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Year 3 - Medicine > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Outline respiratory failure and the 2 types of RF

A

Respiratory failure: inability to maintain adequate oxygen levels or remove carbon dioxide

Type 1:
Low O2
Low/normal CO2

Type 2:
Low O2
High CO2 (retaining)

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2
Q

List some common causes of type 1 and type 2 respiratory failure

A

Type 1 RF:
- V/Q mismatch (PE, COPD, pneumonia, RDS newborn, pulmonary oedema)
- Diffusion defect (lung fibrosis)
- Intra-lung shunt (ARDS)
- Low atmospheric oxygen (high altitude)
- Right-to-left shunt (congenital heart defect)

Type 2 RF:
- Hypoventilation (many, including chest wall disorders, NM junction disorders)
- Increased carbon dioxide production

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3
Q

Outline the difference between acute and chronic respiratory failure

A

Acute:
- Needs urgent treatment
- May need artificial ventilation
- Minimal compensation by kidneys (bicarbonate levels)

Chronic:
- Slow onset and progression, allows for compensation
- Better tolerated, treatment is less urgent
- Compensation by kidneys (bicarbonate levels)

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4
Q

Outline how someone with respiratory failure presents (acute and chronic)

A

Acute:
- Respiratory symptoms e.g. SOB, cough, fever
- Drowsiness / coma
- Confusion
- Warm hands
- Bounding pulse
- Headache

Chronic:
- Mild vasodilation (pink puffers)
- May have no presenting features

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5
Q

List some investigations for suspected respiratory failure

A

ABG - gold standard for respiratory failure!
(gives pH, PaO2, PaCO2 and HCO3-)

May also do:
- Imaging e.g. chest x-ray
- O2 sats probe

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6
Q

List common causes of acute and chronic respiratory failure

A

Acute:
- Opioid overdose
- Head injury
- Severe acute asthma

Chronic:
- Severe COPD (can get acute exacerbations due to LRTI)

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7
Q

Outline the management steps for acute and chronic respiratory failure

A

ABCDE approach!

  1. Correct hypoxaemia/hypoxia with O2
    - Nasal cannula
    - Non-rebreathing mask
    - Venturi mask
  2. Correct hypercapnia / acidosis
    - Correct underlying cause of hypercapnia if known
    - Ventilatory support (non-invasive ventilation or intubation)
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8
Q

List some common asthma triggers

A
  • Pet fluff
  • Dust / dust mites
  • Cold weather
  • Exercise
  • Pollution
  • Cigarette smoke
  • Pollen
  • Damp
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9
Q

Describe the correct inhaler technique

A
  1. Hold inhaler with thumb underneath and finger on top
  2. Breathe out
    Put inhaler into mouth, teeth on the plastic but don’t bite down, form a seal with your lips
  3. Breathe in and press down on top
  4. Keep inhaling until lungs are full
  5. Hold breath for 10 seconds

May use spacer if their inhaler technique is ineffective

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10
Q

Outline occupational lung disease, including occupations that are associated with lung diseases and specific types of occupational lung disease

A

Can occur when there is long term exposure to hazardous / toxic / irritating particles or gases

Occupations:
- Factory workers
- Coal workers
- Farmers
- Worked with asbestos
- Industrial cleaners
- Labourers

Type:
- Coal workers’ pneumoconiosis (Black Lung Disease)
- Asbestosis (presents 20-30 yrs post exposure)
- Silicosis
- Farmers’ lung (allergic alveolitis)

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11
Q

Asbestosis - state the following:
- Pathophysiology
- Those at risk
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Disturbing asbestos can lead to release of fine asbestos particles

At risk:
- Construction worker in 1970-1990s
- Builders/labourers working with older houses

Presentation:
- SOB
- Wheeze
- Chest pain
- Cough
- Fatigue
- Clubbing

Investigations:
- Lung function tests
- Chest x-ray
- CT scan

Management:
- No treatment once damage has occured
Can help
- Pulmonary rehabilitation
- O2 therapy
- Inhalers
- Stop smoking / don’t start smoking
- Ensure vaccinations up to date

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12
Q

Asthma (non-acute) - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Chronic hypersensitivity condition caused by bronchoconstriction and leads to reversible airway obstruction
- Inflammatory response due to eosinophils, mast cells and Th2 cells
- Reversible on bronchodilators

Presentation:
- Wheeze
- SOB
- Dry (nocturnal) cough
- Chest tightness
- Atopic triad (asthma, eczema and hay fever)
- Family history of asthma
- Raised eosinophils

Investigations:
- PEFR
- Spirometry with reversibility with bronchodilators
- Fractional inhaled NO

Management:
Stepwise management
1. Short acting beta 2 agonists (SABA) e.g. Salbutamol
2. Inhaled corticosteroids (ICS) e.g. Beclomethasone
3. Leukotriene antagonists e.g. Montelukast
4. Long acting beta 2 agonists (LABA) e.g. Salmeterol
5. Increase ICS dose
6. Long acting muscarinic antagonists (LAMA) or Theophylline or increase ICS further
7. Refer to specialist
- Trigger avoidance
- Vaccinations up to date
- Yearly asthma review
- Avoid / stop smoking

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13
Q

State the different severities of acute asthma:
- Mild
- Moderate
- Severe
- Life threatening
- Near fatal

A

Mild:
- PEFR > 75%

Moderate:
- PEFR 50-75%

Severe:
- PEFR 33-50%
- Can’t complete full sentences
- RR >25
- HR > 110

Life threatening:
- PEFR < 33%
- Sats < 92%
- Low RR or HR
- Cyanosis
- Silent chest
- Acute type 1 respiratory failure (low O2, low/normal CO2)
- Exhaustion

Near fatal:
- Acute type 2 respiratory failure (low O2, high CO2)

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14
Q

Outline the management for acute asthma
- Non-severe
- Severe
- Life threatening/fatal

A

ABCDE approach!

Non-severe:
- O2 therapy
- Nebulised Salbutamol (5mg)
- Oral Prednisolone 40mg (can use IV hydrocortisone)

Severe:
- Nebulised Ipratropium Bromide (500microg)
- Consider Salbutamol back-to-back

Life threatening/fatal:
- Urgent ITU/anaesthetist assessment
- CXR (portable)
- IV Aminophylline

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15
Q

What needs to be done to ensure safe discharge of a patient after asthma exacerbation

A
  • PEFR > 75%
  • 5 days oral Prednisolone
  • 24 hrs without the use of nebulisers

Follow ups:
- Ensure asthma plan and PEFR tube
- Assess inhaler technique
- GP fu after 2 days
- Respiratory clinic after 4 weeks

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16
Q

COPD - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Chronic obstructive non-reversible disease
- Either chronic bronchitis, emphysema or mixed
- Non-reversible with bronchodilators
- Associated with noxious particles (mostly smoking)

Presentation:
- Productive cough
- Wheeze
- SOB
- Periods of infective exacerbations

Investigations:
- Spirometry which shows non-reversibility with bronchodilators

Management:
- SMOKING CESSATION
- Pulmonary rehabilitation
- Inhalers (beta agonists and ICS)
- Mucolytics
- O2 therapy
- Up to date vaccinations

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17
Q

Outline the management for COPD exacerbations

A

ABCDE approch!

  • O2 support
  • Nebulisers - Salbutamol and Ipratropium
  • Steroids (Prednisolone)
  • Antibiotics if infective cause
  • Consider IV Aminophylline
  • Consider non-invasive ventilation or ITU referral if Type 2 RF
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18
Q

List the common bacteria for pneumonia in:
- Community (CAP)
- Hospital (HAP)
- Atypical bacteria

A

Community (CAP)
- Strep pneumonia
- Haemophilus influenzae
- Moraxella catarrhalis

Hospital (HAP)
- MRSA
- E Coli
- Pseudomonas

Atypical bacteria - can’t be cultured or gram stained and don’t respond to Penicillins
- Legionella
- Mycoplasma pneumoniae
- Chlamydia pneumoniae

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19
Q

Pneumonia - state the following:
- Pathophysiology
- Presentation
- Chest examination findings
- Investigations
- Management

A

Pathophysiology:
- Infection of the lung parenchyma
- Chest x-ray abnormalities with respiratory symptoms

Presentation:
Symptoms
- SOB
- Fever
- Productive cough (yellow/green)
- Haemoptysis
- Pleuritic chest pain
- Fatigue/lethargy
Signs
- Low O2 sats
- Tachycardia
- Tachypnoea
- Hypoxia
- Hypotension

Chest examination findings:
- Bronchial breathing
- Coarse crackles
- Dullness to percussion
- May have reduced chest expansion

Investigations:
- Routine bloods (FBC, U&Es, CRP)
- Calculate CURB-65 score
- Chest x-ray
- Sputum culture (moderate/severe)
- Blood culture (moderate/severe)
- Legionella and pneumococcal urinary antigens (moderate/severe)

Management:
Mild: 5 days oral Abx
Moderate-severe: 7-10 days oral Abx (Flucloxacillin)

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20
Q

Outline the UHL recommended antibiotics for the following scenarios

Community acquired pneumonia (CAP):
- Mild
- Moderate
- Severe

Hospital acquired pneumonia (HAP):
- Mild
- Moderate
- Severe

A

Community acquired pneumonia (CAP):
Mild = Oral Amoxicillin (5 days)
Moderate = Oral Amoxicillin (5 days)
Severe = IV Amoxicillin (5 days)
(Doxycycline second line)

Hospital acquired pneumonia (HAP):
Mild = Oral Co-Amoxiclav (5 days)
Moderate = Oral Co-Amoxiclav (5 days)
Severe = IV Co-Amoxiclav (5 days)
(Doxycycline second line)

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21
Q

Outline the scoring system used for pneumonia severity
- What it’s an indicator of
- What it is used for
- What does CURB-65 stand for?

A

CURB-65 score

  • Predictor of mortality
  • Used to help decide whether a patient needs to be admitted for their pneumonia

Confusion
Urea > 7
Respiratory rate > 30
Blood pressure systolic < 90mmHg OR diastolic < 60
> 65 yrs

Mild score 0-1 = treat at home
Moderate score 2 = admit to hospital
Severe score 3-5 = intensive care

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22
Q

Outline the scoring results for CURB-65 and how it influences treatment

A

0-1 Mild = treat at home (oral abx)
2 Moderate = admit to hospital (oral abx)
3-5 Severe = admit to intensive care (IV abx)

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23
Q

Pulmonary Embolism - state the following:
- Pathophysiology
- Risk factors
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Embolus lodged within the pulmonary arteries
- Main source is usually thrombus dislodged from a DVT

Risk factors:
- Previous DVT/PE
- Prolonged immobilisation / long haul flights
- Recent surgery
- HRT/OC
- Pregnancy
- Malignancy
- Polycythaemia

Presentation:
- Pleuritic chest pain
- Haemoptysis
- Cough
- SOB
- Tachycardia
- Haemodynamic instability if large

Investigations:
1. Calculate Wells’ score
If > 4 (likely) = CTPA
If < 4 (unlikely) = d-dimer, if high then CTPA

Management:
- Immediate anticoagulation with LMWH e.g. Enoxaparin or Dalteparin
- If massive PE, may do thrombolysis e.g. Streptokinase or Alteplase
- Supportive: O2 or analgesia
- Long-term DOACs (3 months if temporary cause, indefinitely if malignancy or unknown) e.g. Apixaban

24
Q

List some reasons why pneumonia may not be resolving (AEIOU)

A

Antibiotic issue - incorrect dose, poor Empyema or abscess
Immunocompromised
absorption
Organism - resistant or atypical
Underlying/secondary diagnosis - e.g. PE

25
Q

Outline the score used to assess the likelihood of a DVT/PE and how the outcome of the score differs based on whether it’s a DVT or PE

A

Wells’ score

DVT
Likely if 2 or more
Unlikely if less than 2

PE:
Likely if 4 or more
Unlikely if less than 4

26
Q

List some other reasons for a high d-dimer (other than a PE)

A
  • PE
  • Recent surgery
  • Pneumonia / infection
  • Pregnancy
  • Malignancy
  • Heart failure
27
Q

Tuberculosis - state the following:
- Pathophysiology
- Common extrapulmonary colonisation sites
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Mycobacterium tuberculosis bacteria
- Inhaled through droplets of an actively infected individual
- Spreads through the lymphatics and blood
- TB can be active or latent

Common extrapulmonary colonisation sites:
- Lymph nodes
- Pleura
- Pericardium
- GI system
- Genitourinary system
- Subcutaneous
- CNS
- Bones and joints

Presentation:
- Weight loss
- Night sweats
- Cough +/- haemoptysis
- Lethargy
- Erythema nodosum
- Lymphadenopathy
- Spinal pain (if spinal TB)

Investigations:
- Mantoux test or QuantiFERON gamma
- Sputum cultures (if suspect active disease)
- Chest x-ray (if suspect active disease)

Management:
Acute pulmonary TB: RIPE
- Rifampicin
- Isoniazid (plus Pyridoxine)
- Pyrazinamide
- Ethambutol
Latent TB (at risk groups): 3 months of Rifampicin and Isoniazid OR 6 months of Isoniazid
Other:
- Test for other infectious disease e.g. HIV, Hepatitis
- Notify Public Health
- Contact tracing
- Isolation in -ve pressure rooms

28
Q

Bronchiectasis - state the following:
- Pathophysiology
- Causes
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Permanent dilation of the bronchi, with paradoxical narrowing due to decreased mucus clearance
- Caused by chronic damage

Causes:
- Post-infection e.g TB
- Recurrent childhood respiratory infections
- Immune deficiency e.g. hypogammaglobinaemia
- Genetic defects in mucus clearance e.g. cystic fibrosis

Presentation:
- Considerable productive cough (white)
- Haemoptysis
- Fatigue
- SOB
- History of risk factors/causes

Investigations:
- Sputum culture
- High resolution CT (gold standard) = signet ring sign
- Lung function tests
- Autoimmune screen / genetic testing

Management:
- Pulmonary rehabilitation
- Stop smoking
- Up to date vaccinations
- Long term O2 therapy
- Mucolytic agents
- Bronchodilators
- Long term abx
- Therapy for any underlying cause

29
Q

Cystic fibrosis - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Autosomal recessive disease affecting CFTR
- Impaired mucus clearance throughout body

Presentation:
- Meconium ileus at birth
- Intestinal malabsorption
- Recurrent respiratory infections
- Pancreatitis / gallstones
- Often found on newborn screening

Investigations:
- Newborn screening or family history
PLUS
- Positive sweat test or genotyping

Management:
- Pulmonary physiotherapy
- Mucolytics
- Pancreatic enzyme replacement therapy
- Up to date vaccinations
- Fat soluble vitamin replacement

30
Q

List some complications of cystic fibrosis and how they are managed

A
  1. Recurrent respiratory infections
    - Prophylactic antibiotics
    - Physiotherapy
  2. Low BMI
    - Nutritional supplements
    - Pancreatic enzyme supplementation
    - May need NG / PEG feeding
  3. Distal intestinal obstruction syndrome (DIOS)
    - Oral Gastrografin (osmotic)
  4. Diabetes
    - Normal management
31
Q

List some lifestyle advice given to patients with cystic fibrosis

A
  • Avoid other CF individuals
  • Avoid stables / hay (aspergillus)
  • Avoid hot tubs (pseudomonas)
  • Stay hydrated and have NaCl replacement in hot weather
  • Don’t smoke
  • Up to date vaccinations
32
Q

Interstitial lung disease - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Inflammation and fibrosis of the lung parenchyma
- Leads to thickening of the basement membrane and impaired gas exchange, particularly O2

Presentation:
- DRY cough
- SOB
- Fatigue/lethargy
- Finger clubbing
- Chest discomfort
- History of causes/risk factors

Investigations:
- Routine bloods
- High Resolution CT
- Lung function tests including Spirometry

Management:
- Limited treatment options (damage is irreversible)
- Manage any risk factors / underlying because
- Smoking cessation
- O2 therapy
- Physiotherapy and pulmonary rehabilitation
- Up to date vaccinations
- Advanced care planning if appropriate
- Perhaps lung transplant

33
Q

Outline the different types of interstitial lung disease (causes)

A

Types/causes:

1) Idiopathic
- Progressive pulmonary fibrosis with no clear because
- Bibasal fine inspiratory crackles and finger clubbing

2) Drug-induced (MAN-C)
- Methotrexate
- Amiodarone
- Nitrofurantoin
- Cyclophosphamide

3) Secondary (R-ASS)
- Secondary to other conditions
- RA
- Alpha-1 antitrypsin deficiency
- SLE
- Systemic sclerosis

4) Hypersensitivity pneumonitis
Type 3 hypersensitivity reaction to an environmental allergen
4 main causes:
- Bird fancier’s lung (bird droppings)
- Farmer’s lung (mould in hay)
- Mushroom worker’s lung (specific mushrooms)
- Malt worker’s lung (mould on barley)

5) Cryptogenic organising pneumonia
- Local inflammation of the lung (almost any trigger)
- Similar presentation to pneumonia and on chest x-ray
- Definitive diagnosis with lung biopsy

6) Asbestosis
- From exposure to asbestos
- Often takes 30-40 yrs to develop

34
Q

Outline the presentation of lung cancer

A
  • Chronic cough > 3 weeks
  • Haemoptysis
  • SOB
  • Finger clubbing
  • Lymphadenopathy (supraclavicular)
  • Recurrent chest infections
  • Weight loss
  • Lethargy
  • Night sweats
    BUT may have no symptoms
35
Q

Outline the common causes of finger clubbing (mnemonic CLUBBING)

A

Cyanotic diseases
Lung abscess
Ulcerative colitis
Bronchiectasis
Brachial AV fistula
Interstitial lung disease / infective endocarditis
Neoplasia (incl. lung / fibroma / mesothelioma)
Graves’ disease

36
Q

Pleural effusion - state the following:
- Pathophysiology
- Presentation
- On examination
- Investigations
- Management

A

Pathophysiology:
- Accumulation of fluid in the pleural cavity (between visceral and parietal pleura)
- Can be transudate or exudate

Presentation:
- SOB only

On examination:
- Dull percussion and reduced breath sounds on auscultation
- May have tracheal deviation if large

Investigations:
- Chest x-ray (blunted costophrenic angles, meniscus, tracheal deviation if large)
- Need to sample fluid with chest drain or aspiration, for analysis

Management:
Dependent on cause
- Small effusions = conservative management
- Pleural aspiration, but may reoccur
- Chest drain, prevents from recurring

37
Q

Outline the main causes of pleural effusion (exudate and transudate and empyema)

A

Exudate (self-producing):
- Pneumonia
- TB
- Lung cancer
- RA

Transudate (due to pressure):
- Congestive heart failure
- Hypoalbuminemia
- Hypothyroidism
- Meig’s syndrome (ovarian malignancy)

Empyema:
- Infected pleural effusion
- Suspect if pneumonia is improving but new/unresolving fever
- Treat with chest drain and abx

38
Q

Pleural infection - state the following:
- Pathophysiology
- Most common organisms
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Infection of the pleural lining

Most common organisms:
- Strep pneumoniae
- Strep pyogenes
- Staph aureus

Presentation:
- Pleuritic chest pain (sharp and well localised)
- Pain worse on inspiration
- Fever
- SOB
- Cough with purulent sputum

Investigations:
- Chest x-ray which shows pleural effusions (from pneumonia) but with failure to improve

Management:
Variable!
- Abx
- Thoracentesis
- Chest drain

39
Q

Pneumothorax - state the following:
- Pathophysiology
- Categories of pneumothorax
- Presentation
- On examination
- Investigations
- Management

A

Pathophysiology:
- Collection of air within the pleural cavity, leading to disruption of the pleural seal

Categories:
- Simple vs tension
- Primary vs secondary
- Spontaneous vs iatrogenic

Presentation:
- Chest pain
- SOB
- Cough
- Evidence of original cause e.g. trauma

Investigations:
- Erect chest x-ray, which shows
1. Hyperlucency
2. Lung border
3. Loss of lung markings
CT thorax can be used if the pneumothorax is too small to be seen on chest x-ray

On examination:
- Hyperresonance
- Decreased breath sounds
- Reduced chest expansion
- Tracheal deviation if large tension

Management:
- Conversative (if small and no SOB) with f/u in 2-4 w
- Thoracentesis (if large OR SOB)
- Chest drain (if large or haemodynamically unstable OR the thoracocentesis fails twice)

40
Q

List some causes of pneumothorax

A

Spontaneous:
- Subpleural blebs

Secondary / pre-existing conditions:
- COPD
- Asthma
- Bronchiectasis / cystic fibrosis
- Lung cancer
- Lung infections e.g. TB / pneumonia
- RA
- Marfan’s syndrome / Ehler’s Danlos syndrome

Traumatic:
- Stab wound
- Needle wound
- Fractured rib

Iatrogenic:
- Chest drain
- Central line
- Any other procedure near the lungs (including apices)

41
Q

Outline the signs and management of tension pneumothorax

A

Signs:
- Tracheal deviation (to unaffected side)
- Reduced air entry on affected side
- Hyperresonance
- Haemodynamically unstable (hypotension and tachycardia)

Management:
1) Thoracocentesis (immediate management)
- Large bore cannula into 2nd intercostal space, midclavicular line
2) Chest drain (definitive management)

42
Q

Outline the safety triangle for a chest drain and where needle should be inserted relative to ribs

A
  1. 5th intercostal space
  2. Mid-axially line
  3. Anterior axillary line

Insert needle above the ribs avoid the neurovascular bundle

43
Q

Obstructive sleep apnoea - state the following:
- Pathophysiology
- Risk factors
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Collapse and obstruction of the pharyngeal airway during sleep
- Apnoea episodes where the patient stops breathing completely for up to a few minutes
- Leads individual to wake many times during the night (often reported by partner)

Risk factors:
- Obesity
- Smoking
- Alcohol
- Middle age
- Male

Presentation:
- Snoring reported by partner
- Reduced O2 sats at night
Problems with tiredness as a result of disrupted sleep
- Poor concentration
- Daytime tiredness / fatigue
- Morning headache

Investigations:
- Referral to ENT specialist or specialist sleep clinic for: Sleep studies

Management:
- Weight loss if appropriate
- Stop smoking / alcohol
- CPAP overnight
- If severe, surgery is UPPP (uvulopharyngoplasty to restructure soft palate and jaw)
*Consider occupation and whether it’s high risk e.g. HGV driver = require urgent referral

44
Q

List causes of obstructive and restrictive lung diseases, as well as the FEV1:FVC ratios for both types of lung disease

A

Obstructive
Causes:
- COPD
- Asthma
FEV1:FVC ratio - < 0.75 (FEV1 reduced)

Restrictive
Causes:
- ILD e.g. pulmonary fibrosis
- Obesity
- Sarcoidosis
- Scoliosis
- Motor neurone disease
FEV1:FVC ratio - > 0.75 (FEV1 and FVC reduced)

45
Q

Non-invasive ventilation - describe the difference between BiPAP vs CPAP and explain when you would use each

A

BiPAP (bilevel positive airway pressure)
- Positive pressure during inspiration to force air into lungs
- Less positive pressure during expiration to allow air to leave
Use: type 2 respiratory failure, with respiratory acidosis that doesn’t respond to treatment

CPAP (continuous positive airway pressure)
- Pressure that is continuous to keep airways open, for airways that are prone to collapse
Use: obstructive sleep apnoea, congestive heart failure and acute pulmonary oedema

46
Q

Influenza - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Viral infection classified by haemagglutinin (H) and neuraminidase (N) surface antigens
- Spread through direct contact or via respiratory droplets

Presentation:
- Fever and chills
- Headache
- Rhinorrhoea
- Cough
- SOB
- Myalgia
- Arthralgia
- Fatigue / malaise

Investigations:
- Only test for influenza if it will change outcomes or if patients are at high risk of complications from influenza
- PCR tests

Management:
- Manage pt in a side room
- Usually supportive e.g. analgesia, fluids, O2 if required
- Oseltamivir if required

47
Q

COVID-19 - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Viral coronavirus infection
- Spread through direct contact or via respiratory droplets

Presentation:
- Fever and chills
- Continuous cough
- Loss / change sense of smell or taste
- SOB
- Sore throat
- Rhinorrhoea
- Myalgia
- Arthralgia
- Fatigue / malaise
- Headache
- Diarrhoea

Investigations:
- Rapid antibody test
- PCR test

Management:
- Manage pt in a side room
- Usually supportive e.g. analgesia, fluids, O2 if required
- Dexamethasone / corticosteroids
- Monoclonal antibody treatment (Casirivimab/Imdevimab)

48
Q

Pulmonary hypertension - state the following:
- Pathophysiology
- Presentation
- Common causes

A

Pathophysiology:
- Increased pressures in the pulmonary vasculature
- Can be either primary or secondary to pulmonary disease
- Often leads to cor pulmonale

Presentation:
Symptoms
- May be asymptomatic
- SOB
- Syncope
- Chest pain
Signs
- Raised JVP
- Peripheral oedema
- Reduced O2 sats / cyanosis
- Hepatomegaly

Common causes:
- Primary pulmonary hypertension
- Large PE
- Interstitial lung disease e.g. pulmonary fibrosis
- COPD
- Cystic fibrosis

Management:
- Treat the underlying cause
- Long-term O2

49
Q

Cor pulmonale - state the following:
- Pathophysiology
- Presentation
- Common causes
- Management

A

Pathophysiology:
- Right-sided heart failure, secondary to respiratory disease (leading to pulmonary hypertension)

Presentation:
Symptoms
- May be asymptomatic
- SOB
- Syncope
- Chest pain
Signs
- Raised JVP
- Peripheral oedema
- Reduced O2 sats / cyanosis
- Hepatomegaly

Common causes:
- Large PE
- Primary pulmonary hypertension
- Interstitial lung disease e.g. pulmonary fibrosis
- COPD
- Cystic fibrosis

Management:
- Treat the underlying cause
- Long-term O2

50
Q

Outline the 5 broad causes of pulmonary hypertension

A

1) Primary pulmonary hypertension or connective tissue disease (e.g. SLE)

2) Left-sided cardiac failure or systemic hypertension

3) Chronic lung conditions e.g. COPD

4) Vasculature issues e.g. PE

5) Miscellaneous e.g. sarcoidosis, haematological disorders

51
Q

Outline the purpose of the MRC dyspnoea scale

and outline the 5 grades

A

Grade 1: breathless only on strenuous exertion

Grade 2: breathless when hurrying on the flat / walking up a slight hill

Grade 3: breathless after 15 minutes walking / walk slower than most people

Grade 4: breathless after a few minutes on the flat / breathless after walking 90m

Grade 5: breathless after undressing / too breathless to leave the house

52
Q

List the 3 interventions that alter prognosis/mortality for patients with COPD

A
  1. SMOKING CESSATION
  2. Long term O2 therapy (used for > 15 hrs per day)
  3. Lung volume reduction surgery
53
Q

List 3 common drug classes that can cause a cough (directly or indirectly)

A
  • ACEi
  • CCB
  • DMARDs
54
Q

Sarcoidosis - state the following:
- Pathophysiology
- Who commonly develops it?
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Multi-system disease characterised by granuloma formation (nodules of inflammation full of macrophages)
- Cause is unknown
- Usually associated with chest symptoms, but can also have multiple extra-pulmonary manifestations e.g. erythema nodosum and lymphadenopathy

Who commonly develops it?
- Young adulthood and aged 60
- Women
- Black ethnicity

Presentation:
- Dry cough
- SOB
- Lymphadenopathy
- Arthralgia
(young black woman, presenting with dry cough and SOB)

Investigations:
- Serum ace
- Chest x-ray (hilar lymphadenopathy)
- HRCT (pulmonary nodules)
- PET scan (active areas of inflammation)
- Histology = gold standard (skin biopsy or bronchoscopy) shows non-caseating granulomas

Management:
May spontaneously resolve in 6 months in 60% of patients
- No treatment needed if no/mild symptoms (often resolves spontaneously)
- Oral corticosteroids (6-24 months)
- Methotrexate or Azathioprine if above doesn’t work

55
Q

Outline the complications of sarcoidosis (how it presents)

A

Lungs (mainly):
- Pulmonary fibrosis
- Nodules
- Mediastinal lymphadenopathy

Systemic:
- Fever
- Weight loss
- Fatigue

Liver:
- Nodules
- Cirrhosis
- Cholestasis

Eyes:
- Uveitis
- Conjunctivitis
- Optic neuritis

Skin:
- Erythema nodosum
- Lupus pernio

Heart:
- Heart block
- Heart failure

Kidneys:
- Kidney stones (hypercalcaemia)
- Calcium deposits
- Interstitial nephritis

CNS:
- Nodules e.g. in brain
- Pituitary involvement e.g. diabetes insipidus
- Encephalopathy

PNS:
- Bell’s palsy

56
Q

Which lung cancer is most associated with non-smokers

A

Adenocarcinomas of the lung

57
Q

Which lung cancer is almost always inoperable on presentation

A

Small cell carcinoma

Year 3 - Medicine (8 decks)

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