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Year 3 Medicine > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What antibiotic would be given to a patient with a CURB score of 2?

A

oral/IV amoxicillin and claritromycin
or just clarithromycin if pen allergic

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2
Q

What are the classical findings on respiratory examination of a patient with COPD?

A

Reduced circo-sternal distance <3cm
Hyper-resonant percussion note
Use of accessory muscles for respiration

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3
Q

What lung cancer has the strongest relationship to smoking?

A

Small cell lung cancer

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4
Q

What is the gold standard treatment for SCLC?

A

Radiotherapy and chemotherapy
Chemotherapy sensitive

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5
Q

What is the criteria for long term oxygen therapy in COPD patients?

A

PaO2 < 7.3
or PaO2 7.3-7 AND peripheral odema, pulmonary HTN, hypoxaemia, secondary polcythaemia

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6
Q

What is the criteria for long term oxygen therapy in COPD patients?

A

PaO2 < 7.3
or PaO2 7.3-7 AND peripheral odema, pulmonary HTN, hypoxaemia, secondary polcythaemia

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7
Q

What is the most common lung cancer in non smokers?

A

Adenocarcinoma

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8
Q

What peripheral stigmata indicate lung adenocarcinoma?

A

clubbing and
hypertrophic pulmonary osteoarthropathy (painful wrist)

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9
Q

How should a secondary pneumothorax in a patient >50 years with a rim of >2cm on CXR be managed?

A

Insert a chest drain 5th intercostal space anterior to the mid-axillary line

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10
Q

Signs consistent with a tension pneumothorax?

A

Hyper-resonant percussion note
Tracheal deviation
Reduced chest expansion

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11
Q

How should a haemodynamically unstable patient with a tension pneumothorax be managed?

A

Insert and IV cannula for emergency needle thoracentesis in the 2nd intercostal space mid-clavicular line.

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12
Q

What is the most common cause of diagnosis of superior vena cava obstruction?

A

Lung cancer

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13
Q

What is the best initial step in the management of SVCO?

A

Dexamethasone after to reduce swelling (after ensuring the airway is secure)

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14
Q

How is curb 65 calculated?

A

C - confusion, ABM <8
U - urea>7 mmol/L
R - RR>/ 30
B - Blood pressure <90 systolic and / or <60mmHg diastolic
65 - ages over 65

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15
Q

Why does a pancoast tumour sometimes cause Horner’s syndrome?

A

IN the apex of the lung, the tumour can invade the sympathetic chain which includes a pre-ganglionic neurones supplying the muscles in the eye and face

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16
Q

What is the most common cause of an exudative pleural effusion?

A

Mallignancy
Infection
Lung injury
(blocked blood vessels and lymph nodes)

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17
Q

What is the most common cause of an transudative pleural effusion?

A

Heart failure.
Pulmonary embolism
Cirrhosis
Post open heart surgery

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18
Q

Pathophysiology of exudative pleural effusion?

A

Caused by fluid leaking out of capillaries with increased permeability, a process which happens when inflammation is present. Due to the increased permeability of the capaillaries, larger molecules like proteins are able to follow out fluid into the pleural space

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19
Q

What causes a transudative pleural effusion?

A

Associated with low protein levels. Fluid filters out through intact capillary walls which do not leave space for larger molecules such as proteins to pass through. Pleural fluid production is not balanced with re-absorption, resulting in its accumulation. This is due to altered hydrostatic and osmotic forces acting across the capillary membrane.

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20
Q

What pleural aspirate is exudative?

A

If the pleural fluid protein is between 25 and 35 g/L

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21
Q

Fissures of the right lung?

A

Horizontal fissure (upper lobe to middle lobe)
Oblique fissure (middle lobe to lower lobe)

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22
Q

Fissures of the left lung?

A

Oblique fissure only (two lobes, upper and lower)

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23
Q

How does pneumothorax affect V/Q ratio?

A

Decreases

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24
Q

What is the first line treatment for COPD?

A

SABA or SAMA

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25
Q

Findings in IPF?

A

Fine bi-basal end inspiratory crackles
Reduced chest expansion
Clubbing of the fingers

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26
Q

Causes of basal lung fibrosis

A

Connective tissue disorders (exlcuding anklosing spondylitis)
Asbestos and drugs (Nitrofurantonin, bleomycin, methotrxate, amiodarone)

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27
Q

Why are fine crackles upon inspiration heard in pulmonary fibrosis?

A

Thickened stiffened walls of the alveoli are moved apart by the air entering

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28
Q

Features of a life threatening asthma attack?

A

Sats <90%
Peak expiratory flow rate <33% of best
Silent chest
Bradycardia
Hypotension
Exhaustion

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29
Q

Following a provoked PE, how long should a patient be anticoagulated for?

A

3 months

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30
Q

Following an unprovoked PE, how long should a patient be anticoagulated for?

A

6 months (or longer if active cancer)

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31
Q

Second line pharmacotherapy for asthma and COPD?

A

Inhaled corticosteroids e.g. beclometasone inhaler

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32
Q

What asthma/COPD treatment is most likely to cause oral thrush?

A

ICS e.g. beclomethasone inhaler

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33
Q

What might a patient present with when they have a respiratory complaint?

A

Dysponea: MRC score, ET, triggers, relieving factors, diurnal variation, orthopnea, PND
Chest pain: site, severity, radiation, triggers, relieving factors, associated symptoms
Wheeze: triggers, relieving factors, diurinal variation, associated cough
Cough: dry or productive, triggers, relieving factors, diurnal variation, associated with eating or dyspepsia, positional, nasal secretions, associated fever
Sputum: how much over 24hrs, colour, consistency
Haemopytsis: quantity and frequency, fever/night sweats, appettite, weight loss

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34
Q

What is the MRC dysponoea score?

A

1 Not troubled by breathlessness related to activites
2 SOB when hurrying or walking up a slight hill
3 Walks slower than contemparies on level ground because of breathlessness, or has to stop for breath when walking at his own pace
4 Stops for breath when hurrying or walking up a slight hill
5 Too breathless to leave the house, or breathless when dressing or undressing

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35
Q

What is particularly relevant in a respiratory patient’s PMH or PSH?

A

Asthma - previous hospitalisations/ITU
COPD
DVT/PE
Nasal polyps
Previous lung infections - including TB
Childhood lung infections
Surgery
Cardiovascular illness
Cancer
Allergies

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36
Q

What are particularly significant aspects of family history in relation to a respiratory patient?

A

Respiratory Disease
Cardiac disease
Cancer
Thrombophillia (if DVT/PE)
Cystic fibrosis (if young and chest infections)

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37
Q

What is significant in the social history of a respiratory patient?

A

Smoking - current (pack years), ex (pack years, when stopped), never or passive, also vaping
Occupation history - asbestos specifically
Pets - cats, birds
Recent forigen travel
Immobility - flights or long car journeys
ADLS
Performance status

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38
Q

Relevant systems review in a respiratory history?

A

Bowels ok? Appetite/weight loss
Any problems with your water works?
Joint pains? Rashes?
Neuro/cardio

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39
Q

What hand signs may be present in resp. exam?

A

Clubbing
Peripheral cyanosis
Nicotine/tar staining
CO2 retention flap
Tremmor

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40
Q

What should be looked out for on a patient’s face during a respiratory examination?

A

Trachea
JVP
Lymph nodes

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41
Q

How might you comment on the quality of a chest x-ray?

A

Rotation
Transparency
Spinous processes
Adequete inspiration

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42
Q

How would you present a chest X Ray

A

Are The Elephants Parading By Here Soon? My Mother Finds All Fun Stuff Silly.

AP or PA
Trachea deviation + corena + bronchus
Expiration - sufficient/uniform/roation
Patchiness
Borders of heart and lung fissures
Hemidiaghpram visable?
Size of heart
Mediastinal shift
Mediastinal contors and hilla visable? Lymphandopathy
Fractures and bony abnormalities
Air under diaphragm
Forigen bodies
Surgical emphysema/soft tissue abnormality
Summerise

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43
Q

What is VC on spirometry?

A

Volume of air expired from the lungs from a maximal inspiration using a slow/relaxed manouvere

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44
Q

What is FVC on spirometry

A

Volume of air that can be forcibly expelled from the lungs from a position of maximal inspiration

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45
Q

What is FEV1

A

Volume of air forcibly expelled from the lungs in the first second following a maximal inspiration

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46
Q

What are the four causes of hypoxia (low PaO2)

A

Hypoventilation
Diffusion impairment
Shunt
V/Q mismatch

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47
Q

Causes of respiratory acidosis?

A

Hypoventillation - e.g. neuromuscular diseases
Alveolar hypoventillation - e.g. COPD

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48
Q

What is a normal A-a gradient in a young person?

A

Less than 2kPa

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49
Q

What is a normal A-a gradient in an older person?

A

<4 kPa

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50
Q

What does an increased A-a gradient mean?

A

Implies lung pathology (rather than another cause ie. stand alone hyperventillation)

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51
Q

How do you calculate PAO2

A

20 - pCO2/0.8

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52
Q

How do you calculate the A-a gradient?

A

PA02 - PO2
(20 - PaCO2/0.8) - PO2

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53
Q

What is anaphylaxis?

A

Serious allergic reaction, sensetised individual exposed to specific antigen.
IgE response to antigen, mast cell and basophill activation, histamine realease and body response
Sympathetic activation

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54
Q

Symptoms of anaphylazis?

A

Pruitis, urticaria & angioedema, hoarseness, progressing to stridor and bronchial obstruction, wheeze and chest tightness from bronchospasam

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55
Q

Management of anaphylaxis?

A

Remove trigger, maintain airway, 100% O2
Intramuscular adrenaline 0.5mg, repeated every 5 minuites as required
IV hydrocortisone 200mg
IV chlorpheniramine 10mg
Life flat and resussiate if hypotension
Treat bronchospasam: NEB salbutamol
Larangenal odema: NEB adrenaline

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56
Q

Features of a mild asthma attack?

A

No features of severe asthma
PEFR>75% of normal

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57
Q

Features of moderate asthma?

A

No features of severe asthma
PEFR 50%-75%

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58
Q

Features of severe asthma?

A

Any one of
PEFR 33-50% of predicted
Cannot complete sentences in 1 breath
RR > 25 /min
HR > 110 /min

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59
Q

Features of life threatening asthma?

A

PEFR <33% of best predicted
Sats <92%
ABG pO2 < 8kPa
Cyanosis, poor respiratory effort, nearly silent chest
Exhaustion
Confusion
Hypotension
Arrhythmias
Normal CO2

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60
Q

What indicates near fatal asthma?

A

Raised pCO2

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61
Q

Management of acute asthma (up to moderate)

A

ABCDE
Aim sats 94% - 98% with O2 as needed
5mg nebulised salbutomol - can repeat after 15 mins
40mg oral Prednisolone STAT (IV hydrocortisone if PO not possible)

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62
Q

Management of severe asthma?

A

ABCDE
Aim sats 94% - 98% with O2 as needed - ABG if <92%
5mg nebulised salbutomol - can repeat after 15 mins - consider back to back
40mg oral Prednisolone STAT (IV hydrocortisone if PO not possible)
Nebulised Ipratropium bromide 500 micrograms

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63
Q

Management of life threatening or near fatal asthma?

A

ABCDE
Aim sats 94% - 98% with O2 as needed - ABG if <92%
5mg nebulised salbutomol - can repeat after 15 mins - consider back to back - consider IV if ineffective
40mg oral Prednisolone STAT (IV hydrocortisone if PO not possible)
Nebulised Ipratropium bromide 500 micrograms
IV aminophyline
Urgent portable CXR
Urgent ITU or anaesthetist assesment

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64
Q

What suggests an infective exaccerbation of COPD?

A

Change in sputum volume/colour
Fever
Raised WCC +/- CRP

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65
Q

When should O2 sats be aimed 88-92% in COPD?

A

Evidence of acute or previous Type 2 Respiratory Failure

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66
Q

What NEBs may be used in an exacerbation of COPD?

A

Salbutomol
Ipratropium

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67
Q

What steroid course should a patient with a COPD exacerbation have?

A

Prednisolone 30mg STAT and OD for 7 days

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68
Q

When should antibiotics be given in an exaccerbation of COPD?

A

Raised CRP
Raised WCC
Purulent sputum

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69
Q

When should NIV be considered in a COPD exaccerbation?

A

Type 2 resp failure and pH 7.25-7.35

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70
Q

Under what pH should ITU referal be considered in a patient with COPD?

A

7.25

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71
Q

What imagine should a patient with an acute exaccerbation of COPD have?

A

CXR

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72
Q

When might IV aminophylline be considered in a respiratory patient?

A

Life threatening or near fatal asthma
COPD exaccerbation

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73
Q

Features of pneumonia?

A

Consolidation on CXR with fever
+/- purulent sputum
+/- raised WCC or CRP

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74
Q

What constitutes massive haemoptysis?

A

> 240mls in 24 hours
100mls/day over consecutive days

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75
Q

How is massive haemoptysis managed?

A

ABCDE
Lie patient on side of suspected lesion if known
Oral tranexamic acid for 5 days or IV
Stop NSAIDs, aspirin, anticoagulants
Antibiotics if any evidence of respiratory tract infection
Consider Vitamin K
CT aortogram - interventional radiologist may be able to undertake bronchial artery embolisation

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76
Q

Management of a tension pneumothorax

A
  • Large bore intravenous cannula into 2nd ICS MCL
  • Chest drain into the affected side
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77
Q

Symptoms of a PE?

A

Chest pain - pleuritic
SOB
Haemoptysis
Low cardiac output followed by collapse (if massive PE)

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78
Q

What is a massive PE?

A

PE with haemodynamic compromise

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79
Q

Risk factors for a provoked PE?

A

Surgery
– Abdominal/pelvic; Knee/ hip replacement
Post-operative spell on ITU
• Obstetric
– Late pregnancy; Caesarian section
• Lower Limb
– Fracture; Varicose veins
• Malignancy
– Abdominal/ Pelvic/ Advanced/ Metastatic
• Reduced Mobility
• Previous proven VTE

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80
Q

What might cause an unprovoked PE?

A

Underlying mallignancy
Thrombophillia

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81
Q

Management of PE?

A

ABCDE
O2 of hypoxic
Analgesia if pain
SC LMWH whilst aawaiting CTPA
CTPA
Fully antiocoagulated once confirmed on CTPA

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82
Q

What is a massive PE?

A

Hypotension
Imminent cardiac arrest
Signs of right heart strain on CT/ECHO
Consider thrombolysis with IV alteplase (risk of intracerbral bleed 4%)

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83
Q

Absolute contraindications to thrombolysis?

A

Haemorrhagic stroke or ischemic stroke < 6 months
CNS neoplasisa
Recent trauma or surgery
GI bleed < 1 month
Bleeding disorder
Aortic dissection

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84
Q

Relative contraindications to thrombylisis?

A

Warfarin/DOAC
Pregnancy
Advanced liver disease
Infective endocarditis

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85
Q

Asthma characteristics?

A

Chronic inflammatory airway disease
Airway obstruction is often reversable, either spontaniously or with treatment
Increased airway responsiveness (airway narrowing) to a variety of stimuli

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86
Q

Wheeze differentials

A

Acute asthma exacerbation
Bronchitis - viral or bacterial
(LESS COMMON):
Pulmonary odema
PE
Vocal cord dysfunction
GORD
Forigen body
Allergy
Hyperventillation/psychosocial
Cardiac disease
Vasculitides - Churg-Stauss syndrome, polyarteritis nodosa, granulomatosis with polyangitis
Carcanoid syndrome with hepatic metasteses - release of HIAA

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87
Q

Pathophysiology of Asthma

A

Airway epithelial damage - shedding and subepithelial fibrosis, brasement membrane thickening
An inflammation reaction characterised by eosinophills, T-lymphocytes (Th2) and mast cells.
Inflammatory mediators released include histamine, leukotrienes, and prostaglandins
Cytokines amplify inflammatory response
Increased number of muscus secreting goblet cells
Smooth muscle hyperplasia and hypertrophy
Mucus plugging in severe asthma

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88
Q

Criteria for safe asthma discharge after exacerbation?

A

PEFR>75%
Stop regular nebulisers for 24 hours prior to discharge
Inpatient asthma nurse review to reasses inhaler technique and adherence
Provide PEFR meter and written asthma action plan
At least 5 days oral prednisolone
GP follow up within 2 working days
Respiratory clinic follow up within 4 weeks

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89
Q

Differentials for eosinophillia

A

Asthma
Hayfever / allergies
Allergic bronchopulmonary aspergillosis
Multiple courses of antibiotics for chronic infection
Eosinophillic granulomatosis with polyangitis
Eosinophillic pneumonia
Parasites e.g. Hookworm
Lymphoma
SLE
Hyperesosinphillic syndrome

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90
Q

Asthma triggers?

A

Smoking
URTI - viral
Allergens - pollen, house dust mite, pets
Exercise - also cold air
Occupational irritants
Pollution
Drugs - aspirin, beta blockers (inducing eye drops)
Food and drink - dairy produce, alcohol, orange juice
Stress
Severe asthma - consider inhaled herorin, pre-menstrual, psychosocial aspect

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91
Q

What is COPD?

A

COPD is characterised by airflow obstruction - usually progressive, not fully reversable, does not change markedly over several months.
Combination of chronic bronchitis and empyshema.

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92
Q

Causes of COPD?

A

Smoking
Alpha-1 antitrypsin deficency
Industrial exposure - soot

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93
Q

Outpatient COPD management?

A

COPD care bundle
Smoking cessation
Pulmonary rehabilitation
Bronchodilators
Antimuscarinics
Steroids
Mucolytics
Diet
LTOT if appropriate
Lung volume reduction if appropriate

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94
Q

Long Term Oxygen Therapy criteria?

A

pO2 consistently below 7.3kPa, or below 8 kPa with cor pulmonale
Patients must be non-smokers and not retain high levels of CO2

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95
Q

Why is LTOT offered?

A

Survival benefit
Treatment to help prevent organ hypoxia
Not a treatment to help prevent organ hypoxia

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96
Q

What is pulmonary rehabilitation?

A

6-12 week programme of supervised exercise, unsupervised home exercise, nutritional advice, and disease

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97
Q

Most common organisms causing community aquired pneumonia?

A

Streptococcus pneumonia
Haemophilus influenza
Moraxella catarrhalis

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98
Q

Atypical organisms that may cause pneumonia?

A

Organisms include legionella pneumphila,
Chlamydia pneumoniae,
Mycoplasma pneumoniae

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99
Q

Hospital acquired pneumonia caustive organisms?

A

Organisms include e.coli
MRSA
Pseudomonas

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100
Q

CXR consolidation common differentials?

A

Pneumonia
TB (usually upper lobe)
Lung cancer
Lobar collapse (blockage of bronchi)
Haemorrhage

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101
Q

What is Legionnaire’s disease?

A

Legionnaire’s disease is a form of pneumonia, usually caused by Legionella pneumophilla
CURB - 65 often high

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102
Q

Pneumonia follow up?

A

HIV test
Immunoglobulins
Pneumococcal IgG serotypes
Haemophilus influenzae b IgG
Follow up in clinic 6 weeks with a repeat CXR to ensure resolution

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103
Q

Causes of a non-resolving pneumonia

A

CHAOS
Complication - empyema, lung abscess
Host - immunocompromised
Antibiotic - inadequete dose, poor oral absorption
Organism - resistant or unexpected organism not covered by empircial
Second diagnosis - PE, cancer, organising pneumonia

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104
Q

Clinical features of respiratory TB?

A

Often fever and nocturnal sweats
Weight loss
Malaise
cough +/- purulent sputum/haemoptysis

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105
Q

Differntial diagnosis of haemoptysis?

A

Infection
- Pneumonia
- Tuberculosis
- Brochiectasis / CF
- Cavitating lung lesion (often fungal)
Mallignnacy
- Lung cancer
- Metasteses
Haemorrhage
- Bronchial artery erosion
- Vasculitis
- Coagulopathy
Other
- PE

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106
Q

TB Risk Factors

A

• Past history of TB
• Known history of TB contact
• Born in a country with high TB incidence
• Foreign travel to country with high incidence of TB
• Evidence of immunosuppression–e.g. IVDU, HIV,
solid organ transplant recipients, renal failure/
dialysis, malnutrition/ low BMI, DM, alcoholism

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107
Q

Management of pulmonary TB?

A

ABCDE
Aim to culture whenever possible
Admit to side room, negative pressure
x3 sputum samples for AAFB and TB culture
Routine bloods (especially LFTS)
HIV testing
Vit D level testing
Bronchoscopy if no productive cough
Consider CT chest if clinical features and CXR are not typical
If ?CAP/?TB start antibiotics as per CURB-65 alongside invetigations
Start ATTT before sputum results if critically unwell and high likelihood of TB (After sputum samples are sent)

Saving

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108
Q

Basics of Anti-TB therapy

A

2 months Rifampicin, Isoniazid, Pyrazinamide, Ethambutol
4 months Rifampicin, Isonazid
Weight dependent dosage
Check baseling LFT’s, and visual acuity (ethambutol)
DOT if needed
Pyridoxine given alongside Isonazid to prevent peripheral neuropathy

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109
Q

Side effects of Rifampicin?

A

Hepatitis
Rash
Fever
Orange/red secretions

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110
Q

Isonazid side effects

A

Hepatitis
Rash
Peripheral neuropathy
Psychosis

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111
Q

Side effects of Pyrazinamide?

A

Hepatitis, rash, vommiting, arthralgia

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112
Q

Common medications rifampicin interacts with?

A

Warfarin
Oral contraceptive pill

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113
Q

What is Bronchiectasis?

A

Chronic dilation of one or more bronchi
The bronchi exhibit poor mucus clearence and there is predisposition to recurrent or chronic bacterial infection

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114
Q

Gold standard diagnostic test for bronchiectasis?

A

High resolution CT

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115
Q

Potential causes of bronchiectasis?

A

Post infective - whooping cough, TB
Immune deficiency - hypogammaglobulinaemia
Genetic/mucocillary clearence defects: CF, primary cilary dyskiesia, Young’s syndrome, Kartagener syndrome
Obstruction - forgien body, tumour, extrensic lymph node
Toxic insult - gastric aspiration, inhilation of toxic chemicals, gases
Allergic bronchopulmonary aspergillosis
Secondary immune deficiency - HIV, mallignancy
RA

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116
Q

What non-respiratory conditions is bronchiectasis associated with?

A

Yellow nail syndrome
IBD

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117
Q

What bloods might help identify the cause of newly diagnosed bronchiectasis?

A

Immunoglobulin levels
CF genotype
Asperegillus IgE/IgG / total IgE
HIV test
RF
Auto antibodies
Alpha-1-antitrypsin level

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118
Q

What ogransims are commonly seen in bronchiectasis?

A

Haemophilus infulenzae
Pseudomonas aerguinosa
Moraxella catarrhalis
Stenotrophomonas maltophillia
Fungi - aspergillus, candida
Non-tuberculous mycobacteria
Less common - staph aureus (CF)

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119
Q

Management of bronchiectasis?

A

Treat underlying cause
Physiotherapy - mucus/airway clearence
Sputum for rotine culture as well as nontuberculous mycobacteria
10-14 days abx as per sputum cultures/sensitivites for any acute exaccerbation

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120
Q

What constitutes an exaccerbation of bronchiectasis?

A

Deterioration in 3 or more of the following for at least 48hrs:
Cough
Sputum volume/consistency
Sputum purulence
Breathlessness and or/ET
Fatigue
Haemoptysis

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121
Q

What causes Allergic Bronchopulmonary Aspergillosis (ABPA?

A

Aspergillus fumigatus exposure

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122
Q

What type of bronchiectasis does Allergic Bronchopulmonary Aspergillosis (ABPA) often lead to?

A

Upper lobe

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123
Q

Which patients does Allergic Bronchopulmonary Aspergillosis (ABPA) tend ot be seen in?

A

Asthma
Bronchiectasis
CF

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124
Q

What types of hypersensitivity reactions occur in Allergic Bronchopulmonary Aspergillosis (ABPA)?

A

Fungal spore inhillation leads to a combination of type 1 and type 3 hypersensitivity reaction

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125
Q

When might steroids be required in Allergic Bronchopulmonary Aspergillosis (ABPA)?

A

If ongoing symptoms and high total IgE level

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126
Q

What is cystic fibrosis?

A

An autosomal recessive disease leading to mutations in the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR)
This can lead to multisystem disease (and part of the body with CFTR) characterised by thickened secretions.

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127
Q

How is CF diagnosed?

A

-One or more of the characteristic pheontypic features OR a history of CF in a sibling OR a positive newborn screening result
-An increased sweat chloride concentration (>60 mmol/L) OR identification of two CF mutations on genotyping OR demonstration of abnormal nasal epithelial ion transport

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128
Q

CF presentations?

A
  1. Meconium ileus
    2.Intestinal malabsorption
  2. Recurrent chest infections
  3. Newborn screening
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129
Q

Potential features of cystic fibrosis?

A

Chronic sinusitis
Nasal polyps
Repeated lower respiratory tract infection
Bronchiectasis
Liver disease
Portal HTN
Gallstones
Abnormal sweat secretions (salty)
Pancreatic insufficiency
Diabetes
Distal intestinal obstruction syndrome
Steatorrhoea
Osteoperosis
Male infertility
Arthoropathy/arthritis

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130
Q

What is meconium ileus?

A

In 15-20% of newborn CF infants bowel is blocked by sticky secretions.
Signs of intestinal obstrcution soon after birth - billous vommiting, adbominal distensions, delay in passing meconium

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131
Q

Common complications of CF?

A

Respiratory infections
Low body weight
Distal intestinal obstruction syndrome
CF related diabetes

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132
Q

How are respiratory infections managed in CF patients?

A

Agressive therapy
Resp physio
Antibiotics (potentially prophylactic to maintain health)

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133
Q

How is low body weight managed in patients with CF?

A

Careful monitoring, may be consequence of pancreatic insufficiency (lack of pancreatic enzymes), therefore patients can be given pancreatic replacement enzymes.
High calorie intake, often extra supplements
May need NG or PEG feeding

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134
Q

What is the difference between DIOS and constipation?

A

DIOS is faecal obstruction in the ileocaecum, versus whole bowel

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135
Q

What causes DIOS in CF patients?

A

Due to intestinal contents in the distal ileum and proximal colon (thick, dehydrate faeces)
Often the result of insufficient replacement of pancreatic enzymes
Salt deficiency, hot weather

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136
Q

How does DIOS present?

A

Palpable RIF mass (faecal)
AXR demonstrating faecal loading at junction of small and large bowel

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137
Q

How is distal intestinal obstrcution syndrome managed?

A

PO gastrografin - this works by drawing water across the bowel wall by osmosis into the bowel lumen, aiming to rehydrate dehydrated faecal mass and allow it to pass

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138
Q

How is CF managed?

A

Physio for airway clearence
Exercise
Mucolytic treatment options also include nebulised DNase (pulmozyme)
Pancreatic enzyme replacement therapy - i.e. Creon
Nutitional supplementation if under weight
Fat soluble vitamin replacement (A D E K)
Long term antibiotics (sometimes inhaled or nebulised)
Optimastion of CF related diabetes - insulin therapy
Novel CFTR modulator/potentiators (e.g. Kaftrio) improve FEV1, weight, quality of life and a reduction in frequeny of infective exacerbations
Long-term monitoring for CF related diabetes, CF releated liver disease and osteoperosis

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139
Q

What lifestyle advice should a CF patient be given?

A

No smoking
Avoid other CF patients
Avoid friends/relatives with colds/infections
Acoid jaxuzzis (pseudomonas)
Clean and dry nebulisers throughouly
Clean and dry nebulisers throughly
Avoid stables, compost or rotting vegetation - risk of asperigillus fumigatus inhalation
Annual influenza immunisation
Sodium chloride tablets in hot weather/vigourous exercise

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140
Q

What is the pleural cavity?

A

Potential space created by pleural surfaces

Serous membrane that folds back on itself
- Outer pleura = parietal (attached to the chest)
- Inner pleura = visceral (covers lungs)

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141
Q

What are the various pleural diseases?

A

Pneumothorax = air in pleural cavity
Pleural effusion = fluid in pleural cavity
Empyema = infected fluid in the pleural cavity
Pleural tumours = benign vs mallignant
Pleural plaques = discrete fibrous areas
Pleural thickening = scarring/calcification causing thickening (benign vs. mallignant)

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142
Q

Pneumothroax types?

A

Spontaneous - primary (no lung disease), secondary (lung disease)
Traumatic
Tension: emergency
Iatrogenic (e.g. post central line or pacemaker insterion)

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143
Q

Pneumothorax Risk Factors

A

Pre-existing lung disease
Height (increasing)
Smoking/cannabis
Diving
Trauma/chest procedure
Association with other conditions e.g. Marfan’s syndrome

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144
Q

How is a primary pneumothorax managed as per BTS guidelines?

A

Sympotomatic and rim of air >2cm on CXR give O2 and aspirate.
If unsucsessful re-aspirate or consider costal drain.
Remove drain after full re-expansion / cessation of air leak

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145
Q

What is the management of a secondary pneumothorax?

A

If symptomatic and rim of air >2cm on
CXR give O2 and aspirate. If unsuccessful
consider re-aspiration or intercostal drain (lower threshold than for primary)
Remove drain after full re-expansion / cessation of air leak.

146
Q

How should a patient with a pneumothorax with a peristent air leak > 5 days be managed?

A

Referral to thoracic surgeons

147
Q

Discharge advice for patients with a pneumothorax?

A

No driving or flying until resolved

148
Q

How should you approach a patient with suspeted pleural effusion?

A

CXR
ECG
Bloods: FBC, U&Es, LFTs, CRP, Vone profule, LDH, clotthing
ECHO (if suspect HF)
Staging CT with conrtast if suspect exudative cause
USS guided pleural aspiration for:
- Cytology
- Microbiology (including AAFB)
- Biochemistry (protein, pH, LDH)
Never inset a chest frain unless diagnosis is well established otherwise may hinder opporutinty to obtain pleural biopsy
Consider thoacoscopy or CT pleural biopsy

149
Q

What is the only indication for an urgent chest drain in a patient with pleural effusion?

A

Underlying empyema (pH of pleural fluid <7.2 or visable pus)

150
Q

What pleural protien indicates a transudative pleural effusion?

A

<30g/L

151
Q

What are the causes of transudative pleural effusion?

A

Heart failure
Cirrhosis
Hypoalbuminaemia (nephrotic syndrome or peritoneal dialysis)
Hypothyroidism, mitral stenosis, PE (less common causes)
Constructive pericarditis, superior vena cava obstruction, Meig’s syndrome (rare)

152
Q

Management of transudative pleural effusion?

A

Treat underlying cause (HF, nephrotic syndrome, cirrhosis)
If resolves stop or reduce treatment
Theraputic aspiration/drainage if effusion persists

153
Q

What pleural protein indicated an exudative effusion?

A

Over 30g/L

154
Q

What may cause an exudate effusion?

A

Mallignancy
Infection (parapneumonic, TB, HIV (kaposi’s)
Inflammatory (RA, pancreatitis, benign asbestos effusion, Dressler’s, pulmonary infarction, PE), lymphatic disorders, connective tissue disease (all less common)
Yellow nail syndrome, fungal infections, drugs (rare)

155
Q

When should Lights criteria be used to decide whether a pleural fluid aspirate is tranusdative or exudative?

A

If fluid protein level is between 25 and 35 g/L (borderline)

156
Q

What is light’s criteria?

A

Pleural fluid is exudative if:
Pleural fluid/serum protein >0.5
Pleural fluid/serum LDH >0.6
Pleural fluid LDH > 2/3 of the upper limit of normal

157
Q

What is interstitial lung disease?

A

Umbrella term describing a number of conditions that affect the lung paranchyma in a diffuse manner includin:
Usual interstitial pneumonia (UIP)
Non-specific interstitial pneumonia (NSIP)
Extriinsic allergic alveolitis
Sarcoidosis
Several other conditions

158
Q

What occupational/enviromental history is relevant in ILD?

A

Silicosis (Dust)
Asbestososis (asbestos)
Pneumoconioisis (coal workers)

159
Q

What will be shown on PFT’s in ILD?

A

Restrictive lung disease pattern

160
Q

What investigations should be ordered following a new diagnosis of ILD?

A

ANA - connective tissue disease or SLE
ENA - connective tissue disease
Rh F - RA
ANCA - vasculitis
Anti-GBM - Pulmonary renal disease
ACE - Sarcoidosis
IgG to serum precipitins e.g. pigeon, budgie - Extrinisic
Allergic alveolitis
HIV

161
Q

What is extrinsic allergic alveolitis?

A

Also known as hypersensitivity pneumonitis
Inhalation of organic antigen to which the individual has been sensitised
Subtype of ILD

162
Q

What is the clinical presentation of Acute hypersensitivity pneumonitis/extrinsic allergic alveolitis?

A

Short period from exposure, 4-8 hours
Usually reversable, spontaneously settled within 1-3 days, can recur

163
Q

What is the clinical presentation of chronic hypersensitivity pneumonitis/extrinsic allergic alveolitis?

A

Chronic exposure (months-years)
Less reversible than acute

164
Q

Common drug caused of extrinsic allergic alveolitis/hypersensitivity pneumonitis?

A

Amiodarone
Belomycin
Methotrexate
Penicilliamine

165
Q

What type of hypersensitivity reaction is hypersensitivity pneumonitis?

A

Type-III
Considered as an immune counterpart of asthma, hypersensitivity pneumonitis is a prototypical type-III allergic inflammatory reaction involving the alveoli and lung interstitium, steered by Th1 cells and IgG and, in its chronic form, accompanied by fibrosis.

166
Q

What type of hypersensitivity reaction is asthma?

A

Type I hypersensitivity

167
Q

What is UIP?

A

Usual interstitial pneumona, most common type of pulmonary fibrosis.
Usually idiopathic

168
Q

Common findings in UIP?

A

Clubbing
Reduced chest expansion
Fine inspiratory creptations (velcro) usually best heard basal/axillary areas
Cardiovascular - may be features of pulmonary HTN

169
Q

What is sarcoidosis?

A

Type of intersitital lung disease
Multisystem inflammatory condition of unknown cause
Non-caseating granulomas (histology important)
Immunological response
Commonly involves resp system but can affect nearly all organs

170
Q

How common is spontaneous remission vs progressive disease in sarcoidosis?

A

50:50

171
Q

How would you investigate sarcoidosis?

A

Investigations:
PFTs: obstructive until fibrosis
CXR: 4 stages
Bloods: renal function, ACE, calcium
Urinary calcium
Cardiac involvement: ECG, 24 tape, ECHO, cardiac MRI
CT/MRI head: headaches - neuro sarcoid

172
Q

What are the treatment principles of ILD?

A

Remove an occupational exposure
Remove any enviromental exposure
Drug associated - avoid drug
Smoking cessation
MDT approach - ?speciallist medications such as pirfendone to slow progression
Treatment of infective exaccerbation
Palliative care
Transplantation

173
Q

What specialist drug may be given to some patients with ILD to slow disease progression?

A

Pirfenidone

174
Q

What are the clinical features/presentation of lung cancer?

A

Asymptomatic- incidental finding
Any respiratory symptom/systemic deterioration
Super vena caval obstruction
Horner’s syndrome
Metastic disease - liver, adrenals (addison’s), bone, pleural, CNS
Paraneoplastic - clubbing, hypercalcemia, anaemia, SIADH, cushing’s syndrome, lamert-eaton myasthenic syndrome
Increased risk of thrombo-embolic disease

175
Q

Risk factors for lung cancer?

A

Large number of smoking pack years
Airflow obstruction
Increasing age
Family history
Exposure to other carcinogens

176
Q

What is the WHO scale performance status?

A

0 Fully active without restriction
1 Restricted in physically strenious acitivty but ambulatory and able to carry out light work e.g. light house work, office work
2 Ambulatory and capable of all self-care but unable to carry out any work activities
3 Capable of only limited self-care, confined to bed or chair more that 50% of waking hours
4 Completely disabled, cannot self care, totally confined to bed or chair
5 Dead

177
Q

What diagnostic tests may be performed in suspected lung cancer?

A

Bloods - FBC, U&E, calcium, LFTs, INR
CXR
Staging CT - spine CT thorax and upper abdo (sratify TNM stage)
Histological
PET scan - helps detect small metastases not seen on staging CT

178
Q

Histological options in lung cancer investigation?

A

US guided neck node FNA for cytology if lymphadenopathy
Bronchoscopy - endobronchial, transbronchial, endobronchial USS (if mediastinal lymphadenopathy)
CT biopsy
Thoracoscopy if pleural effusion

179
Q

Histological classification of lung cancer

A

Small cell (oat cell)
Non small cell
Other: bronchial gland ca, carcinoid tumour

180
Q

What are some examples of non small cell lung cancers?

A

Squamous cell
Adenocarcinoma
Large cell carcinoma
Bronchoalveolar

181
Q

What is the most common type of lung cancer?

A

Adenocarcinoma

182
Q

What type of lung cancer is most common in non-smokers?

A

Adenocarcinoma

183
Q

Which lung cancer has the strongest association with smoking?

A

Small cell lung cancer

184
Q

Which NSCLC have a prognosis of more than 50% 5 year survival following surgical resection?

A

Stage I and stage II

185
Q

Which NSCLC stages have a prognosis of less than 25% 5 year survival?

A

Stage III (20%)
Stage IV (1-5%)

186
Q

What stages of lung cancer are suitable for curative surgery?

A

Stages I and II (Assuming patient fit)

187
Q

Which stage of cancer would you consider surgery and chemotherapy for?

A

Stage IIIa

188
Q

What can be curative for lung cancer patients not fit for surgery (and can also be used in palliation)

A

CHART - continous hyperfractionated accelerated radiotherapy

189
Q

What is the prognosis of SCLC?

A

Rapid growth rate and almost always to extensive for surgery at time of diagnosis - median survival 8-16 weeks or 7-15 months with combination chemotherapy

190
Q

What is the mainstay of treatment for SCLC?

A

Chemotherapy
(+palliative radiotherapy)

191
Q

What is obstructive sleep apnoea?

A

Upper airway narrowing
Provoked by sleep
Causing sufficient sleep fragmentation to result in significant daytime symptoms (usually excessive sleepiness)

192
Q

Risk factors for OSA?

A

Male
Upper body obesity
Relatively undersized or set back mandible
Increasing age

193
Q

Pathophysiology of obstructive sleep apnoea?

A

Upper airway patency depends on dilatory muscle activity, all muscles including pharangeal dilators relax during sleep
Some narrowing of the upper airway is normal
Excessive narrowing can be due to either an already small pharyngeal size during awake state which undergoes a normal degree of muscle relaxation during sleep causing critical narrowing OR excessive narrowing occuring with relaxtion during sleep

194
Q

Causes of small phrangeal size?

A

Fatty infiltartion of phrangeal tissues and external pressure from increased neck fat and/or muscle bulk
Large tonsils
Craniofacial abnormalities
Extra submucosal tissue, e.g. myxoedema

195
Q

Causes of excessive narrowing of the airway during sleep

A

Obesity may enhance residual muscle dilator action
Neuromuscular disease with pharangeal involvement may lead to greater loss of dilator muscle tone (e.g. stroke, MND, myotonic dystrophy)
Muscle relaxants - sedatives, alcohol
Increasing age

196
Q

Clinical affects of OSA?

A

If severe, leads to repetitive upper airway collapse, with arousal required to reactivate the pharangeal dilators. There may be associated hypoxia and hypercapnea which are corrected during the inter-apnoeic hyperventillatory period
Reccurent arousals lead to highly fragmented and unrefresshing sleep
Epworth sleepiness scale score >9
Raise in BP
Nocturia
Less common: nocturnal sweating, reduced libido, oesophageal reflux

197
Q

Points (0= for would never dose, 1= for slight chance, 2 moderate change and 3 for high chance) are awarded in the Epworth Sleepiness Score, for which activities?

A

Sitting and reading
Watching TV
Sitting in a public place, e.g. theatre
Passanger in a car for an hour
Lying down to rest in the afternoon
Sitting and talking
Sitting quietly after lunch without alcohol
In a car, while stopped in traffic

198
Q

What sleep study types are there?

A

Overnight oximetry alone
Limited sleep study - oximetry, snoring, body movement, HR, oronasal flow, ches/abdominal movements, leg movements (normal study of choice)
Full polysomnography - oximetry, snoring, body
movement, heart rate, oronasal flow,
chest/abdominal movements, leg movements, EEG, EMG

199
Q

Simple approaches to OSA management?

A

Weight loss
Sleep decubitus rather than supine
Avoid/reduce evening alcohol intake

200
Q

Management of OSA for patients who snore or have mild disease?

A

Mandibular advancement devices
Consider pharyngeal surgery as last resort

201
Q

Management of significant OSA?

A

Nasal CPAP
Consider gastroplasty/bypass
(Rarely) tracheostomy

202
Q

How is severe OSA & CO2 retention managed?

A

May require period of NIV prior to CPAP if acidotic but compensated CO2 may reverse with CPAP alone

203
Q

OSA driving advice?

A

Do not drive whilst sleepy
Patient must notify DVLA
The doctor can advise drivers to stop altogether (e.g. HGV)

204
Q

How is CPAP given, and how does it help OSA?

A

Usually given via nasal mask, but can use mouth/nose masks
Upper airways splinted open with aproximately 10cm H20 presure - this prevents airways collapse, sleep fragmentation, daytime somnelence
Also opens collapsed alveolia and improves V/Q matching

205
Q

Why is CPAP not considered ventilatory support?

A

CPAP supplies constant positive pressure during inspiration and expiration (and is therefore not a form of ventilatory support)

206
Q

How can CPAP be used?

A

Treat OSA
Helps oxygenation in some patients with acute respiratory failure

207
Q

How does BIPAP provide ventilatory support?

A

Two levels of positive pressure - pressure support provided between selected inspiratory and expiratory positive pressures (IPAP and EPAP)
They can also be set up with back up rates so the machine operates when the respiratory rate drops below a fixed level

208
Q

Examples of SYMPATHOMIMETICS?

A

Short acting: salbutamol, terbutaline
Long acting: formeterol, salmeterol

209
Q

What drug class is salbutamol and how long do its effect last?

A

SABA
4-6 hours

210
Q

What drug class is formeterol and how long do its effects last?

A

LABA
12 hours

211
Q

How are SABAs and LABAs excreted?

A

Urine

212
Q

How are SABAs and LABAs metabolised?

A

Liver

213
Q

Common side affects of SABAs and LABAs

A

Tremor
Headache
GI upset
Palpitations
Tachycardia
Hypokalemia

214
Q

Main indication of SYMPATHOMIMETICS?

A

Bronchospasam

215
Q

What should LABAs be combined with?

A

ICS

216
Q

How do SYMPATHOMIMETICS (LABAs and SABAs) act?

A

B2 selective adrnergic agonist
Increase cAMP in SMC’s resulting in relaxation and thus bronchodilation

217
Q

Examples of antimuscarinics?

A

Short acting: Ipratropium (inhaler or liquid for nebs)
Long acting: Tiotropium

218
Q

Indications of SAMAs and LAMAs?

A

Bronchospasam, typically in COPD

219
Q

Common side effects of SAMAs and LAMAs?

A

Dry mouth
Constipation
COugh
Headache

220
Q

How do SAMAs and LAMAs work?

A

Muscarinic antagonist
Decreases cGMP which affects intracellular calcium resulting in decreased SMC contractility

221
Q

What conditions should SAMAs and LAMAs be used with caution in?

A

Angle-closure glucoma
BPH

222
Q

How are SAMAs and LAMAs metabolised?

A

(Partially) liver

223
Q

How are SAMAs and LAMAs excerted?

A

Urine

224
Q

Examples of Xanthines?

A

Aminophylline
Theophylline

225
Q

Main indications for xanthines?

A

Asthma
COPD

226
Q

How do xanthines such as aminophylline act?

A

Block phosphodiesterases resulting in decreased cAMP breakdown causing bronchidilation
Also have positive chronotropic and inotropic effects, diuretic action

227
Q

What action does cAMP have on bronchial smooth muscle?

A

Bronchodilation

228
Q

How does cGMP affect SMC?

A

Increases contractility (via its affect on intracellular calcium)

229
Q

How are xanthines excerted?

A

Urine

230
Q

How are xanthines metabolised?

A

Liver

231
Q

Common side effects of Xanthines such as Aminophylline and Thenophylline?

A

Headache
GI upset
Reflux
Palpitations
Dizziness

232
Q

What is the threaputic window of Xanthines and what might happen if it is exceeded?

A

Plasma level 10-mg/L
Toxic effects are serious arrhythmias
Seizures
N&V
Hypotension

233
Q

What preparations are xanthines available in?

A

PO and IV
NOTE never give a loading dose of IV aminophyline if patient is on regular PO preperation

234
Q

What should be monitored when a patient is on an IV infusion of aminophylline?

A

BP and heart rate due to risk of arrythmia and hypotension

235
Q

Examples of inhaled corticosteroids?

A

Beclomethasone
Budesonide
Fluticasone

236
Q

Brand name for salbutomol?

A

Ventolin
Blue inhaler

237
Q

What are the brown inhalers asthmatics may take?

A

ICS

238
Q

Which inhaler is red and white?

A

Symbicort
Budesonide (ICS) + formoterol (LABA)

239
Q

Main indications for ICS?

A

Asthma
COPD

240
Q

Mechanisms of ICS (glucocorticoid)?

A

Increase airway calibre by decreasing bronchial inflammation +/- modifying allergic reactions
Also weak mineralcorticoid activity

241
Q

How are ICS excreted?

A

Urine

242
Q

How are ICS metabolised?

A

Liver

243
Q

Common side effects of ICS?

A

Cough
Oral thursh
UNpleasent taste
Hoarseness

244
Q

Examples of corticosteroids (glucocorticoids) and their routes of adminsitration

A

Prednisolone - PO
Hydrocortisone - IM/IV
Dexamethasone - PO/IV
Triamcinolone - IM

245
Q

How do corticosteroids act?

A

Alter gene transcription
Anti-inflammatory
Immunosupressive
INcrease gluconeogensis
Decrease glucose utilisation
Increase protein catabolism

246
Q

How are corticosteroids excreted?

A

Urine

247
Q

How are corticosteroids metabolised?

A

Liver

248
Q

Main indications for corticosteroids?

A

Supress inflammation, allergy and immune response

249
Q

Side effects of corticosteroids?

A

Common:
Adrenal supression (especially courses > 3 weeks)
Hyperglycaemia
Psychosis
Insomnia
Indegestion
Mood swings
Other:
Diabetes
Cataracts
Galucoma
Peptic ulceration
Suscepatbility to infections
Osteoperosis
Muscle wasting
Skin thinning
Cushingoid appearance

250
Q

What may need to be prescribed along side corticosteroids?

A

PPI (reduce GORD)
Bisphosphonates (bone protection)

251
Q

In obstructive lung diease what will FEV1:FVC be and why?

A

Decreased <0.7
FEV1 is decreased

252
Q

What percentage of bronchodilater reversability is indicative of asthma?

A

12%

253
Q

What will FVC be in COPD?

A

Normal
Decreased in severe disease

254
Q

What will FVC be in asthma?

A

Decreased - small airways close permanently

255
Q

If there is air trapping due to small airway collapse, how will TLC and FRC be affected?

A

Increased because of increased RV

256
Q

What is DLCO?

A

Diffusing capacity carbon monoxide

257
Q

What does DLCO determine?

A

How much oxygen travels from alveoli of lungs to bloodstream - i.e. diffusion
Provides information on alveolar-capilary (vascular) membrane

258
Q

IN what conditions may DLCO be decreased and why?

A

Emphysema (decreased surface area)
Alveolar inflammation (increased thickness)
Pulomnary fibrosis (increased thickness)

259
Q

What does an abnormal DLCO with normal CXR and spirometry suggest?

A

Problem with vascular part of alveolar-capillary membrane
Idiopathic PAHTN
Chronic thromboembolic disease of lung

260
Q

How do you differentiate between restirctive lung diseases?

A

Parenchymal lung diseases, such as ILD, will have a restictive pattern on spirometry AND abnormal DLCO
Restricitve lung disease related to abnormalities in the chest wall, such as kyphoscoliosis, will have a normal DCLO
Restrictive lung disease related to neuromuscualr disease, for example myasthenia gravis, will have normal DCLO

261
Q

What will FEV1:FVC ratio be in restrictive lung disease and why?

A

Normal or increased
Because FEV1 will be normal or decreased
And FVC will ALWAYS be decreased

262
Q

What is chronic bronchitis?

A

Daily productive cough that last for 3 months of the year
Occuring for at least two years in a row

263
Q

What is acute bronchitis?

A

Lining of the bronchial tube becomes inflammed, causing cough, mucus SOB and mild fever

264
Q

What is empyhsema?

A

Destruction and dilation of the alveoli of the lungs

265
Q

What is meant by blue bloater - type COPD and what are its features?

A

Chronic bronchitis dominant COPD
Chronic productive cough, purulent sputum
CO2 retention (insensitive to it)
Cyanosis
Crackles/wheeze
Obesity
Peripheral odema

266
Q

What is meant by pink puffer - type COPD and what are its features?

A

Emphysema dominant COPD
Minimal cough
Tachypnea, increased minute ventilation
Co2 responsive - compensatory ventilation
Pink skin
Pursed breathing
Accessory muscle use
Barrel chest
Decreased breath sound
Cachexic appearance

267
Q

What is a type 1 hypersensitivity reaction?

A

Immediate (5 mins)
Allergy/asthma
IgE mediated

268
Q

What is a type 2 hypersensitivity reaction?

A

Antibody mediated 5-12h
Antibody binds with cell surface antigen to activate compliment resulting in cell and organ damage
IgG/IgM mediated

269
Q

What is a type III hypersensitivity reaction?

A

Soluble antigen complex forms causing immune complex to be deposited resulting in damage and disease development
IgG/IgM, immune complex mediated 3- 8 hours

270
Q

What is a type IV hypersensitivity reaction?

A

Cell mediated - delayed, 24 hour to 72 hour

271
Q

What are the two phases of hypersensitivity reaction?

A

Senitisation phase - initial exposure to antigen
Effector phase - re exposure to antigen

272
Q

How is a type I hypersensitivity reaction treated?

A

Allergen desentisiation
Anti IgE antibody
Antihistamine
Leukotrine receptor antagonist (cytokine storm)
Corticosteroids

273
Q

What is type 1 respiratory failure?

A

Low pO2
Normal or low pCO2

274
Q

What is type 2 respiratory failure?

A

low pO2
High pCO2

275
Q

What may cause shunting leading to hypoxaemia?

A

Intrapulmonary shunts - ARDs
Right to left shunts - cyanotic heart disease, blood from the right side of the heart enters the left side without passing through the lungs and taking part in gas exchange

276
Q

Why can excessive oxygen administration can lead to hypercapnic respiratory failure in some COPD patients?

A

increased V/Q mismatch
Haldane effect

277
Q

Why can excessive oxygen administration can lead to hypercapnic respiratory failure in some COPD patients due to V/Q mismatch?

A

In COPD, patients optimise their gas exchange by hypoxic vasoconstriction leading to altered alveolar ventilation perfusion ratio
Excessive oxygen administration overcomes this, leading to increased blood flow to poorly ventilated alveoli, so physiological dead space is increased
This increase in Va/Q mismatch occurs in both CO2 retainers and non-retainers

278
Q

Why can excessive oxygen administration can lead to hypercapnic respiratory failure in some COPD patients due to the Haldane effect?

A

deoxygenated Hb binds CO2 with greater affinity than oxygenated hemoglobin (HbO2)
hence oxygen induces a rightward shift of the CO2 dissociation curve, which is called the Haldane effect
in patients with severe COPD who cannot increased minute ventilation, the Haldane effect accounts for about 25% of the total PaCO2 increase due to O2 administration

279
Q

What is the mechanism of action of bupropion?

A

Norepinephrine and dopamine reuptake inhibitor, and nicotinic antagonist

280
Q

Where should a chest drain be inserted?

A

The triangle of safety for chest drain insertion involves the
base of the axilla,
lateral edge pectoralis major,
5th intercostal space and the
anterior border of latissimus dorsi

281
Q

Esculation of care in asthma attack?

A

The SIGN guidelines give clear instructions on how to escalate care.
1. Oxygen
2. Salbutamol nebulisers
3. Ipratropium bromide nebulisers
4. Hydrocortisone IV OR Oral Prednisolone
5. Magnesium Sulfate IV
6. Aminophylline/ IV salbutamol

282
Q

What is an indication for surgery in bronchiectasis

A

Localised disease is an indication for surgery in bronchiectasis

283
Q

How long after a first dose of inhaler should you wait to adminster the second dose?

A

30 seconds

284
Q

Inhaler technique for metered dose inhaler?

A
  1. Remove cap and shake
  2. Breathe out gently
  3. Put mouthpiece in mouth and as you begin to breathe in, which should be slow and deep, press canister down and continue to inhale steadily and deeply
  4. Hold breath for 10 seconds, or as long as is comfortable
  5. For a second dose wait for approximately 30 seconds before repeating steps 1-4.

Only use the device for the number of doses on the label, then start a new inhaler.

285
Q

How long after resolution of pneumonia should a patient have a repeat x ray?

A

6 weeks

286
Q

Commonest causes of an anterior mediastinum mass?

A

The commonest causes of an anterior mediastinum mass can be remembered by the 4 T’s: teratoma, terrible lymphadenopathy, thymic mass and thyroid mass

287
Q

ACE levels in sarcoidosis?

A

High

288
Q

Smoking cessation treatment in pregnancy?

A

Nicotine replacement therapy
Stop smoking clinic referall
Bupropion and varenicline are contraindicated in women who are pregnant or breastfeeding and should not be offered to these patient.

289
Q

Causes of white lung on CXR

A

consolidation (central trachea)
pleural effusion (trachea pulled away from white out)
collapse (trachea pulled towards white out)
pneumonectomy (Trachea pulled toward the white-out)
specific lesions e.g. tumours (central trachea)
fluid e.g. pulmonary oedema (central trachea)

290
Q

What may be seen on CXR in bronchiectasis?

A

Parallel line shadows (often called tram-lines) are common in bronchiectasis and indicate dilated bronchi due to peribronchial inflammation and fibrosis.

291
Q

What do hyper resonance and reduced breath sounds indicate

A

pneumothorax

292
Q

What can mimic pneumothorax in COPD? What are they and how do they appear on CXR?

A

Bullae are air spaces in the lung measuring >1cm in diameter when distended. The most common cause of bullae is cigarette smoking and emphysema. Large bullae in COPD can frequently mimic a pneumothorax and therefore should be differentiated carefully when chest radiography in a smoker presents with large lucent areas.
On chest radiography, bullae appear as lucency without a visible wall.

293
Q

Contraindications to lung cancer surgery?

A

Contraindications to lung cancer surgery include SVC obstruction, FEV < 1.5, MALIGNANT pleural effusion, and vocal cord paralysis

294
Q

On which side is aspiration pneumonia more common and why?

A

Right
Large caliber and more verticle orientation of the right mainstem bronchus

295
Q

What INR is a relative contraindication to chest drain insertion?

A

INR >1.3 is a relative contraindication for chest drain insertion

296
Q

Treatment of choice for allergic bronchopulmonary aspergillosis

A

Oral glucocorticoids

297
Q

What is atelectasis and when should it be suspected?

A

Atelectasis is a common postoperative complication in which basal alveolar collapse can lead to respiratory difficulty. It is caused when airways become obstructed by bronchial secretions.
suspect in the presentation of dyspnoea and hypoxaemia around 72 hours postoperatively
Position patinet upright and chest physio

298
Q

What common asthma medication can cause oral thrush?

A

Beclomethasone or any other ICS as steroid have an immunosupressive effect and can increase susceptability to infection

299
Q

What type of pleural effusion will a mesothelioma?

A

Exudative pleural effusion

300
Q

What is the definition of a pneumothorax?

A

Presence of air or gas in the pleural cavity which is the potential space between the visceral and parietal pleura

301
Q

What type of effusions are para-pneumonic effusions?

A

Exudative

302
Q

What is the preffered treatment for atelectasis?

A

Chest physio

303
Q

Which condition is also known as ‘farmers lung’?

A

Extrinsic allergic alveolitis

304
Q

How can you classify chest infections?

A

Acute bronchitis
Pneumonia (CAP, HAP)
Infective exacerbation of asthma or COPD

305
Q

What most commonly causes acute bronchitis?

A

Viral infection, therefore usually self limiting and advised rest, drink adequete fluids, take paracetomol/ibuprofen if required

306
Q

What features would make pneumonia the likely cause of chest infection?

A

DEFINITION: X ray consolidation

But tell-tale features might include:
Productive cough
Fever

307
Q

How can squamous cell carcinoma of the lung cause hyperparathyroidism and hypercalcemia?

A

Ectopic production of PTHrP

308
Q

What kind of lesion might SCC produce on CXR?

A

Cavitating lesion

309
Q

Pleural effusion secondary to SLE or RA will have what complement level and will be most likely be what type of effusion and cause which antibody?

A

Low complement level
Exudative effusion
(Raised ANA in SLE)

310
Q

Typical TB CXR

A

Typical findings on chest X-ray in the context of tuberculosis include fibronodular upper lobe opacification; there may or may not be cavitation

311
Q

Classic X Ray finding in sarcoidosis

A

Symmetrical hilar and mediastinal lymphadenopathy is classically seen in patients with sarcoidosis, occurring in > 75% of cases

312
Q

Presentation of sarcoidosis

A

The most commonly affected sites include the respiratory system and skin (i.e. erythema nodosum). The disease also typically presents with constitutional symptoms such as fevers, malaise and arthralgias. Hypercalcaemia is often found and bilateral hilar lymphadenopathy is a classical chest x-ray finding.

313
Q

How is COPD without steroid responsive features or asthma features managed if the pt is not responding to a SABA/SAMA well?

A

COPD - still breathless despite using SABA/SAMA and no asthma/steroid responsive features → add a LABA + LAMA

314
Q

What must be done before NIV to r/o an absolute contraindication?

A

CXR R/O pneumothorax

315
Q

When should pts with COPD be assesed for long term o2 therapy?

A

very severe airflow obstruction (FEV1 < 30% predicted). Assessment should be ‘considered’ for patients with severe airflow obstruction (FEV1 30-49% predicted)
cyanosis
polycythaemia
peripheral oedema
raised jugular venous pressure
oxygen saturations less than or equal to 92% on room air

316
Q

How can COPD lead to increased hb?

A

V/Q mismatch > hypoxaemia > increased erythropoietin release from kidneys > polycythaemia

317
Q

How might a pt with a FEV1/FVC>0.7 ratio be diagnosed with COPD?

A

Patients can now be diagnosed with ‘mild’ COPD if their FEV1 predicted is > 80% if they have symptoms suggestive of COPD.

318
Q

What suggests left lingula consolidation on CXR?

A

The loss of the left heart border is a classic sign of left lingula consolidation.

319
Q

Post-trauma/Neurological disorder + Right Lower Lobe Consolidation

A

aspiration pneumonia

320
Q

What is a flail chest?

A

Multiple rib fractures with > or = 2 rib fractures in more than 2 ribs is diagnosed as a flail chest. This is associated with pulmonary contusion

321
Q

Causes of lower zone fibrosis?

A

R = Rheumatoid arthritis/ connective tissue disease
A = asbestosis
I = idiopathic pulmonary fibrosis
D = drugs –> amiodarone, bleomycin, methotrexate

322
Q

upper zone fibrosis causes

A

cystic fibrosis: see pulmonary manifestations of cystic fibrosis; pulmonary sarcoidosis; Langerhans cell histiocytosis; pulmonary tuberculosis; pneumoconioses. silicosis; allergic bronchopulmonary aspergillosis; chronic h ypersensitivity pneumonitis; histoplasmosis

323
Q

Stage 1 COPD FEV1?

A

80

324
Q

Stage 2 COPD FEV1?

A

50-80%

325
Q

Stage 3 COPD?

A

30-50%

326
Q

Stage 4 COPD?

A

Less than 30% FEV1 of predicted

327
Q

Bronchiectasis management?

A

Mucolynics and chest physio

328
Q

First line management of pulmonary HTN?

A

Prostaglandin:
Epoprostenol

329
Q

CXR pulmonary HTN?

A

DIalated pulmonary arteries
Right ventricular hypertrophy

330
Q

Most common causes of pneumonia in COPD?

A

Haemophilus influenza
Moraxella catarrhalis

331
Q

How long abx course in CAP?

A

Mild: 5 days
Moderate severe : 7 days

332
Q

CXR findings in lung cancer?

A

Hilar enlagement or collapse
PLeural effusion and collapse
Opacity/lesion

333
Q

How does mesothelioma present on CXR

A

Opacity along lung margin and fissures, not a true lung cancer - cancer of mestothelia

334
Q

What is lambert-eaton myasthenic syndrome

A

SCC produces autimmune antibodies that attack motor neurones

Dysphagia
Dry mouth
Slurred speech
aching muscles
difficulty walking and climbing stairs
difficulty lifting objects or raising the arms
drooping eyelids, dry eyes and blurred vision
swallowing problems
dizziness upon standing

335
Q

Exudative pleural effusion is linked to problems with the actual lung such as?

A

TB
Lung cancer
Pneumonia
(RA)

336
Q

Transudative pleural effusion is not related to problems with the lung its self - what are the causes?

A

Hypoalbuminaemia
Hypothyroidism

337
Q

What causes a tension pneumothorax?

A

Trauma to chest

Pressure inside chest pushes trachea way from affected side
Can cause cardiac arrest
Haemodynamic instablity

338
Q

SOB or >2cm simple pneumothorax should be managed how?

A

Aspiration and reasses
If failed or unstable or bilateral chest drain (5th ics mid axilary line)

339
Q

<2cm simple pneumothorax should be managed how if no SOB?

A

Review in 2-4 weeks

340
Q

Calculation of Wells score for PE

A

History of DVT/ PE +1.5
Current mallignancy +1
Haemoptysis +1
Alternative diagnosis less likely than PE +3
Recent surgery or imobilisation +1.5
HR>100 +1
Clinical signs of DVT +3

More than 4 CTPA, less D dimer and CTPA as per result

341
Q

What might happen if a pleural effusion is drained too quickly?

A

If a pleural effusion is drained too quickly, a rare but important complication that can develop is re-expansion pulmonary oedema

342
Q

SEVERE ASTHMA

A

Peak flow less than 50% but more than 33%
Pules over 100
RR over 25
Can’t complete sentences

343
Q

LIFE THREATENING ASTHMA

A

Bradycardia
Silent chest
Peak flow less than 33%
Deminished respiratory effort
Hypotension
Echuastion
Coma
Hypercarbia

344
Q

Why does hypercalcemia occur in sarcoidosis?

A
  1. Uncontrolled syntesis of 1,25-dihydroxyvitamin D3 (calcitrol) by macrophages
  2. Increased resorption of calcium in the bone
345
Q

Treatment of sarcoidosis

A

80% require no treatment - spontaneous remission

Steroids if no improvement, disfiguring skin disease, persisten progressive pulmonary disease

Persistent hypercalcemia - systemic steroids

Uveitis - referal to opthalmology

Hypersplenism - steroids

End organ involvement - steroids

346
Q

Causes of bilateral hilar lymphadenopathy?

A
  1. Sarcoidosis
  2. Tuberculosis
  3. Lymphoma
347
Q

Dull percussion note on ascultation of the chest?

A

Think malignancy

348
Q

Common causes of unilateral effusion common causes?

A

Mallignancy
Pneumonia

Do CT scan diagnostic aspiration

349
Q

Paraneolplastic syndromes?

A

Humoral hypercalcemia -squamous cell carcinoma
Syndrome of inappropriate antidiuretic hormone production - non–small-cell lung cancer (NSCLC)
Cushing’s syndrome - non–small-cell lung cancer (NSCLC)
Acromegaly - squamous cell carcinoma
Carcinoid syndrome - neuroendocrine
Gynecomastia - adenocacinoma
Hyperthyroidism - squamous cell carcinoma

350
Q

Scan changes in TB?

A

Bilateral hetrogenous shaddowing, predominantly in upper lobe - CXR
Thick walled cavity on CT
Upper zone cavity - CXR
Bilateral shaddowing and infiltrateds

351
Q

What resp infection shows acid fast bacili on Ziehl-Neelsen (Acid Fast) Staining procedure ?

A

TB

352
Q

Mechnaism of hypoxia in pneumothorax?

A

V/Q mistmatch

353
Q

Why are recreational drug users at higher risk of pneumothorax?

A

Bleb formation

354
Q

Which side is the trachea deviated to in tension pneumothorax?

A

If one side of the chest cavity has an increase in pressure (such as in the case of a pneumothorax) the trachea will shift towards the opposing side

355
Q

Lung collapse vs massive pleural effusuon?

A

Lung collapse, trachea pulled to affected side
Pleural effusuon, trachea pushed away

356
Q

Symptoms associated with Pancoast tumour (sqaumous cell)

A

Ptosis
Anhydrosis
Miosis (small pupil)

(Hoarse voice)

357
Q

How can lung cancer cause hypercalcemia?

A

Humoral hypercalcemia of malignancy due to parathyroid hormone-related protein
Parathyroid hormone secretion
1,25-dihydroxyvitamin D production
Granulocyte colony-stimulating factor release
Osetolytic activity at the sites of skelteal mets

358
Q

Dermatomyosis signs?

A

Heliotrope rash (face around eyes)
Nail fold changes
Gottron lesions (scaly erythematous patches) on the knuckles, elbows and knees
Photosensitive erythematous rash on the back, shoulders and neck
Purple rash on the face and eyelids
Periorbital oedema (swelling around the eyes)
Subcutaneous calcinosis (calcium deposits in the subcutaneous tissue)

359
Q

How might aspirigilloma present on cxr?

A

target-shaped lesion in the right upper lobe with air crescent sign present.

360
Q

Characteristic findings on CXR due to aspestos exposure

A

The presence of bilateral multiple calcified pleural plaques is characteristic of asbestos exposure, especially if they involve the diaphragmatic pleura.

361
Q

Immediate management of pulmonary odema

A

High flow oxygen therapy via rebreathe mask

Diamorphine 2.5mg IV

Furosemide 40mg IV

Loading dose Digoxin 500micrograms over 30 mins IV

Year 3 Medicine (8 decks)

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