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157 Cards in this Set
- Front
- Back
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Components that affect blood pressure?
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Heart Rate
Arteriolar Tone Myocardial Contractility Blood Volume Venous Capacitance Tone Venous Return (but no drugs treat this) |
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Formula for BP?
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BP = CO x PVR
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What does the short term BP Regulation?
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Baroreceptor Reflex
via Vagal Center and Vasomotor Center |
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What does Long term BP Regulation?
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Kidneys
Renin Angiotensin II (=vasoconstrict + inc. Al) Aldosterone (=keep Na and Water) Overall = Inc. BP |
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Where do Loop Diuretics work?
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Loop of Henle
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Where do Thiazide Diuretics work?
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Distal Convoluted Tubule
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Where do K+ Sparring Diuretics work?
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Na Channel Blockers work at NaCl Channels in collecting duct
Aldosterone Blockers (Antagonists) work in Collecting Duct as well |
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Whats the acute effect of Diuretics?
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Inc. Na and Water Excretion = Dec. Blood Volume = Dec. CO and Preload
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Whats the chronic effect of Diuretics?
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6-8 weeks
Dec. Na in Smooth muscle cells = Dec. PVR |
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Over the Long Term (8-8 weeks) Diuretics Dec. BP how?
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By Decreasing PVR
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What are the 1st line drugs used for Hypertension?
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Thiazides.
(Always use this over Loop and K+ Sparring unless there is a reason to use something else) |
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When do you use Loop Diuretics in Hypertensive pts?
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If pt. has reduced Kidney (renal) function
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What is a disadvantage of using Loop Diuretics in Hypertensive pts (that have renal disease...)
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They have short half lives, so you have to take drug more than once/day
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What do Thiazide and Loop Diuretics have in common?
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Both Dec. K+ via Na+
SO, use Na+ Channel blocker to counteract the K+ loss |
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Why is the K+ loss seen with Loop and Thiazide diuretics troubling?
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It can cause cardiac arrhythmias
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What are the Na+ Channel Blockers we've talked about (a subclass of the K+ sparring drugs)
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Triameterene
Amilioride |
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What are the Aldosterone Blocker Drugs we've talked about (a subclass of the K+ Sparring drugs)
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Spironolactone
Eplerenone |
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What are the three target organs for Beta Blockers when they are used to reduce BP?
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B1 on Heart
B1 on Kidneys (IF B Blocker has ISA = Intrinsic Sympathomimetic Activity) B's in Brain (IF drug has ISA) |
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How do B Blockers Decrease BP by targeting the Heart?
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Heart: B1's blocked --> dec. HR --> dec. Contractility --> dec. CO
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If a B Blocker has ISA (=intrinsic sympathomimetic activity), how does it work to dec. BP via the Kidneys and Brain?
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Kidneys: B1's Blocked --> dec. Renin --> dec. Ang. II --> dec. Al --> dec. BP
Brain: B's Blocked --> dec. Sympathetic Outflow --> dec. BP (works b/c dec. NE = Blood vessels constricted) |
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What should you give a pt post MI "so they don't die...as much"?
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B Blocker
Continue to give it indefinitely |
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What structures do Non-Dihydropyridines work on primarily? Dihydropyridines? (Both are Ca2+ Channel Blockers)
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Non-Dihydropyridines = Heart AND Vessels
Dihydropyridines = Vessels only (these end in -"dipine") |
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What are the two Ca2+ Channel Blockers that are Non-Dihydropyridines?
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Verapamil and Diltiazem
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What is the effect of Verapamil and Diltiazem, both Ca2+ channel blockers (Non-dihydropyridines) on the heart and vessels?
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Vessels:
Ca2+ Blocker = Sm. Muscle Relaxes b/c Ca2+ Channel blocked = Relazation = Vasodilation = Dec. PVR = Dec. BP Heart: Dec. HR = Dec. Conduction = Dec. Force of Contraction = Dec. CO |
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What is the effect of the -"dipines" (=Ca2+ Channel Blockers) on the Vessels?
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Relaxation = Vasodilation = Dec. PVR = Dec. BP
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Which has the potential to cause Rebound Tachycardia, Non-dihydropyridines or Dihydropyridines?
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Dihydropyridines, because Ca2+ channels on HEART are NOT blocked = there is no counter-dec. in PVR and CO to blunt the Tachy
(DHPs only work on the vessels) |
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How do Ca2+ Channel Blockers cause peripheral edema?
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Because they only act on the Arterioles = Veins NOT affected, so they are still constricted = Fluid in Tissues
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What are some of the side effects due to vasodilatory effects of Antihypertensive Drugs?
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Constipation
Flushing Headache Dizziness Peripheral Edema |
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What are the adverse effects of the Non-Dihydropyridine Ca2+ Channel Blockers Verapamil and Diltiazem?
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Sinus Brady
AV Block Exacerbation of Heart Failure or Pulmonary Edema Verapamil (mostly) = GI Constipation (b/c of decreased motility due to Ca2+ Channels being Blocked = Constipation) |
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What are the adverse effects of Dihydropyridines (=-"dipines")?
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Reflex Tachy
Usually in First week of Tx, b/c eventually baroreceptor reflex kicks in to correct Reflex Tachy |
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What is the OVERALL effect of Angiotensin II?
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Inc. BP
Inc. Angiotensin II = Inc. Al = Keep Na+/Water = Inc BP |
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How does Angiotensin II achieve its overall effect in increasing BP?
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3 ways:
Adrenal Gland (= Al release = Keep Na2+ and Water = Inc. BP) Arterioles/Venules (=vasoconstriction) Inc. Sympathetic Activity (=Inc. BP) |
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Whats the progression of hormones from Angiotensinogen to Aldosterone Release?
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Angiotensinogen --> Ang I (via Renin) --> Ang II --> AT1 Receptor --> Adrenal Gland --> Al Release
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Whats the progression of hormones from Kininogen to Bradykinin?
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Kininogen --> Bradykinin --> ACE (metabolizes Brady) --> Inactive Bradykinin
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What step in the Process of Al secretion does Renin Inhibitor affect?
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Affects Renin's ability to turn Angiotensinogen into Ang I = No Al
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What step in the process of Al Secretion do the ACE inhibitors (=Angiotensin Converting Enzyme inhibitor) work on?
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They do not allow for the conversion of Ang I to Ang II
They also inhibits ACE's from breaking down Bradykinin = excess Brady = Arteries dilated |
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What step in the process of Al secretion do ARBs (=Angiotensin Receptor Blocker) work on?
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ARB = Angiotensin Receptor Blocker
Do not allow Ang II to bind to the AT1 receptor |
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Which class of Diuretics protect the Kideys (renoprotective) in Diabetics and Non-diabetic nephropathy?
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ACE Inhibitors
(vs. Loop Diuretics which are for pts with reduced kidney function) |
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How are ACE inhibitors renoprotective in pts. with Kidney damage?
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ACE inhibitor will Dec. BP (because it doesn't allow Ang I to convert to Ang II) And Dilate Efferent Arteriole = Dec. Intraglomerular Hydrostatic Pressure = Less Damage = Dec. Proteinuria
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How can ACE inhibitors and ARBs cause renal insufficiency or failure in select pts?
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Pts with pre-existing renal issues, Dehydration, Heart Failure, or non-steroidal anti-inflammatory drug use can acquire renal insuffiency if put on ACE inhibitors or ARBs
WHY? Dec. GFR = Inc. Serum Creatinine (a measure of kidney function) |
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Whats the effect of ACE inhibitors, ARBs, and Renin Inhibitors (Aliskiren) on K+ Excretion in kidney?
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Inc. K+ = Hyperkalemia
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Whats the effect of Loop and Thiazides on K+ Levels in body?
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BOTH dec. K+ in body via Na+
SO use an Na+ Channel Blocker to COUNTERACT this K+ Loss |
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What are the side effects of ACE Inhibitors?
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Anemia (suppress production of erythropoietin)
Neutropenia (Agranulocytosis, Anemia, Impaired renal function, collagen vascular disease) JUST CAPTOPRIL: Loss of taste, metallic taste, skin rash |
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What are the side effects of ACE inhibitors? Which of those are present with ARBs?
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Angioedema (Lower in ARBs than in ACE inhibs)
Cough |
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Use ACE inhibitors in pregnant women?
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NOPE, they are teratogenic
So use ARBs OR Renin Inhibitors (Aliskiren) |
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What are the compensatory systems activated by Alpha Blockers and Vasodilators?
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A-Blockers and Vasodilators do the following:
Vasodilation --> Reflex Tachy --> Inc. CO DIFFERENCE in: Alpha-Blocker Dec. PVR = Dec. BP Vasodilators cause Reflex Renin Release --> Na+ and water retention (via Al) |
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Which of the Alpha Blockers, Selective or Non-selective, can be used to treat Hypertension?
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Alpha 1-selective CAN be used to treat hypertension
(Block A1s = vasodilation) |
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Where are the Alpha 1 receptors located in the CV System?
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Arteries and Veins
Arteries: Block A1s = Vasodilation = Dec. PVR = Dec. BP Veins: Block A1s = Vasodilation = Dec. Venous Retrun = Dec. CO |
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What are some of the side effects of Alpha Blockers?
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Orthostatic Hypotension
Reflex Tachy Edema (Na+ and water retention) Headache, Weakness, Dizziness |
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What are some of the side effects of Lebetalol, an alpha and beta Blocker?
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Orthostatic Hypotension
Sexual Dysfunction Nausea/Vomiting Bronchospasm Prolong/Enhance Hypoglycemia Vasodilation --> Dec. PVR Dec HR --> Dec. CO |
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Which Anti-Hypertensive agent can cause rebound hypertension if abruptly withdrawn?
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Clonidine
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What do you use instead of Clonidine (a centrally acting A2 Agonist) for Hypertension in pregnant women?
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Methyldopa, because its not teratogenic (and won't cross placenta)
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How do the two Centrally Acting A2 Agonists, Clonidine and Methyldopa work in the brain to reduce Hypertension?
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They Affect A2s in brain. A2 coupled to qi = inhibitory, so they decrease Sympathetic outflow = Dec. PVR, Dec. HR, CO
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What are the adverse effects specific to the Centrally acting A2 Agonist Clonidine?
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Contact Dermatitis
Abrupt Withdrawal leads to Rebound Hypertension |
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What are the adverse effects seen with use of either Clonidine or Methyldopa? (ie which adverse effects are characteristic of both?)
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Sedation, Dry Mouth, Depression, Impotence, Na/Water Retention
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What are the adverse effects specific to the Centrally Acting A2 Agonist Methyldopa?
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Positive Coombs Test (when RBCs lyse its a hypersensitivity rxn ie Igg on RBCs attacked)
SO MONITOR PTS RBC COUNT if they're on Methyldopa Hemolytic Anemia Hepatotoxicity (fever, jaundice) |
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What do you need to monitor in pts. who are on Methyldopa, a centrally acting A2 Agonist?
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RBC Count
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Between Clonidine and Methyldopa, which one only causes Hematologic (=blood) and Liver problems/toxicity?
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Methyldopa
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What are the PARENTERAL drugs used in the treatment of Hypertensive urgency/emergency?
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Direct Vasodilators (Hydralazine, Nitroprusside, Fenoldopam, Sodium Nitroprusside)
Ca2+ Channel Blockers (Nicardipine, Clevidipine) ACE inhibitors (Enalapril) Alpha Blocker (Phentolamine) Beta Blocker (Esmolol, Propranolol) Alpha and Beta Blockers (Lebatalol) |
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Of the Direct Vasodilator PARENTERAL drugs used to treat hypertensive urgency/emergency, which acts on both Arteries AND Veins to dilate them?
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Nitroprusside
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Action of Lebatalol on Alpha and Beta Receptors and effect on PVR and CO?
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Lebatalol = alpha and beta receptor BLOCKER
A1s and B2s on Blood vessels blocked = Vasodilation (b/c there are many more A1s) = Dec. PVR B1s on heart Blocked = Dec. HR, Dec. CO BUT mechanisms catch this so LITTLE EFFECT on HR and CO OVERALL: Dec. PVR, NO CHANGE in CO |
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Hydralazine vs. Minoxidil vs. Nitroprusside dilatory actions on arteries and veins? (All are Direct Vasodilators)
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Hydralazine and Minoxidil Dilate Arteries
Nitroprusside dilates Arteries and Veins OVERALL: Dec. PVR = Dec. BP = Dec. CO |
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Whats the onset of action of Hydralazine vs. Nitroprusside?
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Hydralazine = IV = Rapid and Oral = For CHRONIC hypertension
Nitroprusside = IV = VERY RAPID (seconds but short DOA) |
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What are the adverse effects of Hydralazine? (= a Direct vasodilator)
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Lupus-Like Syndrome
Fever, Arthralgia, Skin Rashes |
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What are the adverse effects of Minoxidil (= a direct vasodilator)
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Hypertrichosis = hair over-growth (just think of Ray Chahoud...)
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What are the adverse effects of Nitroprusside (= a direct vasodilator)
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Cyanide Toxicity
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Where in the kidney do Carbonic Anhydrase Inhibitors work? Loops? Thiazides? K+ Sparring?
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CAI: Proximal Tubule
Loops: Loop on Henle Thiazides: Distal Convoluted Tubule K+ Sparring: Collecting Duct Osmotic Diuresis: From cells to extracellular space |
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Carbonic Anhydrase Inhibitors result in the excretion (loss) of what?
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Bicarb
Na+ K+ |
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Loop Diuretics result in the excretion (loss) of what?
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Ca2+
Na+ Mg2+ Cl- K+ |
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Thiazides result in the excretion (loss) of what?
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Na+
Cl- K+ |
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K+ Sparring Diuretics result in the excretion (loss) of what? RETENTION of what?
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Lose Na+
Retain K+ and H+ |
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Osmotic Diuresis
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Draws water from cells to intracellular space = Proportionally more water than Na+ is excreted
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Why do Carbonic Anhydrase Inhibitors, Thiazides and Loops Inc. K+ excretion?
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Inc. Na+ to Collecting Duct
= Lumen has negative electrochemical potential = K+ driven into tubule Sm. Amt. of Na+ reabsorbed into collecting duct = K+ excreted |
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How do K+ Sparring Diuretics work to correct diuretic-induced Hypokalemia?
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Na Channel Blockers:
(Triameterene and Amilioride) Block Na+ Channel on principle cells of collecting duct Al Blockers: (Spironolactone and Eplerenone) Block Al binding to Mineralcorticoid Receptor = reduces Na+ pump activity in collecting duct =Na+ reabsorption and secretion of K+ and H+ both decreased |
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Loops are used in the treatment of what?
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Edema from Heart Failure (peripheral or pulmonary)
Reduced Renal Function Cirrhosis of the Liver = Ascites (fluid in peritoneal cavity) |
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Thiazides are used in the treatment of what?
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Edema
Use with another Diuretic to create a potentiated effect |
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Carbonic Anhydrase Inhibitors are used to treat edema in pts. with what other condition?
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Metabolic Alkylosis (b/c it helps treat both)
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K+ Sparring Diuretics are used to treat what?
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Secondary Aldosteronism: Cirrhosis of the liver with edema or ascites (specifically Spironolactone)
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How do Carbonic Anhydrase Inhibitors treat open angle Glaucoma?
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Carbonic Anhydrase Inhibitors facilitate the movement of HCO3- from ciliary body to post. chamber
OVERALL: dec. production of Aq. Humor |
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How to Carbonic Anhydrase Inhibitors treat Acute Mt. Sickness?
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Acetazolamide makes blood more acidic b/c bicarbonate is pee'd out = Drug accelerates the process that otherwise happens over several days
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Which Carbonic Anhydrase Inhibitor do you use to specifically treat Open Angle Glaucoma? Acute Mt. Sickness?
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Open Angle Glaucoma = Dorzolamide (topical = less side effects)
Acute Mt. Sickness = Acetazolamide (systemically = Inc. risk of side effects) |
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What is the effect of Carbonic Anhydrase Inhibitors on Urine pH?
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Make Urine BASIC (Alkalization)
= INC. Excretion of Acidic Drugs |
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How do K+ Sparring Diuretics work to treat Aldosteronism?
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They block the Mineralcorticoid Receptor = Al can't bind
= Reduced Na+ Channel and Na+ Pump Activity in Collecting Duct =Na+ Reabsorption and coupled K+ H+ secretion decreased |
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Mechanism of action of Spironolactone in treatment of Hirsutism? (=Hair growth in androgen-sensitive areas, like hairy balls) (also polycystic ovarian syndrome, acne)
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Spironolactone decreases ovarian androgen production and peripheral androgen activity
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Side effects of Thiazides?
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Hyperglycemia
Uric Acid Retention Inc. Cholesterol, LDL, Triglycerides Sulfonamide Derivatives = Hypersensitivity Rxns (Rash, Photosensitivity, exfoliative dermatitis) |
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Side effects of Loops?
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Dehydration, Volume depletion
Dec. Na+ Dec. K+ Dec. MG+ Dec. Ca2+ Hyperglycemia Cholesterol, LDL, triglycerides Sulfonamide Derivatives |
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Adverse Effects of Carbonic Anhydrase Inhibitors
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Hyperkalemic metabolic Acidosis
Dec. K+ Drowsiness, Confusion, Paresthesia Kidney Stones Sulfonamide derivatives = hypersensitivity rxns |
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Adverse Effects of K+ Sparring Diuretics?
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Dec. Na+
Inc. K+ TRIAMETERENE = Kidney stones SPRIONOLACTONE = Androgen effects, wacky periods, impotence, man-boobs |
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Side Effects of Osmotic Diuretics?
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Volume Depletion, = Inc. Na+
Volume Expansion = Dec. Na+ Pulmonary Edema Metabolic Acidosis |
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Why do Thiazides have a higher chance of developing Hyponatremia than Loops?
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Thiazides work in distal tubule
Loops work before that, in Loop of Henle. With Thiazides, there's less "chances" to recover Na+ (NOTE-I'm unsure if this is the correct answer..) |
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Ability of Ethacrynic Acid and Furosemide to cause Allergic Rxns and Ototoxicity?
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Furosemide = Allergic Rxns
Ethacrynic Acid = Ototoxicity (damage to ear) |
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Side Effects of Spironolactone vs. Eplerenone?
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Spironlactone = Menstrual Irregularities, Man-boobs (gynecomastia), Impotence
Eplerenone = no man-boobs, horray. (but the other two apply, menstrual irregularities and Impotence) |
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How does Mannitol (osmotic Diuretic) treat acute renal failure?
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Draws water from cells to extracellular fluid
=maintains urine volume protects kidneys from nephrotoxins by preventing their concentration in the tubular fluid |
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How does Mannitol (osmotic Diuretic) treat cerebral edema/ intraocular pressure?
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Water extracted out of Brain and Eye (b/c of increased osmotic pressure in plasma which draws water OUT)
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Mechanism by which mannitol causes volume depletion?
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Depletion: MUCH water in kidney tubule, not much Na+ = in regards to the CELL, its HypERnatremic (too much Na+) and HyPOvolemic b/c water kept in kidney
Water will leave cells and go into blood vessels |
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Mechanism by which Mannitol (=osmotic diuretic) causes volume Expansion?
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Cells = HyPOnatremic
Water from cells goes into blood to decrease the HypOnatremia |
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What are the sources of cholesterol?
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Food
Blood De Novo |
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Whats the fate of cholesterol in the Liver?
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Cholesterol is made from LDL and Mevalonate (Mevalonate is made from HMG CoA via HMG CoA Reductase)
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Cholesterol and what else are combined to make VLDL in the Liver?
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Cholesterol + TG
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As VLDL travels through the blood, it can eventually become?
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ILD, and then LDL, which can then re-enter the Liver
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Absorption of cholesterol from the GI tract occurs where and how?
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Small Intestine via Bile Acids
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What drugs up-regulate the LDL receptor on the Liver?
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Statins
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How do Statins up-regulate the LDL receptor on the liver?
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Inhibit the enzyme responsible for De Novo Synth. of Cholesterol (HMG CoA Reductase)
Dec. Conc. of Mevalonate = Dec. De Novo Synth of Chol. =Up-Regulation of LDL receptors =Inc. Clearance of LDL out of blood stream |
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How do Bile Acid binding resins dec. a patients cholesterol levels?
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Bile is made from chol. in liver
Bile Acid binding resins bind bile in small intestines Because they are anions, Bile Acid binding resins are NOT absorbed =prevents the liver from re-using any bile = Chol. excreted via excretion of the bile acid/bile complex =Livers need for bile is increased, thus it uses up more chol. to make bile (LDL receptors are up-regulated) |
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How do Cholesterol Absorption Inhibitors work (Ezetimibe)?
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Ezetimibe blocks the chol. up-take protein in the gut lumen, NPC1L1 (Niemann-Pick C1 Like1)
=Chol. is not up-taken =Dec. Chylomicrons made =Less chol. delivered to Liver =Dec. Liver Chol. stores =Up-regulate LDL receptors to help clear chol. (LDL) from blood |
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Why should most statins be taken before bed?
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Most statins ave short half lives
People don't eat while sleeping Liver still needs chol. Liver does max De Novo synth. during sleep Taking statin before bed means it will have max effect |
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Why should Bile Acid Binding Resins be taken before meals?
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Because that's when bile acids are present
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What are the side effects of statins?
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Progressive Muscle Weakness:
Myalgia --> Myositis --> Rhabdomyolysis |
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What are the side effects of Bile Acid Binding Resins?
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GI: Constipation, Nausea, Heart burn, Bloating, Abdominal Pain
Impaired Absorption of: DAK (Fat-soluble vitamins) and Ions (negatively charged anions) |
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What are the side effects of Niacin?
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Flushing, Warm, Itchy
GI: Nausea, Vomitting, Diarhea (leads to inc. histamine) Hyperglycemia (inc. glucose = inc. insulin resistance) Hyperuricemia (=inhibits tubular secretion of uric acid) Abnormal Liver Function Tests = Inc. Transaminase Activity leading to Hepatotoxicity |
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What are the side effects of Omega 3 Fatty Acids?
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Nausea
Smelly Burp (malodorous eructation) |
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Whats the rate-limiting step in cholesterol synthesis?
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HMG CoA --> Mevalonate
Drug thats that block this step by inhibiting HMG CoA Reductase are STATINS |
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What class of drugs blocks the rate-limiting step of Chol. synthesis?
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Statins
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How do Fibric Acid Derivatives lower TGs?
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Activates PPAR-delta
=inc. Extrahepatic Lipoprotein Lipase activity =Inc. VLDL catabolism/clearance =Less small, dense LDLs (=the bad LDL) and more Large buyant LDLs (= the good LDL) |
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How does Niacin Lower TGs?
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Inhibits GPR109A
=less Free Fatty Acids delivered to Liver for TG synth =Less small dense LDLs (=the bad LDL) AND less VLDL, LDL (b/c dec. assembly of ApoB containing Lipoproteins) OVERALL: Less small, dense LDL, more large, buyant LDL |
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How do Omega-3 Fatty Acids Lower TGs?
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Inhibit VLDL release from Liver
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Whats the cause of stable Angina?
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Atheroslerosis = obstruction = can't dilate = ISCHEMIA
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When does Stable angina occur?
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During EXERCISE = Inc. in O2 consumption but no inc. in blood flow
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Whats the cause of Prinzmetals angina?
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Vasospasm = dec. coronary blood flow
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When does Prinzmetals angina occur?
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Rest
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What factors contribute to Myocardial O2 Demand?
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Inc. HR
Inc. Contractility To Inc. ventricular wall tension: Inc. Preload Inc. Afterload |
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B Blockers are used ONLY for
a. Stable b. Prinzmentals |
Stable
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Why use B Blockers to treat pts. with Stable angina?
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Use in pts with recent MI to inc. survival
Prevents stroke in pts with Hypertension |
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What are the contraindications for using B Blockers to treat Stable angina?
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Unstable HF
AV Block Asthma Pheochromocytoma |
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Are B Blockers used Prophylactically or acutely to treat Stable angina?
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Prophylactically
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Use Nitrates to treat
a. Stable b. Prinzmetals? |
BOTH
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Use Nitrates
a. Prophylactically b. Acutely to treat either form of angina? |
BOTH: can be used prophylatically OR acutely to treat EITHER
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Use Ca2+ Channel Blockers
a. Prophylatically or b. Acutely to treat a. Stable b. Prinzmetals? |
Prophylactially
Can treat Either Stable or Prinzmetals |
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Use Ranolazine
a. Prophylactially b. Acutely to treat a. Stable b. Prinzmetals? |
Prophylactically
Only treats Stable |
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What channels are opened/activated during an action potential in a cardiac myocyte?
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Na+ influx = depolarizing current = activates Na+/Ca2+ Exchanger
= can lead to Ca+ Overload |
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Whats the recommended first line drug for the treatment of Stable angina?
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B-Blocker
why? Inc. Survival in pts with recent MI and prevent stroke and Heart Failure in pts. with Hypertension |
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How do B Blockers work to be effective in the treatment of Stable Angina?
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Block B1s on heart
=dec. HR =dec. contractility =dec. O2 Demand BP decreases Also involved: Kidney, Brain |
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Why are B Blockers NOT EFFECTIVE for Prinzmetals?
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If you Block B2s on vessels, vessels won't dilate = more O2 can't get to heart = Not effective for Prinzmetals
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Drugs that do what to O2 DEMAND are effective in treating STABLE angina?
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Dec. O2 demand
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Drugs that do what to O2 SUPPLY are effective in treating PRINZMETALS angina?
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Inc. O2 Supply
prInzmetalS = Inc. Supply Stable = Dec. Demand ("I hope our DD is Stable') |
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How does Nitroglycerin (and all the nitrates for that matter) treat Stable angina?
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High dose Nitrate
=Dilate ARTERIES Dec. PVR Dec. Afterload =Dec. O2 demand =Useful in stable Angina Dilate VEINS: =Inc. venous capacitance =Dec. Preload =Dec. Afterlaod =Dec. Wall stress =Dec. Coronary perfusion =Dec. O2 demand =Useful in stable angina |
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How do nitrates treat Prinzmetals angina?
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Dilate Coronary Resistance Arterioles
=Redistribute blood to Ischemic Areas =Relieve Vasospasm =Inc. O2 supply -Treat Prinzmetals |
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How do organic nitrates cause sm. m. relaxation (in vessels)?
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Organic Nitrate enters endothelial cell
= converted into NO = Diffuses over to sm. m. cell =Via cGMP, causes sm. m. relaxation |
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What form of Nitroglycerin (or Isosorbide Dinitrate) is used to treat Stable and Prinzmetals angina ACUTELY?
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sublingual or IV Nitroglycerin
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What different forms of Nitroglycerin are available to treat Stable and Prinzmetals angina Prophylactically?
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Oral
Transdermal Patch Ointment |
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What form of Isosorbide Dinitrate is available to treat Stable and Prinzmetals angina Prophylactically?
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Oral
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How do you prevent pts. from developing tolerance to Nitrates?
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Have a Nitrate-free interval each day, ie at night while asleep (meaning the drug only works for 12 hrs. or so)
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What are the side effects from vasodilatory action of Nitrates?
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Headache
Flushing Orthstatic Hypotension Dizziness Reflex Tachy |
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What are the side effects from vasodilatory action of Ca2+ Channel Blockers?
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NON-DHPs:
Sinus Brady AV Block Exacerbation of Heart Failure or Pulmonary Edema Dihydropyridines: Reflex Tachy ALL Ca2+ Channel Blockers: Constipation Dizziness Flushing Headache Peripheral Edema |
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What occurs when you combine a Nitrate plus any of the Phosphodiesterase-5 Inhibitors?
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Inc. in cGMP conc. and severe HypOtension
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How do DHP Ca2+ Channel Blockers treat stable angina?
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Block Ca2+ Channel on sm. m. cell in Artery
=Relaxation =Vasodilation =Dec. PVR (=Dec. Afterload, Dec. Wall Stress, Dec. O2 demand) |
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How do Non-DHP Ca2+ Channel Blockers treat Stable Angina?
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Dec. HR
=Dec. Contractility =Dec. O2 Demand Also: Dec. Afterload Dec. Wall Stress Dec. O2 demand |
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Whats the difference in DHPs and NON-DHPs in treatment of Stable and Prinzmetals angina?
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DHPs: Vasodilate = Reduce PVR
Non-DHPs: Reduce HR/Contractility |
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How do ANY of the Ca2+ Channel Blockers treat Prinzmetals?
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Dilate Epicardial Coronary Arteries
=Inc. O2 Supply =No more vasospasm |
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How does Ranolazine treat Ischemia in STABLE angina?
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Blocks late cardiac Na+ Current
=Ca2+ influx doesn't occur =Dec. myocardial O2 consumption |
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Whats the overall effect of Ranolazine in treatment of STABLE angina?
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Dec. freq. of anginal attacks
Inc. Exercise Duration |
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Whats the advantage of using Ranolazine in treatment of Stable Angina?
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It has no effect on HR and BP
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Whats one EKG abnormality that can occur with Ranolazine?
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It can increase the QT interval (Toursades des Pointes)
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What can happen to the QT Interval when Ranolazine is combined with Verpamil or Diltiazem?
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QT can be prolonged even longer that it would be with just Ranolazine itself
Why? Verpamil and Diltiazem are CYP3A inhibitors CYP3A breaks down Ranolazine =More Ranolazine around =More drug around =Inc. QT Interval |
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Can you give a Non-DHP CCB with a B Blocker?
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NO
Both will Dec. HR, and the added effect will be to decrease it too much |
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Can you give a DHP CCB with a B Blocker?
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YES
(=Best to use for Stable angina over Non DHP CCB) |
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Can you give Nitrates with B Blockers?
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YES
(B Blocker = 1st line for stable angina and Nitrates can fix the reflex tachy) |
