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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is Alpha 1 antitrypsin deficiency? | and what 2 organs does it affect.
* 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)
26
Pathophysiology of Alpha 1 antitrypsin Deficiency
* 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 ## Footnote Less common association * Panniculitis (tender skin nodules caused by inflammation of the subcutaneous fat) * Granulomatosis with polyangiitis (a small and medium vessel vasculitis)
27
Presentation of Alpha 1 Antitrypsin Deficiency
* 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)
28
Investigations of Alpha 1 Antitrypsin Deficiency
* Low serum alpha-1 antitrypsin (the screening test) * Genetic testing * spirometry: obstructive picture ## Footnote Liver biopsy shows periodic acid-Schiff positive staining globules in hepatocytes, resistant to diastase treatment. These represent a buildup of the mutant proteins.
29
Management of Alpha 1 Antitrypsin Deficiency
* no smoking * supportive: bronchodilators, physiotherapy * intravenous alpha1-antitrypsin protein concentrates * surgery: lung volume reduction surgery, lung transplantation
30
How is COPD -Emphysema (caused by Alpha 1 Antitrypsin Deficiency) appear on X ray
* Emphysema is most promiment in the lower lobes of the lungs with A1AT deficiency * Usually seen in upper lobes with COPD
31
What is Mesothelioma? ## Footnote Mesothelium: Thin membrane of epithelial cells which line all of body's organs as well as thoracic and abdominal cavity.
Aggresive cancer which affects the mesothelium (mesothelial layer) around the lungs and pleural cavity | linked to asbestos exposure.
32
How does Asbestos exposure cause mesothelioma?
* 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 ## Footnote Unlike smoking risk of cancer is reduced as you stop but asbestos remains dormant and unmetabolised so the risk is everpresent.
33
Presentation of Mesothelioma
* Dysnpnoea * Weight loss * Clubbing * Haemoptysis * Pleural Effusion * More common in R Lung | Metastases to contralateral lung and peritoneum ## Footnote History of asbestos exposure in 85-90%, latent period of 30-40 years
34
Investigations of Mesothelioma
* 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 ## Footnote if an area of pleural nodularity is seen on CT then an image-guided pleural biopsy may be used
35
Management of Mesothelioma
* Symptomatic * Industrial compensation * Chemotherapy, Surgery if operable * Prognosis poor, median survival 12 months
36
Define COPD and give Risk Factors for it?
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 ## Footnote Risk Factors * Smoking (biggest) * Alpha 1 antitrypsin deficiency * Pollutants like; dust, coal, cotton, cement.
37
Pathophsyiology of COPD - Chronic Bronchitis | Mucus Issue
* 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**
38
Pathophysiology of COPD - Emphysema | Structural Issue ## Footnote There are 3 types of Emphysema, which gives greater risk of pneumothorax?
* 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) ## Footnote 1. Centriacinar Emphysema 2. Panacinar Emphysema 3. Distal Acinar Emphysema - risk of **Pneumothrax**
39
Which 3 organisms are responsible for Infective Exacerbation of COPD
* With Chronic Bronchitis there is an increased risk of Pneumonia 1. Haemophilus influenzae - **MOST common** 2. Streptococcus pneumoniae 3. Moraxella catarrhalis
40
# COPD Presentation of Chronic Bronchitis & Emphysema | Bronchitis: Blue Bloater. Emphysema: Pink Puffer
**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 ## Footnote COPD doesn't cuase clubbing, haemoptysis, Chest pain.
41
What Investigations are performed for diagnosing COPD
* 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
42
Severity Grade Scale of COPD (FEV1) | 4 Grades
* 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.
43
What features of COPD are seen on a Chest X-Ray?
* Hyperinflation * Bullae - Singular Bulla (sometimes mimic Pneumothorax) * Flat hemodiaphragm * Important as CXR rules out Lung Cancer and other pathologies
44
What are the first interventions before managing COPD?
* 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
45
# Medication What steps are in the stable management of COPD? | STEPWISE ORDER
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) ## Footnote short acting beta agonist - Salbutamol short acting muscarinic antagonist - Ipratropium Bromide long acting beta agonist - Salmetarol long acting muscarinic antagonist - Tiotropium ICS - Fluticasone
46
What is the NICE criteria to determine whether patient has asthma/steroid Response
* 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%)
47
Managing Severe cases of COPD | Not Acute COPD ## Footnote after SABA SAMA LAMA LABA etc
* Oral **Theophyline** * Prophylactic Abx: **Azithromycin** * Mucolytics: **Carbocyteine** - break down mucus * Oral PDE-4 inhibitors - **Roflumilas** | Specialist cases guided by experts
48
Why is it important to monitior ECG and Liver for someone on Prophylactic Azithromycin for COPD?
* 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
49
What is criteria for Long Term Oxygen Therapy for COPD? | Falls and smoking assesment to be done prior. ## Footnote Patients who receive LTOT should breathe supplementary oxygen for at least 15 hours a day.
* 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
50
What are the complications of Long term COPD?
Hypoxaemic Vasoconstriction (increased pressure and resistance in the pulmonary arteries)-> Pulmonary Hypertension -> RV Hypertrophy -> RHF -> Cor Pulmonale. ## Footnote **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)
51
Treatment of Acute exacerbation of COPD? | Including O2 Therapy
* 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. ## Footnote 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
52
Oxygen Therapy in COPD patients in the acute setting | stepwise
- 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. ## Footnote - 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
53
When giving a patient with COPD Oxygen, what should your target levels be and why?
* 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 ## Footnote 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
ABG Interpretation for Acute COPD | pH, pO2, pCO2, HCO3-
* **Low pH** indicates acidosis * **Low pO2** indicates hypoxia and respiratory failure * **Raised pCO2** indicates CO2 retention (hypercapnia) * **Raised bicarbonate** indicates chronic retention of CO2 ## Footnote * 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
What is Bronchiectasis?
- 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. ## Footnote 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
Risk Factors of Bronchiectasis?
* 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
What is the Triad of Yellow Nail Syndrome | Pt usually well, could be OSCE station
* Bronchiectasis * Yellow Nails * Lymphoedema
58
Presentation of Bronchiectasis?
Symptoms * Persisent Chronic Productive cough - Sputum * Dyspnoea * Recurrent Chest Ix Signs * Clubbing * Cachexia - weight loss * Scattered Crackles + Wheezing (abnormal) ## Footnote Usually leads to Cor Pulmonale - due to Pulmonary HTN
59
Investigations of Bronchiectasis?
**CXR**: Ring Shadows + Tram Track Opacities **Sputum**: *H. Influenzae Pseudomonas Aerigunosa* **Gold Standard**: High Rest CT Chest
60
Management of Bronchiectasis?
* Vaccinate: Flu + Pneumococcal * Respiratory Physiotherapy: Postural drainage * Prophylctic Abx: Azithromyocin * Inspiratory Muscle Training
61
How to manage acute exacerbation of Bronchiectasis?
* 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
What are the histoglogical divisions of Lung caner
**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
How does Lung Cancer Present
* 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
What are paraneoplastic syndromes? ## Footnote 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)
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. ## Footnote Small-cell lung cancer cells contain **neurosecretory granules** that release neuroendocrine hormones. **SCLC may be responsible** for various paraneoplastic syndromes.
65
What are the paraneoplastic features of lung cancer | SCLC, Squamous Cell & Adenocarcinoma ## Footnote Give some extrapulmonary features too
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) ## Footnote 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
Referral Criteria of Lung cancer
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. ## Footnote Offer CXR for 40+ with 2 unexplained symptoms (cough, SOB, Chest pain, Fatigue) 1 unexplained symptom for 40+ Smoker
67
Investigations Lung Cancer
**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
Features of SCLC?
* usually central * arise from APUD* cells
69
Features of NSCLC?
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
Management SCLC
* 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
Management NSCLC
* 20% suitable for surger * Curative or palliative radiotherapy * poor response to chemotherapy ## Footnote **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
RESP OSCE station TIP | keep ranking as 1
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
Define Tuberculosis & Risk factors | Primary vs Secondary
* 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. ## Footnote 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
Describe myobacterium tuberculosis? | are they cultured or gram stained?
* 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
Tuberculosis Presentation
* Cough * Haemoptysis * Lethargy * Night sweats * Weight loss * Lymphadenopathy * Erythema Nodusum: Red nodules on shin * Spinal tuberculosis: Pott's disease of the spine. ## Footnote Tuberculosis typically presents with chronic, gradually worsening symptoms. Most cases involve pulmonary disease, often with systemic symptoms.
76
Pathophysiology of Tuberculosis
* Macrophages migrate to regional lymph nodes forming ghon complex * which forms Granukma with caseous necrosis in the centre * Type 4 Hypersensitivity rxn
77
What is the BCG Vaccine?
* 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 ## Footnote The vaccine protects against severe and complicated TB but less against pulmonary TB.
78
Tuberculosis Screening | Usually for Latent TB ## Footnote 2 tests
* **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
Tuberculosis Diagnosis | For Active TB
* **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. ## Footnote 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
How does Tuberculosis appear on CXR
* **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
Active Tuberculosis Management | RIPE
* Rifampicin - 6m * Isoniazid - 6m * Pyrazinamide - 2m * Ethambutol - 2m | pyridoxine/vitamin B6 co-prescribed ## Footnote * 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
Latent Tuberculosis Treatment
* 3 months of Isoniazid + pyridoxine + rifampicin OR * 6 months of Isoniazid + pyridoxine ## Footnote Pt w/ Latent disease cannot pass the disease on to others, so there is no restriction in terms of employment
83
Tuberculosis treatment side effects
**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
Where should a chest drain be placed anatomically | Safe Triangle ## Footnote * Large bore chest drains are preferred for trauma and haemothorax drainage * Smaller diameter chest drains can be used for pneumothorax or pleural effusion drainage.
* **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 ## Footnote 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
Defintion and Classification of Pneumonia | seen as consolidation on Xray
* 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 ## Footnote Can be bacterial, Viral or Fungal
86
Causes of Pneumonia | Top Causes of bacterial pneumonia
* **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
Pathophysiology & RFs of Pneumonia
* 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 ## Footnote RF * Smoking * Age <5 or >65Y * recent viral ix * COPD and CF * Immunosupressed * IV drug users
88
Presentation of Pneumonia
**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
What is CURB-65 and CRB65? | Severity Assesement for Pneumonia
* **C**onfusion * **U**rea >7mmol * **R**espiratory Rate >30pm * **B**lood Pressure <90/<60 * Age: >**65** | Usage: CRB-65 in Primary and CURB-65 in secondary care ## Footnote NICE Recommendation Home care for: 0 or 1 Hospital Care >2 Intensive Care >3 (High risk)
90
Investigations for Pneumonia | CXR Bloods ABG
**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 ## Footnote CRP < 20 mg/L - No Abx CRP 20 - 100 mg/L - consider a delayed antibiotic prescription CRP > 100 mg/L - offer antibiotic therapy
91
Management of Pneumonia | CAP & HAP
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 ## Footnote 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
What are some complications of Pneumonia
* 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
# hat What is Idiopathic Pulmonary Fibrosis | intersitial lung disease ## Footnote Fibrosis involves the replacement of elastic and functional lung tissue with non-functional scar tissue.
* 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 ## Footnote 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
Diagnosis Idiopathic Pulmonary Fibrosis
* 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 ## Footnote 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
Presentation Idiopathic Pulmonary Fibrosis
* Progressive Dyspnoea * Bibasal **fine** end inspiratory **crepitations** * Dry cough * clubbing
96
Management Idiopathic Pulmonary Fibrosis
* 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 ## Footnote Prognosis is poor. Life expectancy is around 4y
97
What is Sarcoidosis and it's epidiemiology
* 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 ## Footnote Epidemiology * Aged 20-39 or around 60 * Women * Black ethnic origin
98
Presentation of Sarcoidosis | What organs does it affect ## Footnote Lungs, Eyes, skin, Heart, Liver etc.
* **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
Syndromes associated with sarcoidosis
**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
What are the investigations for Sarcoidosis | no one diagnostic test
* **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
Management of Sarcoidosis
**Steroid treatment** - Pt with CXR stage2-3 + symptoms - Asymptoatic stage 2-3 no treatment Methotrexate second line | +Bisphosphonate bcz long term steroids ## Footnote 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
What is Pulmonary Hypertension + causes
* 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
Presentation and Investigation of Pulmonary Hypertension
* 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
Management of Pulmonary Hypertension?
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. ## Footnote Supportive treatments (e.g., oxygen and diuretics) are used for complications such as respiratory failure, oedema and arrhythmias.
105
What is Pleural effusion? | How to classify fluid?
* 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) ## Footnote 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
What are the causes of Pleural Effusion?
**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 ## Footnote 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
How does Pleural Effusion present?
* Dyspnoea * Chest Pain * Non-productive Cough * Dullness on chest percussion * Reduced Breath sounds * Tracheal Deviation (in larger effusions) * Reduced Chest Expansion
108
How to investigate Pleural Effusion?
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 ## Footnote Light's Criteria: pleural fluid protein divided by serum protein >0.5 = exudative
109
Management of Pleural Effusion
* **Conservative managemen**t 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
What is Empyema
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
What is a Pneumothorax and its classifications
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) ## Footnote Primary Spontaneous: Tall, thin, young individuals. Rupture of subpleural blebs/bullae Secondary Spontaenous: COPD, Asthma, CF, Lung cancer, Marfans Syndrome.
112
What is **Catamenial pneumothorax**
* Pneumothorax caused by endometriosis within the thorax. * 3-6% of spontaneous pneumothoraces * occurring in menstruating women.
113
Pathophysiology of **Tension** Pneumothorax | Symptoms? ## Footnote Treatment is with needle decompression and chest tube insertion.
* 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! ## Footnote Symptoms In tension pneumothorax: * respiratory distress * tracheal deviation away from the side of the pneumothorax * hypotension
114
Presentation of Pneumothorax?
Symptoms * Dyspnoea * Chest pain (pleuritic) Signs * Hyper-resonant lung percussion * Reduced breath sounds * Reduced Expansion * Tachypnoea * Tachycardia
115
Investigations of Pneumothorax
* 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. ## Footnote 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
Management of Pneumothorax
**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. ## Footnote 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
# [](http://) What is Hypersensitivity Pneumonitis | AKA **Extrinsic allergic alveolitis**
* 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
Symptoms and Management of Hypersensitivity Pneumonitis | AKA **Extrinsic allergic alveolitis**
**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 ## Footnote **Management** * avoid precipitating factors * oral glucocorticoids
119
What is Allergic bronchopulmonary aspergillosis
* 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
Coal workers' pneumoconiosis | black lung disease ## Footnote Coal worker’s pneumoconiosis makes up around 7% of all Pneumoconiosis.
* 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 ## Footnote *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
Granulomatosis w/ Polyangitis | AKA Wegner's Granulomatosis ## Footnote **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).
* 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% ## Footnote Management: - Steroids - Cyclophosphamide - Plasma Exchange - Median Survival 8-9Y
122
what diseases can asbestos exposure cause | 5 in total
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
Obstructive Sleep Apnoea | hypopnoea syndrome ## Footnote RF * obesity * macroglossia: acromegaly, hypothyroidism, amyloidosis * large tonsils * Marfan's syndrome
* 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
# POST OP What is Atelectasis and how can you resolve it
* 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 ## Footnote **Atelectasis is where a portion of the lung collapses due to under-ventilation** Management * positioning the patient upright * chest physiotherapy: breathing exercises
125
Lung Fibrosis Affecting Upper zones | 8 ## Footnote Fibrosis involves the replacement of elastic and functional lung tissue with non-functional scar tissue. Restrictive disease.
* 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
Lung Fibrosis Affecting Lower Zones | 4 ## Footnote Fibrosis involves the replacement of elastic and functional lung tissue with non-functional scar tissue. Restrictive disease.
* idiopathic pulmonary fibrosis * most connective tissue disorders (except ankylosing spondylitis) e.g. SLE * drug-induced: amiodarone, bleomycin, methotrexate * asbestosis ## Footnote 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
What is Silicosis | RF: Miners, Slate workers, Potteries, Foundries
* 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
Interpreting ABGs
129
Interpreting CXRs
130
Type 1 RF vs Type 2 RF
* Type 1 respiratory failure affects 1 value (PaO2 ↓) * Type 2 respiratory failure affects 2 values (PaO2 ↓ and PaCO2 ↑) ## Footnote Type 1: VQ Mismatches: Pneumonia, Pulmonary Oedema, Pulmonary Embolism Type 2: Hypoventilation: Exacerbation of COPD, Opiate overdose/sedation, Rib fractures, Guillain-Barré syndrome