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Pathology > Neuro > Flashcards

Neuro Flashcards

1
Q

What may cause enlargement of lacrimal gland

A

Sacroidosis-inflammation

Neoplasm-lymphoma, pleomorphic adenoma, adenoid cystic carcinoma

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2
Q

Wegener granulomatous is

A

May start in eye

Necrosis and degenerating collagen with vasculitis

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3
Q

What orbital masses are encapsulated

A

Lacrimal gland

Dermoidneurliemmoma

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4
Q

Non Hodgkin lymphoma eye

A

Can effect entire orbit or be confined to a compartment

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5
Q

Metastatic prostic carcinoma

A

May present like idiopathic orbital inflammation

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6
Q

Metastatic neuroblastoma and wilms

A

Rich vascular neoplasms

Perioculat ecchymoses

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7
Q

What does an eyelid basal cell carcinoma look like

A

Pearly white with depressed central area

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8
Q

Granulomatous associated with systemic sarcoidosis may be detected in __

A

Fornix

50%. Nulomas

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9
Q

Primary lymphoma of conjunctiva in ___

A

Fornix

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10
Q

Prob with conjunctival scarring

A

Reduce goblet cells reduced mucin
Tears don’t adhere even if production ok
XEROPTHALMIA

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11
Q

Delle

A

Depression in corneal tissue from dehydration caused by pniguecula
*not enter cornea though causes uneven distribution of tear film

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12
Q

How does conjunctival melanoma form

A

Phase of intraepihtelial growth called primary acquired mmelanosis with atypia

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13
Q

Who gets immune complex deposition with sclera

A

RA

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14
Q

Major refractive surface of the eye

A

Cornea and tear film

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15
Q

Nonimmunologic grade rejection cornea

A

Loss of endothelial cells and then edema

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16
Q

What causes stromal edema

A

Loss of endothelial cells and deturgence

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17
Q

Descent membrane

A

Thicker with age

Where copper deposition occurs in kayser fleischer

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18
Q

Corneal ulceration

A

Herpes, acanthamoebe
Bacteria fungal prozoa

Keratitis-activation of collagenases and stromal fibroblasts

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19
Q

How visualize corneal ulceration

A

Exudate and cells leaking from the iris and ciliary body vessels can be seen by slit lamp or pen lite
(Hypopyon no organisms) but corneal ulcer infectious

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20
Q

What is keratitis

A

Corneal inflammation

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21
Q

Chronic herpes

A

Keratitis associated with granulomatous reaction involving descent

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22
Q

Oil droplet keratopathy

A

Oil droplet keratopathyactinic band

Actinic band superficial corneal collagen

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23
Q

Keratoconus

A

Thinning of cornea without inflammation. Or vascularization
Corneal degeneration
Descent may rupture
Corneal hydrops cause corneal scarring and vision loss

SUDDEN corneal hydrops

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24
Q

Corneal hydrops

A

Keratoconus
Haab striae (infantile glaucoma)
Obstetric forceps injury

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25
Q

Fuchs

A

Gutatta
Stroma ground glass
Stroma vascularization from edema

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26
Q

Degenerative pants

A

Fuchs
Fibrous CT between epithelium and bowman
Epithelium detaches from basement membrane

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27
Q

Pseudophakic bulbous keratopathy

A

After cataract surgery

Edema vision loss

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28
Q

Stromal dystrophy-discrete opacities in cornea that compromise vision

A

TGFB1 mutation
Keratoepithelin

Or improper folding of keratoepithelin

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29
Q

Pars plicata

A

Of ciliary body make aqueous humour to enter posterior chamber through pupil to anterior

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30
Q

Nuclear sclerosis

A

Age related opacification of lens makes brown cant see blue

Rembrandt yellow

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31
Q

Caues of cataract

A

Age

Galactosemia, diabetes, Wilson, atopic dermatitis, corticosteroids, radiation, intraocular disorders

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32
Q

Posterior subscapular cataract

A

Migration of lens epithelium posterior to lens secondary to enlarged or weird positioned lens epithelium

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33
Q

Phacolytic glaucoma from a morgagnin cataract

A

Lens cortex liquify(mortgaging cataract)
High molecular weight proteins leak thorough lens capsule)phacolysos_
Proteins or contained in macrophages can clog trabecular meshwork and cause ICP and optic nerve damage

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34
Q

What causes increased pressure in open angle glaucoma

A

Increased resistance to flow

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35
Q

Angle closure

A

Iris adhere to meshwork

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36
Q

Glaucoma

A

Most from IOP

Visual field and cup of optic nerve changes

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37
Q

Primary open angle

A

MYOC mycolilin
OPTN optineurin

Risk-hyperopia

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38
Q

Secondary open glaucoma

A

Pseudoexfoliation glaucoma-deposition of fibrillation material throughout anterior segment
Lysyl oxidase 1
Get deposition around CT, liver kidney too
Clog trabecular meshwork

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39
Q

Ghost cell glaucoma

A

High molecular weight from phacolytic, senescent red cells after trauma

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40
Q

Pigmentary glaucoma

A

Iris epithelial pigment granules

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41
Q

Melanomalytic glaucoma

A

Necrotic tumours

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42
Q

Episcleral venous pressure

A

Elevations in pressure on the surface of the eye in the presence of open angle

-sturge Weber syndrome or arterialization of episcleral veins following traumatic carotid cavernous fistula

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43
Q

Primary angle closure

A

Hyperopia
Adhere iris to TM
Pupillary block

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44
Q

Iris bombe

A

Iris move forward in closed angle

Increases pressure in posterior chamber

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45
Q

Glaukomflecken

A

Minute anterior subscapular opacities visible on slit lamp from unremitting elevation in IOP in primary closed angle damage to lens epithelium

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46
Q

What can IOP in closed angle primary cause

A

Glaukomflecken
Corneal edema
Bulbous keratopathy

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47
Q

Secondary closed angle

A

Contraction of pathological membranes over iris can draw it over TM, occluding flow like in neovascular glaucoma

Tumors in iris mechanically compress iris nonto trabecular mesh

Retinoblastoma can induce neovascular glaucoma

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48
Q

Chronic retinal ischemia

A

Upregulation of VEGF and proangiogenic factors which cause the development of thin fibrovascular membranes ont he surface of the iris

Cause secondary closed

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49
Q

What may cause neovascular glaucoma

A

Chronic retinal ischemia upregulated vegf and proangiogenic factors causing development of thin fibrovascular membranes on surface of the iris

Necrotic tumors like retinoblastoma can also induce neovascular glaucoma

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50
Q

Endopthalmitis

A

Inflammation vitreous humour

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51
Q

Anterior syenchiae

A

Adhesion between the iris and TM or cornea

From inflammation-vessels in ciliary body and iris become leaky and allow cells and exudate to accumulate in anterior chamber and adhere to corneal endothelium to form keratic precipitates (slit lamp)

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52
Q

Posterior synechiae

A

Adhesion between iris and anterior surface of lens

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53
Q

Anterior synechia can lead o what

A

Secondary closed angle

IOP and optic nerve damage

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54
Q

Posterior synechiae can lead to what

A

Deprive lens epithelium of aqueous humour and induce fibrous metaplasia of lens epithelium (anterior subscapular character)

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55
Q

Endophthalmitis

A

Vitreous humour inflammation

-damage retina

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56
Q

Exogenous endophthamitis

A

Originating in environment and gain access through wound

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57
Q

Endogenous endopthalmitis

A

Delivered to eye hematogenously

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58
Q

Panophthalmitis

A

Whole eye inflammation including retina, choriod, sclera and extend into orbit

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59
Q

What is uvea

A

Iris, choroid and ciliary body

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60
Q

What is one of the most richly vascularized sites in body

A

Choriod

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61
Q

Uveitis

A

Iris choriod ciliary inflammation

Inflammation to eye

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62
Q

Uveitis may manifest anterior segment

A

Juvenile RA

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63
Q

Uveitis is accompanied by what

A

Retinal pathology

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64
Q

What causes uveitis

A

Pneumocystitis carnii, autoimmune (sympathetic ophthalmia), idiopathic sarcoidosis

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65
Q

Granulomatous uveitis

A

Sarcoidosis
Anterior segment mutton fat keratic precipitates
Posterior segment-choroid and retina where granulomatous can develop

Retina-perivascular inflammation see candle wax dripping

Do conjunctival biopsy to detect granulomas

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66
Q

Retinal toxoplasmosis

A

Uveitis, scleritis

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67
Q

AIDS

A

CMV retinitis, pneumocystitis, mycotic choroiditis

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68
Q

Sympathetic ophthalmia

A

Non infections panuveitis
Bilateral granulomas inflammation
Penetrating eye injury antigens released to conjunctiva and get delayed hypersensitivity weeks to years later

Granulomatous inflammation where eosinophils seen

Give immunosuppressive agent

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69
Q

Most common site of intraocular malignancy

A

Uveal-choroid(5% of melanoma)
SHORT SURVIVAL palliative

85% GNAQ and GNA11 (GPCR oncogenes) gain of function

Loss chromosome 3, delete BPA1, a tumor suppressor on chromosome 2 that encodes a deubiquinating enzyme
In epigenetics-does gene silencing

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70
Q

Uveal nevi

A

10% caucasions
GNAQ and GNA11 (GPCR, oncogenes)
Don’t transform

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71
Q

GNAQ GNA11

A

MAPK promote proliferation

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72
Q

Uveal melanoma morphology

A

1 cell types,
Spindle-fusiform
Epithelioid cells-spherical treated cytology atypicallity
Looping slit like spaces lined by laminitis surround tumors ells that aren’t cellls but act as vessels in a process of vasculogenesis mimicry
-are conduits for nutrients allowto spread

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73
Q

How do uveal melanoma spread

A

HEMATOGENOUS

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74
Q

Clinical uveal melanoma

A

Found by chance
Lateral size of tumor big bad
Epithelial cells bad
Loss of chromosome 3 bad

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75
Q

Iris vs ciliary body and choroid melanoma

A

Ok vs BAD 5 yr survival 80% 10 year 40$ dead increase 1% per year after

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76
Q

Tumor dormancy

A

Uveal melanoma

Metastasis appear out of the blue

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77
Q

What is special about the retina

A

Derivative of diencephalon and undergoes gliosis when damaged -no lymphatics like brain

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78
Q

Hemorrhage in retina nerve fiberslooks like what

A

Horizontal streaks or flames

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79
Q

Hemorrhage in external retina

A

Dots (tips of cylinders perpendicular to retinal surface)

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80
Q

Where does exudate accumulate in retinal

A

Outer plexiform layer, espicially macula

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81
Q

Layers of the retina

A 
Optic fiber layer(light hit)
Ganglion cell layer
Inner plexiform later
Inner nuclear layer
Outer plexiform layer
Outer nuclear layer
Inner segments
Outer segments
RPE choroid
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82
Q

RPE derived from what

A

Primary optic vesicle

Helps maintain outer segments of photoreceptors

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83
Q

Retinal detachment

A

RPE from neurosensory retina

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84
Q

Persistent hyperplastic primary vitreous

A

Fetal vessels do not regress in in vitreous humor (adult in avascular)

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85
Q

What can opacity the vitreous humour

A

Hemorrhage from trauma or retinal neovascularization

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86
Q

Vitreous and aging

A

Liquify and collapse (sensation fo floaters)

Posterior vitreous detachment-posterior face separate from neurosensory retina

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87
Q

Retinal detachment

A

RPE from neurosensory
Rhegmatogenous or non rhegmatougenous

Need to maintain photoreceptors in outer retina

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88
Q

Rhegmatougenous retinal detachment

A

Full thickness tear
From collapse of vitreous and posterior hyaloid exerts traction

Or from proliferative vitreoretinopathy where there is formation of epiretinal or subretinal membranes by retinal glial cells (muller cels) or RPE

Vitreous humour leak into space between RPA and neurosensory

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89
Q

Non rhegmatougenous retinal detachment

A

Without retinal break

From retinal vascular disorders associated with significant exudation and any condition that damages RPE and permits fluid ear from choroidal circulation under retina

Associated with malignant HTM

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90
Q

Retinal hypertension

A

Vessels narrow and extra thickness causes color change from red to copper and silver this is bad bc retainal and arterioles share adventitious sheath so can compress veins when cross causing venous stasis

Damage vessels of retina and choroid with malignant hypertension

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91
Q

Elschnig spots

A

Infarcts of the choroid due to damage of choroid vessels

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92
Q

If there is damage to choriocapillaries I then there could be damage to __

A

RPE and allow exudate to enter and cause detachment

-exudate accumulate in outer plexiform layer

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93
Q

Damage to retinal arterioles causes what

A

Exudate in outer plexiform layer

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94
Q

What are signs or exudate in outer plexiform layer

A

Macular star-spoke like arrangement of exudate in the macula in the setting of malignant hypertension, oblique rather than perpendicular to surface

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95
Q

Occlusion of retinal arterioles causes what

A

Infarcts of nerve fiber later (ganglion) and axons

-axoplasmic transport interrupted, accumulation of mitochondria at swollen ends of axons causes cystic bodies

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96
Q

Characterization of infarct of nerve fiber layer

A

Cystoid bodies(accumulation of mitochondria at the swollen ends of damaged axons)-collections of these seen as cotton wool spots on ophthalascope

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97
Q

Besides HTN, what may cause retinal vasculopathy

A

AIDS

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98
Q

Diabetes eye

A

Thicken BM of epithelium of pars plicata of ciliary body-proliferative or non)

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99
Q

Non proliferative diabetic retinopathy

A

Thick BM of BV
(Decrease in pericytes to endothelial cells)
Microaneusysms and hemorrhages

VEGF makes retinal microcirculation leaky
Cause macular edema -vision loss

Vascular microocclusions can be seen with intravenous fluorescein

Exudate in outer plexiform

Non perfusion of the retina due to microcirculatory change is associated with up regulation of VEGF

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100
Q

Proliferative diabetic retinopathy new vessels from optic nerve head of retina

A

Extend along posterior hyaloid and retinal plane

Can get posterior vitreous detachcausing hemorrhage from ruptured neovascular membranescarring and wrinkle of retina cause vision prob and may cause retinal detachment (traction retinal detachment)

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101
Q

Retinal neovascularization may accompany

A

Iris neovascularization

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102
Q

Retinopathy of prematurity (retro lentil fibroplasia0

A

At term lateral retina is incompletely vascularized , medial is vascularized

Premature baby-immature retinal vessels in temporal constrict making ischemic here..places on O2
Upregulate VEGF and get retinal angiogenesis

Contraction of resulting peripheral retinal neovascular membrane may drag the temporal aspect of the retina toward peripheral zone and displace macula lateral or detach retina

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103
Q

Sickle retinopathy

A

Non proliferative SS SC
Or
Proliferative

Cause vascular occlusion form low O2 tension leading to RBC sickling

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104
Q

Vascular occlusion from sickle retinopathy

A

Pre retinal, intraretinal and sub retinal hemorrhage
Resolution of hemorrhages look like salmon patches, iridescent spots and black sunburst lesions

VEGF-neovascularization seen as sea fans

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105
Q

Organization fo pre retinal hemorrhage may result in retinal traction leading to what

A

Detachment

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106
Q

What are sea fans and why seen

A

Neovascularization in retina from sickle retinopathy, damage to retinal celebs, radiation
Cause ischemia trigger angiogenesis

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107
Q

Complications of retinal neovascularization

A

Hemorrhage, traction detachment

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108
Q

Hollenhorst plaques

A

Fragments of atherosclerotic plaques lodge within the retinal circulation

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109
Q

What get retinal infarct

A

When total retinal artery occluded

110
Q

What happens with retinal infarct

A

Derived from brain
Swell and opaque which blocks view of choroid and fundus appears white instead of orange
WHITE INFARCT from arterial occlusion

111
Q

Diffuse retinal infarct

A

Total occlusion of central retinal artery
Retina white opaque

Fovea thin and unaffected;cherry red spot bc red choroid is visible

112
Q

What do we see cherry red spot in

A

Diffuse infarct retina

Ray Sachs Niemeyer pick

113
Q

Retinal vein occlusion

A

Without ischemia-hemorrhage, exudate, macular edema, no neovascularization

With ischemia-upregulate vegf neovascularization -of retina, optic nerve, iris (can get angle closure glaucoma)

114
Q

AMD

A

Wet or dry8% over 75

115
Q

Dry AMD

A

Drusen deposits in bruch and RPE atrophy

No treat

116
Q

Wet AMD

A

Choroidal neovascularization of vessels that originate from choriocapillaries and penetrates through bruch membrane beneath RPE and can fo through RPE to neurosensory retina

117
Q

Issue with wet AMD

A

Vessels leak and blood organize by RPA macular scare

Can get diffuse vitreous hemorrhage

118
Q

Treat wet AMD

A

VEGF antagonist

119
Q

What may abuse choroidal neovascularization

A

Myopia(fuch spot), disruption of bruch due to trauma, immmune to histoplasmosis

120
Q

Bruch membrane

A

BM or RPE

121
Q

Choriocapillaries

A

Innermost layer of choroidal

122
Q

Genetic AMD

A

CHF complement

Also light

123
Q

Functional unit of AMD

A

RPE, bruch membrane which has BM of RPE and innermost choroidal layer, choriocapillaries

-vision loss from photoreceptor damage to any of these

124
Q

Retinitis pigmentosa

A 
Inherited rod cone RPE mutation
Non inflammatory 
Total blind
Retinal degeneration 
AR, X, AD (AD later in life)
125
Q

What syndromes may retinitis pigmentosa be a part of

A

Bardet-biedl syndrome, usher syndrome, refuse disease

126
Q

Sign of retinitis pigmentosa

A

Rod and cones lost to apoptosis with rode leading to night bling and cones center field blind

127
Q

Retinal atrophy from RP

A

Optic nerve atrophy (waxy pallor of optic disc) and accumulation or retinal pigment around the vessels

128
Q

Genetic mutations of RP

A

Transcription factors, structural genets, catabolic paths

129
Q

Infections retinitis

A

Candida can get to retina via blood causing multiple retinal abscesses

CMV retinitis is a major cause of visual impairment in AIDS

HEMATOGENOUS

130
Q

Retinoblastoma

A

Most common intraocular malignancy in kids

131
Q

What recent of RB is familial

A

40

132
Q

RB is __ of function

A

Loss

133
Q

RB unilateral or bilateral

A

Bilateral

134
Q

What is RB associated with

A

Pinealoblastoma (trilateral retinoblastoma) bad outcome

135
Q

Sporadic RB

A

Two mutations q

136
Q

Morphology RB

A

Diffferentiated0round, small cells of hyperchromic nuclei

Flexing wintersteiner rosettes and fleurettes (photoreceptor differentiation)
-focal zones of dystrophic calcification)

137
Q

Where does RB spread

A

Brain and bone marrow

Not lungs

138
Q

What disintguishes bad prognosis of RB

A

Not differentiation

Extraocular extensiona Nd invasion along optic nerve and by choroidal invasion

139
Q

Retinocytoma/retinopathy

A

Premalignant lesion

-

140
Q

Appearance of retinoblastoma in one eye and retinocytoma in other

A

Heritable retinoblastoma

141
Q

Retinal lymphoma

A

AGGRESSIVE

Involves RPE and neurosensory retina

142
Q

What is special about RPE and neurosensory retina

A

Derived from brain

143
Q

Who gets retinal lymphoma and what does it mimic

A

Old people

Uveitis

144
Q

How may diffuse B cell ymphma spread to brain

A

Optic nerve

145
Q

Pilocytoc astrocytoma

A

Gloomy of optic nerve

146
Q

Anterior ischemic optic neuropathy

A

Similar to stroke

-injuries to optic nerve from ischemia /infarction

147
Q

What does optic nerve in AOIN look Ike

A

Swollen pale

148
Q

Transient AION

A

Vision loss comes back

149
Q

Total occlusion infarct AION

A

Partial or complete vision loss

150
Q

Does optic nerve regenerate

A

No

151
Q

What causes ischemia infarct in AOIN

A

Embolism, thrbomtis

152
Q

Temporal arthritis

A

Optic nerve bilateral infarct causes total blindness

153
Q

Papilledema

A

Edema of head of ON from increased ICP
(Bilateral)
Or neoplasm (unilateral)

154
Q

What does nerve head look like in papilledema

A

Swollen hype remix

155
Q

Is acute papilledema from increased intracranial pressure associated with visual loss

A

No

156
Q

Glaucoma optic nerve damage

A

Loss of ganglion cells and thinning of retinal nerve fiber layers
Optic nerve is cupped and strophic

157
Q

Elevated IOP in kids

A

Diffuse enlargement of eye (buphthalmos) or enlargement of cornea (megalocornea)

158
Q

IOP in adult

A

Thin sclera staphylococcus

159
Q

Methanol and optic neuropathy

A

Sure toxic

160
Q

Lever hereditary optic neuropathy

A

Inherited mitochondrial gene mutations (maternal)

Males 9:1
10-30 yr onset
Clouding of vision and progress to vision loss and optic nerve damage

161
Q

Optic neuritis

A

Loss of vision secondary to optic nerve damage

MS

162
Q

40 yo female with vision loss

A

MS workup

163
Q

Increased risk of MS is

A

Optic neuritis

Evidence of brain lesions via MRI

164
Q

Phthisis bulbi

A

Phthisis bulbiend stage eye shrunken and disorganized atrophy

165
Q

Ciliochoroidal effusion

A

Exudate between ciliary body and scleraand choroid and sclera
Phthisis bulbi
Low IOP (hypotonic)
Square eye

166
Q

Cyclists membrane

A

Membrane from ciliary body to ciliary body

167
Q

Signs of end stage eyes

A 
Phthisis bulbi which see
Ciliochordial effusion
Cyclonic membrane
Chronic retinal detachment 
Optic nerve atrophy
Intraocular bone
Thickened sclera
Square eye
168
Q

Red neuron

A

Intense eosinophilia loss of his SLE and pyknosis and shrinkage

169
Q

Central chromatolysis

A

Axonal injury

170
Q

Gemistocytic astrocytes

A

Injury
Nucleus enlarges becomes pink
Eccentric nucleus with ramifying processes

171
Q

Alzheimer’s type II astrocyte

A

Gray matter cell pale staining LARGE intranuclear glycogen droplet and a prominent nuclear membrane and nucleolus

172
Q

Microglial nodules

A

Aggregates around small foci of tissue necrosis

173
Q

Neuropharmacologist

A

Microglia around cell bodies of dying neurons

174
Q

MSA oligodendrocytes

A

Glial cytoplasmic inclusions with a synuclein

175
Q

PML oligodendrocytes

A

Viral inclusions

176
Q

Injury or apoptosis oligodendrocytes

A

Demylinating disease and leukodystrophies

177
Q

Ependymal

A

Ciliated columnar cells
-CMV viral inclusions

Granulations-inflammation or disption of ependymal lining paired with subependylmal proliferation of astrocytes

178
Q

Response of astrocytes to injury

A

Hypertrophy
Accumulation GFAP
Hyperplasia

179
Q

Vasogenic edema

A

Disrupt BBB and increased vascular permeability

ECF

Non lymphatics in brain to reabsorbed

180
Q

Localized vasogenic edema

A

Adjacent to inflammation or neoplasm

181
Q

Generalized vasogenic edema

A

Ischemic injury

182
Q

Cytotoxic edema

A

BB ok Na K atpas lead to retention in NA

ICF increase from neuronal, glial or endothelial cell membrane injury

183
Q

Cause of cytotoxic edema

A

Generalized hypoxic or ischemic

Components of vasogenic

184
Q

Generalized edema

A

Vasogenic and cytotoxic

185
Q

Signs of generalized edema

A

Gyri flat and narrow sulcu ventricular cavities compressed, herniation

186
Q

Interstitial edema(hydrocephalus edema)

A

Hydrocephalus send CSF to perientricular white matter

187
Q

Choroid plexus papilloma

A

Tumor in choroid hydrocephalus rare

188
Q

Causes of genetic non communicating hydrocephalus

A

Aqueductal stenosis dandy walker

189
Q

Dandy walker

A

Vermis aplasia
4th v big
Hydrocephalus

190
Q

Chronic adhesive arachnoiditis

A

Hydrocephalus from failure of CSF resorption

191
Q

What ind of hydrocephalus is hydrocephalus ex vacuo

A

Communicating

192
Q

Subfalcine herniation

A

Cingulate ACA

193
Q

Transtentorial

A

Medial femoral
CNIII
PCA
Contralateral cerebral peduncle (ipsilateral hemiparesis-weak)

194
Q

Kernohan notch

A

Compression of peduncle in transtentorial herniation

195
Q

Duret hemorrhage

A

Form transtentorial herniation
Secondary hemorrhagic linear of flame shaped lesion in midbrain and pons that often accompany transtentorial herniation
-midline and paramedian regions

Mesencephalon

196
Q

Tonsillarr herniation

A

Brainstem problem

Respiratory fail

197
Q

Symptoms of myelomeningocele

A

Motor and sensory deficits in lower extremities with bowel and bladder dysfunction complicated by superimposing infection that enters thin overlying skin

198
Q

Encephlaocele

A

Brain stick out
Nasal glioma
Or posterior fossa

199
Q

NT defect genetic

A

Highly
Folate defiency
Polymorphism in folate stuff

200
Q

Anencephaly

A

Anterior NT prob
No brain and calvaria
Forebrain development disrupted 28 days of gestation
Only thing remaining is area cerebrovaculosa

201
Q

What is area cerebrovaculoas

A

Flattened remnant of disorganized brain tissue with admired ependymal, choroid plexus, and meningothelial cells frog eye posterior fossa spared

202
Q

What causes microencephaly

A

Decreased migration
FAS, HIV, chromosomal abnormalities

Simplified gyrus folding

203
Q

Lissencephaly

A

Reduced gyri

204
Q

Type 1 lissencephaly

A

Mutations that disrupt the signaling for migration and the cytoskeletal motor proteins that drive migration or neuroblasts

SMOOTH

205
Q

Type 2 lissencephaly

A

Genetic alterations that disrupt stop signal for migrationcobblestone surfaced

Need glycosylated proteins and mutations in enzymes that place the sugars onto the proteins

206
Q

Polymicroglia

A

Small unusually numerous cerebral convolutions 4 or less cortex layers
Entrap meningeal tissue

Tissue injury
Or symmetric and bilateral if genetic

207
Q

Neural heteroropias

A

Neurons in inappropriate
Mutate filament a for assembly of complex meshworks of actin filaments X chromosome
Male fatal
Female-some normal some not

Or Double cortin DCX on X (microtubule associated protein)
Males-lissencephaly
Females-subcortical heterotopias (discrete nodules of neurons sitting in subcortical white matter or complete ribbons that parody overlying cortex)

208
Q

Holoprosencephaly

A

Midline suture defect doesn’t separate
Cyclopes
Less severe absence of olfactory

DEFECT SHH

209
Q

What is holoprosencephaly associated with

A

Trisomy thirteen

210
Q

Agenesis of corpus callosum

A

Bat wing
Common
Fine or mentally retarded

211
Q

Arnold chiari formation II

A 
Vermis downward through foramen magnum
Tenting textual plate
Hydrocephalus
Myelomeningocele
Aqueductal stenosis
Heterotopias
Hydrolysis
212
Q

Chiari type I malformation

A

Cerebellar tonsil down into vertebral canal

Silent of symptomatic

213
Q

Dandy walker

A

Rudimentary cerebellar vermis midline cyst
Lined by ependymal and is contiguous with letpmeninges

Represented roof of expanded fourth ventricle in absence of vermis

214
Q

Joubert syndrome

A

Hypoplasia of vermis , elongation of superior cerebellar peduncle, altered brainstem shape
Molar tooth sign

Mutations of primary cilium

215
Q

Syringomyelia

A

Fluid filled cavity in the inner portion of the cord

216
Q

Syringobulbia

A

Syringomyelia extend into brainstem

217
Q

What is syringomyelia associated with

A

Arnold chiariintraspinal tumor

Traumatic injury

218
Q

Histology syringomyelia

A

Destruction of adjacent grey and white mater surrounded by gliosis

219
Q

When does syringomyelia occur

A

Second or third decade

220
Q

Clinical presentation syringomyelia

A

Loss of pain and temperature in upper extremities from anterior spinal commissure

221
Q

Hydromyelia

A

Expansion of ependymal lined central canal of the rod

222
Q

Histology hydromyelia

A

Destruction of adjacent grey and white matter surrounded by a dense gliosis

223
Q

When does hydromyelia occur

A

Second third decade

224
Q

Cerebral palsy

A

Non progressice neurologic motor deficits -spasticity, dystonia, ataxia/athetosis, paresis attributable to insult that occur in the pre natal and perinatal periods from birth

225
Q

IntraParenchymal hemorrhage

A

Terminal matrix hemorrhage
Intraventricular hemorrhage
Extend into the subarachnoid space (subarachnoid hemorrhage)

226
Q

Sequelaea intraparenchymal hemorrhage

A

Larger hemorrhages can organize in aqueduct of Sylvia’s or 4th centriole foramina to obstruct CSF and lead to a non communicating hydrocephalus

227
Q

Premature infants IntraParenchymal hemorrhage

A

Twenty two to twenty three weeks

High cellularity and vascularity and vulnerable to insults even minor changes in cerebral blood

228
Q

Where does IntraParenchymal hemorrhage occur

A

Junction of developing thalamus and caudate nucleus

229
Q

Periventricular leukamalacia

A

Infarct in supratentorial periventricular white matter
Form of perinatal injury that is caused by hypoxic ischemic events or infections
Premature
In supratentorial periventricular white matter
Chalky yellow plaques consisting of discrete regions of white matter

230
Q

Multicystic encephalopathy

A

Infarct more severe that periventricular leukamalaciagrey and white matter ischemia
Lead to large destructive system throughout hemisphere

231
Q

Symptoms of multicystic encephalopathy

A

Thinned gliotic gyri (ulegyria)
Basal ganglia and thalamus suffer ischemic injury, with patchy neuronal loss and reactive gliosis
Lesions of caudate putamen and thalamus lead to choreoathetosis

232
Q

Status marmoratus

Periventricular leukomalacia

A

Abnormal myelinization that gives rise to a marble like appearance of the deep nuclei

233
Q

Marbelized deep nuclei

A

Malignant peripheral nerve sheath tumors

Multicystic encephalopathy

234
Q

Awake fracture

A

Front

235
Q

Sleeping fracture

A

Back syncopal

236
Q

Basal skull fracture

A

Bruise and CSF ears and eyes

237
Q

Concussion

A

Altered consciousness

No radiologic or pathological findings

238
Q

Repeated concussion

A

Post consussion syndrome longer neurologic recovery

Disabling neuropsychiatric manifestations

239
Q

What part of Brian is most susceptible to direct parenchymal injury

A

Crest of gyri

240
Q

Most commmon site of contusion

A

Frontal temporal

Less frequent occipital brainstem cerebellum

241
Q

Immobile head injury

A

Coup

242
Q

Mobile head injury

A

Coup and counter coup

243
Q

Hyperextension neck injury

A

Values pons from the medulla fromt he cord resulting in instant death

244
Q

Morphology brain contusion

A

Wedge
1-pericapillary edema and hemorrhage
Hours-exravasation of blood through tissue of cerebral cortex, white matter, subarachnoid space
24 hours-pyknosis of the nucleus, eosinophilia, disintegration (EVIDENCE OF NEURONAL INJURY, axonal swelling_

245
Q

Old traumatic lesion

A

Depressed, retracted yellow brown patches involving crest of gyri )plaque Jayne) most commonly of countercoup0inferior frontal cortec, temporal and occipital)

Can become foci of epileptic attacks

Larger cavitation more extensive hemorrhagic region

Gliosis and hemosiderin laden macrophages

246
Q

Diffuse axonal injury

A

Swelling and focal hemorrhagic lesions

-50 percent of patients get coma after trauma without contusion FROM diffuse axonal injury

247
Q

Morphology diffuse axonal swelling

A

Hours of injury
Silver impregnating or immunoperoxidase stainsfor transported proteins
(APP, a synuclein_

Increased microglia

248
Q

Subdural

A

Slowing evolve

Bleeding from low pressure vein s

249
Q

Subarachnoid

A

AVM berry aneurysm
Thunderclap headache
Underlying conditions

250
Q

Trauma intraparenchymal hemorrhage

A

Trauma
Crests of gyri where contact skull
Frontotemporal tips or orbitofrontal sulcus

251
Q

IntraParenchymal hemorrhagic conversions of an ischemic infarction

A

Usually petechial hemorrhages in an area previously ischemic brain following cortical ribbon

252
Q

IntraParenchymal CAA

A

Local hemorrhage involving cerebral cortec, often with extension into subarachnoid space

253
Q

IntraParenchymal hypertension

A

Centers in the deep white matter, thalamus, basal ganglia or brainstem may extend into the ventricular system

254
Q

IntraParenchymal tumor hemorrhage (primary of metastatic

A

Associated with high grade gliomas ormetastases

255
Q

Thrombosis intraparenchymal hemorrhage

A

Thrombosis of an intracranial artery may lead to infarction; infarction may be hemorrhagic hemorrhage typically does not extend into subarachnoid or subdural locations

256
Q

Epidural hematoma

A

Lens shape
Kids who have deformable skill
Vessel tears cause extravasion

257
Q

Lucid interval

A

Epidural hematoma lucid for several hours then bad as bp causes dura to separate and compress brain

258
Q

Subdural hematoma

A

Bridging veins tear veins where penetrate cure
More common in old people bc veins are already stretched or in infants since they have thin walled veins
Is chronis subdural hemorrhage slowly there may not be herniation

259
Q

Morphology acute subdural hematoma

A

Collection freshly clotted blood along the brain surface without extension into depths of sulci
Underlying brain flattened and subarachnoid space clear
Venous bleeding self limited and resulting hematoma is broken down and organized over time (lyse after a week, growth of fibroblasts from the dural surface into hematoma after 2 weeks, hyalinized CT in one to three month_

Lesion retracts to a thin layer of CT called subdural membranes

260
Q

Chronic subdural hematoma

A

Recurrent episodes of bleeding called chronic subdural hematoma that is due to the thin walled vessels of the granulation tissue
Risk is greatest for this int he first few months

261
Q

Clinical subdural hematoma

A

Symptomatic hematoma will typically present within forty eight hours
Along lateral aspects of the cerebral hemispheres and bilateral in ten percent
Headache, confusion, slowly progressive neurological deterioration, but sometimes there is acute decompensation
Treat by evacuating blood

262
Q

Post traumatic hydrocephalus

A

Obstruct csf resorption from hemorrhage into the subarachnoid space

263
Q

Chronis traumatic encephalopathy, dementia pugilistica

A

Cementing illness that develops after repeated head trauma
Repeated conclusion
Brains are strophic with enlarged ventricles, accumulation of tau tangles in pattern involving the superficial frontal and temporal lobe cortex

264
Q

Post traumatic epilepsy

A

Ok

265
Q

Post traumatic dementia

A

From repeated blows to the head often has pathological findings of neurofibrillary tangles and neuritis plaques

266
Q

Spinal cord injury-vulnerable to skeletal encasement

A

Most injuries that damag the cord injury are associated with transient or permanent displacement fo vertebral column

267
Q

Lesions below thoracic level

A

Paraplegia

268
Q

Lesion above c4

A

Quadriplegia and diaphragm issue-respiratoy compromise

269
Q

Acute spinal cord injury

A

Hemorrhage, necrosis, axonal swelling in the surrounding white matter-taper above and below site of injury

270
Q

Spinal cord injury later

A

Central areas become cystic and gliotic
Cord sections above and below injury show secondary ascending and descending wallerian degeneration, respectively, involving the long what matter tracts affected at the site of trauma

Pathology (36 decks)

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