Resp Flashcards
Lung function tests
Obstructive vs restrictive lung disease
Examples for each (3-4)
Obstructive = FEV1:FVC <75%
asthma, COPD.
Restrictive = FEV1: FVC >75%
interstitial lung disease, rib #, MSK - chest deformity/scoliosis, neuro (MND), obesity
COPD
- diagnosed based on clinical presentation + spirometry finding:
- How to asseess for impact of breathlessness?
- severity scale, using FEV1 % of predicted…
- potential genetic underlying cause.
- what can it lead to?
- TLCO?
- All FEV1:FVC <0.7. Severity characterised by the FEV1: >80%, 50%, 30%, <30%
Obstructive picture without dramatic response to reversibility testing. - MRS Dyspnoea scale - Grade 1 - 5 (mild; SoB with strenuous exercise to 5 - house bound).
- Severity: 1-4; FEV1 >80, 70, 50, 30% of predicted.
- A-1 antitrypsin deficency - COPD & CLD.
- Polycythaemia.
- Transfer factor for CO is decreased in COPD.
Long-term mx for COPD
- First line treatment options (2)
Second line depends on whether COPD is steroid responsive/pt has asthmatic features
- Mx if YES; Mx if NO.
- 3rd line mx.
- Additional drugs include (3).
- Bronchodilator therapy (SABA- Salbutatmol, or SAMA - Ipatropium bromide)
- Combination therapy:
if steroid responsive –> LABA + ICS (e.g. Salmeterol + Beclometasone). Keep short acting: SAMA or SABA.
If NOT steroid responsive–> LABA + LAMA (e.g. Tiotropium)
- keep shortacting therapy (SABA only).
- Combination therapy:
- Triple therapy for steroid responsive: LABA + LAMA + ICS (e.g. *Salmeterol + Tiotropium + Beclometasone).
Additionals - oral theophylline, mucolytics (Carbocysteine), abx prophylaxis w Azithromycin
akaif steroid responsive there are more options: you can use steroids an
Mx COPD Exacerbation
1. At home
2. In hospital - admit if severe SOB, confusion/low GCS, cyanosis, <90% O2, social reasons, significant comorbidity
3. If severe; not responding to 1st line
4. Not responding to 1st line/ ABG shows resp acidos - what type of NIV is preferred?
5. Further management
Oxygen therapy
* mask of choice
* target sats before/after ABG
What is Doxapram?
- Pred (30mg OD 5/7)
increase freq of bronchodilartor via inhaler/nebs
antibiotics - Amoxicillin or Clarithromycin (if infective exacerbation - purulent sputum & other signs) - Nebs bronchodilator therapy (SABA/SAMA)
systemic steroids (IV hydrocortisone or oral pred)
Abx (if infective)
chest physio. - If not responsding to neb bronchodilator –> IV Amniophylline –> NIV
- NIV = BiPAP (better for acid-base balance and preventing inhaling exhaled gases)
- Intubation and ventilation/HDU admission
Oxygen
Venturi mask 28% at 4l/min
Assume 88-92% sats (Co2 retainer)
If pCO2 normal on ABG: adjust to 94-98%
A resp stimulant if NIV/intubation not appt.
LTOT:
2 x ABGs with a pO2 of what is an indication for at home oxygen therapy for COPD?
Or between X and X with secondary causes/RFs (4)
<7.3
or 7.3-8 with:
secondary polycythaemia
pulmonary htn
peripheral oedema
cannot be used if smoke
pO2 <7.3 kPA or between 7.3 and 8 with the secondary features
Asthma
* specific sx suggestive of diagnosis
* examination findings
* BTS - can make a diagnosis clinically. NICE advise using a diagnostic hub. What are the first line inv advised by NICE (2)
* Further testing options (2)
* Diagnostic criteria - 2 (post-bronchodilator improvement in FEV1 and of lung volume) and exhaled FENO
- SoB, wheeze, cough, chest tightness - episodic sx with diurnal variability
- widespread polyphonic wheeze
1. Spirometry w bronchodilator reversibility
2. FeNo - Note a neg spirometry test doesn’t rule out asthma.
- Peak flow variability (diary of PEFR several times a day 4 weeks) & direct bronchial challenge test (histamine/methacholine)
Diagnostics
Post bronchodilator therapy:
>200ml lung volume
12% or greater FEV1
Or exhaled FeNO >40p/billion
Asthma mx - adults
- 4 main steps (add on drugs)
- further steps (increasing dose, or using alternatives)
How does this differ from management of asthma in children (5-16)?
And for children under 5?
- SABA
- +low doseICS(Beclometasone inh)
- +LTRA(Montelukast)
- +LABA
- +MART- ICS + SABA -combination therapy in one inhaler (+/- LTRA)- instead of individuals
Further steps
- Increase ICS dose low –> medium
- Try theophylline or LAMA
- Seek expert advice
In paeds; NICE recommend stopping the LTRA when trying out the MART. And the ICS used are “paediatric low dose”.
Children under 5:
1. start on a SABA
2. 8-week trial of a paed moderate-dose ICS - if did not resolve, ? other diagnosis. If resolved - restart moderate dose ICS as maintenance. if resolve but reoccured - repeat trial.
3. SABA + paed low dose ICS + LTRA
4. Stop LTRA and seek expert advice
Acute asthma exacerbation:
PEFR, speech, RR, O2, CO2, signs of shock
Moderate
Severe
Life-threatening
Near fatal
Moderate
PEFR 50-75% predicted
Speech normal
RR<25 and PR <110
Severe
PEFR 33-50%
Unable to complete sentences
RR >25 and RR >110
Life-threatening
PEFR <33%
SpO2 <92%
Silent chest, cyanosis, reduced resp effort.
Normal CO2 - reduced resp effort.
Hypotension; bradycardia
Exhaustion, confusion; coma.
Near fatal
Raised PaCO2 +/- requiring mechanical ventilation with raised inflation pressures (doesn’t use PEFR as a feature)
Mx for acute asthma exacerbation
General
Moderate
Severe
Life-threatening
Near-fatal
General
* A-E(O2 if sats low); ABG
Moderate
* SABA inh/oxygen-driven nebs/PMDI
* + SAMA
(SalbutamolAND Ipatropium bromide)
* + Prednisolone PO or Hydrocortisone IV
Severe
* + IV MgSo4
Life-threatening
* + Aminophylline/IV Salbutamol
* Admission to HDU/ICU –> intubation in worst case/ECMO
Near-fatal
Req Mechanical ventilation
when on salbutamol what must be monitored
serum K+ (salbutamol can cause hypokalaemia)
and note salbutamol induced tachycardia
Bronchiecstasis key points
-definition
- how many weeks of recurrent infections?
- presentation (4)
- findings (CXR and HRCT)
- mx (conservative)
A condition of airways obstruction caused by long-term inflammation from recurrent infections >8 weeks –> lung fibrosis. Presents with long hx of cough with thick sputum +/- haemoptysis, SoB and fever in exacerbations. Diagnosed on CXR (bronchial dilation) and to assess extent of disease on HRCT (tramlines & rings, pools of mucus). Conserv trt for chronic disease- mucolytics, chest physio, smoking cessation.
Features specific to underlying micro-organism causing pneumonia
Typical
Gram +ve
1. Strep p.
2. Staph aures
Gram -ve
2. Haemophilius influenzae
3. Klebsiella
4. Moxarella catarrhalis
5. psuedomonas aureginosa
Atypicals - cannot be identified by gram stain or treated with penicillins
1. Mycoplasma p.
2. Legionella
3. Coxiella burnetti
4. pstiacci
Viral
* influenza A&B
* varicella zoster & herpes simplex
* SARS/COVID-19
Fungal - if immunocompromised
- Pneumocystis jirovecci (PCP)
Typicals
* * Most frequent, rusty sputum, associated with herpes labialis
* common in elderly, or secondary to influenza, and CF
* most common in COPD/existing lung disease - may produced beta-lactamase (abx resistant)
* alcoholics/diabetics; red current jelly sputum, increasing resistance, upper lobe consolidation
* immunocompromised/chronic lung disease
* CF/bronchiecstasis
Atypicals: legions of pstiacci MCQs
1. epidemics; has autoimmune features e.g. erythema multiforme/erythema nodosum rash and cold AIH; GBS or immune-mediated neurolgoical diseases Affects younger patients. Prolonged/gradual onset. Requires mycoplasma serology and agglutination test. Requires Doxy or macrolide.
2. travel related from infected water –> legionnairre’s disease (abdo pain, diarrhoea, mental state cx) - requires urinary antigen testt by urne sample. Hyponatraemia.
3. zoonose - can cause Q fever and infective endocarditis.
Fungal
- HIV associated; req. Septic (Cotrimoxazole)
Severity assessment as a predictor of mortality- pneumonia.
Score 0/1 -
>2 -
»3 -
C(U)RB-65 =
* Confusion, AMTSS <=8
* Urea >7
* RR >30
* BP <90/60
* >65
*
0/1 - consider tx at home
>=2 - hospital admission
>=3 - ITU
Tuberculosis infectious disease caused by mycobacterium tb , an acid fast bacteria staining red with Zeil-Neelsen stain
* stages of disease
* vaccination - contents and preliminary step
* who is offered BCG?
* extra-pulmonary TB (3)- bones, skin, lymph nodes?
* Ix - CXR, sputum cultures and 2 special tests
- active, latent, reactivated, milary (disseminated)
- BCG- live TB, requires Mantoux -ve.
- Neonates born in areas or with FHx of high rates of TB. Older children/adults who recently arrived in country with high rates or who are in cloe contact. Healthcare workers.
- Pott’s disease (TB of the spine); erythema nodosum, lymphadenopathy.
- Mantoux test (+ve in previous, active or latent TB).
- IGRA:interferon gamma release assay (+ve if latent TB - aka no sx and -ve mantoux).
Chest xray findings for TB
- primary
- reactivated
- disseminated
- patchy consolidation, pleural effusions, lymphadenopathy
- nodular consoliation & cavities
- millet seeds
TB medications and side effects
- Rifampicin (orange bodily fluids)
- Isoniazid (peripheral neuropathy)
- Pyrazinamide (hepatoxicity; high uric acid - gout (toe on fire)
- Ethambutol (retinopathy - visual acuity & colour blindness)
Other mx considerations for TB
- PHE notification
- Testing for Hep B and Hep C
- Isolation 2 weeks in negative pressure rooms
- Mx by MDT - esp. extrapulmonary e.g. steroids
- individualised drug regime for MDRTB
Drug induced pulmonary fibrosis (fibrOsis) (4)
- MethOtrexate
- AmiOdarone
- NitrOfurantoin
- CyclOphosphamide
Nitro, cyclo, metho, amio
Acute resp
Pulmonary embolism
* Px
* Risk factors
* Ix
* Wells score takes into account (3)
* How else can a definitive diagnosis be made?
* Mx: stable patients (1st line, 2ndline - c/i)
* Mx: unstable “massive PE” - aka hypotension
* Length of anticoagulation : provoked/unprovoked
- sudden onset chest pain, worse on inspiration with SoB
- O/E - reduced lun sounds and air entry on affected side
- VTE - immobility, blood stasis, anti-phospholipid syndrome
- A-E, O2, CXR, ABG>
- Wells score -pmhx, clinical signs, malignancy- Tachcardia, recent surgery, haemopytis etc - if >2 - PE likely –> CTPA. If <2 - D-dimer to exclude it (unless +ve –> CTPA).
- V-Q scan
PE Management
* 1st line - Anticoagulation: DOACs (apixaban/rivaroxaban) if diagnosis is suspected; includes cancer pts
* 2ndline if DOACs contra-indicated; eGFR <15, APLS aka triple negative - LMWH then Warfarin
* Massive PE: thrombolysis with alteplase
Length of anticoagulation
* provoked: 3 months
* provoked, active cancer: 3-6mo
* unprovoked: 6 months
Spontaneous Pneumothorax
* Define
* Px, O/E
* Risk factors
* Erect CXR findings (–>CT thorax if small)
- air trapped within the pleural space; “collapsed lung”
- sudden onset chest pain, SoB
- O/E - hyperresonant on affected side. Tracheal deviation (towards affected side)
- Spontaneous - Tall, thin males, athletic. Or secondary to other condition.
- CXR - loss of lung markings, visible edge of lung
Spontaneous pneumothorax management: decision algorithm
* No/minimal symptoms?
* List the 6 high risk characteristics
* Symptomatic with H-R C
* Symptomatic WITHOUT H-R C
Which pneumothoraces are deemed safe to intervene, and how?
Explain the management for conservative care and ambulatory care.
High-risk characteristics
1. Haemodynamic compromise (?tension)
2. Significant hypoxia
3. Bilateral
4. Underlying lung disease
5. >=50 with sig smoking hx
6. haemothorax
Treatment algorithm
- No/minimal sx -> conservative
- Not high risk–> conservative, ambulatory device or needle aspiration
- High risk & safe to intervene –> chest drain
Safe to intervene - pneumothorax is 2cm or can be safely accessed with radiological support
Conservative
- primary: OP review 2-4days
- secondary: IP then OP f/up
Ambulatory
- Rocket Pleural Vent - one way valve
Needle aspiration
- once resolved requires discharge and OP f/up
Massive PE
- Definition
- Mx (first-line)
- Recurrent PE mx
PE with haemodynamic instability; e.g. saddle PE
Throbolysis
Or other invasive approaches
IVC filters (stop DVT formation)
