lung Flashcards
normal patho
Pathology
Congenital
Atelectasis
Acute Pulmonary Injury
Obstructive Pulmonary Disease (COPD)
Restrictive (Infiltrative) Pulmonary Disease
Vascular Pulmonary Diseases
INFECTIONS
NEOPLASMS
PLEURA (effusions, pneumothorax, tumors)
congenital
-Agenesis/Hypoplasia
-!!!!!Tracheal/bronchial anomalies, i.e., Tracheo-Esophageal (TE) fistula
-Vascular anomalies
-Congenital Emphysema
-Foregut cysts
-Pulmonary Artery Malformations (CPAM)
-Sequestration (no connection to airways)
-know the 82% picture- food goes back up - emesis -> air goes into stomach
atelectasis
-INCOMPLETE EXPANSION
-COLLAPSE
-Resorption can be from a bronchial obstruction, e.g., tumor.
-Compression can be from a pleural effusion.
-Contraction can be from a diffuse lung fibrotic process.
pulmonary edema
-FOUR main pathologic mechanisms of pulmonary edema
-IN-creased venous pressure
-DE-creased oncotic pressure
-Lymphatic obstruction
-Alveolar injury
acute respiratory distress syndrome (ARDS or D.A.D., ie., diffuse alveolar damage
-Clinical syndrome of progressive respiratory insufficiency caused by !diffuse alveolar damage!
-Sepsis, severe trauma, or diffuse pulmonary infection
-Damage to endothelial and alveolar epithelial cells and secondary inflammation are initiating events and basis of lung damage
-Micro: hyaline membranes lining alveolar walls, accompanied by edema, scattered neutrophils and macrophages, and epithelial necrosis
-COVID
-ventilation does nothing
obstructive vs restrictive lung disease
-Obstructive lung diseases: increase in resistance to airflow due to diffuse airway disease (may affect any level of respiratory tract : COPD (obstructive) can’t exhale
-Restrictive diseases: reduced expansion of lung parenchyma and decreased total lung capacity: Fibrosis (restrictive) can’t inhale
-Clinical distinction based primarily on pulmonary function tests
-FEV 1 /FVC ratio of less than 0.7 generally indicates obstructive disease; usually TLC is increased
-Restrictive diseases: proportionate decreases in both total lung capacity and FEV, so that FEV 1 /FVC ratio usually remains normal
-(1) chest wall disorders (e.g., severe obesity, pleural dxs, kyphoscoliosis,etc.)
-(2) chronic interstitial and infiltrative diseases (e.g., pneumoconioses and interstitial fibrosis)
-Overlapping features may occur
obstructive (COPD)
-EMPHYSEMA (almost always chronic)
-CHRONIC BRONCHITIS -> emphysema
-ASTHMA
-BRONCHIECTASIS
emphysema
-Abnormal permanent enlargement of air spaces distal to terminal bronchioles, accompanied by destruction of alveolar walls without obvious fibrosis
-Leads to reduced gas exchange, changes in airway dynamics that impair expiratory airflow, and progressive air trapping
-Centri-acinar (usually due to cigarette SMOKING), Pan-acinar (usually due to alpha-1-antitrypsin deficiency), Paraseptal, Irregular
-macrophages from smoke
-Role of proteases which break down alveolar walls
-INcreased crepitance, BULLAE (BLEBS)
-Clinically likely to produce recurrent pneumonias, and progressive failure
-wall breakdown due to enzymes
-PANacinar – usually due to alpha-1 antitrypsin (protein that inhibits various proteases) deficiency
intrinsic imbalance in activity of protease/elastase released and an inhibitor of protease - alpha-1 antitrypsin
-1) HYPER-expansion
-2) “flattened” diaphragms (blunted),
-3) “bullae” -> can pop
-4) increased lucency (why?)
-black bc a lot of air
chronic bronchitis
-INHALANTS, POLLUTION, CIGARETTES
-CHRONIC COUGH
-CAN OFTEN PROGRESS TO EMPHYSEMA
-MUCUS hypersecretion, early, i.e. goblet cell increase
-CHRONIC bronchial inflammatory infiltrate
asthma
-Similar to chronic bronchitis but:
-Wheezing is hallmark (bronchospasm)
-STRONG allergic role, i.e., eosinophils, IgE, allergens
-Often starting in CHILDHOOD
-ATOPIC (allergic) or NON-ATOPIC
-Chronic small airway obstruction and infection
-1) Mucus hypersecretion with plugging, 2) lymphocytes/eosinophils, 3) lumen narrowing, 4) smooth muscle hypertrophy
-1) Inflammation
-2) Bronchial narrowing
-3) Increased Mucous
-4) Smooth muscle hyperplasia
-5) Eosinophils (if etiology is allergy)
bronchiectasis
-DILATATION of the BRONCHUS, associated with, often, necrotizing inflammation
-CONGENITAL
-TB, other bacteria, many viruses
-BRONCHIAL OBSTRUCTION (i.e., LARGE AIRWAY, NOT SMALL AIRWAY)
-Rheumatoid Arthritis, SLE, IBD (Inflammatory Bowel Disease)
-necrotizing
-Bronchiectasis is not a specific disease, but a condition in which LARGE bronchi are damaged and DILATED due to a variety of causes.
“-ectasis” is the root word for “dilatation”
restrictive (infiltrative)
-REDUCED COMPLIANCE, reduced gas exchange)
-Are also DIFFUSE
-HETEROGENEOUS
-FIBROSING
-GRANULOMATOUS
-EOSINOPHILIC
-SMOKING RELATED
-PAP (Pulmonary Alveolar Proteinosis
lung with restrictive disease: compliance
-less “spongy”
-reduced compliance.
-In contrast to “obstructive” lung diseases, the chest x-ray shows diffuse INCREASE in density, NOT DECREASED, density.
-“restrictive” lung diseases = anatomic/functional barriers to the classic gas exchange between an endothelial cell and a type-1 pneumocyte
FIBROSING
-!!!“IDIOPATHIC” PULMONARY FIBROSIS (IPF)- -cant inhale -> need lung transplant
-NONSPECIFIC INTERSTITIAL FIBROSIS
-“CRYPTOGENIC” ORGANIZING PNEUMONIA
-“COLLAGEN” VASCULAR DISEASES
-!!!PNEUMOCONIOSES
-DRUG REACTIONS
-RADIATION CHANGES
idiopathic pulmonary fibrosis (usually interstitial penumonia)
-IDIOPATHIC, i.e., not from any usual causes, like lupus, scleroderma)
-FIBROSIS- scarring
-Usual Interstitial Pneumonia
-refers to histology of IPF
etiology pathogenesis of IPF
-Unknown
-Injured epithelial cells may be source of profibrogenic factors, such as TGF-beta
-Innate and adaptive immune cells produce profibrogenic factors as a host response to epithelial cell damage
-Genetic role suggested by familial IPF
-20% of cases are associated with collagen vascular disease including RA, SLE and progressive systemic sclerosis – suggests immune system involvement
-UIP (histological hallmark may) – usual interstitial pneumonia
pneumoconioses
-“OCCUPATIONAL”
-“COAL MINERS LUNG”
-DUST OR CHEMICALS OR ORGANIC MATERIALS:
-Coal (anthracosis)
-Silica
-Asbestos
-Be, FeO, BaSO4, CHEMO
-HAY, FLAX, INSECTICIDES, etc.
-Development depends on
-Amount in lungs
-Size, shape, buoyancy
-Solubility and physiochemical reactivity
-Additional irritants (smoking)
-Most dangerous 1 – 5 um
-Macrophages ingest particles and immune system is stimulated
granulomatous
-sarcoidosis, ie. NON-caseating granulomas (idiopathic)
-hypersensitivity (DUSTS, bacteria, fungi, FARMERS lung, PIGEON BREEDERS lung)
sardoidosis
-Mainly LUNG, but eye, skin or ANYWHERE - systemic
-UNKNOWN ETIOLOGY
-IMMUNE, GENETIC factors
-Usually female > male and African American > Caucasian
hypersensitivity pneumonitis
-Interstitial lung disorders - immune mediated, caused by intense, usually long-term exposure to inhaled organic dusts
-Organic dust usually contains Ags made of spores of thermophilic bacteria, fungi, animal proteins, bacterial products
-Patients have abnormal sensitivity or reactivity to Ag mainly involving alveoli; Most patients have specific Abs against causative agent in serum
-Symptoms 4 – 6 hrs after exposure; may last 12 hrs to days; recur with re-exposure
-non-caseating granulomas (2/3 rds of patients)
-Examples –
-farmer’s lung (exposure to dusts from humid, warm, newly harvested hay, permits proliferation of spores of thermophilic actinomycetes)
-pigeon breeder’s lung (provoked by proteins from serum, excreta, or feather of birds)
-air conditioner lung (caused by thermophilic bacteria in heated water reservoirs)
-goes away once they move away from it
vascular pulmonary diseases
-PULMONARY EMBOLISM (with or usually WITHOUT infarction)
-PULMONARY HYPERTENSION, leading to cor pulmonale
-HEMORRHAGIC SYNDROMES:
-GOODPASTURE SYNDROME
-HEMOSIDEROSIS, idiopathic
-Granulomatosis with polyangiitis
pulmonary embolism
-Usually secondary to debilitated states with immobilization, or following surgery
-Usually deep leg and deep pelvic veins (DVT), NOT superficial veins
-Follows Virchow’s triad, i.e., 1) flow problems 2) endothelial disruption, 3) hypercoagulabilty
-Usually do NOT infarct, usually ventilate -> 2 blood supplies
-When they DO infarct, the infarct is hemorrhagic (why?)
-Decreased PO2, acute chest pain, V/Q MIS-match
-DX: Chest CT, V/Q scan, angiogram
pulmonary HTN
-May occur with:
-COPD- As the alveoli become wider, the arterioles become narrower
-CHD (Congenital HD, increased left atrial pressure)
-Recurrent PEs
-Autoimmune, e.g., PSS (Scleroderma), i.e., fibrotic pulmonary vasculature
-congenital vs acquired (RHF)
hemorrhagic syndromes
-GOODPASTURE Syndrome: Ab’s to the alpha-3 chains of collagen IV, glomerular basement membrane deposits also (kidneys)
-IDIOPATHIC PULMONARY HEMOSIDEROSIS
-Granulomatosis with polyangiitis (Wegener’s granulomatosis): form ofvasculitisthat affects thelungs,kidneysand other organs. Due to its end-organ damage, it can be a serious disease that requires long-termimmunosuppression
primary vs secondary TB
Primary tuberculosis develops in previously unexposed, unsensitized person; usually, primary infection is contained, but sometimes progressive.
Secondary tuberculosis arises in a previously sensitized host, more commonly months to years after the initial infection, usually when host resistance is weakened
local effects of lung cancer
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