Respiratory Flashcards
symptoms of asthma
intermittent dyspnoea, wheeze, cough (often nocturnal), sputum
signs of asthma
tachypnoea, audible (widespread, polyphonic) wheeze, hyper inflated chest, hyper-resonant percussion more, decrease air entry,
def dyspnoea
shortness of breath
def tachypnoea
rapid breathing
tests run for acute attack of asthma
PEF
sputum culture
FBC, UE, CRP, blood cultures
tests run for chronic asthma
PEF
spirometry
CXR
identifying allergens: skin prick tes, histamine challenge, Aspergillus serology
asthma differential diagnosis
pulmonary oedema ('cardiac asthma')
COPD
large airway obstruction (foreign body, tumour etc)
SVC obstruction, pneumothorax, PE, bronchiectasis, obliterative bronchiolitiswhich vaccines to get with asthma
influenza and pneumococcal
def peak expiratory flow rate
maximal rate that a person can exhale during short maximal expiratory effort after a full inspiration
what are the pathological changes in asthma
- smooth muscle and submucosal glands hypertrophy and hyperplasia
- infiltration of eosinophils, mast cells and neutrophils
- globlet cell metaplasia + loss of epithelium (–> mucus plug)
factors contributing to airway narrowing in asthma
- bronchial muscle contraction
- mucosal swelling/inflammation (mast cells and oesinophil degranulation –> release of inflammatory mediators)
- increase mucus production
precipitants in asthma
-cold air and exercise
-emotion
-allergens
-pollution and irritant dusts, vapours and fumes
-drugs (NSAIDs, beta-blockers)
-diet
infection, smoking exacerbate it
What range should body pH be kept
7.35-7.45
how to interpret blood gas results
- look at pH
- look at metabolic component (HCO3)
- look at respiratory component (pCO2)
- combine all of the above info
- check compensation is appropriate
- look at pO2 level
FEV1, FVC, FEV1/FVC ratio, RV and RV/TLC in obstructive lung disease
FEV1: (normal or) decreased FVC: normal od decreased FEV1/FVC ratio; decreased (<70%) \+ coving of the curve (in the flow volume loop) RV increased RV/TLC increased
FEV1, FVC, FEV1/FVC ratio, RV and RV/TLC in restrictive lung disease
FEV1: normal or decreased FVC: decreased FEV1/FVC ratio: normal or increased (>70%) RV decreased RV/TLC decreased
GOLD staging based on FEV1 for COPD
GOLD Stage I: FEV1 > 80%
GOLD Stage II: 50% < FEV1 < 80%
GOLD Stage III: 30 < FEV1 < 50
GOLD Stage IV: FEV1 < 30%
causes of clubbing
lung cancer congenital heart defects bronchiectasis CF lung abscess infective endocarditis interstitial lung disease coeliac disease cirrhosis dysentry grave's disease cancers (liver, GI, hodgkin lymphoma)
questions to ask at an annual asthma review?
- difficulty sleeping due to asthma (in the last month)?
- usual asthma symptoms during the day?
- has asthma interfered with usual daily activities?
in which conditions do you hear bronchial breathing?
- Consolidation
- Lobar Collapse with patent bronchus
- lung Cavity
how do you record serial readings of PEFR and for how long?
for diagnosis: 2-4 weeks (twice daily)
for occupational asthma: 2-4 hourly readings over several weeks
complete asthma control definition
- no daytime symptoms
- no night time waking due to asthma
- no need for rescue meds
- no asthma attacks
- no limitation on activity
- normal lung function (FEV1/PEF)
- minimal side effects from meds
asthma treatment
- SABA (for symptoms relief)
- inhaled corticosteroid as preventer therapy if
- use of inhaled SABA 3x/week and/or
- have asthma symptoms 3x/week+ and/or
- woken at night bt asthma symptoms 1x/week+
- -> use twice daily at first and then adjust dose (1 dose/day good for maintenance)
if symptoms not well controlled:
- recheck adherance, tehnique and trigger factors
- leukotriene receptor antagonist (LTRA) + ICS
- LABA + ICS
- MART (single inhalor with ICS and fast acting LABA)
Check this for adults/children
features of acute exacerbation of asthma
- agitation/connsciousness: signs of hypoxia
- signs of exhaustion, cyanosis and use of acessory muscles while at rest
grading of severity of asthma exacerbation
- moderate: PEFR > 50-75% best or predicted and normal speech, with no features of acute severe or life threatening asthma
- acute severe: PEFR 33-50% best or predicted OR resp rate >/= 25/min (people >12), 30/min (children 5-12) and 40/min (children 2-5) OR pulse rate 110/min (people >12), 125/min (children 5-12) and 140/min (children 2-5) OR inability to complete sentences in one breath, or accessory muscle use OR inability to feed (in infants), w/ O2sats >/= 92%
- life threatening: PEFR < 33% best or predicted OR O2sats < 92% OR altered consciousness OR exhaustion OR cardiac arrhythmias OR hypotension OR cyanosis OR poor rrespiratory effort OR silent chest OR confusion
acute exacerbation of asthma treatment
-O2 (aim 94-98%)
- quadrupling ICS at onset of asthma + oral prednisolone
-SABA: either with nebuliser (5mg (patients>5) and 2.5 mg (pateint 2-5)) or pressurised metered dose inhalor with large volume spacer (adult: 4 puffs initially then 2 puffs every 2 min (up to 10 puffs) repeat every 10-20 min if necessary. for a child: give a puff every 30-60s, up to 10 puffs)
-for life threatening or severe + poor repsonse, add nebulised ipratropium bromide
+magnesium
+ aminophyline (O2sats <92% and rising CO2)
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side effects of ICS
hoarse voice
cough
sore throat
oral thrush
side effects of SABA
trembling nervous tension headaches palpitations muscle cramps
side effects of anticholinergics (ie ipratropium)
dry mouth
constipation
cough
headaches
symptoms of COPD
dyspnoea (exertion) chronic cough sputum production wheeze (winter exacerbation)
COPD def
airflow obstruction, progressive and not fully reversible + does not change markedly over several months
difference between COPD and asthma
asthma reversible by 15%+ nocturnal cough (diurnal variation) in asthma
COPD causation
- smoking (tobacco, cannabis, biomass fuels etc)
- alpha1 anti trypsin deficiency
pathogenesis of inflammation in COPD
- goblet cell hyperplasia: protease
- airway narrowing (inflammation and scarring): fibroblasts
- alveolar destruction (empyema): CD8+ + T cells
what symptoms are associated with what pathophysiology?
- goblet cell hyperplasia: cough and sputum
- airway narrowing: breathless and wheeze
- alveolar destruction: breathlessness
COPD signs
tar staining on fingers central cyanosis tachypnoae chest hyper expansion reduced lateral and reduced vertical chest expansion reduced breath sounds wheeze palpable liver edge
CXR for COPD
-often normal
-hyperexpanction (low flat diaphragm and horizontal ribs)
-elongated and narrow heart
(mainly used to exclude other conditions)
CT scan in COPD
‘holes’ or bull
bronchial wall thickening
blood gases in COPD
T1RF: normal pH, PaO2 and HCO3 and reduced Pa02
T2RF low pH and PaO2 and high PaCO2, HCO3
if raised HCO3: one standing T2RF
natural history of COPD
- progressive decline in lung function
- progressive dyspnoea and disability
- right ventricular failure
- exacerbations
common infective causes of exacerbations in COPD
streptococcus pneumonia viruses moraxella catarrhalis haemophilia influenza pseudomonas aeroginosa
drugs given for COPD
- inhaled bronchodilators (SABA, LABA (activate sympathetic NS), anti muscarinics (activate parasympathetic NS))
- ICS (only for severe or frequent exacerbations)
- oral theophylline (bronchiodilate)
- O2
- mucolytics
- magnesium
COPD treatment pathway
- anti smoking advice
- flu and pneumococcal vaccination
- manage anxiety and depression
- pulmonary rehab
long term management:
- SABA + ICS
- LABA OR short acting anti muscarinic + ICS
- if FEV1/FVC < 50% or frequent exacerbations: add ICS
- if still SoB add LABA OR anti muscarinic
- if still breathless high dose bronchodilators (multi dose SABA or nebuliser)
- consider O2 therapy (nasal cannula)
if acute exacerbation (community):
- can give recovery pack or go to hospital
- antibiotics (if infective exacerbation)
- oral corticosteroids (if exacerbation in hospital or community)
- controlled oxygen therapy (T1RF or T2RF)
- physiotherapy (pos pressure devices to clear sputum)
if acute exacerbation (hospital):
- the above +
- nebulised salbutamol and ibutropium
- NIV
- IV theophylline
COPD complications
exacerbation pneumonia pneumothorax right ventricular failure peripheral neuropathy cachexia
how does magnesium work on the lungs
physiological Ca channel blocker effect (sympathetic pathway)
name a mucolytic
carbocysteine
generic names ICS
clenil
QVAR
pulmicort
flixotide
generic names LABA
servant
generic name LAMA
spiriva
generic name combination inhaler
seretide
symbicort
fostair
def T1RF
hyperaemic failure: Pa02 <8kPa
underlying pathology i.e. oedema, shunt or infection
def T2RF
ventilatory failure: PaCO2 > 7
reduced ventilatory effort results in gas trapping
pathophysiology of T2RD in COPD
- elastic recoil lost: gas trapping and reduced excretion of carbon dioxide (combined with water to form carbonic acid)
- lowers pH but as it is progressive, it is compensated by bicarbonate buffer system (kidneys reabsorb more bicarb)
clinical features of hypercapnia
dilated pupils bounding pulse hand flap myoclonus confusion drowsiness coma
diagnosing COPD pathway
- symptoms
- spirometry
- additionally: CXR (exclude other pathologies), FBC (identify anaemia and polycythaemia), BMI (should be btw 20-25 for COPD patients)
what is clinical effectiveness of influenza vaccine
overall 60-82% with lower protection in elderly subjects
how long does it take for influenza vaccine to be effective?
10-14 days
definition of CAP
songs of lower resp tract infection (fever/cough/phlegm/creps or bronchial breathing) + CXR changes
how do you assess severity of pneumonia
CURB65 -confusion -urea >7 mmol/l -resp rate > 30 BP (systolic < 90 mmHg or diastolic < 60 mmHg) -age >/=65
--> get 1 point per feature severity score: 0-1: low severity -2: moderate -3-5 high
what does NEWS measure?
RR O2sats systolic BP pulse rate level of consciousness/new confusion temperature
aetiologies of resp tract infections (upper, lower and pneumonia)
upper: primary viral
lower: viral and bacterial
pneumonia: viral, bacterial and fungal
(the higher you go, the most likely it is to be viral)
host defence to resp tract infections
- mechanical (nose, larynx, coughing)
- respiratory epithelium (ciliary beat, mucus, antimicrobial proteins)
- specific pathogen recognition
- inflammatory cell recruitment
- humoral and cell mediated immunity
classifications of pneumonia (+ aetiology)
- CAP (G+bact, mycoplasma, influenza)
- HAP (G-bact, staph, aureus) + ventilator-associated pneumonia (VAP)
- pneumonia in immunosuppressed host (unusual organisms, fungi)
- aspiration pneumonia (chemical, mixed flora)
- termnial pneumonia
typical bacteria in CAP
- streptococcus pneumoniae
- haemophilus influenzae
- klebsiella pneumonia
- staphylococcus aureus
atypical bacteria in CAP
- mycoplasma pneumoniae
- legionella pneumophilia
- chlamydia pneumoniae
- chlamydia psittaci
symptoms of pneumonia
- cough + purulent sputum/red + haemoptysis
- rigors/fever
- dyspnoa, orthopnea
- chest pain (pleuritic, sudden onset, worse on coughing)
non pulmonary symptoms:
- confusion (elderly, multi morbid patient)
- abdo pain
- D&V
- myalgia and arthralgia
signs in pneumonia
- high T°
- tachypnoea
- reduced chest expansion on side of infection
- dull percussion over affected area
- bronchial breathing
- focal crackles
- pleural rub
- mental confusion
investigations in CAP
- O2 sats, ABG
- sputum culture/throat swab for virus
- urine pneumococcus and legionella antigen
- bloods:
- FBC: WBC, Hb
- platelets (inflam process)
- CRP
- PCT (procalcitonin)
- U&Es (AKI)
- lactate (sepsis/shock)
- LFTs (reduction in liver perfusion associated with sepsis)
- blood culture
- CXR
treatment for low severity CAP
amoxicillin (or doxycycline or clarithromyocin)
treatment of moderate severity CAP in hospital
amoxicillin and a macrolide (oral or IV)
treatment of severe CAP in hospital
broad spectrum beta lactase stable antibiotic (i.e. co-amoxiclav) + macrolide
complications of CAPs
- parapneumonic effusion
- infectious complications: empyema, lung assess, metastatic infection
- VTE
- worsening of comorbidities
- SE of antibiotics
- sepsis
how do diagnose HAP
new onset symptoms + compatible CXR dvlping after 48h+ of patients admission or within 1 month after discharge
difference between early and late onset HAP
- early onset HAP: occurs within 4-5 days of admission and is usually caused by antibiotic sensitive community organism
- late onset HAP: >5 days: more likely to be caused by antibiotic resistant hospital pathogens
bacterial causes of HAP
- enterobacteria (E coli, Klebsiella, enterobacter)
- staphylococcus aureus
- pseudomonas
- environmental gram neg: acinetobacter, stenotrophomons maltrophilia
risk factors in developing HAP
- ICU stay, mechanical ventilation
- prolonged hospital stay
- severe underlying illness, multiple co-morbidities
- underlying rest disease
- abdominal surgery, vomiting/aspiration
pathophysiology of bacterial pneumonia
- acute inflammation of lung parenchyma
- cellular (neutrophil) infiltration
- inflammatory exudate in th interstitial
- alveolar oedema and haemorrhage
what and which are the ESKAPE pathogens
what: pathogens beyond treatment
which: E. faecium S. aureus K. pneumoniae A. baumanil P. aeruginosa Enterobacter spp
how do antibiotics that are mosquito nets or fly swats work?
mosquito nets: time dependent
fly swats: dose dependent
what is antibiotic stewardship?
right drug at the right time
MIND ME
Microbiology guides therapy wherever possible
Indications should be evidence based
Narrowest spectrum required
Dosage appropriate to the site and type of infection
Minimise duration of therapy
Ensure mono therapy in most situations
difference between typical and atypical organisms
typical organisms can be cultured in lab
atypical ar intracellular and can’t be cultured
fungal cause of pneumonia
pneumocystis jirovecii (in immunocompromised patients)
natural history of patient recovering from pneumonia
1 week: fever should have resolved
4 weeks: chest pain and sputum production should be reduced
6 weeks: cough and breathlessness should be reduced
3 months: most symptoms should have resolved but fatigue still may be present
6 months: should be back to normal
when should you give antibiotics?
- prophylaxis in immunosuppression (ie to prevent organ rejection)
- prophylaxis in significant lung, heart, renal, liver or neuromuscular disease
- prophylaxis in patients >65 w/ 2 of the following: DMT1/2, HF, hospitalisation in the last year or being treated with oral corticosteroids
- therapy
- pre-emptive therapy (presumed infection)
SEPSIS 6?
in:
- O2
- IV antibiotics
- fluid
out:
- blood culture
- lactate
- urine output
TB pathology and natural history (primary infection)
- no specific immunity
- small lung lesion (Ghon focus)
- regional lymph node involvement
- haematogenous spread
- heals with develoment of specific immunity + fibrosis
- asymptomatic in 90%
TB pathology and natural history (post-primary infection)
- reactivation of persisting mycobacteria (latent infection)
- much greater immune response
- usually symptomatic
TB symptoms
- weight loss
- fever
- night sweats
- cough +/- sputum
- haemoptysis
- lymph node enlargement
- pleuritic pain
- bone pain
investigations in TB
-CXR
-ESR/CRP
HIV test
-LFTs (cuz TB can affect liver and drugs given can cause problems in the liver)
-sample for microbiology (sputum smear and culture + aspirate/biopsy i.e. pleura, lymph nodes)
-PCR/histology/cytology
-Mantoux test (for any exposure)
-interferon gamma for active exposure
CXR in post primary disease
- upper lobe consolidation
- hilar pulled up due to fibrosis
- cavitation
- volume loss
- lymphadenopathy
- pleural effusion
- pneumothorax
def of military TB
pulmonary homogenous dissemination of uncontrolled TB infection (usually in the immunocompromised)
poor prognosis
what is the pulmonary nodule called in TB and what is it formed by?
granuloma:
- core of caseating necrosis
- layer of epithelial cells
- outer layer of lymphocytes
def mono-resistance TB
resistance to one antituberculosis drugs
def poly-resistance TB
resistance to more than one antituberculosis drug, other than isoniazid and rifampicin
def multidrug-resistance TB
resistance to at least isoniazid and rifampicin
def extensive drug resistance TB
resistance to any fluoroquinolone, and at least one of three injectable second line drugs (capreomycin, kanamycin and amikacin), in addition to multi drug resistance
treatment of TB
6 months of isoniazid (with pyridoxine) and rifampicin
2 months with pyrazinamide and ethambutol
what is TB caused by?
mycobacterium tuberculosis complex:
- M. tuberculosis
- M. bovis
- M. africanum
3 priorities of TB control
- detect and treat cases of active TB
- detect and treat cases of latent infection (targeted)
- offer BCG vaccine (targeted)
(+wider determinants of health: poverty, malnutrition…)
risk assessment equation in TB
risk = (particles/volume)x exposure time
volume: volume of air/space
red flag symptoms in resp
haemoptysis weight loss persistent cough dyspnoea pain changes in fingers suggesting clubbing pain in limb indicating hypertrophic osteoarthopathy
non metastatic manifestations of lung cancer
-clubbing and hypertrophic pulmonary arthropathy (HPOA)
hormone syndromes:
- Cushing’s syndrome (ACTH)
- SIADH (syndrome of inappropriate antidiuretic hormone secretion)
- hypercalcamia
neuromyopathies:
- Eaton Lambert syndrome
- peripheral neuropathy
- dementia
- cerebellar syndrome
how do you go about breaking bad news
SPIKES framework:
- Setting
- Patient perception
- Invitation to continue with information
- Knowledge in small chunks
- Empathy for shock/other emotions
- summarise/strategise
why are lungs common site for secondary metastatic cancer?
cardiac output going through lungs
types of bronchial carcinoma?
- small cell
- squamous
- adenocarcinoma
- large cell
- alveolar cell carcinoma
- bronchial adenoma
clinical presentation of bronchial carcinoma
cough haemoptysis chest pain breathlessness stridor hoarse voice weight loss facial swelling, headaches (SVC obstruction)
clinical examination in bronchial carcinoma
weight loss finger clubbing lymphadenopathy chest asymmetry focal chest signs (consolidation, fluid) hepatomegaly (metastesis) neuropathy (non metastatic manifestations)
what helps you differentiate between pleural effusion and collapse?
mediastinum + trachea
pleural fusion: pushed away
colapse: pulled towards
what is Pancoast syndrome?
lung tumour arises in apex: grows upwards into base of neck. it can grow into brachial plexus:
- pain in inner aspect of arm
- Horner syndrome due to sympathetic nerve supply comes out at T1, reaches lower part of brachial plexus and follows carotid up to eye (pupil is small + droopy, sullen and dry eye on affected side)
differential diagnosis to bronchial carcinoma
TB
pneumonia
lung metastases from other primary
benign lung tumours
investigations in bronchial carcinoma
CXR, CT scan bloods (LFTS, FBC, calcium) fiberoptic bronchoscopy percutaneous needle biopsy node biopsy mediastinoscopy/mediastinotomy thoracotomy
when is bronchial carcinoma inoperable?
(-smal cell)
- distant metastasis
- mediastinal spread (recurrent laryngeal nerve palsy, phrenic nerve palsy)
- poor pulmonary function
- frequent angina/HF
- psychological failure
how do you treat small cell carcinoma?
chemotherapy
palliation
how do you treat non small cell carcinoma
- surgery
- radical radiotherapy
- palliation (symptomatic, radiotherapy and chemotherapy)
EGFR and lung cancer?
epidermal growth factor receptor: protein found on surface of some NSCLC cells
–> EGFR mutation positive predicts response to specific chemotherapy (gefiinib)
where does bronchial carcinoma spread to?
liver kidney pleura bone adrenal glands
squamous cell carcinoma?
- epidemiology
- location/histology
- clinical presentation
- smokers
- more in bronchi (central), (may see desmosomes or keratin accumulation), invade lympathics
- can secrete hormones (PTH-like CMPD: hyprcalcaemia)
adenocarcinoma?
- epidemiology
- location/histology
- presentation
- non smokers
- peripheral disease, mucus production
- hypertrophic osteoarthritis triad: clubbing, long bone swelling and arthritis
small cell carcinoma?
- epidemiology
- presentation
- smokers (exclusively)
- paraneoplastic syndromes: secretes ACTH, ADH, Eaton Lambert
what is the commonest cause of high serum calcium
malignancy
- breast cancer cells
- squamous lung cell carcinoma
- cholangiocarcinoma
- multiple myeloma
def asbestosis
chronic lung condition associated with lung fibrosis that follows chronic exposure to asbestos (thickening and fibrosis of visceral pleura)
