Resp conditions Flashcards
COPD
What is it?
What are its Risk factors?
What is its biggest cause?
A lung disease state characterised by chronic respiratory symptoms and airflow limitation. It encompasses emphysema and chronic bronchitis.
RF - SMOKING, elderly, air pollution, genetic factors (A1AT deficiency)
PATHOLOGY
Smoking is the biggest cause of COPD.
Chronic bronchitis and emphysema aren’t actually separate conditions AS MOST PATIENTS PRESENT WITH A MIX OF BOTH
Chronic bronchitis
RF
PATHOLOGY
SYMPTOMS
INVESTIGATIONS
TREATMENTS
A type of COPD
RF- Smoking, air pollution
Chronic bronchitis
- Characterised as a productive cough for at least 3 months for at least 2 consecutive years
- Exposure to irritants and chemicals –> hypertrophy and hyperplasia of mucinous glands and goblet cells –> increased mucous secretion –> narrows lumen and can cause airway obstruction (increasing risk of infection and airway trapping)
- Chronic inflammation of the bronchi and bronchioles can lead to progressive fibrosis (and also narrows the lumen)
With airway obstruction –> CO2 is trapped in the lungs and in the blood which can cause cyanosis –> BLUE BLOATER
SYMPTOMS
- Productive cough (mucus) - White sputum
- Dyspnoea
- Cyanosis
- Wheezing (due to airway obstruction)
(Overweight due to oedema)
INVESTIGATIONS
Spirometry - A FEV1/FVC ratio less than 0.7 would indicate airflow obstruction
Diffusing capacity of the lung for carbon monoxide (DLCO) - Low in COPD -< 60% predicted (normal in asthma)
Genetic test for A1AT deficiency
ABG - TYPE 2 RESPIRATORY FAILURE (Hypercapnia, hypoxia and respiratory acidosis)
Chest X-ray –> flattened diaphragm and hyperinflation of the lung - Barrel Chest
TREATMENT
Actual 1st line treatment -
Smoking cessation and preventive vaccines for influenza and pneumococcal (as airway obstruction increases risk of infection)
1st line - Salbutamol (SAB2A)
2nd line - Salbutamol + Salmeterol (LAB2A) + Tiotropium bromide (LAM3A)
(If still doesn’t work add inhaled corticosteroids)
Emphysema
-lifestyle treatment and pharmacological treatment
-2 types of emphysema
RF
PATHOLOGY
SYMPTOMS
INVESTIGATIONS
TREATMENTS
A destruction of the elastin layer in the alveolar sacs and respiratory bronchioles –> as elastin keeps these walls open during expiration (bernouli principle) –> decreased elastin results in alveoloar collapse and air being trapped distal to the blockage and there is difficulty exhaling. (Elastic recoil of lung tissue for exhalation is lost)
Different types of emphysema:
Centriacinar emphysema –> Respiratory bronchioles (and proximal alveoli) - Main cause smoking
Panacinar emphysema –> The entire acinar is affected - associated with Main cause A1AT deficiency
Known as PINK PUFFER
- Minimal cough
- Pursed lip breathing
- Barrel chest
- Hyper-resonance on percussion
(Cachexic - thinner because of muscle loss)
Can lead to bullae rupture (enlarge air sacs/spaces due to airflow obstruction) - possible pneumothorax complication
INVESTIGATIONS
Spirometry - A FEV1/FVC ratio less than 0.7 would indicate airflow obstruction
Diffusing capacity of the lung for carbon monoxide (DLCO) - Low in COPD -< 60% predicted (normal in asthma)
Genetic test for A1AT deficiency
ABG - TYPE 2 RESPIRATORY FAILURE (Hypercapnia, hypoxia and respiratory acidosis)
Chest X-ray –> flattened diaphragm and hyperinflation of the lung - Barrel Chest
TREATMENT
Actual 1st line treatment–> Smoking cessation and preventive vaccines for influenza and pneumococcal (as airway obstruction increases risk of infection)
1st line drug treatment- Salbutamol (SABA)
2nd line - Salbutamol + Salmeterol (LABA) + Tiotropium (LAMA)
(If still doesn’t work add inhaled corticosteroids)
What is a complication of COPD?
Cor pulmonale which is pulmonary hypertension resulting in abnormal enlargement of the right side of the heart
Asthma
- Key symptom
- What would you see on sputum culture
RF
PATHOLOGY
SYMPTOMS
INVESTIGATIONS
TREATMENTS
A chronic inflammatory airway disease that leads to airway obstruction (that is reversible). Characterised by reversible, intermittent airway obstruction and hyper-reactivity.
RF- Family history, allergens/irritants, atopic disease history (asthma is an atopic condition and patients with one atopic condition is likely to have others e.g. eczema, hay fever, food allergies), smoking
PATHOLOGY
Overexpressed T helper 2 cells in airways are exposed to the trigger (hypersensitive airway) –> leads to IgE production and EOSINOPHIL recruitment –> IgE triggers mast cell degranulation releasing prostaglandins and histamines. Eosinophils release Major basic protein - causes release of histamine from mast cells. –> results in bronchial constriction and mucus hypersecretion
Atopic/allergic asthma (70%) - IgE mediated T1 hypersensitivity that occurs due to an environmental trigger e.g. pollen, smoke, dust –> often presents earlier (children)
Non Atopic/allergic asthma (30%) - Non IgE mediated –> mostly associated with smoking and presents later (adults)
SYMPTOMS
- Expiratory wheezing
- DIURNAL VARIATION (worse at night/early morning) and EPISODIC
- Dry cough
- Chest tightness
- Dyspnoea
INVESTIGATIONS
1st line - Spirometry
An FEV1:FVC ratio <70% indicates obstructive pathology (asthma/COPD)
Bronchodilator reversibility - Improvement in FEV1 post bronchodilator administration (irreversible in COPD) >12% improvement in FEV1
Fractional exhaled nitric oxide - Increased (biomarker for asthma - eosinophilic inflammation?)
Expiratory peak flow >20% (checking diurnal variation)
Sputum microscopy
- Charcot leyden crystals - eosniophil breakdown products
- Curshmann spirals- plugs formed from bronchial epithelial shedding
TREATMENT
Algorithm
1) SAB2A (salbutamol) PRN
2) SAB2A + Inhaled corticosteroids (budesonide)
–> Check compliance and inhaler technique if still does not work. If still not ok –> Step 3
3) SAB2A + inhaled corticosteroids + Leukotriene receptor antagonist (montelukast)
4) SAB2A + inhaled corticosteroids + Leukotriene receptor antagonist + LAB2A (salmeterol)
5) Everything + increase dose of inhaled corticosteroid
Environmental triggers that can exacerbate symptoms of asthma
Infection, cold weather, exercise, Drugs - BB, NSAIDS (aspirin), animals
Grading for acute asthma
Peak expiratory flow of 50-75% (moderate exacerbation)
PEF of 33-50% (severe exacerbation) (Resp rate >30)
PEF <33%, SpO2 <92% (life threatening exacerbation) - cyanosis
- Wheeze disappears when the airways are so tight that there is no air entry (Silent Chest - life threatening)
CHEST
C - Cyanosis
H - Hypotension 90/60
E - Exhaution
S - Silent chest
T - Tachycardia
How would you manage exacerbations in asthma
OSHITME
Oxygen
Nebulised salbutamol
Hydrocortisone (or prednisolone)
Nebulised ipratropium bromide
Theophylline
Magnesium sulphate
E- Escalate care (intubate and ventilate)
What is the atopic triad?
Allergic rhinitis, eczema and asthma –>some people have all synonymously
Side effect of salbutamol
Serum potassium should be monitored with salbutamol treatment as it causes potassium to be absorbed from the blood in to the cells - hypokalemia.
It can also cause tachycardia and lactic acidosis.
What is Samter’s triad?
Also known as aspirin exacerbated respiratory disease
Triad of
- Asthma
- Sinus disease with recurrent nasal polyps
- Sensitivity to aspirin (and NSAIDS) that inhibits Cox-1and Cox-2
If people affected take NSAIDS –> It would lead to increased leukotriene production –> increasing bronchoconstriction
Tuberculosis
RF
PATHOLOGY
SYMPTOMS
INVESTIGATIONS
TREATMENTS
An infectious disease caused by Mycobacterium tuberculosis (Gram positive bacillus)
RF - Exposure to infection, birth in an endemic country, HIV, immunocompromised, (Africa and south asia), smoking
PATHOLOGY
TYPE 4 HYPERSENSITIVITY
- Spreads through the air (airborne/inhalation of aerosolised particles containing the bacterium)
- It has a thick waxy capsule which makes it resistant to phagolysosomal killing - so able to remain dormant in lung.
Upon inhalation of M.tuberculosis –> the bacteria is engulfed by alveolar macrophages but it survives and multiplies within the macrophages –> proliferating bacilli kill the macrophages are are released –> T cells and Giant cells (macrophages) form a caseous granuloma (CALLED GHON FOCUS - usually in upper parts of lung) with M tuberculosis which serves to prevent further growth and spread (individuals are considered non infectious and have latent TB).
However Ghon focus can spread to nearby lymph node - known as Ghon complex –> which allows it to spread systemically (Miliary TB - disseminated and severe disease that develops as a result of immune system not being able to control the infection)
(Mostly becomes dormant before progressing to active TB - It commonly involves the lungs but can affect other organ systems e.g. lymph nodes, CNS, liver, bones, GI tract, GU tract)
SYMPTOMS
Presents with chronic gradually worsening symptoms.
– Night sweats
- Weight loss
- Productive cough
- Possible chest pain
- Malaise, lethargy
- Erythema nodosum - tender, red nodules on shins caused by inflammation of subcutaneous fat
INVESTIGATIONS
1st line - Chest X-ray
Shows lung cavitations
Ghon focus/complex
Appearance of millet seeds distributed across lung firlds - indicated disseminated milliary tuberculosis
GS
Sputum culture (3 separate samples collected) - They are acid fast bacilli that stains bright red on a Ziehl-Neelson stain
Lung biopsy - Caseous granulomas
Two tests to look for an immune response to tuberculosis (positive means has an immune response)
Mantoux skin test - (people with latent TB have a positive tuberculin skin test with an induration >5mm after 72 hours)
Interferon Gamma release assays - If WBC have become sensitised to the bacteria antigen in a previous infection/contact with M.tuberculosis, there will release interferon gamma on further contact.
TB TO SPINE - POTT disease
TREATMENT
RI6PE2 (Ripe) - all to be taken at same time
Rifampicin - 6 months
Isoniazid - 6 months
Pyrazinamide - 2 months
Ethambutol - 2 months
Side effect of tuberculosis treatment and what should be co prescribed?
RIPE
Rifampicin, isoniazid, pyrazinamide, ethambutol
Rifampicin - Red bloody urine
Isoniazid can cause peripheral neuropathy –> Pyridoxine/vitamin B6 is given to counter this.
Pyrzinamide- hePatitis, arthralgia, rash
Ethambutol - Eyes - Optic neurities (visual problems)
Pneumonia
RF
PATHOLOGY
SYMPTOMS
INVESTIGATIONS
TREATMENTS
An infection of the lung tissue causing inflammation in the alveolar space and Fluid exudation into alveoli
RF - very young/old, residence in healthcare setting, IVDU, immunocompromised, pre existing respiratory disease
PATHOLOGY
Types:
1) Community acquired pneumonia
- Most commonly due to Streptococcus pneumoniae
- H.influenzae
- S.aureus
- Legionella - Europe (france, italy, spain) –> Water cooler/air conditioner
- Mycoplasma pneumoniae –> Causes atypical pneumonia
(Viral cause include influenza)
2) Hospital acquired pneumoniae (>48 hours of hospital admission)
- Gram negative aerobic bacteria: Pseudomonas aeruginosa, Klebsiella (associated with alcoholism)
- MRSA
3) Aspiration pneumonia - infection develops due to aspiration of food or fluids –> possible in patients with impaired swallowing - following a stroke. (Associated with anaerobic bacteria)
(ventilatory associated pneumonia)
Typical pneumonia - exudate forms inside alveoli lumen - sputum
Atypical pneumonia - exudate forms in interstitium
Fungal cause - -Pneumocystic Jirovecci - in immunocompromised patients
SYMPTOMS
Dyspnoea
Pleuritic chest pain - worse with breathing
Productive cough - (Brown/rusty sputum - s.pneumonia)
INCREASED TACTILE FREMITUS - voice is louder on certain parts of the chest.
Systemic - Fatigue, fever - due to infection
Dullness to percussion - due to lung tissue filled with sputum
Coarse inspiratory crackles (lungs)/crepitation - caused by air passing through sputum in the airways
(In atypical pneumonia - Dry cough with a low grade fever)
INVESTIGATION
1st line - Chest X-ray –> shows consolidation (accumulation of fluid filled (exudate) alveoli and adjoining ducts)
Sputum culture + stain with Ziehl Neelson - Identify the causative organism
ABG - Type 1 respiratory failure
CURB 65 - Assessses severity of penumonia
TREATMENT
Community acquired pneumonia (mild- CURB is 0-1)
1st line - Oral Amoxicillin
If penicillin allergy – Clarithromycin
CURB=2
Oral Amoxicillin + clarithromycin
Community acquired pneumonia (high severity - CURB 3-5)
IV Co amoxiclav + Clarithromycin
For legionnaires disease - clarithromycin (A NOTIFIABLE DISEASE)
3 causes of atypical pneumonia
Legionella pneumophila - usually a patient that went on a cheap holiday (e.g. inhaling infected water from an infected water system like air conditioning units)
Mycoplasma pneumoniae - mild pneumoniae with a rash (Erythema multiforme - pink rings with pale centres)
Chlamydophila pneumoniae
What scoring system is used to assess the severity/mortality of pneumonia?
CURB-65
Confusion
Urea >7 mmol/L
Respiratory rate >30
Blood pressure <90 systolic or <60 diastolic
> 65 years
Score of 0/1 - consider treatment at home
Score of 2 or more - consider hospital admission
Score of 3 or more - consider intensive care
Most common type/cause of pneumonia in HIV patients
Pneumocystis pneumonia caused by the fungus pneumocystis jirovecii.
Cystic fibrosis
RF
PATHOLOGY
SYMPTOMS
INVESTIGATIONS
TREATMENTS
An autosomal recessive condition affecting the mucus glands.
RF- family history of CF, Caucasians
PATHOLOGY
Genetic mutation of the CFTR (Cystic fibrosis transmembrane conductance regulator) gene on chromosome 7. (most common is delta F508 (region) mutation)
Causes an abnormality of the chloride channel lining the lungs, intestines, pancreatic duct, sweat glands and reproductive organs.
Key consequences:
- Thick pancreatic and biliary secretions causing blockage of the ducts –> results in a lack of digestive enzymes e.g. pancreatic lipase in the digestive tract
- Thick airway secretions that reduce airway clearance, resulting in bacterial colonisation and susceptibility to airway infections. (Also ciliary dysfunction)
SYMPTOMS
- Respiratory –> Thick sticky sputum production, chronic cough, recurrent respiratory tract infections,
- Neonates –> Meconium ileus (not passing stool within first 24 hours of bring born, possible vomiting) - due to meconium being thick and sticky, getting stuck and obstructing the bowel
- GI –> Steatorrhoea (lack of lipase enzyme), bowel obstruction, abdominal pain/bloating (malnutrition)
- Others –> atrophy of vas deferens (and so infertility), salty sweat, failure to thrive
(Coarse crackles)
INVESTIGATIONS
GS - Sweat test (measures amount of chloride in the sweat- more chloride than usual) >6ommol/L
Faecal elastase test - decreased due to pancreatic insufficiency
Genetic test for CFTR gene- delta F508 mutation
- Screened for at birth with the newborn bloodspot test (New borns might have high immunoreactive trypsinogen)
TREATMENT
No cure
Conservative –> Chest physiotherapy (clears mucus), exercise (improves resp function), no smoking
Drugs –> Mucolytic drugs (N acetyl cysteine), CREON tablets (+ ADEK fat soluble vitamins for patients with pancreatic insufficiency), bronchodilator (salbutamol)
P.aeruginosa - Ciprofloxacin
S.aureus - Flucloxacillin
Common colonisers (bacteria) in patients with cystic fibrosis
S.aureus
H.influenza
Pseudomonas aeruginosa
Top 3 same as bronchiectasis
Klebsiella pneumoniae
E.coli
Bronchiectasis
RF
PATHOLOGY
SYMPTOMS
INVESTIGATIONS
TREATMENTS
The abnormal permanent dilation of bronchi due to the destruction of the elastic and muscular components of the bronchial wall. (Sputum collects–> chronic cough, continuous sputum production and recurrent infections)
RF - Cystic fibrosis, immunodeficiency, previous infections, HIV
PATHOLOGY
Causes:
- Post infection (pneumonia, whooping cough, TB,)
- Cystic fibrosis
- A1AT deficiency
- Yellow nail syndrome (yellow fingernails, bronchiectasis, lymphoedema)
SYMPTOMS
- Dyspnoea
- Chronic productive cough
- Foul smelling sputum
- Recurrent chest infections
- Weight loss
(Coarse Crackles on pulmonary auscultation)
Finger clubbing
INVESTIGATIONS
Imaging –> 1st line - Chest X ray - Dilated bronchi with thickened walls
GS –> HIGH RESOLUTION CT scan - SIGNET RING SIGN + tram track sign - dilated bronchioles next to each other. (bronchus markedly dilated compared to the pulmonary artery)
Spirometry –> Obstructive with FEV1:FVC ratio <0.7
Sputum culture –> to check for infection (Most common H.influenzae, P.aeruginosa)
TREATMENT
No treatment
Conservative –> Chest physiotherapy (e.g. postural drainage), stop smoking, vaccines against infections (influenza)
Drugs –> Bronchodilators
During infections
P.aeruginosa –> Ciprofloxacin
Pleural effusion
-Investigation
RF
PATHOLOGY
SYMPTOMS
INVESTIGATIONS
TREATMENTS
Collection of fluid in the pleural cavity (between lungs and chest wall)
RF - Congestive heart failure, pneumonia, PE
PATHOLOGY
(Light’s criteria to evaluate if it is a exudate or transudate)
Can be exudative fluid (high protein count)
- Due to inflammation - increased vascular permeability –> protein leaks out of tissues into pleural space (lung cancer, pneumonia, rheumatoid arthritis, TB)
Can be transudative fluid (low protein count)
- Fluid moves across (due to an imbalance of fluid/protein) –> Hypoalbuminaemia - liver cirrhosis, nephrotic syndrome, heart failure, pulmonary hypertension
SYMPTOMS
Dyspnoea
Dullness on percussion (over area of effusion) – Hyper resonant would indicate pneumothorax
Reduced breath sounds (over area of effusion)
Tracheal deviation (massive effusions can push mediastinum and trachea)
Cough
INVESTIGATIONS
1st line + GS Chest X-ray –> blunting of costophrenic angle, fluid in lung fissures and tracheal deviation
To establish the underlying caused via Light’s criteria –> Pleural aspiration (thoracocentesis) –> analyse for protein count, WBC+RBC cell count, pH, glucose, lactate dehydrogenase
TREATMENT
Small effusion
Conservative management –> Treating the chest infection with antibiotics
Large effusion (commonly will be chest drain)
Chest drain
Last resort - Pleurodesis –> surgical fusion of pleural layers to prevent fluid buildup (obliterate pleural space)
Pneumothorax
RF
PATHOLOGY
SYMPTOMS
INVESTIGATIONS
TREATMENTS
Air in the pleural space
PATHOLOGY
Can occur
- Spontaneously - Pleural bleb rupture
- Secondary to trauma (accident), medical intervention (iatrogenic e.g. lung biopsy), lung pathology (infection, asthma, COPD)
SYMPTOMS
Young, tall, thing young man with connective tissue disorders (perhaps smoking cannabis) presenting with
- Shortness of breath
- Sudden Sharp Pleuritic chest pain
that may have occurred while playing sports
- Hyper resonant percussion ipsilaterally (due to increased air)
- Decreased breathing sounds
INVESTIGATIONS
1st line + GS Erect Chest X-ray (patient standing upright) –> Visible rim between lung margin and chest wall, absent lung markings, tracheal deviation to the other side, darker area (collapsed lung)
British thoracic society guidelines to measure the size of a pneumothorax
CT thorax –> can help detect small pneumothorax and accurately assess size of the pneumothorax
TREATMENT
(pleural aspiration for low risk and stable)
High risk - require chest drain
If recurrent - surgical intervention –> Pleurodesis (surgical intervention to obliterate pleural space)
Empyema
Symptoms
Investigations
Treatment
Infected pleural effusion
Would see new/ongoing fever despite improving symptoms
Pleural aspiration would show PUS (due to infection), low pH (acidic), low glucose (due to usage by bacteria), high lactate dehydrogenase
Treatment
Chest drain + antibiotics (Cefotaxime) - S.pneumoniae, Ciprofloxacin- S.aureus
Vancomycin may be needed for MRSA
Tension pneumothorax
Pathology
Symptoms
Treatment
Caused by trauma to the chest well that results in a one way valve that allows air to travel into the pneumothorax but doesn’t let it travel out (of pleural space)
So during inspiration, air is drawn into the pleural space and during expiration, air is trapped in the pleural space. (Pneumothorax gets progressively larger and intrapleural pressure increases with each breath) –> pushes mediastinum across that can lead to cardiorespiratory arrest
Signs
- Tracheal deviation away from affected side
- Hyper resonant on percussion
- Haemodynamic instability due to pressure on the heart –> Tachycardia and hypotension
INVESTIGATIONS
Don’t perform investigations when tension pneumothorax is suspected.
MANAGEMENT
(Open thoracostomy if expertise available then chest drain otherwise)
Needle decompression with a large bore cannula(2nd ICS) and THEN Chest drain can be put in afterwards to definitively get rid of air.
What are interstitial lung diseases and what are some examples?
What are the key presenting features?
Conditions that cause inflammation and fibrosis of the lung parenchyma.
Fibrosis involves the replacement of elastic and functional lung tissue with non functional scar tissue.
E.g.
1) Idiopathic pulmonary fibrosis
2) Secondary pulmonary fibrosis - due to drugs (amiodarone, methotrexate, nitrofurantoin), A1AT deficiency, RA, SLE, Systemic sclerosis, sarcoidosis
3) Hypersensitivity pneumonitis - involving type 3 and 4 hypersensitivity reaction to an environmental allergen
4) Asbestosis - Roofing/insulation - shipyard work
5) Good pastures, vasculitis
Key presenting features:
- Dyspnoea on exertion
- Dry cough
- Fatigue
Pulmonary fibrosis
-Treatment
RF
PATHOLOGY
SYMPTOMS
INVESTIGATIONS
TREATMENTS
MOST COMMON INTERSTITIAL LUNG DISEASE
A life threatening disease characterised by formation of scar tissue within the lungs and progressive dyspnoea.
RF- Advanced age (>50), male, family history, smoking
PATHOLOGY
Idiopathic pulmonary fibrosis - Progressive pulmonary fibrosis with no apparent cause
Secondary pulmonary fibrosis - due to drugs (amiodarone, nitrofurantoin), A1AT deficiency, RA, SLE, Systemic sclerosis, sarcoidosis
Repeated lung microinjury –> fibroblast activation (collagen secretion) - and TGF-B secretion - cause lung fibrosis and scarring
Can lead to TYPE 1 RESPIRATORY FAILURE
Symptoms
- Gradual onset shortness of breath
- Dry cough over more than 3 months. Poor prognosis (2-5 years to live)
(In only idiopathic pulmonary fibrosis)
- Bibasal fine end respiratory crackles
- Finger clubbing
Investigations
Spirometry - FVC <0.8 (restrictive)
High resolution CT –> Honeycombing/traction bronchiectasis
Treatment
- Pirfenidone
- Nintendanib (tyrosine kinase inhibitor)
Occupationally acquired interstitial lung disease (PNEUMOCONIOSIS)
Asbestosis
Silicosis
Lung fibrosis related to asbestos exposure
Asbestos (Automotive repair shops, roofing, insulation, shipyard work)
Asbestos is fibrogenic (can cause lung fibrosis) and oncogenic (can cause cancer) MOSTLY MESOTHELIOMA
Silicosis is inhalation of silicon dioxide that can result in eggshell calcification at the hilar lymph nodes.
Sarcoidosis
-Symptoms and investigations
RF
PATHOLOGY
SYMPTOMS
INVESTIGATIONS
TREATMENTS
A chronic granulomatous inflammatory disorder commonly affecting the lungs, skin and eyes. Characterised by the accumulation of lymphocytes and macrophages and the formation of non caeseating granulomas in the lungs and other organs.
RF - 20-50, family history, black people, females
PATHOLOGY
Unknown aetiology
Lungs and lymph nodes are involved in more than 90% of patients with sarcoidosis
Granulomas secrete Ace and 1 alpha hydroxylase –> activate vitamin D –> Calcium absorption = increased serum calcium
SYMPTOMS
20-40 year old black female presenting with dry cough and dyspnoea (with possible nodules on their shins - erythema nodosum)
Vary from asymptomatic to life threatening
-Dry cough
-Dyspnoea
- Erythema nodosum - tender red nodules on shins
- Lupus pernio - purple colour lesions on tip of nose/across cheeks
- Anterior uveitis
Systemic symptoms - Fever, fatigue, weight loss
Parotid enlargement
LOFGREN’S SYNDROME - Triad of erythema nodosum, bilateral hilar lymphadenopathy, polyarthralgia (Acute presentation of systemic sarcoidosis)
INVESTIGATIONS
1st line - Chest x-ray - Bilateral hilar lymphadenopathy
High resolution CT
U and E - Hypercalcemia
GS- Histology
Biopsy of affected area - shows non caeseating granulomas (with epithelioid cells)
Urine dipstick - proteinuria (renal)
LFTS - liver
ECG - Heart
- Serum ACE - elevated
- Serum calcium - elevated
- Soluble IL-2 - elevated
- CRP - elevated
MANAGEMENT
Mild - No treatment
First line - Corticosteroids (consider giving bisphosphonates to prevent bone loss)
2nd line - Immunosuppressants - methotrexate, azathioprine
What syndrome is associated with Sarcoidosis?
LOFGREN’S SYNDROME - Triad of erythema nodosum, bilateral hilar lymphadenopathy, polyarthralgia (Acute presentation of systemic sarcoidosis)
Pulmonary hypertension
-Treatment
RF
PATHOLOGY
SYMPTOMS
INVESTIGATIONS
TREATMENTS
Defined by a mean pulmonary arterial pressure >20mmHg. (often results in Right sided failure or cor pulmonale.
PATHOLOGY
5 main causes:
Group 1 - Genetics - BMPR 2 gene inactivation
Group 2 - left heart failure (increased fluid pressure transferred back to the lungs)
Group 3 - Chronic lung disease - COPD, pulmonary fibrosis
Group 4 - Pulmonary vascular disease - PE
Group 5 - Others e.g. sarcoidosis
As a result of the above, there is hypoxia which results in reactive pulmonary vasoconstriction –> increasing pulmonary vascular resistance pressure –> Right ventricular hypertrophy and RHS heart failure
SYMPTOMS
DYSPNOEA - main symptom
+ RHS heart failure signs
- Syncope
- Tachycardia
- Raised jugular venous pressure
- Louder S2 than normal
(peripheral oedema)
INVESTIGATIONS
1st - Chest X-ray –> Right ventricular hypertrophy
ECG - P pulmonale - Peaked P waves RVH –? Tall R waves in V1 and 2, Deep S waves in V5 and 6 (RVH) + right atrial enlargement
Echocardiogram - Right ventricular hypertrophy
GS - Right heart catheterisation demonstrating the mean pulmonary arterial pressure is >20mmHg
TREATMENT
Phosphodiesterase 5 inhibitors - Sildenafil
(Also used for treating sexual dysfunction)
Calcium channel blockers
Endothelin receptor antagonists - Bosentan
(diuretics for oedema)
Some systemic manifestations of sarcoidosis
Sarcoidosis leads to:
- Mediastinal lymphadenopathy
- Pulmonary fibrosis
- Pulmonary nodules
- Liver nodules
- liver cirrhosis
- Uveitis
- Conjunctivitis
- Optic neuritis
Can affect heart, CNS, PNS and kidneys also.
Hypersensitivity pneumonitis
RF
PATHOLOGY
SYMPTOMS
INVESTIGATIONS
TREATMENTS
Also called extrinsic allergic alveolitis (due to non IgE mediated immunologic inflammation) - an interstitial lung disease
RF - Smoking, Occupational exposure (e.g farming)
PATHOLOGY
It involves type 3 (mainly) hypersensitivity to an environmental allergen. Antibody antigen complex deposition at the lung tissues causing an immune hyper response. –> alveolar + bronchial inflammation.
Types include:
Farmer’s lung - Reaction to mouldy spores in hay
Malt worker’s lung - Reaction to mould on barley
Bird-fancier’s lung - Reaction to bird droppings
SYMPTOMS
- Exposure to birds/cleaning cages
- Mould in work environment
- Cough, dyspnoea, fever, chills, malaise, weight loss
- Crackles (bibasilar) - lungs
INVESTIGATIONS
Bronchoalveolar lavage - Lymphocytosis (and possible antibodies)
TREATMENT
- Removal of allergen
(May need oxygen/steroids)
Sinusitis
-Causes
RF
PATHOLOGY
SYMPTOMS
INVESTIGATIONS
TREATMENTS
Inflammation of the paranasal sinuses (in the face)
Usually accompanied by inflammation of the nasal cavity (Rhinosinusitis)
Acute >12 weeks
Chronic <12 weeks
PATHOLOGY
Paranasal sinuses produce mucus and drain into the nasal cavity via ostia.
Blockage of the ostia prevents drainage of the sinuses –> Sinusitis
Causes of sinusitis
- Infection (following viral URTI)
- Allergies (e.g. hayfever)
- Obstruction of ostia via foreign body, trauma or polyp
- Smoking
SYMPTOMS
Acute sinusitis –> Usually follows a recent viral URTI
- Nasal congestion
- Nasal discharge
- Facial pain/headache/pressure
- Facial swelling
- Loss of smell
Systemic symptoms in cases of infection: fever, tachycardia
Chronic sinusitis –> More associated with nasal polyps but symptoms the same
INVESTIGATIONS
Most cases - not necessary
Persistent symptoms then - nasal endoscopy
TREATMENT
Mostly less than 10 days (viral causes) - self limiting
Symptoms lasting >10 days - Steroid nasal spray (mometasone)
Chronic treatment
- Saline nasal irrigation
- Steroid nasal spray - Mometasone
(amoxicillin if need antibiotic treatment)
Otitis Media
RF
PATHOLOGY
SYMPTOMS
INVESTIGATIONS
TREATMENTS
An infection of the middle ear (space between the tympanic membrane and the inner ear) –> Where the cochlea, vestibular apparatus and nerves are found.
RF - Young age, family history, day care
PATHOLOGY
Common site of infection oin children.
Most often preceded by a viral URTI where the bacteria enter from the back of the throat via the eustachian tube.
Most common bacteria:
- S.aureus
- H.influenza
Most common virus:
- Influenza virus
- Adenovirus
SYMPTOMS
- Ear pain
- Reduced hearing
- Fever, cough, sore throat
INVESTIGATIONS
Otoscopy shows a red and inflamed tympanic membrane
TREATMENT
Most resolve within 3 days without antibiotics.
1st line antibiotic for systemically unwell patients –> Amoxicillin
Can give simple analgesia (paracetamol) for pain
Pharyngitis
RF
PATHOLOGY
SYMPTOMS
INVESTIGATIONS
TREATMENTS
The onset of sore throat and pharyngeal inflammation with/without exudate
PATHOLOGY
Bacterial causes - Group A haemolytic streptococcus (Strep pyogenes)
Viral causes- EBV, Adenovirus
Spread via aerosols (respiratory droplets - coughing, sneezing)
SYMPTOMS
Sore throat and fever
If viral cause = Rhinorrhea (runny nose), nasal congestion and cough
If bacterial cause = Pharyngeal exudate
MUST RULE OUT RHEUMATIC FEVER especially in children if the cause is bacterial
INVESTIGATIONS
Rapid antigen test for group A strep
(If negative –> do a throat culture especially in children as they are at increased risk of rheumatic fever)
TREATMENT
If bacteria confirmed
1st line - phenoxymethylpenicillin (penicillin V)
If allergic to penicillin –> Clarithromycin
Examples of upper respiratory tract infections
Pharyngitis, sinusitis, otitis media, acute epiglottitis, whooping cough, croup
Epiglottitis
-Caused by?
-Symptoms
RF
PATHOLOGY
SYMPTOMS
INVESTIGATIONS
TREATMENTS
Inflammation and swelling of the epiglottis caused by infection. It has the potential to obscure the airway and is this a surgical emergency.
RF - Not vaccinated against haemophilus influenza type B, immunocompromised, children <5
PATHOLOGY
Usually caused by
- Haemophilus influenza type B
SYMPTOMS
Unvaccinated child presenting with fever, sore throat, difficulty swallowing, that is sitting forward and drooling
- Sore throat and stridor (a type of wheeze?)
- Drooling
- Tripod position - sat forward with a hand on each knee
- Difficulty swallowing
INVESTIGATIONS
GS - Laryngoscopy
Lateral X-ray of the neck –> Shows a thumbprint sign - enlarged epiglottis
TREATMENT
Most children recover without requiring intubated
Secure airway via intubation if required (when sudden upper airway closure occurs)
Tracheotomy in patients who cannot be intubated
IV Cefotaxime/Ceftriaxone
Whooping cough (Pertussis)
RF
PATHOLOGY
SYMPTOMS
INVESTIGATIONS
TREATMENTS
An URTI caused by Bordetella pertussis (gram negative)
RF - Unvaccinated/under-vaccinated individuals, close contact with an infected person
PATHOLOGY
Infection transmitted via respiratory droplets.
Bacteria adhere to ciliated respiratory epithelial cells where they produce toxins which cause ciliary paralysis, local tissue damage and inflammation.
Adenylate cyclase toxin inhibits phagocyte chemotaxis
Pertussis toxin inhibits alveolar macrophages (and also host G protein coupled receptor signalling)
SYMPTOMS
Severe cough starts after a week or more of infection.
- Patient produces a large, loud inspiratory whoop when the coughing ends.
- Coryzal symptoms - runny nose, sneezing, low grade fever
(Infants may present with or without cough)
(Not responsive to OTC medication)
INVESTIGATIONS
Within 2 weeks of symptoms
Nasopharyngeal swab with bacterial culture
More than 2 weeks
Serology for anti pertussis toxin immunoglobulin G
TREATMENT
(Notifiable disease)
1st line - Azithromycin
Close contacts should be given prophylactic antibiotics.
What are Coryzal symptoms?
The hallmark of URTIs. Includes: Nasal congestion, rhinorrhoea, sneezing, sore throat and cough
Croup
RF
PATHOLOGY
SYMPTOMS
INVESTIGATIONS
TREATMENTS
Also known as laryngotracheobronchitis. - Common respiratory disease of childhood characterised by sudden onset of a seal-like barky cough, accompanied by stridor and voice hoarseness.
RF- 6 months - 3 years, males
PATHOLOGY
Usually the result of upper airway obstruction due to inflammation of the airways and oedema of the airways as a result of viral infection (PARAINFLUENZA VIRUS)
Sometimes - respiratory syncytial virus (RSV)
SYMPTOMS
- Barking cough
- Hoarse voice
- Stridor (wheezing during inspiratory phase)
- Low grade fever
INVESTIGATIONS
- Clinical diagnosis
TREATMENT
Usually improves in less than 48 hours.
1st line - Dexamethasone (single dose)
(Supportive care with rest and fluids)
Mesothelioma
RF
PATHOLOGY
SYMPTOMS
INVESTIGATIONS
TREATMENTS
A lung malignancy affecting the mesothelial cells of the PLEURA.
RF- ASBESTOS exposure (not smoking), (50-70 males)
PATHOLOGY
Typically does not present till decades after exposure (latent period)
SYMPTOMS
Cancer symptoms - Weight loss, tired all the time (TATT)
Lung symptoms
- Dyspnoea
- Persistent cough
- Pleuritic chest pain
Tumour may press on nearby structures e.g. recurrent laryngeal nerve –> hoarse voice
Signs of metastases - bone pain
INVESTIGATIONS
1st line - Chest x-ray - pleural thickening with or without effusion
CT scan would provide more detail.
GS - pleural biopsy
TREATMENT
Mostly palliative care
(can try surgery + chemotherapy if found early and operable) - generally resistant to radiotherapy
Small cell lung cancer
- Where do they arise from?
RF
PATHOLOGY
SYMPTOMS
INVESTIGATIONS
TREATMENTS
Malignant epithelial tumour arising from cells lining the lower respiratory tract.
RF - older people, SMOKING, asbestos, radon gas
PATHOLOGY
Arises from neuroendocrine kulchitsky cells.
Approx 2/3 of patients have evidence of distant metastasis at presentation
SCLC cells contain neurosecretory granules that release neuroendocrine hormones which can lead to paraneoplastic syndromes e.g.
- SIADH –> caused by ectopic ADH secreted
- Cushing’s syndrome –> caused by ectopic ACTH secreted
- Lambert eaton myasthenic syndrome - caused by antibodies against SCLC cells.
SYMPTOMS
General
- Cough >3 weeks
- Dyspnoea
- Haemoptysis
- Chest pain
- Weight loss
(Symptoms of cushings, SIADH, lambert eaton)
INVESTIGATIONS
First line- Chest x-ray, CT
GS - Bronchoscopy AND biopsy
MRI staging via TNM
TREATMENT
More aggressive
If early - Chemotherapy, radiotherapy
If metastasised - Palliative
Non small cell lung cancer
What cells do they originate from?
RF
PATHOLOGY
SYMPTOMS
INVESTIGATIONS
TREATMENTS
Accounts for 80% of all lung cancers (SCLS - 20%)
RF - smoking, COPD, family history
3 main types
- Adenocarcinoma - MOST COMMON LUNG CANCER(40%) –> Usually due to asbestos, affects the peripheral lung –> arises from mucus secreting glandular epithelium (can metastasise to bone, brain, adrenals, liver) –> Triad of hypertrophic pulmonary osteoarthropathy : clubbing, arthritis and long bone swelling
- Squamous cell carcinoma (25%) –> Mostly smokers, affects the central lung, possible central necrosis.
–> Can result in hypercalcemia via ectopic parathyroid hormone (metastasise later than adenocarcinoma) - Large cell carcinoma (10%) –> undifferentiated tumours without histological features typical of squamous cell or adenocarcinoma. (affects central lung)
SYMPTOMS
Usually a male smoker
- Cough
- Dyspnoea
- Haemoptysis
- Chest pain
- Weight loss
- Tired all the time
- Decreased breath sounds
Possible signs of metastasis e.g.
- Horner’s syndrome as a result of a pancoast tumour (at pulmonary apex) - pressing on the sympathetic ganglion affecting nerves –> Ptosis, anhidrosis, miosis - seen in adenocarcinoma
INVESTIGATIONS
1st line imaging - Chest X-ray, CT
GS - Bronchoscopy + biopsy
MRI staging - TNM
TREATMENT
Less aggressive than SCLC
Early - Surgical excision of tumour
Metastasised - Chemotherapy, radiotherapy
Are secondary or primary tumours more common in the lung?
Secondary as the lungs oxygenate 100% of the blood –> meaning all blood comes to the lungs and thus there is a high metastasis risk.
From the breast, kidney, bowel, bladder.
What can pneumonia lead to?
Conditions like
- Pleural effusion
- Empyema
Difference between type 1 and 2 respiratory failure
Type 1 - Hypoxia and normo/hypocapnia
Type 2 - Hypoxia and hypercapnia
Type 1 - Restrictive lung disease (difficulty getting air into the lungs), VQ mismatch, low ambient oxygen
Type 2 - Obstructive lung disease (difficulty getting air out of lungs), reduced respiratory drive, obesity
Scale for COPD
MRC dyspnoea scale
1 - breathless with strenuous exercise
2- short on breath when hurrying on level ground or walking up a slight hill
3- walks slower than people of the same age on the same level because of breathlessness or has to stop for breath when walking at own pace
4- Stops for a breath after walking about 100m or after a few minutes on level ground
5- Too breathless to leave the house or breathless when dressing
