Histology/Pathology Flashcards
Where are ependymal cells found? How are the different to epithelial cells?
Ventricles and central canal of spinal cord They have no BM
How many axons does a schwann vs an OD surround?
Schwann surrounds 1, OD surrounds a few
What is this?
What are some consequences?
Diffuse axonal injury- in deep white matter with small haemorrhages
Get gliosis and in this case would see enlarged ventricles
what are the two types of cerebral haemorrhage?
vasogenic; increased BBB permeability, usually in white matter and steroid responsive
cytotoxic; intracellular fluid increases after nerve/glia injury in either matter and non-steroid responsive
What haemorrages can see here?
Transtentorial and subfalacine causing midline shift
What is the clinical definition of a stroke?
What are the 3 pathological processes that lead to a stroke?
Focal or global neurological deficit from a vascular event lasting >24hrs or leading to death
Infarction, haemorrhage and subarachnoid haemorrhage
What are some common sources of emboi that can cause stroke?
Bifurcation of common carotid
Aortic/Mitral valves
Thrombis from atrium from AF
What are some histological changes we see in strokes?
What can we see if the embolus gets broken down?
1st see necrotic eosinophilic neurons
Macrophages predominate by 2 days
Macroscropically just see swelling
Get organiastion and repair and those macrophages become foamy, see proliferating blood vessels and astrocytes
By 7-10 days macroscopically see this liquifactive necrosis
By months just see empty space surrounded by gliosis
If embolus broken down see haemorrhage into the area of infarction
What is most common underlying pathology of lacunar infarcts and where do we mainly see them?
Hypertensive small vessel disease- hyaline arteriosclerosis in diabetic or HT patients
Usually forms a thrombus in deep structures of brain
What is the biggest cause of intracerebral haemorrhage?
Where do we see them?
What about 2nd biggest and where do we see them?
Hypertensive small vessel disease (hyaline areteriosclerosis); walls have more collagen so prone to rupture
See them in deep brain structures, around BG and lobar white matter. Can also see in pons and cerebellum
Amyloid angiopathy next, often see in superficial structures
What are some causes of sub-arachnoid haemorrhages? Where are they most likely to occur and what are some risk factors for developing them?
Berry aneuysm rupture; occuring at sites of cognenital weakness at arterial bifurcations, mostly in anterior circulation
- Hypertension
- Sex and age
Rupture of atherosclerotic vessle
The majority of early onset familial Alz is caused by genes encoding what protein?
Presinilins which form g-secretase- increases length of AB, more prone to plaques
How can AB monomers be damaging?
Which drug is targeting AB oligomers and is reducing the development of alzheimers?
Cause synaptic toxicity
Metal protein attenuating compound (MPAC), stopping monomers being an oligomer
What is the pathology behind Creutzfeldt- Jakob disease?
What is the macroscopic brain pathology?
Caused by prion gotten from cattle (bovine spongiform encephalitis-mad cow), a misfolded protein that cause other proteins to misfold. (PrPres- has beta sheet instead of a-helix)
Causes brain tissue to degenerate and humans get transmissible spongiform encephalopathy (CJD)
What is a genetic pathology behind Parkinsons disease?
What are some clinical symptoms?
Mutation in a-synuclein gene which form insoluble protein aggregates (Lewy body).
This disrupts the vesicle function of DA so get neurodegeneration or less is released
Slowness of movement, rigidity, tremor, also has emotional and autonomic dysfunction
