Pulmonary Flashcards
Viral PNA signs/symptoms
-nonproductive cough
-low grade fever
-low to normal WBC’s
-contagious as long as symptoms
present
Bacterial PNA Signs/symptoms
-productive cough
-purulent sputum
-high fever
-high WBC’s
-infiltrates on xray
-not contagious after 48 hrs on
antibiotics
What is the compensatory mechanism of the lungs in response to hypoxia?
intrapulmonary arteries constrict, diverting blood to better oxygenated lung segments-optimizes V/Q ratio
Diseases with decreased V/Q ratio
-PNA
-Asthma
-ARDS
-Alveolar collapse
-Pulmonary Edema
Diseases with increased V/Q ratio
-PE
-Non-embolic obstruction by tumor
-Emphysema
-radiation therapy
-Cardiovascular shock
V/Q ratio (ventilation/perfusion ratio)
adequate ventilation and sufficient perfusion of blood
normal value= 4:5 or 0.8
What are obstructive lung disorders?
disorders that obstruct airflow, making it difficult to exhale completely
EX) COPD, Asthma
What are restrictive lung disorders?
disorders that reduce total lung capacity by limiting lung expansion
EX) pulmonary fibrosis, hypoventilation syndrome (caused by obesity)
What type of hypersensitivity rxn is responsible for formation of granulomas in TB?
Type IV
What causes cavitation in the lungs in active TB infection?
tissue necrosis-bacteria eat the tissue; hallmark of advanced disease
What are the characteristics of TB bacteria?
-Mycobacterium tuberculosis
-acid fast bacilli (rod shaped)
-has waxy cell wall that prevents
phagocytosis
Initial Pathophysiology of TB
-Droplets inhaled/travel to alveoli–> macrophages ingest bacteria –> granulomas form (macrophages, t cells, b cells, other immune cells) –> macrophages merge into giant multinucleated cells to further create barrier
Latent TB
-contained in granulomas
-asymptomatic/not contagious
becoming immunocompromised can trigger latent TB and it will turn into active infection
Active TB symtpoms
-persistent cough
-hemoptysis
-night sweats
-chest pain
-wt loss
-fatigue
What are the types of asthma?
-Allergic (triggered by allergens)
-Non-allergic
-Exercise induced
-Occupational (triggered by irritating substances in certain occupations)
Role of mast cells in asthma
-degranulate in response to allergen –>
release inflammatory mediators like
histamine, prostaglandins, and
leukotrienes
-drive the early phase of asthma attack
Role of leukotrienes in asthma
cause bronchoconstriction, tissue edema (by increasing blood flow & permeability), increase mucus production, attract leukocytes
Role of eosinophils in asthma
-levels in the blood can help predict severity of asthma
-can damage bronchial walls
-release cytokines that cause inflammation and can lead to remodeling of the airway
Pertinent lab values in asthma
eosinophils >300
Serum IgE >100
Spirometry= FVC1/FVC ratio < 0.70
Acid- Base imbalance in asthma
Initially respiratory alkalosis from breathing off too much CO2; progresses to resp. acidosis as pt becomes more tired and cannot ventilate
signs/symptoms of asthma
Exp. wheezes
chest tightness
SOB
Tachypnea
Anxiety
What is pnuemonia
infection of lung parenchyma
What is the cause of the consolidation appearance on x-ray in PNA
d/t increased capillary permeability, fluid, cells, proteins fill alveoli and cause impaired gas exchange- fluid filled alveoli cause consolidation
How does Alpha 1 Antitrypsin play a role in emphysema
it is an enzyme that prevents elastase from attacking structural fibers in the lung; deficiency causes alveolar destruction
Pathophysiology of Emphysema
Chronic progressive lung disease that damages alveoli; loss of alveolar elasticity leading to air trapping and poor gas exchange
Pulmonary fxn tests in emphysema
FEVC1/FVC ratio <0.70
low O2; high CO2
Risk factors for Emphysema include
smoking, secondhand smoke, air pollution, environmental exposures
Complications of emphysema
-Pulmonary HTN leads to Cor
pulmonale (right HF)
-Pneumothorax-from bullae rupture
-Resp failure-advanced stages
S/s of Emphysema
chronic cough
SOB
pink skin “pink puffer”
barrel chest
cachectic appearance from wt loss
Structural changes in Emphysema
-Bullae formation- lrg air filled spaces
from destroyed alveoli
-Bronchiole collapse-sm airway collapse
d/t loss of structural support
-Diaphragm flattens- r/t chronic hyperinflation
Pathophysiology of Chronic Bronchitis
-persistent inflammation of the bronchi along with excessive mucus production
-thickened bronchial walls and hypertrophy of mucus glands
-goblet cells hyperplasia
S/s of chronic bronchitis
productive cough
SOB
Chest tightness
Frequent resp infections
cyanosis “blue bloaters”
clubbing
Complications of Chronic brochitis
Secondary polycythemia
Pulmonary HTN–> Cor Pulmonale
reactive vasoconstriction from hypoxia
Lab values for Chronic bronchitis
FEV1/FVC ratio <0.70
ABG- hypoxia/increased CO2
CXR-hyperinflation, airway thickening
Which inflammatory cells are involved in chronic bronchitis
Neutrophils- contribute to excess mucus
Macrophages
CD8 t lymphocytes-elevated in smokers
Goblet cells
epithelial cells that fxn to produce mucus
become hyperplastic in chronic bronchitis
