Brainscape's Knowledge GenomeTM

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


See full index

Yr3 Med Conditions > RESP > Flashcards

RESP Flashcards

1
Q

Aspergillus Lung Disease Def.

A

Lung disease associated with Aspergillus lung infection

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

Aspergillus Lung Disease Types & Presentations

A

Aspergilloma
- Fumigatus mycetoma ball in pre-existing lung cavity (post-TB, old infarct)
- Presents: Asymptomatic, haemoptysis
ABPA
- Colonisation of airways, common in asthmatics
-IgE & IgG immune response (proteolytic enzymes, mycotoxins, antibodies) leads to airway damage
- Presents: uncontrollable asthma, recurrent pneumonia with wheeze, cough, fever, malaise
Invase Aspergillosis
- Invasion into lung tissue & fungal dissemination, common in immunocompromised (neutropenia, steroid use, AIDS)
- Presents: Dyspnoea, Rapid Deterioration, Septic Picture

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

Aspergillus Lung Disease Epidemiology

A
  • Elderly & Immunocompromised

- Uncommon

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

Aspergillus Lung Disease SIGNS

A
  • Tracheal Deviation (if large)
  • Dullness in lung
  • Reduced breath sounds
  • Wheeze in ABPA
  • Cyanosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Aspergillus Lung Disease Investigations

A

ASPERGILLOMA
- CXR shows round mass with crescent of air around it
- CT/MRI if unclear
- Sputum cultures negative if there is no communication between cavity colonised by Aspergillus & Bronchial Tree
ABPA
- Skin test reactivity to Asp. antigens
- Bloods: Eosinophilia, increased IgE & IgE/IgG specific to A.fumigatus
- CXR shows transient patchy shadows, collapse, distended mucous-filled bronchi. If complicated then there will also be fibrosis in upper lobes & bronchiectasis
- Lung function tests show reversible airflow limitation (reduced lung vol/ gas transfer)
INVASIVE ASPERGILLOSIS
- Dx via cultures & histological examination
- Bronchoalveolar lavage fluid/ sputum used diagnostically
- Chest CT shows nodules surrounded by ground-glass appearance. (haemorrhage into tissue surrounding area of fungal invasion)

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

Asthma Definition

A

Chronic inflammatory airway disease characterised by reversible airway obstruction, airway hyper-responsiveness and bronchial inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Asthma Risk Factors

A

Genetic: Family History, Atopy (T lymph. drive production of IgE on exposure to antibodies)
Environmental: House mites, pollen, pets, cigarette smoke, viral RTI, Aspergillus spores, occupational allergens

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

Asthma Epidemiology

A

10% children, 5% adults with increasing prevalence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Asthma presenting symptoms

A
  • Episodic Hx
  • Wheeze
  • Breathlessness
  • Cough (worse morning & night)
  • important to ask about previous hospitalisations to gauge severity
  • Precipitated by cold, virus, drugs (Beta-blockers, NSAIDs, exercise, emotions)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Asthma Signs

A

-Tachypnoea
- use of accessory muscles
-prolong expiratory phase
-polyphonic wheeze
-hyper inflated chest
If severe: PEFR<50% predicted, pulse >110, RR >25, incomplete sentences
Life threatening: PEFR <33% predicted, silent chest, cyanosis, bradycardia, hypotension, confusion, coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Asthma Investigations (Acute & Chronic)

A

ACUTE
- Peak flow, pulse ox, ABG, CXR, FBC (increase WCC for infection), CRP, U&Es, Blood & Sputum
CHRONIC
- Peak flow monitor to se diurnal variation, pulmonary function test, bloods (eosinophilia, IgE, A.fumigatus), skin prick, spirometry

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

Management of Acute Asthma

A
  • ABCDE
  • Resuscitate
  • Monitor oxygen sats, ABG & PEFR
  • High air flow Oxygen
  • Salbutamol nebuliser (5mg 2-4hourly)
  • Ipratropium Bromide (0.5mg QDS)
  • Steroid therapy (100-200mg Iv hydrocortisone, followed by 40mg oral prednisone for 5-7 days
  • If no improvement (PEFR<50% predicted) : IV Mg Sulphate infusion , IV salbutamol, IV aminophylline infusion
  • Anaesthetic help if pt is getting exhausted (can tell this because PCO2 will be high as the patient is unable to hyperventilate and blow off CO2)
  • Treat underlying cause e.g ABs if infective exacerbation
  • Monitor electrolytes (bronchodilsators & aminophylline cause a drop in K+)
  • Invasive ventilation may be needed in severe attacks
  • Discharge when:
    PEFR >75% predicted, diurnal variation <25%, inhaler technique checked, stable on discharge meds for 24h, pt. has own PEF meter, steroid & bronchodilator therapy
  • Arrange a follow up
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Management of chronic Asthma (5 Steps)

A

Step 1: inhaled SABA

Step 2: (if SABA used >1/day) add regular low-dose steroids (400mcg/day)

Step 3: Add LABA (Salmeterol). If inadequate, increase steroid dose to 800mcg/day. If no response to LABA, stop it and just use steroids

Step 4: Increase steroid dose (2000mcg/day). Add 4th drug (leyukotrine antagonist, slow-release theophylline/ B2 agonist tablet)

Step 5: Add regular oral steroids and maintain at high-dose, refer to specialist

Advice: teach technique, explain importance of PEFR monitoring, avoid provoking factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Complications of Asthma

A
  • Growth retardation,
  • Chest wall deformity (pigeon chest)
  • Recurrent infections
  • Pneumothorax
  • Respiratory failure
  • Death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Asthma prognosis

A

Many children improve with age, but adult-onset asthma is usually chronic

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

Define Bronchiecstasis

A

Lung airway disease characterised by chronic bronchial dilation, impaired mucociliary clearance and frequent bacterial infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Aetiology/ Risk Factors of bronchiectasis

A

Chronic lung inflammation leads to fibrosis & permanent dilation of the bronchi. Leads to pooling of mucus, predisposing to further infection, damage & fibrosis of bronchial walls
Causes:
- 50% idiopathic
- Post-infectious (pneumonia, whooping cough, TB)
- Host-defence defects (Kartagener’s syndrome, CF)
- Obstruction of bronchi (e.g. foreign body, enlarged lymph nodes)
- GORD
- Inflammatory disorders (Rheumatoid arthritis)

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

Epidemiology of Bronchiecstasis

A
  • mostly arises in childhood
  • incidence has decreased with the use of antibiotics
  • 1/1000 per year
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Presenting symptoms of bronchiecstasis

A
  • Productive cough with purulent sputum or haemoptysis
  • Breathlessness
  • Chest pain
  • Malaise
  • Fever
  • Weight loss
  • Symptoms usually begin after an acute respiratory illness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Signs of Bronchiecstasis on physical examination

A
  • Clubbing
  • Coarse crepitations at lung bases which shift with coughing
  • Wheeze
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Investigations for Bronchiecstasis

A
  • High-resolution CT is the GOLD STANDARD . Shows dilated bronchi with thickened walls
  • Sputum ( culture & sensitivity. Pseudomonas aeruginosa = most common organism)
  • CXR shows dilated bronchi (tramline shadows), fibrosis, atelectasis, pneumonic consolidations, may be normal though
  • Bronchography is rarely used
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Management for Bronchiecstasis

A
  • Treat acute exacerbations with 2 IV antibiotics, which cover Pseudonomas aeruginosa
  • Prophylactic ABs in patients with frequent exacerbations (>3/year)
  • Inhaled corticosteroids (e.g. flucticasone) - reduces inflammation and vol of sputum but doesn’t affect the frequency of exacerbations or lung function
  • Maintain hydration
  • Flu vaccination
  • Phsyiotherapy (mucus clearance to reduce acute exacerbations & aid recovery)
  • Bronchial artery embolisation (if life-threatening haemoptysis due to bronchiectasis)
  • Surgical (localised resection, lung or heart-lung transplantation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Complications of Bronchiecstasis

A
  • Life threatening haemoptysis
  • Persistent infections
  • Empyema
  • Respiratory failure
  • Cor pumonale
  • Multi-organ abscesses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Prognosis of patients with Bronchiecstasis

A

Most patients continue to have symptoms after 10 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Define COPD

A

Chronic, progressive lung disorder characterised by airflow obstruction, with the following:
- Chronic bronchitis (cough&sputum on most days >3months/year over 2 consecutive years)
Narrowing of airways resulting in bronchiolitis, bronchial mucosal oedema, mucous hyper secretion, squamous metaplasia

  • Emphysema (pathological diagnosis of permanent destructive enlargement of air spaces distal to the terminal bronchioles)
    Destruction and enlargement of alveoli leads to loss of elasticity that keeps small airways open in expiration. Progressively larger spaces develop called bullae (diameter >1cm)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Aetiology/ Risk Factors of COPD

A
  • bronchial & alveolar damage caused by environmental toxins (cigarette smoke)
  • Rarely caused by alpha1-antitrypsin deficiency
    (consider this in non-smoking, young patients)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Epidemiology of COPD

A
  • Common (8% prevalence)
  • Presents in middle age or later
  • More common in males (may change bc smoking changes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Presenting symptoms of COPD

A
  • Chronic cough
  • Sputum production
  • Breathlessness
  • Wheeze
  • Reduced exercise tolerance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Signs of COPD on physical examination

A 
Inspection: 
- respiratory distress
- use of accessory muscles
- barrel-shaped over-inflated chest
- decreased cricosternal distances
- cyanosis 
Percussion:
- hyper-resonant chest
- loss of liver and cardiac dullness
Auscultation
- quiet breath sounds
- prolonged expiration 
- wheeze
- rhonchi - rattling, continuous and low pitched breath sounds that sound a bit like snoring. Often caused by secretion in larger airways or obstructions 
- Sometimes crepitations
Signs of CO2 retention:
- bounding pulse
- warm peripheries
- asterixis
- later stages: RHF (cor pumonale) , right ventricular heave, raised JVP, ankle oedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Investigations for COPD

A

Spirometry & Pulmonary function tests:
- obstructive picture
- reduced PEFR, FEV1/FVC
- increased lung volumes
- decreased CO gas transfer coefficient
CXR:
- may appear normal
- hyperinflation (>6 anterior ribs, flattened diaphragm)
- reduced peripheral lung markings
- elongated cardiac silhouette
Bloods:
- FBC- increased Hb & haematocrit due to secondary polycythaemia
-ABG- may show hypoxia, normal/ raised PCO2
- ECG & Echocardiogram - check for cor pulmonale
- Sputum & Blood cultures: useful in acute infective exacerbations
- Alpha1 antitrypsin levels- useful in young patients who have never smoked

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Management for COPD

A
  • Stop smoking
  • Bronchodilators :
    SABA (salbutamol), Anticholinergics (ipratropium bromide), LABA (if more than 2 exacerbations per year)
  • Steroids ( inhaled beclamethasone considered in patients with FEV1<50% predicted OR >2 exacerbations per year) Avoid regular oral steroids
  • Pulmonary rehab
  • Oxygen therapy (only if stopped smoking, indicated if PaO2 <7.3kPa on air during a period of clinical stability
    PaO2: 7.3-8kPa and signs on secondary polycythaemia, nocturnal hyperaemia, peripheral oedema or pulmonary hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Treatment of acute exacerbations of COPD

A
  • 24% O2 via venturi mask
  • increase slowly if no hypercapnia and still hypoxic (do an ABG)
  • corticosteroids
  • empirical ABs if infection
  • respiratory physiotherapy to clear sputum
  • non invasive ventilation if severe
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Complications of COPD

A
  • Acute respiratory failure
  • Infections
  • Pulmonary hypertension
  • RHF
  • Pneumothorax
  • Secondary polycythaemia

Give pneumococcal & influenza vaccination to prevent infective exacerbations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Prognosis of patients with COPD

A
  • high morbidity
  • 3-year survival of 90% if <60 yrs, FEV1>50% predicted
  • 3-year survival of 75% if >90yrs, FEV1: 40-49% predicted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q 
Hypersensitivity Pneumonia 
(Extrinsic Allergic Alveolitis) definition
A

Interstitial inflammatory disease of the distal gas-exchanging parts of the lung caused by inhalation of organic dusts.

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

Aetiology/ Risk Factors for hypersensitivity pneumonitis

A
  • inhalation of antigenic dusts induce a hypersensitivity response in susceptible individuals
  • antigenic dusts include microbes & animal proteins
    e. g. Farmer’s lung (mouldy hay with thermophilic actinomycetes)
  • Pigeon Fancier’s lung - blood on bird feathers and excreta
  • Maltworker’s Lung (barley/ malting containing Aspergillus clavatus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Epidemiology of hypersensitivity pneumonitis

A
  • uncommon
  • 2% occupational lung disease
  • 50% reported cases affect farm workers
  • geographical variation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Presenting symptoms hypersensitivity pneumonitis (Acute vs Chronic)

A 
ACUTE:
- 4-12hours after exposure, involving reversible episodes of:
- dry cough
- dyspnoea
- malaise
-fever
-myalgia
-wheeze and productive cough if repeated high-level exposure
CHRONIC:
- slowly increasing breathlessness
- decreased exercise tolerance 
- weight loss
- chronic exposure may be low-level so no previous acute episode

Important to ask a full occupational Hx and enquire about hobbies and pets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Signs of hypersensitivity pneumonitis (acute vs chronic)

A 
ACUTE:
- rapid shallow breathing
- pyrexia
- inspiratory crepitations
CHRONIC:
- fine inspiratory crepitations
- clubbing (rare)
40
Q

Investigations for hypersensitivity pneumonitis

A 
Bloods: 
- FBC (neutrophilic, lymphopenia) 
- ABG (reduced PO2 &amp; PCO2) 
Serology:
- Test for IgG to fungal or avian antigens 
CXR:
- normal in acute episodes
- fibrosis may be seen in chronic cases 
High Resolution CT-Thorax
- detects early changes
- patchy 'ground glass' shadowing and nodules 
Pulmonary Function Tests: 
- Restrictive defect (low FEV1, low FVC) 
- Preserved or increased FEV1/ FVC ratio
- Reduced total lung capacity
Bronchoalveolar Lavage:
- increased cellularity
- lung biopsy
41
Q

Definition of Idiopathic Pulmonary Fibrosis

A

Inflammatory condition of the lung resulting in fibrosis of the alveoli and interstitial. Previously known as cryptogenic fibrosing alveolitis

42
Q

Aetiology/ Risk Factors Idiopathic Pulmonary Fibrosis

A
  • occurs in genetically predisposed individuals
  • recurrent injury to alveolar epithelial cells results in secretion of cytokines and growth factors
  • Leads to fibroblast activation, recruitment, proliferation, differentiations into myofirboblasts and increased collagen synthesis and deposition
  • Certain drugs can reproduce effects (MTX, amiodarone)
43
Q

Histological patterns of Idiopathic Pulmonary Fibrosis

A

Interstitial pneumonia

44
Q

Risk Factors Idiopathic Pulmonary Fibrosis

A

Smoking
Occupational Exposure to metal or wood
Chronic microaspiration
Animal and vegetable dusts

45
Q

Summarise epidemiology of idiopathic pulmonary fibrosis

A
  • Rare
  • 6/100,000
  • more common in MALES
46
Q

Presenting symptoms Idiopathic pulmonary fibrosis

A
  • gradual-onset, progressive dyspnoea on exertion
  • dry irritating cough
  • no wheeze
  • symptoms may be preceded by a viral-type illness
  • fatigue and weight loss are common
    Important to take a full drug and occupational history
47
Q

Signs of idiopathic pulmonary fibrosis on physical examination

A
  • clubbing (50%)
  • bibasal fine late inspiratory crackles
  • signs of RHF in advanced stages
48
Q

Investigations for Idiopathic Pulmonary Fibrosis

A

Lung Biopsy:
GOLD STANDARD
Bloods:
- ABG: normal in early disease, PO2 decreases with exercise, normal PCO2 which rises in late stage disease
- ANA and Rheumatoid Factor (1/3 all patients positive for either of these)
CXR:
- usually normal
- early disease may show ground glass shadowing
- later stages: reticulonodular shadowing, signs of cor pulmonale and eventually honeycombing
HIGH RES CT:
- more sensitive for early disease
Pulmonary function tests:
- restrictive features
- decreased lung vol, lung compliance, total lung capacity
Bronchoalveolar Lavage:
- exclude infections and malignancy
Echocardiography:
- check for pulmonary hypertension

49
Q

Define Obstructive Sleep Apnoea

A

Disease characterised by recurrent prolapse of pharyngeal airway and apnoea (cessation of airflow >10seconds) during sleep, followed by arousal from sleep.

50
Q

Aetiology/ Risk Factors Obstructive Sleep Apnoea

A
  • Narrowing of upper airways because of collapse of soft tissues of pharynx
  • Decreased tone of pharyngeal dilators during sleep
  • Associated with: weight gain, smoking, alcohol, sedative use, enlarged tonsils & adenoids in children, macroglossia, marfans, craniofacial abnormalities
51
Q

Epidemiology of Obstructive Sleep Apnoea

A
  • common
  • 5-20% men >35yrs
  • 2-5% women >35yrs
  • prevalence increases with age
52
Q

Presenting symptoms of obstructive sleep apnoea

A
  • excessive daytime sleepiness
  • unrefreshing / restless sleep
  • morning headaches
  • difficulty concentration
  • irritability and mood changes
  • partner reporting snoring, nocturnal apnoea episodes or nocturnal choking
53
Q

Signs of obstructive sleep apnoea on physical examination

A
  • large tongue
  • enlarged tonsils
  • long/ thick uvula
  • retrognathia
  • neck circumference (>42cm in males, >40cm in females)
  • obesity
  • HTN
54
Q

Investigations for Obstructive Sleep Apnoea

A
  • Sleep study (monitor airflow, respiratory effort, pulse oximetry & HR)
  • Bloods (TFTs, ABG)
55
Q

Pneumoconiosis definition (and 3 different types)

A

Fibrosing interstitial lung disease caused by chronic inhalation of mineral dusts
Simple: coalworker’s pneumoconiosis or silicosis
Complicated: pneumoconiosis results in loss of lung function
Asbestosis: pneumoconiosis in which different diffuse parenchymal lung fibrosis occurs as a result of prolonged exposure to asbestos

56
Q

Aetiology/ Risk Factors of Pneumoconiosis

A 
Inhalation of particles of:
- coal dusts
- silica
- asbestos
Risk Factors:
- occupational exposure
- risk depends on extent of exposure and particle type
- Individual susceptibility
- Cofactors such as smoking &amp; TB also contribute
57
Q

Epidemiology Pneumoconiosis

A

Increasing incidence in developing countries

Disability and mortality from asbestosis will continue to increase for the next 20-30yrs

58
Q

Presenting symptoms pneumoconiosis

A

Occupational History is very important
Asymptomatic: picked up on routine CXR
Symptomatic:
- insidious onset SOB
- dry cough
- Melanoptysis (coal worker’s pneumoconiosis)
- Pleuritic chest pain (acute asbestos pleurisy)

59
Q

Signs of Pneumoconiosis on physical examination

A
  • Expiration may be normal
  • Coalworkers pneum. & silicosis: decreased breath sounds
  • Asbestosis: end-inspiratory crepitations, clubbing
  • Signs of pleural effusion or RHF (cor-pulmonale)
60
Q

Investigations for pneumoconiosis

A

CXR:
Simple shows micro nodular mottling
Complicated: shows nodular opacities in upper lobes, micro nodular shadowing, eggshell calcification of hilar lymph nodes (in silicosis), bilateral lower zone reticulonodular shadowing and pleural plaques (in asbestosis)

CT scan: fibrotic changes can be visualised early

Bronchoscopy: allows visualisation and bronchoalveolar lavage

Lung Function Tests: restrictive pattern

61
Q

Define Pneumonia

A

Infection of distal lung parenchyma

  • CAP
  • HAP
  • Aspiration pneumonia
  • Pneumonia in the immunocompromised
  • Typical
  • Atypical
62
Q

Aetiology/ Risk factors of pneumonia (HAP & CAP)

A

CAP:

  • 70% Streptococcus pneumoniae
  • Haemophilus influenza
  • Moraxella Catarrhalis (COPD patients)
  • Chlamydia pneumonia
  • Mycoplasma pneumonia
  • Legionella
  • Staphylococcus aureus
  • Coxiella Burnetii
  • TB

HAP:

  • Gram negative enterobacteria (Pseudomonas, Klebsiella)
  • Anaerobes (aspiration pneumonia)

Risk Factors:

  • Age
  • Smoking
  • Alcohol
  • Pre-existing lung disease (COPD)
  • Immunodeficiency
  • Contact with pneumonia patients
63
Q

Epidemiology of pneumonia

A

5-11/ 1000

CAP responsible >60,000 deaths per year in the UK

64
Q

Presenting symptoms of pneumonia (and specifically to atypical)

A
  • Fever
  • Rigors
  • Sweating
  • Malaise
  • Cough
  • Sputum
  • Breathlessness
  • Pleuritic chest pain
  • Confusion
    ATYPICAL
  • headache
  • myalgia
  • diarrhoea/ abdo pain
  • dry cough
65
Q

Recognise signs of pneumonia on physical examination

A
  • pyrexia
  • respiratory distress
  • tachypnoea
  • tachycardia
  • hypotension
  • cyanosis
  • decreased chest expansion
  • dull to percuss over affected area
  • increased tactile vocal fremitus over affected area
  • bronchial breathing over affected area
  • coarse crepitations on affected sides

Chronic suppurative lung disease (empyema, abscess)–> clubbing

66
Q

Investigations for pneumonia

A

Bloods:
FBC- raised WCC, E&Es, LFTs, Blood cultures, ABG, Blood film (mycoplasma causes red cell agglutination)
CXR:
Lobar or patchy shadowing, pleural effusion, (klebsiella affects upper lobes)
Sputum/ Pleural Fluid- MC&S
Urine- pneumococcus and legionella antigens
Atypical viral serology
Bronchoscopy and bronchoalveolar lavage- if pneumocystis carinii pneumonia is suspected, or if pneumonia fails to resolve

67
Q

Management plan for pneumonia

A
  • Assess severity with British Thoracic Society Guidelines
  • Start empirical antibiotics: Oral amoxicillin if 0 markers
    Oral/ IV Amoxicillin & Erythromycin if 1 marker
    IV Cefuroximine/ Cefotaxime/ Co-amoxiclav +Erythromycin (>1 marker)
    Add metronidazole if aspiration, lung abscess of empyema
  • Use AB appropriate to sensitivity
  • Supportive treatment : O2, IV fluids, CPAP BiPAP or ITU care for respiratory failure, and surgical drainage if lung abscesses and empyema
  • Discharge planning
    if two or more features of clinical instability are present (e.g. temp, tachycardia, tachypnoea, hypotension, low O2 sats) there is a high risk of re-admission and mortality
68
Q

Prevention of Pneumonia

A
  • pneumococcal vaccine
  • haemophilus influenza type B vaccine
    (only for high risk groups)
69
Q

Complications of Pneumonia

A
  • Pleural effusion
  • Empyema
  • localised suppuration (e.g. abscess, symptoms are: swinging fever, persistent pneumonia, copious/ foul-smelling sputum)
  • Septic shock
  • ARDS
  • Acute renal failure
  • Extra complications of mycoplasma pneumonia :
    erythema multiforme
    myocarditis
    haemolytic anaemia
    meningoencephalitis
    transverse myelitis
    Guillain-barre syndrome
70
Q

Prognosis for patients with pneumonia

A
  • most resolve with treatment within 1-3 weeks
  • severe pneumonia has high mortality
  • CURB-65 score assesses severity of pneumonia:
    Confusion <8 AMTS
    Urea >7 mmol/L
    RR >30/min
    BP: systolic <90mmHg or diastolic <60mmHg
    Age >65yrs
71
Q

Define Pneumothorax

A

Air in the pleural space

72
Q

Aetiology/ Risk Factors of pneumothorax

A

Spontaneous:
- occurs in ppl with typically normal lungs
- typically tall, thin males
- rupture of sub pleural bleb
Secondary:
- in patients with pre-existing lung disease (COPD, asthma, TB)
Traumatic:
- penetrating injury to the chest
- often iatrogenic (i.e. during jugular venous cannulation)

Risk Factors:
- Collagen disorders (Marfans, Ehlers-Danlos)

73
Q

Epidemiology of pneumothorax

A
  • annual incidence: 9/100,000
  • mainly 20-40yr olds
  • 4x more common in MALES
74
Q

Presenting symptoms of pneumothorax

A
  • may be asymptomatic
  • sudden onset breathlessness
  • pleuritic chest pain
  • distress with rapid shallow breathing (if tension pneumothorax)
75
Q

Signs of pneumothorax on physical examination (and for tension pneumothorax)

A

-none if small
- signs of respiratory distress
- reduced expansion
- hyper-resonance to percussion
- reduced breath sounds
TENSION:
- severe respiratory distress
- tachycardia
- hypotension
- cyanosis
- distended neck veins
- tracheal deviation away from pneumothorax

76
Q

Investigations for pneumothorax

A

CXR:
- dark area of film with no vascular markings
- fluid level may be seen if there is bleeding
ABG:
- check for hyperaemia

77
Q

Management plan for pneumothorax

A

• Tension pneumothorax (emergency):
o Maximum O2, insert large-bore needle into second intercostal space, midclavicular line, on side of pneumothorax to relieve pressure, insert chest drain soon after
• Small pneumothorax (<2 cm lung-pleural margin):
o If there is no underlying lung disease, pleural fluid or clinical compromise, reassure, analgesia if required
• Moderate pneumothorax (>2 cm lung-pleural margin):
o Aspiration using large-bore cannula or catheter with three-way tap: inserted into the second intercostal space in the midclavicular line. Up to 2.5 L of air can be aspirated (stop if patient repeatedly coughs or resistance is felt). Follow-up CXR should be performed just after, 2 h and 2 weeks later. Advised to avoid diving
o Chest drain with water seal: if aspiration fails or if there is fluid in the pleural cavity or after decompression of a tension pneumothorax. It is inserted into the fourth to sixth intercostal space in midaxillary line
• Recurrent pneumothoraces: chemical pleurodesis (visceral and parietal pleura fusion with tetracycline or talc). Surgical pleurectomy
• Advice: Avoiding air travel until follow-up CXR confirms resolution of pneumothorax. Avoid diving unless bilateral surgical pleurectomy

78
Q

Complications of pneumothorax

A
  • recurrent pneumothoraces

- bronchopleural fistula

79
Q

Summarise the prognosis for patients with pneumothorax

A
  • after having one , 20% patients will have another and frequency increases thereafter
80
Q

Define Pulmonary Embolism

A

Occlusion of pulmonary vessels, most commonly by a thrombus that has travelled to the pulmonary vascular system from another site

81
Q

Aetiology / Risk Factors of Pulmonary Embolism

A

Thrombus :
- 95% from DVT
- Rarely arises in right atrium (other than AF patients)
Other:
- amniotic fluid, air, fat, tumour, mycotic

Risk Factors:

  • surgical patients
  • immobility
  • obesity
  • OCP
  • Heart Failure
  • Malignancy
82
Q

Epidemiology of PE

A
  • relatively common

- occur in 10-20% of patients with confirmed proximal DVT

83
Q

Presenting symptoms of PE

A
  • depends on site and size of embolus
  • Small: asymptomatic
  • Moderate: sudden onset SOB, cough, haemoptysis, pleuritic chest pain
  • Large: as above and severe central pleuritic chest pain, shock, collapse, acute RHF, sudden death
  • Multiple recurrent: symptoms of pulmonary HTN
84
Q

Signs of PE on physical examination

A

Small: no clinical signs, maybe tachycardia and tachypnoea

Moderate: tachypnoea, tachycardia, pleural rub, low O2 sats despite supplementation

Large: shock, cyanosis, right hear strain (raised JVP, left parasternal heave, accentuated S2 sound)

Multiple recurrent: signs of pulmonary HTN, RHF signs

85
Q

Investigations for a PE

A
  • Using Wells score
  • <4 Wells = low probability, use D-dimer
  • > 4 Wells, image with CTPA plus additional Ix
  • Bloods: ABG, thrombophilia screen
  • ECG: may be normal, or tachycardia, right axis dev., RBBB, S1Q3T3 pattern
  • CXR: normal, but useful to exclude other Dx
  • Spiral CT Angiogram (1st line) : poor sensitivity for small emboli, very sensitive for medium to large emboli
  • VQ scan: mismatch indicates an area of infarcted lung
  • Pulmonary Angiography: invasive & rarely necessary
  • Doppler US of lower limb: assesses venous thromboembolism
  • Echocardiography: may show right heart strain
86
Q

Management plan for PE

A

Primary prevention:
compression stockings, heparin prophylaxis if at risk, good mobilisation & adequate hydration

Haemodynamically stable:
oxygen, anticoagulation with heparin/ LMWH, switch to oral warfarin for at least 3 months (maintain INR 2-3), analgesia

Haemodynamically unstable (massive PE): 
resuscitate, oxygen, IV fluids, thrombolysis with tPA if cardiac arrest is imminent

Surgical/ Radiological:
embolectomy, IVC filters (for recurrent PEs when anticoagulant is contraindicated/ not working)

87
Q

Complications of PE

A
  • death
  • pulmonary infarction
  • pulmonary HTN
  • RHF
88
Q

Prognosis for patients with PE

A
  • 30% mortality in untreated
  • 8% mortality with treatment
  • Increased risk thromboembolic disease
89
Q

Define Tuberculosis (Primary/ Miliary/ Post-primary)

A

Granulomatous disease caused by Mycobacterium TB

Primary: initial infection may be pulmonary or (rarely) gastrointestinal

Miliary: haematogenous dissemination of TB

Post-primary: caused by reinfection or reactivation

90
Q

Aetiology of TB/ Risk Factors

A

Mycobacterium tuberculosis is an intracellular organism that survives phagocytosis

RF: immunocompromised, infection with TB bacterium

91
Q

Epidemiology of TB

A

Annual mortality= 3million
Annual UK incidence= 6000
Asian immigrants are highest risk group in UK

92
Q

Symptoms & Signs of TB

A

Primary: asymptomatic, fever, malaise, cough, wheeze, erythema nodosum, phlyctenular conjunctivitis

Miliary: fever, weight loss, meningitis, yellow caseous tubercles spread to other organs

Post-primary TB: fever/night sweats, malaise, breathlessness, cough, sputum, haemoptysis, pleuritic chest pain, signs of pleural effusion, collapse, consolidation, fibrosis

Non-pulmonary TB: mainly in the immunocompromised

Lymph Nodes: suppuration of cervical lymph nodes leading to abscesses/ sinuses

CNS: meningitis, tuberculoma

Skin: lupus vulgaris (jellylike reddish-brown glistening plaques

Heart: pericardial effusion, constructive pericarditis

GI: subacute obstruction, change in bowel habit, weight loss, peritonitis, ascites

Genitourinary: UTI symptoms, renal failure, epididymitis, endometrial/ tubal involvement, infertility

Adrenal insufficiency

Bone/ Joint: osteomyelitis, arthritis, vertebral collapse (pott’s disease), spinal cord, compression from an abscess

93
Q

Investigations for TB

A

Sputum/Pleural fluid/ bronchial washings - MC&S

Tuberculin tests: positive is pt has previous exposure to M.tuberculosis/ BCG

Mantoux test: purified protein derivative (PPD) injected intradermally, erythema occurs after 72hours

Heaf Test: drop of PPD on forearm, fire spring-loaded needle gun, check after 3-7 days, graded according to papule size & vesiculation

Interferon Gamma tests: useful in latent TB, exposure of host T cells to TB antigens leads to release of interferon

CXR:
Primary Infections: peripheral consolidation, hilar lymphadenopathy

Miliary Infection: fine shadowing

Post-primary: upper lobe shadowing, streaky fibrosis & cavitation, calcification, pleural effusion, hilar lymphadenopathy

HIV Testing

94
Q

Management of TB

A
  • Antimicrobial therapy: combined to prevent resistance.
  • Directly observed therapy (DOT) may be necessary. Treat for 6 months in pulmonary, 12months for bone or brain.
  • Side effects:
    Rifampicin: orange body fluids, enzyme inducing
    Isoniazid: pyridoxine deficiency, peripheral neuropathy
    Ethambutol: optic neuropathy
    Pyrazinamide: increased rate/ arthralgia, hepatotoxicity
    Streptomycin: only if highly resistant

Advice: explain SEs and consider steroids for pericardial, cerebral or bone involvement

Public Health: notifiable disease, isolate if respiratory until 2 weeks treatment
Contact tracing

Prevent: BCG vaccine (60-80% efficacy. live attenuate strain derived from mycobacterium Bovis)

95
Q

Complications of TB

A

Primary TB: lobar collapse (middle) and bronchiectasis (Brock’s syndrome) , pleural effusion, pneumonic spread, military disease disseminated in lung/ body

Post-primary TB: pleural effusion, empyema, aspergilloma, adenocarcinoma, laryngeal disease, swelling of bronchial lymphatics & airflow obstruction, haemoptysis, distant spread

96
Q

Prognosis of TB

A

Excellent if pulmonary TB & treated. Overall mortality 8% is extra pulmonary TB, relapse because of non-adherence, resistance, cavitation, empyema, latency

Yr3 Med Conditions (9 decks)

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