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
drug cautions with asthmatics
beta blockers - B2 cause airway obstruction
NSAIDS or aspirin block COX-1 -> decrease prostaglandins + overproduction of pro-inflammatory leukotrienes
RCP3 questions
in the last month have you
- had difficulty sleeping due to your asthma symptoms
- have you had your usual asthma symptoms during the day - cough, wheeze, chest tightness, breathlessness?
- interferred with ADLS? - housework, school/work?
asthma management targets
good control on minimal medication
FEV1 and PEFR >80% predicted
how does these medications work? SABA LABA MART ICS LRTA Theophylline SAMA LAMA
SABA - short acting beta2 agonist - relax muscles of airways + inhibit histamine release from lung mast cells - can get tremor
LABA - long acting B2 agonist - same as above
MART - Maintanence and reliever therapy - formoterol (LABA + ICS (budesonide) steroid which prevents + therefore reduces inflammation + swelling
ICS - steroid - reduce the number of inflam cells in the airways by:
- suppress production of chemotactic mediators,
- reduce adhesion molecule expression
- inhibit inflam cell survival in airway
- suppress inflammatory gene expression in airway epithelial cells
examples: beclometasone dipropionate, fluticasone propionate,
s/e oral candidiasis and stunted growth
LRTA - leukotriene receptor antagonist - tablets - they stop leukotrienes which causes your airways to narrow
theophylline - relaxes smooth muscles causing bronchodilation - inhibits leukotriene synthesis and TNF alpha
SAMA - short acting muscarinic antagonists - inhaled anticholinergic agents eg ipratropium - bronchodilation by blocking muscarinic M1/3 receptors
LAMA - tiotropium - block bronchoconstriction effect of acetylcholine on M3 receptors in smooth muscle
what is classed as a low/med/high ICS
low = <400 mcg budesonide
med =400-800
high = >800
asthma management guidelines - NICE
NICE
- SABA - newly diagnosed
- SABA + ICS >3 weeks or night-time waking
- SABA + ICS+ LRTA (might go for LABA first - BTS guidelines)
- SABA + ICS + LABA (continue LTRA if working)
- SABA (+/-LRTA) + MART
- increase ICS in MART
- increase ICS to stand-alone rx + SABA (+/-LRTA) + theophylline
- refer
assessing acute asthma severity and ix
moderate
increasing symps
PEF >50-75% best
not one symp of severe
severe any one of: PEF 33-50% best or pred RR >/= 25/min HR >110/min inability to complete sentences in one breath
life-threatening any one of: PEF <33% best or pred sats <92% pao2 <8kPa normal paco2 4-6kPa altered conciousness exhaustion arryhtmia hypotension cyanosis silent chest poor resp effort
near-fatal
raised paco2 +/or requiring mech ventilation with raised inflation pressures
ix listen to chest hr look at them PEF/ FEV1 pulse oximetry ABG - if severe CXR - if life-threatening, suspected pneumothorax, failure to respond
why is normal paco2 scary in an acute asthma attach
indicates exhaustion
what are the admission criteria for acute asthma
admit if any feature of life-threatening or near-fatal attack
if any severe symp persisting after inital treatment
previous near-fatal attack, preg, attack occuring despite already using oral corticosteroid and pres at night
management of acute asthma + discharge requirements
O SHIT ME
Oxygen - aim 94-98 15L NRB
Salbutamol - 5mg neb (repeat up to 3 times B2B then QDS + PRN)
Hydro/pred within 1 hour - pred = 40mg OD 5/7
Ipratropium - neb (mix in with salb if severe or life-threatening, repeat up to 3x) 0.5mg QDS
Theophylline/amino (IV) - get senior for this
mag sulf -IVI 2g over 20min - patchy evidence for this now
Sab - IV
escalate - ITU/ intubate/ventilate
NOTE - oxygen, saba + ipra will all be given through the one neb
discharge requirements -
peak flow >75% #
12hrs from last nebs, oxygen
inhaler technique checked and recorded
patients GP informed within 24 hours of discharge
near-fatal should be under specialist review indefinitely
resp specialist follow up for severe + for at least 1 year after admission
silicosis who gets it aka pres ix mx
who gets it construction worker pottery miners sandblasters present in some kitchen work tops - think about kitchen fitters
aka
potters rot
pres fibrotic presentation restrictive dry cough dyspnoea SOBOE black sputum long latency upper zones risk factor for developing TB as silica is toxic to macrophages
ix
CXR - EGG SHELL CALCIFICATION of hilar lymph nodes, ground glass and honeycombing
restrictive lung function tests
mx pulm rehab avoid exposure make a claim incurable smoking cessation
Tin exposure (stannosis)
pres
CXR
non-fibrotic
doesnt interfere with lung physiology
makes CXR look mad because of high atomic nature
what occupational exposures do you need to ask about
flour dust asbestos silica lead wood dust
exposures related to occupational asthma
flour isocyanates - spray paints wood dust cleaning materials cutting oils resins glues/adhesives
what can cadmium exposure cause
emphysema
what is pneumoconioses
group of chronic lung diseases by exposure to mineral dust or metal
includes: coal workers, silicosis, asbestosis
long latency
coal - 10 years
asbestos - 15-60 years
notifiable industrial disease - eligible for compensation
coal workers pneumoconiosis aka what is it associations types pres ix mgmt
aka black lung
what is it
simple - particles retained in alveoli - engulfed by macrophage - immune response (enzymes released from dead macrophage) - fibrosis
can -> progressive massive pneumoconiosis - round fibrotic masses in upper lobes -> black sputum
association
caplans syndrome
types
simple - can be asymp, nodular interstitial lung disease
progressive massive fibrosis
pres dry cough dyspnoea SOBOE black sputum 15-20 years after exposure
staging
graded on appearance of CXR
cat 1 - some opacities, normal lung markings
cat 2 - large number of opacities, normal lung markings
cat 3 - large number of opacities, normal lung not visible
ix
CXR - upper zone fibrosis
sputum micro
luFT - restrictive in simple, res/obs in PMF
mgmt avoid exposure incurable claim smoke cessation manage symps of chronic bronchitis
asbestos related disease
what is it
asbestos causes a variety of lung disease
pleural plaques -
- benign
- occur 20-40 years post exposure
pleural thickening
asbestosis - severity related to length of exposure - 15-30 years latency - lower lobe fibrosis - white>brown>blue - dry cough dyspnoea diffuse insp crackles: velcro digital clubbing building trade - fire proofing CXR - ground glass opacification, small nodular opacities (asbestos bodies in alveoli at bases), shaggy cardiac sillhouette
mesothelioma
- malignant disease of the pleura
- up to 50 year latency
- crocidolite (blue) asbestos is most dangerous - white>brown>blue
- progressive SOB, chest pain, pleural effusion
- palliative chemo
- 8-14 month survival
lung cancer
RF
synergistic effect with cigarette smoke
mesothelioma what is it pres causes ix mx
what is it
cancer of the mesothelial layer of pleural cavity
sometimes the mesothelial layers in abdomen affected too
metastasises to contralateral lung and peritoneum
right lung affected more than left
pres dyspnoea b symps - weight loss, fatigue, fever, night sweats chest wall pain clubbing 30% pres as painless pleural effusion latency up to 50 years
ix
CXR - pleural effusion, thickening
pleural CT - thickening, plaques, hilar LN enlargement
pleural fluid sent for MC&S, biochem and cytology - exudate with malignant cells
if pleural nodularity seen on CT then image-guided pleural biopsy - epitheliod mesothelioma
mx symptomatic claim palliative chemo median survival 12 months
when prescribing oxygen what do you need to include in the prescription?
target sats
what can giving oxygen cause in a patient?
resportion atelectasis
reactive oxygen radicals
CO2 retention in susceptible (at risk) individuals: ?hypoxic drive
systemic vasoconstriction
decreased cerebral blood flow 25% in normals
increased afterload -> from vasoconstriction
decreased cardiac output by up to 1/4
increased cardiac work/oxygen requirements
venturi or fixed performance mask
percent o2
how it works
pros and cons
deliver constant oxygen concs was seen to be gold standard 24-40% operate accurately 60% - gives 50% FIo2 with tachypnoea RR >30/min the oxygen supply should be increased by 50% increasing flow doesnt increase the oxygen conc so the litres dont really matter PRECISE - COPD
how to read oxygen flow L/min stick on the wall in the hosp
take the reading from the middle of the ball
in what conditions do you just go straight in with high flow
cardiac arrest shock sepsis major trauma burns drowning major head injury
- give via reservoir mask (NRB)
- maintain until oximetry available
- when stable adjust to target range
you have a patient thats not critically ill, not type 2 that needs o2 but not below 85% sats what do you prescribe?
nasal cannulae 2-6L/min aim 94-98%
you have a non critically ill patient that has type 2 resp failure what o2 do you prescribe
24 or 28% venturi
aim for 88-92% + reduce if sats >92%
if theyre >92% perform abg:
- if acidic and hypercapnic or patient tiring consider NIV or IPPV
- If normal PH and hypercapnic then at risk of over oxygenation then maintain at lowest o2 prescription and repeat ABG in 30-60 mins
transfer factor what is it equation causes of raised TLCO \+ lowered causes of low VA causes of low/high KCO
what is it
the rate at which a gas will diffuse from alveoli into blood.
CO is used to test the rate of diffusion.
results may be given as the total gas transfer (TLCO- a derived value) or transfer coefficient, KCO - (standardised measurement of rate of uptake of CO from alveoli). there is also VA - alveolar volume.
KCO X VA = TLCO
therefore the TLCO cannot be reduced by something in the lung - it has to affect the VA or KCO to therefore effect TLCO
causes of raised TLCO: asthma pulmonary haemorrhage (Wegener's, Goodpasture's) left-to-right cardiac shunts polycythaemia hyperkinetic states male gender, exercise
lower TLCO: pulmonary fibrosis pneumonia pulmonary emboli pulmonary oedema emphysema anaemia low cardiac output
things that decrease VA:
reduced expansion - neuromusclar weakness
discrete loss of units - pneumonectomy, pulm fibrosis
diffuse alveolar damage - emphysema, pulm fibr
poor gas mixing - COPD, bronchiectasis, asthma
KCO increased:
age
conditions with + normal or reduced TLCO:
discrete loss of units - pneumonectomy, lobectomy, consolidation
decrease in alveolar expansion - scoliosis/kyphosis, neuromuscular weakness, ankylosis of costovertebral joints e.g. ankylosing spondylitis
technical artefact - poor insp
polycythaemia or haemorrhage - vasculitis
KCO low:
diffuse alveolar destruction - emphysema/pulm fibrosis
pulm hypertension - heart disease
pulmonary capillary dilation - AV malformations, hepatopulmonary syndrome
anaemia - Hb correction
common causes of dyspnoea
asthma COPD PE ACS interstitial lung disease cardiac tamponade
what does a raised JVP mean
high right atrial pressure due to fluid overload
name diseases that cause an obstructive spirometry
asthma COPD bronchiectasis CF bronchiolitis obliterans some vasculitis tumours solid mechanical obstruction
name diseases that cause an restrictive spirometry
intersitial lung disease neuromuscular weakness (eg motor neurone disease) obesity chest wall deformity - scoliosis
what does the Z-score mean on spirometry?
tells you how far away you are from the central distribution the patient is
in spirometry this should be between -1.64 and 1.64
interstitial lung disease
definition
is a disease of the pulmonary interstitium - between the alveoli and cap basement membrane
distinct cellular infiltrates and extracellular matrix deposition in lung distal to the terminal bronchiole ie alveoli/capillary interface
classification of interstitial lung disease
5 major groupings:
- idiopathic
- associated systemic diseases - rheumatological, vasculitis, vascular arterio-venous malformations
- environmental triggers - drugs, fungal, dusts
- granulomatous disease - build up of immune cells predom macrophages and t- cells in interstitium - sarcoid, wegeners (granulomatosis with polyangiitis)
- other - lymphangiolyomatosis, eosinophilic pneumonia, alveolar proteinosis, langerhans cell histiocytosis
idiopathic interstitial pneumonias and whether they are steroid responsive or not
idiopathic pulmonary fibrosis - histological pattern is usual interstitial pneumonia
non-specific interstitial pneumonia - better than UIP
desquamative interstitial pneumonia - immunological response to smoking - stop smoking and may need steroids
cryptogenic organising pneumonia - inflammatory response not infective - very steroid responsive
if you did a broncho-alveolar lavage investigating an interstitial disease and found high: neuts lymph eosino infection
what diagnosis would it lean towards
neuts - IPF, DIP
lymph - sarcoid (tans-bronchial biopsy for diagnosis), extrinsic allergic alveolitis
eosinophils - eosiniophillic pneumonia
infection - virus, atypical microbes
idiopathic pulm fibrosis what is it pres causes ix mx prognosis comps
what is it
aka cryptogenic fibrosing alveolitis
non underlying cause exists
pres 50-70 2:1 men:w progressive dyspnoea on exertion paroxysmal dry cough, bibasal fine end insp creps on ausc clubbing
ix
histo - usual interstitial pneumonia
CXR - reticular shadowing @ peripheries and bases, shaggy heart border
**HRCT - peripheral subpleural and basal fibrosis - ‘ground glass’
traction bronchiectasis and, if progressed, honeycombing
spirometry - restrictive
impaired gas exchange - reduced TLCO (transfer factor)
check for ANA+ve
mx therapeutic monitoring diagnostic trial of steroids check eligibility for pirfenidone/nintedanib (antifibrotic agents) enrol in clinical trials TRANSPLANT - only rx should to extend survival oxygen pulm rehab
prognosis
3 years
complications pulm HTN -> cor pulmonale T2RF cachexia depression
hypersensitivity pneumonitis/EAA what is it examples pres ix mx
what is it
hypersensitivity induced lung damage (alveoli and distal bronchioles) due to a variety of inhaled organic particles
cause
immune complex mediated tissue damage - type III hypersensitivity although delayed type IV in chronic
non-IgE mediated!!!
examples
bird fanciers - avian proteins
farmers - spores of Saccharopolyspora rectivirgula (formerly Micropolyspora faeni)
malt workers - aspergillus clavatus
mushroom workers - thermophilic actinomycetes
pres acute 4-8 hours after exposure SOB dry cough fever, aches/pains subacute - weeks chronic - months
ix
CXR - upper/mid fibrosis - ground glass + honeycomb
restrictive spiro
decreased TLCO
bronchoalveolar lavage - lymphocytosis (predom CD8)
blood - NO eosinophilia
mx remove exposure acute or sub -oral pred/ o2 chronic - low dose corticosteroid immunosuppressant compensation
what may help treat ILD with rheumatological conditions
steroids and cyclophosphamide
or rituximab
plasma exchange
sarcoidosis what is it pres ix mx lifespan limited by
what is it
multi-system of unknown aetiology
affects any organ but predom lymph nodes and lung
pres
young adults
african
acute - erythema nodosum, swinging fever, polyarthralgia
insidious - dyspnoea, non-prod cough, malaise, weight loss
skin - lupus pernio, painful shin rash
hypercalcaemia - macrophage inside granulomas cause can increased conversion of vit D to its active form (1,25-dihydroxycholecalciferol)
ix biopsy - showing non-caseating granulomas CXR - 0 = normal 1 = bilateral hilar lymphadenopathy 2 = + fine reticular, nodular shadows 3 = diffuse infiltrate only 4= diffuse fibrosis serum ACE - elevated FBC - lymphopenia (being tied up in granulomas), raised ESR, hypercalcaemia ECG - ?24 tape, ?ECHO 24hr urinary calcium if serum normal as this can be first indicator of renal involvement bronchoscopy - transbronchial biopsies
mx Do not treat at stage 1 not asymp at stage 2/3 about half patients require treatment - then they will have a prolonged course of illness pred 0.5mg/kg/day - 30-40mgs for 4 weeks gradually reduce steroids if recurs then methotrexate
lifespan limited by:
cardiac involvement - arryhtmia
- renal involvement - nephrocalcinosis
- lung fibrosis
in ILD which diseases will cause changes on scans in these areas:
upper
lower
upper - ESCHART (granulomatous disease) E - EAA, eosinophilic pneumonia S - sarcoid/silicosis C - coal workers pneumoconiosis, H - histiocytosis X A - ankylosis spondylitis R - radiotherpy T -TB
lower - RASCO (systemic) R - RA A - asbestosis S - SLE C - cryptogenic fibrosing alveolitis O - other (drugs)
4Ds of fibrosis
Dyspnoea
dry cough
diffuse end inspiratory crackles
digital clubbing
drugs that causes pulmonary fibrosis
amiodarone bleomycin methotrexate nitrofurantoin bromocriptine
what does pneumonia normally mean in hospital?
microbial infection + host inflammatory response = symptoms and signs of consolidation and impaired alveolar function
caused by bacteria, viruses, fungus, parasites
occurs from inhalation, aspiration or haematogenous spread
co-morbidities important to ask about when suspecting pneumonia
smoking alcohol abuse immunosuppression resp comorbs neuro renal cardiovascular diabetes liver
classification of pneumonia
CAP
aspiration
HAP
pneumonia in the immunocompromised
respiratory host defences
innate reflexes:
- cough
- mucociliary transport
innate immunity:
- antimicrobial peptides (non-specific) : lysozymes, lactoferrin, defensins, collectins
- phagocytic and inflam cells
adaptive immunity
- immunoglobulins
- macrophages
common organisms for:
CAP
HAP
CAP strep pneumoniae h. influenzae influenze virus adenovirus
HAP staph aureua pseudomonas aeroginosa bacteroids e.coli, klebsiella, proteus
clinical features of pneumonia
history of:
prod cough, breathless, pleuritic chest pain, fever, systemic features
examination:
tachyp/c, localizing chest signs - decreased air entry, dull to percuss, increased vocal reasonance, bronchial breathing, crackles
diagnosis of pneumonia
then assessing severity
short hist of acute lower resp infection
new focal chest signs
new radio consolidation
severity assessment
CURB65
pneumonia severity index
presence of comps
pneumonia investigations
vital signs:
sats, BP, HR, RR
CXR
Bloods - FBC, U/E, LFT, CRP, ABG, PCT
micro - sputum, blood culture, viral swabs, specific serology (legionella)
pneumonia management
oxygen fluids antibiotics resp support monitoring
how to notice a not improving patient in penumonia
+ what you should consider doing if you think this is the case
CRP still >50% at day 4 of abx
reasons: slow response incorrect/missed diagnosis secondary comps - pulmonary (empyema/abscess), extra-pulmonary inappropriate abx or unexpected pathogen impaired immunity
next steps:
consider alternative diagnosis
exclude underlying immunodeficiency/chronic lung disease
repeat CXR/cultures
escalate abx
consider bronchoscopy, pleural fluid sampling
post-discharge tasks for pneumonia admissions
CXR follow up 6/8 weeks to ensure full resolution - if not then CT+ bronchoscopy
seen in clinic - as pneumonia can be a presenting feature of lung cancer
vaccine
- annual flu
- pneumococcal - >65 years
resp pharma - if something ends in: ...mab ...sone ...terol ...lone ...nib
mab - monoclonal antibody sone - corticosteroid terol - bronchodilator lone - corticosteroid nib - kinase inhibitor
delivery systems for inhaled drugs
pressurized metered-dose inhalers (normal inhaler)
spacer devices - allow more of the drug to be inhaled
dry powder inhalers- have no propellant (requires the patient to have sufficient inhalation power to breathe in powder)
benefits of inhaled drugs
lungs are robust and able to safely handle repeated exposure
act direct on lung and faster than IV
rpaid absorption
lungs are naturally permeable
large surface area
fewer drug metabolising enzymes
non-invasive port of entry into the systemic circ
name 4 ICS and why are there different ones
different ones as they can be used in different formats
beclomethasone diproprionate (dry powder inhalation, normal ihaler) budesenide (DPI, PMDI, single dose for nebs) ciclesonide (PMDI) fluticasone proprionate (DPI, PMDI, nebs) mometasone furoate (DPI)
s/e seen in high-dose ICS used over long time
loss of bone density
adrenal suppression
cataracts
glaucoma
how do antifibrotics such as pirfenidone work
anti-fibrotic, anti-inflam, anti-oxidant
reduces:
fibroblast proliferation
collagen production
production of fibrogenic mediators
Whys is mycobacteria resistant to gram stain
so what stain do you use?
high lipid content with mycolic acids in cell wall
use ziehl-neelsen stain for AFB
- carbol fuchsin
- acid alcohol
- methylene blue
most common infectious killer in the world?
TB
risk factors for TB
born in high prev area IVDU homeless alcoholic prison HIV +
how is TB spread?
aerosol lung to lung droplets can only carry a few ft - must inhale droplets actually quite hard to catch it mainly get it from households
what % of people exposed to TB develop TB
5%
natural history of TB
- pulm infection
- bacili settle in lung apex
- macro + lymph seal in and contain and kill majority
in 2-5% they will then go on to develop clinically evident primary pulm disease:
- bacili + macrophages coalesce to form a granuloma (collection of epithelioid histiocytes, caseous necrosis in centre) = primary Ghon focus
- mediastinal lymph nodes enlarge (this plus the focus = primary (Ghon) complex
as granuloma grows it develops cavity - more likely in apex as there is more air and less blood supply /immune cells
if not contained there is haematogenous dissemination which leads to serious non pulm disease (can happen at primary infection or at reactivation):
- TB meningitis + CN palsy or tuberculoma
- pleural TB
- miliary TB
- bone and joint TB - pain or swelling, potts with spinal cord lesion (leads to crush fracture)
- genitourinary TB - epididymitis, frequency, dysuria, haematuria
- abdominal TB - ascites, abdo lymph nodes, ileal malabsorption
primary infection -> progressive primary disease or latent TB
then further down line (1 in 10):
post-primary disease (wherever dormant bacilli are hiding)
then further down line may get re-infected
presentation of TB
systemic features: weight loss* low grade fever anorexia night sweats* malaise
- most indicative of TB
pulm features: cough >3/52 chest pain breathless haemoptysis
may be associated with:
consolidation, collapse, pleural effusion, pericardial effusion (depending on the site of the focus and erosion of the cavity)
miliary TB
TB everywhere
tiny granulomas
diagnosing active TB
non-specific - prolong inflam response
- normochromic normocytic anaemia
- thrombocytosis
- raised CRP/ESR
- hypoalbuminaemia
- hypergammaglobulinaemia
- hypercalcaemia
- sterile pyuria - WCC in renal tract TB
definitive - micro - AFB, PCR, culture
- sputum smear - 3 specimens needed for AFB
- sputum culture - GOLD STANDARD
- urine
- CSF
- pleural fluid
- biopsy specimen: LN, bone etc
suggestive - histopatholgy caseating granulomata + ZN
CXR - upper lobe cavitation, bilateral hilar lymphadenopathy
diagnosing latent TB
not possible to find dormant bacteria
must use an indirect measurement - to detect an immune response to an organism, to check for memory T cells
mantoux - tuberculin skin test
- protein derived from organism injected intradermally
stimulates T4 delayed hypersensitivity reaction
false neg - immunosuppressed or milary TB
only mod specific (false pos)
will get reaction if had BCG vaccine
depends on size whether its posi or not:
>15mm = strongly posi (probs had infection)
6-15mm = posi - shouldn’t be given vaccine as maybe due to infection/previous BCG
<6mm = negative/not significant - can give BCG vaccine
OR can use interferon gamma release assays (IGRAs) - Quantiferon- TB test (4 viles of blood)
- use antigens specific to TB so distinguishes between BCG and TB
- demonstrate exposure not active infection
TB treatment
curable RIPE - 6 months rx Rifampicin - 6 (12 in CNS) Isoniazid - 6 (12 in CNS) Pyrazinamide - first 2 Ethambutol - first 2
why so long?
reactivation of dormant bacilli is opp for killing
compliance is CRITICAL to reduce relapse and remittance
people don’t like them as they make you feel a bit shit!
community TB nursing team essential to ensure compliance
DOTS - directly observed therapy - give meds in supervised fashion 3 + times a week
how they work and common s/e of TB drugs
rifampicin -
bacteriocidal, blocks protein synthesis, effective throughout treatment course
S/E = red urine, hepatitis, drug interactions (contraceptive pill no longer works)
isoniazid -
bacteriocidal for rapidly growing bacilli (blocks cell wall synth), most effective in initial stages
S/E = hepatitis, neuropathy
pyrazinamide -
bacteriocidal initally, less effective later
S/E = hepatitis, arthralgia/gout, rash
ethambutol -
bacteriostatic, blocks cell wall synth
S/E = optic neuritis
preventing TB
active case finding - reduce infectivity
detection and treatment of latent TB - community TB nursing team using Mantoux
- identify and treat to reduce risk of post-primary TB:
(6 months isoniazid, 3 months rifampicin + isoniazid) = reduces risk of development of active TB by 2/3
vaccination
- neonatal BCG - works really well
- limited efficacy but does protect against disseminated TB
people at risk of pneumonia
infants and elderly COPD (chronic lung conditions) immunocomp nursing home residents impaired swallow - neurological conditions diabetes congestive heart disease alc and IVDU
COPD what is it pathogenesis pres causes diagnosis ix stable mx
what is it
obstructive disease
spectrum between chronic bronchitis and emphysema
inflamed mucousy narrowed airways and damaged air sacs
pathogenesis
smoking -> variety of proinflam and oxidative stress cascades to be activated in the lung -> protease production and alveolar cell apoptosis -> lung destruction
chronic bronchitis = cough and sputum >3months a year for 2 consecutive years
emphysema = damage to alveoli, loss of elastic recoil, larger airspaces, therefore lower surface area for gas exchange
features cough - productive dyspnoea wheeze severe - RHF + peripheral oedema systemic effects in later stages of disease: - HTN - osteoporosis - depression - weight loss - reduced muscle/ general weakness
causes
smoking
alpha-1 antitrypsin deficiency, cadium, coal, cotton, cement, grain
diagnosis purely functional (spirometry) diagnosis now eg can have emphysema and not have COPD as will have a FEV1/FVC >70%
ix post-bronchodilator spirometry: FEV1/FVC <70% CXR: - hyperinflation - bullae/pneumothorax - flat hemi's - important to exclude lung cancer FBC - exclude secondary polycythaemia BMI MRC breathlessness scale
severity mild/ 1 = FEV1 >80% mod/ 2 = 50-79% severe/ 3 = 30-49% very severe/ 4 = <30%
management
SMOKING CESSATION - nicotine replacement eg varenicline or bupropion
- annual flu/pneumococcal vaccine
- pulm rehab
- prophylactic abx - azithromycin in selected patients
- mucolytics if chronic prod cough
- cor pulmonale - furose + consider LTOT
BRONCHODILATORS:
1. SABA or SAMA
2. asthmatic features/steroid responsiveness or not?
NO -> add LABA or LAMA -> if on SAMA switch to SABA
YES -> LABA + ICS (beclometh), may also + LAMA
explain blue bloaters and pink puffers
blue bloaters - commonly with chronic bronchitis, lost hypoxia as a drive for ventilation as they have become used to it. They now need hypercapnia to drive it so are in T2RF. Hence cyanotic and bloated probs cos got RHF and oedematous.
pink puffers:
emphysematous patient, maintaining resp effort hence why skinny, increased work of breathing T1RF
pres + common organisms + management of acute exacerbations of COPD
pres
change or increase in sputum
increase in dyspnoea, cough, wheeze, hypoxic +/- acute confusion
common organisms -
h.influenzae, step pneumoniae, moraxella catarrhalis, rhinovirus
management increase broncho use - consider neb pred 30mg for 5 days give abx if clin signs this is bacterial - raised PCT? first line abx = amox or clary or doxy
requirements for LTOT
patients that need it
assessing for it
risk assessments
should breathe 02 at least 15 hours a day
Patients that need to be assessed to receive LTOT are:
- Very severe (<30% predicted) and considered in severe (30-49%)
- Cyanosis
- Polycythaemia
- Peripheral oedema
- Raised jugular venous pressure
- O2 sats <92% on air
Assessment includes:
2x ABG at least 3 weeks apart – offer LTOT when p02 <7.3 kPa or 7.3-8kPa + (secondary polycythaemia or peripheral oedema or pulm HTN)
CANNOT OFFER IF STILL SMOKING – after offering smoking cessation
Must also risk assess before:
- Falls risk over equipment
- Risk of burns fires – do they live with someone who smokes (including e-cigarettes)
what do you need to do before prescribing azithromycin
ECG - long QT syndrome
what inflam cells are commonly seen in COPD or asthma
asthma - mast cells + eosinophils
COPD - neuts + macrophages
ANCA-associated vasculitis
microscopic polyangiitis
granulomatosis with polyangiitis
eosinophilic granulomatosis with polyangiitis
rheumatoid arthritis and the lungs
what can it cause?
pleural effusions
- exudate
- metabolically active, low glucose
fibrosing alveolitis
- relatively treatment resistant
airways disorders
- bronchiolitis, bronchiectasis, obliterative bronchiolitis
- reasonably common
mechanisms of immune-mediated damage
bystander - tissue damage in chronic infection (an infection wont clear as of non-immune defects in CF)
excessive immune response eg eosinophilic asthma in response to harmless allergen
failure to control immune like responses eg alpha-1 anti-trypsin disease: emphysema
on-target immune response: bronchiolitis obliterans of your own airways
off-target immune response: goodpastures (antibodies to type IV collagens after some viral infections)
PCP - pneumocystis pneumonia
typical pres + mgmt
6/52 progressive breathlessness dry cough lymphopenia nearlu always present (CD4) exertional hypoxia
mx - high dose co-trimoxazole (trimeth/sulphawmthoxazole)
supplemental steroids for hypoxia - pred
invasive aspergillosis
classic pres + treatment
fever in neutropenic patient, usually on broad spectrum antibiotics
multiple pulm nodules/infiltrates
mx
amphotericin (renal tox)
caspofungin
liposomal amphotericin
virchows triad
stasis
endothelial injury
hypercoagulable state
what factors in the coagulation cascade does warfarin work on
1972
10, 9, 7, 2
what factors in the coag cascade does lmwh work on
2a
10a
what factors in the coag cascade does NOACs work on
2a, 10a
what factors in the coag cascade does thrombolysis work on
2
pulmonary hypertension what is it pathogenesis pres causes ix mx
disease of small pulm arteries characterised by vascular prolif and remodelling
mean pulm art pressure >25mmhg at rest with pulm cap wedge pressure <15mmhg
pathogen
progressive increase in pulm vascular resistance -> right vent failure -> death
causes
heritable - BMPR2 gene
CREST - systemic sclerosis (connective tissue disease)
lung disease - hypoxic vasconstriction (COPD, interstitial)
heart disease -> valvular failure or heart failure -> increased filing pressures
pres in order: dyspnoea ankle swelling chest pain syncope
ix
ECG - RVH (tall R wave and small s in V), RAD, R atrial enlargement (p wave >2.5mm in II, III and aVF)
spirometry/transfer factor
CXR - pruning (attenuated peripheral arts), enlarged pulm art shadow
transthoracic echo
CTPA
right heart catheterisation
mx CCB - nif or amlo sildenafil - augments pulm vascular response to nitric oxide anticoag - warfarin targ 1.5-2.5 lifestyle - exercise furose - oedema supplemental o2 if needed
what type of reaction is the inflam response in TB
Type 4 hypersensitivity
what can cause a falsely negative mantoux test?
miliary TB sarcoidosis HIV lymphoma very young (<6m)
DVT what is it pres causes ix mx comps
deep vein thrombosis
normally in leg behind valve
pres
unilateral calf swelling
pain along deep venous system
asymmetric oedema + collateral superficial veins
causes
clotting RF
ix
wells criteria:
0-1 - unlikely - do d-dimer within 4 hours
2+ - likely - USS doppler leg within 4 hours (if not within 4 hours then d-dimer + anticoag while waiting)
mx
first line = DOAC (apixaban or rivaroxaban)
if DOAC not suitable then - LMWH followed by dabigatran or edoxaban or warfarin
for >3/12.
then stopped if provoked VTE
in unprovoked VTE then anticoag for 6 months total, and consider testing for antiphos antibodies + hereditary thrombophilia
early immobilisation
avoid pill
TEDs
thromboembolic RF
cancer trauma major surg hospitalisation immobilisation clotting disorders previous DVT/PE oral contraception obesity/preg (high oestrogen) recent long travel
PE what is it pres causes ix mx
what is it
clot in pulmonary vasculature. can be peripheral or central.
life-threatening.
if not treated leads to RHF -> death
pres tachypnoea crackles tachycardia fever chest pain - typically pleuritic haemoptysis
causes
50% of DVT embolise
ix - NICE 2020
all patients clinically suggestive of PE should have hx, exam, CXR (to exclude other causes).
if low probs it being PE do PERC (<15% on clin judgement)
if anything higher do a Wells.
PE likely >4 points - immediate CTPA (delay for this start anticoag anyway - apix or rivar)
unlikely =4 - d-dimer
ECG - sinus tachy, S1Q3T3 large S (present in 20%), RBBB + RAD associated
mx DOAC - api or rivar (same as DVT) low risk PE mx in outpatients - do a PESI - but key requirements are haemodynam stable, support at home, lack of comorbs IF HAEM UNSTABLE (eg hypotensive): first line = thrombolysis eg altepase
advant/disadvant of V/Q or CTPA
CTPA advant - speedier, easier to perform out of hours, reduced need for further imaging and possibility of finding alternative diagnosis if PE is excluded
V/Q is ix of choice if there is renal impairment
wells PE score
clinical signs symps of DVT 3 alt diag less likely than PE 3 HR >100 1.5 immob >3/7 or surg in prev 4 weeks 1.5 prev DVT/PE 1.5 haemoptysis 1 malignancy <6months 1
> 4 = likely
wells DVT score
active cancer <6months 1
paralyses, paresis or recent plaster of lower extremeties 1
recent immob >3 days or maj surg <3 months requiring general or regional anaesthesia 1
localised tenderness along deep venous system 1
entire leg swollen 1
calf swelling >3cm larger to asymp side 1
pitting oedema confined to symp leg 1
collateral superficial veins (non-varicose) 1
prev DVT 1
alt diagnosis at least as likely -2
2+ - likely
compare exudate and transudate effusion for: general cause pathophys aetiologies fluid lights criteria mgmt
exudate: general cause - local pathophys - increase cap perm aetiologies - infections (TB/pneumonia) - infarctions (PE), RA, SLE, cancer fluid - rich in cells eg neuts + protein - <7.4 pH (inflam -> metabolism -> acids) lights criteria need one positive criterion: - effusion/serum >0.5 (protein rich) - LDH in efffus >200U/L - E/S LDH >0.6 mgmt - rx underlying cause
transudate: general cause - systemic pathophys/aetiologies - increase hydrostatic forces eg LVHF - decrease oncotic pressure eg kwashiorkor, cirrhosis, nephrotic, menetrier, malabsorption fluid - ultra-filtrate of plasma - >7.4 lights criteria all three criteria have to be neg - E/S protein <0.5 - LDH in e <200u/l - E/S LDH <0.6 mgmt - give diuretics +/- albumin
chest drain what is it indications CI insertion housekeeping comps removal
creates a one way valve allowing air or liquid out of cavity
indications: Pleural effusion Pneumothorax not suitable for conservative management or aspiration Empyema Haemothorax Haemopneumothorax Chylothorax In some cases of penetrating chest wall injury in ventilated patients
contraindications INR > 1.3 Platelet count < 75 Pulmonary bullae Pleural adhesions
insertion arm behind head 5th intercostal space midaxillary line use USS guidance local anaesthetic - lidocaine 3mg/kg use seldinger technique tubing secured with straight stitch or dressing position confirmed by 'swinging' fluid and CXR
housekeeping
swinging - should be if in right place
bubbling - if air for pneumo
comps: failure of insertion bleeding infection penetration of lung re-expansion of pulm oedema - to avoid clamping regularly to avoid output >1L in <6hours
removal
when no output for >24 hours + imaging shows resolution
if been pneumo - remove when stops bubbling or when patient coughs + imaging
pneumothorax what is it causes rf symps ix mx
Accumulation of air in the pleural space
causes
Primary spontaneous: tall thin males, smoking, Marfan’s, family history (no underlying causes)
Secondary spontaneous: pre-existing lung disease: COPD (bullae), CF, TB, PCP
Traumatic
rf preexisting lung disease marfans, RA ventilation incl NIV SMOKING
patho
Normally Palv > Pip (alveolar and intrapleural)
If communication between alveolus and pleural space gases follow pressure gradient to equalise
Thoracic cavity normally below resting volume, lung above resting volume -> thoracic cavity enlarges and lung shrinks
TENSION:
Medical emergency - occurs when intrapleural pressure > atmospheric -> results from ball valve mechanism letting air in but not out
Lung deflates and mediastinum shifts contralaterally compressing great veins and causing decreased venous return to hear
symps dysnpnoea pleuritic chest pain sweating tachyp/c hyperresonant resp distress trach deviation distended neck veins
ix
CXR
mx
primary
- <2cm + asymp discharge, otherwise aspirate - failure = chest drain
secondary - >50yrs and >2cm/symps = chest drain otherwise aspirate 1-2cm all should be admitted for >24 hours <1cm give o2 and admit for 24 hours
DIVING SHOULD BE PERM AVOIDED
common causes of bilateral hilar lymphadenopathy
TIMES TB inorganic dust malignancy EAA sarcoidosis
bronchiectasis what is it types pres causes ix mx
Permanent dilatation and thickening of the airways due to recurrent infection and inflammation
Failure of mucociliary clearance and impaired immune function -> continued insult to bronchial wall -> chronic inflammation
types
diffuse or focal
pres chronic daily cough foul smelling thick green mucous dyspnoea + wheeze weight loss fatigue recurrent infections clubbing intermittent haemoptysis
causes Post infectious: measles/flu/pertussis, aspergillus fumigatus (ABPA), pneumonia Immunodeficiency: HIV, Ig deficiency Genetic: CF, ciliary dyskinesia, A1ATD Connective tissue disease: RA, Sjogren’s IBD: CD, UC
ix
bacterial colonisation - s.aureus (if abscess), h.inf (most common), s.pneumo, pseudomonas aeruginosa, aspergillus fumigatus, klebsiella
insp coarse crackles (shifts on cough)
high pitched insp squeaks and pops
low pitched rhonci (snoring sounds)
CXR - cysts, dilated bronchi with thick walls, tubular or ovoid opacities
CT - gold - dilated bronchi
FBC - raise eosinophils in ABPA, neutrophilia -> bact infection
sputum culture + sens
- G-ve = pseudomonas aeruginosa
- G+ve = s.aureus, s.pneumonia
mx
lifestyle = exercise, good nutrition
airway clearance physio (postural drainage + percussion)
mucolytics - carbocysteine
bronchodilators
inhaled hypertonic saline
vaccines
pseudomonas? neb tobramycin or aminolycoside: gentamicin
ACUTE exacerbation = oral amox if mild
IV fluoroquinolones eg ciprofloxacin if severe
allergic bronchopulmonary aspergillosis what is it pres ix mx
what is it
Hypersensitivity to aspergillus fumigatus that has colonised airway of pt with asthma or CF
Formation of IgE and IgG aBs -> bronchial obstruction, airway inflammation, mucoid impaction -> bronchiectasis, fibrosis
pres hx of asthma/CF/atopy increased cough mucus plugs wheeze fever (>38.5) pleuritic chest pain
ix skin test for aspergillus fumigatus sensitivity - positive Serum IgE elevated FBC with eosinophil count elevated CXR *upper or middle lobe infiltrates
mx
Oral corticosteroid + environmental control (mould avoid) + optimised Rx CF/ast
*Azole antifungal: itraconazole, co-trimoxazole
what is obesity hypoventilation syndrome?
is when severely overweight people fail to breathe rapidly or deeply enough, resulting in low o2 and high co2
can lead to T2RF
the disease puts strain on the heart which may lead to heart failure and leg swelling
is defined as the combination of obesity and an increased blood carbon dioxide level during the day that is not attributable to another cause of excessively slow or shallow breathing
findings on xray for pneumonia
dense or patchy consolidation, usually unilateral air bronchograms (seen as air tubes going through consolidated lung)
what lung lobes border these structures:
diaphragms
R heart border
L heart border
diaphragm - left and right lower lobes
R heart border - R middle lobe
L heart border - lingula (part of the left upper lobe)
findings on xray for pleural effusion
blunting of costophrenic angles
homogenous opacification
fluid level - meniscus
findings on xray for pulm oedema (baso heart failure findings)
ABCDEF A - alveolar and interstitial shadowing B- kerley B lines C - cardiomegaly - heart shadow >50% of thoracic horizontal on PA D - upper lobe venous blood diversion E - effusion F - fluid in horizontal fissure
findings on xray for pneumothorax
air within pleural space - loss of lung markings
in tension - potential for mediastinal shift
NOTE - inverting imaging is useful to help spot them
findings on xray for lobar collapse
look for loss of volume:
raised hemidiaphragm ipsilaterally
tracheal and mediastinal shift towards collapse
LUL - veil sign - the whole left lung looks opaque ish (cover by a veil sign), luftsichel sign - radiolucent rim around aortic arch due to hyperinflation of the lower lobe
LLL - sail sign (below left heart border there is a straight line the sail of a boat), give impression of double heart border
RUL - concave border of upper lobe, increase opacification, right hilar mass (goldens S sign)
RML - indistinct RH border + tracheal deviation + but preserved right hemidiaphragm
RLL- sail sign.
