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Phase 2a > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is Chronic Obstructive Pulmonary Disease (COPD)?

A

Progressive irreversible airway obstruction and limitation of air flow 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

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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

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5
Q

What are the risk factors for COPD?

A

Cigarette smoking
Air pollution

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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 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

This causes air trapping causing poor exchange of O2 and CO2 and increases risk of infection.

This also stimulates immune cells causing inflammation of the bronchus and bronchioles.

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8
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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9
Q

What are the Signs of Chronic Bronchitis?

A

Wheeze - narrowing of airway creates higher pitch sound.

Crackles - popping open of small airways

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).

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

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10
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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11
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

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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12
Q

What are the different types of Emphysema?

A

Centriacinar Emphysema

Panacinar Emphysema:

Paraseptal Emphysema:

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13
Q

What is Centriacinar Emphysema?

A

Most common

Damage to central/proximal acini due to smoking

Typically affects upper lobes

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14
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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15
Q

What is Paraseptal Emphysema?

A

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

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16
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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17
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

Cough - with some sputum

Pulmonary HTN

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18
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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19
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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20
Q

What are the main complications of COPD?

A

Recurrent Respiratory Tract Infections:
S. pneumoniae
H. influenzae

Cor Pulmonale

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21
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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22
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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23
Q

What are the Symptoms of COPD?

A

Chronic cough - often with sputum

Constant Dyspnoea - not episodic

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24
Q

What are the Signs of COPD?

A

Tachypnoea

Barrel Chest

Wheeze/Crackles

Hyperresonance on percussion

Evidence of Cor Pulmonale

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25
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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26
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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27
Q

How is COPD Diagnosed?

A

Clinical Dx with Spirometry Test

Spirometry shows Obstruction:
FEV1/FVC ration <0.7

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

CXR - Lung hyperinflation + Bullae

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28
Q

How does Asthma respond to Reversibility testing?

A

Bronchodilator (salbutamol) will increase FEV1 by >12%

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29
Q

What is FVC?

A

Forced Vital Capacity:
The total amount of air forcibly expired

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30
Q

What is FEV1?

A

Forced Expiratory Volume in 1 second

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31
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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32
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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33
Q

What does a low FVC suggest?

A

Airway Restriction

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34
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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35
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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36
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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37
Q

How is the severity of COPD and airflow graded?

A

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

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38
Q

What is the treatment of COPD?

A

Stop risk factors - smoking
Prophylactic Vaccines - Pneumonia

Medication:
1. SABA (Salbutamol) OR SAMA (Ipratropium Bromide)

  1. LABA (Salmeterol) + LAMA (Tiotropium

(if they have asthmatic/steroid responsive features then LAMA + inhaled corticosteroid beclometasone)

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39
Q

What management can be provided for severe COPD?

A

Nebulisers - Salbutamol and/or ipratropium
Long term Oxygen therapy

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40
Q

What is an Exacerbation of COPD?

A

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

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41
Q

How are Exacerbations of COPD treated?

A

At Home:
Prednisolone 30mg once daily for 7-14 days
Regular inhalers or home nebulisers
Antibiotics if there is evidence of infection

In Hospital:
Nebulised Bronchodilators
Prednisolone 30mg once daily for 7-14 days
Antibiotics if there is evidence of infection
Physiotherapy

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42
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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43
Q

Define Asthma?

A

Chronic reversible inflammatory airway condition characterised by reversible airway obstruction, airway hyperresponsiveness and inflamed bronchioles

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44
Q

What are the types of Asthma?

A

Allergic (70%) - Extrinsic IgE mediated T1 Hypersensitivity

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

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45
Q

Explain the pathophysiology IgE mediated asthma?

A

Environmental trigger against specific allergens.

This 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 production 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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46
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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47
Q

What is the cause of asthma

A

Causes are unknown:
Genetics may play a factor

Environmental Factors:
Hygiene hypothesis

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48
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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49
Q

What are the risk factors for asthma?

A

History of Atopy
FHx of asthma
Allergens - pollen, fur, smoke

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50
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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51
Q

What drugs can trigger asthma?

A

Aspirin
Beta blockers

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52
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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53
Q

What is the epidemiology of asthma?

A

A very common condition affecting 10% of the US.
More common in children/young people compared to COPD

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54
Q

What are the symptoms of asthma?

A

Chest tightness
Episodic Dyspnoea/SOB
Wheeze
Dry Cough (typically but can be wet)

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55
Q

What are the signs of asthma?

A

Diurnal PEFR variation

Dyspnoea and Expiratory Polyphonic wheeze

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

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56
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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57
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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58
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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59
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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60
Q

What is Samter’s Triad

A

Nasal Polyps
Asthma
Aspirin sensitivity

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61
Q

What is Atopic Triad?

A

Atopic Rhinitis
Asthma
Eczema

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62
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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63
Q

What are the classifications of asthma?

A

Intermittent
Mild Persistent
Moderate Persistent
Severe Persistent

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64
Q

What are the primary investigations for asthma?

A

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

1st Line Ix:
Fractional Exhaled NO
Spirometry w/ Bronchodilator Reversibility
(shows reversible obstruction)

2nd Line:
PEF variation measurements - 2-4 weeks
Direct bronchial challenge test with histamine or methacholine

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65
Q

What is the Treatment algorithm for Chronic asthma?

A

16+:

  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)
4. SABA + ICS + LABA (Salmeterol) +/- LTRA
5. Consider change to MART (maintenance and reliever therapy)
6. Increase ICS Dose

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66
Q

What is the treatment for acute asthma Exacterbations?

A

OSHITME:
O2
Saba (nebulised)
Hydrocortisone (ICS)
IV MgSO4
Theophyline (IV) - MgSO4 / Escalate

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67
Q

What are the complications of Asthma?

A

Asthma Exacerbation

Pneumothorax

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68
Q

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

A

Tuberculosis
Pneumonia

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69
Q

What is Tuberculosis?

A

An infectious disease caused by Mycobacteria characterised by caseating granulomas.

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70
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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71
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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72
Q

What is the epidemiology of TB?

A

1.7Bn people have latent TB
Affects immunocompromised more
More common in South Asia (India, China, Pakistan) and Sub-Saharan Africa

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73
Q

How is TB infection spread?

A

Via airborne transmission

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74
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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75
Q

What are the different types of TB?

A

Active TB - active infection

Latent TB - Previous infection where the immune system has encapsulated and prevented progression of TB

Secondary TB - When Latent TB reactivates

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

Extrapulmonary TB - where TB infects other areas

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76
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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77
Q

What is the pathogenesis of TB?

A

Infection of TB via droplets/aerosol

TB phagocytosed (but resistant to killing)
Granulomatous formation (typically in hilar lymph nodes)

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

Ghon Focus spreads to nearby lymph nodes forming a Ghon Complex

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

Miliary TB:
If TB spreads from Ghon complex
systemically then it becomes Miliary TB

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78
Q

Is latent TB symptomatic?

A

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

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79
Q

What are the symptoms of active TB?

A

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

Cough w/haemoptysis
Dyspnoea
Erythema Nodosum

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80
Q

What are the signs of TB?

A

Auscultation - often normal (may have crackles)

Clubbing

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81
Q

What may be symptoms of Extrapulmonary TB?

A

Meningism
Skin rash
TB pericarditis Sx
Join pain
Spinal Pain (spinal TB)

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82
Q

What are the primary investigations for TB?

A

Latent Disease - Mantoux Test
Interferon Gamma release assay

CXR - patchy consolidation, pleural effusions

Sputum culture - AFB bright red on ZN stain.
NAAT

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83
Q

What is the management of latent TB?

A

Doesnt necessarily need Tx
If risk of reactivation then:
Isoniazid and rifampicin for 3 months
Isoniazid for 6 months

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84
Q

What is the Treatment for Active TB?

A

RIPE:
R – Rifampicin for 6 months
I – Isoniazid for 6 months
P – Pyrazinamide for 2 months
E – Ethambutol for 2 months

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85
Q

What are the side effects of TB treatment?

A

Rifampicin - Haematuria
Isoniazid - Peripheral Neuropathy
Pyrazinamide - Hepatitis
Ethambutol - Optic neuritis/eye problems

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86
Q

What is Pneumonia?

A

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

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87
Q

What are the classifications of Pneumonia?

A

Community Acquired Pneumonia
Hospital Acquired Pneumonia
Aspiration Pneumonia

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88
Q

Define Community Acquired Pneumonia (CAP)?

A

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

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89
Q

Define Hospital Acquired Pneumonia (HAP)?

A

Pneumonia that develops more than 48 hours after hospital admission.

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90
Q

Define Aspiration pneumonia?

A

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

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91
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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92
Q

What are the main cause of CAP?

A

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

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93
Q

What are some less common causes of CAP?

A

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

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94
Q

Where is legionella caused pneumonia typically from?

A

Often from Spain.
Recent Travel Hx and staying in hotels with air conditioning.

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95
Q

What are the main causes of HAP?

A

P. aeruginosa
E. coli
S. aureus
Klebsiella

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96
Q

What is the concern of treating HAP?

A

Most of the causative organisms have multi drug resistance

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97
Q

What is the main cause of aspiration pneumonia?

A

Klebsiella

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98
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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99
Q

What are the causes of atypical pneumonia?

A

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

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100
Q

What is the main cause of fungal pneumonia?

A

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

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101
Q

How is PCP treated?

A

Co-trimoxazole
(combination of Trimethoprim and Sulphamethoxazole)

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102
Q

What are the risk factors for pneumonia?

A

Extremes of age
Preceding infection (viral)
Immunosuppressed
IVDU
Respiratory conditions - asthma, COPD, CF

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103
Q

What is the pathogenesis of typical pneumonia?

A

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

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104
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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105
Q

What are the symptoms of pneumonia?

A

Productive cough w/purulent sputum
Fever - due to infection
Pleuritic chest pain
Dyspnoea

May cause confusion in elderly
Dry cough in atypical pneumonia

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106
Q

What are the signs of pneumonia?

A

Reduced breath sounds
Bronchial Breathing w/ coarse crepitations
Hypoxia
Tachycardia
Pyrexia

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107
Q

What are the primary investigations of pneumonia?

A

1st Line:
CXR (diagnostic) shows consolidation
FBC - Raised WCC
U&E - urea
CRP - raised due to inflammation

Sputum sample and culture to ID organism

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108
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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109
Q

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

A

S. pneumoniae
S. aureus
Legionella

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110
Q

What organisms may show Multiple abscess pneumonic lesions on CXR?

A

S. aureus

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111
Q

What organisms may show upper lobe pneumonic lesions on CXR?

A

Klebsiella

(but first exclude TB)

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112
Q

What is the treatment for pneumonia?

A

Antibiotics:
Mild CAP: Amoxicillin 5 days
Moderate-severe CAP: Amoxicillin + Macrolide 7-10 days

If legionella (notify PHE) and Clarithromycin

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113
Q

What are the major complications of pneumonia?

A

Sepsis
Pleural effusion
Empyema
Lung abscess
Death

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114
Q

What is Cystic Fibrosis?

A

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

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115
Q

What are the genetics for CF?

A

autosomal recessive mutation on Chromosome 7 affecting the AFTR protein.

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

This affects chloride channels.

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116
Q

What is the prevalence of CF?

A

1 in 25 are carriers of the gene

1 in 2500 are affected by CF

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117
Q

What are the risk factors for CF?

A

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

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118
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

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119
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.

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120
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

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121
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.

Failure to thrive

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122
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

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123
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

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124
Q

How can CF lead to male infertility?

A

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

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125
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

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)

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126
Q

What are the signs of CF?

A

Low weight or height on growth charts
Nasal polyps
Finger clubbing
Crackles and wheezes on auscultation
Abdominal distention

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127
Q

What are the primary investigations for CF?

A

New-born Blood spot test

Sweat Test (gold standard)

Genetic testing for CFTR mutation)

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128
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)

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129
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.

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130
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

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131
Q

What is the management of CF?

A

Non curative:
Conservative:
Chest physiotherapy
Exercise
No smoking

Medication:
Anti-mucolytics
Prophylactic Flucloxacillin (prevent S. aureus)
Bronchodilators (SABA)
Vaccinations

Systemic Tx:
Pancreatic enzyme replacement
Vitamin Supplements
High calorie diet.

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132
Q

What is Bronchiectasis?

A

Bronchiectasis is a chronic, debilitating lung disease characterised by the permanent dilation of the bronchi.

(Also have lots of mucus within them)

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133
Q

What is the cause of Bronchiectasis?

A

Chronic bronchial inflammation caused by :
previous infection
Allergy and Inflammatory conditions
Immunodeficiency
Congenital - CF

134
Q

What are the risk factors for Bronchiectasis?

A

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

135
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.

136
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.

137
Q

What are the symptoms of Bronchiectasis?

A

Dyspnoea/SOB
Productive cough
Copious sputum production
Haemoptysis (maybe)

138
Q

What are the signs of Bronchiectasis?

A

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

Clubbing

139
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)

140
Q

What is the treatment for Bronchiectasis?

A

Non curative:

Tx underlying cause if present.
Chest Physiotherapy

Bronchodilator / Mucoactive agent (carbocisteine)

Abx for acute exacerbations

141
Q

Define a Pleural Effusion?

A

Excess fluid accumulation between the visceral and parietal pleura (pleural cavity)

142
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)

143
Q

What are the Exudative causes of pleural effusion?

A

Related to inflammation:
Lung cancer
Pneumonia
Rheumatoid arthritis
Tuberculosis

144
Q

What are the Transudative causes of Pleural effusion?

A

Fluid Moving (transport) across into the pleural space:
Congestive cardiac failure
Hypoalbuminaemia
Hypothroidism
Meig’s syndrome

145
Q

What is Meig’s Syndrome?

A

right sided pleural effusion with ovarian malignancy

146
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.

147
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

148
Q

What is the most common cause of Exudative pleural effusion?

A

Pneumonia and malignancy

149
Q

What is the most common cause of Transudative pleural effusion?

A

Heart failure

150
Q

What are the symptoms of Pleural effusion?

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

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

151
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

152
Q

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

A

Pneumothorax

153
Q

What are the primary investigations for pleural effusion?

A

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

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

154
Q

What is the treatment for Pleural effusion?

A

Conservative Mx:
Small effusions can be treated by Tx of underlying cause

Chest Drain - remove fluid

155
Q

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

A

Pleurodosis:
Surgical fusing of pleural layers to prevent fluid accumulation.

156
Q

What is Empyema?

A

An infected Pleural Effusion

157
Q

What does Empyema Show on pleural aspiration?

A

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

158
Q

What is the treatment for Empyema?

A

chest drain to remove the pus and antibiotics

159
Q

What is a Pneumothorax?

A

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

160
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

161
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

162
Q

What is the Pathophysiology of a Pneumothorax?

A

Pleural space is normally a vacuum (no air)

Breach in the pleura (trauma/CT disorders)
Leads to air entry into pleural cavity

eg. Subpleural bullae burst
eg. Abnormal connection between pleural space and airways

163
Q

What are the symptoms of a pneumothorax?

A

Sudden onset
Sharp Pleuritic Chest pain
SOB

164
Q

What are the signs of a pneumothorax?

A

Reduced breath sounds
Hyper resonant percussion (increased air)

165
Q

What is the primary investigation for a pneumothorax?

A

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

CT thorax can be more sensitive for small pneumothoraxes

166
Q

What is the treatment for a pneumothorax?

A

Small - self healing

Larger:
- Need decompression (suck out air)
- Chest drain (one way air remova)

Surgical if chronically recurrent:
Pleurodosis

167
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

168
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.

169
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

170
Q

What is the treatment for a Tension Pneumothorax?

A

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

Once pressure is relieved then chest drain.

171
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)

172
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.

173
Q

Give some examples of ILDs?

A

Idiopathic Pulmonary Fibrosis
Pneumonoconiosis
Sarcoidosis
Hypersensitivity Pneumonitis

174
Q

What test is generally used to diagnose ILD?

A

High resolution CT:
Shows Ground Glass appearance

Lung Biopsy can confirm diagnosis on Histology

175
Q

What is the general Management for ILD?

A

Generally the damage is reversible 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

176
Q

What is Pulmonary Fibrosis?

A

Progressive fibrosis and scarring of the lung parenchyma.

177
Q

What are the different types of pulmonary fibrosis?

A

Idiopathic PF
Drug induced PF
Secondary PF

178
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.

179
Q

What drugs can induce pulmonary fibrosis?

A

Amiodarone
Cyclophosphamide
Methotrexate
Nitrofurantoin

180
Q

What are secondary causes of Pulmonary Fibrosis?

A

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

181
Q

What are the risk factors for Idiopathic Pulmonary FIbrosis?

A

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

182
Q

What is the pathophysiology of Pulmonary fibrosis?

A

Progressive lung damage
Causes fibroblast activation
Leads to Replacement of damage lung parenchyma with collagen.
Causes excessive scarring and fibrosis.
Lungs fail to expand on inhalation

Can lead to Type 1 Respiratory Failure.

183
Q

What are the symptoms of pulmonary fibrosis?

A

Progressive Dyspnoea
Dry cough (no sputum)
Malaise

184
Q

What are the signs of pulmonary fibrosis?

A

Bibasal fine inspiratory crackles (end respiratory)

Finger clubbing

+ Sx of underlying pathology if Secondary PF

185
Q

What are the diagnostic investigations for pulmonary fibrosis?

A

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

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

186
Q

What is the treatment for Pulmonary Fibrosis?

A

Supportive Tx:
Smoking cessation
Vaccines

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

Consider Lung Transplant

187
Q

What is Pneumonoconiosis?

A

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

188
Q

What are some different types of pneumonoconiosis?

A

Silicosis - Inhalation of silicon dioxide
Asbestosis - Inhalation of asbestos

189
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.

190
Q

What are the risk factors for pneumonoconiosis?

A

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

191
Q

What are the symptoms of pneumonoconiosis?

A

Exertional Dyspnoea
Dry Cough
Haemoptysis
Wheezing
Weight loss

192
Q

What does asbestosis increase the risk of developing?

A

Mesothelioma

193
Q

What are the diagnostic findings for Pneumonoconiosis?

A

CXR:
Nodular opacities in upper lobes (Silicosis/Coal)
Eggshell calcification of hilar lymph nodes

Spirometry: Restrictive and reduced DLCO

High-Res CT chest: interstitial fibrosis

194
Q

what is the management for Pneumonoconiosis?

A

Conservative Mx as incurable:

Stop smoking
Avoid exposure

195
Q

What is Sarcoidosis?

A

An Granulomatous inflammatory condition characterised by non-caseating granulomas

196
Q

What is the cause of sarcoidosis?

A

Unknown: Thought to be a type 4 Hypersensitivity reaction.

Idiopathic

197
Q

What are the risk factors for sarcoidosis?

A

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

198
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.

199
Q

What part of the body is affected by Sarcoidosis?

A

Typically affects the lungs

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

200
Q

What are the Chest symptoms of sarcoidosis?

A

Dry cough
Dyspnoea
Mediastinal lymphadenopathy

Constitutional Sx:
Weight loss, Fatigue and fever

201
Q

What are the Extra-pulmonary symptoms of Sarcoidosis?

A

Liver - Nodules, cholestasis, cirrhosis

Eyes - uveitis, Optic neuritis, conjunctivitis

Skin - Erythema Nodosum, Lupus pernio, Granulomas

Heart - Heart block/bundle branch block

Kidneys - Kidney stones

CNS - Encephalopathy, Diabetes Insipidus

PNS - facial palsy

Bones - Arthralgia, Arthritis

202
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)

203
Q

What are some differential diagnoses of sarcoidosis?

A

Tuberculosis (caseating)
Lymphoma
Hypersensitivity pneumonitis
HIV
Toxoplasmosis
Histoplasmosis

204
Q

What are the primary investigations for sarcoidosis?

A

GS Diagnostic - Biopsy (non caseating granuloma)

CXR /CT - Hilar lymphadenopathy and pulmonary infiltrates/nodules

205
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

206
Q

What is the treatment of Sarcoidosis?

A

ASx/Mild: No Tx is 1st Line

When Tx required: Oral steroids (+bisphosphonates to protect against OP)

2nd Line: Methotrexate/Azathioprine

207
Q

What are the potential complications of Sarcoidosis?

A

Can progress to Pulmonary Fibrosis
Pulmonary HTN

208
Q

What is Hypersensitivity pneumonitis?

A

Type 3 hypersensitivity reaction to an environmental allergen that causes parenchymal inflammation and destruction.

209
Q

Explain the pathophysiology of Hypersensitivity pneumonitis?

A

Allergen is inhaled

antibodies against allergen form Ab-Ag complexes.

These complexes get deposited in the lung tissues and alveoli.

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

210
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

211
Q

How is Hypersensitivity pneumonitis diagnosed?

A

Bronchoscopy with Bronchoalveolar lavage:

This shows raised Lymphocytes and mast cells

212
Q

What is the treatment for hypersensitivity pneumonitis?

A

Remove the allergen

Give oxygen if necessary

213
Q

What is Goodpasture’s Syndrome?

A

An autoimmune disease characterised by Anti-GBM autoantibodies that attack the lungs and kidneys.

214
Q

What is the pathophysiology of Goodpasture’s Syndrome?

A

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 complement system.

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

215
Q

What are the risk factors for Goodpasture’s syndrome?

A

Genetics - HLA-DR15

infection
Smoking
Oxidative stress

216
Q

What are the symptoms of Goodpasture’s Syndrome?

A

Cough
Haemoptysis
Dypsnoea

Kidney Sx:
Haematuria and proteinuria

217
Q

How is Goodpasture’s syndrome diagnosed?

A

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

Serology: Anti-GMB +tve

218
Q

What is the treatment for Goodpasture’s Syndrome?

A

Corticosteroids
Immunosuppressants
Plasmapheresis

219
Q

what is the normal pulmonary blood pressure at rest?

A

8-20mmHg

220
Q

What is defined as pulmonary hypertension?

A

Resting mPAP >25mmHg at rest.

221
Q

How is Pulmonary HTN normally measured?

A

Right heart catheterisation.

222
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.

223
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
224
Q

What is the most common cause of secondary pulmonary HTN?

A

COPD

225
Q

What are the symptoms of Pulmonary HTN?

A

Progressive breathlessness
Exertional Dizziness/syncope
Fatigue

Sx of underlying pathology

226
Q

What are the signs of pulmonary HTN?

A

Loud S2 heart sound
Raised JVP
Pulmonary/Tricuspid regurgitation
Tachycardia
Hepatomegaly
Peripheral oedema
Right parasternal heave

Signs of underlying pathology

227
Q

What are the primary investigations for Pulmonary HTN?

A

1st Line: 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

228
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)

229
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

230
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

231
Q

What is a Mesothelioma?

A

A malignant neoplasm of the mesothelial cells of the pleura

232
Q

What is the primary cause of Mesothelioma?

A

Asbestos Exposure

Typically doesnt present until decades after the exposure

233
Q

What are the risk factors for Mesothelioma?

A

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

234
Q

What are the symptoms of Mesothelioma?

A

SOB
Cough
Pleuritic chest pain

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

Sx of metastases: bone pain etc

235
Q

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

A

Tumour presses on recurrent laryngeal nerve

236
Q

What are the signs of a Mesothelioma?

A

Finger clubbing
Reduced breath sounds
Stony Dull Percussion

Ascites (if peritoneal disease present)

237
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)

238
Q

What is the treatment for Mesothelioma?

A

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

+/- Chemotherapy:
Cisplatin
Pemetrexed

+/- Radiotherapy

239
Q

What is the Main malignancy of the lung parenchyma?

A

Primary Bronchial Carcinomas

240
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%)

241
Q

What are the primary metastasis sites for Lung cancers?

A

Bones
Liver
Adrenal Glands
Brain
Lymph Nodes

242
Q

What is the epidemiology of Lung Cancer?

A

3rd most common cancer in the UK
(behind breast and prostate)

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

243
Q

What are the risk factors for Primary lung Cancer?

A

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

Increasing age
FHx

244
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.

245
Q

Who is typically affected by SCLC?

A

Exclusively smokers

246
Q

What are the paraneoplastic syndroms caused by SCLC?

A

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

247
Q

What is the most common NSCLC?

A

Adenocarcinoma

248
Q

Who is affected by NSCLC adenocarcinoma?

A

Most common cancer in non-smokers.
Commonly associated with asbestos.

249
Q

What is a NSCLC Adenocarcinoma?

A

Arise from mucus secreting glandular epithelium in the lungs

Typically affects the peripheral lung
Commonly metastasises

250
Q

What are the paraneoplastic syndromes associated with NSCLC Adenocarcinoma?

A

Hypertrophic pulmonary osteoarthropathy
Gynaecomastia

251
Q

Who is affected by NSCLC SCC?

A

Mostly smokers

252
Q

What is NSCLC SCC?

A

Arises from lung epithelium.

Typically affects the central lungs and may cause lesions with central necrosis

253
Q

What are the paraneoplastic syndromes associated with NSCLC SCC?

A

Hypertrophic pulmonary osteoarthropathy
PTHrP causing Hypercalcaemia

254
Q

What is a NSCLC Carcinoid tumour?

A

Tumour associated with MEN1 mutation and neurofibromatosis.

It is a neuroendocrine tumour that secretes serotonin.

255
Q

What are the paraneoplastic syndromes associated with a Large Cell Lung Cancer?

A

Ectopic B-hCG production

256
Q

What are the general Symptoms of Lung cancer?

A

Cough w/haemoptysis
Shortness of breath
Pleuritic Chest pain

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

257
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

258
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/MRI scan

GS Diagnostic: Bronchoscopy + Biopsy

259
Q

Which is a more aggressive cancer, SCLC or NSCLC?

A

SCLC is more aggressive

260
Q

What is the treatment for SCLC?

A

Often Diagnosed late and Px have metastatic disease:

Therefore
Chemo/radiotherapy (Cisplatin)
palliative care

261
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)

262
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.

263
Q

What are the common causes of secondary lung cancer?

A

Mets from:
Breast
Kidney
Bowel
Bladder

264
Q

What is a Pancoast Tumour?

A

A tumour in the lung apex that commonly metastasises to the necks sympathetic plexus.

265
Q

What syndrome does a Pancoast tumour cause?

A

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

266
Q

What is a Pulmonary Embolism?

A

Obstruction of the pulmonary vasculature, secondary to an embolus.

267
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)

268
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

Hypercoagulability

269
Q

What are the symptoms of PE?

A

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

270
Q

What are the signs of PE?

A

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

271
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%

272
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.

273
Q

What other investigations are performed for a PE?

A

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

CXR - usually normal

274
Q

What is the treatment of PE is the Px is haemodynamically stable?

A

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

2nd Line: Warfarin

275
Q

What is the treatment of PE is the Px is haemodynamically unstable?

A

Thrombolysis (clot busting) - Alteplase

If fails - Catheter embolectomy

276
Q

What can be used as prophylaxis for a PE?

A

Compression Stockings
Regular walking
SC LMWH

277
Q

Define Dyspnoea?

A

A symptom of difficult or laboured breathing

278
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

279
Q

What are the main acute respiratory causes of Dyspnoea?

A

Pneumonia
Asthma
PE
Pneumothorax

280
Q

What are the main Chronic respiratory causes of Dyspnoea?

A

COPD
Idiopathic Pulmonary Fibrosis
Bronchiectasis

281
Q

What are the main cardiac causes of Dyspnoea?

A

ACS
Stable angina
Chronic HF

282
Q

What are some less common respiratory causes of Dyspnoea?

A

Pleural Effusion
Lung Cancer
Interstitial Lung Disease (pneumonoconiosis)

283
Q

What are some less common cardiac causes of Dyspnoea?

A

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

284
Q

What are some other systemic causes of Dyspnoea?

A

Musculoskeletal
Anxiety
Metabolic acidosis:
- DKA
- Acute renal failure

285
Q

What can cause respiratory failure?

A

Impaired Ventilation:
Neural problems
Mechanical problems (obstruction);
- COPD
- Asthma
- OSA
- Pneumonia

Impaired Perfusion:
Pulm HTN
HF
PE
Shunt (VSD)

Impaired Gas Exchange:
Emphysema
ILD
Idiopathic Pulmonary Fibrosis

286
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.

287
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
288
Q

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

A

Pulmonary Embolism

289
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

290
Q

What is Type 2 Respiratory Failure?

A

Type 2 = 2 changes (O2 & CO2)

  • pO2 is low
  • pCO2 is high
291
Q

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

A

Hypoventilation: Caused by
COPD
Neuromuscular weakness
Obesity
Chest wall deformity
Reduced respiratory drive (opiates)

292
Q

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

A
  • Bounding pulse
  • Flapping tremor
  • Confusion
  • Drowsiness
  • Reduced consciousness
293
Q

What is DLCO a measure of?

A

Transfer Coefficient of oxygen/CO

Measure of ability of oxygen to diffuse across the alveolar membrane

294
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

295
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

296
Q

What causes a low DLCO?

A
  • Severe emphysema
  • Fibrosing alveolitis
  • Anaemia
  • Pulmonary hypertension
  • Idiopathic pulmonary fibrosis
  • COPD
297
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)

298
Q

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

A

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

299
Q

What is Pharyngitis?

A

Inflammation of the pharynx w/wo exudate production

300
Q

What are the causes of pharyngitis?

A

Viral - EBV, Adenovirus

Bacteria - Group A Strep (S. pyogenes)

301
Q

What are the signs of pharyngitis?

A

Sore throat
Fever
Cough (viral + bacterial)
Nasal congestion (viral)
Exudate (bacterial)

302
Q

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

A

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

303
Q

What is the treatment for pharyngitis?

A

Viral - self limiting

Bacterial - Amoxicillin/Flucloxacillin

304
Q

What is Sinusitis?

A

inflamed mucosa of nasal cavity and nasal sinuses

305
Q

What causes sinusitis?

A

Viral infection - Most common
Bacterial infection

306
Q

What is the treatment for Viral sinusitis?

A

Self limiting
Usually lasts <10 days and has non-purulent discharge

307
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)

308
Q

What is Otitis Media?

A

Middle ear infection and inflammation
(commonly affects children)

Presents with ear pain

309
Q

What are the causes of Otitis media?

A

Bacterial or Viral

310
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.

311
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

Alternatives in penicillin allergy:
Clarithromycin
Erythromycin

2nd Line: Co-Amoxiclav

312
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.

313
Q

What is the most common cause of Epiglottitis?

A

Haemophilus Influenza B

314
Q

What are the risk factors for Epiglottitis?

A

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

315
Q

What are the symptoms of Epiglottitis?

A

Rapid Onset:
Dysphagia
Dysphonia (stridor)
Drooling
Distress

316
Q

What are the signs of Epiglottitis?

A

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

317
Q

What is the primary investigation of Epiglottitis?

A

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

Lateral neck radiograph:
Thumb print sign

318
Q

What is the treatment for Epiglottitis?

A

First Line:
- Secure airway
- Nebulised adrenaline
- IV antibiotics

Second Line:
- Dexamethasone

319
Q

What is Croup?

A

Acute infective upper respiratory infection causing oedema in the larynx

320
Q

Who is typically affected by croup?

A

Children between 6 months and 2 years old

321
Q

What are the causes of Croup?

A

Main cause: Parainfluenza virus

Influenza
Adenovirus
Respiratory Syncytial Virus (RSV)

322
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

323
Q

What is the treatment of Croup?

A

Oral Dexamethasone (single dose 150mcg/kg)

324
Q

What is Whooping Cough?

A

Upper respiratory tract infection caused by Bordetella pertussis

325
Q

Who is affected by Whooping cough?

A

Mainly children
90% <5yrs

326
Q

What is the pathogenesis of Whooping cough?

A

Haemagglutinin and fimbriae adhere to cilia of URT.
Adenylate cyclase toxin inhibits phagocyte chemotaxis
Pertussis toxin inhibits alveolar macrophages

327
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

328
Q

What is the characteristic symptom of whooping cough?

A

Whoop sound caused sharp inhalation of breath during coughing bout

329
Q

What are the investigations of Whooping cough?

A

Nasopharyngeal swab/aspirate:
Culture/PCR

Anti-pertussis toxin immunoglobulin G (IgG) serology

330
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

331
Q

What are the complications of Whooping cough?

A

Pneumonia
Encephalopathy
Otitis media
Injuries from coughing - pneumothorax
Seizures.

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