Cardiovascular Microbiology Flashcards by Sarah Gillen

Myocarditis can present as a wide array of symptoms with variable presentation. What are some clinical features of myocarditis?

FEVER, precordial discomfort (chest pain), dyspnea, fatigue

Others include unexplained sinus tachycardia, S3 or S4 or summation gallop, abnormal ECG, abnormal echo, new cardiomegaly on CXR, arrhythmia, partial or complete heart block, new-onset BBB, new-onset or worsening heart failure, acute pericarditis, cardiogenic shock, sudden cardiac death, respiratory distress/tachypnea, hepatomegaly

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Physical exam findings of myocarditis

Soft S3/S4 (impaired ventricular function), new murmur (secondary to valvular insufficiency), pericardial friction rub (if there is extension into pericardium)

Think systolic CHF — decreased contractility, orthopnea, dyspnea on exertion, crackles, PND

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Workup considerations for suspected myocarditis

EKG — assess for arrhythmia (sinus tachycardia most common), transient ST-T wave abnormalities (findings can be nonspecific)

CXR — pt is presenting with CP and/or sx of CHF — must consider all etiologies especially: pulmonary disease, heart failure, dissection. Assess for cardiomegaly

Echocardiogram — assessment of ventricular function and structure; eval of EF, LV size, wall motion abnormalities

PCR — detection of viral genome

Labs — CBC (for leukocytosis), cardiac enzymes (likely elevated secondary to myocyte damage), BNP (heart failure), CPK (muscle damage), ESR and CRP = acute phase reactants

Endomyocardial biopsy can aid in definitive dx

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3 major complications of myocarditis

Dilated cardiomyopathy

Myopericarditis (myocarditis extended into pericardium)

Sudden cardiac death (20%)

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Tx for myocarditis; how is prognosis determined?

Heart failure therapy, therapy for arrhythmias

Beta blocker, ACEI, diuretics

Avoid NSAIDs, EtOH, and exercise (restricted)

Prognosis is dependent upon clinicopathologic types of myocarditis

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Infectious etiologies for myocarditis

Typically Coxsackie B, Trypanosoma cruzi, or Trichinella spiralis

Other considerations: HIV, Chalmydophyla psittaci, Rickettsial sp., Corynebacterium diphtheriae, Neisseria meningitidis, Borrelia burgorferi, Candida

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Morphology, transmission, and peak incidence times for coxsackie B virus

+ssRNA virus, small, naked, icosahedral

Transmission = fecal oral

Peak incidence = summer, fall

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Clinical manifestations of coxsackie B infection

URI, pleurodynia (“devil’s grip” - severe intercostal pain and fever), myocarditis (most common infectious etiology), aseptic meningitis

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Endemic locations and transmission of trypanosoma cruzi (hemoflagellate)

Location: southern US, Mexico, South America

Transmission = reduviid bug, animal carriers

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Phases of Chagas dz

Acute: chagoma, romana sign, fever, malaise, LAD, myocarditis, severe meningoencephalitis (usually in younger pts)

Intermediate: asymptomatic

Chronic: dilated cardiomyopathy, arrhythmia, megacolon, achalasia

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Diagnostics for chagas dz

Peripheral smear for trypomastigotes, xenodiagnosis

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Invasive nematode transmitted via ingestion of cysts from raw pork (boars or horses too)

Trichinella spiralis

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Humans are dead-end hosts for trichinella spiralis - describe its lifecycle

Larvae develop in gut —> mate —> larvae disseminate hematogenously —> penetrate muscle tissue

Affect skeletal m, heart, and brain

It is an invasive cycle that can be lethal with heavy infection

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Symptoms and diagnostics associated with trichinella spiralis infxn

Abdominal pain, diarrhea, fever (while in small intestine); after muscle invasion get myalgias and other sx based on location

Consider the dx if — periorbital edema, mositis, eosinophilia

Dx: Serologic (ELISA, etc.) or latex agglutination, CPK levels, muscle bx

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Infectious agents implicated in pericarditis

Viruses, bacteria, TB (caseating pericarditis), fungi, parasites

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Presentation and clinical features for infectious pericarditis

Chest pain — often sharp, positional, and pleuritic in nature, relieved by leaning forwards

Fever

Palpitations

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Physical exam findings in infectious pericarditis

Friction rub upon cardiac auscultation, rapid or irregular pulse

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What would you see on EKG for infectious pericarditis?

Diffuse ST elevations with reciprocal depressions in leads aVR and V1

PR depression

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What would you find on CXR with infectious pericarditis?

Minimal abnormalities in the majority

Exception: pericardial effusion > 250 mL will cause symmetrically enlarged cardiac sillhouette = “water bottle” sign [diaphragm will appear flat to compensate for weight of effusion]

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If you suspect infectious pericarditis, what test should you do to assess for pericardial effusion and/or tamponade, as it is more sensitive than a CXR?

Transthoracic echocardiogram

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Labs to do when infectious pericarditis suspected

Serial cardiac enzymes
CBC with diff
ESR
CRP
Blood cultures if temp >38 C

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Major complication of infectious pericarditis

Cardiac tamponade (tx with pericardiocentesis) — counsel about activity restrictions

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Tx for infectious pericarditis

High dose ASA TID and colchicine

[ibuprofen, indomethacin options too] — or tx underlying cause!

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_______ are CONTRAINDICATED in pericarditis

Anticoagulants

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Ziehl Neelson and Auramine-rhodamine stains are used to identify which organism that can potentially cause infectious pericarditis?

Mycobacterium tuberculosis [Ziehl Neelson is acid-fast stain that shows red rods; Auramine-rhodamine shows apple green color]

Morphology of M.tuberculosis + virulence factors

Acid fast bacillus (weakly G+), obligate aerobes, facultative intracellular (macrophages) [AFB secondary to mycolic acid cell wall composition — highly resistant to desiccation including NaOH] Virulence: facultative intracellular, sulfatides, cord factor, surface protein can cause a delayed hypersensitivity and cell mediated immunity reaction (utilized for PPD test), Wax D

The major manifestation of mycobacterium tuberculosis is pulmonary TB, how does it cause a caseating pericarditis?

Through direct lymphatic or hematogenous dissemination of the bacteria

Risk factors for infective endocarditis

Age > 60, M>F Poor dentition, IV drug abuse, structural heart dz, congenital heart dz, valvular heart dz, prosthetic valve replacement, RHD

IE manifestations can be variable and generally depend on virulence of organism involved. What are some general clinical manifestations seen with IE?

Constituational sx = onset of sx nonspecific in nature then progress toward fever, chills, weight loss, new/worsening murmur, fatigue, arthralgia, and myalgia

Differentiate some clinical manifestations in acute IE vs. subacute IE

Major difference = timeline — acute will have much more rapid onset (<7d) Acute: rapid progression of sx and cardiac damage; high fever, chills, weakness, SOB, pleuritic CP Subacute: indolent course; low grade fever, weight loss over time, fatigue, arthralgia/myalgia

Complications of IE

CHF, abscess formation, hematogenous spread, embolism, systemic immune reaction, death

Cardiac manifestations in IE (including difference betwen acute vs. subacute)

Heart murmurs - new or worsening Acute IE: R side of heart > L side (tricuspid > aortic; especially with S.aureus involvement) Subacute IE: L side of heart > R side of heart

Diagnostic workup for infective IE

Blood culture x3, CBC with diff, CMP EKG, ESR, CRP, UA (assess for hematuria) Transesophageal echo, CXR

What set of criteria are used for the dx of endocarditis, and how many are needed to qualify for definitive dx?

Modified DUKE criteria for diagnosis of endocarditis (consists of major and minor) Definite dx requires one of the following: 1. Meets 2 major criteria 2. Meets 1 major and 3 minor 3. Meets 5 minor

For infectious endocarditis that presents with cardiogenic shock, primary tx is _____ ASAP. If the pt is toxic, empiric abx should be started immediately, typically including _______ and _______. Culture and sensitivities will then determine how to tailor tx. However, this may not be necessary if the infection is ________

Surgery; vancomycin; gentamycin; subacute

Abx prophylaxis for pts at high risk for IE prior to dental or respiratory procedures

Able to take PO: amoxicillin Need IV: ampicillin or cefazolin or ceftriaxone Allergic to PCN: desensitize or cephalexin or clindamycin or azithromycin

Common vs. rare infectious etiologies for IE

Common = S.aureus, S.epidermidis, S.viridans, Enterococcus (Group D Strep) Rare = HACEK, Coxiella burnetti, brucella sp., S.agalactiae

Morphology of S.aureus

G+ cocci in clusters Coagulase and catalase + Facultative anaerobe [normal flora on skin — can breach and colonize respiratory tract]

Virulence factors of S.aureus

Host cell evasion: Protein A, coagulase, catalase, hemolysins, leukocydins Invasion of tissue and bloodstream (hyaluronidase, staphylokinase, lipase) Toxin

Toxin mediated manifestations of S.aureus

Food poisoning, scalded skin syndrome, TSS

Local manifestations of S.aureus

Skin — impetigo, cellulitis, furuncles, carbuncles Respiratory — pneumonia (cavitary)

Systemic manifestations of S.aureus

Acute endocarditis (tricuspid valve), meningitis, osteomyelitis (#1 cause in adults and kids), septic arthritis

For MSSA [methicillin-susceptible S.aureus], _______ is a great starting point of tx

Nafcillin

Morphology of S.viridans

Gram+ cocci in chains, alpha-hemolytic, catalase negative, facultative anaerobe, optochin resistant Normal oral flora, nasopharynx, and GI tract

Virulence factors and manifestations of S.viridans infection

Extracellular dextran binds heart valves Manifestations = dental caries, subacute endocarditis

Tx for S.viridans

PCN

Morphology of S.epidermidis

``` Gram+ cocci in clusters Coagulase negative Catalase + Novobicin sensitive Facultative anaerobe ``` [normal flora on skin]

Virulence of S.epidermidis

Adhesion polysaccharide capsule — adherence to prosthetic devices, indwelling catheters Biofilm formation

Manifestations of S.epidermidis

Subacute endocarditis, infection and bacteremia in neutropenic pts (susceptible)

Tx of S.epidermidis

Extremely abx resistant — use Vancomycin

Organism that is part of normal flora in human bowel that has extracellular dextran to bind heart valves; gram+ cocci that is catalase negative, facultative anaerobe, variable hemolyic nature (alpha or gamma)

Enterococcus faecalis

Manifestations of E.faecalis infxn

Subacute bacterial endocarditis, UTI, biliary tract infxns

Media requirements for E.faecalis

Can grow on 40% bile AND 6.5% NaCl, blood agar

T/F: vancomycin resistant forms of enterococcus faecalis are not of concern at this time

False — vancomycin resistant forms are on the rise!

What organism associated with subacute bacterial endocarditis is associated with colon cancer and IBD?

Streptococcus bovis (group D strep)

Morphology of S.bovis

Gram+ cocci in chains, catalase negative, facultative anaerobe, variable hemolytic nature [normal flora in human bowel; has virulence factor of extracellular dextran to help bind heart valves]

Manifestations and media specifics for S.bovis

Biliary tract infxns, UTIs, subacute bacterial endocarditis Media: 40% bile, blood agar

The HACEK organisms are a gram _____ group of bacilli, fastidious, suspected cause of “culture negative” endocarditis. Media option of _______ agar should be considered. They are part of the normal ____ flora

Negative; chocolate; oral

What are the HACEK organisms?

``` Haemophilus sp (H.parainfluenzae most common) Aggregatibacter sp Cardiobacterium sp Eikenella corrodens Kingella sp ```

T/F: haemophilus sp should be grown on blood agar

False — Haemophilus have the ability to be grown on chocolate agar (contains Factors V and X, aka NAD+ and Hemin); Haemophilus CANNOT be grown on blood agar One exception — will show stellate growth on blood agar if placed on same place as S.aureus because S.aureus has hemolysins to lyse RBCs

Gram- pleomorphic obligate intracellular, aerobic, zoonotic, aerosol transmitted organism

Coxiella burnetti

Major illness caused by coxiella burnetti

Q fever — flu-like sickness carried by goats, sheep, cows, and other animals Animals spread the germ when they give birth; farmers and vets at higher risk Wind can carry barnyard dust mixed with Q fever germs for miles

A 48 y/o female presents to your office with the CC of fatigue, fever, and abdominal pain. Sx have been occurring over the past 3 weeks. She never feels completely rested and is beginning to take frequent naps. Her abdominal pain is diffuse, 3/10, occasional nausea with no vomiting, no radiation. At home temps have been 38.4◦C and have not been abated with Tylenol. She denies recent travel, sick contacts, insect bites, or rashes. She also denies orthopnea or edema. PMH of PNA 3 weeks ago w/ PICC line for abx infusion. PE is significant for retinal hemorrhages, petechiae on buccal mucosa, III/VI holosystolic murmur at 5th ICS MCL on L, no thrills. CTAB with crackles at b/l lung bases, linear hemorrhages present in b/l nail beds. Based on pts presentation and PE you are suspecting which of the following? a. pericarditis b. acute IE c. subacute IE d. myocarditis e. malingering

c. subacute IE

A 48 y/o female presents to your office with the CC of fatigue, fever, and abdominal pain. Sx have been occurring over the past 3 weeks. She never feels completely rested and is beginning to take frequent naps. Her abdominal pain is diffuse, 3/10, occasional nausea with no vomiting, no radiation. At home temps have been 38.4◦C and have not been abated with Tylenol. She denies recent travel, sick contacts, insect bites, or rashes. She also denies orthopnea or edema. PMH of PNA 3 weeks ago w/ PICC line for abx infusion. PE is significant for retinal hemorrhages, petechiae on buccal mucosa, III/VI holosystolic murmur at 5th ICS MCL on L, no thrills. CTAB with crackles at b/l lung bases, linear hemorrhages present in b/l nail beds. Based on your clinical suspicions, your workup includes blood cultures x3 + which of the following? a. cardiac bx b. trans esophageal US c. trans thoracic US d. abdominal CT e. bronchoscopy

b. trans esophageal US

A 48 y/o female presents to your office with the CC of fatigue, fever, and abdominal pain. Sx have been occurring over the past 3 weeks. She never feels completely rested and is beginning to take frequent naps. Her abdominal pain is diffuse, 3/10, occasional nausea with no vomiting, no radiation. At home temps have been 38.4◦C and have not been abated with Tylenol. She denies recent travel, sick contacts, insect bites, or rashes. She also denies orthopnea or edema. PMH of PNA 3 weeks ago w/ PICC line for abx infusion. PE is significant for retinal hemorrhages, petechiae on buccal mucosa, III/VI holosystolic murmur at 5th ICS MCL on L, no thrills. CTAB with crackles at b/l lung bases, linear hemorrhages present in b/l nail beds. Blood cultures reveal G+ cocci in clusters that are catalase positive, coagulase negative. Based on this information and patient presentation, the most likely etiologic organism is? a. S.aureus b. S.viridans c. E.faecalis d. S.bovis e. S.epidermidis

e. S.epidermidis

A 48 y/o female presents to your office with the CC of fatigue, fever, and abdominal pain. Sx have been occurring over the past 3 weeks. She never feels completely rested and is beginning to take frequent naps. Her abdominal pain is diffuse, 3/10, occasional nausea with no vomiting, no radiation. At home temps have been 38.4◦C and have not been abated with Tylenol. She denies recent travel, sick contacts, insect bites, or rashes. She also denies orthopnea or edema. PMH of PNA 3 weeks ago w/ PICC line for abx infusion. PE is significant for retinal hemorrhages, petechiae on buccal mucosa, III/VI holosystolic murmur at 5th ICS MCL on L, no thrills. CTAB with crackles at b/l lung bases, linear hemorrhages present in b/l nail beds. You suspect that the patient acquired their infection secondary to the PICC line. Cultures confirm that S.epidermidis is the infectious etiology. What virulence factor contributed in this patient’s pathology? a. Protein A b. EC dextran that binds cardiac valves c. Adhesion polysaccharide capsule d. Elaboration of coagulase e. Protein M

c. Adhesion polysaccharide capsule

A 58 y/o male with a PMH of HCV presents with dyspnea and pleuritic chest pain that has progressed over the past 2 days. He states that he was in his previous state of health until this point. The chest pain is pronounced when inhaling and feels like a burning sensation, 7/10, with associated hemoptysis. Pt also states he has developed a non-pruritic rash on his B/L LE. He states that he has also developed fevers, chills, and myalgias. He denies sick contacts, recent travel, exposures to pulmonary irritants, or insect bites. Hx reveals 30 pack year hx, in recovery for drug use. PE reveals hypotension, tachycardia, febrile at 40 C, and 89% on RA, coughing frequently, pale and toxic appearing, diaphoretic, pinpoint pupils, IV/VI blowing holosystolic murmur at LLSB 4th ICS with palpable thrill, CR 4 sec; diffuse coarse crackles in all lung fields, intercostal retractions, poor thoracic expansion and use of accessory mm for breathing, as well as splenomegaly. He also has 3/5 muscle strength in b/l UE and LE as well as diffuse palpable purport on b/l LE, non-blanchable. Based on pt presentation and PE, what is your #1 DDx? a. Active TB b. SCLC c. Acute IE d. Pericarditis e. Subacute IE

c. acute IE

A 58 y/o male with a PMH of HCV presents with dyspnea and pleuritic chest pain that has progressed over the past 2 days. He states that he was in his previous state of health until this point. The chest pain is pronounced when inhaling and feels like a burning sensation, 7/10, with associated hemoptysis. Pt also states he has developed a non-pruritic rash on his B/L LE. He states that he has also developed fevers, chills, and myalgias. He denies sick contacts, recent travel, exposures to pulmonary irritants, or insect bites. Hx reveals 30 pack year hx, in recovery for drug use. PE reveals hypotension, tachycardia, febrile at 40 C, and 89% on RA, coughing frequently, pale and toxic appearing, diaphoretic, pinpoint pupils, IV/VI blowing holosystolic murmur at LLSB 4th ICS with palpable thrill, CR 4 sec; diffuse coarse crackles in all lung fields, intercostal retractions, poor thoracic expansion and use of accessory mm for breathing, as well as splenomegaly. He also has 3/5 muscle strength in b/l UE and LE as well as diffuse palpable purport on b/l LE, non-blanchable. Blood cultures are taken and grown G(+) cocci in clusters that are catalase and coagulase positive. What virulence factor likely contributes to symptom severity? a. EC dextran b. protein A c. biofilm formation d. polysaccharide capsule e. opa proteins

b. protein a

A 58 y/o male with a PMH of HCV presents with dyspnea and pleuritic chest pain that has progressed over the past 2 days. He states that he was in his previous state of health until this point. The chest pain is pronounced when inhaling and feels like a burning sensation, 7/10, with associated hemoptysis. Pt also states he has developed a non-pruritic rash on his B/L LE. He states that he has also developed fevers, chills, and myalgias. He denies sick contacts, recent travel, exposures to pulmonary irritants, or insect bites. Hx reveals 30 pack year hx, in recovery for drug use. PE reveals hypotension, tachycardia, febrile at 40 C, and 89% on RA, coughing frequently, pale and toxic appearing, diaphoretic, pinpoint pupils, IV/VI blowing holosystolic murmur at LLSB 4th ICS with palpable thrill, CR 4 sec; diffuse coarse crackles in all lung fields, intercostal retractions, poor thoracic expansion and use of accessory mm for breathing, as well as splenomegaly. He also has 3/5 muscle strength in b/l UE and LE as well as diffuse palpable purport on b/l LE, non-blanchable. Blood cultures x 3 are immediately sent to the lab. Of the following, which is the best empiric treatment for this patient? a. penicillin and ergocalciferol b. vancomycin +/- gentamycin c. nafcillin and ceftriaxone d. TMP-SMX and ceftriaxone e. amoxicillin and vancomycin

b. vancomycin +/- gentamycin

A 64 y/o male presents to the ED with CP, fever, fatigue, cough, and arthralgias. He admits to experiencing night sweats. His PMH is significant for rheumatic heart disease and a dental procedure a few weeks before admission. He currently does not show any vasculitis or immunologic phenomena of endocarditis on PE, although endocarditis is suspected. What is the likely etiology? a. HACEK organisms b. S.viridans c. E.faecalis d. S.aureus e. S.bovis

b. S.viridans

A 67 y/o male with a PMHx of poorly controlled T1DM is being managed in the ICU after a diagnosis of DKA stemming from an infection. He is currently on Day 2 of IV Vancomycin. 4 days into his hospital stay, he develops a fever. Labs reveal a G(+) cocci that grows in chains. The organism demonstrates growth on 40%bile media and 6.5% NaCl. What is the likely infectious etiology? a. S.bovis b. S.epidermidis c. S.viridans d. E.faecalis e. H.influenzae

d. E.faecalis

A 68 y/o female with a PMHx of MVP with mitral valve replacement presents with fevers of 2 weeks duration. In addition to positive blood cultures, which of the following would confirm a diagnosis of infective endocarditis? a. CXR showing pulmonary edema and anemia b. retinal hemorrhages, temp >38 C c. elevated ESR, thrombocytopenia d. petechial rash, leukocytosis

b. retinal hemorrhages, temp >38

23 y/o male presents with retrosternal chest pain that radiates to the neck and left shoulder. He reports a low grade fever for 3 weeks duration, cough, and difficulty swallowing. He also reports night sweats. He recently emigrated from Peru where he spent the last year in prison for having one kilo of “high quality blow” in his personal possession. He is leaning forwards in the chair during history taking. His PPD skin test is 10mm. His CD4 count is 350, CBC shows leukocytosis at 12,000. EKG shows ST elevations. The most likely cause of his illness? a. evolving acute MI b. pneumocystis pneumonia secondar to HIV/AIDS c. M.tuberculosis pericarditis d. hyperkalemia e. Q fever secondary to coxiella burnetti

c. M.tuberculosis pericarditis

treatment for M.tuberculosis pericarditis? A. Vancomycin + ceftriaxone B. Isoniazid + rifampin + ethambutol+ pyrazinamide C. High dose corticosteroids + colchicine D. High dose aspirin + colchicine E. High dose Indomethacin

B. Isoniazid + rifampin + ethambutol + pyrazinamide

A 28 y/o male with a recent URI presents with substernal chest pain that radiates to B/L shoulders. The pain is central in nature with associated diaphoresis and fever. Cardiac auscultation reveals the following: The most likely etiology of his chest pain is? a. single stranded 8 segmented RNA virus b. dsDNA enveloped virus c. retrovirus d. -ssRNA virus e. +ssRNA naked virus

e. +ssRNA naked virus

The patient in the previous question was subsequently diagnosed with viral pericarditis. Prior to presentation, the patient likely had a recent history of? a. herpangia b. URI c. reduviid bite d. hand, foot, mouth dz e. dysphagia

b. URI

Our patient was diagnosed with acute pericarditis secondary to Coxsackie virus. Patient began a regimen of high dose ASA and colchicine. Aside from EKG stabilization, which laboratory can we monitor to ensure treatment effectiveness? a. CBC b. INR c. CMP d. CRP e. Hemoccult

d. CRP

A 60 y/o female with no significant PMH presents with pleuritic chest pain of 72 hours duration. She is leaning forward and sitting upright. Her temperature is 40°C and she is hemodynamically stable. Of the following, which laboratory result could you expect for this patient’s presentation? a. elevation of cardiac enzymes b. leukopenia c. hematuria d. elevated BUN/Cr e. WNL ESR

a. elevation of cardiac enzymes

A 24 y/o professional football player that was recently discharged from the hospital with viral pericarditis presents to the office for followup. He states he is compliant with his ASA and colchicine treatment and wonders when he can get back on the field. The best response for this athlete is? a. you are cleared for practice b. expect a 3 mo break c. suspended indefinitely d. when an ST normalization is present on EKG e. when there are T wave inversions on EKG

b. expect a 3 mo break