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PHASE 2A > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Define pneumonia

A

Inflammation of the lung parenchyma

Acute low respiratory tract infection

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2
Q

How can pneumonia be anatomically classified?

A
  1. Bronchopneumonia = diffuse, patchy infection of different lobes
  2. Lobar pneumonia = localised consolidation of a single lobe
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3
Q

How can pneumonia be aetiologically classified?

A
  1. Community acquired pneumonia = person with no underlying immunosuppression or malignancy
  2. Hospital acquired pneumonia = >48 hours after hospital admission
  3. Aspiration pneumonia = acute aspiration of gastric contents into lungs
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4
Q

Briefly describe the pathophysiology of pneumonia

A

Pathogen colonises pharynx –> translocated to distal airways –> alveolar macrophage response is overwhelmed
Inflammatory response + pathogenic features –> airway exudate and parenchyma damage

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5
Q

What can cause pneumonia to be severe?

A
  1. Excessive inflammation
  2. Lung injury
  3. Resolution failure
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6
Q

What protective features does the respiratory tract have against pathogens?

A

Teeth, commensal bacteria, swallowing reflex, mucociliary escalator, coughing, sneezing etc.

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7
Q

Name 3 groups of people who might be at risk of pneumonia

A
  1. Elderly
  2. Children
  3. COPD patients
  4. Immunocompromised people
  5. Nursing home residents
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8
Q

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

A
  1. Streptococcus pneumoniae
  2. Haemophilus influenzae
  3. Mycoplasma pneumoniae
  4. Staphylococcus aureus
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9
Q

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

A
  1. Pseudomonas aeruginosa
  2. E.coli
  3. Klebsiella penumoniae
  4. Staphylococcus aureus
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10
Q

Name 3 pathogens that can cause pneumonia in immunocompromised patients

A
  1. Bacterial pathogens (CAP)
  2. Fungal - pneumocystis jirovecii (PCP), Aspergillus
  3. Viral - CMV, adenovirus
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11
Q

What symptoms might you see in someone with pneumonia?

A
  1. Fever, sweats and rigors
  2. Cough +/- rusty sputum
  3. SOB
  4. Pleuritic chest pain
  5. Fatigue and malaise
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12
Q

What signs might you see in someone with pneumonia?

A
  1. Raised HR and RR
  2. Lung consolidation - dull percussion, crackles and wheezes
  3. Pleural effusion
  4. Hypoxia
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13
Q

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

A

CXR = consolidation
FBC (WCC )
Biochemistry - LFTs, renal function, U+Es
CRP and ESR = severity
Microbiology - sputum culture, blood culture, serology

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14
Q

How can you assess the severity of community acquired pneumonia?

A 
CURB65 score (1 point for each)
- Confusion 
- Urea >7 mmol/L
- RR > 30/min
- BP <90/60 mmHg
- Age >65 
Scores
0-1 = mild 
2 = admit to hospital 
3-4 = severe, admit and monitor closely 
5 = ITU transfer
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15
Q

How can pneumonia be prevented?

A

Children have pneumococcal vaccine
At risk groups have pneumococcal and influenza vaccination
Smoking cessation

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16
Q

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

A

Amoxicillin OR clarithromycin

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17
Q

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

A

Amoxicillin AND clarithromycin

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18
Q

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

A

IV co-amoxiclav AND clarithromycin

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19
Q

What is the treatment for someone with Legionella pneumoniae?

A

Fluoroquinolone + clarithromycin

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20
Q

What is the treatment for someone with Pseudomnoas aeruginosa pneumonia?

A

IV ceftazidime + gentamicin

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21
Q

What is the treatment for early onset HAP?

A

Metronidazole OR beta lactam + beta lactase inhibitor

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22
Q

What is the treatment for late onset HAP?

A

Linezolid/vancomycin OR IV colistin

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23
Q

A 66 y/o patient presents to you with fever and a productive cough. On examination you notice they are their confused. Their vital signs are: RR - 35; BP - 80/55 and HR: 130. You measure their urea and it comes back at 8mmol/L

a) What is this patients CURB65 score?
b) Where should they be treated?
c) Describe the treatment for this patient

A

a) Their CURB65 score is 5
b) This patient should be treated in hospital and admitted to critical care
c) The patient should be given IV co-amoxiclav and clarithromyocin

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24
Q

Give 3 potential complications of pneumonia

A
  1. Respiratory failure
  2. Hypotension
  3. Empyema
  4. Lung abscess
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25
Q

What is empyema?

A

Pus filled cavities

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26
Q

Give 3 signs of empyema

A
  1. WBC/CRP don’t settle with Abx
  2. Pain on deep inspiration
  3. Pleural collection
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27
Q

What is the treatment for empyema?

A

Drainage

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28
Q

Give 3 risk factors for lung abscess

A
  1. Aspiration
  2. Alcoholics
  3. Poor dental hygiene
  4. Bronchial obstruction
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29
Q

How is a lung abscess treated?

A

Surgical drainage and antibiotics

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30
Q

Define bronchiectasis

A

Chronic infection of the bronchi/bronchioles leading to permanent dilation and thinning of the airways

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31
Q

Describe the pathophysiology of bronchiectasis

A

Failed mucociliary clearance and impaired immune function –> microbes easily invade and cause infection –> inflammation –> progressive lung damage
Bronchitis –> bronchiectasis –> fibrosis

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32
Q

What can cause bronchiectasis?

A
  1. Congenital = CF
  2. Idiopathic (50%)
  3. Post infection - pneumonia, TB, whopping cough
  4. Bronchial obstruction
  5. RA
  6. Hypogammaglobulinaemia
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33
Q

Which bacteria might cause bronchiectasis?

A
  1. Haemophilus influenza (children)
  2. Pseudomonas aeruginosa (adults)
  3. Staphylococcus aureus (neonates often)
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34
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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35
Q

Give 3 signs of bronchiectasis

A
  1. Finger clubbing
  2. Coarse inspiratory crepitate (crackles)
  3. Wheeze
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36
Q

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

A

CXR = dilated bronchi with thickened walls
High resolution CT = bronchial wall dilation
Spirometry = obstructive lung disease
Sputum culture

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37
Q

Describe the treatment for bronchiectasis

A
  1. Antibiotics
  2. Anti-inflammatories
  3. Bronchodilators
  4. Chest physio
  5. Surgery = lung resection or transplant
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38
Q

Give 3 possible complications of Bronchiectasis

A
  1. Pneumonia
  2. Pleural effusion
  3. Pneumothorax
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39
Q

A lady who has recently had pneumonia presents to you with SOB and chronic cough. She is producing copious amounts of purulent sputum. What is the likely diagnosis?

A

Bronchiectasis

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40
Q

Describe the pathogenesis of Cystic fibrosis

A

AR defect in chromosome 7 coding (commonly F508) CFTR protein
Cl- transport affect
Decrease Cl secretion and increase Na reabsorption –> increase H2O reabsorption –> thickened mucus secretion

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41
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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42
Q

How is CF passed on?

A

Autosomal recessive condition

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43
Q

How does neonate present with CF?

A
  • Failure to thrive
  • Meconium ileus (sticky intestine)
  • Rectal prolapse
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44
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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45
Q

What are 3 possible respiratory complications of CF?

A
  1. Pneumothorax
  2. Respiratory failure
  3. Cor pulmonale
  4. Bronchiectasis
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46
Q

Give 3 signs of CF

A
  1. Clubbing
  2. Cyanosis
  3. Bilateral coarse crepitations
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47
Q

Name 3 associated conditions with CF

A
  1. Osteoporosis
  2. Arthritis
  3. Vasculitis
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48
Q

What investigations might you do to diagnose cystic fibrosis?

A

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
Spirometry

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49
Q

What is the management of CF?

A
  1. Physical therapies (airway clearance) and surveillance
  2. Antibiotics for infections and prophylaxis
  3. Bronchodilators
  4. Pancreatic enzymes replacement (creon)
  5. ADEK vitamin supplements
  6. Screening for consequent conditions - osteoporosis
  7. Bilateral lung transplant
  8. Vaccinations - flu and pneumococcal
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50
Q

Infection with a gram negative bacteria is a particular concern in patients with CF. What is this organism and how can infection be prevented?

A
  • Pseudomonas Aeruginosa

- Nebulised anti-pseudomonal antibiotic therapy and regular sputum cultures

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51
Q

Malignant bronchial tumour can be divided into 2 groups, what are they?

A
  1. Non small cell lung carcinoma (80%)

2. Small cell lung carcinoma (20%)

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52
Q

What type of malignant bronchial tumour tends to have a worse prognosis?

A

Small cell lung carcinomas - often metastasise

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53
Q

From what cells are small cell carcinomas derived from and what is the significance of this?

A

Neuroendocrine cells

Can secrete peptide hormones - ACTH, PTHrP, ADH, HCG

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54
Q

Give 3 main cell types the make up non-small cell lung cancers

A
  1. Squamous cell (20%) - arise from epithelial cells + associated with keratin production
  2. Adenocarcinoma (40%) - originate from mucus-secreting glandular cells
  3. Large cell
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55
Q

Name 3 types of benign lung cancer

A
  1. Hamartoma
  2. Lipoma
  3. Chondroma
  4. Leiomyoma
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56
Q

Give 4 causes of lung cancer

A
  1. Smoking = main cause
  2. Asbestos
  3. Radon
  4. Coal products
  5. Chromium
  6. Arsenic
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57
Q

Which type of NSCC is most common in smokers?

A

Squamous cell carcinoma

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58
Q

Which type of malignant bronchial tumour fits into TNM staging?

A

Non small cell carcinoma

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59
Q

What does TNM stand for in lung cancer?

A 
T = size/invasion = T1 (<3cm) --> T2 (>3cm) --> T3 (chest wall/diaphragm) --> T4 (heart + vessels)
N = nodal involvement = N1 (hilar) --> N2 (ipsilateral mediastinal) --> N3 (contralateral mediastinal)
M = metastases = M0 (no metastases) --> M1 (metastases)
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60
Q

Name 4 places lung cancer can metastasise to

A
  1. Bone
  2. Brain
  3. Lymph nodes
  4. Liver
  5. Adrenal
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61
Q

Name 4 cancers that can metastasise to the lungs

A
  1. Breast
  2. Prostate
  3. Colorectal
  4. Melanoma
  5. Thyroid
  6. Lymphoma
  7. Kidney
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62
Q

Give 4 symptoms of local disease lung cancer

A
  1. Chest pain
  2. SOB
  3. Haemoptysis
  4. Cough
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63
Q

Give 4 symptoms of lung cancer that has metastasised

A
  1. Bone pain
  2. Headaches
  3. Abdominal pain
  4. Seizures
  5. Confusion
  6. Weight loss
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64
Q

What are paraneoplastic syndromes?

A

Disorders triggered by immune response to a neoplasm

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65
Q

Give 3 examples of paraneoplastic syndromes due to lung cancer

A
  1. Anorexia
  2. Weight loss
  3. Finger clubbing (hypertrophy pulmonary OA)
  4. Hypercalcaemia
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66
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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67
Q

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

A 
CXR = consolidation or collapse 
CT scan = tumour staging 
Bronchoscopy = biopsy 
PET scan
Bloods
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68
Q

How does PET scanning work?

A

FDG is taken up by rapidly dividing cells

Tumour therefore appear ‘hot’ on the scan

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69
Q

What can cause:
a) false positive
b) false negative
on a PET scan?

A

a) Infection and inflammation

b) Small lesions

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70
Q

What tests might you do on a patient with lung cancer to determine whether they’re fit for an operation?

A
  1. ECG
  2. Lung function tests
  3. Determine performance status
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71
Q

What is the treatment for NSCLC?

A

Prevention = smoking cessation and avoid enivronemtnal carcinogens
Stage 1-2 = resection –> radio + chemo
Stage 3-4 = chemo + radio –> palliative care

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72
Q

What is the treatment for SCLC?

A

Limited disease = chemo + radio

Extensive = palliative chemo + care

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73
Q

Why is the 5 year lung cancer survival rate so low?

A

Only 8-10%

Often present very late, so treatment is much harder

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74
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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75
Q

What does the medullas detect?

A

The pH (H+ conc) of the CSF

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76
Q

What do carotid and aortic bodies detect?

A

Chemoreceptors respond to increased CO2 and decreased O2 levels

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77
Q

What is type 1 respiratory failure?

A

Hypoxia = low PaO2

PaCO2 is normal or low due hyperventilation

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78
Q

What is type 2 respiratory failure?

A

Hypoxia and hypercapnoea = Low PaO2 and increase PaCO2

There is alveolar hypoventilation (CO2 enters alveoli, but not removed)

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79
Q

Give 3 signs of hypercapnoea

A
  1. Bounding pulse
  2. Flapping tremor
  3. Confusion
  4. Drowsiness
  5. Reduced consciousness
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80
Q

What can cause type 1 respiratory failure?

A
  1. Airway obstruction
  2. Failure of O2 to diffuse into the blood
  3. V/Q mismatch
  4. Alveolar hypoventilation
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81
Q

What can cause type 2 respiratory failure?

A

Alveolar hypoventilation

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82
Q

Give examples of diseases that can obstruct the airway (could lead to type 1 respiratory failure)

A
  1. COPD
  2. Asthma
  3. Obstructive sleep apnoea
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83
Q

Name 3 things that lead to alveolar hypoventilation (could lead to type 1 and type 2 respiratory failure)

A
  1. Emphysema
  2. Obesity
  3. Neuromuscular weakness - MND
  4. Chest wall deformity
  5. Opiates
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84
Q

Give examples of diseases that lead to a failure of O2 to diffuse into the blood (could cause type 1 respiratory failure)

A
  1. Interstitial lung disorders - pulmonary fibrosis, sarcoidosis
  2. Emphysema
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85
Q

Give examples of diseases that lead to V/Q mismatch (could cause type 1 respiratory failure)

A
  1. Cardiac failure
  2. Pulmonary embolism
  3. Shunts
  4. Pulmonary hypertension
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86
Q

Give 4 signs and symptoms of type 1 respiratory failure

A

= Hypoxia

  1. Cyanosis
  2. Tachypnoea
  3. Tachycardia
  4. Hypotension
  5. Confusion
  6. Dyspnoea
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87
Q

Give 4 signs and symptoms of type 2 respiratory failure

A
  1. Dyspnoea
  2. Anxiety
  3. Orthopnoea
  4. Disturbed sleep
  5. Frequent chest infections
  6. Confusion
  7. Flapping temor
  8. Bounding pulses
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88
Q

What treatments might be given for V/Q mismatch?

A

Ventilation support - CPAP, BIPAP

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89
Q

What is continuous airway pressure (CPAP)?

A

Ventilation support given to people with obstructive sleep apnoea
Improves gaseous exchange

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90
Q

What is bilevel positive airway pressure (BIPAP)?

A

Ventilation support given to those who have had acute exacerbation of COPD
Improves ventilation to perfused alveoli - pressure decreases when breathing out, and increases when breathing in

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91
Q

What happens to the FEV1, FVC and FEV1/FVC ratio in an obstructive lung disease?

A

FEV1 < 80% predicted
FVC = normal
FEV1/FVC ratio <0.7

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92
Q

What happens to the FVC and FEV1/FVC ratio in a restrictive lung disease?

A

FVC = reduced

FEV1/FVC ratio = normal

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93
Q

If the trachea, bronchi and bronchioles are involved in a disease process, is this likely to be an obstructive or a restrictive disease?

A

Obstructive

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94
Q

If the lung parenchyma are involved in a disease process, is this likely to be an obstructive or a restrictive disease?

A

Restrictive

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95
Q

If the chest wall is involved in a disease process, is this likely to be an obstructive or a restrictive disease?

A

Restrictive

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96
Q

Give an example of a reversible obstructive lung disease

A

Asthma

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97
Q

Give an example of a irreversible obstructive lung disease

A

COPD

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98
Q

What is the effect of COPD on residual volume and total lung capacity?

A

RV and TLC are increased

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99
Q

Give an example of a restrictive lung disease

A

Pulmonary fibrosis

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100
Q

Is total lung capacity increased or decreased in restrictive lung diseases?

A

Decreased

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101
Q

Is total lung capacity increased or decreased in obstructive lung diseases?

A

Increased

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102
Q

Define inspiratory reserve volume (IRV)

A

The additional volume of air that can be forcibly inhaled after a tidal volume inspiration

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103
Q

Define expiratory reserve volume (ERV)

A

The additional volume of air that can be forcibly exhaled after a tidal volume expiration

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104
Q

Define forced vital capacity (FVC)

A

The maximum volume of air that can be forcibly exhaled after maximal inhalation

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105
Q

Define total lung capacity (TLC)

A

The vital capacity plus the residual volume. It is the maximum amount the lungs can hold
TLC = VC + RV
TLC = TV + FRC + IRV

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106
Q

Define residual volume (RV)

A

The volume of air remaining in the lungs after a maximal exhalation

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107
Q

Define functional residual capacity (FRC)

A

The volume of air remaining in the lungs after a tidal volume exhalation
FRC = ERV + RV

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108
Q

Define tidal volume (TV)

A

The volume of air moved in and out of the lungs during a normal breath
Normal = 500ml

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109
Q

Define FEV1

A

The volume of air that can be forcibly exhaled in 1 second

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110
Q

Define peak expiratory flow (PEF)

A

The greatest rate of airflow that can be obtained during forced expiration. Age, sex and height can all affect PEF

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111
Q

What is the transfer coefficient?

A

The ability of O2 to diffuse across the alveolar membrane

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112
Q

How can you find the transfer coefficient?

A

Inspired small amount of CO then hold breath for 10 seconds at total lung capacity then gas transferred is measured

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113
Q

Name 3 disease that might have a low transfer coefficient

A
  1. Emphysema
  2. Anaemia
  3. Fibrosis alveolitis
  4. Pulmonary hypertension
  5. Pulmonary fibrosis
  6. COPD
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114
Q

Name a disease that might have a high transfer coefficient

A

Pulmonary haemorrhage

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115
Q

What is consolidation on a CXR?

A

Regions of lung filled with liquid

Area appear white - dense

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116
Q

What might be released on mast cell degranulation?

A
  1. Pre-formed histamine
  2. Newly synthesised eicosanoids - cysteine leukotrienes and prostaglandin D2
  3. Cytokines - IL-3,4,5
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117
Q

What is IL-5 responsible for?

A

Pro-inflammatory and eosinophil survival

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118
Q

What is IL-3 responsible for?

A

Increases the number of mast cells

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119
Q

What is IL-4 responsible for?

A

IgE synthesis

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120
Q

What is the eicosanoid pathway?

A

Phospholipid –> arachidonic acid (by phospholipase A2) –> leukotrienes (by 5-lipooxygenase) or prostaglandins (by Cyclooxygenase)

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121
Q

What are the lung mast cell mediators that are responsible for bronchoconstriction?

A

Cysteine leukotrienes and histamine

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122
Q

What are the lung mast cell mediators that are responsible for inflammation?

A

Cysteine leukotrienes, cytokines and histamine

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123
Q

What are the lung mast cell mediators that are responsible for airway remodelling?

A

Cysteine leukotrienes, cytokines and enzymes

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124
Q

Describe asthma

A

Episodic, reversibile airway obstruction due to bronchial hyperactivity to a variety of stimuli

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125
Q

What are the 3 characteristic features of asthma?

A
  1. Airflow obstruction
  2. Hyper-responsive airways to a range of stimuli
  3. Bronchial inflammation
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126
Q

Give 3 reasons why the airways are hyperactive in asthmatics

A
  1. Inflammatory infiltrate
  2. Eosinophils
  3. Epithelium destruction gives easier access to bronchoconstrictors
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127
Q

What is the mechanism behind hyper-reactivity?

A

Neurogenic inflammation

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128
Q

Describe neurogenic infalmmation

A

Sensory nerve activation initiates impulses –> stimulates CGRP (pro-inflammatory) –> activated mast cells and innervates goblet cells

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129
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. Eosinophils play a role
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130
Q

What type of T cell is involved in asthma?

A

CD4+

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131
Q

What 2 categories can asthma be divided into?

A
  1. Allergic asthma (extrinsic), atopic, IgE and mast cell involvement
  2. Non allergic asthma (intrinsic)
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132
Q

Define atopy

A

The tendency to develop IgE mediated response to common aeroallergens

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133
Q

What is allergic asthma?

A

When an innocuous allergen triggers an IgE mediated response
Immune recognition processes are faulty –> increase IgE, IL3,4,5, production

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134
Q

What is non-allergic asthma?

A

Airway obstruction induced by exercise, cold air and stress

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135
Q

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

A

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

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136
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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137
Q

What occupations can be associated with an increase risk of developing asthma?

A
  1. Paint sprayers
  2. Animal breeders
  3. Bakers
  4. Launder workers
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138
Q

What other atopic conditions are associated with asthma?

A

Eczema

Hayfever

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139
Q

What are the symptoms of asthma?

A
  1. Episodic cough
  2. Expiratory wheeze
  3. SOB
  4. Diurnal variation - often worse in morning
  5. Chest tightness
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140
Q

What are the signs of asthma?

A
  1. Tachypnoea
  2. Audible wheeze
  3. Widespread polyphonic wheeze
  4. Cough
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141
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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142
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. PEF < 33% predicted
  6. Cyanosis
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143
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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144
Q

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

A
  1. PEFR
  2. Spirometry = obstructive
  3. CXR
  4. Atopy = skin prick, RAST
  5. Bloods = high IgE, Eosinophils
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145
Q

How can reversibility be tested in asthma?

A

When given a beta agonist there will be a 400ml increase in FEV1 OR a 20% improvement in PEFR

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146
Q

What are the 2 principles of asthma treatment

A
  1. Alleviate symptoms

2. Target inflammation

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147
Q

Describe the management of asthma

A 
Improve control and avoid trigger 
Smoking cessation 
Beta agonist = symptomatic relief 
Inhaled corticosteroid = anti-inflammatory 
Steroids
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148
Q

What is the guideline mediation regime for asthma?

A
  1. SABA
  2. SABA + inhaled corticosteroid
  3. LABA
  4. Oral corticosteroid
  5. Anticholinergics + theophylline
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149
Q

What broad class of drugs are commonly used to alleviate asthmatic symptoms?

A

Bronchodilators

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150
Q

What broad class of drugs are commonly used to reduce inflammation in asthmatics?

A

Steroids

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151
Q

Name 2 types of bronchodilators that are commonly used in asthma

A
  1. Beta agonist

2. Muscarinic antagonists

152
Q

What type of beta adrenergic receptors are found in the lungs?

153
Q

Describe how beta 2 agonists work?

A

Beta 2 interacts with Gs –> activation of adenylate cyclase –> ATP to cAMP –> PKA synthesis –> bronchodilation

154
Q

Give 2 functions of cAMP

A
  1. Stabilisation of mast cells, inhibit mast cell mediator release
  2. Relaxes airway smooth muscle
155
Q

Give an example of a short acting beta 2 agonist (SABA)

A

Salbutamol

Last 4 hours

156
Q

Give an example of a long acting beta 2 agnosia (LABA)

A

Salmeterol, formoterol

Last 12 hours

157
Q

What makes LABA long acting?

A

They have increased lipophilicity

158
Q

How do muscarinic antagonist work?

A

Prevent M3 receptor activation –> reduction in Ca2+ activation –> less MLC kinase –> reduced muscle contraction
Block bronchoconstriction

159
Q

Give an example of a muscarinic antagonist

A

Atropine, ipratropium bromide, tiotropium bromide

160
Q

Where are anti-inflammatory steroids produced?

A

Adrenal cortex

161
Q

How do glucocorticoids work?

A

Interfere with gene transcription to suppress inflammation

162
Q

Give an example of an inhaled corticosteroid

A

Beclomethasone, budesenide

163
Q

What is the advantage of having inhaled medication in the management of asthma?

A

More likely to reach target site and there is reduced chance of side effect

164
Q

Give 3 potential side effect of inhaled corticosteroid use

A
  1. Adrenal suppression
  2. Osteoporosis
  3. Cataracts
  4. Glaucoma
165
Q

Effects of steroids: what is the effect of a positive GRE?

A

= increased transcription

Increase lipocortin production - anti-inflammatory as it inhibits phospholipase A2

166
Q

Effects of steroids: what is the effect of a negative GRE?

A

= suppression of cytokines

167
Q

Give 3 possible complications of asthma

A
  1. Exacerbation
  2. Pneumothorax
  3. Pneumonia
168
Q

Define COPD

A

Progressive obstructive disorder (FEV1/FC < 70%) that is irreversible

169
Q

What can COPD be sub-divided into?

A
  1. Chronic bronchitis

2. Emphysema

170
Q

What is the clinical diagnosis of chronic bronchitis?

A

Cough/sputum for >3 months in 2 consecutive years

171
Q

Describe the pathophysiology of chronic bronchitis

A

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

172
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

173
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

174
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

175
Q

What are the main cells responsible for inflammation in COPD?

A

Neutrophils and macrophages

176
Q

What type of T cell is involved in COPD?

177
Q

What can cause COPD?

A
  1. Genetic = alpha 1 antitrypsin deficiency
  2. Smoking
  3. Air pollution
  4. Occupational factors = dust, chemicals
178
Q

Name 4 symptoms of COPD

A
  1. Dyspnoea
  2. Cough +/- sputum
  3. Expiratory wheeze
  4. Weight loss
179
Q

Give 4 signs of COPD

A
  1. Tachypnoea
  2. Barrel shaped chest
  3. Hyperinflantion
  4. Cyanosis
  5. Pulmonary hypertension
  6. Cor pulmonale
180
Q

Give 3 differential diagnosis’s for COPD

A
  1. Asthma
  2. HF
  3. Pulmonary embolism
  4. Bronchiectasis
  5. Lung cancer
181
Q

What investigations might you do to diagnose someone with COPD?

A 
CXR = hyperinflation, flat hemi-diaphragms, large pulmonary arteries 
CT = Bronchial wall thickening, enlarged air spaces 
ECG = RA and RV hypertrophy 
ABG = decreased PaO2 +/- hypercapnia
182
Q

How can spirometry stage COPD?

A

Stage 1 = FEV1 <80% of predicted value
Stage 2 = FEV1 50-79% of predicted value
Stage 3 = FEV1 30-49% of predicted value
Stage 4 = FEV1 <30% of predicted value

183
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
184
Q

What are the treatments for COPD?

A 
Smoking cessation 
Pulmonary rehabilitation 
SABA/LABA = symptomatic relief 
Inhaled corticosteroids 
Muscarinic antagonist 
Long term O2 therapy 
Alpha 1 antitrypsin replacement if due to deficiency
185
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

186
Q

Give 3 possible complications of COPD

A
  1. Exacerbations
  2. Infection
  3. Respiratory failure
  4. Cor pulmonale
  5. Pneumothorax
187
Q

Define exacerbation

A

An acute event characterised by worsening symptoms beyond normal day to day variation

188
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
189
Q

What is the likely cause for an exacerbation of COPD?

A

Viral URTI

Bacterial infections

190
Q

What are the aims of treatment for exacerbations of COPD?

A
  1. Minimise the impact of the current exacerbation

2. Prevent subsequent exacerbations

191
Q

What is the treatment for an exacerbation of COPD?

A
  1. Oxygen
  2. Bronchodilators
  3. Systemic steroids
  4. Antibiotics if there is breathlessness and sputum production
192
Q

Give 3 ways in which subsequent exacerbations be prevented

A
  1. Smoking cessation
  2. Vaccination
  3. LABA/LAMA/ICS
193
Q

A young person presents to you with breathlessness, wheeze and cough. There appears to be inflammation of the airways. When you do a spirometry test the results are variable. You ask the patient to do a peak flow diary and the results of this show diurnal variation. Is the patient likely to have asthma or COPD?

A

Asthma
Although breathlessness, wheeze and cough are symptoms of both asthma and COPD the fact that the spirometry results are variable is a large indication that this person has asthma!
The patient is also young and COPD tends to be more common in older people

194
Q

An older person presents to you with breathlessness, wheeze and cough. There appears to be inflammation and fibrosis of the airways and also alveolar disruption. You ask the patient to do a peak flow diary and the results of this are all abnormal. Is the patient likely to have asthma or COPD?

A

COPD
Although breathlessness, wheeze and cough are symptoms of both asthma and COPD the fact that the spirometry results are consistently abnormal is a large indication that this person has COPD; in asthma there would be diurnal variation. Fibrosis and alveolar disruption are also signs of COPD and the fact that the patient is an older patient also makes COPD the more likely diagnosis

195
Q

Where might an emboli arise form to cause a pulmonary embolism?

A

Dislodged DVT

196
Q

Name 5 risk factors for a pulmonary embolism

A
  1. Recent surgery
  2. Immobilisation
  3. Oestrogen = HRT, OCP, pregnancy
  4. Malignant
  5. Hypertension
  6. Smoking
  7. Anti-phospholipid syndrome
197
Q

What is the consequence of a small, peripheral PE?

A

Infarction

Ventilation but no perfusion = dead space

198
Q

What is the consequence of a large, central PE?

A

Ischaemia

Resistance to flow –> RHF

199
Q

Give 3 symptoms of a PE

A
  1. Dyspnoea
  2. Pleuritic chest pain
  3. Haemoptysis
200
Q

Give 3 signs of a PE

A
  1. Tachycardia
  2. Tachypnoea
  3. Pleural rub/effusion
  4. Cyanosis
  5. Signs of DVT = red, swollen leg
201
Q

What investigations mighty you in someone to determine whether they have a PE?

A 
ECG = tachycardia, RBBB
V/Q scan = mismatch defect 
Bloods - D-dimer
Doppler US 
ABG = type 1 respiratory failure 
CT pulmonary angiography
202
Q

What is D dimer?

A

A small protein fragment found in blood after a blood clot is degraded by fibrinolysis
Negative D dimer = excludes PE

203
Q

What does the Wells scoring system use to work out the probability of someone having a PE?

A
  1. Clinical signs/symptoms of DVT
  2. HR > 100bpm
  3. Recent immobilisation
  4. Previous DVT/PE
  5. Haemoptysis
  6. Malignancy
    Score >4 - PE likely
204
Q

Describe the treatment for PE

A
  1. Thrombolysis
  2. LMWH and oral warfarin
  3. NOAC
  4. Analgesia
  5. Oxygen
205
Q

What disease might be in the differential diagnosis of PE?

A
  1. Asthma
  2. COPD
  3. Pneumonia
  4. MI
206
Q

How can you prevent a PE?

A

Compression stockings
Early mobilisation
LMWH prophylaxis

207
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
208
Q

What does the pleural fluid contain?

A

Protein - albumin, globulin, fibrinogen

Mesothelial cells, monocytes and lymphocytes

209
Q

How much fluid is contained within the healthy pleural space?

210
Q

What produces and reabsorbs pleural fluid?

A

Parietal pleura

211
Q

Name 3 diseases associated with the pleura

A
  1. Pleural effusion
  2. Pneumothorax
  3. Pleural plaques
212
Q

Define pleural effusion

A

Excess fluid in the pleural space

213
Q

Name the types of pleural effusion

A
  1. Transudate = extravascular fluid with low protein content (<25 g/L)
  2. Exudate = protein rich fluid (>35 g/L)
  3. Chylothorax = lymph in pleural cavity
214
Q

Name 3 causes of a transudate pleural effusion

A
  1. Heart failure
  2. Hypoalbuminaemia
  3. Peritoneal dialysis
  4. Constrictive pericarditis
215
Q

Name 3 causes of a exudate pleural effusion

A
  1. Pneumonia
  2. Malignancy
  3. PE with infarction
216
Q

Name 2 causes of a chylothorax pleural effusion

A
  1. Neoplasm
  2. Trauma
  3. TB
  4. Sarcoidosis
217
Q

How does a pleural effusion present?

A
  • Dyspnoea
  • Pleuritic chest pain
  • Reduced chest wall movement
  • Dull percussion
  • Absent breath sounds
218
Q

How might you diagnose a pleural effusion?

A

CXR = blunt costophrenic angles

Thoracentesis

219
Q

How would you treat a transudate pleural effusion?

A

Treat the underlying cause

220
Q

How would you treat a exudate pleural effusion?

221
Q

What can you do if recurrent pleural effusions occur?

A

Pleurodesis (stick pleura together)

222
Q

What is a pneumothorax?

A

Accumulation of air in the pleural space which can lead to partial or complete lung collapse

223
Q

How can pneumothorax be classified?

A 
Primary = thin, young men = caused by trauma, congenital pleura rupture 
Secondary = associated with chronic lung diseases, infections and malignancies
224
Q

How does a pneumothorax present?

A
  • Sudden onset dyspnoea and pleuritic chest pain
  • Reduced expansion
  • Hyper-resonant percussion
  • Diminished breath sounds
225
Q

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

A

CXR = translucency and collapse

226
Q

What is the treatment for a pneumothorax?

A

Drainage
Oxygenation if hypoxic
Pleurodesis if recurrent

227
Q

Name a possible complication of a pneumothorax

A

Tension pneumothorax

228
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

229
Q

What is the treatment for a tension pneumothorax?

A

Immediate needle decompression
Chest drain insertion
NO CXR

230
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

231
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
232
Q

What are the 4 major features of interstitial lung disease?

A
  1. Cough
  2. Dyspnoea
  3. Restirictve spirometry
  4. Abnormal CXR/CT
233
Q

Would pulmonary function tests taken from someone with interstitial lung disease show a restrictive or obstructive pattern?

A

Restrictive

Decreased gas transfer and a reduction in PaO2

234
Q

What is the pathology of interstitial lung disease?

A

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

235
Q

What kind of disease is sarcoidosis?

A

Granulomatous disease

236
Q

Describe the pathophysiology of sarcoidosis

A

Chronic inflammation –> non-caseating granuloma in various body sites
Focal accumulation of epithelia cells, macrophages and lymphocytes (mainly T cells)

237
Q

Describe the epidemiology of sarcoidosis

A

Women > men

Aged 20-40 years old

238
Q

Give 3 pulmonary symptoms of sarcoidosis

A
  1. Dry cough
  2. Progressive SOB
  3. Wheeze
  4. Chest pain
239
Q

What is the effect of sarcoidosis on the skin?

A

Erythema nodosum

240
Q

What is the effect of sarcoidosis on the eyes?

241
Q

What is the effect of sarcoidosis on the bone?

A

Arthralgia

242
Q

What is the effect of sarcoidosis on the liver?

A

Hepatosplenmeagly

243
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 biopsy = diagnostic = non-caseating granulomata
CXR = staging

244
Q

How can you stage sarcoidosis?

A

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

245
Q

How do you treat acute sarcoidosis?

A

NSAIDs and bed rest

246
Q

How do you treat sarcoidosis if there are pulmonary infiltrates?

A

Prednisolone

+/- immunosuppression

247
Q

Give 2 possible differential diagnosis’s for sarcoidosis

A
  1. Lymphoma

2. Pulmonary TB

248
Q

What is idiopathic pulmonary fibrosis?

A

Progressive fibrosis in the alveoli that limits the patients ability to respire

249
Q

Describe the pathophysiology of idiopathic pulmonary fibrosis

A

Fibroblast proliferation + collagen formation –> restrictive lung disease

250
Q

Give 3 causes of idiopathic pulmonary fibrosis

A
  1. Occupational = coal, asbestos
  2. Smoking
  3. Idiopathic
251
Q

Give 4 signs and symptoms of idiopathic pulmonary fibrosis

A
  1. Dry cough
  2. SOB on exertion
  3. Systemic = malaise, weight loss, arthralgia
  4. Cyanosis
  5. Finger clubbing
  6. Inspiratory crackles/crepitus
252
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
Spirometry = restrictive
Lung biopsy = confirmation

253
Q

What is the treatment for idiopathic pulmonary fibrosis?

A

Lung transplant
Supportive care = oxygen, pulmonary rehab, pain relief
Pirfenidone = antifibrotic agent

254
Q

Give 2 possible complications of idiopathic pulmonary fibrosis

A
  1. Respiratory failure

2. Cor pulmonale

255
Q

What is hypersensitivity pneumonitis (EAA)?

A

Allergic response to inhaled antigen –> type 3 hypersensitivity reaction –> inflammatory response in alveoli and small airways

256
Q

In hypersensitivity pneumonitis (EAA), what can chronic exposure lead to?

A

Granuloma formation and obliterative bronchiolitis

257
Q

Name 3 causes of hypersensitivity pneumonitis (EAA)

A
  1. Farmers lung - mould hay
  2. Bird/pigeon fancier’s lung - proteins in droppings
  3. Malt-workers lung
  4. Cheese workers lung
258
Q

Give 3 symptoms of acute hypersensitivity pneumonitis (EAA)

A

4-6 hours post exposure

  1. Fever
  2. Rigors
  3. Dry cough
  4. Myalgia
  5. Dyspnoea
259
Q

Give 3 symptoms of chronic hypersensitivity pneumonitis (EAA)

A
  1. Cyanosis
  2. Clubbing
  3. Weight loss
  4. Increasing dyspnoea
  5. Type 1 respiratory failure
260
Q

What investigations might you do in someone you suspect to have hypersensitivity pneumonitis (EAA)?

A

Bloods = raised WCC, ESR and neutrophilia
CXR = upper zone fibrotic shadow –> honeycomb lung
Spirometry = restrictive
Bronchoalveolar lavage = increase lymphocytes and mast cells

261
Q

What is the treatment for hypersensitivity pneumonitis (EAA)?

A

Avoid exposure
Steroids
- acute = prednisolone followed by reduced dose
- choric = long term

262
Q

What are occupational lung disorders?

A

Lung disorders due to a response in inhaling something at work - fumes, dust, gas, aerosol

263
Q

Give 4 damage mechanisms of occupational lung disorders

A
  1. Direct injury
  2. Infection
  3. Allergy (e.g. EAA)
  4. Chronic inflammation (e.g. COPD)
  5. Destruction of lung tissue (e.g. emphysema)
  6. Lung fibrosis
  7. Carcinogenesis
264
Q

Give an example of an occupational asthma

A

Baker’s asthma - due to flour

265
Q

Give 3 ways in which occupational lung disorders can be prevented

A
  1. Risk assessment
  2. Legal requirement
  3. Prevent and minimise exposure to harmful substances
  4. Monitor workers health so health problems can be identified early
266
Q

What are potential consequences of occupational lung disorders?

A
  1. Increases morbidity and mortality

2. Loss of income

267
Q

What is the name of a lung disorder group the reflect inhaled dust/toxins?

A

Pneumoconiosis

268
Q

Give an example of pneumoconiosis

A

Coal workers pneumoconiosis
Silicosis
Asbestos exposure
Extrinsic allergic alveolitis

269
Q

What is coal workers pneumoconiosis?

A

Accumulation of dust in lungs and reaction of the tissue to its presence

270
Q

Describe the pathogenesis of coal workers pneumoconiosis

A

Dust ingested by alveolar macrophages in small airways –> alveoli die –> release enzymes –> fibrosis

271
Q

What can the progression of coal workers pneumoconiosis lead to?

A

Progressive massive fibrosis = apical destruction and disruption of lung –> emphysema + airway damage

272
Q

What investigations might you do to diagnose progressive massive fibrosis?

A

CXR = round fibrotic masses in upper lobes

Rheumatoid factor and anti-nuclear antibodies present in serum

273
Q

What is silicosis?

A

Inhalation of silica particles –> toxic to alveolar macrophages –> initiated fibrogenesis
Seen in stonemasons, pottery workers and foundry workers

274
Q

What is shown on a CXR in silicosis?

A

Diffuse nodular pattern in upper and mid-zone and thin streaks of calcification of hilar nodes

275
Q

Give 5 potential consequences of asbestos exposure

A
  1. Plaques
  2. Effusion
  3. Asbestosis
  4. Mesothelioma
  5. Bronchial carcinoma
276
Q

Describe the pathophysiology of asbestosis

A

Asbestos trapped in lungs –> resistant to macrophage and neutrophil enzymatic destruction –> chronic inflammation –> fibrosis

277
Q

Give 4 signs and symptoms of asbestosis

A
  1. Progressive dyspnoea
  2. Finger clubbing
  3. Bilateral basal end-inspiratory crackles
  4. Pleural plaques (increase risk of mesothelioma and bronchial carcinoma)
278
Q

Define mesothelioma

A

A high grade malignancy of the pleura that spreads around the pleural surfaces

279
Q

What is the main cause of mesothelioma?

A

Asbestos exposure

280
Q

What are the signs and symptoms fo mesothelioma?

A
  1. SOB
  2. Cough
  3. Chest pain
  4. Finger clubbing
  5. Weight loss
281
Q

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

A

CXR/CT scan = pleural effusion and thickening

Pleural biopsy

282
Q

What is the treatment for mesothelioma?

A
  1. Symptom control

2. Palliative chemo or radiotherapy

283
Q

What is treatment of mesothelioma so difficult?

A

Incurable as it is resistant to surgery, chemo and radiotherapy
Average time from diagnosis to death = 8 months

284
Q

How does the treatment between local and systemic lung cancer vary?

A 
Local = surgery and radiotherapy 
Systemic = chemotherapy
285
Q

Give 5 side effects of radiotherapy

A
  1. Fatigue
  2. Anorexia
  3. Cougared
  4. Oesophagitits
  5. Systemic symptoms
286
Q

What are the 3 main aims of palliative chemotherapy?

A
  1. Relieve symptoms
  2. Improve quality of life
  3. Shrink tumours
287
Q

Give 4 side effects of chemotherapy

A
  1. Alopecia
  2. Nausea and vomiting
  3. Peripheral neuropathy
  4. Constipation or diarrhoea
288
Q

Define pulmonary hypertension

A

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

289
Q

What can cause an increase in mPAP?

A

Increase resistance to flow

Increased flow rate

290
Q

Give 3 causes of pulmonary hypertension

A
  1. Congenital heart defects - septal defects
  2. SLE
  3. Pulmonary embolism
  4. Portal hypertension
  5. COPD
291
Q

Give 4 symptoms of pulmonary hypertension

A 
Initial 
1. Exertional dyspnoea 
2. Lethargy 
3. Fatigue 
4. Syncope 
After RV failure develops 
5. Peripheral oedema 
6. Abdominal pain (due to hepatic congestion)
292
Q

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

A

CXR = enlarged pulmonary arteries
ECG = ventricular hypertrophy
ECHO = right ventricular dilation and/or hypertrophy
Spirometry

293
Q

Describe the treatment of pulmonary hypertension

A
  1. Oxygenation
  2. Warfarin (for risk of thrombosis)
  3. Diuretics (for oedema)
  4. CCB (pulmonary vasodilation)
  5. Treat underlying cause
294
Q

Give a possible complication of pulmonary hypertension

A

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

295
Q

Describe mycobacterium tuberculosis

A
  1. Acid fast bacilli
  2. Has a waxy capsule
  3. Grows slowly (so hard to culture in a lab)
  4. Resistant to phagolysomal killing –> granulomatous disease
296
Q

What mycobacterium can cause abdominal tuberculosis?

A

Mycobacterium bovis

- found in unpasteurised milk

297
Q

How is TB transmitted?

A

Aerosol transmission

298
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

299
Q

Describe the pathogenesis of pulmonary TB disease

A
  1. Bacilli and macrophages form primary focus
  2. Mediastinal lymph nodes enlarge
  3. Primary focus and enlarged lymph nodes = primary complex = Gohn complex
  4. Granuloma develops into a cavity
  5. Cavity is filled with TB bacilli = expelled when patient coughs
  6. Granuloma can rupture –> spread around the body
300
Q

Describe the disease course of TB

A

Primary infection –> latent TB –> reactivation/immunocompromised

301
Q

Where in the lung is granuloma cavity most likely to develop in TB?

A

Apex of the lung = more air and less blood supply and less immune cells

302
Q

Give 3 risk factors for TB

A
  1. Living in a high prevalence area
  2. IVDU
  3. Homeless
  4. Alcohol
  5. HIV +ve
303
Q

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

A
  1. Weight loss
  2. Night sweats
  3. Anorexia
  4. Malaise
304
Q

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

A
  1. Cough
  2. Chest pain
  3. Breathlessness
  4. Haemoptysis
305
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
306
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

307
Q

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

A

Lowenstein Jenson Slope

308
Q

What test might you do to diagnose latent TB?

A

Tuberculin skin test

Intradermal injection –> stimulates type 4 hypersensitivity reaction

309
Q

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

A

Caseating granuloma

310
Q

What is the drug treatment commonly used for TB?

A 
RHZE 
RH = 6 months 
ZE = 2 months 
R = rifampicin
H = isoniazid 
Z = pyrazinamide
E = ethambutol
311
Q

Give 2 potential side effects of Rifampicin

A
  1. Red urine
  2. Hepatitis
  3. Drug interaction - it’s an enzyme inducer
312
Q

Give 2 potential side effects of Isoniazid

A
  1. Hepatitis

2. Neuropathy

313
Q

Give 2 potential side effects of Pyrazinamide

A
  1. Hepatitis
  2. Gout
  3. Neuropathy
314
Q

Give a potential side effect of Ethambutol

A

Optic neuritis

315
Q

Why is compliance so important when taking TB medication?

A

Resistance and relapse likely if non-compliant

316
Q

Why does TB treatment need to last 6 months?

A

Ensure all dormant bacteria have ‘woken up’ and been killed

317
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
318
Q

How can TB be prevented?

A
  1. Active case finding
  2. Detect and treat latent TB
  3. Vaccination = BCG
319
Q

Name 4 upper respiratory tract infections

A
  1. Rhinosinusitis - common cold
  2. Bacterial sinusitis
  3. Pharyngitis
  4. Epiglottitis
  5. Whooping cough
  6. Influenza
320
Q

What are the causative organisms of influenza?

A

Influenza A (severe outbreaks)
Influenza B
Influenza C

321
Q

What are the main antigens on influenza A?

A

Haemagglutinin - grappling hook binds to cell

Neuraminidase - cuts new viruses out of cell

322
Q

Define antigenic drift

A

Small mutation and minor antigenic variation

Causes seasonal epidemics

323
Q

Define antigenic shift

A

Larger mutations and major antigenic variation

Causes pandemics

324
Q

How can influenza be transmitted?

A

Aerosol

Droplet = hand-to-hand

325
Q

What are the symptoms of influenza?

A

URTI symptoms = cough, sore throat, runny nose

Systemic = fever, headache, myalgia, weakness

326
Q

What is the treatment for influenza?

A

Oxygenation, nutrition and hydration
Treat secondary infection
Antiviral to prevent spread (has no treatment effect)

327
Q

Name a possible compilations of influenza

A

Bacterial pneumonia

328
Q

What factors are there to suggest that future pandemics may be likely?

A
  1. More travel
  2. Increasing world population
  3. Rise in intensive farming
329
Q

What can cause the common cold (rhinitis and sinusitis)?

A
  • Rhinovirus

- Coronavirus

330
Q

What are the symptoms of a common cold?

A
  1. Blocked/runny nose
  2. Sore throat
  3. Cough
  4. Sneezing
  5. Pain, swelling and tenderness around sinuses
331
Q

What is the management for a common cold?

A

Watch and wait

Hydration, plenty of sleep and paracetamol

332
Q

What can cause bacterial sinusitis?

A

Streptococcus pneumoniae

Haemophilius influenzae

333
Q

Give 4 symptoms of bacterial sinusitis

A
  1. Unilateral pain
  2. Purulent discharge
  3. Fever
  4. Sinus headache
334
Q

What is the treatment for bacteria sinusitis?

A

Plenty of rest and hydration
Paracetamol and ibuprofen
Nasal decongestants
Antihistamines

335
Q

What are 2 possible complications of bacterial sinusitis?

A
  1. Brain abscess

2. Sinus vein thrombosis

336
Q

Is sinusitis normally caused by a bacterial or viral infection?

337
Q

Is pharyngitis normally caused by a bacterial or viral infection?

338
Q

What can cause pharyngitis?

A 
Viral 
 - Adenovirus, rhinovirus = common 
 - EBV, acute HIV = rare
Bacterial 
 - Strep pyogenes
339
Q

What is the clinical presentation fo pharyngitis?

A
  1. Sore throat
  2. Fever
  3. Oropharynx and soft palate reddened
  4. Tonsils inflamed or swollen
  5. Lymphadenopathy
340
Q

What is the Centor criteria used for?

A

To determine the likelihood that a sore throat is bacterial

341
Q

What signs make up the Centor criteria?

A 
Tonsillar exudate (1 point)
Cervical lymphadenopathy (1 point)
38oC fever (1 point)
No cough (1 point)
Age 3-14 years (1 point) 
Age >44 years (-1 point) 
0-2 = viral infection
3-4 = 50% bacterial infection
342
Q

What is the main cause of acute epiglottitis?

A

Haemophilius influenza B

343
Q

Give 3 symptoms of acute epiglottitis

A
  1. Odynophagia (pain on swallowing)
  2. Inspiratory stridor
  3. Fever
  4. Fatigue
  5. Malaise
344
Q

What is the management of acute epiglottitis?

A

Prevention = HiB vaccine
Secure airway
Ceftazidime

345
Q

What is Whooping cough caused by?

A

Bordatella pertussis (gram -ve bacilli)

346
Q

Describe the disease course of whooping cough

A

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

347
Q

What are the symptoms of whooping cough?

A

Paroxysmal cough - sudden and severe

Vomiting after cough

348
Q

What is the treatment of whooping cough?

A

Clarithromycin

349
Q

How can you prevent whooping cough?

A

Pertussis vaccination

8, 12 and 16 weeks and a pre school booster

350
Q

Give 2 possible complications of whooping cough

A
  1. Pneumonia
  2. Encephalopathy
  3. Sub-conjunctival haemorrhage
351
Q

What is ANCA?

A

Anti-neutrophil cytoplasmic antibody

Autoimmune disorder

352
Q

What is the mechanism of ANCA?

A

ANCA activates neutrophils and monocytes
Neutrophils adhere to endothelial cells –> degranulaiton –> free radicals released –> damage endothelium
Further neutrophil recruitment –> inflammation of vessel wall = vasculitis

353
Q

What disease can be caused by ANCA?

A

ANCA associated vasculitis

354
Q

What is Goodpastures syndrome?

A

Acute glomerulonephritis and pulmonary alveolar haemorrhage and circulating antibodies directed against an intrinsic antigen to basement membrane of kidney and lungs

355
Q

What are the symptoms of Goodpastures syndrome?

A

Haemoptysis
Cough
Anaemia
URTI symptoms

356
Q

What is seen on a CXR of someone with Goodpastures syndrome?

A

Bilateral lower zone infiltrates (haemorrhage)

357
Q

How do you treat Goodpastures syndrome?

A

Immunosuppression (prednisolone) and plasmapheresis

358
Q

What is Wegener’s granulomatosis?

A

Necrotising granulomatous inflammation and small vessel vasculitis commonly involved with upper and respiratory tracts and kidneys

359
Q

What are the symptoms of Wegener’s granulomatosis?

A
  1. Rhinorrhoea
  2. Cough
  3. Pleuritic chest pain
  4. Haemoptysis
  5. Haematuria and proteinuria
360
Q

What would the serum tests for someone with Wegener’s granulomatosis show?

A

C-ANCA positive

361
Q

What is the treatment for Wegener’s granulomatosis?

A

Glucocorticoids (prednisolone)
+ Immunosuppressive drugs (cyclophosphamide or rituximab)
+ plasma exchange

362
Q

What is the mechanism behind damage in chronic infection?

A

Infection won’t clear
Chronic neutrophil recruitment and persistent cellular activation
Pro-inflammatory mediators are released = tissue damage

363
Q

What is the difference between bronchitis and bronchiolitis?

A 
Bronchitis = inflammation of bronchi epithelium due to irritant and chemical 
Bronchiolitis = Inflammation of bronchioles and increased mucus secretion due to RSV infection
364
Q

Respiratory immunity: describe the innate immune repsonse

A

Mucous, mucociliary escalator, macrophages and neutrophils

Cough reflex and epiglottis closing off trachea on swallowing

365
Q

Respiratory immunity: describe the adaptive immune response

A

B cells proudce mainly IgG and IgA antibodies

T cells = CD4, CD8 and regulatory

366
Q

What can mast cell mediators affect?

A

Airways = bronchoconstriction

Blood vessels = vasodilation

367
Q

What are the 3 types of immunosuppression?

A
  1. Granulocyte defect - associated with chemotherapy
  2. B cell defect - associated with rituximab and haematological malignancy
  3. T cell defect - associated with immunosuppression/HIV
368
Q

Give 2 examples of iatrogenic suppression

A
  1. Corticosteroid use
  2. Chemotherapy
  3. Immune suppression after organ transplant
  4. Rituximab
369
Q

Give 2 examples of non-specific immunosuppression

A
  1. Malnutrition
  2. Alcohol
  3. Sepsis
  4. Trauma
370
Q

Describe the usual presentation of pulmonary infection in the immunocompromised

A
  1. Pyrexia
  2. Lethargy
  3. Cough
  4. Dyspnoea
  5. Hypoxic
371
Q

An immunocompromised person presents with a rapid onset pulmonary infection, is this likely to have a bacterial or viral cause?

A

Rapid onset is likely to be bacterial

372
Q

An immunocompromised person presents with a slow onset pulmonary infection. Is this likely to have a bacterial or viral cause?

A

Slow onset is likely to be CMV, aspergillus or cryptococcus

373
Q

Give 3 radiological indication for bronchoscopy

A
  1. Lobar colapse
  2. Presence of a mass
  3. Persistent consolidation
374
Q

Give 3 non-radiological indication for bronchoscopy

A
  1. Haemoptysis
  2. Cough
  3. Wheeze
  4. Stridor
375
Q

What are the possible complications of a bronchoscopy?

A

Pneumonia

Pneumothorax

376
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

PHASE 2A (16 decks)

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