Respiratory Flashcards
Embryonic stage
- Weeks 4-7
- Lung bud → trachea → mainstem bronchi → secondary (lobar) bronchi → tertiary (segmental) bronchi
- Errors at this stage can lead to TE fistula
Pseudoglandular stage
- Weeks 5-16
- Endodermal tubules → terminal bronchioles
- Surrounded by modest capillary network
- Respiration impossible, incompatible with life
Canalicular stage
- Weeks 16-26
- Terminal bronchioles → respiratory bronchioles → alveolar ducts
- Surrounded by prominent capillary network
- Airways increase in diameter
- Respiration capable at 25 weeks
Saccular stage
- Weeks 26-birth
- Alveolar ducts → terminal sacs
- Terminal sacs separated by primary septae
- Pneumocytes develop
Alveolar stage
- Weeks 32-8 years
- Terminal sacs → adult alveoli (due to secondary septation)
- In utero, breathing occurs via aspiration and expulsion of amniotic fluid → ↑ vascular resistance through gestation
- At birth, fluid gets replaced with air → ↓ pulmonary vascular resistance
Bronchogenic cysts
- Caused by abnormal budding of the foregut and dilation of the terminal or large bronchi
- Discrete, round, sharply defined and air-filled densities on CXR
- Drain poorly and cause chronic infections
Club cells
- Non-ciliated
- Low columnar/cuboidal with secretory granules
- Secrete component of surfactant
- Degrade toxins
- Act as reserve cells
Zone of respiratory tree that has least airway resistance
Terminal bronchioles
Where do cartilage and goblet cells extend to on respiratory tree
End of bronchi
Where do cilia extend to on respiratory tree
Respiratory bronchioles
Inspiratory capacity
IRV + TV
Functional residual capacity
- RV + ERV
- Volume of gas in lungs after normal expiration
- Includes RV (cannot be measure on spirometry)
Vital capacity
- TV + IRV + ERV
- Maximal volume of gas that can be expired after a maximal inspiration
Physiological dead space
- Anatomic dead space of conducting airways plus alveolar dead space
- Apex of healthy lung is larges contributor of alveolar dead space
- Volume of inspired air that does not take part in gas exchange
Physiologic dead space
- Approximately equivalent to anatomic dead space in normal lungs
- May be greater than anatomic dead space in lung diseases with V/Q defects
Pathologic dead space
- When part of respiratory zone becomes unable to perform gas exchange
- Ventilated but not perfused
What determines the combined volume of the lungs
The elastic properties of both chest wall and lungs
Hysteresis
Lung inflation curve follows a different curve than the lung deflation curve due to need to overcome surface tension forces in inflation
How does fetal hemoglobin has an increased affinity for O2
Has a decreased affinity for 2,3-BPG
Perfusion limited
- O2 (normal health), CO2, N2O
- Gas equilibrates early along the length of the capillary
- Diffusion can only be ↑ if blood flow ↑
Diffusion limited
- O2 (emphysema, fibrosis), CO
- Gas does not equilibrate by the time blood reaches the end of the capillary
Haldane and Bohr effects
HALDANE EFFECT:
- Occurs in lungs
- Oxygenation of Hb promotes dissociation of H+ from Hb
- This shifts equilibrium toward CO2 formation
- Therefore, CO2 is released from RBCs
BOHR EFFECT:
- Occurs in peripheral tissue
- ↑ H+ from tissue metabolism shifts curve to right, unloading O2
Response to high altitude
- ↓ atmospheric O2 → ↓ PaO2 → ↑ ventilation → ↓ PaCO2 → respiratory alkalosis → altitude sickness
- Chronic ↑ in ventilation
- ↑ erythropoietin → ↑ hematocrit and Hb (chronic hypoxia)
- ↑ 2,3-BPG, binds Hb so that Hb releases more O2
- Cellular changes (↑ mitochondria)
- ↑ renal excretion of HCO3- to compensate for respiratory alkalosis (can augment with acetazolamide)
- Chronic hypoxic pulmonary vasoconstriction results in pulmonary hypertension and RVH
Response to exercise
- ↑ CO2 production
- ↑ O2 consumption
- ↑ ventilation rate to meet O2 demand
- V/Q ratio from apex to base becomes more uniform
- ↑ pulmonary blood flow due to ↑ cardiac output
- ↓ pH during strenuous exercise (secondary to lactic acidosis)
- No change in PaO2 and PaCO2, but ↑ in venous CO2 content and ↓ in venous O2 content
Epistaxis of anterior segment of nostril
Kiesselbach plexus
Epistaxis of posterior segment of nostril
Sphenopalatine artery, branch of maxillary artery
Homan sign
- Dorsiflexion of foot → calf pain
- DVT
When do cyanosis and hypercapnia occur in chronic bronchitis
- Cyanosis is due to early onset hypoxemia due to shunting
- Late onset dyspnea and CO2 retention (hypercapnia
What is associated with peribronchial cuffing
Asthma
Hypersensitivity pneumonitis
Mixed type III/IV hypersensitivity reaction to environmental antigen → dyspnea, cough, chest tightness, headache. Often seen in farmers and those exposed to birds.
Caplan syndrome
Rheumatoid arthritis and pneumoconioses with intrapulmonary nodules
What causes the initial damage in acute respiratory distress syndrome
Initial damage due to release of neutrophilic substances toxic to alveolar wall, activation of coagulation cascade and oxygen derived free radicals
Causes of acute respiratory distress syndrome
- Sepsis
- Pancreatitis
- Pneumonia
- Aspiration
- uRemia
- Trauma
- Amniotic fluid embolism
- Shock
“SPARTAS”
Obstructive sleep apnea in adults
Excess parapharyngeal tissue
Obstructive sleep apnea in children
Adenotonsillar hypertrophy i
Obesity hypoventilation syndrome
Obesity → hypoventilation → ↓ PaO2 and ↑ PaCO2 during sleep
↑ PaCO2 during waking hours (retention)
Nonheritable causes of pulmonary arterial hypertension
- Drugs (eg amphetamines, cocaine)
- Connective tissue disease
- HIV infection
- Portal hypertension
- Congenital heart disease
- Schistosomiasis
Physical findings of pleural effusion
- ↓ breath sounds
- Dull to percussion
- ↓ fremitus
- No tracheal deviation or might also be away from side of lesion (if large)
Physical findings of atelectasis (bronchial obstruction)
- ↓ breath sounds
- Dull to percussion
- ↓ fremitus
- Tracheal deviation toward side of lesion
Physical findings of simple pneumothorax
- ↓ breath sounds
- Hyperresonant to percussion
- ↓ fremitus
- No tracheal deviation
Physical findings of tension pneumothorax
- ↓ breath sounds
- Hyperresonant to percussion
- ↓ fremitus
- Tracheal deviation away from side of lesion
Physical findings of consolidation (lobar pneumonia, pulmonary edema)
- Bronchial breath sounds; late inspiratory crackles
- Dull to percussion
- ↑ fremitus (this indicates denser or inflamed lung tissue)
- No tracheal deviation
Sites of metastases from lung cancer
- Adrenals
- Brain
- Bone (pathologic fracture)
- Liver (jaundice, hepatomegaly)
Lung metastases
- Usually multiple lesions
- More common than primary neoplasms
- Breast
- Colon
- Prostate
- Bladder cancer
Antibodies produced by small cell (oat cell) carcinoma are against
- Presynaptic Ca2+ channels (Lamber-Eaton myasthenic syndrome)
- Neurons (paraneoplastic myelitis, encephalitis, subacute cerebellar degeneration)
Small cell (oat cell) carcinoma stains for
- Chromogranin A
- Neuron-specific enolase
Adenocarcinoma stains for
Mucin
Bronchioalveolar subtype (adenocarcinoma in situ)
- CXR often shows hazy infiltrates similar to pneumonia
- Better prognosis
- Grows along alveolar septa → apparent “thickening” of alveolar walls
- Tall columnar cells containing mucus
Large cell carcinoma secretes
β-hCG
Bronchial carcinoid tumor stains for
Chromogranin A
