Pulmonology and ABX Flashcards

1
Q

What is a COPD exacerbation and what can cause it?

A

Exacerbation- increased SOB or cough, change in sputum color/quantity, wheezes, prolonged expiration, and use of accessory muscles.

It can be triggered by a URI, physical exertion, and air pollution.
—Infectious causes are H flu, M Catarrhalis, and Strep Pneumo

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2
Q

Treatment for COPD exacerbations

A

—Oxygen
—Nebulized albuterol + Ipratropium
— Oral glucocorticoids

ABX:
—Azithromycin, Levofloxacin/Moxifloxacin, Augmentin, or Doxycycline for 5-7 days

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3
Q

Community Acquired Pneumonia Sx and Causative organisms

A

Fever, productive cough, and infiltrates on CXR

Strep Pneumoniae most commonly
H. Flu
M. Catarrhalis

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4
Q

Community Acquired PNA Treatment

A

Outpatient:
—Macrolide or Doxycycline first line
—FQN only used as first line if comorbid conditions or recent ABX use

Inpatient:
—Beta lactam + either Macrolide (pref) or Doxycycline
OR
—A broad spectrum FQUN

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5
Q

Atypical PNA cause and presentation

A

Caused by Mycoplasma.

Young pt with viral prodrome (Fever, HA, malaise, pharyngitis) + persistent dry cough

Non focal lung exam— scattered wheezes or crackles

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6
Q

Atypical PNA Chest X ray findings

A

Atypical pattern:
—Reticulonodular pattern most common
—Diffuse, patchy, or interstitial infiltrates

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7
Q

Atypical PNA treatment

A

Macrolides
—Azithromycin or Clarithromycin—

Or Doxycycline

**Mycoplasm lacks a cell wall so its naturally resistant to Beta Lactams

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8
Q

Macrolides MOA, Clinical use, and ADRs

A

PO and IV= erythromycin and azithromycin
PO only= Clarithromycin

MOA: Inhibits bacterial protein synthesis by blocking 50S ribosomal subunit

Clinical Use:
—CAP, atypical PNA, pertussis, MAC infections
—Gastroparesis
—Strep throat and AOM if PCN allergy

ADRs:
—GI distress
—QT Prolongation
—Rash
—Relative contraindication in pregnancy
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9
Q

What causes Pertussis and how does it present?

A

Caused by Bordatella pertussis (Gram -)

Catarrhal phase:
—URI sx lasting 1-2 weeks. MOST CONTAGIOUS during this period

Paroxysmal phase:
—Severe paroxysmal coughing fits with inspiratory whooping sound after coughing.
—May have post cough emesis
—often lasts 2-4 weeks

Convalescent phase:
—Resolution of the cough (coughing stage may last for up to 6 weeks)

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10
Q

Diagnosis of Pertussis

A

Clinical diagnosis

When available order both throat cultures and PCR
—Throat culture: most sensitive during first 2 weeks of illness
—PCR of nasopharyngeal swab: sensitive up to 4 weeks of illness

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11
Q

Is lymphocytosis common in pertussis?

A

Yes

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12
Q

Management of Pertussis

A

Supportive is mainstay of treatment:
—oxygenation, nebulization, mechanical ventilation as needed

Antibiotics are used to decrease contagiousness of pt:
—Macrolides are DOC: Azithromycin, erythromycin
—TMP SMX second line

Post exposure prophylaxis for all close contacts regardless of vaccine status

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13
Q

What abx is better tolerated and preferred in children <1 month of age?

A

Azithromycin

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14
Q

How is Pertussis transmitted?

A

Respiratory droplets during coughing fits. If pt is admitted should be on droplet precautions

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15
Q

Complications of pertussis

A

Pneumonia, encephalopathy, otitis media, sinusitis, and seizures.

Increased mortality in infants d/t apnea/cerebral hypoxia associated with coughing fits

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16
Q

Pertussis prevention

A

In the US, 5 doses of DTaP is typically recommended at 2 months, 4 months, 6 months, 15-18 months, and 4-6 years of age.

Booster dose is administered between 11-18 years of age

17
Q

What is the cause and pathophysiology of a Tuberculosis infection?

A

Infection of the respiratory system by Mycobacterium tuberculosis.

After inhalation of airborne droplets, Mtb goes to the alveoli, gets incorporated into the macrophages and can disseminate from there

18
Q

What are the outcomes of infection with tuberculosis?

A
  1. Primary TB
    —the outcome of initial infection (usually self limiting)
    —Primary Rapidly Progressing TB—> active initial infection with clinical progression. Common in children <4yo in endemic areas. These pts are contagious
  2. Chronic Latent Infection
    —About 90% of pts control the initial primary infection via caseating granuloma formation
  3. Secondary Reactivating TB
    —Reactivation of latent TB with waning immune defenses
    —5-10% lifetime incidence
    —Most commonly localized in APEX/UPPER LOBES with CAVITARY LESIONS
    —These pts are contagious
19
Q

What 3 criteria need to be met to be non infectious with a chronic (latent) TB infection?

A
  1. (+) PPD skin test
  2. So sx of infection
  3. no imaging findings of active infection
20
Q

What are caseating granulomas in TB infections?

A

Caseating=necrosis

These granulomas may become caseating= central necrosis and acidic with low oxygen, making it hostile for Mtb to grow

21
Q

Clinical Manifestations of TB

A

Pulmonary:
—Cough (productive or not)
—hemoptysis
—Fever, chills, night sweats and chest pain

Extrapulmonary: can affect any organ
—Cervical lymph nodes Scrofula
—meningitis
—Potts disease (vertebrae)
—Miliary TB
—Adrenal gland involvement
—Genitourinary
22
Q

Chest Radiographs in TB infections

A

Primary TB:
—Middle/Lower Lobe consolidation
—Granuloma=residual evidence of healed primary TB
—Ghon complex= calcified primary focus + lymph node
—Rankes complex=healed fibrocalcific Ghon complex

Reactivation:
—Apical upper lobe fibrocavitary disease most common

Miliary TB:
—small millet seed like nodular lesions 2-4mm