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34 Cards in this Set
- Front
- Back
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FEV1
-Def -Normal -Obstructive -Restrictive |
Forced Expiratory Volume in 1 second time. The volume exhaled during the first second of a forced expiratory maneuver started from the level of total lung capacity. Perform 3 tests and report the LARGEST value of the 3 via extrapolation from the steepest part of the vol-time curve which should not be greater than 5% of FVC or 150mL whichever is greater.
NORMAL= 4.0L OBSTRUCTIVE= 1.3 L (SIg DEC) RESTRICTIVE= 2.3 L (less dec) |
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FVC
-Def -Normal -OBstructive -Restrictive |
Forced vital capacity AKA FEVC (forced EXPIRATORY vital capacity)
volume change of the lung between a full inspiration to total lung capacity and a maximal expiration to residual volume. The measurement is performed during forceful exhalation; the preceding maximal inhalation need not be performed forcefully NORMAL= 5 L OBSTRUCTIVE= 5 L (NO CHANGE) RESTRICTIVE= 3.1 L (DEC) |
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FEV1/FVC
-Def -Normal -OBstructive -Restrictive |
The ratio of these two values are the most commonly used tests (SPirometry PFTs) used to determine pulmonary functionality and ability potential
Normal= 80% OBSTRUCTIVE= DEC bc ONLY FEV1 is usually dec. (25%) RESTRICTIVE= normal to INC bc BOTH FEV1 and FVC DEC. WILl remain 80% if the dec in FEV1 and FVC IS PROPORTIONAL and will INC if the DEC in FVC>>FEV1. (ex 80-90%) |
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Obstructive Lung Diseases
-Def -Exs |
DEC in AIRFLOW in lungs
1)COPD -Emphysema -Chronic Bronchitis -Chronic Bronchioloitis 2) Bronchiectasis 3) Bronchial Asthma -Extrinsic -Intrinsic |
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Restrictive Lung Diseases
-Def -Exs |
*DEC PARHENCHYMAL (functional, epithelial) Expansion
*DEC Lung CAPACITY |
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COPD
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Chronic IRREVERSIBLE OBSTRUCTION (aka dec airflow) Pulmonary Disorders:
1) Emphysema (FUNCTIONAL COPD only) 2)Chronic Bronchitis and Chronic Bronchioloitis *Often COMORBID with each other and with SMOKING! *10% of US population *4th leading cause of death in US |
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Emphysema= PINK PUFFERS
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-FUNCTIONAL rather than STRUCTURAL COPD Irreversible INC in Size of airspaces DISTAL to the TERMINAL BRONCHIOLES (resp bronchioles, alveolr ducts, distal alveoli) w/
-Alveolar wall DESTRUCTION ----I ELASTICITY/recoil so can't push air out -Dyspnea, Tachypnea, w/ NORMAL Hb Oxygenation!, resp insufficiency, poss Cor pulmonale----> Death *weight loss, BARREL CHEST - NO MECHANICAL OBSTRUCTION -Pathogenesis = Indirect and Direct via nicotine activation of PMNs resulting in PROTEASE/antiprotease (ELASTASE/a1-AT) AND tobacco induced OXIDANT/antioxidant (FREE RADS/sod and gth) imbalances lead to DEC Elasticity/recoil of alveolar septal walls making it more diff to expire air so FUNCTIONAL airway obstruction. -Though superimmosed infections may cause scarring, emphysema is due to PARENCHYMAL Lung Loss NOT Fibrosis (so very little scarring) |
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Centriacinar Emphysema
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- UPPER LOBEs of midage MEN
-DOES NOT effect Distal Alveoli -50% of smokers have this - comorbid with chornic bronchitis - prolonged expiration - "Hunch over" when sitting to try to squeeze air out of lung -black and tarry looking |
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Panacinar Emphysema
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-LOWER Lobes of YOUNG WOMEN
-WHOLE ACINUS (resp bronchioles, alveolar ducts AND DISTAL ALVEOLI) -big and pink and puffy looking |
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a1-AT
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an inhibitor (antiprotease) of the protease elastase which normally prevents it from destroying elastin in the alveolar septal walls. When PMNS are activated by nicotine during smoking, they inhibit this elastase inhibitor and also induce elastase activity thus acting as a DBL whammy on breaking down the elastic componenets of the Alveolar septal wall during EMPHYSEMA
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Pure Chronic Bronchitis of large airways (trachea, bronchi)= Blue Bloaters
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A CLINICAL CONDITION of PERIPHERAL HYPERMUCOUS SECRETION in the bronchial tree w/:
-Persistant/PRODUCTIVE cough for 3+mo/year for 2 CONSECUTIVE years. - MidAge men who smoke or live in air polluted (S--, N- Dioxides) cities |
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Pure Chronic Bronchiolitis of small airways (bronchioles)= Blue Bloaters
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*induced by golbic cell /squamous metaplasia of surface epithelium with hypermucous secretion causing mucous plugging of the bronchiolar lumen, inflmmation and periobroncihiolar (wall) FIBROSIS
*almost always comorbid with EMPHYSEMA *likely mediated by local release of T cell cytokines such as IL13 |
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Reid Index
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Ratio of thickness of mucous gland to bronchial wall in lungs
Normal= .4 or less Chronic Bronchitis= INC to .5 or MORE |
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T cell cytokines (IL-13)
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Mediators of the respiratory epithelial effects of environmental irritants that result in small airway disease (chronic bronchiolitis) effects such as muchous hypersecretion
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Bronchiectasis
-Def -Classification -3 etiologies |
*Irreversible Obstructive/Infective Pulmonary Disorder
*Irreversible DILATION of Bronchi(s) AND *DESTRUCTION of STROMA (Elastic suppoort and SMCs) *3 etiologies= 1. Neoplasms 2. Aspirated Foreign Material 3. Cystic Fibrosis |
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Broncial Asthma
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chronic REVERSIBLE airway Lung Obstruction due to bronchospasm w/ EPISODIC:
-Dyspnea -Wheezing -Dry Cough Caused by Chronic Bronchiol Inflammation which causes bronchospasms aka HYPERactive airway response, Eosinophis, SMC Hypertriphy/Hyperplasia 2 types= 70%Extrinsic and 30%Intrinsic |
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Extrinsic Bronchial Asthma
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70%, Childhood,
Atopic Type 1 Hypersensitivity with HIGH IgE and Th2 mediated immune responses to environmental Ags |
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Intrinsic Bronchial Asthma
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30% Adult
Nonatopic (Non-immune) STRESS triggered asthma |
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status Asthmaticus
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Uncontrolled asthma
may lead to death via: -mucous plugging of airways - hyperinflation of lung - |
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Restrictive Lung Disorders
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DEC in PARENCHYMAL lung EXPANSION
DEC LUNG CAPACITY |
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Pneumoconioses
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RESTRICTIVE NON NEOPLASTIC lung reaction of inhaled mineral dusts, organic, or inorganic substances.
Results from chronic irritation of the substances and subsequent macrophage activation resulting in fibrosis form collegen producting fibroblasts-----> Stiff lung with dec. compliance and progressive dyspnea. *Silicosis is an ex. It is the most prevalent occupational chronic diseases in the worlD! |
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Terms to describe inhaled mineral dust pneumonconisoses of:
1. coal dust 2. silica 3. asbestos 4. berylium |
1. Anthracosis
2. Silicosis 3. Asbestosis 4. Berylliosis |
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Silicosis
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*Pneumoconioses of silica
-aka RESTRIVTIVE Nonneoplastic chronic inflammatory disease of inhaled mineral silica dust. *MOST prevalent occupational chronic disease in the world!! *Silica---->macropgages-----> Fibroblasts------>Collagen deposition in NODULAR FOCI----> Stiff fibrotic lung-----> Restricted lung parenchymal expansion------> chronic inflammatory cells contiune to infiltrate and destroy BRONCHIOLES, ALVEOLI, and pulm. BVs.------> Dec lung compliance and capacity-------> Progressive Dyspnea---> Hypoxia----->PHT---->RHF---> Cor Pulmonale----> Death |
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The most common occupational chronic disease in the WORLD!
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Silicosis (aka inhalation of silica dustis)
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Pneumonia
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*INfection of the lung
*6th leading cause US death *may be due to defects in humoral, complement, PMN immunity (-->Pyogenic bac.) or defet in Tcell immunity (---> intracellular mycobac/viral andor LOW VIRULENCE microorganisms) , environmental smoking alchohol |
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Pneumocystis jiroveci
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A low virulent microbe that can cause pneumonia due to T CELL-mediated immune defects.
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Lobar Pneumonia
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Rare in US. virulent bac.-Strep Pneumoniae. which cause ACUTE INFLAMMATORY ALVEOLAR CONSOLIDATION
Healthy Adults Tx w/Ab to dec the classic 4 stage changes: 1. Congestion 2. Red Hepatization 3. Gray Hepatization 4. Resolution- oftene ends in an extreme HYPOTHERMIC CRISIS! |
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Bronchopneumonia
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Common and caused by low virulent bac. like Klibessela SECONDARY to AGE EXTREMES with: immunocompromised, bronchitis, flu, cancer etc.
These bac cause alveolar consolidation AND BRONCHIAL INFLAMMATION |
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Strep Pneumoniae
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A rare rather virulent bacteria that directly causes lobar pneumonia in adults via alveolar consolidation.
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Klebisiella
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A low virulence microbe that very commonly causes bronchopneumonia in age extermes due to complication of: flu, broncihtis, immunosupressed ppl.
*caues broncial inflammation and alveolar consolidaton |
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Conditions that are likely to cause aspiration of upper respiratory tract content include _____ _____ _____ can cause ____________ and inlcude symptoms such as _____ ____ ______. If untreated it will (probably rarely always) resolve on its own and may lead to ______ _____ ______ ________
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werqrews
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What is highly indivacative of a pulmonary infection that has caused aspiration of upper respiratory tract secretions or gastric content?
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werqwe
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Empyema
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Fibrous Pleural thickening and ADHESIONS whic may result from unresolved pulmonary absess from a condition that causes pulmonary infectiosn via aspiration of upper resp tract secretions/gastric content.
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Viral Pneumonia
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ryeawydf
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