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NRSG 220 > Chapter 34: HYPERTENSION (9) > Flashcards

Chapter 34: HYPERTENSION (9) Flashcards

(70 cards)

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1
Q

HTN

A

consistent elevation of systemic arterial BP

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2
Q

HTN factors

A
  1. Genetic factors
  2. Environmental factors
    - diet
    -exercise
    -age
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3
Q

Primary HTN

A

Also called essential, there is NO identifiable cause

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4
Q

Secondary HTN

A

Caused by another disease

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5
Q

Where does prolonged HTN damage?

A
  1. Heart
  2. Eyes
  3. Brain
  4. Kidneys
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6
Q

How does prolonged HTN damage the heart?

A

Hypertrophy, MI, HF

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7
Q

What to watch for with heart damage from HTN

A

Rapid weight gain (5lbs in 2-3/days), SOB, BLE edema

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8
Q

How does prolonged HTN damage the eyes?

A

Blindness - frequent eye checks

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9
Q

How does prolonged HTN affect the brain?

A

Stroke - assess speech changes, drooping face, one sided weakness

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10
Q

How does prolonged HTN affect the kidneys?

A

Kidney failure

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11
Q

What to watch for with the kidneys and prolonged HTN?

A

protein in the urine (micro-macro albuminuria)
Kidneys like fishing nets, let micro pass but not macro
if macro is in urine = kidney problem

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12
Q

What arterial changes occur with prolonged HTN

A

Endothelial inflammation
arteriosclerosis
Atherosclerosis

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13
Q

What do arterial changes with prolonged HTN end with?

A

increased afterload leading to hypertrophy
CAD leading to MI
Cerebrovascular disease leading to stroke

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14
Q

What can lifestyle changes do for HTN

A

May eliminate the need for pharmacotherapy

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15
Q

What are some lifestyle changes to non pharmacologically treat HTN?

A
  1. Limit alcohol
  2. Restrict sodium consumption
  3. Dash diet
  4. Aerobic exercise at least 30 mins 3-5x/week
  5. Tobacco cessation
  6. Stress management
  7. Maintain optimum weight
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16
Q

What is the DASH diet?

A

rich in fruits, veggies, whole grains, and low fat dairy foods (includes meat fish, poultry, nuts and beans)
limited in sugar sweetened foods and drinks, red meat and added fats

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17
Q

What are racial differences associated with HTN treatment

A

Same therapy for blacks and nonblacks with CKD
Different therapy for blacks and nonblacks without CKD
Lower systolic BP with diabetics (decreased resistance to kidneys)

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18
Q

What’s important to note when managing HTN?

A

Not all people with a BP higher than 140/90 need pharmacotherapy

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19
Q

What are the different types of antihypertensives? (9)

A
  1. Diuretics
  2. Angiotensin-converting enzyme inhibits (ACEI)
  3. Angiotensin 2 receptor blockers (ARBS)
  4. Calcium channel blockers (CCBs)
  5. Beta 1 blockers (BBs)
  6. Beta 2 blockers
  7. Alpha 1 blockers
  8. Alpha 2 agonists
  9. Vasodilators
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20
Q

Goal of pharmacotherapy?

A

To reduce morbidity and mortality

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21
Q

What is pharmacotherapy individualized to?

A

Patients risk factors
Comorbid medical conditions
degree of BP elevation

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22
Q

What are some patient adherence factors to consider?

A
  1. Difficult of changing established lifestyle habits
  2. Choose generic forms to decrease cost of drug for pt
  3. occurrence of ADEs
  4. Encourage patient to report ADEs to adjust dosage (BB, depression, fatigue)
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23
Q

Diuretics are

A

often the 1st choice in treating mild-moderate HTN

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24
Q

What diuretic is first line treatment?

A

Thiazide diuretics

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25
What do diuretics do?
Decrease blood volume and decrease pressure
26
ADEs of diuretics
Dehydration Hyponatremia hypokalemia (less with K+ sparing) Nocturne (if given too late in the day) Orthostatic hypotension
27
What are the 3 kinds of diuretics + prototype drug
1. Thiazide/thiazide like diuretics - most common for HTN - HYDROCHLOROTHIAZIDE 2. Potassium-sparing diuretics - TRIAMTERENE, SPIRONOLACTONE 3. Loop (high-ceiling) diuretics - usually not used for HTN - FUROSEMIDE, BUMETANIDE = K+
28
What do ACEIs do?
Vasodilation by reducing angiotensin 2 - decreased aldosterone effects increases effectiveness of diuretics - protect kidney
29
Common ACEI agents
enalpril, lisinopril, captopril
30
ACEI ADEs
Persistent cough postural hypotension hyperkalemia angioedema
31
ARBS
Inhibit effects of angiotensin 2 - similar effects to ACEIs
32
ARBS ADEs
hypotension angioedema (less common compared to ACEIs) more expensive no cough
33
Calcium channel blockers selective drugs
DIHYDROPIRIDINE - relax arterial smooth muscle - nifiedipine, amlodipine
34
CCBs Nonselective drugs
NONDIHYPROPIRIDINE - relax arterial smooth muscle - affect myocardial contraction and HR - verapamil, diltiazem
35
CCBs ADEs
reflex tachycardia peripheral edema exacerbation of some dysrhythmias worsens HF *research shows greater efficacy in African Americans and elderly patients*
36
Adrenergic Antagonists
- used for cardio disorders - block adrenergic receptors in SNS
37
What receptors do adrenergic antagonists block?
1. Beta 1 adrenergic receptors 2. Alpa 1 adrenergic receptors 3. Alpha 2 and beta adrenergic receptors 4. peripheral adrenergic neurons
38
Nonselective ABs and BBs
Carvedilol, labetalol - block both alpha 1 and beta adrenergic receptors
39
How do nonselective ABs and BBs act in the body
decrease CO decrease renin secretion block vasoconstriction of arterioles and veins
40
Nonselective ABs and BBs ADEs
orthostatic hypotension bradycardia bronchoconstriction potential for arrhythmias *watch with asthmatics, COPD, and DMs*
41
What do BBs do
decrease HR, contractility, and cardiac conduction velocity = decreased BP
42
BB agents
Propanolol metoprolol atenolol timolol
43
BB ADEs:
High doses: - fatigue, activity intolerance -erectile dysfunction - masks symptoms of hypoglycemia - clinical depression
44
Direct acting vasodilators
relax arterial smooth muscle directly = decrease resistance and decreased afterload
45
Vasodilators can also affect
some drugs affect veins which decrease preload (eg isosorbide denigrate)
46
Vasodilators ADEs
- reflex tachycardia & hypotension (compensatory increase in HR due to sudden BP drop) - fluid retention (can be minimized with BBs and diuretics)
47
Vasodilators agents
hydralazine, diazoxide, nitroprusside
48
Vasodilators prototype drug?
Hydralazine
49
Hydralazine therapeutic
Antihypertensive
50
Hydralazine pharmacologic
direct vasodilator
51
Hydralazine uses
moderate to severe HTN hypertensive emergiences acute HF
52
Hydralazine MOA
Causes peripheral vasodilation decrease PVR, HR, and CO decreases afterload selective for arterioles
53
Hydralazine ADEs
HA tachycardia palpitations flushing N/V/D Orthostatic Hypotension Lupus like syndrome
54
Hydralazine serious ADEs
Blood dyscrasia
55
Hydralazine contraindications/precautions
Lupus CV disease rheumatic Heart disease renal impairment slow aetylators CAD
56
Hydralazine drug interactions
- severe hypotension with antihypertensives of MAOIs - NSAIDs may decrease antihypertensive action
57
Hydralazine pregnancy category
C
58
Hydralazine OD treatment
- gastric lavage, activated charcoal, administration of a plasma volume expander - treat tachycardia with a beta blocker
59
Hydralazine Considerations
Hx and Px monitor lab tests fro antinuclear antibody timer before and during lab therapy monitor I&O watch for ADEs Assess for rapid drop in BP and subsequent tachycardia
60
What classifies a Hypertensive emergency
Diastolic over 120 evidence of organ damage most common cause is untreated/poorly controlled essential HTN
61
Urgency classification of HTN
Diastolic over 120 no evidence of organ damage more conservative treatment
62
What is the prototype drug used for hypertensive emergencies?
Nitroprusside sodium (nitropress)
63
Nitroprusside therapeutic
Antihypertensive
64
Nitroprusside pharmacologic
direct vasodilators
65
Nitroprusside uses
aggressive, life threatening HTN
66
Nitroprusside MOA
direct relaxation of arteries and veins
67
Nitroprusside ADEs
Hypotension headahce dizziness skin flushing
68
Nitroprusside contraindications
high ICP inadequate cerebral circulation compensatory HTN serious renal impairment
69
Nitroprusside Pregnancy category
C
70
Nitroprusside treatment of OD
Vasopressor for extreme hypotension cyanide antidote kit for cyanide toxicity

NRSG 220 (8 decks)

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