Flashcards in Respiratory- Infection/ventilation Deck (42):
Types, at risk groups, timeline
Acute viral infections of the upper respiratory tract (URT). Generally Seasonal
Types A, B, C (A is most prevalent)
1-4 day incubation period
Elderly, young, health workers, chronically ill are at risk
Where is does tissue damage generally occur with influenza?
Viral injury to epith cells in URT
Inflm response also causes tissue damage
If extension to LRT -> bronchial and alveolar damage
How are respiratory bacterial infections involved?
Secondary bacterial infection (prophylactic abx)
• Body resource focus of viral infection and can allow development of Bronchitis and Pneumonia
MNFTS of Influenza
Lethargy and Myalgia
Tx if influenza
Limit to URT
Antivirals ?? (very rarely amantadine, 2nd gen influenza)
What is Pneumonia?
Inflm of the alveoli and bronchioles
How is pneumonia generally classified
Classification is normally based on agent of injury or Area affected by agent
Based on agent
-> Typical (common bacterial agents) vs atypical (diversity, but mainly viral) Fig 28-3.
Based on location
One lobe (or part) is affected = lobar pneumonia
Diffuse across lung= Bronchopneumonia
NOTE- atypical can also refer to uncommon MNFTS from uncommon pneumonia source. Often patchy alveolar inflm without consolidation. Less exudate, more mild, often leading to secondary infections
What constitutes upper vs lower rest tract
URT- larynx and above
LRT- Trachea and below
Describe all levels of bronchial tree
1* L and R Main Bronchi (separated at Carina)
2* Lobar Bronchi
3* Segmental Bronchi
Conducting Brionchioles (terminal Br. at end)
Respiratory Bronchioles (start of Resp. Zone)
NOTE- L side only 2 lobes (no middle) w/ cardiac notch
-> Higher bronchi more cartilage, bronchioles lots smooth muscle
3 layers of pleura
Pleural cavity (space with a touch of fluid for lubricant)
Is pneumonia infectious or non infectious?
Can be either (e.g smoke inhalation causing inflm)
Describe potential etiological agents of pneumonia
Usually bacterial (Typical Pneumonia)
Fungi (inhaled fungal spores)
Non infectious forms (Aspiration of gastric contents especially damaging or Noxious fumes
Basic Patho of pneumonia
Impaired pulmonary defenses -> Agent enters resp tract and proceeds to lungs (enviro wam, moist and spread is fairly easy) -> Inflm -> pulmonary edema -> impairs gas exchange
What specifically impairs gas exchange in Pneumonia
related to the increased diffusion distance required for gas exchange r/t inflm or exudate at alveoli
What does it mean when exudate and debris solidify in lungs
consolidation – consolidation is often permanent, similar to scar tissue
MNFSTS of Pneumonia
Fever and Chills
Sputum (excess mucous and exudate)
Dx and Tx of Pneumonia
ABx if bacterial
What is COPD and what disorders does it include
COPD is Persistent inflm of airway, parenchyma, vasculature. Often Acute, recurrent and chronic obstruction of airway
Comprises several disorders: chronic bronchitis and emphysema
NOTE: While Asthma can occur concurrently, it is not considered COPD
How closely is smoking related to COPD?
What causes damage?
• Smoking (causes 80-90% of COPD)
Smoke has a variety of irritants in it
Pronounced increase in mucous secretion which leads to Cilia damage and destruction
Causes inflm and damage of Alveoli and vessels and Induces coughing
Other etiological factors for COPD
Recurrent respiratory infections
Ageing (lost stretch in fibers of airways)
Genetic defect of alpha-one antitrypsin
Specifically what are three primary causes for the obstruction of lumen
Hypertrophy or luman wall, mucous obrstruction, compromised elastic fibres
What is Chronic bronchitis
Inflm and obstr of airway
often d/t smoking or chronic recurrent infections
Where does pathological change first occur in chronic Bronchitis?
What are the changes?
1rst change is in the larger primary Airways (larger airways have defenses protecting the lowers airways)
Hypertrophy of the submucosal glands (inc demand r/t mucous production)
Hypersecretion of mucous
What is the second area to change in chronic Bronchitis?
What sort of changes
Smaller airway changes (later)
Inc in number of goblet cells
Inc mucous secretion
Patho of Chronic Bronchitis
Excess mucous -> mucociliary defenses impaired -> infection -> bronchial wall inflm -> lumen obstr -> airway collapse (at level of alveolus) -> air trapped in parts of lung -> dec alveolar ventilation -> ventilation perfusion ratio imbalance -> hypoxemia
How does one accurately measure hypoxemia
Simple Dx of Chronic Bronchitis
Chronic productive cough (> 3 months/yr in 2 consecutive years)
MNFTS of Chronic Bronchtis
Impaired respiratory Fx (Hypoxemia and hypercapnia)
Wheezing and crackles
Why would someone with chronic Bronchitis have prolonged expiration?
You know... I can't really recall
What is emphysema?
Two central Issues that arise from it?
Destruction of alveolar tissue and cap beds causing:
• Loss of compliance
• Enlarged distal airspaces (Reduces exchange surface area)
What do we mean by loss of pulmonary compliance?
Compliance is the ease with which you fill and empty the lungs. (i.e change in volume given a given amount of pressure)
Describe Etiology of Emphysema
Genetic Deficiency of Alpha-one antitrypsin
What is trypsin and what is it's relation to anti trypsin
Trypsin is GI protease enzyme (breaks down proteins. Immune cells also release it in the lungs occasionally to help break down bacteria and other material for recycling.
Antitrypsin is an inhibitor of trypsin. Deficiency in antitrypsin allows protease to “run free” and break down lung str components
How does smoking bring about emphysema?
Smoking inhibits antitrypsin (end up with same issue as genetic deficiency) and also attracts inflm cells to area (inc trypsin)
`Patho of Emphysema
Inc in protease -> destr alveolar walls -> alveoli merge -> dec in surface area
Permanent distended air space -> ventilation impaired
Air traps in between alveoli -> dead space (like trachea)-> Inc work of breathing
Capillary wall destroyed -> impaired perfusion (reduced ventilation/perfusion ratio)
What is the difference between centriacinar and panacinar emphysema?
Centriacinar (more common generally and in smokers) is confined to terminal and respiratory bronchioles
Panacinar- peripheral alveoli are also involved (more likely with antitrypsin def)
MNFTS of emphysema
Inc ventilatory effort including :
Use of accessory muscles
Pursed lip breathing
Note: blue breathers (chr. bronc. and heart failure) and pink puffers (pre dominant emphysema barrel and accessory)
What is barrel chest?
Anterior-Posterior diameter of lungs is normally half the transverse diameter, this can be dec to 1:1 in emphysema. A similar ratio to infants r/t a dependency on diaphragm breathing
What are the normal vs accessory breathing muscles?
Normal- diaphragm and intercostals (quiet breathing)
Accessory- The sternocleidomastoid and the scalene muscles (anterior, middle and posterior scalene) which lift rib cage.
Dx of COPD's
Pulm fx tests (smaller lung capacity and tidal volume)
Tx of COPD's (non pharma)
COPD is progressive (i.e symptom tend to worsen over time and MNGMT is necessary to limit worsening)
Avoid airway irritants (smoke, dust, etc)
Flu and pneumococcal vaccines