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Pharmacology
Midterm
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Created by
Julia Thornton
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Cards (104)
Alpha 1
contracts
vascular
smooth muscle and
relaxes
intestinal
smooth muscle
Alpha 2 decreases
GI motility
and
insulin secretion
Beta 1 increases
HR
and
kidney
function
Beta 2 -
bronchodilation
,
vasodilation
, and
reduces
GI motility
Beta 3
decreases
heart
contractility
and
reduces
bladder contraction
HTN Drugs
Vasodilators
Diuretics
Renin-angiotensin
inhibitors
Sympatholytics
Diuretics
= IDE
thiazide
loop
Potassium sparing
Diuretics adverse effects
OH
Hypokalemia
Increased urinary frequency
Sympatholytics
beta blockers
alpha blockers
ganglionic blockers
Centrally acting drugs
presynaptic adrenergic NT depleters
Beta Blockers =
LOL
blocks
beta 1
Alpha blockers =
SIN
blocks
alpha 1
receptors to reduce
peripheral vascular tone
may cause
tachycardia
and trigger
baroreceptor
reflex
Presynaptic Adrenergic Inhibitors
inhibit the release of
norepi
reduces heart
excitation
relaxes
peripheral vasculature
Bradycardia
,
arrhythmias
,
drowsiness
Centrally acting agents
inhibit sympathetic
discharge from BS
dry mouth
,
dizziness
,
sedation
Ganglionic blockers
are used in emergencies to reduce
BP
because they are vasodilators
OH
,
urinary retention
,
visual disturbances
Vasodilators adverse effects
OH
Tachycardia
dizziness
Renin-angiotensin inhibitor regulates
sodium
and
water
balance to maintain BP
ACE =
pril
ARB =
sartan
ACE
inhibits the conversion of I to II so BP will drop
Side effects of renin-angiotensin inhibitors
Dry mouth
Angiodemia
=
medical emergency
Calcium Channel Blockers =
PINE
safe for those with
kidney
disease
causes
vasodilation
and
reduced vascular resistance
Side effects of CCB:
excessive vasodilation
OH
HR abnormalities
Reflex
tachycardia
Organic nitrates
cause
global vasodilation
reduces
cardiac
workload, it does
not
increase
oxygen
supply
nitroglycerin
Adverse effects:
HA
,
Dizziness
,
OH
,
Nausea
For stable angina =
nitroglycerin sublingually
Variant angina =
CCB
CHF
positive inotropic agents - to
increase myocardial contraction force
Digoxin increases CO
can be
fatal
CHF
positive inotropic agents
dopamine
stimulates
beta 1
receptors
Anticoagulants
prevents clots in the
venous
system
antiplatelets prevents
thrombus
in the
arterial
system
Fibrinolytic
agents are used to reopen occluded vessels in arterial and venous thrombosis
Anticoagulants
Low molecular weight heparin = no
monitoring
replaces heparin for DVT
Heparin
is used for initial treatment for
venous thrombosis
aPTT
normal
21-35
seconds
therapeutic
2-2.5
times normal (
60-109
seconds)
Warfarin (
Coumadin
)
primary drug for
LONG
TERM prevention of
DVT
used for
a-fib
too
interferes with vitamin
K
need
INR
testing
INR
measures how quickly a person clots
normal
0.8-1.2
for stroke 2-2.5
a-fib, PE, VTE 2-3
prosthetic heart valve 2.5-3.5
Direct thrombin
inhibitors and
factor Xa
inhibitors are anticoagulants that have
reversal
effects
Direct thrombin inhibitors (
Pradaxa
) inhibit specific components of the clotting mechanisms and is an alternative to
heparin
Factor Xa
inhibitors (Eliquis and Xarelto) inhibit factor Xa to reduce clotting
Adverse effects of Anticoagulants
bleeding
thrombocytopenia
GI upset
Antiplatelets
COX inhibitor
- ASA
ADP receptor blockers
(Plavix)
more effective than ASA and prevent thrombosis from MI
Glycoprotein lib-IIIa receptor blockers
inhibit fibrinogen to activate platelets
most
powerful
Adverse effects of antiplatelets
bleeding
GI upset
Liver
/
kidney toxicity
Thrombolytics
=
dynamite
for clots
converts
plasminogen
to
plasmin
for
MI
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