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Phase 2a > Conditions - Resp > Flashcards

Conditions - Resp Flashcards

1
Q

COPD definition

A

It is a NON-reversible, long-term, progressive lung disease characterised by airway obstruction.

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2
Q

COPD encompasses which two types of chronic lung disease?

A

Chronic bronchitis and emphysema

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3
Q

COPD epidemiology

A
  • 2% of the UK population are living with DIAGNOSED COPD
  • Each year is accounts for 26% of all lung disease related deaths
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4
Q

COPD aetiology

A
  • Smoking (active and passive)
  • Occupational exposures e.g., mining (v common in Sheffield), cotton, wool, dust
  • Alpha-1 antitrypsin deficiency
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5
Q

Alpha-1 antitrypsin in COPD

A

Alpha-1 antitrypsin deficiency can lead to earlier onset and increased severity of COPD. Alpha-1 antitrypsin is an inhibitor of proteinases enzymes. It is produced in the liver and protects the lung from enzymes which are secreted by neutrophils in response to infection and irritants. The lack of sufficient levels of AAT leads to lung damage by the proteinase enzymes.

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6
Q

What is chronic bronchitis?

A

Involves hypertrophy and hyperplasia of the mucus glands in the bronchi.

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7
Q

What is emphysema?

A

Involves enlargement of the air spaces and destruction of alveolar walls.

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8
Q

COPD clinical presentation

A

Dyspnoea
Cough
Sputum production
Wheeze
Cyanosis
Recurrent respiratory infections
Reduced exercise tolerance
Weight loss
Accessory muscle use for respiration
Pursed lip breathing
Tachypnoea
Reduced chest expansion
Hyper-resonant percussion
Decreased/quiet breath sounds
Cor pulmonale (signs of RHF)
Prolonged expiratory phase

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9
Q

COPD investigations

A

Spirometry showing FEV1/FVC < 0.7
CXR showing a flattened diaphragm
Serum A1AT levels
FBC
BMI
ECG

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10
Q

COPD management

A

Stop smoking (if smoking)
Lifestyle changes
SABA (salbutamol) or SAMA (ipratropium bromide)

If no asthmatic/steroid response: LABA (salmeterol) or LAMA (tiotropium bromide)
If asthmatic/steroid response: LABA (salmeterol) or inhaled corticosteroids

Long-term oxygen therapy

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11
Q

MRC Dyspnoea Scale

A

0 - I only get breathless with strenuous exercise
1 - I get short of breath when hurrying on level ground or walking up slight hills
2 - on level ground, I walk slower than people my age because of breathlessness, or I have to stop for breath when walking at my own pace on level
3 - I stop for breath after walking about 100 yards or after a few minutes on level ground
4 - I am too breathless to leave the house or I am breathless when dressing/undressing

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12
Q

Asthma pathology

A

Chronic inflammation of the airways caused by IgE mediated type I hypersensitivity causing episodic exacerbations of bronchoconstriction

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13
Q

Asthma triggers

A

Infection
Night time/early morning (diurnal variability)
Exercise
Animals
Damp/Cold
Dust
Strong emotions

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14
Q

Asthma clinical presentation

A

Episodic symptoms
Diurnal variability
Dry cough with wheeze and SOB
History of atopic conditions (eczema, hayfever, asthma)
Bilateral widespread “polyphonic” wheeze

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15
Q

Asthma investigations

A

Fractional exhaled nitric oxide
Spirometry showing FEV1/FVC < 0.7
Spirometry with bronchodilator reversibility
Peak flow variability (measured several times per day for 2 weeks)
Direct bronchial challenge test

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16
Q

Asthma management (ongoing)

A

Step 1 - SABA (salbutamol)
Step 2 - SABA + inhaled corticosteroids (beclometasone)
Step 3 - SABA + ICS + LABA (salmeterol)
Step 4 - SABA + LABA + high-dose corticosteroids + considering leukotriene receptor antagonists (montelukast / modified-release theophylline) or LAMA (tiotropium bromide
Step 5 - SABA + LABA + high-dose ICS + daily oral low-dose corticosteroids (prednisolone)

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17
Q

Asthma management (acute)

A

ABCDE O SHIT ME
ABCDE
Oxygen
Salbutamol (nebulised)
Hydrocortisone IV or oral prednisolone
Ipratropium bromide (SAMA)
Theophylline (leukotriene receptor antagonist)
Magnesium sulphate
Escalate care

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18
Q

TB pathology

A
  • Type IV hypersensitivity reaction
  • Results in caseating granulomas
  • Airborne spread through droplets
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19
Q

TB aetiology

A

Mycobacterium Tuberculosis
(Acid-fast bacilli)

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20
Q

TB risk factors

A
  • Known contact with active TB
  • Immigrants from areas of high TB prevalence e.g. South Asia and Africa
  • Immunosuppression e.g. HIV
  • Homeless people, drug users, alcoholics
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21
Q

TB clinical presentation

A

Lethargy
Fever/night sweats
Weight loss
Cough +/- haemoptysis
Lymphadenopathy
Spinal TB -> Erythema nodosum

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22
Q

TB investigations

A

2 tests for an immune response to TB
- Mantoux test (Tuberculin skin testing, >5mm or more = positive)
- Interferon-Gamma Release Assays

CXR

Sputum Culture
- Ziehl-Neelsen Stain -> Bright red
- Cultured with Lowenstein-Jensen Medium

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23
Q

TB management (active)

A

Combination of Antibiotics (+ their SE)
- Rifampicin - 6 months
- Isoniazid - 6 months
Pyrazinamide - 2 months
Ethambutol - 2 months

SE management - Pyridoxine (Vit B6)

24
Q

TB management side effects

A

Rifampicin - red urine/tears (“red-I’m-pissin’”)
Isoniazid - peripheral neuropathy (“I’m-so-numb-azid”)
Pyrazinamide - hyperuricemia - Gout
Ethambutol - colour blindness, decreased visual acuity (“eye-thambutol”)

25
Q

TB prevention

A

BCG vaccination

26
Q

Pneumonia definition

A

Infection-induced inflammatory condition of the lungs

27
Q

Pneumonia pathology

A

Invasion and overgrowth of a pathogen in the lung parenchyma which overwhelms host immune defenses and leads to the production of intra alveolar exudates (which then block the alveoli, impairing gas exchange due to reduced ventilation).

28
Q

Pneumonia clinical features (symptoms)

A

Fever
Cough
Haemoptysis
Purelent sputum
Rigors
Low blood pressure
Dyspnoea
Malaise
Pleuritic chest pain (sharp chest pain worse on inspiration)
Sepsis

29
Q

Pneumonia types

A
  • Community-acquired
  • Hospital-acquired
  • Atypical
  • Aspiration
  • Pneumonia in immunocompromised patients
30
Q

Pneumonia clinical features (signs)

A

Dull to percussion (due to lung collapse and/or consolidation)
Decreased air entry
Bronchial breath sounds (harsh breath sounds which are equally loud of inspiration and expiration- due to consolidation of the lung tissue)
Tachypnoea
Tachycardia
Hypoxia
Hypotension
Increased vocal resonance/ tactile vocal fremitus (due to air passing through the sputum in the airways)
Confusion
Cyanosis

31
Q

Pneumonia aetiology

A

Streptococcus pneumoniae (50%)
Haemophilus influenzae (20%)

32
Q

Pneumonia investigations

A

ABG
CXR showing consolidation
Sputum for microscopy and culture
Blood culture
Bloods including FBC, U&E, ESR, CRP

33
Q

Pneumonia severity score

A

CURB-65

1 point for each of the following:
Confusion
Urea >7
Respiratory rate ≥30
Blood pressure <90 and/or ≤60 diastolic
Age ≥65

0-1= outpatient treatment
2= short stay inpatient or hospital supervised outpatient treatment
3-5= manage as high severity pneumonia

34
Q

Pneumonia management

A

Want to maintain oxygen sats between 94-98% (note: in COPD patients want to maintain oxygen sats between 88-92%)
Use analgesia
IV fluids

CURB-65 guided treatments:
0-1: oral amoxicillin
2: amoxicillin (IV/ oral) and macrolide (clarithromycin or erythromycin)
3+: IV co-amoxiclav and macrolide (clarithromycin or erythromycin)

35
Q

Hospital-acquired pneumonia

A

This is a lower respiratory tract infection that develops more than 48 hours after hospital admission. The most common organisms are Pseudomonas aeruginosa, Staphylococcus aureus and enterobacteria.

36
Q

Aspiration pneumonia

A

This occurs in patients with an unsafe swallow. Risk factors include stroke, myasthenia gravis, bulbar palsy, alcoholism and achalasia. On chest x-ray the right lung is most commonly affected, as the right bronchus is wider and more vertical than the left bronchus, making it more likely to facilitate the passage of aspirate.

37
Q

Atypical pneumonia

A

Bacterial pneumonia caused by atypical organisms that can’t be detected on a gram stain and can’t be cultured using standard methods.

38
Q

Legionella pneumonia

A

It is associated with Legionnaire’s disease, usually in patients who have been exposed to poor hotel air con. Note: can cause hyponatreamia.

39
Q

Pneumocystis pneumonia

A

Associated with patients who are immunosuppressed (malignancy or chemotherapy) or HIV positive. The causative organism is called pneumocystis jiroveci and is a fungus. In patients who are HIV positive the risk of PCP increases when the CD4+ <200 cells/uL. Patient will have symptoms such as a fever, dry cough and exertional dyspnoea.

40
Q

Pneumonia treatment in patients with a penicillin allergy

A

Doxycycline (moderate severity)
Clarithromycin (moderate severity)
Levofloxacin (high severity)

41
Q

Cystic fibrosis aetiology

A

Autosomal recessive condition caused by a mutation of the CFTR gene on chromosome 7

42
Q

Cystic fibrosis pathology

A

Affects mucous glands, causing the glands to produce thick secretions

43
Q

Cystic fibrosis clinical features (1st sign)

A

Meconium ileus
Meconium not passed within 48 hours of birth + abdominal distention and vomiting

44
Q

Cystic fibrosis clinical features (symptoms)

A

Chronic cough
Loose, greasy stools (steatorrhea)
Failure to thrive
Thick sputum production
Recurrent respiratory tract infections
Salty skin

45
Q

Cystic fibrosis clinical features (signs)

A

Nasal polyps
Finger clubbing
Crackles + Wheeze
Abdominal distention

46
Q

Cystic fibrosis complications

A

Infertility (congenital bilateral absence of vas deferens in males)
Pancreatitis
Diabetes
Respiratory tract infections
Bronchiectasis

47
Q

Cystic fibrosis investigations

A

Newborn bloodspot test (screening)
Sweat test
Genetic testing for CFTR gene

48
Q

Cystic fibrosis key colonisers

A

Staph aureus (take prophylactic flucloxacillin)
Pseudomonas aeruginosa (hard to treat + worsens prognosis, take long term nebulised antibiotics)

49
Q

Cystic fibrosis management

A

No cure, LE=50
Chest Physio
Exercise
High calorie diet
CREON tablets
Treat chest infections
Bronchodilators
Nebulised DNase- makes secretions less viscous
Nebulised hypertonic saline
Novel Triple Therapy
Vaccinations
Lung/Liver transplant

50
Q

Bronchiectasis main organisms

A

H. influenzae
Pseudomonas aeruginosa
Strep. pneumoniae

51
Q

Bronchiectasis aetiology

A
  • End point/complication of many lung disease e.g. COPD, CF
  • Post-infection (most common), eg. previous pneumonia or TB
  • Congenital, eg. CF and primary ciliary dyskinesia
52
Q

Bronchiectasis pathology

A
  • Chronic inflammation of the bronchi and bronchioles leading to permanent dilation and thickening of these airways
  • Build up of mucus, increased risk of infections
53
Q

Bronchiectasis clinical features (symptoms)

A

Persistent cough
Copious purulent sputum
Intermittent haemoptysis
Dyspnoea

54
Q

Bronchiectasis clinical features (signs)

A

Finger clubbing
Coarse inspiratory crepitations
recurrent infections

55
Q

Bronchiectasis investigations

A

High-resolution CT (Gold Standard)
Sputum culture to show infection
CXR showing cystic shadows, thickened bronchial walls
Spirometry
Bronchoscopy

56
Q

Bronchiectasis management

A

Can’t be cured

Non-Pharmacological
- Stop smoking
- Vaccinations
- Airway clearance techniques

Pharmacological
- Mucolytic - Carbocysteine
- Antibiotics
- Bronchodilators e.g. nebulised salbutamol
- Corticosteroids e.g. prednisolone

Surgery - may be indicated in localised disease or to control severe haemoptysis

Phase 2a (3 decks)

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