Respiratory Part 2 Flashcards

1
Q

Explain what TB is?

A
  • Tuberculosis is a bacterial infection by mycobacterium tuberculosis which are bacilli
  • Although most commonly TB symptoms are in the lungs TB can affect all systems
  • TB does not gram stain because the bacteria has a waxy coating
  • Infection of TB is by inhalation
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2
Q

7 groups who are at higher risk of TB infection?

A
  • Known contact with active TB
  • Immigrants from areas of high TB prevalence
  • People with relatives or close contacts from countries with a high rate of TB
  • Immunocompromised individuals e.g. HIV, those on immunosuppressive medication
  • Homeless
  • PWID
  • Alcoholics
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3
Q

Describe primary infection with TB?

A
  • Primary infection occurs in those who have not been previously exposed to TB or vaccinated against it
  • A small Ghon focus at the periphery of the lung is the site of infection and there is lymphatic spread to the hilar lymph nodes, some caseous masses may form
  • In most patients the lesions undergo fibrosis or calcification and heal
  • Spread however can occur

Side note: unclear whether you can entirely clear TB from your body after initial infection or if everyone who gets TB goes on to develop latent TB

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4
Q

Describe and explain 4 types of TB?

A
  • Active TB – active infection in various areas within the body
  • Latent TB – immune system encapsulates sites of infection and stops progression – no symptoms but bacteria remain (can remain for years) and can be reactivated
  • Secondary TB – this is when latent TB reactivates, this only occurs if immunocompromised in some way e.g. elderly, HIV, alcoholic, diabetic, immunosuppressant medication
  • Miliary TB – occurs when the immune system is unable to control the disease and it is disseminated and severe
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5
Q

What is a ghon focus?

A

a lesion in the lung that is the site of primary TB infection, they are usually subpleural and predominantly in upper or middle lobe

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6
Q

Presentation of active TB?

A
  • Productive cough (sometimes haemoptysis)
  • Weight loss
  • Fever
  • Night sweats (red flag symptom for TB)
  • Loads of symptoms of TB at other sites
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7
Q

Describe the 2 screening tests for immune response to TB?

A
  • Mantoux test – inject tuberculin (TB proteins) into skin, look for reaction after 72 hours – test will be positive in someone with BCG vaccine, active or latent TB
  • Interferon gamma release assay (IGRA) – blood test looking to see if WBC release interferon gamma in response to TB antigens – this is not affected by BCG vaccine and if positive means latent or active TB
  • Mantoux test is generally done first and then if that is positive you get the IGRA test
  • Those who have a positive Mantoux and IGRA should be assessed for symptoms of active TB and go on to have a CXR to check
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8
Q

Appearance of TB on chest xray?

A
  • Primary TB– patchy consolidation, pleural effusions, hilar lymphadenopathy
  • Reactivated – patchy or nodular consolidation with cavitation
  • Disseminated – miliary TB- millet seeds distributed throughout the lung fields
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9
Q

Staining for TB?

A
  • Ziehl Neelsen staining is traditionally used on sputum samples – it stains acid fast bacilli – i.e. mycobacterium bright red against a blue background
  • Auramine staining is a newer fluorescent dye that is more sensitive
  • These stains can be used on direct smear or on paraffin sections or cultures that have taken time to grow
  • Direct smear testing will provide rapid results but you need a higher bacterial load to see results so it won’t pick up everyone
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10
Q

Describe cultures for TB?

A

Taking cultures allows you to test for resistance however they can take months to grow so treatment is usually started before results are back
also allows you to identify subtypes
Can take:
1. Sputum samples – if patient producing sputum this is easy if not may need to do bronchoalveolar lavage (during bronchoscopy saline solution put through bronchoscope to wash airways and catch a fluid sample)
2. Blood cultures – need special TB blood culture bottle for this
3. Lymph node aspiration/ biopsy

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11
Q

Biopsy for TB shows?

A

caseating granulomas

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12
Q

Investigation overview for TB?

A

Pathology - caseating granulomas

Microbiology
Stain for AFB - presence of mycobacterium
PCR/ NAAT - specific for TB and can also show if rifampicin resistant TB but can pick up dead bacteria
culture - for acuity and further sensitivities - culture takes weeks

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13
Q

Describe management other than drug treatment that should be done in TB?

A
  • Overall management involves informing public health and contact tracing
  • Anyone with active TB needs isolated to avoid spread until established on treatment (usually 2 weeks)
  • Those with TB should also be tested for HIV, Hepatitis B and C
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14
Q

Describe treatment of latent TB?

A
  • These patients don’t necessarily need treatment and are not contagious
  • However, it is recommended due to risk of developing active TB later in life if/ when they may become immunocompromised
  • Treatment of latent TB involves isoniazid and rifampicin for 3 months and isoniazid for a further 3 months
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15
Q

Describe treatment of active TB?

A
  • 2RIPE4RI
  • 2 months of rifampicin, isoniazid, pyranzamide and ethambutol, 4 months of only rifampicin and isoniazid
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16
Q

Describe all the side effects of TB drugs?

A
  • Rifampicin turns body secretion orange/ pink, it is also a potent inducer of cytochrome P450 meaning it reduces the effectiveness of a number of drugs including the COCP
  • Isoniazid causes peripheral neuropathy and should be co-prescribed with pyridoxine (vitamin B6)
  • Pyranzamide can cause hyperuricaemia and gout
  • Ethambutol can cause colour blindness and reduced visual acuity
  • Rifampicin, isoniazid and pyranzamide are all associated with hepatotoxicity
  • Redandorange-picin, isonumbizid, eye-thambutol, pyranzamide (p for painful joints)
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17
Q

What TB drug turns body secretions orange/ pink?

A

rifampicin

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18
Q

What should isoniazid be co-prescribed with and why?

A

pyridoxine (vitamin B6) - because isoniazid causes peripheral neuropathy and this reduces risk of this developing

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19
Q

What TB drug can cause gout?

A

pyranzamide

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20
Q

What TB drug can cause colour blindness and reduced visual acuity?

A

ethambutol

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21
Q

List the 3 TB drugs associated with hepatotoxicity?

A

rifampicin, isoniazid and pyranzamide

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22
Q

List the components of Virchows triad?

A
  • The three main factors leading to thrombus are known as virchows triad: alteration of blood flow (stasis), changes in the composition of blood (hypercoagulability) and endothelial damage
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23
Q

Explain what a pulmonary embolism is?

A
  • Blood clot that forms in the pulmonary arteries usually as a result of a DVT in the legs that has embolised
  • Once in the pulmonary artery flow to the lung tissue is blocked and there is also strain put on the right side of the heart due to this blockage
  • This can cause ischaemia and infarction of lung tissue
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24
Q

List 9 risk factors for VTE?

A
  • Immobility
  • Recent surgery
  • Long haul flights
  • Pregnancy
  • Oestrogen therapy e.g. HRT or COCP
  • Malignancy
  • Polycythaemia
  • SLE and other inflammatory conditions
  • Thrombophilias e.g. anti-phospholipid syndrome, factor V Leiden, protein C deficiency, protein S deficiency etc.
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25
Q

Describe presentation of PE?

A

DVT: swelling in one leg, throbbing or cramping pain, red or darkened skin, swollen veins

PE:
* Symptoms can be very non-specific
* Sudden onset shortness of breath is most common symptom
* Cough
* Pleuritic chest pain
* Haemoptysis
* Hypoxia
* Tachycardia and tachypnoea
* Low grade fever

Note: pleuritic chest pain and haemoptysis are generally only present when infarction has occurred

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26
Q

Explain initially how you would go about making a diagnosis of a PE?

A
  • History
  • Examination – low grade fever, hypotension (sign of right heart strain), tachycardia, tachypnoea, pleural rub (squeaking or grating caused by ischaemic lung tissue coming in contact with the pleura), hypoxia, evidence of DVT
  • CXR – want to rule out other potential causes of these symptoms as DVT is very non-specific
  • NICE recommend at this point you should then go on to do a Wells score which essentially gives you result of either PE likely or PE unlikely
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27
Q

What is the most common ECG finding of a PE? What is the classical ECG finding?

A

most common finding is a sinus tachycardia but the classic finding is S1Q3T3 – a large S wave in lead 1, a Q wave in lead 3 and an inverted T wave in lead 3 indicate acute right heart strain

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28
Q

Describe what you do if PE likely/ unlikely on Wells score?

A

PE likely on Wells Score (more than 4):
* https://www.nice.org.uk/guidance/ng158/chapter/Recommendations#diagnosis-and-initial-management
* offer CTPA immediately, if not possible do a V/Q scan

PE unlikely on Well Score (4 points or less) :
* Offer a d-dimer test
* Only if d-dimer positive should then do a CTPA, if negative consider an alternative diagnosis
* d-dimers are 95% sensitive but not very specific, i.e. if d-dimer is negative that can exclude a PE but if it is positive it does not diagnose it

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29
Q

Initial management of PE?

A
  • For those with diagnosed PE should start treatment with anticoagulants
  • Everyone is also usually given high flow O2 and analgesia
  • If no renal impairment, active cancer or haemodynamic instability first line drugs are apixaban or rivaroxaban
  • LMWH can be used as alternative as well as edoxaban, dabigatran etc.
  • Those who are haemodynamically unstable due to massive PE should be considered for thrombolysis, thrombolysis comes with risk of massive bleeds so should only be used in massive PE, examples include streptokinase, alteplase and Tenecteplase
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30
Q

When may you use thrombolysis in PE? Why do you not use it on everyone?

A
  • Those who are haemodynamically unstable due to massive PE should be considered for thrombolysis, thrombolysis comes with risk of massive bleeds so should only be used in massive PE, examples include streptokinase, alteplase and Tenecteplase
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31
Q

Long term management of PE?

A
  • Anticoagulation should be continued for at least 3 months
  • Should perform investigations to determine underlying cause based on history etc. e.g. do they have a malignancy? Do they have a thrombophilia?
  • At 3 months (3 to 6 months with active cancer), stop and discuss with patients benefits vs risks of stopping vs continuing
  • HERDOO2 score can be used for looking at risks of discontinuing anticoagulation in unprovoked PE
  • HAS-BLED score can look at risk of major haemorrhage if stay on anticoagulation
  • Generally those with a provoked DVT where factor has now been controlled it is okay to stop anticoagulation and those with unprovoked should be encouraged to stay on anticoagulation
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32
Q

Explain what a pneumothorax is?

A
  • Pneumothorax occurs when air gets into the pleural space separating the lung from the chest wall
  • It can occur spontaneously or be due to trauma, medical interventions or lung pathology
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33
Q

Explain what a spontaneous pneumothorax is and classical presentation?

A
  • These generally occur when bullae which are abnormal air pockets that form in the lung rupture
  • A primary spontaneous pneumothorax occurs in someone with no underlying condition and these are more common in thin, tall, adolescent males
  • Spontaneous pneumothorax is also common in Marfan’s syndrome
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34
Q

Presentation of a pneumothorax?

A
  • Small ones can be asymptomatic
  • Acute onset of pleuritic chest pain and SOB
  • Hypoxia
  • Tachycardia
  • Reduced breath sounds on the affected side
  • Hyper-resonance
  • Deviated trachea away from side of pneumothorax in tension pneumothorax
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35
Q

Management of a pneumothorax?

A

Primary:
* If pneumothorax < 2cm and the patient is not short of breath then no treatment is required there should just be a follow up CXR
* If the patient is short of breath or the pneumothorax is > 2cm aspiration should be done
* If aspiration fails (patient still short of breath or pneumothorax > 2cm still) then a chest drain should be inserted

Secondary:
* > 2cm or breathless - chest drain, admit
* 1-2 cm in size - aspirate, admit
< 1cm admit, high flow oxygen, observe for 24 hrs

secondary if age > 50 with significant smoking history or evidence of underlying lung disease on exam or CXR

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36
Q

Describe the triangle of safety for inserting a chest drain?

A

Chest drains should be inserted into the “triangle of safety” – 5th ICS (nipple line), mid axillary line (anterior border of latissimus dorsi), anterior axillary line (lateral border of pectoralis major) – should also make sure you insert just above a rib to avoid hitting a neurovascular bundle (these run beneath each rib)

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37
Q

Explain what a tension pneumothorax is?

A
  • A one way valve forms so air can only move into the chest which results in compression of mediastinal structures and deviation of the trachea away from the involved lung
  • Tension pneumothorax is a medical emergency
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38
Q

Management of a tension pneumothorax?

A
  • Emergency management of a tension pneumothorax involves insertion of a large gauge cannula into the pleural cavity via the 2nd or 3rd intercostal space in the midclavicular line of the side of the tension pneumothorax
  • Definitive management would be with a chest drain
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39
Q

Explain what pulmonary hypertension is?

A
  • Increased resistance and pressure of blood in the pulmonary arteries – this puts strain on the right side of the heart and also causes back pressure of blood into the venous system
  • Variety of causes which can be classified into 5 groups
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40
Q

WHO classification system for pulmonary hypertension?

A
  • Group 1 – idiopathic
  • Group 2 – secondary to left heart disease, valvular heart disease or restrictive cardiomyopathy (because left sided heart failure causes backflow into the lungs)
  • Group 3 – secondary to chronic lung disease and environmental hypoxaemia
  • Group 4 – due to chronic thrombotic disease, embolic disease or both
  • Group 5 – miscellaneous, systemic disorders (e.g. SLE), haematological diseases etc.
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41
Q

Presentation of pulmonary hypertension?

A
  • Progressive breathlessness, weakness and fatigue
  • Syncope
  • Pulmonary oedema can occur late on as increased pressure pushes fluid out of the vessels
  • Loud heart sounds, murmurs, raised JVP, peripheral oedema, ascites, tachycardia
  • May be signs of associated conditions e.g. SLE or liver disease
42
Q

Investigations for pulmonary hypertension?

A
  • Bloods including LFTs, TFTs and autoimmune screening to detect any underlying causes
  • CXR to exclude other lung conditions
  • ECG – may should right ventricular hypertrophy and strain patterns
  • Echocardiography can be used to assess RV function and estimate pulmonary arterial pressure
  • Right heart catheterisation is needed to confirm the diagnosis by directly measuring pulmonary pressure
43
Q

Prognosis of pulmonary hypertension?

A
  • Prognosis depends on underlying cause but is generally poor (max 3 years)
44
Q

Most common cause of pulmonary hypertension?

A

secondary to left heart disease

45
Q

Management of pulmonary hypertension?

A
  • Management of any underlying cause

Medications can have a significant effect on symptoms and exercise tolerance in the short term but evidence suggests they have little effect on long term survival:
o Intravenous prostanoids e.g. epoprostenol
o Endothelin receptor antagonists e.g. maciten
o PDE5 inhibitors e.g. silendafil

  • Supportive treatment
46
Q

What is bronchiolitis and who does it occur in?

A
  • Lower respiratory illness that involves acute inflammatory injury of the bronchioles usually due to infection with RSV
  • Occurs in babies under 18 months old
47
Q

Presentation of bronchiolitis?

A

NICE guidelines advise it should be considered in children under the age of 2 presenting with:
* Persistent cough and
* Either tachypnoea or chest recession (or both) and
* Either wheeze or crackles on chest auscultation (or both)

Other features – wet cough, fever, poor feeding, very young babies may present solely with apnoea

48
Q

Investigations for bronchiolitis?

A
  • Pulse oximetry
  • Viral throat swabs for respiratory viruses
  • CXR and bloods are not advised for routine management unless there is evidence of deterioration and worsening respiratory distress
49
Q

Management for bronchiolitis?

A
  • Most infants have mild self limiting illness that can be managed at home
  • Mainstay of treatment is supportive
  • Anti-pyretics only needed if temperature causing distress to the child
  • In secondary care supportive is still mainstay, high flow nasal oxygen or CPAP may be used
  • Most children make a full recovery in a week
50
Q

Explain what cystic fibrosis is and how it arises?

A
  • Genetic condition
  • CFTR gene mutation results in dysregulation of epithelial fluid transport
  • Causes thicker body secretions as the CFTR transporter usually transports chloride allowing water into secretions
  • Most common gene mutation is delta F508
  • It is an autosomal recessive condition so need 2 copies of the gene to get the disease
  • Multisystem disorder but leading cause of death is lung disease
  • Majority of patients have pancreatic insufficiency
51
Q

Most common gene mutation for cystic fibrosis?

A

delta F508

52
Q

Describe pancreatic presentation of CF?

A
  • The thick secretions can block the ducts in the pancreas meaning less pancreatic fluid can get out to help break down food
  • This results in fat malabsorption, steatorrhoea and a failure to thrive
  • Patients can also get diabetes due to damage of the endocrine portion of the pancreas although this tends to present when older whereas exocrine failure can present from early on
53
Q

Describe lung presentation of CF?

A
  • Sputum and chronic cough
  • Patients develop bronchiectasis due to recurrent RTIs (as sticky mucus means lungs can’t clear pathogens as well) that don’t get fully better
  • Breathlessness
  • Can develop nasal polyps
  • Eventually develop respiratory failure
54
Q

Other signs of CF?

A
  • Those with CF tend to be infertile
  • In males there is often a congenital absence of the vas deferens (causing the infertility)
  • Patients have salty sweat due to increased chloride
  • Neonates can present with meconium ileus (meconium is the first stool passed by a new-born and CF can mean the stool is so sticky that it actually causes a bowel obstruction), this presents with bilious vomiting, abdominal distension and no passage of meconium
  • Clubbing
55
Q

Diagnosis of CF?

A
  • CF screening is offered to all new-borns so it is often picked up then although they don’t check for every mutation so could potentially be missed
  • In adults and children diagnosis is a combination of clinical presentation, sweat test and genetic tests
  • Also, you should offer a test for CF to anyone: under the age of 40 with bronchiectasis or with upper lobe bronchiectasis or with colonization with Staph or infertile or low weight/ failure to thrive
56
Q

Management of CF?

A

Managed by specialist centre:
- Learn airway clearance techniques
- Nebulised therapy to help with mucociliary clearance
- CF patients should not be managed together due to risk of spread of infection
- Broad spectrum antibiotics are used for infections
- Respiratory failure is treated with oxygen and non-invasive ventilation
- Pancreatic enzyme supplements and vitamin tablets are given to those with pancreatic insufficiency
- CF diabetes usually requires insulin
- Ivacaftor and Lumacaftor are new targeted treatments that involve CFTR modulation, these drugs are very expensive

57
Q

Explain what asthma is?

A
  • Asthma is defined as recurrent but reversible obstruction to the airways in response to substances that are not necessarily noxious
  • Asthma is a type 1 hypersensitivity reaction involving eosinophilic inflammation and a TH2 response
  • Chronic asthma can cause permanent changes to the airway such as smooth muscle hypertrophy, increased mucus and epithelial damage with subepithelial fibrosis
58
Q

Causes of asthma?

A
  • Not fully understood
  • Atopic Asthma is part of the atopic triad which includes asthma, hayfever and eczema (people with one of these are more likely to have the others)
  • Increased risk of having asthma if family history of asthma
  • Asthma exacerbations generally have triggers e.g., pollen, dust, air pollution, cold weather
59
Q

Symptoms and signs of asthma?

A
  • Tight chest
  • Widespread wheeze
  • Dry cough
  • Diurnal variation in symptoms
  • Symptoms associated with triggers
60
Q

Investigations for asthma?

A
  • Spriometry: FEV1 is reduced but FVC is normal, the FEV1/ FVC ratio is reduced
  • Should have reversibility on administration of a bronchodilator
  • Peak flow testing is done and people may be given a peak flow diary
  • Normal spirometry does not exclude asthma diagnosis and can also do FeNO and bronchial challenge testing
61
Q

Asthma management?

A
  • Those with a diagnosis of asthma should be prescribed a SABA for relief of symptoms
  • The frequency of use of a SABA is a good measure of asthma severity and control
  • If a preventer is needed inhaled ICS has been shown to be the most effective and is first line in adults and most children
  • Can add on other preventer therapies which seems to be patient dependent on what is prescribed e.g. Leukotriene receptor antagonists (montelukast), LABAs, Sodium cromoglicate and theophylline (methylxanthines)
  • Very unresponsive asthma may be referred for monoclonal antibody treatment
62
Q

What can give a good idea of severity for acute asthma? What are the different categories?

A
  • Peak flow is important in understanding severity – 50-75% of predicted = moderate, 33-50% predicted = severe, < 33% = life threatening
63
Q

Management of acute asthma?

A
  • Oxygen
  • Salbutamol (in moderate can be given by inhaler and spacer, in severe or life threatening by nebuliser)
  • Steroids – prednisolone oral if can manage or hydrocortisone IV if not
  • Ipratropium bromide neubulised
  • IV magnesium sulfate in some patients
  • IV aminophylline but only after consultation with staff
  • Call for help
64
Q

Explain what asthma COPD overlap syndrome is?

A
  • This is subset of patients who have both features of asthma and COPD
  • Features of persistent airflow limitation but a history of asthma or show large bronchodilator reversibility
  • Tend to have worse symptoms than those just with asthma or COPD
65
Q

What is COPD?

A
  • COPD is a progressive disease characterized by poorly reversible airflow obstruction and an abnormal inflammatory response in the lungs
  • Clinically this manifests as a combination of chronic bronchitis and emphysema
66
Q

Explain what chronic bronchitis is?

A
  • Chronic bronchitis is long term inflammation of the bronchi
  • It is usually however a clinical diagnosis defined as a productive cough for at least 3 months of the year for at least 2 years
  • The main cause is smoking where the chemicals from the smoke stimulate hypertrophy and hyperplasia of the bronchial mucinous glands and goblet cells, there is also a reduction in the height of the cilia
67
Q

Explain what emphysema is?

A
  • Emphysema is defined as permanent dilatation of the air spaces distal to the terminal bronchioles due to destruction of their walls without fibrosis
  • The main cause of emphysema is smoking which is thought to cause an imbalance between protease (which break down lung connective tissue) and anti-protease activity
  • Lungs are hyperinflated due to trapped air, this can also be seen on post mortem
68
Q

List some symptoms and signs of COPD?

A
  • Productive cough
  • Breathlessness
  • Wheeze
  • Frequent infective exacerbations
  • Use of accessory muscles of respiration
  • Chest expansion is poor
  • Hyperinflation
  • Loss of cardiac and liver dullness (lungs hyperinflated over these)
69
Q

Investigations for COPD?

A
  • Spirometry – FEV1/ FVC ratio < 0.7 with no dramatic response to a bronchodilator
  • Should also get a CXR to exclude other lung pathologies, FBC to check for polycythaemia or anaemia and a BMI to allow monitoring
  • Additional investigations that may be helpful include: sputum cultures, ECG, echo, CT thorax, serum alpha 1 antitrypsin, TLCO
70
Q

Explain polycythaemia in COPD?

A

secondary polycythaemia (increased red cells) can be a complication of COPD, chronic hypoxia causes increased EPO secretion cause increased red cells, as the kidney cells are stimulated by the hypoxia to secreto EPO

71
Q

Management of COPD?

A
  • Before pharmacological therapy must offer smoking cessation, pneumococcal and influenza vaccines, offer pulmonary rehab, optimize treatment of co-morbidities
  • If struggling with breathlessness and it is limiting their exercise can offer inhaled therapies
  • SABA or SAMA as needed initially
  • If no asthmatic/eosinophils - LABA plus LAMA is next. If asthma features LABA plus ICS then if still bad LABA LAMA ICS

Side note: trellegy ellipta or trimbow is triple therapy and breo ellipta inhaler is dual therapy

72
Q

Management of acute COPD exacerbation?

A

iSOAP
* Ipatropium
* Salbutamol
* Oxygen
* Amoxicillin (if sputum purulent or signs of pneumonia)
* Prednisolone

73
Q

What is pneumonia?

A
  • Pneumonia is defined as a lower respiratory tract infection with new consolidation on X-ray
  • It can be described as CAP (community acquired), HAP (hospital acquired if more than 48 hours after admission) or aspiration (if related to aspiration of foreign material)
  • There are many organisms that can cause pneumonia
74
Q

2 common causes of pneumonia?

A

strep pneumonia is most common cause
another common cause is haemophilus influenzae

75
Q

Describe strep pneumonia?

A
  • Gram positive, alpha haemolytic, streptococci
  • Causes typical pneumonia but can also cause meningitis and blood stream infections
  • Presence can be detected by culture
76
Q

Describe haemophilus influenzae?

A
  • A cause of atypical pneumonia usually in those already with lung disease
  • Can also cause epiglottitis in children and exacerbations of COPD
  • Gram negative organism that is grown on chocolate agar
  • Less common now as there is a vaccine
77
Q

Define atypical pneumonia? List them?

A
  • “Caused by an organism that cannot be cultured in normal way/ gram stained and does not generally respond to penicillin”
  • Legions of psittaci MCQs: legionella, chalmydia psittaci, mycoplasma pneumonia, chlamydophilia pneumonia, Coxiella burnetti
78
Q

How do you test for legionella?

A

urinary antigens

79
Q

Describe legionella pneumonia?

A
  • Legionella – this comes from infected water supplies, can cause SIADH and hyponatraemia – usually someone just come back from cheap holiday abroad/ hot tubs
80
Q

Describe mycoplasma pneumonia?

A
  • Mycoplasma pneumonia – known as walking pneumonia as tends to cause mild symptoms, can cause an erythema multiforme like rash
81
Q

Describe coxiella burnetti pneumonia?

A

due to exposure to animals and their fluids so generally presents in farmer with flu like illness

82
Q

Describe chlamydia psittaci pneumonia?

A

this is from birds e.g. an infected parrot owner

83
Q

Atypical pneumonias
1. from infected water/ hot tub/ cheap holiday
2. farmer with flu like illness
3. parrot owner with pneumonia

A
  1. legionella
  2. coxiella burnetti
  3. chlamydia psittaci
84
Q

Describe klebsiella pneumonia?

A
  • Atypical pneumonia more common in men with a history of excess alcohol, poor dental hygiene and diabetes
  • Can cause a red current jelly sputum
  • Association with empyema as a complication
85
Q

Red currant jelly sputum?

A

klebsiella pneumonia

86
Q

Describe pseudomonas pneumonia?

A
  • Cavitation and abscess formation occurs in the lungs
  • Generally, infection occurs in those with underlying lung disease e.g. COPD or CF or in those who are immunosuppressed
  • Treated with ciprofloxacin
87
Q

Describe pneumocystitis pneumonia?

A
  • Fungal pneumonia caused by infection with pneumocystis jiroveci that occurs in HIV when low CD4 count
  • Causes shortness of breath on exertion, low O2 sats and night sweats
  • Treated with oral co-trimoxazole
  • Those with low CD4 count are usually on prophylactic co-trimoxazole to stop development of this
88
Q

Presentation of pneumonia?

A

Generally depends on organism but common symptoms and signs:
- Cough (usually productive but can be dry)
- Breathlessness
- Fever
- Chest Pain
- Myalgia, arthralgia and malaise
- Headache
- Abdo pain, diarrhea and vomiting
- Can get herpes simplex reactivation in Strep Pneumonia
- Skin rashes in Mycoplasma
- In elderly may become confused

89
Q

Investigations for pneumonia?

A
  • Those with score 0/1 may be able to be kept at home, no investigations and simply empirical treatment
  • Those with higher scores are likely to go to hospital and everyone should get: CXR, FBC (raised WBC), U and E (for urea), CRP (raised)
  • With moderate or severe pneumonia should also take blood and sputum cultures as well as urine to test for legionella and pneumococcal antigens
90
Q

Describe CURB65 score and interpretation?

A
  • This is pneumonia acquired in the community and the CURB65 score can be used as guidance on if treatment is needed (clinical judgement should be used to!)

C= New onset of confusion
U= Urea > 7mmol/L
R= Resp Rate > 30
B= BP < 90 systolic or < 60 diastolic
65= Age 65 or over

  • This score should be used with caution as it may over score an older person as anyone over 65 automatically a score one but equally can underscore a younger person as younger individuals tend to be very good at compensating so these signs may not develop until they are very ill
  • With scores 0/1 – consider treating at home, if > 2 admit to hospital, if > 3 consider need for ITU admission
91
Q

Treatment of CAP?

A
  • CURB65 score 0-2: Amoxicillin orally
  • CURBS65 score 3-5: Co-amoxiclav + doxycycline orally
92
Q

Treatment of HAP?

A
  • Non-Severe: Amoxicillin orally
  • Severe: IV Amoxicillin + Gentamicin
93
Q

Explain what aspiration pneumonia is and causes? What organisms may be involved?

A
  • This occurs due to inhalation of food or infected material from the mouth or oropharynx
  • May be a complication of anaesthesia, coma or occur in conditions where there is frequent reflux e.g. oesophageal obstruction or poor swallowing due to motor neurone disease or stroke
  • may be more anaerobic organisms involved e.g. E coli, klebsiella, pseudomonas
94
Q

Treatment of aspiration pneumonia?

A
  • Non Severe Treatment: Amoxicillin and Metranidazole orally
  • Severe Treatment: IV Amoxicillin, Gentamicin and Metranidazole
95
Q

Complications of pneumonia?

A
  • Pleural Effusions
  • Empyema- pus in the pleural space (D sign on XR), signs of empyema are persistent fever and inflammatory markers despite treatment
  • Lung abscess
  • Sepsis
  • Respiratory Failure
96
Q

Explain what respiratory failure is an the types?

A
  • Respiratory failure occurs when disease of the heart or lungs leads to failure to maintain adequate blood oxygen levels (hypoxia) or increased blood carbon dioxide levels (hypercapnia)
  • Type 1 respiratory failure- lack of oxygen
  • Type 2 respiratory failure – lack of oxygen and too much CO2
  • Respiratory failure can be acute, acute on chronic or chronic
97
Q

What can be used to confirm diagnosis of respiratory failure?

A

ABGs

98
Q

Management of respiratory failure?

A
  • A patient with acute respiratory failure generally needs ITU admission
  • Many patients with chronic respiratory failure can be treated at home
  • Management depends on underlying causes
  • Hypoxaemia can be treated with oxygen therapy, mechanical ventilation, non-invasive ventilation and ECMO
  • NIV involves a mask with positive pressure to provide delivery of oxygen
99
Q

What quick test can be used to diagnose empyema?

A

ph of pleural fluid - ph < 7.2 suggest empyema

100
Q

How to interpret Wells score for DVT?

A

DVT likely wells score 2 or more: offer ultrasound, then d dimer if ultrasound negative

DVT unlikely wells score 1 or less: offer d dimer then only ultrasound if d dimer positive