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Medicine > Resp > Flashcards

Resp Flashcards

1
Q

What are the ABG findings in T1RF?

A

O2 <8 kPa

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2
Q

What are the ABG findings in T2RF?

A

O2 <8 kPa, CO2 >6.5 kPa

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3
Q

In summary, what sort of problem is T1RF?

A

Obstruction problem

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4
Q

What is shunting?

A

Alveoli are perfused but not ventilated, eg due to ARDS or consolidation.
Hypoxia can’t be corrected by increasing FiO2 because poorly-ventilated alveoli will continue to lower systemic pO2

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5
Q

Physiological causes of T1RF

A

Hypoventilation
V/Q mismatch
Shunting
Decrease in inspired pO2

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6
Q

Causes of T1RF

A

Severe acute asthma
Pneumonia
PE
Pulmonary oedema

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7
Q

Causes of T2RF

A

COPD
Asthma
Pneumonia
Pulmonary fibrosis
Obstructive sleep apnoea
Decreased respiratory drive: trauma, CNS trauma, sedatives
Neuromuscular: cervical cord lesion, MG, GBS, diaphragm paralysis

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8
Q

Symptoms and signs of hypoxia

A

SOB, restless/ agitated, reduced GCS, cyanosis

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9
Q

Symptoms and signs of hypercapnia

A

Headache, reduced GCS, tachycardia with bounding pulse, tremor in hands, peripheral vasodilatation, papilloedema

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10
Q

Investigations for hypoxia?

A

ABG
Sputum/ spirometry
ABG
CXR

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11
Q

Management of hypoxia

A

High-flow oxygen

Re-check ABGs

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12
Q

What are the options for NON-invasive respiratory support?

A

Humidified supplemental O2 (for T1RF)
CPAP (for T1RF)
NIV (BIPAP) (for T2RF)

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13
Q

Explain CPAP

A

Expiration against a resistance

opens up alveoli, forces out pulmonary oedema, decreases work of breathing

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14
Q

Explain BIPAP

A

Positive pressure support for inspiration in addition to patient’s own breathing
(clears CO2, decreases work of breathing)

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15
Q

How is INVASIVE mechanical ventilation different?

A

Can set a desired pressure, desired tidal volume, desired RR

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16
Q

What are the indications for invasive mechanical respiration?

A

NIV not tolerated
Severe respiratory failure/ increased work of breathing
Airway protection (eg GCS <8 or burns)
Control pO2 and pCO2 in acute neurological disesase/ increased ICP

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17
Q

Contraindications of invasive mechanical ventilation

A

Tension pneumothorax

Volutrauma, barotrauma

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18
Q

How is invasive mechanical ventilation provided?

A

Most will have ETT (requires anaesthesia, sedation)

Long-term need tracheostomy (little/ no sedation, improved comfort, improved nursing/ oral care)

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19
Q

4 types of pulmonary embolism

A

Thrombosis (usually distant vein)
Fat (fractures)
Amniotic fluid
Air (neck vein cannulation/ bronchial trauma)

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20
Q

Presentation of PE

A

Large can cause sudden death/ small can be hard to diagnose

Symptoms: SOB, dyspnoea, chest pain (pleuritic or retrosternal), cough, haemoptysis

Signs: 
tachypnoea, tachycardia, hypotension
hypoxia
pyrexia
pleuritic pain
increased JVP, gallop rhythm
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21
Q

Investigations for PE?

A

Two-level Wells Score:

LIKELY
CTPA + leg USS
anticoag to buy time
[if can’t have contrast/ renal impairment: V/Q spectroscopy]

If UNLIKELY: D-dimer

ABG
Bloods: FBC, U&amp;Es, baseline clotting, D-dimers, troponin + BNP may be raised due to strain
ECG
CXR
Echo will show thrombus

Consider:
looking for ca (hx, CXR, mammogram, abdomino-pelvic CT)
antiphospholipid antibodies, thrombophilia screen

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22
Q

How might a PE present on ECG?

A

Tachy
RBBB
R axis deviation
S1, Q3, T3

Large PE may show ST depression

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23
Q

How do you manage PE?

A

Ideally LMWH or fondaparinux (at least 5 days whilst awaiting warfarin)

Warfarin for 3 months - INR 2-3

Maybe rivoraxaban (prophylactic)
Surgical embolectomy/ IVC filters
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24
Q

What are the signs of pulmonary oedema?

A

Resp distress: pale, sweaty, tachypnoeic, tachycardic
May be cyanosed, low sats <90% RA
May be signs of associated cause
Basal or widespread crackles
Cardiogenic shock: hypotension, oliguria, low CO2

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25
Q

Investigations for pulmonary oedema

A

Bloods: FBC, U&Es, glucose, cardiac enzymes

ECG

CXR

Echo (to establish LV function once stable)

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26
Q

How does pulmonary oedema appear on CXR?

A

Bilateral patchy shadowing
Kerley B lines
Batwings (increased vascular shadowing)
Pleural effusions

If cardiogenic, maybe cardiomegaly

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27
Q

How do you manage pulmonary oedema?

A

Depends on cause but…

Fluid balance

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28
Q

What is a pneumothorax?

A

Air in pleural space

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29
Q

What are the causes of pneumothorax?

A

SPONTANEOUS: rupture of pleural pleb (congenital weakness) - tall, slim males - often apical

SECONDARY: COPD (emphysematous bullae), TB, pneumonia, bronchial Ca, sarcoidosis, CF, trauma

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30
Q

Causes of pulmonary oedema: lymphatic obstruction

A

Mediastinal carcinamatosis

Silicosis

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31
Q

Causes of pulmonary oedema: neurogenic

A

Status epilepticus
Head injury
Cerebrovascular insult

These happen within a few hours

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32
Q

Causes of pulmonary oedema: increased capillary permeability

A 
ARDS
Increased altitude
Inhaled/ aspirated toxins
Radiation
Liver failure
Fat/ amniotic embolus
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33
Q

Causes of pulmonary oedema: increased pulmonary capillary pressure

A

Heart: MI/ ACS, valvular disease (regurg or severe AS), cardiomyopathy, PE, acute arrhythmia, tamponade, dissection, right-output HF (septicaeia, thyrotoxicosis, anaeia)

Renal: AKI, CKD, renal artery stenosis

Iatrogenic: fluid overload

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34
Q

Causes of pulmonary oedema: airway obstruction

A

Acute or chronic upper airway obstruction

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35
Q

What is ARDS?

A

Non-cardiogenic pulmonary oedema - 30-45% mortality

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36
Q

What are the causes of ARDS?

A

Pulmonary causes: mechanical ventilation, trauma, near drowning, smoke inhalation, gastric contents aspiration, infection

Extrapulmonary causes: Gram-negative septicaemia, pancreatitis, burns, CABG, perforated viscus, DIC, O2 toxicity, drug OD

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37
Q

Management of ARDs

A 
Identify cause + support
-ve fluid balance, as in pulm oedema
PEEP: prevent alveolar walls from collapsing during expiration
Vasodilators
Steroids (late stages)
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38
Q

Presentation of pneumothorax

A

Asymptomatic - esp if small or they’re healthy

or

Sudden unilateral chest pain, SOB, sudden deterioration of existing lung problem

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39
Q

How does pneumothorax present on examination?

A

Reduced chest expansion on that size - hyperresonance - reduced, absent breath sounds

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40
Q

How does pneumothorax present on CXR?

A

Are of increased lucency without lung markings, edge of lung may be visible away from chest wall

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41
Q

Management of pneumothorax

A

Small: often no treatment, r/v 7-10 days
Large: admit for aspiration

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42
Q

Common causes of tension pneumothorax

A

Positive pressure ventilation, stab, rib fracture

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43
Q

Management of tension pneumothorax

A

Large-bore cannula, 2nd ICS, MCL

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44
Q

How does tension pneumothorax present on examination?

A

Tracheal deviation (pulled to contralateral side)
Hyperresonance
Absence of breath sounds
Widened ICS spaces on contralateral side

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45
Q

How does tension pneumothorax present?

A

As pressure increases, venous return to heart is impaired:

Dyspnoea, chest pain, cyanosis, even cardiac arrest

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46
Q

What is a tension pneumothorax?

A

A chest or lung wall injury allowing air into the pleural space. The air rises above atmospheric pressure, compressing the lung and venous return to the heart. Air enters but doesn’t leave.

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47
Q

Which side do aspirated foreign bodies go?

A

R

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48
Q

Presentation of foreign body aspiration?

A

Upper airway: stridor, respiratory distress, cyanosis, resp arrest

Beyond carina: recurrent cough, pneumonia, SOB, haemoptysis

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49
Q

Management of foreign body aspiration

A

Heimlich - suction - bronchoscopy - abx to treat/ prevent pneumonia

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50
Q

Investigations for foreign body aspiration

A

Bloods (inflammatory response) - CXR (if radio-opaque, if pneumonia) - bronchoscopy (direct visualisation)

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51
Q

What is OSA?

A

Intermittent and repeated upper airway collapse during sleep

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52
Q

What should you look for when examining for OSA?

A

No specific signs

Look for: neck fat deposition, small mouth, big tongue, polyps etc

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53
Q

Gold standard for OSA?

Ix

Mx

A

Ix Polysomnography (electrodes on eyes and chin)

Mx CPAP

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54
Q

What are the risks associated with OSA?

A

HTN, CVD, obesity, DM, asthma

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55
Q

What are the options for treating OSA?

A

Lifestyle/ avoid supine sleeping
CPAP

Consider:
Modafinil for sleepiness
Surgery

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56
Q

What is central sleep apnoea?

A

Airway patent but no respiratory effort

Causes hypercapnia that arouses pt

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57
Q

What are the causes of pulmonary hypertension?

A

COPD, interstitial lung disease, others

L cardiac disease, secondary to congenital heart disease

Portal HTN

Idiopathic is rare - poor prognosis - associated with CREST/ autoimmune

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58
Q

How does pulmonary HTN present?

A

Non-specific insidious signs (often diagnosed late)
SOB, malaise, presyncopal

Often picked up as signs of cor pulmonale

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59
Q

How is pulmonary HTN investigated?

A

R heart catheterisation confirms

PAH diagnosed by exclusion: ECG, echo, CXR, CT chest, autoantibodies

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60
Q

How is pulmonary HTN managed?

A

Warfarin to minimise risk of thrombosis
CCBs to decrease pressure of pulmonary vasculature
HF should be treated aggressively

Poor prognosis (2-3 years) - death usually due to RHF

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61
Q

Incidence of asthma

A

20% kids

5% adults

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62
Q

Define asthma

A

Reversible airflow obstruction, airway hyper-responsiveness, inflamed bronchi

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63
Q

What is extrinsic vs intrinsic asthma?

A

EXTRINSIC: atopic childhood asthma, remits in teens

INTRINSIC: usually adult, progressive, less responsive to treatment

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64
Q

How to diagnose asthma?

A

at least 15% improvement in FEV1 after bronchodilator use

There will be an obstructive picture (FEV1/ forced vital capacity reduced)

Residual volume may be increased due to air trapping

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65
Q

Management of asthma (adults and children over 5)

A

Avoid triggers!

STEP 1: inhaled short-acting beta2 agonist - PRN

STEP 2: add inhaled steroid (200-800 mcg) - 400 usually ideal, but titrate

STEP 3: Add LABA
Good response: continue!
Quite good response: continue/ ensure steroids at 800 mcg
No response: steroids at 800 mcg, stop LABA
From this step eligible for SMART (single maintenance and reliever therapy)

STEP 4: add leukotriene receptor antagonist, theophylline, beta2 agonist pill
steroids up to 2000 mcg/day

STEP 5: add daily oral steroid (+ 2000 mcg/day inhaled)

TRY TO STEP DOWN WHERE POSSIBLE

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66
Q

What should every asthmatic have?

A

Asthma action plan

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67
Q

Definition COPD

A

airflow obstruction with little or no reversibility

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68
Q

Incidence of COPD

A

5-15% industrialised countries

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69
Q

What should be considered cause of COPD in under 40s?

A

alpha-1-antitrypsin deficiency (proteases overwhelm antiproteases = increased compliance)

panacinar picture

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70
Q

What are the traditional forms of COPD?

A

Blue bloaters: CHRONIC BRONCHITIS - small airways obstructed by mucus plugs & bacterial colonisation - crackles/ wheeze - peripheral oedema

Pink puffers: EMPHYSEMA - proteases overwhell=m antiproteases - cachectic, pursed-lip breathing, accessory muscles, barrel chest, decreased breath sounds

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71
Q

Signs of COPD

A

I: central cyanosis - barrel chest - use of accessory muscles - pursed lip breathing - flapping tremor - tachypnoea - persistent cough - chronic sputum production - weight loss

P: tacycardia - tracheal tug - reduced expansion

P: hyperresonant lung fields (unless consolidation)

A: wheeze - prolonged expiration

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72
Q

Investigations for COPD

A 
Spirometry (severity based on FEV1)
Pulse oximetry
Sputum
Bloods: FBC, alpha1-antitrypsin level
CXR
ECG/ Echo for cor pulmonale
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73
Q

Management of COPD

A

Yearly influenza jab, 5-yearly pneumococcus jab

Pulmonary rehab: 6-12 weeks, work on exercise tolerance

Medications (these are all symptomatic so only continue if iprovement after 4 weeks):

STEP 1 (breathlessness or exercise limitation): SABA or SAMA

STEP 2 (exacerbations or persistent breathlessness)

FEV > 50% - LABA/ LAMA

FEV < 50% - LABA + ICS / or LAMA (combination inhaler - ICS not used alone in COPD)

STEP 3

LABA –> LABA + ICS
Others –> LAMA + LABA + ICS

ORAL: theophylline, carbocisteine (mucolytic), rescue pack abx

SEVERE/ END-STAGE: home O2 (15h/ day)

Lung transplant an option

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74
Q

Complications of COPD

A

Acute worsening (usually infection, eg influenza or haemophilus influenzae)
T2RF
cor pulmonale

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75
Q

Example SABA

A

Salbutamol

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76
Q

Example SAMA

A

Ipratropium

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77
Q

Example LABA

A

Salmetarol

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78
Q

Example LAMA

A

Tiotropium

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79
Q

Definition cor pulmonale

A

Impairment of right ventricular function as a result of respiratory disease - leading to increased resistance to blood flow in the pulmonary vasculature

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80
Q

General two types of pathology leading to interstitial lung disease

A

Granulomatous or fibrosis

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81
Q

Define pulmonary fibrosis

A

The irreversible end-stage of many respiratory diseases, characterised by scarring of lung tissue which decreases compliance.

An example of interstitial lung disease

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82
Q

Symptoms of pulmonary fibrosis

A

Progressively breathless

Dry, non-productive cough

83
Q

Findings on examination of pulmonary fibrosis

A

Lung expansion is reduced

Fine end-inspiratory crackles

84
Q

Investigations of pulmonary fibrosis

A

CXR may show infiltration in basal area

Gold standard is HRCT: honeycomb, ground-glass appearance (needs specialised radiologist)

Biopsy useful but many patients too frail

Lung function tests show restrictive pattern - good to monitor disease progression

85
Q

Management of pulmonary fibrosis

A

Avoid triggers
Pulmonary rehab
Steroids may dampen inflammatory response
Home oxygen may help

86
Q

Define the pneumoconioses

A

An example of interstitial lung disease. A group of disorders caused by inhalation of mineral or biological dusts - incidence is decreasing as working conditions improve

Examples are coal worker’s pneumoconiosis and asbestosis

87
Q

What is extrinsic allergic alveolitis?

A

An example of interstitial lung disease. A hypersensitivity pneumonitis (type III reaction). Results from individual already being sensitised to the inhaled antigen.

Eg farmer’s lung (mouldy hay) and bird fancier’s (bird faeces)

88
Q

What is the pathogenisis of extrinsic allergic alveolitis?

A

Neutrophils infiltrate small airways and alveolar walls after antigen exposure

Lymphocytes and macrophages then infiltrate, forming non-caseating granulomas

May resolve, or lead to pulmonary fibrosis

89
Q

Investigations for extrinsic allergic alveolitis

A

Bloods: polymorph leucocyte count, precipitating antibodies (evidence of exposure, not disease)

Lung function tests show restrictive pattern

CXR: nodular shadowing
HRCT may show disease if CXR normal

Bronchoalveolar lavage

90
Q

Management of extrinsic allergic alveolitis

A

/most will regress if exposure to antigen prevented

CS may speed up recovery

91
Q

Clinical features of extrinsic allergic alveolitis

A

Cough, SOB
Malaise, fever
Coarse end-inspiratory crackles

92
Q

3 pathological features of asthma

A

Bronchospasm - mucus plugging - smooth muscle hypertrophy

93
Q

Describe the early and late responses in asthma

A

EARLY RESPONSE:
release of preformed mediators (predominantly mast cells) causes vascular leakage and smooth muscle contraction within about 15 mins
(1-2 hours to return to baseline)

LATE RESPONSE:
influx of inflammatory cells (predominantly eosinophils) - these release inflammatory mediators that that cause airway narrowing in 3-4 hours
(maximally at 6-12 hours)

94
Q

When is the annual influenza epidemic?

A

Autumn/ winter

95
Q

When is influenza infective?

A

1 day prior to symptoms

96
Q

When do influenza symptoms resolve?

A

After about 1 week

97
Q

Common complications of influenza

A

Secondary bacterial pneumonia (Staph aureus)
Otitis media
Sinusitis
Encephalitis

98
Q

Groups most at risk of influenza

A 
Children under 2
Elderly
Underlying lung disease
Heart disease
Diabetes
Immunocompromised
99
Q

How is influenza diagnosed during pandemics?

A

Nasopharyngeal aspirate

100
Q

Define pneumonia

A

The presence of symptoms and signs consistent with acute LRTI in association with new radiographic shadowing for which there is no alternative explanation.
UK’s fifth leading cause of death

101
Q

Common risk factors for pneumonia

A

Related to processes that impair lung’s natural immune defences

Age: v young/ old

Lifestyle: smoking, alcohol

Preceding viral infection

Respiratory: any existing disease

Immunosuppression

IV drug use (Staph aureus)

Hospitalisation

Underlying predisposing disease: DM, CVD

Swallowing impairment (aspiration pneumonia)

102
Q

What differentiates diagnosis of HAP from CAP?

A

Been in hospital over 48hrs (nursing home acquired is an important sub-type)

103
Q

Common causes of CAP

A 
Streptococcus pneumoniae
Haemophilus influenzae
Mycoplasma pneumoniae
Chlamydophila pneumoniae
Respiratory viruses
104
Q

Common causes of HAP

A

Staph aureus
Gram negative enterobacteria
Klebsiella
Pseudomonas

105
Q

Common causes of aspiration pneumonia

A

Anaerobes
Gram-negative enterobacteria
Staph aureus

106
Q

Common causes of pneumonia in the immunocompromised

A 
CAP organism
HAP organisms
Viruses (CMV, VZV)
Fungi (aspergillus) 
Mycobacteria
107
Q

Atypical pneumonia: Mycoplasma pneumoniae

A

Epidemics every 3-4 years
Young patients
Flu-like symptoms, followed by persistent dry, hacking cough
Extrapulmonary features: haemolytic anaemia, GBS…

Usually resolves spontaneously over few weeks

108
Q

Atypical pneumonia: Legionella pneumophila

A

Severe pneumonia with high mortality

Extrapulmonary features: D&V, neurological deficit (including focal), hepatitis, hyponatraemia

109
Q

How does pneumonia present on examination?

A

Obs: pyrexial, tachycardic, tachypnoeic
(diagnosis unlikely if no focal chest signs and obs normal)

Resp exam: lung expansion is reduced, dull to percuss, creps, pleural rub, may be coarse crackles as resolves

Confusion (esp elderly)

Look for extrathoracic signs if atypical suspected

110
Q

Ix for pneumonia

A

If managed in community, usually not needed

AMTS
Sputum: examination and culture
ABG if signs of respiratory failure
ECG: AF common

Urine: pneumococcal and legionella urinary antigen tests

Bloods:
FBC
CRP/ ESR
U&amp;Es (dehydration common)
LFTs (can become deranged in atypicals)

Cultures: if pyrexial

CXR (plus follow-up in 6 weeks after recovery)
Consider aspiration of pleural fluid

111
Q

Assessing whether CAP needs hospital admission

A

CRB-65

AMTS 8 or less, or new disorientation in person, place or time

RR above 30

Systolic BP below 90 (or diastoilc below 60)

65 years +

Consider hospital admission if 2 or more

112
Q

Management of CAP in community

A

Rest, drink lots, no smoking

Seek advice if no improvement in 72h

113
Q

Management of CAP in hospital

A

Oxygen for hypoxia
Fluids for dehydration
NSAIDs and paracetamol for mild pleuritic pain
Nebulised saline may help

114
Q

Antibiotics for low-severity CAP

A

5-day course amoxicillin (macroglide or tetracycline if allergic)

Add flucloxacillin if staphylococcal infection suspected

115
Q

Name of atypical pneumonia caused by exposure to ill birds

A

Chlamydophila psittaci

116
Q

Atypical pneumonia: Chlamydia pneumoniae

A

Gradual onset, biphasic (may improve then get worse again)
Incubation 3-4 weeks

Initial non-specific URTI followed by bronchitic symptoms
Most ppl are quite well
Scanty sputum, hoarseness, headache
Symptoms may persist for weeks/ months

117
Q

Complications of pneumonia

A 
Pleural effusion (usually sterile)
Empyema
Lung abscess
DVT
Septicaemia and its spread to cause pericarditis, endocarditis, osteomyelitis, septic arthritis, cerebral abscess, meningitis etc.
Post-infective bronchiectasis
AKI
118
Q

Define TB

A

A chronic granulomatous disease caused by bacteria of the Mycobacterium tuberculosis complex (M. tuberculosis, M. bovis and M. africanum)

119
Q

Describe the difference between secondary TB and miliary TB

A

Secondary is due to subsequent reactivation of semi-dormant M.tuberculosis. Usually reactivated by impaired immune function. Reactivation usually occurs in the lung apex and can spread locally or to distant sites.

Miliary occurs when primary infection is inadequately contained and it invades the bloodstream, resulting in severe disease

120
Q

Most common site of extrapulmonary TB

A

Genitourinary, presenting with pyuria

121
Q

Presentation of primary TB

A

Often asymptomatic or general malaise, fever etc.

122
Q

CXR findings in TB

A

Patchy or nodular shadows in the upper zones, loss of volume, fibrosis, cavitation

Primary TB: central apical portion with a L lower lobe infiltrate + pleural effusion

Reactivated TB: central apical lesion, no pleural effusion

Severe: miliary TB (uniform 1-10 mm shadows throughout lungs)

Extrapulmonary: may still have evidence or original lesion

123
Q

Investigations for TB

A

Sputum MC&S with Ziehl-Neelson stain: at least 3 samples, including early morning - ideally before treatment or within 7 days
(If unable to give, consider broncholavage)

CXR

Bloods: check HIV, hep B and hep C status

124
Q

Management of TB

A

Start and complete meds if clinical signs and symptoms, regardless of sputum culture results

RIPE
Rifampicin - 6 months
Isoniazid - 6 months
Pyrazinamide - 2 months
Ethambutol - 2 months

If co-existing HIV, see HIV guidance

Give prophylactic 10 mg pyridoxine if risk factors for peripheral neuropathy (worsened by isoniazid)

LFTs should be monitored: RIP cause hepatic toxicity, monitor more frequently if alcoholic - expect R to cause some disturbances in first 2 months
U&Es ethambutol should be avoided in renal failure
Visual acuity, colour blindness + visual fields should be checked - ethambutol

Notifiable disease

Contact tracing: Mantoux test for all close contacts - may be positive if had BCG, so interferon gamma testing is second-line

125
Q

Who is offered the BCG?

A

Newborns in high-risk areas
Health workers
New immigrants from countries with high levels of TB
Close contacts of pts with pulmonary TB

126
Q

Signs and symptoms of lung abscess

A

Acute: malaise, anorexia, fever, productive cough, copious foul-smelling sputum

Chronic: dullness to percus, pallor due to anaemia, clubbing

127
Q

Causes of lung abscess

A

Aspiration of infected material
Complication of pneumonia, bronchiectasis or TB
Bronchial obstruction
Pulmonary infarction

128
Q

Define suppurative lung disease

A

range of lung diseases characterised by a chronic wet cough and progressive lung damage

129
Q

Clinical features of bronchiectasis

A

Cough - often productive of foul-smelling sputum
Haemoptysis
Clubbing
Crackles on auscultation - usually lower lobes affected

130
Q

Define bronchiectasis

A

Abnormal and permanent dilation of bronchi

131
Q

Causes of bronchiectasis

A

Acquired:
usually caused by severe childhood illness (pneumonia, measles, whooping cough),
bronchial obstruction followed by infection distal to obstruction (foreign object, tumour, lymph nodes)
bronchopulmonary aspergillosis

Congenital:
problems with ciliary function (eg Kartanger’s)
IgA and other primary antibody deficiency

132
Q

Who should be investigated for bronchiectasis?

A

In adults:
persistent productive cough, esp if young and associated with haemoptysis
pts with COPD who are non-smokers or have frequent exacerbations

133
Q

Investigations for bronchiectasis

A 
Sputum MC &amp; S
Spirometry (obstructive pattern)
Tests for CF
Check immunoglobulins (may demonstrate deficiency)
Aspergillus-specific Ig

CXR: may show bronchial wall thickening, cystic spaces if advanced
HRCT

Consider bronchoscopy:
?foreign object
Bronchoalveolar lavage

134
Q

Management of bronchiectasis

A

Control of infection

Bronchodilators may be helpful

135
Q

Incidence of CF

A

Prevalence of heterozygous carriers is 4%

1:2000 births

136
Q

CF sufferers prone to which infection?

A

Psuedomonas aerginosa

137
Q

Clinical presentation of CF

A

In infancy, GI manifestations: meconium ileus, malabsorption

As older, problems with lungs occur - increasingly more infections - then clubbing and dyspnoea

Almost all men infertile, women subfertile

138
Q

Investigations for CF

A 
Genetic screening if family hx
CVS or amnioscentesis prenatally
Guthrie test
Immunoreactive trypsin test or Sweat Test
CXR
139
Q

How does sarcoidosis present?

A

Depends on organ

90% have pulmonary involvement: dyspnoea, chest pain, dry cough

Non-specific: fatigue, malaise, weight loss, lymphadenopathy

140
Q

Common extrapulmonary manifestations of sarcoid

A

Skin: erythema nodosum/ lupus pernio
Arthralgia
Uveitis
Cranial nerve palsies (neurosarcoid)

141
Q

How is sarcoid investigated?

A

Spirometry: restrictive

Bloods: FBC, U&Es, LFTs, bone profile, ESR
Rule out RA and SLE

CXR: hilar lymphadenopathy
HRCT

GOLD STANDARD: biopsy showing epithelioid non-caseating granulomas

142
Q

How does Goodpasture’s present?

A

Haemoptysis (pulmonary haemorrhage), anaemia, haematuria

143
Q

How does Wegener’s granulomatosis present?

A

affects nose, lungs and kidneys
Rhinorrhea, cough, haemoptysis, dyspnoea
wonky nose

144
Q

How does Churg-Strauss Disease present?

A

Triad: late-onset asthma, eosinophilia, small-vessel vasculitis
Vasospasm common: risks of MI, PE, DVT

145
Q

Respiratory manifestation of RA

A 
10-15% have lung involvement
Diffuse pulmonary fibrosis
Pleural fibrosis
Pleural effusions
Rheumatoid nodules in lung
Others
146
Q

Respiratory manifestation of SLE

A

Pleurisy, with or without effusion

147
Q

Respiratory manifestation of systemic sclerosis

A

Pulmonary fibrosis - rapidly-progressing pulmonary hypertension

148
Q

Respiratory manifestation of ankylosing spondylitis

A

Apical lung fibrosis

149
Q

Lung Ca common sites of metastisis

A 
Lymph nodes
Bone
Liver
Adrenals
Brain (personality change, epilepsy, focal neurology)
150
Q

What % smokers get lung cancer?

A

1 in 5

151
Q

Types of bronchial carcinoma?

Which type has best survival rates?

A

Non-small cell: squamous cell - adenocarcinoma - large cell

Small cell

Best survival: squamous cell/ least likely to metastisise

152
Q

Which bronchial ca may present as paraneoplastic syndrome?

A

Squamous cell
Adenocarcinoma
Small-cell

153
Q

Which bronchial ca doesn’t often present with obstructive symptoms?

A

Adenocarcinoma

Non-smoking old women from East Asia
Often peripheral

154
Q

Which bronchial ca is usually diagnosed by process of elimination?

A

Large-cell anaplastic

No typical clinical or radiological findings

155
Q

How does small-cell carcinoma present?

A

Obstructive symptoms
Paraneoplastic
Mets (via lymphatics)

156
Q

What paraneoplastic syndromes are associated with bronchial ca?

A

SIADH

ectopic ACTH

hypercalcaemia (SCC unless bone mets)

hypertrophic pulmonary osteoarthropathy

gonadotrophins (large cell): gynaecomastia + testicular atrophy

157
Q

Pancoast’s tumour is usually which sub-type?

A

66% SCC

158
Q

Who should be referred under TWR?

A

Anyone over 40 with unexplained haemoptysis

Suspicious CXR findings

159
Q

Which lung ca has no staging?

A

Malignant mesothelioma as so aggressive

160
Q

How does COPD affect Hb?

A

Chronic hypoxia causes secondary polycythaemia - Hb raised

161
Q

When may eosinophils be decreased?

A

Steroid therapy

162
Q

How can streptococcal infection be confirmed?

A

ASO titre (anti-streptolysin O)

163
Q

How does salbutamol affect U&Es?

A

Hyperkalaemia

164
Q

How might bronchial ca cause hyperkalaemia?

A

ACTH-secreting tumour

165
Q

Which lung disease affects ACE?

A

Sarcoid

166
Q

When might calcium be raised

A

SCC of lung
Sarcoid
Bone mets

167
Q

How is GA avoided in flexible bronchoscopy?

A

Topical lidocaine to pharynx and vocal cords

168
Q

Differentiating between transudates and exudates

A

Tran- clear - heart failure, liver failure, kidney failure

Exudates- cloudy - lung ca, pneumonia

169
Q

Normal ABG values

A

pH 7.35 to 7.45
paCO2 35 to 45
HCO3 22 to 26

170
Q

Causes of respiratory acidosis

A

IMPAIRED VENTILATION

asthma, COPD, pneumonia, sleep apnoea, acute PE, severe obesity, neuromuscular problems, scoliosis, sedative OD, arrest

171
Q

Causes of respiratory alkalosis

A

HYPERVENTILATION

heart attack, pain, asthma, fever, COPD, infection, PE, pregnancy

172
Q

Causes of metabolic acidosis

A

DKA, lactic acidosis, renal tubular acidosis, severe diarrhoea

173
Q

Causes of metabolic alkalosis

A

excess vomiting, diuretics, adrenal crisis, alcohol abuse, excess sweating

174
Q

Give 3 key facts to encourage smokers to quit

A

Half will die of smoking-related disease
10 years before non-smokers
Slow, painful deaths like COPD

175
Q

How many weeks of stop smoking therapy?

A

2 weeks and then reassess

176
Q

Which stop smoking method for kids and pregnant/ breastfeeding?

A

NRT

177
Q

What is bupropion?

A

Zyban
Antidepressant with cessation effects
8 week course

178
Q

Contraindications of NRT?

A

Severe cardiovascular disease, recent CVA (inc TIA)

179
Q

Contraindications of Zyban?

A

eating disorders

epilepsy/ risk factors for seizures

180
Q

What is varenicline?

A

Champix
Nicotinic Ach receptor with cessation effects
12 week course

181
Q

Contraindications of Champix?

A

Hx of psych illness - needs v close monitoring

Suicide ideation

182
Q

How are beta agonist nebs usually driven?

A

O2 for asthma

Air for COPD

183
Q

What are the issues with e-cigarettes and vaping?

A

Often contain nicotine
Maybe safer than cigarettes

Long-term effects of vapour unknown
Unregulated so not sure what inhaling
No proof they can help stop smoking

184
Q

Average duration of cough

A

3 weeks

185
Q

Average duration of common cold

A

1.5 weeks

186
Q

Features of clubbing

A

beaked nails
loss of angle between nail bed and finger
increased AP width of finger tip
sponginess of proximal nail bed

187
Q

Resp causes of clubbing

A

common:

lung cancer (not small cell cancer)
chronic pulomnary suppuration
bronchiectasis
lung abscess
empyema
Idiopathic pulmonary fibrosis
cystic fibrosis
asbestosis
pleural mesothelioma or fibroma

uncommon:

Cystic fibrosis
Asbestosis
Pleural mesothelioma (benign fibrous type) or pleural fibroma

188
Q

Features more in keeping with asthma than COPD

A

Chronic unproductive cough
Diurnal or day-to-day variation of breathlessness
Waking at night due to SOB/ wheeze

189
Q

Features of poor asthma control

A

Needing SABA 3+ days/week

1+ night per week up at night due to asthma

190
Q

Illustrative examples of V/Q mismatch

A

High, eg asthma

Low, eg PE

191
Q

What do tramtrack marks on CXR signify?

A

Bronchiectasis

192
Q

Most common organism implicated in IECOPD?

A

Haemophilus influenzae

193
Q

Pneumonia mx based on CURB

A

CURB 0-1:
amoxicillin 500 mg TDS or clarithromycin 500 mg BD for 5 days

CURB 2: inpatient
amoxicillin 500 mg TDS AND clarithromycin 500 mg BD for 7 days (oral or IV)

CURB 3: consider ITU
co-amoxiclav 1.2 g TDS AND clarithromycin 500 mg BD for 7 days (IV)

194
Q

Causes of lung abscess

A

Primary disease: existing pneumonia/ untreated pneumonia or lung disease

Secondary disease: aspiration, alcoholics, septic emboli from R-sided infective endocarditis

195
Q

Presentation of lung abscess

A

Swinging fevers, night sweats, productive cough with purulent sputum

196
Q

TB drug side-effects

A

RED-fampicin: reddish orange secretitions, hepatitis

Iso-NEURO-azid: peripheral neuropathy, granulocytosis, hepatitis

Pyr-OUCH-zinamide: hyperuricaemia (causing gout), myalgia, hepatitis

EYE-thambutol: optic neuritis, renal impairment

197
Q

How to avoid peripheral neuropathy with isoniazid?

A

Supplement with vit B6

198
Q

Most commonly implicated organism in Aspergillus-related lung disease

A

Aspergillus fumigatus

199
Q

Presentation aspergillosis

A

haemoptysis, large amount of blood

200
Q

mx aspergilloma

A

surgical removal and long-term itraconazole

201
Q

Triad of Meig syndrome

A

R-sided pleural effusion (transudate), ascites, benign ovarian tumour

202
Q

Which pleural effusions should be aspirated?

A

Exudates (suspect from hx)

203
Q

where to insert large-bore cannula in tension pneumothorax?

A

2nd ICS, MCL

204
Q

where to insert chest drain?

A

3-5th ICS, MAL

Medicine (30 decks)

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