Resp Flashcards
Pneumonia
aka Pneumonitis
Inflammation of alveoli and bronchioles
Pneumonia: Et?
Bacterial
Viruses and fungi
Aspiration
Noxious fumes
Pneumonia: Patho
1) Respiratory defenses are compromised
2) Agent enters
3) Inflammatory response > Edema > Impairment of gas exchange d/t production of inflamm. exudate = sputum
Pneumonia: types?
Typical - Bacterial (worse d/t presence in alveoli and mucus production inside the air sac)
Atypical - Viral
Consolidation
Solification of inflammatory debris, cells, fluid and any other debris (not tissue).
> Impacts fx of lungs and gas exchange
Pneumonia: mnfts?
Fever Malaise Dyspnea Chest pain Productive cough (with sputum)
Pneumonia: Dx
Hx
Px
Chest X-Ray
Sputum analysis to id the microbe
Pneumonia: Tx
Antibiotic (if bacterial)
Supportive management
COPD
> Obstruction of alveoli, not patent d/t inflammation and increased mucus production
acute during progression of the disease
recurrent and chronic obstruction of airway
may coexist with asthma
COPD: Et and risks
Smoking
recurrent respiratory infections
ageing
genetic deficiency of alpha1 antitrypsin
Compliance
Refers the ease of which we can breathe and fill the lungs with air.
If elastic tissue is damaged, there is a loss of compliance.
Chronic Bronchitis
airway inflammation and obstruction
d/t smoking and recurrent infection
> Increased mucus production
large airway 1st - bronchi small airway (later) - goblet cells increase mucus production
Chronic Bronchitis: Patho
1) increased mucus production
2) Impaired defences and mucociliary blanket
3) Infection
4) Inflammation of airways
5) Alveolar obstruction
6) Alveolar airway collapse »_space;>Air gets trapped in alveolus
Decreased alveolar ventilation > perfusion imbalance > hypoxemia (O2 drops in arterial blood)
Chronic Bronchitis: Mnfts
Hx of productive cough (>3 months over 2 consecutive years)
Dyspnea
Impaired respiratory Fx > hypoxemia and hypercapnia
Activity intolerance
Increased sputum
Wheezing and crackles (wet)
Asthma
Chronic inflammatory condition of airways with acute episodic obstruction of aw and bronchospams
Asthma: triggers?
Allergens
Airway irritants- noxious stimuli (perfume, cold air, smoke, perfume)
Infection
Exercise
Asthma: Et?
Complex trait
- Genetic
- Environmental factors
Asthma: Atopic
Extrinsic pathway
Initiated by a type I hypersensitivity due to allergen exposure
Person usually has other allergic conditions
Mechanism of response:
Early or acute phase- s/s within 10-20 min
Late phase response - 4-8 hours after exposure
Emphysema: definition
Loss of elasticity of lung tissue
Abnormal enlargement of airspaces distal to the terminal bronchioles
Alveolar walls and capillary beds get destroyed resulting in loss of compliance
Emphysema: Et
smoking
genetic deficiency of alpha 1 antitrypsin (controls proteases in alveoli)
Emphysema: Patho
- smoking inhibits antitrypsin and attracts inflammatory cells (cause damage)
Increase of proteases damages alveolar walls
Resulting in permanent distended airspaces that trap the air impairing gas exchange > alveoli merge and surface area decreases
Bullae
Blebs
Emphysema: Mnfts
Dyspnea
Increased ventilatory effort
Asthma: definition
Chronic inflammatory condition of airways with episodic obstruct and bronchospasm
Various triggers provoke inflammation and airway obstruction (allergens, airway irritants= noxious stimuli, infection, exercise)
Asthma: Et
Complex trait
- genetic (familial)
- environmental factors
Goals:
> Reduce inflammation
> Avoid triggers
Asthma: Patho
Activated T-lymphocytes direct further release of inflammatory mediators from eosinophils, mast cells and helper T lymphocytes produce interleukins
Mediators increase vascular permeability and edema
Increase airway responsiveness > bronchospasm
Asthma: Types
- Extrinsic (atopic) — External factors: allergens
- Intrinsic (topic) – Resp Tract Infections, exercise, hyperventilation, cold air, exercise,..
Asthma: Mnfts
Dyspnea wheezing coughing in attempt to open airway bronchospasm increase in the respiratory effort - use of accessory muscles Hypoxemia? Immobilization?
Asthma: Dx
Hx Px Pulm Fx Tests - spirometry Labs Inhalation Challenge tests to decrease hypersensitivity
Asthma: Tx
Goal: Control with minimal meds
Preventative:
avoid allergens, irritants, avoid smoking and exposure
Drugs:
Step 1: short acting inhaled bronchodilators
Step 2: inhaled steroid
Step 3: long acting bronchodilator with steroid
Step 4: short course steroid (PO) and 3rd drug - leukotriene or Theophyline
Atelectasis: def
Partial collapse of lung
Incomplete expansion of lung or portion of a lung
Atelectasis: Et
Airway obstruction Lung compression (pneumothorax or pleural effusion) Contraction - increased recoil of the lung d/t loss of surfactant or secretions
Atelectasis: Mnfts
Dyspnea
Tachypnea and tachycardia (compensatory)
Decrease chest expansion (or not equal)
tracheal midline shift on inhalation
Atelectasis: Dx
Hx Px Chest X ray CT (if small) Bronchoscopy
Atelectasis: Tx
Treat underlying cause
Respiratory support
Pleural Effusion
Fluid accumulation in pleural cavity/space d/t abnormal fluid seepage and/or drainage
Rate of fluid formation exceeds the removal rate
Pleural Effusion: Types
1) Exudate (more proteins)
2) Transudate
3) Empyema
4) Chylothorax
5) Hemothorax
Pleural Effusion: Et
usually CHF
when not cardiogenic: infection, CA, pulmonary infarction
Pleural Effusion: Patho
- Normal fluid entry via parietal capillaries
- Drainage into parietal lymphatics
- if entry exceeds drainage > pleural effusion
Pleural Effusion: Dx
Hx
Px
US
CT
Pleural Effusion: Tx
Treat underlying cause
Thoracocentesis (+fluid analysis to identify type and cause)
Chest tube to drain?
Pulmonary Edema
Accumulation of fluid IN the alveoli
Pulmonary Edema: Et
mostly Left Heart Failure
When non-cardiogenic > IV fluid overload, smoke inhalation, aspiration, IV drug use (increases vessel permeability)
Pulmonary Edema: Patho
- Vascular fluid into interstitial space to alveoli
- Leads to impaired gas exchange d/t greater alveolar-vessel membrane distance
- Less compliance d/t space available
Pulmonary Edema: Mnfts
Dyspnea r/t hypoxia
Coughing to expectorate extra fluid (frothy, productive cough)
Blood tinged sputum d/t capillaries damage
Less compliance
Crackles in LS
Pulmonary Edema: Tx
Address underlying cause
If Cardiogenic- inotrope
Respiratory support: O2, mechanical ventilation?
Paranasal sinuses (air sacs)
Frontal
Ethmoid
Maxillary
Rhinosinusitis
Inflammation of paranasal sinuses
Aka sinusitis
Rhinosinusitis: Patho
Low oxygen content in the sinuses facilitate the growth of microorganisms
Impairs local defenses
Alters the functions of the Immune Response cells
Rhinosinusitis: Et
Obstruction of the narrow ostia that drain the sinuses URT viruses - infections Allergic Rhinitis Nasal Polyps Changes in barometric pressure
Rhinosinusitis: Mnfts
Difficult to differentiate from those of the common cold & allergic rhinitis - facial pain - headache - pain on bending - unilateral maxillary pain - pain in teeth - purulent nasal drainage
Symptoms usually resolve within 5 to 7 days without medical is immuno compromised pts, often there are no signs of inflammation such as purulent drainage are absent.
Rhinosinusitis: Dx
Hx Px Differentiate headache type Transillumination CT scan MRI if neoplasms are suspected
Rhinosinusitis: Tx
Usually mnfts improve after 7 days
If not > 2/3 improve with antibiotic
Tuberculosis
Infectious disease caused by Mycobacterium tuberculosis
- M tuberculosis hominis: airborne spread by inhalation of droplet nuclei
- M tuberculosis avian
Primary TB
- Develops in unexposed previously & unsensitized individuals
- Initiated by inhalation of droplet nuclei that contains the tuberculosis bacillus
Secondary TB
Reinfection from inhaled droplet nuclei or reactivation of a previous “healed” primary infection
Occurs when IR is impaired
TB: Patho
- Inhaled droplet nuclei enters and deposits in the alveoli
- Alveolar macrophages phagocytize but are unable to kill the mycobacteria d/t lipid coated cell wall
- Tubercle bacilli proliferate & multiply
- Infected macrophages expose the antigen and a delayed cell-mediated response is activated - T-cells
- Sensitized T-cells stimulate the production of lytic enzymes in the macrophages (proteases)
- When released proteases damage lung tissue
- Ghon focus - granulomatous lesions that result from cell-mediated IR (usually in upper segments of lower lobes - O2 concentration is higher)
- Ghon complex when lymphatics spread infection > dormant?
TB: Dx
Screening:
- TB Skin test
- CXR
Definitive Dx:
- Culture
- Genotyping
TB: Tx
Multidrug regimen d/t high rate of mutation
INH, Rifampin, Pyrazinamide
> 6 months tx
