Pulmonary Flashcards
Conducting vs respiratory zones
Conducting zone
- large and small airways, as get to smaller airways, have more in parallel and thus less resistance
- anatomic dead space - no gas exchange
- cartilage, goblet cells, pseudostratified columnar epithelium to beginning of terminal bronchioles
- airway smooth muscle cells through terminal bronchioles
Respiratory zone
- respiratory bronchioles, alveolar ducts, and alveoli
- site of gas exchange
- cuboidal epithelium in respiratory bronchioles, simple squamous in alveolar ducts
Type I and type II pneumocytes
Type 1: Make up 97% of alveolar surfaces, squamous
Type 2: secrete surfactant, serve as precursors to type 1
Club cells
nonciliated, cuboidal cells with secretory granules that secrete a component of surfactant
Surfactant
secreted by type II pneumocytes and club cells; made up of lecithins including dipalmitoylphophatidylcholine. Synthesis begins at week 26, mature levels at week 35. Lecithin : sphingomyelin ratio over 2 indicates fetal lung maturity
Aspiration locations
When upright: lower portion of R inf lobe
When supine: sup portion of R inf lobe
Relationship between pulmonary artery and brochus
Righ: pulm artery anterior to main bronchus
Left: pum artery superior to main bronchus
Structures perforating diaphragm
T8: IVC
T10: esophagus and vagus n
T12: aorta
Functional residual capacity
residual volume plus expiratory reserve volume (volume of gas in lungs after normal expiration
Physiologic dead space
=anatomic dead space of conducting airways + alveolar dead space (most is in apex)
Minute ventilation vs alveolar ventilation
Minute ventilation=Total volume of gas entering lungs per minute
=Vt x RR
Alveolar ventilation=Volume of gas per unit time reaching alveoli
Intrapleural pressure
Negative at FRC to prevent pneumothorax
Compliance
Change in lung volume for given change in pressure. Decreased in pulmonary fibrosis, pneumonia, pulmonary edema. Increased in emphysema, aging.
Methemoglobinemia
Oxidized form of Hb with increased affinity for cyanide, decreased affinity for O2
Presents with cyanosis and chocolate-colored blood
Treated with methylene blue
Can induce methemoglobinemia with nitrites to treat cyanide poisoning
Perfusion vs diffusion limited
Perfusion limited: Gas equilibrates early along length of capillary; diffusion increased only if blood flow increased; case in normal lung
Diffusion limited: Gas does not equilibrate by time blood reaches end of capillary; seen in emphysema and pulmonary fibrosis
Alveolar gas equation
PAo2 = PIo2 - PaCO2/R
Causes of hypoxemia
Normal A-a gradient: high altituide, hypoventilation
Increased A-a gradient: V/Q mismatch, diffusion limitation, right to left shunt
V/Q mismatch in normal lung
V/Q high at apex: wasted ventilation
V/Q low at base: wasted perfusion
both ventilation and perfusion greater at base than apex
V/Q approaches 1 with exercise due to vasodilation of apical capillaries
Pathology of V/Q
V/Q=0 airway obstruction (shunt), 100% O2 does not improve
V/Q=infinity blood flow obstruction, 100% O2 improves PaO2
Transport of CO2
90% as HCO3-
5% as HbCO2
5% as dissolved CO2
Vichow triad
1) stasis
2) hypercoagulability
3) endothelial damage: exposed collagen triggers clotting cascade
Homan sign
dorsiflexion of foot causes calf pain; sign of DVT
Lines of Zahn in PE
Interdigitated areas of pink and red found in thrombi that occur prior to death
Classic triad of fat emboli
Hypoxemia + neurologic abnormalities + petechial rash
Amniotic fluid emboli - complication
Can lead to DIC, especially postpartum
Air emboli
Nitrogen bubbles precipitate in ascending divers. Treated with hyperbaric O2
PFTs of obstructive lung disease
Decreased FEV1 and decreased FVC with decreased FEV1/FVC ratio (hallmark)
Chronic bronchitis
Path: hyperplasia of mucus secreting glands
Clinical: productive cough for over 3 mos per year for over 2 years. Wheezes, crackles, cyanosis, hypercapnea, secondary polycythemia
Emphysema - two forms
Centriacinar associated with smoking
Panacrinar associated with alpha1 antitrypsin def
Emphysema findings
Increased elastase activity leading to loss of elastic fibers and increased compliance/decreased recoil
Pathologic findings of asthma
Smooth muscle hypertrophy
Curschmann spirals: shed epithelium forms mucus plugs
Charcot-Leyden crystals: eosinophilic, hexagonal, double pointed crystals from breakdown of eosinophils in sputum
Sarcoidosis findings
Bilateral hilar lymphadenopathy, noncaseating granulomas, increased ACE, increased Ca++
Hypersensitivity pneumonitis
Mixed type III/IV hypersensitivity. Dyspnea, cough, chest tightness, headache. Classically in farmers and those exposed to birds
Asbestosis
Exposure: shipbuilding, roofing, plumbing
Pathology: ivory white calcified supradiaphragmatic and pleural plaques. Golden brown rods in alveolar septum.
Presentation: restrictive lung disease. Risk of cor pulmonale. Risk of lung cancer (bronchogenic carcinoma more than mesothelioma)
Berylliosis
Exposure: aerospace and manufacturing industries
Pathology: granulomas in upper lobes
Presentation: restrictive lung disease
Coal workers pneumoconiosis
Exposure: prolonged coal dust exposure
Pathology: Macrophages laden with carbon, inflammation, fibrosis in upper lobes
Presentation: restirctive lung disease
Silicosis
Exposure: foundries, sandblasting, mines
Pathology: Macrophages release fibrogenic factors in response to silica. Eggshell calcifcation of hilar lymph nodes. Effects upper lobes.
Presentation: Restrictive lung disease. Increased risk for bronchogenic carcinoma
Neonatal respiratory distress syndrome
Pathophysiology: surfactant deficiency causes increased surface tension and alveolar collapse
Imaging: ground glass appearance of lung fields
Treatment: Maternal steroids before birth, artificial surfactant for infant
Complications: PDA due to persistent low O2. Retinopathy, intraventricular hemorrhage, and bronchopulmonary dysplasia due to supplemental O2
ARDS
Presentation: Acute onset resp failure with bilateral lung opacities and decreased PaO2/FiO2 in absence of HF
Pathology: Diffuse alveolar damage results in increased alveolar capillary permeability and protein leak into alveoli. Causes noncardiogenic pulmonary edema with normal PCWP. Formation of intra-alveolar hyaline membranes.
Treatment: mechanical ventilation with low tidal volume
Drugs that cause pulmonary hypertension
Amphetamines, cocaine
Pathology of pulmonary hypertension
pulmonary artery pressure greater than 25 mmHg at rest
Arteriolosclerosis, medial hypertrophy, intimal fibrosis of pulmonary arteries
Tracheal deviation in different respiratory conditions
pleural effusion: none or away from side of lesion
atelectasis: toward side of lesion
tension pneumo: away from side of lesion
simple pneumo: none
Types of pleural effusion
Transudate: due to disruption of starling forces (increased hydrostatic pressure, decreased oncotic pressure) due to HF, nephrotic syndrome, hepatic cirrhosis. Low protein
Exudate: High protein. Due to malignancy, pneumonia, collagen vascular disease, trauma
Lymphatic: High TGs. Due to thoracic duct injury by trauma or malignancy
Types of pneumothorax
Primary spontaneous: rupture of apical blebs or cysts in tall thin young male
Secondary spontaneous: due to diseased lung or high pressure mechanical vent
Traumatic: blunt or penetrating trauma
Tension: Air enters pleural space but can’t get out. Causes trachea to deviate away from affected lung
Lobar pneumonia
Organisms: S pneumo, Legionella, Klebsiella
Pathology: consolidation due to exudate, involves entire lobe or lung
Bronchopneumonia
Organisms: S pneumo, S aureus, H flu, Klebsiella
Pathology: inflammation from bronchioles into adjacent alveoli, patchy distribution
Interstitial pneumonia
Organisms: viruses, mycoplasma, legionella, chlamydia
Pathology: diffuse patchy involvement involving interstial areas
Lung abscesses
Clinical: Classically seen in patients with loss of consciousness and aspiration of oropharyngeal contents or bronchial obstruction
Pathology: Local collection of pus in parenchyma. Due to anaerobes
Imaging: Air-fluid levels
Treatment: Clindamycin
Pancoast tumor
Carcinoma in apex of lung. Can invade cervical sympathetic chain and cause Horner syndrome, SVC syndrome, sensorimotor defects, hoarsness
SVC syndrome
Obstruction of SVC by malignancy or thrombosis preventing blood drainage from head, neck, and upper extremities. Causes facial plethora, JVD, and edema. Can raise intracranial pressure if obstruction severe.
Sites of metastasis for lung cancers
Adrenals, brain, bone, liver
Cancers that metastasize to lung
Breast, colon, prostate, bladder
Small cell carcinoma of lung
Location: central
Pathology: Undifferentiated neuroendocrine cells that appear as small dark blue cells. Chromogranin A+, amplificiation of myc genes
Clinical: Very aggressive. Can made ACTH, cause SIADH, cause myasthenic syndrome, cause paraneoplastic encephtalitis
Adenocarcinoma of lung
Location: peripheral
Clinical: most common lung cancer in nonsmokers, and overall. Clubbing.
Pathology: mutations in KRAS, EGFR, ALK. Glandular pattern. Mucin +
Squamous cell carcinoma of lung
Location: central
Clinical: can cause hypercalcemia through a paraneoplastic syndrome
Pathology: Hilar mass, cavitation, keratin pearls
Large cell carcinoma of lung
Location: peripheral
Clinical: Poor prognosis
Pathology: Highly anaplastic and undifferentiated, pleomorphic giant cells, can secrete beta hcG
Bronchial carcinoid tumor
Pathology: neuroendocrine cell nests; chromogranin A +
Clinical: escellent prognosis, presents with symptoms of mass effect, occasionally cuases carcinoid syndrome
meconium ileus
obstruction of distal ileum by dehydrated meconium. Most commonly cuased by cystic fibrosis. Often is the presenting symptom at birth of CF.
Influenza vaccine
Inactivated vaccine: Induce antibodies against hemagglutinin antigen which inhiibin bindings ot hemagglutinin to host cell receptors, prevneting virus from entering cells.q
Minute ventilation vs alveolar ventilation
Minute ventilation is total volume of new air that enters resp pathways per minute
Alveolar ventilation is only volume of new air reaching gas exchange areas per minute - doesn’t include dead space
piriform recess
Cavities on either side of laryngeal orifice. During swallowing, food diverted into piriform recesses and then into esophagus by epiglottis. Food can get stuck in it and damage the internal laryngeal nerve, which serves as the afferent limb of the cough reflex
DHR flow cytometry
Tests for neutrophil superoxide production to diagnose CGD. Preferred to NBT testing.
First vs second generation H1 blockers
First gen: end in “ine” or “ate” - diphenhydramine, dimenhydrinate, chlorpheniramine
Second gen: end in “adine” - loratadine, fexofenadine, desloratadine, cetirizine
N-acetylcysteine
Mucolytic agent used to loosen mucus plugs in CF patients by disrupting disulfide bonds.
Also is antidote for acetaminophen OD
Dextromethorphan
Synthetic codeine. Antagonizes NMDA glutamate receptors
Nasal decongestants
Names: Pseudophedrine, phenylephrine
MOA: alpha1 agonists, constrict nasal vessels to reduce edema and congestion
ADRs: HTN, CNS stimulation/anxiety
Bosentan
MOA: endothelin-1 receptor antagonist - decreases pulmonary vascular resistance
Use: pulm htn
ADRs: hepatotoxicity
Sildenafil
MOA: Inhibits PDE-5 leading to vasodilation
Use:pulm HTN, ED
Prostacyclin agonists
Names: epoprostenol, iloprost
MOA: vasodilatory effect, inhibits platelet aggregation
ADRs: flushing, jaw pain
Use: pulm htn
Ipratropium
MOA: muscarinic antagonist - prevents bronchoconstriction
Use: asthma, COPD; tiotropium is long acting form
Anti-leukotriene agents
Montelukast and zafirlukast: block leukotriene receptors, good for aspirin-induced asthma
Zileuton: 5-lipoxygenase pathway inhibitor, blocks conversion of AA to leukotrienes
Omalizumab
monoclonal anti-IgE antibody
used in allergic asthma resistant to steroids and B2 agonists
theophylline
MOA: inhibits phosphodiesterase, increasing cAMP and causing bronchodilation
Use: narrow therapeutic index limits use for asthma
Metacholine
MOA: M3 agonist
Use: metacholine challenge to diagnose asthma
Cryptococcus neoformans
Budding yeast with thick capsule. Opportunistic pathogen. Most commonly causes meningoencephalitis. Lung infection usually occurs first but is usually asymptomatic
Normal A-a gradient
Less than 10-15 mmHg
Pancoast syndrome
Caused by tumor at lung apex, often in superior sulcus.
Presents with shoulder pain, Horner syndrome, spinal cord compression
Fat embolism syndrome
Acute onset neurologic abnormalities, hypoxemia, petechial rash
