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Respiratory Flashcards

1
Q

IgE Hypersensitivity

Risk Factors Asthma

Definition

Asthma may be defined as a chronic inflammatory disorder of the airways secondary to type 1 hypersensitivity. The symptoms are variable and recurring and manifest as reversible bronchospasm resulting in airway obstruction.

A
  • FH of Atopy
  • Antenatal factors : maternal smoking, viral infection during pregnancy (especially RSV)
  • Low birth weight
  • Not being breastfed
  • Maternal smoking around child
  • Exposure to high concentrations of allergens (e.g. house dust mite)
  • Air pollution
  • ‘Hygiene hypothesis’: Studies show an increased risk of asthma and other allergic conditions in developed countries. Reduced exposure to infectious agents in childhood prevents normal development of the immune system resulting in a Th2 predominant response

Pt could suffer from hayfever (allergic rhinitis) or Eczema (dermatitis)

A number of patients with asthma are sensitive to aspirin. Patients who are most sensitive to asthma often suffer from nasal polyps

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2
Q

Presentation of Asthma

Signs & Symptoms

A

Symptoms

  • Cough (dry)
  • Dyspnea (SOB)
  • Wheeze (tight chest)

Signs

  • Expiratory wheeze on auscultation
  • Reduced Peak Expiratory Flow Rate (PEFR)

Reduced PEFR indicates a decrease in the ability to blow air out forcefully, which can be a sign of breathing difficulties

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3
Q

(aetiology)

Pathophysiology of Asthma

is it reversible or irreversible obstruction?

Epidiemologically: It affects over 10% of children and around 5-10% of adults, can also be caused by occupation.

A
  • Inhalation of Allergen or Irritant (T1 Hypersensitivity reaction)
  • Inflammation of Airway -> Bronchoconstriction/Bronchospasm -> Airflow Obstruction
  • Asthma is Reversible Obstruction (generally) caused by:
  1. Inflammatory Cells infiltration
  2. Mucus Hypersecretion - with Mucus Plug Formation
  3. Smooth Muscle Contraction
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4
Q

What is Type 1 Hypersensitivity Reaction

People susceptible to T1 hypersensitivity have excesss T Helper 2 cells

A
  • Inhalation of allergen causes release of IL 14, 12 + 5 from excess T helper 2 cells
  • IL 14 + 12 cause IgE release from Plasma cells
  • IgE causes degranulation of Mast cells
  • Mast cells release Histamines, Leukotriens, Prostglandins
  • These cause Obstruction (mentioned in Pathophysiology of Asthma Card)

Excess T helper 2 cells commonly found in Atopic Conditions

IL5 causes released of Eosinophils which cause degranulation of Mast cells

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5
Q

Pathologically what could cause Asthma to become irreversible obstruction?

Due to uncontrolled Asthma

A

Irreversible obstruction is caused by:

  • Basement Membrane Thickening
  • Collagen deposits causing Fibrosis
  • Airway Remodelling by Smooth Muscle Hyperplasia and Hypertrophy

Asthma is reversible obstruction (usually) which is caused by: 1. Inflammatory Cells 2. Mucus Hypersecretion 3. Smooth Muscle Contraction

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6
Q

What is FEV1:FVC

Separate FEV1, FVC, FEV1:FVC

What is the normal FEV1:FVC Value

A

FEV1: Force Exipratory volume in 1 second (amount of air forcefully inhaled in one second - SPEED)
FVC: Forced Vital capacity is the volume of air that can forcibly be blown out after full inspiration (AMOUNT-CAPACITY)
FEV1:FVC: is the ratio of the forced expiratory volume in the first one second to the forced vital capacity of the lungs. (How fast you can blow out to how much you store)

these are measured in L

Normal value of FEV1:FVC is above 0.75-85, though this is age dependent.

  • Values less than 0.70 are suggestive of obstruction
  • Restrictive lung diseases often produce a FEV1/FVC ratio which is either normal or higher
  • Obstruction usually has reduced FEV1 compared to normal lungs
  • Restrictive usually has normal or high FEV1 but reduced capactiy (FVC)
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7
Q

Investigations for Asthma (In Order)

Give positive results for asthma below

A
  1. Identify whether its caused occupationally (refer to specialist)
  2. Spirometry with Bronchodilator reversibility
  3. Fractional Exhaled Nitric Oxide (FeNO) -Test of Inflammation
  4. Peak Flow Variablity Diary - Usually 2 - Weeks
  5. Direct Bronchial Challenge Testing (w/ Histamine)

Results of tests
- FEV1/FVC ratio less than 70% (or below the lower limit of normal if this value is available) is considered obstructive
- Greater than 12% increase in FEV1 on reversibility testing supports a diagnosis of asthma.
- 40ppb in FeNO considered diagnostic/positive (some guidelines see FeNO as useless)
- In children perfrom spiro with broncho dilator - if spiro +ve but bronchodilator -ve then reinvestigate using FeNO
- Serial peak flow measurements at work and at home are used to detect occupational asthma

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8
Q

Long term Management of Asthma?

Mix of NICE and British Throcacic Society

Clarify MART Therapy too

A
  • Newly Diagnosed start Short acting Beta Agonist (SABA - Salbutamol)
  • If uncontrolled add inhaled corticosteroid (ICS - Fluticasone)
  • if symptoms persist then add Leukotriene Receptor Antagonist (LTRA - Montelukast)
  • If they persist then SABA + low-dose ICS + Long-acting beta agonist (LABA - Salmeterol) - continue LTRA depending on patient
  • If persisting then swap ICS/LABA for MART (see below) ( SABA +/ LTRA + MART (symbicot))
  • If they still persist then consider medium dose of MART
  • Persistence: then ditch the MART and add high dose ICS
  • Consider Theophyline or long-acting muscarinic receptor antagonist Such as Tiotropium (Theophyline can be toxic due to narrow therapeutic window)

MART: (Maintenance and reliever therapy) -
* a form of combined ICS and LABA treatment in which a single inhaler, containing both ICS and a fast-acting LABA, is used for both daily maintenance therapy and the relief of symptoms as required
* MART is only available for ICS and LABA combinations in which the LABA has a fast-acting component (for example, formoterol)

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9
Q

What are the features of Acute asthma?

what does an ABG show for Acute Asthma?

A
  • Worsening Dypnea, Wheeze, Cough, Tachypnea
  • Accessory Muscle Use
  • Salbutamol use of no or limited help
  • Usually triggered by infection, excercise, cold weather

On ABG = Respiratory Alkalosis
- Tachypnea leads to drop in CO2
- Normal or Raised CO2 or Low O2 = Respiratory Acidosis - LIFE THREATENING

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10
Q

Grading of Acute Asthma Exacerbations

3 Grades and their descriptions

A

Moderate
- PEFR 50-70%
- Speech Normal

Severe
- PEFR 33-50%
- RR >25
- HR 110bpm
- Struggling to complete sentences

Life Threatening
- PEFR <33%
- Oxygen Below 92%
- Tired, Confused, Cyanosis, Bradycardia
- No Wheeze/Silent Chest
- Haemodynamically Instablity
- pa O2 <8%

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11
Q

Management of Acute Asthma

give criteria for discharge too

Admit Pts to hospital who:
Low O2 Sats
Pregnant
History of Acute Asthma Attacks

A

Moderate

  • Inhaled Salbutamol
  • 4 dose ICS - 2weeks

Severe

  • Nebulised Salbutamol
  • Corticosteroids (50mg Oral Prednislone) or (IV hydrocortisone)

Life threatening

  • Oxygen therapy
  • Nebulised Ipratropium Bromide
  • IV Magnesium sulfate
  • IV Aminophyline (consult senior)
  • Consider intubation (for intubation start early as bronchoconstriction can cause difficulty to intubate)

Abx given if there is evidence of bacterial Ix

Criteria for discharge:
* been stable on their discharge medication (i.e. no nebulisers or oxygen) for 12–24 hours
* inhaler technique checked and recorded
* PEF >75% of best or predicted

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12
Q

How does stepping down treatment work with Asthma?

A
  • Should try and step down treatment every 3 months
  • When reducing the dose of inhaled steroids the BTS advise us to do this by 25-50% at a time.

Clearly patients with stable asthma may only have a formal review on an annual basis but it is likely that if a patient has recently had an escalation of asthma treatment they would be reviewed on a more frequent basis.

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13
Q

What causes Occupational Asthma?

and how should PEFR be measured for diagnosis?

A
  • Most Common cause : Isocyanates (Spray Paint, Foam Moulding)
  • platinum salts
  • soldering flux resin
  • glutaraldehyde
  • flour
  • epoxy resins
  • proteolytic enzymes

Serial measurements of PEFR are recommended at work and away from work.

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14
Q

How does Obstructive Lung disease differ from Restrictive Lung disease?

Give Examples of each one

A

Obstructive lung diseases involve difficulty exhaling due to narrowed airways, while restrictive lung diseases result in difficulty inhaling with reduced lung expansion, and mixed patterns may coexist.

Restrictive

  • Pulmonary fibrosis
  • Asbestosis
  • Sarcoidosis
  • Acute respiratory distress syndrome
  • Infant respiratory distress syndrome
  • Kyphoscoliosis e.g. ankylosing spondylitis
  • Neuromuscular disorders
  • Severe obesity

Obstructive

  • Asthma
  • COPD
  • Bronchieactasis
  • Bronchiolitis Obliterans
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15
Q

Define Pulmonary Emobolism

what makes up VTE?

A

Clot (thrombus) which is found in Pulmonary artery.
Usually travels from lower extremities of the body.
The thrombus will block the blood flow to the lung tissue and strain the right side of the heart

DVTs and PEs are collectively known as venous thromboembolism (VTE).

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16
Q

Risk Factors for Pulmonary Embolism?

A
  • Immobility - long haul journey/surgery
  • Pregnancy
  • HRT - Oestrogen Specificallly
  • Malignancy
  • Polycythemia
  • SLE

VTE Prophylaxis given to all hospital patients: low molecular weight heparin (Contraindication: currently bleeding or already on anticoagulation therapy)
Anti-embolic compression stockings are also used unless contraindicated (e.g., peripheral arterial disease).

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17
Q

Pathophysiology of Pulmonary Embolism

A
  • Thrombus breaks off from lower extremities travels via Inferior Vena Cava into RA -> Rv then into Pulmonary circulation
  • Thrombus blocks perfusion (Q) of CO2 + O2 in Alveoli leading to V/Q mismatch (as ventilation (V) is normal)
  • Theres an Increase in V/Q -> Increased Alveolar Arterial Gradient
  • Low O2 in blood (due to low perfusion) = Hypoxemia.
  • Hypoxemia triggers chemoreceptors in aortic/carotid bodies stimulating CNX and CNIX
  • CNX and CNIX trigger breathing centre in brain (medulla) -> Tachypnoea. (causing CO2 exhalation)
  • This in turn reduced CO2 -> Hypocapnia -> Respiratory Alkalosis
  • Pulmonary Vasoconstriction -> reduces O2 supply to lungs -> Lung Infarction -> Haemoptysis
  • Increased Afterload -> Pulmonary HTN -> RV dilation/dysfunction -> Raised JVP (as blood flows back in to superior vena cava)

Chemoreceptors for Resp, Baro receptors for Cardiac

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18
Q

Signs & Symptoms of Pulmonary Embolism

A
  • Pleuritic Chest pain
  • Dyspnoea (SOB)
  • Cough - leading to Haemoptysis
  • Tachycardia
  • Tachypnoea
  • Fever
  • Hypotension

There may also be signs and symptoms of a deep vein thrombosis, such as unilateral leg swelling and tenderness.

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19
Q

What is Virchow’s Triad and how is it linked to PE?

Presence of 3 factor that predisposes development of vascular thrombosis

A
  1. Stasis of Blood Limited movement of blood can cause clots (blood flow should be laminar)
  2. Hypercoaguability Coagulation gives rise to clots (incl. hypercoaguble conditions)
  3. Endothelial Injury Platelet aggregation causes clot formation

Causes of each below.

  1. Limited movement (planes, post-op, paralysis post CVA), Obesity; causes obstruction of veins, Pregnancy; uterus can compress iliac vein, Varicose veins; prevent flow of blood
  2. Factor V lieden, Prothrombin gene mutation, Oestrogen, Lung + Pancreatic Cancer, Nephrotic Syndrome
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20
Q

recommended by the NICE guidelines (2020)

What is the PERC rule

Pulmonary embolism rule-out criteria (PERC)

A
  • Only performed when low clinical suspiscion
  • All the criteria must be absent to have negative PERC result, i.e. rule-out PE

If suscpicion is >15% then move straight to Wells Score

Includes: Age>50, Tachypnoea, Hypoxaemia, Prev DVT, Unilateral leg swellin, haemoptysis, recent surgery, Oestrogen use.

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21
Q

What is the Well’s Score?

A
  • The Wells score predicts the probability of a patient having a PE
  • Score of > 4 PE likely
  • Score of <4 PE less likely
  • If score above 4 then perform CTPA
  • If there is a delay in getting the CTPA then interim therapeutic anticoagulation should be given until the scan is performed.
  • if CTPA -ve then perform doppler (proximal leg vein) ultrasound to rule out DVT

If score less than 4 then perform D-dimer to be on safe side

Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins) 3
An alternative diagnosis is less likely than PE 3
Heart rate > 100 beats per minute 1.5
Immobilisation for more than 3 days or surgery in the previous 4 weeks 1.5
Previous DVT/PE 1.5
Haemoptysis 1
Malignancy (on treatment, treated in the last 6 months, or palliative) 1

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22
Q

More info on Wells Card

Investigations for Diagnosing Pulmonary embolism

including gold standard

D Dimer if low wells score

A
  • All patients to have chest x-ray to exclude other pathology. (normally clear, sometimes wedge-shaped opacification seen)
  • Perform CTPA if not contraindicated
  • V/Q scan if CTPA contraindicated - RENAL DISEASE as CTPA requires contrast medium
  • Classic ECG changes seen in PE are a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III - ‘S1Q3T3’. Sinus Tachycardia - most common

CTPA is Gold Standard

things which can raise D Dimer
* Pneumonia
* Malignancy
* Heart failure
* Surgery
* Pregnancy

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23
Q

Management of Pulmonary Embolism

Outpatient for haemodynamic stable, lack of comorbidities + home support

Pulmonary Embolism Severity Index (PESI) score used to determine to treat for outpatients or inpatients

A
  • Hospital admission for some - give O2 + analgesia as required
  • 1st line DOAC (apixaban - rivoraxaban) - LMWH is alternative followed by Warfarin (Vit K antagonist)
  • Provoked PE: 3mths Treatment Unprovoked: 6mths

Haemodynamically Unstable
- Hypotension
- Begin thrombolysis with fibrinolytic such as alteplase
- alongside continuous infusion of unfractionated heparin
- risk of bleeding with thrombolysis
- thrombolysis given via peripheral canula or central catheter

ORBIT score can be used to help assess the risk of bleeding

Contraindications for DOAC include: severe renal impairment, antiphospholipid syndrome.

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24
Q

What alternative is there for Patients with constant PEs on adequate anticoagulation

A

Patients who have repeat pulmonary embolisms, despite adequate anticoagulation, may be considered for inferior vena cava (IVC) filters. These work by stopping clots formed in the deep veins of the leg from moving to the pulmonary arteries. IVC filter use is currently supported by NICE

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25
Q

What is Alpha 1 antitrypsin deficiency?

and what 2 organs does it affect.

A
  • Alpha-1 antitrypsin deficiency is a genetic condition caused by low levels of alpha-1 antitrypsin.
  • Chronic obstructive pulmonary disease and bronchiectasis in the lungs (typically after 30 years old)
  • Dysfunction, fibrosis and cirrhosis of the liver (depending on the specific genotype)
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26
Q

Pathophysiology of Alpha 1 antitrypsin Deficiency

A
  • Autosomal Co dominant condition affecting SERPINA1 gene on Chromosome 14
  • A1AT (protease inhibitor) which protects cells from enzymes (neutrophil elastase) - is now low in number or non existent
  • In lungs excess protease enzymes (elastase)-> attack connective (elastin) tissue -> bronchieactasis and emphysema
  • in liver an abnormal mutant version of A1AT is made that gets trapped and builds up inside the liver cells (hepatocytes). These are toxic to the hepatocytes ->inflammation -> fibrosis -> cirrhosis and potentially hepatocellular carcinoma.
  • Liver pathology can occur at any age, including childhood

Lungs: deficient A1AT Liver: defunct A1At

Less common association
* Panniculitis (tender skin nodules caused by inflammation of the subcutaneous fat)
* Granulomatosis with polyangiitis (a small and medium vessel vasculitis)

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27
Q

Presentation of Alpha 1 Antitrypsin Deficiency

A
  • lungs: panacinar emphysema, most marked in lower lobes
  • liver: cirrhosis and hepatocellular carcinoma in adults, cholestasis in children
  • Think of COPD picture in young nonsmoker
  • SOB, Wheeze, Mucus

panacinar: whole acinar (alveoli)

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28
Q

Investigations of Alpha 1 Antitrypsin Deficiency

A
  • Low serum alpha-1 antitrypsin (the screening test)
  • Genetic testing
  • spirometry: obstructive picture

Liver biopsy shows periodic acid-Schiff positive staining globules in hepatocytes, resistant to diastase treatment. These represent a buildup of the mutant proteins.

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29
Q

Management of Alpha 1 Antitrypsin Deficiency

A
  • no smoking
  • supportive: bronchodilators, physiotherapy
  • intravenous alpha1-antitrypsin protein concentrates
  • surgery: lung volume reduction surgery, lung transplantation
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30
Q

How is COPD -Emphysema
(caused by Alpha 1 Antitrypsin Deficiency) appear on X ray

A
  • Emphysema is most promiment in the lower lobes of the lungs with A1AT deficiency
  • Usually seen in upper lobes with COPD
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31
Q

What is Mesothelioma?

Mesothelium: Thin membrane of epithelial cells which line all of body’s organs as well as thoracic and abdominal cavity.

A

Aggresive cancer which affects the mesothelium (mesothelial layer) around the lungs and pleural cavity

linked to asbestos exposure.

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32
Q

How does Asbestos exposure cause mesothelioma?

A
  • Exposure from construction material (most cases lying dormant)
  • Asbestos material is very thin and jagged so gets into interstitial space
  • from where it gets into thin epithelial layer
  • Due to size they never get metabolised so affect individual later on in life
  • Mesothelial Plaques are formed
  • these release Calretinin - which helps differentiate mesothelioma from other cancers

* Asbestos can affect other organs elsewhere but commonly affects lungs

Unlike smoking risk of cancer is reduced as you stop but asbestos remains dormant and unmetabolised so the risk is everpresent.

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33
Q

Presentation of Mesothelioma

A
  • Dysnpnoea
  • Weight loss
  • Clubbing
  • Haemoptysis
  • Pleural Effusion
  • More common in R Lung

Metastases to contralateral lung and peritoneum

History of asbestos exposure in 85-90%, latent period of 30-40 years

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34
Q

Investigations of Mesothelioma

A
  • Chest x-ray showing either a pleural effusion or pleural thickening
  • Perform Pleural CT
  • Local anaesthetic thoracoscopy is increasingly used to investigate cytology negative exudative effusions as it has a high diagnostic yield (around 95%)

Xray in some cases shows pneumothrax

if an area of pleural nodularity is seen on CT then an image-guided pleural biopsy may be used

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35
Q

Management of Mesothelioma

A
  • Symptomatic
  • Industrial compensation
  • Chemotherapy, Surgery if operable
  • Prognosis poor, median survival 12 months
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36
Q

Define COPD and give Risk Factors for it?

A

Chronic Obstructive Pulmonary Disease is a Irreversible obstructive lung condition - umbrella term which includes both emphysema and chronic bronchitis.
* Chronic Bronchitis; inflamed airway -> excess mucus, sputum, chronic cough.
* Emphysema; Damage to the elastin -> alveoli and alveoli sacs

classed as partially reversible by some but unlike asthma

Risk Factors
* Smoking (biggest)
* Alpha 1 antitrypsin deficiency
* Pollutants like; dust, coal, cotton, cement.

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37
Q

Pathophsyiology of COPD - Chronic Bronchitis

Mucus Issue

A
  • Constant exposure to pollutant (smoking) causes Hypertrophy & Hyperplasia of Respiratory Tract
  • This causes increase in Mucus glands and Goblet cells -> More Mucus production
  • Hypertrophy + Hyperplasia -> Cilliary Dysfunction (mucus less motile) so mucus plugs airways
  • O2 can’t get through to Alveoli coz of these plugs, CO2 can’t get out = Air trapping
  • CO2 Buildup leads to V/Q mismatch due to low perfusion (Q) -> Hypercapnia + Hypoxaeimia
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38
Q

Pathophysiology of COPD - Emphysema

Structural Issue

There are 3 types of Emphysema, which gives greater risk of pneumothorax?

A
  • Pollutant (smoke) enters airways -> Macrophages phagocytose pollutant
  • Phagocytosis causes release of Cytokines and Neutrophils -> Inflammation
  • CKs & Neutrophils releaee proteases including Neutrophil Elastase -> breaks down elastin.
  • Lungs lose ability to recoil - keading to airway collapse and air trapping
    Bernoulies Principle:
  • relates to increased airflow velocity in narrowed airways, leading to decreased pressure and contributing to airway collapse due to the loss of elastic recoil in the damaged lung tissues
  • Airway Collapse -> CO2 unable to leave -> Hypercapnia + Hypoxaemia ( Develops in later stage)

  1. Centriacinar Emphysema
  2. Panacinar Emphysema
  3. Distal Acinar Emphysema - risk of Pneumothrax
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39
Q

Which 3 organisms are responsible for Infective Exacerbation of COPD

A
  • With Chronic Bronchitis there is an increased risk of Pneumonia
    1. Haemophilus influenzae - MOST common
    2. Streptococcus pneumoniae
    3. Moraxella catarrhalis
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40
Q

COPD

Presentation of Chronic Bronchitis & Emphysema

Bronchitis: Blue Bloater. Emphysema: Pink Puffer

A

Bronichitis
- Obesity
- Inspiratory Crackles
- Cyanosis

Emphysema
- Pink skin - due to pursed lip breathing
and easy to get air in but hard to get air out.
- Skinny - Weight loss

Both
- Wheezing - expiratory
- SOB - Dyspnoea
- Hyperresonance on percussion
- Increased AP diameter

severe cases, right-sided HF, may develop resulting in peripheral oedema

COPD doesn’t cuase clubbing, haemoptysis, Chest pain.

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41
Q

What Investigations are performed for diagnosing COPD

A
  • Usually Clinical Diagnosis aided with investigations
  • Post-bronchodilator spirometry to demonstrate airflow obstruction: FEV1/FVC ratio less than 70%.
  • Irreversible Obstruction so unlike asthma ratio will not improve.
  • FEV1 and FVC both low
  • Full blood count: exclude secondary polycythaemia
  • CT and CXR to rule out other modalities
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42
Q

Severity Grade Scale of COPD (FEV1)

4 Grades

A
  • Stage 1 (mild): FEV1 more than 80% of predicted
  • Stage 2 (moderate): FEV1 50-79% of predicted
  • Stage 3 (severe): FEV1 30-49% of predicted
  • Stage 4 (very severe): FEV1 less than 30% of predicted

Stage 1: Diagnosis only if Symptoms present.

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43
Q

What features of COPD are seen on a Chest X-Ray?

A
  • Hyperinflation
  • Bullae - Singular Bulla (sometimes mimic Pneumothorax)
  • Flat hemodiaphragm
  • Important as CXR rules out Lung Cancer and other pathologies
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44
Q

What are the first interventions before managing COPD?

A
  • Smoking cessation advice (nicotine patches)
  • Annual Flu Vax
  • Pneumococcal Vax
  • Pulmonary rehabilitation to all people who view themselves as functionally disabled by COPD
  • Consider Inhaler therapy after all this
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45
Q

Medication

What steps are in the stable management of COPD?

STEPWISE ORDER

A
  1. SABA + SAMA
  2. Depending on previous history (asthma/steroid) response
    - No asthmatic resposnse: LABA + LAMA (+SABA)
    - Asmatic/Steroid Response: LABA + ICS (+SABA/SAMA)

3.. LABA + LAMA + ICS inhaler (+SABA)

short acting beta agonist - Salbutamol
short acting muscarinic antagonist - Ipratropium Bromide
long acting beta agonist - Salmetarol
long acting muscarinic antagonist - Tiotropium
ICS - Fluticasone

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46
Q

What is the NICE criteria to determine whether patient has asthma/steroid Response

A
  • any previous, secure diagnosis of asthma or of atopy
  • a higher blood eosinophil count - note that NICE recommend a full blood count for all patients as part of the work-up
  • substantial variation in FEV1 over time (at least 400 ml)
  • substantial diurnal variation in peak expiratory flow (at least 20%)
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47
Q

Managing Severe cases of COPD

Not Acute COPD

after SABA SAMA LAMA LABA etc

A
  • Oral Theophyline
  • Prophylactic Abx: Azithromycin
  • Mucolytics: Carbocyteine - break down mucus
  • Oral PDE-4 inhibitors - Roflumilas

Specialist cases guided by experts

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48
Q

Why is it important to monitior ECG and Liver for someone on Prophylactic Azithromycin for COPD?

A
  • LFTs and an ECG to exclude QT prolongation should be done as azithromycin can prolong the QT interval

to be done before treatment and during

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49
Q

What is criteria for Long Term Oxygen Therapy for COPD?

Falls and smoking assesment to be done prior.

Patients who receive LTOT should breathe supplementary oxygen for at least 15 hours a day.

A
  • Hypoxia O2 <92%
  • FEV1 <30%
  • Polycythaemia
  • Cyanosis
  • Cor Pulmonale

Perform ABGx2 3wks apart
* <7.3KPA O2 = LTOT
* 7.3-8 KPA O2 (symptoms as above incl. Pulmonary HTN, Peripherall Oedema, 2ndry Polycythaemia) = LTOT

Falls because you can trip on wires and smoking because O2 is flammable

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50
Q

What are the complications of Long term COPD?

A

Hypoxaemic Vasoconstriction (increased pressure and resistance in the pulmonary arteries)-> Pulmonary Hypertension -> RV Hypertrophy -> RHF -> Cor Pulmonale.

Cor Pulmonale Presentation
* Shortness of breath
* Breathlessness of exertion
* Syncope (dizziness and fainting)
* Chest pain
* Hypoxia
* Cyanosis
* Raised JVP (due to a back-log of blood in the jugular veins)
* Peripheral oedema
* Parasternal heave
* Loud second heart sound
* Murmurs (e.g., pan-systolic in tricuspid regurgitation)
* Hepatomegaly due to back pressure in the hepatic vein (pulsatile in tricuspid regurgitation)

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51
Q

Treatment of Acute exacerbation
of COPD?

Including O2 Therapy

A
  • Nebulised SABA
  • GIve prednisolone 30 mg daily for 5 days
  • Oral antibiotics ‘if sputum is purulent or there are clinical signs of pneumonia’
  • IV hydrocortisone may sometimes be considered instead of oral prednisolone
  • IV theophyline/Aminophylline - If no response to nebuliser

often triggred by viral or bacterial Ix.

Patients with COPD are prone to develop type 2 respiratory failure. If this develops then non-invasive ventilation NIV may be used
* Typically used for COPD with respiratory acidosis pH 7.25-7.35 + PaCO2 >6

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52
Q

Oxygen Therapy in COPD patients in the acute setting

stepwise

A
  • In a normal COPD pt you would give Venturi mask which allows better control as you can deliver specific amount
  • Low SATS despite treatment then treat with High flow O2 - via Non breather mask
  • Consider NIV in patients with acute hypercapnia and unresolving hypoxaemia
  • if NIV fails consider intubation, ventilation, and ICU or whether palliative care is more appropriate.

  • Patients should have a chest x-ray before NIV to exclude pneumothorax.
  • ABGs every hour until stable then every 4 hours. - whilst on non-invasive ventillation
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53
Q

When giving a patient with COPD Oxygen, what should your target levels be and why?

A
  • COPD patients are at risk of hypercapnia - therefore an initial oxygen saturation target of 88-92% should be used
  • Adjust target range to 94-98% if the pCO2 is normal
  • Use Venturi Masks

Venturi masks are designed to deliver a specific percentage concentration of oxygen. They allow some of the oxygen to leak out the side of the mask and normal air to be inhaled along with oxygen. Environmental air contains 21% oxygen. Venturi masks deliver 24% (blue), 28% (white), 31% (orange), 35% (yellow), 40% (red) or 60% (green) oxygen.

54
Q

ABG Interpretation for Acute COPD

pH, pO2, pCO2, HCO3-

A
  • Low pH indicates acidosis
  • Low pO2 indicates hypoxia and respiratory failure
  • Raised pCO2 indicates CO2 retention (hypercapnia)
  • Raised bicarbonate indicates chronic retention of CO2

  • Low pH with a raised pCO2 suggests they are acutely retaining CO2 - Resp Acidosis
  • Raised bicarbonate indicates they chronically retain CO2 (theoretically normal pH)
    However: During an acute exacerbation, the kidneys cannot keep up with the rising level of CO2, so the blood becomes acidotic despite a raised bicarbonate.
55
Q

What is Bronchiectasis?

A
  • Permanent Dilation of the Bronchi
  • Often caused by damage (inflammation, infection) to the lungs
  • Sputum collects and organisms grow in bronchi -> chronic cough, continuous sputum production and recurrent infections.

TOM TIP: The key features to remember with bronchiectasis are finger clubbing, diagnosis by HRCT, Pseudomonas colonisation and extended courses of 7-14 days of antibiotics for exacerbations.

56
Q

Risk Factors of Bronchiectasis?

A
  • Pneumonia
  • Pertussis
  • Could be Idiopathic
  • Measels
  • Connective Tissue Disorder
  • Cystic Fibrosis
  • Yellow Nail Syndrome

The correct answer is bronchiectasis. This patient presents with chronic cough productive cough for the last three months, with occasional haemoptysis, on a background of premature birth and consequent multiple chest infections. These are characteristic features and risk factors of bronchiectasis

57
Q

What is the Triad of Yellow Nail Syndrome

Pt usually well, could be OSCE station

A
  • Bronchiectasis
  • Yellow Nails
  • Lymphoedema
58
Q

Presentation of Bronchiectasis?

A

Symptoms

  • Persisent Chronic Productive cough - Sputum
  • Dyspnoea
  • Recurrent Chest Ix

Signs

  • Clubbing
  • Cachexia - weight loss
  • Scattered Crackles + Wheezing (abnormal)

Usually leads to Cor Pulmonale - due to Pulmonary HTN

59
Q

Investigations of Bronchiectasis?

A

CXR: Ring Shadows + Tram Track Opacities
Sputum: H. Influenzae Pseudomonas Aerigunosa
Gold Standard: High Rest CT Chest

60
Q

Management of Bronchiectasis?

A
  • Vaccinate: Flu + Pneumococcal
  • Respiratory Physiotherapy: Postural drainage
  • Prophylctic Abx: Azithromyocin
  • Inspiratory Muscle Training
61
Q

How to manage acute exacerbation of Bronchiectasis?

A
  • Usually Infective Exacerbations
    1. Sputum culture
    2. Abx - extended course 7-14 days
    3. Ciprofloxacin - usually for P. Aerigunosa

Haemophilus Influenza and Pseudomonas Aeirugunosa common ones

62
Q

What are the histoglogical divisions of Lung caner

A

Small Cell Lung Cancer (20%) - worse prognosis + associated with smoking

Non Small Cell Lung Cancer (80%)
Most common
Further Divided into:
1. Adenocarcinoma - most common in non smokers
2. Squamous Cell Carcinoma - cavitating leisons
3. Large Cell Carcinoma
4. Alveolar cell carcinoma
5. Bronchial adenoma

63
Q

How does Lung Cancer Present

A
  • Dyspnoea
  • Cough
  • Haemoptysis
  • Weight loss
  • Hoarse Voice (pancoast tumour)
  • Superior Vena Cava Syndrome

Examination
- Fixed monophonic wheeze may be noted
- Lymphadenopathy (supraclavicular nodes)
- Finger clubbing

64
Q

What are paraneoplastic syndromes?

Lung cancer is associated with a lot of extrapulmonary manifestations such as paraneoplastic syndromes - such as pancoast tumours (tumour which start at the apex of the lungs)

A

Paraneoplastic syndromes are rare clinical conditions associated with specific cancers, where remote effects, such as neurological or endocrine manifestations, arise due to the production of bioactive substances by tumor cells or the host’s immune response to the tumor.

Small-cell lung cancer cells contain neurosecretory granules that release neuroendocrine hormones. SCLC may be responsible for various paraneoplastic syndromes.

65
Q

What are the paraneoplastic features of lung cancer

SCLC, Squamous Cell & Adenocarcinoma

Give some extrapulmonary features too

A

Small Cell

  • ADH secretion -> SIADH (hyponatraemia)
  • ACTH Secretion -> Cushing’s
  • Lambert-Eaton myasthenic syndrome is caused by antibodies against small-cell lung cancer cells.
  • Limbic encephalitis is caused by antibodies against small-cell lung cancer cells.

Squamous cell

  • parathyroid hormone-related protein (PTH-rp) secretion causing hypercalcaemia
  • clubbing
  • hypertrophic pulmonary osteoarthropathy (HPOA)

Adenocarcinoma

  • Gynaecomastia
  • hypertrophic pulmonary osteoarthropathy (HPOA)

Superior vena cava obstruction is a complication of lung cancer. It is caused by direct tumour compression on the superior vena cava. It presents with facial swelling, difficulty breathing, and distended neck and upper chest veins.

Pemberton’s sign is where raising the hands over the head causes facial congestion and cyanosis. SVC obstruction is a medical emergency.

Horner’s syndrome is a triad of partial ptosis, anhidrosis and miosis. It can be caused by a Pancoast tumour (tumour in the pulmonary apex) pressing on the sympathetic ganglion.

66
Q

Referral Criteria of Lung cancer

A

CXR within 2 weeks for patients:

  • Over 40
  • Clubbing
  • Lyphadenopathy
  • Recurrent Chest Ix’s
  • Chest signs of lung cancer

Urgent chest x-ray: finger clubbing and supraclavicular lymphadenopathy.

Offer CXR for 40+ with 2 unexplained symptoms (cough, SOB, Chest pain, Fatigue)
1 unexplained symptom for 40+ Smoker

67
Q

Investigations Lung Cancer

A

CXR: Hilar enlargement, peripheral opacity, pleural effusion, collapse.
CT: Investigation of choice - allows tumour staging (TMN) and to see lymph node involvement
Bronchoscopy: allows biopsy for histological diagnodid
PET Scanning: usually in NSCLC to establish treatment path
Bloods: Increased Platelets.

68
Q

Features of SCLC?

A
  • usually central
  • arise from APUD* cells
69
Q

Features of NSCLC?

A

Squamous Cell: Central
Adenocarcinoma: Typically Peripheral, most common in non smokers but most people who develop it are smokers
Large cell: Peripheral, poor prognosis ,may secrete beta hCG.

70
Q

Management SCLC

A
  • usually metastatic disease by time of diagnosis
  • patients with very early stage disease (T1-2a, N0, M0) are now considered for surgery. NICE support this approach in their 2011 guidelines
  • however, most patients with limited disease receive a combination of chemotherapy and radiotherapy
  • patients with more extensive disease are offered palliative chemotherapy
71
Q

Management NSCLC

A
  • 20% suitable for surger
  • Curative or palliative radiotherapy
  • poor response to chemotherapy

Surgery contraindications
* assess general health
* stage IIIb or IV (i.e. metastases present)
* FEV1 < 1.5 litres is considered a general cut-off point*
* malignant pleural effusion
* tumour near hilum
* vocal cord paralysis
* SVC obstruction

72
Q

RESP OSCE station TIP

keep ranking as 1

A

A thoracotomy scar in your OSCEs indicates either a lobectomy, pneumonectomy or lung volume reduction surgery for COPD.

A right-sided mini-thoracotomy incision in a cardiology station likely means minimally invasive mitral valve surgery.

Absent breath sounds on an entire side indicates a pneumonectomy.

Focal absent breath sounds suggest a lobectomy.

Lobectomies and pneumonectomies are used to treat lung cancer. Previously, they were used to treat tuberculosis, so remember this in older patients.

73
Q

Define Tuberculosis & Risk factors

Primary vs Secondary

A
  • Ix caused by Mycobacterium tuberculosis - which commonly affects lungs
  • Primary: Infection in lungs - leison called Ghon focus develops (ghon complex) - in healthy pt’s healng is via fibrosis, in imunnocompromised they may develop disseminated disease (miliary tuberculosis)
  • Seconday: Usually post-primary. latent Ix gets reactivated when pt becomes immunocompromised.
    Usually occurs in Apex of lungs but can occur in:
  • central nervous system (tuberculous meningitis - the most serious complication)
  • vertebral bodies (Pott’s disease)
  • cervical lymph nodes (scrofuloderma)
  • renal
  • gastrointestinal tract

Tuberculosis is spread by inhaling saliva droplets from infected people.

Risk Factors

  • Close contact with active tuberculosis (e.g., a household member)
  • Immigrants from areas with high tuberculosis prevalence
  • People with relatives or close contacts from countries with a high rate of TB
  • Immunocompromised (e.g., HIV or immunosuppressant medications)
  • Malnutrition, homelessness, drug users, smokers and alcoholics
74
Q

Describe myobacterium tuberculosis?

are they cultured or gram stained?

A
  • Small rod-shaped bacteria (bacillus)
  • High O2 requirement so difficult to culture in lab
  • Has a waxy coating that makes gram staining ineffective - as theyre acid fast
  • Ziehl-Neelsen Stain - Bright red on blue background is gold standard

Acid Fast bacilli

75
Q

Tuberculosis Presentation

A
  • Cough
  • Haemoptysis
  • Lethargy
  • Night sweats
  • Weight loss
  • Lymphadenopathy
  • Erythema Nodusum: Red nodules on shin
  • Spinal tuberculosis: Pott’s disease of the spine.

Tuberculosis typically presents with chronic, gradually worsening symptoms. Most cases involve pulmonary disease, often with systemic symptoms.

76
Q

Pathophysiology of Tuberculosis

A
  • Macrophages migrate to regional lymph nodes forming ghon complex
  • which forms Granukma with caseous necrosis in the centre
  • Type 4 Hypersensitivity rxn
77
Q

What is the BCG Vaccine?

A
  • Bacillus Calmette–Guérin (BCG) vaccine involves an intradermal injection of live attenuated (weakened) Mycobacterium bovis bacteria
  • Relative of M. Tuberculosis - not a diseases causer in humans
  • Creates immune response against M. Tuberculosis
  • Pt must be Mantoux: -ve
  • It is not part of the routine vaccination schedule.
  • Offered to patients at increased risk of TB, such as those from areas of high TB prevalence, with close contact with TB

The vaccine protects against severe and complicated TB but less against pulmonary TB.

78
Q

Tuberculosis Screening

Usually for Latent TB

2 tests

A
  • Mantoux test: IM of PPD - results 72h later - >15mm induration = +ve for TB
  • False -ve’s: sarcoidosis, HIV, Lymphoma so you do:
  • Inferon Gamma test: +ve result when Inferon gamma released when mixing blood sample
79
Q

Tuberculosis Diagnosis

For Active TB

A
  • CXR: Upper lobe cavitation & bilateral hilar lymphadenopathy
  • Sputum smear: 3 specimens, rapid, ziehl neels stain (red), decresed sensitivity in HIV
  • Sputum culture: can take 1-3 weeks, can assess drug sensitivity, more sensitive than smear and NAAT

Sputum culture is gold standard.

Deep cough sputum req’d. If not possible then: Sputum induction with nebulised hypertonic saline
Bronchoscopy and bronchoalveolar lavage (saline is used to wash the airways and collect a sample)

80
Q

How does Tuberculosis appear on CXR

A
  • Primary tuberculosis may show patchy consolidation, pleural effusions and hilar lymphadenopathy.
  • Reactivated tuberculosis may show patchy or nodular consolidation with cavitation (gas-filled spaces), typically in the upper zones.
  • Disseminated miliary tuberculosis gives an appearance of millet seeds uniformly distributed across the lung fields.
81
Q

Active Tuberculosis Management

RIPE

A
  • Rifampicin - 6m
  • Isoniazid - 6m
  • Pyrazinamide - 2m
  • Ethambutol - 2m

pyridoxine/vitamin B6 co-prescribed

  • Home isolation for 2 wk or based on med team advice
  • In hospitals, negative pressure rooms are used to prevent airborne spread. Negative pressure rooms have ventilation systems that actively remove air to prevent it from spreading onto the ward.
82
Q

Latent Tuberculosis Treatment

A
  • 3 months of Isoniazid + pyridoxine + rifampicin

OR

  • 6 months of Isoniazid + pyridoxine

Pt w/ Latent disease cannot pass the disease on to others, so there is no restriction in terms of employment

83
Q

Tuberculosis treatment side effects

A

Rifampicin

  • potent liver enzyme inducer
  • hepatitis
  • red/orange secretions (urine/tears)
  • flu-like symptoms

Isoniazid

  • peripheral neuropathy: prevent with pyridoxine (Vitamin B6)
  • hepatitis, agranulocytosis
  • liver enzyme inhibitor

Pyrazinamide

  • hyperuricaemia causing gout
  • arthralgia, myalgia
  • hepatitis

Ethambutol

  • optic neuritis: check visual acuity before and during treatment
84
Q

Where should a chest drain be placed anatomically

Safe Triangle

  • Large bore chest drains are preferred for trauma and haemothorax drainage
  • Smaller diameter chest drains can be used for pneumothorax or pleural effusion drainage.
A
  • Mid axillary line of the 5th intercostal space
    Bordered by:
    Anterior edge latissimus dorsi, the lateral border of pectoralis major, a line superior to the horizontal level of the nipple, and the apex below the axilla.

Inserted using anatomical guidance or through ultrasound guidance

Triangle is formed by

  • The 5th intercostal space (or the inferior nipple line)
  • The midaxillary line (or the lateral edge of the latissimus dorsi)
  • The anterior axillary line (or the lateral edge of the pectoralis major)
85
Q

Defintion and Classification of Pneumonia

seen as consolidation on Xray

A
  • Inflammory condition of the lungs (alveoli) - 2ndry to infection.
  • Community-acquired pneumonia (CAP) develops in the community
  • Hospital-acquired pneumonia (HAP) develops after more than 48 hours in a hospital
  • Ventilator-acquired pneumonia (VAP) develops in intubated patients in the intensive care unit
  • Idiopathic interstitial pneumonia: non-infective cause, e.g cryptogenic organising pneumonia developing with R Arthritis or amiodarone therapy.
  • Aspiration Pneumonia Ix develops due to aspiration of food/fluids in pt with impaired swallowing.

it’s classed as LRTI

Can be bacterial, Viral or Fungal

86
Q

Causes of Pneumonia

Top Causes of bacterial pneumonia

A
  • Streptococcus pneumoniae: 80% of cases - most common CAP- seen with Herpes labialis. AKA Pneumococcus (vaccine available)
  • Haemophilus influenzae: common in COPD
  • Staphylococcus Aureus Post Influenza Ix.
  • Mycoplasma pneumoniae atypical pneumonia (diff signs)
  • Klebsiella pneumoniae Classically seen in alcoholics
  • Pneumocystis jiroveci: patients with HIV
87
Q

Pathophysiology & RFs of Pneumonia

A
  • Pathogen enters LRT
  • Neutrophils migrate to Infected alveoli -> Relase Cytokines -> Immune response -> Inducing fever
  • This process leads to accumulation of fluid and pus.
  • impaired gaseous exchange -> hypoxia

RF

  • Smoking
  • Age <5 or >65Y
  • recent viral ix
  • COPD and CF
  • Immunosupressed
  • IV drug users
88
Q

Presentation of Pneumonia

A

Symptoms

  • Cough (purulent sputum - rusty)
  • Dyspnoea
  • Chest pain (?pleuritic)
  • Fever Malaise

Signs

  • Tachycardia, Hypotension, High temp
  • Tachypnoea (Increase RR)
  • Low O2 sats
  • Dullness on percussion (due to fluid filled lungs)
  • Reduced breath sounds ( (harsh inspiratory and expiratory breath sounds) due to consolidation around the airways)
  • Bronchial breathing & Crepitations/Crackles(caused by air passing through sputum filled airways)
89
Q

What is CURB-65 and CRB65?

Severity Assesement for Pneumonia

A
  • Confusion
  • Urea >7mmol
  • Respiratory Rate >30pm
  • Blood Pressure <90/<60
  • Age: >65

Usage: CRB-65 in Primary and CURB-65 in secondary care

NICE Recommendation
Home care for: 0 or 1
Hospital Care >2
Intensive Care >3 (High risk)

90
Q

Investigations for Pneumonia

CXR Bloods ABG

A

CXR:

  • Consolidation (opacity)
  • Effusion

Bloods:

  • FBC: Raised WCC (Ix)
  • U&E: Urea for CURB65
  • CRP: Raised. Used for monitoring to see abx response
  • Blood cultures
  • Renal Profile: Asses AKI

Sputum Sample:

  • Diagnose causative organism

CRP < 20 mg/L - No Abx

CRP 20 - 100 mg/L - consider a delayed antibiotic prescription

CRP > 100 mg/L - offer antibiotic therapy

91
Q

Management of Pneumonia

CAP & HAP

A

Low Severity:

  • Amoxicillin 5 day course
  • (macrolide/tetracycline in allergy)

Moderate/High:

  • Hospital IV treatment
  • Dual Abx therapy - Amoxicillin + Macroclide (azithromycin)
  • 7-10 day course
  • consider beta-lactamase stable penicillin such as co-amoxiclav in high severity

Discharge Criteria

  • 1 week Fever should have resolved
  • 4 weeks Chest pain and sputum production should have substantially reduced
  • 6 weeks Cough and breathlessness should have substantially reduced
  • 3 months Most symptoms should have resolved but fatigue may still be present
  • 6 months Most people will feel back to normal.
  • Repeat CXR at 6wks post treatment to assess.
92
Q

What are some complications of Pneumonia

A
  • Sepsis
  • Acute respiratory distress syndrome
  • Pleural effusion
  • Empyema
  • Lung abscess
  • Death

Post treatment bloods: C-reactive protein shows a lag in decreasing in comparison to the white cell count in treatment of acute bacterial infection

93
Q

hat

What is Idiopathic Pulmonary Fibrosis

intersitial lung disease

Fibrosis involves the replacement of elastic and functional lung tissue with non-functional scar tissue.

A
  • Pprogrsive fibrosis of interstitium of the lungs with no apparent cause
  • chronic inflammation -> fibroblasts triggered -> excess collagen + ecm protein production -> scar tissue formation -> destroys architecture and elasticity of lungs.
  • Seen in 50-70y. common in M

Restrictive Lung disease

What reduced elasticity here means excess collagen makes them more stiff so can’t take in as much gas compared to emphysema for example

94
Q

Diagnosis Idiopathic Pulmonary Fibrosis

A
  • Spirometry shows restrictive picture: Decreased FVC and Same/Decreased FEV1
  • FEV1/FVC ratio >0.8
  • CXR: bilaterla interstitial shadowing. Groundglass -> honeycomb appearance
  • High res CT: Gold standard

ANA positive in 30%, rheumatoid factor positive in 10% but this does not necessarily mean that the fibrosis is secondary to a connective tissue disease. Titres are usually low

95
Q

Presentation Idiopathic Pulmonary Fibrosis

A
  • Progressive Dyspnoea
  • Bibasal fine end inspiratory crepitations
  • Dry cough
  • clubbing
96
Q

Management Idiopathic Pulmonary Fibrosis

A
  • Pulmonary Rehab
  • Supplementary O2

Medication which may slow progression of disease.

  • Pirfenidone reduces fibrosis and inflammation through various mechanisms
  • Nintedanib reduces fibrosis and inflammation by inhibiting tyrosine kinase

Prognosis is poor. Life expectancy is around 4y

97
Q

What is Sarcoidosis and it’s epidiemiology

A
  • Multisystem disorder of unknown aetiology
  • Chronic granulomatous disorder. Granulomas are inflammatory nodules full of macrophages.
  • Usually associated with Respiratory symptoms but has others such as: erythema nodusum, lymphadenopathy

Epidemiology

  • Aged 20-39 or around 60
  • Women
  • Black ethnic origin
98
Q

Presentation of Sarcoidosis

What organs does it affect

Lungs, Eyes, skin, Heart, Liver etc.

A
  • Bilateral hilar lymphadenopathy
  • Dynspnoea, cough, malaise, wt loss
  • Erythema nodosum: inflamed nodules on the shins. (raised, red, painful)
  • Lupus pernio specific to sarcoidosis: raised purple skin lesions on cheeks and nose.
  • Hypercalcaemia
  • Lung fibrosis
  • Bundle branch block
  • Uveitis, optic neuritis
  • Liver nodues & cirrohosis
99
Q

Syndromes associated with sarcoidosis

A

Lofgren’s syndrome is an acute form of the disease characterised by bilateral hilar lymphadenopathy (BHL), erythema nodosum, fever and polyarthralgia. It usually carries an excellent prognosis

In Mikulicz syndrome* there is enlargement of the parotid and lacrimal glands due to sarcoidosis, tuberculosis or lymphoma

Heerfordt’s syndrome (uveoparotid fever) there is parotid enlargement, fever and uveitis secondary to sarcoidosis

Mikulicz syndrome likended to Sjiorgens

100
Q

What are the investigations for Sarcoidosis

no one diagnostic test

A
  • ACE used as monitoring disease activity and not diagnosis
  • Raised ESR and Ca2+

CXR

  • stage 0 = normal
  • stage 1 = bilateral hilar lymphadenopathy (BHL)
  • stage 2 = BHL + interstitial infiltrates
  • stage 3 = diffuse interstitial infiltrates only
  • stage 4 = diffuse fibrosis

spirometry: may show a restrictive defect
tissue biopsy: non-caseating granulomas

101
Q

Management of Sarcoidosis

A

Steroid treatment
- Pt with CXR stage2-3 + symptoms
- Asymptoatic stage 2-3 no treatment

Methotrexate second line

+Bisphosphonate bcz long term steroids

Self resolving within 2y for 50% patients or leads to pulmonary HTN -> fibrosis

Poor Prognosis
- insidious onset
- no erythema nodusum
- CXR Stage 3-4
- Black

102
Q

What is Pulmonary Hypertension + causes

A
  • increased resistance and pressure in the pulmonary arteries
  • causing strain on RHS of the Heart
  • Causes: Idiopathic, COPD, Fibrosis, PE, Sarcoidossis

Mean pulmonary arterial pressure >20  mmHg.

103
Q

Presentation and Investigation of Pulmonary Hypertension

A
  • Dyspnoea
  • Syncope
  • Tachycardia
  • Raised JP
  • Hepatomegaly
  • Peripheral Oedema

ECG: P pulmonale (peaked p waves). right axis deviation, RBBB
CXR: Dilated Pulmonary arteris, RV Hypertrophy
ECHO: meausure Pulmonary Artery Pressure

104
Q

Management of Pulmonary Hypertension?

A

Idiopathic

  • CCB
  • IV Prostaglandins (epoprostenol)
  • Phosphodiesterase-5 inhibitors (e.g., sildenafil)

Secondary pulmonary hypertension is managed by treating the underlying cause, such as pulmonary embolism, COPD or systemic lupus erythematosus.

Supportive treatments (e.g., oxygen and diuretics) are used for complications such as respiratory failure, oedema and arrhythmias.

105
Q

What is Pleural effusion?

How to classify fluid?

A
  • Abnormal fluid in the pleural space, other than the normal pleural fluid
  • Fluid is divided into 2 categories
    1. Transudative: lower protein content (<30g/L)
    2. Exudative: a high protein content (> 30g/L)

Pleural fluid is secreted by mesothelial cells from both pleural layers and acts to lubricate their surfaces. This lubrication reduces friction between the two layers to prevent trauma during breathing, and creates surface tension that helps maintain the position of the lungs against the thoracic wall.

106
Q

What are the causes of Pleural Effusion?

A

Exudative: (Due to Inflammation -> Proteins leaks out of tissue into pleural space)

  • Cancer
  • Pnemonia - most common
  • Tuberculosis
  • Rheumatoid Arthritis & SLE (Cnective Tissue disorders)
  • yellow nail syndrome
  • PE

Transudative: (fluid move across/shifting into pleural space)

  • Congestive HF - most common
  • Hypoalbuminaemia
  • Hypothyroidism
  • Meigs syndrome

Lights criteria used for establishing an exudative effusion using LDH

Meigs syndrome involves a triad of a benign ovarian tumour (usually a fibroma), pleural effusion and ascites. This often appears in exams. The pleural effusion and ascites resolve with the removal of the tumour.

107
Q

How does Pleural Effusion present?

A
  • Dyspnoea
  • Chest Pain
  • Non-productive Cough
  • Dullness on chest percussion
  • Reduced Breath sounds
  • Tracheal Deviation (in larger effusions)
  • Reduced Chest Expansion
108
Q

How to investigate Pleural Effusion?

A

CXR: (to be done P->A)

  • blunting of costrophrenic angle
  • fluid in lung fissures
  • larger ones will have meniscus at bottom

USS: Preferred

  • likelihood of successful pleural aspiration and is sensitive for detecting pleural fluid septations

CT:

  • Used more for Underlying causes (esp in exudative)

Pleural Fluid Analysis

  • Pleural fluid analysis requires a sample taken by aspiration or chest drain (USE USS to guide).
  • This helps establish the underlying cause by measuring the protein content, LDH, cell count, pH, glucose and microbiology testing.

can also see oesophogeal perforation

Light’s Criteria: pleural fluid protein divided by serum protein >0.5 = exudative

109
Q

Management of Pleural Effusion

A
  • Conservative management may be appropriate as small effusions will resolve with treatment of the underlying cause. More significant effusions often need aspiration or drainage.
  • Pleural aspiration involves sticking a needle through the chest wall into the effusion and aspirating the fluid. Aspiration can temporarily relieve the pressure, but the effusion may recur, and further drainage may be required.
  • Chest drain can be used to drain the effusion and prevent it from recurring.
110
Q

What is Empyema

A

Empyema refers to an infected pleural effusion. Suspect an empyema in a patient with improving pneumonia but a new or ongoing fever.

  • Pleural aspiration shows pus, low pH, low glucose and high LDH.
  • if the fluid is clear but the pH is less than 7.2 in patients with suspected pleural infection a chest tube should be placed

Empyema is treated with a chest drain and antibiotics.

111
Q

What is a Pneumothorax and its classifications

A

Accumulation of air in the pleural space - resulting in partial or complete collapse of lung.
Spontaneous Pneumothorax
- Primay (no disease)
- Secondary (underlying disease)

Traumatic Pneumothorax (result of trauma)
Iatrogenic Pneumothorax (Complication of throcentesis, CV cathetar, ventilation- invasive and non, biopsy of lung)
Tension Pneumothorax (severe pneumothorax resulting in respiratory distress and haemodynamic collapse)

Primary Spontaneous: Tall, thin, young individuals. Rupture of subpleural blebs/bullae
Secondary Spontaenous: COPD, Asthma, CF, Lung cancer, Marfans Syndrome.

112
Q

What is Catamenial pneumothorax

A
  • Pneumothorax caused by endometriosis within the thorax.
  • 3-6% of spontaneous pneumothoraces
  • occurring in menstruating women.
113
Q

Pathophysiology of
Tension Pneumothorax

Symptoms?

Treatment is with needle decompression and chest tube insertion.

A
  • Caused by Trauma
  • Air enters pleural space on inspiration
  • Trauma forms parenchymal flap - which prevents air from leaving during expiration by forming one way valve.
  • Rise in pressure causes shift of organs in mediastinum (trachea deviation)
  • This can lead to respiratory distress then cardioresp arrest

More dangerous as air enters but does not leave pleural space!

Symptoms In tension pneumothorax:
* respiratory distress
* tracheal deviation away from the side of the pneumothorax
* hypotension

114
Q

Presentation of Pneumothorax?

A

Symptoms

  • Dyspnoea
  • Chest pain (pleuritic)

Signs

  • Hyper-resonant lung percussion
  • Reduced breath sounds
  • Reduced Expansion
  • Tachypnoea
  • Tachycardia
115
Q

Investigations of Pneumothorax

A
  • CXR: Diagnostic, There will be a line demarcating the edge of the lung where the lung markings end and the pneumothorax begins.
  • CT Thorax: can detect a pneumothorax that is too small to be seen on a chest x-ray. It can also be used to assess the size of the pneumothorax accurately.

Measuring the size of the pneumothorax on a chest x-ray can be done according to the BTS guidelines (2010). This involves measuring horizontally from the lung edge to the inside of the chest wall at the level of the hilum.

116
Q

Management of Pneumothorax

A

Primary:

  • If rim <2cm + no dyspnoea: self limiting
  • if rim <2cm + symptoms: Aspiration
  • > 2cm Rim - Chest drain.

Secondary:

  • Rim >2cm + 50y+ + SOB -> chest drain
  • 1-2cm Rim: Aspiration
  • If fails -> Chest drain + O2
  • <1cm Rim: resolve with O2

Recurrent Pneumothoraces

  • video-assisted thoracoscopic surgery (VATS)
  • for mechanical/chemical pleurodesis +/- bullectomy.

Discharge Advice
Smoking: Avoid smoking (risk is 10% more than normal non smoker)
Flying: 1 week post chest xray you can fly
Scuba diving: Complete ban unless patient’s had bilateral surgical pleurectomy and has post-op CT to determine that and lung function.

117
Q

What is Hypersensitivity Pneumonitis

AKA Extrinsic allergic alveolitis

A
  • Hypersensitivity induced lung damage
  • Caused by immunune mediated tissue damage - T3 Hypersensitivity rxn
  • inhalation of organic particles like: Bird Breeders Lungs (avian proteins from dropping), Farmers lungs (saccharoppolyspara R from wet hay), Malt Workers Lung’s (Aspergiuls), Mushroom Workers.

delayed hypersensitivity (type IV) is also thought to play a role

118
Q

Symptoms and Management of Hypersensitivity Pneumonitis

AKA Extrinsic allergic alveolitis

A

Acute (occurs 4-8 hrs after exposure)

  • dyspnoea
  • dry cough
  • fever

Chronic (occurs weeks-months after exposure)

  • lethargy
  • dyspnoea
  • productive cough
  • anorexia and weight loss

Investigations

  • Upper/midzone fibrosis (CXR)
  • High Lymphocyte count in Brochoalveolar lavage.
  • No Eosinophilla
  • IgG +ve when compared

Management
* avoid precipitating factors
* oral glucocorticoids

119
Q

What is Allergic bronchopulmonary aspergillosis

A
  • Allergy to Aspergilus Spores
  • Bronchoconstriction: Wheeze, Cough, Dyspnoea
  • Proximal Bronchieactasis
  • Mislabled as asthma
  • Bloods show Eosinophila
  • RAST test +ve
  • Raised IgE
  • Managed with oral glucocorticoids (prednislone)
120
Q

Coal workers’ pneumoconiosis

black lung disease

Coal worker’s pneumoconiosis makes up around 7% of all Pneumoconiosis.

A
  • interstitial lung disease caused by Long term exposure to coal particles
  • Macrophages (usually involved in removing dust particles) begin to accumulate in the alveoli over time, which starts an immune response, causing damage to the lung tissue.
  • Dust exposure causes patients to develop round fibrotic masses
  • Avoid exposure to coal dust and other respiratory irritants (e.g. Smoking).
    Manage symptoms of chronic bronchitis

*Pneumoconiosis = accumulation of dust in the lungs and the response of the bodily tissue to its presence, most commonly used in relation to coal worker’s pneumoconiosis.

121
Q

Granulomatosis w/ Polyangitis

AKA Wegner’s Granulomatosis

necrotizing granulomatous vasculitis
Blood vessel inflammation (vasculitis) leads to the formation of clusters of immune cells (granulomas - usually macrophages), often associated with tissue death (necrotizing).

A
  • Autoimmune condition affecting URT, LRT and Kidneys
  • Epistaxis, sinusitis, nasal crusting, haemoptysis, dyspnoea, glomerulonephritis
  • Saddle shape nose deformity
  • cANCA +ve in 90%
  • pANCA +ve in 25%

Management:
- Steroids
- Cyclophosphamide
- Plasma Exchange
- Median Survival 8-9Y

122
Q

what diseases can asbestos exposure cause

5 in total

A
  1. Pleural Plaques - Benign (ghosts on Xray) - no follow up required
  2. Pleural Thickening
  3. Asbestosis - SOB, Clubbing, End Insp Crackeles, Conservative management
  4. Mesothelioma
  5. Lung Cancer
123
Q

Obstructive Sleep Apnoea

hypopnoea syndrome

RF
* obesity
* macroglossia: acromegaly, hypothyroidism, amyloidosis
* large tonsils
* Marfan’s syndrome

A
  • Day time somnolence (drowsiness)
  • Resp acidosis + HTN
  • Epworth Sleep Scale - Assesment
  • Sleep Studies - Diagnositic
  • Wt loss, CPAP - Management
  • DVLA to be indormed if excess daytime sleepiness
124
Q

POST OP

What is Atelectasis and how can you resolve it

A
  • Common postoperative complication in which basal alveolar collapse can lead to respiratory difficulty. It is caused when airways become obstructed by bronchial secretions.
  • It should be suspected in the presentation of dyspnoea and hypoxaemia around 72 hours postoperatively

Alveoli deflation

Atelectasis is where a portion of the lung collapses due to under-ventilation
Management
* positioning the patient upright
* chest physiotherapy: breathing exercises

125
Q

Lung Fibrosis Affecting Upper zones

8

Fibrosis involves the replacement of elastic and functional lung tissue with non-functional scar tissue. Restrictive disease.

A
  • hypersensitivity pneumonitis (also known as extrinsic allergic alveolitis)
  • coal worker’s pneumoconiosis/progressive massive fibrosis
  • silicosis
  • sarcoidosis
  • ankylosing spondylitis (rare)
  • histiocytosis
  • tuberculosis
  • radiation-induced pulmonary fibrosis (may develop following radiotherapy for breast or lung cancer, typically seen between 6 and 12 months following completion of radiotherapy course)
126
Q

Lung Fibrosis Affecting Lower Zones

4

Fibrosis involves the replacement of elastic and functional lung tissue with non-functional scar tissue. Restrictive disease.

A
  • idiopathic pulmonary fibrosis
  • most connective tissue disorders (except ankylosing spondylitis) e.g. SLE
  • drug-induced: amiodarone, bleomycin, methotrexate
  • asbestosis

HEARTS (upper):
- Histiocytosis
- Extrinsic allergic alveolitis
- Ankylosing spondylitis
- Radiation
- Tuberculosis
- Sarcoidosis & silicosis

RAID (lower):
- Rheumatoid arthritis
- Asbestosis
- Idiopathic
- Drugs (amiodarone, cyclophosphamide, methotrexate, bleomycin, nitrofurantoin, hydralazine)

127
Q

What is Silicosis

RF: Miners, Slate workers, Potteries, Foundries

A
  • Fibrosing lung disease coz of inhalation of crystalline silicon dioxide (silica)
  • Can lead to TB - silica is toxic to macrophages)
  • EGG shell calcification of hilar lymph nodes on CXR
  • Upper zone fibrosis
128
Q

Interpreting ABGs

A
129
Q

Interpreting CXRs

A
130
Q

Type 1 RF vs Type 2 RF

A
  • Type 1 respiratory failure affects 1 value (PaO2 ↓)
  • Type 2 respiratory failure affects 2 values (PaO2 ↓ and PaCO2 ↑)

Type 1: VQ Mismatches: Pneumonia, Pulmonary Oedema, Pulmonary Embolism
Type 2: Hypoventilation: Exacerbation of COPD, Opiate overdose/sedation, Rib fractures, Guillain-Barré syndrome

Main Conditions (15 decks)

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