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CRRAB II Week 7 - WLB > Pulmonary Pathology Part 2 - Witrak > Flashcards

Pulmonary Pathology Part 2 - Witrak Flashcards

1
Q

What does the work up for pneumonia consist of?

A
  • pulse oximetry may show desaturation
  • inflammatory disease markers: leukocytosis (typically neutrophilic)
  • increased erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP)
  • sputum gram stain and urinary antigen testing (pneumococcus and Legionella)
  • Chest x-ray
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2
Q

Why do we get pneumonia?

A

Lungs – normally sterile:
- infection requires either:
(1) defect in host defenses and/or pre-
existing acute or chronic lung disease
(esp. ARDS, mechanical ventilation).
(2) Markedly virulent organism.
(3) Overwhelming infection.

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3
Q

What bug can take down a healthy adult with no risk factors for pneumonia? (Hint: normal flora of nasopharynx)

A

Pneumococcus

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4
Q

What are predisposing factors for pneumonia?

A

(1) Extremes of age: esp. elderly.
(2) Altered consciousness: poor cough/expectoration and increased aspiration risk.
(3) Cigarette smoking: impaired cilia/increased secretions.
(4) COPD.
(5) Pulmonary edema.
(6) Malnutrition.
(7) Immunosuppression: acquired or congenital.
(8) Cystic Fibrosis (thick secretions plug up bronchi)
(9) Immotile cilia syndrome.
(10) Bronchial obstruction due to tumor, foreign body, or stenosis.
(11) Viral respiratory tract infection with secondary bacterial pneumonia: esp. influenza – with subsequent staph. aureus pneumonia.

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5
Q

What is the clinical classification of pneumonia?

A

(1) Community-acquired.
(2) Hospital/health care facility-acquired (nosocomial).
(3) Immunocompromised patients.
(4) Immunocompetent hosts with chronic pneumonia (TB or fungi).

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6
Q

20% of patients may not have what common symptoms of pneumonia? (Hint: especially elderly)

A

Fever

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7
Q

Based on clinical picture alone can you differentiate between common bacterial pneumonia or “atypical” pneumonia?

A

NO, NOT ALWAYS.
While “atypical” pneumonia (mycoplasma, chlamydophilia, viruses) is often milder clinically than common bacterial pneumonia (e.g. pneumococcus): the symptom overlaps do not allow reliable clinical separation.

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8
Q

What pathogens, if identified, are always regarded as significant/causative of pneumonia?

A
  • Legionella
  • Influenza viruses
  • Mycobacterium tuberculosis
  • C. psittaci
  • Agents of bioterrorism: B. anthracis (anthrax), Yersinia pestis (pneumonic plague)
  • Misc: Francisella tularensis (tularemia), Coxiella burnetii (Q Fever), hanta virus.
  • Fungal organisms: histoplasma, blastomyces, coccidioides.

***Above organisms important to ID because most require Rx different than usual empiric antibiotics.

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9
Q

What are the microbiological means of diagnosing pneumonia?

A

1) Respiratory secretions: SPUTUM (deep cough), tracheal aspiration, bronchoscopy with washings/bronchoalveolar lavage:
- quick bug stains (gram, KOH/silver, AFB).
- culture, PCR.
2) Blood culture: if positive for known pathogen usually = pneumonia etiology with high positive predictive value (PPV).
3) Culture of: aspirated pleural/empyema fluid or lung abscess: high PPV.
4) Urinary antigen testing: pneumococcus, Legionella, histoplasmosis: high PPV.
5) Lung Bx – for culture (esp. fungi, mycobacteria) and histology (with bug stains): high PPV.
6) Serology – mycoplasma, chlamydophilia, coccidioides: rarely used for common CAP.
7) Emerging serum test: procalcitonin
- increased in bacterial infection but not viral
disease.

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10
Q

What is the most common cause of community acquired viral pneumonia in adults?

A

Influenza (A, B, avian)

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11
Q

How is viral pneumonia best diagnosed?

A

PCR

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12
Q

What is the most feared and common pathogen causing pneumonia?

A

S. pneumoniae (pneumococcus)

  • colonizes up to 20% of adults
  • commonest cause of bacterial pneumonia: 5-18% of CAP and 65% of bacteremic pneumonia cases (esp. if splenectomy)
  • Dx more definitive if, in addition to sputum, bug grown in blood or pleural fluid culture–or if positive urine antigen test.
  • tendency to produce lobar pneumonia
  • vaccine available against common serotypes for high risk patients
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13
Q

What is the most common bacterial pneumonia complicating COPD patients?

A

Hemophilus influenzae

- like pneumococcus, frequent pharyngeal colonizer.
- pneumonia in adults and children.
- S/P type B vaccine: most infections are non-typable/non-encapsulated forms
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14
Q

What pathogen causes 2 to 9% of community acquired pneumonia and comes from aerosolized water droplets from water reservoirs like artificial aquatic environments?

A

Legionella pneumophilia

  • can have associated URI Sx
  • often epidemic outbreaks: travel Hx.
  • favors patients with predisposing chronic disease.
  • fatality rates up to 50%.
  • Dx by urinary antigen test/growth on selective media.
  • significantly associated with hyponatremia.
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15
Q

What are the fungal pathogens that can cause pneumonia?

A
  1. Histoplasmosis: Ohio/Mississippi river valley regions – bat/bird droppings: cave explorers at high risk
  2. North American blastomycosis: central/southeastern USA/Great Lakes region
    - moist soil with decaying vegetation – direct or indirect (via pets) spore inhalation.
  3. Coccidiomycosis: Southwestern USA/semi-desert/desert climates: aka “Valley Fever”.
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16
Q

What is the most frequent complication of varicella infection in healthy adults?

A

Varicella pneumonia

10-30% mortality

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17
Q

How do you diagnose Histoplasmosis?

A
  • respiratory secretions (sputum or bronchoscopic)
  • tissue Bx - for culture, fungal stains; urine antigen testing, serology.
  • CXR may mimic: sarcoidosis, TB, malignancy; associated with hilar/mediastinal adenopathy
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18
Q

How do you diagnose Blastomycosis?

A
  • respiratory secretions (sputum and bronchial wash)
  • tissue Bx for culture
  • fungal stains
  • emerging PCR methods.
19
Q

What are the symptoms of North American Blastomycosis?

A
  • nonspecific pulmonary Sx: cough, fever, sputum production

- bloodstream dissemination: esp. to skin, bones/joints, GU: disease may present at these sites

20
Q

How do you diagnose Coccidiomycosis?

A
  • respiratory secretions
  • tissue Bx – for culture, fungal stains
  • serology
  • emerging PCR
21
Q

How do you treat active pulmonary fungal disease?

A

Rx with antifungal drugs:

  • usually conazole agents
  • occasionally amphotericin B (toxic)
22
Q

What are the reasons for immunocompromised patients that put them at risk for pneumonia?

A

-congenital or acquired defects in cellular or humoral immunity, phagocytosis, or with severe neutropenia.
In community practice => almost all cases are due to acquired deficiencies:
–HIV/AIDS
–Chronic immunosuppression for auto-immune/rheumatological disease.
–CHEMOTHERAPY/RADIATION for common neoplastic disease: esp. hemic malignancy.
–Transplant patients: allogeneic bone marrow and solid organ.

23
Q

What unusual pathogens can cause pneumonia in immunocompromised patients?

A
  1. Nocardiosis
  2. Pneumocystis jirovecii (formerly carinii).
    • esp. HIV/AIDS patients with very low CD4 counts.
      • may cause dyspnea, cough, and marked
        hypoxemia with minimal CXR changes:
        • may need CT scan to see infiltrates
  3. Cytomegalovirus (CMV) – often a co-infection with pneumocystis
  4. Herpes virus/varicella zoster.
  5. Atypical mycobacteria: esp. MAI.
  6. Invasive fungal disease: candidiasis, cryptococcosis, aspergillus, mucormycosis.
  7. Parasites: esp. toxoplasmosis, strongyloidiasis
24
Q

What causes Pulmonary Edema – i.e. movement of fluid into alveolar spaces (alveolar flooding)?

A
  • 1) Hemodynamically increased alveolar capillary pressure: left heart failure = cardiogenic pulmonary edema: congestive heart failure.
    2) Alveolar microvascular injury:
    • Acute Respiratory Distress Syndrome (ARDS)/Acute lung injury
    • high altitude pulmonary edema
    • neurogenic pulmonary edema
      3) Pulmonary edema with mixed cardiogenic/ARDS features: esp. sepsis.
25
Q

What is the clinical presentation of Cardiogenic pulmonary edema?

A

(1) Acute dyspnea with anxiety, diaphoresis, hypoxia.
(2) More gradual (over 24 hours) onset of dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea with cough ± pink/frothy sputum:
- if associated chest pain: think myocardial
ischemia/infarction or aortic dissection.

26
Q

What is the pathogenesis behind Cardiogenic pulmonary edema?

A
  • increased alveolar capillary pressure due to increased pulmonary venous pressure:
  • leads to increased pulmonary interstitial fluid formation – followed by alveolar flooding = very common cause of respiratory distress in adults.
27
Q

What causes Cardiogenic pulmonary edema?

A
  1. Vast majority of cases = left heart disease/dysfunction (myocardial vs. valvular)
    - LV failure = systolic or diastolic LV dysfunction due to: *coronary disease (myocardial ischemia or infarction), chronic hypertension, cardiomyopathy, aortic valve disease, new-onset arrhythmias, and mitral stenosis (now uncommon).
  2. Minority of cases: volume overload = IV fluid or blood administration exceeding cardiovascular capacity.
28
Q

What are the physical exam findings in patients with Cardiogenic pulmonary edema?

A

Physical exam
- tachypnea, tachycardia, either hypertension
(adrenaline reaction) or hypotension (cardiogenic
shock).
- cool extremities if poor peripheral perfusion.
- lungs: rales ± rhonchi/wheezes first affecting
lung bases.
- cardiac murmurs (S3, valve-related).
- jugular venous distension.

29
Q

What are the laboratory/imaging findings in Cardiogenic pulmonary edema?

A
  1. CXR: bilateral basilar interstitial/alveolar infiltrates ± cardiomegaly.
    • note: CXR changes may be delayed up to 12
      hours in acute edema cases.
  2. EKG: may see evidence of myocardial infarction or new dysrhythmia.
  3. serum B – natriuretic peptide (BNP) – secreted by ventricles secondary to stretching or increased wall tension: if 400 = high positive predictive value.
  4. Echocardiography: very good bedside assessment for evaluating LV systolic/diastolic function, cardiac pressures, valvular disease, pericardial effusion/tamponade.
  5. Cardiac catheterization (Swan-Ganz): pulmonary artery catheter wedged distally (PCWP): normally 8-12 mmHg; if >18 mmHg usually is consistent with cardiogenic pulmonary edema/CHF.
30
Q

What is non-cardiogenic pulmonary edema?

A

Acute respiratory distress syndrome(ARDS)/Acute lung injury (ALI)
ARDS = syndrome of acute respiratory distress characterized by: Dyspnea & Hypoxemia.

31
Q

What are the chest x-ray findings in ARDS?

A

Diffuse pulmonary infiltrates on CXR

32
Q

What is the pathology seen in ARDS?

A

Pathology: diffuse alveolar damage (DAD) with alveolar hyaline membranes evolving to granulation tissue/organizing phase: either resolution or pulmonary fibrosis/death.

33
Q

What is the pathophysiology behind ARDS?

A

Poorly understood:

-alveolar capillary injury due to activated neutrophils releasing toxic oxidants, proteases, etc.(?).

34
Q

How do you treat patients with ARDS?

A

mechanical ventilation and treat underlying initiating event as indicated: e.g. sepsis.

35
Q

What initiating events cause ARDS?

A 
ARDS – by definition: secondary to a precipitating insult within the previous 2-3 days:  
		sepsis
		pulmonary infection
		gastric aspiration
		general trauma/head injury (“shock lung”)
		inhaled irritants
		drug overdoses/near drowning
		transfusion 
		many additional/misc. causes
36
Q

What is Acute Lung Injury?

A

acute interstitial pneumonia

= acute respiratory failure without clear precipitating etiology: may follow URI-like infection.
= similar clinical/radiographic features as ARDS.
= pathology shows organizing DAD
- high mortality (30-70%).

37
Q

What is Interstitial/Diffuse Parenchymal Lung Disease (ILD)?

A

A grouping of clinically diverse diseases (>100 entities).

= non-infectious inflammation of pulmonary interstitium ± involvement of alveolar spaces and distal airways.

38
Q

What is the typical pathology seen in Interstitial/Diffuse Parenchymal Lung Disease (ILD)?

A 
Pathology = typically chronic interstitial inflammation (±granulomatous change) – with  risk of pulmonary fibrosis.
PFT=  most commonly shows a restrictive pattern in chronic/long-standing cases:  decreased TLC/FVC.
39
Q

What is the clinical presentation of Interstitial/Diffuse Parenchymal Lung Disease (ILD)?

A

Onset varies from either acute/subacute pulmonary Sx to usually chronic/progressive dyspnea on exertion or persistent non-productive cough.
-with severe disease: eventual hypoxemia at rest with chronic pulmonary hypertension and eventual cor pulmonale: due to hypoxemic vasoconstriction.

40
Q

What are the findings on chest imaging in Interstitial/Diffuse Parenchymal Lung Disease (ILD)?

A

Chest imaging: CXR/CT scan features can simulate pulmonary infection (esp. in immunocompromised patients): typically see reticular/reticulonodular infiltrates ± alveolar filling pattern: best seen with HRCT.

41
Q

How is Interstitial/Diffuse Parenchymal Lung Disease (ILD) usually classified?

A

Pulmonary Medicine consultation will attempt to classify as either:

     1) Fungal, mycobacterial, or other bug.
     2) Neoplasm simulating pneumonia or ILD.
 3) ILD with known causation
 4) Idiopathic ILD: what subtype?
42
Q

What are the possible classifications of ILD with known cause?

A

1) Inhalational exposure to occupational or environmental particles: inorganic (e.g. silicosis, asbestosis) or organic/antigenic (hypersensitivity pneumonitis).
2) Drug-induced pulmonary toxicity: e.g.
chemo- Rx agents, amiodarone, many others
3) Radiation-induced lung injury.
4) ARDS/diffuse alveolar damage.
*5) Smoking-related: Pulmonary Langerhans
cell histiocytosis (PLCH), desquamative
interstitial pneumonia (DIP)/respiratory
bronchiolitis interstitial lung disease (RB-
ILD), and 70% of idiopathic pulmonary
fibrosis cases (IPF).
6) Familial risk for ILD (esp. IPF).

43
Q

What are the possible classifications of ILD with idiopathic/poorly understood causes?

A

1) SARCOIDOSIS.
2) Idiopathic interstitial lung disease: Acute interstitial pneumonia (AIP), usual interstitial pneumonia (UIP/IPF), non-specific interstitial pneumonia (NSIP), cryptogenic organizing pneumonia (COP), lymphocytic interstitial pneumonia (LIP).
3) ILD associated with connective tissue disease: rheumatoid arthritis, systemic lupus erythematosus, scleroderma, Sjogren’s syndrome.
4) Diffuse pulmonary hemorrhage syndromes: Goodpasture’s, idiopathic pulmonary hemosiderosis, lupus, ANCA vasculitis.
5) Alveolar proteinosis.
6) Eosinophilic pneumonia: often drug-related.
7) Granulomatous/vasculitic –Wegener’s/microscopic polyangiitis/Churg-Strauss (asthma) = ANCA-associated disease.
8) Lymphangioleiomyomatosis (LAM) –females.
9) Misc: inflammatory bowel disease, autoimmune cholangitis/hepatitis, GVHD, inherited disorders.

CRRAB II Week 7 - WLB (12 decks)

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