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147 Cards in this Set
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What are some clinical presentations of acute pericarditis?
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Sharp chest pain, retrosternal, frequently sudden in onset, with inspiration and movement. Pain reduced by leaning forward or sitting up.
Splinted breathing, odynophagia, fever, myalgia, anorexia, anxiety, pericardial friction rub, cardiac dysrhythmias (intermittent), SVT, tachypnea, localized rales |
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When there is a pericardial effusion, how would you relieve pressure?
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Insert an aspiration syringe beneath the xyphoid to the bottom of the pericardium
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What is a pericardial "window"? What are the benefits?
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A pericardial "window" is a flap opened to relieve Tamponade
Helps in performing diagnostic biopsies and collecting cultures, relieves fluid rapidly |
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What would a depressed PR segment usually indicate clinically?
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Pericarditis
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What are some ECG findings in acute pericarditis?
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ST segment elevation (NOT AVR or V1)
PR segment depression Sinus rhythm (sometimes atrial flutter or fibrillation) Decreased QRS voltage Occasionally electrical alternans (usually in setting of tamponade) |
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What is "bread and butter" pericarditis?
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Mild fibrinous pericarditis - the heart has a film if fibrous material over the surface of the heart.
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What are the ECG findings in mild fibrinous pericarditis?
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MIld fibrinous pericarditis, or "bread and butter" pericarditis, show T wave inversion in all leads except AVR and V1. It is isoelectric in lead III.
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What are some drugs and procedures that cause pericarditis (Iatrogenic pericarditis)
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Drug induced lupus like syndrome (hydralazine, procainamide, diphenylhydantoin)
Radiation Anticoagulants Methysergide Cyclosporine Minoxidil Streptokinase CVP, defibrillator or pacemaker catheter placement Cardiac transplantation, CABG and other cardiac surgery Endoscopic sclerotherapy |
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What are some agents that cause infectious pericarditis? (don't need to memorize them all)
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Viral (Coxsackie A, B, echovirus, influenza, adenovirus, Epstein-Barr, varicella, HIV, mumps)
Mycobacterial (M Tb, M. avium intracellulare) Protozoa (Toxoplasmosis, Trypanosoma cruzi) Fungal (histoplasma, coccidioides, blastomycosis, candida, aspergillus) Bacterial (staphylococcus, sterptococcus, gram negative bacilli, meningococcus, pneumococcus, salmonella, brucella, Legionella, campylobacter, hemophilus inf, lyme disease, chylamydia psitaci, ricketsial, clostridium, nocaria, actinomyces, mycloplasma) Parasitic (trichinosis, microfiliaria, echinococcus) |
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When the pericardial sac is opened up, what kind of necrosis may be seen?
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Caseous "cheesy" necrosis
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What is the approximate incidence of tuberculous pericarditis in TB patients? In cases of acute pericarditis? In cases of tamponade? Pericarditis in India?
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1-2% of patients with pulmonary TB develop tuberculous pericarditis
4% of acute pericarditis 7% of tamponade 2% of cases of restrictive pericarditis Most common cause of pericarditis in India About 1/3 of cases require pericardiectomy More common in AIDS patients than general population |
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What are some causes of pericardial complications of AIDS?
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Kaposi's sarcoma, TB, HSV type 2, cytomegalovirus, cryptococcus neoformans, lymphoma, nocardia asteroides, nonspecific pericarditis
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What is postpericardiotomy syndrome?
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There is chest pain, fever, increased sed rate, pericardial effusion, sometimes pulmonary infiltrates. Occurs in 10-40% of patients following cardiac operations within 1-8 weeks of the operation.
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In postpericardiotomy syndrome, how would you describe the pericardial fluid?
Are there ECG changes? |
Pericardial fluid in this case is often serosanguinous
In 50% of cases, ECG resembles acute pericarditis. |
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What three types of infarctions are associated with pericarditis?
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Early infarct associated with pericarditis?
Pericardial infusion - with or without tamponade Postcardiac injury (Dressler's syndome) |
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How does pericarditis in MI present?
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Pericardial rub 5-15% of patients
Usually 11 days to 3 months post infarction |
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Why are NSAIDs NOT used to treat pericarditis following MI?
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Increasing risk of wall rupture, scar thinning, aneurysm
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What are some causes of cardiac tamponade?
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Malignant Tumor
Idiopathic pericarditis Uremia Bacterial infections Anticoagulant therapy Myxedema Radiation Cardiac rupture post infarction Primary Chylopericardium Dissecting aneurysm Diagnostic procedures Tuberculosis Postpericardiotomy Trauma Connective Tissue Disease |
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What are some causes of pulsus paradoxis?
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cardiac tamponade
acute/chronic airway disease constrictive pericarditis restrictive cardiomyopathy pulmonary embolism right ventricular infarction circulatory shock |
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Physical findings in cardiac tamponade (good for boards!)
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Elevated systemic venous pressure 100%
Paradoxical pulse 98% Respiratory rate>20/min 80% Heart rate >100/min 77% Diminished heart sounds 34% Pericardial friction rub 29% Rapidly declining blood pressure 25% |
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What are some ECG findings for cardiac tamponade?
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RA, RV diastolic collapse
LA collapse IVC plethora LV pseudohypertrophy Swinging heart Abnormal inspiratory increase in tricuspid wave flow, abnormal increase in RV dimension with abnormal decrease in LV dimension |
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What are some symptoms of constrictive pericarditis?
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Exertional dyspnea
Fatigue Abdominal swelling/discomfort Orthopnea Cough |
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What are some signs of constrictive pericarditis?
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Elevated venous pressure
Edema, Ascites Hepatomegaly Pleural effusion Kussmaul's sign Pericardial knock Pulsus paradoxis Decreased precordial activity |
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What are some of the more common causes of constrictive pericarditis?
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Idiopathic pericarditis: 40%
Post CABG: 30% Tuberculosis: 10% Radiation induced: 5% Collagen vascular disease: 5% Others (malignant, uremic, purulent): 5% |
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What are some causes of secondary cardiomyopathy?
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Sarcoidosis
Amyloidosis Hemochromatosis Rheumatic infection (viral, Lyme, Chagas) Alcoholic Adriamycin and other toxic drugs |
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List the classes of primary cardiomyopathies (3)
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Hypertrophic cardiomyopathy
Dilative cardiomyopathy Restrictive cardiomyopathy |
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What are some treatments for Obstructive HCM?
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Negative inotropes, pacemaker, or Myectomy
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What are some treatments for Non-Obstructuve/End-Stage HCM?
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Digoxin, Afterload reduction, Diuretics, Transplant surgery
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What is hypertrophic cardiomyopathy (HCM)?
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It is disproportionate hypertrophy of the LV, sometimes RV. Most often the hypertrophy bulges out on the interventricular septum, and LV volume is reduced.
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What is the cause of HCM?
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HCM is an autosomal-dominant genetic disease with incomplete penetrance.
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How does an afterload-reducing agent in a patient with sub-aortic stenosis improve heart performance?
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It decreases perfusion
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What two types of HCM are there?
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Obstructive and Non-Obstructive (which progresses to End-Stage)
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What are the patterns for asymmetric vs symmetric idiopathic HCM?
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Asymmetric Idiopathic HCM: 95%
Ventricular septal - 90%; Apical - 3%; Midventricular - 1%; Other - 1%; Symmetric (concentric) Idiopathic HCM: 5% |
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What is dilated cardiomyopathy?
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Dilation of the left ventricle and/or right ventricle - dilation is severe, and hypertrophy usually accompanies it.
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How does dilated cardiomyopathy present?
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LV/RV dilation, hypertrophy, impaired systolic ventricular function, CHF may be present
Rarely: ventricular or atrial arrhythmias Death may occur at any stage |
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Since dilated cardiomyopathy is essentially irreversible, what problems are treated?
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Hemodynamic/CHF issues
Dysrhythmia Thromboembolic complications Treatment for specific muscle diseases and myocarditis Cardiac transplantation |
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What is used to treat hemodynamic/CHF issues in dilated cardiomyopathy?
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Diuretics
Aggressive afterload reduction Low sodium diet Digoxin, possible role for other inotropics |
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What is used to treat dysrhythmias in patients with dilated cardiomyopathy?
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Amiodarone
Beta-blockers (Metaprolol) Carvedilol Propafenone Implantable Automatic Defibrillator |
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What is used to treat (risk of) thromboembolic complications in dilated cardiomyopathy?
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Warfarin therapy
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What are the treatments for specific muscle diseases and myocarditis which may contribute to the dilated cardiomyopathy?
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Antiparasitic therapy for Chagas and trichinosis
Antibiotic therapy for Lyme disease Treatment of underlying malignancies if present in amyloidosis Chelation for hemochromatosis Various treatments for myocarditis? |
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What are some possible viral causes for myocarditis?
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Coxsackie A, B; Mumps, Influenza, Adenovirus;
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What is the most common cause of sudden death in young athletes?
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HCM
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Why does HCM cause diastolic dysfunction?
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Diastolic dysfunction means a problem with blood filling the left ventricle. Since HCM usually has diminished LV capacity and LV hypertrophy, that would cause diastolic dysfunction.
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What are the principles of ACE inhibitor use?
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Start drug early
Start at a low dose Titrate to maximally tolerated dose Tolerate low peripheral BP Decrease diuretics as needed Decrease potassium replacement as needed |
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What causes an increase in the murmur in patients with HCM? Why?
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The murmur increases with amyl nitrate, valsalva, and isoproterenol - anything that increases LVOT gradient and decreases ventricular volume.
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What causes a decrease in the murmur in patients with HCM? Why?
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Decreases with hand grip, beta blockers, and phenylephrine - so with decreased LVOT gradient and increased ventricular volume
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Why does dilated cardiomyopathy cause systolic dysfunction?
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Dilated cardiomyopathy results in dilated left ventricular and a weaker ejection force of blood. As a result, the heart has more trouble ejecting blood into systemic circulation, blood backs up, and the lungs accumulate fluid, edema.
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How would you recognize cardiac amyloidosis clinically?
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In asymptomatic patients with abnormal ECG
In patients with HF and one of the following without obvious cause: Proteinuria, Gastroenteropathy, Anemia, Plasmacytosis, Peripheral neuropathy, bone pain |
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What kind of work-up would you do for cardiac amyloidosis?
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ECG
Urine for Bence Jones protein Serum for immunoelectrophoresis Bone survey Bone marrow aspiration Biopsy - endomyocardial, abdominal subcutaneous fat, rectal, gingival |
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What is involved in a restrictive cardiomyopathy?
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There is endocardial fibrosis, Loffler's cardiomyopathy, scarring that restricts filling of one or both ventricles, involvement of atrioventricular valves, cavity obliteration is characteristic of advanced cases
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What is acute rheumatic fever?
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A systemic disease of childhood that can follow a beta hemolytic streptococcal infection of the pharynx (NOT skin)
It is a diffuse inflammatory disease of the connective tissue, primarily involving the heart, joints, skin, subcutaneous tissue, and CNS. |
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What are some manifestations of RF?
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Migratory polyarthritis of the major joints (75%)
Pancarditis (endocarditis, myocarditis, pericarditis) in 40-50% can result in permanent heart damage Erythema marginatum and subcutaneous nodules are uncommon, nearly pathognomic Sydenham's chorea from inflammation of the basal ganglia |
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What demographics tend to get acute RF? Under what conditions?
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Peak age-related incidence: 5-15 years
Young adults may be affected, recurrence as late as age 40 Associated with lower standards of living, crowding, poor sanitation |
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About what percent of individuals with untreated group A strep pharyngitis will develop RF?
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0.4-3%
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How does RF develop from strep A infection? What is the specific mechanism?
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RF is a delayed immune response to an untreated group A strep infection which typically occurs after a latent period of 2-4 weeks
Antigen of the outer protein wall of GABHS induces an antibody response that can result in autoimmune damage to heart valves, subcutaneous tissue, tendons, joints, and basal ganglia of the brain |
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What is part of the typical immune response with RF?
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Fibrinoid degeneration of connective tissue
Inflammatory edema Inflammatory cell infiltration |
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What is the single diagnostic sign or laboratory test needed for diagnosis of RF?
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There is no single sign/test that is sufficient
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How does one use the (modified) Jones criteria to diagnose RF?
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A patient must have either two major criteria, or one major criteria and two minor criteria
Plus evidence of of recent strep A infection, by culture or evidence of an immune response go GABHS antibody (anti-streptolysin O, anti-deoxyribonuclease B) |
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What are the major criteria of the Jones criteria?
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Carditis
Migratory polyarthritis Sydenham's chorea Subcutaneous nodules Erythema marginatum |
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What are the minor criteria of the Jones criteria?
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Clinically: Fever, Arthralgia
Laboratory: Elevated acute phase reactants; Prolonged PR interval |
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Describe carditis within the context of RF
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Presents with S/S of one or more of the following: pericarditis, cardiomegaly, right/left side CHF, mitral and/or aortic regurgitation
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What is the only manifestation of RF that leaves permanent damage?
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Carditis
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How many patients with ARF carditis will have mitral valve involvement? What pathologic characteristics are present in the chronic phase?
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~60%
Chronic phase: fibrosis, calcification, stenosis |
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How is ARF carditis diagnosed? (ECG studies, 2D echocardiography)
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Prolonged PR interval (1st degree heart block)
May also see... 2nd/3rd degree blocks ST depression T wave inversion 2D Echocardiography - may reveal valve edema, mitral regurgitation, left atrial/ventricular dilation, pericardial effusion, decreased contractility |
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Describe migratory polyarthritis within the context of RF? How common is it?
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Present in up to 75% of RF patients
Often affects ankles, wrists, knees, elbows - over a period of days. Joints become extremely painful, small joints and hips are usually spared. |
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What is an adequate pharmacological treatment for migratory polyarthritis in ARF?
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Responds well to salicylates and other anti-inflammatory, so important not to prescribe until it is determined whether it is MIGRATORY polyarthritis
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What is the difference between arthralgia and arthritis?
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Arthritis is inflamed joints - with clinically observable S/S
Arthralgia is subjective, the sense of having painful or swollen joints |
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What is Sydenham's chorea within the context of RF? In what population is it most common?
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10% of children with RF develop Sydenham's chorea
Latent period may be up to several months between strep infection and onset of chorea Diagnosis of exclusion - no definitive test FOR Sydenham's chorea |
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What is the logical course of action for a patient with Sydenham's chorea?
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Prophylaxis to prevent recurrent attacks even if they don't seem to have rheumatic fever
Patients who only seem to have chorea have later developed rheumatic valve disease, so must treat it as a serious sign |
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Describe erythema marginatum
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Red circular/blobby outlines on the skin
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What is included in the differential diagnosis for RF?
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Juvenile rheumatoid arthritis
Septic arthritis Sickle-cell arthropathy Kawasaki disease Myocarditis Scarlet fever (exotoxin-mediated) Leukemia |
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What laboratory tests are useful in the diagnosis of ARF?
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Anti-streptolysin O titer is positive in 80-85% of patients with ARF before 6 weeks
Adding anti-DNAse B or anti-hyaluronidase to ASO increases sensitivity to 90% ESR, C-reactive protein (non-specific) Throat culture - reliable only 40% of the time |
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What are the four steps in the treatment of RF?
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Step 1 - primary prevention and treatment (eradication of streptococci with penicillin or erythromycin regardless of culture results)
Step 2 - Anti-inflammatory treatment (aspirin and/or steroids) Step 3 - supportive management and management of complications Step 4 - secondary prevention (prevention of recurrent attacks) |
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What are the conditions for going ahead with step 2 (anti-inflammatory tx) in treating RF?
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Treat with anti-inflammatory drugs...
If ONLY arthritis is present, treat with aspirin If carditis is present, treat with prednisone and add aspirin during the tapering |
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What is considered supportive management and management of complications in step 3?
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Bed rest
Joint rest and supportive splinting Treat CHF with diuretics, digitalis Treat chorea with diazepam or haloperidol |
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What is secondary prophylaxis? What are the three categories and associated durations of treatment?
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Patient is instructed to take ongoing low-dose antibiotics (penicillin, sulfadiazine, erythromycin)
Category I - Rheumatic fever with carditis and persistent valvular disease: Treat 10 years minimum, at age 40 consider lifelong prophylaxis Category II - Rheumatic fever with carditis but no residual valvular disease: treat for 10 years or past age of 40, whichever is longer Category III - Rheumatic fever without carditis: treat for 5 years or until age 21, whichever is longer |
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What is the prognosis for RF? What would make for a better prognosis? Worse prognosis?
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RF can recur whenever the individual experiences new GABHS infection of not on prophylactic medicines - 50% recurrence if untreated
Good prognosis for older group if there was no carditis during initial attack Worse prognosis if younger and had carditis - 30% die within 10 years (more susceptible to RF recurrences) |
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What is required for diagnosis of CHRONIC RHD?
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Persistent valve lesions
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How does chronic valvular disease develop (related to RF)? Incidence of mitral valve disease? Combined MV disease and aortic disease? Tricuspid involvement?
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Chronic valvular disease develops from repeated episodes of RF - rigidity and deformity of valve cusps, fusion of the commisures, or shortening and fusion of the chordae tendinae
60% - mitral valve disease - stenosis or regurgitation 20% - combined MV disease and aortic disease - aortic stenosis and/or regurgitation 10% - tricuspid involvement - stenosis |
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What are the common S/S of Mitral Stenosis within the context of RF?
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Common S/S: dyspnea, orthopnea, paroxysmal nocturnal dyspnea - depends on the degree of left atrial pressure and subsequent right heart failure
May remain asymptomatic until there is a precipitating event - usually with onset of atrial fibrillation (80%) or pregnancy |
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How is Mitral Stenosis diagnosed?
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Characteristic heart sounds - opening snap with a low-pitched mid-diastolic murmur (rumble)
Heard best with patient on left side, listen at apex with bell ECG useful |
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How is Mitral Stenosis treated?
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Warfarin - anticoagulant therapy if atrial fibrillation is present
Conversion to sinus rhythm Surgery - balloon valvuloplasty, open mitral commissurotomy, valve replacement Antibiotic prophylaxis |
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What is infective endocarditis?
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A localized infection which forms a mass (vegetation) comprised of fibrin, platelets, and microorganisms
The vegetation adheres to cardiac valves or to the endothelial surface of injured areas |
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How does IE manifest?
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IE tends to manifest systemically
Fever Cardiac murmurs Anemia Splenomegaly Petechiae Pyruia Peripheral Emboli |
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What is the untreated mortality rate for IE? How may it be paced?
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Without proper treatment, mortality approaches 100%
Pace of symptomatic progression may vary from indolent to fulminant |
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What complications dominate during infection (within context of IE)?
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Extracardiac complications are most common - though many patients with endocarditis will experience none of these
Complications result from bacteria shedding fragments of the infected thrombus from the valve vegetations |
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How long does bacteremia persist? How does the immune system make matters worse? (within the context of IE)
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Bacteremia persists for a very long time, and is a prolonged antigenic challenge to the immune system.
Circulating immune complexes may cause microvascular damage, especially in the kidneys and small blood vessels of the skin |
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What is the impact of embolizing fragments in extracardiac disease (in IE)?
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Embolizing fragments can present as metastatic infection, the worst may result in a brain abscess - other sites include kidney, liver, bone, and lung
Emboli also cause damage by occluding vessels |
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How is acute endocarditis defined?
Subacute endocarditis? Which is more common? |
Acute endocarditis - hectic, febrile disease that will cause death in weeks if untreated
Subacute endocarditis - more indolent course, causing cardiac damage slowly, if at all. Accounts for 2/3 of cases |
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What (largely) determines the course of treatment?
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Acute vs Subacute
Causative organism |
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What pathogens may cause infective endocarditis?
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Staphylococcus aureus - 40%
Strreptococcus viridans - 40% Enterococcus sp. - 11% Gram Negative bacteria - HACEK (Actinobacillus, Cardiobacterium, Eikenella, Kingella), pseudomonas, etc. |
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How do the pathogens that cause IE enter the body?
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S. viridans - oral cavity
S. aureus - skin HACEK organisms - upper respiratory tract |
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What are risk factors for developing IE?
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Using IV drugs - number one risk factor pts < 40 yo
Structural heart disease - 75% of patients with IE have a pre-existing structural cardiac abnormality. Up to 20% have a congenital heart disease. Mitral valve prolapse carries a risk 5-8x higher than general population Aortic valve disease in 30% of IE cases Prosthetic heart valves (1-4% recipients) Nosocomial endocarditis (invasive procedures) HIV (from history of drug abuse) |
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How does IE usually develop?
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Normal endothelium is resistant to infection
Infection is usually a consequence of a prior injury - such as impact by high-velocity blood jets from abnormal hemodynamics, areas of aberrant flow that allows thrombus formation |
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How are RF and IE related?
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Decreased cases of RF also result in fewer cases of IE
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What causative agents are usually behind acute IE? subacute IE?
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Acute IE: beta-hemolytic strep, S. aureus, pneumococci
Subacute IE: S. viridans, enterococci, HACEK group |
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Does IE tend to have a general or specific presentation? How indicative is fever?
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Variable presentations - spans a continuum between acute and subacute
Need to have a high degree of suspicion when a fever occurs in a patient with valve disease or history of drug use. Fever is not a reliable sign in elderly |
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What are some cardiac signs in a clinical presentation of IE?
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New regurgitant murmurs from valve damage and ruptured chordae
Development of intra-cardiac abscesses and fistulae Injury to conduction system leads to heart block |
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What are some non-cardiac signs in a clinical presentation of IE?
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Vegetation >10 mm more likely to embolize early, in these patients, peripheral signs are more likely at presentation
Antibiotic therapy significantly decreases but does not eliminate embolic events |
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List some basic S/S of IE, and how often are they seen in a clinical presentation?
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Fever - 80-90%
Heart Murmur - 80-90% Chills/sweats - 40-75% CHF - 30-40% Arterial emboli - 20-50% Splenomegaly - 15-50% Neurological changes - 20-40% Worsened murmur - 10-40% Peripheral signs - 2-15% |
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What organism is the most common causative agent in IV drug-related IE? Blood cultures positive or negative?
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S. aureus in 50% of cases
Positive blood cultures (usually) |
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What kind of IE is most common in IV drug abusers?
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Right-sided IE with tricuspid valve involvement - about 75% also have septic pulmonary emboli
Usually present without peripheral stigmata Low fatality rate |
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Is a physical exam necessary for an IE dx? Why or why not?
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Physical exams are NOT necessary for an IE dx
Most of the physical findings caused by endocarditis are not specific for dx and must be interpreted in the context of the overall exam and the patient's history There are no physical findings that, if absent, are useful for ruling out the an IE dx *However, the initial exam can assist in establishing the severity and serial exams are absolutely essential to the treatment of endocarditis pts. |
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How does fever usually present in an IE presentation?
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Usually is present, may be intermittent or masked by other conditions such as malnutrition. May have already resolved through inappropriate antibiotic treatment
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How does a cardiac exam (physical exam) lend clues to IE?
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The value initially of a heart murmur may be low if there is no reliable information about the patient's prior condition
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How do physical findings regarding skin, eyes, and the extremities lend clues to IE?
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A careful exam for evidence of vasculitis or emboli, if found, can lend strong support to the diagnosis.
Red nodules (Osler's nodes) Purpura (Janeway lesions) Skin sores, such as from S. aureus, may also be useful. Fingernail beds may have splinter hemorrhages. Eyes - Roth spots |
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What is the tests in the Duke criteria? Is the Duke criteria more sensitive or specific?
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Highly sensitive, not specific - 10% of patients meeting these criteria will NOT have IE
Blood cultures - 3 BC sets from different sites obtained over 24 hours. Repeat in 48-72 hours if first sets are negative, but high suspicion remains Echocardiography - allow anatomic confirmation of vegetation locations and size, and of cardiac function. Trans-esophageal (TEE) is the most sensitive. |
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How does one determine presence of IE using the Duke criteria?
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There must be one of the following:
1) Direct evidence of IE based on histology 2) Gram's stain or culture of organisms obtained at surgery or autopsy 3) Two major criteria 4) One major and any 3 minor criteria 5) Five minor criteria |
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What are the major criteria in the Duke criteria?
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Positive blood cultures - 2 separate cultures with S. viridans, S. bovis, HACEK group, S. aureus, enterococci
Evidence of endocardial involvement by echo of: vegetations, abscesses, or new partial dehiscence of prosthetic valve New valvular regurgitation |
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What are the minor criteria in the Duke criteria?
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Predisposition - heart condition, IV-drugs
Fever > 38 degrees C Vascular development - arterial emboli Immunologic development - glomerulonephritis Microbiological evidence - other than major criteria Echocardiogram - other than major criteria |
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What are the laboratory manifestations of IE?
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Anemia - 70-90%
Leukocytosis - 20-30% Microscopic hematuria - 30-50% Elevated sed rate > 90% Rheumatoid factor 50% Circulating immune complexes 65-100% Decreased serum complement - 5-40% *Do not directly contribute to dx of IE, but are important in managing disease* |
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How is a trans-esophageal echo relevant to IE dx?
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TEE is much more sensitive than transthoracic echocardiograms. Especially useful for detecting vegetations, better in dx of prosthetic valve endocarditis
Approaches 100% negative predictive value for native valve endocarditis TTE is still the 1st dx test for most, as it is less invasive and often makes the dx, but TEE is gaining advocates. All agree it is better and necessary in selected situations |
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What is the general path for diagnosing endocarditis?
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Ancillary laboratory tests, BC x 3, TTE - if Diagnostic, treat.
If nondiagnostic...TEE - if diagnostic, treat. If nondiagnostic, most likely is not endocarditis |
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What are the general principles of antibiotic treatment within the context of endocarditis? What if the causative organism is unknown?
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Antibiotics should be administered parenterally initially
Must reach high serum concentrations that will, through passive diffusion, lead to effective concentrations in the depths of vegetations. Effective therapy requires precise knowledge of the susceptibility of the causative organism If the organism is unknown, start with Vancomycin and Gentamicin - will cover MRSA, gram negatives, and other common causative agents |
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What kind of cardiac surgery is recommended in IE? When should it be considered?
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Surgery recommended when...
Peri-valvular extension of infection Poorly responsive S. aureus infection of valve Persistent unexplained fever over 10 days Relapse of prosthetic valve infection due to resistance Surgery is required for optimal outcome if there is ... Moderate/severe CHF Partially dehisced prosthetic valve S. aureus prosthetic valve endocarditis Relapse of prosthetic valve infection due to resistance |
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What is the prognosis for native valve IE? Prosthetic valve IE?
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Native valve IE - 85-90% survival for all organisms except S. aureus (survival is 55-70%)
Prosthetic valve IE - 50-60% if IE occurs within 2 months of valve placement. Increases to 80-90% thereafter |
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Are preventive steps taken for IE?
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No evidence-based studies show effectiveness of endocarditis prophylaxis, but AHA expert committee has set guidelines for treatments and for how long it should be given
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When is one considered at high risk for IE?
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Prosthetic heart valves
Prior IE Complex cyanotic congenital heart disease Coarctation of the aorta Surgically constructed systemic-pulmonary shunts |
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When is one considered at moderate risk for IE?
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Ventricular septal defect, bicuspid aortic valve
Acquired aortic and mitral valve dysfunction HCM Mitral valve prolapse with regurgitation and/or thickened leaflets |
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Who receives prophylaxis for IE prior to dental procedures?
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As of 2007, it is now limited to those at high risk of adverse outcome from IE - argument is that the risk of IE from normal toothbrushing is higher than occasional dental procedures, and there is a relatively high risk of side effects from antibiotic prophylaxis
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What antibiotics are used for IE prophylaxis?
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PO: Amoxicillin
If PO poorly tolerated: Ampicillin, Cefazolin, Ceftriaxone If PCN allergy: Cephalexin, Clindamycin, Azithromycin, Clarithromycin |
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List a few things in the DDx for chest pain (GI, Mus, Resp, CV)?
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GI: PUD, GERD, esophageal spasm, gastritis
Mus: Costochondritis, rib dysfunction Resp: Pneumonia, pleuritis, bronchitis CV: aortic dissection, pericarditis, acute coronary syndromes |
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What affects the nature of cardiac pain in coronary artery occlusion?
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Location of lesion
Amount of lumen narrowing Duration of ischemia |
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What information is used to determine CAD?
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History: HPI, risk factors
ECG Serum biomarkers Stress testing Angiography IVUS (if they have AWESOME insurance or they're at that step in the formulary) |
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What is the classic presentation for an acute coronary event (eg ischemia)? Atypical presentation? Associated symptoms?
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Classic: substernal pressure with radiation along T1-T6 dermatomes, especially left
Atypical: overwhelming fatigue, sense of impending doom, anxiety Associated symptoms: N/V, diaphoresis, dyspnea, lightheadedness |
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What is included in the Framingham risk score?
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Age, gender, smoking, LDL-C, blood pressure
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Describe the treadmill stress test
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Watch for flat ST depression >2mm x 0.08ms
Stable or decreasing BP and HR Can use adenosine to simulate exercise if the person is physically incapable of moving themselves and it's mind-blowing that they haven't died yet |
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Describe the Thallium (or Technetium) stress test
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Inject Thallium during stressed phase of treadmill stress test
Nuclear scans detect regional ischemia Repeat a nuclear scan 4h later to confirm reversibility of ischemia |
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Describe the pathophysiology of unstable angina - most common cause? What is happening? What is included in the DDx?
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Decreased oxygen supply and increasing myocardial demand superimposed on cardiac obstruction
Most common ins plaque rupture with subtotal DDx: consider spasm, fixed lesion, progressive lesion |
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What are some ECG findings in unstable angina?
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Normal or non-specific
30-50% may have inverted T waves Occasional ST segment depressions (transient ischemia) Check ECG with CP and without for compensation |
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What is Variant (Prinzmetal's) Angina?
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Coronary vasospasm without increased myocardial oxygen demand
Often adjacent to plaque, an active phase of spasms over 1-2 years, no evidence of plaque rupture, dysrhythmias are common, some role played by increased sympathetic tone |
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In what populations is Prinzmetal's Angina more common?
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Typical patient is younger, with fewer risk factors - more common in smokers and cocaine users
ECG shows transient ST elevations Good prognosis overall - some short term risk of MI, mostly from concurrent CAD |
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How does one evaluate and treat a patient with Prinzmetal's Angina?
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Angiography with induction of spasm (via Ergonovine or hyperventilation)
Treatment: Nitroglycerin and a CCB - evaluate for CHD risk, refractory disease managed with surgical sympathetic denervation, in cocaine users avoid CCB and use benzodiazepam for short-term management |
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What is NSTEMI? How does it present?
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Non-ST elevation MI
No ST elevation in ECG Positive evidence of myocardial necrosis (biomarkers) Angina or anginal equivalent Diaphoresis, cool/clammy skin, tachycardia, S3/S4, bibasilar rales, HoTN ECG may have T wave inversions, ST depressions, transient ST elevations (subendocardial ischemia) |
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How is NSTEMI treated?
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Bedrest with continuous telemetry monitor
Sublingual Nitroglycerin, then paste or gtt (drip) BB to goal HR 50-60 Morphine for breakthrough pain Transfuse to goal Hct > 30% Manage coagulation, electrolytes, glucose Determine risk of the patient If low risk, stress test within 72h If high, coronary angiography within 48h (consider GPIIb/IIIa inhibitor) |
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How are coagulation, electrolyte balance, and glycemic control treated in NSTEMI patients?
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Antithrombotics: chew 4 baby ASA, Thienopyridine, LMWH
Glycemic control: goal is glucose 120-150 Electrolyte balance: K+ > 4.0; Mg2+ > 2.0 |
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What should a patient be given for long-term management post-NSTEMI?
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Risk factor modification
Nitroglycerin SL prn, or long-acting BB to decrease triggers and maintain target HR Statins for plaque stabilization ACE-I or ARB for preventing LV remodeling Antithrombotics |
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What is STEMI? How does it present?
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Angina or anginal equivalent
Elevated cardiac biomarkers Elevated ST segments on ECG (transmural ischemia) Pain more severe, lasts longer than anginal pain, not relieved with rest Pt more restless, anxious, sense of impeding doom |
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What may be find in a STEMI physical exam?
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Decreased S1, split S2, S3, S4
Apical impulse diminished Dysrhythmias Hypotension |
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How is a STEMI treated?
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Decrease myocardial oxygen demand: O2, nitroglycerine, bed rest, BB, morphine, transfusion
Antithrombotics - ASA, Thienopyridine, Heparin gtt, Gp IIb/IIIa inhibitors Reperfusion - ST elevated > 2mm in 2 precordial leads or > 1mm in 2 limb leads Hypothermia in VF/VT arrest |
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What are some reperfusion strategies?
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Thrombolytics - systemic "clot-busters" - use within 30 minutes of patient arrival
Percutaneous coronary intervention - balloon angioplasty, localizing thrombolysis, stenting CABG |
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What medications should a patient be started on post-STEMI?
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ACE-I within 24h - reduces ventricular remodeling, decreases risk of CHF, decreases reinfarction rate
BB - PO Statin therapy prior to discharge Consider long-acting nitrate for angina |
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Before discharging a patient post-STEMI, what should be done aside from start them on meds and arrange for follow up care?
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Assess LV function with ECG
Follow ECG to look for Q waves - determine final diagnosis of QWMI or NQWMI |
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What effect do the S-ANS fibers from T1-T6 have related to the heart?
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Increase HR and contractility
Dilate coronary arteries Control diameter of thoracic duct and lymphatic channels |
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What are changes in S-ANS post-MI?
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Increased tone inhibits development of collaterals
Increased risk of coronary vasospasm Vasoconstriction raises total peripheral resistance and increases cardiac work load |
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What are the P-ANS effects on the heart? From where do those fibers originate?
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P-ANS fibers originate in vagus nerve
Effect increased tone to slow HR and conduction Decreased tone accelerates HR and conduction Vagal efferents go to SA node (right) and AV node (left) |
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What are some OMM strategies for an inpatient post-MI?
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Calm sympathetic hyperactivity to prevent arrhythmias
Promote lymphatic drainage but don't overload a weakened heart Focus on acute changes - don't try to fix a lifetime of SD in the acute setting |
