Respiratory Conditions Flashcards
What is acute bronchitis, what is the cause and risk factors
Lower respiratory tract infection characterised by inflammation of the bronchi
Result of inflammation of the trachea and major bronchi and is therefore associated with oedematous large airways and the production of sputum. Usually happens after an upper respiratory tract infection
Chest infection which is usually self-limiting in nature, the disease usually resolves within 30 days
Most commonly viral infection from
- Influenza A
- Influenza B
- Parainfluenza
- RSV
- Coronavirus
- Adenovirus
Risk Factors
- Smoking
- Exposure to infection
CLINICAL FEATURES
- cough that lasts less than 30 days (4 weeks)
- may be a productive cough→ white/clear sputum
- Fever
- Preceding URTI symptoms
- Runny nose
- Sore throat
- Headache
- Wheeze
- No history of chronic resp illness
INVESTIGATIONS
Usually clinical diagnosis
Other investigations:
- Pulmonary function test: will improve over time which rules out asthma bcs asthma wont improve
- Chest Xray: rule out pneumonia as cause
- CRP: see if ABx are needed
MANAGEMENT
Analgesia and good fluid intake. Just observe until reaches 4 weeks then think of whether it might be another pathology
If CRP is 20-100 offer delayed prescription
If CRP over 100/has a comorbidity or systemically unwell: oral doxycycline, can use amoxicillin if pregnant or child
COMP: chronic cough and pneumonia
PROG: self limiting but poorer prog in those with preexisting lung conditions, elderly or immunocompromised
How is acute bronchitis differentiated from pneumonia
- Sputum, wheeze, breathlessness may be absent in acute bronchitis
- At least one tends to be present in pneumonia
- No other focal chest signs (dullness to percussion, crepitations, bronchial breathing) in acute bronchitis other than wheeze (no radiological changes either)
- Systemic features (malaise, myalgia, and fever) may be absent in acute bronchitis whereas they tend to be present in pneumonia
What is bronchiectasis, the types, the causes
Permanent dilation of the airways secondary to chronic infection or inflammation due to destruction of elastic and muscular components of bronchial wall
Classified into:
- CF bronchiectasis
- Non-CF bronchiectasis
Causes:
- Post-infective/recurrent pulmonary infections
- Measles
- Pertussis
- Pneumonia
-Cystic Fibrosis
- TB
- COPD
- Aspiration
- Chronic Inflammatory diseases- coeliac, RA
- Allergic bronchopulmonary aspergillosis (ABPA)
- Primary ciliary dyskinesia (Kartagener’s syndrome)
- Bronchial obstruction (lung cancer or foreign body)
- Immune deficiency (selective IgA (lack of IgA) and hypogammaglobulinaemia)
Obstructive diseases cause bronchiectasis because the mucus plugs form in airways and obstruct
Organisms that most commonly cause:
- Haemophilus influenzae - most common
- Pseudomonas aeruginosa
- Klebsiella spp.
- Streptococcus pneumoniae
CLINICAL FEATURES
- Chronic cough associated with large (copious) amounts of purulent sputum (green/rusty colour). May be worsened by lying flat or on one side
- Haemoptysis
- Recurrent chest infections
- Inspiratory coarse crackles on auscultation
- Clubbing
- SOB (especially on exertion)
- Fever
- Acute exacerbation often presents with fatigue, weight loss and wheezing
INVESTIGATIONS
1st- Chest X-ray : will show obscured hemidiaphragm, thin-walled ring shadows woth/without fluid levels, tubular or ovoid opacities, tram lines (parallel line shadows)
Gold standard is : HRCT : would show thickened dilated airways (widened black dots with thick white walls around), varicose constrictions along airways, cysts and/or in bud tree pattern, signet ring, tram-track sign
Spirometry: Obstructive pattern (<0.7)
Sputum MCS: look for underlying cause like haemophilus influenzae (most common) or psudomonas aeruginosa (common in CF)
CYstic fibrosis sweat test- high chloride
MANAGEMENT
- Exercise and improved nutrition
- Airway clearance therapy (chest physiotherapy)
Postural drainage
Percussion
Vibration
Use of oscillatory devices
Maintenance of oral hydration
- Inhaled bronchodilator (salbutamol)- dilate so help clear mucus
- Mucoactive agent e.g. nebulised hypertonic saline
- Abx → amoxicillin, vancomycin
- Immunisations
Lobectomy in uncontrolled haemoptysis or localised disease
COMP
- Massive haemoptysis
- Respiratory failure
- Cor pulmonale
- Ischaemic stroke
PROG: irreversible has periods of good control and period of exacerbation
What is Cystic Fibrosis, clinical findings, investigations and management
Autosomal recessive disorder causing increased viscosity of secretions due to defect in cystic fibrosis transmembrane regulator (CFTR)
Clinical features
- Recurrent chest infections
- Failure to thrive (delayed puberty)
- Malabsorption (steatorrhoea)
- Short stature
- Male infertility
Investigations: Via sweat test (will have abnormally high sweat chloride)
Screened at birth via heel prick
Management: Chest physiotherapy
What is Allergic bronchopulmonary aspergillosis (ABPA),clinical features, investigations and management
Bronchiectasis + bronchoconstriction caused by hypersensitivity response to aspergillus fungus (mould)
Clinical features?
- Wheeze
- Cough
- Dyspnoea
Bloods show
- Eosinophilia
- Raised IgE
Management
Oral prednisolone
What are the clinical features of primary ciliary dyskinesia (Kartagener’s syndrome
Bronchiectasis + dextrocardia (or complete sinus inversu-heart on wrong sides) + recurrent sinusitis
Male infertility
What is COVID-19, its transmission route and incubation period
Potentially severe acute respiratory infection caused by the novel coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
Transmitted via respiratory droplets
Incubation period is 5 days
CLINICAL FEATURES
- Fever
- Cough
- Dyspnoea
- Altered sense of smell/taste
- Headache
- Sore throat
- Nasal congestion
INVESTIGATIONS
Real-Time Reverse Transcription Polymerase Reaction (RT-PCR) from a nasopharyngeal swab
Pulse oximetry
Chest X-ray if pneumonia is suspected
MANAGEMENT
mild/moderat
isolation + supportive measures + antipyretic/analgesic
severe
hospital admission, VTE prophylactic, oxygen therapy, mechanical ventilation
COMPLICATION
- Thrombosis
- AKI
- Long covid
- Cardiac arrest
- Sepsis
- DIC (disseminated intravascular coagulation)
Prognosis: most die if respiratory failure from ARDS
What diseases come under the term lower respiratory tract infection, how does it compare to URTI and does influenza cause upper or lower
- Pneumonia
- Lung abscess
- Acute bronchitis
LTRI is more serious
Influenza causes upper + lower
CLINICAL FEATURES
-Sneezing
- Sore throat
- Nasal congestion & discharge
- Malaise
- Muscle fatigue
- Pain
What is an upper respiratory tract infection, where in the body does it affect and what are some examples
Consists of
- Nose
- Sinuses
- Pharynx
- Larynx
- Trachea
- Mainly viral
- Bacterial in some instances
- Tonsillitis
- Laryngitis
- Sinusitis
- Otitis media
- Rhinitis
- Common cold
CLINICAL PRESENTATION
- Cough
- Sore throat
- Runny nose & sneezing
- Nasal congestion
- Headache
- Fever
- Facial pressure
MANAGEMENT
Symptomatic support
- Analgesia
- Decongestants
- Cough medicine
If see unilateral polyps then urgent referral to ENT as its a red flag
What is Tuberculosis,the types and risk factors
An infectious, chronic granulomatous disease caused by Mycobacterium tuberculosis
Affects the lungs, especially upper lobes but can spread through blood to cause extrapulmonary TB
- M tuberculosis is dormant in many patients, if host becomes immunocompromised the initial infection may become reactivated into secondary TB
- Primary TB is asymptomatic and happens in immunocompetent individuals who become exposed to M tuberculosis- this usually heals in them
Risk factors:
- Exposure to infection
- Immunosuppression:
- Diabetes
- Cushings
- Steroid use
- Silicosis (form of lung fibrosis)
- HIV
- Malignancy
- Birth in an endemic country
- India
- Bangladesh
- Sub Saharan Africa
- Overcrowded areas
CLINICAL FEATURES
- Cough → productive (may have haemoptysis), doesn’t respond to conventional antibiotic therapy
- Fever
- Weight loss
- Night sweats
- SOB
- Anorexia
- Malaise
- Pleuritic chest pain
- Cervical lymphadenopathy + hilar lymphadenopathy
- Pott’s Disease → spread to bones
similar presentation to cancer so look at age and presence of fever
MANAGEMENT
1st line : Chest X-ray
- Consolidation
- Bilateral hilar lymphadenopathy
- Cavitating lesion in upper lobe (Caseating granulomas)
Gold standard diagnostic test: Sputum culture- most sensitive and specific test
Sputum acid-fast bacilli smear uses a ziehl-neelson stain or auramine stain: If have TB show acid fast bacillus positive
Offer: HIV test
For contacts of infected patients do : Mantoux test to screen for latent TB but immunosuppression can cause a false-negative e.g. in
- sarcoidosis
- steroid use
- lymphoma
- AIDS
MANAGEMENT
Latent TB:
Rifampicin + Isoniazid
Active TB:
Rifampicin + Isoniazid + Pyrazinamide + Ethambutol
- Rifampicin and Isoniazid for 6 months
- Pyrazinamide and ethambutol for 2 months
Pyridoxine supplementation
Before commencing treatment ⇒ U&E’s, LFTs, Vision Testing, FBC
Prevention: tuberculin skin test
COMP
transmission of TB
ARDS
Pneumothorax
Haemoptysis
Bronchiectasis
PROG: without treatment mortality rate over 50%. if treated do well
What are the side effects of the medication used to treat TB
Rifampicin
- Red/orange secretions
- Hepatitis as P450 induces which increases metabolism of warfarin and decreases INR
Isoniazid
- Drug induced lupus
- Peripheral neuropathy: give pyridoxine VitB6
- Hepatitis
Pyrazinamid
- Can cause gout due to hyperuricaemia
- Hepatitis
Ethambutol
May cause optic neuritis
Avoid in CKD
What is influenza, when do most infections occur, how is type A and B spread, what classifications of type A are there, what can prevent the spread and how is influenza categorised
Highly contagious disease caused by influenza viruses A, B, and C
RF: winter, healthcare worker, have diabetes or cardio/resp issue, immunocomprimised, over 65 yrs or 6months to 5 years old
A+B (RNA viruses) spread via person-to-person transmission directly through respiratory droplets and indirectly through contact with contaminated surfaces
A is classified into groups based on glycoproteins of viral envelope
- Haemagglutinin (H)
- Neuraminidase (N)
Hygiene products and vaccination can protect
CLINICAL FEATRES
Characterised by upper + lower respiratory tract symptoms
- Fever
- Acute bronchitis- cough
- Headache
- Arthralgia
- Myalgia
- Fatigue and malaise
INVESTIGATIONS
Clinical Diagnosis
Can do:
Reverse Transcriptase-Polymerase Chain Reaction (RT-PCR)
Viral culture
MANAGEMENT
At risk individuals: antiviral prophylaxis
Antivirals → neuraminidase inhibitors- inhibit release of virus from host cells
- Oseltamivir (’tamiflu’)
- Zanamivir
Influenza vaccination in winter between september and early november for at risk groups such as:
- >65 years
- Chronic respiratory, heart, kidney, liver, neurological disease
- Diabetes mellitus
- Immunosuppressed
- Splenic dysfunction
- Pregnant women
- BMI ≥ 40 kg/m^2
- NHS staff
(Shouldn’t be given to acutely unwell patients, must wait until they have recovered)
Vaccines given routinely to children are live, to the elderly they are inactivated- important because different contraindications
Adults
1st line = paracetomol
If at risk/present within 48 hours: antivirals
If develop bacterial pneumonia: ceftriaxone, cefotaxime, cefuroxime
If develop otitis media: amoxicillin
Children : same, different if develop bacterial pneumonia
but only ceftrixone in bacterial
if staph aureus : oxacillin, naficillin, vancomycin, linezolid
COMPLICATIONS
- Bacterial pneumonia
- Otitis media
- Encephalitis
(influezae infection predisposes to streptococcus pneumoniae infection)
What is pneumonia, what are the types, the different causes and the risk factors
Respiratory infection characterized by inflammation of the alveolar space
Causes
- Bacterial pneumonia- most common- Streptococcus pneumoniae most common pathogen
- Viral
- Fungal (e.g. Pneumocystis jiroveci)
RF
- Old age
- Chronic diseases:
- COPD
- HF
- Bronchiectasis
- Immunosuppression e.g. HIV
- Crowded living conditions
Types: CAP (typical and atypical), HAP, idiopathic interstitial pneumonia and aspiration pneumonia
1) CAP
2 types= typical and atypical
TYPICAL
1) Streptococcus pneumoniae- clinical features
- Gram +ve encapsulated lancet shaped coccobacilli
- Rusty sputum
- Can reactivate HSV and cause cold sores
2) Staphylococcus aureus
- Gram +ve cocci found in clusters
- Common in IVDU
- Also occurs after influenza
- Causes cavitating lesions (gas filled lesions) on CXR
-
3) Haemophilus influenzae
- Gram -ve coccobacilli
- Especially in COPD patients
4) Klebsiella pneumoniae
Gram -ve non motile encapsulated bacillus
- Alcoholics and diabetics
- Causes cavitating lesion (gas filled lesions) on CXR, typically upper lobe
- Blood stained sputum (red-currant jelly)
- Commonly due to aspiration
- Causes lung abscess formation and empyema (pus collection in lungs)
Lung Abscesses: - chest pain
- Subacute productive cough
- Foul smelling sputum
- Night sweats
- Fever
IV ABX, dont usually need to drain
TYPICAL CAP TREATED WITH:
Amoxicillin or Co-Amoxiclav
ATYPICAL
1) Mycoplasma pneumoniae
- Associated with erythema multiforme (ring-shaped rash)
- Autoimmune haemolytic anaemia (cold agglutins, IgM) → RBC agglutination on blood smear
Diagnosed with serology and positive cold agglutination test
2) Legionella pneumophilia
- from faulty air conditioning, recently returned from holiday
Legionella = Low sodium, Liver derangement, Leukopenia
- hyponatraemia
- abnormal LFTs
- leukopenia
Daignosed with urinary antigen
3) Chlamydia psittaci
Associated with pet birds
4) Pneumocystis jirovecii
Affects HIV (any immunosuppressed individual)
causes desaturation on exercise
treated with co-trimoxazole (trimethoprim and sulfamethoxazole)
ATYPICAL CAP TREATED WITH Clarithromycin
2) HAP
- Staphylococcus aureus
Cavitating lesions on CXR
MRSA treated with vancomycin
NMRSA flucloxacillin/rifampcin
- Psudomonas aeruginosa
causes: CF and bronciectasis
treated with tazocin
3) Idiopathic Interstitial Pneumonia
Group of non-infective causes of pneumonia e.g Cryptogenic organising pneumonia → a form of bronchiolitis that may develop as a complication of RA or amiodarone therapy
4) Aspiration Pneumonia
Seen in patients with dysfunctional/unsafe swallow : stroke, MA, bulbar palsy, alcoholics. Aspiration of stomach contents is a cause in patients who have neurological injury or who have been intubated
Right lung usually affected since right bronchus is wider and more vertical. Would see consolidation at right lung base
Treat with amoxicillin and metronidazole
CLINICAL PRESENTATION
TYPICAL PNEUMONIA
- Productive cough with purulent sputum (yellow-greenish)
- High fever and chills
- Pleuritic chest pain
- Malaise
- SOB
- Tachypnoea
- O&E
- Crackles on auscultation (bronchial breathing)
- Decreased breath sounds
- Dullness on percussion
- Increased tactile fremitus
ATYPICAL PNEUMONIA
- More slow onset
- Non productive cough
- SOB
- Fever
- Headache
- Myalgia
- Diarrhoea
INVESTIGATIONS
Chest X-ray
- Alveolar opacification
- Air bronchograms
- Consolidation
patients with pneumonia have to redo X-ray at 6 weeks after clinical resolution to rule out any underlying malignancies that were hidden by penumonia consolidation
Bloods
- FBC- neutrophilia in bacterial infections
- CRP- raised in response to infection
- Urea and electrolytes- Dehydration (high urea)
- Procalcitonin- Increased in lower respiratory tract infections
ABG
- Indicates if the oxygen saturations are low
- If patient has any pre-existing respiratory disease e.g. COPD
Urinary Antigen test
Rapid bedside test for diagnosis of
- Legionella (atypical)
- Streptococcus pneumoniae
Sputum MCS
MANAGEMENT
CAP
1) Amoxicillin- typical cover
2) Clarithromycin- Atypical : give if allergic penicillin, avoid in patients with long QT, give pregnant women erythromycin
3) Doxycycline: if allergic to penicillin
HAP
Co-amoxiclav within 5 days of admission as can cause cholestasis (high ALP, high bilirubin)
If after 5 days Tazocin
Supportive ALL PNEUMONIA
- Oxygen- If hypoxaemic
- IV fluids- If hypotensive or signs of dehydration
If patient also has COPD then give Prednisolone, even if there’s no sign of exacerbation of the COPD
COMP
- Pleural effusions
- ARDS
- Respiratory failure
- Sepsis
PROG
- Mortality increases with age and increasing CURB-65 score
- HAP has higher mortality than CAP
What is the scoring system used for pneumonia
CURB-65
Scoring system used for risk stratification for the management of patients with community acquired pneumonia
- Confusion
- Abbreviated mental test score ≤ 8/10
- Urea > 7 mmol/L
- Respiratory rate ≥ 30/min
- Systolic ≤ 90mmHg or diastolic ≤ 60 mmHg
- Age ≥ 65 years
0-1= Outpatient- treat with amoxicillin
2= Hospitalisation- treat with amoxicillin and clarithromycin
3 or more= ICU level of care- treat with IV co-amoxiclav and clarithromycin
In primary care CRB-65 as cant get serum urea result
0= treatment at home- oral amoxicillin
1 or more= hospitalise
What is allergic disorder, the pathophysiology, causes
Conditions caused by hypersensitivity of the immune system to typically harmless substances
IgE binds to receptor on mast cell or basophil, triggering release of histamine
Causes
- Dust
- Foods
- Latex
- Medications
- Insect stings
- Genetics
- Stress
CLINICAL FEATURES
- Runny nose & sneezing
- Redness & itching of eyes
- Coughing & wheezing
- Rashes & hives (urticaria)
INVESTIGATIONS
Skin prick testing: for type 1 hypersensitivity reactions that caused a systemic reaction
Scratch testing: For contact dermatitis, usually type 4 hypersensitivity
Blood testing- measure concentration of specific IgE antibodies in blood and serum tryptase which is a specific marker of mast cell activation
MANAGEMENT
- Antihistamines e.g. Cetirizine
- Glucocorticoids: nasal beclometosone, nasal budenoside, mometasone nasal or triamcinolone nasal
- Emergency → Adrenaline auto-injectors for self-treatment
- Allergen Immunotherapy
Describe type 1-4 hypersensitivity reactions
Type 1 Anaphylactic/Immediate: Allergens (or antigens) are presented to T-cells by Antigen-presenting cells (APCs) during the sensitization phase of Type I hypersensitivity. T-cells then signal for stimulation of B-cells to produce IgE antibodies, which bind to the FcER1 receptors on mast cells and basophils. Subsequently, the free antigen induces the crosslinking of these mast cell and basophil bound IgE antibodies. This results in the degranulation of the cells and the release of histamine, proteolytic enzymes, and other mediators. Causes :
Anaphylaxis
Atopy (e.g. asthma, eczema, hayfever-allergcic rhinitis)
Type 2 Cell Bound: IgG or IgM binds to antigen on cell surface and destroys. Causes
- Autoimmune haemolytic anaemia
-Haemolytic disease of newborns
- Acute haemolytic transfusion reactions
- ITP
- Goodpasture’s sydrome
- Pernicious anaemia
- Rheumatic fever
- Pemphigus vulgaris/bullous pemphigoid
Type 3 Immune Complex: Free antigen and antibody (IgG, IgA) combine should be cleared by immune system, if not then antibodies start to react and deposited in blood vessel walls causing inflammation, rashes, fever . Causes:
- Serum sickness
- Systemic lupus erythematosus
- Post-streptococcal glomerulonephritis
- Extrinsic allergic alveolitis (especially acute phase)
Type 4 Delayed Hypersensitivity: T cell mediated. Antigen presented to naive T cell. When T cell meets then starts to promote inflammation, is slow so takes 2-3 days
Causes:
- TB
- GvH disease (Graft verses host)
- Allergic contact dermatitis
- Scabies
- Extrinsic allergic alveolitis
- MS
- Guillain-Barre syndrome
What is asbestos-related lung disease, difference between ARLD and asbestoisis, risk factors and the most dangerous form of asbestos
Restrictive interstitial lung disease with symptoms caused by fibrotic changes in the lungs
Asbestoisis is a type of pneumoconiosis caused by inhalation of asbestos fibres. Happens 5-10 years after exposure. Asbestos-related lung disease is classified as asbestoisis when it leads to interstitial lung disease - if its just plaque then not called asbestoisis
Risk factors
- Occupations involving manufacture
- Demolition of ships
- Plumbing
- Roofing
- Insulation
- Smoking
Crocidolite (blue) is the most dangerous
Causes lung changes
- Pleural plaques
- Pleural thickening
- Asbestoisis- causes lower lobe fibrosis so get SOB and reduced exercise tolerance (treat conservatively)
- Mesothelioma- malignant diseases of pleura get progressive SOB, chest pain and pleural effusion (Offered palliative chemotherapy but usual survival 8-14 months)
- Lung cancer
lower lobe and pleura usually the point thats most commonly affected
CLINICAL FEATURES
- Long latent period- most patients asymptomatic 15-20 years after exposure
- Progressive dyspnoea- typically exertional
- Dry cough- productive if develop COPD
- Digital clubbing
- Can see FLAWS and haemoptysis if malignant
INVESTIGATIONS
Chest X ray: see diffuse bilateral infiltrates/fibrosis in lower lobes, pleural thickening
Lung function tests- Restrictive or Obstructive pattern- Reduced DLCO in both.
Restrictive: reduced forced vital capacity (FVC), normal FEV1/FVC ratio, reduced slow vital capacity (SVC), reduced total lung capacity (TLC), reduced lung diffusion capacity testing (DLCO).
Obstructive changes: reduced FEV1, reduced FEV1/FVC ratio, increased residual volume (RV)/TLC ratio, reduced DLCO
High resolution CT- pleural thickening and pleural plaques
Bronchial Lavage: unusual but may find
Lung biopsy if malignancy
ABG (if acute)- Type 1 respiratory failure- Low oxygen with normal CO2
MANAGEMENT
No curative treatment, stop smoking
Oxygen therapy+ pulmonary rehabilitation
If obstructive airways then bronchodilators
Immunisation against influenza and pneumococcal pneumonia
Pleural plaques are benign and dont require therapy
Lung transplant if Pao2 under 60
COMPLICATIONS
- Mesothelioma (malignant tumour of mesothelial cells of the pleura)
- Occurs 20-40 years after exposure
What is mesothelioma, the clinical features, the investigations and what would a CXR show
- Mesothelioma (malignant tumour of mesothelial cells of the pleura)
- Occurs 20-40 years after exposure (asbestos)
- Dry chronic cough
- SOB
- Chest pain
- Weight loss
- Chest X-ray and CT scan
- Pleural tap
- Thoracoscopy- preferred over bronchoscopy as peripherally located
- Histology for diagnosis
- If pleural effusion, should send it for MC&S, biochemistry and cytology
- Pleural effusion
- Pleural thickening
- Mass along the pleura
Surgery+ chemo before or after if operable
chemo and immuno if inoperable
