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234 Cards in this Set
- Front
- Back
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what is the defintion of the solitary pulmonary nodule
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approximaetly round
<3cm diameter usually an incidental finding |
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on routine xray what percentage wil show a solitary pulmonary nodule
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0.09-0.2% each year
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What were the results of the ELCAP study looking at solitary pulmonary nodule?
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1000 high risk pateitns were screened (>60 and smokers)
23% had a non-calcified pulmonary nodule 12% were maligniant and many <1cm (too small for PET result or FNAB) |
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what is the next investigation for asolitary pulmonary nodule in a high risk patient?
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<1cm CT scan
>1cm FNAB |
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what is the Ddx for a solitary pulmonary nodule
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bronchogenic carcinoma
carcinoid tumour metastatic malignancy infections granulomas (TB and fungus) - 80% of benign lesions inflammatory lesions (pneumonias) harmatomas (10% of benign lesions) |
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On the CT scan what are we looking for with the solitary pulmonary nodule
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corona radiata
border - smooth or scalloped calcification harmatorma (50% have fat and cartilage) growth rate. |
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wha is the calcifation pattern of a solitary pulmonary nodule for:
Occupational cancer harmatoma granuloma |
occupational is eccentric patern
harmatoma is popcorn pattern granuloma is a central pattern |
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descfibe the low risk of Ca for a solitary pulomary nodule
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<1.5cm
<45y age never soked or quit >7y smooth margins |
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describe athe intermediate risk for can of solitary pulmonary nodule
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1.5-2.2cm
45-60y current smoker or quit <7y scalloped margins |
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describe the high risk of Ca for a solitary pulmonary nodule
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>2.2cm
>60y current smoker nodule margins: corona radiata or speculated |
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What is the ideal next step after ncidental finding of a solitary pulmonary nodule and what are risks?
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fine neadle aspiration biopsy
particularly for peripheral nodules that are easier to acces risk is causing a pneumothorx - so reconsier in a very high risk pateint for instnace severe COPD for COPD pt or proximal lesion consider bronchoscopy or thoracoscopic procedure. |
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which type of surgery ha the most risk attached for PE
|
orthopeadic - particularly on large joints - hips and knees
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with regards to PE what is regarded as low risk?
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DVT <15% and fatal PE <0.1%
minor surgery or major surgery in young person |
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with regards to PE what is regarded as intermediate risk?
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DVT 10-40% and fatal PE 0.1-1%
major surgery such as abdo, uro, gynae <40 + RF |
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with regards to PE what is regarded as high risk?
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DVT 40-80% and fatal PE 1-5%
ortho surgery or extensive pelvic/ado surgery for Ca |
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what is the gold standard invstigation of venous thrombosis?
|
venogram - rarely used
|
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What ECG findings will you see on recent PE?
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S1 Q3 T3
S wave in lead I Q wave in lead III and inverted T wave in leade III |
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what 2 things are worth 3 points in the Well's criteria?
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clinical signs and symptoms of DVT
Alternative diagnosis is less likely that PE |
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wwhat 3 items are worth 1.5 points in the Wells criteria for PE
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HR >100
Imobilisation or surgery in past 4 weeks previous DVT or PE |
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what 2 items are worth 1 point each in the Wells criteria
|
Haemoptysis
cancer |
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According to the wells criteria what is the risk straification
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<2 is low
2-6 is medium >6 is high |
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what is the treatment for PE
|
LMWH for at least 5 days and overlap with oral anticoagulatnt for at least 4-5 days
can discontiune with INR has been therapeutic for 2 consecutive days treat pts with reersable or time limited RF for at least 3 months proven reginen is warfarin for 6 monthsfollowed by warfarin at 1-5-2 if you decide to continue |
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In the case of a massive PE what is the treatment?
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use of thrombolytic agents
pateints with haemodynamically unstable PE or massive ilio-femoral thrombosis are the best candidates |
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In the case of recurrent PE what is the treatment
|
IVC filter placement recommended if:
- there is contraindications to or failure of antocoagulation for chroic recurrent embolism with pHTN and with concurrent performance of surgical pulmonary embolectmy or pulmonary enartectomy |
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what are the 3 absolute contraindications to anticoagulation therapy
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1. active bleeding
2. severe bleeding diathesis of Pp<2000 3. Neurosurgery or intracranial bleeding in the last 10 days |
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what is the incdience of DVT in pregnancy
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7/1000
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at end expiration what is the gas volume of the lung?
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2.5 L
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how is the density of the lungs distributed
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it is about 1g/mL near the hilum and 0.1g/mL at the periphery
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describe the membranous bronchioles
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they are non-cartilaginous <1mm D are numerous and short
consist of about 5 generations branching to the terminal bronchioles. |
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within the lungs what is the anatomical dead space?
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extrapulmonary (upper) airways and the intrapulmonary bronchi
histologically the bronchioles down to the terminal bronchiles ought to contriibute 25% to the dead space - but in life this is not true becouse of gas phase mixing and mechnanical mixing in the distal airways from cardiac impulse. |
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in the lungs apcal junctional complexes consist of what 3 elements
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zonula occuldens (tight junction)
zonula adherens macula adherens (desmosomes) |
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in the lungs what is the function of the tight junction?
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to restict passive diffusion and
the polarisaition of Cl and Na transprot aloows the airwat epithelium to either secrete or absorb ions |
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bronchial blood flow represetents how much of cadiac output?
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0.5-1.5%
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what is the verticle hieght of the lung at function residual capactiy
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24cm
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what is the mean pulmonart artery pressure taken as
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15mmHg or 20cmH2O
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what is pulmonary venous pressure?
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8cmH2O
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what is a pulmonary sign of pHTN?
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the loss of the capillary pulsation
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what is the normal capillary blood volume
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60-75ml which is 1/3 of the possible capacity at around 200ml
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what occurs to Angiotensin I, bradykinin and prostaglandin E1 as they traveser the lung
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in a single passage through the lungs they are almost completely inactivated
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which potent vasodilator is generalted locally in the lungs
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NO
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what is the erminal respiratory unit made up of
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approximately 100 alveolar ducts and 2000 alveoli.
there are 150000 units in both lungs conbined |
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what is the Acinus
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this contains 10-12 terminal respiratory units (100 alveolar ducts + 2000 alveoli)
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in the lungs what are type II cells
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specialised to be synthetic, secretory and repair factoris.
they proliferate to become both type II and type I cells |
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in the lungs what are type I cells>
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these provide a large, thin celular barrier specialised for gas exchange.
central nucleus, attenuated cytoplasm that form a large surface area for gas exchange vulnerable to injury |
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what is the Hering-Breuer reflex
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myelinated slowly adapting stretch receptors that prevent overinflation of the lugs
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what will the percussive note be for a pleural effusion
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stony dull
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what will the percussive note be for COPD
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normal or hyperresonant
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in which lung condition will the trachea move toward the lesion
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in a collapsed lung - tension pneumothorax
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in which lung conditions may you hear no added sounds on auscultation?
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Pleural effusion
Pneumothorax Collapsed lung (blocked bronchus) |
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If crackles do not clear with a cought what do they indicate?
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there may be pulmonary oedema Ddx ARDS
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when is a pleural friction rub best heard
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on insiration
to differentiate from a pericardial friction rub ask the pateint to hold their breath - the sound will stop with a pleural friction rub |
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what are the 5 stages of lung development
|
1. Embyonic stage to week 5
2. Pseudoglandular stage (w5-17) 3. clnalicular stage (w16-26) - differeintiation of squamous type I and II begins 4. saccular stage; persists from week ~24 to termAlveolar type II undergo maturation - * prior to 22 weeks there is insufficienct surface area in the distal pulmonary tree to support life 5. Alveolar stage - to 18months postnatal life. |
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what are the risk factors for asthma
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childhood infection
allergen exposure indoor pollution dietary deficiency of antioxidants exposure to pets early* family history Atopy |
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what form of hypersinsitivty is asthma
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type I IgE mediated
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was is the maladaptive response of an atopic individual
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a tendency to preferentially activate the Th2 pathway in response toa challenge to the immune system
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IgE antibodiies recruit which cells in asthma
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eosinophils and mast cells
|
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which interleukins are crucial in asthma
|
IL4 and IL5 promost production if IgE, growth of mast cells and activation of eosinophils
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what occurs in the immediate raction phase of asthma
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Bronchoconstriction
oedema mucus secretion |
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what are some of the pathological changes that occur in an asthmatic lung?
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crushmann spirals
goblet cell hyperplasia angiogenesis basement membrane thickeing hyperinflation of the lungs petechial haemorrhage on the pleural surfaces mucus plug |
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what will the spirometry of an asthmatic show
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an obstructive pattern; FEV1/FVC <80% and FEV1 <80%
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what is the minimum degree of severity of a patient with asthma who has been woken by their symtoms at night
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moderate
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what is bronchiectasis
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resuting from the abnormal or permanent distortion of one or more conduction bronchi (>2mmD). May be congenital or acquired
common in CF |
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in bronchiectasis the primary infection is typically:
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Klebsiella sp, staph aureus, M. tuberculosis, mycoplasma pneumonieae + atypical mycobacteria, measles virus, pertussis and HSV
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in bronchiectaisis what are the common secondary infections
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Haemophilus sp. and pseudomonas sp.
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what is the most common pthology of bronchiectasis
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secondary to infection
focal process of a lobe or segment |
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diffuse bronchectaisis is associated with what condition?
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CF
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what is the pathophysiology of bronchiectais
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dilatation caused by weakening or destruction of the muscular and elastic components of he bronchial walls.
transmural inflammation, oedema, scarring and ulceration. |
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what will a CXR of bronchiectais show?
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hyperinflation
crowded lung markings small cytic spaces at base of lungs |
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what will a CT of bronchectasis show?
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the D of the bronchus will be >1.5x the diameter of the adjacent vessel
tramtrack lines radiating from hila or signet ring appearence |
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what is the non pharmacological treatment of bronchiectais
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physiotherapy - use of a 'vest' and posutral drainage etc
smoking cesation O2 |
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blood borne metastasis of lung cancer occur most frequently where?
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the liver, bone, brain, adrenals and skin
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which type oc lung cancer can potentially be cured
|
non-small cell lung cancer
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the presenting symptoms of a central lung mass will be
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haemoptyiss, cough (dry irritating), fever, wheeze,
local obstruction of thoracic structurs |
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what does paraneoplastic syndrome include
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clubbing
HPOA migratory thrombophlebitis, ectopic hormone production and neurological symotms ACTH ADH PTH |
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ademocarcinoma of the lung is:
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tumour with glandular differentiation and/or mucin production by tumour cells
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the most common type of lung cancer is?
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adenocarcinoma ~50%
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what is the epidemiology of adenocarcinoma of the lung
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women
non smokers asians |
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what is the characteristic pathology of adenocarcinoma of the lung
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slow growing, metastesises early and associated with local and diffuse fibrosis.
peripheral and sub pleural location |
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where abouts does adenocarcinoma of the lung occur?
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peripherally and sub pleural
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what subtype of adenocarcinoma grows along the alveoli without invasion
|
Bronchioalveolar carcinoma and can present radiographically as a single mass or diffuse multinodular lesion (fluffy infiltrate)
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true of false
pure BAC is rare usually find an adenocarcinoma with BAC features |
true
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describe large cell lung cancer
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lacks the cytological features of small cell carcinoma and gladular or squamous dfferentiation
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what percentage of lung cancer does large cell Lung cancer account for
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2-5%
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what is the prognosis for large cell lung cancer
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poor; rapid growth with large metastesis
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where do large cell lung cancers occur
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peripherally; they are large (>4cm) in 70% of cases
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large cell lung cancer tumours are associated with what pathological feature?
|
central necrosis of the tumour --> cavernous mass
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large cell lung cancers have sharp or blured margins
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sharp
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what is the prognosis of squamous cell carcinoma in the lung
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relatively better than other lung cancers
more frequent in men |
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which lung cancer most commonly causes pancoast syndrome
|
SCC; caused by a pancoast or superior sulcus tumour which are at the apex of the lung
this cell type is most commony associated with hypercalcaemia due to extopic PTH |
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where are SCC of the lung located?
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2/3 are centrally located
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describe small cell lung cancer?
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poorly differentiated neuroendocrine tumour
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where do small cell lung cancers tend to occur?
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centrally
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what percentage of lung cancer is accounted for by small cell lung cancer?
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15-20%
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which is the most aggressive form of lung cancer?
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small cell - mets present on 2.3 of presenting patients
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how is small cell lung cancer staged?
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limited stage: limited to 1 hemithorax with regional nodes including hilar and ipsilarteral and contralateral mediastinal supraclavicular nodes
Extensive stage: |
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chemotherapy for lung cancer is?
|
cisplatin
carboplatin only in patients not candidates for cisplatin |
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what are the RF for COPD
|
smoking
solid fuel fires ocucpational genetic: alpha1-antitrypsin deficiency |
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what changes occur in the lung walls of COPD patients?
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loss of elastic tissue
inflamation fibrosis |
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chahges to chest wall and pulmonary complicance in COPD lead to:
|
premature airway closure
gas trapping dynamic hyperinflation |
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with relevance to COPD unopposed action of protease and oxidants caues
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desctruction of alveoli and appearacne of emphysema
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what are the 2 processes that lead to COPD
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chronic bronchitis and emphysema
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what might you see on examination of a patient with COPD
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pursed lip breathing, central cyanosis and prlonuged expiration
use of the muscles of respiration barrel chest cardiac apex beat may not be palpable |
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what will arterial blood gases be in mild COPD
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there will be mild hypoxaemia without hypercapnoea
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what will the arterial blood gases be in severe COPD
|
severe hypoxaemia and hypercapnoea
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describe the four stages of COPD
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FEV1
I mild - >80% II moderate - 50-80% III severe - 30-50% IV very severe 0 <30% OR <50% with chronic respiratory failure (type II) |
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what is type II respiratory failure
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hypercapnoeic where pCO2 is >50mmHg with a low pO2 also
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list the 7 components of COPD treatemnt
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1. short acting bronchodilator
2. antobiotics for infection 3. corticosteroids - oral prednisolone 4. O2 5. flu vaccination and pneumoccocal vaccination 6. pulmonary rehab starting in stage II or III 7. Inhaled corticosteroids starting in stage III |
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describe cystic fibrosis
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genetic disease resulting from the mutation in the CF transmembrane conductance regulator (CFTR), a Cl- channel found in cells linging the lungs, intestines, pancreatic ducts, sweat glands and reproductive organs
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what is the most common gene mutation in CF
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delta f508
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CFTR is
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a n anioin channel found in apical membranes of epithelial cells
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what is the result of the mutation in CF
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abnormal salt tansport by epithelial celss --> thich viscous ecretions causing mucus retention in the lungs
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In CF what occursi n the pancreas?
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blockage of the exocrine ducts,early activation of pancreatic enxymes causing autodesctuction
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what occurs in the intestines of a CF patient?
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bulky solid stools and intestinal blockage?
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What is the IRT test
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Immunoreactive trysinogen test for CF by quantifyign serum immunereactive trypsiongen from the heel prick blood spot test
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If liver disease develops in a patient with CF what treatment is recomeded?
|
oral bile acid supplemenation Urodeoxycholic acid
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what are the mainstays of treatment for CF
|
physiotherapy
treatment of respiratory infection pancreatic enzyme repalcement: lipase, amylase and protease (pancreatin) adjused for weight and portion sizes H2 antagonists to provide an alkaline enviromenet for pancreatic juices |
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what vitamins should be supplemetned in CF
|
fat soluble vitamins
A, D, E and K |
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which two age groups are most susceptible to foreign body aspiration?
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children <15 years (1-3 higest risk) and elderly >70y
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which are the 3 anatomical sites for lodgement of inhaled aspirate
|
larync - large object
trachea - large object bronchus |
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which main bronchus is mainly affected in adults who inhale a foreign body
|
the right main bronchus because in adulthood the left becomes very angular
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what are the 3 phases of aspiration
|
intial phase: choking and gasping
asymptomatic phase: lodgement of object and reduciton of reflexes complication phase: erosion occurs or obstruction leads to peumonia |
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true or false
most foreign bodies inhaled can be seen on a plain xray |
false.
up to 80% are radioluscent |
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with foreign body aspiration what can you see on a PA xray?
|
hyperinfation
lobar or segmental atelectasis mediastinal shift pneumomediastinum; pneumothorax from the mediastinum |
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what are the common complications of foreign body aspiration
|
~20% will present with peumonia days or weeks aften aspiration
atelectasis: complete obstruction from foreign body or associated mucoid secretions and granulation tissue can cause this (~20% CXR and ~60% of CT) bronchiectasis (30%) |
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in an HIV+ patient which infection required extravigilant screening for
|
mycobacterium tuberculosis
|
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|
true or false
for an HIV+ patient; in the setting of fulminant disease you cannot reply on the accuracy of a negtive skin test. |
true
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is treatment the same for TB in an HIV+ patient?
|
no - should consult an expert as Rifamipcin induces the hepatic cytochrome P450 enzomes which interacts with antiretroviral therapy
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how is pneumonia included as an AIDS defining illness?
|
2 or more episodes in 12months of recurent bacterial pneumonia is an AIDS defining illness
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in an HIV+ patient multilobar consolidation is typical of
|
s. pneumoniae pneumonia
|
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how does the CD4+ T cell count correlate to the incidence of pneumonia in the HIV+ patient
|
HIV is an independent risk factor but incidnece increasses with a decreasing CD4+ count
for patients with CD4+ of <100 particularly at risk of hospitlisation and AB must cover p. aeruginosa |
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what is the Mycobacterium Avium Complex
|
it consists of 2 mycobacterium species M avium and M intracellulare commonly found in air, soil, water.
colonisation in the intestinal tract is an AIDS defining illness and prior to HAART occured in 20-40% of HIV+ now rare |
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what is the recomended antibiotic therapy for MAC in HIV+
|
clarithromycin - must test suseptibility though
|
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in HIV+ what is PCP?
|
Pneumocystis pneomonia is an infection of the lung caused by the fungal organism Pneumocystis Jirovecii
one of the most common AIDS defiing illness in resource rich countries. Rx is TMP-SMX |
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what is Kaposi Sarcoma
|
low-grade vasoformative neoplasm associated with human herpes virus 8
it is an AIDS defining illness |
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pulmonary hypertension is indicated by what findings
|
mean pulmonary artery pressure >25mmHg at rest or 30mmHg with exercise recoreded during RH catheterisation
elevated peak pulmonary artery pressure of >40mmHg |
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how does BMI corelate with the incidence of OSA
|
30% of people with BMI >30
50% BMI >40 |
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what percentage of people with OSA have HTN?
|
50-70%
|
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which congeintal syndromes are risk factors for OSA
|
pierre-Robin syndrome
Down's syndrome |
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what is the mechanism linking OSA with cardiovascular disease
|
hypoxaemia and decreased sleep, --> hypercapnoea --> altered sympathetic activation, metabolic dysregulatoin, LA enlargementa nd endothelial dysfunction and hypercoagulbility
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which pro-inflammatory cytokines are associated with OSA
|
CRP, IL6, IL18, MMP9 and ROS
|
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what are the STOP questions?
|
do you snore loud enough to hear through a door?
do you feel tired during the daytime? has anyoen observed you to stop sleeping past history of HTN? |
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what ist he Mallampati score?
|
it is related to OSA:
I: fully visible tonsils uvula and soft palate II lower portion of tonsils and uvula not seen III only base of uvula seen IV: only hard palate visible |
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what is the apnoea-hypopnoea index
|
the sum perhour of episodes of apnoeas and hypopnoea
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what is the respiratory distress index
|
the sum per hour of episodes of apnoea, hypopnoea and respirtory effort related arousals.
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how do you define OSA on polysomnography
|
>15 episodes/hour OR ?5.hr and symptoms
|
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what is the treatment for OSA
|
weight loss, smokingcessarion and reduce EtOH
CPAP |
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the most comon cause of community acquired pneumonia is
|
streptococcus pneumonia and mycoplasma pneumonia
Haemophilus influenxza, Chlamydophlia and other respiratory virsus |
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the most common cause of community acquired pneumonia requireing intensive care:
|
s. pneumoniae, staph aureus, legionnet, gram neg bacilli and H. influenza
|
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what is first line treatment in the out patient setting for community acquired pneumonia
|
amoxicillin
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what is the first line tretment for a non-severe in patient with community acquired pneumonia?
|
benzylpenicillin plus dlxycycline and if ID gram neg bacilli PLUS gentamicin
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severe community acquired pneumonia is treated with?
|
ceftriaxome or benzylpenicillin
plus gent plus ceotaxine plus azithromycin |
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what is the defintion of hospital acquired pneumonia?
|
an acute lower respiratory tract infection that is acquicer at least 48 hours after admission to hospital
it is one of the most common nosocomial infections |
|
|
the most likely pathogens in hospital acquired pneumonia
|
gram neg bacilli such as: Pseudomonas aeruginosa, E coli, klebsiella and acinetobactoer sp.
|
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what is a primary spontaneous pnemothorax?
|
without a precedding truama or event
|
|
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what is a secondary spontaneous pneumothorax
|
a complication of underlying primary disease
|
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what is a pneumothorax
|
when air gains access to the pleural space
|
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What is a tension pnemothorax
|
a complcation of any other type of pnemothorax causing a "one way valve"
|
|
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what is the pressure gradient in the chest cavity?
and how does this relate to pneomothorax |
alveolar pressure > atmospheric pressure > intrapleural pressure
if a communication between any two spaces occurs then gas will flow down the pressure gradient into the pleural space. |
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which tpe of pneomothorax is a medical emergency and why?
|
tension pneumothrax:
when intrapleural pressure exceeds atmospheric pressure, especially during expiration, and results in a ball valve mechanism that promotes inspiratory accumlation of pleural gases. The build up of pressure within the pleural space eventually results in hypocaemia and respiraotry failure from compression of the lung |
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what is the immediate treatment of a tension pnemothorax
|
immediate decompression
14 guage catheter 2-3 intercostal space midclavicular line |
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what ist he treatment for a secondary spontaneous pnemothorax
|
ealier active intervention and hospitalisation. intercostal tube drainage necessary except with VERY small at <1cm; simple aspiration is rarely succesful.
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what is Virchows triad
|
endothelial injury
stasis or turbulent blood flow blood hypercoaguability |
|
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what is the systolic BP of someone who has just had a massive PE
|
<90mmHg
|
|
|
what are the signs of an acute PE with infartion?
|
acute onset of pleuritic pain, breathlessness and haemptysis
|
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for someonw with suspected PE what screening tests might you run
|
screening for antithrobin III defciency,
protein C or S deficiency factor V leiden lupus anticoagulant homocysteinuria ANAs RF should also do aD dimer, troponins and FBC |
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|
what should the pressure be in compression stockies worn for rpevious PE
|
30-40mmHg at the ankle worm for 2 years; gradient compression means highest at toes and a gradual decrease to thigh
|
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|
when is vena cava filter indicated in a pateint with PE?
|
only for pateints whith acute venous thromboembolis who have absolute contraindications to anticoagulatn therapy or objectively documented recurrent thromboembolism
|
|
|
describe the pathogen M tuberculosis
|
rod shaped
non-spore forming obligative aerobic bacterium gram postive or neutral acid fast due to mycolic acid and high content of lipid in cell wass |
|
|
how does tuberculosis survive in the macrophage?
|
due to acidification by the inhibition of intracellular calcium release
|
|
|
in tuberculosis the tissue damaging response is due to?
|
a delayed type hypersensitivty reaction to various bacillary antigents.
|
|
|
in tuberculosis, when specific immunity is acquired what occurs?
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large numbers of macrohages accumulate at the site of a primary lesion, granulomatous lesions are then formed and refered to as the Ghon focus
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what is the treatment for tuberculosis
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Rifampicin
Isonazide Pyrazinamide Ethambutol RIPE! |
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in tuberculosis what is DOTS?
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directly observed therapy short course
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where is the highest airway resistance
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in the lower airways
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how do type II alveolar cells in the lungs proliferate
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they prolifeate into both type II and type I cells
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describe Type I alveolar cells?
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they have enormous surface area specifically for gas exchange and may up more tha 90% of the alveolar epithelium
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What is the definition for ARDS?
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Acute resiratory distress sydnrome
An acute conditions charactersied by bilateral pulmonary infiltrates and seere hypoxaemia in the absence of evidence for cardiogenic pulmonary oedema |
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what is the characteristic pathophysiology of ARDS
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increased permeability of the alveolar-capillary barrier.
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what is stridor?
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high pitched harsh sounds on inspiration
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what are the chronic remodelling changes taking place in asthma?
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smooth muscle hypertrophy and hyperplasia, angiogenesis and sub-epithelial fibrosis
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what are some of the acute changes in lung histology duing an asthma attack?
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Oedema and mucus secretion
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which interleukins are critical in asthma
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IL4 and IL5
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how is reversibility in asthma difined?
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demonstrated by an increasse of 15% or of 200ml after a SABA
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what are the radiological findings for ARDS?
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alveolar infiltrates
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what ares ome of theclinical features of ARDS
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acute onset
bilateral infiltrates no evidence of LA HTN (the pulmonar artery occlusion pressure should be <18mmHg) |
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how is ARDS managed?
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oxygen: aiming ofr SpO2 of 88-95%
minimising acidosis pH >7.3 initiate volume pressure ventilation RR <35 |
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what is the most common secondary infection in bronchiectasis
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usually haemophilus
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what tyoe of bronchiectasis is most common?
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cylindrical or tubular
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what are the xray findings of bronchiectasis?
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tram track, signet ring sign, bronchiol wall thickening
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what type of bronchiectasis is seen in CF
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cystic or sacuclar
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what are some examples of gram positive cocci
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staph aureus, strep pneomonia, peptococcus niger
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what are some examples of obligate intracellular parasite
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chlamydia trocomatis, coxiella burnetti, Rickettsia richettisa
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what is the mechanism of action of growth factors analgues (antibiotics)?
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inhibit folate metabolism
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what are the radiological findings for ARDS?
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alveolar infiltrates
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what ares ome of theclinical features of ARDS
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acute onset
bilateral infiltrates no evidence of LA HTN (the pulmonar artery occlusion pressure should be <18mmHg) |
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how is ARDS managed?
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oxygen: aiming ofr SpO2 of 88-95%
minimising acidosis pH >7.3 initiate volume pressure ventilation RR <35 |
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what is the most common secondary infection in bronchiectasis
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usually haemophilus
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what tyoe of bronchiectasis is most common?
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cylindrical or tubular
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what are the xray findings of bronchiectasis?
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tram track, signet ring sign, bronchiol wall thickening
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what type of bronchiectasis is seen in CF
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cystic or sacuclar
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what are some examples of gram positive cocci
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staph aureus, strep pneomonia, peptococcus niger
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what are some examples of obligate intracellular parasite
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chlamydia trocomatis, coxiella burnetti, Rickettsia richettisa
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what is the mechanism of action of growth factors analgues (antibiotics)?
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inhibit folate metabolism
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what is the mechanism of action of beta lactams?
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inhibit cell wall synthesis
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what ist he mechanism of action of quinolones
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inhbit DNA replication?
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what is the mechanism of action of aminoglycosides, macrolides and tatracyclines
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inhibit translation (protein synthesis)
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what is the mechanisms of action of rifamycins
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they inhibit transcription (bacterial RNA polymerase)
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what are some of the histological changes that occur in COPD?
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narrowing and remodelling or airways
increased goblet cell numbers vascular bed changes --> pHTN |
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what are the typical xray findings in COPD?
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flattened diaphragm, hyperinflation, increaed retrosternal air space
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what is the pathogen implicated in croup?
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parainfuenza virus
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describe moderate croup:
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frequent barking cough and easily audible stridor at rest and suprasternal and sternal wall retraction at rest with no or minimal agitation
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if you see a compensatory metabolic acidosis on blood gases what do you suspect?
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this tells is that this is a chronic respiratory acidosis
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what does a high pH and a high bicarb on blood gases tell us?
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this is a primary metabolic alkalosis
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what does paraneoplastic syndrome include:
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clubbing, migratory thrombophlebitis, HPOA, ectopic TSH production
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what is the mechanism of action of the chemotherapy drugs platimun compounds?
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they activate within the cell by displacing Cl- leaving a positively charged molecule that react with DNA
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what is the mechanism of action of the chemotherapy drugs Taxanes (paclitaxel and doicetaxel)?
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promote assemply of tubulin into stable non-functional microtubules and inhibit disembly, arresting the cell cycle in late G2 and M phase
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what is the mechanism of action of the chemotherapy drugs Yramidine nucleoside analogues and cytidine (gemutabine)?
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metabolise intracellularly to active nucleoside that inhibit DNA syntheesis and induces apoptosis
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what is the mechanism of action of the chemotherapy drugs vinca alkaloids (vinorelbine)
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binds to tubulin inhibiting its polymerisation and meabolic function --> mitotic arrest in metaphse
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what is the mechanism of action of the chemotherapy drugs topoisomerase inhibitors (irenotecan)?
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inhibit enzyme topomerase I thereby interfereing with coiling and uncoiling of DNA during replication --> inhibits nucleic acid synthesis
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what is the mechanism of action of the chemotherapy drugs tyrosine kinase inhibitors (imatinib)?
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inhibit specific tyrosine kinases thatare abnormally activated in some cancers (CML and ALL t(9;22) translocation)
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where do andenocarcinomas typically occur
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peripherally
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where do large cell lung cancers typically occur?
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peripherally. they are large tumours with rapid growth and early mets
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what is the prognosis of SCC in the lung
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better; they are slower growing and do not metastesise early
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which cancer is a pancoast tumour most commonly associated with?
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usualy assoiciated with SCC of the lung and horners syndrome
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small cell lung cancer is usually located where?
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centrally
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what type of tumour is a small cell lung cancer?
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this is a poorly differentiated neuroendocrine tumour
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how would you treat an inpateint with non-severe gram neg CAP?
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IV benzyl penicillin or cefriaxoen PLUS poxy/clarithromycin
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what is the most common cause of HAP?
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Neussera spp
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what denotes a poor outcome for CF patients?
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early colonisation by staph aureas
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what is the most common cause of secondary spontaneous pneumothorax
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COPD
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what percentage of people with a BMI over 40 have OSA?
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50%
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what is the apnoea-hypoapnoea index
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sum per hour or episodes of apnoeas and hypoapnoeas
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describe M tuberculosis
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rod shaped, obligative aerobe, gram positive/neutral
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how does M tuberculosis survive in the macrophag
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by inhibiting intracellular Ca release
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