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Phase 2a Gold Standard > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Lobes of the lung

A

Left has 2 (superior, inferior)
Right has 3 (superior, middle, inferior)

These are separated by the horizontal and oblique fissures

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2
Q

Define COPD

A

COPD describes progressive and irreversible obstructive airway disease. Consists of Chronic Bronchitis and Emphysema together.

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3
Q

Risk factors for COPD

A
  • Age (>40)
  • Smoking (biggest)
  • Air pollution
    Occupational exposure (coal, cement, dust, smelting)
  • Frequent respiratory infections
  • Gender (men)
  • Alpha 1 anti-trypsin deficiency- (young patients presenting with COPD!!)
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4
Q

O2 saturation targets for a normal person and for someone with an acute COPD exacerbation. And at what O2 sats is someone considered hypoxic

A

Normal: 95-100%
COPD exacerbation: 88-92% (normal COPD maintained above 92%)

Normal <94%
COPD exacerbation <88%

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5
Q

What 2 organisms usually cause infective exacerbations of COPD

A

H. influenza
S. pneumoniae

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6
Q

If a young patient presents with COPD symptoms without a smoking history, what should be suspected?

A

Alpha 1 Antitrypsin deficiency

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7
Q

Define chronic bronchitis

A

Inflammation of the bronchial tubes. Considered chronic when it causes a productive cough for at least 3 months a year for 2 years.

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8
Q

Pathophysiology of Chronic Bronchitis

A

Overall
- Hypersecretion
- Ciliary dysfunction
- Narrowed lumen

Explanations:

  • Irritation of epithelium of bronchi causes inflammation. This leads to hypertrophy and hyperplasia of the bronchial mucous glands in bronchi, and goblet cells in bronchioles.
  • Epithelial layer becomes ulcerated, eventually replacing the columnar epithelium with squamous (metaplasia), and smoking makes cilia shorter and less mobile
  • Chronic inflammation causes infiltration of epithelium, narrowing lumen.
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9
Q

Why does Chronic Bronchitis increase infection risk

A

Even a small amount of mucus can block lumen, stopping clearance.

Cilia are also shortened and immobile.

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10
Q

Explain the lung spirometry tests (4)

A

1) FVC (Forced vital capacity) - Max air volume in 1 breath (<80%)
2) FEV1 (Forced Expiratory Volume in 1 second) - Max air 1 second (<80%)
3) FEV1:FVC Ratio (<0.7 obstructive)
4) TLC (total lung capacity) (increased in COPD due to air trapping)

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11
Q

Signs/symptoms of Chronic Bronchitis

A

Blue Bloater
- Chronic productive cough
- Cyanosis
- Dyspnoea on exertion
- Usually overweight
- Purulent sputum
- Crackles, wheezes when breathing

Hypoxia/aemia (insufficient oxygen in tissues/blood) and hypercapnia (high CO2)

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12
Q

What are some symptoms of CO2 retention? (as would be seen in COPD)

A
  • Drowsiness
  • Asterixis
  • Confusion
  • Cyanosis
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13
Q

Complications of chronic bronchitis

A
  • Secondary polycythaemia vera
  • Pulmonary HTN due to reactive vasoconstriction to hypoxaemia
  • Cor pulmonale due to chronic pulmonary HTN
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14
Q

Define emphysema

A

Damage to/destruction of the alveolar air sacs. This causes the alveoli to permanently enlarge and lose elasticity. This means the lungs are unable to recoil, so patients have trouble exhaling

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15
Q

Pathophysiology of emphysema

A

Irritants trigger inflammation in lungs, releasing proteases (collagenases, elastases), which break down elastin. Normally, elastin prevents low pressure environment from collapsing. In emphysema, elastin is lost and airways collapse.

This causes:
- Air trapping distal to point of collapse
- Airways stretch during inhalation but cant breath out fully.
- Elastin loss also causes breakdown of thin alveolar walls (Septa), causing neighbouring alveoli to coalesce. This reduces the area for gas exchange.

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16
Q

Types of Emphysema

A

Centriacinar - most common. Damages central/proximal alveoli in each acinus, in the upper lobes of lungs. Seen in smokers.

Pan-acinar - Whole acinus affected. Seen in A1AT, affecting lower lobes.

Para-septal - Distal alveoli, can cause a pneumothorax when alveoli rupture

Irregular - Irregular acinar involvement. Scarring/fibrosis

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17
Q

Signs/symptoms of emphysema

A

Pink puffer
- Pursed lip breathing
- Barrel shaped chest
- Hyperresonance on percussion
- Downward displacement of liver
- Dyspnoea, cough, weight loss

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18
Q

Imaging signs of emphysema (3)

A
  • Increased anterior-posterior diameter
  • Flattened diaphragm
  • Increased lung field lucency
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19
Q

Signs of COPD (6)

A
  • Barrel chest
  • Hyperresonance on percussion
  • Cyanosis
  • Pursed lip breathing
  • Wheezing/crackling
  • Productive cough with purulent sputum
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20
Q

What scale is used to assess breathlessness

A

MRC dyspnoea scale.
Breathlessness:
1 - on exercise
2 - on hurrying/slight hill
3 - walks slower than others/ has to stop to catch breath
4 - Stops to catch breath after 100m
5 - breathless on minimal activity (getting changed)

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21
Q

Investigations in COPD

A

Clinical diagnosis - Over 35, smoking history, signs/symptoms of COPD.

Spirometry
- FEV1<80% expected
- FEV1/FVC <0.7, with no bronchodilator reversibility

Chest X ray -
- Flattened diaphragm
- Hyperinflation
- Bullae

CHECK FBC - COPD causes chronic hypoxia -> polycythaemia vera.

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22
Q

Give the difference between type 1 and 2 resp failure. What investigation helps check this?

A

ABG
1 - low oxygen and normal/low CO2
2 - low oxygen and high CO2

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23
Q

How is COPD classified

A

GOLD classification

Goes down based on FEV1
e.g. FEV1>80% = 1 (mild),
FEV1 50-79 = 2 (moderate) etc
FEV1 49-30 = 3 (Severe)
FEV1 <30 = 4 (very severe)

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24
Q

Name all 5 drugs used in COPD treatment

A

Bronchodilators:
- Short acting Beta 2 agonist (salbutamol)
- Long acting Beta 2 agonist (salmeterol)
-
- Short acting muscarinic antagonists (Ipratropium bromide)
- Long acting muscarinic antagonists (Tiotropium)

Inhaled corticosteroid (Beclometasone)

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25
Q

Treatment algorithm of COPD (inhalers)

A

1) SABA or SAMA
2) LABA and LAMA regularly (ICS if asthma features)
3) LABA + LAMA + ICS

+ SABA at any stage (can still be taken as required)

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26
Q

Other treatments of COPD

A

Long term Oxygen if sats below 92 at rest
Oral Theophylline (bronchodilator)
Oral mucolytic
Prophylactic azithromycin!

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27
Q

Indications of oxygen in COPD

A
  • If O2 Sats <92% at rest (88-92 is during exacerbation)
  • Cyanosis
  • Polycythaemia
  • Raised JVP
  • If FEV1<30%
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28
Q

Oxygen targets in patients on oxygen

A

88-92% if retaining CO2
>94% if not retaining CO2

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29
Q

How do Beta 2 agonists and Muscarinic antagonists work

A

B Agonist - Bind to and activate Beta 2 receptors (which are normally activated by NAd)

M antagonist - Bind to M3 muscarinic receptors. Prevents acetylcholine from binding, preventing bronchoconstriction

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30
Q

Complications of COPD (4)

A
  • Cor pulmonale (RH failure secondary to pulmonary HTN)
  • Pneumothorax
  • Type 1/2 resp failure and respiratory acidosis
  • Infections
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31
Q

How does pulmonary hypertension cause cor pulmonale, and what are its clinical manifestations

A

Pulmonary vasoconstriction and HTN means right heart must pump against high pressures, eventually failing.

Causes peripheral oedema, raised JVP, hepatomegaly

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32
Q

Define COPD exacerbation with ABG finding

A

Acute worsening of symptoms, usually due to infective cause (H influenza, S pneumoniae).

Shows respiratory acidosis (low pH and high CO2). Increased bicarbonate (HCO3-) shows compensation by kidney

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33
Q

Treatment of COPD exacerbation

A

Amoxicillin

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34
Q

What are the criteria for bronchodilator reversibility

A

> 12% increase in FEV1
AND volume increase >200ml post bronchodilator

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35
Q

Define asthma

A

Chronic airway disease characterised by reversible airway obstruction, airway hypersensitivity and inflamed bronchioles, causing recurrent episodes of dyspnoea, wheezing and a productive cough.

This can be allergic/IgE mediated, or non IgE mediated (exercise, cold air and stress)

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36
Q

Define Atopy

A

Predisposition to respond immunologically to a diverse range of allergens, leading to CD4+ Th2 production, and overproduction of IgE.

The 3 atopic diseases are atopic dermatitis, allergic rhinitis and asthma

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37
Q

Risk factors for asthma

A
  • History of atopy
  • Family history
  • Allergen exposure (tobacco, pets, outdoor air pollution, dust, grass, pollen)
  • Viral URTI
  • Growing up in a clean environment (Hygiene hypothesis)
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38
Q

Pathophysiology of asthma

A

Allergen picked up by dendritic cells and presented to Th2 cells, which respond by releasing cytokines, releasing IgE which bind to mast cells, causing mast cell degranulation. This releases histamine, leukotrienes, prostaglandin.

This causes chronic airway inflammation causing:
- Bronchoconstriction and smooth muscle spasm
- Mucus hypersecretion

After a few hours, immune cells release chemical mediators that damage the lung. At first this is reversible, however over time, this causes thickening of epithelial basement membrane, permanently reducing airway diameter.

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39
Q

Precipitating factors of asthma

A
  • Pollen, dust mites, grass
  • Cold air
  • Exercise
  • Pets
  • Tobacco smoke
  • Occupational allergens (bakers, manufacturers, lab work, welding)
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40
Q

Signs/symptoms of asthma

A

Episodic shortness of breath, usually after trigger exposure.
- Diurnal PEFR variation (worse at night/early morning)
- Usually dry cough (but can be productive)
- Expiratory wheezing/dyspnoea/chest tightness

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41
Q

What might microscopy of an asthma patients sputum look like?

A

Will contain spiral mucus plugs - casts from small bronchioles.

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42
Q

Investigations in asthma

A

Spirometry:
- FEV1/FVC <70%
- Bronchodilator shows improvement

Fraction of exhaled nitric oxide (FeNO): >45ppb

Peak Expiratory Flow Rate (PEFR) GOLD. Multiple times a day for 2-4 weeks. Variability >20% throughout day diagnostic

Allergy testing

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43
Q

What is Samter’s triad

A

Inflammation and swelling of airways in response to aspirin/NSAIDs. Leads to:
- Chronic Asthma history
- Recurrent nasal polyps
- Aspirin intolerance/hypersensitivity

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44
Q

Management algorithm of asthma

A

1) SABA (Salbutamol)
2) SABA + low dose ICS (beclomethasone)
3) SABA + low dose ICS + LTRA (leukotriene receptor antagonist) (montelukast)
4) SABA + low dose ICS + LABA (salmeterol), + LTRA in adults, - LTRA in children
5) SABA + MART (Maintenance and reliever therapy - fast acting LABA and ICS)

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45
Q

What does stepwise management mean in asthma?

A
  • Aim to use lowest effective doses possible
  • Only step up treatment if previous doesn’t work
  • Step down treatment every 3 months
  • Annual asthma reviews for stable asthma
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46
Q

Define asthma exacerbation

A

acute/subacute episode of progressive worsening of asthma symptoms (SOB, wheezing, cough, chest tightness)

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47
Q

What suggests severe asthma exacerbation/episode

A

Any of
- PEFR 50-33%
- Resp Rate >25
- Heart rate >110
- Inability to complete sentences in one breath

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48
Q

Signs of life threatening asthma exacerbation

A

Cyanosis
Reduced GCS
Exhaustion causing silent chest
Arrhythmia
Hypotension

PEFR <33%
SpO2 <92%
PO2 <8kPa
Normal PaCO2

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49
Q

Acute management of asthma exacerbation

A

Moderate
- Salbutamol + 5 days prednisolone

Severe/life threatening - hospital
1 - Oxygen (aim for SpO2>94%)
2 - Nebulised bronchodilators (SABA, SAMA)
3 - Oral Prednisolone
3 (if not conscious) - IV bronchodilator (Magnesium sulphate)

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50
Q

At what PEFR can a patient be discharged

A

When it falls back into moderate range, PEFR>75%

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51
Q

Define Tuberculosis

A

Granulomatous infection caused by Mycobacterium tuberculosis. Present in 1.7b people worldwide in latent stage. Common in South Asia and sub saharan Africa

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52
Q

Risk factors for TB

A
  • Recent active TB contact
  • Endemic region travel
  • Homelessness
  • Immunosuppression
  • Alcohol/drug abuse
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53
Q

Pathophysiology of TB

A

Macrophages struggle to clear M tuberculosis due to waxy mycolic capsule, which confers protections and prevents stain binding (acid fast!).

Spreads via respiratory droplets from active disease patients.

Disease has 4 stages (more detail in other cards)
- Primary
- Latent (dormant, asymptomatic)
- Secondary (reactivation)
- Miliary (systemic spread)

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54
Q

Stages of TB infection

A

Primary - TB phagocytosed but resists killing. Focal, caseating granuloma forms in upper part of lung, called a Ghon focus. If there is hilar lymph nodes involvement, it becomes a Ghon complex.

Latent - Bacteria dormant, patient is asymptomatic. Sputum test will be negative but Mantoux will still be positive

Secondary - Immunocompromised patients. Latent TB reactivates, patient is infectious and symptomatic.

Miliary - Lymphatogenous spread to other organs, causing systemic symptoms

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55
Q

Signs/symptoms of TB

A
  • Fever
  • Night sweats
  • Weight loss
  • Cough with haemoptysis
  • Lymphadenopathy
  • Crackling on auscultation
  • Dyspnoea
  • Clubbing if long standing
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56
Q

Extrapulmonary TB symptoms

A

TB Meningitis
TB back/spine pain (Pott’s disease)
TB pericarditis
TB cystitis
Miliary TB (disseminated)

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57
Q

Investigations in latent TB

A

Mantoux screening - Intradermal injection of purified protein derivative tuberculin, causes type IV hypersensitivity reaction. >55 induration positive

Interferon gamma release assay - Blood mixed with TB. If previous contact, interferon gamma released

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58
Q

Causes of false positive TB test results (3)

A

Previous BCG vaccine
Non tuberculous mycobacteria infection
Incorrect tuberculin administration

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59
Q

Causes of false negative TB test results (4)

A

Recent infection (<8 weeks)
HIV
Lymphoma
Sarcoidosis

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60
Q

Investigations in active TB

A

Chest X ray (specific signs, in separate card)

  • Sputum stain/culture - 3 deep cough sputum samples. Will stain red with Ziehl-Neelsen stain. Mycobacterium culture positive.
  • Nucleic-acid Amplification Test (NAAT) - Test conducted on urine or sputum. Done if patient has HIV, or is under 15.
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61
Q

CXR signs in TB

A

Primary
- Patchy consolidations
- Pleural effusion
- Hilar lymphadenopathy

Latent
- Ghon complex

Secondary
- Nodular consolidation with cavitation (gas filled spaces) in upper lung

Miliary
- “Millet seeds” uniformly distributed throughout lung fields

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62
Q

What vaccine helps prevent against TB

A

BCG vaccine

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63
Q

Treatment of active TB

A

RIPE - two months course
Rifampicin
Isoniazid (+ Pyridoxine)
Pyrazinamide
Ethambutol

Then R and I for 4 further months

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64
Q

What is prescribed with isonazid and why?

A

Pyridoxine (vitamin B6)

Helps prevent peripheral neuropathy

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65
Q

Treatment of latent TB

A

RI for 3 months
Rifampicin
Isoniazid (+Pyridoxine)

OR Isoniazid for 6 months

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66
Q

What should be done immediately in active TB patient

A
  • Notify UKHSA
  • Isolate patients, ideally in negative pressure room
  • Contact tracing
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67
Q

Side effects of TB treatment drugs

A

R- rifampicin –> red urine/sweat
I- isoniazid –> peripheral neuropathy
P- pyrazinamide –> gout, hepatitis
E- ethambutol –> optic neuritis

All can also cause hepatitis

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68
Q

MoA of TB drugs

A

Rifampicin - inhibits bacterial RNA polymerase
Isoniazid - Inhibits mycolic acid synthesis
Pyrazinamide - Inhibits Fatty Acid Synthetase, disrupting bacterial membrane function
Ethambutol - Inhibits cell wall synthesis

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69
Q

What is the continuation phase of TB Treatment

A

After initial treatment, Rifampicin and Isoniazid may be given for 4 further months

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70
Q

What are the effects of rifampicin and isoniazid on CYP450

A

R - Liver enzyme inducer
I - Liver enzyme inhibitor

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71
Q

3 ways lung defends itself

A
  • Coughing
  • Mucociliary escalator
  • Alveolar macrophages
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72
Q

Pathophysiology of pneumonia

A

Microorganisms enter lungs triggering immune response. Inflammation and fluid accumulation in alveoli of lung occurs (exudate)

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73
Q

Causes of pneumonia

A

CAP - Community Acquired Pneumonia (typical)
- S. pneumoniae (MC)
- H. influenzae

HAP - Hospital Acquired Pneumonia (most g- aerobic bacilli)
- Pseudomonas aeruginosa
- E. coli
- Klebsiella

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74
Q

Atypical CAP causes

A
  • Mycoplasma pneumoniae (Milder disease, rash called erythema multiforme and includes neurological symptoms)
  • Chlamydophila pneumoniae
  • Legionella pneumonia/ legionnaires’ disease (typically due to infected water supplies or AC units. Causes SIADH/hyponatraemia. Suspect if recent cheap hotel holiday to a place with AC units + hyponatraemia!)
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75
Q

Stages of lobar pneumonia

A
  1. Congestion - Blood vessels and alveoli fill with fluid. Few RBCs and neutrophils in lung
  2. Red Hepatisation - Infiltration of exudate, including RBC, neutrophils, fibrin, filling air spaces, making them look “solid” on imaging. Has red, liver like appearance.
  3. Grey hepatisation - RBCs break down, changing it to grey colour
  4. Resolution
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76
Q

Other types of pneumonia

A
  • Ventilator Associated Pneumonia - microbes on endotracheal tube
  • Aspiration pneumonia - food, drink, saliva, vomit goes into lung, carrying microbes with it. (right lower lobe)
  • Bronchopneumonia - bronchioles affected
  • Atypical - Interstitium of alveoli
  • Lobar - Complete consolidation of lobe
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77
Q

Signs/symptoms of pneumonia

A
  • Productive, coloured sputum cough. Can include haemoptysis
  • Fever and chills
  • Pleuritic chest pain (worse breathing/coughing)
  • Bronchial breathing and coarse crepitations
  • Dullness to percussion
  • Fatigue, confusion and hypoxia
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78
Q

Examination signs of pneumonia

A
  • Dullness to percussion
  • Focal coarse crackles
  • Bronchial breathing sounds
  • Tactile vocal fremitus (more vibrations from person’s chest/back when they talk)
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79
Q

Presentation of atypical pneumonia

A
  • Gradual onset
  • Milder flu like symptoms (cough/dyspnoea)
  • Low/No fever
  • Dry cough
  • Sore throat and myalgia (not really present in typical)
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80
Q

1st and GOLD investigations of pneumonia

A

1st Chest X ray
- Consolidation within alveoli and bronchioles, can be lobar. Air bronchograms visible (air-filled bronchi against background of consolidated lung tissue)
- Consolidation is well defined. Diffuse/nodular in atypical

GOLD Sputum culture

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81
Q

How is CRP used in pneumonia

A

<20 no antibiotics
20-100 consider antibiotics
>100 definitely offer

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82
Q

What classification system is used in Pneumonia

A

CURB 65
Confusion (abbreviated mental test score <8 or disorientation)
Urea (kidney function) - >7mmol/L
Respiratory rate - >30/min
Blood pressure - Systolic <90 or diastolic <60

Age >65

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83
Q

How is CURB 65 score used?

A

HAP
>2 = hospital care

CAP (urea not measurable in primary care etc)
0-1 (low severity) - community care
2 (moderate) - hospital care
3 - intensive care

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84
Q

Management of pneumonia

A

Depends on CURB65
CAP
low (0-1) - 5 day Oral amoxicillin or doxycycline.
Moderate (2) - Oral amoxicillin and clarithromycin if atypical. 5 day course
High (3+) - IV co-amoxiclav and clarithromycin

HAP
Low - oral co-amoxiclav
High - IV ceftriaxone

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85
Q

Treatment of Legionnaire’s pneumonia

A

Legionella needs clarithromycin

Also Legionnaire’s is NOTIFIABLE

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86
Q

What is the most common pneumonia in HIV patients

A

Pneumocystis pneumonia

Fungal infection caused by Pneumocystis jirovecii

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87
Q

Presentation of Pneumocystis pneumonia

A

HIV patient

Chest exam mostly normal

Pyrexia, dry cough, fever.

Shows lymphadenopathy, hepatosplenomegaly, choroid lesions (benign naevi back of eye)

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88
Q

Management of pneumocystis pneumonia

A

Co-trimoxazole (trimethoprim and sulfamethoxazole)

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89
Q

Define cystic fibrosis, with how its caused.

A

Autosomal recessive inherited disease, causing secretions from mucus glands to become thick. Respiratory and pancreatic problems most prominent

Phenylalanine deletion on CFTR (Cystic Fibrosis Transmembrane conductance Regulator) gene on chromosome 7.

90
Q

General pathophysiology of Cystic Fibrosis

A

Phenylalanine deletion on CFTR gene on chromosome 7. CFTR is a channel protein that pumps chlorine into secretions, drawing water into them. Mutated CFTR misfolds, and is unable to migrate to cell membrane. Hence, secretions are thicker than usual.

91
Q

Respiratory pathophysiology in Cystic Fibrosis

A

Dry airways/ impaired mucociliary clearance

Thick immobile secretions harbour bacteria and cause infection. This can lead to chronic inflammation and bronchiectasis, which can lead to respiratory failure and death

92
Q

Pancreatic pathophysiology in cystic fibrosis

A

Thick pancreatic and biliary secretions block ducts. This causes pancreatitis, cholangitis and a lack of digestive enzymes in GI tract, which can lead to malabsorption. Causes failure to thrive, steatorrhoea, and endocrine dysfunction e.g. CF diabetes.

93
Q

Signs/symptoms of cystic fibrosis

A
  • Failure to thrive
  • Chronic, thick sputum cough
  • Crackles/wheeze on auscultation
  • Recurrent URTI
  • Loose, greasy, smelly stools
  • Nasal polyps and finger clubbing
  • Salty tasting child
94
Q

Main sign in neonates of cystic fibrosis

A

Meconium ileus

Meconium usually passed in first 48 hours, but becomes thick and mucusy, causing obstruction.

95
Q

Investigations of cystic fibrosis

A

Screened for in all babies in Guthrie heel prick (Immunoreactive trypsinogen)

GOLD: Chlorine sweat test - Pilocarpine induces sweating. Increased chlorine in sweat (>60mmol/L)

Genetic testing for CFTR gene

Faecal elastase - Pancreatic insufficiency

96
Q

Lifestyle advice for cystic fibrosis

A
  • High calorie, high fat diet
  • No smoking
  • Regular exercise
  • Regular chest physiotherapy
  • Regular flu vaccination
97
Q

Respiratory management of cystic fibrosis

A

Chest physiotherapy and exercise
Bronchodilator (SABA - Salbutamol)
Mucolytic - Dornose alfa

Nebulised Tobramycin for Pseudomonas infection
Prophylactic Flucloxacillin always

98
Q

Digestive management of cystic fibrosis

A

High calorie high fat diet
Fat soluble vitamins (ADEK)

Pancreatic enzyme replacement (Creon tablets)
PPI - omeprazole (aid pancreatic enzyme absorption)

Ursodeoxycholic acid (make bile more soluble)

99
Q

Complications of cystic fibrosis (7)

A
  • Life expectancy ~40 yrs
  • Pancreatic insufficiency
  • CF related diabetes
  • Infertility
  • Recurrent URTI/Lung disease
  • Malabsorption, leading to delayed puberty, osteoporosis, infertility
  • Liver cirrhosis
100
Q

Define Sarcoidosis

A

Idiopathic systemic granulomatous inflammation. Granulomas are non caseating (no necrotic core). Lungs most prominently affected

Type 4 hypersensitivity reaction

101
Q

Pathophysiology of sarcoidosis

A

T cell mediated immune response to antigenic stimulus causes formation of non caseating granulomas. This occurs systemically.

Macrophages can fuse together forming Langhans giant cells.

Mostly affects hilar lymph nodes near where bronchi meet lungs.

102
Q

Signs/symptoms of sarcoidosis

A
  • Cervical and submandibular lymphadenopathy
  • Lupus pernio (type of rash)
  • Erythema nodosum (red nodules on shins)
  • Non productive cough
  • Uveitis (red-eye, photophobia)
  • Polyarthralgia, swinging fever, fatigue, weight loss
103
Q

Associated syndromes with sarcoidosis

A

Lofgren’s - Subset of sarcoidosis. Triad of bilateral hilar infiltration, erythema nodosum, acute polyarthritis
Heerfordt’s - Facial nerve palsy, parotitis/mumps (inflammation of salivary glands)

104
Q

Investigations in sarcoidosis

A

CXR - Bilateral hilar lymphadenopathy and pulmonary infiltrates, used to stage.

Serum calcium - Raised
ACE - Raised

Bronchoscopy and mediastinal lymph node biopsy GOLD - Non caseating granulomas with epithelioid cells

105
Q

CXR staging of sarcoidosis

A

CXR - Bilateral hilar lymphadenopathy (staged 1-4)
0 = normal
1 = Just bilateral hilar lymphadenopathy
2 = + interstitial infiltrates
3 = Pulmonary infiltrates, no lymphadenopathy
4 = Diffuse fibrosis

106
Q

CT signs of sarcoidosis

A

Hilar lymphadenopathy and pulmonary nodules.

Ground glass appearance - reversible
Cystic distortion - irreversible

107
Q

Management of sarcoidosis

A
  1. Corticosteroid - Oral prednisolone
  2. Immunosuppression - methotrexate

IV corticosteroid and ventilation support if resp failure

108
Q

Complications of sarcoidosis (6)

A
  • Pulmonary fibrosis/ HTN
  • Cor pulmonale
  • Liver cirrhosis
  • Kidney stones, interstitial nephritis
  • Encephalopathy, nerve palsy (facial)
  • Optic neuritis
109
Q

Risk factors for idiopathic pulmonary fibrosis

A
  • Age
  • Male
  • Smoking
  • Family history
  • Dust exposure
110
Q

Pathophysiology of pulmonary fibrosis

A

Type 1 pneumocytes release transforming growth factor beta 1, which gets type 2 pneumocytes to stimulate fibroblasts to proliferate into myofibroblasts which lay down reticular and elastic fibres.

In IPF there is type 2 pneumocyte overproliferation, causing fibrosis of the lung. This causes problems with ventilation and oxygenation, decreasing FEV1 and FVC.

Also leads to loss of alveoli

111
Q

Signs/symptoms of IPF

A

Mostly affects lower lobes
- Bibasal fine end inspiratory crackling in lower zones
- Clubbing
- Cyanosis
- non productive cough

112
Q

Investigations in IPF

A

CXR - Bilateral shadowing (ground glass appearance, progressing to honeycombing), mainly in lower zones

Spirometry - restrictive pattern (FEV1 decreased FVC greatly decreased, FEV1/FVC >80%)

High resolution CT thorax GOLD - shows reticulation and honeycombing

113
Q

Management and complications of IPF

A

Supportive care - oxygen and vaccinations against pneumococcus and influenza

Antifibrotic agents (nintendinib and pirefenidone)

Can lead to pulmonary HTN and cor pulmonale

114
Q

Define bronchiectasis

A

Permanent dilation of the bronchi due to the destruction of elastic and muscular components of the bronchial wall.

Obstructive condition, as inflammation causes mucus plugs in airways

115
Q

Pathophysiology of bronchiectasis

A

Usually due to chronic inflammation. Over time, cytokines damage ciliated epithelial cells and destroy elastin fibres in walls of airway, so airway becomes clogged with mucus and permanently dilated. Stiff, mucus filled airways make it a struggle for passage of air. This can cause hypoxia over time, causing the pulmonary arterioles to constrict. This causes pulmonary hypertension, which can lead to cor pulmonale.

116
Q

Signs/symptoms of bronchiectasis

A
  • Productive cough with lost of sputum
  • Dyspnoea
  • Chest pain
  • Inspiratory crepitations
    (usually has post infection, CF etc history)

Long standing hypoxia can cause clubbing!

117
Q

Investigations of bronchiectasis

A

CXR/CT scan - Thickened, dilated bronchi and bronchioles

Spirometry shows obstructive disease

118
Q

Management of bronchiectasis

A

Antibiotics for infections
Chest physio
Mucolytics - dornose alfa

119
Q

Explain how Primary ciliary dyskinesia and cystic fibrosis cause bronchiectasis. Give 2 other causes also

A

PCD - Cilia dont move, allowing mucus and bacteria to stay and fester. Bacteria multiplies causing a pneumonia. Recurrent, can cause chronic inflammation

CF - Mucus is sticky and hard to sweep. Causes stagnation and build up of bacteria -> recurrent pneumonias

  • Post infection (TB, measles, HIV)
  • Airway obstruction (tumour or foreign object) blocks mucociliary escalator (same pathology as aspiration pnuemonia)
120
Q

Define Pleural Effusion

A

Fluid collects between in pleural space (space between visceral and parietal pleura)

parietal pleura - stuck to chest wall, covers mediastinum, diaphragm, ribs etc

visceral pleura - envelopes all lung surfaces

121
Q

Pathophysiology of pleural effusion

A

Can be transudate or exudate

Transudate - <30g/L protein
Exudate - >30g/L protein

Normally fluid is drained by lung lymphatics, but disease which increase filtration rate from vasculature or decrease absorption from lymphatics will result in fluid build up in pleural space.

122
Q

What causes transudative effusion

A

Increased hydrostatic pressure or low oncotic pressure causes fluid movement from capillaries to pleural space. Hence, no/low protein.

Causes include
- Congestive heart failure
- Hypoalbuminaemia (liver problem)
- Hypothyroidism
- Peritoneal dialysis

123
Q

What causes exudative effusion?

A

Inflammation, infection and malignancy cause increased vessel permeability, so fluid and protein leak out of tissues into pleural space.

Causes include
- Malignancy
- Infection
- Trauma
- PE
- Autoimmune/connective tissue disorders

124
Q

Symptoms of pleural effusion

A

Dyspnoea
Cough
Pleuritic chest pain

125
Q

Signs of pleural effusion (5)

A
  • Reduced chest expansion and reduced breath sounds on affected side
  • Decreased tactile and vocal fremitus
  • One sided dullness to percussion
  • Pleural friction rub (raspy breathing) and bronchial breathing at most superior part of effusion
  • Tracheal deviation from effusion if big effusion
126
Q

Underlying features indicative of cause of pleural effusion

A

Peripheral oedema -> Heart failure
Ascites/jaundice -> Liver cirrhosis
Productive cough/fever -> pneumonia
Weight loss (malignancy)

127
Q

What is a chylothorax?

A

Lymphatic effusion

Thoracic duct disrupted, so drainage inefficient. This causes leakage of the lymphatic fluid into the pleural space.

128
Q

Investigations of pleural effusion

A

Chest X ray first
- Blunting of costophrenic angle
- Fluid in lung fissures
- Meniscus in larger effusions
- Tracheal and mediastinal deviation

Pleural fluid and analysis
- Conducted on lateral site, above the ribs

129
Q

What are the following fluid appearances suggestive of in pleural effusion:
- Pale yellow
- Red
- Milky
- Pus
- Food

A

Pale - Transudate
Red - Blood (malignancy, PE, TB)
Milky - Chylothorax
Pus - Empyema
Food - Oesophageal rupture

130
Q

What lab tests are conducted on aspirated pleural effusion?

A

pH
Glucose
Protein (transudate/exudate)
LDH (high in exudate)
Gram stain/culture
Acid fast/Ziehl Neelsen
Amylase (pancreatitis)

131
Q

What criteria is used to classify if effusion is transudative or exudative?

A

Light’s criteria - used when protein 25-35g/L

Essentially high protein or high LDH suggests exudative cause

132
Q

Treatment of pleural effusion

A

Small, non infective effusions can be managed through underlying cause.

Chest tube drainage if infective cause

Thoracentesis for symptomatic, non red flag effusion

133
Q

Indications of chest tube drainage (3)

A
  • Purulent or cloudy pleural fluid
  • Positive gram stain/culture
  • pH <7.2
134
Q

Treatment of recurrent effusion

A
  • Pleurodesis: Scarring pleural space causing adhesion of visceral and parietal pleura
  • Indwelling pleural catheter: Allows for long term repeated drainage
135
Q

Complications of pleural effusion

A
  • Empyema (infective effusion)
  • Pneumothorax
  • Lobar lung collapse
  • Trapped lung/fibrosis
136
Q

Define Empyema

A

Collection of pus in the pleural space, usually due to infection

137
Q

Causes of Empyema

A

Bacterial pneumonia
Recent thoracic surgery
Lung abscess
Chest trauma
Immunodeficiency

138
Q

Define Pneumothorax

A

Abnormal accumulation of air within pleural space (basically pleural effusion for air)

139
Q

Pathophysiology of Pneumothorax

A

Normally intrapleural pressure is lower than both atmospheric and alveolar pressure. This means gases can follow pressure gradients. building up in the pleural space.

Normally, the thoracic cavity is below its resting volume, and the lung is greater than its resting volume. Hence, when a pneumothorax forms, the thoracic cavity enlarges and the lung shrinks.

The more air that builds up, the greater the intrathoracic pressure, the smaller the lung becomes, and the larger the tracheal and mediastinal deviation that occurs.

140
Q

The 3 types of pneumothorax and their main causes

A

Primary Spontaneous - No underlying cause, subpleural bleb rupture in healthy, tall male, possibly whilst playing sports
Secondary Spontaneous - Underlying disease, middle aged COPD patient with sudden onset breathlessness and chest pain
Tension Pneumothorax - Usually occurs secondary to penetrating chest injury (surgery, trauma etc)

141
Q

Risk factors for Primary Spontaneous Pneumothorax

A
  • Tall, slender, young (20-30)
  • Smoking
  • Marfan
  • Rheumatoid arthritis
  • Family history
  • Driving/flying
142
Q

risk factors of Secondary Pneumothorax, and how they form

A

Ruptured bleb or bullae (air filled sacs) in a patient with underlying disease. Bullae form when there is a small leak in the alveoli which allow air to leak out and form an air filled sac. Bullae can break into visceral pleura, forming a pneumothorax/

  • Underlying lung disease (COPD, asthma, lung cancer)
  • TB
  • Pneumocystis Jirovecii
143
Q

Formation of Tension Pneumothorax with risk factors

A

Penetrating chest wall injury rips into parietal pleura from outside, allowing air to enter. Forms a ONE WAY VALVE, meaning air can enter but not leave. Air enters during inspiration but can’t leave. Tracheal deviation small in spontaneous, large in tension
Medical emergency, requires emergency decompression.

  • Recent chest wall trauma
  • Recent penetrative surgery
  • Intubation
  • Mechanical ventilation
144
Q

Signs/symptoms of Pneumothorax

A

Sudden onset breathlessness, pleuritic chest pain, haemodynamic instability, sweating/cyanosis

  • Ipsilateral hyperresonance
  • Ipsilateral reduced breath sounds
  • Ipsilateral hyperexpansion
  • Contralateral tracheal deviation and circulatory shock in tension
145
Q

Investigations in pneumothorax

A

1st - Erect CXR
- Visible visceral pleural edge
- Contralateral mediastinal shift and tracheal deviation
- Collapsed lung

GOLD - CT Chest

No investigations in Tension, go straight to decompression

146
Q

Management of spontaneous pneumothorax

A

No SOB, less than 2cm air on CXR - discharge and follow up
If SOB, >2cm - Needle aspiration or chest drain at 5th intercostal space, mid axillary line

147
Q

Management of tension pneumothorax

A

Immediate emergency large bore cannula in 2nd intercostal space, mid clavicular line. Needle decompression then chest drain.

148
Q

Definitive management of pneumothorax

A

Pleurodesis. Create inflammatory reaction between pleural layers, making them stick together

Pleurectomy

149
Q

Driving and flying rules in pneumothorax

A

Driving - avoid indefinitely, or until bilateral pleurectomy
Flying - 1 week after check X ray after resolved pneumothorax

150
Q

Causes of chronic interstitial lung diseases

A
  • Granulomatosis
  • Hypersensitivity pneumonitis
  • Pulmonary fibrosis
  • Scleroderma, RA
  • Amiodarone
  • Goodpastures
151
Q

Define pulmonary hypertension

A

Pulmonary blood pressure greater than 25mmHg (BP in lungs usually much lower than rest of body)

152
Q

Give 5 causes of pulmonary hypertension

A

1 - Congenital heart defects (left to right shunt)
2 - Connective tissue disease
3 - Left heart failure
4 - Chronic lung disease (COPD etc)
5 - Pulmonary vascular disease (embolism)

153
Q

How do connective tissue disorders cause pulmonary HTN

A

Damage to endothelial cells causes release of chemicals such as serotonin and thromboxane which constrict pulmonary arterioles and cause hypertrophy of surrounding muscle.

No compensatory nitric oxide and prostacyclin production

154
Q

How does left heart failure cause pulmonary HTN

A

Left heart unable to pump efficiently, causing backing up of blood into the pulmonary circulation.

155
Q

How does chronic lung disease cause pulmonary hypertension

A

Hypoxic vasoconstriction

Lung area diseased, cant deliver oxygen to blood, so pulmonary arterioles constrict. If widespread (e.g. in COPD), widespread constriction increases pulmonary vascular pressure.

156
Q

How does pulmonary hypertension cause right heart failure

A

Pulmonary hypertension makes it harder for the right heart to pump blood into pulmonary circulation, causing the right ventricle to hypertrophy. Eventually, oxygen demand exceeds supply causing right heart failure

(When chronic lung disease causes this -> Cor pulmonale)

157
Q

How does right heart failure cause its symptoms

A

Right heart failure causes backing up of blood into venous circulation.

This causes fluid buildup (peripheral oedema), elevated jugular vein pressure and hepatomegaly. Left ventricle must compensate, causing it to pump faster

158
Q

Why does pulmonary HTN cause lung symptoms

A

Fluid is squeezed out of pulmonary vessels, causing pulmonary oedema, making gas exchange difficult.

159
Q

Signs/symptoms of pulmonary hypertension

A
  • Shortness of breath (orthopnoea if caused by LEFT HEART FAILURE)
  • Chest pain
  • Raised JVP
  • Hepatomegaly
160
Q

Investigations of pulmonary hypertension

A
  • Echocardiogram measures pulmonary hypertension
  • ECG (RV hypertrophy shows as large R waves in V1-3)
  • CXR (Dilated pulmonary arteries, RV hypertrophy)
161
Q

Treatment of pulmonary hypertension

A

Oxygen
Decrease BP (CCB)
Endothelin receptor antagonist can be used if CCB contraindicated

162
Q

What is a restrictive lung disease

A

Disease that restricts the lung from filling. FEV1/FVC is usually normal (>0.8 - person can exhale 80% of their FVC in first second)

Examples include:
- Idiopathic pulmonary fibrosis
- Sarcoidosis
- Systemic sclerosis (scleroderma)
- Hypersensitivity pneumonitis

163
Q

Define hypersensitivity pneumonitis

A

Restrictive lung disease. AKA extrinsic allergic alveolitis (but NO IgE involvement). Usually caused by known organic antigen

Type 3 hypersensitivity reaction. Antibody-antigen complex deposition causes inflammation of lung tissue.

Over time, chronic exposure can cause type 4 to occur due to T cell involvement. This leads to non caseating granuloma formation

164
Q

Risk factors for hypersensitivity pneumonitis

A
  • Pre existing lung disease
  • Regular hot tub usage
  • Occupations (farmers, cattle workers, ventilation systems, chemicals, coffee, tobacco)
  • Bird keeping)
165
Q

Signs and symptoms of hypersensitivity pneumonitis

A

Dyspnoea
Cough
Headache
Fever and rigors

Chronic can lead to cyanosis, clubbing and respiratory failure

166
Q

Treatment of hypersensitivity pneumonitis

A

Remove trigger
Steroids can be given

167
Q

Define pneumoconiosis

A

A group of lung diseases caused by inhaling certain types of dust or particles, usually in a workplace environment. These cause inflammation, scarring and damage over time.

168
Q

Substances that cause occupational lung diseases

A
  • Coal/carbon dust
  • Asbestos
  • Silicon dioxide
  • Beryllium
169
Q

5 at risk jobs for occupational lung disease

A
  • Quarry worker
  • Miner
  • Cotton mill worker
  • Plumbers
  • Construction workers
170
Q

Signs/symptoms of occupational lung disease

A

Fine crackles, wheezing and clubbing, weight loss, haemoptysis that develops over time in at risk worker.

Cough that may be productive of black sputum if progressive massive fibrosis

171
Q

What job is at risk of berylliosis and what does berylliosis lead to

A

Aerospace industry and beryllium miners

  • leads to non caseating granuloma formation, upper zone fibrosis and risk of lung cancer
172
Q

What job is at risk of silicosis and what does it lead to

A

Sandblasters, quarry miners, silica miners

  • Increased TB risk, eggshell calcification in hilar lymph nodes.
173
Q

What job is at risk of asbestos and what can it lead to

A

Construction workers, plumbers, shipyard workers

  • Pleural plaques and lower zone fibrosis
  • Leads to increased risk of mesothelioma! and lung cancer
174
Q

Risk factors for lung cancer

A
  • Age
  • Smoking
  • Asbestos
  • Arsenic
  • Air pollution
  • Radiation
175
Q

What are the types of lung cancer and from where do they arise?

A
  • Mesothelioma (arises from pleura) (asbestos)
  • Small cell lung cancer (from neuroendocrine Kulchitsky cells)
  • Non small cell (adenocarcinoma MC non smokers, squamous cell carcinoma MC smokers)
  • Large cell
  • Carcinoid tumours
176
Q

Define Mesothelioma with its main cause

A

Malignancy of the pleura

Main cause is asbestos, but doesn’t present until decades post exposure. Usually occurs in men aged 60+

177
Q

Signs/symptoms of mesothelioma

A

Chronic (>3 weeks) cough, breathlessness, weight loss, fatigue, night sweats

Finger clubbing
Reduced breath sounds
Haemoptysis
Pleuritic chest pain

178
Q

Investigations of mesothelioma

A

CXR - Lower zone fibrosis, pleural thickening, pleural effusion, reduced lung volume

Contrast CT - Pleural plaques and enlarged lymph nodes if metastasis

179
Q

Management of mesothelioma

A

Usually inoperable, as has metastasised by the time it is found.

Operable - Extrapleural pneumonectomy, pleurectomy

Inoperable - Chemotherapy (cisplain, pemetrexed)

180
Q

Complications of Mesothelioma

A

Pneumothorax
Local invasion causing dysphagia, hoarseness, cord compression
Metastasis to
- Other lung
- Peritoneum
- Brian
- Hilar lymph nodes

181
Q

What are primary bronchial carcinomas

A

Cancers of the lung that affect lung parenchyma.

These are categorised into small cell lung cancer (15%) and non small cell lung cancer (85%)

182
Q

Define small cell lung cancer

A

Fast growing, late presenting tumours derived from neuroendocrine cells at central lesions near main bronchus.

These cells usually release ectopic neuroendocrine hormones. E.g.
- ADH = SIADH (and hyponatraemia)
- Cortisol = Cushings

Also cause Lambert Eaton syndrome!!

183
Q

Define Non small cell lung cancer

A

All other lung cancers. Consist of squamous cell carcinoma, adenocarcinoma, carcinoid tumour, large cell tumour

184
Q

Summarise Squamous cell lung cancer

A

RF: Smoking

Usually arises from lung epithelium. Central lesion that produces keratin and can also produce PTH related protein, causing hypercalcaemia.

Causes hypertrophic pulmonary osteoarthropathy (HPO)

185
Q

Summarise lung adenocarcinoma

A

RF: Asbestos

Usually peripheral lesion, arising from mucus producing glandular cells. Causes gynaecomastia and can cause HPO

Metastasis common - Bone, brain, adrenal gland, lymph nodes, liver

186
Q

Summarise carcinoid tumour

A

Genetic Association! MEN1

Arise from mature neuroendocrine cells, causing carcinoid syndrome.

187
Q

What do large cell tumours secrete

A

B-HCG (pregnancy marker!)

188
Q

Signs/symptoms of lung cancer

A

Weight loss, cough, breathlessness, haemoptysis, pleuritic chest pain, fever night sweats fever.

Lymphadenopathy and pneumonia possible and stony dull percussion if pleural effusion.

Clubbing, facial plethora, hoarseness are extrapulmonary manifestations

189
Q

Investigations in lung cancer

A

CXR
- Lung consolidation
- Circular opacity (visible lesion)
- Lung collapse
- Hilar node enlargement
- Pleural effusion (unilateral)

CT with Contrast GOLD

PET scan to check for metastasis.

Biopsy for peripheral lesions and bronchoscopy and ultrasound for central.

190
Q

Management of lung cancer

A

NSCLC can be fixed surgically, SCLC less so as presents late.

191
Q

Lung cancer complications

A

Paraneoplastic syndromes
- Cushings
- SIADH
- Hypercalcaemia
- Lamber Eaton syndrome

Nerve palsy/obstruction
- Laryngeal - hoarse voice
- Phrenic - Diaphragm weakness (breathless)
- Horners syndrome (due to pancoasts tumour)
- Superior vena cava obstruction (presents with pembertons sign)

Metastasis to adrenal gland, liver, bone, brain

192
Q

What bacteria most often causes pharyngitis and otitis media, and what antibiotic is used against this

A

Streptococci (Group A/pyogenes)

Amoxicillin

193
Q

Define pharyngitis

A

Pharyngeal inflammation causing sore throat, usually due to a viral infection

194
Q

Causes of pharyngitis

A

Viral (most common):
Adenovirus
Rhinovirus
Coronavirus
EBV

Bacterial:
Group A Strep (“Strep throat”)

195
Q

Causes of tonsilitis

A

Viral (most common)
Rhinovirus
Coronavirus
Adenovirus

Bacterial
Group A beta haemolytic strep (pyogenes)
H influenzae
Staph aureus

196
Q

Most common cause of recurrent tonsillitis

A

Staph aureus and MRSA

197
Q

Signs/symptoms of tonsillitis and pharyngitis

A

Red, inflamed, throat/tonsils (with exudate/pus = bacterial)
Anterior cervical lymphadenopathy
Sore throat
Fever
Malaise

198
Q

How is pharyngitis and tonsillitis diagnosed

A

Usually clinical

Can also do throat culture and rapid group A strep test

199
Q

When should tonsillectomy be considered?

A

If
- Recurring tonsillitis and complications
- Obstructive sleep breathing in children

200
Q

Define otitis media

A

Inflammation of the middle ear. Can be bacterial or viral

Bacterial:
- strep pneumoniae
- H influenzae
- Staph aureus

Viral
- Rhinovirus
- Adenovirus
- Influenza

201
Q

Otoscopy findings in otitis media

A

Red tympanic membrane
Bulging tympanic membrane
Middle ear efffusion

202
Q

Presentation of otitis media

A

general symptoms (fever malaise, headache etc), with ear pain, reduced hearing in children

203
Q

Define Sinusitis

A

Inflammation of paranasal sinuses.

Acute can last up to 4 weeks, subacute 1-3 months, chronic 3+

204
Q

Presentation of sinusitis

A
  • Purulent rhinorrhoea
  • Facial pain
    General symptoms (headache, fever, malaise, cough)
205
Q

Treatment of sinusitis

A

Acute is usually self resolving
If no improvement: Penicillin V for 5 days

206
Q

What major condition are otitis media and sinusitis associated with?

A

Meningitis

Disease spreads contiguously to paranasal sinuses and ears.

207
Q

Define epiglottitis

A

Inflammation of the epiglottis, causing potentially life threatening airway obstruction. Mostly in children

208
Q

Pathophysiology of epiglottitis

A

Normally, epiglottis prevents food from getting into trachea.

Bacterial infection (H influenzae B (MC), Strep pneumoniae and pyogenes) causes it to inflame. Less common now due to HiB vaccine

209
Q

Symptoms of epiglottitis

A
  • Tripoding (Child sat forwards with knees up, mouth open and tongue out to breathe)
  • Drooling
  • High fever
  • Dysphagia
  • Septic/unwell looking child (STRONG association with septicaemia)
210
Q

Investigations of epiglottitis

A

Investigations should not be done, could distress child and cause catastrophic airway occlusion and respiratory arrest.

Lateral neck radiograph may be appropriate - shows thumb sign, helps to exclude foreign body

211
Q

Treatment of epiglottitis

A

Important to not distress child.
Intubation to secure airway.

Once airway secure, cultures can be done for antibiotics.

IV Ceftriaxone

212
Q

Define whooping cough with its causative organism

A

NOTIFIABLE DISEASE
URTI in which child has severe coughing fits with loud whooping sound, in which child struggles to take air in between coughs.

Caused by Bordetella pertussis - a gram negative coccobacilli

213
Q

What factors enable the virulence of Bordetella pertussis

A
  • Filamentous Haemagglutinin (aids adherence)
  • Adenylate Cyclase Toxin (ACT) (inhibits phagocyte chemotaxis/T cell activation)
  • Tracheal cytotoxin (paralyses cilia)
  • Pertussis toxin (makes blood vessels and resp tissue more sensitive to histamine = greater exudate = harder to breathe)
214
Q

Disease course/symptoms of whooping cough

A

Incubation - 1 week

Catarrhal phase - 2 weeks (extremely contagious)
- low grade symptoms, fever, rhinorrhoea, cough.

Paroxysmal phase 1-6 weeks
- Uninterrupted “whooping” coughing that can result in vomiting, collapsed lung, broken ribs and apnoea
- O2 decrease can cause death

Convalescent phase (2-3 weeks)
- Healing

215
Q

Investigations of whooping cough

A

Nasopharyngeal swab
PCR testing

Anti-pertussis toxin IgG present 2 weeks after cough onset

216
Q

Management of whooping cough

A

Notify UKHSA (health security agency) (formerly Public Health England)
- Azithromycin for older than 1 month
- dTap Vaccine

217
Q

Possible complications of whooping cough

A

Symptoms usually resolve in 8 weeks but severe cough can cause damage:

Bronchiectasis
Pneumonia
Seizures
Rib fractures
Encephalopathy

218
Q

Define Croup

A

Laryngotracheobronchitis - swelling of larynx, trachea, large bronchi

Viral upper resp tract infection caused by parainfluenza

Usually in children under 3

219
Q

Signs/symptoms of Croup

A

Characteristic barking cough
Hoarse voice
Stridor (noisy breathing through obstructed airway)
Intercostal and subcostal recession if respiratory distress
Fever

220
Q

Investigations of Croup

A

Do NOT distress child, could worsen symptoms

Clinical diagnosis.

Westley score can be used to assess severity

221
Q

Management of Croup

A

Simple supportive treatment is usually enough, starts to get better in 48 hrs

If severe, or stridor or chest recession do not improve,
- Oral dexamethasone or prednisolone. OR
- Nebulised steroids OR
- Nebulised adrenaline

222
Q

What indicates a need for hospital admission in croup

A

Moderate/severe croup
Haemodynamically significant congenital heart disease
<3 months old
Inadequate fluid intake

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