W2 Cough

Question 1

What is pneumonia?
Transmission? 3
Classification options? 4

Answer 1

purulent, acute infection filling the alveoli impairing gas exchange

Transmission:
1. Air borne from droplets, typically from a cough or sneeze
2. Via blood
3. Viruses and bacteria commonly found on the nose/throat can infect the lung if inhaled

Different Classification Options:
1. Infectious Agent
2. Setting of Infection (where acquired) → community, hospital (nosocomial), ventilator associated (form on endotracheal tube), or aspiration
3. Area of lung → by affected lobe(s), alveolar, interstitial (around alveoli), bronchopneumonia (throughout the lung → bronchi to alveoli)
4. Mild, moderate, severe

Question 2

Pneumonia, what are the 5 main infection agents?
And the common pathogens under them

Answer 2

Infectious Agents:
1.Bacteria:
—Streptococcus pneumonia
—Haemophilus influenzae
—Staphylococcus aureus
—MRSA

2.Atypical Organisms: “CLaM”
—Legionella pneumophila
—Mycoplasma pneumonia
—Chlamydophila pneumonia

3.Viruses:
—Influenza A and B
—Covid-19
—Middle East respiratory syndrome coronavirus
—severe acute respiratory syndrome (SARS)
—rhinovirus
—adenovirus
—respiratory syncytial virus (RSV)

4.Mycobacterial:
—TB

5.Fungi:
—Pneumocystis Jirovecii (formerly Pneumocystis carinii) usually seen in the immunocompromised like HIV

Question 3

Pneumonia
What are the three main fungal infectious agents?

Answer 3

Question 4

⭐️Pneumonia notes
What is the number 1 cause of CAP?
Treatment?
What causes 10% of CAP, Tx?
What causes 5% of CAP, Tx?
Which agent typically follows influenza virus and can lead to pleural effusion, Tx?
Gram neg Tx?
Pseudomonas Tx?
What agent is seen in alcoholics, diabetes and is red-current jelly sputum?

Answer 4

TYPICAL BACTERIAL PNEUMONIA
Streptococcus Pneumoniae:
—Number one cause of CAP (~70%) with increased frequency in asplenic patients.
—Treatment is ceftriaxone+macrolide OR fluoroquinolone

Haemophilus Influenzae:
—causes ~10% of CAP
—treatment ceftriaxone+macrolide OR fluoroquinolone

Moraxella Catarrhalis:
—causes ~5% of CAP with higher frequency in COPD and immunocompromised.
—Treatment is ceftriaxone+macrolide OR fluoroquinolone.

Staphylococcus Aureus:
—typically infects following an influenza virus and can lead to a pleural effusion.
—Treatment is Oxacillin and if MRSA, Vancomycin

Gram Negative Rods:
—usually secondary to nosocomial infections.
—Treatment is a third generation cephalosporin or fluoroquinolone.

Pseudomonas:
—often seen in cystic fibrosis patients or nosocomial cause.
—Treatment is with an anti pseudomona agent like a fluoroquinolone.

Klebsiella:
—seen in alcoholics, diabetics, or have a nosocomial cause.
—Classically sputum is currant jelly bloody.
—Treatment is a third generation cephalosporin or fluoroquinolone.

Anaerobe:
—seen in aspiration pneumonia secondary to loss of consciousness, alcoholism, drug overdose, or cardiac arrest.
—Usually in dependent lung lobes with a possible abscess formation.
—Treatment includes clindamycin or flagyl.

Question 5

⭐️Pneumonia Notes
Atypical Pneumonia “Walking Pneumonia”
Three main organisms:
Most common
Seen in alcoholics, transplant and COPD? S/S?
Seen in elderly? S/S?

💊 treatment for all three
“Atypical LAD”

Answer 5

Mycoplasma Pneumonia:
—classically seen in young adults and causes ~10% of CAP.
—Has a 2-4 week incubation period with resulting tracheobronchitis and a nocturnal cough.
💊 Treatment is doxycycline, a macrolide (azithromycin), or fluoroquinolone (levofloxacin).

Legionella Pneumophilia:
—seen in alcoholics, transplanted patients, COPD, malignancy, and diabetics.
—Usually a water exposure (air conditioner) and 25% fatality.
—Classic signs/symptoms include hyponatremia, CNS changes, LDH > 700, and diarrhea.
💊 Treatment is doxycycline, a macrolide, or fluoroquinolone.

Chlamydia Pneumonia:
—seen in elderly patients and present with pharyngitis, hoarse voice, and sinusitis.
💊Treatment is doxycycline, a macrolide, or fluoroquinolone.

⚠️Allie said not to pay too much attention to this slide
d. Chlamydia Psittaci: contracted from birds (often parrots). Treatment is doxycycline, a macrolide, or fluoroquinolone.
e. Coxiella Burnetii: called “Q-fever” and contracted from animals (goats, cattle, sheep) due to inhalation or even ingestion of milk products. Treatment is doxycycline, a macrolide, or quinolone.
f. Francisella Tularensis: classically contracted from rabbits with treatment being Streptomycin.
g. Nocardia Asteroides: a gram positive acid fast aerobe mimicking TB. Get eosinophilia with fever and night sweats. Seen in AIDS or other opportunistic infections. Treatment is Bactrim.

Question 6

⭐️Pneumonia Notes
Fungal Pneumonia
Page 9 notebook

Answer 6

Pneumocystis Jirovecii:
—insidious onset of dry cough with SOB.
—Have bilateral infiltrates, sputum with silver stain,
—and an elevated LDH.
—Seen in patients with AIDS; if CD4 counts < 200 then get
—💊prophylaxis with Bactrim

Coccidioides Immitis:
—known as “San Joaquin Valley Fever”
—seen in the southwestern US.
—Sputum will show budding yeast.
—💊 Treatment is with an antifungal (-azoles or Amphotericin B).

Histoplasma:
—seen in Ohio/Mississippi River Valleys especially associated with bat caves and bird dung.
—💊 Treatment is -azoles or Amphotericin B.

Aspergillus:
—seen in immunocompromised and noted as a “fungal ball” with cavitation on chest x-ray.
—💊 Treatment is -azoles or Amphotericin B.

Cryptococcus:
—seen in immunocompromised
—💊 treatment is -azoles or Amphotericin B.

Question 7

⭐️Pneumonia Notes
🦠Viral Pneumonia
How do you treat influenza
COVID-19? 2

Answer 7

Influenza:
—💊 treatment is supportive or oseltamivir/zanamivir

COVID-19:
—💊 antiviral medications like oral Paxlovid or IV Veklury (remdesivir) as well as monoclonal antibody therapy in emergency use (bamlanivimab)

Others:
—Hantavirus, RSV, parainfluenza, and adenovirus

Question 8

Pneumonia
Body defences — 3

Answer 8

1.Cough
2.Mucociliary Escalator:
—lines airway and moves bacteria/debris away from the lungs
3.Macrophages
If these mechanisms fail and a microbe colonizes an alveoli, it can multiple and quickly move into the lung tissue activating an inflammatory response resulting in pneumonia

Question 9

Pneumonia,
What are the 4 stages?

Answer 9

Consolidation:
a.Occur sin first 24 hours
b.Cellular exudates from neutrophils, lymphocytes, and fibrin replace alveolar air
c.Capillaries surrounding the alveolar walls become congested
d.Infection spreads to hilum and pleura
e.Pleurisy develops as does cough

Red Hepatization:
a.Occurs in 2-3 days after consolidation
b.Lungs become hyperemic (increased blood flow) and alveolar capillaries are engorged with blood
c.Fibrin fills alveoli

Grey Hepatization:
a.Occurs in 2-3 days from red hepatization
b.Avascular stage
c.Lungs appear grey-brown to yellow because of fibrinopurulent exudates and disintegration of RBCs (hemosiderin)
d.Pressure of the exudates cause compression of the the capillaries
e.Increased leukocytes

Resolution
f.Macrophages enter alveolar spaces and phagocytosis of bacteria-laden leukocytes occurs
g.Re-aerates and sputum expectoration
h.Day 8 to 3 week

Question 10

Pneumonia
What is the presentation?

Answer 10

Presentation:
—Common symptoms include cough, fever, sputum production, pleuritic chest pain, myalgias, headache, arthralgias, shortness of breath
—Tachycardia and Tachypnea
—Dullness to percussion and increased vocal fremitus, egophony (E -> A)
—Crackles with bronchial breath sounds

Question 11

Pneumonia
Diagnostics
Increased lymphocytes indicate which etiology?
What about increased neutrophils
What is the role of procalcitonin levels, what does it tell you?
What else should you test for ?

Answer 11

Diagnostics:
—Pulse oximetry
—Chest X-Ray: decreased lung expansion and patchy opacity on the affected side
—Sputum culture, blood cultures
—Legionella urine antigen test, pneumococcal antigen test, viral nasal swab
—CBC with differential (increased lymphocytes indicate viral; increased neutrophils bacterial)
—Consider HIV and TB testing in high risk patients
—Increased CRP
—Increased procalcitonin in bacterial infections (procalcitonin is a precursor to calcitonin and the final step is inhibited by cytokines and endotoxins released during bacterial infections)

Question 12

[SKILLS OSCE]
What is this?

Answer 12

Bronchopneumonia
—results in peribronchiolar inflammation following inhalation of causative organism.
—Can spread through spaces between the alveoli and cause consolidation on an entire lobe.
—On x-ray, see multiple small nodular opacities which tend to be patchy and confluent (separated by areas of normal parenchyma).
—Often bilateral, asymmetric, and involves the lung bases.

Question 13

Pneumonia, when do you admit
(Note, pharm lecturer said CURB-65 is not used but PSI/PORT is preferred)

Answer 13

Confusion
Urea >7
Respirations >30
Blood pressure <90 or <60
65 > years old

Question 14

[SKILLS OSCE]
What is this?

Answer 14

Pneumonia of the right middle lobe

Question 15

Pneumonia
What are the complications? 4

Answer 15

Pleural Effusion
➜ fluid in the pleural space further collapsing lung

Empyema
➜ infection in the pleural space

Lung Abscess
➜ if the infection destroys lung tissue and forms a cavity filled with pus

Bacteremia/Sepsis
➜ infection spreads from lungs into bloodstream and can go to other organs such as the meninges, joints (septic arthritis), pericarditis, or endocarditis

Question 16

Pneumonia — treatment — CAP
Healthy out patient?
What about in areas of high resistance to strep pneumonia?
Outpatient w/ underlying issues?
Duration?

Answer 16

CAP:
a.Prompt initiation of antibiotic to which the organism is susceptible; early initiation has improved outcomes

b.Outpatient treatment for healthier patients:
—MACROLIDE.
—In areas with high resistance of Strep pneumonia to macrolides, the recommendation is a
beta-lactam + macrolide or a fluoroquinolone
i.e ceftriaxone + azithromycin OR levofloxacin

c.Outpatient with comorbities or have received antibiotics within 90 days, recommendation is:
—a macrolide: azithromycin
—OR doxycycline plus ceftriaxone (beta-lactam)
—OR monotherapy with a fluoroquinolone

d.Default duration is 5 days; 7 days if other medical issues

Question 17

Pneumonia treatment
CAP
For hospitalised patients?
For ICU
Pseudomonas, MRSA, Enterobacter risk?

Answer 17

a.Hospital
—IV macrolide + a beta-lactam
—OR monotherapy with a fluoroquinolone

b.ICU
—antipneumococcal beta-lactam (cefotaxime, ceftriaxone, augmentin) + either azithromycin or a fluoroquinolone

c.Assess for risk factors for Pseudomonas, MRSA, or Enterobacter (prior exposure, inpatient hospitalization in last 90 days, or IV antibiotic in last 90 days).

If concerned for Pseudomonas:
—antipneumococcal/antipseudomonal agent (zosyn, cefepime, meropenem)
—with azithromycin or fluoroquinolone.
—Alternative is antipneumococcal/antipseudomonal plus aminoglycoside (gentamicin) plus azithromycin or a fluoroquinolone.

If MRSA
—vancomycin or linezolid.
—De-escalate antibiotics as clinically I’m

Question 18

Pneumonia — treatment
HAP and VAP

Hospital acquired (HAP) and Ventilator acquired (VAP) pneumonia
Most common agents?

Answer 18

HAP
—develops 48 hours after admission and VAP occurs in ventilated patients 48 hours after intubation

Different than CAP given different infectious agents, different antibiotic susceptibilities, and patients are usually higher risk

Most common agents
—S aureus (including MRSA)
—P aeruginosa
—gram negative rods (Enterobacter, K pneumoniae, E Coli)
—Acinetobacter and S maltophilia for VAP

Treatment starts empirically based on risk factors for MRSA

Question 19

Pneumonia treatment
Anaerobic pneumonia & Lung abscess

Associated with?
Pathogens? 4
1st line?
2nd line?
Duration?
What requires drainage?

Answer 19

Anaerobic Pneumonia and Lung Abscess
—Usually associated with aspiration (sedation, poor dentition)

Common offenders:
—Prevotella melaninogenica
—Peptostreptococcus
—Fusobacterium nucleatum
—Bacteroides

1st line
—Beta-lactam/lactamase inhibitor combination like carbapenem or clindamycin.

2nd line
—combination of penicillin and metronidazole (flagyl)

Duration
—typically 2-3 weeks or until the abscess has resolved on imaging

Empyema requires drainage

Question 20

Pneumonia
Misc treatments 5

Answer 20

Cough suppressants
Analgesics
Fever reduction
Oxygen therapy and humidification (loosen secretions)
Mobilize patient -> expand chest and loosen secretions

Question 21

Tuberculosis
Latent/active
Transmission/pathogenesis
Once activated

Answer 21

Vast majority (90-95%) are LATENT/dormant however and not symptomatic due to an intact immune system.

If the host’s immune system becomes debilitated, TB can be ACTIVE and cause infection.

Mycobacterium are strict aerobes and need oxygen to survive. They have a cell wall allowing them survive as well as be characteristically acid fast (hold onto a dye despite being exposed to alcohol)

Transmission is inhalation
—goes to the alveoli.
—Macrophages present identify them and phagocytize them.
—TB inhibits macrophage lysosomes allowing to survive and proliferate to create a localized infection known as PRIMARY TUBERCULOSIS.
—Most continue to be asymptomatic.
—Three weeks later the body forms a granuloma around the infection to prevent it from spreading via a CELL MEDIATED IMMUNITY RESPONSE.
—The tissue in the middle of the granuloma dies by CASEOUS NECROSIS.
—This area is known as a GHON FOCUS.
—The tissue encapsulated by the granuloma becomes fibrotic, scars, and the infection ends.
—In some cases the mycobacterium, although walled off, are still viable but dormant.
—If the immune system becomes compromised, it can become activated (i.e., HIV, aging)

Once activated
—typically goes to the upper lobes since there is a greater oxygenation in those lobes (aerobes are oxygen dependent).
Memory T cell immunity
—release cytokines → more caseous necrosis → forms cavities → allows bacteria to disseminate.

Spreads through vascular system and lymph to:
—Other areas of lung causing bronchoalveolar pneumonia
—Other areas of body → SYSTEMIC MILITARY TB

Question 22

Systemic Miliary TB:

Answer 22

a. Cervical lymph nodes (lymphadenopathy)
b. Liver (hepatitis)
c. Adrenal Gland (Addison’s disease)
d. Lumbar Vertebrae (Pott’s disease)
e. Meninges of Brain (meningitis)
f. Kidneys (causes sterile pyuria)
g. Heart (pericarditis)

Question 23

Tuberculosis
Testing 2

Answer 23

PPD (purified protein derivative)
—tuberculin (has a component of the mycobacteria) is injected under the dermis; if patient is previously exposed to TB the immune system will produce a small localized reaction in 2-3 days. >5mm is positive
—A positive test only indicates exposure and can not decipher from active or latent disease.

Interferon Gamma Release Assays (IGRA) or:
—is a blood test that detects previous exposure to TB proteins.
—Does not react to the BCG vaccine

If either of the above are positive, chest x-ray

Question 24

Tuberculosis — who is at risk?

Answer 24

—Close contacts of people exposed to TB
—Foreign born person who have immigrated within the last 5 years from areas that have a high TB incidence
—Healthcare workers who serve high risk patients
—Medically underserved, low income populations
—Persons who inject illicit drugs
—Jail patients
—Low body mass index

Question 25

Tuberculosis
When do you treat
What do you need?
Treatment
Latent
Active

Answer 25

If positive and with classic symptoms (night sweats, weight loss, fever/chills, hemoptysis)
—then need 3 sets of AFB sputum cultures (acid fast bacteria)
—and bronchoalveolar lavage samples

TREATMENT:
Latent TB
—monotherapy with INH (Isoniazid) for 9 months

Active TB
—requires at least 2 drug therapy to prevent a higher frequency of drug resistance; also needs extended therapy given the prolonged generation time of mycobacteria; because adherence to multiple drugs is difficult, directly observed therapy is used on patients
Rifampin, Isoniazid, Pyrazinamide, Ethambutol
—All 4 initially
—if the isolate is susceptible to INH and rifampin than ethambutol can be dropped for a total 8 week course followed by dual therapy with INH and Rifampin for another 16 weeks

Question 26

Tuberculosis.
What if isolate is INH resistant?
Which vitamins do you give?
Which drug for MDR-TB?
Which new oral drug from WHO?

Answer 26

—INH can be discontinued and the three remaining drugs should be taken for a total of 6 months
—Pyridoxine (vitamin B6) should be given with INH to prevent neuropathy
—Needs isolation in negative pressure rooms
—MDR-TB (multidrug drug resistant TB): FDA released Pretomanid
—New WHO guidelines recommend an all oral 6 month regimen of Bedaquiline, Pretomanid, Linezolid, and Moxifloxacin (BPaLM)
—Results in better outcomes, shortens duration of treatment, and improved quality of life

Question 27

Acute bronchitis
What is it?
Causes? 2
At risk includes?

Answer 27

Inflammation of the upper airways commonly following an upper respiratory tract infection (URI)

Causes (pathogen rarely identified):
1.Typically Viral:
—Rhinovirus
—Influenza A and B
—Parainfluenza
—Coronavirus
—Human metapneumovirus
—and Respiratory Syncytial Virus

2.Occasionally Bacterial:
—Mycoplasma pneumonia
—Bordetella pertussis
—and Chlamydia pneumonia

At risk include:
—tobacco (+)
—COPD or other diseases that impair the upper bronchial clearance mechanisms such a cystic fibrosis or bronchiectasis

Question 28

Acute bronchitis
Signs & symptoms
Ascultation?
What symptom is last to resolve?

Answer 28

—Nonproductive or minimally productive cough accompanied or preceded by an URI symptoms
—Dyspnea
—Scattered wheezing and rhonchi
—Sputum may be clear or purulent; occasionally with hemoptysis
—Mild fever (if high or prolonged think more influenza or pneumonia)
—Cough is usually the last symptom to resolve and can take weeks to fully resolve

Question 29

Acute bronchitis
Diagnosis
Differential you should consider?
What is not a helpful diagnostic?

Answer 29

Clinical diagnosis based on history and physical
Chest X-ray is indicated for:
—Findings suggestive of pneumonia (high fever, hypoxia, crackles or concern for a consolidation)
—In the elderly with fever/cough or those with COPD or other lung disorder
—Persistent cough
—Sputum culture typically have no role
—Consider Bordetella Pertussis (whooping cough):
=2-3 months of cough with a high pitched whoop sound/gasp as the patient inhales

Question 30

Acute bronchitis
Treatment
What if wheezing?
What if cough >2w
When should PO abx be considered? If so which ones?

Answer 30

Asymptomatic patients rarely require antibiotics; supportive measures with antipyretics, analgesics, antitussives/cough suppressant, and hydration

Patient with wheezing can benefit from
—an inhaled beta-2 agonist (albuterol)
—or an anticholinergic (albuterol) inhaler for 7 days

If cough persists for > 2 weeks
—consider an inhaled corticosteroid to reduce airway inflammation.

Oral antibiotics should be considered:
—COPD patients with increased cough, sputum production and dyspnea
—Pertussis

Antibiotics:
—Amoxicillin 500 mg tid x 7 days
—Doxycycline 100 mg bid x 7 days,

Question 31

Laryngotracheobronchitis (Croup)
What is it?
What are 4 characteristic features ?
Causes?
Which anatomical structures are affected/impacted?

Answer 31

Self limiting, viral upper airway Inflammation of the larynx and trachea causing airway obstruction and causing the characteristic features:
—Hoarse voice
—Barking cough
—Inspiratory stridor
—Increased work of breathing

Most common infectious cause of airway obstruction in children (typically 6 months to 3 years of age)

Causes:
—Typically viral: Parainfluenza and RSV (more bronchiolitis)
—Possibly bacterial or atypical agents

Upper Airway: nasal cavity, oral cavity, pharynx, and larynx
Lower airway: trachea, bronchi, bronchioles, alveoli
In croup the larynx, pharynx, and trachea are all inflamed

Question 32

Laryngotracheobronchitis (Croup)
Pathophysiology
Diagnosis
Treatment

Answer 32

PATHOPHYSIOLOGY
—Begins with an URI followed by viral infiltration of the larynx and trachea causing an inflammatory reaction with subsequent pain and edema
—Swelling causes partial airway obstruction > increased work of breathing and ((barking cough/stridor** (heard during inspiration)

DIAGNOSIS
—Clinical diagnosis based on history and physical (onset of symptoms with barking cough and stridor)
—If acquire imaging, suggestion is a frontal neck x-ray which will show the steeple sign (subglottic tracheal narrowing within the trachea)

TREATMENT
—Single dose of oral Dexamethasone corticosteroid (can give IV or IM)
—Nebulized epinephrine is effective for moderate-severe croup

Question 33

[SKILLS OSCE]
When would this be seen? What would be the diagnosis?
What’s the treatment?

Answer 33

Laryngotracheobronchitis (Croup)

Single dose of oral Dexamethasone corticosteroid (can give IV or IM)
Nebulized epinephrine is effective for moderate-severe croup

Question 34

Pulmonary Vasculitis

Include WEGENER’s GRANULOMATOSIS and CHURG-STRAUSS SYNDROME

For Wegeners:
Causes
Symptoms
Most common sign?
Labs, + for?
Diagnosis demonstrating what?
Treatment — 2

Answer 34

WEGENER’S (Granulomatosis with polyangiitis):
Idiopathic disease
—causes inflammation of blood vessels, kidney, and respiratory tract
—Combination of glomerulonephritis, necrotizing vasculitis of the upper/lower respiratory tract, and small vessel vasculitis

Common symptoms
—Sinusitis, arthralgias, fever, skin rash, and weight loss

Most common pulmonary sign
—is a nodular pulmonary infiltrate on chest x-ray

Tests
—Elevated ESR/CRP, anemia, thrombocytosis, ANCA (+)

Diagnosis
—Diagnosis is based on biopsy of lung, sinus tissue, or kidney with demonstration on necrotizing granulomatous vasculitis

Treatment
—combo of corticosteroids (prednisone 60 mg/daily tapered) for 3-6 months with
—cyclophosphamide (cytotoxic drug) 1-2 mg/kg/daily for 12 months

Question 35

Pulmonary Vasculitis
Churg-Strauss Syndrome (Eosinophilic Granulomatosis with polyangiitis):

Patho
Three stages
Diagnosis 3
Treatment

Answer 35

Idiopathic
—small and medium sized artery vasculitis that occurs in patients with asthma/allergies
—Affects primarily the lungs and skin but other organs including the heart, GI tract, and peripheral nerves can be affected too

Three stages:
—airway inflammation → asthma/rhinitis
—followed by eosinophilia that causes tissue damage
—followed by vasculitis, thrombosis, and cell death

Can be ANCA (+) but not always
—Histology has evidence of EXTRAVASCULAR EOSINOPHILS
—Chest x-ray can show pulmonary nodules

Treatment the same as Wegener’s
—combo of corticosteroids (prednisone 60 mg/daily tapered) for 3-6 months
—with cyclophosphamide (cytotoxic drug) 1-2 mg/kg/daily for 12 months

Question 36

Alveolar Hemorrhage Syndrome
Goodpasture’s Syndrome (Anti-Glomerular Basement Membrane Disease)
What is it?
Presenting symptom?
Other symptoms?
Diagnosis 2
Treatment? 2

Answer 36

Idiopathic or autoimmune disease in which antibodies attack the basement membrane in the lungs and kidneys leading to alveolar hemorrhage, glomerulonephritis, and kidney failure

Presenting symptom
—Hemoptysis

Other
—Dyspnea, cough, hypoxemia, and diffuse alveolar infiltrates are typical features as well as anemia, arthralgias, weight loss, and fatigue

Diagnosis
—characteristic IgG deposits in glomeruli/alveoli biopsy or serum antibodies
—UA: hematuria, proteinuria and RBC casts

Treatment
—Need to clear anti-GBM antibodies from the serum and suppress new antibodies.
—Recommend plasmapheresis for 2 weeks in combination with
—cyclophosphamide/prednisone for 8 weeks

Question 37

Bronchiolitis Obliterans With Organizing Pneumonia (BOOP)
Aka Cryptogenic Organizing Pneumonia (COP) (Bronchiolitis)
P44
Known as?
what is it?
Symptoms
Signs
Causes
Diagnostic
Treatment

Answer 37

*Also known as Cryptogenic Organizing Pneumonia (COP) -> inflammation of the bronchioles (bronchiolitis) and surrounding interstitium. Suspect the diagnosis if there is radiographic evidence of PNA but no response to antibiotics and negative cultures

—Unresolved PNA with persistent alveolar exudate that undergoes fibrosis.

Symptoms
—fever, chills, weight loss, night sweats, cough, and dyspnea

Signs
—crackles and occasionally clubbing

Causes
—toxins including VAPING, side effect of drugs (amiodarone), inflammatory disorders (lupus, RA, scleroderma), covid, and radiation therapy

Chest X-Ray
—looks like a PNA however more extensive; CT chest improved imaging; biopsy via bronchoscopy

Treatment
—corticosteroid therapy for 6 - 12 months