Resp Flashcards

1
Q

CPAP and BIPAP which is used to treat Type 1 vs 2 resp failure

A

CPAP T1, BIPAP T2

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2
Q

Name 3 types of COPD

A

Chronic bronchitis, emphysema, Alpha-1 Antitrypsin (A1AT) deficiency

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3
Q

What are risk factors for COPD

A

Cigarettes
Air pollution
Genetics (A1AT deficiency)

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4
Q

What inheritance pattern is A1AT deficiency

A

Autosomal co-dominant

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5
Q

What is the pathology of chronic bronchitis

A

Hypertrophy+ hyperplasia of mucous glands (as protective against RF)
Chronic inflammation cells infiltrate bronchi- luminal narrowing
Mucus hypersecretion, ciliary dysfunction, narrowed lumen

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6
Q

How long does someone have a cough for nd cough sputum for to be classed as chronic bronchitis

A

2 periods of Cough with sputum 3+ months over 2 years

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7
Q

What is the pathology of emphysema

A

Destruction of the elastin layer in alveolar ducts/ air sacs and resp bronchioles.
Elastin keeps these walls open during expiration so decreased elastin traps air distal to the blockage

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8
Q

What are different types of emphysema

A

Centriacinar:- resp bronchioles
Panacinar:- r.b, alv, alv sacs
Distal acinar
Irregular

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9
Q

What emphysema are smokers most at risk from

A

Centriacinar

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10
Q

What is the pathology of A1AT deficiency

A

A1AT degrades neutrophil elastase which protects the lungs from excess damage to the elastin layer. A deficiency in liver production of A1AT leads to panacinar emphysema and liver issues.

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11
Q

Where is A1AT produced

A

Liver

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12
Q

Who do you suspect A1AT deficiency in

A

Young/ middle aged men with emphysema with COPD Sx but no history of smoking

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13
Q

What are Sx of COPD

A

Typically older, chronic cough w/ (often purulent) sputum
Extensive smoking Hx and constant dyspnoea

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14
Q

Blue bloater (COPD) Sx

A

Chronic purulent cough
Dyspnoea
Cyanosis
Obesity

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15
Q

Pink puffer (emphysema) Sx

A

Minimal cough
Pursed lip breathing
Cachectic (muscle loss)
Barrel chest+ hyper resonant percussion

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16
Q

What is a complication of emphysema

A

Bullae rupture (Bullae is a large air sac)

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17
Q

What finding do you get on spirometry of obstructive disease

A

FEV1:FEV <0.7

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18
Q

What is difference in change of FEV1 in bronchodilator reversible and irreversible obstruction

A

<12% irreversible (COPD)
>12% reversible (Asthma)

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19
Q

What is a complication of COPD

A

Cor pulmonale
RHS heart failure due to increased pulmonary HTN

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20
Q

What is DlCO

A

Diffsuion capacity of CO across lung

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21
Q

How does DlCO differ in asthma from COPD

A

Low in COPD
Normal in asthma

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22
Q

Other than spirometry and DLCO, what other investigation might you perform in someone with suspected COPD

A

Genetic testing for A1AT
ABG show T2RF
ECG
CXR

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23
Q

What can CXR show in a patient with COPD

A

Flattened diaphragm + bullae formation

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24
Q

What is long term management for COPD

A

Influenze+ pneumococal vaccines
1- SABUTEROL
2- SALBUTEROL+ SALMETEROL+ TIOTROPIUM
3-(2+) Inhaled corticosteroids

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25
Q

What is O2 sat target for patients in hospital with acute COPD attack

A

88-92 because excess O2 is dead space leading to V/Q mismatch and increased CO2 retention (resp acidosis)

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26
Q

What are the 2 types of asthma

A

Allergic 70%
Non-allergic 30%

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27
Q

Differences between allergic and non-allergic asthma

A

Allergic:- IgE mediated, Extrinsic, T1 Hypersensitivity, due to environmental trigger, often early presentation

Non-allergic:- non IgE mediated, intrinsic, may prevent later, harder to treat, associated with smoking

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28
Q

Triggers for asthma

A

Infection, allergies, cold weather, exercise, drugs (beta-blockers, aspirin)

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29
Q

What is the atopic triad

A

Atopic rhinitis, asthma, eczma

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30
Q

What is samters triad

A

Nasal polyps, asthma, aspirin sensitivity

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31
Q

How can aspirin exacerbate Asthma

A

Aspirin inhibits COX-1/2 so shunts more arachidonic acid

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32
Q

Pathology of asthma

A

Overexpressed TH2 cells in airway exposed to trigger. TH2 cytokine release leads to IgE production and eosinophil recruitment. Both lead to bronchial constriction.

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33
Q

What cytokines are released by TH2 in asthma

A

IL-3,4,5,13

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34
Q

How does IgE production lead to bronchial constriction

A

Mast cell degranulation
Histamines
Leukotrienes
Tryptase

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35
Q

How do eosinophils lead to bronchial constriction in asthma

A

Release toxic proteins

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36
Q

What happens over time in asthma

A

Chronic remodelling

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37
Q

What is treatment for chronic Asthma

A

1:- Salbutamol
2:- SAB2A+ Inhaled corticosteroid
(Asses inhaler technique)
3:- SAB2A+ ICS + Leukotriene receptor antagonist
4:- SAB2A + ICS+ Salmeterol +/- LTRA
5:- Increase ICS dose

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38
Q

What is an example of a leukotriene receptor antagonist

A

Montelukast

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39
Q

What is treatment for exacerbations of asthma

A

OSHITME
O2
nebulised Salbutamol
Hydrocortisone (ICS)
IV MgSO4
IV Theophylline
BIPAP
+/- Abx if infection present

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40
Q

What is lung cancer of the plura called (primary)

A

Mesothelioma

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41
Q

If primary lung cancer is in the lung parenchyma what is name

A

Bronchial

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42
Q

How can you divide Bronchial lung cancers

A

Small cell 20%
Non-small cell 80%

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43
Q

What are the non-small cell lung cancers

A

Squamous cell carcinoma 20%
Adenocarcinoma 40%
Carcinoid
Large Cell 10%

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44
Q

What are the main metastisis sites of lung cancer

A

Bone, Liver, Adrenals, Brain, Lymph nodes

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45
Q

What is the main cause of mesothelioma

A

Asbestos (typically don’t present until decades after exposure)

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46
Q

Who is the common presentation for mesothelioma

A

Male 40-70

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47
Q

What are standard cancer symptoms

A

Weight loss, night pain, TATT

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48
Q

What are Sx of lung cancer

A

SOB, persistent cough, pleuritic chest pain

Hoarse voice from tumour pressing on recurrent laryngeal nerve

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49
Q

What is 1st line investigation in lung cancer

A

CXR

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50
Q

What do you see on XR/ CT in mesothelioma

A

Pleural thickening +/- effusion

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51
Q

What is the diagnostic investigation for mesothelioma

A

Biopsy

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52
Q

What antigen is non-specifically raised in mesothelioma

A

Cancer antigen 125
(Raised in many tumour)

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53
Q

What is management for mesothelioma

A

Usually palliative even though unlikely to distantly metastise
If found early can try surgery + chemo/ radio but generally resistant

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54
Q

What is a BALT lymphoma

A

A non-Hodgkin lymphoma originating in bronchi
Bronchus associated lymphoid tissue

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55
Q

Who exclusively suffers from small cell carcinomas

A

Smokers

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56
Q

What are Small cell lung cancers

A

Neurosecretory granules release neuroendocrine hormones. Responsible for many paraneoplastic syndromes such as Cushings and SIADH

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57
Q

What are complications of SCLC

A

Ectopic ACTH:- Cushings
Ectopic: ADH:- SIADH
Lambert Eaton syndrome:- autoimmune vs NMJ
Fast-growing and early metastasis

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58
Q

What is Lambert Eaton Syndrome

A

The result of antibodies produced by the immune system against SCLC also targets voltage-gated calcium channels sited on presynaptic terminals on motor neurons.

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59
Q

What are Sx of Lambert Eaton Syndrome

A

Weakness in proximal muscles
Diplopia (double vision)
ptosis
slurred speech/ dysphagia
Autonomic dysfunction (dry mouth/ dizziness)

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60
Q

Which part of the lung does squamous cell carcinoma affect

A

Central lung

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61
Q

What hormone may lung squamous cell carcinoma secrete

A

PTHrP can lead to hypercalcemia

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62
Q

From where does squamous cancer in the lung arise from

A

Lung epithelium

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63
Q

What is metastasis/ spread of lung squamous cancer

A

Late Mets
Local spread mostly

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64
Q

Most common cause of squamous lung cancer

A

Smokers

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65
Q

Most common cause of lung adenocarcinoma

A

Asbestos

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66
Q

What part of the lung does an adenocarcinoma effect

A

Peripheral lung

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67
Q

From where do lung adenocarcinoma arise

A

Mucus secreting glandular epithelium

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68
Q

What is common mets location for lung adenocarcinoma

A

Bone, brain, adrenals, lymph nodes, liver

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69
Q

What genetics is are lung carcinoid tumours associated with

A

MEN1 mutation
Neurofibromatosis 1

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70
Q

What hormone does a lung carcinoid tumour secrete

A

Serotonin

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71
Q

What scale is used to assess the level of dyspnoea

A

MRC breathlessness scale

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72
Q

When do Sx present with a carcinoid tumour

A

When liver mets present

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73
Q

What is 1st line investigation in suspected lung cancer

A

CXR, CT

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74
Q

What is the diagnostic investigation for lung cancer

A

Bronchoscopy+ biopsy

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75
Q

What test is used to give staging to lung cancer

A

MRI

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76
Q

What is treatment for non small cell cancer

A

Surgical excision is early
Met:- Chemo/ radio MAB therapy

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77
Q

Are primary or secondary lung tumours more likely

A

Secondary as all blood comes through lungs

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78
Q

Which cancers met to lungs often

A

Breast, kidney, bowel, bladder

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79
Q

What is a Pancoast tumour

A

Tumour in lung apex that metastasises to neck’s sympathetic plexus causing Horners Syndrome:- Ptosis, myosis, anhidrosis

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80
Q

Risk factors for PE

A

Anything affecting Virchow’s triad

81
Q

What are Sx of PE

A

Sudden onset SOB+ chest pain(pleuritic), painful swollen calf
Haemophysis
Raised JVP
Tachycardia+ dyspnoea

82
Q

What score is used to assess the probability of PE

A

Wells score
<4 PE unlikely
>4 PE likely

83
Q

What if wells score <4 what investigation

A

D-dimer:- sensitive but not specific

84
Q

What is gold standard investigation for PE

A

CT pulmonary angiogram

85
Q

What are the ECG characteristics of a PE

A

S1Q3T3
S waves deep in lead 1
Q waves deep in lead 3
T waves inverted in lead 3
RBBB IN V1-V3
Right axis deviation
Sinus tachycardia

86
Q

What type of Ultrasound scan may you use to investigate DVT

A

Doppler

87
Q

Why do you do a CXR in suspected PE even though it does show

A

Rule of DDx, Plueral effusion/ pneomthorax

88
Q

Treatment for PE if the patient is haemodynamically stable

A

Anticoagulants
1- DOAC (Rivaroxaban)
if DOAC CI 1- LMWH
2- Warfarin

89
Q

Treatment for PE if the patient is haemodynamically unstable

A

Thrombolysis
If fails catheter embolectomy

90
Q

What are prophylaxis options for PE

A

Compression stockings, regular walking, SC LMWH

91
Q

What is the most common interstitial lung disease

A

Pulmonary Fibrosis

92
Q

What are risk factors for pulmonary fibrosis

A

Smoking, occupational, drugs (methotrexate), viruses

93
Q

What resp failure does PF lead to

A

T1

94
Q

Sx of PF

A

Exertional dyspnoea, dry unproductive cough,

95
Q

Is PF restrictive or obstructive?

A

Restrictive

96
Q

What is GS imaging for PF

A

High res CT chest

97
Q

What does Chest CT show in PF

A

Ground Glass lungs + traction bronchiectasis

98
Q

What are non-pharmological treatment options for PF

A

Smoking cessation + vaccines
Surgery- lung transplant

99
Q

Pharmacological treatment options for PF

A

Pirfenidone
Nintedanib

100
Q

What is sarcoidosis

A

A granulomatous disease in which there is an abnormal collection of inflammatory cells that forms clumps on the lungs, skin or lymph nodes

101
Q

Who is the classic presentation of sarcoidosis

A

Women 20-40, Afro-Caribbean

102
Q

What are Sx of sarcoidosis

A

Fever, fatigue, dry cough, dyspnoea, eye lesions (uveitis), lupus pernio (blue red nodules on nose/ cheeks)

103
Q

What does a CXR show in sarcoidosis

A

Bilateral hilar adenopathy+ pulmonary infiltrates

104
Q

What is the diagnostic investigation for sarcoidosis and what does it show

A

Biopsy shows non-caseating granuloma

105
Q

What blood levels are raised in sarcoidosis

A

Serum Ca
Serum Ace (granulomas)

106
Q

Name 4 granulomatous diseases

A

TB (Casting)
Crohn’s
Sarcoidosis
Leprosy

107
Q

Treatment for symptomatic sarcoidosis

A

Corticosteroids

108
Q

What traid do you see in Lofgrens syndrome

A

Bilateral hilar lymph node infiltration
Erthyema nodosum
Acute polyarthritis (mc ankles)

Is an acute form of sarcoidosis

109
Q

What type of hypersensitivity is hypersensitivity pneumonitis

A

Type 3 (immune Ab-Ag complex deposition @ lung tissues causes hyperresponsive)

110
Q

Risk factor for hypersensitivity pneumonitis

A

Farming/ bird-keeping

111
Q

What is most common hypersensitivity pneumonitis

A

Farmers lung

112
Q

What type of hypersensitivity is good pastures syndrome

A

Type 2

113
Q

What antibody is present in good pastures

A

Anti-GBM (attacks lung + kidneys)

114
Q

What lung + kidney damage do you see on biopsy in good pastures

A

Lung fibrosis
Glomerular nephritis

115
Q

What is pneumonia

A

Infection of the lung causing fluid exudation into alveoli due to inflammation. Typically from inhaled pathogens

116
Q

What are the 2 types of pneumonia

A

Community-acquired pneumonia
Hospital-acquired pneumonia

117
Q

How long after admission to be classed as hospital-acquired pneumonia

A

> 48 hours

118
Q

What bacteria cause CAP with MC

A

S. pneumaniae MC
H. Influenzae
Mycoplasma pneumonia

119
Q

What pneumonia-causing bacteria is associated with air conditioning/ coming back from Spain

A

Legionella

120
Q

What type of bacteria mostly cause HAP

A

Gram -ve aerobic bacilli
P. aeruginosa
E. coli
Klebsiella

121
Q

Which pneumonia is more severe and why

A

HAP:- organisms are more drug resitant

122
Q

RF for pneumonia

A

Immunocompromised (HIV), IVdu, pre-existing resp disease, v young/ old

123
Q

Pathology of typical pneumonia

A

Bacteria invades and exudate forms inside alveoli lumen + sputum

124
Q

Pathology of atypical pneumonia

A

Bacteria invade and exudate forms in interstitium of alveoli + dry cough

125
Q

What are Sx of typical pneumonia

A

Productive cough with nasty-coloured sputum
Pyrexic
Pleuritic chest pain
tachypnoea
Confusion in elderly

126
Q

What is 1st line + diagnostic test for pneumonia and what does it show

A

CXR shows consolidation
air bronchogram:- fluid-filled surrounding alveoli make air-filled bronchi visible

127
Q

What can you do to Identify organisms in pneumonia

A

Sputum sample + culture

128
Q

What is the scoring system to assess the severity of CAP

A

CURB65
Confusion
Urea nitrogen
RR> 30
BP <90/60 (either)
65 y/o +

129
Q

Treatment for pneumonia

A

O2 (94-98), broad spec Abx, NSAIDS,

130
Q

What is antibiotic treatment based on curb score for CAP (what is exception)

A

0 to 2:- Amoxicillin
3-5:- Co-Amoxiclac+ clarithromycin

exception:- legionella needs clarithromycin 1st line

131
Q

What is aspiration pneumonia

A

Seen in Px w/ stroke, bulbar palsy:- aspiration of gastric acid contents into lungs

132
Q

Which pathogens cause atypical pneumonia

A

Mycoplasm pneumoniae
Chlamydia pneumoniae

133
Q

What type of bacteria cause TB

A

Mycobacterium tuberculosis complex

134
Q

What are the mycobacterium tuberculosis complex pathogens

A

M. tuberculosis (MC)
M. africanum
M. microtis
M. bavis (unpasteurised milk)

135
Q

Describe the microbiology of M. Tuberculosis

A

Has waxy coating makes gram stain ineffective.
Are acid-fast bacilli
Use Zeihl-Neelsen stain
Turn bright red

136
Q

Where is TB common

A

China, India, Pakistan
Subsaharan Africa

137
Q

How does TB spread

A

Airborne

138
Q

What are RF for TB

A

Country + travel associated
Immunocompromised
Homeless/ crowded housing
IVDU
Smoking + alcohol
Higher age

139
Q

What is the pathology of TB

A

TB phagocytosed but resists killing then forms caseous granulomatous. T cells recruited + central region of granuloma undergoes caseating necrosis. Primary Gohn Focus in upper parts of the lung. Ghon focus spreads to nearby lymph nodes (ghon complex). In most patients infection contained within granulomas (latent TB) if spreads systemically (miliary TB)

140
Q

Pulmonary Sx of TB

A

Night sweat and weight loss
Pyrexia, chest pain and Px looks unwell

141
Q

What are extrapulmonary Sx of TB

A

Meningitis, skin change, TB pericarditis, joint pain

142
Q

What investigations can be performed in suspected TB

A

Mantoux skin test
Sputum culture X3
CXR biopsy

143
Q

What is the treatment for TB

A

RI(6)PE(2)
Rifampicin:- 6 months
Isoniazid:- 6 months
Pyrazinamide:- 2 months
Ethambutol:- 2 months

144
Q

What is a SE of rifampicin

A

Bloody urine

145
Q

SE of Isoniaziol

A

perIpheral neuropathy
(Tingling hands+ feet)

146
Q

SE of Pyramidine

A

hePatitis

147
Q

SE of ethambutamol

A

Eye problems

148
Q

What is Granulomatosis with polyangiitis

A

Granulomatous Vasculitis affecting small+ medium vessels typically causes ENT, lung + kidney Sx

149
Q

What antibodies is Granulomatosis with polyangiitis associated with

A

c-ANCA

150
Q

What are the Sx of Granulomatosis with polyangiitis

A

Saddle-shaped nose, ear infection
Diffuse alveolar haemorrage
Glomerular nephritis

151
Q

What inheritance pattern of cystic fibrosis

A

Autosomal reccesive

152
Q

What chromosome is mutated in cystic fibrosis

A

Chromosome 7

153
Q

What are the risk factors for cystic fibrosis

A

fHx, caucasian

154
Q

What is the pathophysiology of cystic fibrosis?

A

Defective CFTR gene usually secrets Cl- actively and Na+ passively into ductal secretions making them thin and watery. Now secretions are thicker with increased Na+ and Cl- retention.

155
Q

What are resp Sx of cystic fibrosis?

A

Thick+ sticky sputum, recurrent upper resp tract infections
Bronchiectasis

156
Q

What do you see in neonates with cystic fibrosis

A

Meconium ileus:- first stool to thick/ sticky to pass through bowel- leads to bowel obstruction

Failure to thrive
Finger clubbing
Abdominal distention

157
Q

GIT Sx of cystic fibrosis

A

Thick secretions
Pancreatic insufficiency
Bowel obstruction

158
Q

Other Sx of CF thats not resp/ GIT

A

Atrophy of vas deferens+ epididymis (infertility)
Very salty sweat

159
Q

What is the common mutation that causes CF

A

Delta-f508 on chromosome 7:- codes for CFTR protein

160
Q

What is GS investigation for CF (with levels)

A

Sweat test:- Na+ and CL->60mmol/L in children

161
Q

Other investigations to carry out other than sweat test in CF

A

Faecal elastase reduced due to pancreas blockage
Genetic testing
Blood spot test (picks up mosts cases)

162
Q

Non-pharmological Management for CF

A

Non-curative
Chest physio, no-smoking, exercise
High-calorie diet

163
Q

Pharmacological management of CF

A

Bronchodilator
Prophylactic flucloxacillin
Nebulised dornase alfa
Vaccines (varicells, influenzae, pneumocaccal)
Enzyme replacements

164
Q

How many children have cystic fibrosis

A

1 in 2,500

165
Q

How many people are carriers of CF

A

1/25

166
Q

Causes of finger clubbing in Children

A

Hereditary clubbing
Cyanotic heart disease
Infective endocarditis
CF
TB
IBD
Liver cirrhosis

167
Q

What is pleural effusion?

A

Excess fluid accumulation between the viseral+ parietal plural layer

168
Q

In plural effusion, what are the 2 types of fluid?

A

Transudative (protein <25g/L) (TRANSparent)
Exudative (protein >35g/L) (Cloudy)

169
Q

What causes transudative pleural effusion

A

Increase in hydrostatic pressure or decrease in oncotic pressure
CHF
Liver cirrhosis
Nephrotic syndrome

170
Q

What causes exudative plural effusion

A

Inflammation causing increase in vascular permeability
Cancer
TB
Pnuemonia

171
Q

Sx of Plural effusion

A

Dyspnoea, pleuritic chest pain, cough, decrease in breathing sounds
Dull percussion on ipsilateral side

172
Q

What is GS and 1st investigation in suspected pleural effusion

A

CXR

173
Q

What does CXR show in pleural effusion

A

Blunting of costophrenic angles
Excess fluid appears white
Large effusions have meniscus
Massive effusions have tracheal and mediastinal deviation

174
Q

Other than CXR, what investigation do you perform in pleural effusion

A

Thoracentesis (aspiration of pleural fluid)
pH, lactate, WCC, Microscopy

175
Q

What is the treatment for pleural effusion

A

Chest drain
If recurrent- pleurodesis:- surgical fusing of layers to prevent fluid build-up

176
Q

What is a pneumothorax?

A

Excess air accumulation in pleural space causes collapse

177
Q

What is the typical presentation of pneumothorax

A

Tall thin males with a connective tissue disorder (Marfan’s) +/- smoker, some kind of trauma

178
Q

What is primary vs secondary pneumothorax

A

Primary:- spontaneous
Secondary:- trauma/ pathology

179
Q

Sx of plueral effusion

A

SOB, one-sided sharp pleuritic chest pain, decreases in breathing sounds
Hyporesonant percussion ipsilateral

180
Q

What is GS+ 1st investigation for pneumothorax

A

CXR

181
Q

What do you see on CXR in a pneumothorax?

A

Excess fluid appears black
Tracheal deviation to otherside

182
Q

What is the most sensitive imaging for small pneumothorax

A

CT

183
Q

What are 2 types of pneumothorax

A

Simple
Tension

184
Q

Simple vs tension pneumothorax

A

Simple:- Non-medical emergency, little tracheal diversion, air can flow in+ out of valve, unlikely to worsen
Tension:- Medical emergency with tracheal diversion, one-way vale growths with every breath

185
Q

Treatment for a simple pneumothorax

A

Small:- Self healing
Larger:- Needle decompression
-chest drain (longer term)

186
Q

Treatment for tension pneumothorax

A

If obvious go straight to Tx don’t bother with CXR
Large bore cannula into 2nd intercostal space @ midclavicular line
Needle decompress then chest drain

187
Q

What is resting mPAP that shows Pulmonary Htn

A

> 25mmHg

188
Q

How is pulmonary pressure measured

A

Right heart catheterisation

189
Q

Pre capillary causes of pulmonary Htn

A

Pulmonary Emboli
Primary hypertension

190
Q

Capillary + lung causes of Pul Htn

A

COPD
Asthma

191
Q

Post capillary cause of pul Htn

A

Left heart failure

192
Q

What can cause chronic hypoxia

A

COPD, altitude

193
Q

What Signs/ symtptoms of Pul Htn

A

Exertional dyspnoea + fatigue
Tachycardia, Hepatomegaly
RHF signs:- Raised JVP
Peripheral oedema
Louder S2

194
Q

What are initial investigation to carry out in suspected Pul Htn

A

CXR, ECG, ECHO

195
Q

What do you see on CXR and echo in Pul Htn

A

Echo:- RVH
CXR:- RVH, enlarged proximal pulmonary artery

196
Q

What ECG changes do you see in Pul Ht

A

Large R waves or right sided leads (v1-v3)
Large S waves on left side leads (v4-v6)
Right axis deviation
RBBB

197
Q

What is the diagnostic/ GS investigation for Pul Htn

A

Right heart catheter

198
Q

Treatment for Pul Htn

A

Phosphodiesterase-5 inhibitor:- sildenafil (VIAGRA)
CCB (amlodipine)
Endothelin 1 antagonist/ prostaglandin analogues
Diruretics for oedema

199
Q

What is the treatment for Granulomatosis with polyangiitis

A

Corticosteroids