Respiration

Question 1

Define the mechanics of inspiration

Answer 1

1. inspiratory muscles contract (Diaphragm descends; rib cage rises)
2. Thoracic cavity volume increases
3. Lungs are stretched; intrapulmonary volume increased
4. Intrapulmonary pressure drops (to-1mm HG)
5. Air (gases) flows into lungs down its pressure gradient until intrapulmonary pressure is 0 (equal to atmospheric pressure)

Question 2

Explain the mechanics of expiration.

Answer 2

1. Inspiratory muscles relax (diaphragm rises; rib cage descends due to recoil of costal cartilages)
2. Thoracic cavity volume decreases
3. Elastic Lungs recoil passively; intrapulmonary volume decreases.
4. Intrapulmonary pressure rises (to +1 mm hg)
5. Air (gases) flows out of lungs down its pressure gradient until intrapulmonary pressure is 0

Question 3

what are some patterns of breathing

Answer 3

Eupnoea - Normal (diaphragmatic) breathing - 12-20 breaths/minutes
Tachypnoea - 20 breaths/min
Bradypneoa- (age dependent range) - 12+ years <12 breaths/min
Apnoea- Absence of breathing (short periods)
Hyperpnoea - Increased rate and depth of breathing
Cheyne-Stokes Breathing - alternating deep (varying) and absent
Ataxic/Biotic breathing - alternating breathing (same depth) and absent
Kussmaul Breathing - deep, sighing breath
Apneusis breathing - gasping inhalation, inefficient exhalation

Question 4

What are some pulmonary function tests

Answer 4

Spirometry, gas diffusion test, bronchial provocation test, 6 minute walk test, Arterial Blood Gases, Home oxygen therapy assessments.

Question 5

What is Restrictive pulmonary disease?

Answer 5

Is a reduction in lung volume/compliance
-Pulmonary fibrosis
-Asbestosis, Sarcoidosis
-Atelectasis
-Interstitial Lung Disease
-Rheumatoid arthritis
-Chest Wall disorders (eq anatomical, neuromuscular)

Question 6

What is obstructive pulmonary disorders?

Answer 6

Reduction in airflow
-COPD
-Asthma
-Bronchiectasis
-Cystic Fibrosis
Breathing takes more work than normal

Question 7

Briefly explain the pathophysiology of Asthma (Include intrinsic and extrinsic factors)

Answer 7

Bronchial asthma (narrowing or obstruction of airways to alveoli)
Intrinsic Factors: Nonallergic (Non-atopic)- Imbalance between sympathetic and parasympathetic stimulation of airways.
Extrinsic Factors: Allergic (Atopic) Early Phase and Late Phase.
Mucous formation inflammation
Oedema
Alveolar Damage

Question 8

What are the mechanisms of pathology for asthma?

Answer 8

B2 Adrenoreceptor agonists-
Direct action on B2 receptors on bronchial smooth muscle leads to relaxation (Bronchodilation)
Inhibit chemical mediator release from mast cells and monocytes
Increases mucus clearance on bronchi
Antimuscarinic agents (Muscarinic receptor antagonists)- Inhibition of secretions, can be used as an adjunct to B2 adrenoreceptor agonists and steroids
Corticosteroids- Anti-inflammatory.

Question 9

What are the Treatment Strategies. for asthma?

Answer 9

Prevention- Avoiding triggers is an important part of therapy
Monitoring -
Medications used for prevention and treatment vary with the type of asthma and severity of the attack or symptoms
common drugs: Bronchodilators, anti-inflammatory agents

Question 10

Explain the early (acute) phase response of asthma

Answer 10

Develops within 10-20 minutes of non-primary exposure to antigen (allergen)
Antigen binds to IgE molecules on the Mast cells
Mast cells then release chemicals mediators (Cytokines, interleukins) leading to mucus production, and infiltration of submucosal mast cells which leads to an increase in mucus production, and oedema

Question 11

Explain late phase response of asthma

Answer 11

Develops 4-8 hours after asthma trigger, can last up too 24 hours
Typically with release of even more chemical mediators increasing vascular permeability, oedema, inflammation, recruitment of WBCs, increased airway responsiveness bronchospasm

Question 12

Explain the pathophysiology of emphysema

Answer 12

Is a irreversible degenerative condition
Structural Changes - Permanent enlargement of gaseous airways (decrease gas exchange, increase ventilation-perfusion mismatch)
Destruction of structures supporting the alveoli and capillaries feeding the alveoli, loss of elastic recoil of lung tissue.
Airflow impeded and air trapped in the lungs
Diagnosis is by spirometry , gas diffusion tests, Xrays, CT scans, bronchoscopy, blood test, pulse

Question 13

Explain the treatment options for emphysema

Answer 13

Bronchodilators, Corticosteroids, supplemental oxygen

Question 14

What are the two locations for emphysema?

Answer 14

Centriacinar emphysema: Typically in upper lungs, septal destruction of respiratory bronchioles, Alveoli and Alveolar ducts remain intact initially

Panacinar Emphysema: Initial destruction of alveoli, extending to entual destruction of more central involving entire acinus of the lower parts of the lungs.

Question 15

What where the two types of emphysema?

Answer 15

Primary Emphysema - 1-3% of all cases, linked to deficiency in A1-antitrypsin
Secondary Emphysema- Inability to inhibit proteolytic lung enzyme, Linked to inhaled toxins

Question 16

What are some physical characteristics of emphysema?

Answer 16

Damage to the air sacs (alveoli), progressive destruction of alveoli and the surrounding tissue that supports the alveoli
More Advanced disease: Hyperinflation -> large air cysts develop where normal lung tissue used to be, Air is trapped in the lungs due to a lack of supportive tissue which decreases oxygenation

Question 17

How is Oxygen o2 transported around the body?

Answer 17

Main blood components in whole blood Plasma, Leukocytes and platelets, and Erythrocytes.

Question 18

What decreases the O2 transportation efficiency?

Answer 18

Anemia (blood loss, too many erythrocytes destroyed, not enough erythrocytes produced.
Poor gas exchanged (COPD, Asthma, tuberculosis, lung cancer, altitude.
Poisoning (Carbon Monoxide (CO): Hb has 200-300 times greater affinity for CO than O2

Question 19

Explain oxygen as a treatment

Answer 19

Oxygen therapy for COPD: Adjust to match appropriate Po2 in alveoli absorbed and the alveoli collapse (Atelectasis)

Question 20

Briefly Define the pathophysiology of pulmonary embolism

Answer 20

The clot travels in the blood circulation to the lungs from else in the body than can cause an occlusion of 1+ pulmonary arteries by emboli. The embolism can increase pressure within the right ventricle.
Two Types: Thrombotic (VTE) - typically from deep leg or arm veins
Non-thrombotic- Fat, air amniotic fluid, tumour cells, medical devices.

Question 21

Briefly define the pathophysiology of pulmonary arterial hypertension

Answer 21

Normal pulmonary artery pressure (PAP) is high normal 11-17mmg hypertensive 25mmg
Different types of PAH:
Idiopathic
Genetic
Induced
Associated with conditions such as HIV, portal hypertension, congenital heart disease.

Question 22

Briefly define the pathophysiology of pulmonary oedema

Question 23

What are some management strategies for pulmonary embolism

Question 24

what are some management strategies for pulmonary hypertension

Question 25

What are the drugs involved in the pulmonary embolism

Answer 25

Antithrombotic and fibrinolytic agents
eg Heparin, Warfarin

Question 26

What are the different types of pneumonia and examples?