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Phase2a > respiratory > Flashcards

respiratory Flashcards

1
Q

what FEV1/FVC ratio indicates obstructive lung disease

A

< 70% or FEV1 <80%

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2
Q

what FEV1/FVC ration indicated restrictive lung disease

A

> 80%

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3
Q

define transfer coefficient, which conditions is it low and high in?

A 
measure of ability of oxygen to diffuse across the alveolar membrane
low in 
- emphysema 
-fibrosing alveoli's
-anaemia 
high in 
-pulmonary haemorrhage
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4
Q

why might we perform a bronchoscopy on a patient

A
  • lobar collapse, mass or persistent consolidation detected on X-ray
  • haemoptysis
  • cough, wheeze, stride, dyspnoea
  • suspected aspiration of foreign body
  • therapeutic e.g stent
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5
Q

what is the definition of chronic bronchitis

A
  • productive cough for 3 months in two consecutive years
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6
Q

what are the symptoms and signs of chronic bronchitis

A
  • mucus hyper secretion with bronchial mucus gland hypertrophy
  • hypercapnia and hypoxaemia
  • cyanosis (blue bloaters) - rely on hypoxic drive
  • right heart failure
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7
Q

what are the main organisms associated with chronic bronchitis

A
  • haemophilus influenzae
  • streptococcus pneumoniae
  • viruses (adeno, respiratory syncytial)
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8
Q

describe the pathophysiology of emphysema

A
  • enlargement of alveolar airspaces with destruction of elastin in walls
  • permanent enlargement of airspaces distal to terminal bronchioles due to destruction of walls
  • gas trapping effect prevents full exhalation
  • pulmonary hypertension and poor oxygen delivery to tissues
  • neutrophils recruited and release IL8, TNF and destructive enzymes = tissue damage
  • reduced paCO2, normal PaO2 due to over ventilation
  • pink puffers
  • weight loss due to metabolic demands
  • right heart failure
  • over inflated chest
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9
Q

what is the main genetic abnormality linked to emphysema

A

alpha -1 - antitrypsin deficiency

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10
Q

what are the features of bronchiectasis

A
  • permanent dilation of bronchi and bronchioles due to obstruction and inflammation
  • caused by h. influenzae, strep penumoniae, staph aureus
  • chronic cough with expectation of large quantities of foul smelling sputum with intermitted haemoptysis
  • clubbing
  • wheeze
  • complications include: pneumonia, fungal colonisation, metastatic abscess, amyloidosis, pneumothorax
  • treatment to reduce symptoms rather than cause - mucolytics for hyper secretion
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11
Q

in interstitial lung diseases what happens to TCO, VC, FEV1, FVC and PEFR

A

reduced TCO, VC FVC
high FEV1/FVC ratio
normal PEFR

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12
Q

give one acute and 3 chronic interstitial lung diseases

A

acute - Adult respiratory distress syndrome
chronic - fibrosing alveolitis (Idiopathic pulmonary fibrosis)
- pneumoconiosis
- sarcoidosis

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13
Q

what are the main causes of ARDS

A
  • Trauma
  • shock
  • gastric aspiration
  • drug abuse
  • pneumonia
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14
Q

what are the clinical features of ARDS

A

Tachypnoea, arterial hypoxaemia, cyanosis

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15
Q

what are the features of IPF

A
  • symptoms - dry cough, exertion dyspnoea, clubbing, cyanosis
  • abnormally large irregular spaces separated by thick fibrous septa (honeycomb lung)
  • restrictive lung function tests
  • scarring
  • myofibroblasts secrete exaggerated amounts of ECM that remodel lung architecture
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16
Q

what are the different ways the lung can respond to inhaled dust (causes pneumoconiosis)

A
  • inert - coal workers pneumoconiosis (coal in alveolar macrophages)
  • fibrous - asbestosis, silicosis, progressive massive fibrosis
  • allergic - EAA - granulomatous inflammation
  • neoplastic - mesothelioma, lung cancer
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17
Q

what is the Kviem test for sarcoidosis

A

subcutaneous injection of sterile homogenised sarcoid tissue induces granulomas in affected patients

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18
Q

using an FEV1/FVC ratio what is the definition of COPD

A

< 70% or 0.7

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19
Q

which two diseases does COPD encompass

A
  • emphysema and chronic bronchitis
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20
Q

what are the different delivery systems for inhaled drugs

A
  • pressurised measured dose inhalers (PMDIS) - device activated by user pressing down on the top of container, resulting in the release of a fine spray containing propellant and drug
  • spacer devices - slow down the particles of the drug and allow more time for evaporation of the propellant
  • dry powder inhalers (DPIS) - device releases a small amount of drug in powder form which is then inhaled
  • nebulisers - disperse a liquid into a fine mist which can be inhaled through a mask or mouthpiece
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21
Q

what factors need to be considered to prolong absorption of therapeutic agents from the lungs

A
  • solubility
  • charge and tissue retention
  • encapsulation - allow controlled release by use of excipients (molecules that modify properties of medicines)
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22
Q

what are the advantages of using inhaled drugs

A
  • lungs are robust
  • act directly on lung or enter systemic circulation
  • rapid absorption
  • large sa
  • lungs naturally permeable
  • fewer drug metabolising enzymes
  • non invasive
  • fewer systemic side effects
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23
Q

what is bronchoconstriction due to

A
  • tightening of ASM
  • lumens occlusion by mucus and plasma
  • airway wall thickening
  • in asthma ASM is both primed to contract an is resistant to relaxation
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24
Q

what drugs can we use to relieve bronchoconstriction

A
  • B2 adrenoreceptor agonists - act on sympathetic nervous system to cause bronchodilation :
    smooth muscle relaxation and bronchodilation
    inhibit histamine release from lung mast cells
    SABA - salbutamol
    LABA - formoterol and salmeterol
  • Anticholinergics: block bronchoconstriction (PSNS)
    block Ach binding to muscarinic receptors M1-M5 on ASM glands and nerves
    e,g atropine = naturally occurring anticholinergic (ipratropium bromide and tiotropium bromide are synthetic derivatives with fewer side effects)
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25
Q

Which drugs are the first line treatment for inflammation (and describe how they work + side effects)

A

glucocorticoids

  • inhaled corticosteroids most effective for asthma
  • decreases number of inflammatory cells
  • suppress the production of chemotactic mediators
  • inhibit cell survival in airway
  • reduce adhesion molecule expression
  • suppress inflammatory gene expression in airway epithelial cells
  • side effects: decreased bone density, adrenal suppression, cataracts, glaucoma
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26
Q

why are glucocorticoids and B2 agonists good at working together

A

glucocorticoids increase transcription of B2 receptor gene resulting in increased expression of cell surface receptors

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27
Q

what is the treatment for fibrosis

A
  • transplantation best option
  • prefernidone and nintendanib slow progression of disease
  • prefernidone reduces fibroblast proliferation, collagen production and production of fibrogenic mediators
  • nintendanib is a tyrosine kinase inhibitor, inhibits vascular endothelial GF receptor
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28
Q

what % of bronchial cancers are malignant

A

95%

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29
Q

what are the main causes of lung cancer

A

smoking 80-90%
asbestos
coal tar
radon

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30
Q

what is the difference between small and non small cell neoplasms in the lung

A

small cell - high grade epithelium neoplasm with strong cigarette association
non small cell - variable grade - surgery and radiotherapy main treatment

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31
Q

why may you get a false negative and false positive on a lung PET scan for cancer

A

false negative - BAC, carcinoid, small lesions

false positives - inflammation, infection

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32
Q

what is the clinical presentation of lung cancer

A
  • cough
  • SOB
    -wheeze
    -haemoptysis
    dysphagia
    hoarseness
    chest pain
    head neck and arm swelling
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33
Q

what are the main paraneoplastic changes associated with lung caner

A
  • clubbing
  • secretion of PTH
  • SIADH - syndrome of inappropriate ADH release
  • secretion of ACTH
  • myasthenic syndrome
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34
Q

what is the treatment for lung cancer

A

stage 1/2 - surgery or radical DXRT (deep X-ray therapy)

stage 2/3 palliative chemo, chemo+radio, palliative care

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35
Q

how do each of the mucosal surfaces in the body protect themselves against infection

A

vagina - acidic, commensals, thick mucosa
intestine - acidic stomach, commensal flora, enzymes, thick mucosal barrier, mucosal immune system
urinary system - sterile and flows outwards
skin - waterproof barrier
respiratory tract - mucociliary escalator, sneeze and cough reflex, swelling reflex and epiglottis, innate and adaptive immunity

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36
Q

which microbes can colonise the respiratory tract

A

sinuses - sterile
pharynx - streptococci, gram negative rods and cocci
oral cavity - lactobacillus (teeth), streptococci, membranes streptococci, lactic acid bacteria
nares- staph epidermis and corynebacteria

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37
Q

what may make you more susceptible to an RTI

A
  • swallowing problems
  • colonisation of upper airway
  • altered lung physiology e.g CF, bornchiestatis
  • comorbidities
  • immune dysfunction /immunesuppressed
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38
Q

list the common viruses that cause an upper RTI and what they cause

A
  • rhinovirus - common cold
  • influenza A - flu and systemic symptoms
  • corona virus - runny nose, headache, sore throat, fever
  • adenovirus - cold, acute bronchitis, pneumonia, diarrhoea, pink eye, gastroenteritis, sore throat
  • parainfluenza - cough, fever, runny nose
  • respiratory syncytial virus - in children common cold
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39
Q

what are the main causes of pharyngitis and how is it treated

A
  • viral (70-80%) rhino virus and aden virus

- bacteria - streptococcus pyogenes - lance field group A beta haemolytic streptococci - treat with amoxicillin

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40
Q

what are the four “centor criteria” which make a sore throat likely to be bacterial

A
  • tonsils exudate
  • tender anterior cervical adenopathy
  • absence of cough
  • fever over 38
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41
Q

what are the main causes of sinusitis

A
  • mainly viral
  • if bacterial = unilateral pain purulent discharge and fever
    caused by strep pneumoniae or haemophilus influenzae
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42
Q

what clinical presentation does bordatella pertussis infection cause

A

whooping cough

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43
Q

what are the main virulence factors of bordatella pertussis

A
  • toxin that ADP ribosylates G proteins and inhibits alveolar macrophage host defence
  • ACT toxin that inhibits phagocyte chemotaxis and T cell activation
  • filamentous haemaglutinin and fimbriae aid adherence
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44
Q

what are the phases of a bordatella pertussis infection

A

incubation 5-21d
catarrhal phase 1-2 weeks, rhinorrhoea, conjunctivitis, low grade fever
paroxysmal phase 1-6 weeks coughing spasms, inspiratory whoop
treatment clarithromycin - eliminate carriage, reduce symptoms in catarrhal phase

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45
Q

what does the dTap vaccine protect against

A
  • tetanus
  • diphtheria
  • whooping cough
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46
Q

who is at risk of pneumonia

A
  • elderly
  • infants
  • COPD
  • impaired swallowing
  • immunocompromised
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47
Q

what is the pathogenesis of pneumonia

A
  • pneumococci temporarily colonise pharynx
  • they are micro aspirated and usually cleared by alveolar macrophages
  • in some infections ability to kill becomes overwhelmed
  • produce pro inflammatory response which attracts neutrophils
  • this results in dead bacteria, neutrophils, tissue fluid and inflammatory proteins exudate in airspaces
  • causes collateral damage to lung
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48
Q

what are the symptoms and signs of pneumonia

A

symptoms
-SOB
-sputum - classically rusty
- systemic features - weakness, malaise, fever, sweats, rigors
-pleuritic chest pain (worse on deep breathing)
signs
- increased temp, inc HR, inc RR, dcr BP, dehydration

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49
Q

what may a chest X-ray of pneumonia show

A
  • multi lobar consolidation - S. pneumoniae, s,aureus
  • upper lobe cavity - k.pneumoniae
  • interstitial of diffuse shadowing suggestive of viral or pneumocystis pneumonia (PCP)
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50
Q

describe the CURB-65 scoring system for severity of pneumonia

A 
each of the following scores 1 point
- confusion > 8 on mental test
- urea >7mmol
RR > 30
BP <90/60
0-1 - PO antibiotic amoxicillin 
2 hospital therapy - amoxicillin + clarithryomycin
3 severe ITU - coamoxiclav + clarithryomycin
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51
Q

what drug should be used to treat pneumonia if the patient has a penicillin allergy

A

clarithomycin

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52
Q

what are the typical and atypical pathogens causing community acquired pneumonia

A 
typical 
-s.aureus, streptococcus pneumoniae, H.influenzae, klebsiella pneumoniae
atypicals 
-mycoplasma pneumoniae 
- chylamyclophilia pneumoniae
-legionella pneumoniae
53
Q

what is the main extra pulmonary feature that mycoplasma pneumoniae causes

A
  • haemolytic anaemia
54
Q

what are the main tests used in pneumonia diagnosis

A
  • sputum culture and gram stain
  • FBC and cultures
  • serology
  • urinary antigen
  • PCR
55
Q

what are the main methods of pneumonia prevention

A
  • pneumococcal PPV in adults (23 serotypes)
  • PVC in children (13 serotypes)
  • influenza vaccine
  • smoking cessation
56
Q

describe hospital acquired pneumonia

A
  • > 48 hrs after admission
  • early onset <5d of hospital = organisms similar to CAP
  • late onset >5d = staph aureus including MRSA, pseudomonas aeruginosa, klebsiella pneumoniae, acinetobacter baumanii
57
Q

what is bronchiolitis caused by

A

respiratory syncytial virus

58
Q

what is the pathology of COPD

A 
Airflow limitation due to 
small airways disease 
-airway inflammation 
-fibrosis
-inc airways resistance
parenchymal destruction 
- loss of alveolar attachments
-decrease of elastic recoil
59
Q

what are the symptoms and signs of COPD

A
  • SOB
    -wheeze
    -cough
    -sputum
    signs
    -hyperinflated chest
    -weight loss
    -cor pulmonale
    -cyanosis
    -tachypnoea
  • blue bloater (chronic bronchitis)
  • pink puffer (emphysema)
60
Q

what are the stages of the MRC dyspnoea scale

A
  1. SOB on marked exertion
  2. SOB on hills
  3. slow or stop on flat
  4. 100-200yrds flat
  5. housebound
61
Q

what are the main chemical mediators of COPD

A
  • LTB, IL8, TNFa
62
Q

what are the main chemical mediators of asthma

A
  • histamine, IL4, IL5, LTD
63
Q

what are the main cells active in COPD

A
  • neutrophils
  • CD8 T cells
  • macrophages
64
Q

what are the main cells active in asthma

A
  • mast cells
  • eosinophils
  • cd4 T cells
  • macrophages
65
Q

what is the management of COPD

A
  • smoking cessation
  • regular physical activity - exercise rehab programs
  • mucolytics for chronic bronchitis
  • flu and pneumococcal vaccines
  • SABA/SAMA first line e.g salbutamol/ipratropium
  • then in FEV1>50% - LABA e.g salmeterol or LAMA e.g ipratropium bromide
  • in FEV1<50% - LABA + ICS or LAMA
  • then LABA +ICS or LAMA+LABA/ICS combination inhaler
  • oxygen therapy: long term >15 hours a day
  • ventilatory support
  • lung volume reduction surgery
  • transplantation
66
Q

how is an exacerbation of COPD managed

A
  • nebulized bronchodilators - salbutamol and ipratropium
  • oxygenate if Sao2<88% - start with 24-28% and aim for sats of 88-92%, adjust according to ABG
  • steroids - i.v hydrocortisone and oral prednisolone (7-14d)
  • antibiotics if evidence of infection - amoxicillin, clarithromycin or doxycycline
  • physiotherapy for sputum expectoration
67
Q

what family is the influenza virus part of

A

orthomyxoviridae

68
Q

what are the 2 key surface antigens of the influenza A virus and what do they do

A
  • hameagglutinin (15 subtypes)
    virus binding and entrance to cells, immunity confers protection to specific subtype
  • neuraminidase
    bolt cutters for getting out, cuts newly formed virus loose from infected cells and prevents it clumping together. Immunity to subtype results in less virus being released from cells resulting in less severe disease
69
Q

what is antigenic drift and antigenic shift and how do they happen in influenza virus

A

shift - major genetic change in a virus
drift - minor
- gene reassortment due to virus being 8 single stranded dan segments
- can swap genes during confection with human and avian flu virus
-mutation prone when replicating

70
Q

what is the reproduction number of a disease

A
  • the average number of secondary cases generated by a primary case
71
Q

what is the treatment of flu

A
  • supportive care - oxygenation, hydration, maintain homeostasis, prevent secondary infections
  • antivirals - tamiflu
72
Q

what is the difference between a outbreak, epidemic and pandemic

A

outbreak - 2 or more linked cases
epidemic - in region/country
pandemic - spanning international borders

73
Q

which strain of influenza caused swine flu

A

H1N1

74
Q

what are the phases of containment of flu

A
  • identification of cases
  • treatment
  • contact tracing
  • large scale prophylaxis
75
Q

what does type 2 respiratory failure present on an ABG and why? What symptoms does this cause?

A
  • hypercapnia and hypoxaemia
  • only cause is alveolar hypoventilation
  • CO2 enters the alveoli but is not removed
  • sleepy, bounding pulse, flapping tremor, confusion
76
Q

what does type 1 respiratory failure present on an ABG and why? What symptoms does this cause?

A
  • Hypoxaemia
  • limitation of ventilation, perfusion or diffusion
  • cyanosis, inc RR, accessory muscle use, dcr BP, tachycardia
77
Q

what are the causes of respiratory failure

A
  1. failure to maintain a patent airway (obstruction) - type 1 - asthma, COPD, pneumonia, OSA
  2. alveolar hypoventilation - type 1 or 2 - obesity, chest wall deformity, neuromuscular weakness e.g drug overdose
  3. diffusion limitation - type 1 - emphysema, interstitial lung disease (IPF, sarcoidosis, pneumconosis), drug induced lung disease
  4. V/Q mismatching, type 1 - perfusion without ventilation (shunt), ventilation without perfusion (dead space)
78
Q

what is the treatment of respiratory failure

A
  • continuous positive airways pressure (CPAP)
    type 1 treatment
    positive pressure applied into the lungs to make it easier to take a breath
  • non invasive ventilation
    type 2 treatment
    gives a measured breath - biphasic positive airways pressure
79
Q

describe the pathology of asthma

A
  • Reversible chronic obstructive airways disease
  • Hypersensitivity type 1 reaction
    1. Allergen is inhaled, antigen presenting cells digest it and present its anigen on their surface through major histocompatibility complexes
    2. T helper cells bind to these antigens and release substances that cause B cells plasma cells that produce IgE (allergen specific)
    3. The next time that the allergen enters the body it binds to the IgE that is found on the surface of the mast cells
    4. Mast cells degranulate releasing histamine
    5. Causes bronchoconstriction and smooth muscle contraction
  • Bronchial hyperresponsiveness
  • Increased smooth muscle cells and density
  • Narrowing of lumen
  • Mucus secretion
  • Inflammation
80
Q

what are the two pathological types of asthma

A

eosinophilic
- atopic and non atopic
non eosinophilic
-mainly smoking associated + obesity

81
Q

what are the symptoms and signs or asthma

A

symptoms

  • cough
  • episodic wheeze
  • diurnal variation
  • SOB
  • Sputum

signs

  • tachypnoea
  • audible wheeze
  • hyper inflated chest
  • hyperresonant percussion
82
Q

what are the test results for COPD

A

FBC - increased packed cell volume (PCV)
CXR - hyperinflation, flat hemidiaphragm , bullae, large central pulmonary arteries
CT - bronchial wall thickening, scarring, air space enlargement
ECG - right A+V hypertrophy
ABG - hypoxaemia plus or minus hypercapnia
spirometry - FEV1/FVC < 70%

83
Q

what are the tests for asthma

A

-spirometry - obstructive test ( decreased FEV1/FVC ratio, increased residual volume)
-FBC - eosinophils
- tests for allergy and atopy
-PEFR - peak expiratory flow rate - use a peak flow chart to measure morning and night and a diurnal variation of >20% for 3 or more days a week for 2 weeks is indicative
- reversibility testing - usually a 15% or more increase in FEV1 when treat with a B2 agonist
CXR - hyperinflation

84
Q

what are the differential diagnoses of asthma

A

pulmonary oedema, COPD, large airways obstruction, SVC abnormalities, pneumothorax, pulmonary embolism, bronchiectasis

85
Q

what are the three questions used to assess severity of asthma

A
  • recent nocturnal waking?
  • usual asthma symptoms in a day?
  • interference with ADL’s?
86
Q

what is the ATS consensus definition on severe asthma

A 
1 major + 2 minor
major 
- continuous oral steroids
- high dose inhaled steroids
minor 
daily reliever
persistent airways obstruction 
1 or more emergency visits p.a 
3 or more steroid courses p.a 
near fatal event in past
prompt deterioration with 25% reduction in oral or ICS
87
Q

what are the stages of asthma treatment

A
  1. daily reliever short acting B2 agonist e.g salbutamol
  2. add ICS 200-800mg e.g beclometasone
  3. add LABA e.g salmeterol
    then assess and if still not controlled increase ICS to 800mg, or if no response to LABA stop LABA and just increase ICS to 800mg
  4. high dose ICS 2000mcg
    addition of fourth drug e.g leukotriene receptor antagonist
  5. continous or frequent oral steroids - prednisolone
    maintain ICS at 2000mg
    refer to specialist
88
Q

what is the immediate management of acute asthma

A
  • salbutamol nebulised with o2
  • ventilate - maintain sats 94-98%
  • oxygen 40-60%
  • prednisone oral or iv hydrocortisone
  • ABG
  • assess every 15 mins and repeat salbutamol if PEF<75%
  • single dose magnesium sulfate
89
Q

what are the risk factors for a pulmonary embolism

A
  • recent surgery
  • thrombophilia
  • leg fracture
  • prolonged bed rest
  • maligancy
  • pregnancy
  • previous PE
90
Q

What are the symptoms and signs of pulmonary embolism

A 
symptoms 
- acute breathlessness
-pleuritic chest pain 
-haemoptysis
-dizziness
-syncope
signs 
-pyrexia
- cyanosis
-tachypnoea
-tachycardia
-hypotension
-pleural rub
91
Q

what are the tests for pulmonary embolism

A 
FBC - baseline clotting
CXR - normal or show oligaemia (reduction in blood flow to affected segment)
ABG - hypoxaemia
CT pulmonary angiography = first line
D dimer - DVT evidence
92
Q

what is the treatment for a PE

A
  • Thrombolysis
  • or of a stable clot treat with low molecular weight heparin (anticoagulant) tinzaparin
  • alteplase for big PE
93
Q

what are the causes of a pneumothorax

A
  • rupture of sub pleural bulla
  • asthma
  • COPD
  • TB
  • pneumonia
  • lung absess
  • carcinoma
94
Q

what are the symptoms and signs of a pneumothorax

A 
symptoms 
-dyspnoea
-pleuritic chest pain 
signs 
- reduced expansion
- hyper resonance to percussion 
- diminished breath sounds on effected side
95
Q

what is the difference between transudates and exudates

A

transudates are <25g/l of protein and they are due to increased venous pressure or hypoproteinaemia
exudates are >35g/l of protein and are due to leaky capillaries (infection, inflammation or malignancy)

96
Q

what are the symptoms and signs of pleural effusion

A
  • asymptomatic
  • pleuritic chest pain
  • dyspnoea

signs

  • decreased expansion
  • stony dull percussion note
  • diminished breath sounds
  • tracheal deviation
  • bronchial breathing
97
Q

what are the clinical features of CF

A
  • cough
  • wheeze
  • recurrent infections
  • bronchiectasis
  • haemoptysis
  • cor pulmonale
  • pneumothorax
98
Q

which gene is mutated in CF

A
  • mutation in CF transmembrane conductance regulator gene on chromosome 7
  • Cl channel = defective secretion and more Na absorption
99
Q

what is the management of CF

A
  • physiotherapy - postural drainage, airway clearance
  • antibiotics for acute exacerbations and prophylaxis
  • mucolytics
  • bronchodilators
  • annual CXR
  • DEXA for osteoporosis screening
  • pancreatic enzyme replacement
  • fat soluble vitamin supplements
100
Q

what are the risk factors for tuberculosis

A
  • born in high prevalence area
  • intravenous drug use
  • homeless
  • alcoholic
  • prisons
  • HIV positive
101
Q

which bacteria causes tuberculosis and what are its features

A
  • mycobacterium tuberculosis
  • aerobic, non motile, non sporing
  • acid fast (retain dye when treated with acids)
  • resists phagolysosomal killing by macrophages, hence granuloma
102
Q

what is latent TB

A

95% of people do not have any disease
they have an effective immune response that encapsulates and contains the organism forever
-non contagious
-lifetime risk of reactivation 5-10%

103
Q

what is the pathology of tuberculosis

A
  • bacilli settle in lung apex
  • macrophages and lymphocytes kill majority
  • bacilli and macrophages coalesce to form a granuloma called primary Ghon focus
  • mediastinal lymph nodes enlarge
  • primary focus and mediastinal lymph node = Ghon complex
  • granuloma grows into a cavity
  • more likely in apex as more air and less blood supply
  • cavity full of TB bacilli that are expelled when the patient coughs
104
Q

what are the clinical features of TB

A
  • low grade fever
  • weight loss
  • anorexia
  • night sweats
  • malaise
  • cough
  • chest pain
  • breathlessness
  • haemoptysis
105
Q

what are the complications of TB

A
  • focus can rupture into pleural space with effusion, serous occasionally purulent
  • erosion into bronchus, inhalation and areas of tuberculous bronchopneumonia
  • pericardial effusion post rupture of node through pericardium
  • collapsed lobes
  • bacilli can travel via lymph and cause pleural, military, bone and joint, GU TB
106
Q

what are the diagnostic tests for TB

A
  • Tuberculin skin test “Mantoux”
    -intradermal injection of purified protein derivative (PPD) tuberculin
    -stimulates type 4 delayed hypersensitivity reaction
    -induration on skin 5mm or more = positive for TB w/ risk factors 15mm or more positive for everyone
    – interferon gamma release assays (IGRAs) release from T cells reacting to TB antigen
    demonstrate exposure to TB not active infection
107
Q

what is the UK standard treatment for TB

A
  • rifampicin and isoniazid for 6 months

- pyrazinamide and ethambutol for 2 months

108
Q

what is sarcoidosis

A

granulomatous disease affecting mainly the lungs but also other systems

109
Q

what are the tests for sarcoidosis

A 
Kviem test
CXR shows bilateral hilar lymphadenopathy 
Tissue biopsy diagnostic
Inc ESR 
restrictive LFTs
110
Q

what is the management of sarcoidosis

A
  • bed rest
    NSAIDS
    steroids
111
Q

what is the management of bronchiectasis

A
  • airway clearance techniques and mucolytics
  • antibiotics
    pseudomonas aeruginosa - ciprofloxacin
    haemophilus influenzae - amoxicillin
    staph aureus - flucloxacillin
    strep pneumoniae - benzylpenicillin
  • surgery
    -bronchodilators for those with asthma
  • corticosteroids
112
Q

what are the causes of bronchiectasis

A

congenital - CF, young syndrome
post infection - measles, pneumonia, Tb, HIV, pertussis
other - idiopathic, RA, UC, bronchial obstruction

113
Q

what are the tests for bronchiectasis

A
  • sputum culture
  • CXR - thickened bronchial walls, cystic shadows
  • spirometry - obstructive
  • CF test ( as associated with CF)
  • bronchoscopy to identify location of haemoptysis
114
Q

what is the management of pleural effusion

A
  • of underlying cause
  • drainage - slowly
  • pleurodesis - for recurrent effusions - obliterate pleural space
  • surgery - for persistant collections and increasing pleural thickness (on US)
115
Q

what is goodpastures disease/ antiGBM

A
  • a pulmonary renal syndrome
  • acute glomerulonephritis and lung symptoms
  • caused by antiglomerular basement membrane antibodies (and alveloar membrane)
  • tests - CXR and kidney biopsy
  • immunosuppressive treatment and plasmapherisis
116
Q

what is another name for wegeners granulomatosis and what does it cause

A

granulomatosis with polyangitis

  • vasculitis of small and medium vessels
  • upper airways disease common
  • saddle nose deformity
  • arthritis
  • treat with corticosteroids and rituximab to induce remission
  • methotrexate as maintainence
117
Q

What are the tests for COPD

A
  • FBC - increased PCV
  • CXR - hyperinflation, flat hemidiaphragms, large central pulmonary arteries, decreased peripheral vascular markings, bullae
  • CT - bronchial wall thickening, scarring, airspac eenlargement
  • ECG - right atrial and ventricular hypertrophy (cor pulmonale)
  • ABG - hypoxaemia +/- hypercapnia
  • spirometry - obstructive + air trapping ( FEV1 < 80% of predicted, FEV1:FVC < 70%, increased TLC and RV in emphysema, decreased DCLO (decreased diffusing capacity of lung for carbon monoxide) in emphysema
118
Q

what are the differentials of a COPD exacerbation

A
  • asthma
  • pulmonary oedema
  • upper respiratory tract obstruction
  • pulmonary embolus
  • anaphylaxis
119
Q

what is the treatment of pneumonia by organism type

A 
community
- strep pneumoniae - amoxicillin
- staph aureus - flucloxicillin
- haemophilus influenzae - amoxicillin 
- klebsiella pneumoniae - coamoxiclav
atypicals 
- legionella pneumophila - clarithryomycin 
-chlamydia pneumoniae - tetracycline
- mycoplasma pneumoniae - amoxicillin (cause of haemolytic anaemia)

hospital
- staph aureus/MRSA, enterobacter, pseudomonas aeruginosa - I.V aminoglycoside and penicillin

120
Q

what is the management of pneumonia

A
  1. assess using ABC - treat hypoxia (sats <88%)
  2. treat hypotension/shock from infection, assess for dehydration, consider IV fluid support
  3. investigations
  4. antibiotics
  5. analgesia for pleuritic chest pain
  6. if no improvement consider CPAP to recruit lung parenchyma. if hypercapnic will need non invasive or invasive ventilation
121
Q

what are the extrapulmonary features of CF

A
  • pancreatic insufficiency (DM)
  • gallstones
  • arthritis
  • osteoporosis
  • vasculitis
  • cirrhosis
122
Q

what is the first line investigation for pulmonary embolism

A
  • CT pulmonary angiography
123
Q

what are the signs of type 1 respiratory failure

A 
Cyanosis
Increased resp rate
Accessory muscle use
Tachycardia
Hypotension
Sign of underlying disease
124
Q

what are the signs of type 2 respiratory failure

A

Confusion
Flapping tremor
Bounding pulses
Papilloedema

Disturbed sleep
Frequent chest infections

125
Q

why does A1AT deficiency cause emphysema

A

Causes 2% of emphysema – RARE
inherited
A1AT regulates elastase activity
No A1AT = uncontrolled elastase activity
Elastase builds up in liver, causing cirrhosis
Elastase destroys alveoli leading to emphysema
Always consider in young patients with COPD and deranged LFTs

126
Q

what is asthma exacerbated by

A

cold air, exercise, emotion, allergens, smoking, infection, pollution, obesity

127
Q

which organism is likely to cause an upper RTI in CF patients and what is the treatment

A
  • pseudomonas aeruginosa (+ve oxidase test)

- ciprofloxacin

128
Q

what organism is likely to cause an upper RTI in a HIV patient and what is the treatment

A
  • pneumocystis jirovecci penumonia (PCP)

- cotrimoxazole

129
Q

what is the treatment of a strep infection

A

benzylpenicillin

Phase2a (10 decks)

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