pathology Flashcards

Question

``` Global ischemia /hypoxia (Hypotension, hypoperfusion and low flow states (diffuse hypoxic ischemic encephalopathy )); Defenition? Causes? Features? ```

Answer 1

- generalized reduction of cerebral perfusion ,symptoms(mild- irreversible damage) - cardiac arrest , shock, sever hypotension -Cells: neurons affected > glia, but all if severe and prolonged -Selective Vulnerability of neurons in certain locations : 1-Pyramidal cells in CA1 of hippocampus (Sommer sector) 2-Purkinje cells of the cerebellum 3-Cortical pyramidal neurons - Watershed(Borderzone ) infarcts include : - Boundary between anterior & middle cerebral arteries (Cerebral Convexities)

Answer 2

-Brain swelling -Wide gyri and narrow sulci -Poor demarcation between grey & white matter ``` #Acute : after 12 hrs - RED NEURONS - Infiltration by neutrophils # Subacute changes: 24 hrs – 2 weeks - tissue necrosis, macrophages & gliosis # Repair: after 2 weeks - Removal of necrotic tissue - Loss of normally organized CNS structure - Gliosis ```

Answer 3

1-Presence of collateral circulation 2-Duration of ischemia 3-Magnitude and rapidity of reduction of flow * Result varies from persistent neurological deficit to brain death → Deep coma & flat EEG * Patients maintained by mechanical ventilation →Brain autolysis

Answer 4

-necrosis due to complete and prolonged ischemia ``` #Thrombotic occlusion, mainly due to Atherosclerosis : "Ischemic/ pale" 1.Carotid bifurcation 2.Origin of middle cerebral artery 3.Basilar artery at either end ``` #Embolic occlusion : "hemorrhagic/ red" 1- Source: heart or atherosclerosis in carotid 2- Middle Cerebral artery most affected #Other emboli are fat, bone marrow, air, amniotic fluid

Answer 5

1-Acute white infarct in the distribution of the right middle cerebral artery. 2-Acute red infarct in the distribution of the right anterior cerebral artery. - Size of the infarct - Site of the infarct - State of collateral circulation - Rapidity of onset

Answer 6

-No gross change before 48 hrs - Soft swollen pale or hemorrhagic WEDGE SHAPED infarct involving grey & white matter. -Blurred demarcation -Red infarcts: surrounding hemorrhage due to reperfusion of damaged vessels and tissue -After 10 days-3 weeks : liquefaction - Cavity within 1- 6 months -Very similar to global ischemia but more regional. * *linked to site of infarction: - Contralateral hemiparesis - Loss of sensation - Visual field abnormalities - Aphasia

Answer 7

- Intracerebral (intraparenchymal) - Subarachnoid - Epidural - subdural

Answer 8

``` 1-Commonest is HYPERTENSION 50% 2- CEREBRAL AMYLOID ANGIOPATHY -vasculitis - coagulation disorders - neoplasms ```

Answer 9

- atherosclerosis ;in larger arteries - hyaline arteriolosclerosis ;in smaller vessels—>hemorrhage - arteriolosclerosis ;in vessels <=150micro.m—> lacunar infarcts - charcot bouchard microaneurysms ;in vessels <=300micrometer in basal ganglia —>rupture

Answer 10

``` Lacunar infarcts Slit hemorrhages htpertensive encephalopathy Intracerebral hemorrhage Cerebral amyloid angiopathy ```

Answer 11

Tiny cystic infarcts in hemispheric WM ,basal ganglia &brain stem due to hypertensive arteriolosclerosis of deep penetrating arteries and arterioles - multiple small cavitary infarcts (lake like spaces ,less than 15mm wide) - asymptomatic or sever neurologic impairment

Answer 12

- Rupture of smaller penetrating vessels | - Resorb,leaving behind a slit like cavity

Answer 13

Acute : malignant hypertension -diffuse cerebral dysfunction :headaches , confusion,vomiting,convulsions,coma ``` #chronic: over for many months and yrs ,multi bilateral gray and wm infarcts : Dementia, gait disturbances , pseudobulbar signs ```

Answer 14

- putaman 60%,thalamus , pons, cerebellar hemi and others - acute: extravasation of blood wt compression of adjacent parenchyma - old: cavitary destruction of brain wt a rim of brown discoloration

Answer 15

Deposition of amyloid in wall of medium &small meningeal &cortical vessels —>weak wall—>hemorrhage

Answer 16

1-rupture saccular (berry) aneurysm *commonest cause 2-vascular malformation 3-hematological disturbances 4- tumors

Answer 17

- 5th decade,female - mostly sporadic ,but may be genetic - because it develop over time due to underlying defect in media of vessels - 1.3%/yr - 90% near anterior circulation ,20-30% multi

Answer 18

``` Genetic: – Polycystic kidney disease (autosomal dominant) – Defects in extracellular matrix proteins e.g. Marfan’s syndrome, Others • Non-genetic: – Coarctation(constriction) of aorta • Predisposing conditions: – Hypertension – Cigarette smoking ```

Answer 19

* Size: from few mm to 2-3 cm. * Muscular wall and internal elastic lamina are absent * Aneurysm sac is lined only by thickened hyalinized intima. The adventitia covering the sac is continuous with that of the parent artery. * occurs at the apex of the sac, releasing blood into the subarachnoid space or the substance of the brain, or both

Answer 20

”Worst headache of my entire life”, sudden, excruciating with loss of consciousness - 25-50% die at time of first #Acute: in the first few days – Vasospasm : • Increased risk of additional ischemic injury ``` #Repeat bleeding •Associated with ↑mortality ``` ``` #Chronic (healing phase): Meningeal fibrosis and scarring —>obstruction of CSF flow, interruption of normal pathways of CSF resorption ```

Answer 21

1) Arteriovenous malformations (AVM) 2) Cavernous malformation 3) Venous angioma 4) Capillary telangiectasis **1+2 are the types associated with risk of hemorrhage and development of neurological symptoms.

Answer 22

- males - 10-30yrs - seizures ,intracerebral or subarachnoid hemorrhage - vessels in subarachnoid &cerebrum - prominent pulsatile wormlike vascular channels - enlarged BV separated by gliotic tissue

Answer 23

- dilated thin walled vascular channels devoid of intervening brain tissue - cerebellum ,pons and subcortical region

Answer 24

Microscopic foci of dilated thin walled vascular channels separated by normal brain parenchyma -aggregates of ectatic venous channels -in brain ,SC &meninges Progressive neurological symptoms

Answer 25

•Penetrating or Blunt trauma→ Open or Closed • Mobile or immobile head at time of trauma • Lesions at bony prominences e.g - Frontal, orbital, temporal & occipital poles - Spinal cord • Edema may occur & worsen the condition • Skull fracture

Answer 26

1-parenchymal injury 2-diffuse axonal injury 3- traumatic vascular injuries

Answer 27

``` #Concussion (Traumatic brain injury) : – Instantaneous onset of transient neurologic dysfunction, including loss of consciousness, and loss of reflexes – Due to change in the momentum of the head. – Complete neurologic recovery ``` #Direct Parenchymal injury: Contusions & lacerations: – More on crests of gyri •Contusions :wedge shape broad vase along the surface deep to the point of impact Early: edema and hemorrhage Neuronal injury :take about 24 hr ``` Types: 1-Coup lesions: - Contusions at point of contact - Immobile or mobile head 2-Contrecoup lesions : - Contusions opposite to the point of trauma - Mobile head ```

Answer 28

- 50%wt post traumatic coma even wtout cerebral contusions - affect deep WM (CC, paraventricles ,hippo.)&cerebral peduncles -axonal swelling ,micro hemorrhages ,microglia ,later gliosis

Answer 29

1-epidural hematoma | 2-subdural hematoma

Answer 30

-Usually acute & accompanied by skull fracture • Rupture of middle meningeal artery • Mass effect → Dura & Brain compression”more mass effect” • Clinically : - When blood accumulates slowly: Patient has short LUCID interval followed by rapid loss of consciousness - May expand rapidly → Neurologic emergency

Answer 31

Tearing of Bridging Veins • Gross: Collection of fresh blood • Mass effect → Brain compression • Clinically: - Headache and confusion - Slow progressive neurologic deterioration • Treatment: remove blood and associated organizing tissue.

Answer 32

1- Post traumatic hydrocephalus 2- Post traumatic dementia 3- Epilepsy 4- Infection 5- Psychiatric disorders

Answer 33

- Neonates: group B Streptococci & E.coli - >6M : S.Pneumoniae, H.influenza, - Adolescents & young adults :N. meningitidis - Elderly :S.pneumonia& L.monocytogenes #Fever, headache, vomiting, neck stiffness #Waterhouse Friderichsen Syndrome:1.- Results from meningitis associated septicemia with hemorrhagic infarction of the adrenal glands and cutaneous petechiae. 2.- Occurs with meningococcal and pneumococcal meningitis *CSF:Cloudy or frankly purulant ↑P, ↑Protein, ↓glucose, numerous neutrophils Bacteria may be seen or cultured Morphology:Exudate within the leptomeninges Meningeal vessels: Severely congested May cause cerebritis & ventriculitis May show phlebitis → venous occlusion & hemorrhagic infarction of underlying brain. Fibrosis → Hydrocephalus

Answer 34

Clinical: Less fulminant, self-limiting often seasonal CSF: moderate↑ protein, normal glucose , ↑↑ lymphocytes

Answer 35

- Hematogenous spread from lung → brain - Direct spread from Tuberculous vertebra 1#Diffuse meningoencephalitis: Gelatinous or fibrinous exudate, mostly at the base, obliterating the cisterns, and encasing cranial nerves. 2# Tuberculoma: Single or multiple intraparenchymal mass. *Microscopy: -Mixtures of lymphocytes, plasma cells and macrophages - Caseating granulomas -Obliterative endartritis: inflammation in the wall, marked intimal thickening → arterial occlusion → infarction -Dense fibrous adhesive archnoiditis → Hydrocephalus *CSF : Marked ↑Protein, , glucose normal or ↓, ↑ lymphocytes and neutrophils.

Answer 36

-caused by spirochete (T.pallidum) ,Tertiary stage 1-meningovascular syphilis 2-paretic neurosyphilis 3- tabes dorsalis 4- acute syphilitic meningitis

Answer 37

- Chronic Meningitis - Obliterative endarteritis (Heubner arteritis): Perivascular plasma cells and lymphocytes - Cerebral gummas: Plasma cell-rich mass lesion

Answer 38

#-Invasion of the brain, mainly frontal lobe by T.pallidum ``` #-Insidious, but progressive mental deficits with mood alteration → General paresis of the insane ``` #-Inflammation with parenchymal damage: loss of neurons, proliferation of microglia (ROD CELLS) & gliosis -Granular ependymitis: ependymal cells damage with proliferation of subependymal glia → Hydrocephalus -Spirochetes may be seen in tissue section

Answer 39

``` #- Damage to the sensory nerves in the dorsal root - Loss of axons & myelin → pallor and atrophy of dorsal columns ``` ``` #-clinically: Impaired joint position sense and ataxia (locomotor ataxia), loss of pain sensation → skin and joint damage → Charcot joints - Others: lightning pains, absence of deep tendon reflexes ``` ``` #Acute syphilitic meningitis : - HIV infected patients ```

Answer 40

``` 1- Hydrocephalus 2- Cerebral infarction 3- Cerebral abscess 4- Epilepsy 5- Cranial nerve palsy ``` ``` #Prognosis depends on rapidity of proper antibiotic therapy ```

Answer 41

* Localized : abscess, tuberculoma,toxoplasmosis, parasites * Diffuse : encephalitis, usually viral ``` #-Usually bacterial #-Direct infection from paranasal sinuses,mastoiditis & middle ear Hematogenous route from heart, lungs or after tooth extraction. ``` #Grossly: Discrete lesion with central liquefactive necrosis surrounded by fibroblasts. #Microscopic picture : - Localized suppuration surrounded by granulation tissue , reactive astrocytes & severe edema leading to ↑ ICP . - Fibrous capsule, outer zone of reactive gliosis #CSF : ↑protein, ↑white cells, normal glucose ``` #Clinical presentation: Progressive focal deficit, and signs of ↑ ICP ``` 3Complications : If rupture → ventriculitis, meningitis, venous sinus thrombosis #Treatment: Surgery and antiobiotic

Answer 42

-Sporadic infection : HSV -Latent infections : Herpes Zoster, PML -Neurotropic : Polio, Rabies -Antenatal : CMV, Rubella -Immune deficiency : HIV, CMV, PML, Herpes Zoster

Answer 43

-HSV :Temporal lobe & orbital frontal area -CMV : Subependymal region -Polio : Anterior horn cells of spinal cord -Herpes Zoster: Sensory neurons of dorsal root ganglia

Answer 44

1- Perivascular mononuclear infiltrate 2- Neuronophagia 3- Microglial nodules 4- Nuclear or cytoplasmic inclusions

Answer 45

``` #Children or young adults #Hemorrhagic necrotizing inflammation in temporal lobe & orbital gyri of frontal lobe ``` #Alteration in mood, memory and behavior ``` #All common features of viral encephalitis seen with Cowdry type A intranuclear viral inclusions in neurons & glial cells ``` **HSV-2 in adults may cause meningitis

Answer 46

``` #Chicken pox in children -latent infection in dorsal root ganglia in adults ``` ``` #Reactivation (Shingles): Self limited painful vesicular skin eruption along a dorsal nerve in a single or limited dermatomal distribution. ``` ``` #In immunosuppressed patients, may show acute encephalitis. ``` ``` #Lesion is typical of viral infection ± granulomatous arteritis & infarction ```

Answer 47

1.Severe encephalitis - Transmitted to humans by bite of a rabid animal such as dog - Ascends along peripheral nerve from bite - Incubation period (1-3 months) depends on the distance between the wound and the brain 2-Neuronal degeneration and inflammatory reaction , most severe in brain stem - also can be in basal ganglia, S.C, dorsal root ganglia ``` ##Presence of Negri bodies : cytoplasmic, eosinophilic inclusions in pyramidal neurons of the hippocampus & Purkinje cells of cerebellum, in sites usually devoid of inflammation ```

Answer 48

``` #Enterovirus causing mild gastroenteritis -Involvement of CNS in the non- immunized ``` #- Acute : mononuclear cell perivascular cuffs and neuronophagia of the anterior horn motor neurons of the spinal cord #- Chronic : Loss of neurons and atrophy of the anterior (motor) spinal roots,and neurogenic atrophy of denervated muscle. #Clinical presentation: - Meningitis - Flaccid paralysis with muscle wasting - Death can occur from paralysis of the respiratory muscles

Answer 49

-Caused by JC polyomavirus exposure during childhood -mainly AIDS patients & other immunosuppressed patients -Infect oligodendrocytes ``` #RESULT : Progressive demyelination of white matter ``` #Grossly: Patches of irregular, ill-defined destruction of white matter from mm to extensive involvement of the entire lobe #Microscopy: Patch of demyelination , with scattered lipid laden macrophages at the center, and reduced number of axons -Enlarged oligodendrocyte nuclei with viral inclusions -Large astrocytes are also seen.

Answer 50

#-Disease occurs when the PrP undergoes conformational changes from its normal shape (PrPc) to an abnormal conformation called PrPsc (sc for scrapie) ``` #-Creutzfeldt- Jacob Disease -Fatal Familial Insomnia -Kuru -Scrapie in sheep -bovine spongiform encephalopathy in cattle (“mad cow disease”) ```

Answer 51

-Sporadic cases 85%,Familial cases (15%), younger #Iatrogenic Transmitted ! Contaminated material #Rapidly progressive dementia -Onset of subtle changes in memory and behavior to death is only 7 months -FATAL, no treatment known, like ALL prion diseases #Microscopy: - Multifocal spongiform transformation (Intracellular vacuoles in neurons and glia) of cortex & deep gray matter→ multiple small empty microscopic vacuoles , most in caudate &putamen. **- No inflammatory response - Advanced cases:Neuronal loss ,Gliosis

Answer 52

- Mainly in Immunocompromised patient - Hematogenous or direct invasion - Parenchymal granulomas or abscesses, often associated with meningitis -AIDS patients are prone to cryptococcal meningoencephalitis -Candida, Cryptoccocus , Aspergillus, & Mucor

Answer 53

``` #Candida albicans : Multiple microabscesses, with or without granuloma formation. ``` #Mucormycosis : -Presents as an infection of the nasal cavity or sinuses of a diabetic patient with ketoacidosis. -May spread to the brain through vascular invasion or by direct extension through the cribriform plate. #aspergillus:Widespread septic hemorrhagic infarctions, #Cryptococcus neoformans: -Meningitis or meningoencephalitis -Immunosuppressed patients - Extension into the brain follows vessels in the Virchow-Robin spaces. - As organisms proliferate, these spaces expand, giving rise to a “soap bubble”–like appearance

Answer 54

#Partial failure or reversal of neural tube closure ``` #-Genetic factor. -Folate deficiency during the initial weeks of gestation ``` ``` #- Prenatal Folate vitamins can reduce the risk up to 70%. ``` ``` #The most common defects involve the posterior end of the neural tube , -Spina bifida occulta: Asymptomatic bony defects ``` #others: meningocele , meninigomyelocele , anencephaly ,encephalocele,

Answer 55

#Myelomeningocele:Extension of CNS tissue through a defect in the vertebral column that occurs most commonly in the LS region. **- Motor and sensory deficits in the lower extremities and problems with bowel and bladder control. #meningocele: extension of the meninges wtout the SC

Answer 56

**both are Malformation of the anterior end of the neural tube: ``` #Anencephaly: absence of the brain and the top of skull. ``` #Encephalocele: diverticulum of malformed CNS tissue extending through a defect in the cranium. - It most often involves the occipital region or the posterior fossa.

Answer 57

-Megalencephaly : abnormally large brain ``` Microencephaly: Small, associated with a small head (microcephaly). ``` #- associated with chromosome abnormalities, fetal alcohol syndrome, and (HIV-1) infection acquired in utero.

Answer 58

-Disruption of neuronal migration and differentiation during development #(agyria) : absent gyration leading to a smooth-surfaced brain. #Polymicrogyria: increased number of irregularly formed gyri. #Holoprosencephaly : disruption of the normal midline patterning.

Answer 59

#The Arnold-Chiari malformation (Chiari type II malformation) : - Small posterior fossa - Misshapen midline cerebellum - Downward extension of the vermis through the foramen magnum - hydrocephalus and a lumbar myelomeningocele are also present. #Chiari type I malformation: - low-lying cerebellar tonsils that extend through the foramen magnum.

Answer 60

#Neural tube defects ``` #Hydromyelia : Expansions of the ependyma-lined central canal of the cord ``` #Syringomyelia :Development of fluid-filled cleftlike cavities in the inner portion of the cord

Answer 61

1-acute bacterial 2- acute aseptic(viral) 3-chronic bacterial meningo-encephalitis : •TB •neurosyphilis •neuroborreiosis

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pathology Flashcards

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