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Pulmonary Flashcards

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1
Q

Describe the pathophysiology of asthma.

A

Extrinsic
- pathogenesis of underlying inflammation is clear
- type I hypersensitivity develops
- allergen trigger mucosal mast cells to release mediators
- open epithelial junction
- antigen penetrates submucosal layer
- increased release of inflammatory mediators
- inflammatory cells attracted to area
- inflammatory mediators cause bronchial muscle
contraction, mucosal swelling, mucous production and
nerve stimulation resulting in bronchoconstriction

Intrinsic
- unclear but theorised associated with respiratory viral
respiratory infection or inhaled pollutants
-

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2
Q

Describe the clinical manifestations of asthma.

A

Episodic dyspnea
Cough
Wheezing (difficulty with expiration, whistling noise)

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3
Q

Explain how ventilatory function is measured by spirometry to evaluate airway obstruction in asthma.

A

.

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4
Q

Identify the factors that predispose people to respiratory infection.

A
  • Contact,
  • droplet,
  • inhaling the germs.
  • Family members are sick.
  • Cystic fibrosis increases chances.
  • Nasogastric tube.
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5
Q

Name the causative organisms of most upper respiratory tract infections.

A

rhino-, corona- and adenoviruses

Streptococcus pyogenes

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6
Q

Give 2 reasons why treatment of the common cold is solely to reduce symptoms.

A

It is viral so anti-biotics don’t work.

To give comfort whilst getting better.

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7
Q

Describe the cause of pharyngitis and a potentially serious complication.

A

Rhino, corona and adenoviruses.

  • It can cause scarlet fever,
  • Acute rheumatic fever,
  • Acute glomerulonephritis.
  • bronchitis
  • pneumonia
  • secondary bacterial infections
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8
Q

Explain why vaccinations for influenza are not protective for long and describe the basics of treatment for influenza.

A

There are multiple strains of influenza and the virus (Myxovirus) undergoes antigenic shift (mutation)

  • The basic treatment for influenza to take anti-viral drugs.
  • Get the vaccine regularly
  • Paracetamol
  • Drink water
  • Rest
  • Supportive
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9
Q

Describe the pathogenesis of lobar and bronchopneumonia.

A

Microorganisms reach lung via inhalation, aspiration of oropharyngeal secretions or spread from blood stream

Lobar pneumonia
- infection and consolidation confined to 1 or 2 lobes

Bronchopneumonia
- consolidation and infection occurs throughout lungs

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10
Q

Explain why aspiration of gastric fluid causes serious damage to the lungs.

A

Aspiration of gastric fluids can carry bacteria into the lungs. Pneumonia often develops.

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11
Q

Define pneumothorax

A

Partial or entire collapse of affected lung due to air in the pleural space.

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12
Q

Explain why tension pneumothorax is life-threatening

A

The air cannot get out of the lung and therefore puts pressure on the heart.

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13
Q

Describe how pleural effusions develop and why they are often associated with dyspnoea.

A

They are caused by pneumonia.

Fluid accumulation in the pleural space prevents full lung inflation → hypoxemia and dyspnea. Pain with breathing may occur with inflammatory causes.

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14
Q

Define asthma

A

A chronic disorder of reversible airway obstruction

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15
Q

Diagnoses of asthma

A

Patient history

Airway responsiveness assessed via inhalation challenge test with histamine, cholinergic agonists or cold air

Lung function tests are used to measure peak expiratory flow and the FEV1/FVC ratio

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16
Q

Define pneumonia

A

Infection and inflammation within the lungs

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17
Q

Name the most common causative organism of pneumonia

A

Bacteria, virus, fungi

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18
Q

Indicate the significance of pneumonia as a hospital-acquired condition.

A

15- 30% of cases are hospital acquired.

Leading cause of death in infants and elderly
Major cause of death throughout world
Major cause of intensive care mortality

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19
Q

Risk factors of pneumonia

A 
lung disease (e.g. COPD),
smoking, 
immobilisation, 
altered consciousness,
immune suppression, 
alcoholism
elderly
children
underdeveloped nations,
malnourished, 
crowded and unhygienic environments
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20
Q

Clinical manifestations of pneumonia

A 
Fever
cough (progresses to productive cough)
chest pain
breathlessness,
rapid/shallow breathing 
rales
21
Q

2 causes of pneumothorax

A

Spontaneous
- Rupture of bleb or blister on lung surface secondary to asthma or infection/malignancy. Usually occurs in young people.

Traumatic
- Penetrating chest trauma and non-penetrating trauma (fractured rib) damage the pleural space and lung tissue (may also cause haemothorax).

22
Q

Define pleural effusions

A

Abnormal collection of fluid in the pleural cavity.

23
Q

Difference in severity between upper and lower respiratory infections.

A

Upper respiratory tract infections (URTIs) – usually not
life threatening

Lower respiratory tract is normally sterile, thus infections
often serious

24
Q

What categories do the strains on influenza affect

A

Influenza A affects humans and wide range of animals. Cause of epidemics and pandemics.

Influenza B only affects humans. Cause epidemics but not pandemics

25
Q

What are the antigens on the surface envelope of Myxovirus

A

haemagglutinin (H)

neuraminidase (N)

26
Q

Difference between antigenic drift and antigenic shift

A

Antigenic drift are small constant changes in H and N

Antigenic shift are major, sudden and unpredictable changes in H and N that lead to a new strain of virus

27
Q

Pathogenesis of Influenza

A

Transmission by droplet, highly infectious

Virus adheres to upper respiratory tract epithelium via the H proteins.

1 to 3 days – fever, chills, malaise, muscle pain; runny nose, sore throat and cough may follow; recovery in 1
to 3 weeks

28
Q

Acute Bronchitis

A
  • Caused by virus
  • Initial symptoms similar to pneumonia
  • Self-limiting
  • Treatment symptomatic – no antibiotics
  • Bacterial bronchitis occurs with underlying disease
29
Q

Bronchiolitis

A

Childhood form of bronchitis
• under 2 yrs
• Respiratory Syncytial Virus (RSV) most common cause
• Highly infectious
• Fever, coryza, cough, asthma-like symptoms
• Healthy infants recover well while premature infants with low birth weight may display severe and possibly fatal progression

30
Q

Disorders which limit expiratory flow

A 
asthma
bronchitis
emphysema
brochiectasis
cystic fibrosis
31
Q

Cystic fibrosis

A
  • Autosomal recessive condition linked to gene mutation of transmembrane regulator (CFTR) that functions as a chloride ion channel
  • Cl- is retained in cells which leads to water and Na+ absorption from mucosal surface leading to ↑ viscosity of mucous
  • Clinical manifestations include excessive secretion viscous fluid from epithelial glands of respiratory, gastrointestinal and genitourinary tracts
  • Excessive secretions cause accumulation of viscous bronchial mucous, impaired mucociliary clearance and lung infections
  • Major cause of chronic (non-reversible) respiratory disease in children
32
Q

Define atelectasis

A

collapse of lung segment

33
Q

Define transudate fluid

A

clear fluid from congested lungs due to heart failure, renal and/or liver disorder.

34
Q

Define haemothorax

A

escape of blood into pleural space due to chest trauma,

malignancy and/or vessel rupture.

35
Q

Define exudate fluid

A

protein and inflammatory cells that arise from infection, cancer or DVT.

36
Q

Use of prophylactic anti-inflammatory drugs

A
  • Preventative measure for asthma
  • Crucial for moderate to severe asthma and taken on a
    regular basis:
37
Q

Use of bronchodilators

A

symptomatic relief

38
Q

Use of glucocorticoids

A

Beclomethasone (inhaled) and Prednisone (oral)

↓inflammatory mediators
↓inflammatory cell infiltration
↓ oedema and mucous secretions
↑β2 receptors and sensitivity to β2 agonists

• Inhaled drug avoids severe adverse effects

39
Q

Types of prophylactic anti-inflammatory drugs

A

– Glucocorticoids (anti-inflammatory)
– Leukotriene (pro-inflammatory) modifiers
– Cromolyn (mast cell stabiliser)
– IgE antagonists

40
Q

Types of bronchodilators

A

– Beta2 adrenergic agonists
– Methylxanthines (↓ airflow obstruction, airway
hyperresponsiveness, and airway inflammation)
– Anticholinergics

41
Q

Use of leukotriene modifier

A

– introduced late 90’s; well tolerated
– leukotriene receptor antagonist
– used for intrinsic/extrinsic asthma and allergic rhinitis

42
Q

Use of Cromolyn

A

– ↓histamine release and ↓inflammatory cell activity
– low incidence of adverse effects
– less effective than corticosteroids

43
Q

Use of IgE antagonist

A

– second line drug
– monoclonal antibody attaches/inhibits IgE
– associated with a number of adverse effects including
anaphylaxis

44
Q

Use of Methylxanthines

A

– Widespread use diminished as other treatments safer
– Mechanism of smooth muscle relaxation is unclear,
provide less effective but longer duration of action than
β2 agonists
– Adverse effects include vomiting, diarrhoea,
restlessness, insomnia

45
Q

Use of Muscarinic Antagonists

A

– Recommended for COPD but also used for asthma,
– Administered via inhalation which localises drug in lungs
and thus avoids adverse effects

46
Q

Types of inhalers

A 
Metered-Dose Inhalers (MDI’s)
– hand held pressurised devices
– require hand-breath coordination
– 10% of the drug released reaches lungs
– use of a spacer improves delivery

Dry-Powder Inhalers (DPI’s)
– not pressurised/ breath activated
– little coordination required
– 20% of dose reaches lungs

47
Q

Classification of asthma

A

Intermittent Mild Moderate Severe

≤ 2 d/wk 2-7 d/wk daily Through the day

48
Q

Why does frequent use of bronchodilators cause tachycardia

A

While the drug is selective for beta 2 receptors it does have some beta 1 (cardiac receptors) action. Therefore in higher doses some beta 1 stimulation occurs leading to tachycardia.

z Clinical Science (4 decks)

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