W6 Respiratory Dysfunction

Question 1

Define the following terms: Eupnoea, tachypnoea, bradypnoea, dyspnoea, orthopnoea, hypoventilation, hyperventilation, apnoea, hypocapnia, hypoxaemia, atelectasis, haemoptysis.

Answer 1

Eupnoea: tachypnoea: bradypnoea: dyspnoea: orthopnoea: hypoventilation: hyperventilation: apnoea: hypocapnia: hypoxaemia: atelectasis: haemoptysis:

Question 2

Describe the following respiratory patterns: eupnoea, tachypnoea, bradypnoea, Kussmal repiration, hyperventilation, Cheyne-Stokes, apnoea.

Answer 2

Eupnoea: normal respiratory rate

Tachypnoea: accelerated respiration

Bradypnoea: slow respiration

Kussmaul respiration: deep, rapid respiration in response to low blood pH (acidosis)

• Hyperventilation: e.g. during a panic attack
• Cheyne-Stokes: common in end-of – life and palliative care situations
• Apnoea: central or obstructive reason, common during sleep

Question 3

Explain what is a normal and abnormal ventilation-perfusion ratio.

Answer 3

Question 4

Describe the signs, causes and effects of hypoxaemia and hypercapnia.

Answer 4

Hypoxaemia:

_{PO2 <60 mm Hg Signs of hypoxaemia}

• Cyanosis: a bluish discolouration of the skin or mucous membrane

Causes:

• ↓ oxygen conteent of inspired gas
• hypoventilation
• abnormal ventilation
• perfusion ratio
• diffusion abnormalities

Effects: hypocapnia, respiratory acidosis, tissue dysfunction, organ infarcation.

Hypercapnia

PCO2 > 50 mm Hg in arterial blood.

Signs of hyper capnia

• Disorientation, sleepyness

Causes of hypercapnia:

• Increased concerntration of CO2 in inspired air
• hypo ventilation
• Lung disease

​Effects: respiratory acidosis, ↑ respiration, ↓ nerve firing, carbon dioxide narcosis and coma

Question 5

Describe how the following factors affect ventilation: airway’s diameter and mucocilliary escalator mechanism.

Answer 5

Airway diameter: smooth muscle of bronchial pasages constricts (bronchoconstriction) or relaxs (bronchodilation) changing the size of the lumen.

Bronchoconstriction prevents inhalation of toxic praticle. Bronchodilation ↑ air intake and diffusion

Mucocillary escalator: mechanisim of cleaning up airways from inhaled particles

1. Cilia move the layer upwards to pharynx
2. Flow of mucus that traps inhaled particles - Released by goblet cells Excessive mucous will obstruct the airways limiting gas exchange

Question 6

Explain how normal lung function is determined based on the following measures: tidal volume, residual volume, forced vital capacity (FVC), FEV1, FEV1/FVC ratio

Answer 6

Determined by: Age Sex Height Weight Race

FEV1 naturally declines by 30-35 ml per year (forced expiratory volume).

Forced expiratory volume: the total amount of air that can be forcibly exhaled - marker of lung volume.

FEV1/FVC ratio: the eratio of air exhaled in the first second to the total volume exhaled. (EV1/FVC x 100)

Respiratory rate: number of breathes per minue Tidal volume: the volume of air in a normal inspiration/expiration

Question 7

Define respiratory failure.

Answer 7

Is a condition in which not enough oxygen passes from your lungs can’t propeerly remove carbon dioxide from the blood (or often both).

1. Hypoxemic Respiratory failure: lowering oxygenation of blood (↓ PO2)
2. Hypercapnic/hypoxeemic Rspiratory Failure: ↑ the lvel of carbon diozide (↑ PCO2) and ↓ the oxygenation of blood (↓ PO2) simutaneously

Question 8

Describe how spirometry results change in obstructive and restrictive respiratory disorders

Answer 8

Refer to picture

Question 9

Define asthma and describe the clinical manifestations of an asthma event.

Answer 9

Affects individuals who develop hypersensitivity to a particular substance (allergen) or trigger (cold air, exercise) , responding in an exaggerated way.

Hypersensitivity is triggered by dentritic cells, mast cells, T cells and eosinophils → genetically determind. Manifestations include: coughing, wheezing, chest tightening, tachcardia, fatigue, anxiety

Question 10

Distinguish between intrinsic and extrinsic asthma.

Answer 10

1. Intrinsic (non-allergic) asthma: this formis triggered by irritation to th airways rather than an allergic reaction.

Triggers: smoking, stress, emotion, pollution

2. Exrinsic (allergic) asthma: re-exposure to an allergen the respiratory mounts a Type 1 Hypersensitivy response.

Dominate in mast cells whihc release (histamine, prostaglandins and leukotrines that trigger bronchoconstriction)

Question 11

Describe the pathophysiology of asthma.

Answer 11

T6 10! Histamine. leukotrienes and prostoglandins:

1. Activat smooth muscle in airways to contract (bronchoconstriction).
2. ↑ Vascular permeability (odema)
3. Stimulate goblet cells to screte more mucus

Question 12

Explain how acute asthma progresses to chronic asthma and its long-term effects.

Answer 12

With poor management, the lung begins to remodel itself:

1. Hyperplasia of goblet cells (mucus glands)
2. thickening and fibrosing of the sub-basement membrane.

Chronic changes are permanent and non-responsive to medication

Question 13

Outline and explain the mechanism of action of the drug groups used to manage asthma.

Answer 13

1. Relievers → bronchodilation (SABAS - short acting beta agonists, ventolin)

• Immdiate 5-15min relief through rapid bronchodilation via smooth muscle relaxation.
• best for treat asthma symptoms
• prevent exercise-induceed asthma.

Adverse drug reaction can selt in stimulation of beta 1 adrenergic receprots of the myo cardium → causing tachcardia

• Antimuscarinics and xanthines. LABAs - long acting beta agonists: long acting bronchodilation → not for rapid relief as onset of action is too slow
  2. Preventers → prevent inflammatory repsonse; controls asthma,=. Inhaled corticosterioids and NSAIDS.
  3. Combination THerapy: preventers combined inhalers with LABAs

Question 14

Briefly explain how asthma is managed.

Answer 14

Common symptoms: wheeze, shortness of breath coughing. Signs of worsening asthma nocturnal asthma, ↑ reliever medication use, ↓ physical activity, Signs of an acute exacerbathe inability to speak in full sentences , overuse of accessory breathing muscles.

Question 15

Define COPD and its aetiology.

Answer 15

Chronic Obstructive Pulmonary Disorder.

1. Emphysema: enlargement of air spacs and destruction of lung tissue.
2. Chronic obstructive bronchitis: obstruction of small airways. Smoking is a leading cause - abnormal inflammatory response to noxious sparticles.

Cytokines release cause other problems. FEV1/FVC is less than 70% FEV1 is less than 80% os predicted value → cardiac disease, diabetes, osteoprosis

Question 16

Describe the pathophysiology of COPD.

Answer 16

1. Toxic substance induces macrophages to secrete inflammation mediators.

2 Neutriophiles, monocytes and T cells activation.

3. They release other mediators

• Fibrosis of bronchial wall.
• Hypertrophies mucus glands → excess musus = obstructed airflow,
• Loss of alveolar tissue = surface area for glas exchange
• Loss of elastic lung fibres = air trapping, airway collapse

Question 17

Define chronic bronchitis and describe its clinical manifestations.

Answer 17

Bronchitis is an inflammatory condition affecting the bronchial tissue resulting in excessive mucus production. Sputum produced on most days for at lead 3 motnhs for at least 2 years

Question 18

Define emphysema and describe its clinical manifestations.

Answer 18

A condition of loss of lung lasticity and abnormal nlargement of the air space distal to the terminal bronchiols. - ↑ neutrophil invasion of the lung tissue due to inhald irritants can damage aleveoli. → Neutrophils secrete trypsin = damaging the cell

Question 19

Define emphysema and describe its clinical manifestations.

Answer 19

A condition of loss of lung lasticity and abnormal enlargement of the air space distal to the terminal bronchiols.

• ↑ neutrophil invasion of the lung tissue due to inhald irritants can damage aleveoli. → Neutrophils secrete trypsin = damaging the cell. A condition that causes shortness of breath and coughing.

Long-term alterations

• Loss of capillary bed for gas exchange.
• ↑ volume of alveoli
• Loss of cilia
• Loss of normal elastic recoil of the bronchi which makes expiration more difficult
• Accessory muscle use and laourned breathing
• ↑ risk of chronic bronchitis

Question 20

Compare and contrast the pathogenesis of chronic bronchitis and emphysema

Answer 20

Chronic bronchitis = inflammation and excessive mucus secretions resulting in air sacs becoming inflated.

Emphysema: destruction of alveoli septa and pernamemnt enlargement of alveoli with lungs becoming hyper inflated

Question 21

Outline and explain the mechanism of action of the drug groups used to manage COPD

Answer 21

1. Bronchodilators: SABAs (short acting beta2 agonists) improve lung function and daily breathlessness scores.
   * LABAs used to reduc symptoms and improve exercise toleranc.
2. Inhaled Corticosteriods: slow declince of function and reduce mortality↑ risk of pneumia .
3. Reliving signs and symptoms: - mucolytic agents a class of drugs which clear mucus from airways
4. Treating exacerbation, tx infection = antibiotics

Question 22

Describe the pathogenesis of primary and secondary pulmonary hypertension

Answer 22

Primary pulmonary hypertension: blood vssel walls thickn and constrict (arterial hypertrophy) with no know underlying disase.

• Genetic
• autosomal dominant
• Drug, toxins

Secondary pulmonary hypertentsion:

1. ↑ left atrial pressure → back pressure into the pulmonary vascular system
2. Pulmonary disease that ↑ oedema, reduce ventilation or decrease PaO2: sleep apnea
3. Inflammatory disease that affect vascular calibre: Lupus

Question 23

Describe the pathogenesis and clinical manifestations of pulmonary embolisms.

Answer 23

Blood circulation is obstructed by embolus: a dislodged thrombus, an air bubble or an aggregate of fat. Causes by an occlusion of a portion of the pulmonary vascular bed arising from a deep vein thrombosis in the lower limbs.

Manifestations include

• Chest pain
• Dyspnoea
• ↑ respiratory rate,

Anticoagulant therapy: Heparin inactivating coagulation factors Warfarin: depresses the synthesis of coagulation factors