K-11 Patologi Ao

8/10/2019 K-11 Patologi Ao

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DEPARTEMEN PATOLOGI ANATOMIFAKULTAS KEDOKTERAN

UNIVERSITAS SUMATERA UTARA MEDAN

2013


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PNS

Kumpulan neuron = ganglia

CNS

Kumpulan dari neuron = nuclei

10/23/2014 2DEP. PATOLOGI ANATOMI FK-USU 2013
http://www.abta.org/primer/brain.htm


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10/23/2014 DEP. PATOLOGI ANATOMI FK-USU 2013 3


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BRAIN

Consist in large part of 2 cell types

NEURONS GLIAL



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Have :

Cell body Dendrites

intergrating signals

Axon


NEURONS


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6DEP. PATOLOGI ANATOMI FK-USU 201310/23/2014
http://www.pbrc.hawaii.edu/~kunkel/gallery/medical/page011/08418b.htmlhttp://www.pbrc.hawaii.edu/~kunkel/gallery/medical/page011/08418b.html


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90% of all CNS cells

Stuctural & functional support for neuronal elements

Functions include:

Glia-neuronal signaling

Extracellular buffering electrolytes & metabolites Turnover neurotransmitters


GLIAL


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Glial divided into :

Macroglial

Astrocyte

Oligodendrocyte

Ependymal

Microglial

-



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CELLULAR REACTIONS

Neurons Acute (REDneuron, karyolysis)

Subacute, chronic, cell loss, gliosis

Axonal Inclusions (lipid, prot., carb., viruses)

Glia, gliosis Swelling Fibers

Inclusions10/23/2014 10DEP. PATOLOGI ANATOMI FK-USU 2013


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ACUTE NEURONAL INJURY

RED NEURONS10/23/2014 11DEP. PATOLOGI ANATOMI FK-USU 2013


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Hallmark Chronic CNS injury

Neuronal loss

&

Gliosis


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Normal motor units :

Two adjacent motor units



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Abnormal motor units

Segmental demyelination:

Axon & myocytes remain intact


Random internodes of myelin are injured

Remyelinated by multiple Schwann cells


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Axonal degeneration:

Resulting :


Axon & myelin sheath undergo

anterograde degeneration (green)

Denervation atrophy

of the myocytes within itsmotor unit


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Reinnervation of muscle:

Sprouting of adjacent (red)

uninjured motor axons leads to

fiber type grouping of myocytes

Injured axon attempts axonal

sprouting



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Myopathy :

Scattered myocytes of adjacent

motor units are small

(degenerated / regenerated)

Neurons & nerve fibers are

normal



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20DEP. PATOLOGI ANATOMI FK-USU 201310/23/2014
http://biomed.brown.edu/Courses/BIO189/Lab4/spinalcord.jpghttp://biomed.brown.edu/Courses/BIO189/Lab4/drganglion.jpg


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PERIPHERAL NERVE

Same categories of

disease as other tissues

The pattern of disease,

reflects the unique structure & function of nerves

Inflammatory

Traumatic

Metabolic

Toxic

Genetic

Neoplastic



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INFLAMMATORY NEUROPATHIES

Characterized by inflammatory cell infiltrates in :

Peripheral nerves

Roots

Sensory

Autonomic ganglia

Immune mechanisms

presumed to be the primary cause of the inflammation



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Immune-Mediated Neuropathies

Guillain-Barr Syndrome

(Acute Inflammatory Demyelinating

Polyradiculoneuropathy)

Chronic Inflammatory Demyelinating

Polyradiculoneuropathy



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(Acute Inflammatory Demyelinating Polyradiculoneuropathy)

Is a life-threatening disease PNS

Incidence (U.S.)1 -3 / 100.000

persons



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Characterized clinically :

Weakness

beginning in the distallimbs

Rapidly advancing to affectproximal muscle function("ascending paralysis")

Microscopic :

Inflammation & demyelinationof spinal nerve roots & peripheral nerves

(radiculoneuropathy)



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Chronic Inflammatory DemyelinatingPolyradiculoneuropathy

In some patients :

Acute Guillain-Barrsyndrome

Subacute / chroniccourse

Usually :

Relapses & remissions

over the period ofseveral years

Often symmetric Mixed sensorimotorpolyneuropathy

Some patients

predominantlysensory / motor

impairment



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INFECTIOUS POLYNEUROPATHIES

Many infectious processes affect peripheral nerve

Cause unique and specific pathologic changes in

nerves

Leprosy Diphtheria Varicella zoster



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Evidence of recurrent demyelination

With well-developed onion bulb structures

Remyelination

Steroid treatment

Plasmapheresis

Biopsies of sural nerves show :

Clinical remissionsoccur with :



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Leprosy

Lepromatous &

tuberculoid leprosyPeripheral nerve involvement in

Mycobacterium

leprae

Invade Schwann

cells

Proliferates &

infects other cells



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Diphtheria

Peripheral nerve

involvementEffects of diphtheria exotoxin

Begins withparesthesias

and weakness

Early loss ofproprioception

Vibratorysensation



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Earliest changes seen in :

Sensory ganglia

Incomplete blood-nerve barrierallows

entry of the toxin

Selective demyelination of axonsextends

into adjacent anterior & posterior roots(mixed sensorimotor nerves)



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Varicella zoster

The most common viral infections of PNS

ReactivationPainful,

Vesicular skineruption

Distribution of sensorydermatomes (shingles), most

frequently thoracic ortrigeminal

Chickenpox

Latent infection neurons in

sensory ganglia of spinal cord & brain stem



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Varicella zoster

VirusTransported alongthe sensory nerves

To the skin

(where it establishesan active infection

of epidermal cells)



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Varicella zoster

Ganglia :

Neuronal destruction & loss

Abundant mononuclear

inflammatory infiltrates

Regional necrosis with hemorrhagemay also be found

Peripheral nerve :

Axonal degeneration after thesensory neurons death

Focal destruction of large motorneurons of the anterior horns

/cranial nerve motor nuclei

Intranuclear inclusions in PNS (-)



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Classical Disease Patterns

Degenerative

Inflammatory Neoplastic



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Classical CNSDisease Patterns

Degenerative

Inflammatory Neoplastic

Traumatic



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CNS MALFORMATIONS

Neural Tube

Anencephaly, Encephalocele, Spina Bifida

Forebrain

Polymicrogyria, Holoprosencephaly, Agenesis of Corpus

Callosum

Posterior Fossa (Infratentorial)

Arnold Chiari (infratentorial herniation), Dandy-Walker(cerebellar cyst)

Syringomyelia/Hydromyelia



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Fetal -protein in :

Amniotic fluid &

Maternal circulation



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SPINA

BIFIDA



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POLYMICROGYRIASmall gyri



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HOLOPROSENCEPHALYFailure prosencephalon to develop, and separate, often leads to cyclops.


CEREBRAL EDEMA


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CEREBRAL EDEMA(Normal weight 1200-1300 grams)

Vasogenic

(disrupted BBB)

IntravascularINTER-cellular

[ECS/EXTRACellular Space]

Cytotoxic

INTRA-

cellular space



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Gyrus mendatar

Sulcus menyempit

Rongga ventrikel tertekan

CEREBRAL EDEMA



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CEREBRAL EDEMA

Subfalcine (SUPRA-tentorial)

Cingulate (TENTORIAL)

Cerebellar tonsilar (SUB-tentorial, orINFRA-tentorial)



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CEREBRAL EDEMA

D.D.:

EVERYTHING

SYMPTOMS

HEADACHE

HALLUCINATIONSCOMA

DEATH



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HYDROCEPHALUS Impaired RESORPTION Increased PRODUCTION

OBSTRUCTION

COMMUNICATING (entire)

NON-COMMUNICATING (part)

HIGH Pressure

NORMAL Pressure



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PERINATAL Brain Injuries

Cerebral Palsyrefers to non-progressive diffuse cerebralpathology apparent at childbirth

Three most

common types

of perinatal

brain injuries

Intraparenchymal Hemorrhage

Intraventricular hemorrhage(premies)

Periventricular leukomalacia

(i.e., infarcts)



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Various patterns of CNS injury in newborns



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CNS TRAUMA Skull Fractures

Parenchymal Injuries

Traumatic Vascular Injury

Sequelae

Spinal Cord Trauma



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BRAIN TRAUMA

Contusion (bruise)

Laceration (tear)

Coup/Contre-Coup

Concussion



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HAIRLINE DEPRESSED,aka

DISPLACED10/23/2014 58DEP. PATOLOGI ANATOMI FK-USU 2013

Skull fracture types


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HEMATOMAS/HEMORRHAGE

EPIDURAL(fx)

SUBDURAL(trauma No fx)

SUBARACHNOID(arterial, no trauma)

INTRAPARENCHYMAL(any)

INTRAVENTRICULAR(no trauma, rare in

adults, common in premies)



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EPIDURAL HEMATOMA


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EPIDURAL HEMATOMA


The lucid interval is a classic feature of the epidural

hematoma


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SUBDURAL HEMATOMA


No lucid interval, but instead a sudden &

progressive worsening of symptoms


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SUBARACHNOID10/23/2014 64DEP. PATOLOGI ANATOMI FK-USU 2013


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INTRAPARENCHYMAL10/23/2014 65DEP. PATOLOGI ANATOMI FK-USU 2013


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SPINAL CORD TRAUMA

Parallels BRAIN patterns of injury ona cellular basis

Usually secondary to spinal columndisplacement

Level of injury mirrors motor loss:Death Quadriplegia Paraplegia



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Cerebrovascular Diseases


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Cerebrovascular Diseases

(CVA, Stroke)

Ischemic ( blood and 02) Global

Focal (regional):

ACUTE: edema neuronal microvacuolization pyknosiskaryorrhexis neutrophils

CHRONIC: macrophages gliosis

Hemorrhagic(rupture of artery/aneurysm)



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HYPERTENSIVE CVA

Intracerebral

Basal Ganglia Region(lenticulostriate arteries of internal capsule,putamen)


SUBARACHNOID


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SUBARACHNOID

HEMORRHAGE

Rupture of large intracerebral arterieswhich are the primary branches of the

anatomical circle (of Willis) Congenital(berry aneurysms)

Atherosclerotic(atherosclerotic

aneurysms, or direct wall rupture)



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CNS DEGENERATIVE DISEASES

CORTEX

Dementias

BASAL GANGLIAand BRAIN STEM

Parkinsonism

SPINOCEREBELLAR

Ataxias

MOTOR NEURONS

Muscleatrophy



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THANK YOU

SELAMAT BELAJAR

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