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Clinical > Respiratory > Flashcards

Respiratory Flashcards

1
Q

How do you classify massive haemoptysis?

A

Massive bleeding from the airways below the glottis:
- >400ml/24 hours
- >150-200ml in one episode
- 3 episodes in one week >100ml

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2
Q

How do you manage a primary pneumothorax?

A
  • <2cm and no SOB = supportive mx
  • > 2cm or SOB = attempt aspiration, if this fails insert chest drain
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3
Q

How do you manage a secondary pneumothorax?

A
  • pt >50 OR >2cm OR SOB insert chest drain
  • absence of these = aspiration
  • <1cm give oxygen and monitor for 24 hours
  • persistent air leak (>5days) = pleurodesis (surgical or medical if pt not fit for surgery).
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4
Q

How do you manage a tension pneumothorax?

A

Large bore cannula into 5th intercostal space mid-axillary line

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5
Q

What is the common signs of tension pneumothorax?

A

Distended neck veins, tracheal deviation, no audible breath signs

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6
Q

What is the pathophysiology behind ARDS?

A

Alveolar damage causes fluid infiltration and therefore impaired oxygenation.

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7
Q

What are the signs/sx of ARDS?

A

Dyspnoea, tachycardia, confusion, presyncope/syncope, non-cardiogenic pulmonary oedema and diffuse bilateral opacities on CXR.

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8
Q

What conditions cause ARDS? How is it managed?

A

Pneumonia, sepsis, trauma, aspiration.
Mx: mechanical ventilation with a low tidal volume and limited pressure to avoid ventilator associated injury.

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9
Q

Why does hyperventilation cause the sensation of numbness in the hands, feet, and around the mouth?

A

Hyperventilation = reduced arterial CO2 = incease in blood pH (respiratory alkalosis) = promotes calcium binding to albumin which reduces circulating calcium = symptoms.

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10
Q

How do you differentiate between transudative and exudation pleural effusions?

A

T: <25 protein
E: >35
In between use light’s criteria

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11
Q

What causes transudative and exudative pleural effusions?

A

T: increased pressure e.g., heart failure, liver cirrhosis
E: infection, malignancy, rheumatological conditions

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12
Q

What is the mx for a PE?

A
  • Unprovoked: 6 months anticoagulant (DOAC)
  • Provoked: 3 months of anticoagulant (DOAC)
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13
Q

What is thrombembolic pulmonary HeTN?

A

CTEPH: complication of PE, diagnosed with a right heart catheter to measure pressures. Can lead to right sided heart failure.

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14
Q

What is pulmonary atelectasis?

A

Excessive bronchial secretions causes collapse of the lung: tachycardia, fever, tachypnoea, dull ling bases, reduced fremitus.

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15
Q

What sx do you get with carbon monoxide poisoning? What happens to the oxy-Hb curve?

A

N+V, headaches, confusion.
Severe toxicity: temperatures, arrhythmias, pink skin.
Left shift of the curve.

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16
Q

Presentation of TB?

A

Nights sweats, fever, weight loss, chronic cough, different organ system symptoms.
Often travelled form an endemic country.

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17
Q

What do you see on CXR of TB?

A

Upper lobe opacification known as a ‘ fibronodular appearance’ or ‘fibrocavitary lesions’

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18
Q

How do you diagnose TB?

A

Sputum acid-fast bacilli smear: must have 3 early morning +ve results to confirm diagnosis.
Auramine O and Ziehl-Neelsen are types of stains used for this.

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19
Q

How is TB managed?

A

2 months: isoniazid, rifampicin, pyrazinamide, and ethambutol.
Further 4 months: rifampicin and isoniazid.

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20
Q

If there is CNS involvement, how do you manage TB?

A

2 months of quadruple therapy, 10 further months of double therapy (just rifampicin and isoniazid)

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21
Q

What complications can result from TB?

A
  • Aspergilloma
  • Pott’s disease (degradation of vertebrae due to infiltration of mycobacterium)
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22
Q

What are the elements of the CURB65 score?

A
  • Confused? AMTS less than or equal to 8
  • Urea >7mmol
  • RR >30
  • BP systolic <90, diastolic <60
  • > 65 y/o
    0/1= manage at home
    2= admit for abx and observation
    3/4= consider escalation to critical care
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23
Q

A CURB65 score of 1 can be managed at home, what would you prescribe for them?

A

1g amoxicillin TD for 5 days

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24
Q

Mycoplasma pneumoniae is an atypical pneumonia, what are its complications?

A
  • cold autoimmune haemolytic anaemia,
  • erythema multiforme (after antibiotics you get red raised lesions all over the body)
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25
Q

How does klebsiella gram stain?

A

gram -ce rod

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26
Q

Who is klebsiella pneumonia seen in?

A

Immunocompromised pts: you get an upper lobe cavitating pneumonia and a ‘redcurrant’ sputum.

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27
Q

What is seen on CXR for Klebsiella pneumonia?

A

Consolidation with a discrete area of low attenuation with an air-filled level within it (cavity).

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28
Q

How do you manage an empyema?

A

Insert chest drain via USS guidance.

29
Q

What is the most common cause of epiglottitis?

A

Haemophilus influenza

30
Q

What are the signs of epiglottitis?

A

Tripoding, drooling, inability to speak/swallow/drink, respiratory distress.

31
Q

What are the components of the centor criteria?

A
  • Fever
  • No cough
  • tender cervical LNs
  • tonsillar exudate
    3-4 = give abx as there is an increased risk for GABS
32
Q

Your Centro criteria has dictated that that your pt needs abx, what are you giving them?

A

Phenoxymethylpenicillin or clarithromycin in pen allergic

33
Q

What causes Legionnaires disease? How does it gram stain?

A

Legionella pneumophilia: gram -ve aerobic rod.

34
Q

How can you diagnose Legionnaires disease?

A

urinary antigen enzyme immunoassay

35
Q

Where is legionella pneumophilia found?

A

Water based environments such as hot tubs, air conditioning units, heating, showers.

36
Q

Who may meet criteria for RSV prophylaxis? What is given?

A

Children with haemodynamically significantly heart disease.
Palivizumab given SC once/month during RSV season.

37
Q

What is popcorn lung?

A

Bronchiolitis obliterans caused by adenovirus causes destruction of bronchioles due to inflammation.

38
Q

From where can you get histoplasma Capsulatum infection? What signs do you get on CXR?

A

Fungi endemic to Missouri river in Mississippi.
Bilateral hilar lymphadenopathy with calcified granulomas (healed focal infiltrates).

39
Q

How does histoplasma Capsulatum affect immunocompromised pts?

A

Acute respiratory histoplasmosis (influenza-like sx) and disseminated disease.
Whereas in immunocompetent pts it may be asymptomatic.

40
Q

What causes PCP pneumonia? How do we investigate for it?

A

Pneumocystis jiroveci fungi.
Bronchiolar lavage and silver stains.
CXR: bilateral hilar interstitial infiltrates (may also be clear).

41
Q

Management for PCP?

A

Co-trimoxazole oral of IVs.
Some hypoxic pts may benefit from steroids.

42
Q

What are the signs of COPD?

A

‘Pink Puffer’
Thin, severe dyspnoea, hyperinflation of airways (emphysema), repeated infection leading to dilated distal airways (bronchiectasis).

43
Q

What is a sign of bronchiectasis on imaging?

A

Signet ring

44
Q

How do you manage an acute presentation of COPD?

A

Salbutamol and ipratropium nebs, steroids, aim to improve oxygen sats.
Hypoxic pts can be put on 15L via on rebreathe aiming for 94-98 then once this is achieved titrate down to 88-92 if they are CO2 retainers.

45
Q

What are the stages of COPD using FEV1?

A

1: >80%
2: 50-58%
3: 30-50%
4: <30%

46
Q

What are the signs that a COPD pt has developed pulmonary hypertension and right heart failure?

A

PH: Loud S2 heart sound due to loud closure of the pulmonary valve.
Cor Pulmonale: peripheral swelling, fatigue, raised JVP, organomegally.

47
Q

What is the role of volume reduction surgery in COPD pts? What is the criteria?

A

Removal of the most damage areas to help the healthier parts function better.
Predominant emphysema, FEV1 >20%, PaCO2 <7.3, TICO >20%.

48
Q

Why might someone develop signs of COPD at a younger age alongside signs of liver cirrhosis?

A

Alpha 1 antitrypsin deficiency - unchecked quantities of neutrophil elastase and increased attack of alveolar an liver tissues.

49
Q

What ECG changes might you see in COPD?

A

R axis deviation (right heart strain), prominent P waves in inferior leads (P pulmonale: RA enlargement), inverted Ps in high lateral leads, low voltage QRS, delayed R/S transmission in V1-6. RBBB, multifocal tachycardia.

50
Q

What is the risk of intubating a patient with COPD?

A

Reflex bronchoconstriction during intubation causing collapse of peripheral airways and incomplete alveolar emptying.

51
Q

Cystic Fibrosis is caused by what mutation?

A

Autosomal recessive mutation in the CFTR gene.

52
Q

How do you investigate for CF?

A
  • Genetic analysis/blood spot test
  • Sweat test (salt >60)
  • Immunoreactive trypsinogen (raised in CF)
53
Q

What are the categories of an acute asthma exacerbation?

A

Moderate: PEF >50%, able to talk, SO2 >92%
Acute-Severe: PEF 35-50%, too breathless to talk, SO2 <92%, use of accessory muscles
Life threatening: PEF <33%, SO2<92%, CHEST (cyanosis, hypotension, exhaustion, silent chest, tachyarrhythmias)
Fatal: CO2 starts to fall.

54
Q

How do you manage an acute asthma exacerbation?

A

Moderate: bronchodilator via spacer, consider oral prednisolone
Acute Severe: bronchodilator via nebuliser, oral prednisolone
Life-threatening: bronchodilator and ipratropium nebs, oral prednisolone or IV hydrocortisone.
Fatal: intubation

55
Q

How can you diagnose asthma?

A
  • FEV1 improvement of 15% with beta 2 agonist
  • FEV1/FVC ratio <0.7
56
Q

What are the steps of management of chronic asthma? When should they be referred to a specialist?

A
  • Step 1: short acting beta 2 agonist (salbutamol)
  • Step 2: low dose ICS
  • Step 3: long acting beta 2 agonist (salmeterol)
  • Step 4: leukotriene receptor antagonist, high dose steroid, oral beta 2 agonist, oral theophylline.

Waking at night once/week or having more than 3x day time episodes per week then move to next step.
Refer for those on step 3 or 4.

57
Q

What is chronic Bronchitis?

A

Chronic inflammation of small and large airways, daily productive cough for 3 months or more in the last two consecutive years.
These patients are known as ‘blue bloaters’: overweight, cyanotic, peripheral oedema, wheezy.

58
Q

Why does chronic bronchitis cause a low V/Q ratio?

A

Long term hypoxaemia and reduced RR causes pt to be under ventilated. To compensate, the body to increase cardiac output.
This means there is less ventilation and increased perfusion = low V/Q ratio.

59
Q

What are the cause of ILD in the upper lobes?

A

SCHAART:
- Silicosis
- Coal worker’s pneumoconiosis
- Histiocytosis
- Ankylosing spondylitis
- Allergic bronchopulmonary aspergillosis
- Radiation
- Tuberculosis

60
Q

What are the causes of lower lobe ILD?

A

RASCO:
- Rheumatoid arthritis
- Asbestosis
- Scleroderma
- Cryptogenic fibrosing alveolitis
- Other (drugs, idiopathic)

61
Q

What are the signs/symptoms of Asbestosis?

A

Dyspnoea, chronic cough, crepitations, clubbing cyanosis, reduced chest expansion, history of work in building sites/shipyards.

62
Q

What are the signs/sx of idiopathic pulmonary fibrosis?
What happens to FEV1, FVC, ratio, and TLCO?

A

Fine end bi-basal end inspiratory crackles, reduced chest expansion, clubbing,
Reduced FEV1 and FVC, ratio >70%, TLCO reduced.

63
Q

What medications are used for IPF?

A

Pirfenidone, nintedanib.

64
Q

What are the paraneoplastic syndromes associated with small cell lung cancer?

A
  • SIADH: hyponatraemia, reduced plasma osmolality, increased urinary osmolality
  • Cushing’s: hypertension, high blood glucose, central obesity, buffalo hump, etc
  • LEMs: +ve anti-voltage gated calcium channel antibodies causing muscle weakness, constipation, dysphagia, etc
  • Cerebellar degeneration: perkinjee cell degeneration due to autoimmune attack causing speech, balance, etc problems
  • HPOA: periostitis, digital clubbing, osteoarthropathy of the larger joints
65
Q

What type of lung cancer is most commonly associated with smoking?

A

Squamous cell

66
Q

Why might someone with squamous cell carcinoma of the lung get hypercalcaemic?

A

SCC secretes PTH related peptide which leads to hypercalcaemia (polyuria, polydipsia, constipation, confusion), this is paraneoplastic hyperparathyroidism.

67
Q

What are the complications of a Pancoast Tumour?

A

Tumour at the apex of the lung:
- Horner’s syndrome
- Brachial plexus disorders

68
Q

What is the role of aminophylline in COPD pts? SEs?

A

Non-selective adenosine receptor antagonist and phosphodiesterase inhibitor used IV in exacerbations of COPD to relax smooth muscle in airways, and reduce responsiveness to histamine and other inflammatory substances.
SEs: headaches, nausea, palpitations, seizures.

69
Q
A

Clinical (27 decks)

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