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Phase 2a > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What type of hypersensitivity reaction is asthma?

A

Type I (IgE)

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2
Q

What type of hypersensitivity reaction is Goodpasture’s disease?

A

Type II (IgG)

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3
Q

What type of hypersensitivity reaction is SLE?

A

Type III (immune complex formation)

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4
Q

What type of hypersensitivity reaction is TB?

A

Type 4 (cell mediated)

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5
Q

What is a type I hypersensitivity reaction?

A

Reaction mediated by IgE antibodies.
(Allergy) ie anaphylaxis

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6
Q

What is type II hypersensitivity?

A

Cytotoxic reaction mediated by IgG or IgM antibodies.
(antibody binds to host cell which is perceived to be foreign destruction)
Goodpastures, Graves, Myasthenia Gravis

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7
Q

What is type III hypersensitivity?

A

Reaction mediated by immune complexes – deposited in vessel walls.
RA, post-strep glomerulonephritis, reactive arthritis, SLE

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8
Q

What is type IV hypersensitivity?

A

Delayed reaction mediated by cellular response.
Cytotoxic, cell-mediated.
T helper cell activated by antigen presenting cells.
Antigen presented again in the future causes inflammatory response.
Contact dermatitis, Mantoux test, MS, coeliac

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9
Q

What happens in type I hypersensitivity?

A

IgE mediated, mast cell degranulation, antibody binding to antigen eg asthma, allergy

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10
Q

What happens in type II hypersensitivity?

A

IgG reaction – cytotoxic – IgG binds to cell and kills its – Rhesus haemolytic disease, Goodpastures,

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11
Q

What happens in type III hypersensitivity

A

Immune complex forms (soluble but saturates) – SLE, EAA

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12
Q

What happens in type IV hypersensitivity?

A

Cell mediated delayed (CD-4 cells are sensitized to infection but cant clear it - granuloma) – TB, sarcoid, Wegeners,

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13
Q

What is total lung capacity?

A

(5900ml): max volume of air/gas the lungs can contain/accommodate

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14
Q

What is vital capacity?

A

(4700ml): amount of effort that can be exhaled with max effort after max inspiration

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15
Q

What is tidal volume?

A

(500ml): Volume of air inspired (inhaled) and expired (exhaled) in a normal breath

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16
Q

What is inspiratory capacity?

A

(3500ml): max volume of air that can be inhaled after normal tidal expiration

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17
Q

What is expiratory reserve volume?

A

(1200ml): Volume of air exceeding tidal expiration that can be exhaled with max effort

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18
Q

What is inspiratory reserve volume?

A

(3000ml): Volume of air exceeding tidal inspiration that can be inhaled with max effort

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19
Q

What is functional residual capacity?

A

(2400ml): Volume of air remaining in the lungs after a normal tidal expiration

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20
Q

What is residual volume?

A

(1200ml): Volume of air that remains in lungs after expiration (keeps alveoli inflated)

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21
Q

What is FEV?

A

How much air a person can exhale during a forced breath

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22
Q

What is FEV1?

A

FEV in 1 second

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23
Q

What is FVC?

A

Total volume of air forcefully exhaled during FEV test

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24
Q

What is peak expiratory flow rate (PEFR)?

A

The peak flow rate during expiration

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25
Q

How do you calculate total ventilation per minute?

A

Tidal volume x resp rate

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26
Q

What is COPD?

A

Irreversible progressive disorder of airway obstruction

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27
Q

What does COPD include?

A

Chronic bronchitis and emphysema

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28
Q

What causes COPD?

A

Smoking, fumes and dust, air pollution, genetics

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29
Q

How does COPD present?

A

Dyspnoea, tachypnoea, barrel chest

SOB, chronic cough, recurring chest infections, wheeze

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30
Q

What measurement classifies COPD?

A

FEV1/ FVC <70%

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31
Q

How is COPD managed?

A
  1. SABA/ SAMA
  2. LABA +LAMA OR LABA and ICS (if asthmatic features/ steroid responsive)
  3. triple therapy. + smoking cessation, regular physical activity

Other tx options: oxygen, abx in exacerbation, mucolytics, theophylline.

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32
Q

What might you want to rule out if no smoking history in COPD?

A

Alpha-antitrypsin deficiency

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33
Q

What vaccinations are given to someone with newly diagnosed COPD?

A

Pneumococcal and influenza

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34
Q

How are COPD exacerbations treated?

A

Oral pred. 30mg for 7-14 days

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35
Q

What is spirometry?

A

Post-bronchodilator measurement.

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36
Q

Why might you aim for sats of 88-92% in a patient with COPD?

A

For most COPD patients, a target saturation range of 88%–92% will avoid the risks of hypoxia and hypercapnia

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37
Q

What are the stages of COPD?

A

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

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38
Q

What are chronic bronchitis patients nicknamed?

A

Blue bloaters

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39
Q

What are emphysema patients nicknamed?

A

Pink puffers

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40
Q

What is chronic bronchitis?

A

Airway inflammation and narrowing
Increased mucous production

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41
Q

What is emphysema?

A

Destruction and dilation of air spaces
Can’t recoil and expel air

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42
Q

What is required to be diagnosed with chronic bronchitis?

A

Inflammation of bronchi with a productive cough for 3/12 for at least 2 years

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43
Q

How does chronic bronchitis present?

A

Hypoxemia, hypercapnia, cyanosis, wheeze, rales/ crackles, infection

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44
Q

How do you investigate chronic bronchitis?

A

Spirometry, Reid index

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45
Q

How is chronic bronchitis diagnosed?

A

FEV1/ FVC <0.7, Reid index >40%

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46
Q

How is chronic bronchitis managed?

A

Supplemental O2, abx + as with COPD

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47
Q

What is the pathophysiology of emphysema?

A

Alveoli permanently enlarge and lose elasticity

Inflammatory: proteases break down structural collagen/ elastin in the alveoli

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48
Q

How does emphysema present?

A

Pink puffer: exhaling slowly through pursed lips to increase pressure in bronchi, dyspnoea, weight loss, cough, “barrel chest”

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49
Q

How is emphysema diagnosed?

A

Spirometry, CXR: increase ant-post diameter, flattened diaphragm, increased lung-field lucency (more black)

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50
Q

How is emphysema treated?

A

As with chronic bronchitis/ COPD

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51
Q

What is obstructive lung disease?

A

Narrowed airways – normal lung volume (FVC), long time to exhale (wheeze) ie FEV is low
FEV1/FVC <0.7
Shallow spirometry graph
Asthma (variable) + COPD (fixed)

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52
Q

What is restrictive lung disease?

A

Tissue damage results in reduced lung volume
Low FVC, low FEV1
FEV1/FVC >0.8 - normal ratio

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53
Q

What is the difference between obstructive and restrictive lung disease?

A

If it’s obstructed ie a peanut - the air can eventually all get out it just takes ages to get it out. Whereas in restricted there is some dead tissue that can never be ventilated so can never be fully exhaled.

54
Q

What is type 1 respiratory failure?

A

Type 1 Respiratory failure (1 thing wrong)

PO2 low (hypoxia), PCO2 normal

Damage of lung tissue preventing adequate oxygenation of the blood. The remaining normal lung is still sufficient to excrete co2.

Ventilation (V), Perfusion (Q) mismatch

ie COPD, pneumonia, pulmonary oedema, asthma, pneumothorax, ARDS

55
Q

What is type 2 respiratory failure?

A

Type 2 Respiratory failure (2 things wrong)

PO2 low (hypoxia), PCO2 high (hypercapnia)

Alveolar ventilation insufficient to excrete co2 produced. Either due to reduced ventilatory effort or inability to overcome increased resistance to ventilation- affects lungs as a whole- co2 accumulates

Ie COPD, severe asthma, myasthenia gravis.

56
Q

What is PaO2 in hypoxia?

A

↓ PaO2 (<8kPa), ↓ / ↔ PaCO2

57
Q

What is PaCO2 in hypercapnia?

A

↓ PaO2 (<8kPa), ↑ PaCO2 (>6kPa)

58
Q

What is respiratory failure?

A

Failure to maintain adequate gas exchange and characterised by abnormalities of arterial blood gas tension” = failure to oxygenate blood adequately

59
Q

How is respiratory failure treated?

A

ABC

Treat underlying cause (COPD/Asthma/Pneumonia etc)

Oxygen

Continuous Positive Airway Pressure (CPAP) – Type 1

Non-Invasive Ventilation (NIV) – Type 2

60
Q

What are the respiratory centres?

A

Respiratory stimulus

Act via effects on the brainstem respiratory centres in medulla oblongata and pons

61
Q

What is asthma?

A

Paroxysmal and reversible airway obstruction.

62
Q

What is the pathophysiology of asthma?

A

Airflow limitation

Hypersensitivity

What type?

Inflammation and Airway Remodelling

Hypertrophy of smooth muscle

Increased number of goblet cells

63
Q

What causes asthma?

A

Allergic: Allergen (environmental stimuli), genetics, hygiene hypothesis

Non-Allergic: exercise, cold air, b-blockers (WHY?), infection

64
Q

What exacerbates asthma?

A

Infection, trauma, allergens, pollution, smoking, stress, some medications

65
Q

How does asthma present?

A

Diurnal variation (worse in morning), triggers, worse after NSAIDs/ B-blockers, wheeze, chest tightness, SOBOE, Unproductive cough

66
Q

How is asthma investigated?

A

PEFR- peak flow diary, reversibility testing, asthma control questionnaire, FEV1/FVC <70%

67
Q

How is asthma treated?

A
  1. SABA PRN - salbutamol
  2. Regular ICS - beclometasone
  3. LTRA - montelukast
  4. LABA - salmeterol

+/- Theophylline. If severe IgE mediated ?Omalizumab.

68
Q

How is a severe asthma exacerbation managed?

A

O xygen

S albutamol nebs back to back

H ydrocortisone

I pratropium bromide

T heophylline

M agnesium sulphate

E escalate ie intubate/ ventilate

Theophylline, magnesium, escalate : will not be starting without a senior present

69
Q

What is hypersensitivity pneumonitis?

A

Inflammation of the alveoli within the lung caused by type 3/ 4 hypersensitivity to inhaled organic dusts

70
Q

How does hypersensitivity pneumonitis present?

A

Acute: fever, chills, malaise, cough, SOB, poorly formed granulomas; chronic: cough, progressive SOB, fatigue, weight loss, clubbing, tachypnoea, respiratory distress

71
Q

How is hypersensitivity pneumonitis diagnosed?

A

Hx of symptoms after exposure to allergen, spirometry, lung biopsy- expansion of interstitium

72
Q

How is hypersensitivity pneumonitis treated?

A

Avoid antigen, corticosteroids- prednisolone

73
Q

What is cystic fibrosis?

A

Autosomal recessive mutation of the CFTR gene causing a misfolded CFTR protein. CFTR gene- Cl- channel chromosome 7. Thickens any secretions.

74
Q

How does cystic fibrosis present?

A

Newborns: meconium ileus; childhood: failure to thrive, rectal prolapse. Young Adult: Chronic resp symptoms and infection test it. Pancreatic insufficiency (insulin dependent diabetes or steatorrhoea). Male infertility. Ileus.Lungs: cough, recurrent infection, clubbing, bronchiectasis, course bilateral crackles.

75
Q

How is cystic fibrosis diagnosed?

A

Newborn screening (immunoreative trypsinogen due to damaged pancreas), sweat test: high Cl-

Sweat test Cl- >60mmol.

Faecal elastase for exocrine pancreatic dysfunction

Genetics for common CFTR mutations

Vitamin A, D,E levels - what are the fat soluble vitamins? A d e k

FBC, UANDE, LFT, Clotting factors, annual glucose tolerance test

CXR- hyperinflation, bronchiectasis signs,

Fatty liver, cirrhosis, chronic pancreatitis.

Faecal fat analysis

Aspergilis serology- 20% develop ABPA (FUNGAL)

76
Q

How is cystic fibrosis treated?

A

Nutrition (fat soluble vitamins), chest physio, mucolytics: DNAase, SABAs, N-acetylcysteine, lung transplant

Physiotherapy (postural drainage)

Antibiotics for acute exacerbations or prophylactically

Mucolytics Dnase

Bronchodilators

Pancreatic enzyme supplements

Fat soluble vitamins supplements

Ursodeoxycholic acid

Median survival around 40 years

77
Q

What are the problematic bacteria associated with cystic fibrosis?

A

Problematic bacteria include staph. aureus and pseudomonas aeruginosa

78
Q

What is pneumothorax?

A

Abnormal collection of air in the pleural space leading to partial lung collapse

‘Sudden onset, sharp one sided pleuritic chest pain and SOB’

Air should not be found in the pleural space – there is no pathway for the air for to get in and the air in the lungs and bloodstream are of too low pressure to leak through into it.

The only way for air to enter the pleural space therefore is if there is damage to either the chest wall or the lungs allowing air to leak in, or if there is a micro-organism in the pleural space that is producing gas.

It is a build up of air in the pleural space (the area between the lungs and the chest wall). It causes the lung on the affected side to collapse and unable to inflate, leading to problems with breathing.

79
Q

What causes pneumothorax?

A

Trauma (tension pneumothorax if one-way valve formed), spontaneous - air can move in and out- can heal on its own

Primary: damage to lungs with no underlying lung pathology

Secondary: underlying lung pathology that’s caused it

  1. Primary: no underlying lung disease, but risk factors include MALE, SMOKING, FAMILY HISTORY, CONNECTIVE TISSUE DISEASE (Marfans, Ehlers Danlos)
  2. Secondary: underlying lung pathology that has caused it.
  3. Trauma: injury inside the body (fractured ribs), injury outside the body (stab wound, gunshot, etc), medical procedure (catheter, biopsy, etc).
80
Q

What are the symptoms of pneumothorax?

A

Pleuritic chest pain, SOB, tiredness, tachycardia

Signs: low blood pressure, low oxygen levels, diminished breath sounds on the affected side

•Symptoms: SOB, sharp, ONE SIDED chest pain, altered consciousness

In exam: sudden onset, one sided sharp chest pain, worse when breathing in, and becoming short of breath – lead you to think of pneumothorax.

81
Q

How is pneumothorax investigated?

A

CXR (standing) - Gold standard

Gold standard: CXR

Absent lung markings

Collapsed lung

Tracheal deviation towards the pneumothorax

82
Q

How is pneumothorax treated?

A

Observation, simple aspiration, intercostal tube drainage; tension: Bore needle in MCL 2nd space

Small spontaneous ones can heal on their own (no SOB, underlying lung disease)

  • Treat the underlying cause, e.g. close the hole if there is an open wound causing it
  • Chest drain
  • Can also have surgery if its really bad
83
Q

How does tension pneumothorax present?

A

Sudden onset breathlessness, pleural pain, reduced chest expansion, hyperresonant to percussion, reduced breath sounds. MEDICAL EMERGENCY

84
Q

What is tension pneumothorax?

A

In a pneumothorax in which the hole in the pleura allows air in and out of it, whereas in a tension pneumothorax the hole acts as a one way valve; i.e. air can come into the pleural space but not out. This means that there amount of air in the pleural space increases rapidly – less space for air to come into the lung means the resp rate increases, which actually makes things worse as

Trachea deviated on CXR AWAY from tension pneumothroax – increased pressure on this side.

85
Q

How is tension pneumothorax treated?

A

EMERGENCY > immediately insert a chest drain (insert a needle in the 2nd intercostal space mid clavicular line and drain out the extra air )

Emergency needle thoracotomy

86
Q

What are the different types of lung cancer?

A

Small cell- paraneoplastic syndromes

non-small cell most common (80%)

Adenocarcinoma cell- most common + most common in non smokers

Squamous cell- most common in smokers

Large cell

87
Q

How does lung cancer present?

A

Cough, weight-loss, haemoptysis, dyspnoea, chest pain, anaemia, clubbing,

88
Q

What cancers can metastasise to the lungs?

A

Brain, bone, prostate, breast, thyroid, kidney

89
Q

What can small cell lung cancer cause?

A

Paraneoplastic syndromes - ectopic Cushing’s syndrome, hypertrophic osteoarthroparthy (clubbing), SIADH

90
Q

How is lung cancer investigated?

A

CXR: hilum enlargement, pulmonary opacity, rib bone lesions, pleural effusion, lung collapse. Chest CT. Bronchoscopy. Needle or surgical biopsy

91
Q

How is lung cancer treated?

A

Stage 1/2: surgery, radical DXRT, stage 3/4: chemo/ RT, laser therapy and stenting palliative care

92
Q

What is mesothelioma?

A

What: Cancer of the mesothelium (most commonly; pleura: lining covering the outer surface of the lungs - between that and the chest wall)

  1. Associations: Asbestos exposure, occupational link with delayed onset after exposure
  2. Symptoms: SOB, swollen abdomen, chest wall pain, fatigue, weight loss, fever, persistent cough, clubbing
  3. Dx: CXR and CT, confirmed by tissue biopsy
  4. Tx: Surgery, RT, Chemo (cisplatin and pemetrexed), pleurodesis. Often palliative
93
Q

Why might a lung cancer patient present with a hoarse voice?

A

Laryngeal nerve palsy caused by tumour compression usually in L lung.

94
Q

What is a pancoast tumour?

A

Tumour in apex of lung invades into sympathetic plexus in the neck causing compression of plexus resulting in Horner’s syndrome (ptosis, miosis, anhidrosis)

95
Q

Where do lung cancers most commonly metastasise to outside of the lungs?

A
96
Q

How does the prognosis vary between SCLC and NSCLC?

A

Poorer prognosis for SCLC

Neuroendocrine Tumours

Arise from APUD cells (type of neuroendo cells)

Rapid growing, highly malignant, early mets

Can cause –SIADH – secrete ADH

97
Q

What is Wegener’s granulomatosis?

A

Systemic disorder that involves granulomatosis and polyangitis (autoimmune)

Autoimmune condition (small vessel vasculitis) with granulomas

Affecting the respiratory system and the kidneys

Associated with Cytoplasmic anti-neutrophil cytoplasmic antibodies (cANCAs)- responsible for the inflammation.

98
Q

How does Wegener’s granulomatosis present?

A

Haemoptysis, cough, wheeze, SOB, glomerulonephritis, saddle nose deformity, nosebleeds, hearing loss, sinusitis

99
Q

How is Wegener’s granulomatosis investigated?

A

Test for cANCA, CXR, renal biopsy

100
Q

How is Wegener’s granulomatosis treated?

A

Immunosuppressant drugs:

Cyclophosphamide

Steroids ie prednisolone

plasma exchange

kidney transplant

101
Q

What is pneumonia?

A

Inflammation of the lung parenchyma: lung tissue. Acute LRTI

102
Q

What causes pneumonia?

A

Bacteria- strep. Pneumoniae, staph. aureus, haemophilus influenzae

Atypical: fungal- histoplasmosis, legionella, mycoplasma pneumoniae, viral: Influenza A

Aspiration pneumonia: poor swallow. RF?

Hospital acquired pneumonia: >48 hours after hospital admission

103
Q

How does pneumonia present?

A

SOB, chest pain, productive cough (pus/ bloody sputum), fatigue, fever,

Signs: -Pyrexia -Cyanosis -Confusion, Tachycardia -Tachypnea, Consolidation- diminished expansion dull percussion, tactile vocal fremitus, bronchial breathing, pleural rub.

104
Q

How is pneumonia managed?

A

Amoxicillin +/- clarithromycin (for atypical pneumonia cover)

Co-amoxiclav + clarithromycin for severe

105
Q

How is pneumonia investigated?

A

CXR, bronchopneumonia: patchy areas/ lobar: localised fluid/ atypical: concentrated in peri-hilar region lobar/multilobar infiltration/cavitation/pleural effusion.

Late inspiratory crackles, bronchial breath sounds. bLood cultures. Obs. ABG. Bloods FBC, U&E, CRP, Pulse oximetry, sputum culture and microscopy.

106
Q

What are the risk factors for pneumonia?

A

Stroke, Myasthenia gravis, reduced consciousness, oesophageal disease/ reflux

107
Q

What are the complications of pneumonia?

A

Pleural effusion

Empyema – pus

Lung abscess

Respiratory failure

Septicaemia

Pericarditis

108
Q

What is given to groups at risk of pneumonia?

A

Pneumococcal vaccine given to at risk groups

>65yrs old, Chronic disease, Diabetes mellitus, Immunosuppressed

109
Q

What are the differentials for pneumonia?

A

If it doesn’t get better/ the question sounds weird

Old and just back from holiday?- Legionella disease- water tanks will be involved in the question

HIV/AIDS- PCP pneumocystis jiroveci – need bronchoalveolar lavage for diagnosis

Pseudomonas aeruginosa- green sputum

Bronchiectasis/ Cystic fibrosis patient get it

110
Q

What is CURB-65?

A

Mortality risk assessment for pneumonia

Confusion (abbreviated Mental Test score 8 or less, or new disorientation in person, place or time).

Urea over 7 mmol/litre

Respiratory rate : 30 breaths per minute or more

Blood pressure <90/60mmHg

age 65 years or more.

111
Q

What is TB?

A

Mycobacterium tuberculosis with caseating granulomas that eventually calcify within the lungs. Type 4 hypersensitivty.

112
Q

How does TB present?

A

Systemic: Kidneys- sterile pyuria, brain- meningitis, lumbar vertebrae- Pott’s disease, adrenal glands- Addison’s, liver- hepatitis

Symptoms: Fever, night sweats, weight loss, haemoptysis, productive cough

113
Q

How is TB investigated?

A

Man-toux test, Interferon GammaReleaseAssay, 3 sputum samples with Ziehl- Neelsen stain

114
Q

How is TB treated?

A

Rifampicin: red secretions, isoniazid: peripheral neuropathy, pyrazinamide: gout and rash, ethambutol: optic neuritis (All 4 for 2 months, R and I for 6 months) Latent: Isoniazid ONLY 6 months

NOTIFIABLE DISEASE, contact tracing

115
Q

What is a granuloma?

A

an aggregation of epithelioid histiocytes

116
Q

TB

A

Secret ACE marker for systemic granulomatosis

TB, leprosy, Sarcoidosis, Crohns

Rifampicin: orange/ red discolouration of urine/ tears. Liver failure

Isoniazid- LFT, decreased WCC

Pyrozinomide- hepatitis, arthralgia

Ethambutol: optic neuritis always check ishara test before initiation

Risk factors

Poverty

Alcohol

Tobacco

Contact with TB

Immunosuppression

Biggest killer of HIV patients

Miliary TB

Haematogenous dissemination of TB all over.

Ix

Latent TB: Mantoux test if positive Tspot TB test

Tuberculin skin test- identifies immunity

Active TB: CXR- typically upper lobe consolidation+cavitation

3x sputum sample. 1 early in morning. MC+S Zeihl Neilsen stain - Acid Fast Bacilli

Extrapulmonary TB

Get a sample where you can. Lownstein Jenson medium 12 weeks.

Can go anywhere- meningitis big one.

Bone- collapse

Histology of sample: Caseating granuloma

117
Q

What does A1AT cause?

A

Causes 2% of emphysema – RARE

inherited

118
Q

What is A1AT deficiency?

A

A1AT regulates elastase activity

No A1AT = uncontrolled elastase activity

Elastase builds up in liver, causing cirrhosis

Elastase destroys alveoli leading to emphysema

Always consider in young patients with COPD and deranged LFTs

119
Q

What is PE?

A

Emboli in lungs, usually from DVT below knees

120
Q

What are the risk factors for PE?

A

Recent Immobility - >3 days

Previous DVT/ PE

Pregnancy

Thrombophilic syndromes – antiphospholipid, Factor V Leidens

Malignancy

Hormone Therapy – HRT, COCP

Smoking

121
Q

How does PE present?

A

sudden onset dyspnoea, pleuritic chest pain, ?red swollen leg, haemoptysis, tachycardia, tachypnoea

122
Q

How is PE investigated?

A

CT pulmonary angiogram (GOLD STANDARD), V/Q scan: mis-match, D-dimer (sensitive not specific)

123
Q

How is PE managed?

A

Large clots: Oral anticoagulation (DOAC/ Warfarin), Fondaparinux, Unfractionated Heparin, LMWH then oral anticoagulation.

124
Q

PE

A

Causes of Emboli: thrombosis, fat, amniotic fluid, air

Can get a low grade fever (Doesn’t always mean infection!!)

What score? Well’s >4pts CTPA, <4pts D-dimer.

Well’s Score

<2 – PE unlikely

2-6 – moderate possiblity – do a D-Dimer

6+ - CTPA

What do you need to investigate if unprovoked PE? Cancer

D-Dimer – what does it measure?

Is it accurate? negative excludes PE but positive doe not prove it. If positive, need to do imaging

What is the length of anti-coagulation therapy?

At least 3 months

If risk factors (and cause) have gone then stop

If unknown cause/ prolonged risk then at least 6 months+ - warfarin

SUDDEN ONSET OF SOB + CHEST PAIN WITH PAST HISTORY OF PAINFUL CALVES (DVT) AND RECENT LONG HAUL FLIGHT/IMMOBILISATION = PE.

125
Q

Goodpasture’s syndrome

A
  1. What: Autoantibodies attack the basement membrane in the lungs and kidneys
  2. Symptoms: Lungs: haemoptysis, chest pain, cough, SOB. Kidneys: haematuria, proteinuria, oedema, high blood urea, HTN. Systemic: malaise, weight loss, fatigue, fever
  3. Dx: Biopsy to look for anti-GBM (glomerular basement membrane antibody)
  4. Tx: Plasmapheresis, Immunosuppressant drugs: cyclophosphamide, prednisone, rituximab
  5. Other: Antibodies attack alpha-3 subunit of type IV collagen. Type 2 hypersensitivity.
126
Q

Sarcoidosis

A

Non caseating granulomatous inflammatory condition

Chest symptoms + extra-pulmonary manifestations ie erythema nodosum and lymphadenopathy

Bimodal: youngs adulthood and around 60. Women more than men. > in black people.

4 D’s of interstitial lung disease

o Dry cough

o Digital clubbing

o Dynspnoea

o Diffuse inspiratory crackles

  • Erythema nodosum

Investigation

CXR: Enlarged hilar lymph nodes (bilateral hilar lymphadenopathy)

Raised serum ACE

hypercalcaemia

Gold standard: histology from biopsy (non caseating granulomas)

Management

Oral steroids

Methotrexate or azathioprine

Lung transplant

Granulomas: nodules of inflammation full of macrophages

*NB typical MCQ- 20-40y/o black woman – dry cough and SOB, nodules on shins suggesting erythema nodosum*

127
Q

Pulmonary fibrosis

A

What: Progressive replacement of interstitial lung parenchyma with collagen/ scar tissue

  1. Causes: Over-proliferation of type 2 pneumocytes, stimulating myofibroblasts to produce collagen
  2. Symptom/signs: Coughing, SOB, cyanosis, digital clubbing
  3. Dx: CT chest- “honeycombing” and thickening of interstitial walls, spirometry: decreased TLC, FVC and FEV1
  4. Tx: Supplemental O2, antifibrotics (pirfenidone), lung transplant
128
Q

Pulmonary hypertension

A

Pulmonary artery pressure PAP elevated >25mmHg

Asymptomatic or Shortness of breath on exertion, dyspnoea, syncope

If your pulmonary artery pressure is increased→ R ventricular hypertrophy → R heart failure → ascites/hepatomegaly

Causes: Drugs / congenital /idiopathic Left sided heart defects- MI/ valvular disorders Pulmonary disease- COPD, ILD etc Recurrent pulmonary embolisms

Tx- treat the underlying condition causing pulmonary hypertension

If untreated can lead to cor pulmonale

Cor Pulmonale = R sided HF secondary to pulmonary HTN.

129
Q

Pleural effusion

A

Fluid in pleural space- stony dull to percussion. Decreased tactile vocal fremitus.

Diagnostic aspiration

Transudate <25g/L protein conc.

Causes hypoproteinemia- cirrhosis, nephrotic disease, malabsorption

Increased venous pressure - Cardiac failure, Constrictive pericarditis, Fluid overload

Exudate >35g/L protein conc - Leaky vessels so protein and fluid gets out.

Infection- pneumonia, TB. Inflammation- RA, autoimmune stuff. Malignancy

Large effusion causes tracheal deviation away from the pleural effusion side

130
Q

Bronchiectasis

A

Chronic infection of bronchi/ bronchioles. Causes permanent dilation of airways.

H.influenzae, Strep.pneumoniae Staph aureus Pseudomonas aeruginosa

Causes

Anything that causes chronic inflammation or infection of the airways

CYSTIC FIBROSIS

Primary ciliary dyskinesia

post infection

Bronchopulmonary aspergillosis

Autoimmuine conditions

Symptoms

PERSISTENT cough. COPIOUS PURULENT sputum. haemoptysis

Signs

FINGER CLUBBING, course inspiratory crepitation

Ix

Sputum culture

CXR- TRAMLINE + RING SHADOWS cystic shadows

Spirometry of obstructive

Bronchoscopy- rule out obstruction, sample culture,

CF sweat test, Aspergillosis skin prick test

Tx

Physiotherapy to aid mucous drainage.

Bronchodilators or steroids may be useful depending on other underlying disease

Phase 2a (25 decks)

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