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CVS Pharmacology

Cardiovascular system pharmacology-Malik

What are the uncontrollable factors that increase the risk of hypertension? 1) Old Age (Especially those over 60) 2) Race (Africans are more likely to develop it as opposed to Hispanics)
What are the most recent recommendations of the Joint National Committee for blood pressure patients? *Over 60 Start medications at blood pressure of ≥150/90mmHg and treat to goal of < 150/90mm Hg
What are the most recent recommendations of the Joint National Committee for blood pressure patients? *Under 60 Start medications at blood pressure of ≥140/90mmHg and treat to goal of ≤ 140/90mm Hg
What are the most recent recommendations of the Joint National Committee for blood pressure patients? *Patients with diabetes or kidney disease regardless of age Start medications at blood pressure of ≥140/90mm Hg and treat to goal of <140/90mm Hg
Lifestyle modifications to reduce hypertension risk: Weight loss (10kg- 5-20 mmHg decrease) DASH diet (8-14 mmHg decrease) Dietary sodium reduction (2-8 mmHg decrease) Physical activity (4-9 mmHg decrease) Moderation of alcohol consumption (2-4 mmHg decrease)
What is the DASH diet? A carbohydrate-low, protein-low diet which mainly focuses on eating fibers
What is the function of a2 agonists? Inhibit the release of noradrenaline , which works on feedback inhibition, reducing the sympathetic outflow
Examples of a2 agonists: Methyldopa (best choice in case of pregnancy) Clonidine (best choice in case of renal failure)
Which drugs can deplete adrenaline and noradrenaline? Guanethidine Reserpine (not used any more)
How can we recognize B-blockers? They all end with the suffix (-lol)
Why do we give a1 agonists? To allow vasodilation to occur
Example of a1 agonists: Prazosin
Why do we give hypertensive patients diuretics? They increase excretion of water and reduce the blood volume
Example of diuretics: Thiazide
Function of Angiotensin Converting Enzyme inhibitors (ACE I) Inhibits the synthesis of Angiotensin II which is the strongest vasoconstrictor in the body
What is an example of renin inhibitors? Aliskiren
Action of Ca channel blockers: Reduce action potential; cause vasodilation
Why is increased NO an effective way to reduce hypertension? It causes vasodilation
Potassium channel modulators: Manipulate the concentration of potassium around the membrane
What are the categories of the 11 groups of hypertensive drugs? 4 sympathetic, 4 kidney related and 3 local mediators
Drugs which affect the vasomotor center: 1) Methyl dopa 2) Clonidine 3) Guanabenz 4) Guanfacine
Drugs which affect the sympathetic ganglia: Trimethaphan
Drugs which affect vascular smooth muscle: 1) Hydralazine 2) Minoxidil 3) Nitroprusside 4) Diazoxide 5) Verapamil (Ca channel blockers in general) 6) Fenoldopam Hunky Muscular Dudes Feel Very Nude
Drugs which affect angiotensin receptors of vessels: Losartan, Valsartan, Candesartan, Eprosartan, irbesartan, telmisartan, and olmesartan
Drugs which affect sympathetic nerve terminals 1) Guanethidine 2) Guandrel 3) Reserpine Rude Guys Get--> on my nerves
Main 5 groups of hypertensive drugs: 1) Diuretics 2) ACEIs 3) B-blockers 4) A1-blockers 5) Ca antagonists
When should we use combination therapy for BP patients? If your patient’s BP is 210/140
Reserpine can be used in combination with which 3 drugs? 1) a-blocker like prazosine 2) A2 agonist like clonidine 3) Vasodilators like dihydralazine and minoxidil Rudy loves Pretty Cute Ditzy Missies
What is the initial first-choice therapy for hypertension according to JNC 6 and 7? JNC 6: Diuretic or a beta-blocker JNC 7: Thiazide-type diuretics
According to JNC 8 what is the treatment for non-black patients? Thiazide, ACEI, ARB, or CCB
According to JNC 8 what is the treatment for black patients? Thiazide or CCB
For all patients with Chronic Kidney Disease (CKD); initial (or add-on) therapy for hypertension should include ACEI or ARB (for black and non-black patients)
3 groups of diuretics are used in the treatment of hypertension: 1- Thiazide diuretics : most commonly used 2- Potassium sparing diuretics 3- Loop diuretics
Mechanism of action of Thiazide diuretics: Decrease the blood pressure by depleting the body's Na stores -inhibition of Na+ reabsorption in the distal tubules of the kidneys . First 4 weeks of administration- patient's blood pressure will decrease by decreasing blood volume
In the 4 weeks after administration of diuretics, the patient will experience: Frequent urination
The highest efficacy in reduction of blood pressure by thiazide drugs is about 15 mmHg
This efficacy is considered: Low, so thiazides are used with other drugs
Postural hypotension is rarely observed except: In the elderly
The main site of action of thiazide diuretics is on the distal tubules
What percentage of the reabsorption of Na is inhibited? 3-5%
The main drug of choice of the treatment of hypertension with signs of edema Loop diuretics
Loop diuretics are associated with Hypovolemia and electrolyte imbalance ( hypocalcemia ,hypomagnesemia , hypokalemia )
The most important prototypes of thiazide diuretics are: 1- Chlorothiazide : given orally 1-2 times a day 2- Hydrochlorothiazide : 1-2 times a day
Thiazide is usually administered under low dose of 12.5-25 mg (or up to 50mg in extremes )
Low doses of thiazide exert as much antihypertensive effect: As higher doses
Side effects appear at which dosage of thiazides? Over 50mg
What are the side effects of thiazides? 1) Hypokalemia 2) Hyperglycemia : due to inhibition of K+ dependent insulin release 3) Hyperlipidemia : rise in total LDL level which increases the risk for strokes 4) Hyperuricemia due to drug-drug interaction between thiazide and uric acid
Inhibited excretion of uric acid causes it to accumulate in the body, resulting in gout. This side effect is really prominent in patients taking thiazide over: A long time (about 10 years) even under low doses
The prototype drug of loop diuretics is Furosemide commonly known as Lasix
Lasix must be dosed at least Twice daily
Lasix must be administered during the day or at lunch to avoid Nocturia
Adverse effect of loop diuretics is summarized in: 1) Ototoxicity especially with aminoglycosides 2) Hyperurecemia and hypocalcemia
ACE inhibitors are: The best drugs in the treatment of hypertension regarding the patients situation
ACEI drugs end with the suffix -pril
The main prototype drug of ACEIs is: Captopril
ACE inhibitors inhibit the enzymatic activity of angiotensin converting enzyme found in the lungs and this is going to produce the following actions : 1- Reduce the amount of angiotensin 2 by inhibiting the conversion of angiotensin 1 to angiotensin 2 2- Prevent the conversion of bradykinin to an inactive metabolite by ACE which is going to increase the amounts of bradykinin in the body
Angiotensin 2 has two important functions : 1) Potent vasoconstrictor 2) Stimulates the production of aldosterone from the adrenal cortex which stimulates the reabsorption of Na+ and water from kidney tubules
Inhibition of Angiotensin 2 causes: 1- Vasodilatation of vessels 2- Diuretic action by inhibiting the reabsorption of Na+ and water by kidney tubules
Side effects of ACEIs: 1) Dry cough in 10% of patients 2) Angioedema 3) Hyperkalemia 4) First-dose syncope
In those patients who develop dry cough we switch them into ARBs
Angioedema complications: Excessive vasodilatation and increased vascular permeability Rapid accumulation of fluid in the neck Fluid accumulation in the neck creates a huge risk for airway obstruction and suffocation which is a medical emergency
The only case when the hyperkalemia becomes significant is When we use spironolactone along with ACEI because spironolactone is an aldosterone antagonist
Therapeutic uses of ACEIs 1) Congestive heart failure in order to reduce the levels of angiotensin 2 which further damage the heart 2) Treatment of hypertension in patients with diabetes or chronic renal disease 3) Diabetic nephropathy
Why are ACEIs used in CHF? Angiotensin 2 increases myocardial force of contraction Patients with congestive heart failure have increased level of angiotensin 2 because of hypovolemia caused from the low pumping action of the heart
Why are ACEIs used in treatment of hypertension in patients with diabetes or chronic renal disease: Vasoconstriction of renal arterioles which rises intra glomerulus pressure and reduces glomerular filtration rate is caused by angiotensin 2
Angiotensin 2 receptor antagonists are used: as an alternative to ACEI and are mainly used if the patient can't tolerate the side effects of ACEI
Angiotensin 2 receptor blockers (ARB ) are drugs that end with the suffix -sartan
ARB main prototype is: Losartan
ARB have the same efficacy as ACEI and they have the same: Therapeutic uses and the same side effects EXCEPT dry cough and Angioedema because they don't increase bradykinin levels
ARB and ACEI are Teratogenic drugs Category X, never give to pregnant women
Alternative pathways of angiotensin 2 production other than ACE: 1- Chymase enzyme which converts angiotensin 1 to angiotensin 2 2- Nonrenin protease cathepsin t-PA which converts angiotensinogen to angiotensin 2 directly
Why do we use ARB drugs in this case? This alternative pathway can sometime overcome the inhibition of angiotensin 2 production by ACEI
In the case of ACEI and ARB, we only combine these two drugs because: We really don't want any angiotensin 2 to be produced at all
ACEIs are contraindicated in: 1) Pregnancy 2) Bilateral renal artery stenosis
Which drugs are recommended agents when the preferred first-line agents are contraindicated: Calcium channel blockers
Action of calcium: Calcium enters muscle cells through special channels and produce contractility in them
Mechanism of action of CCBs: CCBs block L-type channels and stop the inward movement of Ca into the cell They exert their hypotensive effect through their vasodilation effect on the vessels It will cause a negative inotropic and chronotropic activity on the heart
Chemical Classes of CCBs: 1- Diphenylalkylamines 2- Benzothiazepines 3- Dihydropyridines
Diphenylalkylamines are represented by: Verapamil
Action of Diphenylalkylamines Have no selectivity towards Ca channels wherever in the body; they block those in vessels and in the heart. They result in hypotension ( vasodilation effect) They produce both negative inotropic and chronotropic effect
Benzothiazepines represented by Diltiazem
Action of Benzothiazepines: Have less selectivity towards the heart that ranges between the 1st and 3rd classes and more selective within the vessels
Dihydropyridines represented by: Nifedipine Amlidopine
Action of Dihydropyridines: Selective within vessels and have no effect on heart channels
Coronary artery dilation is induced by which of these 3 drugs? All of them Can be used in Angina Pectoris
Peripheral artery dilation is induced by which of these 3 drugs? Nifedipine The greatest effect on the vessels and in cases of isolated HTN it’s the drug to be used
Which drugs cause negative inotropic effect? Nifedipine has only little effect on it unlike Varapamil and Diltiazem
Slowing AV conduction is done by which drug? Varapamil Decrease heart rate in addition to its negative inotropic effect. Contraindicated in bradychardic patient
Drug which causes greatest increase in cardiac output? Nifedipine Decreases peripheral resistance against the heart pumping Decreases the afterload and allows for greater cardiac output
Heart rate will increase at very low concentrations of nifedipine. This problem has been overcome by: 1) Designing a sustained release formula called a "one dose daily". Sustained release nifedipine is better than the regular 3-times-a-day nifedipine and avoids the peak and trough transition 2) A drug with a longer half-life
Which drug is used to overcome the problems? NORVASC A form of Amlodipine that has a very long half-life and produces little fluctuation in plasma drug concentration due to its sustained release formula and can be used in angina. These drugs are also one dose daily drugs
Uses of CCBs: 1) Verapamil and Diltiazem are used in arrhythmias because they have an effect on the heart 2) If a patient doesn’t have arrhythmias but has HTN use Nifedipine 3) Nifedipines can be combined with B-blockers
NWhich situations can we not use certain drugs in? In congestive heart failure, Verapamil and Diltiazem are contraindicated Contraindicated in drug with negative inotropic/chronotropic effects with them- we might end up with 2nd/3rd stage AV block Can’t combine them with beta blockers that affect SA AV
The most prominent side effects associated with CCBs are: 1- Headaches 2- Ankle swelling/edema 3- Constipation 4- Gingival hyperplasia
CCBs do not affect concentrations of plasma cholesterol or triglycerides or extracellular calcium hemostasis
Beta-adrenergic Blockers end with the suffix: -lol
B blockers can be which types? 1) Selective 2) Non selective and vasodilating 3) Non selective
Selective target: Beta 1 rather than 2
Non selective and vasodilating target: Beta 1, beta 2, and alpha 1
Non selective target: Beta 1 and 2
Examples of selective B-blockers: Metoprolol Acebutolol Atenolol Esmolol Aristocrats Eat Alligator Meat
Examples of non-selective and vasodilating B-blockers: Labetolol Carvedilol
Examples of non-selective B-blockers: Propanolol Penbutolol Pindolol Timolol Nadolol Sotalol
These drugs were previously used in the 4-drug regimen used to treat HTN. Why did they stop? Low efficacy
Their efficacy is at most 10 mmHg
Uses of B-blockers: Angina pectoris Atrial fibrillation Cardiac arrhythmia CHF Essential tremor Glaucoma Hypertension Migraine prophylaxis: to reduce the stress Mitral valve prolapse Pheochromocytoma with α-blocker Symptomatic control in anxiety & hyperthyroidism
Propranolol is : Non-selective (B1 and B2) Reduces cardiac output and renin release. BlockingB2however is not desirable because it causes bronchospasm Lipophilic, meaning it can cross blood brain barrier easily Drug of choice for prophylaxis against migraines
Atenolol& Metoprolol are: Cardioselective drugs Most widely used blockers in treatment of HTN (affect rennin release) and have no carbohydrate effect
Pindolol & acebutolol & penbutolol are : Partial agonists some sympathomimetic activity. They lower blood pressure by decreasing resistance and appear to depress cardiac output less than other blockers Use in patients with bradyarrythmias or peripheral vascular disease
Labetalol and carvidalol are: Totally nonselective; alpha 1, beta 1 and beta 2 blockers They cause vasodilation by blocking the alpha 1 receptors Useful in the management in pheochromocytoma and hypertensive emergencies Peripheral vascular disease
Characteristics of Esmolol: Rapid onset of action Short half-life 9-10 minutes (through constant I.V infusion). Good drug of choice In management of intra and postoperative hypertension Hypertensive emergencies when associated with tachycardia Vasodilators and muscle dilators
Why shouldn't you stop B-blockers suddenly? Sudden withdrawal may cause rebound hypertension
Why may it cause rebound hypertension? When we give beta-blockers for a long time, our bodies respond by upregulating the number of beta receptors so they become more sensitive toward adrenaline
Examples of selective a1 blockers: 1) Alfuzosin 2) Doxazosin 3) Prazosin 4) Terazosin Alpha Dogs Tread Proudly
Functions of a1 blockers: Alpha 1 receptors cause vasoconstriction Alpha 1 blockade causes vasodilation and reduces blood pressure
Are a1 blockers good drugs for hypertension? No
Then, why are they used? For management of hypertension in patients with prostatic hyperplasia Because they block alpha receptors on the prostate Naïve hypertensive patients, as well
Main side effects of a1 blockers: Hypotension First dose syncope
How is first dose syncope avoided? Start the drug with one-third the dose instead of the full dose
If the patient has prostatic hyperplasia but does not have hypertension then you use: alpha blockers selective for alpha 1-A which is only found on the prostate and not on blood vessels
Example of drug that only blocks alpha1-A and are used for normotensive patients with prostatic hyperplasia is: Silodosin
Examples of Alpha 2 receptor agonist: 1) Clonidine 2) Methyldopa
Function of a2 agonists: alpha 2 receptors cause feedback inhibition on the sympathetic system and noradrenalin release Alpha 2 agonists reduce sympathetic activity and decrease blood pressure
Clonidine is used to treat: Mild to moderate hypertension that has not responded adequately to treatment with diuretics alone
Why is Clonidine used to treat hypertension complicated with renal disease? Does not reduce renal blood flow, unlike ACEIs
Therefore in the cases of bilateral renal artery stenosis, we use: 1) Clonidine 2) CCBs
Difference between action of methyldopa and Clonidine: Clonidine lowers heart rate and cardiac output more than methyldopa
Withdrawal of clonidine after protracted use, particularly with high dosages (more than 1 mg/d), can result in: Life- threatening hypertensive crisis mediated by increased sympathetic nervous activity
After omitting one or two doses of the drug, patients exhibit which symptoms? Nervousness, Tachycardia Headache Sweating
If the patient stops the drug suddenly, this will over-activate α1 & α2. Which drug do we use to block these receptors? Labetalol
The most important thing you need to know about methydopa is: It is the drug of choice used in pregnant women with hypertension
Why is it used in pregnant women? It does not reduce cardiac output and perfusion to the baby
Methyldopa especially valuable in treating hypertension with Renal insufficiency
Before giving methyldopa to pregnant hypertensive women, we give: MgCl2
The most common side effect of methyldopa is: Sedation
Side effects of clonidine and methyldopa include: Dry mouth and nasal mucosa Sedation Hallucination Depression
What are some examples of vasodilators? 1) Fenoldopam 2) Nitroprusside 3) Hydralazine 4) Diazoxide 5) Minoxidil
What is the functions of these vasodilators? Smooth muscle relaxants Reflex stimulation of the heart resulting in increasing the myocardial contractibility, heart rate, and oxygen consumption Increase plasma renin concentration
Reflex stimulation of the heart can cause which unwanted effects? Prompt angina and myocardial Infarction in predisposed individuals
Increased plasma renin concentration causes: sodium and water retention
These unwanted effects can be blocked by combination with a diuretic and a beta blocker
How does Nitroprusside work? By release of nitric oxide
Nitroprusside is the drug of choice in which situation? Hypertensive emergency
Why is it the drug of choice? Because it has activity on BOTH veins and arteries, unlike vasodilators(only arterial)
If there is kidney injury, what should we use instead? And why? Fenoldopam, because Nitroprusside reduces kidney perfusion
What is Fenoldapam? D1 receptor agonist
Function of Hydralazine Smooth muscle relaxant Produces reflex stimulation of the heart Mainly by releasing NO and EDRF
When is Hydralazine used? To treat moderately severe hypertension, in combination with diuretics and beta-blockers
Hydralazine monotherapy is accepted method of controlling blood pressure in Pregnancy induced hypertension AFTER methyldopa
Side effects of Hydralazine: Arrhythmia Precipitation of angina Lupus-like syndrome can occur with high doses, but is reversible
What is a hypertensive emergency? A rare but life threatening condition Normal person: DBP is > 150 mm Hg with SBP > 210 Individuals with preexisting conditions: DBP of > 130 mm Hg
What are some examples of pre existing complications? Encephalopathy Cerebral hemorrhage Left ventricular failure Aortic stenosis
If BP is not reduced rapidly, what will occur? hypoperfusion of vital organs would be compromised
Drugs used for treatment of hypertensive emergency 1) Sodium nitropresside (onset 1-2 min), is the drug of choice is administered IV 2) Labetalol (a and b blocker), (onset 5-10 min) given IV bolus or infusion 3) Fenoldopam (onset 2-5 min), D1 receptor agonist also given as an IV infusion
Major limitation of Labetolol: Long half-life(3-6 hr) that prevents rapid titration
Created by: Ulaisl



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