kidneys
  200. What are the side effects for ACE Inhibitors?
    • 1. Hypotension
    • 2. ARF = stenosis
    • 3. Hyperkalemia (more often renal dz/diabetes)
    • 4. Cough & Angioedema (bradykinin and substance P)
  201. What are some contraindications / cautions for ACE Inhibitors?
    • 1. Pregnancy, 1st trimester (teratogen), 2nd/3rd trimesters (fetal hypotension, anuria, renal failure, malformations, death)
    • 2. Interaction with NSAIDS- Block bradykinin/prostaglandin-mediated vasodilation
  202. What is the purpose of an ARB?
    • 1. Prevent Vasoconstriction
    • 2. Prevent Aldosterone secretion
  203. What is the drug names for ARB?
    • 1. "sartan"
    • 2. losartan
    • 3. valsartan
    • 4. irbesartan, etc…
  204. What is the mechanism action for ARB?
    • 1. No bradykinin activity
    • 2. Compete with Angiotensin II at receptor sites
    • 3. Improves glomerular flow by decreasing resistance and pressure
  205. What is the half life of an ARB?
    • 1. Generally about 12 hours
    • 2. Excreted via kidneys
  206. What are the side effects of ARB?
    • 1. Hypotension
    • 2. ARF=stenosis
    • 3. hyperkalemia
    • 4. Cough - less than ACE
    • 5. Angioedema - Less than ACE
  207. What are some contraindications / cautions for ARB?
    1. Pregnancy
  208. What are the goals when treating a Hypertensive Emergencies?
    • 1. Reduce BP by 25%,
    • 2. NOT normalization.
    • 3. Maintain DBP at no less than 100-110 mm Hg.
  209. What is required when treating a patient with an Hypertensive Emergencies?
    • 1. Monitoring with continuous arterial BP, Meticulous I/O, daily weights.
    • 2. Parenteral antihypertensive agents (direct vasodilators- Na+ nitroprusside, Ca++ channel blockers, etc.) for rapid correction.
    • 3. Initiate oral BP agents for smoother long-term management.
  210. What is the initial therapy options for a compelling indication of: Heart Failure?
    • 1. Thiaz
    • 2. BB
    • 3. ACEI
    • 4. ARB
    • 5. ALDO ANT
  211. What is the initial therapy options for a compelling indication of: Postmyocardial Infarction?
    • 1. BB
    • 2. ACEI
    • 3. ALDO ANT
  212. What is the initial therapy options for a compelling indication of: High CAD risk?
    • 1. THIAZ
    • 2. BB
    • 3. ACE
    • 4. CCB
  213. What is the initial therapy options for a compelling indication of: Diabetes?
    • 1. THIAZ
    • 2. BB
    • 3. ACEI
    • 4. ARB
    • 5. CCB
  214. What is the initial therapy options for a compelling indication of: Chronic Kidney Disease?
    • 1. ACEI
    • 2. ARB
  215. What is the initial therapy options for a compelling indication of: Recurrent stroke prevention?
    • 1. THIAZ
    • 2. ACEI
  216. Latest Evidence …. JNC 8 previews
    • 1. Aggressive BP reduction to <120/80 is not beneficial
    • 2. Treatment of very elderly <150/80 is not beneficial
    • 3. Treatment of very elderly does prevent stroke
    • 4. ACE and ARB are not recommended in combination
    • 5. Combination therapy is recommended
  217. Review tie it all together slide:
    1. Slide 73

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