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Respiratory Flashcards

1
Q

How prevalent is lung cancer?

A

3rd after breast and prostate

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2
Q

What are the types of lung cancer?

A

Non - small cell:

  • SCC
  • Adenocarcinoma
  • Large-cell carcinoma

Small- cell carcinoma

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3
Q

What are some signs of lung cancer?

A
  • SOB
  • Cough
  • Haemoptysis
  • Finger clubbing
  • Recurrent pneumonia
  • Weight loss
  • Lymphadenopathy (supraclavicular lymph nodes)
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4
Q

What are the investigations for lung cancer?

A

CXR (hilar enlargement, peripheral opacity, PE, collapse)

Staging CT (chest, abdo, pelvis contrast enhanced for staging, check lymph node involvement and metastasis, contrast enhanced)

PET CT (inject radioactive tracer (attached to glucose molecules) and taking images using CT scanner and gamma ray detector - shows areas of increased metabolic activity

Bronchoscopy with endobronchial ultrasound (EBUS) - endoscopy of airway with US at end of scope for detailed assessment of tumour and US guided biopsy

Histological diagnosis

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5
Q

Who is present at an MDT for lung cancer?

A

Surgeons

Oncologists

Radiologists

Pathologists

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6
Q

What is offered first line in non-small cell lung cancer? What else can be offered?

A

Sugery - lobectomy or segmentectomy or wedge resection

RT can also be curative when early enough

Adjuvant chemo

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7
Q

What is offered first line in small cell lung cancer?

A

Chemotherapy and RT

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8
Q

What treatment can be used as part of palliative treatment in lung cancer?

A

Stents or debulking to relieve bronchial obstruction

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9
Q

What are the extrapulmonary manifestations of lung cancer?

A

Recurrent laryngeal nerve palsy - hoarse voice as cancer presses on recurrent laryngeal nerve as it passes through the mediastinum

Phrenic nerve palsy - weak diaphragm due to nerve compression

SVC obstruction - facial swelling, difficulty breathing, distended veins - “Pemberton’s sign” = raising of hands over face causes cyanosis

Horners - compression of sympathetic ganglion, partial ptosis, anhidrosis and miosis caused by Pancoast’s tumour

SIADH - caused by ectopic ADH from small cell lung cancer causing hyponatraemia

Cushing’s syndrome - caused by ectopic ACTH from small cell lung cancer

Hypercalcaemia from ectopic parathyroid hormone from a squamous cell carcinoma

Limbic encephalitis - paraneoplastic syndrome small cell lung cancer causes antibodies to brain tissue (specifically limbic system) = short term mem impairment, hallucinations, confusion and seizures (associated with anti-Hu antibodies)

Lambert-Eaton myasthenic syndrome

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10
Q

What paraneoplastic syndrome can occur from small cell lung cancer?

A

SIADH - hyponatraemia

ACTH release - Cushing’s

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11
Q

What paraneoplastic syndrome can occur due to squamous cell carcinoma?

A

Hypercalcaemia from ectopic PTH

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12
Q

What is Lambert-Eaton Myasthenic Syndrome?

A

Antibodies against small cell lung cancer which damage motor neurones (specifically voltage-gated calcium channels on presynaptic terminals)

Leading to weakness in:

Proximal muscles

Intraocular muscles causing diplopia

Levator muscles in the eyelid causing ptosis

Pharygeal muscles causing slurred speech and dysphagia

May also have dry mouth, blurred vision, impotence and dizziness due to autonomic dysfunction

In older smokers with symptoms of Lambert-Eaton syndrome consider small cell lung cancer

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13
Q

Where does meothelioma affect?

A

Mesothelial cells of lung pleura

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14
Q

What is mesothelioma associated with?

A

Asbestos inhalation (long latency period - 45 years)

Prognosis is poor - chemo can improve but essentiallt palliative

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15
Q

What are the 3 types of pneumonia?

A

Hospital acquired (48hrs after admission)

Community acquired

Aspiration pneumonia

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16
Q

How does pneumonia present?

A

SoB

Productive cough

Fever

Haemoptysis

Pleuritic chest pain

Delerium

Sepsis

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17
Q

What are the signs of pneumonia?

A
  • Tachypnoea
  • Tachycardia
  • Hypoxia
  • Hypotension
  • Fever
  • Confusion
  • Bronchial breath sounds (harsh breath sounds equally loud on inspiration/expiration)
  • Dullness to percussion
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18
Q

How is the CURB-65 score measured? (CRB-65 used out of hosp - if above 0 refer to hosp)

A

C – Confusion (new disorientation in person, place or time)

U – Urea > 7

R – Respiratory rate ≥ 30

B – Blood pressure < 90 systolic or ≤ 60 diastolic.

65 – Age ≥ 65

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19
Q

What CURB-65 score would you consider admitting?

A

> or = 2 (predicts mortality)

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20
Q

What are some common causes of pneumonia?

A

Streptococcus pneumoniae (50%)

Haemophilus influenzae (20%)

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21
Q

When is Moraxella catarrhalis seen causing pneumonia?

A

Immunocompromised patients or those with chronic pulmonary disease

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22
Q

When is pseudomonas aeruginosa/ S. aureus seen to cause pneumonia?

A

CF

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23
Q

What is atypical pneumonia?

A
  • Organism cannot be cultures/detected on gram stain
  • Don’t respond to penicillins
  • Do respond to macrolides (e.g. clarithomycin)/fluroquinolones (e.g. levofloxacin) or tetracyclins (e.g. doxycycline)
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24
Q

What are some causes of atypical pneumonia?

A

Legionella pneumophilia

Mycoplasma pneumonia

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25
Q

How does legionella pneumophilia present? What is it normally caused by?

A

Hyponatraemia by causing SIADH (caused by infected water supplies / air conditioning units)

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26
Q

How does pneumonia caused by Mycoplasma pneumoniae present?

A

Rash - erythema multiforme (pink rings with pale centres = target lesions) also causes neurological symptoms

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27
Q

What are three other causes of atypical pneumonia? How do they present / what are they caused by?

A

Chlamydophilia pneumoniae - school aged child with mild / moderate chronic pneumonia and wheeze (may also not be caused)

Coxiella burnetii AKA “Q fever” - linked to exposure to animals / bodily fluids (usually farmer with flu like illness)

Chlamydia psittaci - from infected birds (parrot owners)

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28
Q

How can the 5 causes of atypical pneumonia be remembered?

A

Lesions of psittaci MCQs

Legionella pneumophila

Chlamydia psittaci

Mycoplasma pneumoniae

Chlamydophila pneumoniae

Coxiella burnetii = Q fever

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29
Q

When does pneumonia caused by pneumocystis jiroveci present?

A

In immunocompromised patients

Poorly controlled HIV with low CD4 count

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30
Q

How does PCP present?

A

Dry cough without sputum

SOB on exertion

Night sweats

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31
Q

What is the treatment of PCP?

A

Co-trimoxazole (trimethoprim / sulfamethoxazole) = “Septrin”

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32
Q

What are the investigations for pneumonia?

A

CXR

FBC (for raised WCC)

U&Es (for urea)

CRP (for inflammation)

Sputum cultures

Blood cultures

Urinary antigens (for suspected legionella and pneumococcal)

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33
Q

When may patients with pneumonia not show an inflammatory response?

A

Immunocompromised (normally WBC and CRP are raised in proportion to severity of infection - WBC respond faster)

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34
Q

How is mild and moderate CAP treated respectively?

A

Amoxicillin / macrolide

(both if moderate)

Severe may require IV abx

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35
Q

What are some complications for pneumonia?

A

Sepsis

PE

Empyema

Lung abscess

Death

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36
Q

In spirometry what is FEV1?

FVC?

A

FEV1 = forced expiratory volume in 1 second (reduced in obstruction)

FVC = Forced vital capacity, amount exhaled after full inhalation (reduced in restriction)

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37
Q

What Spirometry result indicates obstruction as the cause?

A

FEV1 is <75% of FVC

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38
Q

What are some causes of obstruction?

A

Asthma

COPD (test for reversibility with brochodilator e.g. salbutamol)

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39
Q

What FEV1/FVC ratio indicates restrictive disease?

A

>75%

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40
Q

What are some causes of restrictive lung disease?

A

ILD

Neurological

Scoliosis

Obesity

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41
Q

How is a peak flow performed? What is it typically used for?

A

Measured using a peak flow meter (useful in obstructive lung disease e.g. asthma)

Patient stands tall, breaths in, makes a seal around device, blows as fast and hard as possible.

Take three attempts and record the best one

Usually recorded as “percentage of predicted”

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42
Q

How is peak flow put into context?

A

Percentage of predicted based on sex, height and age

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43
Q

What is asthma?

A

Chronic inflammation of the airways causing bronchoconstriction

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44
Q

What causes the bronchoconstriction seen in asthma?

A

Hypersensitivity​ of the airways

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45
Q

What are some triggers of asthma?

A
  • Infection
  • Night time/early morning
  • Exercise
  • Animals
  • Cold/damp
  • Dust
  • Strong emotions
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46
Q

What presentation suggests asthma?

A
  • Episodic symptoms
  • Diurnal variability (worse at night)
  • Dry cough with wheeze
  • History of other atopic conditions e.g. eczema, hayfever and food allergies
  • FH
  • Bilateral widespread “polyphonic” wheeze
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47
Q

What presentation indicates a diagnosis other than asthma?

A
  • Wheeze related to coughs / colds = viral
  • Isolated / productive cough
  • No response to treatment
  • Unilateral wheeze
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48
Q

What are the investigations for asthma diagnosis?

A

- Spirometry with bronchodilator reversibility

- Fractional exhaled nitric oxide

If uncertainty following then:

  • Peak flow variability (several times a day for 2-4 weeks)
  • Direct bronchial challenge test with histamine and methacholine
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49
Q

What are the steps of medication for asthma? (NICE)

A

As required SABA (short acting beta 2 adrenergic receptor agonists e.g. salbutamol - effect only lasts for an hour / two acts on bronchioles used as “rescue” medication)

Regular inhaled low dose corticosteroid (e.g. beclometasone used as “preventer”)

Leukotriene receptor antagonist (e.g. oral montelukast and check response) / LABA (e.g. salmetarol)

CONSIDER CHANGING TO A MART REGIME (combining inhaler containing a low dose inhaled corticosteroids and fast acting LABA - single inhaler used as preventer and reliever.

Titrate inhaled corticosteroids up to “moderate dose”

Consider increasing ICS higher or add oral theophylline or inhaled LAMA (e.g. tiotropium)

Refer to specialist

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50
Q

What are leukotrienes and what do they do?

A

Product of the immune system and cause inflammation, bronchoconstriction and mucus secretion (leukotriene receptor antagonists work against this)

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51
Q

What is maintenance and reliever therapy?

A

MART

ICS and LABA - replacing all other inhalers using both regularily and as relief

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52
Q

What does the BTS offer as 3rd line medication instead of Leukotriene receptor antagonist?

A

LABA

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53
Q

How do:

Long-acting muscarinic antagonists (LAMA e.g. tiotropium)

Theophylline

work?

A

LAMA = block acetylcholine receptors (usually stimulated by parasympathetic nervous system causing contraction of bronchial smooth muscles)

Theophylline = relaxes smooth muscle and reduces inflammation (has narrow therapeutic window can be roxic in excess - monitoring of theophylline levels is needed - done 5 days after starting and 3 days after each dose changes)

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54
Q

What are some additional things useful for asthmatics?

What are the rules of the treatment ‘ladder’?

A
  • Individual asthma self-management plan
  • Yearly flu jab
  • Yearly asthma review
  • Advise exercise and avoid smoking

Ladder = start at most appropriate step for severity of symptoms, review at regular intervals, step up and down based on symptoms, achieve no symptoms or exacerbation on lowest dose, check inhaler technique at review

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55
Q

What is an acute exacerbation of asthma?

A

Rapid deterioration in symptoms

Triggered by any typical triggers e.g. infection, exercise, cold, weather

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56
Q

How does acute asthma attacks present?

A

Worsening of SoB

Use of accessory muscles

Fast RR (tachypnoea)

Symmetrical expiratory wheeze on auscultation

Chest can sound “tight” on auscultation with reduced air entry

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57
Q

What is moderate asthma?

A

PEFR 50-75% predicted

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58
Q

What is severe asthma?

A

PEFR 33-50% predicted

RR >25

HR >110

Unable to complete full sentences

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59
Q

What is life threatening asthma?

A

PEFR <33%

Sats <92%

Becomming tired

No wheeze - silent chest

Haemodynamic instability (i.e. shock)

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60
Q

What is the treatment of moderate asthma?

A

NEB SABA and NEB IPRATROPIUM BROMIDE

Steroids (prednisolone or IV hydrocortisone) - continued for 5 days

Abx if bacterial infection suspected

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61
Q

What is the treament of severe asthma?

A

Oxygen (sats 94-98%)

Aminophylline infusion

Maybe IV salbutamol

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62
Q

What is the treatment of life threatening asthma?

A

IV magnesium sulphate infusion

Admission to HDU

Intubation in worse cases

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63
Q

What acute asthma medications are under senior guidance?

A

Aminophylline

IV salbutamol

IV magnesium

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64
Q

How are the ABGs in acute asthma, initially then later on?

A

Respiratory alkalosis as tachypnoea causes drop in CO2

A normal pCO2 or hypoxia indicates life threatening asthma

Respiratory acidosis due to high CO2 is a very bad sign in asthma

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65
Q

How to monitor the response to asthma treatment?

A

Monitor RR

Monitor Respiratory effort

Monitor Peak flow

Monitor oxygen saturations

Chest auscultation

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66
Q

What electrolyte needs to be monitored when on salbutamol?

A

Serum potassium (causes hypokalaemia as cells absorb potassium)

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67
Q

What is a cardiac side effect of salbutamol?

A

Tachycardia

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68
Q

What is COPD?

A

Non-reversible long term deterioration in air flow through lungs caused by damage to lung tissue (almost always result of smoking)

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69
Q

How does COPD present?

A
  • Chronic SoB
  • Cough
  • Sputum production
  • Wheeze
  • Recurrent resp infections
  • NO CLUBBING and unusual for it to cause haemoptysis or chest pain
70
Q

Does COPD normally cause haemoptysis?

A

Not usually

71
Q

What scoring system can be used for breathlessness?

A

MRC Dyspnoea Scale

72
Q

What would grade 5 indicated for MRC dyspnoea score?

A

Unable to leave house due to breathlessness (grade 1 = breathless on strenuous exercise)

73
Q

How is COPD diagnosed?

A

Clinical presentation plus spirometry

74
Q

What pattern does COPD show on spirometry?

A

Obstructive picture with no reversibility

75
Q

How is the severity of COPD graded?

A

FEV1

If >80% then stage 1

if <30% then stage 4

76
Q

What are the other investigations for COPD?

A

CXR to exclude lung cancer

FBC for polycythaemia (response to chronic hypoxia) or anaemia

BMI as baseline to assess later weight loss or weight gain (steroids)

Sputum cultures to assess for chronic infection such as pseudomonas

ECG and Echo for heart function

CT thorax for diagnosis of cancer, fibrosis or bronchiectasis

Serum alpha-1 antitrypsin to look for deficiency

Transfer factor for carbon monoxide (TLCO) is decreased in COPD and gives indication about severity of disease

77
Q

What is the first step of managing COPD?

A

Advise stop smoking

78
Q

What additional preventative measures should be advise for COPD?

A

Pneumococcal and annual flu vaccine

79
Q

What is the first line medication for COPD?

A

SABA or short acting antimuscarinic (e.g. ipratropium bromide)

80
Q

What is the 2nd line medication for patients with COPD:

Non-asthmatic features:

Asthmatic features:

A

Non-asthmatic features: LABA plus LAMA combi inhalor

Asthmatic features (steriod responsive): LABA plus ICS combi inhalor (e.g. fostair, symbicort and seretide)

81
Q

What are the additional options in more severe COPD?

A

Nebulisers (salbutamol / ipratropium)

Oral theophylline

Oral mucolytic therapy to break down sputum (e.g. carbocisteine)

Long term prophylactic antibiotics (e.g. azithromycin)

LTOT

82
Q

When is LTOT offered to patients with COPD?

A

When problems such as chronic hypoxia, polycythaemia, cyanosis or heart failure secondary to cor pulmonale (Cant be used if they smoke)

83
Q

What indicates an exacerbation of COPD?

A

Acute worsening of symptoms of cough, SoB, sputum production and wheeze

Usually triggered by viral / bacterial infection

84
Q

How does CO2 make blood acidotic?

What does that indicate in COPD?

A

Breaks down into carbonic acid (H2CO3)

Low pH and raised pCO2 suggests acute retaining

85
Q

What is type 1 and type 2 respiratory failure respectively?

A

1 is low oxygen

2 is low oxygen and high CO2

86
Q

How to investigate acute exacerbation of COPD?

A

CXR to look for pneumonia

ECG to look for arrythmia

FBC to look for infection

U&E to check electrolytes

Sputum culture

Blood culture if septic

87
Q

Why is too much oxygen in COPD dangerous?

A

Supresses respiratory drive

88
Q

What are venturi masks?

A

Masks which are designed to deliver a specific percentage of oxygen (environmental contains 21%)

89
Q

What are the o2 sats for a COPD patient who is retaining CO2 or not retaining O2?

A

Retaining = 88-92

Not retaining = >94

90
Q

How can you tell if a patient with COPD is retaining CO2?

A

Their bicarb is high to compensate

91
Q

What is the treatment for acute exacerbation of COPD at home?

A

Prednisolone 30mg once daily

Regular inhalers / NEBs

Abx if evidence of infection

92
Q

What is the treatment of acute exacerbation of asthma in hospital?

A

Neb bronchodilators (salbutamol / ipratropium)

Steroids (200mg hydrocortisone/ 30mg oral prednisolone)

ABx (if infection)

Physio (help clear infection)

93
Q

What are the options for treatment of severe acute exacerbation of COPD?

A

IV aminophylline

NIV

Intubation / ventilation with admission to intensive care

Doxapram can be used as respiratory stimulant where NIV / intubation isnt appropriate

94
Q

What are the non-invasive ventiation options?

A

BiPAP

CPAP

95
Q

What does Bipap stand for?

A

Bilevel positive airway pressure (high and low pressure corresponds to patients inspiration and expiration - keeps some pressure during expiration to prevent airway collapse)

Used in type 2 resp failure, typically due to COPD

96
Q

What are the contraindications for BiPAP?

A

Untreated pneumothorax / structural abnormality affecting face, airway or GI tract

97
Q

What does CPAP stand for? What does it involve?

A

Continuous positive airway pressure

Continuous air blown into the lungs keeping airways expanded - maintains airways when they are prone to collapse

98
Q

What are some indications for CPAP?

A
  • Obstructive sleep apnoea
  • Congestive cardiac failure
  • Acute pulmonary oedema
99
Q

What is ILD?

A

Term used to describe conditions which affect lung parenchyma causing inflammation and fibrosis

100
Q

How is ILD diagnosed?

A

Clinical features and high resolution CT of thorax

101
Q

What would a HRCT show for ILD?

A

“ground glass” appearance

102
Q

If a diagnosis for ILD is unclear what can be done?

A

Lung biopsy taken and confirm diagnosis on histology

103
Q

What is the management in general for ILD?

A

Limited management options as damage is irreversible

104
Q

What are the treatment options of ILD?

A
  • Treat underlying cause
  • Home oxygen when hypoxic at rest
  • Stop smoking
  • Physio and pulmonary rehab
  • Penumococcal and flu vaccine
  • Advanced care planning
  • Lung transplant is an option but risks and benfits need consideration
105
Q

What are some types of ILD?

A

Idiopathic pulmonary fibrosis

Drug induced pulmonary fibrosis

Secondary pulmonary fibrosis

Hypersensitivity pneumonitis

Cryptogenic organising pneumonia

Asbestosis

106
Q

What is idiopathic pulmonary fibrosis? How does it present?

A
  • Progressive fibrosis with no clear cause
  • Insidious onset dry cough or more than 3 months
  • Affects adults > 50 years old
  • Examination = bibasal fine inspiratory crackles and finger clubbing
  • Life expectancy 2-5 years from diagnosis
107
Q

Which medications can slow progression of idiopathic pulmonary fibrosis?

A

Pirfenidone (antifibrotic and anti-inflammatory)

Nintedanib (monoclonal antibody targeting tyrosine kinase)

108
Q

What drugs can cause pulmonary fibrosis?

A
  • Amiodarone
  • Cyclophosphamide
  • Methotrexate
  • Nitrofurantoin
109
Q

What can cause secondary pulmonary fibrosis?

A

Alpha-1 antitrypsin deficiency

  • RA
  • SLA
  • Systemic sclerosis
110
Q

What is hypersensitivity pneumonitis? What is it also known as?

A

Inflammation of lung parenchyma due to environmental allergens - type 3 hypersensitivity reaction

Extrinsic allergic alveolitis

111
Q

What would bronchoalveolar lavage show for hypersensitivity pneumonitis? How is it performed?

A

Raised lymphocytes and mast cells

Collecting cells during bronchoscopy by washing airways with fluid then collecting

112
Q

What was cryptogenic organising pneumonia previously known as?

What causes it?

How does it present?

How is it diagnosed and treated?

A

Bronchiolitis obliterans organising pneumonia

Causes focal area of inflammation in lungs

Triggers = infection, inflammatory disorders, medications, radiation or environmental toxins or allergens (can be idiopathic)

Presentation = SoB, cough, fever and lethargy

Diagnosis = lung biopsy

Treatment = systemic corticosteroids

113
Q

What can cause hypersensitivity penumonitis? How is it managed?

A
  • Bird droppings (bird fanciers lung)
  • Mouldy spores in hay (reaction to mouldy spores in hay)
  • Mushroom antigens
  • Malt workers lung (reaction to mould on barley)

Management = remove allergen, give O2 and steroids

114
Q

What can inhalation of asbestos cause?

A

Lung fibrosis

Pleural thickening and pleural plaques

Mesothelioma

Adenocarcinoma

115
Q

What is the difference between an exudate/transudate?

A

Exudate = high protein count

Transudate = low protein count

116
Q

What causes an exuative effusion?

A

Inflammation:

  • Lung cancer
  • Pneumonia
  • RA
  • TB
117
Q

What causes a transudative exudate?

A

Congestive cardiac failure

Hypoalbuminaemia

Hypothyroidism

Meig’s syndrome (right sided pleural effusion with ovarian malignancy)

118
Q

How does a pleural effusion present?

A

SoB

Dullness to percuss over the effusion

Reduced breath sounds

Tracheal deviation away from effusion

119
Q

What appear on the xray for pleural effusion?

A
  • Blunting of the costophrenic angle
  • Fluid in the lung fissures
  • Meniscus
  • Deviation of trachea and mediastinum if its a massive effusion
120
Q

What other investigation can be used for pleural effusion?

A

Sample of pleural fluid for analysis for protein count, cell count, pH, glucose

121
Q

What are the treatment options for pleural effusions?

A

Pleural aspiration - put needle in and aspirate (temporary)

Chest drain - drain effusion and prevent recurring

(conservative may be appropriate as small effusions will resolve with treatment of underlying cause)

122
Q

What is empyema?

How is it treated?

A

Infected pleural effusion

Pleural aspiration shows: pus, acidic pH <7.2, low glucose and high LDH

Chest drain treats

123
Q

What are some causes of pneumothorax?

A
  • Spontaneous
  • Trauma
  • Iatrogenic e.g. lung biopsy
  • Lung pathology e.g. infection, asthma or COPD
124
Q

What is the investigation for pneumothorax?

A

Erect chest X-ray

125
Q

What is the management of pneumothorax?

A

If no SOB and there is a < 2cm rim of air on the chest xray then no treatment required as it will spontaneously resolve. Follow up in 2-4 weeks is recommended.

If SOB and/or there is a > 2cm rim of air on the chest xray then it will require aspiration and reassessment.

If aspiration fails twice it will require a chest drain.

Unstable patients or bilateral or secondary pneumothoraces generally require a chest drain.

126
Q

What causes tension pneumothorax?

A

Trauma to chest wall causing one-way valve letting air in but not out (during inspiration air is drawn into pleural space and during expiration air is trapped)

127
Q

What are some signs of tension pneumothorax?

A

Tracheal deviation away from side of penumothorax

Reduced air entry to affected side

Increased resonant to percussion on affected side

Tachycardia

Hypotension

128
Q

What is the management of tension pneumothorax?

A

Large bore callula into 2nd intercostal space, mid clavicular line

129
Q

Where is a chest drain inserted (for definitive management)?

A

5th intercostal space (inferior nipple line)

Mid axillary line (or lateral edge of latissimus dorsi)

Anterior axillary line (or lateral edge of pectoris major)

130
Q

What are some risk factors for PE?

A
  • Immolbilty
  • Recent surgery
  • Long haul flights
  • Pregnancy
  • HRT with oestrogen
  • Malignancy
  • Polycythaemia
  • SLE
  • Thrombophilia
131
Q

What is commonly used at VTE prophylaxis in hospital?

A

LMWH (enoxaparin)

132
Q

What are some contraindications for LMWH?

A

Active bleeding

Existing anticoagulation with warfarin or a NOAC

133
Q

What is the main contraindication for compression stockings?

A

Peripheral arterial disease

134
Q

What are the presenting features of PE?

A

SoB

Cough (maybe haemoptysis)

Pleuritic chest pain

Hypoxia

Tachycardia

Raised resp rate

Low grade fever

Haemodynamic instability causing hypotension

135
Q

What does the Wells score tell you?

A

Risk of a patient presenting with symptoms actually having a DVT or PE

136
Q

In a suspected PE how do you decide if you CTPA?

A

On outcome of Wells score

137
Q

What are the two main options for diagnosing PE?

A

CTPA = chest CT with IV contrast highlighting pulmonary arteries

VQ scan = using inhaled radioactive isotopes, injected isotopes and gamma camera to compare ventilation with perfusion (used in patients with renal impairment, contrast allergy or at risk from radiation)

138
Q

When would a VQ scan be used over a CTPA to diagnose PE?

What does a ABG show in PEs?

A

Contrast allergy

Resp alkalosis (high resp rate causes them to “blow off” extra CO2

139
Q

What is the supportive management for a PE?

A

- Admit to hospital

- Oxygen

- Analgesia

- Monitor for deterioration

140
Q

What is the inital management for PE?

A

Apixaban / Rivaroxaban

LMWH (e.g. in antiphospholipid syndrome) e.g. enoxaparin or dalteparin

141
Q

Which long term anticoagulants are available for VTE?

A

Warfarin, DOAC or LMWH

142
Q

What are some examples of some DOACs

A

Apixaban

Dabigatran

Rivaroxaban

143
Q

How long is anticoagulation continued for post PE?

A

3 months if reversible cause

> 3 months if cause is unclear

6 months in active cancer

(LMWH is first line in pregnancy / cancer)

144
Q

What can be used for patients with a PE and haemodynamic compromise?

A

Thrombolysis = fibrinolytic agent via cannula or directly into pulmonary arteries (significant risk of bleeding)

e.g. streptokinase, altepase, tenecteplase

Can also be given into pulmonary arteries using central catheter = catheter-directed thrombolysis

145
Q

What are some causes of pulmonary hypertension?

A
  • Primary pulmonary hypertension
  • Connective tissue disease e.g. SLE
  • Left heart failure due to MI
  • Pulmonary vascular disease e.g. pulmonary embolism
  • COPD
  • PE
146
Q

What are some signs and symptoms of pulmonary hypertension?

A

Shortness of breath

  • Syncope
  • Tachycardia
  • Raised JVP
  • Hepatomegaly
  • Peripheral oedema
147
Q

What are the ECG changes in pulmonary hypertension?

A
  • Right ventricular hypertrophy (larger R waves on right sided chest leads V1-V3)
  • Right axis deviation
  • Right BBB
148
Q

What are the CXR changes in pulmonary hypertension?

A
  • Dilated pulmonary arteries
  • Right ventricular hypertrophy
149
Q

What are some other investigations for pulmonary hypertension?

A

Raised NT-proBNP blood test results right ventricular failure

Echo to estimate pulmonary artery pressure

150
Q

What can pulmonary hypertension be treated with?

A

Primary pulmonary hypertension

IV prostanoids (e.g. epoprostenol)

Endothelin receptor antagonists (e.g. macitentan)

Phosphodiesterase-5 inhibitors (e.g. sildenafil)

Supportive = respiratory failure, arrhythmias and HF

151
Q

What is sarcoidosis? What does it cause?

A

Granulomatous inflammatory condition - granulomas = full of macrophages

Extra-pulmonary manifestations e.g. erythema nodosum and lymphadenopathy

Symptoms can be asymptomatic to life-threatening

152
Q

Who typically gets sarcoidosis?

A

20-40 or >60

Women more frequently

Black people

153
Q

Where does sarcoidosis affect and how does it manifest?

A

Lungs (mediastinal lymphadenopathy, pulmonary fibrosis, pulmonary nodules)

Systemic (fever, fatigue, weight loss)

Liver (liver nodules, cirrhosis, cholestasis)

Eyes (conjunctivitis, uveitis, optic neuritis)

Skin (erythema nodosum - tender, red nodules on shins caused by inflammation of subcut fat, lupus pernio - raised, purple skin lesions on cheeks and nose, granulomas develop in scar tissue)

Heart (BBB, heart block)

Kidneys (stones due to hypercalcaemia, nephrocalcinosis, interstitial nephritis)

CNS (nodules, pituitary involvement e.g. diabetes insipidus, encephalopathy)

Peripheral nervous system (facial nerve palsy, mononeuritis multiplex)

Bones (arthralgia, arthritis, myopathy)

154
Q

What is Lofgren’s syndrome?

A

Specific presentation of sarcoidosis, characterised by:

  • Erythema nodosum
  • Bilateral hilar lymphadenopathy
  • Polyarthralgia
155
Q

What may also present like sarcoidosis?

A
  • TB
  • Lymphoma
  • Hypersensitivity pneumonitis
  • HIV
  • Toxoplasmosis
  • Histoplasmosis
156
Q

What is the screening test for sarcoidosis?

A

Raised ACE

157
Q

What blood tests may also be raised for sarcoidosis?

A

Hypercalcaemia

Raised serum soluble interleukin-2 receptor

Raised CRP

Raised Immunoglobulins

158
Q

What should chest XR show for sarcoidosis?

A

Hilar lymphadenopathy

High-resolution CT thorax shoes hilar lymphadenopathy and pulmonary nodules

MRI can show CNS involvement

PET scan shows active inflammation in affected areas

159
Q

What is the gold standard for diagnosing sarcoidosis?

A

Histology from a biopsy from bronchoscopy with US guided biopsy

Histology = non-caseating granulomas with epithelioid cells

160
Q

What are the tests for other organs in sarcoidosis?

A

U&Es for kidney involvement

Urine dip for proteinuria

LFTs for liver involvement

Opthamology for eye involvement

ECG and echo for heart involvement

US abdo for liver / kidney involvement

161
Q

What is the treatment for sarcoidosis?

A

Oral steroids (and bisphosphonates) are 1st line

Second line are methotrexate or azathioprine

Lung transplant is rarely required in severe pulmonary disease

162
Q

What is the prognosis of sarcoidosis (unknown aetiology)?

A

Spontaneous resolvement in around 60% in patiens

Some progress to pulmonary fibrosis and pulmonary hypertension

163
Q

What is obstructive sleep apnoea caused by?

A

Collapse of the pharyngeal airway during sleep

164
Q

What are some risk factors of obstructive sleep apnoea?

A

Middle age

Male

Obese

Alcohol

Smoking

165
Q

What are some features of obstructive sleep apnoea?

A
  • Episodes during sleep
  • Snoring
  • Morning headache
  • Daytime sleepiness
  • Unrefreshed sleep
  • Concentration problems
  • Reduced O2 sats during sleep
166
Q

What scoring system can be used to assess symptoms of sleepiness associated with obstructive sleep apnoea?

A

Epworth sleepiness scale

167
Q

How to manage sleep apnoea?

A

Referral to ENT specialist or specialist sleep clinic for sleep studies (pt sleeps whilst lab staff monitor oxygen sats, HR, RR and breathing to establish any apnoea episodes)

Conservative: Stop smoking, drinking, lose weight

CPAP

Surgery - restructuring of soft palete and jaw (uvulopalatopharyngoplasty)

168
Q

What features describes poorly controlled asthma?

A
  • Difficulty sleeping because of symptoms
  • Interfering with usual activities
  • Decreasing PEFR
169
Q

How can cause of peak flow deterioration be checked?

A
  • Check adherance to treatment
  • Smoking?
  • New pets/job
170
Q

What can be included in educating asthma patients?

A
  • Review inhaler technique
  • Step up management: add Leukotriene receptor antagonist (NICE)
  • Smoking cessation
  • Avoid triggers

Medicine (12 decks)

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