anw so today was NUS-Tutorial day. i took a really long bus ride to sgh, was almost late for the tute but thankfully i arrived earlier than the doctor. this was the best Radiology class i ever had (not that i had many, just that i finally understood certain things that my sch nvr taught me before). so i thought i'd write what i learnt over here.
The following are with regards to either CXR, CT Scan or HRCT:
> hyperinflation of the lungs on CXR
-seen as flattening of the the diaphragm or
-length of more than 6 anterior ribs
>enlarged hilar opacities
-decide if it is a VESSEL or a MASS
-branching opacities are likely to be arteries
>Eisenmenger complex
-Eisenmenger syndrome occurs in patients with large congenital cardiac or surgically created extracardiac left-to-right shunts. These shunts initially cause increased pulmonary blood flow. Subsequently, usually before puberty, pulmonary vascular disease causes pulmonary hypertension, ultimately resulting in reversed or bidirectional shunt flow with variable degrees of cyanosis. (frm emedicine)
-eg. ASD, VSD, PDA
>Bronchiolitis
-inflammation of the small airways
-on expiration, airways collapse
>Fluid from lungs (effusion)
-note the colour
-note whether it is transudative or exudative
TRANSUDATIVE: free flowing, dependent on gravity, e.g. in heart failure
EXUDATIVE: loculated, i.e. the effusion is fixed, not free flowing, not dependent. e.g. inflammatory, infective causes.
>Mesothelioma
-in the pleura
-gives a bumpy appearance on CXR
> Tracheal shift
-compare the medial end of the clavicle with the spinous process
TB will exert a PULL on the trachea
EFFUSION will PUSH
>A decubitus film is used to demonstrate free flowing effusion
> the commonest cause of upper lobe fibrosis is TB
-other causes: interstitial fibrosis (inhaled) e.g. Extrinsic Alveolar Pneumonitis
>Blebs/Bullae
-Blebs are small bullae
-what are bullae? they are thin walled sacs, more than 2cm. walls are almost "pencil-thin"
>Consolidation vs Fibrosis
healing
-consolidation-------------------------------->fibrosis
-CONSOLIDATION:
~lungs secrete stuff
~ no sig. decrease in volume
~ no mediastinal shift
-FIBROSIS
~scarring
~loss of vol.
~ scarring PULLS
~mediastinal/tracheal shift
- so the 2 key questions are:
~is there a shift?
~is there loss of volume?
-consolidation is DENSER than fibrosis. fibrosis tends to be seen as lines rather than opacification
>How to know from HRCT/CT that TB is active?
- can see cavitations
-if it's an old TB, there would be fibrosis
>"fluffy changes" in CT/HRCT
- means alveoli are pathologically filled with pus
- i.e. acute TB
> In a normal CXR
-lung markings are BLOOD VESSELS
- the only airways visible are the larger airways like trachea & main bronchi
> Post-TB sequelae
- upper lobe fibrosis
- fine lines
-loss of volume
> Bronchiectasis
- erect film: pus falls to the bottom of airways, you see a crescent thickening (dependent)
>Blunting of costophrenic angle--> effusion
>Consolidation: very dense, cannot see vessels
>ground glass appearance (HRCT): denser than normal but less than than consolidation, and can see vessels. this means there is alveolitis (idiopathic, drug related, allergy)
> Acute Pulmonary embolism
- seen on the CT scan--> contrast surrounds the thrombus
OK end of Radiology Tutorial. There was a renal tutorial too but i'm too lazy to type it out. maybe another day! :) goodnight then..
