4-21 Flashcards
Nitric oxide is made from which amino acid
Arginine + O2
How does NO cause smooth muscle relaxation
Activates guanylyl cyclase, increase formation of cGMP, activates protein kinase G, reduces cytosolic calcium levels = relaxation
Fatigue and exertional dyspnea 3 weeks after tooth extraction
Bacterial endocarditis from Strep viridans
Culture-negative endocarditis organisms
HACEK (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
Persistent fever w/ tricuspid vegetations/regurg
Bacterial endocarditis from S. aureus in IV drug users
Strep bovis
Bacterial endocarditis in previously normal heart valves, associated with underlying colon cancer
Decrease in systolic blood pressure >10mmHg with inspiration
Pulsus paradoxus (seen in cardiac tamponade, constrictive pericarditis, severe obstructive lung disease, restrictive cardiomyopathy)
Loss of cardiomyoctye contractility occurs within ___ after onset of total ischemia
60 seconds (>30 minutes of ischemia = irreversible damage)
Digoxin activity on AV node
Decreases nodal conduction by increasing parasympathetic tone via action on vagus nerve (used to treat atrial fibrillation)
Major criteria for acute rheumatic fever
JONES - joints (migratory polyarthritis), heart (pancarditis), subcutaneous nodules, erythema marginatum, sydenham chorea
Most common cause of death during acute phase of acute rheumatic fever
Myocarditis (Aschoff bodies with Anitschkow “caterpillar” cells and fibrinoid material)
Elevated ASO or antiDNase B titer 2-3 weeks post pharyngitis in children
Acute rheumatic fever
Mechanism that group A beta-hemolytic strep causes disease
M protein, exhibits molecular mimicry by resembling our own proteins
Complications of Aortic Stenosis
Concentric LV hypertrophy, angina/syncope w/ exercise (limited blood flow across valve), Microangiopathic hemolytic anemia (RBCs damaged while crossing valve)
Systolic ejection click w/ crescendo-decrescendo murmur
Aortic stenosis
If have fusion of aortic valve commisssures and coexisting mitral stenosis, will this be rheumatic disease or just “wear and tear”
Rheumatic disease (since involves mainly mitral valve)
“wear and tear” valvular disease
Aortic stenosis (late adulthood >60 years old)
Early blowing diastolic murmur
Aortic regurgitation
Most common cause of aortic regurgitation
Isolated aortic root dilation (can also be caused by syphilitic anuerysm, aortic dissection or valvular dmg/infectious endocarditis)
Hyperdynamic circulation describes the pathophysiology of which heart disorder
Aortic regurgitation (systolic pressure increases, diastolic pressure decreases, so overall pulse pressure increases)
Ehlers-Danlos and Marfan syndrome may be associated with which heart valve abnormality
Mitral valve prolapse (since myxoid degeneration, “gel-like” of mitral valve making it floppy)
Mid-systolic click, followed by regurg murmur
Mitral valve prolapse
Opening snap followed by diastolic rumble
Mitral stenosis
Phases of cardiac cycle
Systolic (ejection), Diastolic (filling)
Most common valve disorders with acute vs. chronic rheumatic disease
Acute=Mitral valve prolapse, Chronic = mitral stenosis
Bounding water hammer pulses, head bobbing
Aortic regurgitation
Holosystolic blowing murmur
Mitral regurgitation
Clinical features of mitral stenosis
Pulmonary congestion (edema, alveolar hemorrhage), pulmonary htn/R. CHF, atrial fibrillation/risk for mural thrombi = volume overload of Left atrium
What does expiration do to the heart?
increases return to the left atrium
What does squatting do to the heart?
increases systemic resistance so decreases ventricular emptying
Most common overall cause of endocarditis
Bacterial infection with strep viridans (low-virulence organism, so requires previously damaged valves)
Endocarditis does/does not destroy the valve?
Does NOT! Only creates small vegetations that can trap bacteria floating in blood stream
high-virulence organism infecting normal tricuspid valve
Staph. Aureus (causes large vegetations, destroys valve) - common in IV drug users
Staph epidermidis
Associated with endocarditis of prosthetic valves
TEE is a good diagnostic tool in_
Bacterial endocarditis (can detect lesions on valves)
Clinical features of bacterial endocarditis
“Bacteria FROM JANE” - Fever, Roth spots, Osler’s nodes, Murmur, Janeway lesions (erythematous on palms/soles), Anemia of chronic disease, Nail-bed splinter hemorrhages, Emboli
Pt with lupus that has a heart murmur, most likely caused by what?
Libman-Sacks endocarditis (non-bacterial), causes sterile vegetations on both sides of mitral valve, resulting in mitral regurg
Pt with sterile vegetations along lines of mitral valve closure
Nonbacterial thrombotic endocarditis, associated with a hypercoagulable state OR underlying adenocarcinoma
Pt has mitral regurg heard on auscultation w/o history of bacterial infection, what other clinical problems could they potentially encounter?
Underlying adenocarcinoma (this is Non-bacterial thrombotic endocarditis), hypercoagulation state
Most common causes of dilated cardiomyopathy
Genetic (autosomal dominant), Myocarditis from Coxsackie A/B infection, alcohol abuse, drugs/doxorubicin/cocaine, pregnancy
Pt has arrhythmia, mitral & tricuspid regurg, with decreased systolic function
Dilated cardiomyopathy (all 4 chambers affected)
Most common cause of dilated cardiomyopathy
Idiopathic, then myocarditis from coxsackie infection
Pt experiences syncope with exercise, decreased cardiac output from diastolic dysfunction; what will you see on biopsy of heart itssue? Will his son be affected with this?
Hypertrophic cardiomyopathy (thickened left ventricle) decreases compliance so can’t fill properly; will see myofiber disarray; Yes his son will get it since it is autosomal dominant mutation in sarcomere proteins
Child with low-voltage EKG and diminished QRS amplitude
Restrictive cardiomyopathy, caused by ENDOCARDIAL FIBROELASTOSIS
Loeffler syndrome
Endomyocardial fibrosis with eosinophilic infiltrate that causes reduced compliance of ventricle/restricts filling during diastole (Restrictive cardiomyopathy)
Causes of restrictive cardiomyopathy
Amyloidosis, sarcoidosis, hemochromatosis, endocardial ribroelastosis (kids), Loeffler syndrome (eosinophils)
Child with tuberous sclerosis can develop which cardiac tumor
Rhabdomyoma (benign hamartoma of cardiac muscle) in ventricle
Most common primary cardiac tumor in adults
Myxoma (gelatinous appearance)
Pt diagnosed with a myxoma, where is this commonly located and what adverse events may ensue secondary to this?
Pedunculated mass in left atrium can cause syncope due to mitral valve obstruction
Congenital failure of neural crest migration can result in which cardiac abnormalities
Tetralogy of Fallot (skewed aorticopulmonary septum), Transposition of great vessels (failure to spiral), persitent truncus arteriosus (partial AP septum development)
Left and right horns of sinus venosus develop into which structures in the adult heart
Left horn = Coronary sinus, right horn = smooth part of Right atrium
The superior vena cava develops from which embryonic structures?
Right common cardinal vein and right anterior cardinal vein
Eisenmenger’s syndrome
Late reverse of an initial L to R shunt, becoming a R to L shunt, due to onset of pulmonary hypertension (RV builds up more pressure than left side of heart, so blood wants to flow into LV towards lower pressure)
Membranous septal defect causes _
Left to right shunt
Pathogenesis of patent foramen ovale
Failure of septum primum and secundum to fuse after birth
List the locations of fetal erythropoiesis during development
“Young Livers Synthesize Blood” - yolk sac (3-10wks), liver (6wk-birth), spleen (15-30 wks), bone marrow (22wks-adult)
alpha2beta2 hemoglobin seen in fetal or adult blood?
Adult (fetal is alpha2gamma2)
Median umbilical ligament is formed from which embryonic structure
allantois
medial umbilical ligaments formed from which embryonic structure
Umbilical arteries
ligamentum teres from which embryonic structure
umbilical vein
Asymptomatic prolonged PR interval
First degree AV block, PR>200msec
Progressive lengthening of PR interval until a beat is dropped
Mobitz type I Wenckebach, 2nd degree AV block
Completely erratic rhythm with no identifiable waves
Ventricular fibrillation (fatal)
“sawtooth appearance” of waves
Atrial flutter
Chaotic and erratic EKG with no discrete P waves in btwn irregularly spaced QRS complexes
Atrial fibrillation
Atria and ventricles beat independently of each other
Complete 3rd degree AV block
Which disease can result in a 3rd degree AV block
Lyme disease
Dropped QRS complex not preceded by a change in length of PR interval
Mobitz type II, 2nd degree AV block -> progress to 3rd degree
Congenital cardiac abnormality with a wide, fixed split S2
ASD, due to high blood volume passing into RA and RV
Most common cause of early cyanosis
Tetralogy of Fallot
Most common congenital cardiac anomaly
VSD
Kid that learns to squat in order to relieve cyanotic sx
Increases peripheral vascular resistance (afterload) and decreases blood flowing across shunt from RtoL
Hypertension in upper extremities with hypotension in lower extremities seen in adult pt, what is the most common assoicated valvular condition
Bicuspid aortic valve (pt has adult/postductal type coarctation of aorta)
Child with hypotension of lower extremities
Infantile type coarctation of aorta, associated with Turner syndrome
If congenital transposition of great vessels is seen, what is the most common cause (clinical)
Diabetic mother
22q11 syndromes cause which congenital cardiac abnormalities
Truncus arteriosus, tetralogy of Fallot
Pulsus paradoxus w/ distant heart sounds and increased JVD w/ hypotension
Cardiac tamponade
What is pulsus paradoxus
decrease in amplitude of systolic BP by >10mmHg during inspiration
Limiting factor to facilitated diffusion
Carrier proteins present and saturation
Mandibular hypoplasia, facial abrnormalities due to failure of neural crest migration of 1st branchial arch
Treacher-Collins syndrome
What does the 3rd aortic arch develop into in the adult human?
Common carotid artery and proximal part of the internal carotid arteries
What does the 4th aortic arch form in an adult
On the right forms proximal part of R. subclavian artery/on left forms the aortic arch
What does the 6th aortic arch develop into in an adult
On right proximal part of pulmonary arteries, on left the ductus arteriosus
Good way to remember aortic arch derivatives
1st is maximal (maxillary artery), second is stapedial, 3rd/C is 3rd letter of alphabet (carotid), 4th for 4 limbs/systemic (subclavian and aortic arch), 6th (none)
Baby found to have 22q11 deletion, what cardiac defects will it most likely have
This is DiGeorge syndrome, associated with Tetralogy of Fallot and an interrupted aortic arch (also see hypocalcemic tetany and T-cell deficiency)
Pt found to have his heart on the Right side of his body with recurrent sinusitis, what disorder does he most likely have?
Kartagener syndrome (situs inversus, immotile cilia w/ autosomal recessive pattern of inheritance)
What are the boundaries of the femoral triangle
Inguinal ligament superiorly, sartorius muscle laterally, adductor longus muscle medially
Longest vein in the body, can be used for coronary bypass grafting
Great saphenous veina (courses along medial aspect of lower leg and thigh)
If pt has a baker’s cyst, what nerves and vessels can be compromised?
Popliteal artery and vein, Tibial nerve
Child with throat pain and difficulty breathing, no prior vaccination history, what kind of Ab’s would increase his/her chance of survival
Pt has C. diphtheriae (since no DPT vaccine), exotoxin deactivates EF-2 elongation factor, inhibiting protein synthesis -> cardiac and neural toxicity (heart failure, paralysis, coma)
Prazosin, terazosin, doxazosin, tamsulosin activity on heart
Alpha-1 selective blockers, can be used in pts with HTN and diabetes because blocks smooth m. vasoconstriction
2 most common important S/E of digoxin toxicity
AV block and Vtach (also hyperkalemia)
Drugs that cause rash on face and trunk, multiple joint pain, and very high ANA titers
(Drug-induced SLE) Hydralazine (direct vasodilator), Procainamide (class IA antiarrhythmic/Na+ channel blocker), Isoniazid = HIP drugs
MOA of a drug that can be used in severe HTN or CHF, can cause S/E of excess fluid retention, compensatory tachycardia, and lupus-like syndrome
(Hydralazine) Is a selective direct vasodilator that increases cGMP to cause smooth muscle relaxation
Drug that can cause increase in cardiac contractility and decreased vascular resistance
Isoproterenol (Beta-agonist/sympathomimetic) - acts on Beta 1 receptors in heart to increase contractility, acts on Beta-2 in smooth muscle to vasodilate/decrease vascular resistance
If a pt has CHF and a previous MI w/ evidence of cardiomegaly, which drug would be best to control long-term HTN
ACE-I’s because inhibit the chronic effects of AngII-mediated ventricular hypertrophy and remodeling
Drugs used to provide symptomatic relief of pulmonary edema and acute CHF tx
Diuretics
Dobutamine MOA and uses
Sympathomimetic, mainly at Beta-1 receptors; causes increased inotropic effect (increase contractility/CO), positive chronotropic effect (increase HR/myocardial O2 consumption) -> used for acute heart failure associated with cardiogenic shock
Nitroglycerin vs. Dobutamine on myocardial oxygen consumption
Nitroglycerine DECREASES this, vs. Dobutamine INCREASES this (since causes increased myocontractility)
Reflex effects seen with nitroglycerin administration
Causes venous pooling, baroreceptors will sense this as low BP and reflex tachycardia will occur
Primary indication for digoxin administration
Chronic heart failure with LV systolic dysfunction and atrial fibrillation (since slows conduction through AV node)
Nitroprusside MOA
Arterial and venous vasodilation to decrease afterload AND preload
Nesiritide MOA
Synthetic brain natriuretic peptide, can be used to decrease afterload by dilating arteries and veins, improving hemodynamics (stimulating diuresis)
If a pt is experiencing CHF but has bilateral renal artery stenosis, which class of drugs would you NOT give
ACE-I’s
What are the different classes of drugs that can be used to treat HTN
Diuretics, Beta-blockers, ACE-I’s, Angiotensin receptor blockers, direct renin inhibitors, CCBs, alpha-blockers (alpha1), other (clonidine, minoxidil/hydralazine, methyldopa, sodium nitroprusside)
Which diuretic has an additional benefit of diminishing cardiac remodeling that occurs in heart failure
Spironolactone (K+-sparing diuretic & Aldosterone receptor antagonist)
How do beta-blockers help in the treatment of HTN
Decrease CO (block Beta-1 receptors in heart), decrease peripheral resistance (decrease beta-1 renin release & decrease AngII vasoconstriction)
Withdrawal syndrome may occur with which drugs in treatment of HTN
Beta-blockers, Alpha-2 agonist
1st dose phenomenon is seen in which drugs
Apha-1 selective blockers (Prazosin, terazosin, doxazosin)
Good drugs to use in a pt with concomitant HTN and diabetes
ACE-I’s or ARB’s
For CCBs, which drugs have more vascular affects vs. cardiac effects
-dipines’ (Amlodipin, nifedipine) vs. verapamil and diltiazem that have more cardiac effects (decrease HR, contractility)
Is Losartan/valsartan beneficial in an african-american pt
No, they are less responsive to ARB’s/ACE-I’s and more responsive to CCBs and diuretics
“-dipines”
CCBs
Which HTN drugs are contraindicated in pregnancy
Anything that affects Renal function (ACE-Is/ARBs, diuretics)
“-zosins”
Alpha-1 selective blockers
Selective HTN drug that is useful when pts have renal disease
Clonidine & Methyldopa (Alpha-2 selective agonist, centrally-acting), does not have activity on renal blood flow or GFR
Monotherapy for pregnancy-induced HTN
Hydralazine (direct vasodilator by inhbiting IP3-induced Ca+2 release from SR in smooth muscle cells, so muscle does not contract/constrict) and stimulates endothelium to make NO
Which anti-hypertensive drug can also be used to treat malepattern baldness
Minoxidil (S/E causes hypertrichosis)
MOA of minoxidil
Used to treat HTN as a direct vasodilator (decreases the amount of intracellular Ca+2 available for smooth muscle contraction by opening K+ channels)
Immediate continuous IV infusion of which drug is used to treat Hypertensive emergencies
Sodium nitroprusside, since causes prompt vasodilation of both arteries and veins (so will also decrease cardiac preload)
How is fenoldopam a better alternative in hypertensive emergencies
It is a peripheral D1 agonist, so lowers BP while increasing renal perfusion (since it relaxes renal vascular smooth muscle)
Which anti-hypertensive agent can precipitate a hypertensive crisis following abrupt cessation of therapy
Clonidine (Alpha-2 agonist, that could potentially cause rebound hypertension)
Cyanide toxicity is seen with which anti-hypertensive drug
Nitroprusside
Which drug is safe to use in pregnancy that is often given w/ a beta-blocker, but can cause compensatory tachycardia and lupus-like syndrome
Hydralazine
Describe MOA of labetalol and important use
Mixed Alpha/beta antagonist that is used in malignant HTN tx
How do nitrates work to cause vasodilation
Conversion into NO at vascular smooth muscle cell membrane, NO stimulates guanylate cyclase (converts GTP -> cGMP), increased cGMP decreases intracellular Ca+2/myosin dephosphorylation, causing muscle relaxation
If a pt has an allergic rxn to aspirin, what is the next best alternative drug and MOA
Clopidogrel, irreversibly blocks plt surface ADP receptors (necessary for plt activation/aggregation/fibrin binding)
Synergistic effects of 2 drugs used in tx of thromboembolic disease
Aspirin and clopidogrel (different MOA’s)
Which nitrate compound has the highest bioavailability if given orally?
Isosorbide mononitrate, an active metabolite of isosorbide dinitrate (must be swallowed, Nitroglycerin has the most rapid onset of action but is given sublingually)
Cinchonism can be caused by which drug
Quinidine (Class IA antiarrhythmic) , headache, dizziness with tinnitus
Class IA antiarrhythmic drugs
Quinidine, Procainamide, Disopyramide
Which antiarrhythmic can cause systemic sx that mimic an autoimmune disorder
Procainamide (lupus-like syndrome)
___ enhances digoxin toxicity
Quinidine
Best antiarrhythmic drugs to use in case of chronic ventricular arrhythmias if pt has previous hx of MI
Class IB = Best (Lidocaine, Mexiletine, Tocainide); preferntially affects ischemic Purkinje/ventricular tissue
Flecainide and Propafenone are contraindicated in_
pts with structural abnormalities (post-MI, any type of heart conditions) - usually only used as a last resort in refractory cases
Can you use lidocaine IV to treat a supraventricular arrhythmia?
NO! it is ineffective
Tocainide
Class IB
Disopyramide
Class IA
Propafenone
Class IC
Mexiletine
Class IB
Quinidine
Class IA
Activity of Class IA drugs
slow rate of AP rise/increase threshold, prolong AP duration, & prolong ERP (shift curve to right and out)
Activity of Class IB drugs
Decrease AP duration, shorten repolarization (therefore not effective in SVA or Atrial arrhythmias!) -curve is shifted left/in
Activity of Class IC drugs
Slow rate of AP rise/increase threshold, but don’t affect AP duration (curve is pretty close to normal curve)
Activity of Class II drugs
Beta-blockers that block phase 4 depolarization of abnormal pacemakers, decrease SA/AV node activity by decreasing cAMP/Ca+2 currents = increase PR interval (used to treat atrial fib/flutter and SVT)
Which short-acting Class II drug is used in surgery or emergency situations
Esmolol
Dyslipidemia in a pt on a anti-arrhythmic drug
Metoprolol
Exacerbation of vasospasm in a pt on an antiarrhythmic drug
Propranolol
Activity of Class III drugs
K+ channel blockers, diminish outward current during repolarization - prolong AP and ERP (AIDS-Amiodarone, Ibutilide, Dofetilide, Sotalol)
Sotalol
Class III drug
Ibutilide
Class III drug
Dofetilide
Class III drug
Amiodarone
Class III drug
2 major classes of antiarrhythmics that prolong the QT interval
Class IA and Class III
Drug class used to prevent nodal arrhythmias, SVT
Class IV-Ca+2 channel blockers
Pt with sinus node depression, flushing and constipation, most likely on which drug
Class IV -CCC (Verapamil, diltiazem) - other effects seen from vasodilation
Adenosine MOA as antiarrhythmic
At higher doses it increases K+ current outward, hyperpolarizing the cell; Used to abolish SVT
Pt with FLUSHING, HYPOTENSION, CHEST PAIN that gets better with drinking coffee (or giving theophylline), most likely on which anti-arrhythmic
Adenosine (increases K+ efflux/out of cells), hyperpolarizing the cell
If have digoxin toxicity or torsades pointes, can give this
Mg+2
Which antiarrhythmic can predispose a pt to digoxin toxicity
Quinidine
Production of a bidirectional block is useful in tx of
Reentrant arrhythmias; class I drugs prevent this
Muffled heart sounds, elevated JVP, profound hypotension
Pericardial tamponade
QRS prolongation that has little effect on QT interval duration, which phase does this correspond to on a myocyte action potential figure?
Phase 0 (depolarization occurs when rapid movement of sodium in the myocyte)
Pulsus paradoxus
Pericardial pressure >10mmHg, seen in cardiac tamponade; can progresses to collapse of atria (death from cardiogenic shock)
Palpate radial pulse and it disappears during inspiration
Pulsus paradoxus
Pulsus parvus et tardus
Pulse of low magnitude with delayed peak, seen in aortic stenosis
Repeated episodes of palpitations that start and stop abruptly in a young adult pt
Wolff-Parkinson-White pre-excitation syndrome
Triad of WPW on EKG
Shortened PR interval <.12 seconds, wide QRS complex, early upslope delta wave immediately preceding QRS
Head bobbing
Seen in Aortic Regurgitation, sign of widened pulse pressure (increased peak systolic pressure relative to end-diastolic pressure)
If stable angina in a pt, what percentage coronary occlusion by atherosclerotic plaque would you start to see sx
> 75%
Most likely cause of fatigue and new onset murmur in a young adult
Bacterial endocarditis, can progress to acute diffuse proliferative glomerulonephritis
Pt given glucagon to treat overdose of a drug, how does this make pts condition better
Pt probably took Metoprolol which can cause dyslipidemia; glucagon serves to decrease cAMP and Ca+2 currents in cardiac myocytes
Drugs that can result in torsades de pointes
(Those which prolong the QT interval) Class IA antiarrhythmics (Quinidine, Procainamide, Disopyramide) and Class III (Amiodarone, Ibutilide, Dofetilide, Sotalol)
Drug given to abolish supraventricular tachycardia
Adenosine
Pt recently put on new antiarrhythmic, notices blue-grey skin lesions and constipation; HR is bradycardic; labs reveal hypothyroidism; what is MOA of drug
(Amiodarone toxicity) Class III, K+ channel blocker that alters lipid membrane
2 classes of drugs that are better at treating atrial arrhythmias
Class II beta blockers & Class IV CCBs since they both decrease conduction velocity/increase PR interval
Drug that has no effect on AP duration, used only in pts without structural abnormalities
Propafenone, Flecainide (Class IC), contraindicated in post-MI pts
Which drugs preferentially affects ischemic or depolarized cardiac tissue
Class IB, Lidocaine, Mexilitine, Tocainide
Which antiarrhythmic drugs can cause bradycardia, heart block, CHF
Class II beta blockers (-olol’s), Class III K+ channel blocker Amiodarone, Class IV CCBs (verapamil, diltiazem)
Drug that can be used for A-fib and CHF begins to cause T-wave inversion on EKG, nausea, vomiting, diarrhea, blurry yellow vision; what is the MOA
Inhibition of Na+/K+ ATPase and stimulation of vagus nerve (increase intracellular Ca+2 and decrease HR)
Antiarrhythmic drug preferentially used in post-MI pts, can also be used to reverse toxicity of which other drug
Digoxin (this drug is Lidocaine)
Pt recently started on a drug and is found to have high levels of cyanide; what is the MOA of this drug
Cyanide toxicity from administration of Nitroprusside, used to treat Malignant hypertensive emergencies; MOA is to increase cGMP via direct release of NO (smooth muscle relaxation)
Pt recently started on hydralazine and now experiences rapid HR, what other drug could be used concomitantly to prevent this
Beta blocker (prevents reflex tachycardia)
Prolongation of QT interval upon administration of a drug, but does NOT predispose to torsades de pointes
Amiodarone
Asthmatic pt recently started on additional drug for HTN, starts having more frequent asthma attacks; which drug is he most likely on
Beta blocker, can cause exacerbation of asthma, impotence
Most common digoxin S/E
N/V, diarrhea, blurry yellow vision, AV block, arrhythmia, ST scooping/T-wave inversion, SHORTENED QT INTERVAL, prolonged PR interval, HYPERKALEMIA
Male pt w/ erectile dysfunction (that is being treated) takes several tablets to relieve an episode of chest pain. Good or bad idea?
BAD idea, Nitroglycerin (nitrate, vasodilator, increases cGMP conc.) plus Sildenafil/Tadalafil for ED (Phosphodiesterase inhibitor, increases cGMP conc.) will cause profound HYPOTENSION due to extreme vasodilation
Major complication of Doxorubicin
Dilated cardiomyopathy (better to use Dexrazoxane, decreases formation of free radicals)
Reflex tachycardia can be seen with administration of which cardiac drugs
Nitrates and Hydralazine (direct vasodilators)
Non-antiarrhythmic agents that can cause QT prolongation and precipitate torsades
Phenothiazines & tricyclic antidepressants
What should be monitored when pt is started on warfarin/coumadin for loong-term anticoagulation
Prothrombin time (PT)
Which drugs significantly decrease heart failure progression as well as all-cause mortality in patients with CHF
Beta-blockers, particularly CARVEDILOL (should NOT be given in pts with unstable heart failure!)
Pt given esmolol infusion, which portion of EKG does it exert its greatest effects
Slows AV conduction, therefore prolongs the PR interval
Activity of cAMP in myocytes
Increases the conductance of calcium channels in the sarcoplasmic reticulum, more calcium allowed to enter cytoplasm and increase force of contraction
Milrinone
Phosphodiesterase isoenzyme 3 inhibitor that can increase cardiac contractility (positive inotropic agent)
Site of action of K+-sparing diuretics
Collecting duct of renal tubule
Main side effects of Niacin
Cutaneous flushing, warmth, itching that is mediated by Prostaglandin (may be prevented co-administration with aspirin)
Most common S/E of statins
hepatotoxicity, myopathy, rhabdomyolysis
Which statin is drug of choice if pt is on erythromycin
Pravastatin (Erythromycin inhibits cytochrome P450, which metabolizes most statins)
Risk of myopathy with statin use in increased when used in combination with which other drugs
Fibrates (gemfibrozil increases the concentration of statins, fenofibrate causes compouding risk for myopathy)
Which statin has the highest associated risk of myopathy
Simvastatin
Statin MOA
Inhibits HMG-CoA reductase (necessary for cholesterol synthesis), causing up-regulation of hepatocyte LDL receptors
First-dose hypotension can be an adverse effect in pts initiating a drug with which predisposing risk factors
(ACE-I’s) Hyponatremia, hypovolemia secondary to diuretics, low baseline BP, high renin/aldosterone levels, renal impairment, heart failure
Which drugs are particularly useful for the tx of both HTN and BPH
Alpha-1 selective blockers (Prazosin, Terazosin)
