adelaidemedblog

Yeah. I assume we all know what those stand for, I’m too lazy to type properly =)

Just an attempted summary of the content of today’s tute, I’m left some small things out (eg. in coning), although if there’s something you wanna add or correct feel free. If you’re an admin/author jump in and edit the post to make corrections etc, and if not leave a comment =)

*Case 3 stuff (diabetes)*

Diabetes & alcohol
Mech for diabetic ketoacidosis after a few drinkies:
alcohol consumption –> alcohol metabolised –> metabolic byproducts –> cessation of gluconeogenesis in liver –> hypoglycaemia –> fat metabolism –> production of ketone bodies (which are acidic) –> depletion of HCO3- stores (as it is used up “buffering” in order to prevent drop in pH) –> acidosis
-respiratory system: DKA leads to rapid shallow breathing (Kussmaul’s breathing) in order to “blow off” carbon dioxide and thus make the blood less acidic. Occurs almost immediately.
-renal: DKA leads to increased HCO3- reabsorption & decreased H+ reabsorption. Starts in the same timeframe as respiratory system response, but takes 3-4 days to have an effect.

Does hard exudate in retina cause vision problems?
No. The lesions are generally small, not big enough to really affect vision. By the time they are big enough to do so, the patient would have other forms of retinopathy & eye disease (I’m sure there’s a nice medical term for that, sorry…) that would be the main cause of loss of vision.

*Pulmonary embolism*

Symptoms of PE
Shortness of breath, followed by pleuritic pain.
An MI would present with pain, followed by SOB.
-SOB is due to necrosis of the part of the lung supplied by the occluded vessel (usually wedge-shaped with the pointy bit where the vessel is, and the “base” towards the outer of the lung)
-Pain is due to the stimulation of pain receptors in the parietal pleura by inflammatory cytokines (?), and so occurs after SOB as it takes time for these to move through the necrosis and visceral pleura to the parietal pleura.

Causes/States leading to PE
1. Stasis (eg. long plane flight, surgery) - can lead to deep vein thrombosis
2. Coagulopath - more likely to clot
3. Abnormal endothelial lining - also more likely to form thrombus

*Case 4 stuff (weakness)*

Brain anatomy and neural pathways
{this would work a lot better with diagrams :(}
Areas seen in medial cross-section of brain, roughly from superior to inferior:
-cortex (including neocortex)
-corona radiata
-corpus colossum [spelling?]
-medial thalamus
-midbrain
-cerebellum
-pons
-medulla

Neural pathways run from the sensory/motor areas in the cortex to the medial thalamus, where they synapse [?], continue to midbrain and down into medulla.

Lobes of the brain & main functions:
-frontal: controls personality & inhibition of certain behaviours (ie. what makes humans different to (other) animals)
-parietal: sensory perception, spatial coordination, numbers & mathematical thinking
-temporal: memory, hearing
-occipital:vision
-cerebellum: coordination
The surrounding area where the frontal and parietal lobes meet is particularly prone to strokes, due to the anatomy of the artery supplying it. This area also includes the motor and sensory areas in the cortex - hence the possible effects of a stroke…

Cranial nerves
The main ones to know of atm:
-olfactory (I)
-optic (II)
-vagus (X)

Coning [spelling, again?]
A vessel supplying part of the brain gets blocked. Part of brain is ischaemic & necrosis occurs [?]. The clot “dissolves” and reperfusion happens, but the tissue is damaged and so the blood seeps out and pools beside brain. Rising intracranial pressure means the brain becomes cone-shaped as it is sucked downwards. Ew. Fatal.