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Hypertension 33
lewis HTN 33
Question | Answer |
---|---|
What is blood pressure determined by | Systemic vascular resistance and cardiac output |
What does abnormally high blood pressure lead to | excessive contraction of arteries, kidney disease, stroke, and heart attack |
What is cardiac output controlled by | Renin-angiotensin-aldosterone system and Naturitic peptides |
What is systemic vascular resistance controlled by | Vasocontrictors-Angiotensin, norepinephrine Vasodilators-prostaglandins |
What is pulse pressure | difference between SBP and DBP |
When is it increased | atherosclerosis |
When is it decreased | CHF and Hypovolemia |
What is Map and what does it measure | perfusion of organs must be above 60 |
What accounts for 90-95% of cases of HTN | Primary or essential |
When is HTN classified as Pre-HTN | 120-139 or 80-89 |
When is HTN classified as Stage 1 | 140-159 or 90-99 |
When is HTN classified as Stage 2 | greater than 160 or greater than 100 |
What are risk factor for Primary HTN | Age,African American, high sodium intake |
What does altered angiotensin mechanism cause | increased aldosterone and fluid retention |
What does stress and SNS mechanism cause | increased vasoconstriction, HR, and Renin release |
What does insulin resistance and hyperinsulinemia cause | stimulates SNS and vasodilator response |
What is blood pressure determined by | Systemic vascular resistance and cardiac output |
What does abnormally high blood pressure lead to | excessive contraction of arteries, kidney disease, stroke, and heart attack |
What is cardiac output controlled by | Renin-angiotensin-aldosterone system and Naturitic peptides |
What are urinalysis indications of renal disease | protein and hematuria |
What is systemic vascular resistance controlled by | Vasocontrictors-Angiotensin, norepinephrine Vasodilators-prostaglandins |
What serum or blood studies indicate HTN | serum electrolytes, glucose, creatnine, lipids, |
What is pulse pressure | difference between SBP and DBP |
What does ECG show in HTN | ischemic heart disease |
When is it increased | atherosclerosis |
What does echo show | LV hypertrophy |
When is it decreased | CHF and Hypovolemia |
What is Map and what does it measure | perfusion of organs must be above 60 |
What accounts for 90-95% of cases of HTN | Primary or essential |
When is HTN classified as Pre-HTN | 120-139 or 80-89 |
When is HTN classified as Stage 1 | 140-159 or 90-99 |
When is HTN classified as Stage 2 | greater than 160 or greater than 100 |
What are risk factor for Primary HTN | Age,African American, high sodium intake |
What does altered angiotensin mechanism cause | increased aldosterone and fluid retention |
What does stress and SNS mechanism cause | increased vasoconstriction, HR, and Renin release |
What does insulin resistance and hyperinsulinemia cause | stimulates SNS and vasodilator response |
What are symptoms of HTN | Fatigue, reduced activity tolerance, palpitations, angina, dyspnea |
What are complications of HTN | CAD, LVH, HF, kidney damage, PAD, and retinal damage |
What are urinalysis indications of renal disease | protein and hematuria |
What serum or blood studies indicate HTN | serum electrolytes, glucose, creatnine, lipids, |
What does ECG show in HTN | ischemic heart disease |
What does echo show | LV hypertrophy |
What does eye exam show | retinal hemmorhage, AV nicking, and papilldoma |
What eight loss is significant | 10-20 lbs show decrease in BP of 5-20 mmHg |
What exercise level is recommended | 30 min aerobic 3 times per week |
What is DASH diet plan | enphasizes fruits and vegetables, fat free milk products, whole grains, fish and poultry, beans,seeds and nuts |
What is the most important role of the nurse in HTN diagnosis | TEACHING |
Where do central adrenergic antagonist act | vasomotor Block SNS response |
Where do peripheral adrenergic antagosist act | Sympathetic ganglion to vasomotor center Block SNS response |
Where do Beta blockers act | Inhibit Renin release |
Where do ACE inhibitors act | block production of angiotensin I |
Where do angiotensin II blockers act | block angiotensin II from constriction blood vessels |
Where do diuretics act | decrease sodium absorption |
Where do calcium channel blockers, and direct arterial vasodilators act | block vasoconstriction |
What med is used to counteract the baroreceptor | bet blocker |
What med counteracts the concentrating effect of the kidneys | Ace inhibitor, ARB, or aldosterone inhibitor |
What symptoms are often the reason for noncompliance with cardiac meds | Orthostatic hypotension, sexual dysfunction,dry mouth, and frequent urination |
What is the result of diruetics | decrease blood volume, preload, cardiac output, and BP |
What are 4 types of diuretics and where do they act | Loop-loop of henle Thiazide-proximal distal renal tubule Potassium sparing-distal renal tubule and collecting duct Osmotic-creates osmotic force in the lumen of the nephron (proximal convoluted tubule |
Which diuretic is used for massive and quick diuresis and/or renal impairment | Loop Diuretics |
Which diuretics are only PO | Thiazides |
Which diuretics can increase glucose | Loop and Thiazides |
Which diuretics cause skin reactions | thiazide and loop |
Which diuretics can't be given with Sulfa allergy | Loops |
Which diuretics are dosed daily | Thiazide and potassium sparing |
Which diuretics are dosed twice daily | loop |
What are dietary sources of potassium | bananas,orange or yellow fruits and vegetables, beans, potato |
What teaching is needed with diuretics | hyperglycemia, NSAIDs reduce effectiveness and gout flares |
What labs are monitored with diuretics | k+ and Mag |
What are common diuretics | Lasix, HCTZ, spiolactone,diuril,mannitol |
What are central acting adrenergic inhibitors | Catapres,aldomet,wytensin |
What are peripheral acting adrenergic inhibitors | Reserpine,beDta blockers |
How do beta blockers work | block catecholamine production which decreases HR and decreases renin |
Why do you have to wean off BB | in diabetics it blunts hypoglcemia symptoms |
What are common beta blockers | Tenormin, lopressor, toprol and olol's |
What does hydralazine do | dilate arterioles, decrease afterload, and increase CO |
What does Nitro do | dilates veins, decreases preload, CO, |
What are adverse effects of vasodilators | postural hypotension, reflex tachycardia, and increased blood voulume |
What is drug of choice in hypertensive crisis | Nipride-IV, immediate onset |
What NI must be done when administering Nipride | BP every minute |
What are adverse effects of Nipride | extreme hypotension, cyanide posioning, and thiocyanate toxicity |
What is Angiotensin II | Neurohormone that promotes sodium and water retention, stimulates SNS, and promotes atherosclerosis |
What do ACE inhibitors do | block the formation of angiotensin II |
What are NI for Ace inhibitors or ARB | Monitor electrolytes, creatnine, fluid status, and blood pressure |
What is a common side effect of ACE inhibitors or ARB | dry hacking cough |
What teaching for ACE inhibitors or ARB | avoid alcohol and salt subtitutes |
What are Angiotensin Receptor Blocker (ARB) | Block the receptor site of angiotensin II |
What are ARB's | Benicar, coozar, Diovan |
What are drug interactions for ACE inhibitors or ARB | potassium supplements, potassium sparing diuretics, and Lithium |
What is the action of CCB | dilation of arterioles, decreased HR and afterload |
What are S/E of CCB | Bradycardia, headache |
What is a food interaction with CCB | grapefruit juice |
What are some of the reasons for hypertension resistant HTN | Corticosteroids, licorice, erythropoetin, oral contraceptives, excessive alcohol intake |
HTN in older persons | wide gap between korotkoff and subsequent beats white coat hypertension |
What consistutes a Hypertensive crisis or malignant HTN | Severe increase in BP Evidence of acute target organ damage |
How is malignant HTN treated | Direct Vasodilators-titrated to MAP monitor cardiac and renal function Neuro checks Bring BP down gradually investigate cause Teaching |