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Pathology > Neuro 2 > Flashcards

Neuro 2 Flashcards

1
Q

Cerebrovascular disease

A

Brain injury hemorrhagic ischemic

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2
Q

Ischemia

A

Reduced perfusion
Loss of ATP and membrane potential for electrical activity
Increased cytoplasmic Ca-cytotoxic
Excitotoxicity-inappropriate release of excitatory aa
Glutamate-ca through NMDA cytotoxic

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3
Q

Penumbra

A

Area of at risk tissue at region of transition between necrotic tissue and normal brain

  • rescued with anti apoptotic
  • ischemia may cause apoptosis
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4
Q

Are embolisms or thrombosis more common

A

Embolism

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5
Q

Global cerebral ischemia (diffuse ischemic/hypoxic encephalopathy)

A

Generalized decrease renal perfusion

Can be minor or severe

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6
Q

What causes global cerebral ischemia

A

Cardiac arrest, shock, severe hypertension

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7
Q

What cells are most sensitive to global cerebral ischemia

A

Neurons , glial
Pyramidal cells of hippocampus CA1 sommer
Cerebellar purkinje and neocortex bets

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8
Q

Pseudolaminar necrosis

A

Band like pattern cells remain next to meninges

Due to some cells being more sensitive

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9
Q

Symptoms of global cerebral ischemia

A

Total loss of brain function

Patients who survive often are in persistent vegetative state brain dead and brainstem damage

When left on respirator with undergo respirator brain-autolytic processs with gradual liquefaction

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10
Q

Border zone (watershed) infarcts

A

Distal brain or spine or arterial supply, the border between arterial territories

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11
Q

What border zone is most vulnerable to infarct

A

Between ACA(legs and dick) and MCA (convexities)

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12
Q

Linear para sagittal infarction

A

Area of cortex is most at risk and will show a sickle shaped band of necrosis over the cerebral convexities a few cm lateral to the interhemispheric fissure

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13
Q

Why are areas in watershed areas between ACA and MCA most vulnerable

A

Large pyramidal neurons in particular are most sensitive to hypoxic and hypoglycemic stress

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14
Q

When are border zone watershed infarcts seen

A

Hypotensive episodes

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15
Q

Morphology of global ischemia

A

Edema and swollen brain wide gyri narrow sulci
Ongoing liquefication necrosis
Demarcation bt white and grey

12-24 hours-red neuron
2 weeks-necrosis, macrophages, vascular proliferation, gliosis

After-macrophages, remove necrotic tissue, loss of architecture, gliosis

Pseudolaminar necrosis-neuronal loss and gliosis uneven in cortec some layers preserved some not

Fibroblast proliferation rare

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16
Q

Focal cerebral ischemia

A

Reduction or cessation or blood flow to localized area

Sustained get infarction

Damage depends on collateral

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17
Q

Where is there no collateral circulation

A

Deeper areas and white matter

Thalamus, basal ganglia, deep white

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18
Q

Embolism

A

From cardiac mural thrombi

plaque in ICA go to MCA

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19
Q

Where do most embolism events occur

A

Gray white junction where narrowing and acute branching of the vessels trap emboli

MCA location

Supplies convexities of cortec arms and feet on homunculus

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20
Q

What artery is most frequently affected by embolism infarction

A

ICA send to MCA

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21
Q

Shower embolism(like fat emboli after bone break)

A

Generalized cerebral dysfunction with higher cortical function disturbance and consciousness

Widespread white matter hemorrhages -characteristic of embolization of bone marrow after trauma

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22
Q

Thrombotic occlusion

A

Usually from atherosclerosis and plaque rupture

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23
Q

Most common sites of thrombotic occlusions

A

Carotid bifurcation, origin of MCA and either end of basilar artery

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24
Q

Thrombi

A

Progressive narrowing may cause fragmentation

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25
Q

Thrombosis of intracranial artery

A

Infarction , which can be hemorrhagic, but the hemorrhage typically does not extend into subarachnoid or subdural locations-stays confined to intraparenchymal

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26
Q

What may also cause luminal narrowing

A

Vasculitis

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27
Q

Infections vasculitis

A

TB, syphilis, opportunistic CMV and aspergillos

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28
Q

Polyarteritis nodosa

A

Non infectious vasculitis may involve cerebral vessels and cause infarcts in brain

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29
Q

Primary angiitis

A

Granulomatous angiitis of nervous system
Inflammation affects many small to medium parenchymal and subarachnoid vessels
Chronic inflammation, multinucleated giant cells, and destruction of the vessel wall
Patients develop a diffuse encephalitic of multifocal clinical picture with cognitive dysfunction
Patients improve with steroid and immunosuppressive treatment

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30
Q

What are the two types of infarcts

A

Hemorrhagic and non hemorrhagic

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31
Q

Hemorrhagic infarcts

A

When emboli partially occlude a vessel or undergo dissolution

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32
Q

Nonhemorrhagic infarcts

A

More likely to arise from thrombosis over atherosclerotic lesions

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33
Q

Infarcts are typically ___ in the beginning because infarcts are the result of a loss of blood

A

Nonhemorrhagic

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34
Q

With repercussion injury from collaterals or from breakdown of the clot the infarct can becomes __

A

Hemorrhagic

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35
Q

The hemorrhagic infarcts are typically petechial and can be multiple of confluent management.treatment differs greatly as __ __ is contraindicated in hemorrhagic infarcts

A

Thrombocytic therapy

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36
Q

Brain swelling with infarcts

A

No

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37
Q

Non hemorrhagic infarct morphology

A 
Little change in first 6 hrs
From edges inward
12 h-red neurons edema
Loss of tissueendothelial and glial cells begin to swell and myelination falls 
Neutrophils

48 hrspale doft and swollen corticomedullary junction indistinct
Macrophages and microglia are now the dominant cell type and will be 2-3 weeks persist
2-10 days brain becomes gelatinous and friable more distinct demarcation infarct and non..reactive astrocytes
Months-astrocytes response stops and leaves glial fiber meshwork mixed with capillaries and perivascular CT
PIA AND ARACHNOID MATER ARE UNAFFECTED AND DO NOT CONTRIBUTE TO THE HEALING PROCESS

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38
Q

Hemorrhagic infarct morphology

A

Same as hemorrhagic but there is blood extravasation and resorption
Prob if anti coagulant -thrombolytic therapy tPA contraindicated in hemorrhagic infarct

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39
Q

Venous infarcts are often hemorrhagic and can occur after thrombotic occlusion of the superior sagittal sinus or occlusion of other cerebral veins

A

Spinal cord infarction

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40
Q

With hypoperfusion or result of traumatic interruption of the feeding tributaries derived from the aorta

A

Rarely can be due to occlusion of the anterior spinal artery as the result of embolism or vasculitis

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41
Q

Effects of hypertension cerebrovasculardisease

A

Lacunae infarcts, slit hemorrhages, and hypertensive encephalopathy as well as massive hypertensive intracerebral hemorrhage

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42
Q

Lacunar infarcts/occlusion

A

Hypertension affects deep penetrating arteries and arterioles that supply the basal ganglia and hemispheric white matter and brainstem,. These cerebral vessels develop arteriolar sclerosis and can become occluded -associated with widening of perivascular spaces without tissue infarction

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43
Q

What can lacunar infarcts lead to

A

Single or multiple small cavityary infarcts known as lacunas (less than 12 mm wide)

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44
Q

Where do lacuna occur

A

Lenticular nucleus, thalamus, internal capsule, deep white matter, caudate nucleus, pons

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45
Q

Etat crible

A

Lacunar vessels associated with widening or perivascular spaces without tissueinfarction

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46
Q

Slit hemorrhages

A

HTN can cause rupture of small caliber penetrating vessels and the development of small hemorrhage
Hemorrhage will be resorted and leave small slit like cavity that is surrounded by a brownish discoloration

There is focal tissue destruction, pigment laden macrophages and gliosis

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47
Q

Hypertensive encephalopathy

A

From malignant HTN from eye and kidney problems

Diffuse cerebral dysfunction (headache, confusion, vomiting, convulsions, and coma_
Edema and herniation of tonsil or transtentorial

Petechial and fibrinoid necrosis of arterioles in grey and white matter

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48
Q

Vascular dementia

A

From bilateral grey (cortex, thalamus, basal ganglia) and white matter (centrum semiovale) infarcts over many months and years

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49
Q

Clinical vascular dementia

A

Dementia, gait, pseudobulbar signs, neuro deficits

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50
Q

Causes of vascular dementia

A

Cerebral atherosclerosis, vessel thrombosis or embolus, arterial sclerosis

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51
Q

Biswanger disease

A

Pattern of injury preferentially involves large areas of the subcortical white matter with myelin and axon loss. Usually large areas of subcortical white matter with myelin and axon loss

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52
Q

What hemorrhages are associated with trauma

A

Epidural and subdural

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53
Q

Subarachnoid and intraparenchymal hemorrhages

A

Underlying cerebrovascular disease

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54
Q

IntraParenchymal hemorrhage

A

Rupture small vessels with sudden onset of symptoms

Peak 60

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55
Q

Ganglionic hemorrhage

A

In basal ganglia and thalamus from hypertension

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56
Q

Lobar hemorrhage

A

In cerebral hemisphere from CAA

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57
Q

What is risk factor of deep brain parenchymal hemorrhages

A

HTN

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58
Q

Where are hemorrhages associated with HTN

A

Deep white/grey matter followed by brainstem and cerebellum

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59
Q

Duret hemorrhage

A

Pontine , putamen, thalamus, pons

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60
Q

Acute hemorrhage

A

Extravasion of blood with a subsequent compression of surrounding parenchyma

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61
Q

Old hemorrhage

A

Cavitary lesion with a rim of brown (slit hemorrhage) but initially they consist of a central core of clotted blood with a rim of brain tissue with anoxic and glial changes with edema

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62
Q

After intraparenchymal hemorrhage

A

Hemosiderein and lipid laden macrophages and reactive astrocytes along periphery

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63
Q

CAA

A

Lobar hemorrhage
AB40 which weakens walls leading to hemorrhage
Microbleeds

NO FIBROSIS vessels rigid
Only affects leptomeningeal and cerebral cortical arterioles

Amyloid, dense uniform deposits@@@

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64
Q

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy CADSIL

A

AD
NOTCH3 causes misfolding of receptor protein on vascular smooth
Recurrent strokes and dementiafirst seen in white matter around 35 and infarcts 45-50

Concentric thickening of media adventitia

Loss of smooth muscle
Basophils PAs deposits that appear as osmiphilic compact granular material

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65
Q

Clinical CADAIL

A

Devastating if affects large brain portions

Granular resolution after of hematoma its improvement

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66
Q

Saccular aneurysm

A

At birth congenital defect cause dilation later

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67
Q

Subarachnoid hemorrhage

A

Base of brain less likely to cause mass effect

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68
Q

Most common intracranial aneurysm

A

Berry

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69
Q

Where is berry

A

Anterior circulation near arterial branch point

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70
Q

Structural problem with berry

A

Absence of smooth muscle or intimate elastic lamina at birth

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71
Q

Are berry congenital prob

A

No smooth muscle deficit is congenital aneurysm are acquired after

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72
Q

Berry media

A

Ok

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73
Q

Risk factor saccular berry

A

Genetic

AD polycystic kidney disease, helpers danlos, neurofibromatosis type I, Maryam, smoking HTN

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74
Q

Where does rupture of berry aneurysm happen

A

Apex of aneurysm leads to extravasation of blood into subarachnoid space, substance of the brain or both

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75
Q

The wall next to a berry aneurysm has intimacy thickening and attenuation of the media

A

Ok

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76
Q

Why get non communicating hydrocephalus after berry aneurysm

A

Organization of the subarachnoid hemorrhage occluding foramina of luschka and magendie

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77
Q

Risk of saccular aneurysm

A

Organs and stool HTN, female,

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78
Q

Clinical presentation saccular berry

A

Worst headache of life thunderclap headache
Subarachnoid

Then vasospasm in basal subarachnoid hemorrhages that involve major vessels in circle of Willis

Heal-obstruction of csf flow

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79
Q

Arteriovenous malformations

A

In cerebral hemispheres of a young adult
Subarachnoid space or brain
Tangled vessels that show prominent, pulsatile arteriovenous shunting with high blood slow-bypass a capillary bed
Can be respected
Separated by gliotic tissue with evidence of prior hemorrhage
Some vessels show duplication and fragmentation of the internal elastic lamina while others show marked thickening or partial replacement of the media by hyalinized CT

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80
Q

Cavernous malformations

A

Distended loosely organized vascular channels back to back with collagenized walls of variable thickness
No. Brain parenchyma between vessels
In cerebellum, pons, and subcortical regions
Low flow channels that do not participate in AV shunting
There is commonly evidence of prior hemorrhage, infarct or calcification
Familial AD

81
Q

Capillary telangiectasias

A

Microscopic foci of dilated thin walled vessels separated by normal parenchyma
In pons

82
Q

Venous angiomas

A

Aggregates of ecstatic venous channels

83
Q

Foix alajouanine disease (angiodysgenetic necrotizint myelopathy)

A

Venous angiomatous malformation of the spinal cord and overlying meninges
Most common in the lumbosacral region
Associated with ischemic injury to the spinal cord and slowly progressive neurological symptoms

84
Q

AVM

A

Males
10-20 seizure disorder, intracerebral hemorrhage, or subarachnoid hemorrhage
Most common site is the MCA (hands face), espicially posterior branches
Can lead to CHF

85
Q

Stroke

A

Acute onset of neurological deficits resulting from hemorrhagic or obstructive vascular lesion

86
Q

What are the two most common causes of the spontaneous subarachnoid hemorrhage

A

Aneurysm or arteriovenous malformation

87
Q

Infection:four principal routes by which microbes enter the nervous system

A

Hematogenous (venous also sinus)
Meningitis :arachnoid and pia caused by microbes
Meningoencephalitis
Chemical meningitis

88
Q

Acute progenitor meningitis

A

Neutrophilils, elevated protein, reduced glucose

89
Q

Aseptic meningitis poliomyelitis

A

Lymphocytic, moderately elevated, normal glucose

90
Q

Chemical (sterile ) meningitis

A

Neutrophilis elevated protein

Normal glucose

91
Q

Brain abscess, subdural empyema

A

Elevated WBC, elevated protein normal glucose

92
Q

TB meningitis

A

Mixed mononuclear cells and neutrophilis cells

Elevated protein
Normal reduced glucose

93
Q

Arthropod borne viral encephalitis

A

Neutrophilis then rapidly lymphocytic
Elevated protein
Normal glucose

94
Q

Bacterial

A

Increased neutrophils increased protein decreased glucose

Increased pressure

95
Q

Viral

A

Increased lymphocytes increased protein normal glucose

Increased pressure

96
Q

Fungal and mycobacterium

A

Increased lymphocytes increased protein decreased glucose

Increased pressure

97
Q

Acute progenitor meningitis

A

Bacterial

98
Q

Aseptic meningitis

A

Acute or subacute viral

99
Q

Chronic meningitis

A

TB, spirochetal, cryptococcal

100
Q

Meningoencephalitis

A

Inflammation of meninges and brain parenchyma

101
Q

Chemical meningitis

A

Non bacterial irritate into subarachnoid space causes inflammation of meninges

Chemo

102
Q

Neonates acute progenitor meningitis

A

Group b strep (agalactiae)

103
Q

Adolescent acute progenitor meningitis

A

Neisseria meningitidis college

104
Q

Elderly acute progenitor meningitis

A

Strep pneumonia and listeria monocytogenes

105
Q

Most common organism to cause acute progenitor meningitis

A

Strep pneumo

106
Q

Immune suppressed people acute progenitor meningitis

A

Klebsiella or anaerobic organisms

Will have uncharacteristic CSF findings

107
Q

Haemophilus influenza and meningitis

A

Immunization now infants don’t get

108
Q

Clinical presentation of meningitis

A

Headache, photophobia, cloudy consciousness, stiff neck

Bacterial cultured

109
Q

Waterhouse friderichsen syndrome

A

Meningitis associated with septicemia with hemorrhagic infarction rothe adrenal glands and cutaneous petechial
Occurs with meningococcal and pneumococcal meningitis

110
Q

Acute aseptic meningitis

A

Less fulminant than progenitor
Self limited

Enterovirus

111
Q

Morphology bacterial meningitis

A

Exudate in leptomeninges (pia and arachnoid)

H. Influenza-basal distribution
Pneumococcal-cerebral and sagittal sinus distribution

Neutrophils in leptomeningeal vessels (less severe) or subarachnoid space (severe)

112
Q

Fulminant mengitis

A

Inflammatory cells infiltrate the walls of the leptomeningeal veins ad can cause cerebritis

113
Q

Phlebitis

A

Lead to venous thrombosis and hemorrhagic infarction of the underlying brain

114
Q

Leptomeningeal fibrosis can happen after progenitor meningitis and lead to hydrocephalus

A

The capsular polysaccharide of the microbe can make a gelatinous exudate that promotes arachnoid fibrosis known as chronic adhesive arachnoiditis

115
Q

Chronic adhesive arachnoiditis

A

No CSF flow

116
Q

Bacterial meningitis lead to CSF what

A

Obstruction at foramina luschka and magendie making communications hydrocephalus

117
Q

Brain abscesses

A

Localized focus of necrosis of brain tissue with inflammation that is usually caused by bacteria
RING enhancesmtn on CT scans

118
Q

What are ring enhancements of brain abscesses

A

As abscess organized it is ringed by fibroblasts that deposit collagen -characteristic of an abscess in the CNS

119
Q

Describe ring enhancement

A

Granulation tissue with fibrosis is a typical healing inflammatory response reaction to a cerebral abscess, usually caused by bacterial organisms. Collagen deposition ground a ring enhancing lesion is typical for an abscess that organizes. The ring enhancement results from increased vascularity from capillary proliferation and disrupted BBB. A common source for such brain abscess is a lung infection

120
Q

Primary infiltrate of brain abscess

A

Neutrophils

121
Q

What are brain abscesses associated with

A

Fever

122
Q

Where are brain abscesses commonly located

A

Cerebral hemispheres away from the ventricular system

123
Q

What causes brain abscess

A

Direct implantation of microbe , local extension of the microbes from adjacent foci, or hematogenous spread from a primary site like the heart, lungs, extremity bones, or tooth extraction

124
Q

Predisposing conditions for brain abscesses

A

Acute bacterial endocarditis :lead to many abscess
Congenital heart disease with right to left shunting and loss of pulmonary filtration chronic pulmonary sepsis like bronchiectasis
Immune suppression

125
Q

Most common bacteria for brain abscess

A

Strep and staph

126
Q

Brain abscess morphology

A

Central liquefaction necrosis

Leaky vasogenic edema

127
Q

Clinical presentation brain abscess

A

Progressive focal neuro deficit
ICP signs
CSF high white count and increased protein but glucose normal

128
Q

When is glucose decreased in csf

A

Bacterial

129
Q

Complications of brain abscess

A

Rupture with ventriculitis or meningitis and venous sinus thrombosis .=

130
Q

Cubdural empyema

A

Bacterial or fungal infections of the skull bones or air sinuses can spread to the subdural space to produce a subdural empyema

131
Q

Are arachnoid and subarachnoid affected in subdural empyema

A

No

132
Q

Venous occlusion subdural empyema

A

Mass effect of thrombophlebitis of bridging veins that cross the subdural space and infarction

133
Q

Clinical presentation subdural empyema

A

Fever, headache, stiff neck

Csf with white cell, increased protein, normal glucose

134
Q

If leave subdural empyema untreated

A

Focal neuro signs and symptoms , lethargy, coma

135
Q

Treat subdural empyema

A

Residuum and thickened dura

136
Q

Extramural abscess

A

Associated with osteomyelitis
Comes from another source of infection from surgery or sinus

Can cause spinal cord compression if occur in spinal epidural space

137
Q

Cause of bacterial meningoencephalitis

A

TB, syphilis borrelia species

138
Q

TB meningitis

A

Headache, malaise, mental confusion, vomit

CSF pleocytosis of mononuclear cells, elevated protein, normal to moderate reduction of glucose

139
Q

Complication of TB meningitis

A

Arachnoid fibrosis producing hydrocephalus and obliterating endarteritis producing arterial occlusion and infarction of the brain

Nerve roots
Granulomas cause space occupying lesion and symptoms

140
Q

Morphology TB meningitis

A

TB acid fast

Obliterating endarteritis and marked intimacy thickening

141
Q

Tuberculomas

A

Well circumscribed intraparenchymal mass
Caseous necrosis in mussel
Calcification in inactive
Mass space occupying lesion

142
Q

Tertiary syphilis

A

Mix of tabes dorsalis, paretic neurosyphilis, meningovascular neurosyphilis

Taboparesis

143
Q

Neurosyphilis and aids

A

Increase

144
Q

Meningovascular neurosyphilis

A

Chronic involves base of the brain and cerebral convexities and spinal leptomeninges

145
Q

What is meningovascular neurosyphilis associated with

A

Obliterating endarteritis (heubner arteritis) accompanied by perivascular inflammmatiory reaction rich in plasma cells and lymphocytes

Cerebral Gemma’s

146
Q

Paretic neurosyphilis

A

Treponema
Mood changes
General paresis of the insane
Iron deposits demonstrable by Prussian blue stain

147
Q

Tables dorsalis

A

Damage dorsal column
Widen gait
Poor proprioception and locomotor ataxia
Charcot joints-loss of pain leading to skin and joint damage
Lightening Pain and loss of DTR
Pallor and atrophy in the dorsal columns of spinal cord

148
Q

Neuroborreliosis

A

From ticks Lyme disease

Aseptic meningitis, facial nerve palsies, and encephalopathy

149
Q

Arthropod borne viral encephalitis

A

Arboviruses tropical regions

Seizures, confusion, ocular palsies, reflex assymmetry

150
Q

Morphology viral meningoencephalitis

A

Perivascular lymphocytes
Foci of necrosis in grey and white
Single cell neuronal necrosis with phagocytosis of the debris neurophagis

Microglial nodules

151
Q

West nile

A

Polio type encephalitis

152
Q

Herpes encephalitis

A 
TLR4 defect 
Mood memory behavior 
Temporal lobe 
Hemorrhagic lesions of temporal lobes
Necrotizing infection
153
Q

Hsv2

A

Meningitis can pass to kids

HIV-hemorrhage and necrotizing encephalopathy

154
Q

Varicella zoster

A

Chicken pox
Kid come back as shingles
Adult -granulomatous arteritis
Immunocompromised-acute encephalopathy characterized by numerous sharply circumscribed demyelinating lesions that undergo necrosis

155
Q

CMV

A

Microcephalic

Periventricular leukomalacis

156
Q

Poliomyelitis

A

Tropism for anterior horn

Perivascular cuffs, neuronophagia of anterior horn motor neurons of the spinal cord
Neuronophagia of the anterior horn motor neurons of the spinal cord
Affected anterior horns of the spinal cord LMN and atrophy of msucles

157
Q

Polio features

A

LMN-areflexia, atrophy, Antonia, flaccid paralysis

UMN-hyperreflexia, hypertonic, spastic paralysis

158
Q

Polio and diaphragm

A

Death

159
Q

Destroy motor neurons

A

Paresis/paralysis

160
Q

Post polio syndrome

A

Progressive weakness and decreased muscle mass in affected area

161
Q

Rabies

A

Pyramidal neurons of the hippocampus and purkinje cells of cerebellum
Nehru

162
Q

Symptoms rabies

A

Local paresthesia around wound

Conjunction fo thes symptoms with local paresthesia around the wound is nearly diagnostic

163
Q

HIV

A

Acute-lymphocytic meningitis, perivascular inflammation, and some myelin

164
Q

Immune reconstitution inflammation syndrome

A

Paradoxical deterioration after starting therapy from the exuberant reconstituted immune system

165
Q

HIV encephalopathy

A

Chronic inflammation axonal swelling

166
Q

PML

A

JC polyomavirus
Oligodendrocytes demyelination is its principle pathological effect in immune compromised

Glassy amp Philip viral inclusions

167
Q

Clinical PML

A

Focal and relentlessly progressive neuro signs

Image -extensive multifocal lesions in hemispheric or cerebellar white matter

168
Q

Subacute sclerosis’s penencephalitis

A

Kids or young adults months or years after initial measles virus

169
Q

SSPE clinic

A

Progressice cognitive decline , limb spacisitiy and seizures
Widespread gliosis
Lots of viral inclusions that are mostly found in the nuclei of oligodendrocytes and neurons

170
Q

Fungal meningoencephalitis

A

Immunocompromised
Aspergillus, cryptococcal neoforms
-histoplasma capsulatum, coccidiodes immitis and blastomyces dermatitidis can affect cns after an initial pulmonary or cutaneous infection

171
Q

Most fungi et into brain how

A

Hematogenous

172
Q

What are 3 forms of CNS fungal injury

A

Chronic meningitis, vasculitis, parenchymal invasion

173
Q

Vasculitis

A

Mucormycosis, aspergilosis after infect

Love to invade blood cells

174
Q

Parenchymal nfection

A

Granulomas or abscesses
Candida or cryptococcal

Candidiasis causes multiple microabsceses with or without granulomas

175
Q

Cryptococcal meningitis

A

AIDS fulminant and fatal 2 weeks or indolent

Protein CSF and yeast

176
Q

Cryptococcal meningitis morphology

A

Obstruct outflow of CSF from the foramina or luschka and magendie leading to hydrocephalus
Soap bubbles-small cysts within parenchyma espicially the basal ganglia parenchymal lesions consist of aggregates of organisms within perivascular virchow node
INDIA PINK CYSTS

177
Q

Cerebral toxoplasmosis

A

Opportunistic
HIV
Ring enhancing lesion
Pregnancy-TORCH

178
Q

Cerebral toxoplasmosis morphology

A

Affect cerebral cortex and deep grey nuclei

Necrosis, hemorrhage, chronic inflammation, macrophage infiltration and vascular proliferation

179
Q

Cerebral amebiasis

A

Naegleria or acanthamoeba
PAS meth silver

Immunofluoresence sulture and olecular methods

180
Q

Cerebral malaria

A

Rapidly progressing encephalopathy
Complication of infection by plasmodium falciparum with highest mortality rate
Most likely vascular dysfunction

Reduced cerebral blood flow, ataxia, seizures, coma, cognitive deficits

181
Q

Prions

A

Sporadic 90%

182
Q

PrP

A

Polymorphism at 127 M or V homozygous overrepresent CJD

183
Q

Heterozygous 129

A

Protective

184
Q

Morphology prions

A

Spongiform change caused by intracellular cavuoles in neurons and glial cells and progressive dementia

185
Q

PrPsc

A

Proteinase k resistant in tissue

186
Q

CJD

A

Rapidly progressive dementia

187
Q

Gerstmann straussler scheinker syndrome

A

Progressive cerebellar ataxi

188
Q

CJD

A

Familiar
70s
Iatrogenic (corneal transplant, brain electrodes, contaminated Growth hormone)

189
Q

Clinical CJD

A

Subtle changes in memory and behavior followed by rapidl dementia and smartly myoclonus (pronounced involuntary jerking muscle contractions on sudden stimulation’s

190
Q

Survival CJD

A

7 months

191
Q

VCJD

A

Exposure to bovine spongiform encephalopathy from contaminated food or blood transfusion
Young adults
Behavior change
Extensive cortical plaques surround halo of spongiform change

Limited to 129 MET MET homozygous

192
Q

CJD morphology

A

Cyst like spaces (status spongiosus)
Spongiform transformation of cerebral cortec and deep gray
Uneven formations of small and empty microscopic vacuoles within neuropil and perilaryon of neurons

Kuru plaques Congo red and PAs positive in cerebellum

193
Q

Fatal familial insomnia

A

Sleep disturbances in initial stages

Specific mutation in PRNP gene

194
Q

What mutation in FFI PRNP gene

A

Substitution for aspargine at residue 178 of PrPsc result in FFI when is occurs in a PRNP allele encoding methionine at codon 129 but causes CJD when present in tande, with Celine at this spot

195
Q

Asparagine at 178 and M at 129

A

FFI

196
Q

Asparagina at 178 and valine at 129

A

CJD

197
Q

FFI clinical

A

3 years

Then develop ataxia, autonomic disturbances, stupor, and coma

198
Q

Spongiform pathology inFFI

A

No
Characterized by neuronal loss and reactive gliosis in anterior ventral and dorsomedial nuclei of the thalamus instead
Neuronal loss also prominent in inferior olivary nuclei

Pathology (36 decks)

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