Resp Emergencies

Question 1

Restrictive vs Obstructive

Answer 1

Restrictive
* Harder to get air in due to a
reduced lung expansion, and, in
turn, reduced lung volumes,
particularly with reduced total
lung capacity
* Interstitial lung disease
* Obesity
* Scoliosis
* Reduced Forced Lung Capacity
(FLC)

Obstructive
* Harder to get air out due to
narrowing or destruction of the
airways or inflammation
* COPD
* Asthma
* Cystic Fibrosis
* Bronchiectasis

Question 2

Intrinsic vs extrinsic restrictive

Answer 2

Intrinsic disorders come from a problem within the lungs themselves.
* Interstitial lung disease
* Pulmonary Fibrosis

Extrinsic restrictive lung disorders cause lung problems to occur from
disorders outside of the lungs.
* This means that the restriction and lung problems originate from outside of the lungs.
* Sometimes, restriction is caused by weak muscles, stiffness in the chest wall or damaged
nerves.
* Obesity
* Pleural Effusion
* Myasthenia gravis
* Scoliosis
* Neuromuscular disease

Question 3

What is asthma

Answer 3

chronic inflammatory disorder characterized by increased responsiveness of the small airways to multiple stimuli.

Question 4

three main processes in asthma

Answer 4

bronchoconstriction,
* mucus hyper-secretion
* airway inflammation

Question 5

Pathophys of asthma

Answer 5

• Individual previous exposed and sensitized to specific antigen and hence formed antibodies
• allergen reaches the bronchial epithelium, they activate the dendritic cells on cell membrane to take up the allergen and start phagocytosis
• immune response by activating the T-cells (T2)
• Interleuken 4+5 lead to release of histamine and Leukotrienes Causing:
• Bronchoconstriction due to contraction of
  smooth muscle
  ➢ Mucus hyper-secretion due to excess
  goblet cell activation
  ➢ Airway inflammation
  ➢ Increase in vascular permeability

Question 6

mechanics of airflow obstruction

Answer 6

Bronchoconstriction, mucus production and airway inflammation causes a decrease in airway diameter
no issue inspiring as there is still negative intrathoracic pres.
Inspired air cant escape during expiration due to the inflammation and excessive mucus

Question 7

Consequences of Airflow
Obstruction

Answer 7

Increased airway resistance
* Decreased maximum expiratory flow rates
* Air trapping
* Increased airway pressure
* Barotrauma
* Adverse hemodynamic effects
* Ventilation–perfusion imbalance
* Hypoxemia
* Hypercarbia
* Increased work of breathing
* Pulsus paradoxus
* Respiratory muscle fatigue with ventilatory failure

Question 8

Signs and Symptoms of asthma

Answer 8

Cough
* Dyspnea
* Chest tightness
* Shortness of Breath
* Wheezing – may be absent
* Tachypnea
* Prolonged expiration time
* Tachycardia
* Retractions
* Use of accessory respiratory muscles
* Speaking in short sentences
* Anxious
* Diaphoretic
* Pulsus Paradoxis

Question 9

Treatment of Asthma

Answer 9

Treatment
B2 nebulizer
* Binds to B2 receptors on bronchial wall, causing bronchial smooth muscle relaxation and dilation
Anticholinergic nebulizer
* Blocks parasympathetic nervous system to airways, causing bronchial smooth muscle relaxation
Corticosteroids IV
* Stabilization of mast cell membranes, so decrease inflammation and mucus production by Histamine
* Suppression of antibody production

Question 10

b2 stims

Answer 10

Salbutemal 5mg
Fenoterol 1.25mg

Question 11

Hydrocort

Answer 11

5mg/kg IV
precautions
Diabetes
Petic ulcer

Question 12

Anticholernergic Nebulizer

Answer 12

Ipratropium bromide
0.5 mg

Question 13

Status Asthmaticus treatment

Answer 13

IM adrenaline binds to b2 recepters
0.3mg (1:1000). Can be repeated every 20 mins to a
maximum of 3 doses

Mg sulph 2g over 20 mins via syringe drive
decreases uptake of Ca by bromchial smooth muscles causing dilation

Question 14

Chronic Obstructive Pulmonary Disease

Answer 14

persistent respiratory symptoms and airflow
limitation that is due to airway and/or alveolar abnormalities

emphysema and chronic bronchitis

Question 15

Emphysema

Answer 15

abnormal permanent enlargement of air
spaces distal to the terminal bronchioles

Question 16

Chronic bronchitis

Answer 16

chronic productive cough for 3 months during each of 2 consecutive years

Question 17

Risk factors for COPD

Answer 17

• Smoking
• Dust
• Chemicals
• Air pollution

Question 18

Pathophys of chronic bronchitis

Answer 18

Inflammatory response
* Mucus-secreting cells replace cells that normally secrete surfactant and protease inhibitors
* Proteases break down lung parenchyma
Mucus production
* The number and size of Goblet cells as well as bronchial submucosal glands of the airways also increase and secrete more mucus
Destruction of the cilia
* Ciliary dysfunction and motility leads to a decrease in mucus clearance

Air entrapment
* Small airways collapse on expiration, leading to less air being exhaled and air
entrapment
VQ mismatch
* Due to narrowing of the airways and excessive mucus plugs, there is decreased Oxygen reaching the alveoli and less CO2 being expired

• Leads to Type II respiratory failure & Acidosis
  Infection
• Excessive mucus leads to recurring bacterial infections

Question 19

Patho phys emphysema

Answer 19

Destruction of alveoli
* The Protease also leads to the destruction of the alveolar wall and capillary
beds
* Leading to a decrease in perfusion
Air trapping
* Loss of alveolar wall elasticity leads small airways collapse on expiration,
leading to less air being exhaled and air entrapment
* Increase in end expiratory volume
* Barrel chest

VQ mismatch
* Due to the collapsing of the airways, there is decreased Oxygen reaching the
alveoli and less CO2 being expired
* Decrease in perfusion due to destruction of alveolar capillary bed
* Lead to Type II respiratory failure & Acidosis

Question 20

Treatment of COPD

Answer 20

Same as Asthma then CPAP

Question 21

Presentation of COPD exacerbation

Answer 21

Tachypnea and respiratory distress with simple activities
– Use of accessory respiratory muscles and paradoxical indrawing of
lower intercostal spaces (Hoover sign)
– Diaphragm is flat due to increased lung volume, so can’t contract properly
– Cyanosis
– Elevated jugular venous pressure (JVP) & Peripheral edema

Hyperinflation (barrel chest)
* Wheezing – Frequently heard on forced and unforced expiration
* Diffusely decreased breath sounds
* Hyperresonance on percussion
* Prolonged expiration
* Coarse crackles beginning with inspiration in some cases

Question 22

Risk factors for COPD

Answer 22

Suspect COPD in:
* >35 years
* Chronic smoker
* Exertional breathlessness
* Chronic cough
* Regular sputum production
* Frequent winter bronchitis with wheezing
* Infection history
* Trigger history
* Gastric reflux
* Beta blocker use
* Cold weather
* Opioid and sedative hypnotic use

Question 23

Presentation of bronchiectasis

Answer 23

Chronic Symptoms:

Persistent, productive cough with large volumes of purulent sputum.
Hemoptysis in severe cases.
Recurrent Respiratory Infections:

Frequent exacerbations marked by increased sputum production, dyspnea, and systemic symptoms like fever.
Dyspnea and Wheezing:

Resulting from airway obstruction and reduced gas exchange.
Systemic Features:

Fatigue, weight loss, or digital clubbing in advanced disease.

Question 24

Pathophys of Bronchiectasis

Answer 24

Bronchiectasis is a chronic condition characterized by abnormal and permanent dilation of the bronchi and bronchioles due to the destruction of their walls. The underlying mechanisms include:

Cycle of Infection and Inflammation:

Recurrent or chronic infections damage the airway epithelium, leading to impaired mucociliary clearance.
This promotes microbial colonization and persistent inflammation, causing further structural damage.
Structural Changes:

Loss of elastic tissue and smooth muscle in the bronchial walls leads to weakened and dilated airways.
Inflammatory mediators and enzymes (e.g., proteases) contribute to tissue destruction.
Airway Obstruction:

Mucus stasis and thick secretions obstruct airflow, further exacerbating infection and inflammation.

Question 25

Patho phys of bronchiolitis

Answer 25

Common in children inflamation of bronchioles

Viral Infection: Commonly caused by respiratory syncytial virus (RSV), leading to infection of the lower respiratory tract.

Airway Inflammation: Edema, mucus production, and sloughing of epithelial cells narrow the small airways (bronchioles).

Air Trapping: Partial airway obstruction causes hyperinflation, atelectasis, and impaired gas exchange.

Question 26

Presentation of bronchiolitis

Answer 26

Nasal congestion, rhinorrhea, mild cough, and low-grade fever.
Progression: Tachypnea, wheezing, crackles, and increased work of breathing (e.g., nasal flaring, retractions).
Severe Cases: Cyanosis, hypoxemia, and apnea (especially in young infants).

Question 27

Presentation of Bronchopneumonia

Answer 27

Respiratory Symptoms: Cough with purulent sputum, dyspnea, and pleuritic chest pain.
Systemic Symptoms: Fever, chills, and fatigue.
Physical Signs: Crackles, bronchial breath sounds, and dullness to percussion over affected areas.

Question 28

Pathophysiology of Bronchopneumonia

Answer 28

Inflamation of bronchi
Infection: Typically bacterial (e.g., Streptococcus pneumoniae, Staphylococcus aureus), spreading through the airways.
Patchy Inflammation: Affects multiple lobules, causing alveolar congestion and consolidation.
Impaired Gas Exchange: Inflammation and exudate in alveoli reduce oxygenation.

Question 29

Presentation of Pleural Effusion

Answer 29

Symptoms:
Dyspnea (most common).
Pleuritic chest pain (if inflammation is present).
Cough, typically non-productive.
Physical Signs:
Diminished breath sounds.
Dullness to percussion.
Reduced chest expansion on the affected side.

Question 30

Pathophysiology of Pleural Effusion

Answer 30

Excess Fluid Accumulation: Occurs in the pleural space due to:
Increased hydrostatic pressure (e.g., heart failure).
Decreased oncotic pressure (e.g., hypoalbuminemia).
Increased vascular permeability (e.g., infections, malignancy).
Impaired lymphatic drainage (e.g., cancer, trauma).

Question 31

Presentation of Pulmonary TB

Answer 31

Pulmonary Symptoms: Persistent cough (often productive), hemoptysis, and chest pain.
Systemic Symptoms: Fever, night sweats, weight loss, and fatigue.
Physical Signs: May include crackles or bronchial breath sounds over affected areas.

Question 32

Pathophysiology of Pulmonary Tuberculosis (TB)
Infection

Answer 32

: Caused by Mycobacterium tuberculosis, spread via inhaled respiratory droplets.
Primary Infection:
Bacilli are phagocytosed by alveolar macrophages but may survive and replicate.
Formation of granulomas (tubercles) to contain the infection.
Latent TB: Bacteria remain dormant within granulomas, potentially reactivating later.
Active TB: Granuloma breakdown leads to caseating necrosis, cavitation, and spread within the lungs and systemically.