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Year 3 Medicine > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What are the causes of Respiratory acidosis?

A
  • Hypoventilation e.g. neuromuscular diseases
  • “Alveolar hypoventilation” e.g. COPD
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2
Q

What should the A-a values be ?

A
  • Young healthy people: <2 kPa
  • Older people: <4 kPa
  • >4 kPa- lung pathology
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3
Q

What happens in anaphylaxis?

A

Immunological response: – IgE → antigen → mast cell & basophils ‡ → histamine ↑ → body response

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4
Q

Symptoms of Anaphylaxis and Angioedema?

A
  • Pruritus, urticaria & angioedema
  • Hoarseness, progressing to stridor & bronchial obstruction
  • Wheeze & chest tightness from bronchospasm
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5
Q

How is Anaphylaxis treated?

A
  • Remove trigger, maintain airway, 100% O2
  • Intramuscular adrenaline 0.5 mg (Repeat every 5 mins as needed to support CVS)

Management following stabilisation:

  • non-sedating oral antihistamines, in preference to chlorphenamine
  • Serum tryptase levels are sometimes taken in such patients (remain elevated for up to 12 hours)
  • Referral to a specialist allergy clinic
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6
Q

How is mild to moderate asthma defined?

A
  • Mild: No features of severe asthma; PEFR >75% Moderate:
  • No features of severe asthma; PEFR 50-75%
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7
Q

How is severe asthma defined?

A
  • PEFR 33-50%
  • Cannot complete sentences in 1 breath
  • RR > 25/min
  • HR >110 BPM
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8
Q

How is life threatening asthma defined?

A
  • Life threatening (if any one of the following):
    • PEFR < 33% of best or predicted
    • Sats <92% or ABG pO2 < 8kPa
    • Cyanosis, poor respiratory effort, near or fully silent chest
    • Exhaustion, confusion, hypotension or arrhythmias
    • Normal pCO2
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9
Q

How is acute asthma managed?

A
  • ABCDE
  • Aim for SpO2 94-98% with oxygen as needed, ABG if sats <92%
  • 5mg nebulised Salbutamol (can repeat after 15 mins)
  • 40mg oral Prednisolone STAT (IV Hydrocortisone if PO not possible)

If severe:

  • Nebulised Ipratropium Bromide 500ug
  • Consider back to back Salbutamol If life threatening or near fatal:
  • Urgent ITU or anaesthetist assessment
  • Urgent portable CXR
  • IV Aminophylline
  • Consider IV Salbutamol if nebulised route ineffective
  • Magnesium sulphate
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10
Q

What are some of the signs and sx of COPD?

A

Symptoms

  • Cough + sputum
  • Dyspnoea
  • Wheeze
  • Wt. loss

Signs

  • Tachypnoea
  • Prolonged expiratory phase
  • Hyperinflation
    • ↓Cricosternal distance (normal = 3 fingers)
    • Loss of cardiac dullness
    • Displaced liver edge
    • Wheeze
  • May have early-inspiratory crackles
  • Cyanosis
  • Cor pulmonale: ↑JVP, oedema, loud P2
  • Signs of steroid use
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11
Q

How are COPD Exacerbations treated?

A
  • ABCDE
  • Oxygen: - via a fixed performance face mask due to risk of CO2 retention - aim for SaO2 88-92% (use ABGs)
  • NEBs – Salbutamol and Ipratropium
  • Steroids – Prednisolone 30mg STAT and OD for 7 days
  • Abx if raised CRP / WCC or purulent sputum
  • CXR
  • Consider IV aminophylline
  • Consider NIV if Type 2 respiratory failure and pH 7.25-7.35
  • If pH <7.25 consider ITU referral
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12
Q

How is pneumonia investigated?

A
  • Bedside: urine CAP (pneumococcal and legionella ), ECG?, sputum sample MC+S
  • Bloods: FBC, UE, CRP, LFT
  • Imaging: CXR
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13
Q

What are the signs + sx of pneumonia?

A
  • Sx: Fever, rigors, Malaise, anorexia, Dyspnoea, Cough, purulent sputum, haemoptysis, Pleuritic pain
  • Signs: ↑RR, ↑ HR, Cyanosis, Confusion,
    • Consolidation: ↓ expansion, Dull percussion, Bronchial breathing, ↓ air entry, Crackles, Pleural rub , ↑VR
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14
Q

What aids in the diagnosis of pneumonia?

A
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15
Q

What antibiotics are used for the treatment of pneumonia?

A
  • ABCDE - appropriate management
  • Antibiotics
    • CURB65 score 0 or 1 (low severity): amoxicillin 500mg TD 5 days
      • Atypical: Doxycycline (e.g. legionella)
    • CURB65 score 2: Amoxicillin 500mg TD 5 days + Clarithromycin 500 mg BD 5 days
      • Atypical: Doxycycline
    • CURB65 score 3 to 5: Co-amoxiclav (500/125 mg 3 times a day orally or 1.2 g 3 times a day IV) and Clarithromycin (500 mg twice a day orally or IV for 5 days)
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16
Q

What is considered a massive haemoptysis?

A
  • >240mls in 24 hours OR
  • >100mls / day over consecutive days
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17
Q

Define the Management of Massive Haemoptysis?

A
  • ABCDE
  • Lie patient on side of suspected lesion (if known)
  • Oral Tranexamic Acid for 5 days or IV
  • Stop NSAID’s / aspirin / anticoagulants •
  • Antibiotics if any evidence of respiratory tract infection
  • Consider Vitamin K
  • CT aortogram – interventional radiologist may be able to undertake bronchial artery embolisation
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18
Q

How is a tension pneumothorax detected?

A
  • Hypotension
  • Tachycardia
  • Deviation of the trachea away from the side of the pneumothorax
  • Mediastinal shift away from pneumothorax
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19
Q

How is a tension pneumothorax managed?

A
  • Large bore intravenous cannula into 2nd ICS MCL
  • Chest drain into the affected side: 4th ICS MAL
  • Give high flow 02 and admit
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20
Q

What are some of the sx of a PE?

A
  • Chest pain (pleuritic)
  • SOB
  • Haemoptysis
  • Low cardiac output followed by collapse (if Massive PE)
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21
Q

What are some of the Major Risk Factors of a PE?

A
  • Surgery – Abdominal/pelvic; Knee/ hip replacement; Post-op spell on ITU
  • Obstetric – Late pregnancy; C- section
  • Lower Limb – Fracture; Varicose veins
  • Malignancy – Abdominal/ Pelvic/ Advanced/ Metastatic
  • Reduced Mobility
  • Previous proven VTE
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22
Q

How is a PE managed?

A
  • ABCDE
  • Oxygen if hypoxic
  • Fluid resuscitation (if hypotensive)
  • Thrombolysis: if haemodynamically unstable (large PE) - 100mg alteplase IV; (2nd: streptokinase)
  • Anticoagulation
    • LMWH - Dalteparin on admission
    • After admission:
      • 1st line: DOAC - provoked 3 months, unprovoked life long
      • 2nd: LMWH (bridging) + warfarin (check INR 2-3 - warfarin needs 5 days to be effective and is prothombotic)
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23
Q

How do sx and management change for a massive PE?

A
  • Hypotension/ imminent cardiac arrest
  • Signs of right heart strain on CT / Echo
  • Consider thrombolysis with IV alteplase
  • Consider Thrombolysis Contraindications
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24
Q

What are some of the absolute contraindications of thrombolysis?

A
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25
Q

What are some of the relative contraindications of thrombolysis?

A
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26
Q

What are the characteristics of asthma?

A
  • Asthma is a chronic inflammatory disease of the airways
  • Airway obstruction that is reversible, either spontaneously or with treatment
  • Increased airway responsiveness (airway narrowing) to a variety of stimuli
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27
Q

Asthma Pathophysiology

A
  • Airway epithelial damage – shedding and subepithelial fibrosis, basement membrane thickening
  • An inflammatory reaction characterised by eosinophils, T-lymphocytes (Th2) + mast cells. Inflammatory mediators released include histamine, leukotrienes, and prostaglandins
  • Cytokines amplify inflammatory response
  • Increased numbers of mucus secreting goblet cells and smooth muscle hyperplasia and hypertrophy
  • Mucus plugging in fatal and severe asthma
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28
Q

How is Acute Asthma Managed?

A
  • ABCDE
  • Aim for SpO2 94-98% with 02 as needed, ABG if sats <92%
  • 5mg nebulised Salbutamol (can repeat after 15 mins)
  • 40mg oral Prednisolone STAT (IV Hydrocortisone if PO not possible)
  • Severe: ipratroprium bromide 500mg + back to back salbutamol
  • Life threatening fatal: IV aminophylline. IV salbutamol
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29
Q

What are the histological features of asthma?

A
  • Thickening of basement membrane
  • Mucosal thickening
  • Mucus plugging
  • Bronchial wall smooth muscle hypertrophy
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30
Q

How do you treat severe or life threatening asthma?

A
  • If severe: Nebulised Ipratropium Bromide 500 micrograms
  • Consider back to back Salbutamol If life threatening or near fatal
  • Urgent ITU or anaesthetist assessment
  • Urgent portable CXR
  • IV Aminophylline
  • Consider IV Salbutamol if nebulised route ineffective
  • Magnesium sulphate
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31
Q

Criteria for safe asthma discharge after exacerbation

A
  • PEFR >75%
  • Stop regular nebulisers for 24 hours prior to discharge
  • Inpatient asthma nurse review to reassess inhaler technique and adherence
  • Provide PEFR meter and written asthma action plan
  • At least 5 days oral prednisolone
  • GP follow up within 2 working days
  • Respiratory Clinic follow up within 4 weeks
  • For severe or worse, consider psychosocial factors
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32
Q

What are the NICE guidelines for chronic asthma management?

A
  1. SABA
  2. +ICS
  3. +LTRA
  4. +LABA
  5. +SABA=/- LTRA
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33
Q

What is Eosinophilia

A
  • Some patients with asthma have eosinophilic inflammation which typically responds to steroids. However, there are several differentials of eosinophilia:
  • Airways inflammation (asthma or COPD)
  • Hayfever / allergies
  • Allergic Bronchopulmonary Aspergillosis
  • Drugs
  • Churg-Strauss / vasculitis
  • Eosinophilic Pneumonia
  • Parasites
  • Lymphoma
  • SLE
  • Hypereosinophilic syndrome
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34
Q

What is the COPD definition?

A
  • COPD is characterised by airflow obstruction.
  • The airflow obstruction is usually progressive, not fully reversible and does not change markedly over several months.
  • The disease is predominantly caused by smoking
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35
Q

What is the pathophysiology of COPD?

A
  • COPD is an umbrella term which encompasses emphysema and chronic bronchitis
  • Mucous gland hyperplasia
  • Loss of cilial function
  • Emphysema – alveolar wall destruction causing irreversible enlargement of air spaces distal to the terminal bronchiole
  • Chronic inflammation (macrophages and neutrophils) and fibrosis of small airways
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36
Q

What are the common causes of COPD?

A
  • Smoking
  • Inherited α-1-antitrypsin deficiency
  • Industrial exposure, e.g. soot
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37
Q

What outpatient COPD management?

A
  • COPD care bundle
  • Smoking cessation
  • Pulmonary Rehabilitation
  • Bronchodilators
  • Antimuscarinics
  • Steroids
  • Mucolytics
  • Diet
  • LTOT if appropriate
  • Lung volume reduction if appropriate

General Measures

  • Stop smoking
  • Specialist nurse
  • Nicotine replacement therapy
  • Bupropion, varenicline (partial nicotinic agonist)
  • Support programme
  • Pulmonary rehabilitation / exercise
  • Influenza and pneumococcal vaccine

Medications:

  • Mucolytics -Consider if chronic productive cough
    • E.g. Carbocisteine (CI in PUD)
    • Breathlessness and/or exercise limitation
      • SABA and/or SAMA (ipratropium) PRN
      • SABA PRN may continue at all stages

Exacerbations or persistent breathlessness

  • FEV1 ≥50%: LABA or LAMA (tiotropium) (stop SAMA)
  • FEV1 <50%: LABA+ICS combo or LAMA
  • Persistent exacerbations or breathlessness: LABA+LAMA+ICS
  • Roflumilast / theophylline (PDIs) may be considered
  • Consider home nebs

LTOT: Aim: PaO2 ≥8 for ≥15h / day (↑ survival by 50%)

Surgery

  • Recurrent pneumothoraces
  • Isolated bullous disease
  • Lung volume reduction
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38
Q

What are the three types of pneumonia?

A
  • Community Acquired
  • Hospital Acquired
  • Others, e.g. aspiration
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39
Q

How is CAP diagnosed?

A
  • CURB-65 score
  • ABX according to CURB-65 score and patient allergies
  • ABCDE approach - Even if CURB-65 score is low do not ignore signs of sepsis
  • NO DELAY in initiating Abx (or IV fluids if indicated) + / - Paracetamol
  • ITU referral if high CURB-65 score
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40
Q

What other tests are used for CAP diagnosis?

A
  • CXR
  • Bloods: FBC, U&E, CRP and sputum cultures
  • Blood cultures if febrile
  • If high CURB-65 score -
  • Urinary CAP screen - Atypical pneumonia screen – legionella
  • ABG if low sats
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41
Q

What tests are used in a Pneumonia Follow Up?

A
  • HIV test
  • Immunoglobulins
  • Pneumococcal IgG serotypes
  • Haemophilus influenzae b IgG
  • Follow up in clinic in 6 weeks with a repeat CXR to ensure resolution
42
Q

Causes of a non-resolving pneumonia

A

CHAOS

  • Complication – empyema, lung abscess
  • Host – immunocompromised
  • Antibiotic – inadequate dose, poor oral absorption
  • Organism – resistant or unexpected organism not covered by empirical antibiotics
  • Second diagnosis – PE, cancer, organising pneumonia
43
Q

What are some of the clinical features of Tuberculosis?

A
  • Often fever and nocturnal sweats (typically drenching)
  • Weight loss (weeks – months)
  • Malaise
  • Respiratory TB: cough ± purulent sputum/ haemoptysis, may also present with pleural effusion
  • Non-Respiratory TB: Skin (erythema nodosum); Lymphadenopathy; Bone/joint; Abdominal; CNS (meningitis); Genitourinary; Miliary (disseminated); Cardiac (pericardial effusion)
44
Q

What are the risk factors of TB?

A
  • Past history of TB
  • Known history of TB contact
  • Born in a country with high TB incidence
  • Foreign travel to country with high incidence of TB
  • Immunosuppression–e.g. IVDU, HIV, solid organ transplant recipients, renal failure/ dialysis, malnutrition/ low BMI, DM, alcoholism
45
Q

What are the differential diagnosis of Haemoptysis?

A
  • Infection: Pneumonia, Tuberculosis, Bronchiectasis / CF, Cavitating lung lesion (often fungal)
  • Malignancy: Lung cancer, Metastases Haemorrhage, Bronchial artery erosion, Vasculitis, Coagulopathy
  • Others: PE
46
Q

What investigations are performed for TB?

A
  • CXR
  • Sputum acid-fast bacilli (AFB) smear
  • sputum culture
  • Bloods: FBC
  • Gastric aspirate
  • Bronchoscopy and bronchoalveolar lavage (BAL)
  • Tuberculin skin testing (TST)
  • Interferon-gamma release assays (IGRAs)
47
Q

How is respiratory TB managed?

A
  • ABCDE
  • Side room & start infection control measures
  • Productive cough: x3 sputum samples for AAFB&TB culture (early morning samples)
  • No productive cough & pulmonary TB suspected consider bronchoscopy
  • Bloods: LFTs, HIV test + Vit D levels
  • Pulmonary TB: CT chest
  • Military TB: MRI brain/spine followed by LP
  • If diagnosis between pneumonia and TB not clear: start Abx for pneumonia (CURB-65) whilst investigatingTB.
  • Pt critically unwell and high likelihood of TB (no time to wait for sputum results): start anti-TB therapy AFTER sputum samples sent.
  • Notify case to TB nurse specialists TB culture can take 6-8 weeks
48
Q

How is Latent TB diagnosed?

A
  • Mantoux test (tuberculin skin test (TST))
  • Interferon Gamma Test
49
Q

How is Pulmonary TB treated (ATT - AntiTB therapy)?

A
  • 4 antibiotics for the 1st 2 months: (RIPE) Rifampicin, Isoniazid, Pyrazinamide, Ethambutol
  • Followed by 4 months on 2 ABx: Rifampicin, Isoniazid
  • Dose of anti-TB antibiotics is weight dependent
  • Check baseline LFT’s and monitor closely
  • Check visual acuity before giving Ethambutol
  • Pyridoxine: given (while on Isoniazid) as prophylaxis against peripheral neuropathy
  • If CNS TB suspected: MRI Brain is the test of choice, more likely to identify tubercles than CT
50
Q

What are some of the major side effects of TB drugs?

A
  • Rifampicin – Hepatitis, rashes, febrile reaction, orange/red secretions (N.B. contact lenses), drug interactions w/ warfarin and OCP
  • Isoniazid – Hepatitis, rashes, peripheral neuropathy, psychosis
  • Pyrazinamide – Hepatitis, rashes, vomiting, arthralgia
  • Ethambutol – Retrobulbar neuritis

Do baseline visual acuity and LFTs

51
Q

What is CF?

A
  • Autosomal recessive disease leading to mutations in the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR).
  • This leads to a multisystem disease affecting the respiratory and GI systems
  • Characterised by thickened secretions
52
Q

How if CF diagnosed?

A
  • History of CF in a sibling OR
  • Positive newborn screening test result
  • And
    • Increased sweat chloride concentration - SWEAT TEST
    • Identification of 2 CF mutations – genotyping
    • Abnormal nasal epithelial ion transport

Other Ix:

  • Bloods: FBC, LFTs, clotting, ADEK levels, glucose TT
  • Sputum MCS
  • CXR: bronchiectasis
  • Abdo US: fatty liver, cirrhosis, pancreatitis
  • Spirometry: obstructive defect
  • Aspergillus serology / skin test (20% develop ABPA)
53
Q

How does CF present itself?

A
  1. Meconium ileus:
    • Infant bowel blocked by sticky secretions.
    • Intestinal obstruction after birth with bilious vomiting, abdominal distension and delay in passing meconium
  2. Intestinal malabsorption
    • Evident in infancy.
    • Main cause is a severe deficiency of pancreatic enzymes
  3. Recurrent Chest infections
  4. Newborn screening
54
Q

What are some of the common CF complications?

A
  1. Respiratory Infections: physio, Abx and sometimes prophylactic ABx
  2. Low Body Weight: bc of pancreatic insufficiency
  3. Distal Intestinal Obstruction Syndrome (DIOS): faecal obstruction in ileocaecum versus whole bowel. RIF mass.
  4. CF Related Diabetes
55
Q

What are the signs and sx of CF?

A
  • Nose: nasal polyps, sinusitis
  • Resp: cough, wheeze, infections, bronchiectasis, haemoptysis, pneumothorax, cor pulmonale
  • GI:
    • Pancreatic insufficiency: DM, steatorrhoea
    • Distal Intestinal Obstruction Syndrome
    • Gallstones
    • Cirrhosis (2O biliary)
  • Other: male infertility, osteoporosis, vasculitis

Signs

  • Clubbing ± HPOA
  • Cyanosis
  • Bilateral coarse creps
56
Q

What life style advice should be given to those with CF?

A
  • No smoking
  • Avoid other CF patients
  • Avoid friends / relatives with colds / infections
  • Avoid jacuzzis (pseudomonas)
  • Clean and dry nebulisers thoroughly
  • Avoid stables, compost or rotting vegetation – risk of aspergillus fumigatus inhalation
  • Annual influenza immunisation
  • Sodium chloride tablets in hot weather / vigorous exercise
57
Q

How is CF managed?

A
  • Conservative: physiotherapy
  • Pharmacological: abx, mucolytics, bronchodilators
  • GI: pancreatic enzyme replacement (CREON), give fat soluble vitamins (DEAK)
  • Other: treatment of CF related diabetes
  • Advanced lung disease: oxygen, diuretics
  • Dornase Alfa
58
Q

What is the pleural cavity?

A
  • Potential space created by pleural surfaces
  • Serous membrane that folds back on itself to give: –Outer pleura = PARIETAL (attached to chest wall) –Inner pleura = VISCERAL (covers lungs)
59
Q

What can end up in the pleural cavity?

A
  • Pneumothorax = air in pleural cavity
  • Pleural effusion = fluid in pleural cavity
  • Empyema = infected fluid in pleural cavity
  • Pleural tumours = benign vs malignant
  • Pleural plaques = discrete fibrous areas
  • Pleural thickening = scarring/ calcification causing thickening (benign vs malignant)
60
Q

What are the different types of pneumothorax?

A
  1. Spontaneous
  2. Primary (no lung disease)
  3. Secondary (lung disease)
  4. Traumatic
  5. TENSION: emergency
  6. Iatrogenic (e.g. post central line or pacemaker insertion)
61
Q

What are risk factors for pneumothorax?

A
  • Pre-existing lung disease
  • Height - Smoking/ Cannabis
  • Diving
  • Trauma/ Chest procedure
  • Connective tissue disorders: Ehlers danlos, Marfan’s syndrome
62
Q

How are pneumothorax managed?

A
  • Primary
    • <2cm rim of air: discharge and review in 2-4 weeks
    • >2cm rim of air:
      1. Aspirate (2ICSMCL) + oxygen
      2. (If aspirate unsuccessful) - Chest drain (4ICSMAL)
  • Secondary
    • <1cm air: admit for 24 hr
    • 1-2cm air: aspiration -> chest drain
    • >2cm: chest drain
63
Q

How do you deal with Pleural Effusions?

A
  • Ultrasound guided pleural aspiration
  • CXR
  • ECG
  • Bloods: FBC, U&E’s, LFT’s, CRP, Bone profile, LDH, clotting
  • ECHO (if suspect heart failure)
  • Staging CT (with contrast)
64
Q

What are the causes of transudate effusions?

A
  • Heart failure
  • Cirrhosis
  • Hypoalbuminaemia (nephrotic syndrome or peritoneal dialysis)
  • less common: Hypothyroidism, mitral stenosis, pulmonary embolism
65
Q

What is Interstitial Lung Disease?

A
  • Umbrella term describing a number of conditions that affect the lung parenchyma in a diffuse manner including:
    • Usual Interstitial Pneumonia (UIP)
    • Non-specific Interstitial Pneumonia (NSIP)
    • Extrinsic Allergic Alveolitis
    • Sarcoidosis
    • Several other conditions - Important to take a comprehensive occupational / environmental history - Typically restrictive lung diseases on PFT’s
66
Q

What investigations for interstitial lung disease?

A
  • Bloods: FBC (neutrophilia); ↑EST; ABGs; serum antibodies
    • ANA ENA Rh F ANCA Anti-GBM ACE Ig G to serum precipitins (HIV)
  • CXR: upper-zone mottling/consolidation; hilar lymphadenopathy (rare)
  • Lung function tests: Reversible restrictive defect; reduced gas transfer during acute attacks.
67
Q

What are the classification presentation findings of interstitial lung disease?

A
  • 3Cs: Clubbing, coughing, course crackles
  • Reduced chest expansion
  • Auscultation – fine inspiratory crepitations - basal / axillary areas
  • Cardiovascular – may be features of pulmonary hypertension
68
Q

What are the types of interstitial lung disease?

A
  • Sarcoidosis
  • Usual Interstitial Pneumonia (UIP)
  • Non-specific Interstitial Pneumonia (NSIP)
  • Extrinsic Allergic Alveolitis
  • Sarcoidosis
69
Q

What is Extrinsic Allergic Alveolitis?

A
  • Hypersensitivity Pneumonitis
  • Inhalation of organic antigen to which the individual has been sensitised
  • Presentation:
    • ACUTE – Alveoli are infiltrated with acute inflammatory cells
      • Short period from exposure, 4-8 hrs. reversible: spontaneously settle 1-3 days. Can recur.
    • CHRONIC – granuloma formation and obliterative bronchiolitis
      • ​Chronic exposure (months – years). Less reversible
70
Q

What are the causes of Exudate effusions?

A
  • Malignancy
  • Infections: parapneumonic, TB, HIV (kaposi’s)
  • Less common: Inflammatory (rheumatoid arthritis, pancreatitis, benign asbestos effusion, Dressler’s, pulmonary infarction/pulmonary embolus), Lymphatic disorders, Connective tissue disease
71
Q

What is Light’s criteria?

A
  • The Light’s Criteria for Exudative Effusions determines if pleural fluid is exudative
  • Use if pleural fluid protein level is between 25-35 g/L
  • Exudate if:
    • Pleural fluid/ serum protein > 0.5
    • Pleural Fluid/ Serum LDH > 0.6
    • Pleural fluid LDH > 2/3 of the upper limit of normal
72
Q

How would you investigate extrinsic allergic alveolitis? What would you see ?

A

Acute

  • Bloods: FBC, raised ESR, ABG
  • CXR:
    • Upper zone mottling/ consolidation
    • Hilar lymphadenopathy
    • Patchy, nodular infiltrates
    • Fine reticulation may also occur
  • LFTs: reversible and restrictive

Chronic

  • CXR: upper zone fibrosis, honeycomb lung,
  • LFT: persistent changes
  • BAL: increased lymphocytes and mast cells
73
Q

How would you treat Extrinsic allergic alveolitis?

A
  • Remove allergen
  • Oxygen
  • Steroids: prednisalone Po
74
Q

What are the causes of extrinsic allergic alveolitis?

A
  • Bird-fancier’s and pigeon-fancier’s lung (proteins in bird droppings).
  • Farmer’s and mushroom worker’s lung (Micropolyspora faeni, Thermoactinomyces vulgaris).
  • Malt worker’s lung (Aspergillus clavatus).
  • Bagassosis or sugar worker’s lung (Thermoactinomyces sacchari)
75
Q

What are some of the symptoms of extrinsic allergic alveolitis?

A

Fever

Chills

Malaise

Weight loss

Anorexia

Bibasalar rales/ diffuse rales

Clubbing

76
Q

What is Sarcoidosis?

A
  • Multisystem inflammatory condition of unknown cause
  • Non-caseating granulomas (Histology important)
  • Immunological response
  • Commonly involves Resp system BUT can affect nearly all organs
  • 50% get spontaneous remission, others get progressive disease
77
Q

What are the clinical features of sarcoidosis?

A
  • Acute: Erythema nodosum, Polyarthralgia
  • Sx:
    • Dry cough
    • Dyspnoea
    • Reduced exercise tolerance
    • Chest pain
    • Fatigue and arthralgia
78
Q

How is sarcoidosis investigated?

A
  • Pulmonary Function Tests: (obstructive until) fibrosis
  • CXR: 4 stages
  • Bloods: renal function, ↑ESR, lymphopenia, ↑LFTs, ↑serum ACE in ~60% (non-specific), ↑Ca2+, ↑immunoglobulins.
  • 24h urine: Urinary Calcium
  • Cardiac involvement: ECG, 24 tape, ECHO, cardiac MRI
  • CT/MRI head: headaches – Neuro sarcoid
  • Other tests: Bronchoalveolar lavage (bal), USS, Bone X Ray
79
Q

What are the four CXR stages of sarcoidosis?

A
  1. Normal
  2. BHL
  3. BHL + pulmonary infiltrates
  4. BHL - pulmonary infiltrates
  5. Fibrosis + distortion
80
Q

How do you treat sarcoidosis?

A
  • Most recover spontaneously
  • Acute: bed rest, NSAIDs
  • Corticosteroid: prednisalone (if calcium elevated, uveitis, neurological, or parenchymal involvement)
81
Q

What are the ILD Treatment Principles?

A
  • Depends on underlying pathology
  • Occupational exposure – remove
  • Drug associated – avoid
  • Stop smoking
  • ? N-Acetylcysteine ? Immunosuppressant ? Pirfenidone
  • Transplantation
  • Treatment of infections (atypical)
  • Oxygen
  • MDT
  • Palliative care
82
Q

What investigations would you perform for CF?

A
  • CXR
  • High-resolution chest CT
  • Bloods: FBC
  • Sputum culture and sensitivity

Others

  • Bronchial biopsy and electron microscopy of cilia
  • Cystic fibrosis transmembrane regulator (CFTR) protein gene mutation testing
  • Swallow study
  • pH monitoring of oesophagus
83
Q

What is bronchiecstasis?

A
  • Bronchiectasis is the permanent dilation of bronchi due to the destruction of the elastic and muscular components of the bronchial wall
  • It is often caused as a consequence of recurrent and/or severe infections secondary to an underlying disorder.
  • Pt present with a chronic cough and sputum production
84
Q

How does bronchiestasis present?

A
  • Productive cough more than 8 weeks: sputum production
  • Crackles, high-pitched inspiratory squeaks and bronchi
  • Other: fatigue, haemoptysis, rhinosinusitis, weight loss
  • Clubbing
85
Q

How is bronchiecstasis investigated?

A
  • CXR
  • High-resolution chest CT
  • Bloods: FBC, UE, CRP, Se Ig, Aspergillus precipitins, RF, α1-AT level
  • Spirometry
  • Sputum culture and sensitivity
  • Others (for cause): serum a1-antitrypsin deficiency, sweat chloride test (CF), RF (RA), HIV Ab
  • Bronchoscopy + mucosal biopsy
86
Q

What are the signs of bronchiestasis?

A
  • Clubbing
  • Coarse inspiratory creps
  • Wheeze
  • Purulent sputum
  • Cause
    • Situs inversus (+ PCD = Kartagener’s syn.)
    • Splenomegaly: immune deficiency
87
Q

What signs would indicate bronchiecstasis on a HRCT scan?

A
  • Tram-track sign
  • Signet ring sign
  • String of pearls sign
  • Cluster of grapes sign
88
Q

What are some of the common organisms causing bronchiectasis?

A
  • H Influenzae
  • Pseudomonas Aeruginosa
  • Moraxella catarrhalis
  • Fungi
  • Non tuberculous myobacterial
  • Less common - staph
89
Q

How would you manage bronchiecstasis?

A
  • Acute:
  • 1st line: exercise and nutrition,
    • Airway clearance therapy (maintenance of oral hydration, postural drainage, percussion, vibration, and the use of oscillatory devices),
    • Bronchodilator (salbutamol)
    • Mucoactive agent e.g. Nebulised hypertonic saline
  • Acute exacerbation (mild to moderate): + short term oral abx (amoxicillin) - Treatment course: 14 days.
  • Pulmonary rehab
  • Physiotherapy
  • Treat underlying cause
    • CF: DNAase
    • ABPA: Steroids
    • Immune deficiency: IVIg
90
Q

What are some of the symptoms + signs of lung cancer?

A
  • Cough
  • Chest pain
  • Haemoptysis
  • Dyspnoea
  • Weight loss
  • Hoarseness of voice
91
Q

What are some of the clinical complications of lung cancer?

A
  • Recurrent laryngeal nerve palsy; phrenic nerve palsy
  • SVC obstruction
  • Horner’s syndrome (Pancoast’s tumour)
  • Rib erosion
  • Heart: Pericarditis; AF.
  • Metastatic: brain; bone (bone pain, anaemia, ↑Ca2+); liver; adrenals (Addison’s).
  • Paraneoplastic syndrome: clubbing, hypercalcaemia, anaemia, SIADH, Cushing’s, Lambert Eaton myasthenic syndrome
92
Q

What are some of the RFs for lung cancer?

A
  • Smoking
  • Airflow obstruction
  • Age
  • FMH of lung cancer
  • Carcinogens/ occupationl exposure
93
Q

What are some of the investigations you would do for lung cancer?

A
  • Bloods: FBC, UE, CRP, LFT, Ca2+, INR
  • Cytology: sputum, pleural fluid
  • Imaging
    • CXR: peripheral nodule; hilar enlargement; consolidation; lung collapse; pleural effusion; bony secondaries
      • Staging CT (chest abdo pelvis)
    • PET scan (if MDT confirms needed) - for small mets

Histology / biopsy

  • US guided neck FNA for cytology
  • Bronchoscopy - endobronchial, transbronchial, (EBUS) endobronchial US
  • CT biopsy
  • Thoracoscopy
  • Bronchoscopic alveolar lavage (BAL)
94
Q

What is used for the treatment of Pneumocystic Jiroveci pneumonia?

A

Co-trimoxazole

95
Q

How are primary and secondary pneumothoraxes managed? Not tension

A
96
Q

What are some common causes of BHL?

A
  • Infection: TB, mycoplasma
  • Malignancy: lymphoma, carcinoma, mediastinal tumours
  • ILD: extrinsic allergic alveolitis, sarcoidosis
97
Q

When is LTOT offered to COPD patients?

A
  • p02 consistently <7.3 / 8 with cor pulmonale
  • Pt must be non smokers and not retain high levels of C02
98
Q

What are the signs of lung cancer?

A

Chest

  • Consolidation
  • Collapse
  • Pleural effusion

General

  • Cachexia
  • Anaemia
  • Clubbing and HPOA (painful wrist swelling)
  • Supraclavicular and/or axillary LNs

Metastasis

  • Bone tenderness
  • Hepatomegaly
  • Confusion, fits, focal neuro
  • Addison’s

Complications

  • Local
  • Recurrent laryngeal N. palsy
  • Phrenic N. palsy
  • SVC obstruction
  • Horner’s (Pancoast’s tumour)
  • AF

Paraneoplastic

  • Endo
  • ADH → SIADH ( euvolaemic ↓Na+)
  • ACTH → Cushing’s syndrome
  • Serotonin → carcinoid (flushing, diarrhoea)
  • § PTHrP → 1O HPT (↑Ca2+, bone pain) – SCC

Rheum - Dermatomyositis / polymyositis

Neuro

  • Purkinje Cells (CDR2) → cerebellar degeneration
  • Peripheral neuropathy

Derm

  • Acanthosis nigricans (hyperpigmented body folds)
  • Trousseau syndrome: thrombophlebitis migrans
99
Q

How is lung cancer managed?

A

NSCLC

  • Surgical Resection
    • Rx of choice for peripheral lesions c¯ no metastatic spread = stage I/II (~25%)
    • Need good cardiorespiratory function
    • Wedge resection, lobectomy or pneumonectomy
  • ± adjuvant chemo
  • Curative radiotherapy
    • If cardiorespiratory reserve is poor
    • Chemo ± radio for more advanced disease
  • Platinum-based regimens: MAbs targeting EGFR (e.g. cetuximab) or TKI (e.g. erlotinib)

SCLC

  • Typically disseminated @ presentation
  • May respond to chemo but invariably relapse

Palliation

  • Radio: bronchial obstruction, haemoptysis, bone or CNS mets
  • SVCO: stenting + radio + dexamethasone
  • Endobronchial therapy: stenting, brachytherapy
  • Pleural drainage / pleurodesis
  • Analgesia
100
Q

What Ix are used for COPD?

A
  • BMI
  • Bloods: FBC (polycythaemia), α1-AT level, ABG
  • CXR
    • Hyperinflation (> 6 ribs anteriorly)
    • Prominent pulmonary arteries
    • Peripheral oligaemia
    • Bullae
  • ECG:
    • R atrial hypertrophy: P pulmonale
    • RVH, RAD
  • Spirometry: FEV1 <80%, FEV1:FVC <0.70, ↑TLC, ↑RV
  • Echo: PHT

Year 3 Medicine (11 decks)

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