Resp Flashcards
Name 2 features of asthma pres
wheezing, breathlessness, chest tightness, coughing
Worse at night and early morning Wheeze (polyphonic and expiratory) Episodic SOB Chest tightness Cough - *worse at night FHx atopy/nasal polyposis Diurnal variation - *worse in morning
Name 2 triggers of allergic and 2 non allergic asthma
Allergic: house dust mite, pet fur, grass pollen -> IgE
Non: exercise, cold air, stress, strong emotion, viral infx, smoking
2 drugs you need to be careful prescribing asthmatic
Beta blockers - B2 cause airway constriction
NSAIDS or aspirin block COX-1 -> decrease prostaglandins + overproduction of pro-inflammatory leukotrienes
Carboprost
What happens in acute airway inflammation?
Constriction, oedema, mucus hypersecretion
2 Features of chronic airway inflammation
Airway remodelling, airway hyperresponsiveness
Basic pathology of early phase asthma. + Name 2 inflammatory mediators
Allergen ->
Mast cells release IgE
histamine, leukotrienes and TNFa
- > Increase in Vascular permeability and hyper-secretion of mucus
- > airway oedema
+ Increased smooth muscle and airway tone
-> Narrowed airways
Key cell in later phase asthma (6 hrs)? What happens/
eosinophil mediated (recruited by IL4 and IL5)
Increase goblet cells -> hyper-responsive airway
Effect of acute vs chronic inflammation?
Airway remodelling ->?
Acute inflammation = bronchoconstriction,
chronic = airway hyperresponsiveness,
airway remodelling = persistent obstruction
Name 3 questions to assess asthma control?
Inpast 4 weeks:\
How often felt SOB? How often woken from sleep? How often used reliever? How often interfered with normal activities e.g. school/work? How rate asthma control?
What should you always check in asthma (especially if poorly controlled)?
Inhaler technique
Name 3 Ix in asthma
PEFR (peak flow rate) - diurnal variation >20%, according height/weight
Reversibility testing FEV1 improves by 15% with SABA (or PEF - 20%)
Spirometry
FEV1 < 80% + *FEV1/FVC < 70% = obstructive
CXR: normal or hyperinflation
FBC -> ?eosinophilia
Skin prick test
Asthma pharma Mx stages
SABA
SABA + low ICS (<400 mcg budesonide) *step 1 if >3/week
SABA + low ICS + LTRA (montelukast)
SABA (±LTRA) + low ICS + LABA (depending on response LTRA
3 Key Ix in acute exacerbation asthma
PEF + SpO2 + ABG
Mx of acute asthma exacerbation ? If exhausted?
OSHITMS
O2 aim (94-98) Salbutamol (neb) Hydrocortisone /pred within 1 hour IV (4mg/kg hydrocortisone) Ipratropium (neb) Theophylline (IV) Mag Sulf (IV) Salbutamol (IV)
Intubate + ventilate if exhaustion
What is COPD
Chronic obstruction with irreversible airflow obstruction -> air trapping and hyperinflation
COPD genetic cause
A1ATD
Basic pathology of COPD
Chronic inflammation -> increased goblet cells, narrowing of airways, and vascular changes -> pulmonary HTN
Name 2 findings OE of COPD
Barrel chest, CO2 flap, hyperresonant percussion, distant breath sounds (over bullae, hyperinflation and trapping), coarse crackles (exacerbation), wheeze (exacerbation)
Name 3 comps of COPD
Cor pulminale Pneumonia - pneumococcal vaccine and yearly influenza vaccine Depression* Polycythaemia Respiratory failure
2 signs of cor pumonale
raised JVP, distended neck veins, hepatomegaly
Mx cor pulminale
Long term O2 therapy + loop diuretic
Difference between t1/2 resp failure pathology ? Description of people in these types
T1: Ventilation/perfusion mismatch
Pink puffer: emphysema –> old and thin, use of accessory muscles
COPD
T2: Alveolar hypoventilation
Blue bloater: peripheral oedema and overweight from RHF
What spirometry finding in COPD
Obstructive pattern: FEV1/FVC < 0.7
Non-reversible and no diurnal variation
Name 3 Ix in COPD
Spirometry ABG: may see hypoxia +- hypercapnia CXR FBC Sputum culture
Name 2 signs on XR of COPD
Flattened diaphragm
Increased intercostal spaces
Hyperlucent lungs
Increased AP diameter
What might you see on FBC of COPD
polycythaemia +Hb rise. Polycythaemia develops in response to hypoaemia which triggers erythropoietin release by the kidneys
Severity of COPD
Mild: FEV1 > 80%
Mod: FEV1 50-80%
Severe: FEV1 30-50%
V.Severe FEV1 < 30%
4 Non pharma Mx of COPD
Patient education
+ vaccination
+ depression screen
+ COPD nurse
Smoking cessation, exercise, obesity mgmt (pulmonary rehabilitation)
Pharma Mx of non controlled COPD
SABA/SAMA
If FEV1>50%
- LABA
- LABA+ICS
If FEV1<50%
-LABA + ICS
(Or LAMA for either)
Then
LABA+LAMA+ICS
LTOT
pka <7.3
pka >7.3 + one of pulmonary hypertension, polycythaemia
Name 2 bugs commonly causing COPD exacerbation
H. influenza, s. Pneumonia, m. catarrhalis
3 parts of Mx COPD ACUTE exacerbation? If resp insufficiency ?
SABA + SAMA neb (salbuamol + ipratropium)
+ O2 (24% venturi aim for 88-92%)
Oral corticosteroid (prednisolone) - prevents recurrence
Airway clearance - mucolytics + physio
BIPAP if respiratory insufficiency
Abx ….
Infective exacerbation management:
S - steroids H - heparin O - oxygen (88-92) N - nebuliser bronchodilators A - antibiotics
Abx in COPD exacerbation - community vs hospital
Community
amox / doxy
hospital
vanc / tazocin
2 places you might get cultures from in COPD
Blood culture and sputum culture
When would pneumonia be classified as hospital aquired
If LRTI @2 days post admission
Score for pneumonia risk
CURB 65 Confusion Urea > 7 RR > 30 BP < 90 or < 60 diastolic 65
Score
0-1 - low risk, recommend outpatient care
2 - moderate risk - to hospital
3-5 - high risk = to ITU (30 day mortality = 15-40%)
CAP in younger adults - cause? how does it present slightly different?
Mycoplasma pneumoniae
Dry cough + atypical CXR + AI haemolytic anaemia + erythema multiforme
Tx = macrolide (C or E)
HAP in immunocompromised may be caused by fungal pneumocystis jirovecii - Mx?
Co-trimoxazole
3 parts of normal pneumonia pres
Cough with increasing sputum + expectoration
Fever (high in pneumococcal)
Dyspnoea
Pleuritic pain (assoc with bacteraemia)
[Arthralgia + myalgia + confusion]
3 findings OE pneumonia
Increased HR, RR, low BP ?sepsis, temperature
Dullness to percuss
On auscultation -Crackles or bubbling -Reduced air entry (unilateral) -Pleural friction rub -Aegophony (E will sound like A) Vocal fremitus
Name 4 Ix for pneumonia.
When might you check urinary antigen?
FBC, CRP (raised WCC, raised CRP)
ABG: may be low oxygenation
Sputum culture and sensitivity - for causative
CXR - lobar
Blood culture - for causative organism
*Urinary antigen: for legionella and pneumococcus
Name 2 findings on XR of pneumonia
Air bronchograms
Consolidation: homogenous opacification in lobe
Atelectasis if small airway obstruction
What is this describing
diffuse reticular or reticulonodular opacities (affects interstitium)
atypical pneumonia CXR
CURB scores decide the Mx of pneumonia in CAP
0-1
2
2+
Low risk (0-1) CAP: Oral 5 day amoxicillin or clarithro,
Mod (2) CAP:
7-10 days amoxicillin + clarithromycin
Mod and high risk (2+) CAP:
7-10 day
Co-amoxiclav + clarithromycin (IV)
In high risk pneumonia and penicillin allergic what can you use
cefotaxime
Mx of HAP
TAZ
Mx of legionella
Clarithromycin
Mx of chlamydia pneumonia
Doxy
Name 3 comps of pneumonia
Septic shock
ARDS - non-cardiogenic pulmonary oedema
Pleural effusion (50%) + empyema
*Hepatisation (histologically lungs start to look like liver)
Name 3 Rfs for Tb
Birth endemic (asia etc), immunocompromised (e.g. HIV), exposure (v.infective) Poor nutrition, overcrowding, IVDU, homeless, prisons
Screen for TB immunity? the issue with this? If +ve?
Tuberculin skin test: > 5mm
- no distinction between active and latent TB
If +ve - interferon gamma release assay
What type of infection is active TB
Granulomatous
[multinucleate/Langhans giant cell, MP, LC]
3 ix in TB
CXR
3 x sputum acid fast bacilli smear
Sputum culture - Dont get much growth
FBC - leukocytosis and anaemia
NAAT - +ve for m.tuberculosis
?HIV test - for concurrent infection
Stain for TB
Ziehl-Neelsen stain - pink
Seen on CXR of TB
Primary?
Healed primary?
Most important = post primary?
Need to know post primary - focus on that
Primary: consolidation + ipsilateral hilar enlargement (lymphadenopathy)
Healed primary: Ghon focus: large round calcified lesion near hilum
Post primary: fibronodular upper zone opacities with cavitation + calcification + consolidation to hilum
TB mx - What needa to be checked before Mx and monitored?
RIPE DOTS (check LFTs before and monitor, check vision with Snellen)
TB drug Mx and 1 SE of each
6M Rifampicin: liver tox, orange secretions, induces hepatic enzymes (accelerate oestrogens, steroids, anticoagulants, phenytoin)
6M Isoniazid: liver tox, peripheral neuropathy (give w/ pyridoxine B6)
2M Pyrazinamide: liver tox, hepatitis
2M Ethambutol: *visual disturbance: optic neuritis, loss of acuity
[E - for EYES]
What is meant by DOTS in TB Mx
DOTS: directly observed therapy 3x/week
Who gets screened with Dx of TB
Screen household and close contacts
When is infectivity decreased in TB
2 weeks of treatment + 3 consecutive -ve AFB smears
Name 3 systems and pres of extra pulmonary TB
Pleura - pleural TB leads to pleural effusion
LN - scrofula - swelling and discharge
GU - frequency/dysuria/haematuria
Bone - osteomyelitis starting in growth plates of bone Pott’s disease - vertebral fracture associated with TB
Brain - TB meningitis - Rich foci
Abdomen - ascites (peritoneal) and abdominal LN
Whats seen on CT of disseminated TB
millet seed appearance
Liver/spleen/lung
Name 2 thromboembolic and 2 genetic RFs for DVT
Thromboembolic risk factors:
Cancer, trauma, major surgery, hospitalisation, immobilisation, oral contraception, obesity/preg (high oestrogen), recent flight (immobilisation)
Genetic risk factors: (Family history)
Factor V leiden, protein C deficiency, protein S deficiency, antithrombin deficiency, antiphospholipid
What is virchows triad in DVT
venous stasis,
vessel injury,
activation of clotting system
(hypercoaguable state)
DVT score
Wells (>2)
Alternative diagnosis more likely
Symptoms: DVT, haemoptysis, tachy
PMH: previous VTE, immobilisation 4 days, active malignancy
Ix in wells 0-1?
2?
D dimer
if +ve / wells 2
PVUSS - venous duplex USS
2 Main comps of PE
-> RHF and cardiac arrest
Name 3 types of embolus for PE
thrombus Amniotic fluid embolus Fat embolus (at long bone fracture) Air embolus Tumour embolus
Name 3 signs of PE OE
Pleural rub, tachy, tachyp, elevated JVP, hypoxia, shock
Name 2 DDx of PE
ACS, aortic dissection (anticoag fatal), pneumothorax
IX in PE
Wells CXR ECG: sinus tachycardia ABG: reduced PaO2, high lactate D-dimer
Late sign of PE on CXR
wedge shape infarction
Key Ix in PE if wells >4 or D-dimer +ve
CTPA
What OE finding would indicate massive PE
Systolic <90
Initial resus for PE? Mx of haeomdynamically stable / unstable?
100%O2
IV access: fluids
Morphine
stable:
LMWH (dalteparin) or fondaparinux (10a inhibitors)
Haemodynamically unstable (?renal fail): Unfractionated heparin ± thrombolysis (alteplase)
how long do you give Mx in PE?
If active Ca?
What other Mx do you give [always continue on this]?
5 days OR till INR > 2 for 24 hours (longer)
LMWH for 6 months
VKA (warfarin) for 3 months then reassess
mx recurrent DVT + anticoagulation is CI
inferior vena caval filters
Mx symptomatic DVT
Catheter directed thrombolytic - Eg dalteparin
2 methods of prevention VTE
Early mobilisation and hydration post surgery
Avoid the pill
Graduated pressure stockings
Seen on spirometry of pulm fibrosis
restictive
FVC low, FEV1/FVC normal/high
3 things on pres / OE of PF
4Ds: dry cough, dyspnoea, digital clubbing, diffuse inspiratory crackles
Name 3 causes of PF
Connective tissue disease: RA, SLE, SS, Sjogren’s
Occupational exposure: asbestos, coal dust, silica
Medication: amiodarone, bleomycin, methotrexate
Inhalation of irritants: hypersensitivity pneumonitis, birds, mould
Radiation
Name 3 RFs for IPF
Smoking, infectious agent, dust exposure, chronic aspiration (GORD)
Most important q in IPF
Occupation
Main comp of IPF
Pulmonary hypertension -> cor. Pulmonale
Name 3 Ix in IPF
CXR
CT
LuFT - restictive
ANA (SLE…_, RF
lUNG BIOPSY
Name 1 XR findings IPF
reticular shadowing (net-like) of lung peripheries + bases, shaggy heart border
Name 2 findings on High resolution CT of IPF
Ground glass
honeycombing
reticular pattern
General supportive Mx for IPF - 3 things
O2 therapy Physiotherapy Exercise and weight loss Vaccination Smoking cessation
What pharma Mx can be used in IPF
Antifibrotic: pirfenidone (inhibits TGFB collagen synth)
Give 2 differentials for Upper vs Lower lung fibrosis
Upper - ESCHART (granulomatous diseases) Extrinsic allergic alveolitis Sarcoidosis/silicosis Coal worker’s pneumoconiosis Histiocytosis X Ankylosing spondylitis Radiotherapy TB
Lower - RASCO (systemic diseases) RA Asbestosis Systemic sclerosis/SLE Cryptogenic fibrosing alveolitis Other (drugs)
3 main systemic causes of PF
Mx
SLE, RA, systemic sclerosis
Generally immunosuppression with steroids
2 ways RA could lead to PF
Rheumatoid nodules may lead to small effusion
Methotrexate associated pneumonitis -> stop and Rx with steroids
What is caplans syndrome
pulmonary fibrosis in coal workers with RA
EAA - RFs, basic pathology
History of exposure to organic dust
Birds, agricultural, mould
Non-IgE mediated inflammation of alveoli and distal bronchioles
3 Ix in EAA
Raised inflamm markers (WCC, CRP)
CXR: diffuse micronodular interstitial shadowing - upper zone
CT: reticulo-nodular shadowing, ground glass, micronodules
LuFT: restrictive, decreased DLco (diffusing lung capacity of carbon monoxide), decreased SpO2
Inhalation challenge: provocation testing - NP and LC levels, LuFT
BAL (bronchoalveolar lavage): predominant CD8 cells
Mx of EAA ? Acute/chronic?
Allergen avoidance + facemask
Acute or subacute: O2 + prednisolone (oral) taper
Chronic: low dose corticosteroids
What is histiocytosis X also called?
What happens?
Where is affected?
Langerhan’s cell histiocytosis
Usually in kids
clonal proliferation of Langerhan’s cells (Dendritic cell in skin) and CK overproduction
Bone, skin, lung
2 Ix of histocytosis X? Mx?
Bone XR - punched out lytic lesions
Chest XR - reticulo-micronodular infiltration
Tissue biopsy - Langerhan’s cells
Chemotherapy
What are Pneumoconioses? How long for Sx?
What is important to remember?
Group of chronic lung diseases by exposure to mineral dust or metal:
Includes coal workers, silicosis, asbestosis
10 years coal
15-60 years asbestos
Notifiable industrial disease - may be eligible for compensation
Coal worker who has RA will probs have what in exam?
Caplans syndrom
3 Ix in coal workers
Occupational history
LuFT: restrictive
CXR: large nodular fibrotic mass in upper lobes
Sputum microscopy: black
Mx of coal workers lung
Avoid exposure
CXR, CT, LuFT for monitoring - incurable
Financial implications
Smoking cessation
What 2 conditions might give black sputum
coal workers
silicosis
Ix in asbestosis
Occupational history
LuFT: restrictive
CXR: ground glass opacification, small nodular opacities (asbestos bodies - in alveoli at lung bases), shaggy cardiac sillhouette
Sputum microscopy: asbestos bodies
Mx asbestosis
Avoid exposure
CXR, CT, LuFT for monitoring - incurable
Financial implications
Smoking cessation
Usual cause of pleural mesothelioma
asbestosis
3 sx of pleural mesothelioma.
Make sure you know the key recurrent one
Dry cough, dyspnoea, dig club + pleuritic chest pain (*recurrent pleural effusion)
Symp of pleural effusion: diminished breath sounds, dull to percuss
Constitutional symptoms: weight loss, fatigue, fever, night sweats
3 Ix in pleural mesothelioma
CXR
CT
Thoracentesis
pleural biopsy - (*epithelioid mesothelioma)
Seen on thoracentesis of pleural mesothelioma
Exudate with malignant cells
2 things seen on CXR of pleural mesothelioma
Irregular pleural thickening, reduced lung vol, ev asbestosis, unilateral pleural effusion
Mx of pleural mesothelioma
operable at stage 1 + chemo
Chemoradio for others
ENTITLED TO COMPENSATION
What is a pleural effusion
fluid in the potential space between visceral and parietal pleura
What are the 2 main types of effusion and difference? If its hard to tell what can be used?
Transudate (low protein <30g/L)
exudate (high protein >30g/L)
[exercise likes lots of protein]
Light criteria if protein 25-35
Pathology of transudate pleural effusion
disruption of hydrostatic and oncotic forces across pleural membranes (increase venous P or hypoproteinemia)
pathology of exudative pleural effusion
increased permeability of pleura from inflammatio
2 Causes of transudative plerual effusion
Increase hydrostatic or low oncotic:
Heart failure, cirrhosis, hypoalbuminaemia, nephrotic syndrome
What syndrome has pleural transudative effusion and 2 other things?
Meig’s =
right pleural effusion
+ ovarian fibroma
+ ascites
2 Causes of exudative plerual effusion
Pneumonia, malignancy, TB, AI disease (RA) comp of MI (Dressler’s)
3 findings OE pleural effusion
Unilateral reduced chest expansion,
stony dullness on percussion,
decreased breath sounds,
if large -> tracheal deviation away
What CXR finding in small pleural effusion
Blunted costophrenic angle
Unilateral pleural effusion .
Transudative clinical picture mx?
If no transudative picture?
Yes -> treat cause (LVF, hypoalbuminaemia)
No -> USS guided pleural aspiration/thoracentesis
pleural effusion on thoracentesis - if it is
Clear/straw?
turbid / yellow?
red?
Clear/straw = trans or ex
Turbid/yellow = empyema, parapneumonic
Haemorrhagic = haemothorax - malignancy, PE, trauma
Cytology of pleural effusion aspirarion . Neutrophils? Multinucleated giant cells? Abnormal mesothelium? Lymphocytes?
Neutrophils = parapneumonic effusion,
multinucleated giant cells = RA,
abnormal mesothelium = mesothelioma,
Leukocytes = TB, malignancy
Is a bilateral effusion likely to be trans or ex?
transudate
Mx difference between trans and ex effusion
Trans - Do not tap!
Ex - Symptomatic: pleural tap
Max 1.5l - otherwise will result in fluid shift and pulmonary oedema
Mx of malignant cause effusion
pleurodesis (with talc)
Likely to recur
Causes of bilateral hilar lymphadenopathy
TIMES
TB Inorganic dust - silicosis, berylliosis Malignancy: lymphoma, carcinoma, mediastinal EAA: e.g. bird fanciers lung Sarcoidosis
What is a pneumothorax?
Accumulation of air in the pleural space
3 RFs for pneumothorax
Primary spontaneous: tall thin males, smoking, Marfan’s, family history
Secondary spontaneous: pre-existing lung disease: COPD (bullae), CF, TB, PCP
Trauma
What happens in a tension pneumothorax
- occurs when intrapleural pressure > atmospheric -> results from ball valve mechanism letting air in but not out
Lung deflates and mediastinum shifts contralaterally compressing great veins and causing decreased venous return to heart
Pres of pneumothorax
pain *on same side as pneumothorax on breathing in + dyspnoea
2 findings OE of pneumothorax
Hyper-resonant
Reduced expansion
Decreased breath sounds
Pres / OE of tension pneumothorax
Respiratory distress with rapid shallow breathing
Distended neck veins
Tracheal deviation away
Hyperexpanded ipsilateral hemithorax
TachyC/TachyP
2 findings XR of pneumothorax ? extra if tension?
Visceral pleural line
no lung markings
Tension
+ increased intercostal space + contralateral mediastinal shift + depression of hemidiaphragm
Mx pneumothorax? If this doesnt work?
High flow o2
Aspirate 16-18G cannula, 2nd IC space, mid clavicular line
Chest drain and admit
Where does a chest drain go?
Mid axillary IC 4-6
Where do you put needles with regard to ribs for needle thoracostomy
2nd IC mid clavicular
Aim for just above a rib (rather than just below) to avoid neurovascular bundle
Give 3 DDx of pleuritic chest pain
ACS Aortic dissection Pneumothorax PE Pneumonia Malignancy
What is bronchiectasis and characteristic features
Permanent dilatation and thickening of the airways due to recurrent infection and inflammation
Recurrent (chronic daily) cough, excessive sputum
-Prone to infections
Give 3 causes of bronchiectasis
Post infectious: measles/flu/pertussis, aspergillus fumigatus (ABPA), pneumonia
Immunodeficiency: HIV, Ig deficiency
Genetic: CF, ciliary dyskinesia, A1ATD
Connective tissue disease: RA, Sjogren’s
IBD: CD, UC
Name 2 bugs often in bronchiectasis
aspergillus fumigatus
S.aureus, h.inf, s.pneum, pseudomonas aeruginosa
Pres of infective bronchiectasis
Cough and daily sputum (bloody at 50%)
Mild - yellow/green sputum
More severe - khaki sputum
Intermittent haemoptysis
Obstructive symptoms: dyspnoea + wheeze
Weight loss and fatigue
2 findings OE of bronchiectasis
Inspiratory coarse crackles (shift on cough),
high pitched inspiratory squeaks and pops,
low pitched brhonci (snoring sounds),
clubbing
Cause of early vs late inspiratory crackles
Early inspiratory: airway disease e.g. bronchiectasis
Late inspiratory: interstitial disease: e.g. IPF
3 Ix in bronchiectasis and whats seen
CXR
Normal/dilated bronchi with thickened walls + cysts (cystic shadows)
Tubular or ovoid opacities
TRAM-TRACK SIGN
*CT - imaging of choice
Thickened, dilated airways with or without air fluid levels, cysts
FBC - high eosinophils in ABPA, neutrophilia -> bacterial infection
Sputum culture and sensitivity
[For cause Serum A1AT phenotype, serum immunoglobulins (low), sweat test, serum HIV, aspergillus fumigatus skin prick test]
Bronchiectasis bugs if gram +ve vs -ve? Which in CF
G- = pseudomonas aeruginosa (high risk if CF)
G+ = s.aureus, s.pneumonia
Mx bronchiectasis
Exercise + improved nutrition
+ airway clearance physio (postural drainage, percussion)
+ mucolytics
Inhaled bronchodilator
+ inhaled hypertonic saline
Vaccinations and prophylactic antibiotics
Mx recurrent pseudomonas
nebulised gentamicin
Mx severe exacerbation of bronciectasis? Mild?
Iv ciprofloxacin
Oral amoxicillin§
Who gets allergic bronchopulmonary aspergillosis?
what is it?
Asthma / CF
hypersensitivity to aspergilllus fumigatus
-> fibrosis / bronchiectasis
3 Ix allergic bronchopulmonary aspergillosis
Skin test for aspergillus fumigatus sensitivity - positive
Serum IgE elevated
FBC with eosinophil count elevated
CXR *upper or middle lobe infiltrates
Mx allergic bronchopulmonary aspergillosis
Avoid mold
Optomise CF/asthma mx
oral corticosteroid
oral antifungal - Eg co-trimoxazole
Gene in CF ?
CFTR - cl channel
3 organs affected in CF
Lungs, bowel, pancreatic duct, sweat glands, reproductive organs
-> thick sticky secretions
When is screening for CF
Serum immunoreactive trypsinogen on 5d heel prick (Guthrie)
Give 3 parts of Pres of CF
Neonates + infants: failure to pass meconium, failure to thrive, large appetite (pancreatic insufficiency), chronic wet cough
Resp:
Recurrent infection, chronic cough, wheeze, thick mucus, nasal polyps
GI
Gallstones, decreased motility
Panc
Insufficiency -> bulky, greasy, foul smelling stool
May develop DM from autodigestion
Reproductive system
Absent VAS - infertility
Digital clubbing
3 Ix for CF
Serum immunoreactive trypsinogen
Sweat test - high Na/Cl
Genetic testing
pancreatic assessment: feacal elastase
Usual bug in CF - key Ix for this
Pseudomonas aeruginosa (70%) - *highly transmissible
Sputum C+S
2 comps of CF
Bone disease from malnutrition,
depression,
short stature,
cor pulmonale -> RVH
3 parts of the mx for cf
Stop smoking
Chest physio
Inhaled bronchodilator
Inhaled mucolytic: dornase alfa + hypertonic saline
Segregate in hospital
Vaccination: influenza and pneumococcal
Prophylactic ABX: fluclox or amoxi
Pancreatic enzyme replacement, fat soluble vitamins DEAK
Mx of advanced lung disease in CF
Bilateral transplant
What is cor pulmunale
RVH/RHF due to disease of the lungs or the pulmonary blood vessels.(HTN)
pressure for pulm HTN
Mean pulmonary artery pressure >25mmHg at rest
2 egs of vasoconstrictors in pulm vasculature
endothelin-1, thromboxane A2 (+ platelets), low NO
OE pulm HTN
Accentuated P2 (pulmonary component of second heart sound)
Tricuspid regurgitation murmur (high pitched holosystolic)
Pulmonary regurgitation murmur (Graham Steell) - high pitched early diastolic at pulm area (normally if pul HTN secondary to mitral stenosis)
RHF: oedema, exertional syncope, visible RV heave, pulsatile hepatomegaly, ascites, raised pulsatile JVP
3 ix and findings in pulm HTN
CXR: pruning - attenuated peripheral arteries, enlarged pulmonary artery shadow
ECG: RVH (tall R wave and small S in V1), RAD, right atrial enlargement (p-wave > 2.5mm in II, III, aVF)
Transthoracic echo: Tricuspid regurge
Right heart catheterisation (Swan-Ganz) - >25mmHg pul art pressure with pulmonary capillary wedge pressure < 15mmHg
3 parts of Mx pulm HTN
CCB (nifedipine or amlodipine) or sildenafil (PDE5 inhibitor - augments pulmonary vascular response to nitric oxide)
Anticoagulant: warfarin target 1.5 to 2.5
Lifestyle: low level graded exercise
Oedema: furosemide and low salt diet
Supplemental O2 if needed
2 main types and breakdown of lung Ca
Small cell (least common) 15%
Non-small cell (most common) 85%
- Adenocarcinoma
- Squamous cell carcinoma
- Large cell carcinoma
What would get you a 2 week wait for lung Ca
> 40 + 2 of following
Cough, fatigue, SOB, chest pain, weight loss, appetite loss, smoking
Name 2 Paraneoplastic features of small cell lung Ca
ADH, ACTH, Lambert-Eaton syndrome (muscle weakness - NMJ)
SIADH - hyponatraemia
ACTH - HTN, hyperglycaemia, hypokalaemia, alkalosis, muscle weakness
LES - weakness that improves with muscle contraction
Name a paraneoplastic feature os squamous cell Ca
PTH-rp, clubbing, TSH
PTH - bone pain and hypercalcaemia
TSH -> Hyperthyroidism
Name a paraneoplastic feature of adenocarcinoma
gynaecomastia
What tumour is from neuroendocrine cells-? presentation
carcinoid
serotonin secretion -> flushing and diarrhoea
Where are adenocarcinomas usually found
peripheral lung
Where does squamous cell carcinoma usually found? what does this mean for pres?
central airway
-> present as obstructive lesion
Mets in Adeno/squamous/large cell?
Adeno
brain, adrenal, bone
squamou (well differentiated cells)
mets late
Large
mets early
undifferentiated
Where might a pancoast tumour invade? features?
invasion of brachial plexus -> weakness, parasthesia, pain in C8-T1, shoulder pain
Invasion of sympathetic chain -> Horner’s syndrome
Ptosis, miosis, ipsilateral anhydrosis
Recurrent laryngeal nerve -> hoarseness
Where is a pancoast tumour found?
superior sulcus
Signs of Lung Ca
Fixed monophonic wheeze
Pleural effusion -> stony dullness on percussion
Signs of SVC compression - facial congestion, distension of neck veins
Signs of hypertrophic arthropathy - finger clubbing (more common @NSCLC)
Name 2 ways you might get a sample of Lung Ca
Cytology sputum and pleural fluid
Bronchoscopy - for histological diagnosis, endobronchial lesions may be biopsied
Surgical biopsy - transthoracic needle aspiration, peripheral lesions and LNs
Ix for lung Ca
CXR
CT/MRI brain
LuFT
FBC - anaemia
LFT - mets
Bone scan - skeletal mets
U+E: Na, Ca - hyponatraemia = small cell, hyperCa = squamous
Sampling
Common mets of lung Ca
Liver, bones, brain, adrenals
Hilar, mediastinal, supraclavicular LNs
Give 2 times when surgery for NSCLC is CI
Stage 3b or 4 - mets present
*FEV1 < 1.5
Malignant pleural effusion
Vocal cord paralysis/ superior vena cava syndrome
Mx SCLC
Not surgery
chemo (cisplatin + etoposide) 4-6 cycles
+ radio
+ prophylactic cranial irradiation
Palliative support in Lung Ca .
Breathlessness
Obstruction
Pleural effusion
Cough
Hoarseness
SVCO
Bone pain
Spinal cord compression
Breathlessness
Opiate
Obstruction
External beam radiotherapy
Pleural effusion
Aspiration/drainage
Cough
Opiate
Hoarseness
ENT
SVCO
Chemo + radio
Bone pain
Radio
Spinal cord compression
Dex
What is good pastures? presentation? precede?
Anti-glomerular basement membrane disease
Kidney symptoms: oedema, *reduced urine output
Lung symptoms: cough + haemoptysis + SOB + fever
*likely to have had recent URTI
3 Ix goodpastures
Kidney tests:
- Urinalysis - proteinuria + haematuria
- Renal function - raised Ur and Cr (azotaemia - raised nitrogen compounds)
- Renal biopsy - crescentic glomerulonephritis and linear IgG staining on immunofluorescense
Lung tests
-CXR: lower zone pulmonary infiltrates (blood)
Anti GBM titre raised - by immunofluorescence
[ANCA (type 2 cytotoxic reaction therefore may be ANCA +ve)
ANA normal to rule out lupus nephritis
Complement levels - normal to rule out lupus, infection and other nephritis
Anti-streptolysin O to rule out post strep glomerulonephritis]
Mx goodpastures with pulm involvement
Oral corticosteroid
+ plasmapheresis
+ cyclophosphamide (remove and suppress Aab)
O2 +- blood products for severe pulmonary haemorrhage
CO2 levels in 2 types of resp failure? how do they present?
Type 1: hypoxia (<8kPa) without hypercapnia (>6kPa)
Type 2 hypoxia + hypercapnia
T1: COPD (pink puffer), pneumonia, pulmonary oedema, fibrosis, asthma, PE, ARDS
T2: COPD (blue bloater), asthma, myasthenia gravis, polyneuropathy
Ix resp failure
ABG, CXR, FRB, ECG
mx respt failure ? what do you have to be cautious of
Admission and resuscitation
Treat hypoxaemia - aim SATS > 90%
ALWAYS start on high flow
Beware prolonged high conc O2 if lost hypercapnic drive -> elevating PaO2 may reduce RR
Resp failure ventilation options
conscious
O2
BiPAP
Unconcious
O2
Intubate / ventilate
What is ARDS
Non-cardiogenic pulmonary oedema and diffuse lung inflammation
dyspnoea, decreased sats despite ventilation
2 most common causes of ARDS
sepsis
pancreatitis
Who gets ARDS
Low SATS, RFs (sepsis, aspiration, pneumonia, blood trans, panc), respiratory failure
Ix ARDS
Low tidal volume ventilation
CXR (bilateral infiltrates), ABG, blood culture, sputum culture, urine culture
Criteria
- acute
- non-cardiogenic
- CXR pulmonary oedema
- Po2 <40
Mx ARDS
Supportive care - resus and then slightly negative fluid balance
ABX + treat cause
What is seen on an atypical pneumonia CXR
diffuse reticular or reticulonodular opacities (affects interstitium)
