Respiratory- Infection/ventilation Flashcards by Andrew Green

Describe Influenza

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

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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

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How are respiratory bacterial infections involved?

Complications

Secondary bacterial infection (prophylactic abx)
• Body resource focus of viral infection and can allow development of Bronchitis and Pneumonia

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MNFTS of Influenza

Cough
Fever
Lethargy and Myalgia

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Tx if influenza

Immunization (prophylaxis)
Prevent spread
Symptomatic tx
Limit to URT

Antivirals ?? (very rarely amantadine, 2nd gen influenza)

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What is Pneumonia?

(AKA pneumonitis)

Inflm of the alveoli and bronchioles

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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

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What constitutes upper vs lower rest tract

URT- larynx and above

LRT- Trachea and below

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Describe all levels of bronchial tree

Trachea
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)
Alveolar ducts
Alveolar Sac
Alveolus

NOTE- L side only 2 lobes (no middle) w/ cardiac notch
-> Higher bronchi more cartilage, bronchioles lots smooth muscle

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3 layers of pleura

Visceral
Pleural cavity (space with a touch of fluid for lubricant)
Parietal

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Is pneumonia infectious or non infectious?

Can be either (e.g smoke inhalation causing inflm)

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Describe potential etiological agents of pneumonia

Usually bacterial (Typical Pneumonia)

Other atypical:
Viruses
Fungi (inhaled fungal spores)
Non infectious forms (Aspiration of gastric contents especially damaging or Noxious fumes

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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

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What specifically impairs gas exchange in Pneumonia

related to the increased diffusion distance required for gas exchange r/t inflm or exudate at alveoli

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What does it mean when exudate and debris solidify in lungs

consolidation – consolidation is often permanent, similar to scar tissue

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MNFSTS of Pneumonia

Consolidation 
Fever and Chills
Dyspnea
Sputum (excess mucous and exudate)
Headache 
Myalgia
Chest Pain

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Dx and Tx of Pneumonia

DX
Px
CXR
Sputum analysis

TX
ABx if bacterial
Supportive

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

ABG's

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) Activity intolerance Inc sputum Dyspnea Wheezing and crackles Prolonged expiration ```

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

Smoking | 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

Dyspnea + ``` Inc ventilatory effort including : Use of accessory muscles Barrel chest Pursed lip breathing Nasal flaring ``` 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

Hx, Px Labs (ABG’a) CXR 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) Stop smoking Avoid airway irritants (smoke, dust, etc) Flu and pneumococcal vaccines

Tx of COPD's (Pharma)

Drugs (stage based) 1. Short acting Beta agonist and anticholinergics (both bronchodilators) 2. Inhaled steroids 3. Long acting Beta agonist (later stage) Theophylline (bronchodilator w/ some anti inflm properties)