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Year 3 > Week 8 Resp > Flashcards

Week 8 Resp Flashcards

1
Q

Alveolar and arterial O2 gradient

A

Difference between PAO2 and PO2:

2-4: normal

More indicates V/Q mismatch

Less indicates hypoventilation

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2
Q

Spirometry

A

Forced expiration from total lung capacity, followed by a full inspiration

Measures lung function

Disadvantages:

Requires trained technician

Patient is too frail, unwell

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3
Q

Obstructive lung disease

A

FEV1/FVC ratio <70% (FEV1 decreased more than FVC)

Asthma, COPD

Severity of COPD depends on %FEV1

mild = 80%

mod = 50 - 79%

severe = 30 - 49%

very severe = < 30%

If reversible by 15% and 400mL FEV1 with salbutamol then indicates asthma

Residual volume and TLC (total lung capacity) increased - air trapping

Transfer factor reduced due to emphysema

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4
Q

Asthma investigations

A

Spirometry

PEFR

Bronchial provocation - give metocholine or histamine. If there is a decrease in 20% FEV1, indicates asthma

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5
Q

Restrictive lung disease

A

Both FEV1 and FVC reduced so ratio >70%

Flow-volume loop looks same shape but smaller

Causes:

Interstitial lung disease

Kyphoscoliosos

Obesity

Gullain-Barre syndrome

Lung volumes reduced

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6
Q

Transfer factor

A

Give small amount of carbon monoxide and measure expired gas

Measures how well lungs are exchanging gas

Affected by:

alveolar surface

Hb conc

V/Q mismatch

Reduced in:

Interstitial lung disease

Emphysema

Anaemia

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7
Q
A
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8
Q

2 ways to measure residual volume

A

Residual volume - gas left after expiration

Helium dilution - spirometer contains helium, pt breathes it in and out, spirometer measures helium conc

Body plethysmography

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9
Q

Oximetry

A

Non-invasive measurement of saturation of Hb by O2

Does not measure CO2 so no measurement of ventilation

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10
Q

Main causes of hypoxaemia

A

V/Q mismatch (pneumonia, COPD)

Shunt (congenital heart disease)

hypoventialtion (drugs)

low inspired O2 (high altitude)

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11
Q

COPD (def, symptoms, pathophys, signs on CXR)

A

Progressive, non-reversible airway obstruction that does not change markedly over months

Assoc. with smoking

Genetics: Alpha-1-trypsin deficiency (serine proteinase inhibitor)

Symptoms:

Over 35, ex/smoker with:

Chronic cough, sputum production, wheeze, winter bronchitis, exertional breathlessness

Complications:

Hypoxaemia

Can lead to cor pulmonale (hypertrophy of R ventricle due to increase pulmonary hypertension)

Clinical spectrum:

Chronic bronchitis (sputum production on most days for 3 months in 2 years)

  • Leads to hyperplasia of mucus glands in larger airways, and hypersecretion of mucus
  • Chronic inflammatory infiltrate - CD8 T cells, macrophages, neutrophiles
  • Inflammation leads to scarring and thickening of airways

Small airway disease: early process in COPD

  • goblet cell hyperplasia, mucus plugging, inflammation

Emphysema (abnormal enlargment of airspaces distal to terminal bronchioles)

Centri-acinar (damage around resp bronchioles, mostly upper lobes as smoking affects upper lobes.

Pan-acinar (damage to whole acinus distal to resp bronchioles) - due to a1 anti-trypsin deficiency. More severe in lower lobes.

Leads to loss of elastic coil of alveolar sacs and airway collapse on expiration - airway trapping and hyperinflation

Decreased SA for gas exchange

Goblet cell hyperplasia, mucus plugging of lumen, inflammation of airway wall, smooth muscle hypertrophy of bronchial wall and fibrosis

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12
Q

COPD signs on CXR

A

Heart is long and thin

More ribs seen

Hemi diaphraghms are flattened

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13
Q
A
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14
Q

Assessing risk of exacerbations

A

Severity of symptoms and breathlessness

and

Severity of airflow limitation

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15
Q

Treatment COPD

A

Group A

Bronchodilator

Group B

LAMA or LABA

Group C

- LAMA

- LAMA + LABA

Group D

- LAMA + LABA

- LAMA + LABA + ICS (budesonide)

- Roflumilast or Azithromycin

SABA: salbutamol

SAMA: ipatropium bromide

LABA: salmetarol

LAMA: tiotropium

Roflumilast (phosphodiesterase inhibitor 4) - Increases intracellular cAMP, decreasing pro-inflammtory cytokines)

Azithromycin: anti- inflammatory

Carbocisteine - mucolytic, decreases sputum viscosity

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16
Q

Respiratory failure

A

Blue bloater

Type 2 resp failure

Low PO2, high PCO2

Cyanosis

R sided HF

oedema, raised JVP

Confusion

Pink puffer

Type 1 resp failure

Low PO2, low PCO2

Desaturates on exercise

Uses accessory muscles

Wheeze

Breathless

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17
Q

Allergy

A

Clinical reaction based on immunological tolerance

Requires trigger, memory and produces certain clinical features depending on which part of the immune system is activated

Upon first exposire:

IL4, IL-33 leads to activation of IgE on mast cells (immediate)

When re-exposed:

IL-12, IFN leads to activation of reactive T cell (delayed)

Chronic allergy leads to tissue remodelling

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18
Q

Allergy vs hyperreactivity

A

Hyper-reactivity: exagerated but physiological process. Dose dependent effect.

Allergy - occurs no matter the dose of stimulus

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19
Q

Asthma (definition/symptoms, pathophys)

A

Chronic inflammatory condition characterised by recurrent wheeze, breathlessness, chest tightness and cough. Assoc. with bronchoconstriction which is reversible

Patholgical features:

Muscus plugging

Smooth muscle hypertrophy

Increased airway inflammatory cells

Pathophysiology:

Immediate asthma (starts in mins, subsides in hour)

  • bronchoconstriction triggered by direct stimulation of subepithelial vagal receptors, increased mucus production

Late phase:

Follows immediate reaction, sustained airflow limitation

Inflammtion with recruitment of eosinophils, neutrophils, CD4 T cells

Inflammtory cells involved:

CD4 T helper cells: IL-4 (stimulates IgE), IL-5 (stimulates eosinphils), IL-13 (mucus secretion) - maintains allergic phenotype

Eosinophils - attracted to airways by IL-5, chemokines. Release LTC4 (leukotrienes) when activated

Mast cells - increaesd in mucus glands, produce histamine, leukotrienes

Mediators in late phase

Leukotrienes - bronchoconstriction, mucus secretion

histamine - bronchoconstriction

prostaglandins - bronchoconstriction, vasodilation

Airway remodelling in chronic asthma:

Thickening of airway wall

Epithelium - loss of ciliated columnar cells, increased no. of mucus secreeting goblet cells

Smooth muscle hypertrophy

Th1 cells, TNF-a involved

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20
Q

Extrinsic allergic alveolitis (hypersensitivity pneumonitis)

A

Immunological mediated iflammation of alveoli and resp. bronchioles due to inhaled substances

T cell mediated repsonse

Causes:

  • Farmer’s lung (moudly hay)
  • Bird fancier’s lung (due to bird dander)

Symptoms: flu-like illness, cough, high fever (4-8 hrs after exposure)

Chronic: dyspnea, sputum, weight loss

Investigations:

Avian precipitans, aspergillus precipitans

Acute:

4-6 hrs after exposure

Wheeze, cough, fever, headache

Type III hypersensitivity - antibody binds to antigen of trigger and forms immune complexes leading to inflammation

Leads to filling of alveoli with fluid - loss of O2

Sub-acute:

Type IV T cell mediated hypersensitivity

Chronic exposure leads to - pulmonary fibrosis (scarring due to tissue remodelling) and emphysema (interstitial destruction due to neutrophil enzyme release)

Microscopy: Bronchiolocentric pattern, Non-nec granulotamous inflammtion, foamy macrophages

Leads to decreaed passive diffusion between alveoli and blood vessel leading to decrease O2 transport and airspace shadowing on CXR

Management:

Avoid trigger

Corticostreroids

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21
Q

Causes of asthma

A

Atopic (extrinsic) asthma - usually starts in childhood

  • increased IgE

Non-atopic (intrinsic) - starts in middle aged, due to resp viruses, pollutants

Enviromental - hygeine hypothesis. Clean environment predisposes immune system to allergy/T helper cell repsonse. Bacteria predisposes immune system to TH1.

Triggers:

Environmental exposure: house dust mite

Occupational: non Ig E related: isocynates

Ig E related: latex

Irritants: perfume

Cold weather

Genetics: IL4/13

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22
Q

Allergen induced asthma (immediate and late phase)

A

Immediate asthma (starts in mins)

bronchoconstriction triggered by direct stimulation of vagal receptors, increased mucus production

Late-phase

Sustained airflow limitation

inflammation with recruitment of esoinophils, neutrophils, lymphocytes

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23
Q

Cells and immune mediators involved in asthma

A

Cells:

CD4 T helper cells

Eosinophils

Mast cells

Immune mediators

Leukotrienes

Histamine

Ach

Prostaglandins

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24
Q

Asthma treatment: Corticosteroids

A

Budesonide

Binds to activated glucocorticosteroid receptors to supress multiple pro-inflammatory cytokines that are activated in asthmatic airways

Up-regulates B2-adrenoceptors in airways

Indications: Asthma, COPD

Side effects: OP, cushing’s syndrome, immune suppression, thrush

Other points: Increase dose during illness, carry steroid card

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25
Q

Bronchodilators, muscarinics, methylxanthines

A

B2 agonist:

Short acting B2 adrenoceptor agonist

  • Relaxes bronchial smooth muscle, causing bronchodilation
  • Inhibits pro-inf cytokines from mast cells decreasing airway inflammation
  • Stimulates cilia action, increasing mucus clearence

Side effects: tremor, arrythmias, tachycardia, hypokalaemia

SABA: salbutamol, terbutaline

LABA: salmeterol, fometerol

Muscarinics:

Inhibits muscarinic (M1 and M3) receptors in lung leading to decreased parasympathetic mediated bronchoconstriction

Reduces mucus secretion.

Side effects: blurred vision, urinary retention, dry mouth

SAMA: ipotropium bromide

LAMA: tiotropium

Methylxanthines:

Theophylline, Aminophylline

Phosphodiesterase inhibitor - bronchial smooth muscle relaxation

Improves mucociliary clearence

Side effects: hypokalaemia, arrthymias, narrow therapeutic window

Indicated: adjunct to inhaled therapy in asthma, IV for severe exacebations

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26
Q

Leukotriene inhibitors

A

Montekulast

Inhibits LTD4 (leukotriene D4) in smooth muscle cells in airways and airway macrophages leading to smooth muscle relaxation and decreased oedema

Indicated: exercise induced asthma

27
Q

Monoclonal treatments for asthma

A

Omalizumab

Anti-IgE antibody

For persistent, severe asthma

Side effects: hypersensitivity

Mepolizumab

Anti-IL5 antibody

Reduces eosinophils

Side effects: headache

Both given sub cut

28
Q

Stepwise treatment of asthma

A

Step 1: Short acting B2 agonist (salbutamol)

Step 2: + ICS (Budesonide)

Step 3: LABA (salmeterol) + ICS

Add LRTA (Montekulast) or theophylline or oral B2 agonist

Step 4: high dose ICS + regular bronchodilator e.g. nebs, anti-muscarinics

Step 5: Steroid tablet

Omalizumbab (anti-IgE), Mepolizumab (anti-IL-5), Entanercept (Anti-TNFa)

29
Q

Asthma vs COPD (symp, investigations, treatment for exacerbations)

A

Asthma

Symptoms:

Recurring cough, wheeze, chest pain, breathlessness esp in night/early morning

Investigations:

FBC (raised eosinophils), CRP, Uand Es

Sputum (esoinophils)

PEFR

Spirometry - obstructive, imrpoves >400mL and 15% FEV1 after broncholdilator

CXR - may have pneumothorax

sputum culture - resp. viruses

ABG

Treatment for acute exacerbation

40-60% O2 aim >94% sats

Salbutamol and ipatropium bromide nebs

Prednisolone

Life threatning:

IV Mg

IV salbutamol

If pt improving:

40-60% O2, prednisolone (at least 5 days), nebs salbutamol and ipatropium

Cell type involved:

CD4 T cells (secrete IL-4, 5, 13), eosinophils, mast cells

COPD

Symptoms:

Chronic cough, sputum production, wheeze, exertional breathlessness

Investigations:

FBC (polycythaemia (increased Hb) if chronic hypoxaemia), CRP, U and Es

Sputum culture, viral gargle

Spirometry - obstructive. Little improvement after bronchodilator

CXR - hyperinflation, consolidation

Alpha 1 anti-trypsin genetic test

ABG

Treatment acute exacerbation:

24-28% O2, aim 88-92% sats

Salbutamol and ipatropium bromide nebs

Prednisolone

Antibiotics if bacterial infection e.g. purulent sputum - amoxilicillin

Non-invasive ventilation: for acidotic type II resp failiure

Cell types involved:

CD8 T cells, macrophages, neutrophils

30
Q

Pleural effusion

A

Fluid in pleural space

Clinical signs: decreased breath sounds, stony dull to percussion, decreased vocal fremitus

31
Q

CXR appearence pleural effusion vs pneumothorax

A

Pleural effusion

>300mL fluid

Generally white appearence

Blunting of costophrenic angles

Mesnicus at upper edge

Mediastinal shift away

Pneumothorax

Pleural line

Hyperlucent (dark) lung

Tracheal deviation away from affected side

Depression of hemidiapragm

32
Q

Pleural effusion vs pneumothorax

A

Pleural effusion

Accumulation of fluid in pleural cavity

Symptoms:

SOB, pleuritic chest pain, referred pain to shoulder and abdomen

Signs:

Reduced breath sounds, stony dull percussion, reduced vocal fremitus, pleural rub

Causes:

Transudative:

Cardiac failure (increased hydrostatic pressure)

Cirrhosis, hypoalbuminaemia/nephrotic syndrome (decreased oncotic pressure)

Exudative:

Pneumonia (increased vascular permeability), malignancy (decresed lymphatic drainage), TB

Investigations:

Exam, history, CXR - transudate? - treat

If not, pleural aspiration (with US).

Transudate <30 protein, <2/3 LDH ULN, clear, bilateral

Exudate >30 protein, >2/3 LDH ULN, cloudy, unilateral

Pneumothorax

Air in pleural cavity

Breach in pleural cavity leads to collapse of lung

Causes:

Traumatic - rib fracture

Iatrogenic - aspiration, pleural biopsy

Spontaenous - primary (fit, healthy, development subpleural blebs which ruptures and tears visceral pleura leading to lung collapse.

  • secondary (underlying lung disease e.g. COPD - weakness in lung tissue, CF. asthma (increased airway pressure)

Symptoms: SOB, pleuritic chest pain, resp distress

Signs:

Decreased vocal resonance, hyper-resonant to percussion, tracheal deviation if tension pneumo

Investigations:

Observe (via CXR) if small or asymptomatic

Aspiration (if >2cm in primary, or 1-2cm in secondary)

Intercostal chest drain (if >2cm in secondary)

VATS (video assisted transthoracic surgery)

Talc pleurodesis

Tension pneumo:

Medical emergency

One way valve, air enters pleural space but doesn’t leave

Decreased venous return, CO, BP

Treatment: aspiration, chest drain

Empyema

Pus in pleural cavity

Treatment: IV antibiotics, DVT prophylaxis, fibrinolytics

33
Q

Mesothelioma

A

Pirmary tumour of pleura, due to asbestos exposure

Epitheliod or sarcomatoid appearence

34
Q

Adenocarcinoma genetic testing and treatments

A

EGFR inhibitors:

Erlotinib

Cetuximab

Nivolumab - inhibits PD-L1 (receptor on tumour which binds to PD1 on T cells, stopping T cell from killing it)

ALK: Crizotinib

Inhibits ALK which inhibits EML4 ALK- fusion gene (leads to activation of tyrosine kinase, lead to cell proliferation)

35
Q

Lung cancer

A

Symptoms: cough, haemoptysis, weight loss, SOB, chest pain

Signs: finger clubbing, pleural effusion, from metastases - cervical lymphadenopathy, cahexia, Horner’s syndrome (Pancoast tumor), Cushingoid, oedema in face/arm (SVC obstruction)

Small cell carcinoma

  • Chemotherapy, radiotherapy, no surgery

Aggressive

Central

Appearence: small oval/spindle shaped cells, nuclear moudling, scant cytoplasm, finely granular nuclear chromatin (salt and pepper pattern)

Limited or extensive

Non-small cell carcicnoma

Sugery

Radiotherapy

Chemo

Squamous cell carcnioma

Central

Keratinized, intercellular bridges

Can secrete PTHrP

  • p53

Adenocarcinoma

Periphary

TTF-1 (thyroid transcription factor) positive

Glandular, mucin production

Most common in female smokers, and non-smokers

If EGFR +ve, can give EGFR inhibitors

Large cell carcinoma

Diagnosis of exclusion

Undifferentiated malignant epithelial tumour with no features of small cell, squamous or adenocarcinoma

Usually central

Carcinoid

Well diferentiated neuroendocrine tumour

Better prognosis

Yellow-brown tumor

Other treatments:

Endobronchial lasers/stents

Palliative

36
Q

Differentials pulmonary nodules and masses

A

Malignant

Bronchial carcinoma

Metastases

Benign:

Abcess

TB

Sarcoidosis

37
Q

What does the mediastinum consist of?

A

Blood vessels, trachea, oesophagus, thymus, thoracic duct, phrenic nerves

38
Q

Bilateral hilar adenopathy

A

TB

Sarcoidosis

Lyphoma

Malignancy

39
Q

UL collapse

A

Suspect malignancy

Also be mucus plug, foreign body

Golden reverse S sign

40
Q

Left lower lobe collapse

A

Sail boat sign

Can’t see left hemidiaphragm

Remainig left lung is hyperlucent (dark)

41
Q

Causes of opacification (white) lung

A

Mediastinum central:

Pleural effusion

Consolidation

Mediastinum towards:

Collapse

Pneumectomy

Mediastinum away:

Pleural effusion

42
Q
A
43
Q
A
44
Q

Common non-metastatic manifestation lung cancer

A

Weight loss

Hypercalcaemia - increased PTHrP

Cushing’s - increased ACTH

SIADH - increased ADH

Eaton-Lambert syndrome

Finger clubbing

45
Q

Emergency condition assoc. with lung cancer

A

SC compression

Symptoms: leg weakness, reduced bladder/bowel control

Signs: upper motor neuron signs in legs

Treatment: high dose steroids, radiotherapy

SVC obstruction

Symptoms: oedema in face/arms, breathless

Signs: raised JVP, dilated veins in arms

Treatment: high dose steroids, radiotherapy/chemo

46
Q

Interstitial lung disease

A

Unknown

Sarcoidosis

Idiopathic pulmonary fibrosis

Known

Occupation: Asbestos

Drugs: Nitrofurantoin, methotrexate, cocaine

Environment: Hypersensitivity pneumonitis

Connective tissue diseaes: RA, Lupus

47
Q

Sarcoidosis

A

Multi-system inflammatory disease of unknown cause, mostly of lungs and intrathoracic lymph nodes. Diagnosis of exclusion. Characterised by non-necrotising granulomatous inflammation

Causes: Borrelia Burgdorferi, TB

Symptoms:

fever, weight loss, night sweats,

SOB on exertion, cough, chest pain

Diagnosis:

FBC (anaemia), LFTs (AST/ALT high)Ca (high), serum ACE (high)

CXR:

Stage 1: Bilateral lymphadenopathy without hilar infiltration

Stage 2: Bilateral lymphadenopathy with hilar infiltration

Stage 3: infiltration

Stage 4: fibrotic bands, bullae

48
Q

Idiopathic pulmonary fibrosis (IPF)

A

Form of chornic fibrosing interstital pneumonia of unknown aetiology. Characterised by scar tissue in lungs and progressive dyspnoea.

Symptoms: progressive breatlessness, cough, bilateral crackles

Signs: weight loss, finger clubbing

Complications: cor pulmonale

Causes: Abestos, methotrexate, amiodarone, lupus, RA, sarcoid, idiopathic

Diagnosis:

Made by clinical diagnosis, with restrictive pattern and XR changes

Spirometry - restrictive diseasse (both FEV1 and FVC reduced, TLC reduced, CO gas transfer reduced)

ABG (type I resp failure)

CXR: basilar reticular opacities

High Res CT - subpleural reticular abnormalities, honey combing - thick walled cysts in bronchioles

Lung biospy - temporal heterogenity: areas of fibrosis and healthy tissue

fibroblastic foci

Macroscopically - fibrotic areas of lung - firm, rubbery, white

Pathogenesis:

Agent leads to abnormal activation of epithelial cells - abnormal repair - inflammation - formation of fibroblastic foci

Cell types involved:

Damaged epithelial cells - release TGFB1

Fibroblasts - secrete collagen

Type I pneumocytes reduced

MUC5B gene assoc with familial IPF

Treatment

Pirfenidone: anti fibrotic, anti-inflammatory

Nintedenib: inhiibtor of tyrosine kinases

Long term O2, antibiotics, lung transplant

49
Q

Obstructive sleep apnoea

A
50
Q

Obstructive sleep apnoea

A

Recurreing partial/complete airway obstruction during sleeping, leading to intermittent hypoxia

OSAS - daytime sleepliness

Symptoms:

Snoring, daytime sleepliness, fatigue, disruptive sleep, witness apnoeas

Assessment:

History (and from partner), BMI, BP, Neck circumference, craniofacial appearences

Epsworth sleepiness score

Investigations

Limited sleep polysomnography

Full polysomnography

Apnoea-hypoapnoea index: no. of apnoeas (stopping of airflow) and hypoapnoeas (reduced airflow) divded by total hrs slept

AHI >15 = diagnositc OSA

Oxygen desaturation index:

no. of times per hour that SpO2 >4% drop below baseline

Treatment:

Weight lossReduce triggers e.g. alcohol

CPAP - mask over nose directs air in, keeps airway open

Mandicbular advancement device

Sleep position traineres - vibration when pt on back to change position - for supine OSA

51
Q

Untreated OSAS

A

Increased risk of CVA

Accidents at work

RTA

Need to inform DVLA

(if without daytime sleepiness, can still drive)

52
Q
A
53
Q

Lung cancer investigations

A

FBC, CRP, LFTs, UEs

CXR

CT chest and upper abdomen - look for mets

Bronchoscopy (endoscope to see airway)

Others:

US guided aspiration biopsy of supraclavicular lymph nodes

CT-PET - look for mets

Aim of investigations:

To diagnose - whether small cell or non small cell

To stage

To assess fitness for treatment

54
Q

Investigations to assess fitness for lung cancer?

A

Lung function tests

FEV1 > 1.5L

ECG, echo - cardiac disease

55
Q

Common sites of metastasis of lung ca.

A

Lymph nodes - mediastinal (obstructs SVC), cerivcal

Liver

Bone - can cause SC compression

56
Q

None metastatic manisfestation of lung ca.

A

Metabolic

Endocrine

  • ectopic ACTH (Cushing’s)
  • ectopic ADH - water retention - hyponatraemia (sIADH)
  • PTHrP (hypercalcaemia)

Neuro - Lambert-Eaton Syndrome

57
Q

Lung ca emergencies

A

Spinal cord compression

Symptoms: leg weakness and numbness, incontinence

Signs: UMN signs in legs

SVC obstruction

  • due to mediastinal nodes, compressing SVC

Symptoms: SOB, oedema in face and arms

Signs: Raised JVP

Treatment: high dose steroids

58
Q

Type I and type II resp failure

A

Type 2 resp failure “blue bloater” - loss of CO2 sensitivity rely on hypoxic drive to stimulate breathing

Low resp drive, Low PaO2 and high PaCO2

cyanosis, flapping tremor, oedema, right sided heart failure

Type 1 resp failure “pink puffer”

High resp drive, decreased PaO2 and Pa CO2

Weight loss, pursed lip breathing, use accessory muscles,

59
Q

Long term COPD therapy

A

MRC Dyspnoea scale (assesses level of breathlessness) used to assess prognosis

Other: smoking cessation, pulmonary rehabilitation, vaccinations (influenza, pneumococcus)

Long term O2 therapy:

In COPD pts who have

PaO2 < 7.3

or 7.3 - 8 AND pulmonary oedema, pulmonary hyptertension

and non-smokers for 3 months

Resp failure: PaO2 < 8kPa on room air (21%)

60
Q

Asthma (moderate exacerbation, acute severe, life threatning, near fatal)

A

Mod exacerbation

Increasing symptoms

Acute Severe

RR >25

HR> 110

Inabiliy to complete sentences in one breathe

Life threatning

PEF <33%

Normal PaCO2

Near fatal

Raised PaCO2 and/or requires mechiancal ventilation

61
Q

COPD exacerbation definition

A

Sustained worsening of pts symptoms from usual, stable state and acute onset. Common symptoms: worsening breathlessness, increased sputum production, change in sputum colour.

Change in symptoms ususally needs change in medication

62
Q

Insterstial lung disease investigations

A

FBC, UEs, LFTs, ESR (raised in 1st hr), CRP (normal)

Immunology

ANA

ANCA

Serum ACE (sarcoidosis)

Serum immunoglobulins (raised in active sarcoid)

ABG - type 1 resp. failure

  • due to V/Q mismatch

PaCO2 normal or low (due to hypoventilation)

Six minute walk test - test desaturation

Echo - pulm hypertension

CXR - ground glass changes (increased hazy areas in lung due to alveolar wall inflammation, visible bronchial markings), irregular reticulonodular shadowing

CT - subpleural abnormalities

honeycombing (thick walled cysts in resp bronchioles)

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Year 3 (15 decks)

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