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Pharm > CPEE Test 2 > Flashcards

CPEE Test 2 Flashcards

1
Q

What’s the role of NO in VSM relaxation

A
  • Activates Guanylyl Cyclase which creates cGMP
  • cGMP activates myosin light chain phosphatase which takes a phosphate off of myosin light chain
  • Dephosphorylated myosin light chain leads to relaxation of VSM and vasodilation.
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2
Q

Which drugs are the Organic Nitrates

A

-Nitroglycerin and Isosorbide dinitrate

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3
Q

Nitroglycerin

A
  • Prodrug converted to NO by ALDH2 (inhibited by alcohol and some decrease in activity among asian population)
  • ALDH2 deactivation by NO leads to tolerance
  • Primary effect is venous dilation –> decreased preload
  • Reverses ST segment depression but no survival benefit in MI
  • Orthostatic hypotension, reflex tachycardia, flushing headaches
  • Sublingual tablet for fast relief (fast effect short duration of action)
  • Patch or oral formulation for prophylaxis (longer duration of action and slower acting)
  • DON’T TAKE WITH ED drugs.
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4
Q

Isosorbide Dinitrate

A
  • Prodrug that is converted to isosorbide mononitrate which contributes to its efficacy.
  • Longer duration of action that NTG
  • Used when NTG and Beta blockers or CCB aren’t effectively controlling Angina.
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5
Q

Calcium Channel Blocker Drugs

A
  • Dihydropyridines: Nifedipine

- Non-dihydropyridines: Verapamil and diltiazem

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6
Q

Calcium Channel Blockers action

A
  • Block inward flow to Calcium through voltage gated L-type Channels
  • Verapamil and diltizem work at nodal tissue (decrease heart rate) as well as cardiac and VSM
  • Dilators on coronary and peripheral VSM –> decrease in preload
  • Prophylaxis (due to long duration of action) to reduce NTG consumption.
  • Useful in Vasospasm seen in Prinzmetal angina.
  • Efficacy in treating angina = to beta-blockers, but no survival benefit.
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7
Q

Nifedipine

A
  • Dihydropyrimidine
  • Causes reflex tachycardia so it shouldn’t be used
  • Less depression of myocardial contractility and minimal effects on SA node
  • CYP 3A4 (avoid grapefruit juice
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8
Q

Diltiazem and Verapamil

A
  • Same action as Nifedipine with added SA and AV node effects (decreased heart rate and contractility)
  • less potent vasodilators
  • Diltiazem produces less cardiac depression and is generally tolerated better than Verapamil.
  • DONT USE IN SICK SINUS SYNDROME OR AV NODAL BLOCK
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9
Q

Adverse effects of Nifedipine, Diltiazem and Verapamil

A
  • Bradyarrhythmias (VER and DIL)
  • Reflex Tachy (NIFE)
  • Cardiac Depression (VER and DIL)
  • Flushing with peripheral edema (NIFE)
  • Constipation in geriatrics (Ver)
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10
Q

Beta-Blockers

A

-Propranolol

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11
Q

Propranolol

A
  • Beta blocker
  • Decreases: HR, Contractility, Systemic BP
  • Works by decreasing afterload
  • Decreases mortality by decreasing sudden cardiac death
  • Goal is to get resting HR at 55bpm and upper limit is 110 bpm
  • Not useful in Prinzmetal due to unopposed alpha 1 activity
  • Reduces frequency and severity of stable angina attacks
  • Can precipitate acute M.I. after sudden withdrawl
  • Don’t use with B1 agonists
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12
Q

Ranolazine

A
  • Antianginal effects w/o changing heart rate or Blood pressure
  • Stops Calcium overload in ischemic myocytes by inhibiting sodium influx which is later exchanged for calcium
  • Prophylaxis against angina
  • Used for refractory angina because it prolongs QT interval.
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13
Q

1st line Antihypertensives

A

Thiazide diuretics, ACE inhibitors, ARBs, CCBs

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14
Q

3rd line Antihypertensives

A

Beta blockers, Loop diuretics, Alisikiren, Alpha 1 blockers,, vasodilators, Centrally acting alpha-2 agonists, Reserpine, Aldosterone antagonist.

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15
Q

Thiazide

A
  • Chlorthalidone
  • Anti hypertensive not hypotensive
  • Initially increase renal secretion of Na+ and H20 but TPR increases due to sympathetic reflex and activation of RAAS
  • Later on decrease TPR, probably lack of sodium –> altered Na/Ca exchange in VSM
  • No change in HR or CO
  • Low dose mono therapy for stage I (10-15mmHg 4-6 weeks after onset of therapy)
  • reduce Na retention caused by vasodilators
  • Partially effective in volume dependent HTN
  • Hypokalemia, Hyperuricemia, ED
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16
Q

Loop Diuretics

A
  • Furosemide
  • mostly malignant HTN and volume dependent patients w/ renal disease
  • Ototoxicity
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17
Q

RAS System drugs

A
  • Captopril (ACE inhibitor)
  • Losartan (ARB)
  • Eplerenone (Aldosterone agonists)
  • Aliskiren (Renin inhibitors)
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18
Q

ACE inhibitor

A
  • Captopril
  • Inhibits Ang I –> Ang II conversion decrease TPR
  • Antihypertensive (effective even in patients with normal PRA)
  • First dose phenom
  • Doesnt interfere with cardiovascular reflexes or bronchial asthma.
  • Reduce risk of HTN associated cardiovascular mortality
  • hyperkalema, cough, angioedema, teratogenicity
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19
Q

ARBs

A
  • Losartan
  • AT1 receptor antagonists
  • Alternative for patients who don’t like ACEI
  • No cough or angioedema
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20
Q

Aldosterone antagonists

A
  • Eplerenone
  • selective aldosterone antagonist (more selective in this regard than spironolactone)
  • Promotes Na and H2O excretion in kidney
  • Prevent reverse cardiac remodeling
  • Used for additional decrease in BP in Pts taking ACEI or ARB
  • HYPERKALEMIA
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21
Q

Direct Renin inhibitor

A
  • Aliskiren
  • Blocks angiotensinogen –> ATI
  • Used alone or in combo
  • hyperkalemia
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22
Q

Calcium Channel Blockers

A

Nifedipine, Verapamil, Diltiazem

  • Blocks voltage gated L-Ca channels in VSM –> decrease TPR
  • Ver and Dil slow HR
  • First line for mild to mod HTN
  • Nif used for PAH
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23
Q

Vasodilators

A

Nitroprusside, Hydralazine, Minoxidil, Epoprostenol, Bosentan

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24
Q

Nitroprusside

A
  • Decomposes to release NO w/ enzyme (no tolerance)
  • Arterial and venous dilation
  • Immediate effect with short DOA (unstable and light sensitive in solution)
  • Produces CN- that is metabolized in liver by rhodanase (thiosulfate antidote)
  • Hypertensive emergencies, hypotensive during surgery, need to give furosemide to avoid edema
  • Excessive vasodilation and hypotension, cyanide, hypothyroidism (thiocynate accumulations)
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25
Q

Hydralizine

A
  • ARTERIOLAR dilation to decrease TPR
  • High first pass metabolism, NAT-2 inactivates drugs (slow acetylators)
  • SEVERE HTN 3rd line, HTN crisis
  • Combo w/ isosorbide dinitrate for CHF/HTN in AA
  • Reflex tachy, lupus like syndrome in slow acetylators
26
Q

Minoxidil

A
  • Arterial Dilation via K+ efflux –> membrane hyperpolarization
  • Reflex increase in HR and contractility
  • Prodrug, liver –> minoxidil sulfate
  • Seldom used unless extreme HTN due to side effects
  • Rogaine
  • Edema due to Na and H2O retention (diuretic), Pericardial effusion, Reflex tachycardia (beta blocker), Hypertrichosis
27
Q

Prostacyclin

A
  • Epoprostenol
  • Mimics endogenous PGI2 on VSM, binds to GPCR and stimulates cAMP synthesis
  • Vascular relaxation, suppresses VSM growth, inhibits platelet agg.
  • used in PAH to increase short term survival
  • Flushing, headache, nausea, increased risk of bleeding
28
Q

Endothelin-1 Antagonist

A
  • Bosentan
  • Endothelin 1 is endothelial derived vasoconstrictor peptide (POTENT)
  • induces inflammation, fibrosis, and prolif of VSM, levels elevated in PAH
  • Antagonist at ETa and ETb receptors
  • PAH treatment but use limited due to toxicity
29
Q

Sympatholytics

A

-Clonidine and methyldopa

30
Q

Centrally acting Alpha 2 adrenergic agonists

A
  • Clonidine
  • Decrease sympathetic outflow, pre-synaptic alpha 2a receptors in medulla decreased CO and TPR
  • produces compensatory sodium and H2O retention
  • Antihypertensive for patients who haven’t responded to other drugs
  • Sedation, dry mouth, sex dysfunction, postural hypotension
  • abrupt withdrawal symptom
31
Q

Methyldopa

A
  • -> Methyl-NE
  • similar to clonidine but no rebound effect, hemolytic anemia
  • use during pregnancy
32
Q

Beta-Blockers

A
  • Propranolol, metoprolol, atenolol (last 2 are cardioselective)
  • Reduces CO (initial decrease in BP)
  • Inhibits beta-1 mediated release of renin
  • CNS reduces sympathetic outflow
  • no longer recommended unless there is a specific indication (MI, CHF, SIHD) or intolerance to first line agents
  • Less effective in AA and geriatrics
  • Brady, bronchoconstriction, reduced exercise capacity, sex dysfunction
33
Q

Alpha Blockers

A
  • Terazosin
  • Block Alpha 1 on VSM
  • Salt and water retention
  • Used as antiHTN add on
  • first dose effect, reflex tachy, nasal congestion, inhibition of eject
34
Q

HMG-CoA Reductase inhibitors: MOA and effects

A
  • Atorvastatin (Lipitor)
  • Compet inhib of HMG CoA reductase (rate limiting step in cholesterol synth)
  • Increase LDL hepatic receptors –> increased removal of LDL
  • enhance clearance and production of LDL precursors (VLDL IDL)
  • 20-55% dec LDL
  • 20% dec Triglycerides
  • 5-10% incr HDL
  • 1st line hypercholesterolemia due to elevated LDL
35
Q

HMG-CoA Reductase inhibitors: Potential cardioprotective effects, PK, drug interactions, Adverse effects

A

-Cardioprotective effects: Dec C-Reactive protein
-Anti inflam
-Enhance NO synth
-Stabilize plaque
-Reduce lipoprotein agg
-reduce plate agg
Pharmkinects: Orally, at night, extensive 1st pass metabolism, excreted by liver into bile
Drug interactions: Other statins
Adverse effects: GI irritation, headache and rash, hepatotoxicity, myopathy (creatine phosphokinase) NO PREGNANCY!

36
Q

Fibric Acids: MOA and effects

A
  • Fenofibrate
  • agonists at PPAR-alpha
  • Inc. FA Oxidation
  • Inc. act of lipoprotein lipase
  • Reduce expression ApoC-III –> inc. clearance of VLDL
  • ApoA-I and ApoA-II expression –> inc. HDL levels
  • Inhib of coag and incr. fibrinoylsis
  • Total effects: Dec. VLDL lowering Triglycerides and incr. HDL
37
Q

Fibric Acids: Uses, PK, Drug interactions, and adverse effects

A
  • Fenofibrate
  • Uses:
    • Type III hyperlipoproteinemai
    • Severe Hypertriglyceridemia (risk for pancreatitis)
    • Hypertriglyceridemia with low HDL
  • PK: absorbed rapidly and efficiently, T1/2 1-20 hrs, excreted as glucuronides
  • Interactions: warfarin effects may be incr., w/ statins myositis and myopathy
  • Adverse Effects: GI disturbances, skin rash, utricaria, hair loss, myalgias, fatigue and headache
  • NO PREGNANCY RENAL AND HEPATIC FAILURE
38
Q

Bile Acid Binding Resins

A
  • Colesevelam
  • Prevents bile acid reabsorption in the intestines –> incr. breakdown of hepatic cholesterol to bile acids
  • Also increases hepatic LDL receptors like statins, but accompanied by increase in HMG CoA activity
  • Lower LDL levels (10-20%) with a small increase in HDL levels (5%)
  • Familial or primary hypercholesterolemia w/ very high LDL usually used with Statin
  • Not absorbed after oral administration stays in GI tract
  • Bloating, dyspepsia, and Constipation, steatorrhea
39
Q

Niacin: MOA

A
  • Inhibits lipolysis of TGs in adipose tissue which reduces hepatic TG synthesis
  • Inhibits both the synthesis and esterification of FA’s which leads to decrease of TG synthesis. Dec. TG synthesis –> dec. Hepatic VLDL production –> decreased LDL
  • Decreases fractional clearance of HDL ApoA-I (makes HDL)
40
Q

Niacin: Effects, uses, PK, and Adverse effects

A
  • Effects: rapidly lowers TG levels, more gradual lowering of LDL levels, increases HDL
  • Uses: Hypertriglyceridemia and elevate LDL, useful in patients with Hypertriglyceridemia and low HDL
  • PK: Readily absorbed in all part of intestinal tract, short T1/2, metabolized in the liver and excreted unchanged
  • Adverse effects: Myopathy, flush, GI disturbances, Hepatic toxicity, ulcer, hyperglycemia, hyperuricemia
  • Pregnancy, hepatic disease, ulcer, arthritis
41
Q

Ezetimibe (Zetia)

A
  • Inhibits intestinal absorption of cholesterol, reabsorption of cholesterol excreted in bile, inhibits cholesterol transport protein NPC-1L1
  • Primary effect is to reduce LDL levels
  • Primarily used with Statins but study shows no more efficacy than solo statins
  • Orally, feces, 22% conjugated in liver glucuronidation
    • Fibrinates = increase Ezetimibe levels increase levels of cholelithiasis
    • Niacin incr. levels which incr. risk of myopathies
    • Warfarin = incr. prothrombin time
  • Diarrhea
42
Q

Drugs used for altered automaticity

A

-Na+ and Ca+ channel blockers (Reduce phase 4 depolarization rate and reduce excitability)

43
Q

Drugs used for EAD

A

-Reduce K+ channel blockers or and Na+ and Ca+ channel blockers (increase rate of repolarization or suppress depolarization)

44
Q

Drugs for DAD

A

-Na+ or Ca+ channel blockers (reduce Ca+ overload)

45
Q

Reentry Fast tissue

A

-Na+ channel blockers (Decrease excitability and prolong refractory period) K+ channel blocker (prolong APD and prolong refractory period)

46
Q

Reentry Slow tissue

A

-Ca+ Channel blockers (decrease excitability and prolong refractory period)

47
Q

Class IA antiarrhythmics

A

Na+ channel blockers with 1-10 second dissociation.

  • Moderate reduction in rate of depolarization and conduction velocity in normal cells
  • Prolong refractory period and APD (K+ effect)
  • Widen QRS and QT
  • Low [K+] leads to increased pro arrhythmic effects
48
Q

Quinidine

A
  • Class IA
  • Blocks Na+ and K+ channels
  • Alpha adrenergic blockade
  • Anticholinergic
  • Maintain Sinus rhythm in A fib and A flutter
  • Suppresses supraventricular and ventricular tachycardias
  • Prolongs QT –> incr. risk of torsades
  • Incr. levels of digoxin
49
Q

Procainamide

A
  • Class IA
  • N-Acetyl procainamide blocks K+ but not Na+ channels which prolongs QT leading to Torsades
  • Lupus like syndrome in slow acetylators
50
Q

Disopyramide

A
  • Class Ia
  • Stronger anti-cholinergic effects than quinidine
  • Neg. Inotropic effects (Bad in CHF)
51
Q

Class Ib Antiarrhythmics

A
  • Na+ channel blockers
  • Fast dissociation (less than 1 second)
  • Minimal phase 0 and conduction velocity reduction in normal cells. (Functions more on ischemic cells
52
Q

Lidocaine

A
  • Class Ib
  • Selective for ventricular over atrial cells
  • Acute IV therapy for ventricular arrhythmias after MI (Not effective against Atrial arrhythmias
  • Seizures with rapid IV administration
  • Depression of Cardiac function
  • Local anesthetic
53
Q

Class IC

A
  • Very long dissociation (greater than 10 seconds)
  • marked effect on rate of phase 0 depolarization and conduction in normal cells
  • small effect on APD and refractory period
  • Widens QRS and prolongs PR and QT intervals
54
Q

Flecainide

A
  • Class Ic
  • Blocks Na+ channels (selective for cells with a high rate but also blocks cells with a normal rate more than class Ia and Ib
  • Blocks K+ channels (prolongs refractory periods)
  • Suppresses Suprvent tachyarrhythmias
  • Life threatening vent arrhythmias
  • increases mortality in patients recovering from MI
  • Blurred vision
  • Proarrhythmic especially in the presence of severe heart disease
  • Blocks Ca + channels and suppresses LV function
55
Q

Propafenone

A
  • Class IC
  • Beta-adrenergic blockade
  • flecainide and propafenone are metabolized by CYP2D6 but only propafenone levels are increased in the blood in slow CYP2D6 metabolizers
56
Q

Class II

A
  • Beta Blockers
  • Metroprolol
  • Blocks Beta-1 adrenergic receptor regulated activity of Ca++ and K+ channels in myocardium
  • Blocks sympathetic influence on cardiac automaticity
  • Blocks sympathetic induced EAD and DAD
  • Increases refractory period at AV node (incr. PR interval)
  • Decreases mortality after MI (only other drug amiodarone)
  • SA and AV node block
  • Sudden withdrawal may worsen angina and arrhythmias
  • Decrease vent. function
57
Q

Class III

A 
-K+ Channel blockers (prolong APD)
MECHANISM:
-Blocks K+ leading to prolonged refractory period
-Blocks Na+ channels Decreased excitability 
-Blocks Ca++ channels 
-Prolongs PR, QRS and QT intervals
USES:
-Refractory vent tachycardia or fib
-Maintain sinus rhythm in a fib
SIDE EFFECTS:
Pulmonary fibrosis  with long-term use
Thyroid dysfunction (Hypo or Hyper)
Other:
Lipophilic long half life
Many drug interactions due to inhibition of CYP 3A4 2C9 and P-glycoprotein
58
Q

Sotalol

A
  • Class III K+ Channel blocker
  • Non-selectiv Beta blocker that also blocks K+ channels
  • Approved for patients with vent tachy, severe a flutter, or a fib
  • Torsades in overdose
59
Q

Dofeltilide

A

Class III K+ channel blocker

  • Potent and pure K+ channel blocker (no extra cardiac effects)
  • Restricted distribution to main sinus rhythm in patient w/ A fib
  • Torsades
60
Q

Class IV

A

-Ca++ Channel blockers
-Verapamil
MECHANISM:
-Blocks Ca++ Channels and decreases slow tissue automaticity and excitability
-Effects similar to Beta-blockers
-Depresses AV node conduction
USES:
-Control vent rate in atrial flutter fib
-Supravent tachy due to AV node reentry
EFFECTS:
-Depresses Cardiac force of contraction (NO CHF)
-Constipation most common side effect
OTHER:
-Interaction with other drugs that inhibit AV and SA node (beta blockers and digoxin)

61
Q

Adenosine

A 
MECHANISM:
-Stimulates A1 GCPR --> Dec cAMP
-Activate K channels in SA and AV leading to Hyperpolarization
-Reduces AV node Ca++ currents
-Increases PR interval
USES:
-Acute termination of AV node reentry
-WPW syndrome (don't use with A FIB)
Effects:
-Relatively safe due to short action, brief asystole
-Flushing and metallic taste
Other:
-IV 
-Inactivated by adenosine deaminase
-interaction with caffeine

Pharm (8 decks)

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