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48 Cards in this Set

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DDx Pleural Effusion
Pul oedema
Consolidation –pneumonia
Exacerbation of chronic lung disease- COPD, asthma
Lung cancer
Pneumothorax if breathless
Investigations for Pleural Effusion
Beside- sputum, PEFR, temperature
-FBC- signs of infection, look at Hb chronic infection
-U&E- in terms of suspected malignant cause it is important to have a baseline as contrast is used in CT which will be part of workup.
-CRP- inflammation
-Thoracocentesis- look for color, biochemistry, gram stain, cell count and differentiation, cytopathology
-CT PET if suspected malignancy
MGMT Pleural Effusion
-transudate: manage underlying cause
-drain gradually to prevent rapid shift of mediastinum
-if not adequately drained by needle/small bore catheter, surgical intervention
-chemical pleurodesis with talc/bleomycin for recurrent
-pleurx catheter also for refractory
Transudate vs. exudate
transudate <30g protein (caused by decreased oncotic pressure/increased hydrostatic pressure)
exudate >30 g protein. altered permeability of membranes/capillaries.
Light criteria for pleural effusion
if ratio of protein pleural:serum >.5
if ratio of LDH pleural:serum >.6
definition of pleural effusion
abnormal collection of fluid between the pleura due to increased production/impaired reabsorption. normally 1 ml.
atypical pneumonia
legionella, mycoplasma, PCP, chlamydia psittici
CURB 65 score
predicts mortality and guides management with abx.
C: confusion amts 8 or less
U: urea >7
R: rr >30
B: BP systolic >90, diastolic<60

0-1- outpatient treatment
2 short stay in hospital
3-5 hosp/ICU
characteristics of interstitial lung dz/ pulm fibrosis
scar tissue in lungs
decreased compliance (restrictive pattern on PFT-
endstage honeycomb lung, cystic spaces
. can be localised (pneumonia), bilateral (tb), widespread (ipf)
causes of pul fibrosis
systemic sclerosis
connective tissue disorders
occupation (coal workers pneumoconiosis, farmers extrinsic allergic alveolitis)
idiopathic (most common)
drugs (mtx, amiodorone, cyclophosphamide, gold)
Pulmonary fibrosis si/sx
(4 D's)
dry cough, dyspnoea, digital clubbing, diffuse inspiratory crackles

also, reduced chest expansion, fine late crackles, central cynaosis, cor pulm, pul htn late in dz.
MGMT idiopathic PF
high dose prednisolone for 6 weeks followed by taper. few respond well.
can also use immunosuppression (azothioprine and cyclophosphimide)
poor prog- most die within 5 yrs
Asbestos exposure related lung dz
blue is worst, white is lest dangerous
lag of 20-40 years from exposure
pleural plaques and thickening
ca. bronchus
extrinsic allergic alveolitis features:
type III (Immune complexes) and IV (cell mediated) HS.
acute: SOB, cough, fever within hours
chronic- fibrosis Sx
CXR: upper zone fibrosis
extrinsic allergic alveolitis
remove from allergen.
acute: o2, hydrocortisone 200 mg IV, oral pred 40 mg.
chronic: long term steroids
extrinsic allergic alveolitis
COPD, asthma, bronchiectasis, CHF, atypical pneumonia, lung Ca
extrinsic allergic alveolitis
fbc- anemia
ANA (+30%), RF (+50%)
PFT- restrictive. follow progression
reduced TLC, RC, RV, TF
CXR may be normal, or shot reticular/nodular opacities. honeycomb is late.
HRCT more sensitive- ground glass
Bronchiectasis defn
a COPD with inflamed airways that are easily collapsible. result in obstruction and SOB. impaired clearance of secretions.
Bronchiectasis causes
mechanical obstruction (extrinsic or intrinsic),
diffuse lung dz (ipf),
immune deficiency,
mucociliary clearance defects.
Bronchiectasis classic si/sx
sx: chronic cough, excessive sputum, foetor, hemoptysis at some stage, chronic sinusitis.

si: anemia CD, cyanosis, crackles, wheeze, corpulm.
Bronchiectasis Investigations
cxr- normal in 10%. ring shadows/tramlines/cysts
HRCT- confirms. signet rings. 97% sensitive
sputum: C & S for abx
Serum Ig for cause
sinux xray
saccharin test- mucociliary clearance
PFT- obstructive
Bronchiectasis MGMT
postural drainage- physio
bronchodilators- beta ags, antichol, and inh. steroid
ABX- high dose and longer (10-14 days) ie cefaclor, cipro, fluclox if SA
O2, LTOT if chronic
Lobe resection if massive hemoptysis.
Transplant if young and fev1<30
CF presenting complaints
Perinatal- screening, meconium ileus
Child/adult: malabsorption, RTI's +purulent sputum, atypiccal asthma, electrolyte disturbance
adult: bronchiectasis, infertility in males
CF complications
liver dz,
wt. loss,
resp. failure,
nasal polyps,
infertility (males)
CF signs
cough + purulent sputum
obstructive pattern
maybe cor pulm
CF investigations
sweat test (98% sens)
cftr gene
sinus xr/ct shows opacification
cxr/ct lung
pft. only reliable after age 6
sputum micro
fbc, u/e, glucose, lft only abnormal of >4x normal. vitamin adek
CF MGMT- prevention
prevention: physio for clearance
Inhaled mannitol, pulmozyme for increased clearance
reduce exacerbations with inhaled tobramycin, bronchodilators, high dose ibuprofen

CF MGMT- complications
pnemonia- abx, hemoptysis, pneumothorax, RF. Tx may be necessary
nasal polyps: topical steroids, or -ectomy
pancreatic insuff: enzymes (creon) before meals
nutriton: adek vitamins and high protein meals
liver dz- ursodoexycholic acid improves bile flow/transplant
DM- insulin
reproductive- IVF and gene counceling
osteoporosis- ca, vit d, dexa scans, bisphosphonates
asthma defn
chronic obstructive inflammatory disease leading to narrowing of airways and causing reversible airway obstruction
hypersensitivity of airways- triggers cause bronchospasm and excessive secretion
asthma features
polyphonic wheeze, sob, cough, chest tightness. worse at night, with dust, air and exercise.
asthma exam points
breathing: fast? laboured? anxious? speaking in full sentences? acessory muscles? pursed lips? cyanosis? hypervenilation?
ratio of insp: exp normal is 2:1
chronic asthma may have harrison's sulci - childhood
asthma Dx
mainly clinical, spirometry is preferred.
divide into high, int, low probability based on sx.
High: FEV1/FVC <.7 trial of Rx.
Int: FEV1/FVC>.7 investigate
low: investigate/treat other condition

a 400 ml improvement in FEV1 after salbutamol is considered significant.

peak flow less sensitive. look for diurnal variation % greater than 20% over 2 weeks.
ASTHMA stepwise MGMT
control extrinsic factors
1. mild intermittent: inhaled SABA as req.

2. regular preventer: +inhaled steroid (200-800 mcg/d). 400 starting

3. initial add on: a. LABA b. assess control- if good, continue. if inadequate, LABA + more steroid (800). if no response to LABA, stop LABA and increase steroid to 800. try LR antag/theophylline

4. persistent poor control: consider increasing steroid to 2000 mcg/d, add LRA, THeo, B2 ag tablet

5. use of steroids: daily steroid in lowest dose to maintain control. refer.
1. O2- via facemask/cannulae. 94-98%

2. B2 ag in nebulizer or IV for those who cant inhale. repeat 15-30 min or continuous 5-10 mcg.hr
3. steroid- pred 40-50 mg po or IV hydrocortisone 400 mg/day. continue pred for atleast 5 days
4. Ipra. add to b2 ag treatment if life threatening or poor response. .5 mg/4-6 hourly
5. MgSo4. single dose 1.2-2 IV over 20 min when poor response or life threatenting.
when to refer asthma to ITU
requires ventilation
acute severe not respondin:
falling PEF, worsening or persistent hypoxia, hypercapnia, ABG- acidosis, exaustion/confusion, respiratory arrest.
signs of severe asthma
cant complete sentences in one breath
tachy >110
rr >25
<50% PEFR
signs of life threatening asthma attack
<33 pefr
<92% sat
Cyanosis- 84-85%
Silent Chest
Tachy/Brady cardia
Progressive, irreversible airway obstruction usually due to smoking- incl chronic bronchitis, emphysema or both.
although may not have any
pursed lips
accessory muscles
paradoxical mvmt of lower ribs
reduced cricosternal distance
wheeze/quiet breath sounds
reduced cardiac dullness on percussion
peripheral edema
raised JVP
FEV1/FVC <.7 if FEV1 >80%, dx should only be makde in presence of sx.

pts over 35 who have a risk factor and prsent with one or more:
exertional breathlessness (MRC scalre_
chronic cough
regular sputum production
frequent winter bronchitis
ask about wight loss, exercise intolerance, night waking, ankle swelling, fatigue
MRC breathlessness scale
1- only on strenuous excercise
2-sob when hurrying or walking on slight hill
3-walks slower than contemporaries on level ground, or stops for breath at own pace
4- stops for breath after 100 m or few minutes on level ground
5- cant leave house, breathless when dressing
stop smoking.
annual vaccination-flu
one off pneumonia vaccine
if still breathless/exacerbations, Rx determined by Fev1
FEV1 >50%, LABA, or LAMA
FEV1<50% combo inhaler LABA + ICS or LAMA

oral theo, mucolytics, cor pulm: loop D, LTOT
things that can improve survival in stable COPD
smoking cessation
lung volume reduction surgery (remove bullae, allows reinflation)
COPD Investigations
spirometry. however, poor predictor of QOL and disability

Dx if FEV1/FVC <.7 and FEV1 <80%

stage1: mild 80% or above with Sx
stage 2 moderate: 50-79%
3: severe 30-49%
4 very severe <30% or FEV1 <50 but with resp. failure.

if reversible with bronchodilators- reconsider Dx

FBC- anemia/polycy
CXR to exclude
alpha 1 anti trypsin if early or non-smoker
TLCO to ix symptoms out of proportion to pft
pulse ox to assess need for LTOT, if cor pulp, cyanosis, or fev1<50

peak flow no use.
copd complications:
cold weather
Haem. infl., S. Pneum, M. Catarr, Viruses (30%)

patients with frequent infective exacerbations should be given home course of steroid and abx and encouraged to use if purulent sputum.

Cor Pulm due to vasocontriction in lung due to hypoxia
managing complications of copd
broncodilators by nebuliser: SABA 2.5-5 mg & SAMA 500mcg with pred 30 mg/day 5-7 days

if hx of purulent sputum or CXR consolidation, ABX (RD & E say doxy po 200 stat hen 100 mg OD 5/7)
O2 aim for 88-92 via venturi mask at home or 24% in hospital pending ABG
if still acidotic, NIV
at least 15 hrs a day
if obs very severe (<30% fev)
consider if severe (30-49)
cyanosis, poly cy, edema, JVP, o2 <92 on room air

measure abg 3 weeks apart

offer LTOT to those with pa02 7.3-8 AND 2ndary polycy, noctural hypoxemia, edema, pulm htn.

decreases risk of cor pulm.
COPD pathophys, main points
chronic inflammation taht affects central airways, periph. airways, parenchyma and alveoli, and vasculature of lung
narrowing and remodelling of airways. increased number of goblet cells (reid index), enlargement of mucus secreting glands of central airways, and vascular bed changes leading to hypertension.
inflammatory- macrophages, neuts, leuks
not eosinophils (unlike asthma).
emphysema- elastin breakdown and loss of alveolar integrity.
chr. bronchitis- ciliary dysfunction and increased goblet cell size and number, more mucus secretion.
increased airway resistance. decreased recoil, fibrotic changes in parenchyma, and luminal obstruction all contribut to resistance.
expiratory flow limitiation contributes to hyperinflation. these changes lead to hypoxia. vascular smooth muscle thickening with subsequent pulm hypertension which is late and indicates poor prog.