Daymar College
Lisa H. Young, RN, BSN, MA Ed
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Classifications and Prototype Drugs (Pr)
Pregnancy Category
Controlled Substances
Availability
Uses and Unlabeled Uses
Action and Therapeutic Effect
Contraindications and Cautious Use
Route and Dosage
Administration
Intravenous Drug Administration
Adverse Effects
Diagnostic Test Interference
Interactions
Pharmacokinetics
Clinical Implications
Therapeutic Effectiveness
http://www.youtube.com/
watch?v=Jh_U8V9-Htw
http://www.youtube.com/
watch?v=9mcqPJFB3UE
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Drug Names
Generic name
Brand name/Proprietary name
Chemical name
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Indications and Usage
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Contraindications
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Drug Interactions
◦ “Red Flag” Drugs: Warfarin
Aspirin
Cimetinde
Theophylline
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Drug Reactions
Adverse reaction
Side effects
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Drug Administration
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Enteral Routes
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Parenteral Routes
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Topicals & Transdermal
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Pharmacokinetics
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Absorption
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Bioavailability
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Therapeutic range
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Distribution
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Metabolism
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Elimination
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Pharmacodynamics
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Tolerance
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Half-Life
◦ Digoxin
◦ Warfarin
◦ Heparin
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30-60 hours
0.5 – 3 days
1 – 2 days
Poisonings/Toxicity
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Prescription Drugs
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Nonprescription Drugs
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Controlled Substances
Drug Abuse
Drub dependency
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Prescription Orders
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Patient Name (superscription)
Address
Drug name (inscription)
Drug dose
Route (subscription)
Frequency of administration
Number to be dispensed
Number of refills allowed
DEA #
MD Name/signature
MD address
MD Phone number
http://www.youtube.com
/watch?v=Mhqe12Aj1dE
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http://www.youtube.com/watch?v=S0oqYJp9t
2o
http://www.youtube.com/watch?v=hRdGLzyl
ovM
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Ten Rights
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Right
Right
Right
Right
Right
Right
Right
Right
Right
Right
patient name
drug
dosage
route & technique
time
documentation
client education
to refuse
assessment
evaluation
http://www.youtube.com/watc
h?v=cm7GexPKNOc&list=PLxd
OP8vuQhz9SNJLTWjTGzh3yOTs
Esd6l
http://www.youtube.com/watc
h?v=kdB0PmsX2ng
http://www.youtube.com
/watch?v=yhHq-pV6HOw
Abbreviation
Meaning
Abbreviation
Meaning
Ac
before meals
qhs
every night
Bid
twice daily
Rx
take
c
with
s
without
DC
discontinue
SL
sublingual
dx
diagnosis
SOA
short of air
NPO
nothing by
mouth
ss
half
NS
normal saline
suppos
suppository
p
after
tid
3 times daily
PR
per rectum
top
topical
prn
as needed
ung
ointment
q
every
UT
under tongue
Examples of charting:
A. 9/1/12 9:00 a.m. nitroglycerin, 1 tab, sublingually. Written
instructions given to pt. Precautions explained. Told to call
office at 1:00p.m. today to report progress of his
condition….M. Richards, CMA (AAMA)
B. 1/19/12 11:00 a.m. B 12 vitamin, 10000mcg given IM to left
deltoid muscle without complications and band aid applied to
injection site. Pt tolerated injection well. Pt. given written
instructions for possible side effects and considerations. Pt to
return in one monthly to receive monthly B 12 injections as
ordered……L.Young, CCT.
C. 10/10/2012 1:00 p.m. Mantoux test, 0.01 ml. Tuberculin
Purified Protein Derivative, Left forearm, subcutaneous, small
wheal noted. Pt. instructed not to rub or cover the are and to
return for reading on 10/12/12…..M. Richards, CMA (AAMA)
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Client’s own words
Clarity
Completeness
Conciseness
Chronological
Confidentiality
http://www.youtube.com/wa
tch?v=mYGf0AdhhI4
http://www.youtube.com/wa
tch?v=SDcmXqSvP7A
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Date/time of entry
Legible handwriting
Permanent black ink
Proper terminology, correct spelling and
correct grammar
http://www.youtube.c
Document in sequence
om/watch?v=pe2TQJK
XZIs
Be concise
http://www.youtube.c
Correct errors
om/watch?v=GMVwoR
Sign every entry
0YU-I
http://www.youtube.c
om/watch?v=Bkoic2dL
FmY
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gr = grain
dr = dram
oz = ounce
lb = pound
m = minims
fl dr = fluid drams
fl oz = fluid ounce
pt = pint
qt - quart
gal = gallon
qt iii = 3 quarts
ix = 9
qt i = 1 quart
gr ½ = ½ grain
pt iiiss = 3 ½ pints
1 grain = 60 mg
Metric Conversion Value Chart
Kilo – Hecto-Deka-Base-Deci-Centi-Milli-X-X-Micro
Gram
Liter
Meter
http://www.youtube.com
/watch?v=2QR9yCkAEpE
45.2 grams = 45200.0 milligrams
1cubic centimeter (cc) = 1 milliliters (ml)
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Dosage unit
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Dosage strength
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Dosage ordered
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Desired dose
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Dose on hand
Amount to administer
Drug Calculation: Formula Method
Ordered Dose
Available Dose
X Available Amount
Amount to give
Ordered dose: 500 mg
Available dose: 1000 mg
Available amount: 1 ml
http://www.youtube.com/wa
tch?v=b69Wr008dzM
http://www.youtube.com/watc
h?v=BMDOk3RAHC4
http://www.youtube.com/watch?v=
Wa9Zi64_HJk
Apothecary
Metric
1 fluid oz
30 mL or cc
1 quart
1000 mL or cc
1 grain
0.065 gram
15 grains
1 gram
2.2 pounds
1 kilogram
Household
Metric
1 drop
0.06 mL
1 tsp
4-5 mL
1T
15-16 mL
1 cup
250 mL
2 cups
500 mL
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Clark’s Rule
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Fried’s Rule
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Young’s Law
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West’s nomogram
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Body Weight method
http://www.youtube.com/watch?v
=AQaeAON4GUM
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Assessment
Plan
Implementing
Document
Evaluate
Special Needs
Noncompliance
http://www.youtube.com/watch
?v=1HQHdpAov-I
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Cultural Considerations
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The Life Span
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Understanding and knowledgeable about
medication
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In the Workplace
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The Law
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http://www.youtube.com/watch?v=eboZYnTF
6vs
http://www.youtube.com/watch
?v=mQirK5RxhFo
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Sympathetic Nervous System
Adrenergic Response
_ Catecholamines
_ Adrenaline
_ Beta 1-Adrenergic Receptors
_ Alpha 1-Adrenergic Receptors
http://www.youtube.com/watch?v=lw1A
g86SvlY
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Baroreceptors
_ Pressure receptors
_Mechanoreceptors
_Efferent pathways
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Chemoreceptors
_ carotid artery
_ Elevated arterial carbon dioxide level
_ Heart rate increases
_ Vasoconstriction
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Parasympathetic Nervous System
Vagal Response
_ Cholinergic Response
_ Acetylcholine
_ Nicotinic Cholinergic Receptors
_ Muscarinic Cholinergic Receptors
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Renin-Angiotensin-Aldosterone System
_ Release of Renin
_ Angiotensin I → Angiotensin II
_ Angiotensin-converting enzyme (ACE)
http://www.youtube.com/watch?v=M0vpn6YVwiI
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Preload
The stretching of the ventricle at the end of
diastole.
_ Increasing Preload
Administer extracellular fluid expander
Decrease dose of stop drugs that cause venous
vasodilation
_ Decreasing Preload
Stop or decrease fluid
Diuretics
ACE inhibitors
Aldosterone antagonists
Venous vasodilators
http://www.youtube.com/watch
?v=FjdJdoZcbyA
http://www.youtube.com/w
atch?v=lPK017oR3bw
http://www.youtube.com/watch
?v=mQirK5RxhFo
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Afterload
The resistance that the ventricle must overcome
to eject its contents.
_ Increasing Afterload
Sympathomimetics (stimulate alpha receptors)
ADH
_ Decreasing Afterload
Smooth muscle relaxants
Calcium channel blockers
Alpha receptor blockers
ACE inhibitors
ARBs & PDE
http://www.youtube.com/
watch?v=NFcg62I54w8
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Contractility
_Increasing Contractility
Sympathomimetics (stimulate B1 receptors)
PDE inhibitors
Cardiac glycosides
_Decreasing Contractility
Beta-blockers
Calcium channel blockers
http://www.youtube.com/watc
h?v=_sxiloNshfE
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Heart Rate
Cardiac output = heart rate X stroke volume
Increasing heart rate
Parasympatholytics
Sympathomimetics (stimulate B1 receptors)
Decreasing heart rate
Beta-blockers (block B1 receptors)
Calcium channel blockers
Cardiac glycosides
http://www.youtube.com/wa
Other antiarrhythmics
tch?v=PJ8WsZOywgo
http://www.youtube.com/wa
tch?v=OVVwyCCyH8E
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Stimulate the sympathetic nervous system
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Increase heart rate
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Increase contractility
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Increase afterload
http://www.youtube.com/wat
ch?v=HklZH5QdOeE
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Stimulates: B1 & B2 (low dose) & Alpha
receptors (high doses)
Results: increased contractility, automaticity,
bronchodilation and selective
vasoconstriction
Uses: advanced cardiac life support,
anaphylactic shock, hypotension/profound
bradycardia
Considerations: instant onset, peak 20
minutes and given IV every 3 – 5 minutes for
cardiac standstill
http://www.youtube.com/wa
tch?v=9cpD8lG6DvY
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Stimulates: primarily B1, some alpha
receptors and modest B2
Results: increased contractility, increased AV
node conduction, modest vasoconstriction
Uses: as an inotrope with modest afterload
reduction
Considerations: onset 1 – 2 minutes, peak 10
minutes, blood pressure is variable: B2
causes vasodilation, increased cardiac output
increases blood pressure
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Stimulates: dopaminergic and some B1 at low
doses, B1 at moderate doses, pure alpha
stimulation at high doses (>10 mcg/kg/min)
Results: increased contractility at small and
moderate doses, increased conduction,
vasoconstriction at high doses, does not treat
or prevent renal failure at low doses
Uses: refractory hypotension and shock
Considerations: IV onset 1 – 2 minutes &
peak 10 minutes
http://www.youtube.com/watch?v
=YrEn_1FBBsw
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Stimulates: primarily alpha stimulation, some B1
Results: potent vasoconstriction (vasopressor) and
some increased contractility (positive inotrope)
Uses: refractory hypotension, shock, used as
vsopressor but with inotrope properties
Considerations: Rapid IV onset, duration 1-2
minutes
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Stimulates: direct effect is dominant alpha
stimulation, no substantial B1 effect at
therapeutic doses, indirect effect; causes
release of norepinephrine
Results: potent vasoconstriction (vasopressor)
Uses: refractory hypotension
Considerations: rapid IV onset, duration of
action 10 – 15 minutes
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Arginine vasopressin used as vasopressor
Milrinone (phosphodiesterase inhibitor) used
as an inotrope
◦ Side effects: ventricular dysrhythmias
exacerbation of accelerated ventricular
rate with atrial dysrhythmias
Angiotensin-Converting Enzymes (ACE) Inhibitors
 prevent conversion of angiotensin I to angiotensin
II
 inhibits angiotensin-converting enzyme
 promotes arterial vasodilation
 reduces afterload
Benazepril
Lisinopril
Captopril
Quinapril
Enalapril
Ramipril
Fosinopril
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Blocks angiotensin II
Similar hemodynamic effects as ACE
inhibitors
Used in place of ACE inhibitors if they are not
tolerated due to intractable cough or
angioedema
ARBs end with “sartan”
Candesartan, first drug approved by FDA for
heart failure
Candesartan
Irbesartan
Telmisartan
Eprosartan
Losartan
Valsartan
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mineralocorticoid hormone
hold sodium and water and excrete potassium
potassium-sparing diuretics
decrease in preload
minimized release of catecholamines
improved endothelial function
antithrombotic effects
decreased vascular inflammation and myocardial
fibrosis
Spironolactone
Eplerenone
http://www.youtube.com/watch?v=OAkb
KN6AuWE
block B1 or B2 receptors
 decrease heart rate and contractility
 bronchial and peripheral vasoconstriction
 management of heart failure
 management of stable angina
 management of acute coronary syndromes
 decrease myocardial oxygen demand
 increase coronary perfusion
 management of hypertension
Atenolol
Metoprolol
Propranolol Esmolol
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decrease the flux of calcium
decrease heart rate, contractility and
afterload
degree of negative inotropic effect
reduce coronary and systemic vascular
resistance
decreasing myocardial oxygen demand
not indicated in the treatment of heart failure
adverse effects: peripheral edema, worsening
heart failure, hypotension and constipation
Verapamil Dihydropyridine CCB Diltiazem
Action
Verapamil
Dihydropyridine
calcium channel
blockers
Diltiazem
Heart rate
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⇑
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AV nodal
conduction
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Neutral
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Contractility
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Arterial
vasodilation
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Nitroglycerin and Nitrates
 IV a primary venous vasodilator
 sublingual produces both venous and arterial
vasodilation
 decreases preload
 reducing myocardial oxygen demand
 higher doses = coronary artery dilation
 exhibits antithrombotic and antiplatelet
effects
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mixed venous and arterial vasodilative
arterial vasodilator
indicated in hypertensive crisis
cardiac emergencies
hypotension side effect
possible thiocyanate toxicity
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synthetic brain natriuretic peptide (BNP)
counteract the effects of RAAS
venous and arterial vasodilative effects
management of acute decompensated heart
failure
decrease preload and afterload
lowers blood pressure
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cardiac glycoside
weak inotropic properties
parpasympathetic properties
used in treatment of heart failure
narrow therapeutic range
easy to develop toxicity
electrolyte increase effect of digoxin
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reduce preload
ascending loop of Henle
promote venous vasodilation
reduce preload
rapid onset and short duration of action
high-ceiling diuretics
effective for renal dysfunction
Bumex
Lasix
Demadex
Inhibit reabsorption of sodium & chloride
 Less potent than loop diuretics
 Decreased effectiveness with renal dysfunction
 Low-ceiling diuretics
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Bendrofluazide
Hydrochlorothiazide
Indapamide
Metolazone
Cyclothiazide
Chlorothiazide
Polythiazide
Trichlormethiazide
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Direct renin inhibitors – Aliskiren
_ treatment of hypertension
_ impact RAAS
Vasopressin 2 Antagonists – Tolvaptan
_ oral medication
_ renal collecting ducts
_ treatment of heart failure with volume
overload
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Low-Density Lipoprotein Cholesterol
primary goal in the management of
coronary heart disease
HMG-CoA reductase inhibitors (statins)
Bile acid resins
Nicotine acid
Dose dependent effect on LDL-C
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Nicotinic acid (Niacin)
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Fibrates
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Statins
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Bile acid resins
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Bile acid sequestrants
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Combine with bile acids
Hepatic circulation
More production of cholesterol
Breaks cholesterol to make bile acids
Increases LDL-C receptors
Net decrease in total cholesterol
Net decrease in LDL-C
Constipation
Questran
Colestid
WelChol
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B complex vitamin
Dilates the cutaneous blood vessels
Increases blood flow to face, neck and chest
Vasodilation – “flush”
Increase gastric acid secretion
Decrease mortality in MI
Decrease VLDL-C production
Decreases lipolysis of triglycerides
Decreases hepatic triglyceride synthesis
Niacor
Slo-Niacin
Niaspan
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Fibric acid agents
Not fully understood
Stimulate lipoprotein lipase activity
Decrease hepatic triglyceride production
Decrease cholesterol synthesis
Increase mobilization of cholesterol
Enhance the removal of cholesterol
Increase cholesterol excretion
Raise HDL-C levels
Atromid-S
Tricor
Lopid
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Statins
Reduced lipid levels
Reduced future coronary events
Reduce the risk of coronary mortality &
morbidity
Inhibition of HMG-CoA reductase
Reduce the quantity of mevalonic acid
Mevacor
Zocor
Lescol
Lipitor Crestor
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Newest class of lipid-lowering medications
May be combined with HMG-CoA reductase
inhibitor
Ezetimibe
Blocks the absorption of cholesterol in the
small intestine
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To protect the integrity of the vessels and
prevent harmful bleeding
To maintain the fluid state of the blood
These two goals must be achieved
simultaneously to maintain health
Platelet Aggregation
Release Thromoboplastin
Prothrombin
Thrombin
Fibrinogen
http://www.youtube.com/watch?v=IEuFUSuGc
xE&list=PL2UREUiTlHRn3iW9DhoeLjxNDM7Ly5
vrA
Type
Actions/ Physiologic
Effect
Agents
Fibrin specific
Plasminogen activation Tissue plasminogen
Rapid clot lysis
activators (t-PAs)
Clot specific
Alteplase
Reteplase
Tenecteplase
Nonfibrin specific
Systemic lysis
Slow clot lysis
More prolonged,
systemic effect
Streptokinase
Anistreplase (APSAC)
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Earliest “clot busting” medication
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Dissolves clots during an acute MI
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Produce antistreptokinase antibodies
Contraindicated to use streptokinase in these
patients
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Anisoylated plasminogen streptokinase
activator complex
Altered form of streptokinase
Converts circulating plasminogen into
plasmin
May be given as an IV bolus over 2 – 5
minutes
Particular affinity for fibrin
Activates the plasminogen that is bound to
fibrin
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Unfractionated Heparin (UFH)
◦ Antithrombotic agent
◦ Prevents the conversion of prothrombin to thrombin
◦ Binds to plasma proteins, blood cells, and
endothelial cells
◦ Administered intravenously
◦ Weight-based protocol
◦ Administrated subcutaneoulsy
◦ aPTT , PT, INR, platelet count, hemoglobin level and
hematocrit
◦ Bleeding potential complication
◦ Thrombocytopenia
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Low-molecular-weight Heparin (LMWH)
Accelerating the activity of antithrombin III
Longer half-life than UFH
No clotting times need to be monitored
Lower incidence of HIT
Higher rate of minor bleeding
Special dosing required for patients with chronic
renal insufficiency
◦ Protamine used for reversing effects
◦ Administered subcutaneously
◦ Enoxaparin
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Direct Thrombin Inhibitors
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Treatment of thrombosis in patients with HIT
Ability to inactivate fibrin-bound thrombin
Lepirudin and desirudin
Argatroban
Bivalirudin
Pradaxa
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Factor Xa Inhibitors
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New class of anticoagulants
Fondaparinux
DVT and PE prophylaxis treatment
Antithrombotic action by neutralizing factor Xa
Subcutaneous injection
No need for laboratory monitoring
No reports of HIT
Contraindicated in severe renal dysfunction
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Warfarin (Coumadin)
◦ Oral anticoagulant
◦ Inhibition of the synthesis of factor II (prothrombin)
◦ Altering the synthesis of other vitamin K-dependent
factors
◦ Primarily bound to albumin in the blood
◦ Monitor PT and INR levels
◦ Lifelong therapy for atrial fibrillation
◦ Many drugs interact with warfarin
◦ No aspirin, ibuprofen or naprosyn
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Glycoprotein Iib/IIIa Inhibitors
◦ Interfere with the final pathway of platelet
aggregation
◦ Prevent fibrinogen binding
◦ Administrated intravenously
◦ May be given with aspirin, clopidogrel & heparin
◦ Abciximab (ReoPro)
◦ Monitor platelet count and hemoglobin level
◦ Treatment of unstable angina and non-STEMI
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Adenosine Diphosphate Inhibitors
◦ Clopidogrel (Plavix)
◦ Prevents adenosine diphosphate (ADP) activation of
platelets
◦ Treatment of unstable angina & non-STEMI
◦ Avoid use of omeprazole (Prilosec)
◦ Warning for patients who are poor metabolizers
◦ Prasugrel
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Aspirin
◦ Anti-inflammatory, analgesic, antipyretic &
antithrombotic
◦ Treatment of acute or chronic ischemic heart
disease
◦ Inhibiting cyclooxygenase and inhibiting the
synthesis of thromboxane A2.
◦ Inhibits endothelial production of prostabladin I2
◦ Chewing aspirin accelerates absorption
◦ GI side effects
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Oxygen
Aspirin
Sublingual or Intravenous Nitroglycerin
Intravenous Beta Blocker
Unfractionated Heparin
Glycoprotein IIb/IIIa Receptor Blocker
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Stops irregular beats and maintain regular
heart beat
Medications must be taken on time
Take pulse before each dose
Limit fluid and salt intake
Avoid antacids and limit citrus, some
vegetables
Monitor for tiredness
Some are light sensitivity
Regular monitoring
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Four Classes of Antiarrhythmics
Class I
◦ Sodium Channel Blockers
◦ Class I A: treat a wide variety of atrial & ventricular
arrhythmias
 Control arrhythmias by altering the myocardial cell
membrane and interfering with ANS control of
pacemaker cells
 Blocking sodium channels in cell membrane during an
action potential
 Block parasympathetic stimulation of the SA & AV node
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Class I B
◦ Blocks rapid influx of sodium ions during
depolarization phase
◦ Decreased refractory period
◦ Affects Purkinje fibers & myocardial cells in the
ventricles
◦ Used only to treat ventricular arrhythmias
◦ May exhibit additive or antagonistic effects when
administered with other antiarrhythmics
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Class IC
◦ Primarily slows conduction along the conduction
pathway
◦ Used to treat severe, refractory ventricular
arrhythmias
◦ May be used for treatment of SVT
◦ Treat life threatening ventricular arrhythmias
Adenosine
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Class II
◦ Composed of beta-adrenergic antagonists (beta
blockers)
◦ Block beta-adrenergic receptor sites in the
conduction system of the heart
◦ SA node firing is slowed
◦ AV node and other cells receive and conduct
impulses slowly
◦ Reduces strength of contraction
◦ Slow ventricular rates in afib, aflutter and PAT
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Class III
◦ Treat ventricular arrhythmias
◦ Asymptomatic A fib and A flutter treatment is
possible
◦ Amiodarone is first line drug choice for the
treatment of VT and V Fib.
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Class IV
◦ Calcium Channel Blockers
◦ Treat SVT with rapid rates
◦ Inhibits calcium ion influx across cardiac and
smooth muscle cells
◦ Decrease contractility and oxygen demand
◦ Dilate coronary arteries and arterioles
◦ Used to relieve angina, lower blood pressure, and
restore normal sinus rhythm