Upper respiratory infections (URIs); e.g., viral, bacterial (S. pneumoniae) Deviated nasal septum Allergic rhinitis, barotrauma, and smoking cigarettes

Respi Assessment Flashcards by Aserah Blank

Unilateral or bilateral bony (90% of cases) or membranous (10% of cases) septum between the nose and the pharynx

Choanal Atresia

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Nonneoplastic tumefactions tgat develop as a response to chronic inflammation

Nasal polyps

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The most common polyp.
Most often seen in adults with a history of IgE-mediated allergies. Nasal smear shows numerous Eosinophils

Allergic polyps

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excessive snoring with intervals of breath cessation (apnea)

Obstructive Sleep Apnea (OSA)

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Most common cause of OSA where Pharyngeal muscles collapse due to the weight of tissue in the neck.

Obesity

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Other causes of Obstructive Sleep Apnea (OSA)

tonsillar hypertrophy
nasal septum deviation
hypothyroidism
acromegaly

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Excessive snoring with episodes of apnea. Daytime somnolence often simulating narcolepsy

Obstructive Sleep Apnea (OSA)

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PaO2 and O2 saturation (Sa O2) decrease and
PaCO2 increases (respiratory acidosis) during apneic episodes.

Obstructive Sleep Apnea (OSA)

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Inflammation of the mucous membranes lining one or more of the paranasal sinuses.

Sinusitis

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Most common malignant tumor of the nasopharynx. Male dominant
Increased in Chinese (common in adults) and African populations (common in children). Causal relationship with Epstein-Barr virus (EBV)

Nasopharyngeal (NP) Carcinoma

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Occurs followed by right ventricular hypertrophy (RVH) the right ventricle becomes hypertrophied (called cor pulmonale).

Pulmonary hypertension (PH)

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Hypoxemic stimulus for erythropoietin release leads to RBC hyperplasia and secondary polycythemia.

Secondary polycythemia

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Location of Sinusitis

• Adult
Children

Adults- maxillary sinus

Children - ethmoid sinus

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Causes of Sinusitis

Upper respiratory infections (URIs); e.g., viral, bacterial (S. pneumoniae)
Deviated nasal septum
Allergic rhinitis, barotrauma, and smoking cigarettes

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Pathologic findings of Nasopharyngeal (NP) Carcinoma

Squamous cell carcinoma (SCC), nonkeratinizing squamous carcinoma, or undifferentiated cancer
Metastasizes to cervical lymph nodes (70% of cases)

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Treatment for Nasopharyngeal (NP) Carcinoma

Radiotherapy

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Risk factors Laryngeal carcinoma

•Cigarette smoking (most common cause)
• Alcohol (synergistic effect with smoking)
• Squamous papillomas and papillomatosis
-Human papillomavirus types 6 and 11 association.
- Majority located on true vocal cords

• Majority are keratinizing SCCs

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Persistent hoarseness often associated with cervical lymphadenopathy

Laryngeal carcinoma

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Upper Respiratory Tract disease

Choanal Atresia
Obstructive Sleep Apnea (OSA)
Sinusitis
Nasopharyngeal (NP) Carcinoma
Nasal polyps

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Loss of lung volume due to inadequate expansion of the airspaces (collapse)

Atelectasis

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Airway obstruction by thick secretions prevents air from reaching the alveoli. Obstruction occurs in bronchi, segmental bronchi, or terminal bronchioles.

Resorption Atelectasis

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Causes of obstruction
of Resorption Atelectasis

Mucus or mucopurulent plugs after surgery
Aspiration of foreign material
Centrally located bronchogenic carcinoma

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Cause of alveolar collapse

Lack of air and distal resorption of preexisting air. Following obstruction, circulating blood in the pulmonary capillary absorbs the preexisting air in the peripheral alveoli, leading to alveolar collapse and an airless state within a few hours.

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Fever and dyspnea
Symptoms occur within 24 to 36 hours of collapse.

Absent breath sounds
Absent vocal vibratory sensation (tactile fremitus) Alveoli are collapsed.

Clinical findings of Atelectasis

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Treatment for Atelectasis

* Incentive spirometry after surgery * CPAP by face mask * Positive end-expiratory pressure (PEEP) on mechanical ventilation

Air or fluid in the pleural cavity under increased pressure collapses small airways beneath the pleura

Compression Atelectasis

Examples of Compression Atelectasis

* Tension pneumothorax where air compresses the lung | * Pleural effusion where fluid compresses the lung

Atelectasis due to loss of surfactant.

Tension pneumothorax

Synthesize surfactant which is stored in lamellar bodies and synthesis begins in 28th week of gestation.

Type II pneumocytes

Has a decreased surfactant in the fetal lungs caused by prematurity (most common cause), maternal diabetes (poorly controlled) [Fetal hyperglycemia increases insulin release.], Cesarean section (C-section) from lack of stress-induced increase in cortisol from a vaginal delivery

Respiratory distress syndrome (RDS) in newborns

Widespread atelectasis results in _____ from Perfusion without ventilation. Collapsed alveoli are lined by hyaline membranes Derived from proteins leaking out of damaged pulmonary vessels.

massive intrapulmonary shunting.

Respiratory difficulty begins within a few hours after birth. Grunting Tachypnea Intercostal retractions Infants develop hypoxemia and respiratory acidosis.

Respiratory distress syndrome (RDS) in newborns

Diagnosis of Respiratory distress syndrome (RDS) in newborns

Chest radiograph shows a “ground glass” appearance

• Increased hydrostatic pressure (HP) in pulmonary capillaries - Left-sided heart failure, volume overload, and mitral stenosis • Decreased oncotic pressure (OP) - Nephrotic syndrome and cirrhosis

Edema due to alterations in Starling pressure (transudate)

Edema due to microvascular or alveolar injury

exudate

Noncardiogenic pulmonary edema resulting from acute alveolar-capillary damage.

Adult Respiratory Distress Syndrome (ARDS)

Due to direct injury to the lungs or systemic diseases

Adult Respiratory Distress Syndrome (ARDS) | Hyaline Membrane Disease

Main causes are: Severe Acute Respiratory Syndrome (SARS)* Hantavirus

Severe Acute Respiratory Syndrome

Other causes of SARS

* heroin * smoke inhalation * acute pancreatitis * cardiopulmonary bypass * disseminated intravascular coagulation * amniotic fluid embolism * fat embolism

Arrange the following regarding the pathogenesis of the SARS 1. Cytokines are chemotactic to neutrophils. 2. Neutrophils transmigrate into the alveoli through pulmonary capillaries. 3. Capillary damage causes leakage of a protein-rich exudate producing hyaline membranes. 4. Neutrophils damage type I and II pneumocytes. 5. Decrease in surfactant causes atelectasis with intrapulmonary shunting.

1. Cytokines are chemotactic to neutrophils. 2. Neutrophils transmigrate into the alveoli through pulmonary capillaries. 3. Capillary damage causes leakage of a protein-rich exudate producing hyaline membranes. 4. Neutrophils damage type I and II pneumocytes. 5. Decrease in surfactant causes atelectasis with intrapulmonary shunting.

Important to distinguish ARDS from cardiogenic pulmonary edema, where PA wedge pressure is

> 18 mm Hg

Bilateral interstitial infiltrates initially Progresses to widespread alveolar consolidation with air bronchograms (80%)

SARS Corona Virus

Treatment for SAR COV

* Treat underlying disease * Hemodynamic monitoring * Mechanical ventilation * Nitric oxide inhalation, corticosteroids

Sixth leading cause of death in the United States that the majority are caused by bacterial pathogens. Most often due to Streptococcus pneumoniae (50%– 75% of cases)

Typical community-acquired pneumonia

Microaspiration of oropharyngeal contents during sleep • Inhalation of aerosol drops ranging in size from 0.5 to 1 µm • Bloodstream infection

Typical community-acquired pneumonia

It begins as an acute bronchitis and spreads locally into the lungs. The lower lobes or right middle lobe are usually involved. The lung has patchy areas of consolidation with noted microabscesses

Bronchopneumonia

Complete or almost complete consolidation of a lobe of lung

Loba pneumonia

Syages of Lobar Pneumonia

1. Congestion (1st 24hrs)- the affected lobe is red, heavy and boggy. It is vascular dilation and avoelar exudate contain bacteria in microscope 2. Red hepatization (day 2-3)- red firm lobe (liver-like consistency). Avoelar exudate contains neutrophil, erythrocytes, fibrin 3. Gray hepatization (4-6 days) Gray-brown firm lobe. Same with #3 but RBC disintegrate 4. Resolution- restoration of normal architect. Enzymatic digestion of exudate

Signs of consolidation (alveolar exudate)

* Dullness to percussion * Increased vocal tactile fremitus * Sound is transmitted well through alveolar consolidations. * Late inspiratory crackles * Bronchial breath sounds, bronchophony and egophony

gold standard screen in Patchy infiltrates (bronchopneumonia) or lobar consolidation with a sensitivity 50% to 85%

Cgest radiograph

Usually caused by Mycoplasma pneumoniae

Atypical community-acquired pneumonia

Clinical findings of Atypical community-acquired pneumonia

•Insidious onset, low-grade fever • Nonproductive cough • Chest pain • Flu-like symptoms - Pharyngitis, laryngitis, myalgias, headache • No signs of consolidation

Mononuclear infiltrate and alveolar spaces usually free of exudate

Patchy interstitial pneumonia

Gram-negative bacteria- Pseudomonas aeruginosa (respirators), Escherichia coli Gram-positive bacteria (e.g., Staphylococcus aureus)

Nosocomial pneumonia

Common opportunistic infections of Pneumonia in immunocompromised hosts

• Cytomegalovirus • Pneumocystis jiroveci - TMP-SMX is used for prophylaxis and treatment. • Aspergillus fumigatus

Contracted by inhalation of Mycobacterium tuberculosis and the Organism resides in phagosomes of alveolar macrophages

Tuberculosis (TB)

Virulence factor Of Strict aerobe, acid-fast TB

Cord Factor

Purified protein derivative (PPD) intradermal skin test | Does not distinguish active from inactive disease

Screening of TB

Responsible for positive PPD

Protein in cell wall

Chromosome mutations involving mycolic acid | Chromosome mutations involving catalase peroxidase

Drug resistance in TB

Does not distinguish active vs inactive TB

PPD

Nodes: Subpleural location

* Upper part of the lower lobes or lower part of the upper lobes * Ghon focus (caseous necrosis) in periphery * Ghon complex (caseous necrosis) in hilar lymph

Secondary (reactivation) TB

* Due to reactivation of a previous primary TB site * Involves one or both apices in upper lobes * Ventilation (oxygenation ) is greatest in the upper lobes. * M. tuberculosis is a strict aerobe. Reactivation TB: upper lobe cavitary lesion(s)

Complications of Cavitary lesion due to release of cytokines from memory T cells

Miliary spread in lungs due to invasion into the bronchus or lymphatics

Clinical findings of Cavitary lesion due to release of cytokines from memory T cells

* Fever * drenching night sweats * weight loss TB: drenching night sweats * weight loss

extrapulmonary site TB

Kidneys

* Spread is due to invasion of pulmonary vein tributaries. * Kidney is the most common extrapulmonary site. * Adrenal involvement may result in Addison disease.

Miliary spread to extrapulmonary sites

Granulomatous hepatitis, spread to vertebrae (Pott disease) TB in vertebrae

Pott disease

Cavitary lesion treatment

• Isoniazid + rifampin + pyrazinamide • Noninfectious in 2 to 3 weeks (3) Treat for additional 9 to 12 months

* Atypical mycobacterium * Most common TB in AIDS (often disseminates) * Occurs when CD4 helper T cell (T H) count falls < 50 cells/mm3 MAC: MC TB in AIDS

Mycobacterium avium-intracellulare complex (MAC)

Treatment for Mycobacterium avium-intracellulare complex (MAC)

• Clarithromycin + rifabutin + ethambutol

It is cuased most often due to aspiration of oropharyngeal material (e.g., tonsillar material)

Lung abscess

Risk factos for Lung Abscess

* Alcoholism * Loss of consciousness * Recent dental work * Microbial pathogens * Aerobic and anaerobic streptococci Staphylococcus * Prevotella * Fusobacterium * Anaerobes in 60% of cases Lung abscesses: mixed aerobic/ anaerobic infection

From 10% to 15% of abscesses are behind a bronchus obstructed by cancer.

Obstructive lung neoplasia

Infective endocarditis

Septic embolism

Spiking fever and productive cough (foul-smelling sputum) are common. Chest imaging shows cavitation with an air-fluid level

Lung Abscess

Treatment for Lung Abscess

* Clindamycin | * Bronchoscopy if it does not resolve

term applied to peripheral lung nodule < 5 cm

Solitary Pulmonary Nodule

Etiology of Lung Tumor

* Granuloma * Primary lung CA * Bronchial Carcinoid

Patients less than 35 years old risk: Patients more than 50 years old risk:

Patients less than 35 years old risk: < 1% Patients more than 50 years old risk: 50 to 60%

The source of the most common lung tumor that is metastatic and appears as multiple lesions.

Breast

Clinical Findings of Lung CA

Cough (75%) Weight Loss Hemoptysis

Produces Horner syndrome which is a superior sulcus tumor. The tumor is usually a primary SCC located at the extreme apex of the lung.

Pancoast Tumor

Is the most common fatal cancer in both men and women worldwide.

Primary Lung Cancer

The most common cause of lung cancer

Smoking

Most common oncogenes

* KRAS * MYC family * HER-2/ neu * BCL-2 * EGFR (Epidermal Growth Factor Receptor)

Classification of Lung Cell

Small Cell Carcinoma (15%) | Non Small Cell Carcinoma (85%)