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Block 9: Cardio, Renal and Resp II > Week 7 (Genetic, Malignant, and Environmental Lung Disease) > Flashcards

Week 7 (Genetic, Malignant, and Environmental Lung Disease) Flashcards

1
Q

Mortality of lung cancer

A

Case fatality rate >90%

Overall 5 year survival <15%

More deaths anually than colon, breast, prostate and pancreatic cancer combined!

Rates declining in men but may be reaching plateau in women

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2
Q

Etiology of lung cancer

A

Cigarette smoking causes 87% of lung cancer

Second hand smoke

Radon

Occupational exposures: asbestos, uranium, arsenic, nickel radiation, chromium, chloromethyl ether, vinyl chloride

Asbestos and smoking multiply risk of lung cancer 10+ fold

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3
Q

Lung cancer and tobacco risk ratio (RR)

A
  1. 5 PPD = 15%
  2. 5-1 PPD = 17%

1-2 PPD = 42%

>2 PPD = 64%

Cigar = 3%

Pipe = 8%

Marijuana conflicting data

Second hand smoke = 1-2%

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4
Q

Risk factors for lung cancer other than tobacco

A

Pre-existing lung disease (COPD)

Previous tobacco-related cancer (ENT)

Interstitial fibrosis?

Nutrition?

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5
Q

Hypothesis of field cancerization

A

Exposure of respiratory tract to carcinogens (smoke) induces abnormalities in multiple areas with eventual development of carcinoma

Synchronous or metachronous cancer lesions in up to 14% of patients

Second primary cancers in 3-5% of patients/year

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6
Q

Does having another aerodigestive tract malignancy influence chance of getting lung cancer?

A

As many as 35% of patients with head and neck squamous cell carcinoma develop lung cancer

Similar risk in patients with esophageal cancers

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7
Q

Lung cancer evolutionary model

A

Pluripotent epithelial stem cell –> reserve cell, mucous cell, Clara cell, type II pneumocyte

Exposure to carcinogens (tobacco smoke) –> DNA damage

Diversion to premalignant and malignant conditions

Mucosal changes indistinguishable prior to transformation to malignancy

Growth promoted by cytokines and oncogenes

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8
Q

Functional classification of lung cancer

A

Non-small cell carcinoma: surgical resection for cure

Small cell carcinoma: not curable; can’t surgically resect but do chemotherapy

Carcinoid: typically slower growing; malignant potential related to local effects

Metastatic carcinoma: rare resectable lesion

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9
Q

WHO classification of lung cancer

A

Epithelial: benign (papillomas, adenomas), pre-invasive (carcinoma in situ), malignant (squamous cell, adenocarcinoma, large cell, small cell, sarcomatoid, carcinoid, salivary gland and unclasified)

Soft tissue (fibrous tumors)

Mesothelial (benign and malignant)

Miscellaneous (hamartoma, thymoma)

Lymphoproliferative

Other (unclassified, tumor-like)

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10
Q

IASLC/ATS/ERS lung adenocarcinoma

A

Preinvasive lesions

Minimally invasive adenocarcinoma

Invasive adenocarcinoma

Variants of invasive adenocarcinoma

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11
Q

Lung cancer based on location and appearance on radiograph

A

Central: squamous cell, small cell carcinoma

Peripheral: adenocarcinoma, large cell carcinoma

Cavitating: squamous cell carcinoma, occasionally large cell carcinoma

Superior sulcus tumors: more frequently squamous cell, also adenocarcinoma

Solitary pulmonary nodule: all cell types, less likely small cell carcinoma

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12
Q

How often is lung cancer asymptomatic?

A

Only 5% of the time

Solitary pulmonary nodule: if in high risk patient then suspect malignancy

Lack of growth over 2 years suggests benign (doubling of volume = 1.26 x diameter)

Can do serial scans, biopsy or resect

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13
Q

Patterns of appearance of solitary pulmonary nodule

A

Size: most not seen until 5-7 mm on chest x-ray

Spiculation and ill-defined margins suggests malignancy

Calcifications (central, ring, popcorn) suggest benign (but eccentric (off to the side) calcifications in lung cancer)

Mass lesions (>3cm) more likely malignant

Other findings in malignancy: pleural effusion, hemidiaphragm elevation, mediastinal adenopathy, rib or bony destruction, volume loss

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14
Q

Benign and malignant causes of solitary pulmonary nodule

A

Benign: infectious granuloma (cocci, histo, TB), infection, abscess, hamartoma, Wegner’s/GPA, rheumatoid nodule, pulmonary infarction, bronchogenic cyst, pneumonia, amyloidoma

Malignant: bronchogenic cancer (adenocarcinoma, squamous cell, large cell, small cell), metastatic cancer, bronchial carcinoid, pulmonary sarcoma

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15
Q

Clinical presentation of lung cancer

A

Asymptomatic (5%)

Symptoms related to site and extent of tumor

Invasion or obstruction of local structures: pain (chest, shoulder, radiculopathy), hoarseness, Horner’s syndrome (ptosis, miosis, anhydrosis), SVC syndrome, dyspnea, cough, hemoptysis, pleural effusions, diaphragm paralysis

Metastases to distant sites (adrenal, bone, brain, liver)

Paraneoplastic effects (SIADH, hypercalcemia, ACTH, Eaton-Lambert syndrome)

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16
Q

Features of progressive disease in lung cancer

A

Intrathoracic spread: tracheal obstruction, dysphagia, recurrent laryngeal nerve (hoareness), phrenic nerve (elevated hemidiaphragm), SVC syndrome, Horner’s syndrome, superior sulcus tumor, pericardial effusion, lymphatic obstruction, pleural effusion

Extrathoracic spread: lymph nodes (supraclavicular), brain, liver, adrenal, spinal cord, bone (contiguous and distant), subcutaneous

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17
Q

Paraneoplastic syndromes in lung cancer

A

Systemic: anorexia, cachexia, dermatomyositis, polymyositis

Endocrine: hypercalcemia, hyponatremia (SIADH), ACTH production

Neurologic: Lambert-Eaton syndrome (myasthenia), peripheral neuropathy

Cutaneous: clubbing, HPO, acanthosis nigrans

Hematologic: anemia, dysproteinemia

Renal: nephrotic syndrome, glomerulonephritis

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18
Q

Hypercalcemia in lung cancer

A

Ectopic hormone, bony metastases, immobility

Most commonly associated with squamous cell carcinoma

Bony metastases more common in adenocarcinoma and small cell carcinoma but hypercalcemia is rare

PTHrP (parathyroid hormone-related peptide) is ectopically produced by squamous cell carcinoma; binds PTH receptor to increase Ca2+ mobilization; PGE2 and IL-1 may be involved; clinical manifestations are weakness, lethargy, confusion, polyuria, renal failure

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19
Q

SIADH in lung cancer

A

Related to ectopic production of ADH usually by small cell lung cancer cells

Hyponatremia hallmark of presentation

Inappropriate ADH is when serum osmolality is low (<280 mOsm/kg) and don’t need to retain water; urine Na+ is >20 mEq/L

About 11% of small cell lung cancer patients have clinical hyponatremia

ANP is also secreted and can cause hyponatremia, and in this case ADH will be normal

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20
Q

Obtaining tissue for diagnosis in lung cancer

A

Sputum for cytology

Bronchoscopy: washings, bruchings, biopsies, needle aspiration

Transthoracic needle biopsy

Thoracentesis/pleural biopsy

Mediastinoscopy

Operative specimens (open lung biopsy)

Others: soft tissue mass, bone lesions, bone marrow, lymph node

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21
Q

Key issues in managing lung cancer

A

Establish diagnosis (benign vs. malignant)

Identify tissue (small cell vs. non-small cell)

Determine stage (clinical vs. pathologic)

Determine if candidate for surgical resection

Evaluate non-surgical treatment options

Role of screening for lung cancer

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22
Q

Early stage disease characteristics key to survival

A

Primary tumor localized without invasion of vertebrae or great vessels

Tumor >2cm from carina

Nodal spread limited to hilar nodes

Mediastinal nodes limited to same side of tumor

Local extension acceptable as long as areas can be resected (ribs, chest wall, etc)

Pleural effusions acceptable if non-malignant (inflammatory)

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23
Q

TNM staging of lung cancer

A

T: tumor size; confined to lung or spread to local structures

N: nodes involved; N1 is hilar or lobar; N2 is mediastinal; N3a?is ipsilateral; N3b? is extra-thoracic

M: metastasis

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24
Q

Are metastatic lung cancer patients ever operable?

A

Patients with single solitary brain met and localized primary tumor are operable

All other metastases are inoperable

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25
Q

Treatment for non-small cell lung cancer

A

Stage I and II: surgery

Stage IIIA: surgery on select cases; chemo (adjuvant or neoadjuvant); cisplatin or carboplatin based

Stage IIIB and IV: palliative (radiation, stereotactic body radiation therapy (SBRT), chemo, thoracentesis/pleurodesis, laser therapy; bronchial stents)

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26
Q

EGFR-TKI

A

Epidermal growth factor receptor-tyrosine kinase inhibitor

Binding of TK domain produces a signal transduction cascade –> tumor growth and proliferation

Monoclonal antibodies compete with binding and therefore block signals for tumor proliferation, invasion, metastasis, angiogenesis, inhibition of apoptosis

Imatinib (Gleevac); gefitinib (Iressa), cetuximab (Erbitux), erlotinib (Tarceva)

Used alone or in conjunction with other chemotherapy

Greater response and survival with EGFR mutations treated with gefitinib and erlotinib (exon 18, 19, 21), worse (20)

Greater response in females, Asian, adenocarcinoma

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27
Q

Anaplastic lymphoma kinase (ALK)

A

Cell membrane protein involved in central and peripheral nervous systems

Present in childhood neuroblastoma, lymphoma, non-small cell lung cancer

Translocation results in fusion protein (ELM4-ALK) with activity in tyrosine kinase domain

In 3-7% of non-small cell lung cancer but in 13% of light or non-smokers

No overlap in patients with EGFR mutations

Typically adenocarcinoma, younger, male, light or non-smoker

Target therapy with crizotinib (Xalkori) effective in 60%

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28
Q

Limited vs. extensive small cell lung cancer (staging)

A

Limited (30% at presentation): primary tumor confined to hemithorax and/or mediastinum; disease confined to single radiation port; equivalent to stages I-IIIA of non-small cell carcinoma (pleural and pericardial disease not considered limited disease)

Extensive (70% at presentation): metastases to contralateral lung; distant metastases (brain, bone marrow, liver, adrenals); usually with some response to chemo and/or radiation

New staging to change to stage I-III classification

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29
Q

Treatment of small cell carcinoma

A

Surgery: usually not recommended because likely micrometastatic disease and rapid growth; rare solitary lesion amenable to resection

Chemo: always; 15-20 agents; etoposide and cisplatin most active

Radiation: improves local control from 10-60%; improved survival; prophylactic cranial radiation after chemo response

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30
Q

Survival in small cell carcinoma

A

Untreated: 6-17 weeks

Treated: 40-70 weeks; <1% at 5 years

Limited disease: 14-20 months; 20-40% at 3 years

Extensive disease: 8-13 months; <5% at 3 years

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31
Q

Recommendations for lung cancer screening

A

Middle aged (55-74 yo)

>/= 30 pack year current smokers or have quit within the past 15 years

Current smokers encouraged on smoking cessation

General good health without signs or symptoms of lung cancer

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32
Q

Pleural fluid formation and drainage

A

Lymphatic stomata insert directly into parietal pleura

Subpleural lymphatics adjacent to visceral pleura

Fluid enters pleural space through parietal pleura via Starling’s forces and drained through visceral pleura

Proteins, particles, cells drained via lymphatic stomata in parietal pleura

0.5-1L absorbed and reabsorbed from pleural space each day

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33
Q

Normal pleural fluid characteristics

A

pH > 7.6

WBC < 1500 nucleated cells/mm3 (75% macrophages, 23% lymphocytes, 1% mesothelial cells, no eosinophils)

Protein is 15% of plasma levels (1-1.5 g/dL)

Glucose = plasma levels

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34
Q

Transudate vs. exudate

A

Transudate (bland fluid): increase in hydrostatic pressure = CHF; decrease in colloid oncotic pressure = anasarca albumin or nephrotic syndrome; increased negative pressure in pleural space = atelectasis; increased transport of peritoneal fluid through diaphragm = ascites, peritoneal dialysis

Exudate (turbid fluid): results from pleural inflammation, lung inflammation (increased capillary permeability = inflammation), impaired lymphatic drainage = malignancy

Most common causes of transudate: CHF, cirrhosis, PE

Most common causes of exudate: pneumonia, cancer, PE

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35
Q

Formation of pneumothorax (PTX)

A

Breach of pleural space (trauma to parietal or visceral pleura)

Air collects within pleural cavity

Pleural pressure equilibrates with atmospheric pressure

Air slowly resorbs through vasculature

Tension pneumothorax: one way air valve is created so on inspiration, air enters one hemithorax from tear in lung or hole in chest wall and does not exit on expiration; pleural pressure exceeds atmospheric pressure during entire respiratory cycle

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36
Q

Presentation of pleural effusion

A

Blunting of costophrenic angle

Meniscus sign

Contralateral displacement of trachea and mediastinum

Free flowing vs. loculated

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37
Q

Presentation of pneumothorax

A

Loss of lung markings

Pleural reflection

Deep sulcus sign in supine patient

Tension PTX has contralateral displacement of trachea and mediastinum

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38
Q

Thoracentesis

A

Tap effusion when significant amount of fluid (>10mm on decubitus film or significant fluid on US) AND unknown diagnosis; OR when respiratory compromise

Insert thoracentesis needle above the rib because artery, nerve and vein run below the rib

Removal of more than 1-1.5L at a time may lead to re-expansion edema

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39
Q

Light’s criteria for exudate

A

Pleural/serum protein >0.5

Pleural/serum LDH >0.6

Pleural LDH > 2/3 of institution normal

Need to fulfill only 1 criteria

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40
Q

Where do we see the transudate in different types of pleural effusion?

A

CHF: bilateral R >> L

Cirrhosis and peritoneal dialysis: R side

Nephrotic syndrome, hypoalbuminemic states: bilateral with diffuse edema

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41
Q

Unusual transudate from over-diuresed CHF

A

Pleural/serum protein > 0.5

Pleural/serum LDH < 0.6

Pleural LDH < 2/3 of institution normal

Transudate if: serum-pleural albumin ratio > 1.2

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42
Q

Exudates masquerading as transudates (unusual transudate)

A

Hypothyroidism

Heart disease, ascites

PE

23% transudative due to atelectasis

Malignancy

Early lymphatic obstruction, concomitant CHF

Sarcoidosis

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43
Q

All causes of exudate

A

Infectious

Malignant

Inflammatory: connective tissue disease

PE

Pancreatitis

Postcardiotomy syndrome

Drug induced

Esophageal rupture

Subdiaphragmatic abscess

Hypothyroidism

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44
Q

Additional studies to evaluate an exudate in pleural effusion

A

Cell count and diff

pH

Glucose

Culture and sensitivity

Cytology

Hct

Amylase

Adenosine deaminase

Triglycerides

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45
Q

Cell count and diff for pleural effusion

A

Neutrophilic “acute process”: pneumonia, PE, pancreatitis

Lymphocytic: malignant, TB, fungal, chylothorax

Eosinophilic: blood, air, drug reaction (dantrolene, bromocriptine, nitrofurantoin), asbestos exposure, paragonimiasis, Churg-Strauss syndrome

Bloody: Hct 1-20% (cancer, PE, trauma), Hct > 50% of peripheral Hct (hemothorax)

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46
Q

Triglycerides in pleural effusion

A

TG >/= 110

Chylothorax: milky white fluid, chylomicrons, due to disruption of thoracic duct (iatrogenic, lymphoma), unilateral

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47
Q

pH and glucose in pleura effusion

A

Empyema: pH 5.5-7.29, glucose <40

Esophageal rupture: pH 5.5-7, glucose <60

Rheumatoid pleuritis: pH 7, glucose 0-30

Malignancy: pH 6.95-7.29, glucose 30-59

TB: pH 7-7.29, glucose 30-59

Lupus pleuritis: pH 7-7.29, glucose 30-59

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48
Q

Amylase in pleural effusion

A

Pancreatis/pancreatic pseudocyst: pancreatic amylase

Carcinoma lung: salivary amylase

Adenocarcinoma ovary: salivary amylase

Lymphoma: macroamylase/salivary amylase

Esophageal rupture: salivary amylase

Pneumonia: salivary amylase

Ruptured ectopic pregnancy: prob salivary amylase

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49
Q

Adenosine deaminase in pleural effusion

A

Elevated levels in TB pleurisy, empyema, rheumatoid pleurisy, malignancy

Normal level is highly specific for absence of TB

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50
Q

Parapneumonic effusions

A

Simple: 40-57% of patients with pneumonia will develop a simple effusion; pH > 7.2; LDH < 1000; Glucose >/= 0.5 of plasma level

Complicated: 10-15% of patients with pneumonia will develop a complicated effusion; pH < 7.2; LDH > 1000; >1/2 hemithorax; glucose <0.5 of serum level; loculations

Empyema: 5% of patients with pneumonia will develop an empyema; gram stain or culture positive; frank pus

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51
Q

Treatment for parapneumonic effusion

A

Antibiotics

Simple: no drainage, re-tap if patient is not doing well

Complicated: complete drainage (thoracentesis; chest tube +/- fibrinolytics via chest tube; VATS/decortication)

Empyema: chest tube +/- fibrinolytics via chest tube; VATS/decortication

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52
Q

Malignant pleural effusion

A

Approximately 60% of malignant effusions can be diagnosed by cytology

Increased diagnostic yield with repeat thoracentesis: 65% diagnosed with first cytology; another 27% diagnosed with second cytology (however ONLY another 5% diagnosed with third cytology, so don’t do 3)

If suspect malignant effusion, do closed pleural biopsy (dx additional 7% of malignant disease when used in addition to cytology); video assisted thoracoscopic surgery (VATS) has 90% overall diagnosis rate

Treatment: observation, therapeutic thoracentesis, chest tube insertion with intrapleural sclerosant, thoracoscopy with talc poudrage (put talc in pleural space), long term indwelling catheter drainage, pleuroperitoneal shunt, pleurectomy

Note: sclerosis causes inflammation of the pleural tissue and adherence of the visceral pleura to the parietal pleura; need to re-expand lung and have apposition of pleural surfaces prior to sclerosis

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53
Q

Pneumothorax

A

Spontaneous primary: no clinically evident lung disease, no trauma or iatrogenic cause, usually subpleural apical blebs

Spontaneous secondary: due to underlying lung disease

Iatrogenic: direct trauma to visceral or parietal pleura

Traumatic

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54
Q

Spontaneous pneumothorax: primary

A

Young thin male 10-30 years old

Smoking increases risk 20 fold

Chest imaging with subpleural blebs

R/o connective tissue disease (Marfans)

Risk of recurrence 30% after first incidence, 60% after second, 90% after third

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55
Q

Spontaneous pneumothorax: secondary

A

Airways disease: COPD, CF, status asthmaticus

Interstitial lung disease: eosinophilic granulomatosis, sarcoidosis, LAM, tuberous sclerosis, rheumatoid lung disease, IPF, radiation fibrosis

Infectious disease: PCP PNA, staphylococcal PNA, necrotizing gram negative PNA

Other: ARDS barotrauma, Marfans, EDS

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56
Q

Iatrogenic pneumothorax

A

Central line insertion: neck/subclavian

Transbronchial lung biopsy

Transthoracic lung biopsy

Mechanical ventilation

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57
Q

Treatment for primary spontaneous pneumothorax

A

First occurence:

Stable patient with small PTX (<3cm apex to cupola) –> observation in ED 3-6 hours; if no change d/c with f/u in 12-48 hours

Stable patient with large PTX (>/= 3cm apex to cupola) –> re-expand lung, hospitalization preferable but can d/c home with Heimlich valve

Unstable patient with large PTX –> re-expand lung and hospitalize patient

Consider sclerosis if activities include high risk if PTX recurred (pilot, scuba diver), persistent air leak

Second occurrence: sclerosis recommended

VATS preferred intervention for sclerosis: 95-100% success via VATS compared with 78-91% success with chest tube instillation; VATS bullectomy to remove apical bullae

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58
Q

Treatment for secondary spontaneous pneumothorax

A

Stable patient with small PTX (<3cm apex to cupola) –> hospitalize +/- re-expansion of lung

Stable patient with large PTX (>/= 3cm apex to cupola) –> re-expand lung and hospitalize patient

Unstable patient with large PTX –> re-expand lung and hospitalize patient

Proceed with VATS pleurodesis +/- bullectomy as needed

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59
Q

Pneumonia

A

Inflammation of the lung parenchyma (pneumonitis) secondary to infection

Most common cause of infectious death in US

Overall mortality rate for community-acquired bacterial pneumonia 14%

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60
Q

Host defenses against pneumonia

A

Mucocilliary covering in conducting airways

Immunoglobulin A in mucosal secretions

Macrophages in respiratory parenchyma can phagocytize microorganisms and if overwhelmed recruit neutrophils from capillaries

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61
Q

Consolidation

A

Filling of alveoli with neutrophil-rich exudate

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62
Q

Bronchopneumonia vs. lobar pneumonia

A

Bronchopneumonia: pattern of consolidation typically involves more than one lobe with bronchiolocentric distribution (patchy)

Lobar pneumonia: uncommon due to availability of antibiotics

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63
Q

Clues on history for pneumonia

A

Cough in more than 90% of patients

Dyspnea in 66% of patients

Sputum production in 66% of patients

Pleuritic chest pain in 50% of patients

Fever

Malaise

Elderly patients may have few symptoms

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64
Q

Physical exam in pneumonia

A

Inspiratory crackles is most sensitive finding with any type of pneumonia

Increased tactile fremitus over consolidated lobe

Dull percussion over consolidated lobe

Bronchovesicular, egophony, whispered pectoriloquy over consolidated lobe

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65
Q

Chest radiography for pneumonia

A

All definitions of pneumonia include visualizing an infiltrate on a radiograph

Limited value in predicting the pathogen

Great value in determining extent of pneumonia and detecting complications like parapneumonic effusions or lung abscesses

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66
Q

Pneumonia syndromes

A

1) Community acquired acute pneumonia
2) Community acquired atypical pneumonia
3) Healthcare associated pneumonia
4) Aspiration pneumonia
5) Chronic pneumonia
6) Necrotizing pneumonia and lung abscess
7) Pneumonia in the immunocompromised host

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67
Q

Community acquired pneumonia (CAP)

A

Infectious pneumonia that develops in a patient who is not hospitalized or who has been hospitalized for less than 48 hours and has not been admitted to a hospital or extended health care facility in the past 90 days

Common pathogens: Strep pneumo, H influenzae, Moraxella catarrhalis, Staph aureus, Leigonella pneumophilia, Klebsiella pneumoniae

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68
Q

Pneumococcus as prototypical community-acquired acute pneumonia

A

Strep pneumo most common cause of community-acquired pneumonia (15-25% of cases)

Most common cause of lobar pneumonia

Paired diplococci seen on sputum gram stain

Can cause “rust colored sputum”

Encapsulated organism: may disseminate quickly in asplenic patients

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69
Q

Staph aureus pneumonia

A

Typically causes bronchopneumonia with multiple abscesses

Risk factors are recent influenza infection, IVDU

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70
Q

Klebsiella pneumoniae pneumonia

A

Most common gram negative bacillus to cause bacterial pneumonia

Can cause bronchopneumonia, lobar pneumonia and/or lung abscess

Abrupt onset of symptoms

Cough productive of gelatinous currant jelly sputum

Risk factors are alcoholism, debilitation (cause aspiration), malnourishment

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71
Q

Legionella pneumophilia

A

Gram negative bacillus, lives in water

Responsible for 5% of community acquired pneumonias

Fatal in 15% of cases

Usually causes bronchopneumonia

Presents with high fever, GI symptoms (diarrhea, vomiting)

Patients commonly lethargic with headache

Lab findings: hyponatremia is common as are hematuria and proteinuria and indicators of hepatic dysfunction; sputum gram stain with many neutrophils but few if any microorganisms; positive urinary legionella antigen

Risk factors: old age, organ transplantation, chronic lung, heart, kidney disease and hematologic disease

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72
Q

Community acquired atypical pneumonia

A

Atypical symptoms: nonproductive cough, headache, myalgias, upper respiratory symptoms, walking pneumonia

Atypical physical exam, lab and radiographic findings: unremarkable physical exam, minimal leukocytosis, lack of lobar consolidation on CXR

Atypical (not pneumococcus) pathogens: bacteria that do not have a cell wall or intracellular bacteria; viruses

Atypical pathogens: mycoplasma pneumoniae, legionella, chlamydia pneumoniae, chlamydia psittaci, coxiella burnetti, (MLC) influenza A and B, parainfluenza virus (children), metapneumovirus, adenovirus, SARS virus

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73
Q

Mycoplasma pneumonia special features

A

Lacks cell wall so not visible on gram stain

Fewer than 10% of people infected develop lower respiratory tract symptoms

Most common in younger patients (school-aged children and college students)

Upper airway symptoms (rhinitis)

Notable for nonpulmonary features: erythema nodosum, erythema multiforme, neurologic abnormalities (meningitis, encephalitis, transverse myelitis, cranial nerve palsies, cerebellar ataxia), cold agglutinins occasionally with hemolysis

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74
Q

Influenza special features

A

Upper airway symptoms are cough, rhinorrhea and sore throat (viral damage to airways)

Systemic symptoms abrupt onset of fever and myalgia (caused by interferon production)

May cause lower airway infection (pneumonia) on its own: much less common than upper airway infection

Damage to lung epithelial layer also leads to risk of secondary infections (commonly pneumococcus and Staph aureus)

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75
Q

Most common CAP pathogens

A

Outpatient: strep pneumo, mycoplasma pneumoniae, H influenzae, respiratory viruses

Inpatient (non-ICU): strep pneumo, mycoplasma pneumoniae, chlamydia pneumoniae, H influenzae, Legionella, aspiration (of mixed oropharyngeal flora), respiratory viruses

Inpatient (ICU): strep pneumo, Legionella, staph aureus, gram negative bacilli, H influenzae

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76
Q

Initial workup for pneumonia

A

PA and lateral CXR

Blood cultures prior to antibiotics (3-14% will be positive in setting of CAP): quality measure tracked by medicare

Possible urine antigen testing for Legionella and Strep pneumo

Sputum culture: optional given that its useful only 14% of the time

CBC and complete metabolic panel

Thoracentesis should be done if pleural effusion present

77
Q

CURB-65 score

A

1 point for:

Confusion

BUN > 19

RR > 30

SBP < 90 or DBP < 60

Age 65 or above

78
Q

Outpatient treatment of CAP

A

Macrolide antibiotic preferred if patient does not have significant comorbidities (azithromycin, clarithromycin)

Respiratory fluoroquinolone if patient has comorbidities (levofloxacin, moxifloxacin)

79
Q

Duration of antibiotic treatment for CAP

A

By convention most physicians treat for 7-10 days

One study shows levofloxacin x 5 days is equivalent

Certain organisms (Staph aureus, Legionella) may need prolonged treatment

80
Q

What if patient fails to improve on this medication regimen?

A

If patient not improving after 48 hours of treatment, consider pathogen reisstant to chosen antibiotics or spread of infection beyond the alveoli (complicated parapneumonic effusion, empyema, suppurative pericarditis)

81
Q

Vaccines

A

Pneumococcal polysaccharide vaccine (Pneumovax 23): given once to adults >65 decreases risk of bacteremia and death in patients who get a pneumococcal pneumonia

Influenza: recommended yearly for everybody more than 6 years old

82
Q

Smoking cessation counseling

A

Should be addressed before patient with CAP discharged from hospital

Medicare and medicaid quality measure

Quitting smoking reduces risk of pneumococcal disease by 14% each year thereafter

83
Q

What can PPIs and NSAIDs do to contribute to pneumonia?

A

PPIs may be emerging risk factor for community-acquired bacterial pneumonia

NSAIDs are associated with blunted inflammatory response which can lead to delay in presentation and higher risk for pleuorpulmonary complications in patients with pneumonia

84
Q

Healthcare-associated pneumonia (HCAP)

A

Includes hospital-acquired pneumonia (HAP or nosocomial pneumonia) and ventilator-associated pneumonia (VAP), and includes patients who have resided in extended care facility or hospital in previous 90 days and those receiving outpatient hemodialysis, chemo and wound care

85
Q

Hospital-acquired pneumonia (HAP or nosocomial pneumonia)

A

Develops more than 48 hours after hospitalization

86
Q

Ventilator-associated pneumonia (VAP)

A

Develops more than 48 hours after intubation

87
Q

Preventing hospital-acquired pneumonias

A

Avoid endotracheal intubation (consider BiPAP in right settings)

Keep head of bed at 30-45 degrees

Maintain patient’s oral hygiene

Hand washing by all medical staff

88
Q

Risk factors for multidrug resistant pathogens causing HAP or HCAP

A

Antimicrobial therapy in last 90 days

Current hospitalization for longer than 5 days

High-frequency of antibiotic resistance in the hospital or the community

Immunosuppressive disease or therapy

Residence in nursing facility

Family member with multidrug-resistant pathogen

89
Q

Potential pathogens for HAP and HCAP

A

Standard pathogens: Strep pneumo, H influenzae, E coli, Proteus, serratia marcescens, klebsiella pneumonia, legionella pneumophilia

Multidrug resistant pathogens: pseudomonas aeruginosa, MRSA, klebsiella with extended-spectrum beta lactamase (ESBL) activity, acinetobacter

90
Q

Empiric antibiotic therapy for patients with risk factors for multidrug resistant HAP or HCAP

A

Anti-psuedomonal cephalosporin (cefepime or ceftazidime) or anti-psuedomonal carbapenem (imipenem or meropenem) or beta lactam + beta lactamase inhibitor (piperacillin/tazobactam)

PLUS

Anti-pseudomonal fluoroquinolone (ciprofloxacin) or aminoglycoside (amikacin, gentamicin, tobramycin)

PLUS

Linezolid or vancomycin

91
Q

HAP/HCAP duration of treatment

A

Can change broad-spectrum antibiotic therapy to more tailored regimen based on identification of responsible pathogen and deliniation of drug sensitivities

Treat common pathogens for at least 7 days and multidrug-resistant pathogens for at least 14 days

92
Q

Where does aspirated material go?

A

If patient upright: usually basal segment of lower lobe (all the way down)

If patient supine: usually posterior segment of upper lobe or apical segment of lower lobe (not all the way down)

93
Q

Why do you get night sweats and not during the day?

A

Lowest hypothalamic set point for temperature is late at night

Body wants to be cool in the middle of the night but you’re warm because of infection so get really sweaty to try to cool down more!

94
Q

Coccidiodomycosis

A

Caused by inhaling spores of coccidioies immitis a dimorphic fungus found in the southwestern and far western US

Granulomatous pneumonia

Lung lesions, cough, pleuritic chest pain, fever, erythema nodosum or erythema multiforme = San Joaquin Valley Fever Complex

Disseminated disease can involve skin, bone and meninges

95
Q

Histoplasmosis

A

Dimorphic fungus endemic to the Mississippi River Valley

Lives in soils enriched by bird or bat droppings

Like M tuberculosis an intracellular parasite of macrophages

Presentation can mimic that of TB

96
Q

Blastomycosis

A

Blastomyces dermatitidis: soil-inhabiting dimorphic fungus

Pulmonary blastomycosis can present as an abrupt illness with productive cough, fever and upper lung involvement on CXR

Macrophages have limited ability to kill B dermatitidis, thus neutrophils are recruited (suppurative granulomatous inflammation)

Can cause epithelial hyperplasia that can be mistaken for cancer

Midwest and east coast

Broad based budding yeast

97
Q

Actinomyces israelii

A

Gram positive, thin branching filamentous bacterium

Anaerobic, not acid fast (NO and NO!)

Colonies yellow and smell bad and look like sulfur granules

Risk factor is COPD

Causes chronic pneumonia

98
Q

Necrotizing pneumonia and lung abscess common pathogens

A

Anaerobic bacteria

Staph aureus

Klebsiella pneumoniae

Strep pyogenes

Strep pneumo type 3 (only type of strep pneumo that cavitates!)

99
Q

Special consideration for lung abscesses

A

10-15% of abscesses are related to carcinoma obstructing an airway (so look for proximal obstructive tumor)

Right-sided bacterial endocarditis can result in lung abscess (usually see multiple abscesses)

Treat with antibiotics until radiographic resolution (do NOT stick needle into abscess to drain it)

100
Q

Pneumocystis pneumonia

A

Now is called pneumocystis jiroveci but used to be pneumocystis carinii (PCP)

Classified as fungus (but similar to protozoa)

AIDS, occurs when CD4 count <200

Presents with non-specific symptoms: subtle onset progressive dyspnea, nonproductive cough, low-grade fever

PE has tachypnea and tachycardia but normal lung sounds

Elevated serum LDH is non-specific (released by injured lung)

Bilateral perihilar interstitial infiltrates that becomes increasingly homogeneous and diffuse as disease progresses; less often see nodules, pneumatoceles or normal CXR

Diagnose with direct fluorescent antibody (DFA) testing of sputum induced with hypertonic saline

Treatment: TMP-SMX and corticosteroids at the same time (esp in patients with PaO2 <70 on room air or A-a gradient >35)! Want to reduce inflammation that is caused by treating PCP

101
Q

Aspergillus

A

Angioinvasive molds that often induce thrombosis and infarction with subsequent suppuration

Hematogenous spread common with involvement of heart valves and brain

Often seen in transplant patients on corticosteroids or patients with hematologic malignancies

Often diagnosed with aspergillus EIA

Treated with voriconazole and by decreasing immunosuppressant medications

Halo sign: angioinvasive causes bleeding during invasion

Aspergilloma will NOT invade, but see air crescent sign on CXR

102
Q

Nontuberculous mycobacterial infection

A

Ubiquitous mycobacteria found in water and soil

Opportunistic pathogens in patients with cell-mediated immunodeficiency or underlying structural bronchopulmonary disease

M avium and M intracellulare grouped together as M avium complex (MAC)

HIV infected patients can get both pulmonary disease and disseminated disease

Multiple cavitary or nodular opacities on imaging

103
Q

Nocardia asteroides

A

Gram positive, branching filaments

Aerobic and partially acid fast (YES and YES!)

Causes indolent bronchopneumonia with abscess formation

1/5 of infections involve CNS

Most infected patients have defect in T cell-mediated immunity (prolonged steroid use, HIV, diabetes)

Treated with prolonged course of TMP-SMX

104
Q

Key word associations

A

Rust colored sputum = pneumococcus

Currant jelly sputum = klebsiella

Alcoholic = klebsiella, aspiration pneumonitis

Seizure = aspiration pneumonitis

Lung and brain infection (indolent) = nocardia

Lung and brain infection (fulminant) = aspergillus

Putrid sputum = lung abscess (anaerobes)

Sulfur granules = actinomyces

Acid fast = M. tuberculosis, atypical mycobacterium, nocardia

Pneumonia with bullous myringitis = mycoplasma

Walking pneumonia = mycoplasma

Pneumonia with unusually high LDH = PCP pneumonia

Night sweats = TB

Pneumonia after earthquake = coccidiodomycosis

Poor dentition = anaerobes

Pneumonia on ventilator = MRSA, pseudomonas

Foreign born = TB (remember, BCG called “FOB vaccine”)

Cerebrovascular accident = aspiration pneumonia

Dementia = aspiration pneumonia

Diplococci = pneumococcus

Dysphagia = aspiration pneumonia

Coughing with eating = aspiration pneumonia

Sickle cell disease = functional asplenia, risk of sepsis with encapsulated organisms (SHiNE SKiS: strep pneumo, H influenza B, Neisseria meningitidis, E coli, Salmonella, Klebsiella, group B Strep)

Pneumonia with high fever, hyponatremia, and hematuria = legionella

Bird or bat droppings = histoplasmosis

105
Q

Occupational lung diseases

A

Occupational lung diseases: any disorder of the lungs that results from extrinsic etiology related to the workplace

Lung must eliminate particles without excessive inflammation (but appropriately respond to infectious particles)

Often found incidentally on chest imaging and radiographic findings may be out of proportion to symptoms

May exacerbate pre-existing lung disease (increased deposition and decreased clearance of fibers)

Occupational asthma and asbestos-related diseases are most common in US

106
Q

Pneumoconioses

A

“Dust diseases” due to accumulation of inorganic dusts within the lungs and the tissue reaction to their presence

Can be fibrotic or non-fibrotic

Examples: coal worker’s pneumoconiosis, asbestos, silicosis

Primary prevention is key because no treatment other than symptomatic (eliminate hazard, use ventilator, respirator)

Clues: clusters, young age, slower progression of ILD

Easily missed: 25% of “IPF” biopsies had mineral deposits and 6% of “sarcoidosis” patients had + beryllium lymphocyte proliferation test!

107
Q

Classification of occupational lung diseases

A

Parenchymal/interstitial lung disease: pneumoconioses, hypersensitivity pneumonitis, drug-induced lung disease

Airway: occupational asthma, COPD, bronchiolitis obliterans

Physiology: high altitude/diving

Smoking, radiation, etc –> malignancies

108
Q

Fibrogenic vs. low-fibrogenic pneumoconioses

A

Fibrogenic: silica (silicon dioxide), silicates (asbestos is lower and talc and kaolin are upper), coal dust, aluminum

Low-fibrogenic: deposits of iron, tin, barium, titanium, glass wool; granulomatous is beryllium

109
Q

Silicosis

A

Inhalation of crystalline silica (quartz) found in sand and rock

Seen in hard rock/coal mining, construction, quarrying, masonry, sandblasting, foundry, glass workers, ceramics, granite, stonework

Silica generates O2 radicals and injures alveolar macrophages

Note: coal workers can get CWP and silicosis!

110
Q

Three presentations of silicosis

A

Chronic simple silicosis: latency 10-30 years, low exposure with variable course; usually see upper lung zone nodular opacities, can be calcified, have enlarged LN with eggshell calcifications

Accelerated silicosis: develops within 10 years of initial exposure, associated with high-level exposure, more severe and often progressive, progressive massive fibrosis (PMF) refers to progressive coalescence of silicotic nodules leading to respiratory impairment

Acute silicoproteinosis or acute silicosis: exposure to high concentrations of silica, symptoms occur within a few weeks to a few years after initial exposure, poor prognosis (dyspnea, cyanosis, cor pulmonale, respiratory failure and death within 4 years); see bilateral alveolar filling process in both lower lobes

111
Q

Complications of silicosis

A

Complicated silicosis or PMF

Increased risk of TB and non-TB mycobacterial disease, connective tissue disease, lung cancer, chronic bronchitis

Caplan’s syndrome is when you have RA and silicosis

Treatment is supportive, very rarely lung transplant

112
Q

Coal workers’ pneumoconiosis (CWP)

A

Inhalation of coal dust

More prevalent in underground workers (higher concentration)

Alveolar macrophages engulf coal dust and release toxic proteases and cytokines leading to fibrosis and emphysema

Black lung

Also ask about loading ships with coal, manufacture of carbon electrodes and graphite mining

Simple, complicated and progressive massive fibrosis

Caplan’s syndrome is also RA plus CWP

113
Q

Exposure risk for CWP and silicosis

A

Highest exposure risk is cutting machine operator that cuts coal directly

Roof bolters drill through rock (exposed to silica too); continuous mine operator, loading machine operator, shot firer

Train operators drop sand onto tracks for traction and may develop silicosis

Motormen, brakemen, drivers, shuttle car operators have less dust exposure because coal already been cut at this point

Mechanics, electricians and maintenance men have least amount of dust exposure

114
Q

CXR findings in CWP

A

Upper zone predominant nodules

Can develop progressive massive fibrosis and emphysema

In complicated CWP, micronodules have coalesced to form PMF (person will die soon)

115
Q

Simple pneumoconiosis vs PMF

A

Simple pneumoconiosis: usually no functional deficits

Progressive massive fibrosis (PMF): larger (>1cm) opacities, significant functional deficits

Workers with simple pneumoconiosis have much greater risk of getting PMF

116
Q

Asbestos

A

Asbestos is a type of silicate (“magic mineral”) that is cheap, easy to mine and multiple applications

Two forms are serpentine (chrysotile/white >90%) and amphibole (crocidolite/blue, tremolite, etc)

Astestos fiber is critical in disease pathogenesis: released during mining, milling, fabrication, installation (<3 microns in diameter)

117
Q

Jobs with asbestos exposure

A

Shipbuilding, repair or refitting (WWII vets)

Building fireproofing, maintenance, or demolition

Brake work

Construction

Thermal insulation

Plumbers, electricians, welders, present in many rocks

Additionally: launderers of asbestos workers’ clothes, living or working in buildings constructed in early post-WWII period, houses built between 1930-50 (in inuslation), textured paint and patching in ceiling/walls before 1977, hot water and steam pipe blankets and insulation in older homes, some vinyl floor tiles/backing

118
Q

Forms of asbestos-related lung disease

A

Asbestos plaques

Diffuse pleural thickening

Asbestosis: pulmonary parenchymal fibrosis

Bronchogenic carcinoma

Malignant mesothelioma

Benign exudative or bloody pleural effusion

Anxiety

119
Q

Pleural plaques in asbestos exposure

A

Detectable on CXR

Very common in asbestos-exposed workers (shipyard workers)

Plaques usually develop first

Does not predispose to lung cancer?

120
Q

Asbestosis

A

Pulmonary parenchymal fibrosis

Clear dose response relationship

Latency period ranges 15-40 years

Dyspnea, cough, crackles, clubbing

Restrictive lung disease with diffusion impairment

Biospies not required for diagnosis

20-40% progress

Higher subsequent risk of lung cancer

Progression is slower (15-20 years) compared to IPF (2-3 years)

121
Q

Imaging in asbestosis

A

Bilateral reticular/linear opacities at lung bases

Honeycombing (cysts pulled taut)

Usually have associated pleural disease/plaques

Usually basilar and subpleural distribution

If see pleural plaques with lung fibrosis, call it asbestosis!

122
Q

Malignant mesothelioma

A

Rare malignancy of pleura or peritoneum very closely associated with asbestos and not affected by smoking

Occurs even with low levels of exposure especially with amphibole

Presents with large pleural effusion and dyspnea

Prognosis poor with limited treatment options (only live 1-1.5 years after this)

123
Q

Bronchogenic carcinoma

A

Strong synergy between asbestos and tobacco (up to 40-60x increase in exposed smokers)

Asbestosis markedly increases risk of lung cancer and all histologic subtypes seen

Also linked to other malignancies

124
Q

Occupational airway diseases

A

Work-related asthma: occupational asthma (with latency/sensitization, without latency/RADS) and work-exacerbated asthma

COPD

Bronchiolitis obliterans

125
Q

Diagnostic testing for occupational airway diseases

A

Spirometry pre and post-bronchodilator

Methacholine challenge testing

Skin testing

Specific agent inhalation challenges

Antibody tests

126
Q

Occupational asthma with latency

A

Results from allergic sensitization to a specific workplace chemical

Once sensitized a very low dose can cause an asthma attack

Health care workers and latex

Isocyanate in auto spray paints, polyurethane foams, adhesives, surface coatings, elastomers, or in manufacture of plastics or rubber

Carpenters and wood dust

Risk factors: atopy, smoking, genetics

>50% of patients have persistent symptoms/asthma despite cessation of the exposure

Workers who remain exposed have worse prognosis so early diagnosis matters

Treated similarly to non-occupational asthma

127
Q

Occupational asthma without latency

A

Reactive airways dysfunction syndrome (RADS)

Results from single high-level exposure to highly toxic material

Symptoms occur within 24 hours

Paper mill explosions (SO2), chlorine, mustard gas

Direct mucosal injury –> airway hyperresponsiveness

Can be fatal acutely and treated with oral/inhaled corticosteroids

May not improve with time

128
Q

Occupational COPD

A

Not just tobacco!

Coal

Hard rock mining

Concrete products

Dust fumes, gas, diesel exhaust

Wood stoves

129
Q

Chief complaint of cough in a kid

A

Duration of symptoms: acute vs. chronic

Characteristics: sputum production; daytime vs. nighttime symptoms (nighttime = asthma)

Associated symptoms: fever, conjunctivitis, runny nose, ear pain, sore throat, nausea, vomiting, abdominal pain, rash

Factors/tx that makes it better or worse

Additional medical history (birth history)

130
Q

Upper airway diseases with cough

A

Viral URI

Otitis media

Sinusitis

Pharyngitis: strep, peritonsillar/retropharyngeal abscess, epiglottitis

Croup

Foreign body aspiration

131
Q

Lower airways diseases with cough

A

Bronchiolitis

Asthma

Pneumonia

132
Q

Viral URI

A

Pathogenesis: rhinoviruses (50%), RSV, influenza, parainfluenza, coronavirus, adenovirus, enterovirus, immune response to the virus

Symptoms: fever at onset (typically 24-48 hours), rhinorrhea, earache, sore throat, cough, malaise, headache, duration 10-14 days

Treatment: no OTC cough/cold meds for kids less than 2 yo and lack of efficacy and potential toxicity of OTC meds for kids less than 6 years old too; supportive care (anti-pyretics (Tylenol, Advil > 6mo?), cool mist humidifier, nasal bulb suction)

133
Q

Otitis media

A

Pathogenesis: antecedent URI (AOM is a bacterial superinfection on top of viral URI?), colonization with bacterial otopathogen (strep pneumo, H influenzae, moraxella catarrhalis)

Acute otitis media (suppurative infection)

Otitis media with effusion (inflammation with effusion; can happen with any viral URI; is fluid in back of ear that makes it pop)

Diagnosis: recent, abrupt onset of signs/symptoms (fever, irritability, URI symptoms); presence of middle ear effusion (bulging TM, limited mobility of TM, air fluid level behind TM, otorrhea); signs or sx of middle ear inflammation (erythema of TM, otalgia)

Treatment: 6mo-2yr antibiotics if otorrhea w/AOM, uni/bilateral AOM with severe sx, bilateral AOM w/o otorrhea, but if unilateral AOM without otorrhea can do observation; >2yr antibiotics if otorrhea w/AOM, uni/bilateral AOM with severe sx, but if uni/bilateral AOM without otorrhea can do observation; use amoxicillin (cefdnir, azithromycin)

134
Q

Sinusitis

A

Viral: acute, self-limited rhinosinusitis, usually less than 14 days

Bacterial: superinfection with otopathogen (Strep pneumo, nontypeable H influenzae, Moraxella catarrhalis)

Timing of sinus development: ethmoidal and maxillary at birth (maxillary sinuses are pneumatized by 4yrs); sphenoidal 5yrs; frontal 8-12yrs

Diagnosis: antecedent URI, including purulent nasal discharge, fever and cough; symptoms persisting for greater than 10-14 days without improvement

Treatment: antibiotic (amoxicillin (bactrim, azithromycin))

135
Q

Pharyngitis

A

Viral: adenoviruses, coronaviruses, enteroviruses, rhinoviruses, RSV, HIV, EBV (infectious mononucleosis)

Bacterial: group A beta-hemolytic streptococcus, corynebacterium diphtheriae, mycoplasma pneumoniae, neisseria gonorrhoeae, H influenzae, strep pneumo

136
Q

Symptoms of strep throat

A

Rapid onset fever and sore throat

No cough

Headache and abdominal pain, nausea or vomiting

Tonsillar enlargement, white exudates, petechiae on palate

Painful cervical lymphadenopathy

Symptoms of scarlet fever: circumoral pallor and strawberry tongue, red papular sandpaper rash

137
Q

Treatment of GAS pharyngitis

A

Reduce clinical symptoms of fever and pain

Reduce suppurative complications (peritonsillar or retropharyngeal abscess)

Reduce non-suppurative complications (acute rheumatic fever, glomerulonephritis), however can still get glomerulonephritis even if you treat strep throat

Treatment: penicillin (amoxicillin), cephalosporins, macrolides

138
Q

Epiglottitis (supraglottitis)

A

Pathogenesis: H influenza B (Hib), but not much anymore because we vaccinate

Symptoms: rapid onset of fever, sore throat, dyspnea, drooling, tripod-ing

Diagnosis: lateral neck radiographs (thumb sign), direct visualization

Management and treatment: establish airway (nasotracheal intubation, tracheostomy), calming measures (avoid unnecessary exams, blood draws, etc), antibiotics (third gen cephalosporin, vancomycin if MRSA is concern)

139
Q

Croup (laryngotracheobronchitis)

A

Pathogenesis: viral infection of glottis and subglottis (parainfluenza, influenza, RSV, adenovirus, enterovirus)

Symptoms: rhinorrhea, cough, pharyngitis, fever, “barking” cough, hoarseness, inspiratory stridor (high fever at night, cough and stridor worse at night)

Treatment: supportive care (anti-pyretics, fluids, cool mist, oral dexamethasone, racemic epi)

Clinical course: improves within 5-7 days, nighttime symptoms gradually improve

140
Q

Foreign body aspiration

A

Symptoms: initially sudden onset coughing, gagging, possible airway obstruction; in asymptomatic period object becomes lodged, reflexes fatigue out; complications are obstruction, erosion, infection (fever, hemoptysis, pneumonia, new-onset wheezing)

History is key!

Location: right bronchus >50% of cases, trachea approximately 10% of cases

High-risk objects: toys, food (nuts, globular objects (hot dogs, grapes))

Treatment: endoscopic removal

141
Q

Wheezing

A

Inflammation (bronchiolitis): viral infections

Asthma

Anatomic abnormalities

Mucociliary clearance disorders (CF)

Aspiration

Non-pulmonary conditions: heart failure, foreign body aspiration

142
Q

Bronchiolitis

A

Pathogenesis: acute inflammation with edema, mucus and cellular debris in the bronchioles, predominantly viral etiology (RSV >50% of cases, parainfluenza, adenovirus, mycoplasma)

90% of children infected with RSV by age 2 (40% of those will have bronchiolitis)

Risk factors for severe disease: age less than 12 wks, history of prematurity, congenital heart disease, chronic pulmonary disease, history of CF, immunodeficiency, environmental risk factors (older siblings, childcare attendance)

History: birth hx, NICU hx, prior episodes of wheezing, fam hx of wheezing, sick contacts/daycare exposure

PE: vitals (oxygenation and RR; don’t be fooled by absence of wheezing), accessory muscle use

Diagnosis: primarily clinical, chest radiograph, viral testing (RSV, influenza, parainfluenza, pertussis)

Treatment: supportive care, trial of bronchodilators, humidified air, supplemental oxygen, Palivizumab only for high risk kids and is very expensive

143
Q

Palivizumab (Synagis)

A

Treatment for bronchiolitis

Monoclonal antibody designed to prevent serious lower respiratory tract disease caused by RSV in high-risk children only

Dose and schedule: IM injection, given monthly Nov-March, $900 per dose

144
Q

Asthma

A

Pathogenesis: airway inflammation, bronchial hyperreactivity and reversibility of obstruction

Most diagnosed before 6yo, most who wheeze in childhood are NOT later diagnosed with asthma, AA have more ER visits, hospitalizations, deaths

Risk factors: fam hx of parental asthma, allergic history (eczema, allergic rhinitis, food allergy), bronchiolitis requiring hospitalization, penumonia, male, environmental tobacco smoke exposure, low birthweight

Symptoms: dry cough, chest tightness (persistent nighttime cough, associated with exercise), expiratory wheezing

Triggers: physical activity, airway irritants, cold or dry air, infection

Evaluation: FEV1/FVC <0.8, low FEV1, bronchodilator response (improve FEV1 >12%), exercise challenge (worsening FEV1 >15%); peak flow monitoring (daily variation >20%)

Management: assessment and monitoring of disease activity, education of patient and family, ID triggers and co-morbid conditions, appropriate meds, treat co-morbidity (allergic rhinitis, GERD)

145
Q

Classification of asthma severity

A

Mild intermittent: daytime sx <2 days/wk

Mild persistent: daytime sx >2 days/wk but not daily

Moderate persistent: daily sx

Severe persistent: daily sx throughout the day

146
Q

Classification of asthma control

A

Well-controleld: sx <2 days/wk and once per day

Not well-controlled: sx >2 days/wk or more than twice per day on 2 days/wk

Very poorly controlled: sx throughout the day

147
Q

Asthma medications

A

Beta agonists: SABA. LABA

Inhaled corticosteroids: low- or medium- or high-dose inhaled corticosteroid

Oral corticosteroids

Leukotriene receptor antagonist

Cromolyn (prevents mast cell degranulation), montelukast (leukotriene receptor blocker)

Step-wise approach to management

148
Q

Pneumonia

A

Leading cause of under-5 deaths

However, abx and vaccinations (Hib and pneumococcal conjugate) caused 97% decrease since 1939!

Treatment: empiric antibiotics based on age and risk factors, consider hospitalization (age <6mo, immunocompromised, toxic appearance, moderate-severe respiratory distress, hypoxia, vomiting/dehydration, failure of oral antibiotic therapy, social factors)

149
Q

Frequent pathogens causing pneumonia

A

Neonates: Group B strep, E coli, Strep pneumo, H influenzae

3 wks-3mos: RSV, influenza/parainfluenza/adenovirus, strep pneumo, H influenzae, C trachomatis

4mo-4yrs: RSV, influenza/parainfluenza/adenovirus, strep pneumo, H influenzae, C trachomatis, group A strep

>5yrs: M pneumoniae, Strep pneumo, Clamydophila pneumoniae, H influenzae, influenza and other viruses, legionella

Runts may cough chunky sputum: RSV, Mycoplasma, chlamydia trachomatis, C pneumoniae, strep pneumo

150
Q

Cystic fibrosis

A

Autosomal recessive

CF gene is CFTR protein which is expressed on epithelial cells of airways, GI tract, sweat glands, GU system

Failure to clear mucous secretions, paucity of water in mucous secretions, elevated salt content in sweat, chronic respiratory infections

151
Q

Airway epithelial cell pathology in CF

A

Inability to secrete salt and water

Excessive reabsorption of salt and water

Insufficient water on airway surface to hydrate secretions

Altered microenvironment (more acidic) aggravates mucociliary clearance

Airway colonization with staph aureus, pseudomonas, burkholderia cepacia

152
Q

Pathology of CF

A

Lungs develop bronchiolitis –> bronchitis –> bronchiolectasis –> bronchiectasis –> bronchiolar obliteration

Paranasal sinuses contain inflammatory products

Pancreas is usually small and fibrotic

Focal biliary cirrhosis develops with time

Uterine cervix glands are often distended with mucus

Epididymis, vas deferens, seminal vesicles are obliterated or atretic in most cases

153
Q

Clinical presentation of CF

A

Respiratory: cough with purulent sputum, recurrent wheezing/bronchiolitis, prolonged infections, often requiring hospitalization

GI: meconium ileus (abdominal distention, emesis, failure to pass stool within 24-48 hours of life), frequent greasy stools (due to exocrine pancreatic insufficiency), failure to thrive (eat but don’t gain weight)

154
Q

Diagnosis of CF

A

Positive quantitative sweat test

AND

Chronic obstructive pulmonary disease

Documented exocrine pancreatic insufficiency

Positive fam hx

Can do genetic testing and newborn screening

155
Q

Pulmonary treatment

A

CFTR modulators: Ivacaftor (designed for patients with G551D mutation in at least one CFTR gnee)

Antibiotics: azithromycin, nebulized tobramycin directed at pseudomonas

Bronchodilators

Agents to promote airway secretion clearance (inhaled DNAse I cleaves long strands of denatured DNA, hypertonic saline)

Chest physiotherapy

Vaccination (influenza and pneumococcal)

Nutritional treatment: pancreatic enzyme replacement, vitamin supplementation (K, A, D, E), parenteral supplenemtation

Lung transplantation: but non-pulmonary manifestations are unchanged

Multi-disciplinary approach is critical to success (primary care, pulmonology, respiratory therapy, gastroenterology, nutrition, social work, etc)

Transition from pediatric to adult providers of care is critical to success (physical, social, economic changes and challenges need to be anticipated for success)

156
Q

Normal pulmonary circulation

A

High compliance

Low resistance

Therefore, usually low pressures

Normal pressures:

Systolic: 15-30 mmHg

Diastolic: 3-12 mmHg

Mean: <20 mmHg

Mean PA pressure >25 mmHg = pulmonary HTN

157
Q

Three factors that independently increase pulmonary blood pressure

A

Left atrial pressure (LAP)

Pulmonary vascular resistance (PVR)

Pulmonary blood flow (PBF)

158
Q

Hemodynamic classification of pulmonary hypertension

A

Precapillary (increased PVR): primary PH, secondary collagen vascular disease, liver disease, HIV, thromboembolic disease, hypoxemic PH (hypoxic pulmonary vasoconstriction, lung disease)

Postcapillary (increased LA pressure): LV systolic or diastolic heart failure, aortic and mitral valve disease

Mixed: chronic LV failure, chronic aortic and mitral valvular disease

Increased pulmonary blood flow: congenital heart disease (ASD, VSD, PDA), high output failure, liver disease, anemia

159
Q

WHO classification

A

Based on different treatment options

Pulmonary arterial HTN: problems in vasculature of lungs

Pulmonary venous HTN: cardiac conditions

Hypoxic induced: affects circulation of lungs

Thrombotic emboli: obstruct proximal portion of pulmonary circulation

Miscellaneous: tumor obstructing circulation, etc

160
Q

Idiopathic/primary PH

A

More female than male

Etiology unclear

Genetic: familial form, AD, mutation in BMPR2

Coagulation defects, hormonal (association with pregnancy)

161
Q

Secondary PH

A

Collagen vascular disease (scleroderma 20% (especially CREST 50%), mixed connective tissue disease 30-40%, SLE 5%)

Portal HTN (2-5% with cirrhosis, 8% at liver transplant)

Drugs (cocaine, amphetamines, anorexins)

Hemoglobinopathies (sickle cell anemia, chronic hemolytic anemia)

HIV

Congenital heart disease (L to R shunts)

Other: schistosomiasis, Gaucher’s disease, hereditary hemorrhagic telangiectasia, persistent pulmonary hypertension of the newborn and thyroid disorders

162
Q

Pathogenesis of PH

A

Vasoconstriction: impaired synthesis of NO and prostacyclin; enhanced production of endothelin and thromboxane

Vascular wall remodeling: concentric medial hypertrophy due to smooth muscle and endothelial cell proliferation; BMPR2 genetic defect (normally inhibits vascular smooth muscle proliferation and favors apoptosis)

Thrombosis: injury to endothelium, abnormal fibrinolysis, enhanced procoagulant activity, platelet abnormalities

163
Q

Vascular change in PH

A

Normal

Mild to moderate PH: intimal hyperplasia and medial hypertrophy

Severe PH: plexiform lesion (abnormal angiogenesis, aneurysmal formation)

164
Q

Symptoms of PH

A

Exertional dyspnea (60%)

Decreased exercise tolerance

Dyspnea at rest

Anginal chest pain

Syncope

165
Q

WHO functional status classification for PH

A

No limitation of usual physical activity

Mild limitation of physical activity. No discomfort at rest. Normal physical activity causes increased dyspnea and fatigue. (This is because decreased CO which is fine at rest but you feel it when you start exercising)

Marked limitation in physical activity. No discomfort at rest.

Unable to perform any physical activity. Dyspnea and/or fatigue may be present at rest.

166
Q

Physical exam in PH

A

Accentuated pulmonary component of 2nd heart sound in >90% (louder and delayed)

Early systolic ejection click (RVH)

RV S4 gallop (RVH)

Prominent jugular “a” wave (RVH)

Diastolic murmur of pulmonary regurg, or holosystolic murmur of tricuspid regurg

Jugular “v” waves with pulsatile liver

Peripheral edema and ascites

167
Q

EKG of RVH

A

R axis deviation

R atrial enlargement

Q wave in V1

ST-T inversion in V1-6

Of course RVH because pressing against high pressure of pulmonary circulation

168
Q

CXR findings in PH

A

Enlarged main pulmonary artery shadows

Pruning: attenuation of peripheral vascular markings

169
Q

PGI2 and TxA2

A

Endothelial cells have prostacyclin synthetase and make prostacyclin (PGI2), causing vasodilation and platelet aggregation inhibition

Platelets contain thromboxane synthase and make thromboxane (TxA2) causing vasoconstriction and platelet adhesion and aggregation

170
Q

Medical treatment of PH

A

CCBs: diltiazem, nifedipine or amlodipine in large doses; avoid in pts with right heart failure; not commonly used now

Endothelin antagonists: endothelin causes pulmonary vasoconstriction and vascular smooth muscle cell proliferation; bosentan (Tracleer) is oral, nonselective endothelin receptor blocker with hepatic toxicity, contraindicated in pregnancy but first line treatment despite $$$; ambrisentan

Prostacyclin analogues: epoprostenol (Flolan; potent vasodilation, inhibits platelet aggregation, reduces SM proliferation and migration, delivered continuously through catheter via infusion pump, $$); Iloprost (Ventavis; inhaled and can be delivered via nebulizer); Treprostinil (Remodulin; subQ pump or IV administration)

NO: inhaled; potent vasodilator at the area that is being ventilated so has local action (passes from alveolus to endothelial cell causing direct relaxation and improving V/Q mismatch, inactivated by binding to Hgb and no systemic effects if gets into systemic circulation)

Phosphodiesterase inhibitors: sildenafil (Viagra), Tadalafil (Levitra), verdenafil (Cialis; inhibit PDE which converts cGMP to GMP, used in ED, contraindicated with nitrates)

Anticoagulation: pts with PH at high risk for intrapulmonary thrombosis and thromboembolism so use coumadin (warfarin)

171
Q

Surgical treatment for PH

A

Atrial septostomy: increased CO, concomitant loss in arterial saturation, very high mortality rate

Lung transplant: indicated if pt unresponsive to medications

172
Q

Virchow’s triad

A

1) Hypercoagulability
2) Stasis of blood turbulent flow
3) Endothelial injury

Lines of Zahn confirm thrombus occurred over time

173
Q

Risk factors for DVT and PE

A

Immobilization (air travel)

Recent trauma and surgery in past 3 months

Previous PE or DVT

Stroke with limb paresis

Obesity

Malignancy

Significant history of cigarette smoking

Oral contraceptives, pregnancy, hormone replacement

Thrombophilia: factor V Leiden mutation (AD point mutation gives resistance to activated protein C)

174
Q

Pathophysiology of PE

A

Most venous thrombus emboli originate in pelvis or deep veins of the leg

Large emboli can lodge at bifurcation of PAs (saddle emboli), more commonly in second, third and fourth branches

Increased PVR causes PH and acute RH failure

Impaired gas exchange (increased dead space, R to L shunting, V/Q mismatch secondary to atelectasis, lung infarct)

Alveolar hyperventilation (reflex) with low PaCO2

Bronchoconstriction

Decreased lung compliance from pulmonary edema and hemorrhage

175
Q

Symptoms and signs of PE

A

All highly non-specific!

Dyspnea in 84%

Pleuritic chest pain in 74%

Cough

Hemoptysis

Tachypnea (>16) in 92%

Tachycardia

Accentuated pulmonic component of second heart sound

Cardiovascular collapse

176
Q

Lab abnormalities in PE

A

ABG: hypoxemia, hypocapnia, alkalosis, if circulatory collapse then hypercapnia and acidosis

Non-specific lab findings: leukocytosis, increase ESR, elevated LDH, AST, BNP

EKG: normal but could have tachycardia, non-specific T wave changes, RH hypertrophy

CXR: atelectasis, pulmonary parenchymal abnormality and/or pleural effusion (transudate and exudate), but normal CXR in 30%

177
Q

Other causes of PE

A

Air

CO2

Foreign particles due to IVDA (especially talc)

Amniotic fluid

Bone fragments and marrow

Fat

Cement (from ortho surgery)

FAT BAT: fat, air, thrombus, bacteria, amniotic fluid, tumor

178
Q

Chronic thromboembolic pulmonary hypertension (CTEPH)

A

Pulmonary HTN (mean >25 mmHg) that persists 6 months after diagnosis PE

Occurs in 2-4% pts with PE

Presents with all symptoms and findings of pulmonary HTN

Treatment is pulmonary endarterectomy

179
Q

Acute PE

A

Correct diagnosis is important because anticoagulation is life saving but also can cause morbidity

No definitive way to identify whether pt has PE (clinical eval alone inaccurate and more definitive testing may be inaccurate too) therefore treatment based on both clinical suspicion and testing

180
Q

Wells criteria for PE

A

Suspected DVT = 3

Alternative dx less likely than PE = 3

HR > 100 = 1.5

Immobilization/surgery 4wks = 1.5

History DVT or PE = 1.5

Hemoptysis = 1

Malignancy = 1

<!--= 2 is low probability (<4%)</p-->

3-6 is moderate (20%)

>6 is high probability (66%)

181
Q

Diagnostic tests for PE

A

Assessment for DVT: ultrasound lower extremities, D-dimer (plasmin derived fibrin degradation product that is highly sensitive for DVT)

V/Q scan

Spiral (helical) CT angiography scan: excellent with proximal arteries

Pulmonary angiogram: gold standard but rarely done today

182
Q

Treatment if hemodynamically unstable

A

Hospital mortality 58%

Thrombolysis

Surgical embolectomy (requires cardiopulmonary bypass): restricted to pts with absolute contraindication to thrombolysis, extremely high mortality rate (only do this if absolute contraindication to thrombolysis)

183
Q

Treatment if hemodynamically stable

A

Hydration, oxygen, monitoring

Rapid anticoagulation: unfractionated heparin, low molecular weight heparin (subQ; enoxaparin (Lovenox)), fondaparinux

Long term anticoagulation: warfarin (coumadin) for at least 3 months to indefinitely, depending on condition

184
Q

In-hospital prevention of PE

A

Compression stockings or other pneumatic compression devices for lower extremities

Pharmacologic prophylaxis: unfractionated heparin or low molecular weight heparin, coumadin, maybe aspirin

IVC filter (umbrella)

185
Q

Pertussis

A

Whooping cough

Bordatella pertussis infection

Clinical presentation: Catarrhal stage 1-2 weeks (common cold sx); paroxysmal stage 4-6 weeks (severe cough with distinctive “whoop”, cyanosis, post-tussive emesis); convalescent stage 4-6 weeks (gradual improvement)

Complications: apnea, seizures, death

Diagnosis: acute cough lasting 14 days with at least one: paroxysms of cough, inspiratory whoop, post-tussive emesis

Lab dx: culture of nasopharyngeal secretions, PCR

Treatment: macrolide antibiotics, most helpful if started in catarrhal stage within 1-2 weeks of coughing, post-exposure prophylaxis

Vaccination: DTaP for age 6 and younger; TdaP for ages 7 and older (just different concentrations but both diphtheria, tetanus and acellular pertussis)

186
Q

When do you drain a parapneumonic effusion?

A

Large, free-flowing effusion

Loculated effusion

Effusion with thickened parietal pleura

You culture an organism from the effusion fluid

Pus in effusion (empyema!)

187
Q

How do you rule out TB as cause of pleural effusion?

A

If the ADA is normal, it is NOT TB

If there are mesothelial cells in fluid, it is NOT TB (TB encases pleural space and you don’t get mesothelial cells)

188
Q

How do you decide if a patient is ready for discharge?

A

Vitals stable for 24 hours

Able to take oral antibiotics

Able to maintain adequate hydration and nutrition

Mental status normal (or at base line level)

No other active clinical or psychosocial problems requiring hospitalization

189
Q

Conditions that do NOT usually cause pleural effusion

A

Silicosis

Berylium exposure

Occupational asthma

Hypersensitivity pneumonitis

Block 9: Cardio, Renal and Resp II (8 decks)

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