Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

3rd Year Conditions > Resp > Flashcards

Resp Flashcards

1
Q

What is obstructive sleep apnoea?

A

Collapse of the pharyngeal airway during sleep resulting in apnoea episodes where the person will stop breathing periodically for up to a few minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the risk factors for developing OSA?

A

Middle aged, male, obese, alcohol, smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Symptoms of OSA?

A

Apnoea episodes, snoring, morning headache, waking up unrefreshed, daytime sleepiness, concentration problems, reduced SATs during sleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Management of OSA

A

Refer to ENT specialist or specialist sleep clinic

Advise them to stop smoking, drinking and lose weight

Use CPAP

Surgical reconstruction of soft palate and jaw

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is a pneumothorax?

A

when air gets into the pleural space, separating the lung from the chest wall.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What can cause a pneumothorax? What are some risk factors?

A
  • spontaneous (usually tall, thin males)
  • trauma
  • iatrogenic (lung biopsy, mechanical ventilation or central line insertion)
  • lung pathologies such as infection, asthma or COPD
  • Collagen disorders such as Marfan’s, Ehlers-Danlos
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Epidemiology of a pneumothorax

A

annual incidence 9/100,000

20-40 yr olds

4 times more common in males

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does a pneumothorax present?

A
  • asymptomatic if small
  • signs of respiratory distress
  • reduced expansion
  • hyper-resonant
  • reduced breath sounds
  • tension pneumothorax would cause severe distress, tachycardia, hypotension, cyanosis, distended neck veins, tracheal deviation away
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Investigations for a pneumothorax

A
  1. Chest x-ray will show a dark area of film with no vascular markings
  2. ABG to check for hypoxaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How to manage a pneumothorax

A
  1. If no shortness of breath and less than a 2cm rim of air on CXR then no treatment is required and follow up in 2-4 weeks
  2. If shortness of breath and/or more than a 2cm rim then aspiration followed by reassessment, if that fails twice then go for a chest drain
  3. Unstable, bilateral or secondary pneumothoraces require a chest drain
  4. Surgery if chest drain fails, persistent leak in drain or if pneumothorax is recurrent, abrasive or chemical pleurodesis or pleurectomy
  5. If tension then large bore cannula into second intercostal space at the midclavicular line, then do chest drain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the safe triangle for a chest drain?

A

5th intercostal space, midaxillary line (lateral edge of latissimus dorsi and anterior axillary line (lateral edge of pec major)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the different types of pneumonia?

A
  • community acquired
  • hospital acquired
  • aspiration pneumonia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Triggers for asthma

A
  • infection
  • night time or early morning
  • exercise
  • animals
  • cold/damp
  • dust
  • strong emotions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How would asthma present?

A

Acute: worsening SOB, use of accessory muscles, tachypnoea, symmetrical wheeze,

Chronic: episodic symptoms, diurnal variability, dry cough with wheeze and SOB, personal/family history of atopic conditions, bilateral wheeze

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is asthma investigated?

A

1st line = fractional exhaled nitric oxide and spirometry with bronchodilator

2nd line = peak flow variability, direct bronchial challenge test with histamine or methacholine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is acute asthma graded?

A
  1. Moderate = PEFR 50-70% predicted
  2. Severe = PEFR 33-50% predicted, resp rate above 25, heart rate above 110, unable to complete sentences
  3. Life-threatening = PEFR below 33%, sats below 92%, tired, no wheeze, haemodynamic instability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is acute asthma treated?

A

Moderate:

Nebulised beta-2 agonists (i.e. salbutamol 5mg repeated as often as required)

Nebulised ipratropium bromide

Steroids: Oral prednisolone or IV hydrocortisone. These are continued for 5 days
Antibiotics if there is convincing evidence of bacterial infection

Severe:

Oxygen if required to maintain sats 94-98%

Aminophylline infusion

Consider IV salbutamol

Life threatening:

IV magnesium sulphate infusion
Admission to HDU / ICU
Intubation in worst cases – however this decision should be made early because it is very difficult to intubate with severe bronchoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Side effects of salbutamol

A
  • causes potassium to be absorbed into the cells

- causes tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Why is a normal pCO2 concerning during an asthma attack?

A

patients will have a respiratory alkalosis as tachypnoea causes a drop in CO2 so if the pCO2 is high then is suggests they’re fatiguing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Long term management of asthma

A
  • Short acting beta 2 adrenergic receptor agonists for short term relaxation of smooth muscle
  • Inhaled corticosteroids (beclometasone) to reduce inflammation and reactivity, used as maintenance or preventer medications
  • Long acting beta 2 agonists (salmeterol)
  • Long acting muscarinic antagonists (tiotropium) which block acetylcholine receptors which prevents the PNS from causing contraction of bronchial smooth muscles
  • Leukotriene receptor antagonists (montelukast) which stop leukotrienes from causing inflammation, bronchoconstriction and mucus secretion
  • Theophylline relaxes smooth muscle and reduces inflammation. Only has a narrow therapeutic window and can be toxic in excess. So needs monitoring.

Maintenance and reliever therapy which is a combination inhaler with low dose inhaled corticosteroid and a fast acting LABA. Acts as a preventer and reliever.

NICE:

  1. SABA
  2. ICS
  3. Leukotriene receptor antagonist
  4. LABA
  5. Maintenance and reliever therapy
  6. Increase ICS dose to moderate
  7. High dose ICS or oral theophylline or inhaled LAMA
  8. Specialist
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is sarcoidosis?

A
  • multisystem granulomatous inflammatory condition

- nodules of inflammation full of macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Who is affected by sarcoidosis?

A
  • young adults and 60 year olds

- usually 20-40 year old black woman with a dry cough and SOB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How does sarcoidosis usually present?

A
  • 50% are asymptomatic
  • dry cough
  • SOB
  • erythema nodosum
  • hilar lymphadenopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Which organs are affected by sarcoidosis?

A
  1. Lungs - hilar lymphadenopathy, pulmonary fibrosis, pulmonary nodules
  2. Systemic - fever, fatigue, weight loss
  3. Liver - liver nodules, cirrhosis, cholestasis
  4. Eyes - uveitis, conjunctivitis, optic neuritis
  5. Skin - erythema nodosum, lupus pernio, granulomas in scar tissue
  6. Heart - bundle branch block, heart block, myocardial muscle involvement
  7. Kidneys - stones, nephritis
  8. CNS - nodules, diabetes insipidus, encephalopathy
  9. PNS - facial nerve palsy, mononeuritis complex
  10. Bones - arthralgia, arthritis, myopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is Lofgren’s syndrome?

A

specific presentation of sarcoidosis: erythema nodosum, bilateral hilar lymphadenopathy, polyarthralgia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How is sarcoidosis investigated?

A
  • raised serum ACE
  • raised serum calcium
  • raised serum soluble interleukin-2 receptor
  • raised CRP
  • raised immunoglobulins
  • CXR - hilar lymphadenopathy
  • CT shows hilar lymphadenopathy and pulmonary nodules
  • MRI shows CNS involvement
  • PET scan shows active inflammation
  • histology is gold standard for diagnosis (from bronchoscopy with US guided biopsy of mediastinal lymph nodes)
  • shows non-caseating granulomas with epithelioid cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How is sarcoidosis treated?

A

no treatment if no/mild symptoms as it usually resolves spontaneously within 6 months

oral steroids

bisphosphonates to protect against osteoporosis

methotrexate or azathioprine

lung transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Prognosis of sarcoidosis

A

resolves within 6 months in around 60% of patients

  • pulmonary fibrosis or pulmonary hypertension in some patients which may require lung transplant
  • death caused by arrhythmias or CNS issue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Presentation and signs of COPD

A
  • long-term smoker
  • SOB
  • productive cough
  • wheeze
  • recurrent respiratory infections
  • use of accessory muscles
  • cyanosis
  • barrel chest
  • prolonged expiration
  • signs of CO2 retention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

MRC breathless scale

A 
Grade 1 = on strenuous exercise
Grade 2 = up a hill
Grade 3 = on a flat
Grade 4 = 100 metres on flat
Grade 5 = can't leave home
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Diagnosis of COPD

A
  • clinical presentation and spirometry
  • FEV/FVC < 0.7
  • FEV >80% of predicted is stage 1
  • FEV 50-79% of predicted is stage 2
  • FEV 30-49% of predicted is stage 3
  • FEV <30% of predicted is stage 4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How is COPD managed?

A

SABA + Short acting antimuscarinic (ipratropium bromide)

LABA + long acting antimuscarinic combination

LABA + ICS

ABG in acute setting

Prednisolone, antibiotics, inhaler

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Risk factors for PE

A
  • immobility
  • recent surgery
  • long haul flight
  • COCP
  • thrombophilia
  • polycythaemia
  • pregnancy
  • malignancy
  • SLE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is VTE prophylaxis and what is given to patients?

A
  • risk of VTE for patients in hospital
  • increased risk means LMWH should be given (enoxaparin) unless on warfarin or DOAC
  • anti-embolic stockings unless peripheral arterial disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Contraindication to anti-embolic stocking

A

peripheral arterial disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Contraindication to LMWH

A

active bleeding (thrombophilia) or warfarin or DOACs

37
Q

How does PE present?

A
  • SOB
  • cough with or without haemoptysis
  • pleuritic chest pain
  • hypoxia
  • tachycardia
  • tachypnoea
  • low grade fever
  • hypotension
38
Q

What is the Wells score?

A

risk of symptomatic patient actually having a PE

takes into account recent surgery, clinical findings and haemoptysis

39
Q

Describe how a PE is diagnosed/investigated?

A
  1. History, exam and CXR to calculate Wells score
  2. Wells score >4 = CT pulmonary angiogram
  3. If Wells 4 or less then do a d-dimer, if that’s positive then do a CT pulmonary angiogram
40
Q

What can cause a raised d-dimer?

A

very sensitive but not specific so good at ruling out VTE

venous thromboembolism, pneumonia, cancer, heart failure, recent surgery, pregnancy

41
Q

On an ABG, patients with a PE often have ___________

A

respiratory alkalosis due to high RR blowing off CO2 and low O2 due to perfusion issue

42
Q

How should a PE be managed?

A
  1. Apixaban or rivaroxaban (DOACs), LMWH (enoxaparin or dalteparin) as an alternative
  2. Warfarin, DOAC or LMWH in the long-term

Target an INR of 2-3

When switching to warfarin continue LMWH for 5 days or when INR is 2-3 for 24 hours

LMWH for cancer or pregnancy

DOACs (apixaban, dabigatran, rivaroxaban)

3 months if clear reversible cause
Over 3months if unclear cause or recurrent VTE or irreversible underlying cause
6 months in cancer

43
Q

When should thrombolysis be given for a PE?

A
  • haemodynamically unstable patients
  • very high risk of bleeding
  • used in massive PE
  • streptokinase, alteplase, tenecteplase
44
Q

How does pneumonia present?

A
  • SOB
  • productive cough
  • fever
  • haemoptysis
  • pleuritic chest pain
  • delirium
  • sepsis
45
Q

Signs of pneumonia

A
  • possible sepsis
  • tachypnoea
  • tachycardia
  • hypoxia
  • hypotension
  • fever
  • confusion
  • bronchial breath sounds (harsh sounds, equal on inspiration and expiration)
  • coarse crackles (air passing through sputum)
  • dullness to percussion due to lung tissue collapse and/or consolidation
46
Q

Describe the CURB-65 scoring system

A
  • Confusion
  • Urea greater than 7
  • RR 30 or more
  • BP systolic below 90, diastolic 60 or less
  • age 65 or above

0 or 1 = under 5% mortality
above 2 = consider hospital
above 3 = ICU assessment

47
Q

What are the many causes of pneumonia?

A

Common: Streptococcus pneumoniae and Haemophilus influenzae

Other: Moraxella catarrhalis (immunocompromised or chronic pulmonary disease), Pseudomonas aeruginosa (CF or bronchiectasis) or Staphylococcus aureus (CF)

Atypical: Legionella pneumophila (infected water causing SIADH causing hyponatraemia), Mycoplasma pneumoniae (erythema multiforme), Chlamydia pneumoniae, Coxiella burnnetii (animal bodily fluids), Chlamydia psittaci (infected birds)

LEGIONS OF PSITACCI MCQs

Fungal: Pneumocystis jiroveci, treated with co-trimoxazole, SOB on exertion and night sweats

48
Q

Investigations for pneumonia

A

CXR, FBC, U&Es, CRP

Sputum culture, blood culture, legionella ad pneumococcal urinary antigens

49
Q

Treatment for pneumonia

A
  • moderate to severe = 7 to 10 days of dual antibiotics (amoxicillin and macrolide)
  • mild = 5 day course of amoxicillin or macrolide)
50
Q

Complications of pneumonia

A

sepsis, pleural effusion, empyema, lung abscess, death

51
Q

What are the 2 different types of pleural effusion and what causes them?

A
  1. Exudative (protein count greater than 3g/dl) related to inflammation causing protein to leak out into the pleural space, lung cancer, pneumonia, RA, TB
  2. Transudative (protein count lower than 3g/dl) related to fluid movement into pleural space, congestive heart failure, hypoalbuminaemia, hypothyroidism, Meig’s syndrome (right sided pleural effusion with ovarian malignancy)
52
Q

Presentation of pleural effusion

A

SOB, dullness over effusion, reduced breath sounds, tracheal deviation

53
Q

Investigations for pleural effusion

A
  1. CXR: blunting of costophrenic angle, fluid in lung fissures, meniscus in large pleural effusions, tracheal and mediastinal shift
  2. Pleural fluid analysis
54
Q

Treatment for a pleural effusion

A
  • Conservative management for small effusions
  • Pleural aspiration
  • Chest drain
55
Q

What is empyema?

A
  • infected pleural effusion
  • suspect if improving pneumonia but new or ongoing fever
  • aspiration shows pus
  • acidic pH, low glucose, high LDH
  • remove the pus using a chest drain and give antibiotics
56
Q

What are the different causes of pulmonary hypertension?

A

Group 1: primary or connective tissue disorder

Group 2: left sided heart failure due to MI or systemic hypertension

Group 3: COPD

Group 4: pulmonary vascular disease

Group 5: miscellaneous (sarcoidosis, glycogen storage disease, haematological disorders)

57
Q

Signs and symptoms of pulmonary hypertension

A

SOB, syncope, tachycardia, raised JVP, hepatomegaly, peripheral oedema

58
Q

Investigations for pulmonary hypertension

A

ECG: will show larger R waves on V1-3 and larger S waves V4-6

Right axis deviation

CXR: dilated pulmonary arteries, right ventricular hypertrophy

Bloods: raised NT-proBNP in right ventricular failure

Echocardiogram

59
Q

Management of pulmonary hypertension

A

Primary: IV prostanoids, endothelin receptor antagonist, phosphodiesterase-5 inhibitors

Secondary: treat underlying cause

60
Q

How should pulmonary fibrosis be diagnosed?

A
  • clinical features and high resolution CT
  • lung biopsy if unclear
  • Spirometry (FEV1:FVC >0.7, decreased FVC) and impaired gas exchange
61
Q

How does pulmonary fibrosis present?

A

SOB, dry cough, fatigue, weight loss, clubbing

62
Q

How should pulmonary fibrosis be managed?

A
  • treat underlying cause, O2, stop smoking, pulmonary rehab, flu vaccine, lung transplant
63
Q

What drugs can cause pulmonary fibrosis?

A

amiodarone, cyclophosphamide, methotrexate, nitrofurantoin

64
Q

What can cause secondary pulmonary fibrosis?

A

alpha-1 antitrypsin deficiency

RA

SLE

Systemic sclerosis

65
Q

How should primary pulmonary fibrosis be treated?

A

pirfenidone (antifibrotic, anti-inflammatory)

nintedanib (monoclonal antibody)

66
Q

Give some examples of hypersensitivity pneumonitis

A

bird fanciers lung
farmers lung
mushroom workers
malt workers

67
Q

What is acute bronchitis?

A

inflammation of the trachea and major bronchi

associated with oedematous large airways and sputum production

68
Q

How does acute bronchitis present?

A

cough (may or may not be productive)

sore throat

rhinorrhoea

wheeze

69
Q

How can you distinguish acute bronchitis with pneumonia?

A

History, wheeze, breathlessness may be absent in acute bronchitis whereas at least one of those is present in pneumonia

no focal chest signs in acute bronchitis other than possible wheeze

systemic features tend to be absent in acute bronchitis

70
Q

How is acute bronchitis managed?

A

analgesia

good fluid intake

consider Abx if systemically unwell, comorbidities, or high CRP

doxycycline first-line but not in pregnant women

can also use amoxicillin

71
Q

What respiratory issues can asbestos cause?

A
  • pleural plaques which are benign (so not a big issue)
  • pleural thickening
  • asbestosis (lower lobe fibrosis)
  • mesothelioma (malignant disease of the pleura, SOB, chest pain, pleural effusion)
  • lung cancer
72
Q

What stain is needed for TB?

A

Zeihl-Neelsen

Red against a blue background

73
Q

Presentation of TB

A

chronic, worsening symptoms

lethargy, fever or night sweats, weight loss, cough with or without sputum, lymphadenopathy, erythema nodosum, spinal pain

74
Q

Investigations for TB

A

Mantoux test and interferon gramma release assay

Positive mantoux test = over 5mm

Sensitised WBCs will release interferon gamma (blood sample mixed with TB proteins)

CXR: consolidation, pleural effusion, hilar lymphadenopathy

75
Q

How should TB be managed?

A

Latent TB = left alone or if at risk: Isoniazid (6 months) or Isoniazid + Rifampicin (3 months)

Active TB: RIPE
Rifampicin for 6 months
Isoniazid for 6 months
Pyrazinamide for 2 months 
Ethambutol for 2 months

Give pyridoxine too to prevent peripheral neuropathy

76
Q

Side effects of RIPE drugs

A

Rifampicin causes red/orange urine, tears

Isoniazid causes peripheral neuropathy so give pyridoxine

Pyrazinamide causes hyperuricaemia

Ethambutol causes colour blindness and reduced visual acuity

77
Q

What is bronchiectasis and what are some causes?

A
  • permanent dilatation of the airways secondary to a chronic infection or inflammation
  • post-infective: TB, measles, pertussis, pneumonia
  • CF
  • bronchial obstruction
  • immune deficiency
  • allergic bronchopulmonary aspergillosis
  • ciliary dyskinetic syndromes
  • yellow nail syndrome
78
Q

Management of bronchiectasis

A
  • assess for treatable cause
  • physical training
  • postural drainage
  • antibiotics for exacerbations
  • bronchodilators in selected cases
79
Q

What are the different types of influenza?

A

A,B and C
A and B are more common

A has H and N subtypes
H1N1 = swine flu
H5N1 = avian flu

80
Q

Who is at higher risk of developing the flu?

A 
aged 65 or above
young children
pregnant women
asthma, COPD, HF, diabetes
healthcare workers and carers
81
Q

How does flu present?

A 
fever
coryzal symptoms
lethargy and fatigue
anorexia
muscle and joint aches
headache
dry cough
sore throat
82
Q

How is the flu diagnosed?

A

history, risk factors and presentation

Viral nasal or throat swabs for PCR analysis

83
Q

How is the flu treated?

A

Only patients at risk of complications need treatment

  • Oral oseltamivir 75mg twice daily for 5 days
  • Inhaled zanamivir 10mg twice daily for 5 days

Start treatment within 48 hours of onset of symptoms

84
Q

Complications of the flu

A

otitis media, sinusitis and bronchitis

viral pneumonia

secondary bacterial pneumonia

worsening of chronic conditions

encephalitis

85
Q

What are the different types of respiratory failure?

A

Low PaO2 indicates hypoxia and respiratory failure

Normal pCO2 with low PaO2 indicates type 1 respiratory failure (only one is affected)

Raised pCO2 with low PaO2 indicates type 2 respiratory failure (two are affected)

86
Q

Which cancers commonly spread to the lungs?

A

Bladder, breast, colon, kidney, neuroblastoma, prostate, sarcoma, Wilm’s tumour

87
Q

Where does lung cancer commonly spread?

A

other lung, adrenals, lymph nodes, bones, brain, liver

88
Q

Lung metastases symptoms

A

persistent cough, haemoptysis, chest pain, SOB, wheezing, weakness, sudden weight loss

3rd Year Conditions (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions