UNIT 4 Hypertension Flashcards

(46 cards)

1
Q

ThiaSystolic Blood Pressure

A

contraction phase; highest amount of pressure

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1
Q

Hypertension

A

increased pressure on arterial walls;
“silent killer”;
asymptomatic;
may lead to other complications: heart failure, cerebral hemorrhage - stroke, kidney failure, MI

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2
Q

Diastolic Pressure

A

relaxation phase; lowest amount of pressure

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3
Q

Normal Blood Pressure

A

Systolic: less than 120
Diastolic: less than 80

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4
Q

Two Types of Hypertension

A

Primary Hypertension/Essential Hypertension (most common)
Secondary Hypertension (a medical condition present)

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5
Q

Primary Hypertension/Essential Hypertension

A

most common;
cause is unknown;
risk factors: smoking, obesity, racial predisposition, family history, stress, sedentary lifestyle, high-fat diet

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6
Q

Seondary Hypertension

A

a medical condition present;
pregnancy, renal disease, drug-induces

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7
Q

Risk Factors for Hypertension

A

Stress, age: over 60, family history, gender: men and postmenopausal women, increased cholesterol, high sodium diet, sedentary lifestyles, smoking, diabetes

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8
Q

Baroreceptors

A

located in the internal walls of carotid arteries and the aortic arch and other vessels in the body sense the change in BP;
sensors that control BP

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9
Q

Blood Pressure Control

A

if BP decreases, baroreceptors sense the change; EPI and NE are released to constrict smooth muscle of the vessels; this increases BP

if BP increases, baroreceptors sense the change; vagus nerve is stimulated; HR, FOC, CO decrease; vasodilation occurs; this decreases BP

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10
Q

Renin-Angiotensin-Aldosterone System (RAAS)

A

maintains normal BP and blood volume
Angiotensin I is secreted by the kidney (is a vasoconstrictor; increases TPR and BP)
ACE is secreted by the liver
Angiotensin II is formed in the plasma; works on adrenal cortex and is a potent vasoconstrictor
Aldosterone is released by the adrenal cortex

Aldosterone works on the kidneys to conserve Na+ and H2O; this increases blood volume and BP

Angiotensin II stimulates the release of Antidiuretic hormone from the posterior lobe of the pituitary gland;
this stimulates the thirst center (higher fluid intake -> higher volume of blood)
this hormone also stimulates the kidney to pull water from the urine back into blood (higher blood volume); it is also a potent vasoconstrictor

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11
Q

Kidney

A

filter the blood, maintain water and electrolyte balance, maintains the acid-base balance, secretes urine, allows the blood to gain the necessary nutrients (water and electrolytes), is composed of nephrons

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12
Q

Nephron

A

a structure of the kidney;
consists of a glomerulus, a proximal collecting tubule, a loop of Henle, a distal convoluted tubule and a collecting duct

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13
Q

Rules with ions in kidneys

A

If Na+ goes out, so does H2O
If Na+ goes in, K+ comes out
If H+ goes in, Na+ goes out
If Cl- goes in, Na+ goes out

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14
Q

Urine Formation

A

Filtration - H2O, salts, sugars, acids, drugs, nitrogenous wastes leave the blood; large particles stay (proteins and blood cells)

Tubular Reabsorption - body retains H2O, salts, sugars

Tubular Secretion - substances from blood go back into the renal tubule (drugs, acids, nitrogenous wastes, salts and H2O) as wastes products to be excreted

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15
Q

Reabsorption

A

Glomerulus - filtration occurs

Tubular Reabsorption -
PCT & DCT - H+ is secreted; Na+ and H2O is reabsorbed
DCT - Aldosterone is secreted along with K+; Na+ and H2O are reabsorbed (increase in aldosterone may cause hyperkalemia)
Loop of Henle - CL- is reabsorbed along with Na+ and H2O
Collecting duct - ADH maintains the water balance, decrease in urine output, increase in blood volume
- No ADH: increase in urine output and decrease in blood volume

Tubular Secretion - occurs when ions from blood go into the tubules

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16
Q

Non-pharmacological Treatment of HTN

A

decrease sodium input, reduce fat intake, decrease stress, increase physical activity, rest, moderate alcohol intake, weight loss

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17
Q

Antihypertensive Pharmacological Treatment

A

Vasodilators, CCB, BB, diuretics, ACE inhibitors, ARB, renin inhibitors, combo therapy

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18
Q

Diuretics

A

USES: CHF, HTN, edema, anuria, renal disease

Types: Osmotic Diuretics, Thiazide/Thiazide-like Diuretics, Loop Diuretics (Organic Acid Diuretics)

19
Q

Osmotic Diuretic

A

decreased ICP; pulls water from tissues (changes plasma osmolality)
mannitol (Osmitrol)

20
Q

Thiazide/Thiazide-like Diuretics

A

do not spare K+;
block reabsorption of Na+, diuresis, Na+ and H2O loss
- sulfa derivative, if allergic to sulfonamides, these are contradicted

Thiazide Diuretic:
hydrochlorothiazide (HCTZ) (Hydrodiuril)

Thiazide-like Diuretic:
chlorthalidone (Hygroton)
indapamide (Lozol)
metolazone (Zaroxolyn)

21
Q

Loop Diuretics (Organic Acid Diuretics)

A

do not spare K+ (secreted through urine)

USES: edema, HTN, pulmonary congestion, liver and kidney disease

MOA: inhibit Na+ and Cl- transport in Loop of Henle -> this increases Na+, Cl- and H2O secretion

DRUGS:
furosemide (Lasix)
torsemide (Demadex)

22
Q

Potassium Sparing Diuretics (Aldosterone Receptor Antagonists)

A

control K+ depletion through urine

DRUGS:
amiloride (Midamor)
sprinolactane (Aldactone)
triamterene (Dyrenium)

(possible hyperkalemia and gynecomastia)

23
Q

Diuretics (Common Side Effects)

A

Hypotension,
orthostatic hypotension,
reflex tachycardia,
thirsty/dry mouth,
nausea

24
Diuretics Patient Teaching
Take medication exactly as prescribed; taking medication as prescribed helps control high BP and prevent complications; syncope may be experienced (fainting may occur due to blood volume depletion, low BP, and low blood flow and O2 level) Due to taking a diuretic, an increase in HR should be reported; a reflex tachycardia may occur due to lowering of BP); if taking a diuretic and a cardiac glycoside, monitor pulse; orthostatic hypotension may occur - be careful with changing positions; patients should monitor and journal their daily weight; monitor for fluid gain; monitor input and output for patients in hospitals
25
Thiazide Diuretics: Patient Teaching
Side Effects: hypercalcemia, hyperglycemia, hyperlipidemia, hyperuricemia, hypokalemia ( may need to supplement with (dietary): bananas, papayas, mangos, lima beans, artichoke, cantaloupe, watermelon, apricots, nuts, oranges, dates and fish) Symptoms Include: leg cramps, muscle weakness, less alert, lethargy, constipation, arrhythmias
26
Sympatholytics (lower HTN)
Beta Adrenergic Blockers, Peripheral Alpha-1 Blockers, Alpha-2 Central Agonists
27
Beta Adrenergic Blockers (Sympatholytics; lower HTN)
MOA: block beta-1 receptors - decrease BP and CO block release of renin by kidneys - interferes with the RAAS USES: HTN, CHF, angina, migraines, glaucoma, tachyarrhythmias DRUGS: metoprolol (Lopressor) propranolol (Inderal) PATIENT TEACHING/SIDE EFFECTS: drowsiness, GI upset, bradycardia, CNS depression, monitor serum lipid levels, mental depression, monitor blood glucose levels in diabetics
27
Peripheral Alpha-1 Antagonists/Blockers (azosin)
USES: HTN, angina, BPH MOA: block NE from binding to adrenergic alpha-1 receptors -> vasodilation DRUGS: prazosin (Minipress) doxazosin (Cardura) terazosin (Hytrin) PATIENT TEACHING/ SIDE EFFECTS: orthostatic hypotension - caution with changing positions, reflex tachycardia, GI upset, increased urination
27
Alpha-2 Central Agonists
USES: HTN, angina MOA: inhibits CNS activity, lowers BP, acts on alpha-2 receptors -> vasodilation DRUGS: clonidine (Catapres) methyldopa (Aldomet) PATIENT TEACHING/SIDE EFFECTS: hypotension, dry mouth, drowsiness
27
Vasodilators (lower HTN)
MOA: relaxes smooth muscle of the vessels USES: HTN, CHF, CAD DRUGS: hydralazine minoxidil (Loniten, Rogaine) nitroprusside (Nipride, Nitropress) PATIENT TEACHING/SIDE EFFECTS: flushing, HA, hypotension, N/V, rapid heartbeat, cannot be used with ED meds
28
Hypotension (Symptoms)
dizziness, lightheadedness, syncope, nausea
29
Hypotension (Treatment)
rest - lay down, elevate legs, give O2, force fluids
30
Renin-Angiotensin II-Aldosterone System
Renin is secreted by the kidneys; Angiotensin I is secreted by the liver (is a vasoconstrictor); ACE is released by the lungs; Angiotensin II is formed in the plasma; Angiotensin II stimulates adrenal cortex to release aldosterone; Angiotensin II stimulates posterior pituitary to release ADH, Angiotensin II is a potent vasoconstrictor; Angiotensin II stimulates the thirst center (more fluid intake, higher blood volume, higher BP) Aldosterone works on the kidneys; they reabsorb Na+ and water back into blood (higher blood volume, higher BP) AntiDiuretic Hormone works on the kidneys to take fluid from urine back into blood; is a vasoconstrictor
31
ACE Inhibitors (work against HTN)
Normal Process: ACE -> Angiotensin II MOA: inhibits the ACE; decrease of release of aldosterone; decreased reabsorption of Na+ and H2O; vasodilation USES: HTN DRUGS: captoprin (Capoten) enalapril (Vasotec) lisinopril (Zesttril) benazepril (Lotensin) quinapril (Accupril) ramipril (Altace) PATIENT TEACHING/SIDE EFFECTS: Where does K+ go? -> K+ levels rise -> causing hyperkalemia, hypotension, angioedema, dizziness, HA, GI upset, rash, arrhythmias, coughing
32
Angiotensin II Receptor Blockers/Antagonists (ARBs) (work against HTN)
MOA: block effects of Angiotensin II; blocks the release of aldosterone, vasodilation - No significant effects on K+, no angioedema USES: HTN DRUGS: olmesartan (Belicar) PATIENT TEACHING/SIDE EFFECTS: hypotension, dizziness, HA, drowsiness, cough, N, monitor K+ levels
33
Renin Inhibitors (work against HTN)
MOA: inhibit actions of renin USES: HTN DRUGS: aliskiren (Tekturna) PATIENT TEACHING/SIDE EFFECTS: hypotension, dizziness, upset stomach, HA, cough, lightheadedness
34
Calcium Channel Blockers (CCBs) (work against HTN)
MOA: interfere with Ca2+ entry into the cardiac muscle cells and smooth muscle cells of the vessels; this results in a decrease of a venous return, decrease of BP, increase of blood flow in the coronary arteries, slower conduction; vasodilation USES: HTN, tachyarrhythmias, angina DRUGS: nifedipine (Procardia), nisoldipine (Sular), amlodipine (Norvasc), verapamil (Calan), diltiazem (Cardizem) PATIENT TEACHING/SIDE EFFECTS: hypotension, dizziness, HA, facial flushing, constipation, reflex tachycardia, xerostomia
35
BP Thresholds
1) Normal BP: less than 120/80 mm Hg 2) Elevated BP: 120-129/less than 80 mmHg 3) Stage 1 HTN: 130-139/80-89 mm Hg 4) Stage 2 HTN: equal or greater than 140/90 MM Hg
36
Normal BP recommendations
promote optimal lifestyle habits: healthy diet, weigh loss if needed, tobacco use cessation, alcohol moderation, physical activity; reassess in a year
37
Elevated BP recommendations
Nonpharmacological treatment (Class I); reassess in 3 to 6 months; weight loss for overweight or obese patients; healthy diet (DASH); Sodium restriction; potassium supplementation; increased physical activity with structured exercise program; limited alcohol: 1 per day (in women) and 2 per day (in men)
38
Stage 1 HTN (ASCVD or estimated 10-y CVD risk greater than or equals to 10%)
BP: 130-139/80-89 mm Hg; Nonpharmacological treatment and BP lowering medication (Class I); reassess in 1 month (Class I); if BP goal is met, reassess in 3 to 6 months (Class I); if BP goal is not met, assess and optimize adherence to therapy (consider intensification of therapy)
39
Stage 1 HTN (130-139/80-89) (no ASCVD or risk of CV of or greater than 10 %)
Nonpharmacologic therapy (Class I); reassess in 3 to 6 months (Class I)
40
Stage 2 HTN
BP equals or is greater than 140/90; nonpharmacologic treatment and BP lowering medication (Class I)
41
Stepped Care Approach to HTN
First-line options (single or in combination): -ACE Inhibitors, ARBs, CCBs, and thiazide diuretics -beta-blockers can be used in patients who have any of the following: CAD, dysrhythmia, post-myocardial infarction, and heart failure (those older than 60 yrs old should not take beta blockers as initial agents; have not shown effective at preventing CV events -for moderate HTN of >20 mm Hg: take an ARBs or ACE Inhibitors with a diuretic or a dihydropyridine (DHP) calcium channel blocker (such as amlodipine, nifedipine, or felodipine) combination -start with a low dose and titrate upwards -if hypertension has not been controlled, the following may be added in the stepwise order: *CCB or a thiazide diuretic (chlorthalidone is more potent than hydrochlorothiazide (HCTE); add whichever one has not been used); can use a combination low dose amiloride/HCTZ in appropriate patients; -a vasodilating beta-blocker (such as carvedilol or nebivolol) and/or aldosterone blocker -alpha-blockers, direct vasodilators; consider referral
42
Treatment Recommendations for Specific Patient Populations
-African-Americans should be prescribed CCB 1first -those with chronic kidney disease, should be prescribe ACE Inhibitors or ARBs -differences in ARBs agents and diuretics *Losartan (Cozaar): weakest ARB; may require twice a day dosing; *Valsartan (Diovan), telmisartan (Micardis), irbesartan (Avapro), candesartan (Attacand), olmesartan (Benicar) are all generic (except Edarbi) and can be used everyday *more potent ARBs include olmesartan and azilsartan (which is the most potent) *chlorthalidone is more potent than HCTZ -for hypertension that is difficult to control: *make sure that the patient is on sodium restricted diet of 1500-2000 mg per day and not taking OTC nonsteroidal or anti-inflammatory medication or drinking excess alcohol *if a patient is on ACE Inhibitor/ARB with a thiazide diuretic and systolic pressure remains uncontrolled, change ACE inhibitor to ARBs, if a patient is on losartan, change to a more daily, once-daily ARB *if the patient is on a beta-blocker for some other reason, the drug cab be changes to a vasodilating beta-blocker *clinicians may use a dihydropyridine CCB; do not use nifedipine with LV systolic dysfunction *may add an aldosterone blocker if BP remains unchanged *clinicians may change HCTZ to chlorthalidone (more potent patient thiazide diuretic) -for elevated isolated systolic pressure: the Canadian guidelines recommend using an ARB, a thiazide diuretic, and/or dihydropyridine CCBs