airways disease CCL Flashcards
asthma S+S
mechanism, Ix,
pesentation: dry cough at night (anti-inflam cortisol drops), SOB, tightness, wheeze, FEV1/FVC < 0.7. Atopic triad.
Allergic: type 1 hypersensitivity. IgE.
exposed- adaptive immune prod antiibodies to it.
2nd exposure- Th2 –> Il4,% (IgE and eosinophil activation) IgE cross bind to mast cells- degranulation- bronchoconstriction and edema.
Ix: spiro with reversibility testing (improvement of FEV1 more than 12%). FBC with eosinophilia, CXR, Peak flow dary, Fno3. (Fno3 + spiro gold standard)
asthma Mx + emergency Mx
1st SABA
2nd ICS Beclamethasone
3rd LABA (Salmeterol)
acute: O2, Sab nebs 5mg repeated every 20-30 mins.
100mg hydrocostisons/ oral pred 40mg.
ipatropium bromide nebs (500mcg- once only)
escalate as needed.
do a peak flow diary, off nebs for 24 hours before home.
anaphylaxis, describe, mechanism and how to diagnose
an IgE mediated hypersensitivity reaction.
profound histamine and serotonin release from basophil and mast cell degranulation.
primeraly a clinical diagnosis can do serum tryptase (from mast cells) take at 1,6,24 hrs. if more than 15ng/ml significant. can also do the skinprick testing after 6 weeks of initial incident.
management of anaphylaxis.
stop trigger, position supine, O2 (100% if poss) exclude alternatives.
if pulse: Adrenaline 0.5mg IM. IV acc, fluid if SBP<90. promethazine 25-50mg IV. hydrocortisone 250mg IV. repeat adrenaline 5mins if persistant hypoTN/ Bronchospasm. infusion if after 10 min no improvement.
if no pulse: CPR, Raise legs, 2 large IV access. 2L IVF. increacing adrenaline IM 1-4Mg. H1 and H2 antag.
admit if severe, uncontrolled asthma, slow response, need for fluid bolus, or 2nd adrenaline dose.
COPD overview
airflow limitaion, not fully reversable, doesn’t change markedly over several months.
chronic bronchitis(sputum for most days of 3 months for 2 consecutive years. and emphysema(enlarged airspaces)
atiology: more than 20 pack years. occupational exposure, poorly mamanged asthma.
chronic bronchitis pathology.
smoking- inflam change-> mucociliary dysfunction -> goblet cell increace + defective and paralysed cilia -> reduced mucous clerance.
metaplasia of resp epithelium to squamous epithelium. (cilia loss)
mucous plugging created reservoirs for infection.
neutrophil + chronically lymphocites. leads to scaring and thickening
wheeze on expiration, poor alveolar ventilation. progressed to hypoxia and hypercapnia.
Hypoxia causes inc in EPO-> inc Hb -> polycythaemia.
cyanosis but not symptomatic- Co2 receptors desensitised.
hypoxia causes vasoconstiction of pulm vessels- pulm HTN- raised JVP + right heart faliure.
emphysema overview.
destruction of alveolar walls distal to terminal bronchioles.
macrophages in alveoli stim inflamation, macrophages migrate. release free radicals (inhib A1- antitryptase). cytokines release neutrophils- releasing elastase- breaking down suppiorts for alveoli and causing wall destruction. air trapping and bullae result.
pts apper breathless due to inc wob to expel air due to dec elastase.
talk about blue bloaters vs pink puffers
Ix of COPD
Spiro- FEV1/FVC < 0.7. not reversable with SABA. peak flow should be low. inc residual volume.
Cxr: overinflation, flattened diaphragm, bullae
CT- emphasematous changes
ECG- in advanced RHS, P waves prominent.
very much a clinical diagnosis.
ABG
FBC
Sputum culture.
discuss respiratory faliure. causes, Ix, Rx.
type 1 - hypoxia (o2<8)
type 2- hypoxia with hypercapnea (Co2>6.5)
only cause of hypercapnea is insifficient alveolar ventilation (bronchitis, obesity, severe asthma, drug OD, myasthenia gravis)
Ix: ABG- if inc co2 think resp issue. CXR, Sputum/ blood, spiro.
Rx: type 1- Rx underlying cause, assist vent is Po2<8 when fi02>60%.
type 2- increace alveolar ventilation- NIV or intubation.
pneumothorax overview.
risk factors, differentials, presentation.
rupture in either one or both of the pleural membranes. air into pleural space.
primary- no resp illness
secondary- resp illness.
risk factors- tall, thin, smoking, connective tissue disorder, cannabis, COPD.
presentation- Acute SOB, pleuritic chest pain worse on inspiration, dec chest expansion. if ventilates- large sudden inc in ventilation pressures and hypoxia.
investigations and treatment of pneumothorax.
Ix: CXR, ABG. if tension Rx as ABCDE emergency.
primary:
if less than 2cm rim on cxr- send home and monitor.
if more than 2cm aspirate- if unsuccessful chest drain.
2nd- If SOB + 2cm rim or pt is over 50 + symptomatic - chest drain
if 1-2cm aspirate,
if less than 1cm- admit for 24 hrs and monitor.
ref to surgeons if after 2 days bubbles when cough. should have healed.
how does tension pneumothorax differ and what is its management.
air in pleura compressing contralateral mediastinum. trachea will deviate to contralateral side.
heart squished- TP is a cause of pulseless electrical activity.
Rx: arrest call,
large bore needle with syringe 2nd intercostal space in mid clav line, draw air out. OR venflon in same location.
pneumonia overview. Ix, Rx,causative organisms for the types you can get
inflammation of lung parenchyma. bacterial (common) or viral (uncommon)
no destruction of underlying architecture, alveoli fill with fluid.
CAP- strep Pneumonia or H influenzae
HAP- gram -ve, pseudomanias, ecoli. (give coamox for these)
aspiration- klebsiella
Ix: ABG, Cxr, FBC, sputum, urine, bronchoscopy if on ITU.
Rx: symptomatic treatment. 1st line usually amox, if severe dual Abx.
discuss curb 65 for pneumonia+ link with clinical signs of pneumonia.
in addition- what is the post acute management of pneumonia
re-CXR at 6 weeks to ensure eradication of disease and to rule out any undderlying pathology.
pulmonary embolism presentation
clot or blockage in the pulmonary vasculature.
small- segmental artery blocked
recurrent small- sub clinical episodes gradual pulm htn
massive- saddle or blocking pulm trunk. puml vasoconstriction and inc pulm pressures. Rright heart strain. can lead to collapse and death.
Presentation: sudden SOB + Pain, low grade fever, tacycardia, Hypotension, haemoptysis, raised JVP, syncope + dizzyness.
ABG can show resp alkylosis with low o2 (blowing off co2)
PE Ix, Rx.
FBC, D-dimer, U+E, clotting.
CXR +ECG to rule out pneumothorax. (PE sinus tacy with right vent strain)
CTPA gold standard.
should calculate a wells score if 4 or more CTPA.
Rx ABCDE, symptomatic relief,
if stable- DOAC
cancer/pregnancy- warfarin until birth/ treatment.
3 months anticoag if provoked, 6 if unprovoked.
if massive PE- thrombectomy or thrombolysis.
DVT treatment, and wells criteria.
rarely go to lungs if below calf.
D dimer + USS if wells indicates.
LWMH or DOAC 3/12.
pulmonary TB, presentation, risk factors, Ix.
mycobacterium tuberculosis. pulmonary and throat are only infectious elements.
social depravation, crowded housing, HIV, migration,
presents with Cough, (2-3/52+) dry then productive, hemoptasis. fevers, wt loss, nt sweats, lymphadenopathy.
Ix: Cxr triple sample sputum, Ziel-Neelson staining under light microscope.
management of TB
RIPE for 2 months
4 months further of RI
Rifampicin (makes everything orange)
Iosoniazid- causes periferal neuropathy (need to prescribe B6 pyridoxine)
Pyrazinamide- cant not give this one
Ethambutol- optic neuritis- reversable.
need to contact trace- is a notifiable disease.
pathophysiology of TB
initial infection engulfed by macrophage, attempted digestion.
thick waxy wall prevents- sits and hides
macrophage recruits neuts, lymphs - forms clump (granuloma)
in good immune- nice organised grauloma switch off.
can caseate- replicate in granuloma and then burst.
calcified-means eradication.
miliary tb is where it gets into a vein, then can spread
cyctic fibrosis overview
autosomal recessive condition.
leads to cysts + fibrosis
common in caucasians Defect in CTFR gene chromasone 7. CTFR channel pumps chloride into secretions. f508 del most common allele.
S+S: faliure to thrive in infants, rectal prolapse, meconium ilius, recurrent infections, pancreatic insufficiency.
CF Ix, Rx
glucose tolerance test, Cxr, Spiro- obstructive defect.
fecal fat analysis.
immunoreactive trypsinogen - released into blood when panc is damaged.
cl- sweat test. more than 60 is diagnostic.
Rx: healthy weight gain, fat soluable vits. replace pancreatic enzymes.
physio 2x daily, inc 45 mins gym session.
KAftrio (triple therapy elexacaftor, tezacaftor, ivacaftor) chloride channel opener, CFTR modulators.
bronchiectasis-definitoin,S+S, causes Ix, Rx.
chronic inflam of the bronchi and bronchioles leading to permanent dilation and thinning.
H influenzas, pesudomonas, strep, pneumonia.
can be congenital, post infection, due to obstruction.
S+S: persistant cough, clubbing, copious purelent sputum, intermittent haemoptysis, coarse inspiratory crackles.
Ix: CXR- cystic shadows, thickened bronchial walls. sputum culture. Bronc. CT scan definative- looking for signet ring and tramline signs.
Rx: chest physio, Abx, if aspergillosis use cortocosteroids. localised disease is an indication for surgery
