patho Flashcards
Respiratory failure due to multiple pulmonary insults
▪Injury to Type1 pneumocytes and capillary endothelial cells of the lung
▪ Can result from burns, near-drowning, dialysis, Lyme disease, and viral infections
▪ Causes respiratory distress, hypoxemia, pulmonary fibrosis, poor pulmonary
compliance, pulmonary edema
▪ Develops between 24-48 hours after an injury
▪ Very low PaO2, normal or low PaCO2, and elevated pH
▪ Diffuse bilateral alveolar infiltrates
ARDS (Acute Respiratory Distress Syndome)
● Resp failure w/ widespread rapid inflammation of the lungs
● Etiology: direct/indirect lung injury from airway (pneumonia) or circulation (sepsis)
● Sx: severe resp distress within 24-48 hrs, cyanosis, intercostal retractions, hypoxemia, pulmonary edema
o Initial hyperventilation -> respiratory alkalosis (low PO2, high pH, low or normal PCO2 since its being expelled at faster rate)
● Dx: CXR shows bilateral alveolar infiltrates or opacities, but cardiac shape is normal
ARDS (Acute Respiratory Distress Syndome)
▪ Excessive collagen levels in the connective tissue matrix of the lungs
▪ Causes progressive restriction of the lungs leading to dyspnea, cyanosis, weight loss, chronic disability
● Excess collagen in CT matrix of lungs -> difficult for lungs to expand (worsens)
● RFs: differ for upper vs lower lobes
o Upper (CHARTS): Coal worker pneumoconiosis, Histiocytosis X, Ankylosing spondylitis, Radiation, TB, Sarcoidosis/Silicosis
o Lower (SCAR): Systemic sclerosis, Cryptogenic fibrosing alveolitis, Asbestosis, Rheumatoid arthritis
● Sx: dyspnea, cough, cyanosis, weight loss, chronic disability; 2-5 yr life expectancy
idiopathic pulmonary fibrosis
● Systemic; Autoimmune; rare; noncaseating epithelioid granulomas everywhere in the body
granuloma of immune cells desrtoying pathogens form -> accumulate in lymph nodes, esp. hilum of lungs
in severe cases can lead to pro-inflamm. cytokines -> fibrosis
● RFs: 20-40 y/o, Northern European & African American descent
● Sx: fever, weight loss, arthralgia, peripheral lymphadenopathy, skin lesions, impaired organ function d/t fibrosis or granuloma presence, erythema nodusum (red, on legs)
Sarcoidisis
Interstitial fibrosis from inhalation of inorganic dust/braod category that involve occupational exposure
o Anthracosis (black lung) – inhalation of carbon dust in urban areas (no damage)
o Coal worker’s pneumoconiosis – coal dust containing carbon & silica
o Silicosis – silica dust
o Asbestosis – asbestos fibers (construction/shipyard workers)
pneumoconiosis
extrinsic or intrinsic asthma:
childhood, type I hypersensitivity w/ IgE bound to mast cells
▪ Hyperresponsive airway -> immune response -> swelling -> broncho-constriction -> air trapped (wheezing) -> intra-alveolar pressure rises -> decreases hydrostatic pressure -> fluid leaves capillaries -> airway edema -> chronic airway remodelling (BUT asthma can be reversible)
extrinsic
intrinsic or extrinsic asthma:
adulthood, not associated w/ allergies but a neural reflex to a chronic insult or inflammation -> recurrent bronchoconstriction & increased mucus
intrinsic asthma
● Episodic irritation & constriction of the bronchioles; chronic inflammation & narrowing of airways
RFs: idiopathic, Western world, lack of breastfeeding, pollution, high omega 6 intake, lack of childhood infections, sedentary lifestyle; young boys in poverty often affected
Sx: episodic cough, chest tightness, wheezing, dyspnea < at night or w/ triggers
Complications: recurrent infection, disease progression -> fatal, pneumothorax, atelectasis, status asthmaticus (asthma bout lasts for days, unresponsive to tx)
Dx: spirometry shows reduced FEV1 (like COPD)
asthma
Curshmann spirals and Charcot Leyden crystals are seen in which cdx?
asthma
● Wide airways (bronchi) -> mucus forms -> can’t clear -> stinky sputum
● RFs: COPD or infection (main causes) + A SICK AIRWAY…
o Airway lesion/obstruction, Sequestration (unattached piece of lung tissue), I nfection, Cystic Fibrosis, K artagener syndrome (genetic, triad w/ situs inversus & chronic sinusitis), Aspergillosis (mold), Immunodeficiency, Reflux, William’s Campbell Syndrome (congenital, no cartilage in bronchi), Aspiration, Yellow nail syndrome (swollen arms/legs from lymph accum., nails yellow)
● Sx: longstanding cough, stinky sputum; Complications: abscess or bronchial obstruct.
Bronchiectasis
● “Blue Bloater”; overweight and cyanotic; RFs: smoking, occupational exposure
● Chronic obstruction of terminal airways (NOT alveoli) from excess mucus
o Initial insult -> impaired -> bacteria colonize -> chronic inflammation (cycle)
● Sx: mild dyspnea, productive cough, cough w/ hemoptysis, purulent sputum, cyanosis, clubbing, use of accessory muscles for respiration, barrel chest (lung hyperinflation)
● Complications: recurrent acute bronchitis, cor pulmonale (RHF)
● Dx: productive cough > 3 months OR > 2 years
● Spirometry: decreased FEV1, increased PCO2, v low PO2
Chronic Bronchitis
“Pink Puffer”; permanent enlargement & destruction of air spaces (alveolar walls) -> increased RV w/out fibrosis
causes: smoking, A1AT def.
o Centrilobular emphysema: dilation of respiratory bronchioles
o Panacinar emphysema: dilation of entire acinus (gas exchange unit including resp. bronchioles, alveolar ducts/sacs, alveoli)
o Paraseptal emphysema: dilation at distal acinus
o Irregular emphysema: irregular involvement of acinus
● RFs: smoking, occupational exposure, biomass fuel cooking exposure
● Sx: significant dyspnea!, minimal cough, tachypnea, pink skin, cachexia, barrel chest (lung hyperinflation)
● Complications – weight loss, pneumothorax
Emphysema
● Accumulation of milky, lipid-rich fluid in the pleural cavity d/t lymphatic obstruction
Chylothorax
● Blood in pleural space d/t trauma or vessel rupture (ex: rib fracture, clotting disorder)
Hemothorax
▪ Collapse or closure of a lung resulting in reduced or absent gas exchange.
▪ Can affect part or all of a lung
▪ Usually unilateral
▪ Cough, chest pain, dyspnea, low oxygen saturation, pleural effusion, cyanosis (late stage), increased heart rate
▪ Most commonly occurs after surgery
OBSTRUCTIVE ATELECTASIS
▪ Fibrosis of the visceral pleura so that part or all of a lung becomes covered with a plaque or a thick layer of nonexpansible fibrous tissue
PLEURAL FIBROSIS
▪ Chronic inflammatory and scarring disease of the lung tissue
▪ Severe shortness of breath
▪ Increased risk for certain cancer
Pleural Fibrosis - Asbestosis
Passage for air to travel between pleural layers
o Closed – air accumulates between alveoli & visceral pleura
o Open – chest wall trauma; could be just parietal or also visceral
● Etiology: traumatic (stab wound, fracture) or spontaneous (ruptured air-filled lesion)
Sx: acute onset pleuritic chest pain, dyspnea
o PE: + trachea deviated AWAY (air occupying space) + decreased breath sounds + hyper resonant + decreased tactile fremitus + friction rub
Complications: free entry of air into lungs -> lose (-) pressure gradient -> lung collapse
o If pneumothorax severe enough, mediastinum shifts -> compresses other lung
Pneumothorax
▪ Pleural cavity contains air.
▪ Due to perforation of the pleura from outside the lung or from inside the lung
▪ Causes loss of negative pressure and collapse of the lung.
▪ If severe enough it can cause the mediastinum to shift to the other side and cause a tension pneumothorax of the opposite lung.
Pneumothorax
● RFs: smoking (1st or 2nd hand), asbestos exposure, occupation exposure, radiation
● Sx: asx for long time ->
1. Bronchial sx: hemoptysis, chronic cough, dyspnea, chest pain
2. Intra-thoracic spread: chest wall invasion, reflux, hoarse (from recurrent laryngeal nerve paralysis), Horner syndrome, Pancoast’s tumor (located at apex), pleural effusion, phrenic nerve paralysis, SVC obstruction
3. Extra-thoracic spread: fatigue, anorexia, bone pain & fractures, seizures, confusion, personality change (brain meta), high alk phos, headache, N/V, LNs
● Complications: metastasis to hilar & mediastinal LNs, nerve compression
lung cancer
Pathophysiology:
Bronchial Adenoma: benign, from glandular tissue of bronchi, rarely carcinoma
Adenocarcinoma: most common, arises in bronchi, non-smoking (radiation, toxins),
o Originates peripherally, good prognosis & responds to removal
Squamous Cell Carcinoma: begins centrally & strong association w/ smoking
o May cause hypercalcemia by secreting parathyroid-like substance
Small Cell Carcinoma: most aggressive, w/ smoking, highly malignant
o Responds well to chemotherapy
o Can cause hyponatremia & Cushing’s syndrome from inappropriate ADH secretion
● Large Cell Carcinoma: unclear precursor, minimal association w/ smoking
Bronchial Carcinoid Tumor:
o Unrelated to smoking, excellent prognosis; occurs in patients < 40 yoa
o Sx: mass sx (cough, hemoptysis) + flushing, cyanosis, tachycardia, diarrhea
lung cancer
Types:
Adenocarcinoma
1. Cells of mucus-secreting glans in the esophagus
2. More common in lower part of the esophagus
Squamous cell carcinoma
1. Typically in the middle of the esophagus
Sxs: dysphagia, UWL, chest pain (burning or pressure), indigestion, GERD, cough, hoarseness
RFs: alcohol, bile reflux, drinking hot fluids, GERD, Berrett’s esophagus, smoking
esophageal cancer
● Squamous cell carcinoma m/c (in larynx)
RFs: men > 40 yoa, smoking & alcoholism together
● Types: glottic (m/c, arises from true vocal cords), supra- & sub-glottic (poor prog)
Laryngeal Cancer
● Highly aggressive malignant tumor located in the pleura (not actual lung)
● RFs: asbestos exposure, not smoking; very poor prognosis (lung enclosed in tumor)
Mesothelioma