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Y3 med old > RESPIRATORY > Flashcards

RESPIRATORY Flashcards

1
Q

What is the characteristic finding on high resolution CT thorax with Interstitial Lung disease?

A

Ground glass appearance
May also be described as honeycombing

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2
Q

What is the prognosis of interstitial lung disease?

A

Prognosis is poor as damage is irreversible

Management is mainly supportive

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3
Q

How does Idiopathic Pulmonary Fibrosis present?

A

Insidious onset
dry cough
Shortness of breath
over more than 3 months

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4
Q

Define pulmonary embolism

A

Where a thrombus forms in the pulmonary arteries.

Usually result of DVT that has developed in legs and embolised (moved from one part of circulation to another) through the venous system

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5
Q

How does pulmonary embolism affect blood flow?

A

Once in pulmonary arteries, blocks blood flow to lung tissue.

Creates strain on R side of heart

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6
Q

Risk factors for PE?

A 
Immobility / long flights
Pregnancy 
Obesity (>29 kg/m2)
Recent surgery (>30min procedures)
DVT or previous VTE
Contraception - OCP, hormone therapy with oestrogen 
Tumours 
Thrombophillia 
Polycythemia 
SLE (as SLE is an inflammatory condition). 
Age (40+)

Booklet has it grouped as follows:

1) Surgery - Abdo, pelvic; Knee, hip replacement, post-op
2) Obstetris - late pregnancy, C section
3) LL - fracture, varicose veins
4) Malignancy - Abdo, pelvic, mets, advanced
5) Reduced mobility
6) Previous VTE.

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7
Q

Presentation of PE?

Give symptoms and signs

A

Symptoms :

Dyspnoea / SOB - most common.
Pleuritic chest pain
Cough +/- haemoptysis

Signs:

Hypoxia 
Tachycardia 
Hypotension - haemodynamic instability 
Raised RR 
Low grade fever

Note: may have S+S of a DVT - unilateral leg swelling, tenderness.

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8
Q

What scoring system can be used when patient presents with S+S of PE?

A

Wells score

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9
Q

What does Wells score predict?

A

The risk of a patient presenting with symptoms ACTUALLY having a DVT or PE.
Ca

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10
Q

Criteria in Wells score for PE?

A

Clinical S+S of DVT?
Is PE top differential?
HR >100?
Immobilised for 3 days or surgery in last 4 weeks?
Previous PE or DVT?
Haemoptysis?
Malignancy w/ treatment within 6 months or have palliative care for it?

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11
Q

Causes of bronchiectasis?

A

Post infective- Whooping cough/TB
Immune deficiency- Hypogammaglobulinaemia
Genetic- CF, primary cilary kinesia, young’s syndrome, kartagener syndrome
Obstruction- foreign body, tumour
Toxic insult- gastric aspiration,
Secondary immune deficiency- HIV

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12
Q

Next step if Wells score outcome is: Unlikely?

A

D-dimer. If this is positive - then do CTPA

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13
Q

Conditions that cause raised d-dimer?

A 
DVT, PE 
Pneumonia 
Malignancy 
Heart Failure 
Surgery 
Pregnancy
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14
Q

Investigations for suspected PE?

A

CTPA - IV contrast highlights pulmonary arteries
VQ scan - compare ventilation with perfusion. Used if CTPA is unsuitable. In PE, there will be deficit in perfusion.
D-dimer
Echocardiogram (if pt can not have CTPA)
FBC - thrombocytopenia, or anaemia, polycythaemia.
ECG
U+Es - for renal fuction to assess what drugs to use, and whether contrast can be used in CTPA
Coag screen - baseline before staring anticoagulant
LFTs - help choice of anticoagulant

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15
Q

ABG shows respiratory alkalosis for PE. So does hyperventilation. How to differentiate these two differentials?

A

PE = resp alkalosis with low pO2.

Hyperventilation = resp alkalosis with high pO2

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16
Q

Appearance of bronchiectasis on CT?

A

Signet rings

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17
Q

What is Young’s syndrome?

A

Triad of bronchiectasis, sinusitis, and reduced fertility

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18
Q

Methods of thrombolysis for PE?

A

IV - use peripheral cannula

Catheter-directed thrombolysis = directly into pulmonary arteries using central catheter

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19
Q

Risk of catheter-directed thrombolysis in PE?

A

Damage to pulmonary arteries

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20
Q

Bronchiectasis common organisms?

A 
Haemophilius influenzae
Non- tuberculous mycobacteria 
Fungi- aspergillus, candida 
Pseudomonas aeruginosa
Moraxella catarrhalis
Stenotrophomonas maltophilia
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21
Q

Management of bronchiectasis?

A

Treat underlying cause
Antibiotics/ IV for severe infection
Flu and Covid vaccines
Bronchodilators
Antibiotic prophylaxis for those with recurrent infections
Physiotherapy for mucus/airway clearance
Pulmonary Rehab – MRC Dyspnoea Score >3

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22
Q

What is the MRC dyspnoea score?

A

Used to assess the degree of baseline functional disability due to dyspnoea.

Breatheless with strenuous exercise-0

Breathless when walking up slight hill 1

Walk slower than people their age due to breathlessness/ has to stop walking due to breathlessness 2

Stop walking after 100m as am breathless 3

Too breathless to leave the house/ breathless when dressing/ undressing- 4

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23
Q

How to identify pt with acute exacerbation of bronchiectasis

A

A person with bronchiectasis with a deterioration in 3 or more key symptoms for at least 48 hours:
Cough
Sputum volume and / or consistency
Sputum purulence
Breathlessness and / or exercise tolerance
Fatigue
Haemoptysis

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24
Q

Management of PE

A

ABCDE
Oxygen if hypoxic
Analgesia if pain
Subcut LMWH (enoxaparin, dalteparin) whilst awaiting CTPA
Confirmed PE on CTPA - long term anticoagulant needed (warfarin, doac, LMWH).

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25
Q

Pt has massive PE. What is management?

A 
ABCDE
Oxygen if hypoxic 
Analgesia 
Subcut LMWH while waiting for CTPA 
Thrombolysis with IV alteplase
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26
Q

What is thrombolysis?

A

Inject fibrinolytic meds that break down clot rapidly.

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27
Q

Risk of thrombolysis?

A

Bleeding risk

There is 4% risk of an intracranial bleed

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28
Q

Examples of thrombolytic agents?

A

Alteplase
Streptokinase
Tenecteplase

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29
Q

What is Allergic Bronchopulmonary Aspergillosis (ABPA)

A

Caused by aspergillus fumigatus exposure

Combination of Type 1 and 3 hypersensitivity reactions following inhalation of fungal spores

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30
Q

What can ABPA cause?

A

Bronchiectasis

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31
Q

Who is at risk of ABPA?

A

Asthma, bronchiectasis and CF

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32
Q

How do you diagnose ABPA?

A

Dry cough, wheeze,

Raised Aspergillus IgE level, high Total IgE and high eosinophils

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33
Q

Risk of catheter-directed thrombolysis?

A

Damage to pulmonary arteries

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34
Q

Absolute contraindications for thrombolysis?

A 
Haemorrhagic stroke or ischaemic stroke within 6 months 
CNS neoplasia 
Recent trauma/surgery 
GI bleed less than 1month ago 
Bleeding disorder
Aortic dissection
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35
Q

Relative contraindications for thrombolysis?

A

Warfarin/DOAC use
Pregnancy
Advanced liver disease
Infective endocarditis

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36
Q

Presentation of pleural effusion?

A 
SOB - gradual 
Pleuritic chest pain 
Non productive cough - not as common
(productive cough - only if due to pneumonia)
Tachycardia
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37
Q

Investigations for pleural effusion?

A

Imaging: PA CXR. USS . Contrast CT (good for exudative effusions). ECHO (if suspect HF)

Pleural aspiration: fluid sent for pH, protein, MC&S, glucose.

Bloods: FBC. CRP, blood culture, U+Es, LFTs, bone profile, LDH, clotting

Sputum: sputum gram stain and culture

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38
Q

RF for pleural effusion?

A

CCF
Malignancy
Pneumonia

Weaker RF:
SLE, RA, recent MI, renal failure, nephrotic syndrome, drug induced - e.g. nitrofurantoin,

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39
Q

Management for pleural effusion?

A

Ultrasound guided pleural aspiration
Conservative management if small
Chest drain

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40
Q

Examination findings/ signs in pleural effusion?

A 
Reduced chest movement on affected side 
Stony dull percussion 
Reduced/absent breath sounds 
Reduced vocal resonance 
Tracheal deviation
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41
Q

Define exudate and transudate classification of pleural effusion

A

Exudate: Pleural protein concentration more than 30g/L

Transudate: less than 30g/L protein.

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42
Q

Transudate causes of pleural effusion?

A

Transudative = fluid moving across into the pleural space

Heart Failure
Hypoalbuminaemia (nephrotic syndrome or peritoneal dialysis)
Liver cirrhosis 
Hypothyroidism 
Pulmonary embolism 
Mitral stenosis

Rare:
Meigs’ syndrome (triad of benign ovarian tumor with ascites and pleural effusion that resolves after resection of the tumor).
Constrictive pericarditis
Superior vena cava obstruction

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43
Q

Exudate causes of pleural effusion?

A

Exudative = inflammation related - causes protein to leak out of tissue and into pleural space

Infection - pneumonia, TB, subphrenic abscess, TB. HIV (kaposi’s).
Malignancy - lung cancer, mets
Inflammatory causes - Connective tissue disease, RA, SLE, Pancreatitis, lymphatic disorders, PE

Rare: yellow nail syndrome, fungal infections, drugs

Z2F : main ones - lung cancer, pneumonia, RA, Tb

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44
Q

Define empyema

A

Infected pleural effusion.

Z2F: suspect when pt has improving pneumonia but new or ongoing fever.
Pleural aspiration shows pus, acidic <7.2, low glucose and high LDH

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45
Q

How is empyema managed?

A
  • Chest drain - remove pus.
  • antibiotics based on sensitivity - usually for 3 weeks
  • supportive care - pain relief, IV fluids, early mobilisation.

bmj bes practice

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46
Q

What can CF be diagnosed based on?

A

One or more characteristic phenotypic features OR history of CF in a sibling OR positive newborn screening test result

PLUS:

Increased sweat chloride concentration (>60mmol/L Na+, Cl-) in sweat test
OR
Identify of two CF mutations - genotyping
OR
Demonstration of abnormal nasal epithelial ion transport

Note: Quesbook says the following:

  • Neonatal heel prick day between day 5 and day 9
  • Sweat test: sweat sodium and chloride >60mmol/L
  • Faecal elastase: this can provide evidence for abnormal pancreatic exocrine function.
  • Genetic screening: This can identify CF mutations
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47
Q

Pathophysiology of CF?

A

Autosomal receive condition.
Mutation in CFTR gene (which usually regulates sodium channel called ENAC)
Mutation in CFTR gene
—> increases Na+ absorption
—> get abnormal Chloride secretion (as CFTR usually codes cAMP regulated chloride channel) in epithelial cells lining the airways,
—>less water secreted
—> OVERALL: get thicker mucus= impair cilia function

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48
Q

Presenting features of CF?

A

Presenting features:
- Meconium ileus:
is in newborns, bowel is blocked by sticky secretions. Have signs of intestinal obstruction soon after birth - billows vomiting, abdominal distension, delay in passing meconium.

  • Intestinal malabsorption:
    main cause is severe deficiency of pancreatic enzymes
  • Recurrent chest infections
  • Newborn screening
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49
Q

Respiratory features of CF?

A 
Chronic sinusitis 
Nasal polyps 
Cough
Wheeze 
Haemoptysis 
Recurrent LRTI
Bronchiectasis 
Pneumothorax
Cor pulmonale 
Respiratory failure
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50
Q

Apart from respiratory system, CF causes multi-organ damage. What are features of damage in:
1. GI system?

A
  1. Pancreatic insufficiency, so have DM and/or steatorrhea
    Cirrhosis
    Portal HTN
    Gallstones
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51
Q

Apart from respiratory system, CF causes multi-organ damage. What are features of damage in:
2.. Reproductive system?

A
  1. Male infertility
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52
Q

Apart from respiratory system, CF causes multi-organ damage. What are features of damage in:
3. MSK?

A
  1. Clubbing
    Arthritis
    Osteoporosis
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53
Q

Investigations in known CF patients (to monitor disease aseverity, assess symptoms etc)?

A 
Sputum culture - chest infection
Glucose tolerance test - assess DM 
Bloods - FBC, U+Es, coat screen, vitamins, blood sugar, bone profile
Spirometry: obstructive defect
Aspergillus skin prick test or serology

Imaging: CXR - bronchiectasis, hyperinflation
Abdominal ultrasound - Distal Intestinal Obstruction, liver cirrhosis, chronic pancreatitis

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54
Q

Lifestyle advice for pts with CF?

A

No smoking
Avoid other CF pts
Avoid friends/relatives with colds and infections
Avoid jaccuzis (pseudomonas)
Clean and dry nebulisers thoroughly
Avoid stables, compost or rotting veg - Aspergillus inhalation
Annual flu vaccine
Sodium chloride tablets in hot weather/exercise

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55
Q

Medical management for infective exacerbation of CF?

A
  • Antibiotics, although for patients with recurrent chest infections prophylactic long-term antibiotics may be prescribed.
  • Nebulised mucolytics (Dornase Alfa)
  • Bronchodilators (Inhaled corticosteroids or B2-agonists)
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56
Q

Medical management for pancreatic insufficiency in CF?

A

Insulin replacement
Creon - exocrine enzymatic replacement
Vitamins - A, D, E, K

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57
Q

Medical management for worsening progressive lung disease in CF?

A

Oxygen therapy
Ventilation
Diuretics (especially if have cor pulmonale)

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58
Q

Presentation of asthma:

a) Symptoms?
b) Signs?

A 
a) Symptoms: 
Wheeze
Dyspnoea
Cough (may be nocturnal)
Chest tightness
Diurnal variation (symptoms often worse in the morning)
b) Signs:
Tachypnoea
Hyperinflated chest
Hyper-resonance on chest percussion
Decreased air entry (sign of severe illness: silent chest)
Wheeze on auscultation
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59
Q

Investigations for suspected asthma?

A
  1. Peak flow: variability >20%
  2. Fractional exhaled nitric oxide (FeNO): >40 ppb in adults or >35 ppb in children
  3. Spirometry with bronchodilator reversibility: FEV1/FVC < 0.7 (obstructive spirometry). Improvement of FEV1 > 12% after bronchodilator therapy is diagnostic
  4. Bloods - FBC, U+Es, ABG
  5. CXR
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60
Q

Non - pharmacological management of asthma? (not an acute attack)

A

Smoking cessation
Avoidance of precipitating factors (eg. known allergens - dust, animal hair, cold air etc)
Review inhaler technique

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61
Q

Pharmacological management of asthma? (not an acute attack)

A

Step 1: short-acting inhaled B2-agonist (eg. Salbutamol)
Step 2: add low-dose inhaled corticosteroid steroid (ICS)
Step 3: add long-acting B2-agonist (eg. Salmeterol). If no benefit, stop this and increase ICS dose; if benefit but inadequate control, continue and increase ICS dose.
Step 4: Trial oral leukotriene receptor antagonist, high-dose steroid, oral B2-agonist

(from Quesmed - see NICE guidelines too)

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62
Q

Investigations for acute asthma attack?

A

ABG: type 2 respiratory failure (low PaO2 and high PaCO2) is a sign of a life-threatening attack.

Routine blood tests (including FBC, CRP): to look for precipitating causes of an asthma attack, such as an infection.

Chest x-ray: to exclude differentials and possibly identify a precipitating infection.

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63
Q

Management of acute asthma attack?

A
  • ABCDE - Ensure a patent airway
  • Ensure oxygen saturations of 94-98%, ABG if O2 sats <92%
  • Nebulisers: Salbutamol 5mg (can repeat after 15mins).
  • Steroids: oral Prednisolone 40mg STAT or IV Hydrocortisone (if PO not possible)
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64
Q

Differential diagnosis for asthma?

A 
Bronchiectasis 
COPD 
CF 
Foreign body aspiration (especially in children)
GORD 
HF 
Interstitial lung disease 
Lung cancer 
Pertussis
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65
Q

2 Main types of lung cancer?

A

Small cell- 15% of cases and worse prognosis

Non-small cell- more common

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66
Q

Types of non-small cell lung cancer?

A

Adenocarcinoma
Squamous cell carcinoma
Large cell carcinoma

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67
Q

Most common type of lung cancer?

A

Adenocarcinoma

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68
Q

Symptoms of lung cancer?

A 
Persistent cough 
Haemoptysis 
Dyspnoea 
Chest pain 
Weight loss and anorexia 
SVC obstruction
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69
Q

What type of tumour causes a hoarse voice?

A

Pancoast tumour pressing on the recurrent laryngeal nerve

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70
Q

Sign of lung cancer?

A

Cachexia
Finger Clubbing
Hypertrophic pulmonary osteoarthropathy
Anaemia
Horner’s syndrome (if the tumour is apical)
Enlargement of supraclavicular and axillary lymph nodes
Paraneoplastic syndromes: Cushing’s syndrome, SIADH, and Lambert-Eaton syndrome (suggest small-cell), hyperparathyroidism (suggests squamous cell)

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71
Q

On auscultation of the lungs, how might lung cancer sound?

A

Features of consolidation (pneumonia); collapse (absent breath sounds, ipsilateral tracheal deviation); pleural effusion (Stony dull percussion, decreased vocal resonance and breath sounds)

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72
Q

Features of squamous cell carcinoma?

A

Typically central tumour
Associated with PTHrP- hypercalcaemia, finger clubbing and hypertrophic pulmonary osteoarthropathy
May also get hyperthyroidism due to ectopic TSH

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73
Q

Features of large cell carcinoma?

A

Peripheral
Usually anaplastic and poorly differentiated with poor prognosis
May secrete B-hCG

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74
Q

Features of small cell carcinoma?

A

Associated with ectopic ADH–> hyponatraemia
ectopic ACTH–> hyperglycaemia, hypertension, hypokalaemia, alkalosis, muscle weakness–> may get bilateral hyperplasia of the adrenal glands
Lambert- Eaton syndrome

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75
Q

What is Lambert- Eaton syndrome?

A

Antibodies to voltage gated calcium channel–> myasthenic like symptoms

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76
Q

What is SVC obstruction?

A

Oncological emergency

Compression of the SVC most commonly due to lung cancer

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77
Q

Features of SVC obstruction?

A 
Dyspnoea 
Swelling of face and neck, conjunctival and periorbital oedema 
Headache- often worse in the morning 
Visual disturbance 
Pulseless jugular venous distension
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78
Q

Management options for SVC obstruction?

A

Dependent on pt, options range from:
endovascular stenting for symptoms relief
Radical chemo or chemo-radio therapy
Glucocorticoids are usually given but evidence is weak

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79
Q

Investigations in suspected lung cancer?

A

Cxr- may see nodules, lung collapse, pleural effusion, consolidation, and bony metastases

CT- confirm diagnosis and to stage it, ensure adrenals and liver are also scanned to have a look

Bronchoscopy- allow biopsy to be taken

PET scanning- usually in non-small cell lung cancer–> eligibility for curative treatment. Uses 18-fluorodeoxygenase which is preferentially taken up by neoplastic tissue

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80
Q

Management of small cell lung cancer?

A

Most pts will be on palliative chemo

May try chemo-radiotherapy for some patients, however prognosis is poor

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81
Q

Management of Non-small cell lung cancer?

A

Only 20% suitable for surgery, before surgery mediastinoscopy performed as CT doesn’t always show mediastinal involvement

Curative or palliative radiotherapy
Chemo may be offered palliatively

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82
Q

Ddx for lung cancer?

A

pneumonia, bronchitis, exacerbation of COPD, mets from another site, sarcoidosis, TB

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83
Q

What blood abnormality would you most likely see in lung cancer?

A

Raised platelets

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84
Q

What is a pneumothorax?

A

When air gets into the pleural space separating lung from chest wall

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85
Q

Whats the difference between primary and secondary pneumothorax?

A

Primary- no underlying lung pathology

Secondary- if there is underlying lung disease

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86
Q

Causes of pneumothorax?

A

Spontaneous
Trauma
Iatrogenic- lung biopsy, mechanical ventilation, central line insertion
Lung pathology- asthma, COPD

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87
Q

What is catamenial pneumothorax?

A

Due to endometrisosis in the thorax. Occurs during/ after menstruation

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88
Q

Presentation of pneumothorax?

A 
Sudden onset:
Dyspnoea
chest pain: often pleuritic
sweating
tachypnoea
tachycardia
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89
Q

Investigations for pneumothorax?

A

Erect Cxr

CT thorax for small pneumothorax and can accurately asses the size of the pneumothorax

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90
Q

How do you manage a primary pneumothorax?

A

rim of air is < 2cm and the patient is not short of breath then discharge should be considered
otherwise, aspiration should be attempted

if this fails (defined as > 2 cm or still short of breath) then a chest drain should be inserted

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91
Q

How do you manage a secondary pneumothorax?

A

patient is > 50 years old and the rim of air is > 2cm and/or the patient is short of breath then a chest drain should be inserted.
otherwise aspiration should be attempted if the rim of air is between 1-2cm.

If aspiration fails a chest drain should be inserted.

All patients should be admitted for at least 24 hours
if the pneumothorax is less the 1cm then the BTS guidelines suggest giving oxygen and admitting for 24 hours

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92
Q

Where do you insert a chest drain?

A 
Safe triangle:
5th IC space 
Mid axillary line 
anterior axillary line 
within this triangle
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93
Q

What is a tension pneumothorax?

A

One way valve, not allowing air to escape, leading pressure to rise

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94
Q

Typical pneumothorax pt?

A

Young, tall and thin man presenting with SOB

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95
Q

Signs of tension pneumothorax?

A 
Tracheal deviation AWAY from side of the pneumothorax 
Reduced air entry on affected side 
Increased resonance on affected side 
Tachycardia 
Hypotension
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96
Q

Management of tension pneumothorax?

A

Insert a large bore cannula into the second IC space mid clavicular line

Then use a chest drain for definitive management

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97
Q

How does a patient with COPD present? divide into symptoms and signs

A 
Symptoms:
Productive cough sputum 
Wheeze
Dyspnoea
Reduced exercise tolerance
Signs :
Accessory muscle use
Tachypnoea
Hyperinflation
Reduced cricosternal distance
Reduced chest expansion
Hyper-resonant percussion
Decreased/quiet breath sounds
Wheeze
Cyanosis
Cor pulmonale (signs of right heart failure)
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98
Q

what DDx should you consider when thinking about COPD

A

Lung cancer
Heart failure
lung fibrosis

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99
Q

What might you see on examination of a pt with COPD?

A 
Tacchypnoea
Resp distress
accessory muscle use
intercostal retraction
barrel chest
wheezing 
coarse crackles
cyanosis 
Right sided heart failure (+ neck veins, heptatomegaly, LL oedema)
Asterexis -hypercapnia
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100
Q

Pneumonia on a chest xray?

A

Consolidation and air bronchogram

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101
Q

Signs of pneumonia

A 
Usually signs of sepsis:
Tachycardia
Tachypnoea
Hypoxia
Hypotension
Fever
Confusion
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102
Q

Chest signs of pneumonia

A

Bronchial breath sounds-
Focal coarse crackles
Dullness to percussion

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103
Q

Severity assessment for pneumonia

A 
CURB-65 (CRB-65 in community)
C- Confusion
U- Urea> 7
R- RR> 30
B- BP < 90 systolic or < or equal to 60 diastolic
65- age greater than or equal to 65
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104
Q

What is atypical pneumonia?

A

Pneumonia caused by organisms that cannot be cultured by gram staining

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105
Q

What are bronchial breath sounds?

A

In pneumonia- harsh breath sounds equally loud on inspiration and expiration

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106
Q

What are focal coarse crackles?

A

Air passing through sputum in airways similar to using a straw blow air through a drink

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107
Q

What is CURB-65 for?

A

Predicts mortality: (1= 5% 3= 15%, score 4/5= 25%) and whether pt should be treated at hospital
0/1- consider treatment at home
greater than/equal to 2- consider treatment at hospital
greater than/equal to 3- consider intensive care assessment

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108
Q

How do you get Legionnaires’ disease?

A

Infected water supply or air condition units

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109
Q

What complication can Legionnaires’ disease cause?

i.e. note on bloods as a clue

A

Hyponatraemia–> SIADH

Lymphopenia

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110
Q

Typical Legionnaires’ exam patient?

A

Cheap hotel holiday and presents with hyponatraemia and lymphopenia

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111
Q

What are some investigations you might do for lung abscess?

A

CXR :

  • Fluid-filled space within an area of consolidation
  • air-fluid level is typically seen

sputum and blood cultures

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112
Q

Complications of mycoplasma pneumoniae?

A 
haemolytic anaemia 
Erythema multiforme 
meningioenchepalitis 
Guillan barre syndrome 
bullous myringitis: painful vesicles on the tympanic membrane
pericarditis/myocarditis
gastrointestinal: hepatitis, pancreatitis
renal: acute glomerulonephritis
113
Q

Causative organism for fungal pneumonia?

A

Pneumocystis jiroveci

114
Q

Who is at risk of fungal pneumonia?

A

Immunocompromised- esp HIV patients with low CD4 count

115
Q

How does fungal pneumonia present?

A

Dry cough with sputum production
SOB on exertion
Night sweats

116
Q

What are RF for empyema ?

A

recent pneumonia

iatrogenic intervention in the pleural space

thorax trauma

Immunocompromised e.g. diabetes, HIV , chemo, malnutrition

co-morbidities make pneumonia more likely aspiration - stoke/NG tube

lung disease

male sex

young or old age

alcohol abuse

117
Q

In a pt w/ symptoms and signs of infection + a significant pleural effusion what must be done urgently?

A

thoracentesis (pleural aspiration)

118
Q

Complications of pneumonia?

A 
Sepsis
Pleural effusion
Empyema
Lung abscess
Death
119
Q

Causes of pneumonia?

A

Streptococcus pneumoniae (accounts for around 80% of cases)
Haemophilus influenzae
Staphylococcus aureus: commonly after influenza infection
atypical pneumonias (e.g. Due to Mycoplasma pneumoniae)

120
Q

What are the most common bacterial organisms that cause infection exacerbations of COPD?

A

Haemophilus influenzae (most common cause)

Streptococcus pneumoniae

Moraxella catarrhalis

121
Q

What would you see on CXR with a patient with COPD?

A

hyperinflation
Bullae: if large, may sometimes mimic a pneumothorax
flat hemidiaphragm

122
Q

What is a lung abscess?

A

well-circumscribed infection within the lung parenchyma

123
Q

What are the causes / RF for a lung abscess?

A

Secondary to aspiration pneumonia e.g.
Poor dental hygiene
stroke (reduced consciousness)

infective endocarditis - haematogenous spread

direct extension - empyema

Bronchial osbtruction (secondary to lung tumour)

124
Q

What are some of the microbial causes of lung abscess?

A

often polymicrobial

Monomicrobial causes:
Staphylococcus aureus
Klebsiella pneumonia
Pseudomonas aeruginosa

125
Q

What are some of the symptoms of lung abscess?

A

Develop over weeks (like subacute pneumonia)

Systemic: night sweats / weight loss
Fever
productive cough (foul sputum, rarely haemoptysis)
chest pain 
SOB
126
Q

What are some of the signs you would see on examination of a lung abscess?

A

dull percussion

bronchial breathing

clubbing may be seen

127
Q

What are some investigatioins you might do for lung abscess?

A

CXR :

  • Fluid-filled space within an area of consolidation
  • air-fluid level is typically seen

sputum and blood cultures

128
Q

How would you manage a lung abscess?

A

IV antibiotics

Percutaneous drainage may be required

Rare: surgical resection

129
Q

What is an empyema?

A

Empyema is defined as the presence of frank pus in the pleural space

130
Q

What is a Parapneumonic effusion?

A

Parapneumonic effusions are effusions caused by an underlying pneumonia.

Simple - not infected

Complicated- effusion develops once infection has spread to the pleural space.

131
Q

How is empyema, a simple parapneumonic effusion and complicated parapneumonic effusion related?

A

Three conditions = a spectrum of pleural inflammation in response to infection.

From a simple parapneumonic effusion to empyema.

132
Q

What are RF for empyema ?

A 
recent pneumonia
iatrogenic intervention in the pleural space
thorax trauma 
Immunocompromised e.g. diabetes
co-morbidities make pneumonia more likely 
lung disease 
male sex
young or old age
alcohol abuse
133
Q

If empyema or a complicated parapneumonic effusion is diagnosed what must be done urgently?

A

Insert a chest drain

+ long course of AB

if no improvement with AB and drainage - surgery or fibrinolytics

134
Q

How do causative pathogens differ from comminity acquired and hospital acquired empyema?

A

Community: Streptococcus pneumoniae, and staphylococci

Hospital: staphylococci (particularly MRSA)

135
Q

How would a pt with empyema present?

A

Constitutional symp:
Malaise, anorexia, weight loss, fatigue
Pyrexia
Rigors

Examination:
dullness at the lung base
reduced breath sounds
reduced vocal resonance 
signs of sepsis
136
Q

What investigations for empyema?

A

Bloods:
Blood cultures - AB choice
FBC - WCC count
CRP

Imaging:
CXR - see effusion, loculated effusion suggests empyema. consolidation due to pneumonia.

Special tests: 
Thoracentesis : pleaural fluid:
appearance; pus diagnostic
Odor: putrid - anaerobic
PH: <7.2
total protein context > 30 g/l
LDH level >2-3 x upper limit of serum 
Glucose
WCC - lymphocytes -TB / malignancy
 MC&S
137
Q

What is type 1 respiratory failure?

A

Pa02<8kPa; PaC02 Normal

138
Q

Causes of type 1 respiratory failure?

A 
Asthma 
Congestive HF 
Pulmonary Embolism 
Pneumonia 
Pneumothorax
139
Q

What is type 2 respiratory failure?

A

Pa02<8kPa; PaC02 > 6kPa

140
Q

Causes of type 2 respiratory failure?

A

Obstructive lung disease e.g. COPD
Restrictive lung disease e.g. IDL
Depression of respiratory centre e.g. opiates
NMJ disease e.g. Guillan barre syndrome, MND
Thoracic wall disease- rib fracture

141
Q

What is ARDS?

A

Increased permeability of alveolar capillaries–> fluid accumulation in alveoli- non-cardiogenic pulmonary oedema

142
Q

Causes of ARDS?

A

Pulmonary: chest sepsis, aspiration, pneumonia, trauma, smoke inhalation
Non-pulmonary: DIC, acute pancreatitis, drug OD

143
Q

Presentation of ARDS?

A

Acute onset respiratory failure which fails to improve with supplemental O2.

Symptoms of severe dyspnoea, tachypnoea, confusion and presyncope

144
Q

Examination findings in ARDS?

A

fine bibasal crackles but no other signs of HF

145
Q

Investigations for ARDS?

A

Cxr with bilateral alveolar infiltrates w/o any other features of HF

146
Q

Management of ARDS

A 
V serious 
ICU 
Ventilatory support 
Haemodynamic support 
DVT prophylaxis 
Abx only if infectious cause for ARDS
147
Q

Characteristics of asthma? i.e. what is it?

A

Chronic inflammation disease of the airways
Obstructive but reversible (spontaneously or w treatment)
Increased airway responsiveness (i.e. narrowing) to variety of stimuli.

148
Q

Pt has a wheeze. What are most likely/common differentials?

A

Acute asthma exacerbation
Bronchitis - bacterial or viral

Less common:
Pulm oedema 
PE
GORD
Allergy 
Hyperventilation
Cardiac disease 
Churg-Strauss syndrome
149
Q

Define MILD asthma exacerbation based on:

1) PEFR %

2) features of severe asthma

A

1) >75%

2) no features of severe asthma

150
Q

Define MODERATE asthma exacerbation based on:

1) PEFR %

2) features of severe asthma

A

1) 50-75%

2) no features of severe asthma

151
Q

Define SEVERE asthma exacerbation based on:

1) PEFR %

2) features of severe asthma

A

1) 33-50%
2) Cannot complete sentences in one breath
RR>25
HR>110

(ANY ONE OF THESE PRESENT = SEVERE ASTHMA ATTACK)

152
Q

Define LIFE THREATENING asthma exacerbation based on:

1) PEFR %

2) features of severe asthma

A

1) <33%
2) Sats<92% or ABG pO2<8kPa
Cyanosis, poor response effort, silent chest
Exhaustion, confusion
Hypotension, arrythmias
normal pCO2

153
Q

Define NEAR FATAL asthma exacerbation based on features of severe asthma

A

RAISED pCO2

154
Q

Management of SEVERE (PEFR 33-50%) asthma attack?

A

Same as acute asthma attack

  • ABCDE - Ensure a patent airway
  • Ensure oxygen saturations of 94-98%, ABG if O2 sats <92%
  • Nebulisers: Salbutamol 5mg (can repeat after 15mins).
  • Steroids: oral Prednisolone 40mg STAT or IV Hydrocortisone (if PO not possible)

PLUS:

  • Nebulised ipratropium bromide 500micrograms
  • back to back salbutamol if needed
155
Q

Management of LIFE THREATENING (PEFR <33%) asthma attack?

A

Same as acute asthma attack PLUS

  • urgent ITU or anaesthetist assessment
  • Urgent portable CXR
  • IV aminophylline
  • Consider IV salbutamol if nebuliser route is ineffective.
156
Q

Criteria for safe asthma discharge after exacerbation?

A

PEFR >75%
Stop nebulisers 24hrs before discharge
Inpatient asthma nurse review to reassess inhaler technique and adherence
Provide PEFR meter and written asthma action plan
At least 5 day course of oral prednisolone
GP follow up within 2 working days
Resp clinic follow up within 4 weeks
Psychosocial factors considered before discharge

157
Q

Differentials of eosinophilia?

A 
Airway inflammation = COPD or asthma 
Hayfever/allergies 
Multiple courses of abx for chronic infections 
Eosinophillic pneumonia 
Parasites 
Lymphoma 
SLE
158
Q

Asthma triggers?

A 
Smoking 
Cold air 
Allergens - dust, pollen, pets
URTI - mainly viral
Occupational irritants
Pollution 
Drugs - aspirin, Bblocker
Food and drink - dairy, alcohol, orange juice
Stress
159
Q

How to manage chronic asthma?

A

Use BTS stepwise management guidelines
Assess and teach inhaler technique
Self management plans
Avoid triggers

160
Q

Management of CF?

A 
Physio airway clearance 
Exercise
Mucolytic treatment 
Pancreatic enzyme replacement therapy 
Fat soluble vitamin replacement 
Long term abx
Optimise CF related DM - insulin therapy 
Novel CFTR modulators = Kaftrio 
Long term monitoring for CF related DM, CF related liver disease, osteoporosis.
161
Q

(SARS-CoV-2) can cause viral pneumonia. What is the triad of symptoms hospitalised patients get?

A

Hypoxia
Lymphopenia
Bilateral, lower zone changes on CXR

162
Q

What is hospital management for SARS-CoV-2?

A
  1. O2 supplementation
    some may need CPAP / invasive ventilation
  2. Dexamethasone ( consider Tocilizumab +/- Remdesivir)
  3. AB may be needed if superadded bacterial infection
163
Q

What is Influenza?

A

Flu

Single stranded RNA virus.

most common cuaes of viral pneumonia in immunocompromised adults

164
Q

What serotypes of inluenza are there?

A

Three serotypes of influenza - A, B and C

Serotype- determined by surface antigens haemagglutinin and neuraminidase. These are rearranged in host organisms e.g. birds /animals = different strains e.g. Influenza A H5N1 (avian influenza)

165
Q

How is influenza transmitted?

A

via respiratory secretions

VVV contagious

166
Q

How long is incubation period for influenza?

A

typically 1-4 days

167
Q

How long is a pt infectious for with influenza after incubation period ?

A

patients can remain infectious for 7-21 days

168
Q

What are the symptoms of influenza?

A

Fever ≥ 37.8°C

Non-productive cough

Myalgia

Headache

Malaise

Sore throat

Rhinitis

169
Q

What are some pulmonary complications of Influenza?

A

Viral pneumonia,

secondary bacterial pneumonia,

worsening of chronic conditions e.g. COPD and asthma

170
Q

What are some Cardiovascular complications of Influenza?

A

Myocarditis

Heart failure

171
Q

What are some neurological complications of Influenza?

A

Encephalopathy

172
Q

What are some GI complications of Influenza?

A

Anorexia and vomiting are common

173
Q

How do you diagnose Influenza?

A

Routine viral culture

Rapid reverse transcriptase PCR tests are now available.

174
Q

What is the management of Influenza?

A
  1. Supportive (analgesia, antipyretic, fluids, oxygen)
  2. Antiviral treatment with neuraminidase inhibitors e.g. Oseltamivir (‘Tamiflu’)
  3. Infection control and respiratory isolation to prevent onward transmission
175
Q

What are the vaccine options for Influenza? Who is it recommended for?

A
  1. Inactivated vaccine tailored each year according to recent outbreaks.
    It provides partial protection against influenza
  2. those over 65, with chronic conditions. Healthcare workers and nursing home residents.
176
Q

What are some general clinical features of TB?

A
  1. Fever
  2. Night sweats
    drenching)
  3. Weight loss (weeks – months)
  4. Malaise
177
Q

What are some clinical features of Respiratory TB?

A

cough ± purulent sputum/haemoptysis

pleural effusion

178
Q

What are some clinical features of NON- Respiratory TB?

A

Skin (erythema nodosum)

Lymphadenopathy;

Bone/joint; (stiffness, abscess, swelling)

Abdominal; (pain/diarrhoea/distention)

CNS
(meningitis);

Genitourinary; (flank pain, dysuria, polyuria)

Miliary (disseminated);

Cardiac (pericardial effusion)

179
Q

What are you differentials for Haemoptysis : infection related?

A

Pneumonia

Tuberculosis

Bronchiectasis / CF

Cavitating lung lesion (often fungal

180
Q

What are you differentials for Haemoptysis : Malignancy related?

A

Lung cancer

metastases

181
Q

What are you differentials for Haemoptysis : Haemorrhage related?

A

Bronchial artery erosion

Vasculitis

Coagulopathy

182
Q

What are some differentials for Haemoptysis? Other (resp = clue)

A

PE!

183
Q

List some RISK FACTORS for TB ?

A

Past history of TB

TB contact

Born in a country with high TB incidence

Travel to country with high incidence of TB

Immunosuppression–e.g. IVDU, HIV, organ transplant, renal failure/
dialysis, malnutrition/ low BMI, DM, alcoholism

184
Q

What are the immediate management principals for a pt with Resp TB (before investigations)

A

ABCDE approach

Admit to side room + start infective control measure (e.g. masks + negative pressure room.)

185
Q

What are the management principals for a pt with Resp TB (lab investigations)

A
  1. Productive cough - 3 x sputum samples (acid-fast Ziehl-Neelsen stain) + TB culture
  2. NO productive cough - consider bronchoscopy
  3. Routine bloods
    LFTs + HIV test + vit D levels
186
Q

What are the management principals for a pt with Resp TB (imaging)

A
  • CXR

- Consider CT chest if suspect pulmonary TB (CXR normal / no clinical features)

187
Q

What to do if your diagnosis is split between pneumonia and TB?

A

Start Antibiotics for pneumonia as per CURB-65

188
Q

What should you do if pt is critically unwell and there is a likelihood of TB?

A

Start TB treatment AFTER samples sent

189
Q

How long does TB culture take? What does this mean?

A

Culture takes 6-8 weeks.

Means treatment often started before confirmed diagnosis.

Novel PCR test (Gene Xpert) available in some centre - gives immediate info on drug sensitivites / resistance.

190
Q

What role do specialist nurses play in TB management?

A

Notify pt cases to specialist nurses as they:

support pt during investigation, treatment, pubic health issues AND initiate contact tracing!

191
Q

What is standard Anti-TB therapy regimen?

A

FIRST 2 MONTHS:
4: (Rifampicin, Isoniazid, Pyrazinamide, Ethambutol)

NEXT 4 MONTHS
2: (Rifampicin, Isoniazid)

TOTAL: 6 months minimum (can vary)

192
Q

Why is weight important in Anti-TB therapy?

A

dose of anti-TB is weight dependant.

193
Q

Which bloods is it essential to check before commencing anti-TB treatment?

A

LFTS

194
Q

Which anti-malarial drug requires eye test?

A

Ethambutol (E for eyes)
need to check visual acuity before giving.

Side effect - can cause Retrobullar neuritis

195
Q

What strategies can be used to ensure compliance ?

A

Directly observed Therapy (DOT)

196
Q

What investigation if suspect CNS TB?

A

MRI Brain

197
Q

What are major side effects of Rifampicin?

A

Hepatitis
rashes
febril reactions
orange / red secretions - sweat / urine / contact lenses

Drug interactions - warfarin / COCP

198
Q

What are major side effects of Isoniazid?

A

Hepatitis
rashes
peripheral neuropathy
psychosis

199
Q

What are major side effects of Pyrazinamide?

A

Hepatitis
rashes
vomitting
arthralgia

200
Q

What is pathophysiology of COPD?

A

Eemphysema and chronic bronchitis

Mucous gland (goblet cells) hyperplasia

Loss of cilial function

Emphysema – alveolar wall destruction causing
irreversible enlargement of air spaces distal to the
terminal bronchiole

Chronic inflammation (macrophages and
neutrophils) and fibrosis / remodelling of small airways
201
Q

What is the definition of COPD?

A

COPD is characterised by airflow obstruction. Airflow obstruction is progressive, not fully reversible and does not change markedly over several months.

The disease is predominantly caused by smoking

202
Q

What are the cuases of COPD?

A

Smoking

Inherited - α-1-antitrypsin deficiency

Industrial exposure - e.g. soot from coal

203
Q

What is outpatient COPD Management?

A
  • ‘COPD Care Bundle’
  • SMOKING CESSATION
  • Pulmonary Rehabilitation
  • Bronchodilators
  • Antimuscarinics
  • Steroids
  • Mucolytics
  • Diet
  • LTOT if appropriate
  • Lung Volume reduction if appropriate
204
Q

What does the ‘COPD care Bundle’ involve?

A

Assessment of inhaler technique

Provision of a written patient self-management action plan

(where appropriate) an emergency drug pack

The offer of referral for support to stop smoking

Access to a treatment programme that can help people with a lung condition stay active (pulmonary rehabilitation)

Appropriate follow-up arrangements.

205
Q

Who is in the multidisciplinary team for COPD patient care?

A 
Physicians 
GPs
specialist nurses
Physiotherapists
pharmacists 
Occupational therapsits 
Dieticians.
206
Q

What are the indications for long term oxygen therapy for a patient with COPD?

A

pO2 below 7.3 kPa, or 8 kPa (cor pulmonale)

Non-smokers

Balance loss of
independence/ reduced activity

Note: 02 not a treatment for breathlessness; to prevent organ hypoxia

207
Q

Why is long term oxygen therapy good for COPD patients?

A

Hypoxia can causes renal and cardiac damage - LTOT reduces this

208
Q

How long do COPD pts need to use long term oxygen therapy for a day to get a survival benefit ? (LTOT)

A

at least 16 hours a day

209
Q

What is pulmonary rehabilitation?

A

MDT 6-12 week programme:

supervised
exercise

unsupervised home exercise

nutritional advice

disease education

210
Q

Why is pulmonary rehabilitation good for COPD pts?

A

COPD pts avoid exercise / physical activity as breathless.

Leads to vicious cycle of increasing social isolation, depression, muscle weakness and inactivity making symptoms worse

211
Q

How would you judge a pt with COPD to be in the midst of an infective exacerbation ?

A

Change in sputum volume / colour

Fever

Raised WCC +/- CRP

212
Q

How would you manage a pt with COPD who is having an exacerbation?

A

ABCDE approach

O2- aim for 94-98% but if evidence of (raised pCO2 on ABG) or Type 2 Resp Failure, then target SaO2 88-92%

NEBs – Salbutamol and Ipratropium

Steroids – Prednisolone 30mg STAT and OD for 7
days

Antibiotics if raised CRP / WCC or purulent sputum

CXR

Consider IV aminophylline

Non invasive ventilation if Type 2 respiratory failure and pH
7.25-7.35

pH <7.25 consider ITU referral

213
Q

What is interstitial lung disease?

A

Umbrella term describing a number of conditions that affect the lung parenchyma in a diffuse manner. an umbrella term used for a large group of diseases that cause scarring (fibrosis) of the lungs.

214
Q

What are some examples of interstitial lung disease?

A

Usual Interstitial Pneumonia (UIP)

Non-specific Interstitial Pneumonia (NSIP)

Extrinsic Allergic Alveolitis

Sarcoidosis

Several other conditions

215
Q

What are important things to cover in hx taking from a pt with ILD? Why?

A
  • comprehensive occupational / environmental history
    e. g.

inhalation of dust - Silicosis
Inhalation of asbestos - Asbestosis
Pneumoconioisis (coal workers)

216
Q

What results to do you get in PFTs for ILD?

A

Typically restrictive lung diseases on PFT’s

217
Q

What autoimmune / immunological investigations do you need to do for ILD?

(Looking for conditions associated with developing ILD)

A

ANA – connective tissue disease OR SLE

ENA – connective tissue disease

Rh F – Rheumatoid Arthritis

ANCA – Vasculitis

Anti-GBM – Pulmonary Renal disease

ACE – Sarcoidosis

Ig G to serum precipitins e.g. pigeon, budgie – Extrinsic Allergic Alveolitis

HIV

218
Q

What is the most common ILD causing lung fibrosis?

A

Usual Interstitial Pneumonia (UIP)

often idiopathic

219
Q

What findings do you see with Usual Interstitial Pneumonia (UIP) and ILD?

A

`Examination : clubbing, reduced chest expansion

Auscultation: fine inspiratory crepitations (pulling Velcro slowly) – best heard basal / axillary areas

Cardiovascular – features of pulmonary
hypertension

(note L (UIP) is a form of lung disease characterised by progressive scarring of both lungs - interstitial lung disease)

220
Q

What is Extrinsic Allergic Alevolitis? (ILD)

A

Also known as Hypersensitivity Pneumonitis

Inhalation of organic antigen to which the individual has been sensitised

221
Q

How does Extrinsic Allergic Alevolitis? (ILD) present acutely?

A

short period from exposure - 4-8 hrs.

Usually reversible - spontaneously settle 1-3 days.

Can reocur

222
Q

How does Extrinsic Allergic Alevolitis? (ILD) present Chronically?

A

chronic exposure (months – years). Less reversible.

223
Q

What are some drug causes of ILD? Extrinsic Allergic Alevolitis?

A 
Amiodarone
Bleomycin
Methotrexate
Nitrofurantoin
Penicillamin
224
Q

What is Sarcoidosis ? (ILD)

What do you see on histology?

A

Multisystem (often resp) inflammatory condition of unknown cause

50% remission, 50% progressive disease

Non-caseating granulomas on Histology

225
Q

What investigations for Sarcoidosis?

A

Definitive: tissue biopsy (e.g., lung, lymph nodes), which typically reveals non-caseating granulomas

Bedside: PFTs: restrictive pattern (fibrosis) -(obstructive- an early sign)

Bloods:
* raised ESR
* ACE (not specific or diagnostic)
* U&Es
* raised calcium levels
* lymphocytes may be reduced

Imaging:
* CXR: 4 stages of changes from Sarcoid

Cardiac involvement:
* ECG, 24 tape, ECHO, cardiac MRI

  • CT/MRI head: headaches – Neuro sarcoid
226
Q

What are ILD treatment principals?

A

Remove trigger exposure e.g. occupational / environment

Stop smoking

MDT approach – Pirfenidone to slow progression

Treatment of infective exacerbations

Oxygen if respiratory failure

Palliative care

Transplantation

227
Q

Stages of sarcoidosis on CXR?

A

Stage 1 - Bilateral hilar lymphadenopathy (BHL)
Stage 2 - BHL with peripheral infiltrates
Stage 3 - Peripheral infiltrates alone
Stage 4 - Pulmonary fibrosis

228
Q

What is sarcoidosis?

A

Sarcoidosis is a multi-system disease that is characterised by the formation of granulomas, leading to widespread inflammatory changes and complications across multiple body systems.

229
Q

Clinical definition of obstructive sleep apnoea?

A

Upper airway narrowing, provoked by sleep, causing sufficient sleep fragmentation. Results in daytime sleeping

230
Q

Signs and symptoms of Acute Sarcoidosis?

A

Signs and symptoms of acute sarcoidosis, also known as Löfgren syndrome, include:

Fever
Polyarthralgia
Erythema nodosum
Bilateral hilar lymphadenopathy

231
Q

Characteristic physical features of pt with obstructive sleep apnoea?

A

Male
Upper body obesity - collar size >17inches
Undersized/set back mandible

232
Q

Common manifestations of Chronic Sarcoidosis?

Involving other organs / systems

A
  • Pulmonary: Dry cough, dyspnoea, reduced exercise tolerance, and crepitations on examination
  • Constitutional: Fatigue, weight loss, arthralgia, low-grade fever, lymphadenopathy, and enlarged parotid glands
  • Neurological: Meningitis, peripheral neuropathy, bilateral Bell’s palsy
  • Ocular: Uveitis, keratoconjunctivitis sicca
  • Cardiac: Arrhythmias, restrictive cardiomyopathy
  • Abdominal: Hepatomegaly, splenomegaly, renal stones
  • Dermatological: Erythema nodosum, lupus pernio
233
Q

Definition and Pathophysiology of obstructive sleep apnoea?

A

Obstructive sleep apnoea (OSA) is a sleep disorder caused by recurrent episodes of complete or partial collapse of the upper airway, causing obstruction of airflow and therefore apnoeic episodes.

It is normal for muscle tone to reduce when asleep, in these patients the innate tone of the pharynx is overcome, which causes it to collapse on itself, obstructing the airway. This induces hypoxia and therefore a reactive episode of transient arousal to reopen the airway. Overall overnight ventilation is impaired and CO2 levels increase.

234
Q

Management of sarcoidosis?

A
  • Bilateral hilar lymphadenopathy alone: Usually self-limiting and often does not require treatment
  • Acute sarcoidosis: Bed rest and NSAIDs for symptom control
  • Steroid treatment: Oral or intravenous, depending on the severity of the disease
  • Immunosuppressants: Used in severe disease.
235
Q

Causes of small pharyngeal size?

Obstructive Sleep apnoea

A

Fatty infiltration of pharyngeal tissues and external pressure from increased neck fat/muscle bulk
Large tonsils
Craniofacial abnormalities
Extra submucosal tissue = e.g in myxoedema

236
Q

Causes of excessive narrowing of the airway during sleep?

A

Obesity
Neuromuscular disease with pharyngeal involvement - leads to greater loss of dilator muscle tone e.g stroke, myotonic dystrophy, motor neurone disease
Muscle relaxants - sedatives, alcohol
Increasing age

237
Q

Clinical features (signs and symptoms) of obstructive sleep apnoea?

A

Unrefreshed sleep
Snoring and apnoea attacks witnessed by partner
Excessive daytime sleepiness
Nocturia

Less common in booklet: Nocturnal sweating, reduced libido, oesophageal reflux

238
Q

What is Epworth sleepiness scale?

A

A questionnaire completed by patient +/- partner to assess chance of having obstructive sleep apnoea. 0 = would not doze. 1 = slight chance. 2 = moderate chance. 3 = high chance. 0-3 given for each question, score out of 24 given.

239
Q

What kind of questions are asked in Epworth sleepiness scale?

A

Sleep when:

  1. sitting and reading
  2. watching tv
  3. sitting in public place
  4. passenger in a car for an hour
  5. lying down to rest in the afternoon
  6. sitting and talking
  7. sitting quietly after lunch without alcohol
  8. in a car, while stopped in traffic
240
Q

What sleep studies can be done to diagnose obstructive sleep apnoea?

A

Overnight oximetry alone
Limited sleep study
Full polysomnography

241
Q

What is included in limited sleep study to diagnose obstructive sleep apnoea?

A
  • Oximetry
  • Snoring
  • body movement
  • HR
  • oronasal flow
242
Q

What simple approaches can you suggest for obstructive sleep apnoea managed?

A

Note: Treatment is based on symptoms/QofL. Need to consider livelihood too

Simple approaches: Weigh loss, sleep on side (decubitus), not supine. Avoid or reduce evening alcohol intake

243
Q

How to manage mild obstructive sleep apnoea/ snorers?

A

Mandibular advancement devices

Consider pharyngeal surgery

244
Q

How to manage significant obstructive sleep apnoea?

A

Nasal CPAP, consider gastric bypass.

Rare: tracheostomy

245
Q

How to manage severe obstructive sleep apnoea and CO2 retention?

A

Non-invasive ventilation before CPAP if acidotic.

Note: compensated CO2 may reverse with CPAP only. (So treatment here is individualised).

246
Q

What is CPAP in obstructive sleep apnoea?

A

Continuous positive airway pressure - helps keep airway open so prevents sleep apnoea

247
Q

How is CPAP delivered?

What is air pressure?

A

Via nasal mask. Can also use mouth and nose mask.

Air pressure is 10cm H2O pressure = this splints open the upper airways.

248
Q

Benefit of CPAP for obstructive sleep apnoea?

A

Prevents airways collapse
Prevents fragmented sleep
Prevents daytime somnolence
Opens collapsed alveoli - improves V/Q match

249
Q

CPAP (continous positive airway pressure) vs NIV (non-invasive ventilation)?

A

Biggest contrast:
CPAP supplies constant positive pressure in inspiration and expiration = so is NOT a form of ventilatory support.
NIV has two levels of positive pressure - one for inspiration and one for expiration = so IS A form of ventilatory support.

Additional from booklet:
CPAP can be used in patients with acute respiratory failure (palm oedema) to help oxygenation,
NIV can be set up with back up rates so the machine operates when RR drops below a certain level.

250
Q

How is pleural effusion diagnosed (1st line)?

A

Do CXR

Ultrasound guided pleural aspiration

251
Q

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

A

If there is an underlying empyema

252
Q

pH of pleural fluid in empyema plural effusion?

A

pH <7.2

253
Q

From a US guided pleural aspiration, what is tested?

A

Biochemistry —> protein, pH, LDH

Cytology

Microbiology (including acid alkali fast bacteria)

254
Q

Disadvantage of draining all fluid from pleura without understanding Dx?

A

Draining all the fluid = prevents opportunity to take pleural biopsies.

255
Q

Options available to biopsy pleura (e.g. if malignancy is found in cytology from aspiration sample|)?

A

Thoracoscopy

CT pleural biopsy

256
Q

How to manage pleural effusion that is found to be transudate?

A

Treat underlying cause

257
Q

Pt has transudative pleural effusion. You have treated the underlying cause but pt still has effusion. What is appropriate next step?

A

Effusion has persisted even after treating underlying cause - so now need to use therapeutic aspiration/drainage

258
Q

When is Light’s criteria used?

A

If pleural protein level is between 25-35g/L

259
Q

Lights criteria to identify exudative pleural effusion?

A

Pleural fluid/Serum protein >0.5
Pleural fluid/ Serum LDH >0.6
Pleural fluid LDH >2/3rds of the upper limit of normal

260
Q

What type of shock can PE lead to ?

A

Mechanical shock

261
Q

What is pathophysiology of mechanical shock from a massive PE?

A

Embolus occludes the large pulmonary artery.
Pulmonary artery pressure is high. Occlusion means RV can not empty, and central venous pressure increases.

So, get reduced return of blood to the left side of the heart and there is limited filling of the left heart.
Left atrial pressure is low, so arterial BP is low, leading to shock.

262
Q

Context:Pt has lung cancer.

What scale is used to interpret a patient’s level of fitness?

A

WHO scale to find out performance status

263
Q

WHO scale for fitness level in pts with lung cancer is from 0 to 5. Describe each level.

A

0 - normal fitness - fully active without restriction
1 - restricted in physically strenuous activity. Ok with light work e.g. office work, light house work
2 - capable of all self care, ambulatory but can not carry out work activities. Active (up and about ) over 50% of waking hours
3 - capable of only limited self care. Confined to bed or chair for more than 50% of waking hours
4 - completely disabled. Can no self care. Totally confined to bed or chair.
5 - dead.

264
Q

Gold standard investigation for bronchiectasis?

A

High resolution (1/2) CT (1/)

265
Q

Salbutamol side effects?

A

Hypokalaemia

266
Q

X-ray findings for ILD?

A

Fluffy appearance- reticulonodular shadowing

267
Q

Causes of ILD?

A 
Medication e.g. amiodarone, bleomycin, methotrexate, nitrofurantoin 
Sacroidosis 
Hypersensitivity pneumonitis 
coal worker's pneumoconiosis
TB
268
Q

Indication for LTOTs?

A

paO2<7.3
paO2<8 in cor pulmonale
Not smoking

269
Q

What is a restrictive pattern on spirometry?

A

FEV1:FVC ratio the same >0.7 but the FEV1:FVC values have decreased

270
Q

Causes of non-resolving pneumonia?

A

CHAOS
Complication - empyema, lung abscess
Host - immunocompromised
Antibiotics - inadequate dose or poor oral absorption
Organism - resistant or unexpected, so empirical abx did not cover this organism
Second diagnosis - PE, cancer, organising pneumonia

271
Q

ECG findings for a PE?

A

Sinus tachycardia
“S1Q3T3” pattern of acute cor pulmonale is classic; this is termed the McGinn-White Sign.
—> A large S wave in lead I, a Q wave in lead III and an inverted T wave in lead III together indicate acute right heart strain

272
Q

Which oxygen delivery device is commonly used in patients with COPD, and why?

A

Venturi masks are calibrated to deliver Fio2 between 24% and 50%, allowing Po2 to be titrated.

minimising the risk of CO2 retention (hypercarbia) associated with uncontrolled oxygen therapy

273
Q

How should beta-2 agonists be delivered in patients with hypercapnia, in the context of acute COPD exacerbation?

A

Use a nebuliser driven by compressed air rather than oxygen (to avoid worsening hypercapnia).

274
Q

Describe the management of acute COPD exacerbation if there is no response to an initial dose of a bronchodilator

A

Repeat doses of salbutamol at 15-30 minute intervals
Give continuous nebulised salbutamol at 5-10 mg/hour

275
Q

When are oral corticosteroids indicated in an acute exacerbation of COPD and what is the recommended prescription?

A

Consider oral corticosteroids for people with a significant increase in breathlessness that interferes with daily activities.
Offer 30mg oral prednisolone once daily for 5 days

276
Q

Describe the management of patients with acute COPD exacerbation that do not respond to first or second-line drug treatments

A

Escalate the patient’s care to senior medical staff to consider further management, including:

Non-invasive ventilation (NIV) for persistent hypercapnic respiratory failure.
Respiratory stimulants and intravenous theophylline.

277
Q

Describe the GOLD staging criteria

A

Used for staging COPD
4 categories based on the FEV1
Stage 1 is classed as an FEV1 >80%
Stage 2 50-79%,
Stage 3 30-49%
Stage 4 <30%.

see Geeky medics - COPD

278
Q

Name four complications of COPD

A

Cor pulmonale
Pneumothorax
Secondary polycythemia
Hypercapnic respiratory failure

Cor pulmonale is right-sided heart failure due to high pressure in the p

279
Q

Name three clinical signs associated with cor pulmonale

A
  • Distended neck veins
  • Hepatomegaly
  • Peripheral oedema

Y3 med old (8 decks)

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