respiratory Flashcards
steroid side effects
HTN osteoporosis stomach ulcers skin conditions eg acne cushionian like features
what happens if you suddenly stop long term steroids
addinsonian crisis
preventing pneumonia in elderly
oral hygiene
head position when sleeping -45 degrees
SALT assessment
pneumococcal and flu preventative vaccines
the trick to remember how long consolidation takes to clear
works in decades
eg 80 year old person will take 8 weeks for consolidation to clear
cxr to check its gone in 6-8 weeks - to ensure not malignant
s/e of co-amox that is forgotten
can cause hepatic cholestasis
method to read x-rays
AP or PA?
1- details
2- rotated film? is trachea in middle of clavicles?
3 - inspiration - 6 ribs anteriorly, 10 posteriorly
4- penetration - can you see a spine through the heart (how good the xray is)
OBVIOUS ABNORMALITIES
5 - A airways (trachea in middle of spine)
- B breathing - check lung fields (apices, behind heart, angles, hilar, diaphragms)
- C = cardiomegaly
- D = diaphragms
- E = everything else - bones, soft tissue, pneumomdiastinum/peritoeneum
6 - Lines - endotracheal/nasogastric/central
7 - review areas - apices, hila, behind heart, costophrenic angles
8 - SUMMARISE - include differentials (with ur clinical judgement suggest management)
pe scores
- wells
- perc
- pesi
WELLS
- clinical signs/symps of DVT +3
- PE is number 1 diagnosis +3
- HR >100 +1.5
- immobilised - reduced mobility >3 days/ surgery within 4 weeks +1.5
- previous PE/DVT +1.5
- malignancy - active/past 6 months/palliative +1
- haemoptysis +1
score = 4 PE unlikely -> D-Dimer
- if high then CTPA/VQ scan
- if low no PE
>/5 PE likely -> CTPA/VQ scan
PERC - pulmonary embolism rule-out criteria - allowing you to feel confident to rule out PE and safely discharge age >/=50 HR >/= 100 02 sat on room air <95% unilateral leg swelling haemoptysis recent surg/trauma = 4 weeks ago prior PE or DVT hormone use
PESI - PE severity index predicts 30 day outcome of patients with PE - age sex hx of cancer history HF hx of chronic lung cancer HR >/= 110 systolic BP <100 RR >/=30 T <36 altered mental status o2 sats<90
how to assess SOB severity - options
WHO functional class
MRC breathlessness scale
Borg scale
NYHA class
what are the steps of the MRC breathlessness scale?
Grade 1 - are you troubled by breathlessness except on strenuous exertion?
Grade 2 - are you breathless when hurrying on the level or uphill?
Grade 3 - do you have to walk much slower on the flat than other people? Do you have stop after a mile or so on the level at ur own pace?
Grade 4 - do you have to stop for breath after walking on the level after 100 yards (or after a few mins)
Grade 5 - are you too breathless to leave the house, or breathless after undressing?
what drugs are notorious for changes in lungs
nitrofurantoin
anti rheumatoid drugs
why is giving lots of o2 potentially dangerous for those in type 2 resp failure?
as they rely on hypercapnia to drive ventilation there by replacing the 02 you are removing that drive
what is Procalcitonin used for?
to determine between viral or bacterial infections
if low avoid abx
what is Procalcitonin used for?
to determine between viral or bacterial infections
if low avoid abx
released in response to TNF-alpha and IL-6
CURB 65
confusion - <8/10 AMT urea >7mmol/l RR >30 BP <90 or <60 age >/65
0 = communitu
1 = mortality low - home care if 02 >92% air + CXR shows no bilateral/multilobar shadowing
2 = mortality intermediate - hosp
3 + = mortality high - hosp/ITU? 30% dead in 30 days
acute eosinophilic pneumonia what is it pres causes ix mx comps
what is it
- uncommon
- the rapid accumulation of eosinophils in the lungs
pres
- progressive dyspnoea of rapid onset and poss acute resp failure
- cough
- fatigue
- night sweats
- fever
- unintended weight loss
- 20-40 year olds
causes
- smoking
- inhaled recreational drugs
- medicines
- infections - parasites, fungi, viruses
- mainly unknown tho - above are more triggers
ix - FBC
CXR
ABG
bronchoalveolar lavage - diagnosis
chest CT - alveolar bilateral consolidation + effusion, interlobular septal thickening
pulm function test show restrictive pattern
mx - oral corticosteroids
what is the commonest form of occupational lung disease
mesothelioma - asbestosis
nasal cannula oxygen percentage delivery of: 1L/min 2L/min 3L/min 4L/min
pros and cons
1L - 24%
2L - 28%
3L - 32%
4L - 36%
varies massively on the patient minute volume, inspiratory flow and pattern of breathing comfortable no re-breathing low cost preferred by patients can be used in type 1 and 2 failure
maximum flo rate of simple face mask
pros and cons
40-60% 15L/min
used for patients with type 1 after surgery - reason for this as you create a dead space within the mask and if this is not cleared you will rebreathe the CO2
flow must be at least 5L/min to avoid CO2 build up and resistance to breathing
non-rebreather mask
% and flo rate
60-90%
used in emergency
10-15L/min
amount of fluid needing to be in pleural space before you see it on CXR
250mls
eosinophilic lung diseases, name:
- idiopathic
- secondary
- eosinophilic vasculitis
idiopathic -
- simple pulmonary eosinophilia
- acute eosinophilia pneumonia
- chronic
- idopathic hypereosinophilic syndrome
secondary
- bronchocentric granulomatosis
- parasitic infection
- allergic bronchopulmonary aspergilosis
- drug reaction
eosinophilic vasculitis
- allergic angitis
- granulomatosis (churg-strauss syndrome)
churg-strauss syndrome aka what is it pres causes ix mx comps
aka eosinophilic granulomatosis with polyangiitis (wegeners - has extra features)
what is it
ANCA associated small-medium vessel vasculitis
LTRA may precipitate the symps
pres
THINK - adult onset asthma!!
TRIAD - tissue eosinophilia, granulomatous inflammation, vasculitis
diagnosis criteria - asthma (wheeze), oesinophilia in peripheral blood (>10%), paranasal sinusitis, plumonary infiltrates, histo confirmation of vasculitis, mononeuritis multiplex
haemoptysis - more wegeners
purpura/skin nodules
ix
p-ANCA - 60%
FBC - oesinophilia + anaemia, elevated ESR/CRP
CXR - plum infiltrates
Pukm CT -peripheral consolidation - ground-glass attenuation
biopdy - small necrotising granulomas and necrotising vasculitis
FIVE FACTOR SCORE (if positive then wegener’s granulomatosis aka granulomatosis with polyangiitis) - proteinuria, serum creat, GI involve, cardiomyopathy, CNS involvement = higher mort
mx
corticosteroids
- for remission - IV methylpred 3/7 then oral pred
- if five factor score +ve - then add cyclophosphamide
+asthma management
sleep architecture (stages)
wakefulness REM - when you are dreaming N1 - light sleep N2 - 45-50% of total sleep N3 - slow wave sleep first half of night more deep, second half more likely to dream
classification of sleep disorders
ICSD 3rd edition
severn major catagories
- insomnia (short term, chronic, other)
- sleep-related breathing disorders (CSA, OSA, hypoventilation)
- central disorders of hypersomnolence (narcolepsy, idiopathic hypersomnia)
- circadian rhythm sleep-wake disorders (shift work, advanced/delayed sleep wake phase disorder)
- parasomnias (NREM, REM, other)
- sleep-related movement disorders (restless legs, periodic limb movements, bruxism)
- other (unclassified)
symptoms of sleep disorders
daytime sleepiness unrefreshed sleep snoring sleepwalking sleeptalking irritable morning headache poor conc poor progress in school HF/pulm HTN cataplexy hallucinations
obstructive sleep apnoea what is it pres predisposing factors consequences causes ix mx
what is it repeated partial (hypopnoea) or complete (apnoea) closure of the upper airway during sleep
pres daytime sleepiness imparied conc, poor mem, mood changes loss of libido weight gain snoring - very loud stopping breathing and waking up sensation of drowning
predisposing factors
- obesity
- macroglossia: acromegaly, hypothyroidism, amyloidosis
- large tonsils
- marfans
consequences
- daytime somnolence
- compensated resp acidosis
- hypertension
ix POLYSOMNOGRAPHY - diagnostic: - repeated dips in blood o2 - o2 oximetry - repeated pulse rate rises - measure airflow in nose - thoracic and abdomen paradoxing - not moving at same time - very loud snoring - EEG -arousal from sleep reduced sleep qual
epworth sleepiness scale - questionnaire by pt/partner
multiple sleep latency test - EEG - measures time to fall asleep in dark room
mx CPAP mandibular advancement devices lifestyle - weight loss - position retraining - no sleeping on back - reduce alc intake surgery - tonsillectomy, bariatric surg - inform DVLA
central sleep apnoea what is it pres causes ix mx
what is it
repetitive cessation of both airflow and ventilatory effort during sleep
- idiopathic
- secondary (cheyne-stokes, high altitude, drugs etc)
pres
common in HF _ intracranial pathology
diagnosis
history - v v important
questionnaires/screening
sleep studies
ix -
tier 3 limited channel studies - flat lining, no movement from chest/abdo, no airflow
questionnaire points for sleep disorders
OSA symps
anthropometry - BMI, neck circ
demo - gender, age (hertiage - south asians have large tongues)
co-morbs - hypertension, stroke, CAD, etc
how likely to fall asleep in these scenarios questionnaire
STOPBang questionnaire - sleep apnoea S - do you snore loudly T - do you often feel tired during daytime? O - has someone observed you stop breathing during you sleep? P - high blood pressure? B - BMI >35 A - age >50 N - neck circ >16 inch G- gender male
high-risk of OSA - 5-8
inter - 3
low - 0-2
investigating sleep disorders
pulse/o2 oximetry
limited channel studies - most common first line study, completed at home
narcolepsy deficiency of what pres ix mgmt
very rare
1 in 100,000
deficiency or absence of hypocretin - CSF (protein responsible for controlling appetite and sleep patterns)
HLA DR2
cataplexy - involuntary loss of muscle tone
sleepiness - sleep attacks
hypnagogic hallucinations/sleep paralysis
multiple sleep arousals at night
distorted sleep architecture
can have OSA/PLMS
onset - teenage years
IX
reduced REM latency (<60 mins)
multiple sleep latency testing - EEG
mx
modafinil - stimulant, wakefulness drug
sodiu, oxybate - powerful sedative, anti-cataplectic
pitolisant - novel histamine H3 receptor antagonist
lung cancer - epidemiology
world leading cause of cancer deaths for men
2:1 men:women
40k new cases in UK per annum
90% are smoking related
2 main types of lung cancer
small cell lung cancer 20-25% of all lung cancers most aggressive - usually disseminated by time of diagnosis, freq to liver, bones, adrenals, brain SIADH common chemo/radiosensitive surg not an option untreated - 6/52 to live arise from APUD (amine precurser uptake decarboxylase) cells usually central
non small cell commonest - 75-80% 4 types: - squamous - adenocarcinoma - bronchialveolar carcinoma (adenocarcinoma in situ, alveolar - mainly not smoking related, ++sputum, bronchial - mostly carcinoid) - large cell carcinoma
histology of adenocarinoma of lung
typical acinar pattern of glandular differentiation observed
challenges of lung cancer
majority of patients present in advanced stages
not always symptomatic/non-specific
poor resp physiology (other co-exisiting lung pathology)
direct link between cancer and social deprivation index
common symptoms/signs of lung cancer - most to least (including atypical)
cough haemoptysis dyspnoea chest pain unexplained weight loss paraneoplastic symptoms - SIADH, neurological syndromes
O/E - fixed monophonic wheeze, supraclavicular lymphadenopathy or persistent cervical, clubbing
atypical - SVCO T1 wasting hoarse voice (seen in pancoast tumour pressing on recurrent laryngeal nerve) horners
paraneoplastic features small cell squam adeno large cell
small cell
ADH -> SIADH -> hyponatraemia
ACTH - not typical, hypertension, hyperglycaemia, hypokalaemia, alkalosis and muscle weakness are more common than buffalo hump etc (cushings)
lambert-eaton syndrome
squam
- central
- parathyroid hormone-related protein secretion causing hypercalcaemia
clubbing
- hypertrophic pulmonary osteoarthropathy - bone pain
- hyperthyroidism due to ectopic TSH
adenocarcinoma
- peripheral
- gynaecomastia
- hypertrophic pulmonary osteoarthropathy
large cell
- B-hCG
- anaplastic
- poorly differentiated with poor prognosis
lambert-eaton syndrome what is it pres causes ix mx
myasthenic syndrome
seen in association with small cell lung cancer and sometimes breast/ovarian
may occur independantly as autoimmune disorder
pres
repeated muscle contractions -> increased muscle strength - only seen in 50%
limb-girdle weakness (affects lower limb first)
hyporeflexia
autonomic symptoms: dry mouth, impotence, difficulty micturating
ophthalmoplegia and ptosis not commonly a feature
causes
antibody directed against presynaptic voltage-gated calcium channel in peripheral nervous system
ix
ElectroMyoGraphy - incremental respinse to repetitive electrical stimulation
mx
rx underlying cancer
immunosuppression - pred +/or azathioprine
3,4-diaminopyridine currently being trialled
IV IG and plasma exchange
inital tests in lung cancer
CXR
- neither sensitive or specific
- low dose radiation
staging CT (chest + upper abdomen- includes adrenals)
- standard for diagnosing
- highly sensitive/specific
- requires contrast - so not good if they have poor kidney function
PET-CT - using radioactive Fluorodeoxy-glucose)
- gold standard for staging
inital tests in lung cancer
CXR
- neither sensitive or specific
- low dose radiation
staging CT (chest + upper abdomen- includes adrenals)
- standard for diagnosing
- highly sensitive/specific
- requires contrast - so not good if they have poor kidney function
PET-CT - using radioactive Fluorodeoxy-glucose)
- gold standard for staging
- shows areas of high metabolism as use the glucose = malignant areas
used for non-small cell
bloods
- raised platelets maybe
staging lung cancers + their survival
TNM
TNM
T1: < 3cm
T2: 3-7cm, assoc atelectasis, involves main bronchus >2cm to carina, invades visceral pleura
T3: >7cm and directly invades chest wall, diaphragm, phrenic, mediastinal pleura, parietal pericardium
T4: invasion of mediastinal organs: oesophagus, trachea, great vessels, heart, malignant pleural effusion, recurrent laryngeal
N1: ipsilateral bronchopulmonary or hilar
N2: ipsilateral mediastinal or subcarinal
N3: contralateral mediastinal, hilar or any supraclavicular
M1: mets present, contralat lung or malignant pleural effusion
stage 1 = T1/T2, N0, M0
2 = T1/T2 + N1 or T3 + N0
3 = Any N3, T1/T2 N2 or T3 N1 or any T4
4 = Any M1
2 year survival from top to bottom goes from 97% to 10% incrementally
most common mutation in lung adenocarinoma
Unknown then
KRAS then
EGFR- sensitising
further tests for diagnosis in lung cancer
bronchoscopic biopsy + camera (literally see it)
CT guided biopsy - accessed from outside body
management of lung cancer
MDT
follow national optimal lung cancer pathway - certain time frames for things
small cell - only considered for surg T1-2a, N0M0.
most chemo, radio
extensive? palliative chemo
radical treatment
- surgery - only 20% suitable
- radiotherapy - stereotactic ablative radiotherapy, external beam radiotherapy
- chemo-radio - concurrent or sequential
advanced cancer
- palliative intent (chemo, radio for brain/bony mets, pain/haemoptysis, targeted molecular therapy/immunotherapy)
- symptomatic management (pain,breathlessness, o2, palliative care)
things to consider in lung cancer management
managing expectations
patient wishes
risks vs benefits
think about why you want to treat - surviving longer? maintaining qual of life..
carcinoid
slow growing
excessive secretion of serotonin: flushing + diarrhoea
from neuroendocrine cells (kulchitsky cell - small cell)
lung cancer referral NICE guidelines
a suspected cancer pathway referral for:
- CXR findings that suggest lung cancer
- are aged 40 and over with unexplained haemoptysis
offer an urgent CXR (within 2/52) for >40 + 2 or more, or smoker + 1 or more of: - cough - fatigue - SOB chest pain weight loss appetite loss
consider urgent CXR in >40 with any of :
- persistent or recurrent chest infection
- finger clubbing
- supraclavicular lymphadenopathy or persistent cervical lymphadenopathy
chest signs consistent with cancer
thrombocytosis
surgery contraindications in lung cancer
assess general health
stage IIIb or IV (i.e. metastases present)
FEV1 < 1.5 litres is considered a general cut-off point*
malignant pleural effusion
tumour near hilum
vocal cord paralysis
SVC obstruction
pancoasts tumour
what is it
pres
tumour of the pulm apex
normal lung cancer symps + invasion of brachial plexus so weakness, parasthesia, pain in C8-T1, shoulder pain
invasion of sympathetic chain - horners syndrome (ptosis, miosis, ipsilateral anhydrosis)
pneumonia what is it causes pres ix mx discharge criteria + safety netting
strictly any inflammation of the alveoli - vast majority is caused by a bacterial infection
causes- bacterial, viral, fungal
- Streptococcus pneumoniae - pneumococcus accounts for 80%, vaccine available
- Haemophilus influenzae - COPD
Staphylococcus aureus - often post influenza
mycoplasma pneumoniae - atypical (autoimmune haemolytic anaemia and erytherma multiforme may be see)
legionella pneumophilia - atypical, holidays (secondary to infected air con units), hyponat + lymphopenia common
klebsiella pneumoniae - alcoholics
pneumocystis jiroveci - HIV, dry cough, exercise-induced desats and absence of chest signs
idiopathic interstital pneumonia - group of no-infective causes eg broncholitis from comps of RA or amiodarone
pres
cough, sputum, dyspnoea, pleuritic chest pain, fever, tachycardic, low 02 sats, reduced breath sounds, bronchial breathing
ix CXR - consolidation bloods - FBC, U+E, CRP, ABG sputum culture blood culture pneumococcal and legionella urinary antigen tests
mx abx - PCT, CRP LOW SEV CAP - first - amoxicillin - pen allergy? macrolide (erytho/azitho/clary) or tetracylcine - 5/7 MED SEV CAP - dual abx - amox + macrolide -7-10/7 HIGH SEV CAP beta-lactamase stable pen eg co-amox, ceftriaxone or tazocin(piperacillin eith tazobactam) + macrolide supportive - O2, fluids CURB-65
discharge criteria + safety netting cannot go home if in last 24 hours had: fever >37.5 RR >24 HR >100 SBP <90 sats <90% air abnormal mental status inability to eat without assistance
pleural effusion what is it types + path causes criteria pres ix mx
what is it
excessive fluid in potential space between visceral and parietal pleura
restrictive lung disease
types
- transudate - low protein <30g/l
- disruption of hydrostatic and oncotic forces across pleural membrane (increase venous P or hypoproteinaemia)
- eg increase in hydrostatic is LHF, decreased oncotic pressure = kwashiorkor, severe liver disease, nephrotic, malabsorption - exudate - high protein >30g/l
- increased permeability of the pleura from inflammation
- eg sickle cell disease, pneumonia, TB, lung abscess, bronchiectasis, primary myelofibrosis, cancers, SLE, PE, asbestos - chylous
- pseudochylous
- haemorrhagic
causes 1 - pulm 2 - pleural 3 - extrapulm more likely to be benign than malignant if is malignant - 40% lung mets, 25% breat mets, 10% malignant mesothelioma
Light criteria if protein 25-35g protein:
LDH measurement + protein in pleural fluid and serum
for exudate:
- pleural to serum protein >0.5 or
- pleural to serum LDH >0.6 or
- pleural LDH >2/3 upper limit of normal
pres dyspnoea cough unequal chest movements decreased tactile vocal fremitus (as gone from solid to liquid) tracheal shift dullness to percuss diminished breath sounds
ix
CXR - PA in everyone
USS recommended - increase likelihood of successful aspiration + can see septations
thoracentesis - 21G needle and 50ml syringe -> fluid sent to lab for cytology, MC&S, AFB, LDH, protein, glucose, amylase, RF- characteristic findings aside from lights:
- low glucose: RA, TB
- raised amylase: panc, oesoph perf
- heavy blood: mesothelioma, PE, TB
all patients with effusion secondary to infection need fluid sampling - if purulent or turbid/cloudy = chest drain, if clear but pH <7.2 = chest drain
mgmt do NOT tap transudate if recurrent: - recurrent aspiration - pleurodesis (talc) - indwelling pleural catheter - opioids to relieve dyspnoea - abx if infection
comps
large? compress lung
parapneumonic effusion -> organizing pleural fibrosis -> lung cannot expand
how can CRP help you decide whether you need abx or not for pneumonia
<20mg/L - NO
20-100mg/L - delayed abx
CRP > 100 - abx
why is it resp acidosis when co2 is high
as when breathing is inadequate CO2 accumulates. The extra co2 molecules combine with water to form carbonic acid which contributes to an acid pH. the treatment is all else fails is to lower the pco2 by breathing for the patient using a ventilator
if an abg shows metabolic acidosis explain the physiology behind this
when normal metabolism is impaired acid forms - poor blood supply stops oxidative metabolism and lactic acid forms. if severe patient may be in shock and require treatment, normally by neutralizing excess acid with bicarb possibly by allowing time for excretion/metabolism
where is the metabolism component on an abg controlled by in the body?
kidneys
if the paco2 is high on abg what are the two potential causes for this
resp acid
resp compensation for met alk
if pac02 is low on abg what are the two potential causes for this
resp alk
resp comp for met acid
if HCO3 is low (<22) on abg what are the two potential causes for this
met acid
or renal comp for resp alk
if HCO3 is high (>26) on abg what are the two potential causes for this
met alk
or renal comp for resp acid
what is the difference between the terms pao2 and fio2
pao2 - arterial oxygen partial pressure in mmHg - basically the amount of oxygen in arteries
fio2 - fractional inspired oxygen - conc of oxygen that a person inhales
what is the henderson equation
h+ is proportional to co2/HCO3
h+ = k x (co2/Hco3)
what can you get on an ABG
pH co2 bicarb sodium, pot, calc, chloride, glucose lactate, haemoglobin oxygen sats CO hb Fi02
two main things to elicit that are important in an asthma history
- day-to-day control
- exacerbation history
questions to ask to gather severity of asthma
- risk of life-threatening episodes (exacerbation history)
- how many times in the last 12 months have you needed a course of steroids from your GP?
- how many times have you been to A+E/admitted/ITU/ventilated? - day-to-day symps
RCP3 questions
gold-standard investigation for asthma/COPD
spirometry lung function test looking at obstructive or restrictive
asthma - FEV1 before and after bronchodilator, should see a change (reversibility)
whats a good test to see if inflammatory response in lung - eg allergic asthma
exhaled nitric oxide, gas thats made from inflamed lung
also good to monitor and guide treatment
someone has mild asthma, bit wheezy but always seem quite well whats a good test for them
measure if lungs are twitchy by doing a bronchiohyperesponsive challenge (BHR) to a common lung irritant like mannitol or histamine, and how easy they begin wheezing gives you an idea of how twitchy the airway is
what is asthma generally
inflammation underpinned by bronchial hyperresponsiveness
reversibility - comes and goes which causes the wheezy
inflam - mucous
triggers!!
asthma types
pro-atopic pro-eosinophilic group (TH2 high)
non-atopic non-eosinophilic group (TH2 low)
how much asthma may be occupational
10%
dont miss it out in social history
key management of asthma - one answer
inhaled corticosteroid
what do you have to warn patients about before starting them on a LRTA
montelukast can cause nightmares
tablets
neuropsychiatric reactions, including speech impairment and obsessive-compulsive symptoms
really severe asthma resistant treatment - what can we give
biologics - end in -mab, monoclonal antibodies
REALLY expensive - £30,000/year/person
work on different phenotypes:
- ones that work on IL-5 all treat the eosinophilic asthmas as IL-5 is used to create cytokines
omaluzumab - removes IgE, good for allergic asthma and hayfever
LIFECHANGING
asthma what is it pathophysiology causes/rf triggers pres ix mx comps
what is it
chronic inflammatory disorder of the airways secondary to type 1 sensitivity. symptoms are variable and recurring and manifest as reversible bronchospasm resulting in airway obstruction
pathophysiology
ATOPIC
- irritant/allergen -> binds to IgE -> mast cells cause increase in -> leukotrienes, histamine, TNFa
- this leads to increase smooth muscle contractility, hypersecretion of mucus, increase vascular permeability
- 6hrs later -> airway remodelling, increased airway hypersensitivity, increase goblet cells
causes/rf
- maternal smoking
- atopy - personal or fh
- hygiene hypothesis - causes TH2 predom response
- viral illness (in children they wheeze with this, difficult to differentiate) - during preg espesh RSV
- occupation - flour
- not breastfed
- exposure to high conc of allergens
- air pollution
- low birth weight
triggers
- house dust mite
- infection
- pollen/pets
- stress
- cold
- exercise
- emotion
- smoking
pres
diurnal variation of (worse at night/early morn):
- cough - often worse at night
-wheeze
-SOB
- chest tightness
hyperinflation of chest
harrison’s sulci - dent below costal margin
nasal polyps - in severe asthma
10-15% of adult asthma is occupational - isocyanates + flour!
expiratory polyphonic wheeze on auscultation
ix Lung function: PEFR - diurnal variation >20%, or with SABA FEV1 - significantly reduced, should improve by 15% with SABA FVC - normal FEV1/FVC - <70% fractional exhaled nitric oxide - rises when eosinophils present FBC - eosinophilia skin prick test weekday/weekend asthma diary for occupational ?CXR - adult + smoker questions in history - how often felt SOB? - often wake up from sleep? - often used reliver? - affect ADL? - do you think its under control - inhaler technique
mx (general)
- SABA
- SABA +ICS (<400mcg budesonide)
- SABA + ICS + LRTA (montelukast)
- swap LRTA for LABA
- SABA +/- LRTA + MART (steroid + laba)
- increase ICS dose in MART
- SABA +/- LRTA theophylline
- refer
triad of atopy
igE mediated asthma
allergic rhinitis
atopic dermatitis
