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Antihypertensives Flashcards

1
Q

Cardiovascular disease (CVD) is usually managed with

A

with exercise, diet, stress management and a variety of pharmacological and surgical approaches

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2
Q

CVS provides the body’s cells with

A

nutrients and removes their metabolic waste efficiently

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3
Q

The response to heightened tissue demands is to:

A

Increase BP
Increase HR
Redirect blood flow to prioritize tissues under stress

***These responses are normal but are intended to be short-term immediate reactions

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4
Q

Cardiovascular medications:

A

Anti-hypertensives
Drugs to manage heart failure and angina
Drugs that interfere with coagulation

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5
Q

Drugs to treat respiratory conditions

A

Bronchodilators
Inhaled steroids
Antihistamines
Decongestants

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6
Q

BP = CO x TPR

A

CO: cardiac output is the volume of blood the heart pumps per minute. Reflects the pumping strength of the heart, its rate and rhythm, and the volume of blood returned to the heart
TPR: all the elements that create resistance to the flow of blood. Most important factor is blood vessel diameters in the systemic and pulmonary circulations

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7
Q

Average BP is

A

120/80 mm Hg

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8
Q

Hypertension – AKA the silent killer

A

140/90 mm Hg

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9
Q

Average normal resting heart rate is

A

70-72 beats per minute

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10
Q

Within physiological limits, the faster the heart beats

A

the more blood it can pump

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11
Q

A rapid HR reduces the time frame in which the heart wall itself can

A

be perfused with fresh blood

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12
Q

When drugs are used in the treatment of CVD, they are often directed at managing

A

BP or strengthening heart function, or BOTH

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13
Q

CVD Medications are grouped by function:

A 
Improve heart function
Increase blood vessel diameter
Alter blood coagulation mechanisms
Reduce blood volume
Lower blood lipid levels (reduce blood vessel blockage)
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14
Q

Sites of action for cardiovascular medications

A 
CNS-Alpha-2 agonists
Kidneys- Diuretics
Heart-Beta blockers/
Alpha-1 antagonists/
Calcium channel blockers
BOTH-Angiotensin-
     converting enzyme 
     inhibitors (ACE-i)
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15
Q

Drugs that Improve Heart Function

A

BETA BLOCKERS

Cardiac Glycosides

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16
Q

Betablockers

A

metoprolol, atenolol, propranol, lavetolol

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17
Q

Betablockers act on

A

beta-adrenergic receptors located on the surface of the heart

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18
Q

receptors are normally activated when sympathetic neurotransmitters like _________
are released during stress

A

adrenaline

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19
Q

adrenaline when activated increase _____ _____ and ______as part of ‘flight or fight’
response

A

heart’s rate and force of contraction

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20
Q

unnecessary or chronic stimulation of the beta receptors

A

begin to weaken the heart from overstress and reduce perfusion

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21
Q

Cardiac Glycosides

A

commonly called digitalis (Digoxin)

- derived from a number of naturally occurring plants such as foxglove

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22
Q

Drugs that Improve ↑ blood vessel diameter

A

Vasodilators
Alpha receptor Drugs
Ca+ Channel Blockers
Angiotensin Converting Enzyme(ACE) Inhibitor

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23
Q

Angiotensin Converting Enzyme(ACE) Inhibitor

A

lisinopri l(Zestril), captopril (Copoten), enalapril (Vasotec)

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24
Q

Ca+ Channel Blockers

A

verapamil (Isoptin), nifedipine (Procardia), ditiazem

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25
Q

Alpha receptor Drugs

A

Alpha-1 receptor antagonist (Prazosin, doxazosin) and Alpha-2-receptor Agonist (Clonidine)

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26
Q

Vasodilators

A

Nitroglycerine vasodilators belong to a group of drugs that are chemically related to nitrates

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27
Q

nitroglycerine can be administered through a wide variety of routes

A

IV,

transdermally (patch, cream), sublingually, and via oral spray

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28
Q

other anti-anginal drugs that have similar mechanisms of action to antihypertensives

A

includes calcium-channel blockers and beta-blockers

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29
Q

nitroglycerine almost complete first-pass metabolism, so never given

A

orally (swallowed)

but may be sublingually, and via oral spray

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30
Q

Alpha 1 and 2 receptor found in

A

the CNS and the smooth muscle of blood vessel walls

  • alpha-1 receptors located on vascular smooth muscle cells
  • alpha-2 receptors found in synapses in the autonomic nervous system
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31
Q

the alpha receptors respond to sympathetic NT epinephrine and norepinephrine to

A

alter
blood vessel tone
- alpha-1 receptor activation has a direct effect to produce vasoconstriction
- alpha-2 receptor activation results in a decrease in sympathetic impulses leaving the
vasomotor centre resulting in peripheral vasodilation

32
Q

Ca+ Channel Blockers commonly used to treat

A

high blood pressure by exerting their effects by influencing smooth
muscle tone in blood vessel walls

33
Q

Angiotensin Converting Enzyme(ACE) Inhibitor

produces vasodilation by interrupting

A

the activities of one of the enzymes in the renin-angiotensin system (this system plays a role in long-term blood pressure control )

34
Q

Drugs that Improve
alter blood coagulation mechanisms- there are 3 categories of drugs used in the treatment of CVD that influence blood
coagulation

A

anticoagulants (affect blood clotting)

  • antithrombotics (inhibit thrombosis by altering how platelets adhere together)
  • thrombolytics (break down clots and thrombi that have already formed)
35
Q
  • blood coagulation is a necessary process to stop
A

bleeding
- too much clot formation- can lead to thrombosis which can obstruct the blood
vessel
- inadequate clot formation- can lead to excessive bleeding

36
Q
  • anticoagulants (affect blood clotting)
  • antithrombotics (inhibit thrombosis by altering how platelets adhere together)
  • thrombolytics (break down clots and thrombi that have already formed)
A

Anticoagulants -Heparin (administered parenterally), coumadin- warfarin (admin orally)
Antithrombotic -(asprin, persantin)
Thrombolytics -(streptokinase, tPA)

37
Q

Drugs that Improve ↓ blood volume

A

Diurectics -hydrochlorothiazide (Diuril), furosemide

38
Q

Drugs that Improve

↓ blood lipid levels (↓BV blockage)

A
  1. Bile acid sequestrants
  2. Nicotineic acid
  3. Fibric acid derivatives
  4. HMG Co A reductase inhibitors
39
Q 
Beta blockers: metoprolol 
(lopressor), atenolol, 
propranolol (Inderal), 
labetalol
MoA
A 
Hypertension: reduce 
cardiac output, 
therefore reducing 
blood pressure
Ischemic heart 
disease: reduced 
heart rate and cardiac 
output reduce the 
workload of the heart
Heart Failure: some 
beta blockers reduce 
peripheral resistance 
and workload of the 
heart
40
Q 
Beta blockers: metoprolol 
(lopressor), atenolol, 
propranolol (Inderal), 
labetalol
Adverse Effects
A 
GI: nausea and 
diarrhea
Resp: bronchospasm 
(mostly asthmatics or 
COPD)
Cardio: hypotension, 
heart failure, 
orthostatic 
hypotension, 
bradycardia
Endocrine:
hypoglycemia, 
especially in diabetics
CNS: fatigue, 
dizziness, depression
41
Q 
Beta blockers: metoprolol 
(lopressor), atenolol, 
propranolol (Inderal), 
labetalol Massage Therapy 
Guidelines
A 
Massage: postural 
hypotension. May not 
tolerate lying down. 
May cause peripheral 
edema
Hydrotherapy:
systemic treatments 
pose a high risk of 
hypotension, 
dizziness, falls. 
Beware of increasing 
cardiac workload
Exercise: beta 
blockers notorious for 
causing fatigue during 
exercise
42
Q

CARDIAC GLYCOSIDES

(Digoxin) MoA

A 
Heart failure: reduces 
heart rate, but 
increases strength of 
contraction of the 
heart
43
Q

CARDIAC GLYCOSIDES

(Digoxin) Adverse Effects

A

Toxicity: fatigue, nausea, vomiting, visual disturbances, HA, bradycardia-EMERGENCY.
Cardio: bradycardia ,hypotension

44
Q

CARDIAC GLYCOSIDES
(Digoxin) Massage Therapy
Guidelines

A 
dysrhythmias are 
common side effects. 
Be aware of dyspnea, 
angina symptoms 
while working
Hydrotherapy: see 
general guidelines for 
heart failure
45
Q

VASODILATORS

(Nitroglycerine) MoA

A 
Angina: vasodilation 
of coronary arteries 
improves blood flow to 
heart; vasodilation of 
veins and systemic 
arteries decrease 
preload and afterload 
(decreases workload 
of the heart)
46
Q

VASODILATORS

(Nitroglycerine) Adverse Effects

A

Hypotension

Headache

47
Q

VASODILATORS
(Nitroglycerine) Massage Therapy
Guidelines

A

Considerations as for
clients with ischemic
heart disease

48
Q

ALPHA RECEPTOR DRUGS- Alpha-2-receptor
agonist
(clonidine) MoA

A

Hypertension: acts
on the CNS to cause
peripheral vasodilation

49
Q

ALPHA RECEPTOR DRUGS- Alpha-2-receptor
agonist
(clonidine) Adverse Effects

A 
CNS: fatigue, 
drowsiness, sedation
Cardio: orthostatic 
hypotension, 
hypotension
50
Q

ALPHA RECEPTOR DRUGS- Alpha-2-receptor
agonist
(clonidine) Massage Therapy
Guidelines

A 
Massage: postural 
hypotension
Hydrotherapy: 
systemic heat 
treatments increase 
risk of hypotension 
and syncope
51
Q

ALPHA RECEPTOR DRUGS-Alpha-1-receptor
antagonist
( Prazosin,
doxazosin) MoA

A 
Hypertension: 
vasodilation and 
reduces the force of 
contraction of the 
heart
Angina: reduces the 
workload of the heart 
by reducing 
contractility
52
Q

ALPHA RECEPTOR DRUGS-Alpha-1-receptor
antagonist
( Prazosin,
doxazosin) Adverse Effects

A 
Cardio: edema, 
bradycardia, 
congestive heart
failure, hypotension, 
dizziness
53
Q 
ALPHA RECEPTOR DRUGS-Alpha-1-receptor 
antagonist
( Prazosin, 
doxazosin) Massage Therapy 
Guidelines
A 
Massage: postural 
hypotension-take care 
when changing 
positions. Peripheral 
edema-poorly treated 
with massage
Hydrotherapy: 
systemic heat 
treatments increase 
risk of hypotension 
and syncope
54
Q

Calcium Channel
Blockers: verapamil
(Isoptin), nifedipine
(Procardia), ditiazem MoA

A 
Hypertension: 
vasodilation and 
reduces the force of 
contraction of the 
heart
Angina: reduces the 
workload of the heart 
by reducing 
contractility
55
Q

Calcium Channel
Blockers: verapamil
(Isoptin), nifedipine
(Procardia), ditiazem Adverse Effects

A 
Cardio: edema, 
bradycardia, 
congestive heart 
failure, hypotension, 
dizziness
56
Q 
Calcium Channel 
Blockers: verapamil 
(Isoptin), nifedipine 
(Procardia), ditiazem Massage Therapy 
Guidelines
A 
Massage: postural 
hypotension, 
peripheral edema
Hydrotherapy: 
systemic heat 
treatments increase 
risk of hypotension 
and syncope
57
Q

ACE Inhibitors: lisinopril
(Zestril), captopril
(Copoten), enalapril
(Vasotec) MoA

A 
Hypertension: 
vasodilation and 
reduces blood volume, 
due to reduced 
angiotensin II 
formation
58
Q

ACE Inhibitors: lisinopril
(Zestril), captopril
(Copoten), enalapril
(Vasotec) Adverse Effects

A

Cardio: dizziness,
hypotension
Resp: cough
Fluids: hyperkalemia

59
Q 
ACE Inhibitors: lisinopril 
(Zestril), captopril 
(Copoten), enalapril 
(Vasotec) Massage Therapy 
Guidelines
A 
hypotension-take care 
when changing 
position. May not 
tolerate prone position
Hydrotherapy: see 
calcium channel 
blockers
60
Q 
Anticoagulants: Heparin 
(administered 
parenterally), 
coumadin- warfarin 
(administered orally) MoA
A 
Heparin: activation of 
antithrombin III and 
decreased activity of 
thrombin
Coumadin (warfarin): 
antagonizes vitamin K, 
needed for clotting 
factors II, IV, IX, and X
61
Q 
Anticoagulants: Heparin 
(administered 
parenterally), 
coumadin- warfarin 
(administered orally) Adverse Effects
A 
Cardio: hemorrhage, 
ecchymosis
Note: Coumadin levels 
can be altered by a 
wide range of food 
and drugs, resulting in 
under or overdose
62
Q 
Anticoagulants: Heparin 
(administered 
parenterally), 
coumadin- warfarin 
(administered orally) Massage Guidelines
A 
Massage: these 
agents are much more 
likely to cause 
hematomas or 
eccymoses with deep 
work. Light modalities 
are necessary
63
Q

Antithrombotics prevent or impair

A

platelet aggregation reduce the risk of dangerous thrombus

formation —> ANTIPLATELET DRUGS

64
Q

Antithrombotics used in prevention of

A

arterial thrombosis, especially in the coronary and cerebral arteries

65
Q

thrombi develop as a result of platelet activation with the presence of

A

thromboxane A2

causing platelets to aggregate

66
Q

thrombi typically comprises of

A

aggregated platelets, entrapped red blood cells, and fibrin

67
Q

platelets are important in controlling bleeding but thrombi can be dangerous if

A

they obstruct

blood vessels

68
Q

aspirin: inhibits

A

the formation of thromboxanes

69
Q

single dose of aspirin can inhibit platelet aggregation for up to

A

a week

70
Q

a platelets lifespan is only 6-10 days, so aspirin can inactivate platelets for

A

most or

all of their short lifespan

71
Q

Thrombolytics

promote disintegration of

A

clots and thrombi that have already formed

72
Q

disintegration of clots and thrombi depends on the presence of

A

plasmin (enzyme responsible for breaking down fibrin

mesh)

73
Q

any drug that increases plasmin formation has the potential to be used to

A

promote clot and

thrombus dissolution

74
Q

streptokinase: drug that is an enzyme that combines with plasminogen to form a

A

plasminogen-streptokinase complex which facilitates plasmin formation

75
Q

thrombolytics (tPA) are used in the treatment of

A

arterial and venous thrombi, after strokes and

heart attacks, and to clear IV catheters and other such devices

Pharm (4 decks)

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