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48 Cards in this Set
- Front
- Back
DDx Pleural Effusion
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Pul oedema
Consolidation –pneumonia Exacerbation of chronic lung disease- COPD, asthma Lung cancer Pneumothorax if breathless |
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Investigations for Pleural Effusion
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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 -Spirometry -CXR -Thoracocentesis- look for color, biochemistry, gram stain, cell count and differentiation, cytopathology -CT PET if suspected malignancy |
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MGMT Pleural Effusion
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-transudate: manage underlying cause
-drain gradually to prevent rapid shift of mediastinum CXR -if not adequately drained by needle/small bore catheter, surgical intervention -chemical pleurodesis with talc/bleomycin for recurrent -pleurx catheter also for refractory |
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Transudate vs. exudate
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transudate <30g protein (caused by decreased oncotic pressure/increased hydrostatic pressure)
exudate >30 g protein. altered permeability of membranes/capillaries. |
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Light criteria for pleural effusion
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EXUDATE
if ratio of protein pleural:serum >.5 if ratio of LDH pleural:serum >.6 |
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definition of pleural effusion
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abnormal collection of fluid between the pleura due to increased production/impaired reabsorption. normally 1 ml.
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atypical pneumonia
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legionella, mycoplasma, PCP, chlamydia psittici
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CURB 65 score
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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 >65. 0-1- outpatient treatment 2 short stay in hospital 3-5 hosp/ICU |
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characteristics of interstitial lung dz/ pulm fibrosis
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scar tissue in lungs
decreased compliance (restrictive pattern on PFT- Fev1/FCV>80%) endstage honeycomb lung, cystic spaces . can be localised (pneumonia), bilateral (tb), widespread (ipf) |
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causes of pul fibrosis
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think SARCOID
systemic sclerosis asbtestosis rheumatoid connective tissue disorders occupation (coal workers pneumoconiosis, farmers extrinsic allergic alveolitis) idiopathic (most common) drugs (mtx, amiodorone, cyclophosphamide, gold) |
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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. |
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MGMT idiopathic PF
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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 |
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Asbestos exposure related lung dz
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blue is worst, white is lest dangerous
lag of 20-40 years from exposure pleural plaques and thickening ca. bronchus asbestosis mesothelioma |
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extrinsic allergic alveolitis features:
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type III (Immune complexes) and IV (cell mediated) HS.
acute: SOB, cough, fever within hours chronic- fibrosis Sx CXR: upper zone fibrosis |
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mgmt
extrinsic allergic alveolitis |
remove from allergen.
acute: o2, hydrocortisone 200 mg IV, oral pred 40 mg. chronic: long term steroids |
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DDX
extrinsic allergic alveolitis |
COPD, asthma, bronchiectasis, CHF, atypical pneumonia, lung Ca
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Investigations
extrinsic allergic alveolitis |
fbc- anemia
ESR/CRP ANA (+30%), RF (+50%) ABG 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 Bx |
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Bronchiectasis defn
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a COPD with inflamed airways that are easily collapsible. result in obstruction and SOB. impaired clearance of secretions.
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Bronchiectasis causes
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congenital,
mechanical obstruction (extrinsic or intrinsic), post-infective, granuloma, diffuse lung dz (ipf), immune deficiency, mucociliary clearance defects. |
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Bronchiectasis classic si/sx
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sx: chronic cough, excessive sputum, foetor, hemoptysis at some stage, chronic sinusitis.
si: anemia CD, cyanosis, crackles, wheeze, corpulm. |
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Bronchiectasis Investigations
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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 ABG if RF |
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Bronchiectasis MGMT
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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 |
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CF presenting complaints
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Perinatal- screening, meconium ileus
Child/adult: malabsorption, RTI's +purulent sputum, atypiccal asthma, electrolyte disturbance adult: bronchiectasis, infertility in males |
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CF complications
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liver dz,
wt. loss, hemoptysis, pneumothorax, resp. failure, osteoporosis, nasal polyps, DM, infertility (males) |
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CF signs
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clubbing
cough + purulent sputum crackles wheezes obstructive pattern maybe cor pulm |
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CF investigations
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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 |
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CF MGMT- prevention
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prevention: physio for clearance
Inhaled mannitol, pulmozyme for increased clearance reduce exacerbations with inhaled tobramycin, bronchodilators, high dose ibuprofen complications: pnemonia |
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CF MGMT- complications
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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 |
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asthma defn
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chronic obstructive inflammatory disease leading to narrowing of airways and causing reversible airway obstruction
hypersensitivity of airways- triggers cause bronchospasm and excessive secretion |
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asthma features
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polyphonic wheeze, sob, cough, chest tightness. worse at night, with dust, air and exercise.
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asthma exam points
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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 |
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asthma Dx
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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. |
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ASTHMA stepwise MGMT
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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. |
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ASTHMA acute MGMT
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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. |
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when to refer asthma to ITU
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requires ventilation
acute severe not respondin: falling PEF, worsening or persistent hypoxia, hypercapnia, ABG- acidosis, exaustion/confusion, respiratory arrest. |
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signs of severe asthma
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cant complete sentences in one breath
tachy >110 rr >25 <50% PEFR |
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signs of life threatening asthma attack
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<33 pefr
<92% sat Cyanosis- 84-85% Hypotension Exhaustion Silent Chest Tachy/Brady cardia |
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COPD Def
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Progressive, irreversible airway obstruction usually due to smoking- incl chronic bronchitis, emphysema or both.
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COPD Si
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although may not have any
cachexia hyperinflation pursed lips accessory muscles paradoxical mvmt of lower ribs reduced cricosternal distance wheeze/quiet breath sounds reduced cardiac dullness on percussion peripheral edema cyanosis raised JVP |
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COPD Dx
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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 wheeze ask about wight loss, exercise intolerance, night waking, ankle swelling, fatigue |
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MRC breathlessness scale
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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 |
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COPD MGMT
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stop smoking.
annual vaccination-flu one off pneumonia vaccine SABA/SAMA 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 |
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things that can improve survival in stable COPD
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smoking cessation
LTOT lung volume reduction surgery (remove bullae, allows reinflation) |
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COPD Investigations
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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 BMI 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. |
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copd complications:
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cold weather
infective: 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 |
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managing complications of copd
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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 |
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LTOT
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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. |
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COPD pathophys, main points
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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. both are PROGRESSIVE AND NOT REVERSIBLE 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. |