Microbiology DSA Flashcards

1
Q

Essentials of diagnosis of Acute Inflammatory Pericarditis

A

o Anterior pleuritic chest pain worse supine than upright
o Pericardial rub
o Fever common
o Erythocyte sedimentation rate elevated
o ECG: diffuse ST-segment elevation with associated PR depression

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2
Q

Viral causes of pericarditis

A
o	Coxsackieviruses
o	Echoviruses
o	Influenza
o	Epstein Barr
o	Varicella
o	Hepatitis
o	Mumps
o	HIV
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3
Q

Viral pericarditis dx

A

o dx made clinically, leukocytosis often present
o Rising viral titers – rarely done
o Cardiac enzymes slightly elevated – epicardial myocarditis component
o Echocardiogram normal, or trivial amount of extra fluid during acute inflammatory process

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4
Q

Tuberculous Pericarditis

A

direct lymphatic or hematogenous spread
o Clinical pulmonary involvement absent or minor, pleural effusions common
o S/S: subacute, fever, night sweats, fatigue for days to months
o Acid-fast bacilli found elsewhere
o Low yield of organisms by pericardiocentesis, pericardial biopsy higher yield but may also be negative, pericardiectomy may be required
o Tx: antituberculous drug therapy, constrictive pericarditis can occur

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5
Q

Bacterial pericarditis

A

direct extension from pulmonary infections
o Pneumococci
o Borrelia burgdorferi – myopericarditis, occasional heart block
o Patients appear toxic, often critically ill
o Suspected on clinical grounds, pericardiocentesis confirmatory

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6
Q

Uremic pericarditis

A

complication of CKD
o Untreated uremia and stable dialysis patients
o w/ or w/o symptoms – fever absent
o If not on dialysis – incidence correlates to level of BUN and Cr
o “Shaggy” pericardium and effusion is hemorrhagic and exudative
o Tx dialysis

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7
Q

Myxedema pericarditis

A

hypothyroidism

cholesterol crystals within fluids

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8
Q

Neoplastic pericarditis

A

most frequent causes of pericardium tamponade
• Hodgkin Disease
• Lymphomas
• Painless, presenting symptoms related to hemodynamic compromise or primary disease
• Pericardial effusion may be very large, consistent with chronic nature
• Cytologic examination of effusion or pericardial biopsy
• Difficult to establish clinically if medialstinal radiation within previous year
• Pericardial effusions develop over long period of time, may become quite large (2L+)
• Poor prognosis, drain effusion percutaneously initially, pericardial window
• Chemotherapeutic agents or tetracycline reduce recurrence rate

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9
Q

Radiation pericarditis

A

4000 cGy delivered to 30%+ of heart
• Initiate fibrinous and fibrotic process in pericardium
• Presents as subacute pericarditis or constriction
• Within first year, may delayed for many years before constriction evident
• Symptomatic therapy, recurrent effusions and constriction require surgery

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10
Q

Drug toxicity causing pericarditis

A
  • Minoxidil
  • Penicillins
  • Clozapine
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11
Q

Dressler Syndrome

A

postcardiotomy pericarditis, post MI
o Days to weeks after MI or open heart surgery
o Recurrence of pain with pleural-pericardial features
o Rub audible
o Repolarization changes on ECG may be confused with ischemia
o Pain, fever, malaise, leukocytosis
o Autoimmune disorder symptoms – joint pain, fever
o Tamponade rare after MI, but not postoperatively
o High sedimentation rate helps confirm dx
o Large pericardial effusions and accompanying pleural effusions frequent

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12
Q

Pericarditis post MI

A

occur 2-5 days after infarct due to inflammatory reaction to transmural myocardial necrosis

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13
Q

S/S of pericarditis

A
  • Substernal pain, may radiate to neck, shoulders, back, or epigastrium
  • Dyspnea
  • Febrile
  • Characteristic pericardial friction rub with or without evidence of fluid accumulation or constriction
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14
Q

ECG findings in pericarditis

A
  • ST and T wave changes
  • Begins with diffuse ST elevation
  • Followed by return to baseline
  • Then to T wave inversion

• Atrial injury manifested by PR depression in limb leads

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15
Q

CXR findings in pericarditis

A

frequently normal, may show cardiac enlargement if pericardial fluid present
• Pulmonary disease signs
• Mass lesions and enlarged LNs suggest neoplastic process

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16
Q

Echocardiography in pericarditis

A

mild pericardial effusion in 60%

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17
Q

MRI and CT in pericarditis

A

visualize tumor

• Screening to ensure no extracardiac diseases contiguous to pericardium

18
Q

CRP and late gadolinium in pericarditis

A

elevated CRP

late gadolinium enhancement of pericardium

19
Q

Treatment of pericarditis

A

o Restrict activity until symptom resolution

o Athletes: restriction until resolution of symptoms and normalization of all lab tests – generally 3 mo

o Aspirin 750-1000 mg Q8h for 1-2 weeks with taper by decreasing dose 250-500 mg every 1-2 weeks or ibuprofen 600 mg Q8h for 1-2 weeks with taper by decreasing dose by 200-400 mg every 1-2 weeks.
• GI protection with colchicine 0.5-0.6 mg once (under 70 kg) or twice (over 70kg) daily for 3 months
• Taper: Reduce dose every other day for patients 70 kg or under, or once a day for over 70 kg in last week.

  • Use Aspirin and Colchine in postMI (Dressler syndrome)
  • NSAIDs have adverse effect on MI healing

• Use Colchine for at least 6 mo in all refractory cases and in recurrent pericarditis

o CRP used to assess effectiveness of treatment – once normal, tapering initiated

20
Q

Indomethacin

A

25-50 mg Q8h in recurrent pericarditis in place of ibuprofen

21
Q

Systemic corticosteroids

A

severe symptoms, refractory cases, with immune-mediated etiologies
• Higher risk of recurrence, prolonged illness
• Recommend colchicine with corticosteroids for at least 3 mo to help prevent recurrences
• Prednisone 0.25-0.5 mg/kg/d orally with taper over 4-6 week period

22
Q

Treatment if colchicine therapy fails or cannot be tolerated

A

immunosuppression required
• Cyclophosphamide, azathioprine, IV human Ig, interleukin-1 receptor agonsits (anakinra), methotrexate

o If colchicine and significant immunosuppression fails – surgical pericardial stripping considered in recurrent cases even without clinical evidence for constrictive pericarditis

23
Q

Tamponade

A

early complication, less than 5% of patients

treated with partial pericardiectomy (pericardial window)

24
Q

Characteristics of Picornaviridae family

A

Enteroviruses

i. Spread fecal-oral route, respiratory secretions, infect intestinal epithelial and lymphoid cells (tonsils, Peyer’s patches)
ii. Positive single stranded RNA viruses, smallest RNA viruses
iii. Naked icosahedral symmetry
iv. Replication in cytoplasm

25
Q

Symptoms of Picornaviridae family

A

i. Asymptomatic or mild febrile infections
ii. Respiratory symptoms “colds”
iii. Rashes
iv. Aseptic meningitis

26
Q

Coxsackie B pathology

A

a. Heart, brain, liver, pancreas, skeletal muscle damage

b. Pleurodynia:
i. Fever, headache, severe lower thoracic pain on breathing (pleuritic pain)

c. Myocarditis/Pericarditis
i. Infection and inflammation of the heart muscle and pericardial membrane
ii. Self-limited CP or more serious arrhythmias, cardiomyopathy, heart failure

27
Q

M. tuberculosis morphology

A

i. 40% lipid
ii. composed of mycolic acids
iii. Thin rods
iv. Non-motile

28
Q

M. tuberculosis metabolism

A

i. Aerobic
ii. Catalase-positive
iii. Slow growth rate

29
Q

M. tuberculosis virulence

A

i. Mycosides:
1. Cord factor – only found in virulent strains – release TNF (cachectin) causing wt loss
2. Sulfatides – inhibit phagosome-lysosome fusion
3. Wax D – acts as adjuvant

ii. Iron siderophore – mycobactin
iii. Faculative intracellular growth – can survive and multiply in macrophages
iv. Non-motile, no capsule, no attachment pili

30
Q

Clinical presentation of M. tuberculosis

A

i. Primary tuberculosis – asymptomatic or overt disease involving lungs or other organs
ii. Reactivation or secondary tuberculosis –
1. Pulmonary, pleural or pericardial, LN infection, kidney, skeletal, joints, CNS, miliary TB

31
Q

Diagnostic studies for M. tuberculosis

A

i. Acid-fast stain
ii. Rapid culture – bactec radiometric culture – liquid broth in a bottle with radioactive palmitate, measurble carbon source, allowing for early detection (1-2 weeks) before colony seen
iii. PPD skin test - positive
1. >5mm in immunosuppressed host
2. >10 mm – chronic disease or risk factors for exposure to TB
3. >15 mm all others
4. Can get false negatives in AIDS or malnourished
iv. IGRA – interferon gamma release assay
v. CXR
vi. Gene Xpert MTB/Rif (similar PCR studies)

32
Q

First line medications for Mycobacterium endocarditis

A

a. Isoniazid – INH
b. Rifampin
c. Pyrazinamide
d. Ethambutol
e. Streptomycin

33
Q

Immunologically mediated pericarditis agents

A

i. Rheumatic fever
ii. SLE
iii. Scleroderma
iv. Postcardiotomy
v. Postmyocardial infarction (Dressler) syndrome
vi. Drug hypersensitivity reaction

34
Q

Fibrinous and serofibrinous pericarditis

A

i. Serous fluid variably admixed with fibrinous exudate
1. Fibrin may be lysed with resolution of the exudate or can become organized

ii. Fibrinous: Surface is dry with fine granular roughening.
iii. Serofibrinous: more intense inflammatory process, larger amounts of yellow to brown turbid fluid containing leukocytes, erythrocytes, and fibrin

35
Q

Fibrinous pericarditis S/S

A

i. pain – sharp, pleuritic, position dependent
ii. fever
iii. CHF may be present
iv. Characteristic loud pericardial friction rub
1. Serous fluid can prevent rubbing by separating the two layers of pericardium

36
Q

Purulent or Suppurative Pericarditis

A

active infection in pericardial space

  1. Spread:
    a. Direct extension: empyema of pleural cavity, lobar pneumonia, medialstinal infections, extension of ring abscess through myocardium or aortic root
    b. Seeding from blood
    c. Lymphatic extension
    d. Direction introduction during cardiotomy
  2. Exudate: thin cloudy fluid to frank pus up to 400-500 mL
  3. Serosal surfaces reddened, granular, coated with exudate
  4. Acute inflammatory reaction can induce medialstinopericarditis
  5. Complete resolution infrequent, organization by scarring is usual outcome producing constrictive pericarditis
  6. Clinical findings: resemble fibrinous pericarditis, frank infection leads to marked systemic symptoms: spiking fevers, rigors
37
Q

Caseous pericarditis

A

TB origin

  1. Infrequently fungal origin
  2. Antecedent of disabling, fibrocalcific, chronic constrictive pericarditis
38
Q

Hemorrhagic pericarditis

A

neoplastic

  1. Exudate: blood mixed with fibrinous or suppurative effusion
  2. Spread of malignant neoplasm into pericardial space
  3. Fluid contains neoplastic cells
39
Q

Adhesive mediastinopericarditis

A

follow infectious pericarditis, surgery, irradiation

i. Pericardial sac obliterated, adherence of external aspect to surrounding structures strains cardiac function
ii. Each systolic contraction – heart pulls against parietal pericardium and attached surrounding structures
iii. Systolic retraction of rib cage and diaphragm, pulsus paradoxus
iv. Increased workload causes severe cardiac hypertrophy and dilation

40
Q

Constrictive pericarditis

A

i. Heart encased in dense fibrous or fibrocalcific scar limiting diastolic expansion and cardiac output
1. Mimics restrictive cardiomyopathy
ii. Pericardial space obliterated, sometimes calcified
iii. Concretio cordis – extreme cases resemble plaster mold
iv. Cardiac hypertrophy and dilation cannot occur
v. Cardiac output reduced at rest, little capacity to increase output in response to systemic demands
vi. Distant or muffled heart sounds, elevated jugular venous pressure, peripheral edema
vii. Tx: surgical resection of the shell of constricting fibrous tissue - pericardiectomy