High Yield
-
-
What organ systems/body parts do PNS dominate/affect? What about SNS?
Left-sided HF VS right-sided HF
Common side effects of loop diuretics, ACE inhibitors, CCBs, BBs
What is endocarditis?
Digoxin
- MOA
- Side effects
- What to do before administering meds?
- Relationship with potassium?
Beta blockers and the different generations – which receptors they each affect?
What do those receptors affect in the body?
General anatomy of the heart (pericardium, veins, arteries, atrium, ventricle, SA
node, valves, etc)
Stable VS unstable anginas + STEMI VS NSTEMI, how to differentiate from each
other?
Angina medications and MOA
Atherosclerosis pathophysiology + what are foam cells?
Heparin toxicity antidote? Muscarinic agonist toxicity antidote? Muscarinic
antagonist toxicity antidote? Warfarin toxicity antidote?
Different classes of dysarrthymic medications
Veins VS arteries function
Diastolic failure VS systolic failure
Warfarin and what is important to know – SE, labs, etc
Statins and what side effects to look out for?
What is Frank-Starling law?
Anticoagulants MOA
HDL = good, LDL = bad – relation with atherosclerosis
Risk factors of HTN
Why are beta blockers taken with nifidepine?
Neurotransmitters of PNS and SNS
Peripheral VS arterial vascular disease
Valve issues (stenosis, prolapse, regurgitation)
Know CO = HR x SV and BP = CO x SVR
HTN medications
Autonomic Nervous System
PNS/Parasympathomimetic
(cholinergic) PREDOMINATES
Function
●
Decrease HR
SNS/Parasympatholytic (adrenergic)
●
Increase HR
●
●
Vasodilation + glands
Increase GI activity (saliva,
gastric, bowel, bladder)
Constrict pupils
Contract bronchi
●
●
●
●
Vasoconstriction + glands, esp sweat
Decrease GI activity
Dilate pupils
Dilate bronchi
●
ACh
●
●
ACh
Epinephrine – all alpha/beta but no
dopamine
Norepinephrine – A1, A2, B1, but not B2,
dopamine
Dopamine – A1, B1, dopamine
●
●
Neuro
transmitters
●
●
Receptors
●
●
●
●
Baroreceptors
NicotinicN - nerve
NicotinicM - skeletal muscle
contraction
Muscarinic - to all PNS
●
●
●
●
●
●
Pathway
Long preganglionic → ACh → short
postganglionic with Nicotinic receptors →
ACh → target effector with Muscarinic
receptors
Baroreceptors
Alpha1 – eyes, vessels, genitals
Alpha2 – inhibition of transmitter
release
Beta1 – increase
chronotropic/inotropic/dromotropic +
release renin from kidney
Beta2 – dilated bronchi, glycogenesis of
liver and skeletal muscle, relax uterus
Dopamine – dilation of kidney
Short preganglionic → ACh → long
postganglionic with Nicotinic receptors → NE →
target effector with Alpha/Beta receptors
Postganglionic → ACh → sweat gland with
Muscrinic receptor
Preganglionic → ACh → adrenal gland with
Nicotinic receptor to release E
What is Beers Criteria? → List of drugs that are potentially dangerous for >65 y/o as it increase risk for AE;
especially ANTICHOLINERGIC DRUGS
ANS Drugs (blue: PNS, red: SNS)
Drug Class
Prototype
MOA + Use
Side Effects
Good to Know
Muscarinic
Agonist
Bethanechol
(Urecholine)
Bind reversibly to
muscarinic receptors to
cause activation
hypotension,
bradycardia, diarrhea,
salivation, abd cramps,
bronchoconstriction,
sweat
Treatment for OD
= atropine
Xerostomia (dry mouth,
tooth decay), blurred
vision, photophobia,
increased intraocular
pressure, urinary
retention, constipation,
anhydrosis,
Treatment for OD
= physostigmine
For urinary retention
Muscarinic
Antagonist
Atropine
Competitive blockage @
muscarinic receptors to
prevention activation by
ACh
For prevent/treat
bradycardia, decrease
Caution for pts
with asthma,
hyperthyroidism,
GI obstruction,
urinary tract
blockage
secretion during
preanesthesia, treat GI
hypermotility, reverse OD
for bethanechol
Cholinestera
se Inhibitors
Oxybutynin
(Ditropan) &
Tolterodine
(Detrol)
For OAB: oxybutynin
selective for M3 and
tolerodine non-selective
Neostigmine
(prostigmin)
Decreases activity of
cholinesterase; leads to
increased amounts of ACh
available
–stigmine
Physostigmine
Neuromuscul
ar Blocking
Agent
Turbocurarine,
vecuronium
Myasthenia gravis
(autoimmune destruction
of ACh receptors); reverse
atropine poisoning
(physostigmine
preferred)
Nondepolarizing binding
to nicotinicM
receptor-ACh cannot bind,
→ paralysis of muscles by
blocking action at the
nicotinicM receptor site
For surgery, intubation,
mechanical ventilation
Succinylcholin
e
Depolarizing binding to
nicotinicM and initiate a
contraction, then stays
bound so the membrane
remains depolarized →
paralysis of muscles by
blocking action at the
nicotinicM receptor site
constipation,
tachycardia
Same as muscarinic
agonist > hypotension,
bradycardia, diarrhea,
salivation, abd cramps,
bronchoconstriction,
sweat
positive charge
CANNOT cross
membrane
resp arrest,
hypotension
Keep in mind:
must be given
thru IV, CANNOT
pass thru BBB +
placenta, DOES
NOT alter pain
perception +
consciousness
Specific to
Succinylcholine:
Malignant
hyperthermia (increase
in body temp due to
hypercatabolic state);
post-op muscle pain;
hyperkalemia (due to
promotion of release of
K+ from tissues)
no charge CAN
cross membranes
For surgery, intubation,
mechanical ventilation
Adrenergic
Antagonist
ALPHA
Prazosin
(Minipress) for
HTN
-sin
Tamsulosin
(Flomax) for
BPH enlarged
prostate
Adrenergic
Antagonist
BETA
Propranolol
(Inderal): 1st
gen,
nonselective
-lol
Metoprolol
HTN, BPH, Raynaud’s
disease,
pheochromocytoma
Orthostatic hypotension, relfex tachycardia,
congestion, ejaculation inhibition
For heart and vessels:
angina, HTN, MI, heart
failure, dysrhythmia
SE for B1: bradycardia/reduce CO/AV
block/rebound excitation
SE for B2:
bronchoconstriction, glycogenolysis
inhibition
(Lopressor):
2nd gen, beta1
selective
Carvedilol
(Coreg): 3rd
gen, B1, B2, A1
for
vasodilation
Adrenergic Agonists = -cholamines = directly stimulating adrenergic receptors + can promote NE
release, inhibit NE reuptake, or inhibit NE inactivation
Catecholamine = non-oral, no cross BBB, short ½ life
Noncatecholamine = oral, cross BBB, long ½ life
Receptor
Use
SE
Alpha 1
Promotion of hemostasis, nasal
decongestion, combined with/adjunct
with local anesthesia, treatment of
decreased BP, pupil dilation
hypertension, necrosis, bradycardia
Alpha 2:
Clonidine
(Catapress)
for HTN, pain, ADHD by activating α2
receptors in the CNS; decreases
sympathetic outflow to vessel and heart
to decrease HR + BP
drowsiness, xerostomia, rebound HTN, abuse
potential/euphoria, teratogenic
Alpha 2:
Methyldopa
HTN by convert methylnorepinephrine
neurons + activate α2, only decrease BP
Beta 1
treatment of cardiac arrest, heart
failure/shock, AV block
dysrhythmias, angina
Beta 2
for asthma, delay preterm labor
Hyperglycemia, tremor
Dopamine
treatment for shock/heart failure
tachycardia/dysrhythmia, angina, renal damage
Atherosclerosis: Thickening and hardening of vessel walls, caused by accumulation of lipid-laded
macrophages within the arterial wall, leading to formation of a lesion = plaque, important to consider
cholesterol level
1. Injury
2. Inflammation
3. adhesion m’c with macrophages - damage endothelium = free radicals
4. engulf oxidized LDL = fatty streak/foam cell = more free radicals
5. smooth muscle cell proliferation = fibrous plaque
6. plaque rupture = complicated plaque = ischemia or infarction
Total cholesterol level = <100
● LDL = < 100
● HDL = > 60
● TG = < 150
Metabolic syndrome = increases triglyceride levels in pts, often those who are inactive, smokers,
alcoholic, genetic hx, high cholesterol diet; Cluster of conditions that increase the risk of heart
disease, stroke, DM (has to meet 3 parameters)
Anti-Hyperlipidemia (Statins & NFE)
Drug
Class
Prototype
MOA + Use
Side Effects
Good to Know
Statins
Atorvastatin
(Lipitor),
Rosuvastatin
(Crestor),
Simvastatin
(Zocor)
Inhibits enzyme critical
in the cholesterol
biosynthesis pathway =
decreased cholesterol
production ‒> liver to
take up cholesterol from
bloodstream = reduces
LDL (MOST
IMPORTANT) and
triglycerides, increases
HDL
muscle pain,
rhabdomyolysis SO
LOOK FOR COKE
COLA URINE (look out
for muscle pain and
coke urine,
discontinue + report to
provider immediately),
liver damage,
increased risk for
diabetes (CI for
pregnancy and
muscle disorder)
Given at night
-statin
Promote plaque stability,
reduce inflammation at
plaque site, slow
progressing of coronary
artery calcification,
enhance vasodilation,
reduced risk for
thrombosis and platelet
deosition, suppress
produpction of thrombin
Exercise to increase HDL
Other
antihyperl
ipemics
Niacin
(nicotinic acid)
Reduce LDL &
triglycerides + increase
HDL
Flushing, GI upset
Used in
conjuncti
on with
statins
No longer a
recommendation since
not as effective as statins
and no evidence of CV
risk reduction
ONLY used when statins
cannot be used
Fibrates
Reduce triglycerides, no
effect on LDL
FIBER
REDUCE FAT
Ezetimibe
(Zetia) - bile
acid
EXCLUDE
CHOLESTERO
L
GI upset, highly
protein boundinteract with warfarin
Inhibit dietary
absorption/reabsorptio
n of cholesterol in
intestines - increase
excretion in feces
Anti-HTN (Red: diuretic, orange: sympatholytics, green: CCBs, blue:
RAAS) due to excessive activation of RAAS
Drug Class
Prototype
MOA + Use
Side Effects
Good to Know
Thiazide
diuretics
Hydrochlorot
hiazide
block reabsorption of Na+
and Cl- at distal CT; not
useful in severe renal
impairment
similar to loop
diuretics but less
severe and no
ototoxicity
first line for HTN, edema
Loop Diuretic
K+-sparing
diuretics:
Aldosterone
antagonist
Furosemide
(Lasix)
Spironolacto
ne
(Aldactone)
Blocks reabsorption of Na+
and Cl- in the thick segment
of ascending loop of henle.
20% of filtered sodium and
chloride is reabsorbed here,
so diuresis is
profound-strongest diuretics
require rapid or massive
mobilization of fluid; should
be avoided when other
diuretics will suffice as it
has more severe SE, for
severe renal impairment
hypokalemia,
ototoxicity,
hyponatremia,
hypochloremia,
dehydration,
hypotension
Blocks aldosterone @ distal
nephron = retention of K+
and increased excretion of
Na+; minimal diuretics
hyperkalemia,
similar to
hormones (affect
menstrual cycle,
deepen voice,
hirsutism)
Drug interaction:
combined with
thiazide and loop
diuretics, careful
with agents that
increase K+ levels
hyperkalemia, GI
upset
careful with agents
that increase K+
levels
Eplerenone
-one
HTN + edema (used with
loop or thiazide) heart
failure
Disrupt Na+ and K exchange
@ distal nephron by inhibit
mechanism; minimal diuretics
Drug interactions:
Digoxin (increased
toxicity for those
w/ hypokalemia),
ototoxic drugs,
potassium-sparing
drugs (to
counteract K+
wasting)
Dose: LAst 6 hrs
(Lasix), BID
K+-sparing
diuretics:
Non-aldostero
ne antagonist
Triameterne
(Dyrenium)
Osmotic
diuretics .. not
important
Mannitol
(Osmoitrol)
given thru IV, filtered at glomerulus, undergo minimal reabsorption +
metabolism, pharmacologically inert
Beta blocker
Prototypes
Propranolol
(Inderal)
decrease HR, CO, contractility
bradycardia,
hypotension,
insomnia
Alpha 1 blocker
Prototype
Prazosin
(Minipress)
prevent stimulation of A1
receptors = prevent
vasoconstriction
Orthostatic
hypotension so
not first line for
HTN
Alpha/Beta
Blockers
Carvedilol
(Coreg)
Blocks B1, B2, A1 for
decrease HR, RR, and BP so
bradycardia,
hypotension =
Alone or combined w/ other
diuretics to treat HTN and
edema
Caution with
diabetics, you can
mask S&S of
hypoglycemia and
ability to raise
blood glucose +
less effect in
blacks than
whites
Prototype
CAUTION with resp disease
heart block
Central Active
Alpha2 Agonist
Prototype
Clonidine
(Catapress)
A2 inhibit neurotransmitter
release so it suppress
sympathetic outflow from
brain stem to heart and
vessels = vasodilation and
reduced CO
dry mouth,
sedation, rebound
HTN, orthostatic
hypotension
Direct
vasodilators
Hydralazine
(Apresoline)
Dilates arterioles, given
frequently for HTN crisis
for HTN,
angina, heart
failure to
decrease
afterload
(resistance) in
arterioles and
preload
(stretch) in
veins =
decrease
workload, CO,
perfusion
Minoxidil
(Lonitan)
Very potent, also dilates
arterioles
Topical: Rogaine for hair
growth
Nitrates
(nitroglycerin
e, isosorbide
dinitrate)
Dilates veins and coronary
arteries
expansion of blood
volume by body
attempt to restore
BP, reflex
tachycardia
because
baroreceptors
sense drop and
trigger SNS,
orthostatic
hypotension
Dihydropyridin
es
Nifedipine
(Procardia)
For HTN and angina, selective
calcium channels in
arterioles to decreased BP
and increase coronary
perfusion, HR, contractility
toxic dose can lead
to non-selectivity +
cardiac
suppression, ankle
edema, reflex
tachycardia
(combine with beta
blocker to prevent
this)
Why would a beta
blocker be given
with a CCB?: to
prevent reflex
tachycardia
Verapamil
For HTN, arrhythmias, angina;
block calcium channel in
vascular smooth muscle +
heart to cause negative
chronotrope, inotrope,
dromotrope, and
vasodilation
constipation,
hypotension, can
exerbate
dysfunction with
cardiac disease,
caution with
heart failure and
hypotension
because can AV
block
Drug/food
interactions:
Digoxin +
beta-adrenergic
blocker (cardiac
suppression),
grapefruit juice
(decrease
metabolism =
toxicity = can lead
to
hypotension/cardio
toxicity)
Enalapril
(Vasotex),
Lisinopril
(Zestril)
reduce levels of
angiotensin II and increase
levels of bradykinin thru
inhibition of ACE and kinase
II, prevents cardiac
remodeling/myocytes
changes
ACE: Angioedema
(should not use
med again), cough
from bradykinin,
elevated K+
(hyperkalemia),
first-dose
hypotension,
vasodilation, fetal
Drug interaction:
diuretics (first-dose
hypotension),
antihypertensive
agents, agents that
increase K+
-pine
Acts on
arterioles for
HTN
Orphans
Acts on
arterioles +
heart for HTN
and
dysrhythmias
Angiotensin-C
onvertng
Enzyme
Inhibitors
(ACEIs)
-pril
HTN, heart failure, MI,
Caution: pts with
renal
Angiotensin II
Receptor
Blockers
(ARBs)
Valsartan
(Diovan)
-sartan
diabetic/nondiabetic
nephropathy, prevent
diabetic neuropathy, prevent
MI/stroke/death
injury, decrease
remodeling and
blood volume
insufficiency
given low dosage
since its excreted
by kidneys,
pregnant women
block action of angiotensin II
at receptor; only for decrease
cardiac morbidity and
mortality
Angioedema, fetal
injury, similar to
ACEIs but lower
cough and
hyperkalemia
Drug interaction:
antihypertensives
HTN, heart failure, diabetic
nephropathy, MI, stroke,
diabetic retinopathy
Caution: pts with
renal
insufficiency
given low dosage
since its excreted
by kidneys,
pregnant women
Renin Inhibitor
Aliskiren
(Tekturna,
Rasilez)
bind to renin to inhibit
production of angiotensin I,
only for HTN
less cough +
angioedema but
fetal injury
Caution with
pregnant women
Aldosterone
Antagonists
Eplerenone
(Inspra)
block aldosterone receptor
hyperkalemia
Drug interactions:
Drugs that increase
K+
HTN, heart failure
Common Dysrhythmias
Atrial
fibrillation
most common dysrhythmia caused by multiple atrial impulses firing randomly = stroke,
clot; treated by cardioversion, drugs to control rate/rhythm (beta blocker/CCB or
antiarrhythmics, anticoagulant, ablation
Atrial flutter
fast atrial rate with a fixed or variable ventricular rate; similar treatment as Afib
Supraventric
ular
tachycardia
(SVT)
AV node affected; HR of 150-250 bpm = increase CO but can get too fast to have enough
blood filled up in heart eventually decrease CO; treated with Valsalva maneuver/bearing down
to slow rate down when rapid or dump baby head in ice water
Ventricular
tachycardia
(VT)
150-250 bpm; emergency need cardioversion ASAP, Amiodarone IV, defibrillator implant
Ventricular
fibrillation
(Vfib)
No meaningful CO = emergency with async discharge of ventricules, localized twitching
around ventricles, will eventually stop pumping; treatment with defibrillation, ICD placement,
Amiodarone
Premature
ventricular
contractions
(PVCs)
common like from caffeine but can lead to decrease of CO; ventricle fires prematurely without
atrial stimulation
Torsades de
Pointes
tachydysrhythmia, form of VT, caused by prolonged QT interval as SE of drug, fatal if not
treated by cardioversion IV Mg+
Atrioventricu
lar (AV) block
impaired transmission from atria to ventricles has 3 degrees
1.
First degree: P wave normal but QRS complex is late but regular
2.
3.
4.
Second degree Type I: P wave normal but QRS complex gradually is late until it is
gone
Second degree Type II: P wave normal but QRS complex sometimes does not occur
and sometimes occurs but when it does its regular – requires pacemaker
Third degree: P wave and QRS complex no longer in sync – requires pacemaker
Antidysrhythmic (SBPC, O)
Drug Class
Prototype
MOA + Use
Side Effects
Good to Know
Class I:
Sodium
Channel
Blockers
Lidocaine
short-term treatment of
ventricular dysrhythmias
by slow
atrial/ventricular
conduction and
accelerate
repolarization
drowsiness, confusion
rapidly metabolized
by liver
Class II:
Betablockers
Propranolol
non-selective beta
blocker to slow
ventricular rate &
decrease contractility
hypotension, AV block,
bronchospasm
Caution with pt with
resp issue
Class III:
Potassium
Channel
Blockers
Amiodarone
HIGHLY effective
short-term against
atrial + ventricular
dysrhythmias by delay
repolarization
has SERIOUS toxicity
(lung damage, impaired
visual, thyroid/liver
toxic, teratogenic,
photosensitivity)
Class IV: CCBs
Verapamil &
Diltiazem
cause negative
chronotrope, inotrope,
dromotrope, and
vasodilation
constipation,
hypotension, can
exerbate dysfunction
with cardiac disease,
caution with heart
failure and
hypotension because
can AV block
Drug/food
interactions: Digoxin
+ beta-adrenergic
blocker (cardiac
suppression),
grapefruit juice
Others
Adenosine
& Digoxin
slow conduction thru AV
node
dysrhythmias risk for
digoxin and increase
risk for it with
hypokalemia
Adenosine has rapid
half-life + terminate
SVT
Digoxin leads to positive
inotrope, negative
chronotrope and
dromotrope + suppress
renin and SNS
Must count HR before
admin digoxin
Left VS Right HF
Left
sided HF
More common, can lead to right sided
Forward effects = decreased tissue perfusion + RAAS activation
Backward effects = pulmonary congestion symptoms: dyspnea on exertion, orthopnea, cough,
paroxysmal nocturnal dyspnea, cyanosis, crackles at base of lungs
Right
Most likely caused by left sided HF
sided HF
Forward effects = decreased tissue perfusion + RAAS activation
Backward effects = systemic congestion symptoms: hepatomegaly, ascites (fluid in abdomen),
splenomegaly, anorexia, subcutaneous edema, jugular vein distention
Anti-Heart Failure (DRAASBS)
Drug Class
Prototype
MOA
Good to Know
Diuretics
thiazide, loop,
spironolactone,
caution with
k-spring diuretic
decrease venous pressure,
afterload, pulmonary/peripheral
edema, cardiac dilation
decrease symptoms BUT NOT
survival time
Agents that
inhibit RAAS:
ACE inhibitors
—pril
suppress production of
angiotensin II
improve symptoms and survival
time
Agents that
inhibit RAAS:
Aldosterone
antagonist
spirolactone/epler
enone
blocks aldosterone receptors
improve symptoms and survival
time
Agents that
inhibit RAAS:
Arnis
Sacubitril +
Valsartan
inhibit neprilysin to
vasodilation and reduce volume
SE: similar to ARBs and dementia
Beta blockers
Propranolol,
Metoprolol,
Carvedilol
blocks beta receptors depending
on generation to decrease HR
and BP
start with LOW does because can
suppress cardiac function with
SE of bradycardia, hypotension,
another HF
SGLT-2
inhibtors
Canagliflozin
(Invokana)
inhibit SGLT-2 in kidney to inhibit
RAAS, promote excretion, reduce
SNS, reduce preload/afterload
SE: vaginal fungal infection, UTIs
SE: hyperkalemia
Anginas
Acute Coronary
Syndrome =
complete
occlusion of
coronary artery
by thrombosis
Angina
pain beneath sternum and radiate to left jaw, shoulder, arm because
decrease O2 flow to heart caused by atherosclerosis treated with BB,
nitrates, CCB
Chronic stable
angina
(exertional
angina)
caused by coronary artery disease (CAD) + atherosclerosis = decrease
blood supply, triggered by exertion, emotional stress, cold, but no pain
at rest; treated by increase supply/decrease demand, stop smoking,
exercise, treat hyperlipidemia
Variant angina
(Prinzmetal’s)
rare, caused by coronary artery spasm from cold, stress, substance use
Unstable angina
EMERGENCY! Unstable plaque! Unpredictable pain! Acute coronary
syndrome, may have normal, undetermined, or abnormal EKG (but NOT
ST-segment elevation) + no troponin rise
STEMI
(ST-Elevation
persistent ST-segment elevation indicating blockage of coronary
artery and imbalance of O2 supply and demand = cell death within 20
MONA
(morphine, O2,
nitroglycerine,
aspirin
CHEWED)
Myocardial
Infarction)
min if no intervention
crushing radiating pain, last 20-30 min, can look different for women
like crushing, stabbing, cold sweat, dizziness, nausea, fatigue, SOB, EKG
change, elevated serum cardiac marker
NSTEMI
(Non-ST-Elevati
on Myocardial
Infarction)
may have normal, undetermined, or abnormal EKG (but NOT
ST-segment elevation) + Troponin rise
Antianginals (NBC)
Drug Class
Prototype
MOA + Use
Side Effects
Good to
Know
Nitrates
NTG
(Nitroglycerine),
Imdur (Isosorbide)
decrease O2 demand/preload by
vasodilation in VENOUS system
primarily and CORONARY
ARTERIES
hypotension,
tachycardia
do not
abruptly
stop med
Beta blockers
Metoprolol
(Lopressor) +
Propranolol
decrease O2 demand by decrease
HR and contractility
Calcium-Channel
blocker
Verapamil
(ORPHAN) +
Enalapril
decrease O2 demand by
vasodilation
ORPHAN can decrease afterload,
preload, contractility (decrease
SV)
Anticoagulants (HEF + WDR)= prevent thrombosis in veins and atria by
prevent formation of fibrin
Drug Class
Prototype
MOA + Use
Good to Know
Activating
Antithrombin
Heparin (IV)
(unfractionated
binds antithrombin,
increase ability to
inactivate factor Xa and
thrombin; HIGHEST RISK
for HIT (Look for PLT
counts) to prevent DVT
or Afib
aPTT= partial thrombosis time = to measure
contact activation and common pathways for
heparin use with
Normal as < 40 sec
TR = 60-80 sec
we want to 2x their normal = TR (40*2 = 80)
BLEEDING + BRUISING RISK
rapid onset,
enhancing
activity of
antithrombin
and inactivate
thrombin and
factor Xa to
decrease
thrombin BUT
differ in equal
effects on
thrombin and
If TR too high = hemorrhage
Treatment for OD = protamine sulfate
Enoxaparin
(SubQ)
(low-molecularweight (LMW)
inactivate Xa, and thrombin to small extent; low risk for HIT
factor Xa
Vitamin K
Antagonists
heparin)
Fondaparinux
(SubQ)
only inactivate Xa; no risk for HIT
Warfarin (PO)
(Coumadin)
suppress coagulation by
decrease production of vit
K-dependent clotting
factors to prevent DVT
and PE for pts with Afib or
cardiac valve
replacement; dosing
highly variable because
of genetics and dietary vit
K intake (kept steady) +
delayed onset
Treatment for OD = vitamin K
(phytonadione)
If INR too high = vitamin K + fresh frozen
plasma
If INR too low = continue
Caution: drugs that promote bleed, albumin
bound, inhibit metabolizing enzymes,
increase risk for peptic ulcer formation + pts
with liver disease, alcohol, pregnant, vit K
deficiency
Educate: frequent INR monitoring, keep vit
K intake consistent, BLEEDING + BRUISING
RISK ensure all prescribers know warfarin
use, avoid OTC pain relievers, S&S of
hemorrhage, discuss contraception with child
bearing age
Normal INR = <1.1 (0.8-1.1) (we want to 3x
more than normal = TR)
TR: 2.0-3.0 or 2.5-3.5 (for higher risk to
develop clot)
If TR too high = bleeding
Direct
Thrombin
Inhibitors
Dabigatran (PO)
(Pradaxa)
bind to thrombin when
free and within clots
Direct Factor
Xa Inhibitors
Rivaroxaban
(PO)
bind to active center of
Xa, which inhibit
activation of thrombin
Compared to warfarin –
Advantages: rapid onset, no monitoring
needed, few drug/food interaction, same
does for all pts, low risk of bleed
Disadvantages: short duration of action (so
need to take at prescribed time for sure), no
antidote for OD, limited experience, not
approved for mechanical valve replacement
so still must use warfarin
Antiplatelets (ACA) = prevent thrombosis in arteries and platelet
aggregation
Prototype
MOA + Use
Side Effects
Good to Know
Aspirin (COX
inhibitor)
irreversible inhibition of COX leading to decreased
platelet aggregation by decrease TXA2 (thromoxane
A2) (for vasoconstriction) to prevent stroke and MI
bleeds
do not give to
anyone under
18 yo
Clopidogrel (P2Y12
ADP receptor
antagonist)
irreversible blockage of P2Y12 ADP receptors leading
to decrease platelet aggregation to use as secondary
prevention for atherosclerotic events for pts with
angina, MI, coronary stents
bleed, risk for
thrombotic
thrombocytop
enic purpura
usually used
with ASA
Abciximab (GP
IIb/IIIa receptor
antagonist)
super aspirins, most effective, reversible blockage
at receptor = no platelet aggregation; used short
term for those undergo cardiac angiography or acute
coronary syndrome
has 2x risk for
bleed
Thrombolytics
Alteplase (tPA/Activase) = catalyze conversion of plasminogen to plasmin to digest fibrin
clots of new thrombi that have already formed which is used acutely for MI, PE, stroke;
SERIOUS RISK FOR BLEEDING! Only use after ruling out potential risks
What is the biggest risk factor of thrombolytic medications?: hemorrhage when giving
thrombolytic and another drug that interfere with clotting; educate pt S&S of increased
HR and decreased BP, petichiae/hematoma/excessive bruise, black/red stool, discolored
urine, pain and location