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Medicine Phase 2a > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is Chronic Obstructive Pulmonary Disease (COPD)?

A

Progressive irreversible airway obstruction characterised by persistent airflow limitation caused by long term damage to lung tissue.

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2
Q

What are the conditions that are classed as COPD?

A

Chronic Bronchitis
Emphysema

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3
Q

What is the epidemiology of COPD?

A

1.2 million people with COPD in the UK
4th leading cause of death globally
Typically diagnosed >45 yrs
More common in males
Strongly related to Smoking.

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4
Q

What are the risk factors for COPD?

A

Cigarette smoking
Air pollution
Occupational exposure to dusts, chemical agents, and fumes
A1AT deficiency - can lead to early onset COPD

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5
Q

What is the most important cause/aetiological factor for COPD?

A

Cigarette smoking

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6
Q

Define Chronic Bronchitis?

A

A inflammatory lung condition that develops over time in which the bronchi and bronchioles become inflamed and scarred.

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7
Q

What is Chronic Bronchitis as a clinical definitions?

A

Chronic Bronchitis is a clinical term relating to a chronic productive cough for at least 3 months over 2 consecutive years.
Alternative explanations for the cough should also be excluded.

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8
Q

What is Emphysema as a pathological Definition?

A

Refers to abnormal air space enlargement distal to terminal bronchioles with evidence of alveoli destruction and no obvious fibrosis.

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9
Q

What is the pathophysiology of Chronic Bronchitis?

A
  • Initial exposure to irritants and chemicals (cigarette smoke)
  • Hypertrophy and hyperplasia of bronchial mucinous glands and goblet cells. There is also ciliary destruction.
  • This increases the production of mucus in the lumen causing narrowing and obstruction
  • Epithelial layer becomes ulcerated and there is the stimulation of immune cells causing inflammation of the bronchus and bronchioles.
  • This leads to scarring and thickening of the walls further narrowing the airways.
  • This causes air trapping causing poor exchange of O2 and CO2 and increases risk of infection.
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10
Q

What are the pathological changes that occur in Chronic Bronchitis?

A

Goblet cell hyperplasia
Mucus hypersecretion
Chronic inflammation and fibrosis
Narrowing of small airways

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11
Q

What are the symptoms of chronic bronchitis?

A

Chronic Cough - high sputum production

Dyspnoea

Wheeze

Recurrent respiratory tract infections - due to mucus plugging

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12
Q

What are the Signs of Chronic Bronchitis?

A

Wheeze - narrowing of airway creates higher pitch sound.

Crackles - popping open of small airways

Obesity

Hypoxaemia and Hypercapnia - mucus plugs block airflow and lead to partial pressures of CO2 to rise and subsequent decline of O2.

Cyanosis (if hypoxaemia is really bad leading to the term blue bloaters).
Peripheral Oedema

Pulmonary Hypertension - due to Hypoxic vasoconstriction leading to increased pulmonary vascular resistance

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13
Q

What is Emphysema?

A

A lung disease characterised by dilatation and destruction of the lung tissue causing enlarged air spaces distal to the terminal bronchioles

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14
Q

What is the Pathophysiology of Emphysema?

A

Occurs in the ACINUS

Irritants/chemicals lead to damage and destruction of the alveoli wall.

Causes and inflammatory reaction and immune cell infiltration releasing Leukotriene B4, IL-8 and TNF-a

Neutrophil Proteases (elastases and collagenases) are also produced which break down alveolar wall structural proteins.

This leads to permanent enlargement of the alveoli and loss of their elasticity.

Alveolar wall septa break down reducing the total surface area. This leads to gas exchange dysfunction.

Loss of elasticity in the airways means that the airways collapse upon exhalation causing air trapping distally.

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15
Q

What are the different types of Emphysema?

A

Centriacinar Emphysema

Panacinar Emphysema:

Paraseptal Emphysema:

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16
Q

What is Centriacinar Emphysema?

A

Most common

Damage to central/proximal acini due to smoking

Typically affects upper lobes

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17
Q

What is Panacinar Emphysema?

A

Entire acinus affected

Due to A1AT Deficiency (protease inhibitor deficiency) cannot prevent breakdown.

Typically affects Lower lobes

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18
Q

What is Paraseptal Emphysema?

A

Affects peripheral lung tissue.
Peripheral ballooned alveoli can rupture causing pneumothorax

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19
Q

What are the pathological changes seen in emphysema?

A

Related to loss of Elastin:
Collapse and bullae formation: the alveoli are prone to collapse leading to bullae formation.
Dilation: alveoli dilate and may eventually join with neighbouring alveoli reducing surface area

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20
Q

How is Chronic Bronchitis and Emphysema classified differently?

A

Chronic Bronchitis is defined by clinical features

Emphysema is defined by structural changes (enlarged alveoli)

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21
Q

What are the symptoms of Emphysema?

A

Dyspnoea - diminished gas exchange
( can improve this by exhaling slowly through pursed lips giving the name pink puffers)

Hypoxaemia

Weight loss - older and thinner

Cough - with some sputum

Pulmonary HTN

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22
Q

What are the main features of COPD phenotypes (emphysema/chronic Bronchitis)?

A

Pink puffer - emphysema
- Weight loss
- Breathless
- Emphysematous
- Maintained pO2

Blue bloater – chronic bronchitis
- Cough
- Phlegm
- Cor pulmonale
- Type 2 Respiratory failure

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23
Q

How does Emphysema lead to pulmonary hypertension?

A

Widespread Hypoxic vasoconstriction.

Too many blood vessels are constricted increasing the pressures in others.

Leads to pulmonary hypertension.

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24
Q

What is the cause of the barrel shaped chest in COPD?

A

Both chronic bronchitis and emphysema leads to air trapping within the Bronchi/acini.

This leads to Hyperinflation of the lungs giving a barrel chest appearance.

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25
Q

What are the main complications of COPD?

A

Recurrent Respiratory Tract Infections: S. pneumoniae/H. influenzae
Respiratory failure
Pneumothorax: rupture of bullous disease
Polycythaemia or anaemia
Depression

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26
Q

What is a the most serious complication of COPD?

A

Cor Pulmonale:

Both Chronic bronchitis and Emphysema will lead to pulmonary hypertension due to excessive hypoxic vasoconstriction.

This causes R sided ventricular hypertrophy which will eventually lead to RHF and “Cor Pulmonale”

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27
Q

Who typically presents with COPD?

A

Older Px
Long term smokers
Occupational exposure: such as dust, cadmium (in smelting), coal, cotton, cement and grain

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28
Q

What are the Symptoms of COPD?

A

Chronic cough: usually productive
Sputum production
Breathlessness: usually on exertion in early stages
Frequent episodes of ‘bronchitis’: usually in the winter
Wheeze

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29
Q

What are the Signs of COPD?

A
  • Dyspnoea
  • Pursed lip breathing: (prevents alveolar collapse by increasing the positive end expiratory pressure)
  • Wheeze
  • Coarse crackles
  • Cyanosis
  • Loss of cardiac dullness: due to hyperexpansion of lungs from emphysema
  • Downward displacement of liver: due to hyperexpansion of lungs from emphysema
  • Signs of C02 retention
    Drowsy
    Asterixis
    Confusion
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30
Q

What symptoms may be concerning in a COPD patient that suggests an alternative pathology?

A

Weight loss
Haemoptysis
Anorexia
Chest pain
Lymphadenopathy
Finger clubbing
Unexplained fatigue

May suggest cancer

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31
Q

Do patients with COPD typically present with Chronic Bronchitis or Emphysema?

A

Often Px will present with both conditions as COPD due to the same triggers causing both.

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32
Q

What is an acute exacerbation of COPD?

A

Presents similarly to chronic stable COPD however there is an acute and sustained worsening of symptoms in the patient

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33
Q

Who typically presents with COPD?

A

Older Px
Long term smokers
Occupational exposure: such as dust, cadmium (in smelting), coal, cotton, cement and grain

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34
Q

How is COPD Diagnosed?

A

Clinical Dx with Spirometry Test for confirmation

Spirometry shows Obstruction:
FEV1/FVC ration <0.7
FEV1 < 0.8 of predicted

Negative Reversibility Testing: <12% Inc FEV1
Obstruction does not show good response to salbutamol.

CXR - Lung hyperinflation + Bullae + flattened hemidiaphragms

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35
Q

What other investigations may be done in COPD on top of spirometry?

A

Bloods: FBC (assess for anaemia/polycythaemia)

ABG - for T2RF

A1AT serology

CXR: Hyperexpanded, Bullae, flattened hemidiaphragms, hypodense, Saber sheath trachea

ECHO if Cor Pulmonale Suspected

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36
Q

What features of a Px are supportive of a COPD diagnosis?

A

Smoker or ex-smoker
Symptoms in older adults (> 35 years old)
Chronic productive cough
Persistent/progressive breathlessness
Night time waking with symptoms uncommon
Variability uncommon (diurnal or day-to-day)

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37
Q

How is Breathlessness assessed in COPD?

A

Using the MRC Dyspnoea Scale:

  1. Breathlessness on strenuous exercise.
  2. Breathlessness on hurrying or slight hill.
  3. Walks slower than contemporaries on ground level due to breathlessness OR have to stop to catch breath when walking at own pace.
  4. Stops to catch breath after 100 metres OR a few minutes of walking
  5. Breathlessness on minimal activity (dressing) or unable to leave the house due to breathlessness
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38
Q

How does Asthma respond to Reversibility testing?

A

Bronchodilator (salbutamol) will increase FEV1 by >12%
AND
must increase FEV1 by 200ml

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39
Q

What is FVC?

A

Forced Vital Capacity:
The total amount of air forcibly expired

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40
Q

What is FEV1?

A

Forced Expiratory Volume in 1 second

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41
Q

What is an Abnormal FEV1?

A
  • The result is compared with the predicted values, if the FEV1 is 80% or
    greater than the predicted value = NORMAL
  • Thus is the FEV1 is less than 80% of the predicted value = LOW i.e
    abnormal
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42
Q

What is an Abnormal FVC?

A
  • The result is compared with the predicted values, if the FVC is 80% or
    greater than the predicted value = NORMAL
  • Thus is the FVC is less than 80% of the predicted value = LOW i.e
    abnormal
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43
Q

What does a low FVC suggest?

A

Airway Restriction

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44
Q

What does a Low FEV1/FVC ratio suggest?

A

<0.7 = Airway Obstruction

If FEV1/FVC ratio is high/normal but FVC is low (<80%) then airway restriction.

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45
Q

Do patients with COPD typically present with Chronic Bronchitis or Emphysema?

A

Often Px will present with both conditions as COPD due to the same triggers causing both.

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46
Q

What other tests may be done to look for the cause of COPD?

A

DLCO (diffusing capacity of CO across lung):
Low in COPD, Normal in Asthma

Genetic testing for A1AT Def.

ABG - may show T2RF
ECG - heart function
CXR - flattened diaphragm
Bloods - anaemia

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47
Q

How is the severity of COPD and airflow graded?

A

Post Bronchodilator when FEV1/FVC ratio < 70%
Stage 1: Mild - FEV1 >80% of predicted
Stage 2: Moderate - FEV1 50-79% of predicted
Stage 3: Severe - FEV1 30-49% of predicted
Stage 4: Very Severe - FEV1 <30% of predicted

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48
Q

What are the management Principles for COPD?

A

Education
Smoking cessation
Vaccination
Pulmonary rehabilitation
Self-management plans
Management of co-morbidities
Pharmacotherapy

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49
Q

What is the treatment of COPD?

A

Stop risk factors - smoking
Prophylactic Vaccines - Pneumonia

Medication:
1. SABA (Salbutamol) OR SAMA (Ipratropium Bromide) PRN at all stages

  1. (a = Non steroid Responsive. B = Steroid Responsive)
    a. LABA (Salmeterol) + LAMA (Tiotropium
    b. Steroid Responsive = LABA + ICS (Beclometasone)

3.
a. 3 Month Trial of LABA + LAMA + ICS
b. Steroid Responsive = LABA + LAMA + ICS

Long term oxygen therapy if very severe

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50
Q

What management can be provided for severe COPD?

A

Nebulisers - Salbutamol and/or ipratropium
Long term Oxygen therapy

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51
Q

When should COPD Patients be put on Oxygen?

A

O2 sats </= 92 on room air

FEV1 <30% predicted
Cyanosis
Polycythaemia
Peripheral Oedema
Raised JVP

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52
Q

What is an Exacerbation of COPD?

What is it often caused by?

A

worsening of symptoms such as cough, shortness of breath, sputum production and wheeze. It is usually triggered by a viral or bacterial infection.

Haemophilus Influenzae

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53
Q

How are Exacerbations of COPD treated?

A

Oxygen - carefully monitored
Nebulised Bronchodilators
Oral Prednisolone 30mg once daily for 7-14 days
Assess Acid-Base status on ABG for T2RF
CPAP - Continuous positive airway pressure

Antibiotics if there is evidence of infection
Physiotherapy

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54
Q

What is the main risk of COPD exacerbations?

A

Respiratory Failure:
COPD patients are chronic retainers of CO2 and therefore their kidneys adapt to produce extra HCO3 to compensate the acidotic state.

In acute exacerbations the kidneys cannot produce enough HCO3 quickly leading to RF.

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55
Q

What are some Impacts of COPD exacerbations?

A

Negative impact on quality of life
Impact on symptoms and lung function
Increased economic costs
Increased mortality
Accelerated lung function decline

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56
Q

What are the differential Diagnoses of COPD?

A

Asthma
Heart Failure

Other causes of SOB:
Bronchiectasis (airways become abnormally widened resulting in build-up of excess mucus making lungs more susceptible to infection)
Allergic fibrosing alveolitis
Pneumoconiosis
Pulmonary Embolus
Lung cancer
Asbestosis

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57
Q

What are the indications for hospital admission in a Px with COPD?

A

Marked increases in symptom intensity
Severe underlying COPD
Onset of new physical signs
Failure of an exacerbation to respond to initial medical management
Presence of serious comorbidities
Frequent exacerbation
Older age
Insufficient home support

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58
Q

Define Asthma?

A

Chronic reversible inflammatory airway condition characterised by reversible airway obstruction, airway hyperresponsiveness, Bronchial inflammation and airflow limitation from bronchoconstriction

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59
Q

What are the types of Asthma?

A

Eosinophilic (Allergic) (70%) - Extrinsic IgE mediated T1 Hypersensitivity

Non-Eosinophilic (Non Allergic) (30%) - Intrinsic non IgE mediated.

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60
Q

Explain the pathophysiology IgE mediated asthma?

A

Environmental trigger against specific allergens leads to sensitisation reaction where IgE Abs against antigen bind to mast cells.

Secondary exposure leads to an immune system activation and activation of Th2 cells.

Th2 cells produce cytokines such as IL3, 4, 5, 13.
IL-4 leads to IgE Crosslinking and degranulation of mast cells releasing histamine and leukotrienes.

IL-5 leads to eosinophil activation and release of proteins

This leads to a Hypersensitivity Rxn which causes Smooth muscle bronchospasm and increased mucus production leading to narrow airways and airway obstruction.

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61
Q

What happens to the airways in chronic asthma?

A

Initially asthma and inflammation of the airways is reversible.

Over chronic asthma the inflammation in the airways causes irreversible damage such as scarring and fibrosis causing thickening of the epithelial BM causing permanent narrowing of the airways.

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62
Q

What pathological changes are responsible for airway narrowing in Asthma?

A
  • Increased number of and hypertrophy of smooth muscle
  • Constriction of smooth muscle cells (bronchoconstriction)
  • Increased mucous production
  • Swelling and inflammation (of mucosa)
  • Thickened basement membrane
  • Airway hyperreactivity, cellular infiltration
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63
Q

What is the cause of asthma

A

Causes are unknown:
Genetics may play a factor

Environmental Factors:
Hygiene hypothesis

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64
Q

What is the Hygiene Hypothesis?

A

Reduced early exposure of bacteria and viruses when young leads to an altered proportion of immune cells.
This can subsequently lead to later onset asthma

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65
Q

What are the risk factors for asthma?

A

History of Atopy
FHx of asthma
Allergens - pollen, fur, smoke
Occupation
Obesity
Premature Birth

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66
Q

What are some triggers for asthma?

A

Infection
Night time or early morning
Exercise
Animals
Cold/damp
Dust
Strong emotions
Drugs

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67
Q

What drugs can trigger asthma?

A

Aspirin
Beta blockers

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68
Q

How can aspirin trigger asthma?

A

Aspirin inhibits COX1/2
Shunts more arachidonic acid down LPOX pathway.
Produces leukotrienes (LTB4, 5, 6)
These are proinflammatory

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69
Q

What is the epidemiology of asthma?

A

5.4 Million in UK receiving treatment
More common in developed countries
More common in children/young people compared to COPD
Commonly starts age 3-5. Peak prevalence age 5-15

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70
Q

What are the symptoms of asthma?

A

Chest tightness
Episodic Dyspnoea/SOB
Wheeze
Dry Cough (typically but can be wet) - often nocturnal
Diurnal Variation

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71
Q

What are the signs of asthma?

A

Diurnal PEFR variation

Tachypnoea

Dyspnoea and Expiratory Polyphonic wheeze

Hyper resonant Percussion

Hx of Atopy

Samter’s Triad: Nasal polyps, Aspirin sensitivity, Asthma

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72
Q

What are some addition signs of an acute asthma attack?

A

Signs of Respiratory Failure

Tachypnoea
Tachycardia
Inability to complete sentences
Exhaustion
Reduced respiratory effort
Silent chest
Altered conscious level

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73
Q

What may be found in sputum from an asthmatic?

A

Curschmann spirals:
Mucus plugs that look like casts of the small bronchi

Charcot-Leyden crystals:
From break down of eosiophils.

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74
Q

How may a patient present indicating asthma?

A

Episodic symptoms

Diurnal variability. Typically worse at night.

Dry cough with wheeze and shortness of breath

A history of other atopic conditions such as eczema, hayfever and food allergies

Family history

Bilateral widespread “polyphonic” wheeze

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75
Q

How may a patient present indicating a different diagnosis to asthma?

A

Wheeze related to coughs and colds more suggestive of viral induced wheeze

Isolated or productive cough

Normal investigations

No response to treatment

Unilateral wheeze. This suggests a focal lesion or infection.

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76
Q

What are the signs of asthma?

A

Diurnal PEFR variation

Dyspnoea and Expiratory Polyphonic wheeze

Samter’s Triad: Nasal polyps, Aspirin sensitivity, Asthma

Atopic Triad: Atopic Rhinitis, Asthma, Eczema

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77
Q

What is Samter’s Triad

A

Nasal Polyps
Asthma
Aspirin sensitivity

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78
Q

What is Atopic Triad?

A

Atopic Rhinitis (Hayfever)
Allergic Asthma (Asthma)
Atopic Dermatitis (Eczema)

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79
Q

How is asthma classified?

A

According to:
Frequency of symptoms (night/early morning)
FEV1
PEFR (peak expiratory flow rate)
Frequency of medication use

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80
Q

What are the classifications of asthma?

A

Intermittent
Mild Persistent
Moderate Persistent
Severe Persistent

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81
Q

What are the primary investigations for asthma?

A

NICE advise to carry out tests and not make a clinical Dx:

1st Line Ix:
- Spirometry w/ Bronchodilator Reversibility
(shows reversible obstruction 200ml AND 12% increase)
- if spirometry normal - do Bronchial challenge

2nd Line:
FeNO3
PEF diary (variation measurements - 2-4 weeks)
Direct bronchial challenge test with histamine or methacholine
Bloods
CXR

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82
Q

What are the targets of treating asthma?

A

Dampen inflammation:
Corticosteroids
LRTAs
biologics
Macrolides

Relax Smooth Muscle Airways:
Bronchodilators
Antimuscarinics
Theophylline

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83
Q

What is the Treatment algorithm for Chronic asthma in adults?

A

16+: Avoid Triggers

  1. SABA (salbutamol)
  2. SABA + ICS (beclomethasone)

3a. Before adding more drugs assess inhaler technique and compliance

3b. SABA + ICS + Leukotriene Receptor Antagonist (LTRA = montelukast)

  1. SABA + ICS + LABA (Salmeterol) +/- LTRA
  2. Consider change to MART (maintenance and reliever therapy)
  3. Increase ICS Dose
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84
Q

What is the treatment algorithm for chronic asthma in children?

A
  1. SABA (salbutamol)
  2. SABA + ICS (beclomethasone)

3a. Before adding more drugs assess inhaler technique and compliance

3b. SABA + ICS + Leukotriene Receptor Antagonist (LTRA = montelukast)

  1. SABA + ICS + LABA (STOP LRTA)
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85
Q

When should you move asthma treatment from step 1 to step 2?

A

When the Patient has asthma related symptoms more than 3 times a week or waking up at night!

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86
Q

What are indications for good asthma control?

A

No Night time symptoms
Inhaler no more than 3 times a week
No breathing difficulties, cough or wheeze most days
Able to exercise without symptoms
Normal Lung Function Tests

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87
Q

What are some side effects of Beclomethasone ICS?

A

Oral Candida
Stunted Growth

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88
Q

What is the first line treatment for an acute asthma exacerbation?

A

Oxygen Driven Salbutamol Nebuliser

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89
Q

What are the main side effects of Salbutamol?

A

Fine Tremor
HYPOKALAEMIA
Headache
Palpitations
Muscle cramps

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90
Q

What are the Severities of Asthma?

A

Moderate PEFR 50-75%
Acute Severe PEFR 33-50%
Very Severe (life threatening) PEFR <33%

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91
Q

What indicates a Severe Asthma Attack?

A

Inability to complete sentences
Pulse >110bpm
Respiratory Rate > 25/min
PEF 33-50% predicted

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92
Q

What indicates a severe life threatening asthma attack?

A

33, 92, CHEST:
PEF < 33% predicted
<92% - Oxygen Stats
Cyanosis
Hypotension
Exhaustion
Silent Chest
Tachycardia

ALSO CONFUSION/AMS

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93
Q

What is the treatment for acute asthma Exacerbations?

A

ABCDE - OSHITME
ABCDE

Oxygen - maintain Sats 94-98%
Salbutamol (nebulised)
Hydrocortisone (IV)
Ipratropium Bromide
Theophylline
Magnesium Sulphate (IV)
Escalate (intubation and ventilation)

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94
Q

What are the complications of Asthma?

A

Asthma Exacerbation

Pneumothorax

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95
Q

What is the histological characterisation of asthma?

A

Characterised by eosinophilic inflammation:
Lots of inflammation
Smooth muscle hypertrophy
Basement membrane thickening
Little fibrosis and little alveolar disruption

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96
Q

What is the Histological Characterisation of COPD?

A

Characterised by neutrophilic inflammation:
Lots of inflammation
Lots of fibrosis
Lots of alveolar disruption
Little smooth muscle hypertrophy and basement membrane thickening

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97
Q

What are the main conditions that are caused by Lower respiratory Tract Infections (LRTL)?

A

Tuberculosis
Pneumonia

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98
Q

What is Tuberculosis?

A

An infectious disease caused by Mycobacteria characterised by caseating granulomas.

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99
Q

What are the organisms classified as Mycobacterium Tuberculosis Complex (MTC)?

A

MTC organisms = TB causing:

M. tuberculosis
M. africanum
M. microtis
M. bovis (from unpasteurised milk)

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100
Q

What is the morphology of M. TB?

A

Gram Positive Rod Bacilli
Non motile + non spore forming

Mycolic acid capsule: Acid fast staining (w/ ZN)

Resistant to phagocytic killing.

Slow growing (15-20 hrs)

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101
Q

What is the epidemiology of TB?

A

1.7Bn people have latent TB
Top infectious killer in the world and in top 10 killers in the world (of anything)
Affects immunocompromised more
More common in South Asia (India, China, Pakistan) and Sub-Saharan Africa

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102
Q

How is TB infection spread?

A

Via airborne transmission

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103
Q

What are the risk factors for TB infection?

A

Contact with someone w/ active TB
Country/recent travel to associated countries
Immunocompromised (HIV etc)
IVDU
Homelessness
Smoking and alcohol
Increased age

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104
Q

What are the different types of TB?

A

Active TB - active infection

Latent TB (95% of cases) - Previous infection where the immune system has encapsulated and prevented progression of TB

Secondary TB - When Latent TB reactivates - often in immunocompromised

Miliary TB - Where immune system cannot control the infection and it becomes disseminated

Extrapulmonary TB - where TB infects other areas

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105
Q

What Extra-pulmonary sites can TB infect?

A

Lymph nodes
Pleura
Central nervous system
Pericardium
Gastrointestinal system
Genitourinary system
Bones and joints
Cutaneous TB affecting the skin

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106
Q

What is the pathogenesis of TB?

A

Infection of TB via droplets/aerosol

TB phagocytosed (but resistant to killing). (primary TB)

Over the next few weeks the immune system is activated and will form a granuloma around the infected macrophage which typically occurs in the lung apex.

T cells recruited and Centre of granuloma undergoes caseating necrosis (1’ Ghon Focus)

Ghon Focus spreads to nearby Hilar lymph nodes forming a Ghon Complex

Latent TB:
In most people TB is contained within granuloma will lie dormant and becomes latent TB.

Miliary TB:
If immune system becomes compromised TB can become reactivated.
TB spreads from Ghon complex throughout pulmonary system and then systemically then it becomes Miliary TB

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107
Q

Why does TB typically occur in the Upper lobes of the lung?

A

Upper lobes are better oxygenated (less perfused due to V/Q mismatch and gravity)

TB is aerobic and therefore perfers this environment.

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108
Q

How does TB resist gram staining?

A

High lipid content with mycolic acids in cell wall makes mycobacteria resistant to gram stain

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109
Q

Is latent TB symptomatic?

A

No - ASx as bacteria is contained within granuloma and causes no Sx

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110
Q

What are the symptoms of active TB?

A

Systemic Sx:
Fatigue
Fever + night sweats + weight loss (characteristic of TB)
Lymphadenopathy

Cough w/haemoptysis >3 weeks
Chest pain
Dyspnoea
Erythema Nodosum

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111
Q

What are the signs of TB?

A

Auscultation - often normal (may have crackles)
Consolidation in lung
Lung Collapse
Clubbing

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112
Q

What may be symptoms of Extrapulmonary TB?

A

Lymph Node TB (most common)
CNS - Meningism
Skin rash
Cardiac - TB pericarditis Sx
Bone - Join pain
Spinal Pain (spinal TB)
GU - Epididymitis, LUTS
Abdo - Ascites

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113
Q

What are some screening Tests for TB/diagnosis of latent TB?

A

Latent Disease - Mantoux Test

Interferon Gamma release assay
(This can distinguish between TB exposure and TB vaccine)

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114
Q

What are the primary investigations for Active TB?

A

CXR - UPPER LOBE patchy consolidation/cavitation, pleural effusions, Granulomata in chest

Sputum culture and Microscopy:
Microscopy - AFB bright red on ZN stain.
PCR - NAAT/PCR
Culture - Solid Culture on Lowenstein-Jensen Agar

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115
Q

What would you see on CXR in TB?

A

UPPER LOBE PRIMARILY

Patchy Consolidation
Ghon Complex
Granulomatous Lesions
Hilar Lymphadenopathy
Pleural Effusion
Millet Seeds in millary

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116
Q

What is the Mantoux Test?

A

Protein derived from organism (Tuberculin)
Inject intradermally
Stimulates type 4 delayed hypersensitivity reaction

  • within 2 days the APCs and T cells would be activated if there has been exposure to Tb and an immune response would have occurred

Not sensitive – immunosuppressed or miliary TB won’t react (false negatives)

Only moderately specific (false positives)

Won’t easily distinguish infection from disease

Drawback of Tuberculin skin test:
If patient has had BCG vaccine, there will be a reaction
Cannot tell if patient has latent TB

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117
Q

What is the management of latent TB?

A

Doesnt necessarily need Tx
If risk of reactivation then:
6 months of isoniazid with pyridoxine (6H) or
3 months of isoniazid (with pyridoxine) and rifampicin (3HR)

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118
Q

What is the Treatment for Active TB?
When would Tx be given for 12 months?

A

RIPE: Combination Abx for 6-12 months
R – Rifampicin for 6 months
I – Isoniazid for 6 months
P – Pyrazinamide for first 2 months
E – Ethambutol for first 2 months

Tx for 12 months if CNS TB

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119
Q

Why is TB Treatment given for so long?

A

To ensure the TB is cleared to prevent re-occurrence
Also to prevent Drug resistance developing.

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120
Q

What are the side effects of TB treatment?

A

Rifampicin - red/orange Urine + Hepatitis
Isoniazid - Peripheral Neuropathy / inhibitor of CYP450/ Hepatitis
Pyrazinamide - Hepatitis and gout
Ethambutol - Optic neuritis/eye problems

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121
Q

What is often Co-Prescribed with Isoniazid and Why?

A

Pyridoxine (Vit B6)
Helps to reduce the risk of peripheral neuropathy development

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122
Q

What must be done if TB is diagnosed?

A

Inform Public Health England

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123
Q

How can TB be prevented?

A

Vaccination - BCG vaccine for neonates

Detection and Tx of latent TB via Mantoux Test and Treat

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124
Q

What is the treatment for Latent TB?

A

6 months of isoniazid with pyridoxine (6H) or
3 months of isoniazid (with pyridoxine) and rifampicin (3HR)

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125
Q

What is Pneumonia?

A

Infection of the lung parenchyma leading to inflammation of the lung tissue and fluid exudation (sputum) collecting in the alveoli.

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126
Q

What is the Epidemiology of Pneumonia?

A

Incidence 350/100, 000/year (>1 in 300)
20-50% hospitalised, 5-10% require ITU
Hospitalisation average 6-8 days
Mortality
1% in community, 10% in hospital, 30% in ITU
UK 2012, 28,952, 5.1% of all deaths
Costs > £400 million/year to UK
Significant short- and long-term mortality from other causes after pneumonia

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127
Q

Who is at risk of developing pneumonia?

A

Extremes of age
COPD and other respiratory diseases
Immunocompromised
Nursing home residents
Impaired swallow
Diabetes
Congestive Heart Failure
Alcoholics
IVDU

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128
Q

What are the classifications of Pneumonia?

A

Classified by the setting in which a Px has contracted infection
Community Acquired Pneumonia
Hospital Acquired Pneumonia
Aspiration Pneumonia

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129
Q

Define Community Acquired Pneumonia (CAP)?

A

Pneumonia that develops out in the community or <48hrs after hospital admission

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130
Q

Define Hospital Acquired Pneumonia (HAP)?

A

Pneumonia that develops more than 48 hours after hospital admission.

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131
Q

Define Aspiration pneumonia?

A

Pneumonia that develops as a result of inhaling foreign material (food etc)

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132
Q

What is the main type of organism that causes pneumonia?

A

Bacterial infection

Can also be Viral (Influenza/CMV) or fungal (P. jirovecii)

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133
Q

What are the main cause of CAP?

A

S. pneumonia (50%)
H. influenzae (20%)
Mycoplasma pneumoniae (Atypical pneumonia)
H. Influenzae
Legionella

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134
Q

What are some less common causes of CAP?

A

S. aureus
Legionella (atypical)
Moraxella
Chlamydia pneumoniae (atypical)

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135
Q

Where is legionella caused pneumonia typically from?

A

Often from Spain/ warmer countries
Recent Travel Hx and staying in hotels with air conditioning.
Or WARM water

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136
Q

What are the risk factors for HAP?

A

Elderly
Ventilator associated
Post Operative

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137
Q

What are the main causes of HAP?

A

S. aureus
Gram Neg Enterobacter:
- P. aeruginosa
- E. coli
- Klebsiella

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138
Q

What is the concern of treating HAP?

A

Most of the causative organisms have multi drug resistance

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139
Q

What is the main cause of aspiration pneumonia?

A

Klebsiella

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140
Q

What is atypical pneumonia?
How are they Tx?

A

pneumonia caused by an organism that cannot be cultured in the normal way or detected using a gram stain.

They dont respond to penicillins

Tx with Macrolides, Fluoroquinolones and tetracyclines.

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141
Q

What are the causes of atypical pneumonia?

A

Legionella
Chlamydia psittaci
Mycoplasma pneumoniae
Chlamydophila pneumonia
Q fever (Coxiella)

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142
Q

What is the main cause of fungal pneumonia?

A

Pneumocystis jiroveci (PCP)
Occurs in immunocompromised Px
AIDS defining illness

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143
Q

How is PCP treated?

A

Co-trimoxazole
(combination of Trimethoprim and Sulphamethoxazole)

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144
Q

What are the risk factors for pneumonia?

A

Extremes of age
Preceding infection (viral)
Immunosuppressed
IVDU
Smoking
CO-Morbidities - DM, HIV
Respiratory conditions - asthma, COPD, CF

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145
Q

What is the pathogenesis of typical pneumonia?

A
  • Bacteria “translocate” to normally sterile distal airway - bacteria from URT that has either came in quickly or colonised for a while are micro-aspirated into lower lung
  • Resident host cells become overwhelmed
  • Develop an inflammatory response – neutrophils and inflammatory exudate fill alveolar space
  • Pus collects in the lung causing consolidation

Resolution phase – when bacteria cleared

  • Inflammatory cells removed by apoptosis
  • Resolution phase leads to complete recovery

Simple:
Bacteria invades
Infection and inflammation
Exudate forms inside alveolar lumen
Sputum production

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146
Q

What is the pathogenesis of atypical pneumonia?

A

Bacteria invades
Infection and inflammation
Exudate forms in interstitium of alveoli
Dry cough

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147
Q

What are the symptoms of pneumonia?

A

Productive cough w/purulent sputum (classically rusty may suggest S. pneumonia)
Fever, Sweat and Rigors - due to infection
Pleuritic chest pain
SOB
Malaise

May cause confusion in elderly
Dry cough in atypical pneumonia

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148
Q

What are the signs of pneumonia?

A

Deranged Vital Signs (HR, BP, RR, PP)
Consolidation:
- Reduced Chest Expansion
- Dull Percussion
- Bronchial Breathing

Bronchial Breath Sounds
Focal Coarse Crackles
Dullness to Percussion

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149
Q

What are some classical symptoms of Pneumonia infection?

A

Fever
Sweats
Rigors

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150
Q

What are the primary investigations of pneumonia?

A

1st Line:
CXR (diagnostic) shows consolidation

Sputum Microscopy culture and Sensitivities (MC+S) + Gram Stain to ID organism

FBC - Raised WCC
U&E - urea
CRP - raised due to inflammation
Legionella Urinary Antigen - Doesn’t respond well to Abx

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151
Q

How is pneumonia assessed for severity?

A

CURB65:
C – Confusion
U – Urea > 7
R – Respiratory rate ≥ 30
B – Blood pressure < 90 systolic or ≤ 60 diastolic.
65 – Age ≥ 65

Score 0/1: Consider treatment at home
Score ≥ 2: Consider hospital admission
Score ≥ 3: Consider intensive care assessment

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152
Q

How can CURB65 be used to assess mortality in Pneumonia?

A

0 = Low risk (<1% mortality)
1-2 = Intermediate risk (1-10% mortality)
3-4 = High Risk (>10% mortality)

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153
Q

What organisms may show multi-lobar pneumonic lesions on CXR?

A

S. pneumoniae
S. aureus
Legionella

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154
Q

What organisms may show Multiple abscess pneumonic lesions on CXR?

A

S. aureus

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155
Q

What organisms may show upper lobe pneumonic lesions on CXR?

A

Klebsiella

(but first exclude TB)

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156
Q

What is the Initial treatment for CAP pneumonia?

A

Oxygen Saturation 94-98% (If COPD then sats 88-92%)
IV Fluids if dehydrated
Appropriate Analgesia - Paracetamol/NSAIDs

Antibiotics: Initially start on Broad Spec:

  • Mild CAP (CURB65 0-1): Amoxicillin PO 5 days (clarithromycin/Doxycycline if allergic)
  • Moderate-severe CAP (CURB65 2): Amoxicillin + Macrolide (clarithromycin) PO 7-10 days
  • Admit to hospital
  • Severe CAP (CURB65 3-5): IV Co-Amoxiclav + IV Macrolide (Clarithromycin) 7-10 days or 14-21 if S.aureus

(If legionella (notify PHE) and Clarithromycin)

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157
Q

After Treating Pneumonia, What should be done in the elderly (>50yrs)

A

Follow-up CXR to ensure that there is not a lung tumour causing the infection as the consolidation from the pneumonia will hide this.

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158
Q

What is the treatment for pneumonia when the causative organism is known?

A

S. pneumoniae - Amoxicillin (Clarithromycin/Cefotaxime)
H. Influenzae - Doxycycline/Co-amoxiclav
S. aureus - Flucloxacillin (cefuroxime)
MRSA - Vancomycin
Klebsiella - Cephalosporins (cefotaxime) or carbapenems
P. Aeruginosa - Piperacillin-Tazobactam (Tazocin)
Atypical - Macrolides/Fluoroquinolones

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159
Q

What are the treatments for HAP?

A

Broader spectrum Empirical Tx first:

Early Onset <5 days - IV aminoglycoside (gentamicin) + Tazocin

Later Onset >5 days -IV Tazocin

Then once cultures ID organism - targeted Abx

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160
Q

What can be done to prevent pneumonia?

A
  • Polysaccharide pneumococcal vaccine – protects against 23 serotypes
  • Pneumonococcal Conjugate Vaccine
  • Influenza vaccination to those >65, immunocompromised or with medical co-morbidities
  • Smoking cessation
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161
Q

What are the major complications of pneumonia?

A

Sepsis - Used to grade severity - CURB65
Parapneumonic Pleural effusion in 57% of CAP
Empyema
Respiratory Failure
Lung abscess
Death

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162
Q

What is Cystic Fibrosis?

A

An autosomal recessive condition that affects the mucus glands multi-systemically

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163
Q

What are the genetics for CF?

A

autosomal recessive mutation on Chromosome 7 affecting the CFTR protein.

There are multiple mutations but Del-F508.
(phenylalanine is deleted)

CFTR = Cystic Fibrosis Transmembrane Conductance Regulatory Gene

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164
Q

What is the prevalence of CF?

A

1 in 25 are carriers of the gene

1 in 2500 are affected by CF

165
Q

What are the risk factors for CF?

A

FHx
Known parental carriers
Caucasian (CF is the most common inherited condition in caucasians)

166
Q

What is the CFTR protein?

A

CFTR is an epithelial cAMP regulated chloride channel that normally actively secretes Cl- ions and passively secretes Na+ ions along with water into ductal secretions

This makes the ductal secretions thin and watery

167
Q

What is the pathophysiology of CFTR protein?

A

Mutation in CFTR causes it to become dysfunctional.

CFTR has reduced function meaning that less Cl-, Na+ and water are released into ductal secretions leading to the thickening of the mucus secretion.

168
Q

What is the pathophysiology of a CFTR dysfunction in relation to the lungs?

A

CFTR mutation leads to thick mucus secretions.

This causes impaired mucociliary clearance as the mucus is extra thick.

This leads to stagnation of mucus that contains pathogens which leads to increased infection risk.

The thicker mucus causes difficulty breathing

Trapping of mucosal pathogens can cause a inflammatory reaction which leads to an increased risk of bronchiectasis

169
Q

What is the pathophysiology of a CFTR dysfunction in relation to neonates?

A

Can lead to Meconium Ileus:
Stool becomes too thick to pass through the bowel leading to bowel obstruction therefore they do not have their first Meconium (poo) in first 24 hrs

170
Q

What is the pathophysiology of a CFTR dysfunction in relation to the GI Tract?

A

Thick secretions from the pancreas can lead to pancreatic duct obstruction.
Pancreatic insufficiency and malabsorption of foods.
Bowel obstructions

171
Q

What is the pathophysiology of a CFTR dysfunction in relation to the Hepatobiliary system?

A

Thicker biliary secretions leads to an increased risk of biliary obstruction.

Could lead to liver cirrhosis

172
Q

How can CF lead to male infertility?

A

CFTR mutation can cause atrophy of the vas deferens leading to infertility

173
Q

What are the symptoms of CF?

A

Chronic cough w/Thick sputum production

Recurrent respiratory tract infections

Loose, greasy stools (steatorrhoea) due to a lack of fat digesting lipase enzymes

Abdominal pain and bloating

Most common cause of Meconium Ileus in infants

Parents may report the child tastes particularly salty when they kiss them, due to the concentrated salt in the sweat

Poor weight and height gain (failure to thrive)

174
Q

What are the signs of CF?

A

Meconium Ileus is first sign
Low weight or height on growth charts
Nasal polyps
Recurrent respiratory infections
Neonatal jaundice
Salty Sweat
Pancreatic Insufficiency
Finger clubbing
Crackles and wheezes on auscultation
Abdominal distention

175
Q

What are the primary investigations for CF?

A

New-born Blood spot test (Immuno-reactive Trypsin Test)

Sweat Electrolyte Test (gold standard)

Genetic testing for CFTR mutation)

Faecal Elastase Test - Pancreatic Insufficiency

CXR - Hyperinflation, Increased Pulmonary Markings, Bronchiectasis

176
Q

What is the CF Sweat test?

A

Pilocarpine and electrodes placed on skin make it sweat.

Tested for Chloride Concentration.

A result of > 60 mmol/L (sweat chloride) is positive and requires referral to a cystic fibrosis specialist (normal value < 40 mmol/Ll)

177
Q

Why are people with CF at a massively increased risk of recurrent respiratory tract infections?

A

Patients with cystic fibrosis struggle to clear the secretions in their airways.
This creates a perfect environment with plenty of moisture and oxygen for colonies of bacteria to live and replicate.

178
Q

What are the key microbial organisms that colonise the respiratory tract in CF?

A

S. aureus
P. aeruginosa

+Haemophilus influenza
Klebsiella pneumoniae
Escherichia coli

179
Q

What is the management of CF?

A

Conservative:

  • Chest physiotherapy
  • Exercise
  • No smoking

Medication:

  • Anti-mucolytics - rhDNase (Dornase Alfa)
  • Prophylactic Flucloxacillin (prevent S. aureus), Amoxicillin (H. Influ), Ciprofloxacin (p.aeur)
  • Bronchodilators (SABA) + ICS
  • Vaccinations - Pneumococcal, Influenza, Varicella
  • Lung Transplant in progressive RF

Systemic Tx:

  • Pancreatic enzyme replacement
  • Vitamin Supplements (A,D,E,K)
  • High calorie diet.
180
Q

What is Bronchiectasis?

A

Chronic inflammation of the bronchi and bronchioles leading to permanent dilatation of central and medium-sized airways. This is due to inflammatory destruction of airway walls resulting in persistently infected mucous.

Commonly occurs secondary to CF

181
Q

What is the Epidemiology of Bronchiectasis?

A

More common in women than men
May develop after lung infections
Pathological end point of many disease
Presents at any age but incidence increase with age

182
Q

What are the possible causes of Bronchiectasis?

A

Idiopathic - 50%
Chronic bronchial inflammation caused by :

  • Obstruction - Foreign bodies, Tumour, Thick Mucus
  • Previous infection - P. aeruginosa, TB
  • Allergy and Inflammatory conditions
  • Immunodeficiency - AIDS, Immunoglobulin Deficiency
  • Congenital - CF
183
Q

What are the risk factors for Bronchiectasis?

A

Post Infection (TB/Pneumonia)
Increased Age
Smoking
Females
Genetics
CF

184
Q

What is the pathogenesis of Bronchiectasis?

A

Infection or chronic inflammatory conditions cause immune system activation.

This will secrete proteases that break down elastin in the bronchi walls leading to irreversible dilation of the bronchi

This leads to increased risk of microbial colonisation.

This causes mucus hypersecretion and trapping due to the dilated bronchi and damaged cilia there is impaired mucociliary escalator

This will lead to airway obstruction.

185
Q

How are bronchiectasis and emphysema different?

A

Emphysema is dilation of the acini and alveoli due to loss of elastin.

Bronchiectasis is dilation of the bronchi due to loss of elastin.

186
Q

What are the symptoms of Bronchiectasis?

A

Dyspnoea/SOB
Productive cough with Copious sputum production
Haemoptysis (maybe)
Wheeze
Chest Pain
Recurrent chest infections

187
Q

What are the signs of Bronchiectasis?

A

Hx of Chronic Productive cough and recurrent Chest infections
Foul Smelling Sputum

Auscultation:
Coarse Crackles on inspiration
High pitched inspiratory crepitations
Ronchi - Low pitch snore

Finger Clubbing

188
Q

What are the primary investigations for Bronchiectasis?

A

High resolution CT Chest: Gold Standard:
shows bronchial dilation and bronchial wall thickening (signet ring sign)

CXR - dilated airways with thickened walls appear as ‘tram-tracks’

Sputum cultures - infective organisms

Spirometry: Obstructive (FEV1/FVC < 0.7)

189
Q

What are some differential Diagnoses for Bronchiectasis?

A

COPD
Asthma
TB
Chronic sinusitis
Pneumonia
Pulmonary fibrosis
Inhalation of foreign body

190
Q

What is the treatment for Bronchiectasis?

A

Non curative: Tx underlying cause if present.
Reduce RFs (stop smoking) and Chest Physiotherapy

Mucoactive agent (carbocisteine)
Bronchodilator - for asthma/COPD sufferers
Prophylactic Abx for acute exacerbations: (Pseudo (Ciproflox), Haem (Doxyc), S.aureus (fluclox)

191
Q

What are some complications of Bronchiectasis?

A

Infective exacerbation
Chronic respiratory failure
Haemoptysis (may be massive and life-threatening)
pneumonia
Pneumothorax
Chest pain

192
Q

Define a Pleural Effusion?

A

Excess fluid accumulation between the visceral and parietal pleura (pleural cavity)
Clinically detected when >500ml present
Detected on CXR when >300ml Present

193
Q

What are the different types of Pleural effusion?

A

Whether the fluid is:

Exudative - high protein count (>3g/dL)

Transudative - lower protein count (<3g/dL)

194
Q

What are the main pathology relating to a Exudative and Transudative Pleural Effusion?

A

Exudative:
Occurs due to increased permeability and therefore leakiness of pleural space and/or capillaries, usually as a result of inflammation, infection or malignancy

Transudative:
Occurs when the balance of hydrostatic forces in chest favour accumulation of pleural fluid i.e. increased pressure due to the backing up of blood in left-sided congestive HF

195
Q

What are the Exudative causes of pleural effusion?

A

Related to inflammation:
Trauma
Lung cancer
Pneumonia
Empyema
Rheumatoid arthritis
Tuberculosis

196
Q

What are the Transudative causes of Pleural effusion?

A

Fluid Moving (transport) across into the pleural space:
Increase Hydrostatic Pressure:
Congestive cardiac failure
Fluid Overload
Constrictive pericarditis
Meig’s syndrome

Decreased Oncotic Pressure:
Hypoalbuminaemia
Hypothroidism
Nephrotic Syndrome

197
Q

What is Meig’s Syndrome?

A

right sided pleural effusion with ovarian malignancy

198
Q

What is the pathophysiology of an Exudative pleural effusion?

A

Inflammation leading to increased vascular permeability

This leads to increased protein leaking out of the vessels and accumulates in the pleural cavity.

Increased pleural oncotic pressure draws fluid into the pleural cavity leading to pleural effusion

199
Q

What is the pathophysiology of an Transudative pleural effusion?

A

Fluid shifting due to and increase in hydrostatic pressure (eg. in HF) or a decrease in oncotic pressure (eg.hypoalbuminaemia) causing leaking of fluid into pleural cavity

200
Q

What is the most common cause of Exudative pleural effusion?

A

Pneumonia and malignancy

201
Q

What is the most common cause of Transudative pleural effusion?

A

(congestive) Heart failure

202
Q

What are the symptoms of Pleural effusion?

A

May be ASx

  • Dyspnoea
  • Pleuritic chest pain (often exudate due to pleural inflammation/irritation)
  • Cough

Sx of underlying pathology:
Peripheral oedema - HF
Ascites - LF
Cough & fever - RTI

203
Q

What are the signs of pleural effusion?

A

Reduced Chest expansion on affected side
Reduce breath sounds on affected side

Dull percussion (increased fluid)

Pleural friction rub/bronchial breathing

Tracheal Deviation

204
Q

What may be a differential diagnosis with a hyper resonant percussion?

A

Pneumothorax

205
Q

What are the primary investigations for pleural effusion?
What would you see?

A

GS + 1st Line: CXR:
Shows Blunting of Costophrenic angles
Fluid in lung fissures (fluid appears white)
Tracheal/Mediastinal deviation (if massive effusion)
Meniscus

Thoracocentesis (Pleural fluid aspiration):
pH, Lactate, WCC, Microscopy
Determine Transudate or Exudate

206
Q

Where would you see transudates or exudates on CXR in pleural effusion?

A

Transudates - Bilateral (TB)
Exudates - Unilateral (EU)

207
Q

What would you see in thoracocentesis to aid in determining whether a pleural effusion is exudative or transudative?

A

Transudate – clear
Exudate – cloudy
Lymphatic – looks like milk

208
Q

What is the treatment for Pleural effusion?

A

Conservative Mx:
Small effusions can be treated by Tx of underlying cause (often Transudative) - eg. loop diuretics for HF

Infective Effusions:
Chest Drain - remove fluid (often Exudative) + Abx

Non-malignant:
Thoracocentesis - needle drainage for Sx effusions.

Recurrent:
Pleurodesis - injection that adheres visceral and parietal pleural

209
Q

What should be done if a patient is having chronic recurrent pleural effusions?

A

Pleurodesis:
Surgical fusing/injection that adheres the pleural layers together to prevent fluid accumulation between them

210
Q

What is Empyema?

A

An infected Pleural Effusion (pus collects in pleural cavity)

211
Q

What does Empyema Show on pleural aspiration?

A

PHAL:
Pus,
High LDH.
Acidic pH (pH < 7.2),
Low glucose

212
Q

What is the treatment for Empyema?

A

chest drain to remove the pus and antibiotics

213
Q

What is a Pneumothorax?

A

An excess accumulation of air within the pleural space causing ipsilateral lung collapse.

214
Q

What is the Epidemiology of a Pneumothorax?

A

Occurs spontaneously or secondary to chest trauma
Spontaneous pneumothorax most common in young males
Generally, more common in males
Patients often tall and thin
Most commonly occurs between 20-40

215
Q

What are the causes of Pneumothorax?

A

Spontaneous

Trauma

Iatrogenic - lung biopsy, mechanical ventilation or central line insertion

Lung pathology - infection, asthma or

COPD

216
Q

What are the risk factors for a pneumothorax?

A

Tall thin males
Connective tissue disorders (MF, EHD)
FHx
Smoking
Underlying Lung disease - COPD, Asthma
RA

217
Q

What is the Pathophysiology of a Pneumothorax?

A

Pleural space is normally a vacuum (no air) with a negative pressure

Breach in the pleura (trauma/CT disorders)
Leads to air entry into pleural cavity
Elastic recoil of the lung causes it to deflate

Closed - air leaks from lung into pleural cavity (intact chest wall)

Open - Trauma to chest wall

218
Q

What are the symptoms of a pneumothorax?

A

Sudden onset
Sharp Pleuritic Chest pain
SOB

As pneumothorax enlarges, patient becomes more breathless and may develop pallor and tachycardia

219
Q

What are the signs of a pneumothorax?

A

Reduced breath sounds on affected side
Hyper resonant percussion (increased air)
Reduced chest expansion
Trachea Deviation away

Tachycardia/Tachypnoea
Hypotension - in Tension Pneumothorax

220
Q

What is the primary investigation for a pneumothorax?

A

If suspected Tension Pneumothorax - Do not wait for Ix

GS + 1st Line: erect CXR
Excess air appears black
Tracheal Deviation to other side

CT thorax can be more sensitive for small pneumothoraxes (GS for smaller Pneumothoraxes)

221
Q

What is seen on CXR in a pneumothorax?
When should you avoid requesting a CXR?

A

Loss of lung markings
Visible visceral pleural edge
Radiolucent space

Avoid request in Tension-Pneumothorax as this wastes time

222
Q

What is the treatment for a Primary, secondary and Tension pneumothorax?

A

Primary:

  • No SOB / <2cm - Self limiting and discharge
  • SOB/>2CM - Needle aspiration

Secondary:

  • NO SOB/<1cm - Self limiting and Discharge
  • NO SOB/1-2cm - Needle Aspiration
  • SOB & >2cm - Chest Drain (5th ICS)

Tension:

  • Urgent Needle Decompression
  • ABCDE Management
  • High Flow Oxygen
223
Q

What is a Tension Pneumothorax?

A

MEDICAL EMERGENCY:
Caused by trauma to the pneumothorax where air can flow into the pleural space but it cannot lead due to the creation of a one way valve

224
Q

What is the pathogenesis of a Tension pneumothorax?

A

Trauma creates a one way valve

During inspiration air is drawn into the pleural space and during expiration, the air is trapped in the pleural space.

More air keeps getting drawn into the pleural space with each breath and cannot escape.

Creates pressure inside the thorax that will push the mediastinum across, kink the big vessels in the mediastinum and cause cardiorespiratory arrest.

225
Q

What are the signs of a tension pneumothorax?

A

Tracheal deviation away from side of pneumothorax
Reduced air entry to affected side
Increased resonant to percussion on affected side
Tachycardia
Hypotension

226
Q

What is the treatment for a Tension Pneumothorax?

A

High Flow Oxygen and Urgent Needle Decompression

LEARN BY HEART:
“Insert a large bore cannula into the second intercostal space in the midclavicular line on the side of the pneumothorax.”

Once pressure is relieved then chest drain.

227
Q

Where would you insert a chest drain?

A

Triangle of Safety:
The 5th intercostal space (or the inferior nipple line)
The mid axillary line (or the lateral edge of the latissimus dorsi)
The anterior axillary line (or the lateral edge of the pectoris major)

228
Q

What is an Interstitial Lung Disease (ILD)?

A

Umbrella term to describe conditions that affect the lung parenchyma (the lung tissue) causing inflammation and fibrosis.

229
Q

Give some examples of ILDs?

A

Idiopathic Pulmonary Fibrosis
Pneumonoconiosis
Sarcoidosis
Hypersensitivity Pneumonitis

230
Q

What test is generally used to diagnose ILD?

A

CXR - nodular opacities

High resolution CT Thorax:
Shows Ground Glass appearance and honeycombing (mainly in the lower zones)

Spirometry - Restrictive Pattern

Lung Biopsy can confirm diagnosis on Histology

231
Q

What is the general Management for ILD?

A

Generally the damage is irreversible and so supportive Tx to prevent progression.

Mx options:
Remove or treat the underlying cause
Home oxygen where they are hypoxic at rest
Stop smoking
Physiotherapy and pulmonary rehabilitation
Pneumococcal and flu vaccine

232
Q

What is Pulmonary Fibrosis?

A

Progressive fibrosis and scarring of the lung parenchyma.

233
Q

What are the different types of pulmonary fibrosis?

A

Idiopathic PF
Drug induced PF
Secondary PF

234
Q

What is Idiopathic Pulmonary Fibrosis?

A

Condition of PF where there is no clear cause.

This is the most common ILD that is typically seen in older men who smoke.

235
Q

What drugs can induce pulmonary fibrosis?

A

Bleomycin
Amiodarone
Cyclophosphamide
Methotrexate
Nitrofurantoin

236
Q

What are secondary causes of Pulmonary Fibrosis?

A

Alpha-1 antitripsin deficiency
Rheumatoid arthritis
Systemic lupus erythematosus (SLE)
Systemic sclerosis

237
Q

What are the risk factors for Idiopathic Pulmonary FIbrosis?

A

Smoking
Occupational causes (dust)
Increased age (60-70s)
Male
FHx

238
Q

What is the pathophysiology of Pulmonary fibrosis?

A
  • Progressive chronic lung damage
  • Causes Type II pneumonocytes to over proliferate during repair leading to excessive myofibroblast activation
  • Leads to Replacement of damaged lung parenchyma with collagen.
  • Causes excessive scarring and fibrosis.
  • Lungs fail to expand on inhalation
  • Thickens the interstitium between the capillary and alveoli causing impaired gas exchange

Can lead to Type 1 Respiratory Failure.

239
Q

What can cause pulmonary fibrosis in the upper respiratory zones?

A

Upper Zone: ASPENT
Aspergillosis
Sarcoidosis
Pneumoconiosis (Coal, Silica)
Extrinsic allergic alveolitis (hypersensitivity Pneumonitis)
Negative. ser-arthropathy Ankylosing Spondylitis
Tb

240
Q

What can cause Pulmonary Fibrosis in the Lower Respiratory Zones?

A

Lower Zone: AIDS
Asbestosis
Idiopathic Pulmonary Fibrosis
Drug induced Fibrosis (Methotrexate, Amiodarone, Nitrofurantoin)
SLE/Scleroderma and other CT diseases

241
Q

What are the symptoms of pulmonary fibrosis?

A

4 Ds:
Dyspnoea
Dry Cough
Diffuse Inspiratory crackles
Digits (clubbing)

and malaise

242
Q

What are the signs of pulmonary fibrosis?

A

Bibasal fine inspiratory crackles (end respiratory)

Finger clubbing

Cyanosis

+ Sx of underlying pathology if Secondary PF

243
Q

What are the diagnostic investigations for pulmonary fibrosis?

A

Spirometry: Restriction (FVC reduced, FEV1/FVC normal)

CXR - non specific but can be used to exclude other DDx

Gold Standard:
High CT thorax to confirm diagnosis = Ground glass & Honeycombing

244
Q

What is the treatment for Pulmonary Fibrosis?

A

Supportive Tx:
Smoking cessation
Pulmonary Rehabilitation
Oxygen Therapy
Vaccines

Antifibrotic Agents:
Pirfenidone or nintedanib (indicated if FVC is 50% - 80% of predicted)

Consider Lung Transplant

245
Q

What is the prognosis like for IPF?

A

IPF has a poor prognosis, with median survival ranging from 2.5 - 3.5 years after diagnosis.

246
Q

What is Pneumonoconiosis?

A

Interstitial lung fibrosis that occurs secondary to inhalation of occupational triggering antigens that cause an inflammatory reaction.

247
Q

What are some different types of pneumonoconiosis?

A

Silicosis - Inhalation of silicon dioxide
Asbestosis - Inhalation of asbestos

248
Q

Explain the pathogenesis of pneumonoconiosis?

A

Particles (Dust, asbestos, silica) are inhaled, they reach the terminal bronchioles and are ingested by interstitial and alveolar macrophages.

Dust particles are carried by macrophages and expelled as mucus.

In chronic exposure (occupation), this process is no longer functional and macrophages accumulate in alveoli,

Resulting in immune system activation and lung tissue damage.

Fibroblasts then arrive and deposit excess collagen to cause lung fibrosis

249
Q

What are the risk factors for pneumonoconiosis?

A

Male
Increasing age
Substance exposure - Coal, dust, silicon, asbestos etc

250
Q

What are the symptoms of pneumonoconiosis?

A

Exertional Dyspnoea
Dry Cough
Haemoptysis
Wheezing
Weight loss

251
Q

What does asbestosis increase the risk of developing?

A

Mesothelioma

252
Q

What are the diagnostic findings for Pneumonoconiosis?

A

CXR:
Coal Workers Lung - Nodular opacities in upper lobes
Silicosis - Eggshell calcification of hilar lymph nodes
Asbestosis - Pleural Thickening and Calcification

Spirometry: Restrictive and reduced DLCO

High-Res CT chest: interstitial fibrosis

Microscopic Exam - Ferruginous Bodies - Asbestos fibres coated in macrophages

253
Q

what is the management for Pneumonoconiosis?

A

Conservative Mx as incurable:

Stop smoking
Avoid exposure

254
Q

What is Sarcoidosis?

A

A Type of Interstitial Lung disease

A multi-systemic Granulomatous inflammatory condition characterised by non-caseating granulomas depositing in many tissues of unknown cause

255
Q

What type of hypersensitivity reaction is sarcoidosis thought to be?

A

Thought to be a type 4 Hypersensitivity reaction.

Idiopathic

256
Q

What are the risk factors for sarcoidosis?

A

Afro-Caribbean and Scandinavian ethnicity
Young adults: 20-40 yrs
Female gender
Family history

257
Q

What is the Typical presentation of Sarcoidosis?

A

Sx can range from ASx to life threatening

Typical patient:
patient is a 20-40 year old black woman presenting with a dry cough and shortness of breath. They may have nodules on their shins suggesting erythema nodosum.

258
Q

What part of the body is affected by Sarcoidosis?

A

Typically affects the lungs (90%)

But can present will many extra-pulmonary symptoms as it can affect any system of the body

259
Q

What are the Chest symptoms of sarcoidosis?

A

Dry cough
Dyspnoea
Mediastinal lymphadenopathy

Constitutional Sx:
Weight loss, Fatigue and fever

260
Q

What are the Extra-pulmonary of features Sarcoidosis?

A

GRANULOMAS:
General - Fever, Weight loss, rigors
Respiratory issues - Dry cough, Dyspnoea
Arthralgia
Neurological - polyneuropathy
Urinary signs - Hypercalcaemia
Low Hormones - Amenorrhoea
Ophthalmology - Anterior Uveitis
Myocardial - restrictive cardiomyopathy
Abdominal - Hepatomegaly
Skin - Erythema Nodosum

261
Q

What is Lofgren’s Syndrome?

A

specific presentation of sarcoidosis. It is characteristic by a triad of:

Erythema nodosum
Bilateral hilar lymphadenopathy
Polyarthralgia (joint pain in multiple joints)

262
Q

What are some differential diagnoses of sarcoidosis?

A

Tuberculosis (caseating)
Lymphoma
Hypersensitivity pneumonitis
HIV
Toxoplasmosis
Histoplasmosis

263
Q

What are the primary investigations for sarcoidosis?

A

First Line:

  • CXR - Bilateral Hilar lymphadenopathy and pulmonary infiltrates/nodules
  • CXR often used for staging

CT Chest (may also be used)

GS Diagnostic:

  • Biopsy (non caseating granuloma)

Other:

  • Spirometry - Restrictive
  • Bloods:
    • HYPERCALCAEMIA - Excess Vit D produced by macrophage
    • Elevated ACE due to granulomas
264
Q

What electrolyte is commonly found increased in Sarcoidosis?

A

Hypercalcaemia

265
Q

What would be seen on CXR to stage Sarcoidosis?

A

Staging
Stage 0 – no changes
Stage I – bilateral hilar lymphadenopathy
Stage II – bilateral hilar lymphadenopathy and diffuse interstitial disease
Stage III – interstitial disease only (reticulonodular pattern)
Stage IV – pulmonary fibrosis (honeycombing)

266
Q

What other investigations would be done for sarcoidosis to check for extra-pulmonary involvement?

A

U&Es - kidney involvement
Urine dipstick - proteinuria indicating nephritis
LFTs - liver
Ophthalmology review - eye
ECG/ECHO - heart
Abdo USS - liver and kidney

267
Q

What is the treatment of Sarcoidosis?

A

ASx/Mild: No Tx is 1st Line:
85% of stage 1 resolve spontaneously
50% of stage 2 resolve spontaneously

When Tx required:
1st Line: Oral Prednisolone (+bisphosphonates to protect against OP)

2nd Line: Methotrexate/Azathioprine

268
Q

What are the potential complications of Sarcoidosis?

A

Can progress to Pulmonary Fibrosis
Pulmonary HTN

269
Q

What is Hypersensitivity pneumonitis?

A

Type 3 hypersensitivity reaction (Non-IgE) to an environmental inhaled allergen that causes parenchymal inflammation and destruction to the alveoli and distal bronchioles

270
Q

Explain the pathophysiology of Hypersensitivity pneumonitis?

A

Allergen is inhaled and picked up by alveolar macrophages which take it to the nearest lymph node.

antibodies against allergen (IgG) form Ab-Ag complexes.

These complexes get deposited in the lung tissues and alveoli.

Complement is activated which causes acute inflammation of the lung tissue causing pneumonitis

Chronically this can lead to pulmonary fibrosis

271
Q

What are some different allergens/occupations that can lead to hypersensitivity pneumonitis?

A

Bird-fanciers lung is a reaction to bird droppings

Farmers lung is a reaction to mouldy spores in hay

Mushroom workers’ lung is a reaction to specific mushroom antigens

Malt workers lung is a reaction to mould on barley

272
Q

What are the classifications of Hypersensitivity Pneumonitis?

A

Acute - Sx develop <12 hrs post exposure and resolve typically < 48 hrs

Chronic - Develop often after lower levels but prolonged exposure to allergens

273
Q

What are the acute clinical manifestations of Hypersensitivity Pneumonitis?

A

Sx develop <12 hrs after a good amount of exposure and resolve after 48 hrs

  • Fever
  • Rigors
  • Headache
  • Malaise
  • Shortness of breath
  • Cough
  • Chest tightness
274
Q

What are the Chronic clinical manifestations of Hypersensitivity Pneumonitis?

A

Sx develop over prolonged exposure (often lower levels for long time)

Progressive cough
Progressive Dyspnoea
Fatigue
Weight loss

Fibrosis is evident

275
Q

How is Hypersensitivity pneumonitis diagnosed?

A

Acute:
Bloods
CXR
Lung Function Tests - Spirometry

Chronic:
Bronchoscopy with Bronchoalveolar lavage:
Biopsy shows raised T Lymphocytes and mast cells in bronchi, alveoli and non-caseating granulomas

CXR - Infiltrates, nodular or patchy fibrosis

High Res CT - Ground glass (upper lobes) and centrilobular nodules fibrosis in chronic. Reticulonodular infiltrates in acute

Spirometry/ Pulmonary function test - Restrictive

Serology - Specific Igs

276
Q

What is the treatment for hypersensitivity pneumonitis?

A

Remove the allergen

Steroids (glucocorticoids) can help with symptoms

Give oxygen if necessary

277
Q

What is Goodpasture’s Syndrome?

A

An autoimmune disease characterised by Anti-GBM autoantibodies that attack the lungs and kidneys.
A type of Pulmonary Vasculitis

278
Q

What is the pathophysiology of Goodpasture’s Syndrome?

A

Type II Hypersensitivity Reaction

Lung alveolar basement membranes and kidney glomerular basement membranes are made up of Type IV collagen (containing alpha 3, 4, and 5 strands)

Environmental toxins (smoking/infection) pass through the kidneys (via blood) or the lungs (inhalation) and damage the collagen exposing the strands.

Autoantibodies against the alpha3 chain of collagen bind and activate the Classical complement system.

This leads to inflammation of the lungs and kidneys that can cause pulmonary fibrosis and glomerular nephritis.

279
Q

What are the risk factors for Goodpasture’s syndrome?

A

Genetics - HLA-DR15

infection
Smoking
Oxidative stress

280
Q

What are the symptoms of Goodpasture’s Syndrome?

A

Constitutional Sx:
Lethargy
Fever
Anorexia
Weight loss
Myalgia

Pulmonary Sx:
Cough
Haemoptysis
Dypsnoea

Kidney Sx:
Haematuria and proteinuria

281
Q

How is Goodpasture’s syndrome diagnosed?

A

Biopsy often of kidney /lung:
Shows inflammation of BM and fluorescence testing for auto Abs
Microscopy - Crescent Glomerulonephritis

Serology: Anti-GMB +tve

282
Q

What is the treatment for Goodpasture’s Syndrome?

A

Corticosteroids
Immunosuppressants - Cyclophosphamide
Plasmapheresis

283
Q

what is the normal pulmonary blood pressure at rest?

A

8-20mmHg

284
Q

what is the definition of 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

285
Q

What is defined as pulmonary hypertension (mPAP)?

A

Resting mPAP >25mmHg at rest.

286
Q

How is Pulmonary HTN normally measured?

A

Right heart catheterisation.

287
Q

What is the pathophysiology of pulmonary HTN?

A

Reactive pulmonary vasoconstriction due to hypoxaemia

The increased resistance in the pulmonary vasculature leads to increased pressure in the right ventricle

This results in increased ventricular filling and stroke volume, which further increases pulmonary arterial pressure

Over time, right ventricular hypertrophy develops as it compensates for the increased afterload.

288
Q

What are the different groups of causes of pulmonary HTN?

A
  1. Primary pulmonary HTN - Idiopathic/CT disorders (MF, EHD)
  2. Left heart disease - VHD, HF, HOCM
  3. Chronic Lung disease - COPD, Asthma
  4. Pulmonary vascular disease - PE/Tumour
  5. Unclear/multifactorial - Sarcoidosis, Haematological disorders
289
Q

What is the most common cause of secondary pulmonary HTN?

A

COPD

290
Q

What are the symptoms of Pulmonary HTN?

A

Progressive breathlessness
Exertional Dizziness/syncope
Fatigue

Sx of underlying pathology

291
Q

What are the signs of pulmonary HTN?

A

Loud S2 heart sound - pulmonary side
Raised JVP
Pulmonary/Tricuspid regurgitation
Tachycardia
Hepatomegaly
Peripheral oedema
Right parasternal heave - due to RV hypertrophy

Signs of underlying pathology

292
Q

What are the primary investigations for Pulmonary HTN?

A

1st Line: (TEE) ECHO:
RV function, enlargement and Pressures

Gold Standard (diagnostic) Right heart Catheter

CXR - RVH, Enlarged proximal PA

ECG:
Right Ventricular Hypertrophy
Right axis deviation
Right bundle branch block

293
Q

What does Right ventricular hypertrophy look like on an ECG?

A

Larger R waves on the right sided chest leads (V1-3) and S waves on the left sided chest leads (V4-6)

294
Q

What is the treatment for pulmonary HTN?

A

Primary P HTN:
Phosphodiesterase-5 inhibitors (SILDENAFIL)
IV prostanoids (Epoprostenol)
Endothelin receptor antagonists (Macitentan)

Secondary P HTN:
Tx underlying cause

Supportive Tx for complications:
Respiratory failure, HF, arrythmias

295
Q

What are the main complications of pulmonary HTN?

A

Right heart failure: due to increasing pulmonary pressures
(Can lead to biventricular failure)

Pericardial effusion and tamponade

Hepatic congestion: due to worsening right heart failure

296
Q

What is a Mesothelioma?

A

A malignant neoplasm of the mesothelial cells of the pleura

297
Q

What is the primary cause of Mesothelioma?

A

Asbestos Exposure

Typically doesnt present until decades after the exposure

298
Q

What are the risk factors for Mesothelioma?

A

Asbestos Exposure (85% of cases have Hx)
Increasing age (40-70)
Males

299
Q

What is the epidemiology of a Mesothelioma?

A

More common in men
Often presents between 40-70
Latent period between exposure and development of tumour may be up to 45 years

300
Q

What are the symptoms of Mesothelioma?

A

SOB
Cough
Persistent Pleuritic chest pain

Constitutional Cancer Sx:
Fatigue, fever, night sweats, weight loss

Sx of metastases: bone pain etc

301
Q

Why may a patient with a mesothelioma have a hoarse voice?

A

Tumour presses on recurrent laryngeal nerve

302
Q

What are the signs of a Mesothelioma?

A

Finger clubbing
Reduced breath sounds
Stony Dull Percussion

Ascites (if peritoneal disease present)

303
Q

What are the primary investigations for mesothelioma?

A

First Line: Imaging:
CXR - pleural thickening +/- effusion
Contrast Enhanced CT

Bronchoscopy + Biopsy (Gold Standard for Dx)

304
Q

What is the treatment for Mesothelioma?

A

Surgery (if operable) otherwise Palliative:
Extrapleural pneumonectomy
Pleurectomy with decortication
Rarely curative

+/- Chemotherapy:
Cisplatin
Pemetrexed

+/- Radiotherapy

305
Q

What is the Main malignancy of the lung parenchyma?

A

Primary Bronchial Carcinomas

306
Q

How are Primary Lung cancers classified?

A

By Histology:

Small Cell Lung Cancer (SCLC): 20%

Non-Small Cell Lung Cancer (NSCLC): 80%
- Adenocarcinoma (40%)
- Squamous cell Carcinoma (20%)
- Large Cell Carcinoma (10%)
- Carcinoid/other (10%)

307
Q

What are the primary metastasis sites for Lung cancers?

A

Bones
Liver
Adrenal Glands
Brain
Lymph Nodes

308
Q

What is the epidemiology of Lung Cancer?

A

3rd most common cancer in the UK and 1/3rd of all cancer deaths
(behind breast and prostate)

Male:Female - 2:1

Kills 35,000 people in the UK
(more than Breast and Colorectal combined)

309
Q

What are the risk factors for Primary lung Cancer?

A

Smoking (BIGGEST CAUSE)
Asbestos
Coal
Ionising radiation
Underlying lung disease

Increasing age
FHx

310
Q

What are the causes of Lung Cancer?

A

SHOE:
Smoking (most common - 90%)
Host factors - Pre-existing lung disease, Genetics, HIV
Occupational - Coal, Asbestos, Nickel
Environmental - Ionising Radiation, Radon

311
Q

What is a Small cell lung cancer?

A

15% of primary lung cancers.
Derived from neuroendocrine APUD cells
Has Central lung lesions

Rapidly grows and Px often present at an advanced stage.

312
Q

Who is typically affected by SCLC?

A

Exclusively smokers

313
Q

What are the features of a SCLC?
Number of cases:
Location:
Derivation:
Paraneoplastic Syndromes

A

No of Cases - 15% of Lung Cancer

Location - Central lesions near main bronchus

Derived - From neuroendocrine cells - makes them responsible for paraneoplastic syndromes

Paraneoplastic Syndromes:
Ectopic ACTH - Cushing’s
Ectopic ADH - SIADH
Lambert Eaton Syndrome (NMJ disorder)

314
Q

What is the most common NSCLC?

A

Adenocarcinoma

315
Q

What are the features of an Adenocarcinoma NSCLC?
Number of cases:
Location:
Originates:
Affects:
Paraneoplastic Syndromes

A

Number of cases: 40% of NSCLC

Location: Peripheral Lesion

Originates: Mucus Secreting Glandular Cells

Affects: Non-smokers mainly

Paraneoplastic Syndromes:
- Hypertrophic Pulmonary Osteoarthropathy
- Gynaecomastia

316
Q

What are the Features of a Squamous Cell Carcinoma NSCLC?
Number of cases:
Location:
Originates:
Affects:
Paraneoplastic Syndromes

A

Number of cases: 20% NSCLC

Location: Central Lesion

Originates: From Lung Epithelium and has central necrosis

Affects: Smokers typically

Paraneoplastic Syndromes:
- Hypertrophic Pulmonary Osteoarthropathy
- PTHrp - Hypercalcaemia

317
Q

What are the Features of a Carcinoid NSCLC?
Number of cases:
Location:
Originates:
Affects:
Paraneoplastic Syndromes

A

Number of cases: <10% NSCLC

Location: Rare Peripheral

Originates: From mature Neuroendocrine cells related to MEN1 mutation

Affects: MEN1 mutations and neurofibromatosis

Paraneoplastic Syndromes
Secretes Serotonin

318
Q

What are the Features of a Large-cell Carcinoma NSCLC?
Number of cases:
Location:
Originates:
Affects:
Paraneoplastic Syndromes

A

Number of cases: <10% NSCLC
Location: Peripheral lesion commonly but can be found anywhere in lungs
Originates: Lacks both glandular and squamous differentiation

Paraneoplastic Syndromes
- Ectopic B-hCG production

319
Q

What are the general Symptoms of Lung cancer?

A

Persistent Cough w/haemoptysis
Shortness of breath
Pleuritic Chest pain

Constitutional Sx of Cancer:
Fever
Night sweats
Weight loss
Loss of appetite

320
Q

What are the general signs of Lung Cancer?

A

Reduced Breath sounds
Stony Dull Percussion - suggests malignant pleural effusion
Hoarseness (press on RLN)
Lymphadenopathy
Clubbing
Recurrent chest infections
Paraneoplastic Changes

321
Q

What are the primary investigations for lung cancer?

A

First line: CXR
Hilar enlargement
Peripheral opacity – a visible lesion in the lung field
Pleural effusion – usually unilateral in cancer
Collapse

Staging - CT Thorax with contrast scan if abnormal CXR

GS Diagnostic: Bronchoscopy + Biopsy w/ Histology

322
Q

How are Lung Cancers Graded?

A

TNM classification
Tumour – how big it is
T1 – <3cm
T2 - >3cm
T3 – invades chest wall, diaphragm and pericardium
T4 – invades mediastinum, heart, great vessels, trachea, oesophagus, vertebra, carina

Nodes – how many and where they are
N0 - none
N1 – Hilar nodes
N2 – same side mediastinal nodes or subcarinal
N3 – contralateral mediastinum or supraclavicular

Metastases
0 - none
1a – tumour on same side
1b – tumour elsewhere
X - unknown

323
Q

Which is a more aggressive cancer, SCLC or NSCLC?

A

SCLC is more aggressive

324
Q

What is the treatment for SCLC?

A

Often Diagnosed late and Px have metastatic disease:

Therefore
Chemo/radiotherapy (Cisplatin)
palliative care

325
Q

What is the treatment for NSCLC?

A

Early: Surgical Excision + adjuvant therapy

Late/Metastatic:
palliative treatment with immunotherapy, chemotherapy, and radiotherapy

(Nb. NSCLC has poor response to chemotherapy)

326
Q

What are some complications for lung cancer?

A

Recurrent laryngeal nerve palsy
Horner’s syndrome (Pancoast tumour)
SVC obstruction - shown as pembertons sign (red head when elevating arms)
Paraneoplastic Syndromes
Bone pain/Hypercalcaemia

327
Q

What is more common, Primary or secondary lung cancer?

A

Secondary are More common than Primary:

Lungs oxygenate 100% of blood and therefore they come into contact with all blood. This increases the risk of metastasis.

328
Q

What are the common causes of secondary lung cancer?

A

Mets from:
Breast
Kidney
Bowel
Bladder

329
Q

What is a Pancoast Tumour?

A

A tumour in the lung apex that commonly metastasises to the necks sympathetic plexus and can press on the sympathetic ganglion causing Horner’s Syndrome:
Triad of Ptosis, Miosis and Anhidrosis

330
Q

What syndrome does a Pancoast tumour cause?

A

HORNERS Syndrome characterised by:
Ptosis - Droopy eyelids
Myosis - Excessive Pupil Constriction
Anhidrosis - Lack of sweating

331
Q

What is a Pulmonary Embolism?

A

Obstruction of the pulmonary vasculature, secondary to an embolus.

332
Q

What is the pathophysiology of a PE?

A

Embolus enters Right heart via IVC
It enters pulmonary vasculature
This causes occlusion of small blood vessels
Causes V/Q mismatch as blood cannot gas exchange.
Causes Hypoxic vasoconstriction and reactive bronchoconstriction.
Narrows airways leading to Dyspnoea

Hypoxic vasoconstriction increases pulmonary vascular resistance causing Pulm HTN.
This causes RV heart strain and hypertrophy.
Eventually this leads to RHF (Cor Pulmonale)

333
Q

What are the risk factors of a PE?

A

Anything affecting Virchow’s Triad:

Endothelial Injury:
Smoking, HTN, Trauma

Venous Stasis:
Immobility, Post surgery, AF, Obesity

Hypercoagulability - OCP, Polycythaemia, Malignancy

334
Q

What are the symptoms of PE?

A

Sudden onset Shortness of breath
Cough with or without blood (haemoptysis)
Pleuritic chest pain
Dyspnoea/Tachypnoea
Syncope (RED FLAG)

335
Q

What are the signs of PE?

A

Hypotension
Tachypnoea
Tachycardia
Raised respiratory rate
Low grade fever
Haemodynamic instability causing hypotension
Raised JVP
Hypoxia

336
Q

What are the common features that are highly suggestive of PE on examination?

A

Tachypnoea (RR >16/minute): 96%
Crackles: 58%
Tachycardia (HR >100): 44%
Fever (temp >37.8°C): 43%

337
Q

How is PE diagnosed?

A

WELLS Score:
<4 Unlikely PE - perform D-dimer. - if >500ng/ml then perform CT Pulmonary Angiogram.

> 4 Likely PE - Perform CTPA (GS): Will diagnose PE clot.

CXR - Exclude other pathology (typically normal in PE)
ECG - S1Q3T3

338
Q

What other investigations are performed for a PE?

A

ECG: S1Q3T3
Deep S waves in lead I
Deep Q waves in lead III
T waves inverted in Lead III
RBBB V1-3 & Sinus Tachycardia

CXR - usually normal

CTPA - GS diagnostic

Bloods:
D-Dimer
Anti-phospholipid Abs - in unprovoked DVT/PE

339
Q

What is the treatment of PE is the Px is haemodynamically stable (non-massive PE)?

A

Anticoagulants:
1st Line:
DOAC (Rivaroxaban, Apixaban)
(LMWH if DOAC CI)

2nd Line: Warfarin

340
Q

What is the treatment of PE is the Px is haemodynamically unstable (Massive PE)?

A

Thrombolysis (clot busting) - Alteplase

If fails - Catheter embolectomy

341
Q

What can be used as prophylaxis for a PE?

A

Compression Stockings
Regular walking
SC LMWH

342
Q

Define Dyspnoea?

A

A symptom of difficult or laboured breathing

343
Q

What is the MRC Dyspnoea Scale?

A

Assess degree of baseline functional disability due to Dyspnoea

Grade 0: I only get breathless with strenuous exercise

Grade 1: I get short of breath when hurrying on level ground or walking up a slight hill

Grade 2: On ground level I stop for breath when walking at own pace

Grade 3: I stop for breath after walking about 100 yards or after a few minutes on level ground

Grade 4: I am too breathless to leave the house or I am breathless when dressing/undressing

344
Q

What are the main acute respiratory causes of Dyspnoea?

A

Pneumonia
Asthma
PE
Pneumothorax

345
Q

What are the main Chronic respiratory causes of Dyspnoea?

A

COPD
Idiopathic Pulmonary Fibrosis
Bronchiectasis

346
Q

What are the main cardiac causes of Dyspnoea?

A

ACS
Stable angina
Chronic HF
Pericarditis

347
Q

What are some less common respiratory causes of Dyspnoea?

A

Pleural Effusion
Lung Cancer
Interstitial Lung Disease (pneumonoconiosis)

348
Q

What are some less common cardiac causes of Dyspnoea?

A

Carditis (end, myo, peri)
Valvular dysfunction
Cardiomyopathy
Acute HF

349
Q

What are some other systemic causes of Dyspnoea?

A

Musculoskeletal
Anxiety
Metabolic acidosis:
- DKA
- Acute renal failure

350
Q

What can cause respiratory failure?

A
  1. Low oxygen delivery - anaemia, high altitude
  2. Airway obstruction - Asthma, COPD
  3. Gas exchange limitation - lung fibrosis, IDLs
  4. V/Q Mismatch - Pneumonia, PE, Pulm HTN
  5. Alveolar hypoventilation - emphysema, reduced resp drive, obesity, Muscular weakness
351
Q

What is the main pathophysiology of type 1 respiratory failure?

A

Type 1 respiratory failure occurs when the respiratory system cannot adequately provide oxygen to the body, leading to hypoxemia.

352
Q

What is Type 1Respiratory Failure?

A

Type 1 = 1 change (O2)

  • pO2 (partial O2 pressure) is low
  • pCO2 (partial CO2 pressure) is low or normal
353
Q

What condition is the most common cause for Type 1 Respiratory failure?

A

Pulmonary Embolism
Pneumonia

354
Q

What is the main pathophysiology of type 2 respiratory failure?

A

Type 2 respiratory failure occurs when the respiratory system cannot sufficiently remove carbon dioxide from the body, leading to hypercapnia

355
Q

What is Type 2 Respiratory Failure?

A

Type 2 = 2 changes (O2 & CO2)

  • pO2 is low
  • pCO2 is high
356
Q

What is the most common cause of Type 2 Respiratory Failure?

A

Hypoventilation:
Caused by Obstruction:
COPD

Alveolar Hypoventilation:
Neuromuscular weakness
Obesity
Chest wall deformity
Reduced respiratory drive (opiates)

357
Q

What are the signs of Hypercapnia seen in type 2 respiratory failure?

A
  • Bounding pulse
  • Flapping tremor (asterixis)
  • Confusion
  • Drowsiness
  • Reduced consciousness
358
Q

How would you interpret the results of an ABG to determine if it is respiratory or metabolic acid/alkalosis?

A

pH - Down = acid/ Up= Alkalosis
CO2 - Rise = acid
O2 - if low then respiratory cause
HCO3 when O2 low if it rises then compensatory

Partial compensation when mechanisms working but pH still not back to normal.
If pH returns to normal then complete compensation

359
Q

What is DLCO a measure of?

A

Transfer Coefficient of oxygen/CO

the ability of the lungs to transfer gas from inhaled air to the red blood cells in pulmonary capillaries

360
Q

How is DLCO measured?

A

Can calculate by inspiring a small amount of carbon monoxide (not too much since can kill)
hold breath for 10 seconds at total lung capacity (TLC) then the gas transferred is measured

361
Q

What causes a high DLCO?

A

Pulmonary haemorrhage - can absorb O2 very efficiently due to bleeding resulting in more red blood cells being available

362
Q

What causes a low DLCO?

A
  • Severe emphysema
  • Fibrosing alveolitis
  • Anaemia
  • Pulmonary hypertension
  • Idiopathic pulmonary fibrosis
  • COPD
363
Q

Why in airway restriction is FVC low but FEV1 normal?

A

Due to restriction, lung volumes are small (lower TLC and therefore FVC) and most of breath is out in first second (normal FEV1)

364
Q

What are the main Upper Respiratory Tract Infections (URTI)?

A

Epiglottitis.
Laryngitis.
Pharyngitis (sore throat).
Sinusitis (sinus infection).
Whooping Cough
Croup
(Otitis Media)

365
Q

Where does an URTI go from?

A

Between the nose to the larynx above the vocal cords

366
Q

What are some risk factors impairing Lung Defences?

A

Old age
Smoking
Alcohol use
ETT/nasotracheal intubation
Respiratory therapy
Hypoxaemia
Acidosis
Toxin inhalation
Immunosuppression
Malnutrition

367
Q

What is the epidemiology of URTIs?

A

Adults will have 2-3 URTIs each year.
Most commonly caused by Viruses (rhinovirus)

368
Q

What are the most common causes of URTIs?

A

Rhinoviruses (45-50%)
Influenza A virus (25-30%)
Coronaviruses (10-15%)
Parainfluenza viruses (5%)
Respiratory syncytial viruses (5%

369
Q

What are the general Symptoms of a URTI?

A

Coryzal Sx:
Nasal stuffiness, runny nose, sneezing, sore throat, and cough.

370
Q

What is Pharyngitis?

A

Inflammation of the pharynx w/wo exudate production

371
Q

What are the causes of pharyngitis?

A

Viral (70-80%) - Rhinovirus, Adenovirus, EBV/HIV

Bacteria (20%) - Group A Strep (S. pyogenes)

372
Q

What are the signs of pharyngitis?

A

Sore throat
Fever
Cough (viral)
Nasal congestion (viral)
Exudate (bacterial)
Cervical adenopathy (bacterial)

373
Q

What must be ruled out if a Px (especially child) has pharyngitis?

A

Rheumatic fever
(typically 2-4 weeks post S. pyogenes infection.

374
Q

What is the treatment for pharyngitis?

A

Viral - self limiting

Bacterial - Amoxicillin/Flucloxacillin
Likely Strep pyogenes so amoxicillin

375
Q

What is Sinusitis?

A

inflamed mucosa of nasal cavity and nasal sinuses

376
Q

What causes sinusitis?

A

Viral infection - Most common
Bacterial infection - S. Pneumo / H. Influ

377
Q

What are the signs and symptoms of sinusitis?

A

Symptoms
Fontal headache
Facial pain
Fever

Signs
Purulent nasal discharge
Tenderness

378
Q

What is the treatment for Viral sinusitis?

A

Self limiting
Usually lasts <10 days and has non-purulent discharge
Inhalation of water vapour can help

379
Q

What is the treatment for Bacterial Sinusitis?

A

May last >10 days and have purulent discharge

Symptoms for less than 10 days: No antibiotics.

No improvement after 10 days: 2 weeks of high-dose steroid nasal spray

No improvement after 10 days and likely bacterial cause: consider delayed or immediate prescription of antibiotics (Amoxicillin)

380
Q

What is Otitis Media?

A

Middle ear infection and inflammation
(commonly affects children)

Presents with ear pain

381
Q

What are the causes of Otitis media?

A

Viral - RSV, Rhinovirus, adenovirus, influenza

Bacterial - H. influenza, S. pneumoniae, Moraxella catarrhalis

382
Q

What is the diagnostic findings for otitis media?

A

Otoscopy examination will reveal a bulging red tympanic membrane.

If the ear drum perforates there can be discharge from the ear.

383
Q

What is the treatment for otitis media?

A

Otitis media usually resolves within 3-7 days without antibiotics.

An appropriate initial antibiotic in the community:
Amoxicillin 5-7 days

Alternatives in penicillin allergy:
Clarithromycin
Erythromycin

2nd Line: Co-Amoxiclav

384
Q

What is Acute Epiglotitis?

A

Epiglottitis refers to inflammation and localised oedema of the epiglottis, which can result in potentially life-threatening airway obstruction.

385
Q

What is the most common cause of Epiglottitis?

A

Haemophilus Influenza B
Often secondary to immunocompromisation (such as following HIV)

386
Q

What are the risk factors for Epiglottitis?

A

Peak age 6-12 (can occur at any)
Male gender
Unvaccinated
Immunocompromised

387
Q

What are the symptoms of Epiglottitis?

A

Rapid Onset:
Dysphagia
Dysphonia (stridor)
Drooling
Distress

388
Q

What are the signs of Epiglottitis?

A

Stridor - whistling
Tripod Position: A sign of respiratory Distress
Lean forward, mouth open, tongue out = max air in)
Pyrexia

389
Q

What is the primary investigation of Epiglottitis?

A

If acutely unwell then NO Ix but immediate Tx

Laryngoscopy (GS):
swelling and inflammation of the epiglottis or supraglottis.

Lateral neck radiograph:
Thumb print sign

390
Q

What is the treatment for Epiglottitis?

A

EMERGENCY
First Line:
- Secure airway
- Nebulised adrenaline
- IV antibiotics - Doxycycline, Co-Amoxiclav, Erythromycin,

Second Line:
- Dexamethasone

391
Q

What is Croup?

A

Acute infective upper respiratory infection causing oedema in the larynx
(Acute Larygnotracheobronchitis)

392
Q

Who is typically affected by croup?

A

Children between 6 months and 2 years old

393
Q

What are the causes of Croup?

A

Main cause: Parainfluenza virus

Influenza
Adenovirus
Respiratory Syncytial Virus (RSV)

394
Q

What is the presentation of Croup?

A

Usually improves in <48 hours

Increased work of breathing
“Barking” cough, occurring in clusters of coughing episodes
Hoarse voice
Stridor
Low grade fever

395
Q

What is the treatment of Croup?

A

Oral Dexamethasone (single dose 150mcg/kg)

396
Q

What is Whooping Cough?

A

Upper respiratory tract infection caused by Bordetella pertussis

397
Q

Who is affected by Whooping cough?

A

Mainly children
90% <5yrs

398
Q

What is the pathogenesis of Whooping cough?

A

Haemagglutinin and fimbriae adhere to cilia of URT.
Adenylate cyclase toxin inhibits phagocyte chemotaxis (Lots of virulence factors)
Pertussis toxin inhibits alveolar macrophages
Leads to lymphoid hyperplasia skewing the immune response

399
Q

What are the stages of whooping cough presentation?

A

Catarrhal stage (1-2 weeks):
- Dry, unproductive cough
- Low-grade fever
- Conjunctivitis
- Coryzal symptoms

Paroxysmal stage (1-6 weeks):
- Coughing fits: typically consist of a short expiratory burst followed by an inspiratory gasp, causing the ‘whoop’ sound
- Post-tussive vomiting

Convalescent stage (lasts up to 6 months):
Gradual improvement in symptoms

400
Q

What is the characteristic symptom of whooping cough?

A

Whoop sound caused sharp inhalation of breath during coughing bout

401
Q

What are the investigations of Whooping cough?

A

Nasopharyngeal swab/aspirate:
Culture/PCR

Anti-pertussis toxin immunoglobulin G (IgG) serology

402
Q

What is the treatment for Whooping cough?

A

Notify PHE
Hospital admission if severe

Antibiotics: if Cough Sx is within 21 days
Macrolids - Clarithromycin, Azithromycin

School work absence: highly contagious

403
Q

What are the complications of Whooping cough?

A

Pneumonia
Encephalopathy
Otitis media
Injuries from coughing - pneumothorax
Seizures.

404
Q

What can cause the oxygen dissociation curve to shift to the left?

A

Rule of L:
Shifts to L → Lower oxygen delivery, caused by
Low [H+] (alkali)
Low pCO2
Low 2,3-DPG
Low temperature

405
Q

What can cause the oxygen dissociation curve to shift to the right?

A

‘CADET, face Right!’
For CO2, Acid, 2,3-DPG, Exercise and Temperature

Raised [H+] (acidic) (from exercise)
Raised pCO2
Raised 2,3-DPG*
Raised temperature

406
Q

How are upper respiratory viral infections diagnosed?

A

Green Viral Throat swab + PCR

Some Point of Care tests for some viruses (influenza, SARS-CoV-2)

407
Q
A
408
Q
A

Medicine Phase 2a (20 decks)

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