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Dannys Medicine Finals > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Causes of ARDS?

A

(SHAFT)
Sepsis

Head injury (sympathetic nervous stimulation which then leads to pulmonary HTN)

Acute pancreatitis

Fractures of long bone or multiple fractures (through fat embolism)

Trauma/ direct lung injury

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2
Q

How do you exclude Pulmonary Oedema?

A

normal pulmonary capillary wedge pressure

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3
Q

How would you describe ARDS

A

acute condition characterized by bilateral pulmonary infiltrates and severe hypoxemia in the absence of evidence for cardiogenic pulmonary oedema

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4
Q

causes of upper lobe fibrosis?

A

CHARTS

Coal workers’ pneumoconiosis
Histiocytosis
Ankylosing spondylitis/Allergic bronchopulmonary aspergillosis
Radiation
Tuberculosis
Silicosis (progressive massive fibrosis), sarcoidosis

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5
Q

Describe Chronic Bronchitis

A

productive cough for more than 3 months in two consecutive years

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6
Q

Describe Emphysema

A

Destruction of lung parenchyma - abnormal airspace enlargement from distal to terminal bronchioles + alveoli destruction

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7
Q

What does chronic bronchitis lead to?

A

1) chronic inflammation / fibrosis
2) goblet cell hyperplasia
3) mucuous hypersecretion
4) narrowing of small airways

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8
Q

Causes of Emphysema?

A 
Smoking
A1AT deficiency (uninhibited neutrophil elastase breaks down alveoli)
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9
Q

What is Cor Pulmonale and what are the signs?

A

RV impairment due to pulmonary disease

1) peripheral oedema
2) left heave (RVH)
3) Raised JVP
4) Hepatomegaly

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10
Q

Difference in inflammation between COPD and Asthma?

A

COPD - inflammayion with neutrophils, CD8 T lymphocytes and macrophages

Asthma - Mainly eosinophilic infiltration with CD4+ T lymphocytes

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11
Q

CO2 retention signs?

A

Asterixis
Drowsy
Confusion

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12
Q

Symptoms of COPD

A 
Wheeze
Sputum
Cough
breathless
Bronchitis
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13
Q

Signs of COPD?

A

Dyspnoea
Pursed lips
Coarse crackles
bronchial sounds

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14
Q

Diagnosis on Spirometry?

A

FVC decreased
FEV1 decreased
FEV1 / FVC <70%

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15
Q

How is COPD staged?

A

FEV1% of prediced

1 >80%
2 50-79%
3 30-49%
4 <30%

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16
Q

Medical management of COPD?

A

1st - SABA/SAMA

2nd - Asthmatic features = LABA + ICS

No asthmatic features = LABA + LAMA

3rd - Triple Therapy = LABA, LAMA , ICS

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17
Q

give examples of SAMA and LAMA

A

SAMA - Ipratropium

LAMA - Tiotropium / Glycopyrronium

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18
Q

Give examples of a Mucolytic

A

Mucinex (guaifenesin)

Carbocisteine.

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19
Q

What is Seretide made up of

A

LABA + ICS (Salmeterol + Fluticasone)

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20
Q

What is Trimbow made up of

A

LABA + LAMA + ICS (formoterol, glycopyrronium, beclometasone)

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21
Q

What is Ultibro made up of

A

LABA + LAMA (indacaterol + glycopyrronium)

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22
Q

Appropriate bedside tests for COPD

A 
O2 sats
sputum pot
ECG
ABG
BMI
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23
Q

When should someone be admitted to hospital if they have a COPD exacerbation

A
  • cant cope at home
  • severe co-morbidities
  • severe symptoms (low sats <90%)
  • confined to bed
  • already on LTOT
  • CXR changes
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24
Q

what are the PaCO2 and PaO2 figures in T2RF?

A

PaO2 <8kPa

PaCO2 >6.7kPa

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25
Q

further complications of COPD?

A 
Pneumona
Pneumothorax
Polycythaemia / anaemia 
Depression
respiratory failure
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26
Q

Describe the 5 stages of the MRC Dyspnoea Scale

A 
1 - breathless on strenuous exercise
2 - " a hill / hurrying
3 - " normal walk 
4 - " after 100m / few minutes of walk 
5 - " minimal activity (dressing etc - cant leave house)
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27
Q

Treatment of COPD Exacerbation?

A 
Oxygen (aim for 88-92% sats) 
Salbutamol (2.5mg neb)
Ipratropium bromide (500mcg neb)
Prednisolone (30mg for 5 daysa) 
Doxycycline (200g stat then 100mg for 7 days)
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28
Q

What is Obstructive Sleep Apnoea

A

collapse of the pharyngeal airway during sleep. It is characterised by apnoea episodes during sleep where the person will stop breathing periodically for up to a few minutes.

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29
Q

Obstructive Sleep Apnoea

Risk Factors?

A 
Middle age
Male
Obesity
Alcohol
Smoking

macroglossia: acromegaly, hypothyroidism, amyloidosis

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30
Q

Obstructive Sleep Apnoea

Features?

A

Partner complains of excessive snoring and apnoea episodes

  • morning headache
  • daytime sleepiness

Severe cases can cause hypertension, heart failure and can increase the risk of myocardial infarction and stroke.

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31
Q

Obstructive Sleep Apnoea

Assessment of sleepiness?

Diagnosis?

A

Epworth Sleepiness Scale

sleep studies (polysomnography)

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32
Q

Obstructive Sleep Apnoea

Treatment?

indication of urgent referral?

A

weight loss

continuous positive airway pressure (CPAP) is first line

Patients that need to be fully alert for work, for example heavy goods vehicle operators, require urgent referral

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33
Q

ASTHMA

How does inhalation of allergens lead to histamine release?

A

Inhalation of allergens results in type 1 hypersensitivity which causes IgE antibody release

IgE bind to mast cells which degranulate to cause histamine release

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34
Q

ASTHMA

How does histamine release cause airway obstruction

A

1) Smooth muscle contraction
2) Bronchoconstriction
3) Mucous production

all cause obstruction

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35
Q

ASTHMA

How is it diagnosed

A

Spirometry and peak flow

Fractional Exhaled Nitric Oxide (FeNO)

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36
Q

ASTHMA

How are FeNO results interpreted?

A

> 40ppb = dx of asthma

25-39ppb = suggestive of dx

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37
Q

ASTHMA

Management (7 steps)

A

1) SABA
2) SABA + ICS
3) SABA + ICS + LTRA
4) SABA + ICS + LABA (+/- LTRA)
5) SABA + MART
6) SABA + Moderate dose MART (increase ICS dose)
7) additional theophylline or MRA

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38
Q

ASTHMA

Management of under 5 years?

A

1) SABA
2) 8 week trial of ICS
3) Add LTRA

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39
Q

ASTHMA

Acute management?

A
  1. Oxygen
  2. Salbutamol nebulisers
  3. Ipratropium bromide nebulisers
  4. Hydrocortisone IV OR Oral Prednisolone
  5. Magnesium Sulfate IV
  6. Aminophylline/ IV salbutamol
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40
Q

When can a patient after an acute asthma attack be discharged?

A

If peak flow is >75% of best with <25% diurnal variation

If peak flow <50% then 5 days minimum prednisolone required

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41
Q

BRONCHIECTASIS

What is it?

A

Irreversible and abnormal dilation of the airways

Commonly secondary to cystic fibrosis

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42
Q

BRONCHIECTASIS

how does infection lead to further predisposition to infection?

A

infection - inflammation - destruction - dilation - further predisposition

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43
Q

BRONCHIECTASIS

Causes?

A

immunodeficiency
primary ciliary dyskinesia / kartagener syndrome
airway obstruction
young syndrome

Allergic bronchopulmonary aspergillosis (sensitive to fungus Aspergillus)

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44
Q

What is Young Syndrome?

A

condition characterized by

  • male infertility
  • bronchiectasis
  • sinusitis
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45
Q

What is Kartagener’s syndrome?

A

autosomal recessive genetic ciliary disorder comprising the triad of:

  • situs inversus
  • chronic sinusitis
  • bronchiectasis
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46
Q

BRONCHIECTASIS

clinical features?

A

Persistent sputum production + cough

+ dyspnoea
+ haemoptysis
+ weight loss

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47
Q

BRONCHIECTASIS

Signs on examination?

A

Wheeze

high pitch inspiratory crackles

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48
Q

BRONCHIECTASIS

Gold standard dx?

A

CT of chest (Signet Ring Sign = dilated bronchus)

CXR (tramtrack airways + ring shadows)

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49
Q

BRONCHIECTASIS

Basic necessary investigations?

A

sputum / blood cultures
kidney function
serum immunoglobulins

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50
Q

BRONCHIECTASIS

Management?

A

1) Airway clearance techniques
2) Mucolytic agents
3) Antibiotic prophylaxis

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51
Q

What mucoactive should NOT be used in Bronchiectasis

A

Recombinant human DNase

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52
Q

BRONCHIECTASIS

Long terrm antibiotics are given if a patient has over 3 exacerbations a month. Which should be given?

A

Pseudomonas aeruginosa colonised :

1st - Inhaled Colistin / gentamicin
2nd - Oral Macrolides

Non P. aeruginosa:

1) Macrolides
2) Inhaled Gent

+ bronchodilators

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53
Q

BRONCHIECTASIS

Complications?

A

haemoptysis

Respiratory failure

Cor Pulmonale

Pneumothorax

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54
Q

LUNG CANCER

Types?

A

Non small cell (NSCLC)

  • Adenocarcinoma
  • Squamous cell carcinoma
  • large cell

Small Cell (SCLC)

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55
Q

LUNG CANCER

Describe Adenocarcinoma

e. g
- % of incidence
- where cancer tends to be

A

Most common type (38%) - cancer of mucous secreting cells

tends to be lung peripheries

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56
Q

LUNG CANCER

Describe squamous cell carcinoma

e. g
- % of incidence
- where cancer tends to be
- how it presents
- mets?

A

(20% incidence)
SMOKING - most common cause

Tends to be central - often presents with pneumonia secondary to obstructed bronchus

mets tend to be LATE and histology shows keratin

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57
Q

LUNG CANCER

What is large cell and does it metastasise early or late

A

Metastises early and large cell LC is undifferentiated neoplasms with poor prognosis

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58
Q

LUNG CANCER

Describe small cell LC

cancer of ..
% of incidence
mets early or late

A

15%

Cancer if APUD cells (neuroendocrine cells in lung so causes paraneoplastic syndromes)

early mets with POOR prognosis

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59
Q

LUNG CANCER

Possible symptoms

A 
SVCO 
cough
malaise
haemoptysis
weight loss
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60
Q

How is SVCO clincially diagnosed and what is it?

A

Superior vena cava obstruction due to compression by tumour or mediastinal lymphadenopathy

diagnosed by presence of neck and facial swelling and distended veins over the anterior chest wall.

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61
Q

LUNG CANCER

Signs on examination?

A 
Lymphadenopathy
Stridor
Clubbing 
HPOA 
Signs of effusion
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62
Q

What is HPOA

A

Hypertrophic pulmonary osteoarthropathy (HPOA) syndrome characterized by the triad

  • periostitis
  • digital clubbing
  • painful arthropathy of the large joints (especially lower limbs)
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63
Q

LUNG CANCER

Likely mets?

A

Bone (bone pain + raised ALP)
Brain
Liver (abnormal mets)
Adrenal glands

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64
Q

LUNG CANCER

Signs of Pancoast tumour?

A

Tumour of the apex

horners syndrome

hoarseness due to pressure on recurrent laryngeal nerve

pain/ atrophy of upper limb + oedema

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65
Q

What cancer does Asbestos cause

A

Mesothelioma classically and adenocarcinoma

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66
Q

Name some Paraneoplastic Syndromes

A

Hypercalcaemia

SiADH 
Hyponatraemia 
Cushings 
Lambert Eaton 
HPOA
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67
Q

What is the incidence of Hypercalcaemia in various lung cancers?

A

50% in SCC
20% in adenocarcinoma
15% in small cell

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68
Q

how can Lung Cancer cause Cushings?

A

Lung cancer producing ectopic ACTH (SCLC)

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69
Q

What is Lambert Eaton Syndrome?

A

Antibodies form to Calcium gated channels in the nerves to muscles resulting in PROXIMAL and OCULAR WEAKNESS

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70
Q

LUNG CANCER

Investigations?

A

CXR - CT - PET

Tissue biopsy via Bronchoscopy

Cytology from aspiration / washings / secretions

71
Q

LUNG CANCER

How are NSCLC and SCLC staged?

A

NSCLC - TMN

SCLC - VALSG

72
Q

LUNG CANCER

Management of NSCLC and SCLC?

A

NSCLC - Surgical for stage 1/2
chemo
palliative radio to improve symptoms

SCLC - surgical only if early enough (<5% cases even in T1/2)

73
Q

LUNG CANCER

5 year survival?

A

16% - poor prognosis

highest cancer related death

74
Q

LUNG CANCER

5 year survival?

A

16% - poor prognosis

highest cancer related death

75
Q

Murmur heard in Patent ductus Arteriosus?

A

continuous machinery murmur

76
Q

What is Barlow syndrome?

A

click murmur heard in mitral valve prolapse found in 5-10% of world population

77
Q

What is Austin Flint murmur

A

Rumbling diastolic murmur heard in AR

78
Q

What is Graham Steell Murmur

A

early diastolic murmur due to pulmonary incompetence caused by pulmonary hypertension

79
Q

What is Carey Coombs murmur

A

Mid diastolic (mitral stenosis from rheumatic fever)

80
Q

What is the mutation in Cystic Fibrosis

A

Mutation to CFTR gene on chromosome 7

81
Q

Cystic Fibrosis

Why is there mucociliary dysfunction

A

Dehydration of airway surface fluid causes this as well as impaired biliary and pancreatic drainage

82
Q

What does impaired biliary and pancreatic drainage in CF lead to?

A

Impaired digestion and malabsorption

83
Q

What does mucociliary dysfunction lead to?

A

1) Reduced mucous clearance
2) Airway obstruction
3) predisposition to infection - leads to Bronchiectasis

84
Q

Associated problems as well as respiratory CF?

A

Pancreatic insufficiency - (Steatorrhoea due to pancreatic blocking of exocrine digestive enzymes)
CF related diabetes
Infertility

85
Q

CF

How is it diagnosed early on?

A

Skin heel prick on day 5 OR

Meconium Ileus / constipation in first few days of life

86
Q

How is CF confirmed?

A

Sweat test (chloride over 60mmol/L)

immunoreactive trypsin test

87
Q

How is CF pulmonary disease managed?

A

1) Airway clearance techniques
2) Mucolytic agents
3) Antibiotic prophylaxis
4) Bilateral sequential lung transplant

88
Q

Name some mucolytic agents

A

rhDNase (not used in bronchiectasis)

hypertonic saline

mannitol dry powder

89
Q

Management of CF extra pulmonary disease?

A

1) Pancreatic enzyme replacement
2) Liver screening annually + ursodeoxycholic acid
3) Diabetes screening (OGTT / CGM)

90
Q

What is the name of new CF drugs?

what is the median age of life?

A

CFTR modulator drugs

49 years

91
Q

Idiopathic Pulmonary Fibrosis

Name some symptoms

A

Chronic exertional dyspnoea

Dry cough

fatigue

92
Q

Idiopathic Pulmonary Fibrosis

Name some signs

A

Bilateral inspiratory crackles
Clubbing
Acrocyanosis (peripheral discolouration)

93
Q

Idiopathic Pulmonary Fibrosis

What pattern is shown on lung function testing

A

Restrictive

Reduced lung volume

reduced DLCO

94
Q

Idiopathic Pulmonary Fibrosis

What does CT show?

A

honeycombing
reduced lung volume
reticular opacities

(seen in bases and peripheries)

95
Q

Idiopathic Pulmonary Fibrosis

Methods of gathering pathological specimens?

A

bronchoalveolar lavage

Transbronchial biopsy

Surgical lung biopsy

96
Q

Idiopathic Pulmonary Fibrosis

Management of breathlessness?

A

Oxygen

Physio

97
Q

Idiopathic Pulmonary Fibrosis

Name some IPF modifying drugs and when they can be given

A

Pirfenidone

Nintedanib

If FVC is 50-80% of predicted

98
Q

Idiopathic Pulmonary Fibrosis

Name some medication that can be given for symptomatic relief

A

Benzos and Opioids

99
Q

PLEURAL EFFUSION

Sign on X-ray?

A

Blunting of costophrenic angles

100
Q

PLEURAL EFFUSION

If the protein level is between 25-35 g/L, Light’s criteria should be applied. An exudate is likely if at least one of the following criteria are met:

A

pleural fluid protein divided by serum protein >0.5

pleural fluid LDH divided by serum LDH >0.6

pleural fluid LDH more than two-thirds the upper limits of normal serum LDH

101
Q

PLEURAL EFFUSION

Why may fluid enter the pleural space?

A

1) Microvascular pressure (increased hydrostatic pressure in venous system - HF)
2) Vasculature permeability (leaky vessels - infection/malignancy)
3) Decreased plasma oncotic pressure (hypoproteinaemia)

102
Q

PLEURAL EFFUSION

Transudate and Exudates

Whats the difference and are they bilateral or unilateral

A

Transudates tend to be bilateral and minimal protein

Exudates tend to be unilateral and protein count of >30g/L

103
Q

PLEURAL EFFUSION

Transudate causes?

A
  • Heart failure
  • Hypoalbuminaemia
  • Constrictive pericarditis
  • Peritoneal dialysis
  • Meig’s syndrome (benign ovarian tumour)
104
Q

PLEURAL EFFUSION

why might someone have hypoalbuminaemia and what type of effusion does it cause

A

Nephrotic syndrome
liver disease / cirrhosis
malabsorption

Transudate

105
Q

PLEURAL EFFUSION

Exudate causes

A
  • Connective tissue disease (RA, SLE)
  • Cancer/ Malignancy (lung / breast)
  • TB
  • Pneumonia (secondary to MOST COMMON)
  • PE
  • Pancreatitis

CC T TRIPLE P

106
Q

PLEURAL EFFUSION

Signs on examination?

A

REDUCED:
breath sounds
vocal resonance
chest expansion

DULL percussion
Tracheal deviation AWAY from effusion

107
Q

PLEURAL EFFUSION

Imaging?

A

Initially X-ray

Contrast CT for investigating cause

PLEURAL PARACENTESIS
US with aspiration to reduce complication rate

108
Q

PLEURAL EFFUSION

Management?

What should the fluid be sent for:

A

ASPIRATION
- 21G needle and 50ml syringe should be used

fluid should be sent for ; 
pH
protein
lactate dehydrogenase (LDH)
cytology and microbiology
109
Q

PLEURAL EFFUSION

Management if infected?

A

pleural effusion in association with sepsis or a pneumonic illness require diagnostic pleural fluid sampling

If the fluid is purulent or turbid/cloudy = CHEST TUBE

if the fluid is clear but the pH is less than 7.2 in suspected infection = CHEST TUBE

110
Q

PLEURAL EFFUSION

Transudate management?

A

Treat with diuretics - aspiration should be avoided

111
Q

PNEUMONIA

Common organism in CAP?

A

Strep pneumoniae

H. influenza

112
Q

What type of bacteria is Strep Pneumoniae

A

Gram POSITIVE alpha haemolytic strep

113
Q

PNEUMONIA

Common organism in HAP?

What patients is this organism common in CAP?

A

Pseudomonas Aureginosa

IN CF and Bronchiectasis - common in CAP

114
Q

PNEUMONIA

Types of Atypical Pneumonia?

A

Mycoplasma

Legionella

Chlamydophila

Psittacosis (BIRDS e.g parrots)

Q fever

Tularemia

115
Q

What is Q fever?

A

a disease caused by the bacteria Coxiella burnetii

infected farm animals

116
Q

Extrapulmonary symptoms of Mycoplasma?

A

HAEM

Haemolytic Anaemia
Arthralgia
Erythema Multiforme
Myocarditis / Pericarditis

117
Q

Extrapulmonary symptoms of Legionella?

How is it diagnosed?

A

Hyponatraemia secondary to SiADH

Hypophosphataemia and Raised serum ferritin

Diagnosed with urinary antigen testing

118
Q

How can Klebsiella causing Pneumonia be recognised?

A

‘red currant jelly’ sputum

119
Q

What is PCP and its antibiotic treatment?

A

Pneumocystis jirovecii - fungi causing pneumonia - aids defining illness

Treated with Co - trimoxazole

120
Q

What is Co- trimoxazole made up of

A

Trimethoprim and Sulfamethoxazole

121
Q

PNEUMONIA

Which patients is aspiration pneumonia more common in

A

Those with reduced conscious level / neuro disorders

122
Q

PNEUMONIA

Signs on examination?

A

Dull percussion
Bronchial breathing
Coarse crepitations

123
Q

PNEUMONIA

Investigations?

A

CXR
blood and sputum Cultures
FBC, U+Es, CRP

124
Q

PNEUMONIA

What is CURB-65

A

Method of determining severity of pneumonia

0: low risk (less than 1% mortality risk)
1 or 2: intermediate risk (1-10% mortality risk)
3 or 4: high risk (more than 10% mortality risk- urgent admission)

Confusion
Urea >7mmol
Respiratory rate >30
BP <90 systolic or <60 diastolic 
>65 years old
125
Q

PNEUMONIA

Management?

A

Fluids, Analgesics, Antibiotics:

Low risk : amoxicillin / doxycycline / clarithromycin

Intermediate: Amoxicillin + Macrolide (clarithromycin)

High : an IV beta-lactamase stable penicillin such as co-amoxiclav, ceftriaxone or piperacillin with tazobactam + Macrolide (clarithromycin)

126
Q

Link between Pneumonia and Lung cancer?

A

11% of patients who smoke over the age of 50 with pneumonia have lung cancer

127
Q

Major risk factors of PE?

A
  • DVT
  • Previous VTE
  • Active Cancer
  • Recent surgery / immobilisation / flight
  • Pregnancy
  • COCP
  • Thrombophilia
  • Obesity
128
Q

What is Virchows Triad

A

3 factors that are critically important in the development of venous thrombosis:

(1) venous stasis,
(2) activation of blood coagulation (hypercoaguable state) (3) vein damage (endothelial injury)

129
Q

Symptoms of PE?

A 
Dyspnoea
Pleuritic chest pain (worse on inspiration) 
Cough 
Haemoptysis 
Syncope
leg swelling
130
Q

Frequency of clinical signs in PE?

A

Tachypnea (respiratory rate >16/min) - 96%
Crackles - 58%
Tachycardia (heart rate >100/min) - 44%
Fever (temperature >37.8°C) - 43%

131
Q

Signs of Right heart failure?

A

Increased JVP
Hypotension
Pansystolic tricuspid regurgitation murmur
Split S2

132
Q

Describe the 2- level PE Wells Score

A

/12.5

if >4 points do immediate CTPA

if <4 points do d-dimer, if positive do CTPA

Score itself:
\+3 signs of DVT
\+3 PE most likely dx
\+1.5 Immobilised for >3 days / recent surgery/ flight
\+1.5 Previous DVT/ PE
\+1 Haemoptysis
\+1 Malignancy <6 months
133
Q

What should be done if Wells under 4 points and the d-dimer is negative?

A

Stop anticoagulation and consider alternative diagnosis

134
Q

What should be given if PE suspected

A

immediate anticoagulation

LMWH is empirical but DOAC recommended

135
Q

What anticoagulation should be given if PE diagnosed and:

Stable?
Unstable?
Active cancer?
Renal impairment?

A

Stable - Apixiban / Rivaroxaban

Unstable - Thrombolysis / UFH

Active cancer- Edoxaban, 2nd line - LMWH

Renal impairment - CrCl <15ml/min offer LMWH/ UFH followed by VKA

136
Q

What should be given if Apixiban / Rivaroxaban not suitable in PE?

A

LMWH followed by dabigatran or edoxaban
OR
LMWH followed by a vitamin K antagonist (VKA, i.e. warfarin)

137
Q

How long should anticoagulation in PE last?

A

At least 3 months

If unprovoked at least 6 months and test for thrombophilia / cancer

138
Q

Indications for thrombolysis in PE?

A

Cardiac arrest with confirmed PE

No improvement after anticoagulation

haemodynamically unstable (e.g. BP under 90 for over 15 mins)

139
Q

PULMONARY HYPERTENSION

How does it occur?

A

Increased resistance / pressure in pulmonary arteries leads to right heart strain and back pressure into venous system

140
Q

PULMONARY HYPERTENSION

Causes?

A

GROUP 1: Primary pulmonary HTN (connective tissue disorders e.g. SLE)

2: Left heart failure due to MI / systemic hypertension
3: chronic lung disease (COPD)
4: Vascular (PE)
5: Miscellaneous (sarcoidosis)

141
Q

PULMONARY HYPERTENSION

Signs?

A 
SHORTS
SOB
Hepatomegaly
Oedema
Raised JVP
Tachycardia
Syncope
142
Q

PULMONARY HYPERTENSION

Signs on ECG?

Signs of RVH on ECG?

A

Right heart strain - RVH, RAD, RBBB

RVH :
V1-3 larger R waves
V4-6 deeper S waves

143
Q

PULMONARY HYPERTENSION

Signs on X-ray?

which blood marker is classically raised?

A

Dilated pulmonary arteries
RVH

RAISED BNP (NT proBNP)

144
Q

PULMONARY HYPERTENSION

Give examples of?

Prostanoids

A

Epoprestenol

145
Q

PULMONARY HYPERTENSION

Primary treatment?

A

1) IV Prostanoids
2) Endothelin Receptor Antagonists
3) Phosphodiesterase - 5 - inhibitors

146
Q

PULMONARY HYPERTENSION

Give examples of?

Phosphodiesterase - 5 - inhibitors

A

Sildenafil

147
Q

PULMONARY HYPERTENSION

Give examples of?
Endothelin receptor Antagonists

A

Macitentan

148
Q

Signs of Acute Bronchitis?

A

normal CXR with clear sputum and low grade fever

149
Q

When should antibiotic therapy be given in acute bronchitis?

Which Abx is first line

A

1) Systemically unwell
2) Pre existing co morbidities
3) CRP >100

if CRP 20-100 give delayed prescription

DOXYCYCLINE

150
Q

What is Heerfordt’s Syndrome?

A

Uveoparotid fever

Parotid enlargement and uveitis secondary to Sarcoidosis

+ facial nerve palsy

151
Q

Stages of Pulmonary Sarcoidosis?

A

1- Biliteral hilar lymphaedenopathy (BHL)
2- BHL + interstitial infiltrates
3 - diffuse interstitial infiltrates
4 - diffuse fibrosis

152
Q

Signs of Diffuse fibrosis?

what may it lead to?

A

Fine inspiratory crackles, clubbing and exertional desaturation

may lead to pulmonary hypetension and cor pulmonale

153
Q

Sarcoidosis spirometry findings?

A

RESTRICTIVE (reduced FVC)

154
Q

Treatment and causes of secondary Pneumothorax?

A

<1cm - observe
1-2cm - treat with needle aspiration
>2cm - small bore chest drain

causes - pre-existing lung disease e.g.
COPD
fibrosis
asthma
bronchiectasis
TB
Sarcoidosis
155
Q

What is goodpastures syndrome now known as?

What is it?

A

Anti Glomerular basement membrane disease (GBM)

type 2 hypersensitivity small vessel vasculitis more common in men (20-30s, 60-70s)

156
Q

ANTI-GBM DISEASE

Classical disease?

A

Pulmonary haemorrhage (haemoptysis)

Rapid progressive glomerulonephritis / rapid onset AKI

systemically unwell: fever, nausea

157
Q

ANTI-GBM DISEASE

Cause?

Associated HLA?

A

Anti GBM antibodies against type 4 collagen - small vessel vasculitis

HLA-DR2

158
Q

Signs of Eosinophilic granulomatosis with polyangiitis?

A 
asthma
blood eosinophilia (e.g. > 10%)
paranasal sinusitis
mononeuritis multiplex
pANCA positive in 60%
159
Q

What is Churg Strauss Syndrome?

A

Eosinophilic granulomatosis with polyangiitis

ANCA associated small-medium vessel vasculitis

160
Q

Eosinophilic granulomatosis with polyangiitis

What may precipitate disease?

A

Leukotriene receptor antagonists

161
Q

ANTI-GBM DISEASE

Investigations?

A

Renal biopsy - linear IgG deposits on basement membrane

Increased transfer factor secondary to pulmonary haemorrhage

162
Q

ANTI-GBM DISEASE

Management?

A

plasma exchange (plasmapheresis)
steroids
cyclophosphamide

163
Q

What is Wegener’s Granulomatosis known as now?

A

Granulomatosis with Polyangiitis

164
Q

Management of Granulomatosis with Polyangiitis ?

A

Same as Anti GBM:

plasma exchange (plasmapheresis)
steroids
cyclophosphamide

165
Q

ANTI-GBM DISEASE

Factors which increase the likelihood of Pulmonary Haemorrhage?

A 
smoking
lower respiratory tract infection
pulmonary oedema
inhalation of hydrocarbons
young males
166
Q

Features of Granulomatosis with Polyangiitis ??

A

upper respiratory tract: epistaxis, sinusitis, nasal crusting

lower respiratory tract: dyspnoea, haemoptysis

kidneys: rapidly progressive glomerulonephritis (‘pauci-immune’, 80% of patients)

saddle-shape nose deformity

also: vasculitic rash, eye involvement (e.g. proptosis), cranial nerve lesions

167
Q

Investigations of Granulomatosis with Polyangiitis ?

A

cANCA positive in 90%

renal biopsy shows epithelial crescents in Bowman’s capsule

168
Q

What is Granulomatosis with Polyangiitis ?

A

autoimmune condition associated with a necrotizing granulomatous vasculitis, affecting:

1) upper and lower respiratory tract
2) kidneys.

169
Q

Prophylactic Abx of choice in a patient with COPD who has frequent exacerbations?

A

Azithromycin

170
Q

KEY SYMPTOMS of:

Mitral stenosis?

A

Dyspnoea
Atrial Fibrillation
Malar flush on cheeks
Mid-diastolic murmur

171
Q

KEY SYMPTOMS of:

Aspergilloma?

A

Often past history of TB
Haemoptysis may be severe
CXR shows rounded opacity

172
Q

KEY SYMPTOMS of:

Pulmonary Oedema?

A

Dyspnoea
Bibasal crackles
S3

173
Q

What may be seen on X-ray in idiopathic pulmonary fibrosis?

A

bilateral interstitial shadowing (typically small, irregular, peripheral opacities - ‘ground-glass’ - later progressing to ‘honeycombing’

174
Q

Causes of lower lobe fibrosis?

A
  • idiopathic pulmonary fibrosis
  • most connective tissue disorders (except ankylosing spondylitis) e.g. SLE
  • drug-induced: amiodarone, bleomycin, methotrexate
  • asbestosis

Dannys Medicine Finals (9 decks)

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