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Block 4 - Cardio > Pharmacology > Flashcards

Pharmacology Flashcards

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
What are the effects of calcium channel blockers?
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
25
Adenosine - actions, effects, use, adverse effects, pharmacokinetics
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
26
Digoxin - effects, use
Hyper polarizes atrium, shortens atrial AP, increases AV nodal refractoriness Control ventricular rate in a fib and terminate reeentries involving AV node
27
Which drugs are good for terminating AV reeentries?
Adenosine - acute Beta blockers - either Calcium channel blockers - either Class Ic antiarrhythmics - chronic
28
What drugs can terminate acute a fib?
Beta blockers Calcium channel blockers Digoxin Amiodarone
29
What are the most powerful diuretics?
Loop diuretics
30
Hydrochlorthiazide and metolazone - mechanism and effects
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
31
Hydrochlorothiazide and metolazone - adverse effects
Due to abnormalities of fluid and electrolyte balance Adverse generally only at higher doses Decrease glucose tolerance and can unmask diabetes Multiple drug interactions
32
Hydrochlorothiazide and metolazone - uses
Hypertension Edema from CHF, liver disease, renal disease Reduce Ca so useful in calcium disorders * most are ineffective if GFR <30-40 ml/min
33
Furosemide and torsemide - mechanism and effects
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
34
Furosemide and torsemide - adverse effects
Interactions with probenecid and other diuretics Due to abnormalities in fluid or electrolyte balance Ototoxic
35
Furosemide and torsemide - uses
Acute pulm edema Chronic CHF Hypertension Mobilize edema due to cardiac, liver, or kidney disease
36
Triamterene and amiloride - mechanism and effects
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
37
Triamterene and amiloride - adverse effects
Hyperkalemia | Multiple interactions
38
Triamterene and amiloride - uses
Typically used in combo for hypertension | Aerosolized triamterene used in CF
39
Spironolactone - mechanism and effects
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
40
Spironolactone - adverse effects
Hyperkalemia
41
Spironolactone - uses
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
42
What 3 factors control renin release?
Rate of sodium absorption in thick ascending limb BP in Pre-glomerular cells Sympathetic nervous system
43
How does angiotensin II act?
Mostly AT1 receptors - couple to Gq then phospholipase c beta to IP3 and DAG --> smooth muscle contraction
44
Captopril and enalapril - mechanisms and effects
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
45
ACE inhibitors - adverse effects
Generally well tolerated Hypotension Cough Hyperkalemia in patients with abnormal renal function Acute renal failure Fetopathic potential in 2nd and 3rd trimesters
46
ACE inhibitors - uses
Hypertension CHF with LV systolic dysfunction First choice antihypertensive for diabetics
47
Losartan - mechanism and effects
Angiotensin II receptor antagonist
48
Losartan - adverse effects
Don't cause cough Hypotension Hyperkalemia
49
Aliskiren - mechanism and effects
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
Aliskiren - adverse effects
Similar to ACE inhibitors Lower incidence of cough Irritates GI tract and causes diarrhea
51
Aliskiren - uses
Mono therapy of hypertension and combo | Good add on for high renin hypertension and patients resistant to ACEIs or ARBs
52
Calcium channel antagonists (for hypertension) - basics
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
Calcium channel blockers - adverse effects
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
What kind of hypertension are calcium blockers particularly good for?
Low renin - don't cause much fluid retention
55
Beta blockers - effects
Initially decrease CO with increase in PVR and no change in BP PVR will return to normal
56
Why is co admin of a diuretic not generally needed with beta blockers?
They do not cause retention of salt and water
57
What is the role of clonidine in hypertension?
Alpha 2 agonist that reduces sympathetic outflow | Only used as supplemental agent in patients who haven't responded to combos of other drugs
58
What is the role of prazosin in hypertension?
Alpha 1 antagonist Decreased venous return and PVR decreases BP Useful in hypertensive men with BPH
59
Hydralazine - effects
Direct vasodilator Acts on smooth muscle of arterioles Oral, IV and IM all possible Bioavailability depends on individual rates of acetylation
60
Hydralazine - adverse effects
Effects from vasodilation Alone could cause salt retention and development of CHF Immunological reactions
61
Hydralazine - uses
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
Minoxidil - mechanism and effects
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
Minoxidil - adverse effects
Fluid and salt retention Cardiovascular effects - caution in patients with ischemic disease Hypertrichosis - hair growth
64
Minoxidil - use
Third line agent for hypertension | Never use alone - always give with diuretic and beta blocker
65
Sodium nitroprusside - mechanism and effects
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
Sodium nitroprusside - adverse effects
Short term due to vasodilation and hypotension Accumulation of cyanide at too fast infusion rates Concomitant admin of sodium thiosulfate can reduce toxicity
67
Sodium nitroprusside - use
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
How much overweight must you be for weight loss to have a significant effect on BP?
At least 20 lbs
69
What are the exceptions to the rule of thiazides diuretics being the first consideration for medical management of hypertension?
Diabetes - give ace inhibitor first | CAD/angina/previous MI - first give beta blocker
70
What is the recommended BP threshold for patients who already have hypertension?
130/80
71
How is hypertension managed in the older patient (>65)?
Start treating at 150/90 | Thiazides plus an ACEI works really well - start one at a time
72
What is the most COMMON side effect of ACEIs?
Cough
73
How is a hypertensive emergency vs. urgency treated?
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
What are the categories of meds given in chronic heart failure and what are the general risks?
Beta blockers ACEIs Aldo antagonists Risks - hypotension, decompensation
75
What are the categories of drugs given in acute (decompensated heart failure) and what are the general risks?
``` Diuretics Vasodilators Inotropic drugs IV if needed Risks- hypotension, ischemia, arrhythmias ```
76
What is the main effect of digoxin?
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
What are the indirect effects of cardiac glycosides like digoxin?
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
What are the electrophysiological effects of digoxin?
Decreases automaticity in nodes due to increase in vagal tone and decrease in symp activity Toxic at higher effects
79
What are the pharmacokinetics of digoxin?
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
What are the adverse effects and toxicity of digoxin?
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
What are the important drug interactions with digoxin?
Quinidine - elevates levels by decreasing clearance and Vd Verapamil, diltiazem, amiodarone, flecainide, and spironolactone all increase levels Hypokalemia can potentiate induced arrhythmias
82
What are the therapeutic uses of digoxin?
CHF - reduces symptoms, may not increase survival | Termination of AVNRT or controlling ventricular rate in a fib
83
What are the main actions of ACEIs in heart failure?
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
What do nitrates do in CHF?
Reduce ventricular filling pressures in acute and chronic | Primarily preload reduction
85
What is BiDil?
Combo of hydralazine (dilates arterioles) and isosorbide dinitrate (dilates venous) Particularly effective in African American population
86
When are inotropic agents used during heart failure?
Only for short term positive inotropic intervention to maintain adequate blood flow
87
What are the two inotropic agents used in heart failure?
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
Milrinone - mechanism of action, effects, use
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
In addition to CHD, what conditions can hyperlipoproteinemia cause?
Life threatening pancreatitis | Xanthomas
90
How are triglycerides transported in the serum?
Chylomicrons and VLDL | Very responsive to ingestion of food and normally low in fasting state
91
What are the five different types of lipoproteins in order from largest to smallest?
``` Chylomicrons VLDL IDL LDL HDL ```
92
How are triglycerides and cholesterol absorbed from the intestine (exogenous pathway)?
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
What is the endogenous pathway for lipoprotein delivery?
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
What mutation is responsible for familial hypercholesterolemia?
Genetic defects in LDL receptor
95
What do high levels of intracellular cholesterol do to its metabolic pathway?
Inhibit synthesis of HMG-CoA reductase = rate limiting enzyme in cholesterol biosynthesis Decrease production of LDL receptors Increase rate of cholesterol esterification
96
What are the guidelines for treatment of patients with high cholesterol and no other risk factors?
If borderline - advise diet | If high - treat with goal of borderline to normal levels (<160 LDL)
97
What are the guidelines of treatment of a patient with high cholesterol and two or more other risk factors?
If borderline - advise diet and exercise, potential drug treatment with goal of <100
98
What are the guidelines for treatment of a patient with high cholesterol when CHD, diabetes, or atherosclerotic disease is already present?
LDL of 100-130 consider drug therapy | LDL >130 drug therapy with goal of <70
99
What are the levels of HDL and TGs for which treatment should start being considered in high risk patients?
HDL 200
100
Statins - mechanism of action
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
Statins - uses and effects
Choice for hypercholesterolemia Lowers total and LDL cholesterol Lowering of moderately high TGs Modest increase in HDL
102
What are two available statins and what p450 metabolizes it?
Atorvastatin Lovastatin Both by CYP 3A4
103
What are the major but infrequent side effects of statins?
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
What are the drug interactions of statins?
Other drugs metabolized by the same enzyme - erythromycin, warfarin, etc. - increase levels and risk of myopathy Grapefruit increases concentrations (not observed with prevastatin)
105
Cholesterol uptake inhibitors - mechanism
Inhibits absorption from small intestine reducing intake of exogenous cholesterol and reabsorption of secreted cholesterol
106
Cholesterol uptake inhibitors (ezetimibe) - uses and effects
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
Ezetimibe - adverse effects
Similar to statins Generally well tolerated Contraindicated for hepatic insufficiency
108
Cholestyramine - mechanism
Bile acid sequestration - binds in gut to prevent reabsorption, bile acid synthesis from cholesterol is increased
109
Cholestyramine - uses and effects
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
Cholestyramine - problems
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
Nicotinic acid (niacin) - effects
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
Niacin - uses
``` 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
Niacin - problems
Severe cutaneous flushing Compliance better with newer once daily admins Nausea, abdominal discomfort, pruritis, and dryness of skin
114
What are the contraindications for use of niacin and the problems each would cause?
Type II diabetes - hyperglycemia Gout - hyperuricemia PUD - peptic ulcer disease Abnormalities of liver function - liver dysfunction
115
Fibrates (gemfibrozil) - mechanism of action
Activation of PPARs which leads to: Decreased apoprotein CIII synthesis Decreased hepatic triglyceride synthesis Increased activity of LPL - increases circulating triglycerides
116
Gemfibrozil - effects
``` Decreased VLDL Conversion of IDL decreased chylomicrons Modest increase in HDL LDL may decrease slightly or increase ```
117
Gemfibrozil - use
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
Gemfibrozil - problems
``` 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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