Pulmonology and ABX Flashcards
What is a COPD exacerbation and what can cause it?
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
Treatment for COPD exacerbations
—Oxygen
—Nebulized albuterol + Ipratropium
— Oral glucocorticoids
ABX:
—Azithromycin, Levofloxacin/Moxifloxacin, Augmentin, or Doxycycline for 5-7 days
Community Acquired Pneumonia Sx and Causative organisms
Fever, productive cough, and infiltrates on CXR
Strep Pneumoniae most commonly
H. Flu
M. Catarrhalis
Community Acquired PNA Treatment
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
Atypical PNA cause and presentation
Caused by Mycoplasma.
Young pt with viral prodrome (Fever, HA, malaise, pharyngitis) + persistent dry cough
Non focal lung exam— scattered wheezes or crackles
Atypical PNA Chest X ray findings
Atypical pattern:
—Reticulonodular pattern most common
—Diffuse, patchy, or interstitial infiltrates
Atypical PNA treatment
Macrolides
—Azithromycin or Clarithromycin—
Or Doxycycline
**Mycoplasm lacks a cell wall so its naturally resistant to Beta Lactams
Macrolides MOA, Clinical use, and ADRs
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
What causes Pertussis and how does it present?
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)
Diagnosis of Pertussis
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
Is lymphocytosis common in pertussis?
Yes
Management of Pertussis
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
What abx is better tolerated and preferred in children <1 month of age?
Azithromycin
How is Pertussis transmitted?
Respiratory droplets during coughing fits. If pt is admitted should be on droplet precautions
Complications of pertussis
Pneumonia, encephalopathy, otitis media, sinusitis, and seizures.
Increased mortality in infants d/t apnea/cerebral hypoxia associated with coughing fits
Pertussis prevention
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
What is the cause and pathophysiology of a Tuberculosis infection?
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
What are the outcomes of infection with tuberculosis?
- 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 - Chronic Latent Infection
—About 90% of pts control the initial primary infection via caseating granuloma formation - 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
What 3 criteria need to be met to be non infectious with a chronic (latent) TB infection?
- (+) PPD skin test
- So sx of infection
- no imaging findings of active infection
What are caseating granulomas in TB infections?
Caseating=necrosis
These granulomas may become caseating= central necrosis and acidic with low oxygen, making it hostile for Mtb to grow
Clinical Manifestations of TB
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
Chest Radiographs in TB infections
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