Deck 1 Flashcards
How does Digoxin work?
- it is an Na/K+ ATPase blocker that increases Na+ concetration, which exchanges for Ca2+. This leads to an increase in Ca+ increases heart contractility, and positive inotropy
- has parasympathommetic effects via direct stimulation of the vagus nerve, leading to AV nodal inhibition
digoxin is used to treat
chronic systolic HF and atrial arrythmias like Afib and Aflutter
does digoxin reduce mortility?
no!
when do you give digoxin
when ace inhibitors and diuretcs have failed
side effects if digoxin
hyperkalemia, PVCs, St scopps, bradychardia, AV nodal block / heart block , GI symptoms, yellow vision
what are the EKG change shown with digitalis poisoning
scooped concave ST segments
do not use digoxin in
pts w significant SA or AV nodal block
on b-blockers
pts w hypokalemia
renal dysf(x)
Milrinone - how does it work?
is a phosphodiesterase inhibitor that leads to the breakdown of cAMP
effects of Milrinone
Milrinone is inotropic and vasodillitory (decreased after load)
main side effect to watch out for with milrinone:
hypotension
Nesiritde is a synthetic form of and does what in a cell
BNP, which increases cGMP, which leads to a relaxation of smooth muscle
nesiritde effect
venous AND arterial vasodillation, and increases natriuresis. reduces pre load and afterload, along with Na+ excretion
ACE inhibitors act how
block the concersion of Angiotensin I –> ATII
down stream effects of ACE
decreased BP –> low arteriolar resistance, high venous capacitance and low CO
do ace inhibitos prevent cardiac remodeling?
yes
who do you not give ACE inhibitors to
pregnant nasty women, patients with chronic renal disease and patients with CHF
side effects of ACE inhibitors
dry cough due to bradykinin buildup and angioedema
hypokalemia
Aliskiren works how
it is an angiotensin inhibitor that blocks renin, so angiotensinogen cannot be converted to angioensin I
what do all angiotensin receptor blockers end in
“sartan”
what do all ace inhibitors end in
pril
Calcium channel blockers / dihydropyridines target
L-type calcium channels in smooth muscle. They reduce the frequency of Ca channgel opening, leading to relaxation of the muscle and in cardiac musle
duhydropyridines are used to treat
hypertension, reynauds
use nifedipine
in pregnant women w HTN
what is the caveot of amlodipine?
it takes a long time to take efect, so you have to use others until it starts working
non-dyhidropyridines do what
target calcium channels in the AV an SA node in the heart
which calcium channel blocker is used to treat antiarrhythmias
verapamil
side effects of non-dihydropyrimidines
constipation
side effects of calcium channels
flushing dizziness, peripheral edema
Furosimide is a
Loop Diuretic that is K+ wasting
how does furosimide work
causes net excretion of Na+, K+ and Mg+ and Ca+ excretion
side effect of furosimide
metabolic acidosis and more renal stones
Chlorothiazide and hydrochlorothiazide are
Thiazide diuretics, K+ wasting that block a pump in the PCT to resorb NaCl
thiazide diuretics are helpful in pts w
hypercalcemia w recurrent urinary stones
be careful using what drugs in gout
thiazide diuretics due to hypruricemia
what are the three K+ sparing diuretics that we care about
Spiroolactone, eplerenone and triamterene
spironolactone and eplerenone work on
an ATP dependent pump on interstitial side –> inability to reabsrob Na and retention of K
side effect of spironolactone
takes a few days to start working and gynecomastia
how does triamterene work
blocks Na_ influx into the cell
Methylopa is an
alpha 2 agonist that decreases sympathetic stimuli from the brain
how does methyldopa work
is replaces precursors of NE with breakdown products of methyldopa, which produces an altered neurotransmitter –> stimulation of alpha 2 receptors
use methydopa in patients with
parkinsons and pregnany patients with hypertension
side effects of methydopa
sedation, nightmares, depressio vertigo, + coombs test
Clonidine acts how and are used in what
alpha 2 agonist, leading to decreased NE,
effects of clonidine
decreases BP and HR
do not use clonidine in pts with
taking tricyclic antidepressants
side effect of clonidine
depression
Guanethidine ats how
blocks the release of NE from the SNSnby replacing it in the vesicle
which drugs block the action of guanethidine
cocaine, amphetamine and tricyclic antidepressants since they block the uptake of the drug in the first place q
side effects of guanethidine
postural hypotension, retrograde ejaculation, hypotenie crisis
how does resperine work
it blocks vesicle membrane associated transport (VMAT) that takes up bioenic amines, IRREVERSIBLY. so you get less sympathetic action through a1 receptors
Phentolamine is a
non-selectie alpha blocker, REVERSIBLE
give phentolamine to pateints with
pheochromocytoma
side effect of resperine
reflex tachyardia
phenoxybenzamine is a
aLPHA blocker, IRREVERSIBLE
selective alpha 1 antagonists end in
OSIN, example tamsulosin
selective apha 1 antagonists cause
vasodilation
tamsulosin is used for
BPH
which b blocker is used first line for HTN in pregnancy
labetolol
how does labetalol work
alpha and beta: but more b blockade than a blockade, so vasodillator effects due to a1 blocking while also blocking b1/b2
what is cervedilol
nonselective peripheral alpha and beta blocking agent. PERIPHERAL. leads to vasodilation
wht do we use cervedilol in
CHF
Hydralzine
dillates the arteries only
use hydralazine in pts w
HTN or HF
have to use hydralazine in combination w
nitrates
minoxodil is a
arterial vasodillator
how does minoxodil work
it opens K+ channels leading to hyperpolarization of the smooth muscle and less depolarization
side effects of minoxodil
hair growth
what drugs would you give alone w minoxodil
loop diuretics
notroprusside acts on what
acts on veins and arteries, but mainly arteries
how does nitroprusside work
NO –> guanylte cyclase –> cGMP –> kinases and relaxation of ARTERIAL smooth muscle
side effects of nitroprusside
cyanide toxicity which leads to bradycardia, acidosis, convulsions and confusion arrhythmias
hiocynate toxicity –> nausea and vomiting
diazoxide is
a vasodillator of arteries and veins
diazoxide is used when and how
IV in the ICU during a hypertensive crisis
what is the vasodillator that is best used in African American
hydralazine
what vasodillator so we use to treat insulin secreting tumors in the pancreas
diazoxide
Fenoldopam does what
dillates arteries and veins by acting as a D1 dopamine receptor agonist
avoid fendolopam in
patients with glaucoma
B1 receptors
increase HR, contractility and conduction speed
B2 receptors induce
fight or flight!
A1 receptors lead to
vasoconstiction
A2 receptors
tone town the SNS tone in the CNS
treat general population >60 when
SBP> 150 or DBP >90
in population <60 initiate treatment when
SBP>140 or DBP >90
in pts w diabetes initiate treatment when
SBP> 140 or DBP>90
avoid non-dihydropyrimidines in
heart failure, sick sinus syndrome or heart block
regression of fibrosis in the liver, heart and lung have been found due to what drug
ARBs
three major indications for the use of BB
cardiac arrhythmias, protecting from a 2nd MI, control of HTN
what 2 beta blockers also have vasodillatory effects
carvedilol and labetalol
Clonidine
centrally acting a2 adrenergic agonists –> decrease in SNs tone and decrease in peripheral vascular resistance
drugs to use in treating HTN in pregnancy
hydralazine, methyldopa, labetalol
avoid aspirin use in patients with
severe hepatic failure because it is metabolized in the iver by CYP2C9 (also metabolizes warfarin)
clopidogrel
is a P2Y12 inhibitor, so block GPiib/IIIa for the rest of the platelet lifespan
clopidogrel is metabolized by
CYP2C19
eptafibitide is a
GP IIb/IIIa inhibitor with immediate activity
abciximab is a
GP IIb/IIIa inhibitor
wht patients are given GPiib/iiia inhibitors
high risk patients
Bivalirusin works by
direct thrombin inhibitor, it binds to thrombin and preents cleavage of fibrinogen –> fibrin
Fondaparinux
ATIII mediated inhibition of factor Xa
what does tPa do?
it activates plaminogen into plasmin which cleaves fibrin
door - needle time for thrombolytics
30
door- balloon time for PCI
90 mins
major contraindiciations for beta blockers
heart failure, heart block, asthma, hypotension, significnt bradychardia
way to remeber types of antiarrhythmics
Some Block Potassium Channels
Na blocker, B Blockers, K+ blocker, Ca L-type blocker
in general, what do type I antiarrhythmcs do?
they slow the upstroke of the AP by blocking the fast Na+ channels that allow for depolarization
what do class I antiarrhythmics bind to
open or inactivated Na+ channels
explain use dependence in the context of type I antiarrhythmic drugs
type 1 = Na+ channel blockers, which can bind in the open or inactivated state. this includes phase 0, 2 and 3. As the HR increases, the heart spends more time in phase 0,2 and 3 and less in the closed state. So tissues undergoing constant depolariztions are more susceptible to blockage
which type of drugs exhibit use dependence?
type I antiarrhythmics
what will you see on an ECG as a result of a type I antiarrhythmic
slow down the depolarization and decrease conduction velocity, leading to widened QRScomplex
Class Ia drugs
Quinidine, Procainimide and disopyramide
sodium channel binding strentgh of clss Ia srugs in order
1c>1a>1b
class Ia antiarrhythmics result in
medium binding, intermediate use dependence and moderate slowing of AP
Quinidine is used to treat
supraventricular and ventricular arrhythmia
what other channel, in addition to Na+ channels do type Ia antiarrhythmics block?
K+channels
what is the ultimate effect of quinidine
prolonged QT interval and wide QRS
side effects of quinidine
tinitus, thrombocytopenia, GI side effects
ultime effect of procainamide on EKG
prolongs to AP and QT interval
Procainamide is used to treat
Afib in WPW syndrome
side effects of procainamide
drug induced lupus
Disopyramide can excacerbate
heart failure
general risk of type I antiarrhythmics
toursades de pointe syndrome due to prolonging QT interval from the K+ current inhibition
how do you reveal brugada syndrome
by giving procainimide in the presence of brugada syndrome can lead to ST elevations in V1, V2, V3
wha tis brugada syndrome
K+ channel deficiency that makes you susceptible to long QT syndrome and sudden death
class Ib antiarrhythmics
Lidocaine, phenytoin and Mexiiletine
class Ib antiarrhythmics have a _____ affinity for Na+ channels
very low
what do class Ib do to an EKG
they shorten the phase 3 repolarization by blocking Na+ curent during the action potential and decrease QT interval
type Ib most useful in treating
ischemia induced ventricular arrhythmias
the side effects of 1b antiarrhythmics are
neurological
type Ic antiarrhythmics are
flecainimide and propafenone
class Ic bind _____ to na+
strongly and exhibit the strongest use dependence
class Ic effect on EKG
have the largest QRS duration, in a rate dependent manner
use Ic to treat
atrial fibrillation
do not give 1c to patients with
Heart failure or coronary artery disease, or ANY history of any heart disease since they can cause a delay in production speed, leading to arrhythmias in patients with ischemia
what are the class III antiarrhythmics
defetilide, ibutilide , sotolol, amniodarone
class III antiarrhythmics treat
supraventricular and ventricular arrhythmis
A fib
which b blocker do you use for long QT syndrome and sudden death syndromes
Nadolol
class III toxicities (amniodarone)
neurological toxicity, gray corneal sunglasss, hypothyroidism or hyperthyroidism, pulmonary fibrosis (most important), heart block, heart failure with rapid IV admin, hepatitis, grey-blue skin discoloration / photodermatitis, toursades
which drug can cause either hypo or hyper thyroidism
amniodarone
amniodarone can decrease the metablism of
warfarin through P450 interactions
prolongation of the QT interval is associated with and caused by what drugs
toursades, polymophc ventricular tachycardia, due to Class III drugs ibutilide and deftilide, and sotolol and Class1a
diltiazem and verapamil are used to treat
supraventricular arrhythmias since they work on the AV and SA node Ca channels
does digoxin do rate or rhythm control?
rate control since it delays conduction through the AV node
use magneium to treat
Toursades rhythm
hyperkalemia EKG changes
tall peaked T waves with a shortened QT interval
hypokalemia EKG changes
decrease in the amplitude of P waves, and a U wave at the end of the t wave, for two bumps after the QRS
Adenosine acts how
it activates inhibitory A1 receptors on the myocardium and at the SA and AV nodes. causes an outwad K+ current leading to hyperpolarization. mostly @the AV node, to increase AV nodal refractory period
adenosine causes
transient heart block
adenosine used to treat
supraventricular arrhythmias
epinephrine main effects
a1 agonist, leading to vasoconstriction
B1 agonist, leading to increased HR
increased HR + vasoconstriction
Ne main effects
a1 agonist: vasoconstriction (less potent than Epi)
b1 agonist: tachycardia
phenylephrine effects
a1 agonist only –> vasoconstriction
what vasopressor works well in acidotic pateints
vasopressin
if i only want to increase SVR and not increase Hr, what drug do i give?
phenylephrine
dopamine does what
increases CO, contractility through a1, and peripheral vasodilltion through b1. also increases HR
what does dobutamine do
mostly B1 effects –> increases HR,
vasodillation through B2
milrinone does what
is a PDEIII inhibitor that is inotropic thorough a1 and vasodilitory. drops the BP alot. small impact on HR
Nitroglycerin does what
it is a venous dillator, not really much arterial dillation
Nitroprusside is a _____ dillator
arterial dillator
when do you find fibrinous necrosis
in malignant HTN, where the HTN increases rapidly and uncontrolled
Metoprolol is a
beta 1 antagonist
Metoprolol is used to treat
bradycardia, arrhythmias and heart block
tizanidine works as an ____ and is used to treat_____
alpha 2 agonist used to treat HTN
Modafinil acts how
it displaces catecholamines to increase catecholamines in the synapse
modafinil used to treat
narcolepsy
epinephrine acts as a
at low doses acts on beta –> incr HR, contracility
at high doses acts on alpha —> vasconstriction and MAP
isoproterenol is a
Beta 1 and 2 agonist that increases HR, and decreases diastolic pressure
dobutamine is used to treat
cardiogenic shock and heart failure
isoprenterol works as a
beta 1 and 2 agonist
NE is a ______ agonist
alpha 1 and 2, beta 1 agonist
phenylephrine is a
alpha 1 agonist
side effect of phenylephrine
reflex bradychardia
side effect of NE
reflex tachycardia
oxybutynin acts as an ____ leading to treatent for _____
M3 antagonist, –> bladder control
tiotropium is an
M3 agonist
effects of tiotropium
M3 antagonist that leads to bronchodilation and reduction of bronchia seretions
scopalamine is a
M1 agonist
scopalamine used to treat
sea sickness
Atropine is
muscarining 1, 2 and 3 antagonist leading to iincreased HR, increased sweating, bronchodilation
side effects of atropine
mad as a hatter, dry as a cracker, how as a haire, blint as a bat
rivastigmine acts as a
indirect cholinomimetiv where it binds to Achase –> Ach breakdown and increase of Ach at the junction
what b blockers can be used in hypertensive emergencies
esmolol and meoprolol can be adminisered IV
side effect of hydralazine
reflex tachycardia and exacerbation of angina
lupus
fenoldipams most important role is to
dilate renal arteries
suffix of all of the ACHase inhibitor drugs
STIGMINE
most important use of acetylcholinesterase inhibitors is for the treatment of
myasthenia gravis
ACHase inhibitors to treat MG
edrofonium, pyridostigmine, and neostigmine
use what drug to diagnose if its a cholinergic crisis or MG
edrophonium
depolarizing neurouscular blockade caused by
succinylcholine
neostigmine is used to treat
postoperative bladder distention
physostigmine is used to
treat atropine overdose - atropine is a muscarinic antagonist, so my using physostigmine to block ACHase which increases ACH, this blockade can be overcome
if you see THIO in a drug think
that it is an insecticide and also a cholinesterase inhibitor
rivastigmine, galanthastigmine and doneprezil are all
ACHase inhibitors that can pentrate the CNS to treat alzheimers
is aspirin reversible or irreversible
irreversible
mechanism of aspirin
it irreversible blocks cox1 and cox2 so you get decreased prostaglandins and thromboxane
what does the P2Y12 receptor do
it is involved int he ADP dependent activation of GPIIb/IIIa
major side effect of thienopyradines
bleeding
metabolism of clopidogrel
it is a prodrug, the requires transofrmation by CYP2C19 - delayed onst
the newer classes of thienopyridines are assocaited wtih
more intense platelet inhibition and associated higher risks of bleeding
onset of prasugrel?
rapid and higher level of platelet inhibition
what special about ticragrelor? and what is it
it is a P2Y12 inhibitor, that is reversivle
when is ticragrelor better to use than clopidogrel
in acute coronary syndrome
when do you use a GP11a/IIIb inhibitor?
when you already have ASA and a P@Y12 on board and still not responding and on way to cath kab
what is eptafibitide
it is a gpIIb/IIIa inhibitor
what is abcixumab
a IIb/IIIa inhibitor
onset of action of eptifibitide
immediate
contraindications to eptafibitde administration
renal disease
take home point: what should a high risk patient w a UA/STEMI be treated with
ASA, clopidogrel and a IIb/IIIa inhibitor like abcixumab or eptafibitide
a direct thrombin inhibitor is
bivalirudin,
want to give pateints who have had an MI ACE inhibitors in what time period
NOT FIRST 24 HRS afterna MI
metolazone is a
thiazide-like diuretic
lupus is induced by
hydralazine, procainimie and methyldopa
