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pharm > exam 2: lecture 2 > Flashcards

exam 2: lecture 2 Flashcards

1
Q

what is the MOA of CCB? how many subunit does CCB have ?

A

BLOCKS L type ca channel and T type ca channel

5 subunits- 2a b g d

V + D binds to the A1 subunit and dihydro binds to the a1 subunit but on a DIFF PLACE = accounts for specificity

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2
Q

what are the nondihydro and dibhydro CCB meds?

A

non-dihydro - VD - verapamil, diltz

Dihydro: NNFAC
nifedipine - 1st drug in class casues tachycardia since blood vessles dialte fast
nicardine
felodipine
amlodipine - LONGEST half life
clevidipijne - only in IV form

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3
Q

where does nondihyfro and dihydro work best?

A

nondihydro works best in myocardium

dihydro works best in peripheral vascualr smooth musucles

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4
Q

what binds to T type channels CCB?

A

they are found in SA and AV nodes and non-dihydro drugs bind to it more which accounts for tissue specificity

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5
Q

what are the effects on the myocardium, arterial smooth musucles, coronary aa from CCB?

A

mycardium - slows contraction, reduces O2 requirement, usefull in angina. slows AV/SA nodes, decreases HR, decreases O2 requiremetns

arteiral smooth muscules - STOPS ca influx so casues vasodilation which decreases aterial presure

coronary aa - stops contraction stops spasm helps w prinz metal angina

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6
Q

what does amlodipine do to NO?

A

amlodipine worsk as a ACEi which leads to buildup of bradykinin –> increases NO –>. vasodilation

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7
Q

how does Vereapamil and diltiazem have sympatehtic antagonist effects?

A

if you give someone diltiazem, there is no relfex tachycardia due to sympaethtic blockage = vasodialtion, no tachycarida!!!

unlike nifidepine which has tachy effect

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8
Q

what are some indication for CCB and how do some of them work?

A
  • HTN = dihydro drugs like amlodipine
  • variant angina = diltizaem + isosorbide dinitrate (will explain in diff card)
  • supraventricular arrhytmias = dilz, vera = targets T CA channels (t challens leads to depolarization)
  • raynauds = dihydro (nifedipine) prevetns constriction, casues dialtion to fingers

-achalasia= dihydro (nifedipine) presents vasocontriction and casues relaxation

  • migraines
  • intracranila vasospams = dihydro = prevetns spasm after a stroke
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9
Q

what are some untoward effects to CCB?

A

cardiac depression - can slow down condcution and casue bradycarida and heart block

Hypotension = orthostasisi
GERD - VERY COMMON
Hyperglycemia - CCB can block calcium channels to stop releasing insulin leading to hyperglycemia!! ==> Metabolic ketoacidosis!!

Edema = due to redistruction of fluid and space

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10
Q

when is non dihydro CCB contraindiacated?

A

AV NODE BLOCK

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11
Q

what is the sig to papaver somniferum? what does the opium contain?

A

its an illegal plant that contains a crude opium (morphone, codein, pavaverine, thebaine).

this is why in drug test its positive

in 1964 reserchers realzied that the opiates are great vasodilators and they modfied papaverine to verapamil

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12
Q

what was the first drug in the nondihydro (year) and dihydro class?

A

non dihydro - verapamil 1964 but FDA approved in 1982

dihydro - nifedipine

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13
Q

waht is the MOA and pharmokinetics for minoxdil? what year was it made?

A

made in the 60s which has an untaught effect of hypertrichosis!!

MOA = OPENS K channels in arterial smooth musucles which hyperpolarizes making it harder to transmit a signal.

AFFECTS ONLY ARTERIES NOT VEINS!

pharmokinetics = taken PO. its a prodrug so liver can convert it to active sulfate metabolite!

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14
Q

what are the indication and untowards effect for minoxdil?

A

indications are:
- HTN = NOT FIRST IN LINE, its used for refractory HTN. only give this is nothing else works

  • +diuretic and BB - you need to give it w either these two drugs or else it will casue bad vasodilation –> bad edema and bad tachycardia

untoward effects:
- CV - tachycardia, palpitation, angina, death
- hypertrichosis

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15
Q

what is the MOA of hydralazine?

A

normally, Gq activates IP3 but hydralazine inhibits IP3 so theres less contraction OR IT COULD ALSO open up calcium channels who knows

net effect: arterioles vasodilators

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16
Q

what is the pharmokineteics for hydralazine? think about metformin (mommy)

A

PO

hydralzies is metabolzied in liver by acetylate
fast metabolism = 15%
slow metabolism = 35-40%

17
Q

what are the indication for hydralazine?

A

you give it to someone wiht HTN w angina.

you would combine hydralazine +isosorbide dinitrate = BIDEL

18
Q

whats the significance of BIDEL?

A

so normally tachypalaxis effect happen when you give someone NO and body respond by making ROS to cancel out NO.

but if you give someone BIDEL, then this cancels the ROS so BIDEL gets rid of tachyphalyaxis effect

19
Q

why is BIDEL effective in black pt than white? think of the study

A

study showed that BIDEL decreased M/M sig in black pateitns

more in black bc black has more ROS than anyone else so BIDEL works better

20
Q

what are the untoward effect for hydralazine?

A

HYPOtension, headahce, lupus like syndrome

21
Q

which drug has lupus like syndrome as their untoward effect? explain

A

hydralazine!!

lupus like syndrome consist of malasie, rash, fever, muscule joint but NO RENAL DYSFUNCTION

its an auotimmune mediated reaction developing months after taking the rx

if you stop the drug lupus like syndrome can get back to normal

more prone in SLOW metabolizers since drug lingers in their body logner for effects to happen

22
Q

which two vasodilator rx would you combine with +isosobirde dinitrate and what is it used for ?

A

CCB for variant angina: combine ditazem + Isosobide = FOR preventing tachycardia reflux

Hydralazine for HTN w angina: combine hydra + isosorbide = FOR preventing tachyphylaxsis

23
Q

what is the MOA for milrinone?

A

normally in the cell, cAMP is converted to 5AMP by PDE3 (phosphodiesterase 3)

BUT milrinone inhibits PDE3

so the effect is increase cAMP therefore increase in PKA which will release MORE CA –> POSTIVE INOTROPIC EFFECT TO HEART

24
Q

whats the pharmokinectic, when would u give it, and untwoard effect for milrinone?

A

given IV

given for HF or acute cardiac decompenstation for THAT JOLT for inotropic effect (contractility)

effects are GI disturbances :( and arrhythmias sine were contracting

25
Q

what are some untoward effect of nitrates?

A
  • HYPOtension duh
  • tachycardia
  • cyanide = sodium nitroprusside can increase build up of cyanide whcih interferes w ETC
  • HYPOthryoidism - sodium nitrorusside affects iodine uptake and thyroid glands
  • dont mix sildefil and nitrate = bad hypotension
  • tolerance
26
Q

exaplin the foxglove plant and the two people in the picture?

A

the black and white pic: William withering is holding a foxglove plant that can go to three feet high, diff colors comes out in spring

he is slouching and looks comfy from neck down but head looks good

on the color pic, van gough painted his doctor Paul GOSHAE who tx him w heart failture - was on digoxin

van gough portrayed him the same way at withering

27
Q

what are the indication/untoward effect for digoxin?

A

indication = HF (+ inotropic effect) and arrhthmias

untoward effect =
- arrthymia - AV block, bradycarida
- GI issues
- neuro: HA, fatigeu
- visual = yellow tint cone cells affected

  • toxicity: (how would u tx it)
    • atropine: it helps w w slow HR
    • K+ = given IV will prevent dixogin from bidning
    • AB - antibodies will bind to digoxin and kill it and take it out of circulation
28
Q

where doe NO come from? what molecule and which layers does it go through?

A

ARG is converted to NO and Nitrate goes into the tunica intima and tunica media to do its thing

29
Q

what are the three exogenous nitrate examples and when do u use it/how does it work?

A
  1. nitroglyerine
    - sublingual or transdermal to avoid first pass effect
    - used for angina BUT NOT VARIANT ANGINA
  2. isosorbide dinirate
    - HTN w hydralziine
    - variant angina w CCB = for spasm help
  3. sodium nitropursside
    - given IV
    - for aortic dissection, HTN emergencies, acute MI which will decrease O2 requirements
30
Q

when NO gets to the smooth muscules, what does it get activated to? what is the pathway step by step

A

in the smooth muscules,
1. NO gets converted to sGC –>cGMP
2. cGMP activates –> PKG
3. PKG has many effects of stopping CA influx and release

31
Q

which gets activated with NO: MLCK or MLCP?

A

MLCP gets activated –> casues vasodilation and relaxtion of the smooth muscules

32
Q

what recepetor does NO interact with in the heart? what is the effect?

A

NO interacts w cardiac ryanodine receptor!

this regulates CA flux in a positive way –>increases inotropic effect of the heart

33
Q

how do u turn off nitrate system?

A

you use PDE phosphidiesterase which will BREAK DOWN cGMP

34
Q

what is contraindicated with nitrate?

A

do not give nitrate with outflow obstruction!!!! since it can cause POOR preload!!

AND
with sidenafil :( severe vasodialtion bruh

35
Q

what is vericuguat? what drug class is it ass with?

A

ass with nitrate. its. NEW DRUG!
- it activates sCG directly so it bypasses production of NO!

without making NO, we dont get tachphylaxis = better affect on ryanoidde receptor

36
Q

what does sildenafil (viagra) do?

A

it can cause vasodilalation!

in the penis = corpus cavernosa,
- PDE5 normally break down cGMP. sildenafil binds to the PDE5 so cGMP is not broken down so high levels of cGMP increases vasodilation of the penis :)

PDE6 is found in the retina - sildenafil binds to PDE6 blocks it = halo effect

pharm (13 decks)

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