CH 26: Hypertension Flashcards

1
Q

homeostasis resulting from increased blood pressure in the cardiovascular system

A

vasodilation
decreased stroke volume
decreased HR
decreased CO
blood pressure back to normal

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2
Q

homeostasis resulting from increased blood pressure in the kidneys

A

increased urine output
decreased blood volume
blood pressure returns to normal

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3
Q

primary HTN

A

no identifiable cause

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4
Q

secondary HTN caused by:

A

 Diseases: for example, Cushing’s, hyperthyroid, CKD
 Drugs: corticosteroids, contraceptives, alcohol, amphetamines,
caffeine, decongestants,
Many times there are no symptoms

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5
Q

4 organs most affected by prolonged HTN or uncontrolled HTN

A

 Heart
 Brain
 Kidneys
 Retina

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6
Q

consequences of HTN

A

 Heart must work harder
o Excessive workload can ultimately cause heart to fail = heart
failure (HF)
 Damage to the blood vessels
o Can result in transient ischemic attacks and strokes
 Damage to the arteries of the kidneys
o Can result in CKD
 Damage to the vessels in the retina
o Can result in rupture or occlusion = visual impairment and
blindness
 If HTN continues, damage to the organs and tissues can be irreversible

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7
Q

lifestyle recommendations for HTN

A

 Limit intake of alcohol.
 Restrict sodium consumption and increase potassium intake.
 Reduce intake of saturated fat and cholesterol and increase
consumption of fresh fruits and vegetables.
 Increase physical activity.
 Discontinue use of tobacco products.
 Reduce sources of stress and learn to implement coping strategies.
 Maintain optimal weight.

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8
Q

goal of pharmacotherapy for HTN

A

reduce morbidity and mortality

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9
Q

Alpha2 Agonists action

A

Decrease SNS impulses to heart and arterioles = vasodilation

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10
Q

Alpha 1 Blockers action

A

inhibit SNS action on arterioles = vasodilation

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11
Q

direct vasodilators

A

Act on smooth muscle of arterioles = vasodilation

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12
Q

calcium channel blockers

A

Block calcium ion channels in arteries causing vasodilation

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13
Q

Angiotensin receptor blockers

A

Prevent angiotensin II from reaching the receptors = vasodilation

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14
Q

ACE inhibitors (angiotensin-converting enzyme)

A

Block formation of angiotensin II = vasodilation AND block aldosterone secretion = decrease fluid volume

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15
Q

diuretics

A

Increase urine output = decrease fluid volume

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16
Q

Beta blockers

A

Decrease heart rate and myocardial contractility = reduce CO

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17
Q

treatment begins at systolic greater than 120 with:

A

non-pharmacologic changes

18
Q

drug treatment starts with systolic greater than

A

130

19
Q

therapeutic effects of lisinopril (ACE inhibitors)

A

Block formation of angiotensin II = vasodilation AND block
aldosterone secretion = decrease fluid volume

19
Q

adverse effects of lisinopril (ACE inhibitors)

A

Headache,
dizziness,
orthostatic hypotension,
rash,
cough
Angioedema,
acute renal failure,
first-dose phenomenon,
fetal toxicity,
hyperkalemia

20
Q

monitoring for lisinopril (ACE INHIBITORS)

A

Persistant cough
Postural hypotension– first dose phenomenon
Hyperkalemia with potassium sparing diurectics
Monitor labs for glucose,
eletrolytes, AST, ALT, BUN, creatinine
Potassium!

21
Q

safety for lisinopril (ACE inhibitors)

A

angioedema - emergency!
No use during pregnancy
NSAIDs can reduce the effect
Alcohol may increase hypotension
Can lead to lithium toxicity

22
Q

adverse effects of losartan (ARBs)

A

Headache,
dizziness,
orthostatic
hypotension,
diarrhea,
fatigue,
upper respiratory tract infection
Angioedema,
acute renal
failure,
first-dose phenomenon,
fetal toxicity,
hyperkalemia,
nephrotoxicity
(aliskiren)

23
Q

safety and monitoring for losartan (ARBs)

A

Hypoglycemia
UTIs
anemia
Dizziness and fainting after first couple of doses
Fetal injury and death when taken with pregnancy

24
Q

therapeutic effects of nifedipine (selective CCB) and diltiazem (non-selective CCB)

A

Block calcium ion channels in arteries causing vasodilation
Nifedipine: decrease HTN and angina

25
Q

adverse effects of nifedipine (selective CCB) and diltiazem (non-selective CCB)

A

Flushed skin,
headache,
dizziness,
peripheral edema,
lightheadedness,
nausea,
constipation,
fatigue,
sexual dysfunction
Hepatotoxicity,
MI, HF,
confusion,
mood changes,
angioedema

26
Q

safety and monitoring of nifedipine (selective CCB) and diltiazem (non-selective CCB)

A

monitor for digoxin toxicity
do not crush or divide
alcohol increases vasodilation and can lead to syncope

27
Q

therapeutic effects of atenolol (beta blocker)

A

Decrease heart rate and myocardial contractility = reduce cardiac output
Reduced blood pressure
Reduce angina
Heart failure,
MI
Migraines

28
Q

adverse effects of atenolol (beta blocker)

A

Fatigue,
insomnia,
drowsiness,
impotence or decreased libido,
bradycardia,
confusion
Agranulocytosis,
laryngospasm,
Stevens-Johnson syndrome,
anaphylaxis; if the drug is abruptly withdrawn,
palpitations,
rebound HTN,
dysrhythmias,
MI

29
Q

safety and monitoring for atenolol (beta blocker)

A

Broncho-constriction
Fatigue and intolerance
Caution in patients with asthma or HF
Do not stop abruptly!
Can result in rebound hypertension and MI

30
Q

therapeutic effects of doxazosin (alpha 1 - alpha blockers)

A

Inhibit SNS activation in arterioles = vasodilation
Lower blood pressure
Bph symptoms

31
Q

adverse effects of doxazosin (alpha 1 - alpha blockers)

A

Orthostatic
hypotension,
dizziness,
headache,
fatigue
First-dose phenomenon,
tachycardia,
dyspnea

32
Q

safety and monitoring of doxazosin (alpha 1 - alpha blockers)

A

Orthostatic hypotension
HYPOTENSION
Sedation and dizziness
Hemolytic
anemia,
leukopenia,
thrombo-
cytopenia,
lupus.
Caution with erectile dysfunction drug = low bp
NSAIDs can decrease effect

33
Q

therapeutic effects of clonidine (alpha 2 adrenergic blockers)

A

Decrease SNS impulses
to heart and arterioles
= vasodilation

34
Q

adverse effects of clonidine (alpha 2 adrenergic blockers)

A

Peripheral edema,
sedation,
depression,
headache,
dry mouth,
decreased
libido
Hepatotoxicity,
hemolytic anemia,
granulocytopenia

35
Q

therapeutic effects of hydralazine (direct acting vasodilators)

A

Act on the smooth muscle of arterioles = vasodilation
Not first choice due
to side effects

36
Q

adverse effects of hydralazine (direct acting vasodilators)

A

Orthostatic hypotension, fluid retention,
headache,
palpitations
Lupus-like reaction
(hydralazine),
severe hypotension,
MI,
dysrhythmias,
shock

37
Q

safety and monitoring of hydralazine (direct acting vasodilators)

A

Reflex tachycardia**
Sodium and water retention
Can develop tolerance
over time
DO NOT STOP ABRUPTLY
Severe hypotension with other anti-hypertensives

38
Q

swelling around the lips, eyes, throat, and other body regions.

A

angioedema

39
Q

compensatory response to the sudden decrease in blood pressure caused by the
drug.

A

reflex tachycardia