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Phase 2A revision > respiratory to work on > Flashcards

respiratory to work on Flashcards

1
Q

Briefly describe the pathophysiology of pneumonia

A
  • invasion and overgrowth of a pathogen in lung parenchyma
  • overwhelming of host immune defences
  • production of intra-alveolar exudates
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2
Q

Name 3 pathogens that can cause community acquired pneumonia (CAP)

A
  1. Streptococcus pneumoniae (most common)
  2. Haemophilus influenzae
  3. Mycoplasma pneumoniae
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3
Q

Name 3 pathogens that can cause hospital acquired pneumonia (HAP)

A

mainly gram negative

  1. Pseudomonas aeruginosa
  2. E.coli
  3. Klebsiella penumoniae
  4. Staphylococcus aureus
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4
Q

What symptoms might you see in someone with pneumonia?

A 
SOB
cough
sputum
fever
pleuritic chest pain
delirium
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5
Q

What signs might you see in someone with pneumonia?

A
  • increased resp rate and HR
  • hypotension
  • decreased O2 saturation
  • dull to percuss
  • increased tactile fremitus
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6
Q

What investigations might you do on someone you suspect has pneumonia?

A
  • FBC, U&E, CRP– increased WCC, urea and CRP
  • Sputum culture - MC+S
    Chest X ray: localised/widespread consolidation, effusion, abscesses, empyema
    Multi-lobar – strep pneumoniae, s. aureus
    Multiple abscesses – s. aureus
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7
Q

What is the treatment for someone with mild CAP (CRUB65 score 0-1)?

A

oral amoxicillin at home

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8
Q

What is the treatment for someone with moderate CAP (CRUB65 score 2)?

A

consider hospitalising, amoxicillin (IV or oral) + macrolide (clarithromycin)

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9
Q

What is the treatment for someone with severe CAP (CRUB65 score 3-5)?

A

consider ITU,

IV Co-Amoxiclav + macrolide (clarithromycin)

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10
Q

What is the treatment for someone with Legionella pneumoniae?

A

Fluoroquinolone + clarithromycin

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11
Q

What is the treatment for someone with Pseudomonas aeruginosa pneumonia?

A

IV ceftazidime + gentamicin

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12
Q

Give 3 potential complications of pneumonia

A
  1. Respiratory failure
  2. Hypotension
  3. Empyema
  4. Lung abscess
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13
Q

Describe the pathophysiology of bronchiectasis

A

Failed mucociliary clearance and impaired immune function means microbes easily invade and cause infection

This causes inflammation and progressive lung damage

Bronchitis –> bronchiectasis –> fibrosis

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14
Q

What can cause bronchiectasis?

A
  1. Congenital = Cystic fibrosis
  2. Idiopathic (50%)
  3. Post infection - (most common)
    • pneumonia,
    • TB,
    • whopping cough
  4. Bronchial obstruction
  5. RA
  6. Hypogammaglobulinaemia
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15
Q

Which bacteria might cause bronchiectasis?

A
  1. Haemophilus influenza (children)
  2. Pseudomonas aeruginosa (adults)
  3. Staphylococcus aureus (neonates often)
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16
Q

Give 3 symptoms of bronchiectasis

A
  1. Chronic productive cough
  2. Purulent sputum
  3. Intermittent haemoptysis
  4. Dyspnoea
  5. Fever, weight loss
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17
Q

Give 3 signs of bronchiectasis

A
  1. Finger clubbing
  2. Coarse inspiratory crepitate (crackles)
  3. Wheeze
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18
Q

What investigations might you do on someone to determine whether they have bronchiectasis?

A

CXR = kerley B lines, dilated bronchi with thickened walls, multiple cysts containing fluid

High resolution CT = bronchial wall dilation

Spirometry = obstructive lung disease

Sputum culture - h.influenzae is most common

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19
Q

Describe the treatment for bronchiectasis

A
  1. Antibiotics
  2. Anti-inflammatories (azithromycin)
  3. Bronchodilators (nebulised salbutamol)
  4. Chest physio - physical training
  5. Surgery = lung resection or transplant
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20
Q

Give 3 possible complications of Bronchiectasis

A
  1. Pneumonia
  2. Pleural effusion
  3. Pneumothorax
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21
Q

What are the main systemic consequences of CF?

A

Pancreatic insufficiency = dehydrated secretion –> enzymes stagnation
GI = intraluminal water deficiency –> concentrated bile
Resp = thick mucus can’t be cleared –> infection risk and inflammatory damage

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22
Q

How do children/young adults present with CF?

A
  • Cough and wheeze
  • Recurrent infections
  • Haemoptysis
  • Pancreatic insufficiency
  • Malabsorption
  • Male infertility
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23
Q

What are 3 possible respiratory complications of CF?

A
  1. Pneumothorax
  2. Respiratory failure
  3. Cor pulmonale
  4. Bronchiectasis
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24
Q

Give 3 signs of CF

A
  1. Clubbing
  2. Cyanosis
  3. Bilateral coarse crepitations
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25
Q

Name 3 associated conditions with CF

A
  1. Osteoporosis
  2. Arthritis
  3. Vasculitis
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26
Q

What investigations might you do to diagnose cystic fibrosis?

A

heel prick test - newborns

Sweat test = Na and Cl < 60 mmol/L

Genetic screening for common mutations

Faecal elastase - tests pancreatic enzyme function

Absent vas deferent and epididymis (males)

Microbiology - for infections

Spirometry

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27
Q

What is the management of CF?

A
  1. Physical therapies (airway clearance) and surveillance
  2. Antibiotics for infections and prophylaxis
  3. Bronchodilators
    - B2 agonist (SALBUTAMOL) and inhaled corticosteroids (BECLOMETASONE)
  4. Pancreatic enzymes replacement (creon)
  5. ADEK vitamin supplements
  6. Screening for consequent conditions - osteoporosis
  7. Bilateral lung transplant
    • must not have m. abscessus
  8. Vaccinations - flu and pneumococcal
  9. high calorie, high fat diet
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28
Q

what are the risk factors of lung cancer

A
  1. Smoking = main cause
  2. Asbestos
  3. Radon exposure
  4. Coal products
  5. pulmonary fibrosis
  6. HIV
  7. genetic factors
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29
Q

Which type of NSCC is most common in smokers?

A

Squamous cell carcinoma - it is most stronlgy associated with cigarette smoking

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30
Q

where does lung cancer commonly metastasise to?

A
  1. Bone
  2. Brain
  3. Lymph nodes
  4. Liver
  5. Adrenal
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31
Q

Give 4 symptoms of local disease lung cancer

A 
Persistent cough 
Shortness of breath
Haemoptysis
Weight loss
Chest pain, wheeze, recurrent infections
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32
Q

Give 4 symptoms of lung cancer that has metastasised

A
  1. Bone pain
  2. Headaches
  3. Abdominal pain
  4. Seizures
  5. Neuro deficit - Confusion
  6. Weight loss
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33
Q

Give 3 examples of paraneoplastic syndromes due to lung cancer

A
  • ↑PTH -> Hyperparathyroidism
  • ↑ADH -> SIADH
  • ↑ACTH -> Cushing’s disease
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34
Q

Name 3 differential diagnosis’s of lung cancer

A
  1. Oesophageal varices
  2. COPD
  3. Asthma
  4. Pneumonia
  5. Bronchiectasis
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35
Q

What investigations might you done on someone to determine whether they have lung cancer?

A

First line:
- CXR - central mass, hilar lymphadenopathy, pleural effusion
(a negative CXR does not rule out cancer)

  • CT chest, liver & adrenal glands – for staging
  • Sputum cytology - malignant cells in sputum
    (high specificity but mixed sensitivity)

diagnostic = biopsy + histology

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36
Q

What is the treatment for NSCLC?

A
  • Surgical excision for peripheral tumours with no metastatic spread
  • Curative radiotherapy is an alternative if respiratory reserve is poor - complications include radiation pneumonitis + fibrosis
  • Chemotherapy +/- radiotherapy for more advanced disease e.g. with monoclonal antibodies e.g. CETUXIMAB
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37
Q

What is the treatment for SCLC?

A

Limited disease = chemo + radio
Extensive = palliative chemo + care

• Superior vena cava stent + radiotherapy + dexamethasone for superior
vena cava obstruction

• Endobronchial therapy - used to treat symptoms of airway narrowing:

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38
Q

Give 4 possible complications of lung cancer

A
  1. SVC obstruction
  2. ADH secretion –> SIADH
  3. ACTH secretion –> Cushing’s
  4. Serotonin secretion –> carcinoid
  5. Peripheral neuropathy
  6. Pathological fractures
  7. Hepatic failure
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39
Q

Describe asthma

A

Chronic, inflammatory condition, causing episodes of reversible airway obstruction, due to:
Bronchoconstriction
Excessive secretion production

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40
Q

What are the 3 characteristic features of asthma?

A
  • Airflow limitation - usually reversible spontaneously or with treatment
  • Airway hyper-responsiveness
  • Bronchial inflammation with T lymphocytes, mast cells, eosinophils with associated plasma exudation
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41
Q

What is the mechanism behind hyper-reactivity?

A

Neurogenic inflammation

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42
Q

Describe neurogenic infalmmation

A

Sensory nerve activation initiates impulses which stimulates CGRP (pro-inflammatory)
this activates mast cells and innervates goblet cells

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43
Q

Describe the process of airway remodelling in asthma

A
  1. Hypertrophy and hyperplasia of smooth muscle cells narrow the airway lumen
  2. Deposition of collagen below the BM thickens the airway wall
  3. metaplasia occurs with an increase in number of mucus-secreting goblet cells
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44
Q

What type of T cell is involved in asthma?

A

CD4+

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45
Q

Extrinsic asthma: what happens when IgE binds to mast cells?

A

Vasodilative substances are released causing bronchoconstriction, oedema, bronchial inflammation and mucus hyper-secretion

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46
Q

Name 4 factors that can exacerbate asthma

A
  1. Allergens
  2. Viral infection
  3. Cold air
  4. Exercise
  5. Stress
  6. Cigarette smoke
  7. Drugs - NSAIDs/BB
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47
Q

What are the symptoms of asthma?

A
  1. Episodic cough
  2. Expiratory wheeze
  3. SOB
  4. often worse at night (and in the morning)
  5. Chest tightness
  6. dyspnoea
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48
Q

What are the signs of asthma?

A
  1. Tachypnoea - rapid breathing
  2. Audible wheeze
  3. Widespread polyphonic wheeze
  4. Cough
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49
Q

What are the signs of an acute asthma attack?

A
  1. Can’t complete sentences
  2. HR > 110 bpm
  3. RR > 35/min
  4. PEF < 50% predicted
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50
Q

What are the signs of a life threatening asthma attack?

A
  1. Hypoxia = PaO2 <8 kPa, SaO2 <92%
  2. Silent chest
  3. Bradycardia
  4. Confusion
  5. PEFR < 33% predicted
  6. Cyanosis
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51
Q

Give 3 differential diagnosis’s of asthma

A
  1. COPD
  2. Bronchial obstruction
  3. Pulmonary oedema
  4. Pulmonary embolism
  5. Bronchiectasis
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52
Q

What investigations might you do someone to determine whether they have asthma?

A
  1. PEFR
  2. Spirometry with reversibility testing (>5 years)
    - Obstructive pattern:
    • FEV1 <80% of predicted normal (reduced)
    • FVC = normal
    • FEV1/FVC ratio <0.7
      Peak flow measurement (reduced)
  3. CXR
  4. Atopy = skin prick, RAST
  5. Bloods = high IgE, Eosinophils
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53
Q

What is the long-term guideline mediation regime for asthma?

A
  1. SABA
  2. SABA + ICS
  3. SABA + ICS + LTRA
  4. SABA + ICS + LTRA/LABA + MART
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54
Q

Give 3 possible complications of asthma

A
  1. Exacerbation
  2. Pneumothorax
  3. Pneumonia
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55
Q

Describe the pathophysiology of chronic bronchitis

A

Airway inflammation –> fibrosis and luminal plugs –> decreased alveolar ventilation

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56
Q

Would a patient with chronic bronchitis be a ‘pink puffer’ or a ‘blue bloater’?

A

Blue bloater
Patient have low PaO2 and high PaCo2 –> cyanosis –> cor pulmonale
Cyanosis = blue

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57
Q

Describe the pathophysiology of emphysema

A

Dilation and destruction of the lung tissue distal to the terminal bronchioles
Enlarged alveoli + loss of elastic recoil = increased alveolar ventilation

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58
Q

Would a patient with emphysema be a ‘pink puffer’ or a ‘blue bloater’?

A

Pink puffer
Breathless but not cyanosed
Type 1 respiratory failure
Normal or near normal PaO2 and normal or low PaCO2

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59
Q

What are the main cells responsible for inflammation in COPD?

A

Neutrophils and macrophages

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60
Q

What type of T cell is involved in COPD?

A

CD8+

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61
Q

What can cause COPD?

A
  1. Genetic = alpha 1 antitrypsin deficiency
  2. Smoking = major cause
  3. Air pollution
  4. Occupational factors = dust, chemicals
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62
Q

Name 4 symptoms of COPD

A
  1. Dyspnoea
  2. Cough +/- sputum
  3. Expiratory wheeze
  4. Weight loss
  5. SOB
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63
Q

Give 4 signs of COPD

A
  1. Tachypnoea
  2. Barrel shaped chest
  3. Hyperinflantion
  4. Cyanosis
  5. Pulmonary hypertension
  6. Cor pulmonale
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64
Q

Give 3 differential diagnosis’s for COPD

A
  1. Asthma
  2. HF
  3. Pulmonary embolism
  4. Bronchiectasis
  5. Lung cancer
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65
Q

What investigations might you do to diagnose someone with COPD?

A 
Spirometry = FEV1:FVC < 0.7
CXR = hyperinflation, bullae, flat hemi-diaphragms, large pulmonary arteries 
FBC = exclude secondary polycythaemia
CT = Bronchial wall thickening, enlarged air spaces 
ECG = RA and RV hypertrophy 
ABG = decreased PaO2 +/- hypercapnia
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66
Q

Give 3 factors that can be used to establish a diagnosis of COPD

A
  1. Progressive airflow obstruction
  2. FEV1/FVC ratio < 0.7
  3. Lack of reversibility
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67
Q

What are the treatments for COPD?

A

general:

  • stop smoking (refer to cessation services)
  • pneumococcal vaccine
  • annual flu vaccine

step 1:
- SABA (salbutamol or terbutaline) or SAMA (ipratropium bromide)

step 2:

  • If no asthmatic / steroid response:
    • LABA (salmeterol)
    • LAMA (tiotropium)
  • If asthmatic / steroid response:
    • LABA (i.e. salmeterol)
    • ICS (i.e. budesonide)

step 3:
- long term oxygen therapy

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68
Q

Give 3 advantages and 1 disadvantage of using ICS in the treatment of COPD?

A

Advantages

  1. Improve QOL
  2. Improve lung function
  3. Reduce the likelihood of exacerbations

Disadvantages:
1. There is an increased risk of pneumonia

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69
Q

Give 3 possible complications of COPD

A
  1. Exacerbations
  2. Infection
  3. Respiratory failure
  4. Cor pulmonale
  5. Pneumothorax
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70
Q

Give 2 potential consequences of exacerbations of COPD/asthma

A
  1. Worsened symptoms
  2. Decreased lung function
  3. Negative impact of QOL
  4. Increased mortality
  5. Huge economic cost
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71
Q

What is the likely cause for an exacerbation of COPD?

A

Viral URTI

Bacterial infections

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72
Q

What is the treatment for an exacerbation of COPD?

A

Steroids (hydrocortisone / prednisolone)
+
nebulised bronchodilators (salbutamol / ipratropium bromide)
+
antibiotics

Physiotherapy → sputum clearance

If severe:
IV aminophylline (bronchodilator),
NIV (CPAP / BIPAP)

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73
Q

Give 3 ways in which subsequent exacerbations of COPD can be prevented

A
  1. Smoking cessation
  2. Vaccination
  3. LABA/LAMA/ICS
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74
Q

Give 3 functions of pleura

A
  1. Allows movement of the lung against the chest wall
  2. Coupling system between the lungs and chest wall
  3. Clearing fluid from the pulmonary interstitium
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75
Q

What does the pleural fluid contain?

A

Protein - albumin, globulin, fibrinogen

Mesothelial cells, monocytes and lymphocytes

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76
Q

what are the causes of a transudate pleural effusion?

A

fluid movement (systemic causes)

  1. Heart failure
  2. fluid overload
  3. Peritoneal dialysis
  4. Constrictive pericarditis
  5. hypoproteinaemia
    • cirrhosis
    • hypoaluminaemia
    • nephrotic syndrome
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77
Q

Name 3 causes of a exudate pleural effusion

A

inflammatory (local causes)

  1. Pneumonia
  2. Malignancy
  3. TB
  4. pulmonary infarction
  5. lymphoma
  6. mesothelioma
  7. asbestos exposure
  8. MI
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78
Q

How does a pleural effusion present?

A
  • SOB especially on exertion
  • Dyspnoea
  • Pleuritic chest pain
  • cough
  • Loss of weight (malignancy)
  • Chest expansion reduced on side of effusion
  • In large effusion the trachea may be deviated away from effusion
  • Stony dull percussion note on affected side
  • Diminished breath sounds on affected side
  • Decreased tactile vocal fremitus (vibration of chest wall when speaking)
  • Loss of vocal resonance
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79
Q

How might you diagnose a pleural effusion?

A

1st line: CXR =
blunt costophrenic angles, fluid in lung fissures, meniscus, tracheal and mediastinal deviation

USS - identify pleural fluid

aspiration (thoracentesis/pleural tap)

  • purulent = empyema (pus)
  • turbid (cloudy) = infected
  • milky = chylothorax
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80
Q

How would you treat a pleural effusion?

A

Dependent on cause
Fluid overload or congestive HF - diuretic
Infective - antibiotics
Large effusions often need aspiration or drainage

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81
Q

How can pneumothorax be classified?

A 
Spontaneous pneumothorax
Traumatic pneumothorax
Iatrogenic pneumothorax
Lung Pathology
Tension pneumothorax
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82
Q

How does a pneumothorax present?

A
  • Sudden onset dyspnoea and pleuritic chest pain
  • as the pneumothorax enlarges the patient becomes more breathless and may develop pallor and tachycardia
  • Reduced expansion
  • Hyper-resonant percussion
  • Diminished breath sounds
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83
Q

What investigation might you do in someone you suspect to have a pneumothorax?

A

CXR = translucency and collapse

ABG = in dyspnoeic patients check for hypoxia

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84
Q

What is the treatment for a pneumothorax?

A

Small primary spontaneous PTX (visible rim ≤ 2cm) and not SOB
- Consider discharge and follow up CXR in review

Large primary spontaneous PTX (visible rim >2cm) and/or SOB
- Needle aspiration
If not <2cm on repeat CXR insert chest drain and supplemental O2 if needed, admit.

  • Secondary Pneumothorax – requires chest drain if large/ needle aspiration if small, admission and high flow O2
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85
Q

Name a possible complication of a pneumothorax

A

Tension pneumothorax

86
Q

Describe the pathophysiology of a tension penumothorax

A

Pleural tear creates 1 way valve - air only goes into cavity –> increased unilateral pressure –> respiratory distress, shock and cardiac arrest

87
Q

What is the treatment for a tension pneumothorax?

A 
Put out cardiac arrest call
Start high flow O2
Immediate decompression
Unless tension PTX due to trauma:
“Insert a large bore cannula into the pleural space through the second intercostal space in the mid-clavicular line”

Hiss sound confirms diagnosis

88
Q

Define interstitial lung diseases

A

Distant cellular infiltrate and extracellular matrix deposition in lung distal to the terminal bronchioles - disease of the alveolar/capillary interface

89
Q

What are 5 major categories of interstitial lung disease

A
  1. Associated with systemic disease - rheumatological
  2. Environmental aetiology - fungal, dusts
  3. Granulomatous disease - sarcoidosis
  4. Idiopathic - idiopathic pulmonary fibrosis
  5. Other
90
Q

What are the 4 major features of interstitial lung disease?

A
  1. Cough
  2. Dyspnoea
  3. Restirictve spirometry
  4. Abnormal CXR/CT
91
Q

What is the pathology of interstitial lung disease?

A

Increased fibrous tissue within the lung parenchyma resulting in increased stiffness and decreased expansion

92
Q

What kind of disease is sarcoidosis?

A

Granulomatous disease - type of interstitial lung disease

93
Q

Describe the pathophysiology of sarcoidosis

A

Chronic inflammation –> non-caseating granuloma in various body sites

Typical sarcoid granulomas consist of focal accumulations of epithelioid cells, macrophages and lymphocytes - mainly T cells

94
Q

Give 3 pulmonary symptoms of sarcoidosis

A
  1. Dry cough
  2. Progressive SOB
  3. Wheeze
  4. Chest pain
95
Q

What is the effect of sarcoidosis on the skin?

A

Erythema nodosum

96
Q

What is the effect of sarcoidosis on the eyes?

A

Uveitis

97
Q

What is the effect of sarcoidosis on the bone?

A

Arthralgia

98
Q

What is the effect of sarcoidosis on the liver?

A

Hepatosplenmeagly

99
Q

What investigations might you do in someone who you suspect to have sarcoidosis?

A

Bloods = increase ESR, lymphopenia, increase CAE, raised LFTs

Bronchoalveolar lavage = increased lymphocytes

Lung tissue biopsy = diagnostic = non-caseating granulomata (increased lymphocytes in active disease and increased neutrophils in pulmonary fibrosis)

CXR = staging

100
Q

How can you stage sarcoidosis?

A

Using CXR
Stage 1 = bilateral hilar lymphadenopathy (BHL)
Stage 2 = pulmonary infiltrates with BHL
Stage 3 = pulmonary infiltrates without BHL
Stage 4 = progressive pulmonary fibrosis, bulla formation and bronchiectasis

101
Q

How do you treat acute sarcoidosis?

A

NSAIDs and bed rest

102
Q

How do you treat sarcoidosis?

A

do not treat symptomatic stage 1, and asymptomatic stage 2 or 3
patients with BHL do not need treatment - most recover spontaneously

acute = bed rest and NSAIDs

prednisolone orally
if severe = IV methylprednisolone
if steroid resistant = methotrexate (requires close monitoring)

lung transplant in severe cases

103
Q

Give 2 possible differential diagnosis’s for sarcoidosis

A
  1. Lymphoma

2. Pulmonary TB

104
Q

Describe the pathophysiology of idiopathic pulmonary fibrosis

A

repetitive injury to the alveoli epithelium causes wound healing mechanisms to become uncontrolled

this leads to fibroblast over-production and increased fibrosis

this leads to a loss of elasticity and ability to perform gas exchange is impaired -> restrictive lung disease and progressive respiratory failure

105
Q

what are the risk factors of idiopathic pulmonary fibrosis?

A
  • cigarette smoking
  • infectious agents - CMV, Hep C, EBV
  • occupational dust exposure
  • drugs - methotrexate, imipramine
  • GORD
  • genetic predisposition
106
Q

what are the clinical features of idiopathic pulmonary fibrosis

A
  1. Dry cough
  2. SOB on exertion
  3. Systemic = malaise, weight loss, arthralgia
  4. Cyanosis
  5. Finger clubbing
  6. bibasal crackles (Inspiratory crackles/crepitus)
  7. dyspnoea
107
Q

What investigations might you do in someone you suspect to have idiopathic pulmonary fibrosis?

A

ABG = type 1 respiratory failure

Bloods = raised CRP, immunoglobulins and check autoantibodies

CXR/CT = degreased lung volume + honeycomb lung

High resolution CT = ground glass appearance

Spirometry = restrictive

Lung biopsy = confirmation

108
Q

What is the treatment for idiopathic pulmonary fibrosis?

A

Pharmacological: Pirfenidone, nintedanib - antifibrotic

Non pharmacological: Smoking cessation, physiotherapy, vaccines up to date

Lung transplantation last resort

109
Q

what are the possible complications of idiopathic pulmonary fibrosis

A
  1. Respiratory failure

2. Cor pulmonale

110
Q

Define pulmonary hypertension

A

A disease of the small pulmonary arteries characterised by vascular proliferation and remodelling. It results in a progressive increase in pulmonary vascular resistance (PVR)

Increase in mean pulmonary arterial pressure >25 mmHg and secondary right ventricular failure

111
Q

What can cause an increase in mPAP?

A

Increase resistance to flow

Increased flow rate

112
Q

what are the causes of pulmonary hypertension

A
  • pre-capillary
    • multiple small PE’s
    • left-to-right shunts
    • primary
  • capillary
    • emphysema
    • COPD
  • Post-capillary
    • backlog of blood causes secondary hypertension
    • LV failure
  • chronic hypoxaemia
    • living at high altitude
    • COPD
113
Q

what is the clinical presenation of pulmonary hypertension

A

initial features - due to an inability to increase cardiac output

  • exertional dyspnoea
  • lethargy and fatigue
  • ankle swelling
  • Accentuated pulmonic component to the 2nd heart sound
  • Tricuspid regurgitation murmur
  • peripheral oedema, cyanosis
  • cor pulmonale
114
Q

What investigations might you do in someone to determine whether they have pulmonary hypertension?

A

Initial tests:
- CXR - Enlarged main pulmonary artery, enlarged hilar vessels and pruning.

  • ECG - right ventricular hypertrophy,right axis deviation, right atrial enlargement. (A normal ECG does not rule out the presence of significant pulmonary hypertension)
  • TTE - (trans-thoracic echocardiogram)

Diagnostic test: Right heart catheterisation

115
Q

Describe the treatment of pulmonary hypertension

A 
General supportive therapy:
       Treat underlying cause
       - Oral anticoagulants - WARFARIN
       - diuretics for oedema
       - oxygen 
       - oral CCBs
       - Supervised exercise training
       Avoiding pregnancy

In treatment-resistant patients:
Balloon atrial septostomy - produces right-to-left shunting that decompresses the right atrium and right ventricle, increases systemic cardiac output, and decreases systemic arterial oxygen saturation
Lung transplantation

116
Q

Give a possible complication of pulmonary hypertension

A

Cor pulmonale (RS HF) –> pleural effusion + death

117
Q

How is TB transmitted?

A

Aerosol transmission

118
Q

Describe pulmonary infection of TB

A

Bacilli settle in lung apex

Macrophages and lymphocytes mount an effective immune response that encapsulate and contains the organism forever

119
Q

Describe the pathogenesis of pulmonary TB disease

A

TB spread via respiratory droplets as it is an airborne infection
1. Alveolar macrophages ingest bacteria and the rods proliferate inside.

  1. Drain into hilar lymph nodes 🡪 present antigen to T lymphocytes 🡪 cellular immune response.
  2. Delayed hypersensitivity reaction 🡪 tissue necrosis and granuloma formation: caseating.
    • Primary Ghon Focus
    • Ghon Complex – Ghon focus + lymph nodes
120
Q

Give 3 risk factors for TB

A
  1. Living in a high prevalence area
  2. IVDU
  3. Homeless
  4. Alcohol
  5. HIV +ve
121
Q

What systemic symptoms might you see as a result of TB?

A
  1. Weight loss
  2. Night sweats
  3. Anorexia
  4. Malaise
  5. low grade fever
122
Q

What pulmonary symptoms might you see as a result of TB?

A 
Productive cough
Haemoptysis
Cough >3 weeks (dry or productive)
Breathlessness
Sometimes chest pain
123
Q

Name 3 places where TB might spread to?

A
  1. Bone and joint = pain and swelling
  2. Lymph nodes = pain and discharge
  3. CNS = TB meningitis
  4. Biliary TB = disseminated
  5. Abdominal TB = ascites, malabsorption
  6. GU TB = sterile pyuria, WBC in GU tract
124
Q

What investigations might you do to determine whether someone has TB?

A

Inflammatory markers = raised CRP, hyperalbuminaemia, thromobocytosis, high B cell count
CXR = consolidation, collapse, pleural effusion
Microbiology - sputum/biopsy = Ziehl-Neelson stain and culture

125
Q

A special culture medium is needed to grow TB, what is it called?

A

Lowenstein Jenson Slope

126
Q

What might a lymph node biopsy from someone with TB show?

A

Caseating granuloma

127
Q

What is the drug treatment commonly used for TB?

A

RIPE
RI = 6 months
PE = for first 2 months

R = rifampicin
I = isoniazid 
P = pyrazinamide
E = ethambutol
128
Q

Give 2 potential side effects of Rifampicin

A
  1. Red urine
  2. Hepatitis
  3. Drug interaction - it’s an enzyme inducer
129
Q

Give 2 potential side effects of Isoniazid

A
  1. Hepatitis

2. Neuropathy

130
Q

Give 2 potential side effects of Pyrazinamide

A
  1. Hepatitis
  2. Gout
  3. Neuropathy
131
Q

Give a potential side effect of Ethambutol

A

Optic neuritis

132
Q

Give 2 factors that can increase the risk of drug resistance in TB

A
  1. If the patient has had previous treatment
  2. If they live in a high risk area
  3. If they have contact with resistant TB
  4. If they have a poor response to therapy
133
Q

What is Whooping cough caused by?

A

Bordatella pertussis (gram -ve coccobacilli) - rod

134
Q

Describe the disease course of whooping cough

A

7-10 day incubation –> 1-2 week catarrhal stage –> 1-6 week paroxysmal stage

135
Q

What are the symptoms of whooping cough?

A

Paroxysmal cough - sudden and severe

Vomiting after cough

136
Q

What is the treatment of whooping cough?

A

Clarithromycin - in catarrhal or early paroxysmal stages

  • have little effect on disease course in paroxysmal stage
137
Q

How can you prevent whooping cough?

A

Pertussis vaccination

8, 12 and 16 weeks and a pre school booster

138
Q

Give 2 possible complications of whooping cough

A
  1. Pneumonia
  2. Encephalopathy
  3. Sub-conjunctival haemorrhage
139
Q

A patient presents with breathlessness. On examination they have absent breath sounds and their chest produces a stony dull sound on percussion. They have a PMH of heart failure. What is the likely cause of their symptoms?

A

Pleural effusion

140
Q

what is CFTR and what is it’s function?

A

• Transport protein on membrane of epithelial cells that acts as a chloride
channel
• Transports chloride ions
• Normally; it actively exports NEGATIVE IONS especially Cl- and Na+ passively follows causing an osmotic gradient and movement of water out of the cell and into the mucus

141
Q

what is the clinical presentation of the alimentary effects of cystic fibrosis?

A

• Thick secretions
• Reduced pancreatic enzymes (due to mucus blocking pancreatic duct)
• Pancreatic insufficiency (diabetes mellitus & steatorrhoea (fatty stools
since enzymes not released to digest fat)
• Distal intestinal obstruction syndrome - bowel obstruction (equivalent of
meconium ileus) resulting in reduced GI motility
• Reduced bicarbonate (HCO3-)
• Maldigestion & malabsorption thus poor nutrition (associated with
pulmonary sepsis)
• Cholesterol Gallstones (in increased frequency) & cirrhosis
• Increased incidence of peptic ulcers & malignancy

142
Q

what are the risk factors for pleural effusion?

A
  • Previous lung damage

- Asbestos exposure

143
Q

what are the risk factors for pneumothorax?

A 
Smoking
Family history
Male
Tall and slender build
Young age 
Presence of underlying lung disease
144
Q

what is the pathophysiology of pneumothorax?

A

Normally intrapleural pressure is negative

When there is a bridge between alveoli and pleural space or atmosphere and pleural space

Flow of air in until communication closed or gradient closed.

145
Q

what is the clinical presentation of a tension pneumothorax?

A 
Cardiopulmonary deterioration:
Hypotension – imminent cardiac arrest
Respiratory distress
Low sats
Tachycardia
Shock
Severe chest Pain
146
Q

what are the clinical features of a tension pneumothorax?

A

Tracheal deviation to contralateral side

Ipsilateral reduced breath sounds
Hyperresonance on percussion

Hypoxia

147
Q

what are the causes of pneumothorax?

A
  • In patients over 40 years of age the usual cause is underlying COPD
  • Other/rarer causes include:
    • Bronchial asthma
    • Carcinoma
    • Breakdown of a lung abscess leading to bronchopleural fistula
    • Severe pulmonary fibrosis with cyst formation
    • TB
    • Pneumonia
    • Cystic fibrosis
    • Trauma (penetrating or rib fracture)
    • Iatrogenic e.g. pacemakers or central lines
148
Q

what is the catarrhal phase of whooping cough?

A
  • Patient highly infectious
  • Cultures from respiratory cultures are positive in 90% of cases
  • Malaise
  • Anorexia
  • Rhinorhoea (nasal cavity congested with significant amount of mucus)
  • Conjunctivitis
149
Q

what is the paroxysmal phase of whooping cough?

A

• Begins 1 week later from catarrhal phase
• Coughing spasms
• Classic inspiratory whoop is only seen in younger individuals in whom
the lumen of the respiratory tract is compromised by mucus secretion
and mucosal oedema
• These coughing spasms usually terminate in vomiting
• Cough for more than 14 days

150
Q

what are the investigations for whooping cough?

A
  • Chronic cough and one clinical feature indicated pertussis
  • Chronic cough and history of contact or microbiological diagnosis is used to confirm pertussis
  • Suggested clinically by the characteristic whoop and history of contact with an infected individual
  • PCR test
  • But culture of a nasopharyngeal swab = definitive diagnosis
151
Q

what are the signs of TB?

A 
Signs of bronchial breathing
Dullness to percuss
Decreased breathing
fever
crackles
152
Q

what is the treatment for pneumonia?

A

Maintaining O2 Sats between 94-98%
In COPD patients: maintain O2 sats between 88-92%
Analgesia: paracetamol or NSAIDs
IV fluids

153
Q

which bacteria causes rusty sputum in pneumonia?

A

strep pneumoniae

154
Q

what are the common organisms that cause atypical pneumonia?

A

Mycoplasma pneumoniae,
Chlamydophila pneumoniae,
Legionella pneumophila
coxiella burnetii

155
Q

what are the characteristic symptoms of atypical pneumonia?

A

headache
low-grade fever
cough
malaise

156
Q

what is the mechanism of action for rifampicin for TB?

A

bactericidal - blocks protein synthesis

157
Q

what is the mechanism of action of isoniazid for TB?

A

bactericidal - blocks cell wall synthesis

158
Q

what is the mechanism of action for pyrazinamide for TB?

A

bactericidal initially, less effective later

159
Q

what is the mechanism of action for ethambutol

A

bacteriostatic - blocks cell wall synthesis

160
Q

what antibiotics are used for bronchiectasis?

A
  • pseudomonas aeruginosa = oral ciprofloxacin
  • h.influenzae = oral amoxycillin, co-amoxyclav or doxycycline
  • staph aureus = flucloxacillin
161
Q

what is the pathophysiology of goodpasture’s syndrome?

A

Specific autoimmune disease caused by a type II antigen-antibody reaction leading to diffuse pulmonary haemorrhage, glomerulonephritis (and often acute kidney injury and chronic kidney disease)

  • There are circulating anti-glomerular basement membrane (anti-GBM) antibodies
162
Q

what is the characteristic presentation of COPD?

A 
productive cough
white or clear sputum
wheeze
SOB
following many years of smoking
163
Q

what are the systemic effects of COPD?

A 
hypertension
osteoporosis
depression
weight loss
reduced muscle mass with general weakness
164
Q

which is the most common lung cancer in non-smokers?

A

adenocarcinoma

165
Q

where does adenocarcinoma arise from?

A

mucus-secreting glandular cells

166
Q

what is the pathophysiology of pulmonary hypertension?

A

The main vascular changes are:
Vasoconstriction
Smooth-muscle cell and endothelial cell proliferation
Thrombosis

167
Q

what is centri-acinar emphysema?

A
  • Distension and damage of lung tissue is concentrated around the respiratory bronchioles, whilst the more distal alveolar ducts and alveoli tend to be well preserved
  • Extremely common
168
Q

what is pan-acinar emphysema?

A
  • Less common
  • Distension and destruction affect the whole acinus and in severe cases the lung is just a collection of bullae
  • Associated with alpha-1 antitrypsin deficiency
169
Q

what is irregular emphysema?

A

• Scarring and damage that affects the lung parenchyma

patchily, independent of acinar structure

170
Q

what are the signs of emphysema?

A 
Dyspnoea / Tachypnoea
Minimal cough
Pink skin, pursed-lip breathing
Accessory muscle use
Cachexia
Hyperinflation (barrel chest)
Weight loss (due to increased work of breathing and cachexia)
171
Q

what are the complications of emphysema?

A

Pneumothorax due to bullae

172
Q

what are the investigations for IE COPD?

A

ABG

  • CO2 retention → acidosis
  • Raised pCO2 + low pO2 = T2RF

Chest X-Ray, sputum culture + sensitivities for antibiotic therapy, FBC + U&E

173
Q

what is extrinsic (atopic) allergic asthma?

A
  • Occurs most frequently in atopic individuals

- Childhood asthma often accompanied by eczema

174
Q

what is intrinsic allergic asthma?

A
  • Often starts in middle-aged and attacks are usually triggered by respiratory infections
175
Q

what are the genetic factors for asthma?

A
  • Genes controlling the production of cytokines IL-3,-4,-5,-9 & -13
  • ADAM33 is associated with airway hyper-responsiveness and tissue remodelling
176
Q

what are the environmental factors for asthma?

A

• Early childhood exposure to allergens and maternal smoking has a
major influence on IgE production
• Growing up in a ‘clean’ environment may predispose towards an IgE
response to allergens whereas growing up in a ‘dirtier’ environment may
allow the immune system to avoid developing allergic responses

177
Q

what are the risk factors for developing asthma

A
  • Personal history of atopy
  • Family history of asthma or atopy
  • Obesity
  • Inner-city environment
  • Premature birth (low birth weight, not breast-fed)
  • Socio-economic deprivation
  • exposure to allergens
178
Q

which drugs can trigger asthma attacks?

A

NSAIDs and aspirin

beta blockers - results in bronchoconstriction which results in airflow limitation and potential attack

179
Q

what is the acute management of asthma?

A
  1. oxygen
  2. salbutamol nebuliser
  3. ipratropium bromide nebuliser
  4. hydrocortisone IV or oral prednisolone
  5. IV magnesium sulfate
  6. aminophylline / IV salbutamol
180
Q

give 2 examples of SABAs

A
  • salbutamol (partial agonist)

- terbutaline

181
Q

what is the mechanism of action for SABAs?

A
  • are beta-2 selective

- bind to B2 receptor causing more cAMP which leads to more bronchodilation

182
Q

give 2 examples of LABAs

A
  • salmeterol

- formoterol (full agonist)

183
Q

what is the mechanism of action for LABAs?

A
  • are beta-2 selective
  • bind to B2 receptor causing more cAMP which leads to more bronchodilation
  • are longer acting since more lipophilic so remain in the body for longer
184
Q

give an example of a SAMA

A

ipratropium

185
Q

what is the mechanism of action for SAMA?

A
  • Act on airway M3 receptors

- prevent ACh from binding since they bind to the M3 receptor thereby blocking ACh action

186
Q

give an example of a LAMA

A

tiotropium

187
Q

what is the mechanism of action for LAMA?

A
  • Act on airway M3 receptors
  • prevent ACh from binding since they bind to the M3 receptor thereby blocking ACh action
  • has high affinity and disassociates slowly from muscarinic receptors
188
Q

what is the mechanism of action for ICS?

A
  • They reduce the number of inflammatory cells in the airways
  • Suppress production of chemotactic mediators
  • Reduce adhesion molecular expression
  • Inhibit inflammatory cell survival in the airway
  • Suppress inflammatory gene expression in airway epithelial cells
189
Q

what are the side effects of ICS?

A

Loss of bone density
Adrenal suppression
Cataracts
Glaucoma

190
Q

what is the effect of interaction between beta-2 agonists and glucocorticoids in the treatment of asthma?

A
  • glucocorticoids increase the transcription of B2-receptor gene, resulting in increased expression of cell surface receptors
  • Long acting B2 agonists increase the translocation of GR from cytoplasm to the nucleus after activation by glucocorticoids
  • Leads to greater overall efficacy and need for lower doses
191
Q

what are the advantages of inhaled drugs?

A
  • lungs are robust -> can handle repeated exposure
  • very rapid absorption
  • large SA
  • fewer drug metabolising enzymes
  • non-invasive port of entry
  • fewer systemic side effects
192
Q

what are the risk factors for developing pneumonia?

A
  • under 16 or over 65
  • HIV infection
  • DM
  • CF
  • COPD
  • smoking
  • excess alcohol
  • IVDU
  • immunosuppressant therapy
193
Q

what is a Ghon complex?

A

Ghon focus + lymph nodes

194
Q

what are the extra-pulmonary manifestations of lung cancer?

A

Recurrent laryngeal nerve palsy - hoarse voice

Superior vena cava obstruction - facial swelling, distended veins in neck and upper chest, Pemberton’s sign

Horner’s syndrome - ptosis, miosis, anhidrosis

195
Q

what scoring system is used to measure the risk of PE?

A

Wells score

196
Q

what is the management for PE?

A
  • if investigations are delayed start anticoagulation

1st line = apixaban/rivaroxaban

LMWH for 5 days followed by dabigatran
3 months for provoked
>3 months for unprovoked

IVC filter

197
Q

what is the management for haemodynamic instability caused by a PE?

A
  • IV thrombolysis - alteplase
  • catheter directed thrombolysis
  • embolectomy
198
Q

what are the most common causes of pharyngitis?

A

group A strep = most common

EBV

199
Q

what are the clinical features of pharyngitis?

A 
Sore throat → difficulty swallowing
Fever 
Headache
Joint pain/ muscle ache
Skin rashes
Swollen lymph nodes in neck
200
Q

what are the clincial features of pharyngitis that suggest a viral cause?

A

runny nose, blocked nose, sneezing, cough

201
Q

what are the clinical features of pharyngitis that suggest a bacterial cause?

A

fever, pharyngeal exudate, cervical lymphadenopathy, absence of cough + runny nose

202
Q

what are the investigations for pharyngitis?

A

rapid antigen detection test (RADT)

throat culture

203
Q

what is the management for pharnygitis?

A

group A strep = phenoxymethylpenicillin (clarithromycin if allergic to penicillin)

viral = self resolving, supportive care

204
Q

what are the most common causes of sinusitis?

A

Common infectious agents:
Streptococcus pneumoniae
Haemophilus influenzae
Rhinoviruses

205
Q

what are the risk factors for sinusitis?

A

nasal pathology e.g. septal deviation or nasal polyps
recent local infection e.g. rhinitis or dental extraction
swimming/diving
smoking

206
Q

what is the clinical presentation of sinusitis caused by bacteria?

A 
symptoms > 10 days
purulent nasal discharge
nasal obstruction
dental/facial pain
headache
207
Q

what is the clincial presentation of sinusitis caused by virus?

A

symptoms < 10 days
clear nasal discharge
fever
sore throat

208
Q

what is the management for sinusitis?

A

Symptom management with analgesia and intranasal decongestants

intranasal corticosteroids considered if symptoms have been present for >10 days

Antibiotic therapy not normally required but may be given for severe presentations (phenoxymethylpenicillin first-line)

209
Q

what is the clinical diagnosis of chronic bronchitis?

A

cough/sputum for more than 3 months in 2 consecutive years

210
Q

what are the signs of COPD on CXR?

A

hyperinflation
bullae
flat hemidiaphragm

211
Q

what are the signs that long term oxygen therapy is required in COPD?

A
  • FEV1 < 30% predicted value
  • cyanosis
  • polycythaemia
  • peripheral oedema
  • raised JVP
  • O2 less than or equal to 92% on room air
212
Q

what is the treatment for latent TB?

A

rifampicin
isoniazid

RI for 6 months
I for 3 months

Phase 2A revision (38 decks)

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