Patho Test 2 Hypertension/CCB/Vasodilators Review

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Categories of BP in adults
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Categories of BP in adults
Normal: <120 and <80
Elevated: 120-129 and <80
Stage 1: 130-139 or 80-89
Stage 2: >/equal to 140 or >/or equal to 90
-Go with the worst category if both levels are high
For black population
use a thiazide diuretic or Ca channel blocker in the general black population
Primary (essential) hypertension
No identifiable cause
Chronic, progressive disorder
Population: older adults, African Americans, postmenopausal women
Treated but not cured (lifelong condition)
-Risk= Lifestyle, diet, age, gender (higher in males), obesity
secondary hypertension
high blood pressure caused by the effects of another disease
-Identifiable primary cause
-Possible to treat the cause directly
-Some can be cured
Causes of Primary hypertension
-Caused by water and Na retention
-Insulin resistance and hyperinsulinemia
--Increase in insulin -> Stimulates SNS -> Increase BP / Impairs nitric oxide-medicated vasodilation also in increasing BP
-Altered renin-angiotensin mechanism: High plasma renin activity
-Endothelial cell dysfunction
consequences of hypertension
Heart disease
Myocardial infarction (MI)
Heart failure
Angina pectoris
Kidney disease
Stroke (CVA)
Patho of complicated hypertension
-Chronic hypertensive damage to the walls of systemic blood vessels
-Smooth muscle cells undergo hypertrophy and hyperplasia with fibrosis of the tunica intima and media
-Affects heart, kidneys, retina (END ORGAN DAMAGE)

-Can result in transient ischemic attack/stroke, cerebral thrombosis, aneurysm, dementia
Sodium restoration level
2300 mg/day
Arterial pressure =
cardiac output x peripheral resistance (systemic vascular resistance)
Sympathetic Baroreceptor Reflex
In carotid bodies and aortic arch
-When they sense low BP the send signals to increase RAAS and Aldosterone
capacitance vesselsthe term for veins because they have the ability to stretch. they have a large diameter and are more distensible to hold more blood. this reduces stress on the heart.Sympatholytics (antiadrenergic drugs)-Beta-adrenergenic blockers (-lol) -Alpha 1 blockers -Alpha/Beta blockers: Carvedilol and labetalol -Direct-acting vasodilators: Hydralazine and minoxidil -Calcium channel blockers -Drugs that suppress RAAS --ACE inhibitors (-prils) --AngioII receptor blockers (-sartan) --Aldosterone antagonist (-one) -Direct renin inhibitors: Type 2 diabetes mellitus precautions (should not be on ACE or ARBs at the same time bc will drop BP to much)Severe increase in BP (hypertensive crisis)Diastolic that exceed 120 mmHg -Often occurs in patient with a history of HTN who have failed to comply with medications or who have been under medicatedHypertensive crisis clinical manifestation-Hypertensive emergency= Evidence of acute END organ damage: --Hypertensive encephalopathy (severe HA, N/V, Sz, confusion, and coma) --Cerebral hemorrhage --Acute renal failure --Myocardial infarction -Heart failure with pulmonary edemaDrugs for Hypertensive emergenciesSodium nitroprusside (Nipride) Labetalol (Trandate) -Both IV onlyWhat are the elderly at risk for?Orthostatic hypotension (drop when lay to stand) so they need to get up slowly -This is because they have varying degrees of impaired baroreceptors relax mechanismsAngiotensin-converting enzyme (ACE) inhibitors: MOA-reducing levels of angiotensin II -increasing levels of bradykinin by blocking kinase II (vasodilation)Decreased levels of Angiotensin II causes-vasodilation -decreased blood volume -decreased cardiac and vascular remodeling -potassium retention -fetal injuryIncreased levels of bradykinin results in:-vasodilation -cough (#1 reason ppl stop taking this ACE inhibitor) -angioedemaAngiotensin-Converting Enzyme Inhibitors: Therapeutic uses-hypertension -prevention of MI, stroke, and death in patients at high cardiovascular risk -diabetic and non diabetic nephropathy (when kidneys show signs of bad renal functioning)ACE Inhibitors: Adverse effects-first dose hypotension -cough -angioedema -hyperkalemia -renal failureACE Inhibitors: Drug interactions-diuretics -antihypertensive agents -drugs that raise potassium levels (life threatening arrhythmias) -lithium -non-steroidal anti-inflammatory drugsACE prep, dosage, and admin-except for enalaprit, all ACE inhibitors are administered orally -except for captopril and moexipril, all formulations may be administered without regard to meals. these two have to be given on an empty stomach before meals or 2 hrs afterARBs MOA-blocks angiotensin II -cause dilation of arterioles and veins -prevent angiotensin II from inducing pathologic changes in cardiac structure -reduce excretion of potassium -increase renal excretion of sodium and water -does not inhibit kinase II, so does not increase levels of bradykinin. Therefore, the pt is less likely to have coughARB Adverse effects-angioedema (low risk) -fetal harm -renal failure -possibility of promoting cancer -additive effects with antihypertensivesAldosterone AntagonistsSpironolactone -blocks aldosterone -binds with receptors for other steroid hormonesAldosterone Antagonists adverse effects-hyperkalemia*** -menstrual irregularities -impotence -deepening of the voiceCardiac Calcium Channels OverviewBeta agonist (Epi and NE) act on B receptor cause Ca channels to open causing -Increase HR -Increase Conduction velocity -Increase force of contraction (increase heart workload)Calcium Channel Blockers (CCB) Used to treat-Hypertension -Angina -Cardiac dysrhythmias (only CCB can do) -Drop in BP causes stimulation of baroreceptors, this increases sympathetic response but bc Ca are blocked the net effect is decrease HR and BPVerapamil (Phenylalanine) and Diltiazem (Benzothiazepine)CCB agents that act on arterioles (vascular smooth muscle) and the heart -Phen and Benzo= Can treat cardiac arrhythmiasDihydropyridines (nifedipine) (end in -pine)CCB agent that act mainly on arterioles (vascular smooth muscle) (only cause vasodilation and can not treat arrhythmias)Calcium channel blocked=vasodilationCCB therapeutic doses-Selective on peripheral arterioles and arteries and arterioles of the heart -No significant effect on veinsDirect hemodynamic effects of CCB1. Blockade at peripheral arterioles --Reduces arterial pressure 2. Blockade at arteries and arterioles of heart --Increases coronary circulation** 3. Blockade of SA node --Reduces heat rate 4. Blockade in the myocardium, --Decreases force of contraction --Decrease workloadVerapamil therapeutic usesAngina pectoris Essential hypertension (first line agent) Cardiac dysrhythmias*** MigraineVerapamil adverse effects-Decreased HR to much -Edema of ankles and feet -Most common complaint= Constipation caused by CCB in intestines (especially severe for the elderly) -Treatment: --Ambulate, Increase fluids (if not contraindicated), Increase fiberVerapamil drug/food interactions-Digoxin and beta blockers (both slow HR) -Grapefruit (get toxic) Toxicity= Hypotension Bradycardia Ventricular tachydysrhythmiasIV verapamil for dysrhythmias can causesevere cardiovascular effects. -So don't give ti fast and must put on monitorDiltiazem Actions and Uses-Blocks calcium channels in the heart and bloods vessels (similar to verapamil) -Lowers BP (arteriole dilation)diltiazem therapeutic usesAngina pectoris Hypertension Cardiac dysrhythmias (used to slow HR) --Atrial flutter, atrial fibrillation, paroxysmal tachycardiaDiltiazem adverse effects-Similar to verapamil, except for less constipation -Exacerbates bradycardia, sick sinus syndrome, HF, second or third degree heart block -Headache -Dizziness -Edema of the ankles and feetDiltiazem interactionsBeta-adrengic Blockers may increase digoxin* levelsNifedipine-Agents that act mainly on Vascular Smooth muscle -Does not effect HR -Significant blockade of calcium in blood vessel -Minimal blockade of calcium channels in the heartWhy can Nifedipine not be used to treat tachydysrhythmias?Do not effect conduction system of the heartNifedipine direct effects-Limited to blockade of Ca channels in vascular smooth muscle (VSM) -So only cause vasodilation, and lower arterial pressureNifedipine indirect effects-lowered BP activates baroreceptor reflex, which cause sympathetic stimulation of heart -primarily w/ fast acting vs. sustain release (Want to give pt. long acting)nifedipine therapeutic uses-Angina pectoris -Hypertension -Investigational basis to relieve migraine headache and to suppress preterm laborNifedipine adverse effects-Peripheral edema -Gingival hyperplasia -Reflex tachycardia -Rapid acting nifedipine (not sustained) --Has been associated with increased mortality in patients with MI and unstable angina --No cause and effect relationships establishedreflex tachycardia-temporary increase in heart rate that occurs when blood pressure falls (from Nifedipine) -Increased cardiac O2 demand -Can increase pain for angina patients -Can prevent by combining with a beta blockerBeta blockers decrease* the adverse effects of Nifedipine, butcan intensify* the adverse cardiac effects of verapamil and diltiazenHemodynamic Effects-Drugs that dilate resistance vessels (arterioles) cause a decrease in cardiac afterload -Drugs that dilate capacitance vessels (veins) reduce the force with which blood is returned to the heart, thus reducing preloadTherapeutic uses of vasodilators-Essential hypertension -Hypertensive crisis -Heart failureAdverse effects of vasodilators-Postural hypotension -Reflex tachycardia= When BP drops the baroreceptors sense it and send a message to SNS to increase BP and can cause tachycardia -Pooling of blood volumeHydralazine (Apresoline) MOA-Selective dilation of arterioles, no effect on veins -HR increasesHydralazine (Apresoline) adverse effectsReflex tachycardia Systemic lupus erythematosus-like syndrome Headache, dizziness, weakness, and fatigueHydralazine (Apresoline) drug interactions-Other antihypertensive agents (make BP to low) -Avoid excessive hypotension** -Combined with beta blocker to protect against reflex tachycardia and diuretics to prevent sodium and water retention and expansion of blood volumeNitroprusside (Nipride)-Fast acting antihypertensive agent -Causes venous and arteriolar dilation -Administration: IV infusion -Onset: immediate (BP returns to pretreatment level in minutes when stopped) (1/2 life is very short) -Therapeutic uses: --Used for hypertensive emergencies -Adverse effects? --Excessive hypotension --Cyanide poisoning (very excessive dosage)