WEEK 1: Respiratory Symptoms and Signs Flashcards

1
Q

Example 1/4
60/M Entrepreneur, Smoker
Breathlessness, Productive cough x 3/12
Wheezing 1/52
Similar problem every winter for over 10 years
Mild symptoms persist throughout the year

What is the diagnosis?

A

Ex 1 =Chronic Bronchitis/COPD

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2
Q

Example 2/4
20/M Medical Student
Sore Throat, Runny Nose x 2days
Dry and painful cough x 1 day
Fever x 1 day

What is the diagnosis?

A

Ex 2= Upper Respiratory Tract Infection

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3
Q

Example 3/4
50/M Teacher
Dry cough x 2 weeks
Recently started on treatment for High Blood Pressure (Amlodipine & Enalapril)

What is the diagnosis?

A

Ex 3= Angiotensin Converting Enzyme (ACE) inhibitor induced cough

They prevent the inbition of Bradykinin which can stimulate the cough mechanoreceptors in the lungs.

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4
Q

Example 4/4
40/F Nurse
Productive cough x 2 months
Weight loss, Fever x 2 months
Blood in sputum x 2days

What is the diagnosis?

A

Pulmonary TB

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5
Q

The respiratory system has several key functions.

State the principal ones.

Gas exchange is achieved by exposing thin-walled capillaries to the alveolar gas and matching ventilation to blood flow through the pulmonary capillary bed.

The lungs expose a large surface area of body tissue to the external environment in order to achieve gas exchange hence they can be damaged by dusts, gases and infective agents.

Host defense is therefore a key priority for the lung and is achieved by a combination of structural and immunological defenses.

The pulmonary circulation responds readily to increased oxygen demands in exercise and also plays a role in innate immunity: for example, in de-priming neutrophils.

A

The respiratory system has several key functions, the principal ones being to extract oxygen from the external environment and to dispose of carbon dioxide.

Gas exchange is achieved by exposing thin-walled capillaries to the alveolar gas and matching ventilation to blood flow through the pulmonary capillary bed.

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6
Q

Describe the pathway of the upper respiratory tract.

A

The upper respiratory tract (URT) is the portion of the respiratory system that includes the nose, nasal cavity, pharynx, and larynx.

Upper respiratory vs lower respiratory tracts
The conduction of air through the nose-nasopharynx-oropharynx-laryngopharynx allows for filtration, warming, water saturation of air from nose to alveoli

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7
Q

Describe the pathway of the lower respiratory tract.

A

Trachea
Main bronchi (right and left)
Secondary (lobar bronchi)
Tertary (Segmental bronchi)
Bronchioles
Terminal bronchioles
Respiratory bronchioles
Alveolar ducts
Alveoli
Capillaries (surrounding alveoli)

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8
Q

Where does the carina lie?

A

The trachea lies slightly to the right of the midline and divides at the carina into right and left main bronchi.

The carina lies under the junction of the manubrium sterni and the second right costal cartilage.Strenal angle. T4/T5.

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9
Q

Compare right and left lung.

A

The right main bronchus is more vertical than the left and inhaled material is therefore more likely to end up in the right lung.

The right main bronchus divides into the upper lobe bronchus and the intermediate bronchus, which further subdivides into the middle and lower lobe bronchi. On the left, the main bronchus divides into upper and lower lobe bronchi only.

Each lobar bronchus further divides into segmental and subsegmental bronchi.

2 Fissures on the right and 1 on the left; resulting in 3 lobes on the right and 2 on the left.

Fissures and lobes determine whether clinical signs are anterior or posterior e.g …

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10
Q

What is pleura?
Describe the 2 types found at the lungs.

State the key inspiratory muscles.

What feature of the lungs does expiration depends on?

A

Boundaries: Spine, Heart, Mediastinum, Diaphragm

Lung movement facilitated by visceral & parietal pleura.

The pleura is a layer of connective tissue; The visceral pleura covers the surface of the lung, lines the interlobar fissures, and is continuous at the hilum with the parietal pleura, which lines the inside of the hemithorax.

Key inspiratory muscles: Diaphragm, IC muscles

Expiration: passive-elastic recoil

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11
Q

There are about how many divisions between the trachea and the alveoli?

The first 7 divisions are bronchi. Describe bronchi.

The next 16–18 divisions are bronchioles. Describe bronchioles.

What is the function of the ciliated epithelium?

There are approximately how many alveoli in each lung, with a large surface area for gas exchange by diffusion?

What is an Acinus? -

State the 2 types of cells lining the alveoli and their functions.

Phospholipid rich fluid that counteracts alveoli collapse. What is it?

Whatis the function of type I pneumocytes?

A

There are about 25 divisions between the trachea and the alveoli.

The first 7 divisions are bronchi that have walls consisting of cartilage and smooth muscle, an epithelial lining with cilia and goblet cells, submucosal mucus-secreting glands endocrine cells.

The next 16–18 divisions are bronchioles that have: no cartilage but have a muscular layer, a layer of ciliated cells but very few goblet cells, Clara cells that produce a surfactant-like substance.

The ciliated epithelium is a key defense mechanism as it moves Mucus, which contains macrophages, cell debris, inhaled particles and bacteria, towards the larynx: the ‘mucociliary escalator.’

There are approximately 300 million alveoli in each lung, with a large surface area for gas exchange by diffusion.

Acinus-unit of gas exchange; composed of respiratory bronchiole and clusters of alveoli.

Alveoli lined with Type 1 & 2 epithelial cells/pneumocytes.

Type 2-surfactant-phospholipid rich fluid that counteracts alveoli collapse.

Barrier Maintenance: Type I pneumocytes form the structure of the alveoli. Their primary function is to maintain a barrier that prevents the leakage of fluid and proteins across the alveolar wall into the air spaces. Simultaneously, they allow gases (such as oxygen and carbon dioxide) to freely cross the air-blood barrier 12.

Gas Exchange: These flat and thin cells cover approximately 95% of the alveolar surface. Their thinness facilitates rapid diffusion of gases between the alveoli and capillaries. During inspiration and expiration, their flat extensions overlap, aiding in efficient gas exchange 1.

Regeneration: Interestingly, type I pneumocytes cannot replicate when exposed to toxicity. However, they have a backup plan! If damaged, type II pneumocytes differentiate into type I cells to compensate for the injury

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12
Q

Describe the blood supply to the lung and venous drainage.

A

The lungs are supplied with deoxygenated blood by the paired pulmonary arteries. Once the blood has received oxygenation, it leaves the lungs via four pulmonary veins (two for each lung).

The bronchi, lung roots, visceral pleura and supporting lung tissues require an extra nutritive blood supply. This is delivered by the bronchial arteries, which arise from the descending aorta.

The bronchial veins provide venous drainage. The right bronchial vein drains into the azygos vein, whilst the left drains into the accessory hemiazygos vein.

The venous drainage to the left atrium follows the interlobular septa.

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13
Q

State the 2 types of fibers that are found in the alveolar walls and their functions.

A

Healthy alveolar walls contain a fine network of elastin and collagen fibers.

Elastin fibers allow the lung to be easily distended at physiological lung volumes.

Collagen fibers cause increasing stiffness at full inflation, to avoid overinflation.

Elastin fibers in alveolar walls maintain small airway patency.

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14
Q

What is emphysema?

Describe what happens in emphysema.

A

Emphysema is a chronic and progressive respiratory disease that falls under the umbrella term of chronic obstructive pulmonary disease (COPD).

It is characterized by the gradual destruction of the air sacs (alveoli) in the lungs and the accompanying loss of lung elasticity. Emphysema, along with chronic bronchitis, is a major contributing factor to COPD.

In emphysema, there is loss of alveolar walls, which leaves the small airways unsupported, resulting in their collapse on expiration. This causes air trapping and limits expiration.

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15
Q

What is lung compliance?

A

Lung compliance: a measure of the lung’s ability to stretch and expand.

Low compliance = stiff lung; extra work is required to bring in normal air volume; e.g thick balloon; seen in lung fibrosis

High compliance = pliable lung, with low elastic recoil; the elastic tissue is damaged by enzymes, resulting in difficulty exhaling air e.g., grocery bag/emphysema

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16
Q

What is the difference between elasticity and compliance?

A

Elasticity:

Definition: Elasticity refers to the ability of a material to return to its original shape and size after deformation or stretching.

In the Lungs: In the respiratory system, lung elasticity is a crucial property. The lung tissue, particularly the alveoli and surrounding connective tissue, possesses elasticity.

During inhalation, the lungs stretch, and elastic recoil occurs during exhalation.

This elasticity aids in the passive recoil of the lungs and chest wall, allowing them to return to their resting state after each breath.

Clinical Significance: Reduced lung elasticity, as seen in conditions like emphysema, can lead to a loss of the lungs’ natural recoil, making exhalation more difficult and contributing to symptoms like shortness of breath.

Compliance:
Definition: Compliance refers to the ease with which a structure can be stretched or distended. It is the reciprocal of stiffness.

In the Lungs: Lung compliance specifically refers to the ease with which the lungs can expand.

High compliance means the lungs can easily expand, while low compliance indicates that the lungs are stiff and resistant to expansion.

Compliance is influenced by the elastic properties of the lung tissue, the surface tension of the alveoli, and the flexibility of the chest wall.

Clinical Significance: Reduced lung compliance is associated with conditions like fibrosis, where lung tissue becomes stiff and less distensible. This can result in difficulty in fully expanding the lungs during inhalation.

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17
Q

CONTROL OF BREATHING

Where are respiratory motor neurons found?

State the 4 main control stations for respiratory systemm and their inputs.

A

Ventilation is controlled by a combination of neurogenic and chemical factors, however voluntary control through Cortical (volitional) and limbic (emotional) influences can override the automatic control of breathing.

Respiratory motor neurons are found in the medulla oblongata and are the origin of the respiratory cycle, modulated by multiple inputs;

*pH & PaCO2 -Central chemoreceptors
*Hypoxemia -carotid bodies
*Mechanical load -muscle spindles
*Stretch, inhaled toxins, interstitial disease- Vagal sensory fibers.

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18
Q

In healthy individuals, what is the main driver for respiration?

Sensitivity to this may be lost in chronic obstructive pulmonary disease: In these patients, what is the chief stimulus to respiratory drive?

State 2 factors that can depress the respiratory center.

A

In healthy individuals the main driver for respiration is the arterial pH, which is due to a rise in PaCO2, which increases [H+] in cerebrospinal fluid.
Sensitivity to this may be lost in chronic obstructive pulmonary disease: In these patients, hypoxemia is the chief stimulus to respiratory drive; oxygen treatment may therefore reduce respiratory drive and lead to a further rise in PaCO2.

The respiratory center is depressed by severe hypoxemia and sedatives (e.g. opiates).

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19
Q

Outline the COMMON RESPIRATORY SYMPTOMS.

A

Cough
Sputum
Hemoptysis
Dyspnea
Wheeze
Chest Pain
Hoarseness,
Constitutional symptoms

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20
Q

What is a cough?

State the purpose of a cough.

Outline the triggers of a cough.

A

Explosive expiration against a closed glottis

Purpose: clearance of foreign bodies & secretions from the airways.

Triggers
*Exogenous: Smoke, Dust, Foreign Bodies, Fumes

*Endogenous: Secretions, Gastric contents, specific pathologies (next slides)

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21
Q

A cough is a protective superficial reflex. Outline the afferent and efferent innervation.

A

Afferent: Trigeminal, Glossopharyngeal, Superficial Laryngeal (Vagus) Nerves

Efferent-Recurrent Laryngeal (Vagus) and Spinal Nerves

22
Q

OUTLINE QUESTIONS TO ASK A PATIENT WITH COUGH.

A

Age, Occupation
Pre-existing disease e.g., HIV, Heart/Lung Disease, Sinusitis
Duration & timing of the day
Risk Factors e.g. smoking, medications, contact history.
Sputum production & character
Associated symptoms
Fever, dyspnea, wheezing

23
Q

Review tables on slides.

A
24
Q

What is hemoptysis?

What is the source of bleeding?

A

Expectoration of blood from the lower respiratory tract.

ALWAYS ALARMING

Differentiate from Nasopharyngeal bleed, Epistaxis, Hematemesis

Source of Bleeding
*Bronchial arteries: ~90%
*Pulmonary arteries: ~5%
*Systemic arteries: ~5%
*Diffuse Alveolar Hemorrhage: <1%

Quantify
Streaks/Rusty/Mixed
Mild vs Massive (definition evolving)

25
Q

Define the following.
*Nasopharyngeal bleed
*Epistaxis
*Hematemesis

A
  1. Nasopharyngeal Bleed:
    Definition: A nasopharyngeal bleed refers to bleeding that originates from the nasopharynx, which is the upper part of the throat located behind the nasal cavity and above the soft palate.

Common Causes: Nasopharyngeal bleeds can result from various factors, including irritation, trauma, infections, or underlying medical conditions.

  1. Epistaxis:
    Definition: Epistaxis is a medical term for a nosebleed. It involves bleeding from the blood vessels in the nose, typically from the anterior part of the nasal septum. Kiesselbach’s area or triangle.

Common Causes: Common causes of epistaxis include dry or irritated nasal passages, trauma, sinus infections, nasal fractures, or certain medical conditions that affect blood clotting.

  1. Hematemesis:
    Definition: Hematemesis refers to the vomiting of blood. It occurs when blood from the upper gastrointestinal tract, such as the esophagus, stomach, or upper part of the small intestine, is regurgitated and expelled through the mouth.

Common Causes: Hematemesis can be caused by various conditions, including peptic ulcers, esophageal varices, gastritis, Mallory-Weiss tears (tears in the esophagus), or other gastrointestinal bleeding disorders.

26
Q

Outline the causes of hemoptysis.

A

PULMONMARY
*Tracheobronchial
-Foreign body
-Bronchogenic Carcinoma
-Acute/Chronic Bronchitis
-Bronchiectasis

*Parenchyma
-Pneumonia
-Cavity (TB, Abscess, Aspergilloma)

*Vasculature
-Pulmonary Embolism/Infarction
-Vasculitis/Vascular Malformation (AVM, Aneurysm, Fistula)

CARDIAC
-Mitral Stenosis/Pulmonary Hypertension
-Congestive Heart Failure

HEMATOLOGIC
-Thrombophilia/Coagulopathy e.g., Hemophilia, –Anticoagulants

OTHERS
-Trauma (lung contusion)
-Iatrogenic (e.g., Lung biopsy)
-Catamenial

It is often used in medical contexts to describe phenomena or conditions that are associated with or influenced by the menstrual cycle in women.

27
Q

What is dyspnea?

State other synonyms for dyspnea.

A

The awareness that an abnormal amount of effort is required for breathing.

Synonyms: Breathlessness, difficulty breathing, shortness of breath (SOB)

28
Q

Describe the process of inhalation.

A

Inspiration (Inhalation):

  1. Diaphragmatic Contraction:
    The primary muscle involved in inspiration is the diaphragm, a dome-shaped muscle below the lungs.
    Contraction of the diaphragm flattens it, increasing the vertical dimension of the thoracic cavity.
  2. External Intercostal Muscles:
    External intercostal muscles, located between the ribs, also assist in inspiration.

These muscles contract, lifting and expanding the ribcage, which further increases the thoracic volume.

  1. Thoracic Volume Expansion:
    The combined action of the diaphragm and external intercostal muscles expands the thoracic cavity in both vertical and horizontal dimensions.

As the thoracic volume increases, the intrathoracic pressure decreases.

  1. Intrapulmonary Pressure Changes:
    The decrease in intrathoracic pressure causes a pressure gradient between the atmosphere and the alveoli (air sacs in the lungs).

Air moves from the higher-pressure atmosphere into the lower-pressure alveoli, resulting in inhalation.

29
Q

Describe the process of expiration.

A

Expiration (Exhalation):
Passive Process (At Rest):

Expiration is typically a passive process at rest, driven by elastic recoil.

During inspiration, the lung tissues and chest wall structures are stretched, and they naturally recoil during expiration.

Forced Expiration:

During forced expiration, such as during exercise or coughing, additional muscles come into play.

  1. Internal intercostal muscles and abdominal muscles contract to further reduce thoracic volume.
  2. Increased Intrathoracic Pressure:
    The reduction in thoracic volume increases intrathoracic pressure.

Air is forced out of the lungs, moving from an area of higher pressure within the alveoli to the lower-pressure atmosphere.

30
Q

Describe the mechanism of breathing.

A

Mechanism is complex.

Stimulation of intrapulmonary sensory nerves
increasing mechanical load on respiratory muscles
Stimulation of chemoreceptors/carotid body

31
Q

Describe the control of breathing.

A
  1. Stimulation of Intrapulmonary Sensory Nerves:

Location: Intrapulmonary sensory nerves are distributed within the lung tissue, especially in the airways and lung parenchyma.

Function: These nerves detect various stimuli, including irritants, stretch, and changes in lung volume.

Mechanism: When irritants or excessive stretching occurs, intrapulmonary sensory nerves transmit signals to the respiratory centers in the brainstem, initiating reflex responses.

  1. Increasing Mechanical Load on Respiratory Muscles:

Definition: Mechanical load refers to the resistance or effort required to move air in and out of the lungs.

Effect on Respiratory Muscles: An increased mechanical load, such as during exercise or respiratory distress, requires more effort from respiratory muscles.

Feedback to Respiratory Centers: This increased load is sensed by receptors in the muscles and joints, and feedback is sent to the respiratory centers to adjust the rate and depth of breathing.

  1. Stimulation of Chemoreceptors/Carotid Body:

Location: The carotid bodies are specialized chemoreceptors located near the bifurcation of the common carotid arteries in the neck.

Function: Carotid bodies are sensitive to changes in arterial blood oxygen (O2), carbon dioxide (CO2), and pH levels.

Mechanism: When arterial blood O2 levels decrease (hypoxemia) or CO2 levels increase (hypercapnia), or when there is an increase in acidity (acidosis), the carotid bodies are stimulated.

Effect on Breathing: Stimulation of carotid bodies sends signals to the respiratory centers in the brainstem, resulting in an increase in the rate and depth of breathing to restore oxygen and carbon dioxide levels to within normal ranges.

32
Q
A
32
Q

Outline the respiratory causes of dyspnea.

A

AIRWAY DISEASE
*COPD, Asthma
*Bronchiectasis, Cystic Fibrosis
*Laryngeal/Pharyngeal Tumor
*Tracheal Obstruction/Stenosis

PARENCHYMAL DISEASE
*Pneumonia
*Interstitial Lung Disease/Fibrosis
*ARDS
*Lung Cancer

PULMONARY VASCULAR
*Pulmonary Embolism
*Pulmonary Hypertension

PLEURAL
*Effusion, Pneumothorax
*Pleural Tumor

CHEST WALL
*Neuromuscular disease
*Kyphoscoliosis: Kyphoscoliosis is a medical condition characterized by the presence of both kyphosis and scoliosis in the spine.
*Fractured ribs

33
Q

Outline the NON-RESPIRATORY CAUSES OF DYSPNEA.

A

CARDIAC
-Left Ventricular Failure
-Mitral Valve Disease
-Pericardial Effusion
-Cyanotic Heart Disease
-Anemia
-Compensation for Metabolic Acidosis
-Psychogenic
-Hypothalamic/Brain stem lesions

34
Q

DISCUSS QUESTIONS TO ASK A PATIENT WITH DYSPNEA.

A

QUESTIONS TO ASK A PATIENT WITH DYSPNEA

Age, Occupation, Pre-existing diseases, Risk factors e.g Smoking

Duration (sudden onset vs acute vs gradual)

Symptom scale: How much exercise can you do before your SOB stops you

Associated symptoms/Precipitating events

Sleeping supine (flat): Pulmonary Edema/Heart Failure

Numbness and tingling around lips/anxious: Anxiety/panic attack w/ hyperventilation.

Painful when breathing: Pneumothorax, Pleural effusion, Pneumonia, PE

Chest heaviness: Angina

Wheeze: Asthma, COPD
Fever, cough

35
Q

Review notes for acute, subacute and chronic causes of dyspnea table.

A
36
Q

What does wheezing result from?
State causes of wheezing.

A

Wheezing
Wheezing is a common complaint and results from airflow limitation due to any cause.

Causes include asthma, vocal cord dysfunction, bronchiolitis, CCF (congestive cardiac failure) and COPD.

37
Q

Chest pain
The most common type of chest pain reported in respiratory disease is a localized sharp pain, often termed pleuritic; made worse by deep breathing or coughing and the patient can usually localize it.

What are the following chest pains likely to be?

  1. Localized anterior chest pain with tenderness of a costochondral junction.
  2. Shoulder tip pain.
  3. Central chest pain radiating to the neck and arms.
A
  1. Localized anterior chest pain with tenderness of a costochondral junction is caused by costochondritis.

Description: Costochondritis is the inflammation of the costal cartilage, where the upper ribs attach to the sternum (breastbone).

  1. Shoulder tip pain suggests irritation of the diaphragmatic pleura.
  2. Central chest pain radiating to the neck and arms is likely to be cardiac.
38
Q

What is pleural effusion?

What does accumulation of the following in the pleural space called?

  1. frank pus
  2. blood
  3. chyle

What is chyle?

A

Accumulation of fluid within the pleural space

frank pus = empyema
blood = hemothorax
chyle =chylothorax

Chyle is a milky fluid that consists of lymph and emulsified fats, typically formed in the small intestine during the digestion and absorption of dietary fats.

39
Q

State reasons for accumulation of pleural fluid.

A

Pleural fluid accumulates as a result of either:

*Increased hydrostatic pressure (e.g., heart/renal failure) OR decreased oncotic pressure (liver failure, nephrotic syndrome): Transudative

*Increased microvascular pressure due to disease of the pleura or injury in the adjacent lung (‘exudative’ effusion)

The causes of pleural effusions are identified by a thorough history, examination, relevant investigations.

40
Q

What is pneumothorax?

State the risk factors for:

*Primary spontaneous pneumothorax
*Secondary pneumothorax

A

Presence of air in the pleural space.

*Spontaneous
*Trauma to the lung or chest wall OR Iatrogenic injury

Primary spontaneous pneumothorax: no history of lung disease

Risk Factors:
The main risk factors include smoking, tall stature (possibly related to increased lung height and apical stress), and the presence of apical subpleural blebs (small air-filled cysts or sacs).

Secondary pneumothorax affects patients with pre-existing lung disease.

Associated Conditions:

It is often associated with underlying lung diseases such as chronic obstructive pulmonary disease (COPD), lung fibrosis, or infections like Pneumocystis jirovecii pneumonia (PJP).

Connective tissue disorders like Marfan syndrome can also increase the risk.

41
Q

Describe the following:
Tension pneumothorax.
Closed pneumothorax
Open pneumothorax

A
  1. Tension Pneumothorax:

Cause: It occurs when air enters the pleural space, but it cannot exit, leading to increasing pressure within the pleural cavity.

Mechanism: As more air accumulates, it causes progressive collapse of the affected lung and shifts the mediastinum (central structures of the chest) to the opposite side.

Clinical Features:
Severe respiratory distress.
Absent breath sounds on the affected side.
Tracheal deviation away from the affected side.
Hemodynamic compromise (e.g., hypotension).

Emergency: Tension pneumothorax is a medical emergency and requires immediate decompression with a chest tube or needle thoracostomy.

  1. Closed Pneumothorax:

Cause: It occurs when there is no communication between the pleural space and the external environment.

Mechanism: Air enters the pleural space through an internal injury, often due to a spontaneous rupture of a bleb (small air-filled sac on the lung) or as a complication of underlying lung disease.

Clinical Features:
Chest pain.
Decreased breath sounds on the affected side.
Possible respiratory distress depending on the size of the pneumothorax.

Management: Treatment may involve observation, supplemental oxygen, or, in more severe cases, chest tube insertion.

  1. Open Pneumothorax (Sucking Chest Wound):

Cause: It occurs when there is a communication between the pleural space and the external environment, often due to a penetrating chest injury.

Mechanism: Air is drawn into the pleural space during inspiration and expelled during expiration, causing a “sucking” sound.

Clinical Features:
Visible or audible wound on the chest wall.
Paradoxical chest wall movement (chest moves inward during inspiration).

Management: Emergency treatment involves covering the wound with an airtight dressing to prevent air entry and converting the open pneumothorax into a closed one.

42
Q

Define AIRWAY OBSTRUCTION AND AIRFLOW LIMITATION

State the acute and chronic causes of airway obstruction.

A

Inability to move air above the larynx (Upper Airway) or below the larynx (Lower Airway)

Acute: Anatomic blockage e.g., angioedema, aspiration, foreign object

Chronic:
*Anatomic blockage (e.g., tumors, bronchial strictures).
*Neoplastic conditions.
*Inflammation (e.g., chronic bronchitis, bronchiolitis).
*Deposition disorders (e.g., granulomatous diseases).
*Infectious conditions (e.g., chronic pneumonia).

Common causes: Asthma, COPD

43
Q

Describe asthma and COPD pathophysiology.

A

Asthma is a disease of diffuse airway inflammation caused by a variety of triggering stimuli resulting in;
*Partial or completely reversible bronchoconstriction
*Airway edema and inflammation
*Airway hyperreactivity
*Airway remodeling

COPD is airflow limitation caused by an inflammatory response to inhaled toxins, often cigarette smoke.
Rarely caused by Alpha-1 antitrypsin deficiency.

Alpha-1 antitrypsin (AAT) is a protein that is made in the liver and released into the bloodstream. It belongs to the serpin superfamily and is encoded by the SERPINA1 gene1. It is a protease inhibitor that protects the lungs from the damaging effects of proteases.

44
Q

DESCRIBE MECHANISMS OF AIRWAY OBSTRUCTION AND AIRFLOW LIMITATION: ASTHMA

A

Gene predisposing to allergies and lack of TH1 activation result in elevated TH2 expression.

TH2 cells release IL-4 & IL-13 which activate B cells.

Activated B cells will then activate IgE antibody and mast cells.

Mast cells can also be activated by external factors such as allergens, viruses, exercise, cold and irritants.

Mast cells release leukotrienes, cytokines and histamine.

Physiologic effects such as oedema, bronchoconstriction, bronchospasms and airway obstruction take place.

Inflammatory response may persist to chronic inflammation and tissue remodeling.

45
Q
A
45
Q

Describe the process of airway or tissue remodeling in asthma.

A

TH2 cells and other cell types—notably, eosinophils and mast cells form an extensive inflammatory infiltrate in the airway epithelium and smooth muscle, leading to airway remodeling.

*Desquamation,
*Subepithelial fibrosis,
*Angiogenesis,
*Smooth muscle hypertrophy-narrows the airways and increases reactivity to allergens, infections, irritants, parasympathetic stimulation and other triggers of bronchoconstriction.

Mucus plugging and peripheral blood eosinophilia are additional classic findings in asthma and may be epiphenomena of airway inflammation.

However, not all patients with asthma have eosinophilia.

46
Q

Discuss MECHANISMS OF AIRWAY OBSTRUCTION AND AIRFLOW LIMITATION: COPD process.

A

Inhalational exposures can trigger an inflammatory response in airways and alveoli that leads to disease in genetically susceptible people.

The process is mediated by an increase in protease activity and a decrease in antiprotease activity.

Lung proteases, such as neutrophil elastase, matrix metalloproteinases, and cathepsins, break down elastin and connective tissue in the normal process of tissue repair.

Their activity is normally balanced by antiproteases, such as alpha-1 antitrypsin.

In patients with COPD, activated neutrophils and other inflammatory cells release proteases as part of the inflammatory process; protease activity exceeds antiprotease activity, and tissue destruction and mucus hypersecretion result.

Neutrophil and macrophage activation also leads to accumulation of free radicals, superoxide anions, andhydrogen peroxide, which inhibit antiproteases and cause bronchoconstriction, mucosal edema, and mucous hypersecretion.

Neutrophil-induced oxidative damage, release of profibrotic neuropeptides (eg, bombesin), and reduced levels of vascular endothelial growth factor may contribute to apoptotic destruction of lung parenchyma.

47
Q

Define lung fibrosis.

A

Lung fibrosis refers to a condition where there is excessive scarring and fibrous tissue formation in the lung parenchyma (lung tissue).

48
Q

Discuss the PATHOPHYSIOLOGY OF LUNG FIBROSIS.

A
  1. Injury or Insult:
    Lung fibrosis often begins with an initial injury or insult to the lung tissue. This can result from various causes, including environmental exposures (e.g., asbestos, silica, pollutants), infections, autoimmune diseases, radiation, or idiopathic factors.
  2. Inflammatory Response:
    The initial insult triggers an inflammatory response in the lung tissue. Inflammation involves the recruitment of immune cells, release of inflammatory mediators, and activation of signaling pathways.
  3. Fibroblast Activation:
    Chronic inflammation leads to the activation of fibroblasts, which are cells responsible for synthesizing collagen and other components of the extracellular matrix.
  4. Excessive Collagen Deposition:
    Activated fibroblasts produce excessive amounts of collagen and other connective tissue proteins.

This collagen deposition results in the formation of scar tissue within the lung parenchyma.

  1. Altered Tissue Architecture:
    The progressive deposition of collagen disrupts the normal architecture of the lung tissue. This fibrotic tissue is less elastic and flexible than healthy lung tissue, impairing lung function.
  2. Reduced Lung Compliance:
    The increased stiffness of the fibrotic tissue reduces lung compliance, making it more difficult for the lungs to expand and contract during breathing.
  3. Impaired Gas Exchange:
    The altered tissue architecture and reduced compliance impair the efficiency of gas exchange in the lungs. This can lead to hypoxemia (low oxygen levels in the blood) and respiratory symptoms.
49
Q

The onset is characterized by both injury and susceptibility to the formation of progressive fibrosis.

Many different injurious agents have been identified that lead to epithelial and endothelial damage, vascular leak and fibrin clot formation.

b) This is followed by an abnormal repair process characterized by an abnormal re-epithelialization, abundance of myofibroblasts and the formation of a collagen matrix.

c) The process proceeds to excessive matrix formation leading to architectural distortion and finally death.

Name the pathology described above.

A

Lung fibrosis

50
Q

COMPARISONS OF CLINICAL SIGNS IN COMMON RESPIRATORY PATHOLOGIES

Review table on slides.

A