Week 8 Resp Flashcards

(63 cards)

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
Bronchodilators, muscarinics, methylxanthines
**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
26
Leukotriene inhibitors
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
Monoclonal treatments for asthma
**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
Stepwise treatment of asthma
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)
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Asthma vs COPD (symp, investigations, treatment for exacerbations)
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
Pleural effusion
Fluid in pleural space Clinical signs: decreased breath sounds, stony dull to percussion, decreased vocal fremitus
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CXR appearence pleural effusion vs pneumothorax
**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
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Pleural effusion vs pneumothorax
**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
Mesothelioma
Pirmary tumour of pleura, due to asbestos exposure Epitheliod or sarcomatoid appearence
34
Adenocarcinoma genetic testing and treatments
**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
Lung cancer
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
Differentials pulmonary nodules and masses
**Malignant** Bronchial carcinoma Metastases **Benign:** Abcess TB Sarcoidosis
37
What does the mediastinum consist of?
Blood vessels, trachea, oesophagus, thymus, thoracic duct, phrenic nerves
38
Bilateral hilar adenopathy
TB Sarcoidosis Lyphoma Malignancy
39
UL collapse
Suspect malignancy Also be mucus plug, foreign body Golden reverse S sign
40
Left lower lobe collapse
Sail boat sign Can't see left hemidiaphragm Remainig left lung is hyperlucent (dark)
41
Causes of opacification (white) lung
**Mediastinum central:** Pleural effusion Consolidation **Mediastinum towards:** Collapse Pneumectomy **Mediastinum away:** Pleural effusion
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Common non-metastatic manifestation lung cancer
Weight loss Hypercalcaemia - increased PTHrP Cushing's - increased ACTH SIADH - increased ADH Eaton-Lambert syndrome Finger clubbing
45
Emergency condition assoc. with lung cancer
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
Interstitial lung disease
Unknown Sarcoidosis Idiopathic pulmonary fibrosis Known Occupation: Asbestos Drugs: Nitrofurantoin, methotrexate, cocaine Environment: Hypersensitivity pneumonitis Connective tissue diseaes: RA, Lupus
47
Sarcoidosis
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
Idiopathic pulmonary fibrosis (IPF)
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
Obstructive sleep apnoea
50
Obstructive sleep apnoea
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
Untreated OSAS
Increased risk of CVA Accidents at work RTA Need to inform DVLA (if without daytime sleepiness, can still drive)
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53
Lung cancer investigations
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
Investigations to assess fitness for lung cancer?
Lung function tests FEV1 \> 1.5L ECG, echo - cardiac disease
55
Common sites of metastasis of lung ca.
Lymph nodes - mediastinal (obstructs SVC), cerivcal Liver Bone - can cause SC compression
56
None metastatic manisfestation of lung ca.
Metabolic Endocrine - ectopic ACTH (Cushing's) - ectopic ADH - water retention - hyponatraemia (sIADH) - PTHrP (hypercalcaemia) Neuro - Lambert-Eaton Syndrome
57
Lung ca emergencies
**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
Type I and type II resp failure
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,
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Long term COPD therapy
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
Asthma (moderate exacerbation, acute severe, life threatning, near fatal)
**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
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COPD exacerbation definition
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
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Insterstial lung disease investigations
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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