Pulmonary Flashcards
Embryonic
weeks 4-7
lung bud –> trachea –> bronchial buds –> mainstem bronchi –> secondary bronchi –> tertiary bronchi
ERROR => tracheoesophageal fistula
Pseudoglandular
Weeks 5-17
endodermal tubules –> terminal bronchioles
surrounded by capillary network
RESPIRATION IMPOSSIBLE
Canalicular
Weeks 16-25
Terminal bronchioles –> respiratory bronchioles –> alveolar ducts
Surrounded by prominent capillary network
airways increase in diameter
Respiration at 25 weeks
Pneumocytes develop at 20 weeks
Saccular
week 26-birth
alveolar ducts –> terminal sacs (separated by sepate)
Alveolar
week 36- 8 years
Terminal sacs –> adult alveoli
in utero breathing via aspiration and expulsion of amniotic fluid –> increase vascular resistance
at birth fluid gets replaced with air –> decrease pulmonary vascular resistance
Pulmonary hypoplasia
poorly developed bronchial tree with abnormal histo
Associated with congenital diaphragmatic hernia (L side), bilateral renal agenesis (potter)
Bronchogenic cysts
caused by abnormal budding of the foregut and dilation of terminal/large bronchi
Discrete round, sharply defined fluid filled density on CXR
asymptomatic, drain poorly –> airway compression or recurrent respiratory infection
club cells
nonciliated low columnar/cuboidal with secretory granules
Located in bronchioles
Degrade toxins, secrete component of surfactant
Type 1 pneumocytes
squamous
thinly line alveoli for optimal gas exchange
Type 2 pneumocytes
cuboidal and clustered
stem cell for Type 1 and Type 2 pneumocytes and secrete surfactant.
Surfactant
decrease alveolar surface tension, decrease alveolar collapse, decrease lung recoil and increase compliance
Composed of lechithins (DPPC)
synthesis begins 20 weeks and achieves mature levels at week 35
CORTICOSTEROIDS –> surfactant
Alveolar macrophages
phagocytes
release cytokines and alveolar proteases
hemosiderin macrophages found in pulmonary edema or alveolar hemorrhage
Neonatal RDS
surfactant deficiency –> high surface tension –> alveolar collapse, ground glas
risk: premature, Maternal DM, C section
Tx: maternal steroids before birth, exogenous surfactant
Therapeutic O2 –> retinopathy, intraventricular hemorrhage, bronchopulmonary dysplasia
L/S >2 is healthy
Conducting zone of Respiratory tree
large airways consist of nose, pharynx, larynx, bronchi
airway resistance highest in large to medium bronchi
Warm, humidifies and filters air BUT NO GAS EXCHANGE
Cartilage and goblet cells extend to bronchi
Pseudostratified ciliated columnar cells= bronchus to beginning of terminal bronchioles then transition to cuboidal cells
Respiratory zone of respiratory tree
lung parenchyma (respiratory bronchioles, alveolar ducts, alveoli.
PARTICIPATE IN GAS EXCHANGE
cuboidal cells in respiratory bronchioles –> simple squamous
cilia terminate in respiratory bronchioles
alveolar macrophages clear debris
Lingula homologous to
right middle lobe
Relation of pulmonary artery to bronchus
Right anterior, Left superior
Carina position
posterior to ascending aorta and anteromedial to descending aorta
Most common site for inhaled foreign bodies
right lung
supine: superior segment of right lower lobe
lying on right side- right upper lobe
upright- enter right lower lobe
T8 Diaphragm
IVC
right phrenic N
T10 Diaphragm
esophagus
Vagus N
T12 Diaphragm
aorta
thoracic duct
azygous vein
Inspiratory reserve volume
air that can still be breathed in after normal inspiration
Tidal volume
air that moves into lung with each quiet inspiration (500)
Expiratory reserve volume
air that can still be breathed out after normal expiration
Residual volume
air in lung after maximal expiration
RV and any lung capacity that includes RV cannot be measured by spirometry
Inspiratory Capacity
IRV+TV
air that be breathed in after normal exhalation
Functional residual capacity
RV + ERV
volume of gas in lungs after normal expiration
Vital capacity
TV + IRV + ERV
Maximum volume of gas that can be expired
Total Lung Capacity
IRV + TV + ERV + RV
volume of gas present in lungs after a maximal inspiration
Elastic recoil
Tendency of lungs to collapse inward and chest wall to spring outward
At FRC airway and alveolar pressure = Patm and intrapleural pressure is negative, PVR at minimum
Compliance
change in lung volume for a change in pressure
inversely proportional to wall stiffness and increased by surfactant
High compliance –> lung easy to fill (emphysema, aging)
Low compliance –> lung hard to fill (pulm fibrosis, pneumonia, ARDS, pulm edema)
Hysteresis
lung inflation follows a different pressure volume curve than lung deflation due to need to overcome surface tension forces in inflation.
Respiratory system changes in the elderly
TLC remains the same
increased compliance, RV, V/G mismatch, A-a gradient
Decreased chest wall compliance, FVC and FEV1, respiratory muscle strength, ventilatory response to hypoxia
CO poisoning
Normal Hb conc
low O2 sat Hb
Normal dissolved O2
low total O2
Anemia
Low Hb conc
Normal O2 sat Hb
Normal Dissolved O2
Low total O2
Polycythemia
High Hb concentration
Normal O2 sat Hb
Normal dissolved O2
High total O2 content
Methemoglobin
Iron in Hb is normally reduced (2+)
oxidized Iron (3+) does not bind O2 readily but has increased affinity to CN- –> tissue hypoxia from low O2 saturation and low O2 content
CYANOSIS AND CHOCOLATE COLORED BLOOD
Shift right on ODC
low Hb affinity for O2 --> high P50 low pH high PCO2 Exercise high 2,3 BPG High altitude high temperature
Shift left on ODC
low O2 unloading --> renal hypoxia --> high EPO synthesis --> compensatory erythrocytosis basic low PCO2 low 2,3 BPG low temp high CO high MetHb high HbF
CN- poisoning
Byproduct of combustion
Tx: hydrocobalamin, nitrites, sodium thiosulfate
Sx: breath has bitter almond odor, CV collapse
ODC normal
CO poisoning
odorless gas from fires, car exhaust or has heaters
Tx: 100% O2
Sx: HA, dizzy, bilateral globus pallidus lesions on MRI
Left shift in curve, bind competitively to Hb
Pulmonary circulation
Low resistance, high compliance
low PaO2 –> hypoxic vasoconstriction that shifts blood away from poorly ventilated region
Perfusion limited
O2, CO2, N2O
gas equilibrates early along the length of the capillary. Exchange can be high only if blood flow high
Diffusion limited
O2, CO
gases does not equilibrate by the time blood reaches the end of the capillary
Ventilation/ perfusion mismatch
High at apex and low at base
with exercise there is vasodilation of apical capillaries so ratio approaches 1
V/Q = 0
obstruction
100% O2 does not improve PaO2
V/Q = infinity
blood flow obstruction
100% O2 improves PaO2
Response to high altitude
low atmospheric oxygen–> low PaO2 –> high ventilation –> low PaCO2 –> respiratory alkalosis –>altitude sickness
increase EPO, 2,3 BPG, mitochondria, renal excretion of HCO3-
Vasoconstriction –> pulmonary HTN and RVH
Response to exercise
High CO2 production, high O2 consumption
Right shift
high ventilation rate meet O2 demand
V/Q ratio from apex to base becomes more uniform
increase pulmonary blood flow due to increased cardiac output
low pH
Rhinosinusitis
obstruction of sinus drainage into nasal cavity –> inflammation and pain over are (Maxillary –> drain against gravity)
superior meatus- drain sphenoid, posterior ethmoid
middle meatus- drain frontal, maxillary and anterior ethmoid
inferior meatus0 drain nasolacrimal duct
VIRAL URI + H. influenz, S. pneumoniae, M. catarrhalis
Epistaxis
most common in anterior segment of nostril
life threatening in posterior segment
caused by foreign body, trauma, allergic rhinitis and nasal angiofibromas
Head and neck cancer
SCC
Risk: tobacco, alcohol, HPV 16, EBV
Field cancerization: carcinogen damages wide mucosal area –> multiple tumors that develop independently
DVT
blood clot within deep vein –> swelling, redness, warmth, pain
predisposed: stasis, hypercoaguability, endothelial damage
D dimer –> rule out DVT
Imaging with compression US with Doppler
use unfractioned heparin or LMWH for acute management
oral anticoagulants for long term prevention
Pulmonary emboli
V/Q mismatch, hypoxemia, respiratory alkalosis
sudden onset dyspnea, pleuritic chest pain, tachypnea
CT pulmonary angiography
Lines of Zahn
platelets and fibrin- RBC streaks
ONLY IN THROMBI
postmortem finding
Fat emboli
associated with long bone fractures and liposuction
hypoxemia, neuro abnormalities, petechial rash
Air emboli
nitrogen bubbles precipitate in ascending divers. treat with hyperbaric O2
Amniotic fluid emboli
during labor or postpartum
due to uterine trauma
lead to DIC
Mediastinal mass anterior
Thyroid, thymic neoplasia, Teratoma, Lymphoma
Mediastinal mass Middle
esophageal carcinoma, metastases, hiatal hernia, bronchogenic cysts
Mediastinal mass Posterior
neurogenic tumor, multiple myeloma
Mediastinitis
post op complication of cardiothoracic procedures, esophageal perforation, infection
fever tachy leukocytosis, chest pain, sternal wound drainage
chronic mediastinitis
high proliferative connective tissue
Histoplasma capsulatum
fever tachy leukocytosis, chest pain, sternal wound drainage
pneumomediastinum
presence of gas in mediastinum
via rupture of pulmonary bleb, trauma, Boerhaave syndrome
ruptured alveoli allow tracking of air into the mediastinum via peribronchial and perivascular sheaths
chest pain, dyspnea, voice change, subcutaneous emphysema, + Hamman sign
Obstructive Lung Disease
Air trapping in lungs, airways close prematurely at high lung volumes
High RV, FRC, TLC
LOW FEV1, FVC, FEV1:FVC
V/Q mismatch, chronic hypoxic vasoconstriction can lead to cor pulmonale
COPD, chronic bronchitis, emphysema
Restrictive lung disease
Low RV, FRC, TLC, FEV1, FVC
Normal or high FEV1: FVC
Chronic bronchitis
wheezing, crackles, cyanosis, dyspnea CO2 retention, secondary polycythemia
Hypertrophy and hyperplasia of mucus secreting glands in bronchi
DLCO normal
Productive cough for > 3 months in a year for > 2 consecutive years
Sarcoidosis
immune mediated widespread noncaseating granulomas
high ACE levels, high CD4/CD8 ratio
enlarged LN
bilateral adenopathy and coarse reticular opacities
Associated Bells Palsy, Uveitis, granulomas, Lupus pernio, Intersititial fibrosis, erythema nodosum, RA like, high Ca
Tx steroids
Inhalation injury sequelae
chemical tracheobronchitis, edema, pneumonia, ARDS
secondary to burns, CO, CN, arsenic
singed nasal hairs or soot
severe edema, congestion of bronchus and soot deposition
Asbestosis
Shipbuilding, roofing, plumbing
ivory white calcified supradiaphragmatic and pleural plaques
Bronchogenic carcinoma > mesothelioma, increase risk of Caplan syndrome
LOWER LOBES
ferruginous bodes are golden brown fusiform rods resembling dumb ells
increase risk pleural effusion
Berylliosis
aerospace and manufacturing industry
granulomatous
increase risk of cancer and cor pulmonale
UPPER LOBES
Coal Workers
macrophages with carbon –> inflammation and fibrosis
increase risk of Caplan
UPPER LOBES
small rounded nodular opacities
Caplan Syndrome
RA, pneumoconioses with intrapulmonary nodules
silicosis
sandblasint, foundries, mines
macrophages release fibrinogenic factors –> fibrosis
increase susceptibility to Tb, increase risk of cancer, cor pulmonale, Caplan syndrome
UPPER LOBES
eggshell calcifications of hilar LN
Mesothelioma
malignancy of pleura associated with asbestosis
may result in hemorrhagic pleural effusion, pleural thickening
Psammoma bodies
Calretinin and cytokertain +
ARDS
alveolar insult –> pro inflammatory cytokines –> neutrophils –> endothelial damage and increasesed permeability –> hyaline membranes
Loss of surfactant –> alveolar collapse
via sepsis, aspiration, pneumonia, trauma, pancreatitis
Dx: bilateral lung opacities, resp failure, low PaO2/FiO2, hypoxemia, not HF issues
impaired gas exchange, low lung compliance, pum HTN
Sleep apnea
repeated cessation of breathing > 10 seconds during sleep –> disrupted sleep –> daytime somnolence
Dx sleep study
Nocturnal hypoxia –> systemic/ pulm HTN, arrhythmias, sudden death
Hypoxia –> increase EPO –> increase erythropoiesis
Obstructive sleep apnea
respiratory effort against airway obstruction
Normal PaO2during the day
Associated with obesity, loud snoring, daytime sleepiness
caused by parapharyngeal tissue in adults, adenotonsillar hypertrophy in children.
Tx weight loss, CPAP, dental device
Central sleep apnea
impaired respiratory effot due to CNS injury, HF, opioids
Associated wtih Cheyne Stokes respirations
Obesity hypoventilation syndrome
obesity –> hypoventilation –> high PaCO2 during waking hours, low PaO2 and high PaCO2 during sleep
Pickwickian syndrome
Pulm HTN
normal 10-14
HTN >25 at rest
results in arteriosclerosis, medial hypertrophy, intimal fibrosis of pulmonary A, plexiform lesions
severe resp distress –> cyanosis and RVH –> death from decompensated cor pulmonale
Pulm A HTN
Heritable can be due to inactivation of BMPR2 gene
poor prognosis
increase vasoconstrictors and decrease vasodilators
Left Heart Disease
caused by systolic/ diastolic dysfunction and valvular disease
Lung diseases or hypoxia
destruction of lung parenchyma, lung inflammation/ fibrosis, hypoxemic vasoconstriction
Chronic thromboembolic
recurrent microthrombi –> decreased cross sectional area of pulmonary vascular bed
Multifactorial pulm HTN
hematologic, systemic, metabolic disorders, compression of pulmonary vasculature by a tumor
Pleural effusion
Excess accumulation of fluid between pleural layers --> restricted lung expansion during inspiration decreased breath sounds dull to percussion decreased fremitus Tracheal deviation none
Atelectasis
Alveolar collapse decreased breath sounds dull to percussion decreased fremitus trachea deviate to side of lesion
Simple pneumothorax
accumulation of air in pleural space Sx dyspnea, uneven chest expansion, chest pain decreased breath sounds hyperresonant decreased fremitus
Tension pneumothorax
air enters pleural space but cannot exit. Increasing trapped air
decreased breath sounds
Hyperresonant
decreased fremitus
Tracheal deviation away from side of lesion –> mediastinal displacement –> kinking IVC –> decrease venous return –> decreased cardiac output
Consolidation
bronchial breath sounds, late respiratory crackles, egophony
dull to percussion
increased fremitus
Causes of atelectasis
obstructive: prevent new air reaching distal airways, old air resorbed
Compressive: external compression on lung decreases lung volumes
Contraction: scarring of lung parenchyma that distorts alveoli
Adhesive: due to lack of surfactant
Lymphatic Pleural effusion
thoracic duct injury from trauma or malignancy
Milky appearing fluid high TG
Exudate pleural effusion
high protein content, cloudy
due to malignancy, inflammation, trauma
MUST BE DRAINED DUE TO RISK OF INFECTION
Transudate effusion
low protein, clear
via increased hydrostatic pressure or decreased oncotic pressure
Primary spontaneous pneumothorax
due to rupture of apical subpleural bleb or cyst
in tall thin young males and smokers
Secondary spontaneous pneumothorax
due to diseased lung, mechanical ventilation with use of high pressure
Traumatic pneumothorax
blunt, penetrating or iatrogenic trauma
Lobar Pneumonia
S. pneumoniae, Legionella, Klebsiella
intra alveolar exudate
Bronchopneumonia
S. pneumoniae, S. aureus, H. influenzae, Klebsiella
acute inflammatory infiltrates from bronchioles into adjacent alveoli
Patchy distribution in >1 lobe
interstitial pneumonia
Mycoplasma, chlamydophila pneumoniae, chlamydophila psittai, Legionella, viruses
diffuse patchy infiltrate localized to interstitial areas of alveolar wall
bilateral multifocal opacities
Indolent
Cryptogenic organizing pneumonia
chronic inflammatory diseases or medication (amiodarone) - sputum culture
Noninfectious with inflammation of bronchioles and surrounding structures
Lung cancer
cough, hemoptysis, bronchial obstruction, wheezing, coin lesion
Metastasize to liver, adrenals, bone, brain,
Metastasis from breast, colon, prostate, bladder
Complications: SVC syndrome, pancoast tumor, Horner syndrome, endocrine, recurrent laryngeal N compression, effusions
Risk factors: smoking, radon, asbestos, fam hx
Small cell carcinoma of the lung
Central location undifferentiated (very aggressive) May produce ACTH, ADH, Lambert Eaton Amplification of myc oncogenes Neoplasm of neuroendocrine Kulchitsky cells Chromogranin A + Neuron specific enolase + synaptophysin +
Adenocarcinoma of the lung
Peripheral location nonsmoking women activate KRAS, EGFR, ALK associated with clubbing glandular pattern on histo mucin + Bronchioalveolar subtype grows along alveolar septa --> thickening of alveolar walls. Tall, columnar cells containing mucus
Squamous cell carcinoma of the lung
Central location
Hilar mass arising from the bronchus
cavitation, cigarettes, hypercalcemia
keratin pearls and intracellular bridges
Large cell carcinoma of the lung
Peripheral location highly anaplastic undifferentiated tumor poor prognosis less responsive to chemo STRONG ASSOCIATION WITH SMOKING pleomorphic giant cells
Bronchial carcinoid tumor
central or peripheral excellent prognosis mass effect or carcinoid syndrome nests of neuroendocrine cells chromogranin A +
Lung abscess
pus within parenchyma
caused by aspiration of oropharyngeal contents or bronchial obstruction
Air fluid levels seen on CXR
Due to anaerobes
Pancoast tumor
apex of the lung
can compress recurrent laryngeal N, stellate ganglion, SVC, brachiocephalic V, brachial plexus, phrenic N
SVC syndrome
impair blood drainage from the head, neck, upper extremities.
Caused by malignancy and thrombosis
MEDICAL EMERGENCY
can rain intracranial pressure –> HA dizzy, increased risk of aneurysm
Histamine 1 blockers first generation
Diphenhydramine,dimenhydrinate, chlorpheniramine, doxylamine
used for allergy, motion sickness, sleep aid
adverse: sedation, antimuscarinic, anti a adrenergic
Histamine 1 blockers second generation
-adine
used for allergy
Adverse: far less sedating than 1st generation because of low entry into CNS
Guaifenesin
thins respiratory secretions, does not suppress cough reflex
N acetylcysteine
liquifies mucus in chronic bronchopulmonary diseases by disrupting disulfide bonds
Dextromethorphan
antagonize NMDA glutamate receptors
Has mild opioid effect when used in excess
Naloxone can be given for overdose
mild abuse potential
May cause 5HT syndrome if combined with other serotonerigic agents
Pseudoephedrine, phenylephrine
a adrenergic agonists
used to reduce hyperemia, edema, open obstructed eustachian tubes
Adverse: HTN. rebound congestion if used more than 4-6 days
Can also cause CNS stimulation, anxiety
Endothelin receptor antagonists
decrease pulmonary vascular resistance
Hepatotox
treat pulm HTN
PDE5 inhibitors
increase cGMP –> prolonged vasodilatory effect of NO
treat pulm HTN and erectile dysfunction
don’t use nitro
Prostacyclin analogs
inhibit platelet aggregation
treat pulm HTN
side effects: flushing, jaw pain
Albuterol
B2 agonist
relax bronchial smooth M
acute exacerbation of asthma
can cause tremor arrhythmia
Salmeterol, formoterol
B2 agonist for asthma
long acting agents for prophylaxis
cause tremor arrhythmias
Fluticasone, budesonide
inhaled corticosteroids for asthma
inhibit synthesis of all cytokines
Inactivate NFkB
1st line therapy for chronic asthma
Tiotropium, ipratropium
muscarinic antagonist for asthma
prevent bronchoconstriction
used for COPD
Montelukast, zafirlukast
block leukotriene receptors (CysLT1)
good for aspirin induced and exercise induced asthma
Zileuton
5 lipoxygenase pathway inhibitor
blocks conversion of arachidonic acid to leukotrienes
Hepatoxic
Omalizumab
anti IgE monoclonal therapy
bind unbound IgE and blocks binding to FceRI
used in allergic asthma with high IgE levels resistant to inhaled steroids and long acting B2 agonists
Theophylline
methylxanthines for astma
likely causes bronchodilation by inhibiting phosphodiesterase –> high cAMP due to low cAMP hydrolysis
limited use due to narrow therapeutic index
cardiotox, neurotox
block actions of adenosine
Anti IL5 monoclonal therapy
prevent eosinophil differentiation maturation, activation and survival mediated by IL5 stimulation.
Mepolizumab, reslizumab –> against IL5
Benralizumab –> against IL5 receptor a
