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Acute respiratory failure
state of disturbed gas exchange
Acute respiratory failure blood gas values
PaO2 less than 60, PaCO2 higher than 50
Acute respiratory failure etiology
hypoxemia - poorly matched ventilation and perfusion, hypercapnia - poor alveolar ventilation in relation to CO2 production
Acute respiratory failure diagnosis
low PaO2, high PaCO2, low potassium and sodium, increased WBCs or decreased RBC and Hb
Pulmonary hypertension
sustained increase in pulmonary arterial pressure gradient
Secondary pulmonary hypertension
vasoconstriction seen in chronic bronchitis and emphysema
Pulmonary hypertension chest XR
enlargement of pulmonary arteries and right ventricle, abnormal vessel contours
Pulmonary hypertension EKG
right ventricular hypertrophy, mitral valve stenosis, left arterial myxma, and right heart enlargement
Pulmonary hypertension treatment
vasodilators - prostacyclin, diuretics - furosemide, spironolactone
Pulmonary embolism
circulation distal to obstruction is impaired leads to ischemic hypoxia
Pulmonary embolism Virchow’s triad - risk factors
venous sluggishness, hyper coagulability, and damage to venous wall
Pulmonary embolism diagnosis
mismatched ventilation and perfusion seen on scan, low PaO2 and PaCO2, and increased pH
Lung cancer
squamous cell carcinoma, adenocarcinoma, large cell carcinoma, small cell carcinoma, and bronchoalveolar carcinoma
squamous cell carcinoma
originates in central bronchi near hilus as intraluminal growth
squamous cell carcinoma doubling time, metastasizes
100 days, lymph nodes
adenocarcinoma
appears in periphery of lung, acinar bronchoalveolar and papillary tumors
adenocarcinoma doubling time, metastasizes
180 days, distant organs
large cell carcinoma
develops in periphery, large clusters
large cell carcinoma doubling time, metastasizes
100 days, distant organs
small cell carcinoma
originates in central bronchus region compressing and narrowing airway, associated w/ lesion in chromo 3
small cell carcinoma doubling time, metastasizes
33 days, widespread
bronchoalveolar carcinoma
originates in periphery, metastasizes through lymphatics, not associated w/ smoking
Asthma types
intrinsic, extrinsic, exercise induced, occupational, and drug induced
asthma etiology
airway obstruction and inflammation, increased airway responsiveness
asthma pathogenesis
IgE mediated activation of mast cells and cytokines, normal epithelium replaced by goblet cells
extrinsic asthma
allergic, pediatric onset
intrinsic asthma
nonallergic, adult onset
drug induced asthma
aspirin and NSAIDs
asthma diagnosis
forced expiratory volume decrease, FEV1/FVC less than 75, elevated WBCs and eosinophils
asthma treatment
B2 agonists, corticosteroids, leukotriene modifiers, and mast cell inhibitors
Acute bronchitis
acute inflammation of trachea and bronchi. viral and nonviral
Chronic bronchitis
Type B COPD, usually w/ emphysema
Chronic bronchitis etiology
Elevated IL-8 (neutrophil activation) and CD8 T cells and fibrotic changes extend into surrounding alveoli
Chronic bronchitis pathogenesis
increased bronchial wall thickness, high airflow resistance, hypoxemia and hypercarbia
Chronic bronchitis pulmonary function test
normal TLC, increased residual volume and FEV1
Chronic bronchitis arterial blood gas
elevated PaCO2 and decreased PaO2Chronic bronchitis
Chronic bronchitis EKG
artial arrhythmia and right ventricular hypertrophy
Chronic bronchitis treatment
B2 agonists (bronchodilation), anticholinergic bronchodilators, and corticosteriods
Emphysema
Type A COPD. destructive changes of alveolar walls and abnormal enlargement in distal air sacs
Emphysema clinical manifestations
exertional dyspnea, thin, pursed lip breathing, etc
Emphysema pulmonary function test
increased FRC, RV, and TLC. decreased FEV1 and FVC
Bronchiectasis
Obstruction of bronchi due to inflammation, infection, and dilation of wall. H influenza most common cause
Bronchiectasis clinical man
chronic productive cough, purulent foul smelling green sputum, hemoptysis, etc
Bronchiectasis ABG
decreased PaO2 and increase PaCO2
Bronchiolitis
widespread inflammation of bronchioles, half from RSV
Bronchiolitis pathogenesis
proliferation and necrosis epithelium produce obstruction and increase mucus
Bronchiolitis 3 mechanisms of obstruction
inflammatory exudate, release of chemical mediators lead to constriction, and inflammation induced fibrosis which narrows airway
Cystic fibrosis
hypersecretion of abnormal, thich mucus obstructs exocrine glands and ducts. autosomal recessive disorder
Cystic fibrosis pathogenesis
mutations - alters Cl and H2 transport = thick mucus obstructions
Cystic fibrosis diagnosis
stool sample - 95%
Epiglottitis
Rapid progressive cellulitis of epiglottis and soft tissue. mainly caused by H. influenza B
Epiglottis clinical man
pain w swallowing, drooling, etc
Epiglottis diagnosis
neck radio shows thumbprint sign
Croup syndrome
acute viral and inflammatory diseases of larynx, trachea, and bronchic
Croup syndrome diseases
Laryngotrachrobronchitis - viral, bacterial tracheitisCroup syndrome
Croup syndrome causes
parainfluenza type I, RSV, mycoplasma pneumoniae
Diffuse interstitial lung disease
restrictive disease w/ thickening of alveolar interstitial
Diffuse interstitial lung disease clinical manifestations
clubbing of nail beds, velcro rales
Sarcoidosis
systemic disease w/ immunological origin Sarcoidosis
Sarcoidosis pathogenesis
multiple, uniform, and noncaseating epithelioid granulomas = abnormal t cell function
Hypersensitivity pneumonitis
inhalation of organic particles responsible for inflammatory process
Hypersensitivity pneumonitis pathogenesis
type II hypersensitivity reaction
Occupational lung disease
chronic inhalation of toxic gasses or foreign particles
Occupational lung disease pathogenesis
particles paralyze ciliary action
Acute respiratory distress syndrome
damage to alveolar-capillary membrane
Acute respiratory distress syndrome pathogenesis
result of stiff, noncompliant lungs w/ presence of alveolar edema and exudate that exaggerates surface tension
Infant respiratory distress syndrome
hemorrhagic pulmonary edema, patchy atelectasis, and hyaline glassy membranes. under 25 weeks gestation is high risk
Infant respiratory distress syndrome pathogenesis
lack of pulmonary surfactant - increased surface tension and decreased lung compliance
Pneumothorax
accumulation of air in pleural space
Primary Pneumothorax
spontaneous, rupture of small subpleural blebs in apices
secondary Pneumothorax
complication of another disease, ruptured cyst or bleb
Tension Pneumothorax
trauma induced, buildup of pressure
Pneumothorax ABG
decreased PaO2 and acute respiratory alkalosis
Pleural effusion
pathological collection of fluid or pus in pleural cavity
Pleural effusion transudates
increased hydrostatic or decreased osmotic pressure
Pleural effusion exudate
increased production of fluid due to increased permeability of pleural membrane or impaired lymphatic drainagePleural effusion
Pleural effusion diagnosis
Thoracentesis
Pneumonia
inflammatory reaction to alveoli and interstitium of the lung
SARS
alveolar collapse w/ vascular injury occurring at same time
MERS
infection in monocytes and macrophages
TB
caused by mycobacterium tuberculosis
TB pathogenesis
T cells and macrophages surround bacteria in granulomas, limit replication, form necrotic nodules that become fibrotic and calcified
ECV Volume deficit
removal of sodium-containing fluid. flat neck veins
ECV volume excess
excessive aldosterone secretion. neck vein distention
Hyponatremia
low sodium, ECF too diluted - cells enlarge
Hypernatremia
high sodium, ECF too concentrated - cells shrivel
Clinical dehydration
combo of ECV deficit and hypernatremia
Edema
accumulation of excess fluid in interstitial compartment
Edema - increased capillary hydrostatic pressure
pushes fluid out of vessels into interstitial tissue
Edema - increased interstitial colloid osmotic pressure
pulls fluid from vasculature
Edema - blockage of lymphatic drainage (lymphedema)
pulls fluid from vasculature
Edema - decreased capillary osmotic pressure
fluid follows osmotic gradient out of vasculature interstitium
Hypokalemia
low potassium - shift into cells. hyperpolarization - less response to stimuli
Hypokalemia treatment
K wasting diuretics - thiazide, corticosteroids - prednisone
Hyperkalemia
high potassium - shift into ECF. hypopolarization - muscle dysfunction
Hyperkalemia treatment
K sparing diuretics - spironolactone
Hypocalemia
low calcium, decrease in threshold potential, hyper-excitability of neuromuscular cells
Hypercalcemia
high calcium, increase in threshold potential, decreasing neuromuscular excitability, cardiac dysrthemias
Hypomagnesemia
low magnesium, more AcH released, increased neuromuscular excitability
Hypomagnesemia clinical man
hyperactive reflexes, nystagmus