Pulmonary Flashcards

(48 cards)

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
What are the antigens on the surface envelope of Myxovirus
haemagglutinin (H) | neuraminidase (N)
26
Difference between antigenic drift and antigenic shift
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
Pathogenesis of Influenza
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
Acute Bronchitis
* Caused by virus * Initial symptoms similar to pneumonia * Self-limiting * Treatment symptomatic – no antibiotics * Bacterial bronchitis occurs with underlying disease
29
Bronchiolitis
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
Disorders which limit expiratory flow
``` asthma bronchitis emphysema brochiectasis cystic fibrosis ```
31
Cystic fibrosis
* 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
Define atelectasis
collapse of lung segment
33
Define transudate fluid
clear fluid from congested lungs due to heart failure, renal and/or liver disorder.
34
Define haemothorax
escape of blood into pleural space due to chest trauma, | malignancy and/or vessel rupture.
35
Define exudate fluid
protein and inflammatory cells that arise from infection, cancer or DVT.
36
Use of prophylactic anti-inflammatory drugs
- Preventative measure for asthma - Crucial for moderate to severe asthma and taken on a regular basis:
37
Use of bronchodilators
symptomatic relief
38
Use of glucocorticoids
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
Types of prophylactic anti-inflammatory drugs
– Glucocorticoids (anti-inflammatory) – Leukotriene (pro-inflammatory) modifiers – Cromolyn (mast cell stabiliser) – IgE antagonists
40
Types of bronchodilators
– Beta2 adrenergic agonists – Methylxanthines (↓ airflow obstruction, airway hyperresponsiveness, and airway inflammation) – Anticholinergics
41
Use of leukotriene modifier
– introduced late 90’s; well tolerated – leukotriene receptor antagonist – used for intrinsic/extrinsic asthma and allergic rhinitis
42
Use of Cromolyn
– ↓histamine release and ↓inflammatory cell activity – low incidence of adverse effects – less effective than corticosteroids
43
Use of IgE antagonist
– second line drug – monoclonal antibody attaches/inhibits IgE – associated with a number of adverse effects including anaphylaxis
44
Use of Methylxanthines
– 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
Use of Muscarinic Antagonists
– Recommended for COPD but also used for asthma, – Administered via inhalation which localises drug in lungs and thus avoids adverse effects
46
Types of inhalers
``` 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
Classification of asthma
Intermittent Mild Moderate Severe | ≤ 2 d/wk 2-7 d/wk daily Through the day
48
Why does frequent use of bronchodilators cause tachycardia
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.