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Block 4 - Cardio > Pharmacology > Flashcards

Pharmacology Flashcards

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0
Q

What is the role of calcium channels during the cardiac action potential?

A

Closed at resting potential
Responsible for phase 2 plateau - open at more positive potential than sodium channels and inactivate slowly
Switch from inactive to closed during phase 3 repolarization

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1
Q

What is the role of sodium channels in the cardiac action potential?

A

Maintained in resting or closed state at negative resting potential
Responsible for phase 0 depolarization - local currents raise potential so they all open
Rapidly switch to inactive state and remain inactivated during phase 2 plateau
Switch back to resting or closed during phase 3 = recovery

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2
Q

What is the role of potassium channels in the cardiac action potential?

A

Delayed rectifier channels - closed at resting potential
Responsible for phase 3 repolarization - move down gradient
Don’t inactivate - just close when potential approaches resting

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3
Q

At what membrane potential do a critical number of sodium and calcium channels typically become available to fire another action potential?

A

-50 mV

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4
Q

When do delayed afterdepolarizations occur?

A

During phase 4 of the action potential

Most commonly associated with calcium overload - SR can spontaneously release immediately following repolarization

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5
Q

What four main mechanisms do antiarrhythmics use?

A

Block sodium channels
Decrease adrenergic stimulation to heart
Block potassium channels
Block calcium channels

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6
Q

What are the four Vaughan Williams classes of anti arrhythmic drugs?

A

I - sodium channel blockers
II - beta blockers (esp beta 1 selective)
III - potassium blockers - prolong AP
IV - calcium channel blockers/antagonists

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7
Q

What are the mechanisms of sodium channel blockers?

A

Bind mostly to sodium channels, a little to the others
Bind with more affinity to open or inactivated than closed state = use dependent action - bind more at faster rates
Must dissociate for channel to return to closed - delays refractory period

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8
Q

What are the effects of sodium channel blockers?

A 
Increase threshold for impulse conduction - reduce available channels so larger proportion must be activated, reduces propagation of abnormal impulses (DADs)
Increase effective refractory period (w/o affecting repolarization) - can block reentry 
Slow conduction (phase 0 less steep and wider QRS) - can increase risk of reentry
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9
Q

What are the mechanisms of potassium channel blockers?

A

Block delayed rectifier channels and inhibits potassium current
Can interact with other types of channels

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10
Q

What are the effects of potassium channel blockers?

A

Increase refractory period - decreases rate of phase 3 repolarization which prolongs AP duration
Increase in QT segment of EKG
Delay allows calcium channel recovery and can cause early afterdepolarizations
Major action is to slow or terminate reentry

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11
Q

What are the molecular mechanisms of calcium channel blockers?

A

Bind selectively to open or inactivated calcium channels
Raise threshold for excitement
Slow voltage dependent recovery of calcium channels

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12
Q

What are the effects of calcium channels blockers?

A

Major action in slow response tissues = nodes
Slow HR
slow AV node conduction - slows ventricular rate
Increase AV node refractoriness - can terminate AVNRT

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13
Q

How are the class I antiarrhythmics subdivided?

A

Ia - intermediate dissociation rates
Ib - fast dissociation rates
Ic - slow dissociation rates (most effective at preventing arrhythmias)

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14
Q

What is an example of each of class Ia, Ib, and Ic sodium channel blockers?

A

Ia - quinidine
Ib - lidocaine
Ic - flecainide

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15
Q

Quinidine - actions, effects, use, adverse effects

A

Sodium and potassium channel block
Raises threshold, widens QRS, prolongs QT and refractoriness
Maintain sinus rhythm in patient with a flutter or a fib and prevent recurrence of v tach or v fib - rarely used now
Can get marked QT prolongation and torsades de pointes

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16
Q

Lidocaine - action, effects, use

A

Sodium channel block
Not useful in atrial arrhythmias
Used occasionally IV for ventricular arrhythmias

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17
Q

Flecainide - actions, effects, use, adverse effects

A

Blocks sodium and potassium current, weak effect on calcium
Increases threshold and refractoriness, slowed conduction and repolarization, increases AP duration, increases PR interval, widens qrs, and increases QT interval, works better at faster rates
Paroxysmal supraventricular tachs, paroxysmal a fib/flutter in patients WITHOUT STRUCTURAL HEART DISEASE
Can cause new or worsened arrhythmias, negative inotropic effect can worsen CHF

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18
Q

Amiodarone - actions, effects, use

A

Class III potassium blocker
Blocks all channels and non competitive adrenergic blocking
Slows conduction, increases QRS, slows AV node conduction, increases PR interval, increases AP duration and QT interval, inhibits abnormal automaticity, can cause sinus bradycardia
Oral therapy for recurrent v tach or v fib resistant to others, maintains sinus rhythm with a fib, IV for acute termination of v tach or v fib

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19
Q

What are the adverse effects of IV amiodarone?

A

Hypotension
Bradycardia and AV block
May worsen or precipitate new arrhythmias
QT prolongation can cause torsades de pointe or VF

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20
Q

What are the effect of oral amiodarone?

A

Pulmonary toxicity/fibrosis - usually at higher doses
Worsened arrhythmias
Liver injury - higher enzymes, usually asymptomatic
Hypo or hyper thyroidism

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21
Q

What are the pharmacokinetic of amiodarone?

A

Metabolized in liver no active metabolite
Elim slowly by hepatic metabolism and biliary excretion
Lots of drug interactions because of p450 metabolism

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22
Q

Dofetilide - actions, effects, use, adverse effects

A

Pure potassium channel blockers, specific to cardiac muscle
Prolonged AP, increased QT interval, no effect on sinus node or conduction (pr or qrs)
Terminates reentrant tachycardias and inhibit re-induction, conversion of symptomatic a fib/flutter and maintenance of normal sinus rhythm
Always initiated in hospital or clinic, generally well tolerated but can cause new or worsening arrhythmia

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23
Q

What the effects of beta blockers?

A

Decrease calcium current in slow response tissue (nodes)
Decrease pacemaker current
Decrease after depolarization mediated arrhythmias
Increased AV nodal conduction time (PR interval), prolonged AV refractoriness
Terminate reentrant arrhythmias that involve AV node and control ventricular rate in a fib or flutter

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24
Q

What are the effects of calcium channel blockers?

A

Block in slow response tissues
HR slowed, but hypotension can cause reflex symp and tach
Can terminate reentrant circuits involving AV node
Reduce ventricular rate in a fib or flutter

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25
Q

Adenosine - actions, effects, use, adverse effects, pharmacokinetics

A

Agonist at adenosine receptor = GPCR that increaes k conductance, decreases Ca conductance, and antagonizes cAMP in cardiac cells
Shortens atrial APD, slows or blocks AV nodal conduction
Termination of supraventricular tachs
Well tolerated, short lived effects
IV only, has drug interactions

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26
Q

Digoxin - effects, use

A

Hyper polarizes atrium, shortens atrial AP, increases AV nodal refractoriness
Control ventricular rate in a fib and terminate reeentries involving AV node

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27
Q

Which drugs are good for terminating AV reeentries?

A

Adenosine - acute
Beta blockers - either
Calcium channel blockers - either
Class Ic antiarrhythmics - chronic

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28
Q

What drugs can terminate acute a fib?

A

Beta blockers
Calcium channel blockers
Digoxin
Amiodarone

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29
Q

What are the most powerful diuretics?

A

Loop diuretics

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30
Q

Hydrochlorthiazide and metolazone - mechanism and effects

A

Thiazides diuretics - inhibit NaCl symporter in distal convoluted tubule and increases their secretion
Modest efficacy
Increased secretion of K and H+
Secreted into proximal tubule by organic acid transporter, interact probenecid

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31
Q

Hydrochlorothiazide and metolazone - adverse effects

A

Due to abnormalities of fluid and electrolyte balance
Adverse generally only at higher doses
Decrease glucose tolerance and can unmask diabetes
Multiple drug interactions

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32
Q

Hydrochlorothiazide and metolazone - uses

A

Hypertension
Edema from CHF, liver disease, renal disease
Reduce Ca so useful in calcium disorders
* most are ineffective if GFR <30-40 ml/min

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33
Q

Furosemide and torsemide - mechanism and effects

A

Loop diuretics
Inhibit symporter in thick ascending limb and inhibit Ca and Mg reabsorption
Increase excretion of Na, Cl, Ca, Mg, K, and H
Powerful stimulators of renin release
Entry into lumen inhibited by inhibitors of organic acid transporter

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34
Q

Furosemide and torsemide - adverse effects

A

Interactions with probenecid and other diuretics
Due to abnormalities in fluid or electrolyte balance
Ototoxic

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35
Q

Furosemide and torsemide - uses

A

Acute pulm edema
Chronic CHF
Hypertension
Mobilize edema due to cardiac, liver, or kidney disease

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36
Q

Triamterene and amiloride - mechanism and effects

A

Act on principal cells in late distal and collecting duct
Inhibit sodium channels and decrease sodium transport - causes less K secretion
Minor increase in Na and Cl excretion
Increased reabsorption of Mg and Ca
Renal failure can enhance toxicity
Liver disease can decrease clearance of triamterene

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37
Q

Triamterene and amiloride - adverse effects

A

Hyperkalemia

Multiple interactions

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38
Q

Triamterene and amiloride - uses

A

Typically used in combo for hypertension

Aerosolized triamterene used in CF

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39
Q

Spironolactone - mechanism and effects

A

Aldosterone antagonist and potassium sparing
Bind mineralocorticoid receptor in distal tubule and collecting duct and prevent Aldo from binding
Higher aldosterone means greater effect
Similar effects to potassium sparing diuretics

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40
Q

Spironolactone - adverse effects

A

Hyperkalemia

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41
Q

Spironolactone - uses

A

Used in combo for edema and hypertension
Treats hyperaldosteronism
Diuretic of choice in patients with hepatic cirrhosis
Long term benefit in slowing progression of heart failure

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42
Q

What 3 factors control renin release?

A

Rate of sodium absorption in thick ascending limb
BP in Pre-glomerular cells
Sympathetic nervous system

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43
Q

How does angiotensin II act?

A

Mostly AT1 receptors - couple to Gq then phospholipase c beta to IP3 and DAG –> smooth muscle contraction

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44
Q

Captopril and enalapril - mechanisms and effects

A

ACE inhibitors
Lower BP by decreasing peripheral vascular resistance
Do not cause reflex symp activation - can be used in ischemic heart disease
Cleared by kidney - impaired renal function decreases clearance

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45
Q

ACE inhibitors - adverse effects

A

Generally well tolerated
Hypotension
Cough
Hyperkalemia in patients with abnormal renal function
Acute renal failure
Fetopathic potential in 2nd and 3rd trimesters

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46
Q

ACE inhibitors - uses

A

Hypertension
CHF with LV systolic dysfunction
First choice antihypertensive for diabetics

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47
Q

Losartan - mechanism and effects

A

Angiotensin II receptor antagonist

48
Q

Losartan - adverse effects

A

Don’t cause cough
Hypotension
Hyperkalemia

49
Q

Aliskiren - mechanism and effects

A

Renin inhibitor - competitive at active site
Similar effects to ACE inhibitors
Don’t cause elevation of AI or AII or bradykinin - might be advantage

50
Q

Aliskiren - adverse effects

A

Similar to ACE inhibitors
Lower incidence of cough
Irritates GI tract and causes diarrhea

51
Q

Aliskiren - uses

A

Mono therapy of hypertension and combo

Good add on for high renin hypertension and patients resistant to ACEIs or ARBs

52
Q

Calcium channel antagonists (for hypertension) - basics

A

Nifedipine - dihydropyridine
Verapamil and diltiazem - non-dihydropyridine class - reflex tach abolished by negative chronotropic effect
Selective for arterial smooth muscle dilation and little effect on venous
Cause mild reflex sympathetic response
All metabolized to inactive drugs in liver

53
Q

Calcium channel blockers - adverse effects

A

Effects due to vasodilation
Aggravation of ischemia with short acting
Bradycardia but usually only IV in patient with nodal disturbances
Constipation
Don’t use in patients with nodal abnormalities of CHF

54
Q

What kind of hypertension are calcium blockers particularly good for?

A

Low renin - don’t cause much fluid retention

55
Q

Beta blockers - effects

A

Initially decrease CO with increase in PVR and no change in BP
PVR will return to normal

56
Q

Why is co admin of a diuretic not generally needed with beta blockers?

A

They do not cause retention of salt and water

57
Q

What is the role of clonidine in hypertension?

A

Alpha 2 agonist that reduces sympathetic outflow

Only used as supplemental agent in patients who haven’t responded to combos of other drugs

58
Q

What is the role of prazosin in hypertension?

A

Alpha 1 antagonist
Decreased venous return and PVR decreases BP
Useful in hypertensive men with BPH

59
Q

Hydralazine - effects

A

Direct vasodilator
Acts on smooth muscle of arterioles
Oral, IV and IM all possible
Bioavailability depends on individual rates of acetylation

60
Q

Hydralazine - adverse effects

A

Effects from vasodilation
Alone could cause salt retention and development of CHF
Immunological reactions

61
Q

Hydralazine - uses

A

Chronic treatment of hypertension only when combos of other drugs aren’t working
Never use alone
Not used in patients with CHD or in elderly

62
Q

Minoxidil - mechanism and effects

A

Activates ATP sensitive k channel in vascular smooth muscle and causes hyperpolarization
Powerful vasodilator of arterioles - no effect on veins or capillaries
Causes strong reflex sympathetic activation - stimulates renin
Oral absorbed, hepatic elim

63
Q

Minoxidil - adverse effects

A

Fluid and salt retention
Cardiovascular effects - caution in patients with ischemic disease
Hypertrichosis - hair growth

64
Q

Minoxidil - use

A

Third line agent for hypertension

Never use alone - always give with diuretic and beta blocker

65
Q

Sodium nitroprusside - mechanism and effects

A

Decomposed to NO in smooth muscle
Dilates both arterioles and venules
Causes only modest increase in heart rate
Plasma renin activity increases
IV prep only
Reacts with sulfhydryls to form NO and cyanide - metabolized in liver and excreted in urine

66
Q

Sodium nitroprusside - adverse effects

A

Short term due to vasodilation and hypotension
Accumulation of cyanide at too fast infusion rates
Concomitant admin of sodium thiosulfate can reduce toxicity

67
Q

Sodium nitroprusside - use

A

Treatment of hypertensive emergencies
Acute aortic dissection - also needs beta blocker
Increase CO in acute heart failure
Temporarily decrease oxygen demand after MI
induce controlled hypotension to reduce bleeding during surgery

68
Q

How much overweight must you be for weight loss to have a significant effect on BP?

A

At least 20 lbs

69
Q

What are the exceptions to the rule of thiazides diuretics being the first consideration for medical management of hypertension?

A

Diabetes - give ace inhibitor first

CAD/angina/previous MI - first give beta blocker

70
Q

What is the recommended BP threshold for patients who already have hypertension?

A

130/80

71
Q

How is hypertension managed in the older patient (>65)?

A

Start treating at 150/90

Thiazides plus an ACEI works really well - start one at a time

72
Q

What is the most COMMON side effect of ACEIs?

A

Cough

73
Q

How is a hypertensive emergency vs. urgency treated?

A

When BP is at least 160/100 - if its progressing its am emergency, if its stable its urgency
Emergency - IV - most often nitroprusside
Urgency - oral Rx in ER

74
Q

What are the categories of meds given in chronic heart failure and what are the general risks?

A

Beta blockers
ACEIs
Aldo antagonists
Risks - hypotension, decompensation

75
Q

What are the categories of drugs given in acute (decompensated heart failure) and what are the general risks?

A 
Diuretics
Vasodilators
Inotropic drugs
IV if needed
Risks- hypotension, ischemia, arrhythmias
76
Q

What is the main effect of digoxin?

A

Direct positive inotropic effect
Binds to and inhibits Na-K pump - reduced Na gradient drives Na-Ca exchange
Increased intracellular Ca taken into SR and is available to contractile elements

77
Q

What are the indirect effects of cardiac glycosides like digoxin?

A

Decreased sympathetic tone - reflex withdrawal following increase in CO, additional withdrawal due to increased baroreceptor sensitivity - leads to vasodilation and electrophysiological effects
Increased vagal tone - CNS - leads to electrophysiological effects like bradycardia and AV block

78
Q

What are the electrophysiological effects of digoxin?

A

Decreases automaticity in nodes due to increase in vagal tone and decrease in symp activity
Toxic at higher effects

79
Q

What are the pharmacokinetics of digoxin?

A

Oral and IV
Bioavailability is high
Excreted unchanged by kidney
Large Vd - loads in skeletal muscle not fat –> dose based on lean body mass

80
Q

What are the adverse effects and toxicity of digoxin?

A

Low therapeutic index
Arrhythmias, nausea, disturbances of cognitive function
Ectopic beats, first degree AV block, slow ventricular response to a fib, or accelerated AV pacemaker - from DADs
Anti digoxin antibody treatment is effective antidote

81
Q

What are the important drug interactions with digoxin?

A

Quinidine - elevates levels by decreasing clearance and Vd
Verapamil, diltiazem, amiodarone, flecainide, and spironolactone all increase levels
Hypokalemia can potentiate induced arrhythmias

82
Q

What are the therapeutic uses of digoxin?

A

CHF - reduces symptoms, may not increase survival

Termination of AVNRT or controlling ventricular rate in a fib

83
Q

What are the main actions of ACEIs in heart failure?

A

Vasodilators that can restore CO
increased bradykinin-sustained vasodilation
Reduction in intrarenal vasoconstrictor effects of AII
Decreased generation of AII in heart
Decreased AII mediated release of Aldo
Decrease sympathetic activation

84
Q

What do nitrates do in CHF?

A

Reduce ventricular filling pressures in acute and chronic

Primarily preload reduction

85
Q

What is BiDil?

A

Combo of hydralazine (dilates arterioles) and isosorbide dinitrate (dilates venous)
Particularly effective in African American population

86
Q

When are inotropic agents used during heart failure?

A

Only for short term positive inotropic intervention to maintain adequate blood flow

87
Q

What are the two inotropic agents used in heart failure?

A

Dobutamine - beta 1 agonist with activity at beta 2, less tach and arrhythmias than other agonists, IV for short term treatment of acute HF, vasodilator that rescues systemic vascular resistance and afterload
Dopamine - IV infusion, d1 receptors, beta 1 agonist, alpha 1 agonist

88
Q

Milrinone - mechanism of action, effects, use

A

Phosphodiesterase inhibitor - inhibits type III cAMP that normally degrades cAMP - increases cAMP which increases Ca and contractility
increases force of contractility and velocity of relaxation, vasodilates to reduce afterload
Parenteral for short term acute, side effects exclude long term use

89
Q

In addition to CHD, what conditions can hyperlipoproteinemia cause?

A

Life threatening pancreatitis

Xanthomas

90
Q

How are triglycerides transported in the serum?

A

Chylomicrons and VLDL

Very responsive to ingestion of food and normally low in fasting state

91
Q

What are the five different types of lipoproteins in order from largest to smallest?

A 
Chylomicrons
VLDL
IDL
LDL
HDL
92
Q

How are triglycerides and cholesterol absorbed from the intestine (exogenous pathway)?

A

Assembled into chylomicrons - pass through capillaries of adipose tissue and muscle and hydrolyzed by LPL to be absorbed
Chylomicron remnants absorbed by liver through receptor mediated endocytosis

93
Q

What is the endogenous pathway for lipoprotein delivery?

A

Delivers cholesterol to extra hepatic tissues
Delivers endogenously synthesized triglyceride to storage tissues
Triglycerides and cholesterol ester released from liver as VLDL - in capillaries LPL action converts it to IDL - removed by liver or converted to LDL which is absorbed by tissues that have receptor
HDL is cholesterol that is released as cells die or membranes turn over - transferred to VLDL or LDL by CETP

94
Q

What mutation is responsible for familial hypercholesterolemia?

A

Genetic defects in LDL receptor

95
Q

What do high levels of intracellular cholesterol do to its metabolic pathway?

A

Inhibit synthesis of HMG-CoA reductase = rate limiting enzyme in cholesterol biosynthesis
Decrease production of LDL receptors
Increase rate of cholesterol esterification

96
Q

What are the guidelines for treatment of patients with high cholesterol and no other risk factors?

A

If borderline - advise diet

If high - treat with goal of borderline to normal levels (<160 LDL)

97
Q

What are the guidelines of treatment of a patient with high cholesterol and two or more other risk factors?

A

If borderline - advise diet and exercise, potential drug treatment with goal of <100

98
Q

What are the guidelines for treatment of a patient with high cholesterol when CHD, diabetes, or atherosclerotic disease is already present?

A

LDL of 100-130 consider drug therapy

LDL >130 drug therapy with goal of <70

99
Q

What are the levels of HDL and TGs for which treatment should start being considered in high risk patients?

A

HDL 200

100
Q

Statins - mechanism of action

A

Inhibit HMG-CoA reductase:
Decreased synthesis of cholesterol
Increased clearance of LDL and LDL precursors through increase in LDL receptors
Some decreased VLDL production

101
Q

Statins - uses and effects

A

Choice for hypercholesterolemia
Lowers total and LDL cholesterol
Lowering of moderately high TGs
Modest increase in HDL

102
Q

What are two available statins and what p450 metabolizes it?

A

Atorvastatin
Lovastatin
Both by CYP 3A4

103
Q

What are the major but infrequent side effects of statins?

A

Increased liver enzymes due to decreased liver function
Proximal muscle myopathy - high levels of creatinine kinase, can lead to acute renal failure if not recognized
Dose dependent and reversible

104
Q

What are the drug interactions of statins?

A

Other drugs metabolized by the same enzyme - erythromycin, warfarin, etc. - increase levels and risk of myopathy
Grapefruit increases concentrations (not observed with prevastatin)

105
Q

Cholesterol uptake inhibitors - mechanism

A

Inhibits absorption from small intestine reducing intake of exogenous cholesterol and reabsorption of secreted cholesterol

106
Q

Cholesterol uptake inhibitors (ezetimibe) - uses and effects

A

Treatment of hypercholesterolemia and sitosterolemia (accumulation of plant sterols in blood)
Lowers total and LDL cholesterol
Modest decrease in TGs
Some increase in HDL
Efficacy lowered by upregulation of HMG-CoA reductase
Reduce uptake of plant sterols

107
Q

Ezetimibe - adverse effects

A

Similar to statins
Generally well tolerated
Contraindicated for hepatic insufficiency

108
Q

Cholestyramine - mechanism

A

Bile acid sequestration - binds in gut to prevent reabsorption, bile acid synthesis from cholesterol is increased

109
Q

Cholestyramine - uses and effects

A

Treatment of hypercholesterolemia
Lowers total and LDL
Efficacy limited by upregulation of HMG-CoA reductase (can also cause increased TGs - don’t use in combined hyperlipidemia)
No systemic absorption or metabolism - fairly safe

110
Q

Cholestyramine - problems

A

Poor palatability and constipation - newer formulations have increased compliance
Ion exchange resins can bind it - give other drugs 1 hr before or 3-4 hrs after and consider vitamin supplements for long term

111
Q

Nicotinic acid (niacin) - effects

A

Mechanism unclear
Inhibits lipolysis in adipose tissue
Decreased hepatic synthesis of TGs
Decreased secretion of apoB containing lipoproteins
Reduced concentration of circulating lipoprotein
Altered metabolism of HDL
Effective doses are vastly in excess of nutritional role of niacin as a vitamin

112
Q

Niacin - uses

A 
Can lower total cholesterol and TGs
Potential decreases in VLDL
Potential decreases of LDL
Increased HDL 
Drug of choice in younger patients, may be used to control hyperTGs during pregnancy
113
Q

Niacin - problems

A

Severe cutaneous flushing
Compliance better with newer once daily admins
Nausea, abdominal discomfort, pruritis, and dryness of skin

114
Q

What are the contraindications for use of niacin and the problems each would cause?

A

Type II diabetes - hyperglycemia
Gout - hyperuricemia
PUD - peptic ulcer disease
Abnormalities of liver function - liver dysfunction

115
Q

Fibrates (gemfibrozil) - mechanism of action

A

Activation of PPARs which leads to:
Decreased apoprotein CIII synthesis
Decreased hepatic triglyceride synthesis
Increased activity of LPL - increases circulating triglycerides

116
Q

Gemfibrozil - effects

A 
Decreased VLDL 
Conversion of IDL
decreased chylomicrons
Modest increase in HDL 
LDL may decrease slightly or increase
117
Q

Gemfibrozil - use

A

Primarily for treating severe triglyceridemia
Especially associated with highly elevated fasting VLDL and IDL, to prevent pancreatitis, and where nicotinic acid is not effective and/or contraindicated
Useful in diabetics

118
Q

Gemfibrozil - problems

A 
Generally well tolerated
Some risk of myopathy 
Contraindications are hepatic dysfunction or gallstones due to potential to increase biliary lithogenicity 
Potential for tumor promotion 
Not used in children or pregnant women

Block 4 - Cardio (15 decks)

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