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Respiratory, Drugs - Coggle Diagram

- - - - hair, cilia, mucus, normal flora
    - - lysozyme
    - - immunoglobulin A
    - - resident macrophages, monocytes, neutrophils, eosinophils
  - - - case, carrier, environment
    - - own flora, aspiration, secondary bacterial
  - - - Common cold: Children 3-8 viral respiratory illnesses per year
        
        Adults 2-4 colds, >60yrs, fewer than 1 cold per year
        
        Children 3-8 viral respiratory illnesses per year
      - Pharyngitis: Peaks in children, 4-7 years old
      - Epiglottitis: Children aged 2-7 years, peaks in 3 year olds
      - Laryngitis & laryngotracheobronchitis: Usually, 6 months to 6 years, peaks in second year
    - - Rhinitis: Hormonal changes during the middle of the menstrual cycle & during pregnancy: hyperaemia of the nasal & sinus mucosa
      - Nasopharyngitis: Occurs frequently in women aged 20-30
      - Epiglottitis & laryngotracheobronchitis: Male:female ratio 3:2
    - - Rhinovirus, from March-October, Coronavirus from December-April, Enterovirus from June- October, Respiratory syntical virus and group A strep from November-May, Influenza from November-March, Parainfluenza virus (PIV-3) from March-July, Parainfluenza virus (PIV2,3) form August- November
  - - - Coughing/sneezing – droplets spread x 6-8 metres
  - - - Not part of normal flora
      - Vast number of serotypes
      - Frequent changes in antigenicity
    - - Symptoms
        
        Sore throat
        
        Cough
        
        Rhinitis
      - common cause
        
        Rhinoviruses
        
        Coronaviruses
        
        RSV
      - other causes
        
        Influenza viruses
        
        Parainfluenza viruses
        
        Enteroviruses
        
        Adenoviruses
        
        Human metapneumoviruses
    - - Symptoms
        
        More systemic symptoms (fever, malaise, headache)
        
        Sore throat
        
        Rhinitis
        
        Viral pneumonia
      - Common cause: Influenza viruses
      - Other causes:
        
        Parainfluenza viruses
        
        Adenoviruses
  - - - Viral
        
        Rhinovirus
        
        Influenza
        
        Parainfluenza
        
        Often follows a cold
        
        May be due to virus or inflammatory mediators
        
        Cough
        
        Sneeze
        
        Nasal discharge
        
        Headache
      - Bacterial
        
        S. pneumoniae
        
        M. catarrhalis
        
        H. influenzae
        
        Gp A streptococci
        
        S. aureus
        
        Anaerobes
        
        May follow a viral infection
        
        High fever
        
        Facial pain
        
        Headache
        
        Nasal discharge
      - Fungal
        
        Aspergillus spp.
        
        Mucor spp.
        
        Candida
        
        May be non-invasive or invasive (hospitalised or immunocompromised patients)
        
        May be acute or chronic
        
        Fever
        
        Cough
        
        Nasal discharge
        
        Headache
        
        Confusion (invasive)
      - Non-infective
        
        Tumour
        
        Allergy
        
        Foreign body
        
        Wegeners granulomatous
      - Associated with:
        
        common cold
        
        allergy
        
        Swimming
        
        nasal obstruction
        
        ciliary dysfunction
      - INVESTIGATIONS
        
        Sinus X-ray, often normal but may show air-fluid level +/- thickening of soft tissue
        
        CT sinuses, occasionally required
        
        Sinus aspirate for culture if fluid present
      - Treatment
        
        Many cases resolve spontaneously (viral)
        
        Features of a true bacterial sinusitis
        
        Fever & symptom duration > 10 days
        
        Maxillary toothache
        
        Initial symptom improvement and then deterioration
        
        Cacosmia – (sense of bad odour in the nose)
        
        Unilateral facial pain
        
        Empirical antibiotics
        
        e.g. amoxicillin or clarithromycin if purulent discharge that persists
        
        5 days
        
        Decongestants
        
        Analgesia
        
        Sinus puncture & lavage
        
        Particularly if don’t respond to antibiotics
        
        Fungal
        
        Surgical debridement
        
        Anti-fungal agent
      - COMPLICATIONS
        
        (Most cases uncomplicated)
        
        Meningitis
        
        Brain abscess
        
        Drainage
        
        Prolonged antibiotics
        
        Orbital cellulitis
        
        Bronchitis
    - - Presence of fluid in the middle ear with signs or symptoms of acute illness
      - Usually arises as a complication of a preceding viral URTI: Dysfunction of Eustachian tube due to mucosal congestion leading to accumulation of middle ear secretion –> bacterial replication
      - Incidence
        
        Peak in first three years
        
        Male > female
        
        Associated with group day care
        
        Passive smoking
      - Causative organisms: As per sinusitis, but bacterial predominates (S. pneumoniae)
      - Clinical features
        
        Fever, lethargy, irritability
        
        Ear pain, ear discharge, hearing loss
        
        Reddened tympanic membrane
        
        Severe: moderate-severe otalgia, temp >39
      - Diagnosis
        
        Otoscopy
        
        Tympanocentesis
      - Treatment
        
        Antibiotics if severe
        
        e.g. amoxicillin, clarithromycin, co-amoxiclav x 5 days
        
        Analgesia
      - Complications
        
        Mastoiditis:
        
        Extension of infection into mastoid antrum
        
        Severe pain & high fever
        
        Risk of spread to cranium
        
        Antibiotics & mastoidectomy
        
        Chronic otitis media: Tympanostomy tubes
        
        Attic infection
        
        Damage to high roof of middle ear cavity
        
        Cholesteatoma: consists of squamous epithelium that is trapped in the skull base. Squamous epithelium trapped within the temporal bone (ie, middle ear or mastoid) can expand only at the expense of the bone that surrounds and contains it. Consequently, a growing cholesteatoma can erode and destroy important structures within the temporal bone.
        Secondary acquired cholesteatomas result directly from an injury to the tympanic membrane. This injury can be a perforation caused by acute otitis media or trauma, or it may be due to surgical manipulation of the drum.
  - - - Viral pharyngitis
      - Tonsillitis
      - Streptococcal pharyngitis
      - Infectious mononucleosis
    - - Epiglottitis
      - Retropharyngeal / tonsillar abscess
      - Diphtheria
      - Gonococcal infection
    - - Clinical history
        
        Could diphtheria be a possibility??
        
        GAS
        
        EBV
        
        Gonococcus
      - Examination findings
        
        Epiglottis – drooling, acutely unwell
        
        Bull neck or pseudomembrane – diphtheria
        
        Unilateral tonsillar swelling - abscess
      - Microbiological
        
        Throat swab (routine culture & viral)
        
        If diphtheria suspect – alert laboratory
        
        ?Point of care test for GAS
        
        Monospot / EBV serology
        
        Blood cultures if epiglottitis
    - - Most patients do not benefit from antibiotics
      - Symptoms take about 8 days to resolve.
      - Consider antibiotics if 3 of 4 Centor criteria
        
        History of fever, purulent tonsils, cervical adenopathy, absence of cough or history of otitis media
        
        Or if positive culture results
      - Supportive for viral infection, e.g. analgesia
      - Treatment in diphtheria
        
        Treatment in diphtheria
        
        Diphtheria antitoxin
        
        It is used only for treatment, not prophylaxis
        
        Antitoxin neutralizes only unbound toxin
        
        Before toxin binds to cell and is internalised
        Diphtheria toxoid immunization during their convalescence since natural infection does not reliably induce immunity.
        
        Antibiotics - penicillin G / erythromycin
        
        Airway management / ECG & enzymes / Neuro
        
        IPC: Droplet precautions
        
        Follow-up
        
        cultures to ensure eradication
        
        Subsequent vaccination to ensure immunity
        
        Notifiable infection- contacts, antibiotic prophylaxis plus vax booster
  - - - Gp A Strep
      - S. pneumoniae
    - - Dysphagia
      - Drooling
      - Fever
      - Stridor
      - Dyspnoea
      - Lethargy
    - - Urgent Hospital Admission
      - Secure airway (ITU admission)
      - Blood cultures
      - Epiglottic cultures
        
        Only if airway secure
      - Antibiotics
        
        IV Cefotaxime
  - - - Parainfluenza
      - Influenza
      - Respiratory syncytial virus (RSV)
    - - Clinical
      - NB to distinguish from epiglottitis: More rapid course, generally more unwell without ‘croup-like’ cough
    - - Corticosteroids
      - Humidified oxygen
  - - - Influenza
      - Parainfluenza
      - Rhinoviruses
    - - H. influenzae
      - S. pneumoniae
      - M. catarrhalis
    - - Amoxicillin / clarithromycin / doxycycline x 5-7 days
      - Corticosteroids
      - Bronchodilators
    - - Influenza vaccine – annually
      - Pneumococcal vaccine – every 5 years
      - Smoking cessation
  - - - Cough – may last several weeks, typically non-productive
      - +/- substernal pain (severe tracheal inflammation)
      - +/- fever
    - - Symptomatic – control of cough
      - Antibiotics – amoxicillin, clarithromycin, tetracycline (only if bacterial cause)
      - Severe disease may require ventilatory support
- - - - Economy-class syndrome
      - Flights greater than 4 hours
      - Hydration
      - Ambulation / Exercise
      - Compression stockings
      - ? Low molecular weight heparin in high risk
  - - - Byproduct of fibrin cross- linkage
      - Sensitive but not specific
  - - - dyspnoea
      - pleuritic chest pain
      - haemoptysis
    - - tachycardia
      - fever
      - tachypnoea
      - pleural rub or effusion (later) Massive PE usually fatal
  - - - loss of vascular markings or
      - wedge shaped consolidation
    - - prominent P waves
      - ST segment depression
      - T-wave inversion in leads III, aVF, V1, V2, V3
  - - - Low Molecular Weight Heparin (LMWH)
        
        Treatment of choice Given subcutaneously
        
        Dose proportional to based on body weight No need for monitoring
        
        Almost immediate effect
      - Heparin: Unfractionated. Given as continuous IV infusion. Dose guided by serum APTT levels
      - Maintenance therapy:
        
        Warfarin
        
        Aim for INR of 2.0 – 3.0
        
        Continue therapy for 3-6mths
        
        Consider life-long therapy in patients with recurrent episodes
  - - - Acute
        
        Cardiac arrest
        
        Pulmonary infarction
        
        Haemoptysis
        
        Pneumonia
      - Chronic:
        
        Chronic breathlessness
        
        Pulmonary hypertension
      - DVT: Chronic venous insufficiency: Damage to bicuspid valves allows backflow, pooling of blood and venous hypertension
        
        Clinical Features:
        
        Ache and heaviness
        
        Oedema
        
        Ulceration
        
        Varicose veins
        
        Lipodermatosclerosis- also known as sclerosing panniculitis and hypodermitis sclerodermiformis, is an inflammation of the subcutaneous fat,
  - - - What is the differential diagnosis for this presentation?
        
        (2 hour history of pleuritic chest pain, dyspnoea, haemoptysis and pleural rub);
        
        Pulmonary Embolus
        
        Pneumonia with Pleuritic Involvement
        
        Chronic / long standing conditions unlikely causes of 2 hour history
        
        Bronchiestasis / Chronic Bronchitis
        
        Chronic infections such as TB or lung abscess
        
        Lung Cancer
        
        Inflammatory condition such as Sarcoidosis, Goodpasture’s Syndrome
    - - Apixaban: Direct Factor Xa Activator
      - Rivaroxaban : Direct Factor Xa Activator
      - Dabigatran: Direct Thrombin Inhibitor
      - Low molecular weight heparin: Indirect Inhibitor of Factor Xa
      - Unfractionated heparin: Indirect Inhibitor of both Factor Xa and Thrombin
      - Warfarin: Interferes with the synthesis of clotting factors by preventing the reduction of vitamin K.
      - Edoxaban: Direct Factor Xa Inhibitor
      - Mechanisms of Action & Monitoring of Effects of Current and New Anticoagulants
        
        Parenteral
        
        Unfractionated Heparin (UFH) – intravenous infusion; complexes with and activates anti-thrombin, and is therefore an indirect inhibitor of factor Xa and thrombin – monitored by APTT.
        
        Low molecular weight heparin (LMWH) eg enoxaparin – subcutaneous injection; complexes with and activates anti-thrombin, and is therefore an indirect inhibitor of factor Xa – laboratory monitoring usually not indicated.
        
        Oral
        
        Warfarin – interferes with the synthesis of clotting factors by preventing the reduction of vitamin K. – monitored by INR.
        
        Dabigatran – direct thrombin inhibitor (binds thrombin and prevents the cleavage of fibrinogen to fibrin). Laboratory monitoring not indicated.
        
        Rivaroxaban, edoxaban and apixaban – reversible direct inhibitors of factor Xa. Laboratory monitoring not indicated
    - - As the woman is haemodynamically stable (no hypotension) there are 5 correct answers to this question;
        
        Subcutaneous Low Molecular Weight Heparin eg Enoxaparin 1 mg/kg subcut twice daily.
        
        Direct oral anticoagulants have been shown to be equally effective, to result in less major bleeding events, and no need to monitor anticoagulant effect
        
        Apixaban
        
        Rivaroxaban
        
        Dabigatran
        
        Edoxaban
    - - What is the likely explanation for this deterioration?
        It appears highly likely that the woman has now suffered a second pulmonary embolus, as;
        
        New left-sided pleuritic chest pain
        
        More breathless
        
        Frightened
        
        More tachycardic and hypotensive
        
        Tachypnoea and hypoxic
        
        Now has signs of right ventricular strain
        
        Left parasternal heave
        
        ECG right axis deviation.
      - Should you proceed with the LMWH or new oral anti-coagulant therapy or Should the management plan now be altered?
        
        In view of the hypoxia and hypotension,
        
        She should be admitted to the Intensive Care Unit (ICU)
        
        Active resuscitation with oxygen should be commenced immediately.
        
        Intravenous fluid and possibly inotropic agents (vasopressors such as norepinephine, dopamine or dobutamine) should be commenced immediately.
        
        Given the presence of hypotension (SBP <90mmHg) systemically administrated thrombolytic therapy is indicated (Intravenous tPA) followed by intravenous unfractionated heparin (IV UFH).
        
        Initial intravenous heparin bolus: 80 units/kg.
        
        Continuous intravenous heparin infusion: 18 units/kg/hour
        
        If no improvement gained surgical or catheter embolectomy could be considered.
    - - Spiral (Helical) CT scanning with intravenous contrast [CT pulmonary angiography (CTPA)]
      - Ventilation Perfusion (aka VQ) Scan
      - Pulmonary angiography (with intra-arterial contrast)
      - Are all possible confirmatory investigations – CTPA most commonly used.
    - - Oral anticoagulant therapy should be commenced once the diagnosis of pulmonary embolus is confirmed.
      - Warfarin was most commonly prescribed.
      - Recent trial data suggest that Dabigatran, Apixaban, Edoxaban and Rivaroxaban;
      - Provide very similar protection against recurrent thrombosis,
      - Cause less bleeding,
      - Need less/no monitoring,
      - Monoclonal antibody binders acting as reversal agents now available
    - - Typically anticoagulation continued for at least 3 months for a first episode of pulmonary embolus in a patient with identifiable reversible or temporary risk factors (as in this woman).
      - However, in patients <50 yrs with recurrent VTE and strong FHx, also check for irreversible risk factors (under guidance from Haematology):
      - Antithrombin III deficiency, protein C deficiency, protein S deficiency, factor V Leiden gene mutation, prothrombin 20210 gene mutation, homocysteinemia, high factor VIII levels, antiphospholipid antibodies.
      - Anticoagulation therapy recommended for 6 - 12 months for patients with PE and any one irreversible risk factors.
      - Anticoagulation recommended for at least 12 months (and possibly indefinitely) for patients with PE and either antiphospholipid antibodies or > 2 irreversible risk factors or patients with unprovoked PE.
- - - - Primary valve failure/reflux
      - Incompetent perforating veins
      - Venous thrombosis
    - - Chronic deep venous insufficiency
      - Deep venous or IVC obstruction (cirrhosis)
      - Trauma
      - Pelvic tumors
  - - - Oedema
      - Hyperpigmentation
      - Lipodermatosclerosis
      - Venous Ulcer
  - - - Improvement of symptoms
      - Improvement of appearance
      - Reduction of oedema
      - Healing of ulcers
    - - Endothermal ablation = 1st line treatment
        
        radiofrequency or laser
        
        Pre op vein mapping
        
        U/S guided venous access
        
        Catheter tip 2cm distal to SFJ
        
        Tumescence
        
        Occludes vessel by fibrosis
      - Foam injection sclerotherapy = useful alternative
      - Open surgery becoming obsolete
- - - - Personal risk factors
        
        Smokers
        
        Malnourished
        
        Immunocompromised
        
        Recurrent RTI’s
        
        Medications
        
        Elderly >65 years
      - Environmental risk factors: Seasonal; more common in winter
      - Organism virulence
    - - Bacteria
        
        Streptococcus pneumoniae (60% of CAP)
        
        •Commonest cause of community acquired pneumonia
        
        •Presentation:
        
        Abrupt onset of illness followed by sustained fever
        
        Purulent sputum
        
        Pleuritic chest pain
        
        Associated with bloodstream infection if severe
        
        Parapneumonic effusions in 25%, rarely empyema
        
        •10-20% mortality
        
        How is it diagnosed?
        
        Sputum culture
        
        Blood culture
        
        Urinary antigen
        
        TREATMENT (targeted to culture results)
        
        Benzylpenicillin IV Amoxicillin for oral switch
        
        Ceftriaxone IV, if penicillin-resistant
        
        Empiric cover in LRTI: eg. Amoxicillin or Co-amoxiclav or Clarithromycin
        
        PREVENTION: Pneumococcal vaccine
        
        Childhood vaccination programme
        
        Adults > 65 years
        
        Clinical risk groups
        
        Haemophilus influenzae
        
        A ‘typical’ CAP pathogen
        
        Risk Factors: Age/ smoking/ COPD
        
        Diagnosis: Sputum culture
        
        Treatment: 20% produce β-lactamase so are resistant to penicillin/ amoxicillin but covered by co-amoxiclav
        
        N.B. H. influenzae is NOT the cause of influenza (“the flu”)
        
        H. influenzae = bacteria which can cause pneumonia
        
        Influenza (“the flu”) is caused by influenza virus
        
        Staphylococcus aureus
        
        Who gets it?
        
        Mostly patients post-influenza
        
        S. aureus producing the PVL toxin can cause severe necrotising pneumonia in previously healthy young people
        
        Clinical Features: Multifocal pneumonia, abscess formation
        
        associated with severe CAP, patient may require ICU
        
        Mycoplasma pneumoniae (atypical)
        
        School-age children and young adults (common in this group)
        
        Mostly seen in GP/ outpatient setting
        
        Prominent cough
        
        Extrapulmonary complications
        
        Diagnosis: Serology (blood sample) or PCR (sputum)
        
        Treatment: Has no cell wall so use an antibiotic with a different mechanism of action (macrolides e.g. clarithromycin or tetracyclines e.g. doxycycline)
        
        Legionella pneumophilia (atypical)
        
        Acquisition: Inhalation of aerosols from contaminated water
        
        Risks: Smoking / Age/ Immunocompromised
        
        Clinical Features: Pontiac fever/ Legionnaire’s disease
        
        Diagnosis: Urinary antigen/ sputum culture
        
        Treatment: Macrolide (e.g. clarithromycin) or quinolone (e.g. levofloxacin)
        
        What is atypical pneumonia?
        
        Term previously used to define infections caused by:
        
        Mycoplasma pneumoniae
        
        Legionella pneumophila
        
        Chlamydophila pneumoniae
        
        Intracellular pathogens: can’t be grown on routine culture Detected by serology or PCR
        
        Causes LRTI including pneumonia
        
        <1% of cases of CAP
        
        Mild, self-limiting
        
        Chlamydophila psittaci
        
        Intracellular pathogens: can’t be grown on routine culture Detected by serology or PCR
        
        Pneumonia with systemic involvement (fever, anorexia, sore throat, photophobia, headache)
        
        Occasionally endocarditis
        
        Mortality up to 20% untreated
        
        Inhalation of dried, infected bird droppings
        
        Coxiella burnetii
        
        Zoonosis
        
        Occupational exposure (farmers/vets/abattoir workers) via aerosols from infected sheep/cattle/goats
        
        Acute Q fever:
        
        Self-limiting, flu-like febrile illness
        
        May get pneumonia or hepatitis
        
        Chronic Q fever: Endocarditis
        
        Diagnosis: Serology
        
        ‘Atypical pathogens’ more appropriate term than ‘atypical pneumonia’
        
        These ‘atypical pathogens’ are characterised by being:
        
        Difficult to diagnose early in the illness
        
        Sensitive to antibiotics other than β-lactams
        
        e.g. macrolides, tetracyclines or fluoroquinolones
        
        Klebsiella pneumoniae (a gram-negative bacillus)
        
        Who gets it?
        
        Alcoholics, elderly, aspiration, malignancy, diabetes
        
        Clinical Features
        
        Cavitating pneumonia, abscess formation
        
        associated with severe CAP, patient may require ICU
        
        Other causes of community acquired pneumonia (less common): Staphylococcus aureus & Klebsiella pneumoniae
      - Viral
        
        Influenza pneumoniae
        
        Respiratory syncytial virus
        
        SARS-CoV-2 (COVID-19)
      - Fungal
        Rare; immunocompromised
        PCP
    - - Organisms in alveoli multiply
      - Immune cells attack
      - Influx of white blood cells, protein, fluid, red cells
      - Release of cytokines
      - Release of vasodilators increase vascular permeability causing congestion
      - Alveoli filled with fluid = CONSOLIDATION
      - Hampers O2 flow –> Shortness of breath
      - Bronchoconstriction and increase in mucus secretion stimulates Cough reflex
      - Pain receptor on alveoli –> Chest pain
      - Cytokine release -> Pyrexia
    - - Source of organism
        
        Hospital acquired pneumonia (HAP) (HCAP)
        
        Ventilator associated pneumonia (VAP)
        
        Type of HAP that develops more than 48 hours after endotracheal intubation
        
        Can occur in 10-20% of patients ventilated for >48 hrs, Mortality 25-50%
        
        What is it? Pneumonia that occurs that occurs 48 hours or more after admission (=“nosocomial” pneumonia / HAP)
        
        Why is it different to CAP? Different bugs involved so different antibiotics required
        
        “Healthcare-associated” pneumonia previously included in same guideline but recent research has shown infections in this category are more like CAP than HAP
        
        RISK FACTORS
        
        Mechanical ventilation (VAP)
        
        General anaesthesia
        
        Surgery
        
        Opiate analgesia
        
        Immunosuppression
        
        Decreased level of consciousness
        
        Residence in a healthcare facility (hospital, nursing home etc.)
        
        HAP & VAP: Different bugs to CAP!
        
        Gram negative bacilli: including multidrug resistant ones
        
        E. coli
        
        Klebsiella spp.
        
        Enterobacter spp.
        
        Pseudomonas spp.
        
        Staphylococcus aureus: including MRSA
        
        Legionella pneumophila
        
        Viruses – influenza, RSV etc.
        
        Choosing an antibiotic
        
        Always check if recent positive microbiology or history of antibiotic resistant organisms (e.g. MRSA)
        
        Check your hospital guidelines – different antibiotics to community acquired pneumonia! e.g. Piperacillin-tazobactam
        
        PREVENTION OF HAP / VAP
        
        Standard precautions: Hand hygiene, environmental cleaning
        
        Avoid excessive sedation
        
        Oral hygiene
        
        Legionella control strategies
        
        Plus, if ventilated:
        
        Implementation of VAP care bundle
        
        Suction secretions
        
        Appropriate cuff size of endotracheal tube
        
        Elevate head of bed
        
        Review need for ventilation
        
        Community acquired pneumonia (CAP)
        
        Atypical Pneumonia
        
        “Walking well”
        
        Also called Interstitial pneumonia
        
        CXR: Reticulonodular pattern; linear threadlike opacities in lung
        
        Infiltrate is outside / around the alveoli i.e. NO CONSOLIDATION
        
        Patchy interstitial lymphocytic inflammatory infiltrate
        
        Symptoms tend to be milder and gradual onset; “flu-like” symptoms
        
        Cough is non-productive / Dry
        
        Low grade pyrexia
        
        Breath sound: rales
        
        WCC: normal or only slightly raised
        
        Other extra pulmonary symptoms: sore throat, myalgia, fatigue, diarrhoea
        
        Mycoplasma pneumoniae
        
        Chlamydia pneumoniae
        
        Legionella pneumoniae
        
        Mycobacteria
        
        Viruses e.g. Influenza, respiratory syncytial virus, adenovirus, SARS-CoV-2
        
        Important to distinguish as different causative organisms
        (and thus different empiric antibiotics)
        
        Aspiration Pneumonia
        (May be community or hospital- acquired)
        
        Risk factors:
        
        Impaired cough reflex (e.g. Stroke, neurologic disorder, C2H5OH xs, drug overdose)
        
        Unconscious
        
        Pyloric stenosis
        
        Oesophageal obstruction
        
        Hiatus hernia
        
        Aspirate non sterile contents eg food, drink, gastric contents (including gastric acid)
        
        Pneumonia – generally will cause a widespread bronchopneumonia
        
        Can cause chemical pneumonitis -> further weaken immune system
        
        Loss of gag reflex
        
        Post-anaesthesia
        
        Stroke or other neurological disorder
        
        Head injury
        
        Organisms
        
        Anaerobes
        
        Streptococcus spp.
        
        Staphylococcus aureus
        
        Escherichia coli & other Gram-negative bacilli
      - Anatomical
        
        Lobar pneumonia (right)
        
        Affects a sections of a lobe
        
        Starts distally and spreads to involve entire lobe
        
        signs and symptoms:
        
        Decrease in chest expansion
        
        Shortness of breath (SOB)
        
        Cough
        
        Chest pain
        
        Pyrexia
        
        Dull to percussion
        
        Tactile fremitus
        
        Bronchial breathing, crackles
        
        Vocal resonance
        
        4 Stages
        
        Pathological appearance
        
        M>F; 3:1; neglected people; alcoholics
        
        95% of cases of Lobar pneumonia are due to Streptococcus Pneumoniae
        
        Pathological Stages of Lobar Pneumonia
        
        Congestion — Lung is heavy and red due to vascular engorgement and intra-alveolar fluid with few neutrophils
        
        Red Hepatization — Massive confluent exudation with red cells, neutrophils and fibrin into alveolar spaces. Lobes are distinctly red, firm and airless, with liver-like consistency
        
        Gray Hepatization — Follows with progressive disintegration of red cells and persistence of a fibrino-suppurative exudate resulting in grayish dry appearance
        
        Resolution or scarring — Resolution due to clearance of the infection and enzymatic digest of exudate which can be reabsorbed, ingested by macrophages cleared via muco-cilliary escalator. Scarring due to organization of exudate, infiltration of fibroblasts and deposition of collagen
        
        BRONCHOPNEUMONIA (left)
        
        Starts proximally in the BRONCHIOLES
        
        Patchy infiltrate, often throughout both lungs
        
        Generally affects the extremes of age: elderly and very young
        
        Elderly: risk factors include COPD, stroke, immunocompromised
        
        Young: immature immune system
        
        Patchy consolidation
        
        Signs and symptoms: productive cough, pyrexia, chest pain, dyspnoea, crackles on auscultation
        
        Complications include microabscess formation
    - - Post organ transplant
      - Chemotherapy
      - AIDS
      - Organisms:
        
        Pneumocystis (PCP)
        
        Cytomegalovirus (CMV)
        
        Unusual mycobacteria
        
        Toxoplasma
  - - - WCC, inflammatory markers, e.g. CRP, ESR
      - Sputum for Gram stain & culture
      - Blood cultures
      - Blood gases/ lactate
      - Urinary antigen for legionella / pneumococcus
      - Nose / throat swab for SARS-CoV-2, influenza PCR (seasonal), other respiratory viruses
      - Serology (discuss with microbiology)
  - - - Blood cultures
      - Sputum culture
      - Specific organisms e.g. influenza, PCP
    - - CURB-65
        
        Confusion
        
        Blood urea nitrogen
        
        Respiratory rate > 30
        
        Blood pressure low
        
        Age: 65 years old
      - Pneumonia severity index (PSI)
      - These determine management strategy
  - - - Empyema
        
        Complication of pneumonia
        
        Investigations:
        
        CXR
        
        aspirate pleural fluid for cytology and microbiology
        
        Collection of pus within the pleural cavity
        
        Pleural fluid: exudate containing abundant neutrophils.
        
        Treatment: Antibiotics, +/- chest drain +/- surgical decortication if complex
    - - Localised area of suppurative necrosis within the pulmonary parenchyma, leading to formation of one or more cavities
      - “necrotising pneumonia”
      - Anaerobic bacteria are present in almost all lung abscesses
      - Tx: Antibiotic =? surgical drainage if necessary
      - Aetiology:
        
        Aspiration of infected material
        
        Aspiration of gastric contents
        
        Complication of bacterial pneumonia
        
        Bronchial obstruction e.g. neoplasm
        
        Septic embolus
        
        Haematogenous spread of bacteria
      - Morphology:
        
        Vary in size; mm to large cavities
        
        Site depends on mode of development i.e. aspiration more common on right side (more vertical airways), in posterior segment of upper lobe
        
        As the focus of suppuration enlarges, ruptures into airways and may partially drain giving an “air-fluid” level on CXR
        
        May rupture into pleural space -> bronchopleural fistula or pneumothorax or empyema
        
        May embolize septic material to brain -> meningitis or brain abscess
        
        Clinical course:
        
        Manifestations include cough, copious amounts of foul smelling sputum
        
        Spiking fevers, malaise
        
        Clubbing, weight loss, anaemia
        
        Secondary amyloidosis in chronic cases
        
        10% mortality rate
    - - Congestive cardiac failure
      - Pulmonary embolism
      - Pulmonary vasculitis
      - Malignancy
  - - - What patient groups are we talking about?
        
        Neutropenia
        
        Stem cell & solid organ transplantation
        
        High dose steroids
        
        Other immunosuppressive agents, e.g. methotrexate
        
        HIV
      - Two groups of organisms
        
        Common causes of LRTI / pneumonia e.g. pneumococcus
        
        Opportunistic pathogens
      - In addition to the commonly encountered pathogens, need to consider and investigate for opportunistic pathogens:
        
        Pneumocystis jiroveci (“PCP”)
        
        Fungi:
        
        Aspergillus fumigatus
        
        Cryptococcus neoformans
        
        Viruses
        
        Herpes simplex (HSV)
        
        Cytomegalovirus (CMV)
        
        Mycobacteria: Atypical mycobacteria & M. tuberculosis
    - - Pulmonary infection involving destruction of parenchyma to produce cavitation
      - Risk factors
        
        Aspiration – altered consciousness/ dysphagia
        
        Periodontal disease
        
        Bronchiectasis
        
        Bronchial carcinoma
        
        Bacteraemia
        
        IVDU (Intravenous drug users)
    - - Respiratory viruses
        
        Sars-CoV-2 (Covid-19)
        
        Influenza A&B
        
        RSV: small children & immunocompromised
        
        Others
      - As part of systemic infection
        
        Varicella-zoster (chickenpox)- esp. pregnancy, immunosuppressed
        
        Measles: unvaccinated children
        
        CMV: immunosuppressed
    - - symptoms
        
        Productive Cough
        
        Haemoptysis
        
        Fever / Night sweats
        
        Anorexia
        
        Weight loss
        
        Haemoptysis
      - LRTI unresponsive to antibiotics
      - If TB suspected – isolate, airborne precautions and inform infection prevention & control team
      - History of TB
        
        1882 – Robert Koch – staining technique for MTB
        
        1921 – Calmette & Guerin – BCG vaccine
        
        1944 - Streptomycin
      - Transmission of M. tuberculosis
        
        Spread by droplet nuclei
        
        Expelled when person with infectious TB coughs, sneezes, speaks, or sings
        
        Close contacts at highest risk of becoming infected
        
        Transmission occurs from person with infectious TB disease (not latent TB infection)
      - Risk Factors
        
        Originating/living in a country where TB is endemic
        
        Previous history of TB or exposure to TB
        
        HIV/AIDS
        
        Socioeconomic issues
        
        Overcrowding, institutions, prisons
        
        Lifestyle
        
        Other medical conditions e.g. Diabetes
        
        Immunosuppressive medications
        
        TNF inhibitors
        
        **Anyone can get TB. Above risk factors are not a pre-requisite
      - Taking a history
        
        Cough
        
        Dry or productive – not specific
        
        Sputum colour – not specific
        
        Duration – weeks to months - suspicion
        
        Unresponsive/ partially responsive to standard antibiotics
        
        Haemoptysis
        
        Mild to moderate
        
        Intermittent
        
        Painless
        
        **Similar to lung ca
        
        Fever
        
        Spiking temperature
        
        PUO – raises the suspicion of TB
        
        Night sweats: Drenching sweats
        
        Shortness of breath
        
        Generally only if underlying respiratory disease e.g. COPD
        
        Occurs if there is a pleural effusion
      - Signs
        
        None
        
        Weight loss
        
        Pleural effusion
        
        Lymphadenopathy
        
        Clubbing
        
        Monoarthropathy
        
        Erythema nodosum
        
        Cutaneous TB; Several different types of cutaneous TB exist. Direct infection of the skin or mucous membranes from an outside source of mycobacteria results in an initial lesion called the tuberculous chancre. The chancres are firm shallow ulcers with a granular base. They appear about 2-4 weeks after mycobacteria enter through broken skin. The immune response of the patient and the virulence of the mycobacteria determine the type and severity of cutaneous TB. Scrofuloderma, Skin lesions result from direct extension of underlying TB infection of lymph nodes, bone or joints, Often associated with TB of the lungs, Firm, painless lesions that eventually ulcerate with a granular base, May heal even without treatment but this takes years and leaves unsightly scars
      - Differential Diagnosis
        
        Lung cancer – similar symptoms – persistent cough, haemoptysis, weight loss, cavitating lung lesion (on CXR)
        
        Sarcoidosis – radiological similarities – upper lobe infiltrates, lympadenopathy. Relatively asymptomatic.
        
        Lymphoma – spiking fever, night sweats. Lymphadenopathy on imaging
      - Spectrum of disease
        
        Pulmonary TB – variable anti-mycobacterial immune response
        
        Treatment
        
        Isoniazid, rifampicin, pyrazinamide, ethambutol × 2 months
        
        Isoniazid, rifampicin × 4 months
        
        *Total of 6 months treatment
        
        Pleural TB – strong anti-mycobacterial immune response
        
        Extra-pulmonary TB – Bone, renal, skin, adenitis
        
        Duration of Tx
        
        9-12 months
        
        Corticosteroids
        
        Neuro, miliary TB
        
        Meningeal TB
        
        Miliary TB- poor anti-mycobacterial immune response
        
        Tuberculin skin test : Also known as: Mantoux test, or PPD (purified protein derivative) test
        
        Inject intradermally 0.1 ml of 2TU PPD tuberculin initially.
        
        Produce wheal 6 mm to 10mm in diameter
        
        Reading the Tuberculin Skin Test:
        
        Read reaction 48-72 hours after injection
        
        Measure only induration
        
        Record reaction in millimeters
        
        Classifying the Tuberculin Reaction
        
        5 mm is classified as positive in high risk patients e.g. HIV-positive persons and recent contacts of TB case
        
        10 mm is classified as positive in moderate risk patients e.g. Recent arrivals from high-prevalence countries, IVDU
        
        15 mm is classified as positive in Persons with no known risk factors for TB
        
        Tuberculin Skin Test: Interpretation
        
        Positive Mantoux interpretation
        
        Active TB
        
        Recent exposure/ latent TB
        
        Negative Mantoux interpretation: No exposure to TB
        
        Factors that May Affect the Skin Test Reaction
        
        Type of Reaction : False-positive, Possible Cause : Nontuberculous mycobacteria, BCG vaccination
        
        Type of Reaction : False-negative, Possible Cause Anergy (e.g. Sarcoidosis) --Recent TB infection, Very young age (< 6 months old), Live-virus vaccination, Overwhelming TB disease
        
        Likely due to Cytokine gene polymorphisms – low IL-10 , high IFN-g
        
        Ethnicity may determine mode of presentation, disease manifestations
      - Investigations
        
        Sputum testing – ZN stain + TB culture
        
        Interpretation
        
        Smear +ve, Culture +ve, Infectious risk & need for isolation
        
        Smear –ve, Culture +ve
        
        Smear +ve Culture –ve
        
        CXR
        
        Mantoux test ( 2TU)
        
        ESR
      - Molecular techniques
        
        Nucleic acid amplification techniques are increasingly important in the diagnosis of TB e.g. PCR
        
        Rapid (90mins) diagnosis at point of care
        
        Can detect some drug resistant strains also
        
        Very important in the developing world
      - Radiology
        
        Abnormalities often seen in apical or posterior segments of upper lobe or superior segments of lower lobe
        
        Classically – cavitating infiltrates
        
        May have unusual appearance in HIV-positive persons
      - TB drugs
        
        TB Drug Side effects
        
        Rifampicin: Hepatotoxicity, Enz. Inducer, orange secretions, “rifampicin flu” (intermittent tx)
        
        Pyrazinamide: Hepatotoxicity
        
        Ethambutol: Optic neuritis, colour blindness (ophthalmology review prior to starting). Renal excretion
        
        Streptomycin: Ototoxicity, nephrotoxicity. Renal excretion. Unsafe in pregnancy
        
        TB Drug Induced Hepatotoxicity
        
        Monitoring: Pretreatment LFT’s & 2 weeks after starting treatment
        
        Discontinue all drugs when transaminases > 5´ normal
        
        Reintroduce anti TB drugs individually and sequentially (every 2 weeks)
        
        Isoniazid: Hepatotoxocity, peripheral neuropathy (pyridoxine)
        
        Drug resistant TB: Definition
        
        MDR-TB : multi-drug resistant TB: Resistance to at least Isoniazid & Rifampicin
        
        XDR-TB : extremely drug resistant TB: Additionally resistant to three or more classes of 2nd line agents
      - Latent TB
        
        Latent TB Infection (LTBI): Diagnosis
        
        Interferon g release assays
        
        T-SPOT.TB & QuantiFERON-TB Gold
        
        May reduce false positive & negatives inherent in the Mantoux skin test
        
        Mantoux test
        
        Low sensitivity in immuno-compromised patients
        
        Low specificity in BCG vaccinated patients
        
        Treatment of LTBI with Isoniazid (INH)
        
        9-month regimen considered optimal, Pyridoxine (Vitamin B6)
        
        Children should receive 9 months of therapy
        
        Can be given twice-weekly if directly observed (DOT)
        
        Alternative regimes:
        
        Rifampicin x 4/12
        
        Rifapentine & Isoniazid x 3/12 (DOT)
        
        Before treatment for LTBI is started, clinicians should
        
        Rule out possibility of TB disease
        
        Determine history of treatment for LTBI or disease
        
        Determine contraindications to treatment
        
        Obtain information about current and previous drug therapy
        
        Recommend HIV testing if risk factors are present
      - BCG Vaccination
        
        Contraindications for BCG vaccine: Contraindicated in immunosuppressed individuals e.g.
        
        HIV infection
        
        HIV & TB
        
        HAART and Anti-TB drugs
        
        Medication burden and compliance
        
        Cost issues (in the developing world)
        
        toxicity
        
        Interactions
        
        Major cause of TB resurgence
        
        Congenital immunodeficiency
        
        Leukemia
        
        Receiving chemotherapy etc.
        
        Variable efficacy against adult pulmonary TB
        
        High efficacy against childhood TB meningitis and miliary TB
        
        Highly cost effective intervention in high incidence countries
      - TB: Summary
        
        Significant global impact
        
        Endemic in many parts of the world
        
        Prolonged cough – main symptom
        
        Similar symptoms to lung ca
        
        Treatment is with a combination of anti-TB drugs for a minimum of 6 months – to eradicate/cure and prevent resistance
        
        Hepatotoxicity – main anti-TB drugs SE
        
        LTBI becoming an important issue
    - - Causes
        
        Childhood infection, e.g. whooping cough
        
        Congenital e.g. cystic fibrosis / congenital malformations
        
        Obstruction / inhalation foreign body
        
        Bronchial carcinoma
        
        Tuberculosis
      - Causes of Infection
        
        H. influenzae
        
        S. pneumoniae
        
        S. aureus
        
        P. aeruginosa
      - Clinical features: Excess production of purulent foul-smelling sputum
      - X-ray appearances: Collapse / consolidation / bronchial dilation
      - Abnormal irreversible dilatation of the bronchi caused by destruction of the muscle and elastic tissue
      - Classified as an obstructive lung disease
      - Disease involves a vicious circle of transmural infection and inflammation with mediator release
      - Prognosis depends on underlying cause and extent of lung involved
      - Causes of Bronchiectasis
        
        Infection
        
        Sequel to bronchopneumonia and bronchiolitis in childhood which has imperfectly resolved
        
        Pneumonia complicating measles or whooping cough. Incidence reduced due to effective childhood immunisation strategies
        
        Allergic Bronchopulmonary Aspergillosis (ABPA)
        
        Chronic tuberculous cavities
        
        Primary Mycobacterium avium complex infection
        
        Congenital Conditions
        
        •Primary ciliary dyskinesia: Poorly functioning cilia contribute to retention of secretions & recurrent infections
        
        •Alpha-1-antitrypsin deficiency
        
        •Cystic Fibrosis
        
        •Young’s syndrome
        
        Chronic sinopulmonary infections
        
        Male infertility
        
        •Marfan syndrome (very rarely)
        
        •Kartageners Syndrome
        
        Characterised by a triad of dextrocardia, bronchiectasis and severe sinusitis.
        
        Autosomal recessively inherited condition
        
        Affects the mobility of the cilia
        
        Immunodeficiency
        
        Persons with humoral immunodeficiency syndromes involving deficiencies of IgG, IgM and IgA (i.e. Hypogammaglobulinaemia)
        
        Immunodeficiency due to malignancy e.g. myeloma, lymphoma
        
        Immunoglobulin replacement reduces the frequency of infections and prevents ongoing airway destruction
        
        Bronchial Obstruction, Obstruction of central bronchi by:
        
        Inhaled / aspirated foreign bodies
        
        Tumour
        
        Mucus plugs in asthma
        
        Compressive lymphadenopathy
        
        Chronic aspiration
        
        Rheumatic Conditions
        
        Sjogrens Syndrome
        
        Systemic Lupus Erythematosus
        
        Rheumatoid arthritis
        
        Also associated with inflammatory bowel disease especially ulcerative colitis
      - Focal & Diffuse Presentations
        
        Lower lobes; left > right
        
        Often bilateral
        
        Bronchi are dilated and contain thick mucopurulent secretions
        
        The wall is destroyed with chronic inflammation and lymphoid follicles
        
        Bronchial arteries are increased in size
      - PATHOLOGY Classification of bronchiectasis
        
        Cylindrical bronchiectasis – uniformally dilated
        
        Varicose bronchiectasis – irregular bulging contours
        
        Cystic or saccular bronchiectasis – more severe form, cystic pus filled cavities
      - Symptoms
        
        Productive cough with purulent sputum
        
        Sputum may be mucoid, mucopurulent, thick or viscous
        
        Blood streaked sputum or copious haemoptysis may result from erosive airway damage due to acute infection
        
        Dyspnoea and wheezing in 75%
        
        Pleuritic pain in 50%
        
        Recurrent LRTI
      - Physical Findings
        
        Crackles, coarse crepitations and rhonchi on auscultation
        
        Clubbing a common finding in the past, rare now 3%
        
        Major confounding disease is COPD
      - COMPLICATIONS OF BRONCHIECTASIS
        
        Massive haemoptysis
        
        Respiratory failure
        
        Pneumonia
        
        Pleural effusion
        
        Accumulation of fluid in the pleural space
        
        Empyema: accumulation of infected fluid in the pleural space
        
        Normally a small amount of thin, pale yellow fluid is present in the pleural space to allow movement of the visceral pleural against the parietal pleura
        
        Pleural effusions are classified as:
        
        TRANSUDATE: have low specific gravity, low protein and few cells.Causes include heart failure, fluid overload, nephrotic syndrome, Peritoneal dialysis
        
        EXUDATE: have high specific gravity, high protein and lots of cells.Causes include infection, malignancy, pulmonary emboli
        
        Pathophysiology:
        
        •Pleural fluid will accumulate when the rate of pleural fluid formation is greater that the rate of pleural fluid removal by the lymphatics
        
        •A transudative effusion occurs when alterations in the systemic factors that influence pleural fluid movement result in a pleural effusion. Examples are elevated visceral pleural capillary pressure with left heart failure, elevated parietal pleural capillary pressure with right heart failure, decreased serum oncotic pressure with nephrotic syndrome, hepatic cirrhosis
        
        •A exudative effusion occurs when the pleural surfaces are altered. Inflammation of the pleura, leading to increased protein in the pleural space is the most common cause of exudative effusion
        
        Clinical features
        
        •History
        
        •Depends on underlying cause
        
        •Physical examination:
        
        Dyspnoea
        
        Pleuritic chest pain
        
        Cough, haemoptysis
        
        Weight loss
        
        Trauma
        
        History of other malignancy
        
        Cardiac surgery
        
        Decreased breath sounds over side of effusion
        
        Bronchial breath sounds immediately above effusion
        
        Dull to percussion
        
        Absent / reduced tactile fremitus
        
        Other findings (depending on underlying cause): Ascites, JVP, peripheral oedema, friction rub, unilateral leg swelling etc.
        
        Management
        
        CXR
        
        without/with CT Thorax
        
        Blood tests
        
        Thoracocentesis
        
        •Indicated if effusion persists > 3 days
        
        •Performed at the bedside; but may require radiological guidance, particularly if small or loculated
        
        •Gross appearance of fluid helpful (Usually thin and yellow)
        
        Bloody
        
        Cloudy
        
        Malodorous
        
        •Ratio of pleural fluid protein to serum protein measured
        
        •Glucose, LDH, +/- amylase
        
        •Cytology: inflammatory cells, malignant cells
        
        •Culture & Sensitivity
        
        Brain abscess
        
        Amyloidosis
        
        Respiratory pathogens are staphylococcus aureus, haemophlyus influenza, pseudomonas aeruginosa
      - Investigations
        
        Bloods
        
        FBC, U&E
        
        Exclude / confirm aetiologies e.g. autoantibody screen, sweat test, serum immunoglobulins, IgE, alpha-1-AT levels etc.
        
        Microbiology
        
        Sputum C&S
        
        Blood cultures if clinically indicated
        
        Exclude infectious aetiologies (e.g. TB, aspergillus etc.)
        
        Radiology
        
        CXR
        
        High resolution computed tomography (CT) thorax
        
        Bronchoscopy
        
        Obstruction
        
        Culture and cytology of washings
        
        PFT’s
      - Management
        
        Confirm correct diagnosis
        
        Treat infectious exacerbations
        
        Reduce risk factors
        
        Vaccinations (including Influenza vaccine and pneumococcal vaccine)
        
        Chest physiotherapy
        
        Nebulised DNAase, Nebulised antibiotics
        
        Maintenance antibiotics +/-
        
        Surgery +/- indicated perhaps if focal
    - - Infection is important in Cystic Fibrosis
      - Primary cause of morbidity & mortality is persistent bacterial infection of the airways, with subsequent bronchiectasis, fibrosis & obstructive lung disease
      - Chronic respiratory infection with resultant respiratory failure accounts for >90% of deaths in CF
      - Why do CF patients get infection?
        
        Defects in microbial clearance
        
        Altered salt content in airway surface liquid inactivates antimicrobial defensins and impairs neutrophil killing
        
        Receptor for P. aeruginosa
        
        Decreased nitric oxide (antibacterial) predisposes to lung infection
        
        Airways hyper inflammatory
      - The most common life-shortening autosomal recessive disorder in Western Caucasian populations
      - Abnormal apical membrane chloride channel defect resulting in reduced volume and increased hyperviscosity of mucosal secretions leading to end –organ damage.
      - It is a multisystem disorder but most commonly affects the respiratory and gastrointestinal tracts.
      - The majority of deaths are due to respiratory disease and failure.
      - In the past the majority of deaths occurred in childhood. Now most of the deaths occur in the adult patient population.
      - History
        
        1938 – CF as a specific entity (Dorothy Andersen)
        
        1940’s
        
        Autosomal recessive inheritance
        
        Nutrition major problem
        
        1950’s
        
        Sweat testing – pilocarpine iontophoresis
        
        Antibiotic standard therapy
        
        1960’s
        
        National (U.S.) & International CF organizations
        
        Neonatal screening – immunoreactive trypsin blood spot test
        
        1980’s
        
        Chloride channel defect
        
        1989 – CF gene identified
      - Epidemiology
        
        CF gene mutation frequency
        
        1:35 Continental Europe
        
        1:25 U.K. Anglo Saxon descent
        
        1:17 Irish Celtic descent
        
        Incidence (live birth prevalence)
        
        1:2500 (U.S. & Continental Europe)
        
        1:1700 (IRL) ~ 35-40 new PWCF/ annum
      - Gene defect to chloride channel
        
        MUTATION CLASSES
        
        1500 mutations identified
        
        Class I Defective synthesis
        
        e.g.G542X, 621+1 G→T
        
        Class II Defective processing e.g. delF508
        
        Class III Defective regulation e.g. G551D, Y569D
        
        Class IV Defective conductance e.g. R117H
        
        Class V Reduced quantity e.g. 3849+10kb→T
        
        Class VI Increased turnover
        
        CF: Genotype/Phenotype
        
        1000 CFTR gene mutations
        
        Irish Population:
        
        delta F508 (92%), G551D (15.5%), R117H (5.9%)
        
        All other mutations < 4% of CF population
        
        delta F508
        
        Class II mutation
        
        reduced lung function and reduced survival in homozygotes
        
        delta F508/ delta F508 ~ 56% of Irish CF population
        
        Genotype – Phenotype correlation
  - - - Use hospital guidelines: Usually based on the likely organisms that can cause community-acquired pneumonia i.e., you need to know some of the bugs to help you choose antibiotics!
      - Other general considerations: Recent antibiotics? Allergies? Previous resistant organisms/ previous positive microbiology? (Check the laboratory computer system)
      - Other considerations in pneumonia : Recent travel? Pneumococcal / influenza vaccine? Animal / bird contact (more unusual organisms)?Any history of immunocompromise?
    - - At 24-48 hours after starting antibiotics, we must make an Antimicrobial Prescribing Decision:
        
        Review the clinical diagnosis : Pneumonia
        
        Review laboratory/radiology results: S. pneumoniae, penicillin-susceptible, WCC down to 7
        
        Reassess clinically : Doing well / fever settled / eating & drinking
      - Choose one of the five prescribing decision options: What do you want to do foe your patient: A) Stop antibiotics, B)Switch route, C) Change antibiotics, D) Continue same, E) OPAT, Answers : B+C
    - - Clinically improving
      - Afebrile x 24- 48 hours
      - Inflammatory markers (WCC, CRP) improved
      - Tolerating oral intake
      - No specific indication for prolonged IVs (e.g. endocarditis/ septic arthritis)
      - Suitable oral alternative available
    - - Switch IV to PO
      - Change co-amoxiclav to amoxicillin (narrower spectrum)
      - Stop clarithromycin
      - Plan for 7 -10 days total of antibiotics i.e. 5-8 more days of oral amoxicillin
      - What else should we do before discharge?
        
        Discuss vaccination
        
        Pneumococcal (once-off)
        
        Influenza (annual)
        
        Smoking cessation support and referral
  - - - Need to know the bugs to choose the correct antibiotic!
      - Relevant questions
    - - If critically ill, needing ICU admission, immunocompromised or risk of resistant pathogens
      - If not responding to empiric therapy
- - - - Larynx, trachea, bronchi, bronchioles
  - - - •Loss of cough reflex
        
        e.g. Coma; Anaesthesia
      - • Injured mucociliary apparatus
        
        e.g. Smoking
      - • Decrease in alveolar macrophages
        
        e.g. Alcohol, smoking
      - • Pulmonary congestion / oedema
      - • Accumulation of secretions
      - • Obstruction
- - - - Presenting symptoms:
        
        Core Respiratory Symptoms
        
        Sputum
        
        Sputum production DDx
        
        Upper respiratory tract: Post nasal drip
        
        Lower respiratory tract
        
        LRTI / Pneumonia
        
        TB
        
        Bronchiectasis
        
        COPD
        
        Haemoptysis
        
        Haemoptysis DDx
        
        Bronchogenic neoplasm
        
        Pneumonia
        
        TB
        
        Bronchiectasis
        
        PE
        
        Out rule epistaxis, haematemesis
        *CCF – pink frothy sputum
        
        Pleuritic Chest Pain
        
        Pleurtic chest pain DDx
        
        Pulmonary Embolus
        
        Pneumonia
        
        Pneumothorax
        
        *Pleural effusion- chest discomfort, not classically pleuritic
        
        Wheeze
        
        Wheeze DDx
        
        Asthma
        
        COPD
        
        Bronchiectasis
        
        Type 1 hypersensitivity allergic reaction
        
        **Hallmark of obstructive airways disease
        
        Chest tightness:
        May be cardiac or respiratory
        Out rule cardiac features
        
        Fever/Chills
        
        Symptoms of infection
        
        URTI / Pharyngitis / Sinusitis
        
        LRTI / Pneumonia
        
        Night sweats/Rigors
        
        Rigors
        
        *Violent shivering – rocking the bed!
        
        Septicaemia (pneumonia)
        
        TB
        
        Empyema
        
        Lung abscess
        
        Non pulmonary DDx - pyelonephritis
        
        Night Sweats
        
        *Drenching sweats unrelated to room temperature, where the patient has to change clothes and bed clothes. Not just sweating at night!
        
        ** Prolonged symptom – weeks to months
        
        TB
        
        Empyema
        
        Lung abscess
        
        Non pulmonary DDx – Lymphoma, Renal cell carcinoma
        
        Weight loss
        
        Wt loss on it’s own, is a very non-specific symptom, present in many non-pulmonary conditions. The underlying cause is usually non – pulmonary e.g. Gastrointestinal.
        
        Bronchogenic neoplasm
        
        TB
        
        Empyema
        
        End stage COPD
        
        Cough
        
        System based DDx for Cough
        
        Upper Respiratory Tract
        
        URTI
        
        Sinusitis
        
        Rhinitis
        
        Post nasal drip
        
        Lower Respiratory Tract
        
        LRTI / Pneumonia
        
        TB
        
        Asthma
        
        COPD
        
        Gastrointestinal: GORD
        
        Drugs: ACE inhibs, Beta blockers, aspirin
        
        Shortness of Breath
      - Initial DDx —> Specific DDx symptoms
        
        COPD
        
        Smoker > 20 pack years
        
        Age > 50 years
        
        Duration of symptoms – years
        
        SOB on exertion progressing to SOB at rest
        
        with/ without Productive cough
        
        Acute exacerbations
        
        increased SOB, wheeze, chest tightness
        
        Associated LRTI – dirty sputum
        
        Onset- days to weeks
        
        Relief with bronchodilators, steroids, antibiotics
        
        Frequent hospital & GP visits
        
        Decompensated Heart Failure
        
        Age > 50 years
        
        Background: IHD (Ischemic heart disease) , Valvular HD
        
        SOB on exertion progressing to SOB at rest
        
        Orthopnoea, PND, ankle oedema
        
        Paroxysmal nocturnal dyspnea (PND) is a sensation of shortness of breath that awakens the patient, often after 1 or 2 hours of sleep, and is usually relieved in the upright position.
        
        Orthopnea is the sensation of breathlessness in the recumbent position, relieved by sitting or standing.
        
        Relieved by diuretics
        
        Chronic CCF ( congestive cardiac failure) onset: weeks to months
        
        Acute pulmonary oedema: minutes to hours
        
        Asthma
        
        Intermittent symptoms**
        
        SOB, wheeze, dry cough, chest tightness
        
        Nocturnal, occupational, exercise induced symptoms
        
        Relieved by Beta 2 agonists or oral steroids
        
        Being younger or being a non-smoker makes asthma a more likely diagnosis as other DDX’s are less likely
        
        However asthma can happen at any age, and can present in smokers too
        
        New onset makes asthma more likely
        
        However it is possible that a patient may have had undiagnosed asthma for years
        
        Acute exacerbation: Onset: hours to days
        
        Precipitating factors: URTI, dust, perfumes, food substances, animal dander, seasonal variation, stress, exercise induced.
        
        Personal Hx: Eczema, hay fever, atopy
        
        Family history
        
        Pulmonary Embolism
        
        Main symptoms: SOB++, Pleuritic chest pain+
        
        with/ without Cough, with/without haemoptysis
        
        Unilateral calf swelling + tenderness
        
        Absence of obstructive airways disease or infective symptoms
        
        Risk factors
        
        Idiopathic Pulmonary Fibrosis
        
        Age > 60 years
        
        M > F
        
        Presenting symptom: SOB on exertion
        
        Onset of symptoms: 6 to 12 months
        
        Progressive: from SOB on Exertion to SOB at rest
        
        with/without Dry cough
        
        Upper respiratory tract infection
        
        Pharyngitis, sinusitis, rhinitis, coryza
        
        Short, acute Hx (1-3 days)
        
        Very common, all age groups
        
        Fever, chills, myalgia
        
        Sore throat
        
        Blocked/runny nose, sneezing
        
        Dry or productive cough
        
        LRTI / Pneumonia
        
        Acute onset: Hours - few days
        
        All age groups
        
        Fever, chills ,sweats
        
        Productive cough, purulent sputum, with/without haemoptysis
        
        Pleuritic chest pain
        
        (Pneumonia – clinical or radiological features of consolidation)
        
        Atypical Pneumonia
        
        Prolonged Hx - 2 to 4 weeks
        
        Malaise, myalgia, headaches
        
        Ear pain, diarrhoea
        
        Dry cough, SOB
        
        Unresponsive to penicillins/cephalosporins
        
        Lung Cancer
        
        Ever Smokers are at highest risk
        
        Symptom duration: Weeks --> Months
        
        Haemoptysis
        
        SOB (pleural effusion, atelectasis)
        
        Weight loss
        
        Prolonged dry cough
        
        Persistent hoarseness
        
        Bone pain, jaundice, headaches (metastases)
        
        Bronchiectasis
        
        Productive Cough, Viscid mucus
        
        Recurrent LRTIs
        
        Wheeze
        
        Haemoptysis
        
        Chronic/ long history - years
        
        Aetiology
        
        Cystic Fibrosis
        
        Primary cilliary dyskinesia , Young’s syndrome (Kartagener’s syndrome – triad)
        
        Immunoglobulin deficiency syndromes
        
        Allergic Bronchopulmonary Aspergillosis
        
        alpha-1 antitrypsin def
        
        Recurrent aspiration
        
        Idiopathic
        
        Previous infections
        
        Tuberculosis
        
        Measles
        
        Pertusis (Whooping cough)
        
        Pneumothorax
        
        Acute unilateral pleuritic pain
        
        Acute SOB
        
        Any age group
        
        Marfanoid features (rare)
        
        Definite clinical signs ( with/ without CXR) – confirm diagnosis
        
        Empyema
        
        Pus in the pleural space
        
        Duration : weeks to months
        
        Fever, chills , rigors, night sweats, weight loss, chest discomfort, SOB
        
        At risk: Elderly, intellectual disability, long term care, aspiration/swallowing difficulties, poor dentition, alcohol abuse.
        
        Lung abscess
        
        Pus within a pathological cavity
        
        Similar symptoms to empyema
        
        Productive cough / foul smelling sputum (as an abcess may communicate with a bronchus)
  - - - Signs of CO2 retention:
        warm bounding pulse, dilated veins, asterixes – almost exclusive to chronic severe COPD
      - Clubbing:
        
        Malignancy – lung carcinoma, mesothelioma
        
        Pulmonary fibrosis - cryptogenic fibrosing alveolitis , asbestosis
        
        Suppurative lung diseases – empyema, lung abscess, bronchiectasis
    - - Description: Central or displaced
      - Pulled towards the abnormal side: telectasis, pneumothorax, unilateral fibrosis, pneumonectomy
      - Pushed away from the abnormal side: large pleural effusion, tension pneumothorax
    - - Description: Normal or reduced
      - If reduced, state whether symmetrical or unilateral
      - Symmetrically reduced
        
        Symmetrically reduced
        
        Obstructive lung disease
        
        Restrictive lung disease
      - Unilaterally reduced
        
        Pneumothorax
        
        Pleural effusion
    - - Feels the transmission of sound waves from the trachea to the chest wall.
      - i.e. lung has to be in contact with the chest wall
      - Increased / normal / decreased/ absent
      - Increased – only one condition: consolidation (pneumonia)
      - Decreased or absent – pleural effusion, pneumothorax, atelectasis
    - - •Intensity of Breath Sounds/Air entry: normal or decreased
        
        It will be decreased in any lung pathology
      - •Nature of Breath Sounds: vesicular or bronchial
        
        Assume its vesicular
        
        Bronchial breathing
        
        Direct transmission of tracheal sounds to chest wall
        
        i.e. very loud and clear
        
        Due to consolidation
      - •Symmetry:
      - •Added sounds:
        
        Wheeze (rhonchi):
        
        is always an expiratory sound although there may also be an inspiratory component in severe disease
        
        Is almost always bilateral
        
        Indicates obstructive airways disease i.e. Asthma, COPD, bronchiectasis, type 1 allergic reaction
        
        Creps (crackles/ rales)
        
        Is always an inspiratory sound
        
        Indicative of fluid in the alveoli
        
        Pneumonia, fibrosis, bronchiectasis, pulmonary oedema
        
        Rub
        
        Rare
        
        Is heard throughout inspiration and expiration
        
        Indicates pleural inflammation
        
        Pulmonary infarct, pneumonia, chest drain
    - - Assesses the density of whatever is under the chest wall (doesn’t have to be lung)
      - Hyper-resonant/ Resonant/ Dull/ Stony dull
      - Air > lung > consolidation > fluid
      - Hyper-resonant - pneumothorax, COPD
      - Resonant – normal
      - Dull – pneumonia, atelectasis, tumour
      - Stony dull – pleural effusion (includes haemothorax, chylothorax, empyema).
    - - Bilateral lung signs
        
        CCF
        
        Idiopathic pulmonary fibrosis
        
        Bronchiectasis
        
        COPD
      - Unilateral lung signs
        
        Pleural effusion
        
        Pneumothorax
        
        Pneumonia
        
        Atelectasis
        
        Empyema
        
        Lung cancer
        
        Old TB
        
        Lobectomy/ Pneumonectomy
    - - Wheeze
        
        Asthma
        
        COPD
        
        Bronchiectasis
        
        Type 1 allergic reaction
      - Bibasal Creps
        
        Common
        
        Pulmonary oedema
        
        Idiopathic Pulmonary Fibrosis
        
        Bronchiectasis
        
        Less common: Bibasal pneumonia
      - Unilateral Creps
        
        Common: Pneumonia
        
        Less common
        
        Bronchiectasis
        
        Congestive cardiac failure
        
        Idiopathic Pulmonary Fibrosis
      - Bilateral Effusions
        
        Congestive cardiac failure
        
        Liver failure
        
        Renal failure
        
        **The effusions for the above are usually transudates
      - Unilateral Effusion
        
        Parapneumonic (Post Pneumonia)
        
        Neoplasia (1 lung or metastatic)
        
        TB
        
        Pulmonary infarction (from a PE) – usually small effusion
        
        *These effusions are usually exudates
    - - COPD
        
        Signs of CO2 retention
        
        Warm sweaty palms/ Dilated veins
        
        Bounding pulse
        
        Chemosis
        
        Asterixes
        
        (only in chronic severe COPD)
        
        Signs of Hyperinflation
        
        Barrell shaped chest
        
        Decreased cricosternal distance
        
        Reduced chest expansion
        
        Impalpable apex beat
        
        Hyper-resonance on percussion
        
        Absent cardiac dullness on percussion
        
        Liver ptosis (on percussion)
        
        Chest Signs
        
        Trachea: central, decreased cricosternal distance
        
        Chest expansion: decreasedsymmetrically
        
        Tactile fremitus: normal
        
        Percussion: hyper-resonant bilaterally
        
        Auscultation: diminished intensity vesicular breath sounds bilaterally, with expiratory wheeze throughout both lung fields (during an exacerbation)
      - Decompensated Heart Failure
        
        Tachypnoea , tachycardia, low volume pulse, with/without hypotension
        
        Palpation, fremitus, percussion: unimpressive
        
        Auscultation Diminished intensity vesicular breath sounds bilaterally, with crepitations bibasally
        
        Peripheral signs: increased JVP, with/without hepatomegaly (mild, tender), with/without ascites, bilateral ankle oedema or sacral oedema
      - Idiopathic Pulmonary Fibrosis
        
        Tachypnoea,
        
        Finger clubbing
        
        reduced Chest expansion
        
        Tactile fremitus, percussion: unremarkable
        
        Auscultation: diminished intensity vesicular breath sounds with fine end inspiratory crepitations bibasally
      - Pulmonary embolism
        
        Common findings
        
        Tachypnoea, tachycardia
        
        Normal chest findings
- - - - Unfractionated Heparin (UFH) – intravenous infusion; complexes with and activates anti-thrombin, and is therefore an indirect inhibitor of factor Xa and thrombin – monitored by APTT.
      - Low molecular weight heparin (LMWH) eg enoxaparin – subcutaneous injection; complexes with and activates anti-thrombin, and is therefore an indirect inhibitor of factor Xa – laboratory monitoring usually not indicated.
    - - Warfarin – interferes with the synthesis of clotting factors by preventing the reduction of vitamin K. – monitored by INR.
      - Dabigatran – direct thrombin inhibitor (binds thrombin and prevents the cleavage of fibrinogen to fibrin). Laboratory monitoring not indicated.
      - Rivaroxaban, edoxaban and apixaban – reversible direct inhibitors of factor Xa. Laboratory monitoring not indicated