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Core Conditions > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is the definition of asthma?

A

Asthma is a chronic inflammatory airway disease characterised by intermittent airway obstruction and hyper-reactivity.

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2
Q

What are the three pathological hallmarks of asthma?

A
  1. bronchoconstriction
  2. oedema
  3. mucus hypersecretion
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3
Q

What questions do you ask when taking an asthma history?

A

Symptoms: SOB, cough, wheeze
Severity: does it wake you up at night? How often do you take your puffer? Have you ever been hospitalised/intubated?
Social: how does it affect your life?
Medications: puffer, preventer, oral pred
Triggers: exercise, cold, pollutants
Atopy: eczema, hayfever, allergies

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4
Q

What signs will you find on examination of a patient with asthma?

A 
Hyperinflated chest (gas trapping)
Tachypnoea
Use of accessory muscles
Pursed lip breathing
Cyanosis
Prolonged expiratory wheeze
Reduced breath sounds on auscultation
Possibly decreased heart sounds (increased chest volume)
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5
Q

What are some triggers for asthma?

A 
Allergens
Pollutants
Tobacco smoke
Occupational exposure
URTIs
Exercise
Cold air
Medication: aspirin, beta blockers
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6
Q

How do we diagnose asthma?

A

Spirometry: airflow obstruction is when FEV1/FVC (FER) <70%

We need to prove that the bronchoconstriction is reversible, so look for an increase in FEV1 following Ventolin.

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7
Q

What are the goals of treatment for asthma?

A

Control symptoms
Prevent exacerbations
Maximise lung function and prevent future lung function decline
Maintain normal levels of activity
Lower dose of amedication to achieve suitable asthma control and minimise side effects

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8
Q

What are the pharmacological treatments for asthma?

A

Relievers: beta2 agonists (relax smooth muscle but do not change underlying inflammation)
Preventer: inhaled GCS (reduce inflamm and AHR)
Oral GCS
Combination inhalers (ICS + LABA)
LT-receptor antagonists (for aspirin-sensitive asthma)
Long-acting anticholinergics
Anti-IgE

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9
Q

What are the signs of an acute asthma attack?

A

Low oxygen
Respiratory muscle fatigue = no hyperventilation = not alkalotic
Silent chest

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10
Q

How do we treat an acute asthma attack?

A

Oxygen is essential.
Oral prednisolone or IV hydrocortisone
Regular bronchodilators
Urgent ICU assessment for observation - possible intubation
IV magnesium (bronchodilation properties)

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11
Q

What is the definition of COPD?

A

COPD is a preventable and treatable disease, characterised by airflow limitation that is not fully reversible.

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12
Q

What are the three major components of COPD?

A
  1. Emphysema
  2. Chronic bronchitis
  3. Small airways disease
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13
Q

What is emphysema?

A

Alveolar wall destruction with irreversible enlargement of the air spaces distal to the terminal bronchioles and without evidence of fibrosis

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14
Q

What would you find on examination for a patient with COPD?

A

Early (note: there are often not many signs early on in COPD):

  • nicotine staining
  • prolonged expiratory phase +/- wheeze on forced exhalation

Later:
- hyperinflation (barrel chest)

End stage:

  • pursed lip breathing
  • accessory muscle use
  • cyanosis
  • asterixis (metabolic encephalopathy due to high CO2 levels)
  • engorged liver
  • RV heave
  • engorged neck veins due to increased intrathoracic pressure
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15
Q

What investigations should you perform to diagnose COPD?

A

Pulmonary function tests: spirometry, flow-volume loop, lung volumes
CXR
HRCT
ABGs

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16
Q

What would you see on CXR for a patient with COPD?

A 
Hyperinflation:
- flat hemidiaphragms
- increased lucency
- tapered vascular shadows peripherally
Bullae
- large cysts in the lung (increase risk of pneumothorax)
17
Q

What are the management principles for patients with COPD?

A

Remember COPX:
C = confirm diagnosis
O = optimise function (smoking cessation, treat other comorbidities)
P = prevent deterioration (smoking cessation, flu vacc to decrease risk of exacerbations)
D: develop support network and self-management plan
X: management of exacerbations

18
Q

What is the definition of pulmonary oedema?

A

Pulmonary oedema is the accumulation of fluid in the alveolar sacs of the lung.

19
Q

What are some causes of pulmonary oedema?

A 
Cardiogenic causes:
- left heart failure
- mitral regurgitation
Non-cardiogenic causes:
- fluid overload
- pulmonary embolus
- ARDS
20
Q

What is the definition of pleural effusion?

A

Pleural effusion is the accumulation of fluid in the space between the visceral and parietal pleura.

21
Q

What are some causes of pleural effusion?

A 
Transudate:
- left heart failure (increased pulmonary capillary pressure)
- right heart failure (increased parietal pleural capillary pressure)
- cirrhosis
- pulmonary embolism
- kidney failure
- hypoalbuminuria
Exudate:
- pneumonia
- malignancy
22
Q

What might you find on history and examination of a patient with pleural effusion?

A 
History
1. Pleuritic chest pain, worse on inspiration and movement
2. If caused by pneumonia, may be associated with productive cough. Transudative pleural effusions cause non-productive cough.
3. Dyspnoea 
Examination 
1. Dullness to percussion 'stony dull'
2. Reduced breath sounds over effusion
3. Reduced vocal resonance
4. Reduced chest expansion
23
Q

What are common causes of typical pneumonia?

A 
Streptococcus pneumoniae
Haemophilus influenzae
Klebsiella pneumonia
Staphylococcus aureus
Moraxella catarrhalis
24
Q

What are common causes of atypical pneumonia?

A 
Mycoplasma pneumoniae
Chlamydia pneumoniae
Chlamydia psittaci
Legional penumophila
Coxiella burnetii
25
Q

What are the three main categories of lung disease? List some examples of each.

A
  1. Airways disease
    - e.g. asthma, COPD, bronchiectasis
  2. Diffuse lung diseases
    e. g. pulmonary oedema, pulmonary fibrosis, lung injury by drugs/fumes
  3. Pulmonary vascular diseases
    e. g. pulmonary embolus, pulmonary hypertension
26
Q

What kind of processes can acutely cause a diffuse lung pattern?

A

Due to the presence of:

  • water: from altered starling forces in pulmonary oedema
  • inflammation: due to acute inhalational injury from toxic fumes or acute drug toxicity; acute infection, e.g. influenza
  • blood: diffuse leakage from inflamed vessels in vasculitis
27
Q

What kind of processes can cause a subacute or chronic diffuse lung pattern?

A

Interstitial diseases:

  1. Idiopathic pulmonary fibrosis
  2. Sarcoidosis
  3. Occupational: asbestosis
  4. Extrinsic allergic alveolitis (e.g. bird fanciers, farmer’s lung)
  5. Drugs (e.g. methotrexate, amiodarone, bleomycin, nitrofurantoin)
  6. Radiotherapy
  7. Pulmonary fibrosis associated with connective tissue disease
  8. Vasculitis
28
Q

What are the symptoms of airways disease, diffuse lung diseases and pulmonary vascular diseases?

A
  1. airways diseases: wheeze, cough, sputum, dyspnoea
  2. diffuse lung diseases: cough, dyspnoea (wheeze unusual)
  3. pulmonary vascular diseases: dyspnoea, pleuritic pain, haemoptysis
29
Q

What are the causes of respiratory alkalosis?

A

Respiratory alkalosis is caused by hyperventilation –> overbreathing causing loss of CO2

Causes:

  • asthma
  • anxiety
  • cardiac failure
  • sepsis
  • hypoxia
30
Q

What is the rule for acute respiratory acidosis? (in terms of CO2 and HCO3 levels)

A

For every 10 mmHg CO2 rises, HCO3 rises by 1 mmHg

31
Q

What is the rule fo acute respiratory alkalosis? (in terms of CO2 and HCO3 levels)

A

For every 10 mmHg CO2 decreases, HCO3 decreases by 2.5 mmHg

32
Q

How does the body compensate in respiratory acidosis/alkalosis?

A

The kidneys will either retain or excrete bicarbonate. This will not occur in an acute setting.

33
Q

What are the causes of metabolic acidosis?

A

Increase in H+:

  • ketoacids
  • lactic acid
  • poisons
  • amino acids
  • HCl

Loss of HCO3-:

  • pancreas
  • kidneys
  • GIT
34
Q

What is the anion gap and how are its results interpreted?

A

We use the anion gap in the case of metabolic acidosis.
Anion gap = (Na + K) - (Cl + HCO3)

If increased anion gap, the metabolic acidosis is caused by lactate, ketoacids or ethanol.
If normal anion gap, the metabolic acidosis is caused by HCl, amino acids or loss of HCO3.

35
Q

What are the causes of metabolic alkalosis?

A

Addition of HCO3: exogenous

Loss of H+: vomiting, NG aspirate

36
Q

What is the rule for compensated metabolic acidosis/alkalosis?

A

CO2 same as last 2 digits of pH

HCO3 +15 is same as last 2 digits of pH

Core Conditions (13 decks)

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