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Nur 3010 exams > HTN > Flashcards

HTN Flashcards

1
Q

describe HTN

A
  • most common chronic condition among adults in the US
  • based on average 2 or more BPs taken 1- 4 weeks apart by health care provider
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2
Q

normal BP

A

<120 sys. / <80 dias.

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3
Q

elevated BP

A

120-129 sys. / <80 dias.

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4
Q

HTN stage 1

A

130-139 sys. / 80-89 dias.

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5
Q

HTN stage 2

A

140 or higher sys. / 90 or higher dias.

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6
Q

HTN crisis

A

> 180 sys. / >120 dias.

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7
Q

primary HTN

A
  • essential
  • 95% of patients; unidentifiable cause
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8
Q

secondary HTN

A
  • 5% of patients; identifiable cause! (rare, harder to identify)
  • renal disease, sleep apnea, pregnancy related
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9
Q

HTN incidence

A
  • about 33% of the adult population of US has HTN
  • about 46% DO NOT have it under control
  • highest prevalence in African Americans
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10
Q

pathophysiology HTN (SNS activation) (4)

A
  • Epi and norepirelease
  • increased vasoconstriction
  • increased contractility
  • increased release of Renin -> stimulates RAAS -> Angio I -> Angio II
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11
Q

pathophysiology HTN (renin -> angiotensin II) (3)

A
  • further vasoconstriction
  • release of aldosterone from adrenals (retention Na/H2O)
  • release of cortisol from adrenals (no direct affect, affects binding sites)
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12
Q

primary/essential HTN

A
  • unidentified antecedent to HTN
  • 95% of all cases
  • earlier onset (22-55yr) (younger patients, not taken seriously)
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13
Q

secondary HTN

A
  • S/D to some other cause
  • 5% of all cases
  • later onset
  • typically higher numbers (180/100 - secondary to other issues)
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14
Q

potential antecedents to primary HTN (6)

A

1) increased SNS activity -> more epi/norepi
- increased vasoconstriction and BP
- activates RAAS system

2) increased RAAS activity -> Na & H2O retention + increased systemic resistance
- vasoconstriction and more volume

3) increased renal resorption of Na & H2O: retain more vol. w/o renin d/t melanin
- occurs in the absence of Renin (aka low-renin HTN)
- more prevalent in African Americans

4) decreased vascular dilation secondary to vascular endothelial dysfunction

5) resistance to insulin, hypertriglyceridemia, T2DM

6) inappropriate activation of inflammatory pathways (autoimmune, oxidized stress)

how to stop RAAS: ace inhibitors, thiazides = help w/ volume issues

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15
Q

how does CO increase BP

A

normal CO + lots of resistance

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16
Q

how does CO decrease BP

A

okay CO + decreased resistance

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17
Q

Secondary HTN - renal disease (4)

A
  • glomerulonrphritis (impaired filtration)
  • diabetic nephropathy (impairs filtration)
  • polycystic kidnery disease (impairs output)
  • renal artery stenosis (not enough blood going into the kidneys -> RAAS) -> extra release renin
18
Q

Secondary HTN - endocrine (adrenal glands)

A
  • Cann syndrome -> increased aldosterone production (Na, H2O retention)
  • Cushings -> increased cortisol -> increased api/norepi receptor sensitivity (steroids)
  • pheochromocytoma -> Increased epi/norepi (rare, tumor in adrenal glands)
19
Q

Secondary HTN - endocrine (thyroids)

A
  • hyperthyroidism -> increased T3/T4 -> increased HR and epidural/norepi
  • hypothyroidism -> increased sodium retention (and water)
20
Q

Secondary HTN - endocrine (parathyroid)

A
  • hyperparathyroidism -> increased Ca+ in blood -> increased vasoconstriction
21
Q

Secondary HTN - intracranial pressure increases

A
  • swelling -> increased brain pressure -> body compensates by increase pressure everywhere
  • Cushing’s triad -> HTN, decreased HR, decreased RR
22
Q

risk factors for primary HTN (8)

A
  • HTN
  • smoking / obesity
  • physical inactivity
  • dyslipidemia
  • DM (uncontrolled)
  • microalbuminuria or GFR <60 mL/min (kidney ds.)
  • older age
  • family hx.
23
Q

assessment HTN (6)

A
  • history and risk factors: diet? exercise? lifestyle? drugs? alcohol?
  • assess potential symptoms of target organ damage (angina, SOB, altered speech, altered vision, nosebleeds, dizziness, balance problems, nocturia (urine in sleep), cardiovascular assessment (apical and peripheral pulses))
  • personal, social, financial factors that will influence the condition or its treatment (ace, thiazides)
  • physical examination (retinal exam, bp)
  • lab tests (urinalysis (kidney damage, protein in urine - big indicator) (blood chemistry: Na, K, other lytes, BUN/Cr, GFR, lipid panel)
  • ECG (not everyone)
24
Q

measuring BP (home, practitioner, patient)

A
  • home use: auto upper-arm device w/ digital display
  • practitioner use: validated electronic device w/ appropriately sized arm cuff
  • patient teaching: avoid caffeine, nicotine, activity 30 min prior, empty bladder, sit for 5 min pre-measurement, sits comfortably w/ back supported, forearm at heart level, both feet on ground, avoid talking, no crossing legs
25
Q

measuring BP - practitioner teaching (7)

A
  • use appropriately sized cuff
  • wrap cuff firmly around arm, with cuff bladder over brachial artery
  • position patients arm at heart level
  • record BP of both arms, normal variation should not exceed 5 mmHg
  • take two readings 1-2 minutes apart, average these
  • record position of arm for standardization (know which side you use)
  • inform patient of their reading and implications (don’t use on arm w/ fistula, side of breast cancer)
26
Q

signs & (rarely) symptoms

A

1) usually no symptoms other than elevated blood pressure

2) symptoms r/t organ damage are seen late and are serious:
- retinal and other eye changes
- renal damage (kidney damages)
- myocardial infarction (heart damage)
- cardiac hypertrophy
- stroke

27
Q

management HTN (maintenance, lifestyle, pharm, meds)

A
  • maintain BP (<140/90 mmHg, stage 2 HTN) (<150/90 mmHg for older adults - ortho)
  • lifestyle medications (wt. reduction, DASH diet, decreased sodium intake, regular physical activity, reduced alcohol consumption)
  • pharmacologic therapy (decreased peripheral resistance, blood volume) (decrease strength and rate of myocardial contraction)
  • meds: diuretics, beta-blockers, alpha 1 blockers, combined alpha & beta blockers, vasodilators, ACE inhibitors, ARBs, calcium channel blockers, dihydropyridines, and direct renin inhibitors
28
Q

Ace inhibitors (suffix, fact, action, function, risk, contraindication, side effect, considerations gero)

A
  • meds: -pril
  • first line agents (caucasians)
  • action: inhibit conversion of angio I -> angio II
  • function: lower total peripheral resistance (vasodilation)
  • risk: angioedema (rare, fatal)
  • contraindications: concomitant use of ARB, renin inhibitor, potassium sparing diuretic, potassium supplements, BL renal artery stenosis, pregnancy, hx. angioedema with prior use of ACE inhibitor, hyperkalemia
  • side effects: cough
  • gerontologic considerations: require reduced dosages and addition of loop diuretics when there is renal dysfunction
29
Q

ARBs (suffix, fact, action, function, risk, contraindication, side effect)

A
  • meds: -sartan
  • alternative to ACE
  • action: block the effects of angio II at the receptor
  • function: reduce peripheral resistance
  • risk: minimal
  • contraindications: concomitant use of an ACE inhibitor, renin inhibitor, potassium sparing diuretic, potassium supplements, BL renal artery stenosis, hx. angioedema, pregnancy, lactation, renovasuclar disease
  • side effects: hyperkalemia, hx. angioedema from ACE inhibitor
30
Q

calcium channel blockers - dihydropyridines (suffix, fact, action, function, contraindication, side effect, route, report)

A
  • meds: -pine
  • no affect on HR
  • action: inhibit calcium ion influx across membranes, vasodilatory effects
  • function: rapid action, effective by oral or sublingual route
  • contraindication: HFrEF (systolic dysfunction)
  • side effects: pedal edema (more common in women)
  • route: administer on empty stomach, recommend eating small, frequent meals if complaint of nausea, use with caution in patients with diabetes (decreased dose) muscle cramps, joint stiffness, sexual dysfunction
    report: irregular HR, constipation, SOB, edema, dizziness
31
Q

calcium channels - nondihydropyridines (suffix, fact, action, avoid, contraindication, side effect)

A
  • meds: diltiazem
  • affect on HR (decreases)
  • action: inhibit calcium ion influx, reduce cardiac afterload, slow velocity of conduction of cardiac impulse
  • avoid concomitant dosing with beta blockers
  • contraindications: HFrEF (systolic dysfunction), sinus node dysfunction, AV block
  • side effects: do not discontinue suddenly, observe for hTN, report irregular heartbeat, dizziness, edema, instruct on regular dental care of potential gingivitis
32
Q

diuretics - loop (suffix, action, use, contraindication, risk, gero consideration)

A
  • meds: bumetanide, furosemide
  • action: volume depletion, block reabsorption of sodium, chloride, and water in renal tubules (release fluid)
  • use: patients with symptomatic HF and for patient patients with moderate to severe CKD
  • contraindications: same as for thiazide diuretics
  • risk: volume and electrolyte depletion, monitor for hypokalemia
  • gerontologic considerations: risk for orthostatic hTN
33
Q

pharmacologic’s stage 1 HTN (4)

A
  • african american and patients: calcium channel blocker or thiazide diuretics
  • non African american and patients: ACE-I or ARB
  • low doses are initiated, medication dosage is increased gradually if blood pressure does not reach target goal
  • multiple medications may be needed to control BP
34
Q

gerontologic considerations HTN (5)

A
  • medication regimen can be difficult to remember
  • expense can be a challenge (BP meds affordable)
  • monotherapy: if appropriate, may simplify the medication regimen and make it less expensive
  • ensure that older patients understand the regimen and can see and read instructions, open medication containers, and get prescriptions refilled (biggest concern = ortho HTN)
  • include family and caregivers in educational program (biggest motivator: erectile dysfunction)
35
Q

potential complications HTN (9)

A
  • L ventricular hypertrophy
  • myocardial infarction (heart attack)
  • heart failure
  • atherosclerosis
  • abdominal aortic aneurysm (AAA) development and subsequent rupture
  • transient ischemic attack (TIA)
  • cerebrovascular disease (CVA, stroke, brain attack)
  • renal insufficiency and chronic kidney disease
  • retinal hemorrhage
36
Q

hypertensive crisis (emergency vs urgency)

A
  • hypertensive emergency: BP >180/120 mmHg & signs of DAMAGE TO TARGET ORGANS (blood in urine, chest pain, vision changes)
  • hypertensive urgency: BP is very elevated but no evidence of immediate or progressive target organ damage
37
Q

HTN emergency mgmt (6)

A
  • reduce bp 20% to 25% in first hour
  • reduce to 160/100 mmhm over 6 hours
  • gradual normalization occurring in 24-48 hours (gradual unless stroke)
  • exceptions are ischemic stroke and aortic dissection (emergencies which require immediate tx.)
  • meds: IV vasodilators, sodium nitroprusside, nicardipine, fenoldopam mesylate, enalaprilat, nitroglycerin
  • needs frequent monitoring of BP and cardioversion status
38
Q

HTN emergency s/sx (7)

A
  • blurred vision/vision changes/vision loss
  • hypertensive retinopathy (causes exudates and hemorrhages within retina)
  • chest pain (not enough O2 -> issues to heart)
  • hematuria
  • seizures
  • mental status changes
  • vascular damage
39
Q

HTN emergency - aortic dissection (RF, occurs with, etiology, s/sx, goals tx)

A
  • HTN: big risk factor for aortic dissection
  • occurs in conjunction with aortic aneurysm (vessel has weak spot that is ruptured by HTN)
  • blood tears through endothelium -> into arterial media to create second lumen
  • tamponades the true lumen (blocks BF -> lumen)
  • s/sx: increase BP, pain response: tearing, ripping pain in back
  • goals tx: type and screen patient pre-op, lower BP (while we wait for OR), stent or graft aorta in the OR, risk reduction to follow surgery
40
Q

hypertensive urgency - can be handled outpatient (4)

A
  • oral agents can be administered with goal of normalizing BP within 24-48 hours (250/100 BP), assess s/sx internal organ damage)
  • fast acting oral agents: beta-adrenergic blocker (labatalol), angiotensin-converting enzyme inhibitor (captopril), alpha 2 agonist (clonidine)
  • patient requires close monitoring of BP and cardiovascular status (be specific)
  • assess for potential evidence of target organ damage (nurse)

Nur 3010 exams (13 decks)

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