PHTY208 Lecture Notes - Lecture 15: Chest Injury, Kyphosis, Pancreatic Duct

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School
Department
Course
Disorders of ventilation
Learning Outcomes
o For the following respiratory disorders, describe the:
pathology
aetiology
pathogenesis
effects on chest wall compliance, lung compliance, airway resistance and respirato
ry mechanics (pathophysiology)
effects on O2, CO2 and secretion movement (pathophysiology)
clinical manifestations
o Infective disorders
Acute bronchitis
Pneumonia
o Obstructive disorders
Chronic bronchitis
Emphysema
Asthma
o Restrictive disorders
Interstitial lung disease
Chest wall disorders
o Suppurative disorders
Cystic fibrosis
No‐CF bronchiectasis
o Disorders of the pleural space
Pneumothorax
Haemothorax
Pleural effusion
o Disorders of the pulmonary circulation
Right heart failure
Cor pulmonale
Revision of terminology
o Pathology
The interruption, cessation, disorder or disease of a body system or organ
structure
o Aetiology
the cause, set of causes, or manner of causation of a disease or condition
o Pathogenesis
The sequence of cellular and tissue events that take place from the time of
initial contact with an aetiological agent until the ultimate expression of the
disease i.e. how the disease process evolves
o Pathophysiology
The study of the ods response to dysfunction or disease.
o Clinical manifestations
Symptoms
Patient reported subjective outcomes
Signs
Objective outcomes measured by observations, examination, tests, scales
Airways defence mechanisms
o Normal airways defence mechanisms
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Lungs are usually sterile
Upper airway is colonised by benign anaerobic bacteria which limit invasion
by more pathogenic bacteria
o 3 major risks to the respiratory system
Inspired air
Pulmonary circulation
Flooding of the alveoli
o Mechanical and Anatomical defences
Nasal passages
Filter & humidify air
Upper airway reflexes
Epiglottis & bulbar muscles minimise aspiration
Mucociliary escalator
Mucous glycoprotein produced by goblet cells, trap particles
Traps & clears foreign particles
Cough
Clear mucous & particles from lower airways
Lymphatics
Drain fluid from interstitium & assist immune response
o Cellular Lung Defences
Alveolar macrophages reside in alveoli and survey alveolus for foreign material
which they internalise, phagocytose and inactivate
They also release chemical mediators to recruit neutrophils.
Neutrophils increase phagocytic activity due to large numbers that are rapidly recr
uited
Natural killer lymphocytes target virally infected and other o‐
self cells for apoptosis by releasing membrane permeabilising enzymes.
o Molecular Lung Defences
Include cytokines, prostaglandin E2, cell wall hydrolases, iron binding proteins, co
mplement components, defensins, anti-proteinases, surfactant proteins and
antioxidants
Surfactant protects alveoli from collapse according to Laplace's Law P=4T/r
Infective Disorders
o Upper respiratory tract infection (URTI)
Definition
Infection of the respiratory system involving anatomical structures including
the larynx and above e.g. the common cold
Aetiology
Usually viral (±bacterial)
Pathogenesis
Immune and inflammatory response
Clinical manifestations
Increased mucus production
Constitutional symptoms (see acute bronchitis)
o Acute bronchitis
Definition
Reversible bronchial inflammation and mucus production
Aetiology
Infection of the lower respiratory tract in 95% of cases viral in origin
(influenza)
Fifth most common condition diagnosed by Australian GPs
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Pathogenesis
An infectious or non infectious trigger leads to bronchial epithelial injury,
which causes an inflammatory response with airway hyper responsiveness
and mucus production.
Clinical manifestations
Signs and symptoms
Cough illness lasting less than 2 to 3 weeks
±Sputum
Dyspnoea
Frequently accompanied by other upper respiratory tract and
constitutional symptoms
Headache, fever, myalgia, malaise, sore throat, rhinorrhoea
Auscultation
±Wheeze
±Crackles
o Pneumonia
Definition
Inflammation of the lung parenchyma due to the presence of a micro-
organism
May be acute or chronic
Aetiology
Bacteria, fungal or viral
Aspiration of pathogens from oropharyngeal or nasopharyngeal flora (most
common)
Inhalation of other irritating substances e.g. gastric contents
Inhalation of iro‐orgaiss e.g. legionella
Bacteria are spread into the lungs in the blood from bacteraemia e.g.
infected IV site
Direct inoculation or spread e.g. tracheal intubation, stabbing
Infection only occurs when organisms overcome the normally effective
lung defence mechanisms - as a result of either lungs' defences being
defective or overwhelmed by the virulence or quantity of organisms
Risk factors
Age
Immunocompromised individuals
Chronic respiratory disease
Alcoholism
Altered level of consciousness
Smoking
Malnutrition
Immobilisation
Acute pneumonia
Usually bacterial
Induces primarily neutrophilic exudate in alveoli, bronchioles and bronchi
Chronic pneumonia
Usually fungi, parasites and intracellular bacteria
Chronic inflammatory response
Pathology: common microorganisms
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Document Summary

Learning outcomes: for the following respiratory disorders, describe the, pathology aetiology, pathogenesis, effects on chest wall compliance, lung compliance, airway resistance and respirato ry mechanics (pathophysiology, effects on o2, co2 and secretion movement (pathophysiology) clinical manifestations. Infective disorders: acute bronchitis, pneumonia, obstructive disorders, chronic bronchitis, emphysema, asthma, restrictive disorders. Signs: objective outcomes measured by observations, examination, tests, scales, airways defence mechanisms, normal airways defence mechanisms. Lungs are usually sterile: upper airway is colonised by benign anaerobic bacteria which limit invasion by more pathogenic bacteria, 3 major risks to the respiratory system. Flooding of the alveoli: mechanical and anatomical defences, nasal passages. Filter & humidify air: upper airway reflexes, epiglottis & bulbar muscles minimise aspiration, mucociliary escalator, mucous glycoprotein produced by goblet cells, trap particles, traps & clears foreign particles, cough, clear mucous & particles from lower airways. Include cytokines, prostaglandin e2, cell wall hydrolases, iron binding proteins, co mplement components, defensins, anti-proteinases, surfactant proteins and antioxidants.

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