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.
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.
