Pathology Flashcards
(522 cards)
Disc prolapse reason
Degeneration of annulus fibrosus -> nucleus pulposus forced out
Why is spinal cord injury serious (pathological changes)
1) neuron regeneration impossible 2) primary injury will lead to secondary injury due to hemorrhage, oedema and accumulation of necrotic cells ——— 1) Neuronal and glial cell death (1º & 2º) 2) Axontomy and intrinsic changes of injured neurons 3) Demyelination 4) Glial Scars 5) Inhibit molecules 6) Poor blood supply
Occlusion of PICA
Lateral medullary syndrome (Wallenberg syndrome) 1) Spinal trigeminal nucleus -> ipsilateral facial analgesia and thermoanesthesia 2) Spinothalamic tract -> contralateral analgesia and thermoanesthesia below neck 3) nucleus ambiguus -> dysphagia, hoarseness of voice; ipsilateral paralysis of palatal and laryngeal muscles 4) sympathetic nerve -> Horner’s syndrome
Wallenberg syndrome
PICA occlusion: Lateral medullary syndrome (Wallenberg syndrome) 1) Spinal trigeminal nucleus -> ipsilateral facial analgesia and thermoanesthesia 2) Spinothalamic tract -> contralateral analgesia and thermoanesthesia below neck 3) nucleus ambiguus -> dysphagia, hoarseness of voice; ipsilateral paralysis of palatal and laryngeal muscles 4) sympathetic nerve -> Horner’s syndrome
Occlusion of vertebral artery or ASA
Medial medullary syndrome 1) medial lemniscus -> contralateral impaired sensation of position and movement and tactile discrimination 2) corticospinal tract -> contralateral hemiparesis 3) CN XII -> ipsilateral tongue paralysis; deviation to ipsilateral side when protrude
Reticular formation lesion
Loss of life function -> death Interrupt ARAS -> sleep and coma
Brown-séquard syndrome
Hemisection of spinal cord 1) ipsilateral loss of discriminative touch and proprioceptive sense below lesion (DC/ML pathway) 2) contralateral analgesia and thermoanesthesia below lesion (spinothalamic pathway) 3) loss of all sensation at the lesion level 4) ipsilateral UMN sign below lesion (corticospinal tract) 5) ipsilateral LMN sign at lesion level
Pathological manifestation of cerebellar dysfunctions
1) Ataxia and unsteady gait 2) Error in movement range and force (intention tremor, past-pointing, dysmetria) 3) Error in movement rate and regularity (dyssynergia, dysdiadochokinesia) 4) nystagmus (normally purkinje cells exert inhibitory influence to VOR neural network) 5) Delay in initiating responses 6) hypotonus
Horner’s syndrome
Lesion of spinal cord above T1 -> sympathetic ganglion damage PAM Ptosis Anhidrosis Miosis
definition of raises ICP
Elevation of mean CSF pressure above 15mmHg when measured in lateral decubitus position
Raised ICP signs
Headache (meningeal stretching) Vomiting (brainstem distortion) Cushing’s reflex (irregular respiration, bradycardia, hypertension) Unilateral mydriasis (CN III lesion) —- Infant: separation of sutures Long term: skull bone erosion, brain atrophy
Brain herniation types
1) Subfalcine/ supra callosal 2) transtentorial/ uncal 3) reverse tentorial 4) cerebellar tonsil herniation (coning) 5) transcalvarial/ fungus
Raised ICP effect consideration
1) Age 2) stage of spatial compensation 3) rate of development 4) pressure gradient
Transtentorial herniation effects
1) compress ipsilateral CN III -> mydriasis, ophalmplegia (downward outward) 2) optic nerve and retinal vein compression -> papilloedema 2) compress aqueduct of sylvius -> hydrocephalus 3) compress vital structure - midbrain and pontine infarction and haemorrhage (loss of consciousness, bradycardia, respiration changes, hypertension) 4) contralateral cerebral peduncle pushed against tentorium -> ipsilateral hemiplegia (false localising sign) 5) compress posterior cerebral artery -> ipsilateral occipital cortex infarction -> cortical blindness
Tonsillar herniation effects
Displacement of cerebellar tonsils through foramen magnum: - compression and distortion of medulla -> apnoea
Hydrocephalus definition
CSF increase in ventricles and/or subarachnoid space
Brain swelling causes
1) cerebral oedema (vasogenic, cytotoxic, hydrocephalic) 2) congestive brain swelling due to vasodilation alone (in hypoxia, hypercapnia, loss of vasomotor tone)
UNN vs LMN lesion
Location: CNS vs CNS/PNS Structure: cortex/corticospinal tract/ corticobulbar tract vs alpha motor neurons/ motor fibres in cranial or spinal nerves Distribution: groups of muscles vs segmental muscle fibres Spastic paralysis vs flaccid paralysis Hyperreflexia vs hyporeflexia Mild disuse muscle atrophy vs pronounced muscle atrophy Babinski sign vs none
Common sites of metastatic intracranial tumour
~25% Lung, breast, kidney and malignant melanoma Metastatic choriocarcinoma common in Chinese female
Primary intracranial carcinoma classified by origin
- Neuroectodermal tumours a. Glial cells (gliomas) - astrocytoma - ependymoma - oligodendroglioma - etc b. Neurons and primitive cells - neuroblastoma - medulloblastoma 2. Other structure tumours E.g. Meningioma, schwannoma, pituitary adenoma, carniopharngioma, haemangioblastomas
Supratentorial intracranial tumours
CEREBRAL LOBE AND DEEP HEMISPHERE - astrocytoma - glioblastoma - meningioma - metastatic tumours SELLA TURCICA - pituitary adenoma - carniopharyngioma
Intracranial tumours in ventricular system
Ependymoma Choroid plexus papilloma
Sites of cerebral astrocytoma, glioblastoma and oligodendroglioma
Commonly in frontal and temporal lobe; uncommon in occipital lobe
Biological malignancy of intracranial tumours
1) while histologically well differentiated, neuroectodermal tumours are rarely encapsulated and diffusely infiltrate tissues 2) may be in inoperable sites e.g medulla, pons, midbrain or deep hemisphere 3) may become histologically malignant with years, esp astrocytoma to glioblastomas multiforme