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88 Cards in this Set
- Front
- Back
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What are "Sartan" drugs? Name two of them.
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They are Angiotensin I Receptor blockers
1) Valsartan 2) Lolsartan |
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What are "pril" drugs? Name them
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They are ACE inhibitor.
1) Captopril 2) Enalapril 3) Lisinopril |
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T/F: Na+ loss causes increase response of arterioles to norepinephrin?
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False. Na+ loss will cause decrease response
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With sodium loss, what happens to arteriol resistance? why?
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Decrease,because arterioles are less responsive to the vasoconstrictive effect of NE.
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Which selecting a diuretic to treat HTN, which one do you choose first?
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Thiazide
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Is thiazide alone good enough for stage 1 HTN?
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YEs
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When is a loop diuretic used for HTN? what route?
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When there's HTN and renal insufficiency.
Also use IV for Hypertensive emergency |
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Are K+ drugs used alone? if not with what other drugs?
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No. use with loop or diuretic
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What are the advantages of diuretics for HTN?
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Frequently, adequately effective by themselves
Combat Na+ retention (many anti-hypertensives promote Na+ retention, particularly the vasodilators and alpha-blockers) Potentiate effects of other antihypertensive drugs Elderly respond well Minimal hypotension with thiazides Loop diuretics are effective even in the presence of a high degree of renal failure |
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True/False: Caucasians respond better to thiazide than Black
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False. Blacks respond better
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Do thiazides cause hyperuricemia, how about gout?
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THey may cause hyperuricemia but gout is uncommon in used in modest doage
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Do thiazides cause significant change in lipid profile?
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It does change lipid profile but NOT significantly.
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What is the biggest disadvantage of thiazides? How do you reduce it when using this drug?
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Hypokalemia.
-Add K+ supplement -Add potassium sparing diuretic |
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ARB(s) block which angiotensin II receptor?
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AT1
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AT1 mediates what effects?
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Constriction of vascular smooth muscle
Release of aldosterone CNS activation of sympathetic discharge Enhanced responsiveness of vascular smooth muscle to sympathetic activation |
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ARB and ACEI, which has worse side effects?
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ACEI
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What accounts for the side effects caused by ACEI?
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The ACE also break down bradykinin. ACEI blocks this process and bradykinin builds up giving the side effects.
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What are the common side effects of ACEI?
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Cough
Angioedema |
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How does ARB blunt the hypokalemia caused by diureticss?
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It decreases the release aldosterone
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ARB can be used for pregnancy?
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NO. It's ok to take before pregnancy but not during pregnancy. It's toxic to the developing kidney.
GIVE ACEI instead if pregnant |
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What is one benifit of ACHI that ARB doesn't have
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ACEI improve mortality in CHF! ARB doesn't
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What are the mechanims of ACEI?
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Block Angiotensin I conversion into angiotensin II. --> decrease release of aldosterone
Decrease breakdown of bradykinin(side effect) Decrease overly active SNS All lead to dec preload and dec after load --> dec BP. |
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What is Kininase II?
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Same enzyme as ACE
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What are the effects of bradykinin
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Tissue irritant
Vasodilator -A candidate for why ACE-I drugs inhibit cardiac hypertrophy |
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T/F ACEI inhibits cardiac hypertrophy?
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True
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Angiotensinogen is to Renin as Kininogen is to _______?
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Kalikrein - converts kininogen to bradykinin
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What are the uses of "pril" drug in hypertension?
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Essential hypertension
Efficacious and relatively minimal side-effects High plasma renin Diabetes mellitus (preferred anti-HTN -- reduces proteinuria) Renal insufficiency CHF (preferred anti-HTN – decreases mortality) |
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What is the best drug to treat HTN in CHF patient?
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an ACEI--> decreases mortality
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Is there any correlation bt high plasma renin and Anti-HTN reponse to "pril" drug?
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No clear correlation between plasma renin and anti-HTN response to prils
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T/F Diabetes increase Pgc and causes glomerular hypertrophy.
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True
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Which drug is contraindicated in Diabetic pt with HTN? why?
Which drug is prefered? |
ARB -it dialates afferent arteriole causing further increase in Pgc --> glomerular hypertrophy.
ACEI --> dilate EFFERENT arteriole --> dec Pgc |
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Two most common cause of Renal insufficiency.
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Diabetic glomerulosclerosis
Hypertensive nephrosclerosis |
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Why are "pril" drugs prefered for CHF pts w/ HTN?
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90% of CHF pts have hypertension
Prils slow the rate of cardiac remodelling, resulting in improved mortality. Use of prils in CHF is discussed in detail in Cardio2. Note: ARBs do not share this effect |
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Advantages of ACE-I?
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Predictable, typically mild, dose-related side-effects
Blunt the hypokalemia caused by diuretics Decrease aldosterone release Little orthostatic hypotension or SNS activation No effect on triglycerides, cholesterol |
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Disadvantages of ACE-I
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Cough (see below)
Initial dose hypotension, esp. if hypovolemic Skin rashes/neutropenia (is captopril worse than others?) Acute renal failure in renal artery stenosis (see below) Angioedema Can be life threatening African-Americans and elderly may not respond well Contraindicated in 2nd & 3rd trimester pregnancy Fetal malformations, hypotension and renal failure Hyperkalemia possible (esp. if combined with other drugs that increase K) |
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Why is ACE-I bad for renal artery stenosis pts?
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ACE-I will dilate efferent arteriole causing further decrease in Pglomerulus--> dec GFR
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Name all the b-blockers.
(MAAP mnemonic) |
Metoprolol - b1 short acting
Atenolol - b1 Acebutolol - b1 partial agonist Propanolol - b1, b2 |
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These drugs end in "osin". Name them
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Alpha 1 selective blocker
Doxazosin Prazosin - (short acting) Terazosin "Don't Play Tetris" |
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Phenoxybenzamine is what type of drug?
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Irreversible Alpha blocker
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Name the CNS active agents.
Hint (CA) |
Clonidine
Alpha-methyl DOPA |
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Name the sympatholytics
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Reserpine
Guanithidine |
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b1 stimulation will cause what?
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^ HR
^ cardiac contractility ^ AV node conduction ^ electrical excitability of the heart ^ renin release in the kidney |
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b2 stimulation will cause
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^ bronchodilation
^ arteriole dilation ^ relaxation of the uterus ^ glycogenolysis ^ insulin release |
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What does b-blocker do to the heart?
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Decrease heart rate.
In the absence of reflexes, these effects should lead to BP. In reality, if CO falls, sympathetic tone is increased. In the presence of a beta-blocker sympathetic activation doesn’t do much to cardiac function; however, through alpha-receptors, peripheral resistance increases |
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T/F: Renin release is controlled by Na+ concentration by a cAMP mechanism.
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True
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T/F b1 also increase cAMP production so also partly control renin release.
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True
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T/F B1 blocker is likely to block renin release and helps to decrease blood pressure
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true
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What is propanolol? is it selective or non selective
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It's a non selective b blocker
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What is metoprolol.
What limits its utilitiy |
It's a b1 selective blocker.
It has a short half life. |
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To what patients is metoprolol preferred?
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In Pts w/:
Asthmatic Diabetes Peripheral vascular dz |
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What is atenolol. How is it different from metoprolol
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B1 selective blocker.
It has a longer halflife |
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Which drug has "intrinsic sympathomemimetic activity" and acts as a partial agonist.
The partial agonist effects act on which receptors? So how is it used? |
Acebutolol.
Partial agonist at B2 receptors Used as a vasodiating b blocker due to its effect on b2 receptors. |
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What are the side effects of b blocker?
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-AV block
-Severe bradycardia -Bronchospasm and respiratory distress in asthma, COPD -Exaceration of CHF and pulmonary edema -Delay of recovery from hypoglycemia -Hypertriglyceridemia, decreased HDL cholesterol -Impotence, depression |
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How does alpha-1 antagonist (blocker) work?
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-Block post synaptic alpha1 receptors
-Decrease sympathetic nervous system effect on vasculature -Decrease preload and afterload --> decrease BP |
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Prazosin
Doxazosin Terazosin which is short acting? |
Prazosin
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How are Alpha-1 antagonists used?
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They are not first line drugs.
Used w/ other drugs classes Useful for benign prostatif hypertrophy (BPH) |
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So what are the advantages of alpha-1 antagonist?
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Don't change serum lipid
Useful for BPH -Increase risk for aggravity or causing CHF -First dose hypotension (severe) -Nasal congestion -Salt and water retention (need diuretic) -Orthostatic hypotension including chronic fatigue, light headedness |
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Clonidine and methyldopa are what kind of agents again?
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CNS active agents
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Oh what receptor do clonidine and methyldopa work?
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ALpha 2 (agonist)
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What does Alpha 2 receptor do in the periphery? In the brain?
Where is the main site of effect for HTN? |
Autoreceptor on norepinephrine nerve terminals. THey decrease the release of NE when stimulated.
In brain it decrease responsiveness to sympathetic system (regulate sympathetic nerve activity) Brain stem |
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What is clonidine not the first line drug?
When is it ok to use it? What do you prescribe along with clonidine, why? How is it useful in opoid withdrawal? |
It causes withdraw hypertension
Useful in emergency hypertensive states in those with large sympathetic component A diuretic, to reduce Na+ retention It calms the sympathetic components of the withdrawal |
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What are the side effects of clonidine?
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CNS: drowsiness, drymouth, depression
Rebound HTN- severe hypertensive crisis (tested on boards) |
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If a women is hypertensive before pregnancy, what is the best drug to give during pregnancy? why?
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Methyldopa
Don't know why |
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What are two sympatholytic agents?
what do they do Are they still used clinically? |
Reserpine
Guanethidine Block vesicular uptake and storage of NE (and othe monoamines)--> depletion of monoamines throughout the body including the CNS. Not really |
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What are side effects of reserpine? when do you not use it?
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Depression, nightmares.
Nasal stuffiness Unopposed parasympathetic activity: miosis, bradycardia, aggravation of ulcers, diarhea Fluid retention Don't use if pt has history of depression |
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What is the mechanism of guanethidine?
Does it get into the CNS? Do they cause water and salt retention? |
Inh release of NE from sympathetic nerves and depletes NE from storage granules. Must be taken up via NE reuptake pump.
NO- it is highly polar Yes=give with diuretic |
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Ca+ channel blockers block which type of calcium channels?
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L type calcium channels
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T/F: "pine" drugs are preferred over verapamil and diltiazem for hypertension.
Which are cardio selective, vascular selective? |
True.
Diltiazem and verapamil are cardio selective, "pines" are vascular selective |
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Name the arterial dilators.
Name the arteriovenodilators |
hydralazine, minoxidil, diazoxide
Nitroprusside |
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Name the drugs used in HTN crisis.
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Nitroprusside
Nitroglycerine Hydralazine Labetalol Fenoldopam |
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contrast nifedipine to verapamil/diltiazem
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Nifedipine is vascular selective. "pine" drugs
-Nifedipine decrease Ca++ influx and results in smooth muscle relaxation -diltiazem/verapamil decreae cardiac contractility and cardiac output |
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What activates myosin in smooth muscle?
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Myosin light chain kinase.
Calcium activates calmodulin which actives the MLCK. Block Ca++ and this won't happen |
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How does NO promote smooth muscle relaxation
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Cyclic GMP dephosphorylates myosine. NO activates guanylyl cyclase which promotes formation of cGMP from GTP--> smooth muscle relaxation
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What are the "non cardiac" side effects of calcium blockers?
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Headache
Postural dzness * Flushing * Peripheral edema * "pine" major side effects Constipation Other GI problems Paresthiasis |
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What are two uses of Ca++ blocker?
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HTN, Angina
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Do Ca++ blockers have more or less side effects than ACE-I or ARB
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They have more side effects
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When is Ca++ more useful?
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They efficacious for isolated systolic HTN
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Verapamil and diltiazem are not used with what drugs, why?
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b blockers. Might cause heart block
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What is a significant side effect of vasodilators?
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Orthostatic Hypotension
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Hydralazine, diazoxide, and minoxidil are what drugs again? mechanism?
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Arterial vasodilators.
They dilate arterioles==> > peripheral resistence==> compensatory response ==> < sympethetic nervous system | < renin/Angiotensin system |
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What is the consequence of SNS and RAS activation caused by arterial vasodilators?
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-Increase SNS w/ arterial block but venous constriction ==> increase HR and CO
-Na and H20 retention => edema - < myocardial O2 consumption(angina) - < myocardial work (CHF likely) - hypotension side effects (palpitation, headache, flush) |
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Arterial dilators mustbe combined w/ what two drugs?
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b blocker and diuretic
Becareful when using it in CHF and angina |
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1)what is hydralazine used for?
2) What are side effects? |
1)severe HTN, pregnancy
2)tachyphylaxis, hirsutism, headache, palpitation, GI, SLE (reversible) |
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Minoxidil is indicated in? used w/ what?
Side effects? |
Severe hypertension, used with b blocker and diuretic
SNS activation, angina, edema, HIRSUTISM |
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What is fenodolpam?
When is it used? route of admission) |
arteriodilator, D1 agonist (maintains renal blood flow)
Hypertensive emergency (given IV) |
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What is nitroprusside again?
What is the mechanism? Does it increase or decrease myocardial o2 demand |
Venoarteriodilator (dilates arteries and mostly veins)
NO formation ->increase cGMP -->relaxation Decrease |
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When is nitroprusside used?
What are the toxicity? |
HTN emergencies (IV) --must monitor pressure
CHF w/ hydralazine Surgery (for controlled hypotension) Tox: Excess hypotension, cyanide/thiocyanate toxicity |
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What happens in rapid decrease in BP?
AVOID THIS |
Cerebral or cardiac hypoperfusion
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