Pharm-Part 2

Front 1

how Tx Alz?

Back 1

carbamate, and other AChase inhibitors like donepezil

Front 2

chol agonists

Back 2

CarbaCHOL
BethaneCHOL
MethaCHOLine

Front 3

methacholine

Back 3

methaCHOLine=Ach+

*Dx asthma (d/t bronchoconstriction<==Ach)

S/E: Ach+ ==>
flushing
sweating (SNS CHOLinergic)
salivation,
GI cramping,
bronchoconstriction

Front 4

bethanechol

Back 4

Tx: urinary retention
(muscarinic agonist)

Front 5

Tx: urinary retention

Back 5

bethanechol

Front 6

Tx Park Dz

Back 6

benztropine
(muscarinic antagonist;
in Park Dz: no DA, so ACh predominates)

Front 7

Tx psychotic pt

Back 7

typical antipsychotic (thioridazine)

Front 8

choline esters
-ex?
-affects what receptors?
-PE?

Back 8

eg- ACh, CarcbaCHOL

-affects nicotinic/muscarinic receptors

PE:
*decr BP via NO released from vascular endothelial cells (muscarinic receptors)

*decr BP blocked by atropine

Front 9

what can block the decr BP caused by ACh or carbachol (choline esters)?

Back 9

atropine (muscarinic antagonist)

Front 10

pilocarpine

Back 10

(pilocarpine=chol agonist)

Tx: glaucoma

PE:
*miosis (via sphincter pupillae)
*cycloplegia (paralysis of ciliary muscle) via contraction of ciliary muscle
==>decr IOP via incr AH outflow

S/E: bronchoconstrict, salivation

Front 11

nicotine
-desc
-PE
-S/E

Back 11

tertiary amine; not hydrolyzed by plasma AChase, metabolized by liver

PE:
-incr SNS: incr HR/BP, cutaneous vc
-incr resp & GI motility

S/E:
-muscle fasciculations folloed by depolarization blockade (large doses)
-CNS: convulsions (OD)

Front 12

carbamates
-what are they
-ex's

Back 12

=types of AChase -

-ex:
physostigmine(3')-ENTERS brain
==>CNS effects

neostigmine (4')-does NOT enter brain
edrophonium (4')-does NOT enter brain
==>NO CNS effects, only peripheral effects

(reversible)

Front 13

physostigmine

Back 13

3' AChase -

==>enters brain

Front 14

edrophonium:

Back 14

4' AChase -does NOT enter brain
==>NO CNS effects, only peripheral effects

(reversible)

*diagnosis of myasthenia gravis (MG)
*differentiate b/w
“myasthenic” & “cholinergic” crisis in patients tx w
neostigmine
*used with atropine (musc-) to reverse NMB caused by non-depolarizing drugs (d-tc, pancuronium)

Front 15

neostigmine

Back 15

4' AChase -does NOT enter brain
==>NO CNS effects, only peripheral effects

(reversible)

Tx:
*MG (always used with atropine to prevent indirect musc S/E)
*used w/glycoporrolate to reverse NMB caused by non-depolarizing drugs

Front 16

organophosphates
-ex?

Back 16

malathion
parathion
isofluophate (DFP)

organophosphate=AChase inhibitor
- irreversible due to phosphorylation (covalent bond) of AChase active site

Front 17

USMLE: Scientist tries to commit suicide with “common laboratory chemical” or “chemical used in protein reactions.” What do you Tx him with?

Back 17

The chemical was isofluophate (organophosphate). Tx him with atropine and pralidoxime

Front 18

What do these Sx indicate:

lacrimation, salivation, miosis, dyspnea, no change BP, skeletal muscle fasciculations

-how Tx?

Back 18

no change BP (N1)
SkM fascic (N2)

These indicate organophosphate (OP) poisoning.

-organophosphate=AChase inhibitor
* irreversible due to phosphorylation (covalent bond) of AChase active site


Tx w/atropine and pralidoxine (2-PAM): regenerates phosphorylated AChase

Front 19

how Tx poisoning with plants that causes incr Ach?

Back 19

(incr Ach is like giving physostigmine: 3' AChase inhibitor ==>DOES enter brain)

Tx w/atropine (3' musc - ==>cross BBB, placenta)

Front 20

how Tx poisoning with plants that causes decr Ach?

Back 20

decr ACh is like giving atropine (3' musc - ==>enters brain)

Tx w/physostigmine (3' AChase inhibitor: DOES enter brain)

Front 21

muscarinic antagonist

Back 21

3' (cross BBB, placenta)
aTROPINE
benzTROPINE
cyclopentolate
scopolamine

4' (do not cross BBB)
"N-METHYL-PIG: imagine a PIG with methyls on it" :

N-methylATROPINE
Propantheline - GI spasticity
Ipratropium - (Tx bronchoconstriction in asthma)
Glycopyrrolate

Front 22

Sx of muscarinic receptor blockade

Back 22

OD of atropine-like drugs
(atropine=musc - ==>incr SNS):

*red as a beet (cutaneous dilation bc shunting blood to skin==>sweat and reduce heat)

*hot as a pistol (hot skin bc cant sweat away heat; sweating=sympathetic CHOLINERGIC innervation, & atropine inhibits cholinergics)

*dry as a desert:
--inhibition of sweating
--saliva is thick (not watery)==>mouth feels dry
==>difficulty swallowing

*mad as a hatter (hallucinations/delerium)
(think how cocaine (incr SNS)==>hallucinations/delerium)

Front 23

Tx glaucoma:
-ex?
-MOA

Back 23

A. Decr production of AH:

1. BB: timolol, propanolol
2. CA-: acetoZOLAMIDE, dorZOLAMIDE


B.Inc outfow of AH via nl path:
1. A1 receptor:
EpinEPHRINE
dipivEFRIN

2. OP ACHase - :
isofluOPHATE
echothiOPHATE

(mneum: "OP"=OP ACHase-)

3. Musc agonist: pilocarpine

C. Inc outflow of AH via uveoscleral pathway
(contract ciliary muscle SmM):

Latanoprost (PGF2a analog)

Front 24

ganglionic blocking drugs:
ex's?
effects?

Back 24

trimethaphan
hexamethonium (mneum: put an “hex” on the autonomic NS)

These block SNS and PSNS:
1. Block SNS:
-arteriodilation lowers TPR
-venodilation==>decr preload
-decr dp/dt
-decr preload & dp/dt ==> decr CO
-decr TPR & CO==>hypotension
-decr sweating
-impotence (no ejaculation)

2. Block PSNS:
tachycardia
mydriasis & cycloplegia
decr GI motility
constipation, urinary retention
decr salivation & lacrimation
impotence (no erection)

Front 25

NMB drugs

Back 25

Depolarizing (non-comp):
*succinylcholine
*dexamthenoium

-Stage 1: MEP depol
-Stage 2: repol, but still refractory

-fasciculations prior to flaccid paralysis (b/c depol)
-Uses: NMB, ECT


Non-depolarizing (competitive)
"the --curiums & --roniums":
*d-tubocurarine (d-tc; curare)
*pancuronium

-MEP never depol==>no fasciculations prior to flaccid paralysis
-Use: NMB

Front 26

effects of
a) succinylcholine
b) curare

on
1) MG,
2) burns,
3) denervation?

Back 26

1) MG
*decr Ach receptor density
*succinylcholine: effect decr
*curare: effect incr

2) burns
*incr Ach receptor density
*succinylcholine: effect incr (hyperkalemia)
*curare: effect decr

3) denervation
*incr Ach receptor density
*succinylcholine: effect incr (hyperkalemia)
*curare: effect decr


*↓ Ach receptor density ==>
↑ effect of curare b/c not as many receptors to stimulate, so works really well

• Ach receptor density is directly related to effect of succinylcholine and inversely related to effect of curare

With burns and denervation, you get hyperkalemia with succinylcholine.

-Succinylcholine binds and constantly depolarizes; you try to repolarize (by ship K+ out of the cell to try to make cell interior (-) again), but it doesn’t repolarize, so just keep shipping out K+ ==>hyperkalemia.

-Since burns and denervation have increased succinylcholine effect (d/t incr Ach receptor density), ship out even more K+.

Front 27

metyrosine

Back 27

inhibits production of DA, NE, and Epi via:

1. inhibit Tyrosine Hydroxylase
[catalyzes Tyrosine==>DA]

2. inhibit DA Hydroxylase
[catalyses DA==>NE]

3.prevent release of ATP with NE release

Front 28

causes incr NE overflow

Back 28

AngII & B2 stimulation
a1 block (3 P's)
cocaine (blocks NE uptake1)
TCA's

Front 29

causes decr NE overflow

Back 29

musc (ACh) & a2 stimulation (clonidine)
PGE's

Front 30

site of action at sympathetic nerve jxn:

-a1, a2, B1, B2
-D1, D2
-MAO-A and MAO-B

Back 30

site of action at sympathetic nerve jxn (Module 1, p.209)

*a1 [IP3 & DAG]...Semo: DAG caues DIRECT incr Ca2+ in SR


-SNS post-jxn sites @ effector organs, tissues, & glands

*a2:

-SNS post-jxn on effector organs, tissues, & glands
[inhibit AC==>decr cAMP]

-SNS pre-jxn= "Autoreceptors"
[Gi increaed K+ conductance]

-PSNS post-jxn= "Heteroreceptors" [Gi ==> incr K+ conductance] at:
--SA node
--sphincter muscle of iris
--GI


*B1 [AC]:
-post-jxn @
--cardiac
--adipocytes
--JG cells of renal aff art

*B2:

-Post-jxn @
--arterioles, venules
--lung (bronchioles)
--liver
--GI
--uterus

Prejxn on sympathetic neuron="Heteroreceptors"

*D1 [AC]
-Post-jxn @
--VSM of renal aff art==>vd

*D2 [inhibit AC==>incr K+]
-At synapse in CNS:
--corpus striatum,
--hypothalamus
--CTZ (4th ventricle & limbic system)

-MAO-A and MAO-B vacuum up xs Epi and NE in pre-synaptic cytoplasm
-Thus, MAOi
==>incr Epi and NE in pre-synaptic cytoplasm
==>Epi & NE leaks out into synapse via channel
==>incr Epi and NE in synapse

Front 31

what is rate-limiting step of catecholamine syntehsis ?
-what prevents it

Back 31

(catecholamines=NE, Epi)

rate-limiting step in syntehsis is tyrosine hydroxylase, which converts
L-TYRO==>DA

MeTYROSINE inhibits TYROSINE hydroxylase

Front 32

CV effects of Epi, NE, DA

Back 32

*Epi: (B2>B1>A)
-Incr: ("fight-or-flight")
*VR (relax hepatic resistance)
*dp/dt (B1)
*CO/SV==>incr SBP/PP
*incr coronary blood flow

-Decr:
*TPR/DBP (B2>A, so B2 effects of vd SkM,liver outweighs A effect of constricting kidney/GI)

*NE: (A >>> B)
-NE via IV decr HR via baroreflex (NE==>vc==>incr BP==>decr HR via baroreflex)
--this decr HR blocked by atropine

*DA: (D1>B1>B2>A)
-low dose: D1 incr RBF/GFR
-med dose: B1 incr CO/SV, D1 incr RBF/GFR
-high dose: A==>vc==>incr TPR==>decr CO/SV

Front 33

USMLE:
-Give drug iv
==>incr BP, decr HR

-Then give atropine.
==>incr BP, incr HR

What is the drug

Back 33

NE

(BP incr, but decr HR d/t baroreflex. Atropine blocks muscarinic effects like the baroreflex)

Front 34

what blocks incr RBF/mesenteric BF caused by DA?

Back 34

haloperidol (DA antagonist)

Front 35

effects of epi

Back 35

Epi: B2>B1>A

incr SkM BF (B2)
decr skin, renal, GI BF (A)

-incr dp/dt, SV/CO (B1)
-incr VR (relax hepatic resistance) (B2)
-decr DBP (relax arteriole resistance) (B2)

Front 36

what's the advantage of DA

Back 36

can incr BP without decreasing RBF

(both NE and Epi decr RBF [via A] a lot--very bad)


*DA: (D1>B1>B2>A)

-low dose: D1 incr RBF/GFR
-med dose: B1 incr CO/SV, D1 incr RBF/GFR
-high dose: A==>vc==>incr TPR==>decr CO/SV

Front 37

Epi + what drug can cause arrhythmias?

Back 37

halothane (inhalational anesthetic)

Front 38

Epi reversal + phentolamine==>what effects?

Back 38

phentolamine= alpha blocker

(Epi: B2>B1>A)

Thus, Epi + alpha blocker==>
only B effects:
B2:
*incr VR (decrease hepatic resistance)
*decr TPR/DBP (vd SkM,liver)

B1: incr dp/dt, SV/CO

Front 39

Epi + propanolol

Back 39

propanolol=B blocker

Epi+ B blocker==>only a effects (incr BP)

Front 40

what add to local anesthetic

Back 40

Epi (to prevent systemic absorprtion b/c Epi vc)

Front 41

phenylephrine

Back 41

=a1-agonist= mydriasis w/o cycloplegia

Front 42

ritodrine

Back 42

=B2-agonist=decr uterine contraction in premature labor

Front 43

bronchodilation w/incr HR caused by what drug

Back 43

isoproterenol (B1=B2, AKA non-selective B1 and B2 agonist)

Front 44

bronchodilation w/very little HR-->caused by what drug

Back 44

albuterol, terbutaline (selective B2 agonists)

Front 45

clonidine

Back 45

pre and post-synaptic a2 agonist (Module 1 syll,p. 209: alpha-2 is inhibitory to SNS)

-this α2-agonist enters & works in brain to DECREASE SNS
==>decr BP and HR

mneum: "get clobbered by clonidine"

(give to psych pts to calm them down)

Front 46

indrect adrenergic agonists
-ex?
-MOA

Back 46

-Tyramine (in fermented foods: beer, cheese)
-amphetamine

MOA: release of stored NE

*NO EFFECT if pre-treat with:

1. reserpine/guanethidine (sympatholytic: thus can't release stored NE)

2. cocaine (blocks NE uptake1, so NE is in the cytoplasm instead of in the pre-synaptic strores)

3. "3 P's" (alpha blockers): phentolamine, prazosin, phenoxybenzamine (PBZ)

Front 47

For what drugs are you not supposed to eat cheese or beer?

Back 47

Fermented foods like cheese and beer contain Tyramine (indirect adrenergic agonist: release stored NE).

Thus, tyramine is contraindicated if taking phenelzine or tranylcypromine, which are MAOi and thus incr NE in synapse. Since cheese/beer (Tyramine) release stored NE, this would increase NE even more==>hypertensive crisis

Front 48

incr BP d/t tyramine and amphetamine can be blocked by

Back 48

(Recall: tyramine and amphetamine are indirect adrenergic agonists, MOA=released stored NE)

*NO EFFECT if pre-treat with:

1. reserpine/guanethidine (sympatholytic: thus can't release stored NE)

2. cocaine (blocks NE uptake1, so NE is in the cytoplasm instead of in the pre-synaptic strores)

3. "3 P's" (alpha blockers): phentolamine, prazosin, phenoxybenzamine (PBZ)

Front 49

Tx ADHD?
-S/E:

Back 49

methylphenidate (Ritalin)

MOA: stim NE release and block NE uptake1

S/E: insomnia, decr linear growth rate, depression

Front 50

amphetamine toxicity
-Sx?
-how Tx?

Back 50

-nervous, excited, agitated
-convulsions
-formication (think have ants under skin)==>excoriation (cut yourself)

Tx w/chlorpromazine (typical antipsychotic: blocks DA in brain)

Front 51

the following are Sx of toxicity/withdrawal from what?

-nervous, excited, agitated
-convulsions
-formication (think have ants under skin)==>excoriation (cut yourself)

Back 51

amphetamine toxicity (looks like cocaine)

Front 52

ephedrine

Back 52

diret B1 and B2
indirect a--thus no a effects after reserpine

Front 53

alpha blockers
-ex?
-PE?
-S/E?

Back 53

"3 P's":
phentolamine
prazosin
phenoxybenzamine (PBZ):

-PBZ causes IRREV (non-competitive) blockade of alpha receptors

-phentolamine/phenoxybenzamine (PBZ) incr HR via baroreflex
-prazosin has no effecton HR

Epi reversal: These REVERSE the vasopressor (vasopressor=incr BP via vc) of supraphysiological dose of Epi (B2>B1>A)
==>VASODEPRESSOR

S/E: orthostatic hypotension
(alpha receptors prevent you from fainting when you stand up)

Front 54

Tx migraine

Back 54

partial a agonists:
ERGOTAMINE
dihydroERGOTAMINE

("ERG, you GOT A MINE migraine pills")

Front 55

Tx BPH
-Rx?
-MOA

Back 55

tamsulosin

MOA: block a1A receptors in GU tract==>void

Front 56

pheo tumor
-Tx?
-PE?

Back 56

phentolamine (A-blocker)

PE: decr BP (Epi reversal)

Front 57

how reverse Epi?

Back 57

A-blockers: "3 P's"
phentolamine
phenoxybenzine (PBZ)
prazolin

These REVERSE the vasopressor (vasopressor=incr BP via vc) of supraphysiological dose of Epi (B2>B1>A)
==>VASODEPRESSOR

Front 58

selective B1 blockers

Back 58

atenolol, metaprolol (sp?)

mneum: ppl get heart attacks in he morning (AM), so give “AM” drugs to block B1 (heart attack)

Front 59

block B1 and B2

Back 59

timolol, propanolol

Front 60

Beta blockers
-Rx?
-Tx?
-S/E

Back 60

B1-selective:
*Atenolol
*Metoprolol

non-selective (B1 and B2):
*propnaolol
*timolol- decr IOP w/o cycloplegia (do not use propanolol b/c causes local anesthesia of cornea)

Tx:
1. angina: decr O2 demand by decr dp/dt & HR, but LV-EDV incr (d/t decr HR)

2. decr HR, AV conduction, dp/dt

3. Hyperthyroidism: decr tachycardia and tremor, also prevents conversion of T4-->T3

4. block incr HR caused by hemorrhage, minoxidil, hydralazine, diazoxide, nitroprusside, nitroglycerin

5. decr Oxygen demand via decr HR, dp/dt, afterload/DBP
[Nitroglycerin decr O2 demand by decr VR and LV-EDV)

-S/E:
-CHF, AV block
-bronchospasm
-delayed recovery of [glucose] in Type I DM after s.c. injxn of too much insulin

Front 61

Pt Tx w/BB for angina, then d/c drug. Now, angina and MI.

Why?

Back 61

BB Withdrawal Syndrome
(Sx=tachycardia, palpitations, tremor, chest pain)

BB==>upreg B receptors
==>d/c drug
==>incr cardiac B receptor stimulation
==>incr O2 demand
`==>Angina and MI

Front 62

reserpine

Back 62

sympatholytic:

1. decr NE release by poisoning NE storage vesicles

2. no effect of TAP drugs (Tyramine, Amphetamine, Propanolamine= Indirect Adrenergic Agonist) if pre-Tx with reserpine

3. no alpha effects of ephedrine if pre-Tx with reserpine

Front 63

guanethidine

Back 63

sympatholytic:

1. decr nerve-stimulated release of NE

2. competitive inhibitor of NE uptake1 (vs. cocaine=non-competitive inhibitor of NE uptake1)
==>inhibits vesicular storage of NE (sympatholytic)

3. anti-HTN effect blocked by TCA's b/c TCA's block entry of guanethidine into neuron

Front 64

cocaine
-PE
-MOA
-toxicity
-withdrawal

Back 64

1. blocks uptake1 of NE, Epi, DA, adn 5-HT in CNS

2. blocks uptake1 in peripheral sympathetic neurons--potentiates effects of NE and Epi, but not isoproterenol (B1=B2 agonist)

3. euphoria via DA release in nucleus accumbens

4. local anesthetic effect via blockade of Na channels in sensory neurons

Toxicity:
dilated pupils
excitation, euphoria,
halo vision
itchy skin
incr BP/HR
convulsions

Withdrawal:
sleepiness
depression
anhedonia (inability to feel pleasure)

Front 65

what do these Sx indicate:
-dilated pupils
incr BP/HR
euphoria
hallucinations
halo vision
itchy skin
convulsions

Back 65

cocaine toxicity

Front 66

what do these Sx suggest:
sleepiness
depression
anhedonia

Back 66

(anhedonia=inab to feel pleasure)

cocaine withdrawal

Front 67

MAOi's
-Rx?
-Tx
-MOA
-S/E

Back 67

Rx
-inhibit MAO-A and MAO-B:
*phenelzine
*tranylcypromine

-inhibit MAO-B to prevent breakdown of DA in CNS:
*selegiline

Tx: depression

S/E:
cheese rxn (cheese, pickled herring): inhibition of MAO-A (thus, phenelzine and tranylcypromine (not selegiline)) allows dietary tyramine to enter circulation and release NE==>HTN and tachycardia

Front 68

clonidine

Back 68

Tx: HTN (give to psych pts to calm them down: "get CLObbered by CLOnidine")

MOA: decr SNS activity via stim of a2 receptors in CNS (mimics baroreceptor input==>decr SNS)
==>decr NE and renin activity,
decr HR

s/E: sedation, dry mouth, edema

Withdrawal syndrome: sweating, incr HR, abrupt return of BP to HTN value,
abdominal pain,
tremor,
H/A,
apprehension

(vs. BB withdrawal syndrome:
incr HR w/palpitations,
but not tremor, sweating, ab pain, or incr BP)

Front 69

alpha methyl-dopa

Back 69

Tx: HTN in pregnant women
MOA: decr SNS by stim a2 receptors in CNS (mimics baroreceptor input)
==>decr NE and renin,
decr HR

S/E: (+)Coombs test (Goljan),
heptatitis, "flu" syndrome

Front 70

drugs that decr plasms NE

Back 70

clonidine
alpha methyl-dopa
reserpine
guanethine

Front 71

drugs that incr plasma NE

Back 71

-alpha blockers (3 P's: phenotolamine, phenoxybenzine, prazosin)
-arterial vasodilators (hydralazine, minoxidil, diazoxide)
-HCTZ (anti-HTN: inhibit NA abs)
-sodium nitroprusside
-

Front 72

arterial vasodilators
-Rx?
-PE?
-MOA?
-SE?

Back 72

arterial vasodilator (hydralazine, minoxidil, diazoxide)

-dilate resistence vessels (arterioles)
==>decr TPR, BP
==>incr dp/dt, CO, PRA, NE

-S/E:
*hydralazine (sHip drug):
==>lupus-like syndrome
==>d/c hydralazine & tx with steroid

minoxidil: hirsuitism, effective additive w/finasteride; edema

diazoxide: inhibit insulin release==>hyperglycemia;
edema

Front 73

hydralazine

Back 73

arterial vasodilator (hydralazine, minoxidil, diazoxide)

-dilate resistence vessels (arterioles)
==>decr TPR, BP
==>incr dp/dt, CO, PRA, NE

-S/E:
*hydralazine (sHip drug):
==>lupus-like syndrome
==>d/c hydralazine & tx with steroid

Front 74

minoxidil

Back 74

-dilate resistence vessels (arterioles)
==>decr TPR, BP
==>incr dp/dt, CO, PRA, NE

S/E of minoxidil:
-hirsuitism
-effective additive w/finasteride
-edema

Front 75

diazoxide

Back 75

arterial vasodilator (hydralazine, minoxidil, diazoxide)

-dilate resistence vessels (arterioles)
==>decr TPR, BP
==>incr dp/dt, CO, PRA, NE

S/E: inhibit insulin release==>
hyperglycemia; edema

Front 76

sodium nitroprusside

Back 76

Tx:
*hypertensive emergency (Goljan)
*CHF

MOA: dilates artieres & veins via release of NO from sodium nitroprusside molecule

PE: balanced vasodilation
dilate arteries==>decr TPR/DBP
dilate veins==>decr VR

In normotensive pt, these effects cancel out, so no change in CO.

In CHF pt, CO incr (b/c VR is too high in CHF pt, can't pump blood out, so reducing VR actually helps incr CO (good!).

Thus, both the decrease in DBP and decrease in VR lead to incr CO in CHF pts.)

Front 77

what happens in infuse sodium nitroprusside into a pt with poor renal fxn
-how tx?

Back 77

thiocyanate toxicity (muscle weakness, spasm, disorientation)

Tx with thiosulfate

Front 78

how Tx cyanide toxicity

Back 78

Tx with nitrate or thiosulfate

Front 79

Ca++ blockers

Back 79

verapamil
diltiazem
nifedipine

(mneum: "Valentine's Day" (heart)="VD"=Verapimil, Diltiazem)

Tx:
-HTN
-exertional & vasospastic angina
-AVNRT

1. block Ca++ channels at SA/AV nodes, cardiac myocytes, arterial VSM
2. decr BP: Nifedipine>Diltiazem>Verapamil
3. decr AV conduction via incr ERP: verapamil>diltiazem
4. nifedipine- incr HR with little/n.c. AV conduction
5. angina-decr O2 (decr dp/dt, HR, afterload) w/incr O2 delivery via dilation of coronary artieres

Front 80

Rx that decr dp/dt

Back 80

BB,
Ca++ blockers
diisopyramide

Front 81

effects of AngII

Back 81

relese ALDO & ADH
incr BP
incr SNS
incr NE release
block NE uptake 1
decr mesenteric BF

Front 82

Tx GI bleeding
-rx?
-MOA?

Back 82

MOA: decr mesenteric BF

Rx:
NE & AngII (get escape),
ADH (AKA AVP) & octreotide--no escape

Front 83

Tx Portal HTN
-rx?
-MOA?

Back 83

MOA: constrict arterial BF to GI tract-->less blood going from GI to liver

Rx: ADH & octreotide (somatostatin analog)--
"no escape"

Front 84

ACEi

Back 84

"--pril": captopril, enalapril

Tx:
*lower BP;
*CHF (incr CO by decr preload and afterload; reverses cardiac remodeling caused by AngII)
*HTN w/DM (ACEi lowers BP and proteinuria (protects kidney))

MOA: prevent conversion of AngI==>AngII in every vascular endothelial cell

PE:
-decr BP/TPR without changing CO, HR
-
S/E:
fetal toxicity (Category X)
K+retension
cough (ACEi blocks metabolism of bradykinin==>incr BK==>incr PG==>cough)
*can prevent cough by giving aspirin, or d/c ACEi and switch to ARB (sartan, i.e.losartan)

Front 85

person on ACEi develops cough. what do you do?

Back 85

d/c ACEi switch to ARB (sartan)

Front 86

what can you give along with ACEi to prevent cough?

Back 86

aspirin

Front 87

why give ACEi to CHF pt?

Back 87

*incr CO by decrasing preload and afterload
*reverse cardiac remodeling by AngII

Front 88

what give to HTN pt w/DM

Back 88

ACEi:
*decr BP
*decr proteinuria (protects kidney)

Front 89

acetozolamide

Back 89

Tx:
glaucoma
aspirin OD
altitude sickness

MOA: inh CA in PT and DT to prevent reabs of bicarb

PE:
*inhibits formation of aq humor and CSF (CA invovled in production of aq humor & CSF)
==>Tx glaucoma
*incr excretion of bicarb, Na, K
*makes urine more alkaline==>enhances clearance of aspirin (acid)
*prevents reabs of bicarb and Na
*causes met acid==>stimulates resp alkalosis (good for altitude sickness)

S/E:
-metabolic acid
-hyperchloremic

Front 90

what Rx stimulates respiration?

Back 90

caffeine, theophylline
nicotine
Epi
acetozolamide (met acid==>compensatory resp alk)

Front 91

what Tx depress respiration?

Back 91

EtOH
baribiturates
opiates (i.e. morphine)
benzodiazepine (ie. diazepam)

Front 92

how enhance renal clearance of acidic drugs?

Back 92

make urine alkaline via CA inhibitor or Na bicarbonate

Front 93

how enhance renal clearance of basic drugs?

Back 93

make urine acidic via ammonium cloride (NH3Cl)

Front 94

furosemide

Back 94

Loop diuretic (furosemide, ethacrynic acid)

Tx:
*fluid overload d/t CHF, pulmonary edema, periph edema
*hypercalcemia (Goljan)

MOA:
*inhibits Tri-transporter in TAL (Na:K:2Cl)
*inhibits Na transport in macula densa of DT

PE:
-loss of Na, K, Cl, Ca, Mg, water

-K loss worsened b/c Na not reabosrbed in TAL, so later on CD principal cells reabsorb more Na (and thus wastes more K)
-blocks Na transport in macula densa of DT==>no Na sensed==>secondary hyper-ALDO worsens K loss

S/E:
-ototoxicity; potentiated by aminoglycosides (e.g. gentamicin)

-enhances digoxin toxicity:
loop diuretic causees hypokalemia, so less K to compete with digoxin
-hypochloremic met alkalosis
(lose Cl-, so retain HCO3-)
-hypomagnesemia
-hyperglycemia (d/t enhanced reabsorption in PT)
-dilutional hyponatremia--cannot make a dilute urine in order to excrete free water
-hyperuricemia (bad for gout) and Li+ toxicity b/c enhanced reabs in PT

Front 95

ethacrynic acid

Back 95

Loop diuretic

Tx:
*fluid overload d/t CHF, pulmonary edema, periph edema
*hypercalcemia (Goljan)

MOA:
*inhibits Tri-transporter in TAL (Na:K:2Cl)
*inhibits Na transport in macula densa of DT

PE:
-loss of Na, K, Cl, Ca, Mg, water

-K loss worsened b/c Na not reabosrbed in TAL, so later on CD principal cells reabsorb more Na (and thus wastes more K)
-blocks Na transport in macula densa of DT==>no Na sensed==>secondary hyper-ALDO worsens K loss

S/E:
-ototoxicity; potentiated by aminoglycosides (e.g. gentamicin)

-enhances digoxin toxicity:
loop diuretic causees hypokalemia, so less K to compete with digoxin
-hypochloremic met alkalosis
(lose Cl-, so retain HCO3-)
-hypomagnesemia
-hyperglycemia (d/t enhanced reabsorption in PT)
-dilutional hyponatremia--cannot make a dilute urine in order to excrete free water
-hyperuricemia (bad for gout) and Li+ toxicity b/c enhanced reabs in PT

Front 96

hydrochlorothiazide

Back 96

MOA:
-site of action=DT
-decr GFR in all pts

-blocks NaCl symporter in DT==> incr excretion of Na, Cl, Mg, K
-decreased free water clearance: urine always hypertonic
==>dilutional hyponatremia ("emia"=blood)
-decr Ca+ excretion (thus, decr formation of kidney stones)
-increased Na delivery to distal tubule worsens K loss
-blocks Na transport in macula densa
==>no Na sensed
==>secondary hyperALDO

S/E:
-hyponatremia, hypokalemia w/alkalosis, hypomagnesia, hyponatremia, hypergluyemia
==>all uniformly decr GFR

-enhances digoxin toxicity via hypokalemia - less K+ to compete with digoxin for
Na+-K+ ATPase binding sites
-hyperuricemia (bad for gout) and Li+ toxicity (bipolar) b/c enhanced reabs of uric acid and Li+ in prox tubule

Front 97

K+ sparing diuretics

Back 97

mneum: "the K+ STAys"

S=Spironolactone
*ALDO antagonist in CCT (Cortical Collecting Tubule)

T=triamterene & A=amiloride:
*block Na channels in CCT principal cells
==>no Na/K exchange (usually, Na is absorbed and K excreted via Na/K exchange)

*block Na channels in CCT intercalated cells
==>no Na/H exchange (usually, Na is absorbed and H excreted via Na/H exchange)
==>no H excreted
==>urine more alkaline

S/E: hyperkalemia! DO NOT USE IN RENAL INSUFFICIENCY B/C CAN CAUSE FATAL HYPERKALEMIA

Front 98

Triamterene

Back 98

K-sparing diuretic

mneum: "the K+ STAys"

S=Spironolactone
*ALDO antagonist in CCT (Cortical Collecting Tubule)

T=triamterene & A=amiloride:
*block Na channels in CCT principal cells
==>no Na/K exchange (usually, Na is absorbed and K excreted via Na/K exchange)

*block Na channels in CCT intercalated cells
==>no Na/H exchange (usually, Na is absorbed and H excreted via Na/H exchange)
==>no H excreted
==>urine more alkaline

S/E: hyperkalemia! DO NOT USE IN RENAL INSUFFICIENCY B/C CAN CAUSE FATAL HYPERKALEMIA

Front 99

amiloride

Back 99

mneum: "the K+ STAys"

S=Spironolactone
*ALDO antagonist in CCT (Cortical Collecting Tubule)

T=triamterene & A=amiloride:
*block Na channels in CCT principal cells
==>no Na/K exchange (usually, Na is absorbed and K excreted via Na/K exchange)

*block Na channels in CCT intercalated cells
==>no Na/H exchange (usually, Na is absorbed and H excreted via Na/H exchange)
==>no H excreted
==>urine more alkaline

S/E: hyperkalemia! DO NOT USE IN RENAL INSUFFICIENCY B/C CAN CAUSE FATAL HYPERKALEMIA

Front 100

spironolactone

Back 100

K+ sparing diuretic

MOA: ALDO-antagonist in CCT (Cortical Collecting Tubule)
==>incr Na excretion, decr K excretion
-no effect on adrenalectomized pts (b/c no adrenal cortex, so no ALDO for spironolactone to antagonize)

-Tx: secondary hyperaldosteronism assoc w/cirrhosis, nephrotic syndrome
-reverses cardiac remodeling caused by ALDO in HF pts

S/E:
-hyperkalemia
-spironolactone is a partial sex agonist, so can get==>
-males: gynecomastia
-females: hirsutism, deep voice
-can treat hirsutism in pts taking OCP's (OCP's contain the progestin northethindrone, which are sex hormone agonists; spironolactone is a partial sex agonist so can act as antagonist in presence of full agonist like norethindrone)

Front 101

Tx: secondary hyperaldosteronism in pats with cirrhosis, nephrotic syndrome

Back 101

spironolactone

spironolactone is a partial sex agonist so can act as antagonist in presence of full agonist

Front 102

Tx: hirsutism in postmenopausal woman

Back 102

spironolactone

spironolactone is a partial sex agonist so can act as antagonist in presence of full agonist

Front 103

Tx: hirusutism in woman taking OCP's

Back 103

spironolactone

spironolactone is a partial sex agonist so can act as antagonist in presence of full agonist

Front 104

pt with adrenal tumor has high BP and low bicarb, K, and PRA, nl Na

-Dx?
-Tx?

Back 104

conn's syndrome (adrenal tumor secreting ALDO)

Tx: spironolactone (ALDO antagonist)

Front 105

how can you prevent hypokalemia from furosemide and HCTZ?

Back 105

K-sparing diuretics,
ACEi,
BB,
po K supplements

Front 106

graph on the effects of diuretics on
urinary flow, pH, and electrolyte composition

--how distinguish b/w diuretics?

Back 106

A. Look at urine flow rate. 1. If flow=8-10 ml/min
==>fureosemide, mannitol
2. If flow=2-3 ml/min
==>acetozolamide, thiazide, K+ sparing

B. Now look at quantitative changes in electroylate composition.
1. Distinguish b/w furosemide and mannitol b/c furosemide has more excretion of Na, K, Cl
2. Distinguish b/w acetozolamde, thiazide, and K+ sparing:
-high excretion of bicarb (thus high urine pH)==>acetozolamide
-less excretion of K+ sparing
==>K+ sparing
-the one that remains is thiazide

Front 107

digoxin, digitoxin

Back 107

Tx: control (decr) ventricular rate in pts with Atrial flutter/fib

Meet the 3 (Italian) Digitali bros.!!!
1. Good ME (incr dp/dt via inhibit Na/K)
2. Good EE (vagal activity, decr AV conduction)
3. Bad EE (PVCs/PACs, AV block)

MOA:
(1) acts centrally to incr PSNS

(2) acts centrally to decr SNS

(3) partial inhibition of Na/K ATPase:

==>can't pump out Na+
==>Na+ builds up inside cell
==>Na/Ca antiport cannot work (usually pumps out Ca, pumps in Na)
==>Ca builds up inside the cell
==>more Ca in SR, so DIRECTLY incr dp/dt!!


Automaticity in fast fibers
("bad EE": PVC's/PAC's, AV block) d/t:

a. Inhibited Na-K pump
==>Na builds up inside cell (decreases membrane potential (more +)==>depolarized)==>automaticity

b. Hypokalemia (low K+ outside the cell) potentiates inhibition of Na-K ATPase b/c not enough extracellular K+ to pump into cell in order to pump Na+ out
==>Na/K ATPase doesn't work
==>Na builds up inside the cell and makes it +
==>spontaneous depolarization= “automaticity”==>decr ERP in ventricles

d. High Ca++: Ca++ overload inside cells causes automaticity (Goljan: decreasing depolarization threshold)

d. Low Mg++: same as Ca++ overload inside cells - causes automaticity


PE:
(1)&(2):
*decr HR
*decr conduction velocity
*incr ERP in AV node >> controls (reduces) V rate in A fib/flutter

(3) incr SV via increased dp/dt (thus, OK for HF)

*half-life of digitoxin >> half-life of digoxin (7 days vs. 1 day);

mneum: digitoxin is a longer word than digoxin, so it has a longer half-life


*Digitoxin cleared hepatically
(reduce dose in CHF, cirrhosis)

*Digoxin is cleared renally (reduce dose if decr GFR);

-older pt on digoxin--
low Vd ==>decr loading dose
low GFR==>decr maintenance dose

-MOA: inhibits N-Ka pump
==>incr dp/dt,
==>but also incr automaticity

S/E:
AV block
PVC's (d/t automaticity)
N/V (CTZ)
CNS-abnl color vision, halo vision
*quinidine incr plasma digoxin from SkM and decr renal Cl==>incr digoxin (toxic!)

Front 108

quinidine

Back 108

Tx: A and V dysrhythmias
(A fib/flutter, PVC's)

MOA:
1. block Na channels (in fast fibers: A, V, Purk)
2. block K channels (in fast fibers: A, V, Purk)
3. block a-adrenoceptors
4. block musc-receptors

PE:
1. suppress spontaneous depol(incr depol threshold) & slope of phase 0
==>slows conduction velocity (wider QRS)
==>PVC's

2. incr APD/ERP (b/c no K+ to repolarize)
-in atria==>decr AV conduct
-in vent ==>incr QT (Toursaud)

3. dilate arterioles & venules

4. tachycardia, incr AV conduction

*SA Node: no direct effect
*AV node: decr AV conduction d/t block K+ receptors (#2), but incr AV condution d/t block muscarinic (#4)

*give digoxin before quinidine in A fib/flutter pt so that digoxin can prevent incr QT interval d/t atropine-like effect of quinidine casued by blocking musc receptors

S/E:
Toursaud (incr QT interval)
hypotension (a-block)
decr dp/dt
diarrhea
tinnitus

Front 109

pt with A fib given quinidine to slow ventricular rate, but instead ventricular rate rises immediately.
-why?
-how Tx?

Back 109

incr vent rate d/t immediate anti-muscarinic effect of quinidine

Tx w/verapamil or diltiazem (Ca+ channel blockers, Tx AVNRT) to decr AV conduction

Front 110

procainamide

Back 110

shiP: SLE and arthritis in slow aceylators, who cannot clear drug by hepatic biotransformation

Tx:
-ACUTE control of V rate in A fib/flutter and PVC's

MOA: block Na and K channels
==>suppress phase 4 automaticity in fast fibers
==>decr conduction veloc (widens QRS)

Front 111

disopyramide

Back 111

PE:marked decrease in dp/dt

S/E: marked antimuscarinic effects:
-dry mouth
-constip
-contraindicated in BPH and glaucoma

Front 112

lidocaine

Back 112

Tx: DOC for PVC's (only for ventricular arrthythmias)

MOA: block Na+ channnels in fast fibers (A,V,Purk)
-give IV d/t low F

PE:
-decr phase 4 automaticity (prevent PVC's)
-no effect on SA or AV nodes, BP, or dp/dt
-local anesthetic effect by blocking Na+ channels

S/E:
seizures (b/c blocks Na channels in brain too well)
==>tx w/BZ (benzodiazepine)

Front 113

DOC for PVC's

Back 113

lidocaine

MOA: block Na+ channnels in fast fibers (A, V, Purkinje)
-give IV d/t low F

PE:
-decr phase 4 automaticity
(prevent PVC's)
-no effect on SA or AV nodes, BP, or dp/dt
-local anesthetic effect by blocking Na+ channels

S/E:
seizures (b/c blocks Na channels in brain too well)
==>tx w/BZ (benzodiazepine)

Front 114

amiodarone

Back 114

Tx: recurrent V tach/fib

MOA: block Na and K channels in fast fibers

PE:
-block K fibers
==>can't repolarize
==>incr APD/ERP
==>incr QT (but never Toursaud!)
==>slows AV conduction (incr PR_

-block Na fibers
==>suppress phse 4 automaticity

S/E:
-pulmonary fibrosis
-hyper/hypothyroidism
-corneal microdeposits

Front 115

verapamil

Back 115

mneum: VD=Valentine's Day (heart=cardiovascular)
=Verapamil & Diltiazem

Ca+ Channel blockers

Tx: AVNRT
MOA: blocks L-type channels at SA and AV nodes & cardiac myocytes

PE:

block at SA node:
==>decr HR

block at AV node:
==>decr conduction velocity and incr ERP
==>fewer signals from A to V

block at myocytes:
==?decr dp/dt==>decr CO

S/E:
AV block
decr dp/dt
decr CO in HF

Front 116

patient with A fib and no GR has palpitations and dizziness. Tx w/verapamil:

MOA?

Back 116

incr ERP of AV node slows AV conduction
==>more time for ventricles to fill
==>incr CO

Front 117

antiplatelet drugs

Back 117

1. Aspirin:
irreversibly inhibits both COX-1 & COX-2
==>prevent conversion of AA to PG's (incl. TxA2)
==>lack of TxA2 inhibits GP2b/3a expression (which use fibrinogen to bind platelets together)
on activated platelets
==>platelets can't aggregate

2. Ticlopidine, clopidogrel :
irreversibly blocks ADP receptors
==>inhibits GP2b/3a expression (which use fibrinogen to bind platelets together)on activated platelets
==>platelets can't aggregate

3. Abciximab, Tirofiban, Eptifibatide ("ATE"):
antagonize GP2b/GP3a
==>no platelet aggregation

(AbcixiMAB is Monoclonal AB that binds GP2b/3a)

Front 118

a patient requires antiplatelet rug after MI or drug, but they have aspirin hypreseensitivity. how tx?

Back 118

clopidogrel or ticlopidine

Front 119

heparin

Back 119

Tx: MI, DVT's

MOA: enhances binding of ATIII to activated clotting factors 2, 9-12
(Intrinsic Path: 12,11,9)
(Common Path: 10, 2)

-must give iv (not po)
-incr aPTT (intrinsic pathway) > incr PT (extrinsic pathway)
-antagonist: protamine sulfate

S/E: bleeding

Front 120

ticlopidine

Back 120

Ticlopidine, clopidogrel :
irreversibly blocks ADP receptors
==>inhibits GP2b/3a expression (which use fibrinogen to bind platelets together)on activated platelets
==>platelets can't aggregate

Front 121

clopidogrel

Back 121

Ticlopidine, clopidogrel :
irreversibly blocks ADP receptors
==>inhibits GP2b/3a expression (which use fibrinogen to bind platelets together)on activated platelets
==>platelets can't aggregate

Front 122

Abciximab,

Back 122

Abciximab, Tirofiban, Eptifibatide ("ATE"):
antagonize GP2b/GP3a (which use fibrinogen to bind platelets together)
==>no platelet aggregation

Front 123

Eptifibatide

Back 123

Abciximab, Tirofiban, Eptifibatide ("ATE"):
antagonize GP2b/GP3a (which use fibrinogen to bind platelets together)
==>no platelet aggregation

Front 124

Tirofiban

Back 124

Abciximab, Tirofiban, Eptifibatide ("ATE"):
antagonize GP2b/GP3a (which use fibrinogen to bind platelets together)
==>no platelet aggregation

Front 125

LMW heparins

Back 125

="--PARINS" (~hePARIN)
-eg: ardeparin, dalteparinm, enoxaparin
clreaed by kidneys instad of RE system (ReticuloEndothelial syste)
-longer half-life than heparin
-wroks mostly on 10a, so little effect to incr aPTT

Front 126

warfarin

Back 126

MOA=alters shape of factors 2,7,9,and 10, so that Ca2+ cannot bind to them and thus they cannot be gamma-carboxylated by Vit K1
-incr PT/INR (extrinsic system) > incr aPTT (Goljan)
-OD with warfarin incr both PR and aPTT (according to Keeton, nl dose of
warfarin does not inc aPTT)
-antidote: Vit K1 (phytonadione)
-many drug-drug interactions==>displacement of warfarin from plasma protein has 2 effects:
1. incr PT
2. incr clearance of warfarin

-Tx:
*MI,
*DVT,
*prevent emboli in pts with cardiac valves
*prevent thrombotic stroke in pts with A fib

-metabolized by CYP450; thus warfarin & PT/INR incr if CYP450 inhibited

Inhibition of CYP450:
"I C a KEG"
-isoniazid (INH) (Tx tb)
-cimetidine
-ketoconazole
-erythromycin
-grapefruit juice

Induction of CYP450(==>decr warfarin/PT):
-chronic EtOH (smoking)
-benzopyrene (cig's)
-carbamazepine (tx seizure)
-phenobarbital (tx seizure)
-phenytoin (tx seizure)
-rifampin (tx TB)

Front 127

what drug give post-DVT

Back 127

warfarin

Front 128

what drug give post-MI

Back 128

warfarin

Front 129

person OD's with rat poison. what happens to clotting times?

Back 129

both aPTT and PT incr
(nl dose=only PT(INR) incr.
OD =both aPTT and PT incr

Front 130

what cardiac dysrhythmia req Tx with warfarin?

Back 130

A fib

Front 131

things that inhibit CYP450

Back 131

Inhibition of CYP450:

"I C a KEG"

-isoniazid (INH) (Tx tb)
-cimetidine
-ketoconazole
-erythromycin
-grapefruit juice

Front 132

things that induce CYP450

Back 132

-chronic EtOH (smoking)
-benzopyrene (cig's)
-carbamazepine (tx seizure)
-phenobarbital (tx seizure)
-phenytoin (tx seizure)
-rifampin (tx TB)

Front 133

thrombolytic drugs

Back 133

activate plasminogen==>plasmin

-plasmin destroys fibrin to lyse clots (fibrin catches RBC's into its net, just like a fishing net catches fish. Then plasmin acts like scissors to cut the fibrin (fishing net))

1. urokinase: directly activates plasminogen==>plasmin

2. tPA: (direct activator)
when tPA and plasminogen bind to fibrin in loose proximity, tPA activates plasminogen==>plasmin

3. streptokinase (indirect activator): exposes protease binding site on plasminogen,
which activates other plasminogen molecules==>plasmin

S/E: systemic destruction of clotting factors 5 & 8
-->bleeding, esp in CNS (hemorrhagic stroke)

Front 134

pt with MI treated with several drugs, then develops intacranial bleeding. what drug casued this?

Back 134

streptokinase (indirectly activates plasminogen==>plasmin)

Front 135

anti-fibrolytic drug?

Back 135

aminocaproic acid

MOA: lysine analog, binds lysine-binding sites on plasmin and prevents it from binding fibrin

Front 136

aminocaproic acid

Back 136

anti-fibrinolytic

MOA: lysine analog, binds lysine binding sites on plasmin
==>prevents plasmin from binding fibrin

Front 137

lovastatin

Back 137

(and all other statins)

MOA: inhibit hepatic HMG CoA reductase
==>decr intracellular hepatic sterol pool
==>upreg HMG CoA reductase & LDL receptors

-Net effect:
decr LDL, total cholest, TG;
slight incr HDL

S/E:
-myosities/myopathy: muscle pain and weakness d/t incr CPK
-muscle damange
==>incr CPK & myoglobinuria
==>can progress to rhabdomyolysis (can kill you)

Front 138

ezetimibe

Back 138

MOA: inhibit GI abs of chol
==>decr sterol pool
==>incr gene expression of hepatic LDL receptors
==>decr total chol & LDL
(but no change HDL)
-Tx pts who get myositis on a statin: if pt on statin gets myositis, you can lower statin dose to lowest level and give ezetimibe (just as effective as highest dose of statin!)

Front 139

pt on lovastatin develops myosiit. what drug can you switch them to?

Back 139

ezetimibe

Front 140

if pt on statin gets myositis, what can you do?

Back 140

you can lower statin dose to lowest level and give ezetimibe (just as effective as highest dose of statin!)

Front 141

Tx hypertriglyceridemia

Back 141

gemfibrozil, fenofibrate

Front 142

dicumerol

Back 142

same as warfarin:

MOA=alters shape of factors 2,7,9,and 10, so that Ca2+ cannot bind to them and thus they cannot be gamma-carboxylated by Vit K1
-incr PT/INR (extrinsic system) > incr aPTT (Goljan)
-OD with warfarin incr both PR and aPTT (according to Keeton, nl dose of
warfarin does not inc aPTT)
-antidote: Vit K1 (phytonadione)
-many drug-drug interactions==>displacement of warfarin from plasma protein has 2 effects:
1. incr PT
2. incr clearance of warfarin

-Tx:
*MI,
*DVT,
*prevent emboli in pts with cardiac valves
*prevent thrombotic stroke in pts with A fib

-metabolized by CYP450; thus warfarin & PT/INR incr if CYP450 inhibited

Inhibition of CYP450:
"I C a KEG"
-isoniazid (INH) (Tx tb)
-cimetidine
-ketoconazole
-erythromycin
-grapefruit juice

Induction of CYP450(==>decr warfarin/PT):
-chronic EtOH (smoking)
-benzopyrene (cig's)
-carbamazepine (tx seizure)
-phenobarbital (tx seizure)
-phenytoin (tx seizure)
-rifampin (tx TB)

Front 143

gemfibrozil

Back 143

Tx: hypertriglyceridemia

MOA: inhibits lipoprotein lipase (esp in SkM)
==>decr VLDL synthesis
==>decr total chol, LDL, VLDL, TG;
-slight incr HDL

S/E:
-myositis/myopathy = musc pain/weakness assoc w/high CPK
-muscle damage can progress to rhabdomyolysis

Front 144

niacin

Back 144

MOA: unknown
-used to incr HDL
-S/E: flushing itchiness in face and upper body

Front 145

what drug used to incr HDL

Back 145

niacin

Front 146

antianginal drugs

Back 146

*all decr O2 demand and/or incr O2 supply
*all incr endocardial blood flow (incr diastole & decr HR)

1. Beta blockers ("--olol")
atenolol, metoprolol,
timolol, propolol

MOA:
*negative chronotropic (HR) and inotropic (decr dp/dt)
==>decr rate-pressure product (HRxSBP)
==>decr O2 Demand
*decr afterload==>decr D(O2)

B. Nitrates=nitroglycerin
NITROGLYCERIN
AKA GLYCERyl triNITRATE
AKA isosorbide mono- and diNITRATE

MOA: NO donors selectively venodilate
==>decr VR (preload)
==>decr D(O2)

*drug tolerance is big problem

C. CCB:
Verapamil, Diltiazem,
amLODIPINE, feLODIPINE

Verapamid & Diltiazem
(Valentines Day):

1. negative chlonotropic (HR) and inotropic (decr dp/dt)
==>decr rate-pressure product (HRxSBP)
==>decr D(O2)

2. decr afterload==>decr D(O2)

3. dilate epicardial vessels
& small endocardial resistance vessels
==>incr S(O2)

amLODIPINE, feLODIPINE:
*decr afterload==>decr D(O2)

*dilate epicardial vessels
& small endocardial resistance vessels
==>incr S(O2)

Front 147

atenolol

Back 147

"--olol"=Beta blocker
(also metoprolol, timolol, propanolol)

MOA:
*negative chronotropic (HR) and inotropic (dp/dt)
==>decr rate-pressure product (HRxSBP)
==>decr O2 Demand
*decr afterload==>decr D(O2)

Front 148

nitroglycerin

Back 148

*all decr O2 demand and/or incr O2 supply
*all incr endocardial blood flow (incr diastole & decr HR)

NITROGLYCERIN
AKA GLYCERyl triNITRATE
AKA isosorbide mono- and diNITRATE

MOA: NO donors selectively venodilate
==>decr VR (preload)
==>decr D(O2)

*drug tolerance is big problem

Front 149

Verapimil

Back 149

*all decr O2 demand and/or incr O2 supply
*all incr endocardial blood flow (incr diastole & decr HR)

Verapamil & Diltiazem
(Valentines Day):

1. negative chlonotropic (HR) and inotropic (decr dp/dt)
==>decr rate-pressure product (HRxSBP)
==>decr D(O2)

2. decr afterload==>decr D(O2)

3. dilate epicardial vessels
& small endocardial resistance vessels
==>incr S(O2)

Front 150

Diltiazem

Back 150

*all decr O2 demand and/or incr O2 supply
*all decr O2 demand and/or incr O2 supply
*all incr endocardial blood flow (incr diastole & decr HR)

Verapamil & Diltiazem
(Valentines Day):

1. negative chlonotropic (HR) and inotropic (decr dp/dt)
==>decr rate-pressure product (HRxSBP)
==>decr D(O2)

2. decr afterload==>decr D(O2)

3. dilate epicardial vessels
& small endocardial resistance vessels
==>incr S(O2)

Front 151

amlodipine

Back 151

*all decr D(O2)and/or incr S(O2)
*all incr endocardial blood flow (decr HR==>incr diastole)

amLODIPINE, feLODIPINE:
-decr afterload==>decr D(O2)
-dilate epicardial vessels
& small endocardial resistance vessels
==>incr S(O2)

Front 152

glyceryl trinitrate

Back 152

*all decr O2 demand and/or incr O2 supply
*all incr endocardial blood flow (incr diastole & decr HR)

NITROGLYCERIN
AKA GLYCERyl triNITRATE
AKA isosorbide mono- and diNITRATE

MOA: NO donors selectively venodilate
==>decr VR (preload)
==>decr D(O2)

*drug tolerance is big problem

Front 153

isosorbide dinitrate

Back 153

AKA nitroglycerin
AKA glyceryl trinitrate

*all decr O2 demand and/or incr O2 supply
*all incr endocardial blood flow (incr diastole & decr HR)


MOA: NO donors selectively venodilate
==>decr VR (preload)
(decr D(O2))
*drug tolerance is big problem

Front 154

Tx Congestive Heart Failure

Back 154

=systolic dysfxn

1. decr preload w/diuretic
2. decr preload & afterload (balanced vasodilation) w/ACEi or ARB
3. incr cardiac dp/dt w/digoxin
4. reverse cardiac remodeling caused by AngII w/ACEi or ARB
5. reverse cardiac remodeling caused by ALDO w/spironolactone
6. reverse cardiac remodeling caused by SNS w/carvedilol
7. add digoxin to Tx when ACEi + diuretic isn't working or when pt is in chronic A fib

Front 155

how decr preload in CHF

Back 155

diuretics (preload only)
ACEi or ARB (balanced vd
==?decr preload & afterload)

Front 156

how enhance dp/dt in CHF

Back 156

digoxin

Front 157

how reverse cardiac remodeling in CHF caused by AngII

Back 157

ACEi or ARB

Front 158

how reverse cardiac remodeling in CHF caused by ALDO

Back 158

spironolactone

Front 159

how reverse cardiac remodeling in CHF caused by SNS

Back 159

carvedilol

Front 160

what add to Tx in CHF when ACEi + diuretic not working?

Back 160

digoxin

Front 161

how Tx chronic A fib in CHF?

Back 161

digoxin