1
Q
What is the pathophysiology of COPD?
A
- Increased numbers of mucus-secreting goblet cells within the bronchial mucosa, especially in the larger bronchi
- In advanced cases, the bronchi become overtly inflamed and pus in seen in the lumen
- Most have emphysema and chronic bronchitis and the combination of these severely limits airflow
- V/Q mismatch from damage and mucus plugging
- Cigarette smoke causes mucus gland hypertrophy in larger airways, leading to an increase in neutrophils, macrophages and lymphocytes in the airways
- These cells release inflammatory mediator, attracting inflammatory cells, inducing structural changes and breaking down connective tissue in the lung → emphysema
2
Q
What are the risk factors of COPD?
A
- CIGARETTE SMOKING
- Pollutants at work (mining, building and chemical industries)
- Outdoor air pollution
- Inhalation of smoke from biomass fuels
3
Q
What is the clinical presentation of COPD?
A
- Characteristic symptoms are productive cough with white or clear sputum, wheeze and breathlessness (usually follows many years of a smoker’s cough)
- Colds seem to settle on the chest and frequent infective exacerbations occur with purulent sputum (contains pus)
- Symptoms worsened by cold or damp weather and atmospheric pollution
- Systemic effects: hypertension, osteoporosis, depression, weight loss, reduced muscle mass with general weakness
- Severe disease = breathless at rest with prolonged expiration, poor chest expansion and hyperinflated lungs (barrel chest)
- Pursed lips on expiration (helps to prevent airway collapse)
- Later stages are characterised by respiratory failure
- May develop pulmonary hypertension in advanced disease
4
Q
What are the differential diagnoses of COPD?
A
- Asthma
- Congestive heart failure
- Bronchiectasis
- Allergic fibrosing alveolitis
- Pneumoconiosis
- Asbestosis
5
Q
How is COPD diagnosed?
A
- Based on a history of breathlessness and sputum production in a chronic smoker
- If there is no history of smoking, it’s more likely to be asthma unless there’s a family history suggesting alpha-1 antitrypsin deficiency
- Lung function tests show progressive airflow limitation with increasing severity and breathlessness
6
Q
How is COPD managed?
A
- SMOKING CESSATION
- Bronchodilators: inhaled tiotropium bromide with salbutamol
- Corticosteroids in symptomatic patients with moderate/severe COPD prednisolone daily
- Oxygen therapy
- Antimucolytic agents can reduce sputum viscosity
- Diuretics
- Pulmonary rehabilitation to increase exercise capacity
- Good diet to reduce weight
- Alpha-1 antitrypsin replacement
7
Q
What is the pathophysiology of chronic bronchitis?
A
- Airway narrowing and airway limitation from hypertrophy and hyperplasia of mucus secreting glands of the bronchial tree, bronchial wall inflammation and mucosal oedema
- Infiltration of the bronchi/bronchiole walls with acute and chronic inflammatory cells
- Epithelial layer becomes ulcerated and eventually squamous epithelium replaces the columnar cells (=squamous metaplasia) when the ulcer heals
- Inflammation is followed by scarring and thickening of the walls, narrowing the small airways
- Small airways are particularly affected in early disease
- Initial inflammation is reversible so improvement in airway function can happen is smoking is stopped early (in later stages, inflammation continues even if smoking is stopped)
8
Q
What is the classic clinical presentation of chronic bronchitis?
A
- ‘Blue bloaters’
- Cough with phlegm
- Cor pulmonale
- Respiratory failure (usually T2)
9
Q
What is the pathophysiology of emphysema?
A
- Dilatation and destruction of the lung tissue distal to the terminal bronchioles
- Results in loss of elastic recoil, causing expiratory airflow limitation and air trapping
- Premature closure of airways limits expiratory flow while the loss of alveoli decrease capacity for gas transfer
10
Q
What is the classic clinical presentation of emphysema?
A
- ‘Pink puffers’
- Weight loss
- Breathless
- Maintained pO2
11
Q
What is the aetiology of asthma?
- Allergic/ eosinophilic
- Non allergic/ non-eosinophilic
- Genetic factors
- Environmental factors
A
Two main categories:
- Atopy: IgE antibodies readily produced against common exposures.
- Increased responsiveness of airways to inhaled stimuli: histamine and methacholine
ALLERGIC/ EOSINOPHILIC:
- Allergens (e.g. fungal allergens and pets etc) and atopy
NON-ALLERGIC/ NON-EOSINOPHILIC:
- Exercise, cold air and stress
- Smoking and non-smoking associated
- Obesity associated
GENETIC FACTORS:
- No single gene, but several genes in combination with environmental factors
- Genes controlling the production of different cytokines
- ADAM33 is associated with hyper-responsiveness and tissue remodelling
ENVIRONMENTAL FACTORS:
- Early childhood exposure to allergens and maternal smoking has a major influence on IgE production
- Growing up in a ‘clean’ environment may predispose towards an IgE response to allergens
12
Q
What is the pathophysiology of asthma? (Inflammation and muscular changes)
A
INFLAMMATION:
- Triggers cause an inflammatory cascade in the bronchial tree
- Mast cells, eosinophils, T lymphocytes and dendritic cells increased in bronchial wall, membranes and secretions
- Lymphocytes produce ILs to start cascade → IgE produced
MUSCULAR:
- Increased contraction of smooth muscle in bronchial wall
- Remodelling causes more muscle mass in wall and increased number of goblet cells
13
Q
What are the risk factors of asthma?
A
- Personal history of atopy
- Family history of asthma or atopy
- Obesity
- Inner-city environment
- Premature birth, socio-economic deprivation
14
Q
What is the clinical presentation of asthma?
General, during attack, uncontrolled attack, severe attack, life threatening attack
A
- Intermittent dyspnoea
- Wheeze
- Cough (especially nocturnal)
- Sputum
- Symptoms worse at night
- Episodic shortness of breath
- Provoking factors: allergens, infection, menstrual cycle, exercise, cold air
DURING ATTACK:
- There is reduced chest expansion
- Prolonged expiratory time
- Bilateral expiratory polyphonic wheezes
- Tachypnoea
UNCONTROLLED ATTACK:
- PEFR < 50% expected
- Resp rate < 25/m
- Pulse < 110bpm
- Normal speech
SEVERE ATTACK:
- Inability to complete sentences
- Pulse > 110bpm
- Resp rate > 25/m
LIFE-TREATENING ATTACK:
- Silent chest
- Confusion and exhaustion
- Cyanosis (PaO2 < 8kPa)
- Bradycardia
- PEFR < 33%
15
Q
What are the differential diagnoses of asthma?
A
- Pulmonary oedema
- COPD (may co-exist)
- Large airway obstruction caused by a foreign body/ tumour
- Pneumothorax
- Bronchiectasis
16
Q
How is asthma diagnosed?
A
- History and evidence of obstruction (PEF/ spirometry) during episodes
- RCP3 questions: recent nocturnal waking, usual symptoms in a day, interference with activities of daily living
- Lung function tests (PEFR, spirometry)
- Exercise tests
- Trial or corticosteroids
- Exhaled nitric oxide (measure of eosinophilic inflammation)
- Blood and sputum tests
- Skin prick tests to identify allergens
17
Q
How is asthma managed?
normal, non-emergency management
A
- Avoid triggers
BRONCHODILATORS: → Beta2-agonists: - SABA last 4h e.g. salbutamol - LABA last 12h e.g. salmeterol → Muscarinic agents: - SAMA e.g. ipratropium - LAMA e.g. tiotropium → Methylxanthines: - Theophylline
ANTI-INFLAMMATORY STEROIDS (inhaled corticosteroids)
- For all patients with regular persistent symptoms
- E.g. prednisolone, beclomethasone, budesonide
18
Q
What is the immediate management for a life-threatening asthma attack?
A
- Oxygen therapy to maintain O2 sat (94-98%)
- Nebulised 5mg salbutamol (+ ipratropium if life threatening) – repeat/ IV infusion
- Prednisolone (± IV hydrocortisone)
- Take ABG and repeat within 2 hours if severe or if deteriorating
- CXR if fails to respond to treatment
- Check PEFR within 15-30m / regularly
- Oximetry to ensure SaO2>92%
19
Q
What is the aetiology of mesothelioma?
A
Asbestos exposure
20
Q
What is the pathophysiology of mesothelioma?
A
- High grade malignancy of the pleura that spreads around pleural surfaces
- Can also start in the pericardial space, peritoneal space and paratesticular space
- Tumour begins as nodules in the pleura which extend as a confluent sheet to surround the lung and extend into fissures
- The chest wall if often invaded with infiltration of intercostal nerves, giving severe intractable pain
- Lymphatics may be invaded, giving hilar node metastases
21
Q
What is the main risk factor for mesothelioma?
A
Asbestos exposure
22
Q
What is the clinical presentation of mesothelioma?
A
- Chest pain
- Dyspnoea
- Weight loss
- Finger clubbing
- Recurrent pleural effusions
- Breathlessness
- Signs of metastases: lymphadenopathy, hepatomegaly, bone pain/tenderness, abdominal pain/obstruction
23
Q
How is mesothelioma diagnosed?
A
- CXR and CT: unilateral pleural effusion, pleural thickening
- Blood/straw coloured pleural fluid
- Pleural biopsy
24
Q
How is mesothelioma managed?
A
- Surgery for extremely localised mesothelioma
- Generally resistant to surgery, chemotherapy and radiotherapy
- Average time from diagnosis to death is 8m
- Refer all mesothelioma deaths to HM coroner
- Poor prognosis
25
What is the pathophysiology of a small cell lung carcinoma?
- Often arises from endocrine cells in a central bronchus
| - Secretes polypeptide hormones and have early development of widespread metastases
26
What is the pathophysiology of a squamous cell carcinoma (type of non-small cell lung carcinoma)?
- Tumours are usually central in location and frequently cavitate with central necrosis
- Arise from epithelial cells and are associated with keratin production
- Cause obstructive lesions of bronchus with post-obstructive infection
- Local spread common and metastases relatively late
27
What is the pathophysiology of an adenocarcinoma (type of non-small cell lung carcinoma)?
- May be central or peripheral
- Usually single lesions but they can arise in a multifocal pattern, sometimes bilaterally
- Originate from mucus-secreting glandular cells
- Most common type in non-smokers
- Often cause peripheral lesions on CXR/ CT
- Metastases common to pleura, lymph nodes, brain, bones and adrenal glands
Carcinoid tumours:
- Characteristic neuroendocrine secreting cells and relatively low rates of invasion and growth
28
What is the pathophysiology of lymphomas (type of non-small cell lung carcinoma)?
- Involve the lung primarily but are usually a component of disseminated disease
- Main lung lymphoma is a B cell lymphoma
29
What is the pathophysiology of benign non-small cell lung tumours (hamartomas)?
- Irregular proliferations of benign/normal tissues not normally found in this pattern within the lung
- Most common one in the lung is chondroid hamartoma
30
What are the risk factors for lung cancers?
| general, occupational, environmental, host factors
- Cigarette smoking (including passive smoking)
- OCCUPATIONAL: asbestos, coal (and products of coal combustion), chromium, arsenic, nickel, petroleum products, iron oxide
- ENVIRONMENTAL: radon exposure, ionising radiation
- HOST FACTORS: pre-existing lung disease such as pulmonary fibrosis, HIV infection, genetic factors
31
What is the clinical presentation of lung cancers? (local and metastatic disease)
LOCAL DISEASE:
- Cough
- Breathlessness
- Haemoptysis
- Chest pain
- Wheeze
- Recurrent infections e.g. pneumonia
- Clubbing
METASTATIC DISEASE:
- Bone pain
- Headache
- Seizures
- Neurological deficit
- Hepatic pain
- Abdominal pain
32
How are lung cancers diagnosed?
- TNM classification
- CXR: appear as round shadow, edge has a fluffy spiked appearance, hilar enlargement, consolidation, lung collapse, pleural effusion
- CT for staging
- Bronchoscopy to give histology and assess operability
- Cytology for sputum and pleural fluid
- Bloods: low FBC
33
How are small cell lung cancers managed?
- Limited disease is treated with combined chemo and radiotherapy
- Extensive disease treated with chemotherapy
- Palliation to relieve symptoms; radiotherapy used for bronchial obstruction, haemoptysis, bone pain and cerebral metastases
- Superior vena cava stent + radiotherapy + dexamethasone for superior vena cava obstruction
- Endobronchial therapy used to treat symptoms of airway narrowing (tracheal stenting, cryotherapy, brachytherapy)
- Pleural drainage for symptomatic relief
- Drugs: analgesia, steroids, antiemetics, codeine, bronchodilators, antidepressants
34
How are non-small cell lung cancers managed?
- Surgical excision for peripheral tumours with no metastatic spread
- Curative radiotherapy if respiratory reserve is poor
- Chemo ± radiotherapy for more advanced disease
35
What is the pathophysiology of a pulmonary embolism?
- Circulatory stasis, endothelial injury and hypercoagulable state
- Arise from venous thrombosis in the pelvis or legs, clots break up and pass through the IVC → right side of heart → pulmonary circulation
- Becomes lodged in the small capillaries supplying the alveoli, causing a PE
- After a PE, lung tissue is ventilated but not perfused, resulting in intrapulmonary dead space and impaired gas exchange
- After a while, the non-perfused lung no longer produced surfactant, resulting in alveolar collapse, exaggerating hypoxaemia
36
What are the risk factors of a pulmonary embolism?
- Change in blood flow: immobility (paralysis/ post op), obesity, pregnancy
- Change in blood vessel: smoking, hypertension
- Change in blood constituents: dehydration, malignancy, high oestrogen (e.g. combined oral contraceptive pill), nephrotic syndrome, polycythaemia, inherited
- Recent surgery (esp. abdo/pelvic or hip/knee replacement)
- Leg fracture
- Aged >60y
37
What is the clinical presentation of a pulmonary embolism?
- Depends on the number, size and distribution of emboli (small ones may be asymptomatic, large ones are often fatal)
- Sudden onset unexplained dyspnoea is the most common symptoms (may be only symptom)
- Pleuritic chest pain and haemoptysis when infarction has occurred
- Dizziness
- Past history/ family history of thromboembolism
- Pyrexia
- Cyanosis
- Tachypnoea
- Tachycardiac
- Hypotension
- Raised jugular venous pressure
- Pleural rub (audible sign on stethoscope)
- Pleural effusion
38
What are the differential diagnoses of a pulmonary embolism?
- Asthma
- COPD
- MI
- Pneumonia
- Heart failure
39
How is a pulmonary embolism diagnosed?
CT pulmonary angiography:
- Gold standard test
CXR:
- Often normal
- Decreased vascular markings
- Blunting of costophrenic angle
- Wedge-shaped areas of infarction
- Pulmonary oligaemia in massive embolism
ECG:
- May be normal
- May show sinus tachycardia
- Right atrial dilation with tall peaked P waves in lead II
- Right BBB
- Right ventricular strain (inverted T wave in V1 to V4)
Blood gasses:
- May be normal
- Arterial hypoxaemia with significant PE
Plasma D-dimer:
- Elevated
- Not specific to PE therefore not diagnostic
USS:
- Look at legs and pelvis for clots
40
How is a pulmonary embolism managed?
| standard, non-massive PE
- High flow oxygen (60-100%)
- Anticoagulants (low molecular weight heparin)
- IV fluids and inotropic agents in severe cases (improves pumping of right heart)
- Thrombolysis for massive PE to improve pulmonary perfusion
- Surgical embolectomy
- Vena cava filter in patients who still develop emboli after anticoagulation
41
How are pulmonary emboli prevented?
Prevention:
- Vitamin K antagonist e.g. warfarin
- Early mobilisation
- TED stockings
42
How is a massive PE managed?
- Oxygen if hypoxic
- Morphine with anti-emetic if patient is in pain or very distressed
- Consider immediate thrombolysis if critically ill
- Rapid colloid infusion if systolic BP <90mmHg
- Warfarin if systolic BP >90mmHg
43
What is the aetiology of TB?
Caused by 4 main mycobacterial species:
- Mycobacterium tuberculosis (most common)
- Mycobacterium bovis (from unpasteurised milk)
- Mycobacterium africanum
- Mycobacterium microti
44
What is the pathophysiology of primary TB?
| full detail of process
- First infection with a mycobacteria
- Alveolar macrophages ingest the inhaled bacteria
- Bacteria proliferate inside macrophages, causing the release of neutrophil chemo-attractants and cytokines
- This results in a cellular immune response and a delayed hypersensitivity-type reaction, causing tissue necrosis and granuloma formation
- Initial granuloma = Primary Ghon Focus (found in upper region of lung in sub-pleural region)
- Primary lesion can also occur in the GI tract
- The caveated areas heal completely and may become calcified
- Some of the calcified nodes contain bacteria which can lie dormant for many years
- If the bacteria can’t be contained, there is dissemination of the primary infection → miliary TB (it spreads to other organs)
45
What is the pathophysiology of latent TB?
Immune system contains the infection and the patient develops cell-mediated immunity memory of the bacteria
46
What is the pathophysiology of reactivation TB?
When there’s a depression of host immunity causing latent TB to reactivate
47
What are the risk factors for TB?
- Origination from a high-incidence country e.g. sub-Saharan Africa
- HIV +immunosuppression
- Immunosuppressant therapy (chemo or MAB)
- Diabetes mellitus
- IVDU
- Ageing
- Malnutrition
- Homeless i.e. poverty
- Prisons
- Smoking
- Alcohol
48
What are the systemic clinical features of TB?
- Weight loss and night sweats = most predictive
- Low grade fever
- Anorexia
- Malaise
49
What are the pulmonary clinical features of TB?
- Can be asymptomatic
- Productive cough with occasional haemoptysis
- Cough for >3w
- Can be pleuritic pain if pleural involvement
- Chest pain
- Breathlessness
- Can be hoarse voice if laryngeal involvement
- Associated with consolidation, pleural effusion and pulmonary collapse
50
What are the extra-pulmonary clinical features of TB?
| lymph nodes, bone, abdominal, GU, CNS
LYMPH NODES: swelling ± discharge
BONE: joint pain/ swelling, Potts disease (spinal cord/ vertebral TB)
ABDOMINAL: ascites, abdo lymph nodes, ileal malabsorption
GU: epididymitis, frequency, dysuria, haematuria
CNS: bacilli in CSF, meningeal inflammation (produces thick exudate leading to cranial nerve strangulation and raised ICP), low grade meningitis, random cranial palsies and symptoms of raised ICP
51
How is TB diagnosed?
| non-miliary
- CXR: patchy/nodular shadows in upper zones with loss of volume and fibrosis; consolidation; may be normal in miliary TB
- Sputum: stain for bacteria (e.g. red with Ziehl-Neelsen)
- Bronchoscopy if no sputum available
- Culture and histology
- Nucleic acid amplification (useful for differentiating between tuberculosis and non-tuberculosis mycobacterium)
- Lumbar puncture and CSF examination for miliary TB
52
How is miliary TB diagnosed?
TUBERCULIN SKIN TEST (Mantoux)
- TB antigen is injected intradermally
- Cell-mediated response at 48-72h is recorded as a type 4 hypersensitivity reaction should be stimulated
- Positive results indicated immunity and therefore contact with TB
- Immunosuppressed or miliary TB won’t react (false negative)
- Will react with BCG vaccine (false positive)
INTERFERON GAMMA RELEASE ASSAYS (IGRAs)
- Use antigens specific to M. tuberculosis to distinguish between BCG vaccine or environmental bacteria
- Demonstrates exposure to M. tuberculosis but not active infection
53
How is TB treated?
Patients with fully sensitive TB require 6m of treatment (12m if CNS TB):
- RIFAMPICIN for 6m (bactericidal, blocks protein synthesis, effective throughout treatment)
- ISONIAZID for 6m (bactericidal for rapidly growing bacilli)
- PYRAZINAMIDE for first 2m (bactericidal initially, but less effective later on)
- ETHAMBUTOL for first 2m (bacteriostatic, blocks cell wall synthesis)
54
How is TB prevented?
- Active case finding to reduce infectivity
- Detection and treatment of TB via community nursing team using Mantoux and IGRAs
- Vaccination: neonatal BCG
55
What is the aetiology of community-acquired pneumonia?
- Most common cause is Streptococcus pneumoniae
| - Atypical causes include Haemophilus influenzae and Mycoplasma pneumoniae
56
What is the aetiology of hospital-acquired pneumonia?
- Aerobic G-ve bacilli
| - Pseudomonas aeruginosa, Escherichia coli, Klebsiella pneumoniae
57
What is the pathophysiology of pneumonia?
- Spread by respiratory droplets
- Bacteria translocate to the normally sterile distal airway where they overwhelm resident host defence
- Alveolar macrophages change roles coordinate the response instead of fulfilling their normal roles
- E.g. they cause stimulation of neutrophils to fill alveolar space and produce inflammatory exudate (→ pneumonia)
- Thus is normally resolved when inflammatory cells are removed by apoptosis
- Severe disease occurs if there is excessive inflammation, lung injury of failure to resolve without lung damage
58
What are the risk factors of pneumonia?
- Under 16 and over 65
- Comorbidities: HIV infection, diabetes mellitus, cystic fibrosis, COPD, bronchiectasis
- Smoking
- Excess alcohol
- IVDU
- Immunosuppressant therapy
59
What is the clinical presentation of pneumonia?
- Pneumonia is likely if there are no upper respiratory tract symptoms, but there’s fever, night sweats, raised resp. rate and productive cough
- Symptoms vary depending on infecting agent
- Fever ± raised resp rate, heart rate and low BP
- Rigors
- Malaise
- Anorexia
- Dyspnoea and breathlessness
- Signs of consolidation and auscultation
- Dry of productive cough (dry is non-productive in atypical causes)
- Purulent sputum
- Pleuritic chest pain
- Cyanosis
- Confusion (might be only sign in elderly patients)
60
What are the differential diagnoses of pneumonia?
- TB
| - Lung cancer
61
How is pneumonia diagnosed?
| diagnosis + severity indicator
- CXR: air bronchogram (black branch) in consolidated area (multi-lobar suggests S.pneumoniae, S.aureus and Legionella spp., upper lobe cavity = klebsiella
- Blood tests: FBC (look for raised WCC as a marker of severity)
- Biochemistry: U&E, electrolytes, LFTs, renal function for severity
- Microbiological tests: sputum culture and antibiotic sensitivities ± gram stain, blood culture, serology for viruses and atypical organisms
CURB-65 to assess severity: one point each for confusion, urea>7mmol/L, respiratory rate> 30/min, BP < 90mmHg systolic and/or 60mmHg diastolic, age > 65
Implications of CURB-65:
- 0-1 = mild, only admit if social circumstance or single worrying feature
- 2 = moderate, admit to hospital
- 3-5 = severe, admit and monitor closely
- 4-5 = consider admission to ICU
62
How is pneumonia managed?
- Maintain O2 sats between 94-98% (unless COPD then lower)
- First dose of antibiotics within 4h of presentation in hospital
- Narrow spectrum antibiotics if mild → amoxicillin
- IV antibiotics if severe → co-amoxiclav or clarithromycin
- Analgesia e.g. paracetamol or NSAID for pleuritic pain
Special cases:
- Severe legionella spp. Pneumonia → fluoroquinolone ± clarithromycin
- Necrotising pneumonia → IV linezoid, IV clindamycin, IV rifampicin
- Pseudomonas aeruginosa → IV ceftazidime with gentamicin
63
How is pneumonia prevented?
- Polysaccharide pneumococcal vaccine
- Influenza vaccine to those >65y, immuno-compromised or with co-morbidities
- Smoking cessation
64
What is the aetiology of pharyngitis/ tonsillitis?
- Most common viral cause are adenoviruses
- Can also be rhinovirus, EBV and acute HIV infection
- Bacterial causes include Lancefield Group A Beta-haemolytic streptococci e.g. strep pyogenes
65
What is the clinical presentation of pharyngitis/ tonsillitis?
- Sore throat
- Fever
- Inflamed, swollen tonsils with exudate
- Tender anterior cervical lymph nodes
- Reddened oropharynx and soft palette
66
How is pharyngitis/ tonsillitis diagnosed?
Clinical diagnosis
67
How is pharyngitis/ tonsillitis managed?
- Self-limiting disease
- Symptomatic treatment
- No antibiotics required
- Persistent and severe tonsillitis should be treated with phenoxymethylpenicillin or cefaclor
68
What is the aetiology of sinusitis?
Bacterial: streptococcus pneumoniae, haemophilus influenzae
69
What is the clinical presentation of sinusitis?
- Frontal headache
- Purulent rhinorrhoea (nasal cavity filled with a significant amount of mucus fluid)
- Bacterial sinusutis presents with unilateral pain and purulent discharge ± fever for >10d
70
How is sinusitis diagnosed?
Clinical diagnosis
71
How is sinusitis managed?
- Nasal decongestants e.g. xylometazoline
| - Broad spectrum antibiotics e.g. co-amoxiclav
72
What is the aetiology of acute epiglottis?
- Disease in adults is most severe due to Haemophilus influenzae
- Hib vaccine has made this rare
73
What is the clinical presentation of acute epiglottis?
- High fever
- Severe airflow obstruction
- Meningitis
- Septic arthritis
- Osteomyelitis
74
How is acute epiglottis diagnosed?
Clinical diagnosis
75
How is acute epiglottis managed?
- Requires urgent endotracheal intubation
| - IV antibiotics e.g. ceftazidime
76
What is the aetiology of whooping cough?
Caused by Bordetella pertussis (G-ve coccobacillus)
77
What is the pathophysiology of whooping cough?
Spreads by droplet infection
78
What is the clinical presentation of whooping cough? (general, catarrhal and paroxysmal phases)
- Chronic cough and one clinical feature indicated pertussis
- Characteristic whoop and history of contact with an infected individual
CATARRHAL PHASE (1-2w):
- Patient highly infectious
- Malaise
- Anorexia
- Rhinorrhoea
- Conjunctivitis
PAROXYSMAL PHASE (1-6w):
- Coughing spasms
- Classic inspiratory whoop in younger individuals
- Spasms usually end by vomiting
- Cough for >14d
- May be associated with complications like pneumonia, encephalopathy and sub-conjunctival haemorrhage
79
How is whooping cough diagnosed?
- Chronic cough and history of contact/ microbiological diagnosis
- PCR tests
- Culture of a nasopharyngeal swab is needed for definitive diagnosis
80
How is whooping cough managed?
- Antimicrobials (macrolides e.g. clarithromycin) to eliminate carriage of bacteria
- Antibiotics have little role to play in the paroxysmal stage
- Vaccination against acellular pertussis as part of the dTap vaccine
2a high tier
flashcards
Decks in class (10)
# Cards
