Term
| This causes what? Edema and tumors will increase brain tissue volume; Tumor and edema increases brain tissue volume; hydrocephalus accumulation of CSF in ventricular system from impaired flow, HTN, hemorrhage, VD |
|
Definition
|
|
Term
|
Definition
| increases brain tissue volume |
|
|
Term
|
Definition
| increases brain tissue volume |
|
|
Term
|
Definition
| increases brain tissue volume |
|
|
Term
| How does hydrocephalus increase ICP |
|
Definition
| CSF accumulates in ventricular system from impaired flow, reabsorption or overproduction of csf |
|
|
Term
| What does HTN and hemorrhage, VD cause to ICP |
|
Definition
|
|
Term
| Clniical: Retinal edema, decreased perfusion , tissue atrophy due to compression, reflex increase in BP to maintain perfusion, change in LOC due to ischemia, herniation |
|
Definition
|
|
Term
| Ischemia, altered neuronal conduction, compression of cortical structure or compression of ascending reticular activating system or other cognition pathways |
|
Definition
| Change in LOC in Increased ICP |
|
|
Term
|
Definition
Epidural
Subdural
Subarachnoid hemorrhage/intraparenchymal |
|
|
Term
| Collection of arterial blood between the dura mater and cranium, Expands Rapidly |
|
Definition
| Epidural (extradural) hematoma |
|
|
Term
| Collection of blood between the dura and arachnoid, usually venous--slower blood |
|
Definition
|
|
Term
| Blood escapes into the subarachnoid space, intraparenchymal hemorrhage |
|
Definition
| Subarachnoid hemorrhage/intraparenchymal hematomas |
|
|
Term
| Irritation of meninges, disruption of CSF circulation/absorption --causes rise in ICP |
|
Definition
| Blood escaping into subarachnoid space during hematoma |
|
|
Term
| What does intraparenchymal hemorrhage cause? |
|
Definition
|
|
Term
| Brief and reversible impairment of neurologic function due to interruption of blood flow |
|
Definition
|
|
Term
| Neuronal cell death from ischemia or hypoxia, sx last seconds to hours |
|
Definition
| TIA, neurological function impairment due to blood flow disruption |
|
|
Term
| Risk for reoccurence of TIA |
|
Definition
| 30% at 3 mo. 60% at 6 mo, 80% one year |
|
|
Term
| Sudden onset of focal neurologic deficit that persists for at least 24 hours; due to an abnormality of cerebral circulation |
|
Definition
|
|
Term
| Thrombotic, Lacunar, Embolic |
|
Definition
|
|
Term
Common sites of ?type of ischemic stroke?
internal carotid, middle cerebral artery, posterior cerebral artery, basilar artery |
|
Definition
| Thrombotic-ischemic stroke |
|
|
Term
| This causes what ? type of ischemic stroke? microinfarcts that involve small arteries |
|
Definition
| Lacunar type of ischemic stroke |
|
|
Term
| This causes what? type of ischemic stroke: emboli traveling heart, aorta, carotid, occluding middle cerebral artery, and emboli in vertebral and basilar arteries, occludes basilar artery and posterior cerebral arteries |
|
Definition
| Embolic type of ischemic stroke |
|
|
Term
| This causes what? type of ischemic stroke: emboli traveling heart, aorta, carotid, occluding middle cerebral artery, and emboli in vertebral and basilar arteries, occludes basilar artery and posterior cerebral arteries |
|
Definition
| Embolic type of ischemic stroke |
|
|
Term
| What artery carries 80% of blood flow to cerebral hemispheres? |
|
Definition
| Middle cerebral artery--common site for embolic ischemic stroke, emboli traveling heart, aorta and carotids |
|
|
Term
| What arteries do emboli traveling vertebral and basilar arteries occlude? |
|
Definition
| basilar artery, posterior cerebral arteries |
|
|
Term
| Patho: nerve cells in the ischemic focus are damaged and killed by energy deprivation, neurons die at the edges from excessive stimulation of glutamate receptors: Neuronal Excitotoxicity |
|
Definition
|
|
Term
|
Definition
|
|
Term
| depletion of energy supplies-inhibits Na+K+ATPase-loss of normal transmembrane ion gradient |
|
Definition
| Ischemia depletes brain tissue energy supplies in patho of ischemic stroke |
|
|
Term
| Neuronal excitotoxicity (glutamate toxicity) |
|
Definition
| neurons die from excesive stimulationof glutamate receptors |
|
|
Term
| Cause of increased intracellular Na+ and increased extracellular K+ in patho of ischemic stroke |
|
Definition
| ischemia depleting brain tissue energy supplies: inhibits Na,K, ATPase-loss of normal transmembrane ion gradient |
|
|
Term
| increased intracellular Na+ in patho of ischemic stroke does what to Na+ dependent glutamate uptake? |
|
Definition
| Reduces Na+ dependent glutamate uptake |
|
|
Term
| Increased K+ depolarizes nerve termials in patho of ischemic stroke and causes? |
|
Definition
| release of glutamate from nerve terminals |
|
|
Term
| What does increased K+ depolarizing nerve terminals release from the nerve terminals? |
|
Definition
| glutamine: patho of ischemic stroke |
|
|
Term
| What happens with increased levels of extracellular glutamate? |
|
Definition
| excessive stimulation of glutamate receptors: increase in Ca2+ influx, directly stimulates NO production in neurons (patho of ischemic stroke) |
|
|
Term
| Stimulates sustained activation of enzymes that cause protein breakdown, free radical formation, lipid peroxidation, fragmentation of DNA and nuclear breakdown in the neuron |
|
Definition
| Increase of Ca2+ influx due to increased glutamate causing stimulation of glutamate receptors: patho of ischemic stroke |
|
|
Term
| Sustained activation of enzymes from increased Ca2+ influx causes? in ischemic stroke patho? |
|
Definition
| Cell death, glutamate receptor antagonists given to reduce size of ischemic lesions, and causes neuronal brain injury. Cell body shrinkage, nucleolus disappears and Nissl substance loss. |
|
|
Term
| Shrinkage of cell body, nucleolus disappearance, nissl substance loss; Injured axons swell and transport disrupted; Inflammatory response |
|
Definition
| Neuronal injury to the brain from sustained activation of enzymes during patho of ischemic stroke |
|
|
Term
| Wallerian degeneration followed by sprouting; proper guidance for sprouts is generally lacking; neuronal loss can't be replaced |
|
Definition
| Injured axons swelling and axonal transport disrupted: patho of ischemic stroke from cell death |
|
|
Term
| Inflammatory response in neuronal injury of the brain causes? |
|
Definition
| Vasodation leading to increased ICP |
|
|
Term
Patho of:?
-nerve cells damaged and killed by energy deprivation
-neurons die from excessive stimulation of glutamate receptors
-activation of astrocytes
-activation of microglia |
|
Definition
|
|
Term
| astrocytes undergo hypertrophy, hyperplasia; responsible for repair and scar formation that can lead to seizure focus |
|
Definition
| Astrocyte activation; patho of ischemic stroke |
|
|
Term
| Microglia proliferate, function as phagocytes of CNS |
|
Definition
| Activation of microglia in patho of ischemic stroke |
|
|
Term
| Etiology?: hypertension (Charcot-Bouchard) , Rupture of aneurysm or AV malformation or weakened vessel; spontaneous from platelet and coagulation disorders; cocaine and amphetamines |
|
Definition
|
|
Term
| How does hypertension (Charcot-Bouchard) cause a hemorrhagic CVA? |
|
Definition
| rupture of small intraparenchymal vessels, common are small vessels supplying the basal ganglia, thalamus, pons and cerebellum |
|
|
Term
| Common site of hemorrhagic CVA |
|
Definition
| small vessels to the basal ganglia, thalamus, pons and cerebellum |
|
|
Term
| most common form of aneurysm |
|
Definition
| congenital (berry): rupture will cause hemorrhagic CVA |
|
|
Term
| tangle of fragile abnormally tortuous misshapen vessels |
|
Definition
|
|
Term
| How does cocaine and amphetamines cause hemorrhagic stroke? |
|
Definition
| rapid elevation of BP or drug induced vasculitis |
|
|
Term
| Patho: Hemorrhage and inflammation and edema causes inc ICP, secondary vasospasm from blood toxicity causes ischemia; compression ischemia/neuronal cell death |
|
Definition
|
|
Term
|
Definition
|
|
Term
| responsible for maintenance of a waking state and arousal |
|
Definition
| RAS: reticular activating system |
|
|
Term
| What is cognition mediated by? |
|
Definition
| Functional cerebral cortex |
|
|
Term
| Etiology of?: destructive mechanisms in brain (lesions in RAS, hemorrhages, etc.), or Compressive Mechanisms; Metabolic-Toxic Mechanisms; Psychogenic arousal alterations |
|
Definition
| Disorders of Arousal and Cognition |
|
|
Term
| Disorders of Arousal and Cognition |
|
Definition
| Types of Mechanisms: Destructive, Compressive, Metabolic-Toxic, and psychogenic arousal alterations |
|
|
Term
What type of mechanism causing an arousal or cognition disorder are these?
Lesions in the RAS
Hemorrhages, ischemic infactions, absesses or tumors in cerebral hemi
Deposition of neuritic plaques/neurofibrillary tangles, amyloid deposits |
|
Definition
| Destructive Mechanisms of arousal/cognition disorders |
|
|
Term
| What type of mechanism are the following: substrate depletion, hypoxia, toxins, fluid and lytes imbalance (in arousal/cognition disorders) |
|
Definition
| Metabolic-toxic mechanisms |
|
|
Term
| Intermittent disturbance in cerebral function caused by abnormal syndhronous discharge of cortical neurons |
|
Definition
|
|
Term
|
Definition
|
|
Term
Patho of?: epileptogenic focus
spread of local discharge
synchronous discharge of seizure |
|
Definition
|
|
Term
| abnormally excitable area of the brain |
|
Definition
Epileptogenic focus--has three factors:
-patho excitable neurons-maybe low threshhold, inc perm or chronic state of partial depol
-more excitatory glutamate transmission
-inhibitory system (usu GABA) disrupted |
|
|
Term
inhibitory system disrupted (usu GABA)
incr excitatory glutamate transmission
-excitable neurons with low threshold, inc perm or always in a state of partial depol |
|
Definition
| epileptogenic focus: abnormally excitable area: patho of seizure |
|
|
Term
| Step in a seizure after a epileptogenic focus |
|
Definition
| Spread of local discharge: enhancement of excitatory stimuli (due to three reasons: extracell K+ depolarized near neurons; more disharges CA+ influx; and less inhibitory stimuli |
|
|
Term
| How does extracellular K+ enhance excitatory stimuli in spreading of local discharge during a seizure? |
|
Definition
| Extra cell K+ accumulates around the epileptogenic focus; when neuron depolarizes Na IN, K out, it depolarizes nearby neurons |
|
|
Term
| How does increased freq of discharges cause epileptogenic focus to spread a seizure? |
|
Definition
| The increased frequency of discharge (from K+ influx) enhances CA+ influx into nerve terminals and that increases neurotransmitter release at excitatory synapses |
|
|
Term
| What happens to fibers from excitatory neurons in secondary epilepsy? |
|
Definition
| fibers from excitation neurons sprout |
|
|
Term
| How does a reduction in inhibitory stimuli cause the spread of a local discharge in epilepsy? |
|
Definition
| Desensitization of GABA receptors with hi freq stimulation, and in secondary epilepsy: loss of inhibitory circuits |
|
|
Term
| synchronous discharge in the brain |
|
Definition
|
|
Term
| Sudden attack of altered consciousness, motor activity or sensory phenomena |
|
Definition
|
|
Term
| In what phase do inhibiting neurons in other parts of the brain inhibit cortical excitation to cause the interruption in seizures, thus control? |
|
Definition
| Clonic: Tonic,Clonic,Post-ictal confusion |
|
|
Term
| autoimmune demyleinating disorder characterized by episodes of neurologic deficits, due to diffuse demyleinating white matter lesions |
|
Definition
|
|
Term
| Patho: CD4 T autoreact to myelin basic protein (MBP), protein on sheath; TH1 secretion of cyto and inflam, CD8T and B activate against MBP, get demylelinated patches (axons OK), Remylelinate with thin sheath, exacerbations with permanent disruption in conduction |
|
Definition
|
|
Term
| patho: CD4 T cell autoreactivity to a single myelin basic protein(MBP), protein in membrane of myelin sheath |
|
Definition
|
|
Term
| patho: Th1 secretion of cytokines/inflamm response reacts to ?? in patho of MS? |
|
Definition
| CD4 T cell autoreactivity to single MBP-protein in membrane of myelin sheath |
|
|
Term
| Patho: What do macrophage (microglia), CD8 T cell and B cell activation react against in MS |
|
Definition
| Myelin basic Protein (MBP) protein in myelin sheath |
|
|
Term
| What happens to axons when demyleinated patches or placques develop in MS? |
|
Definition
|
|
Term
| Repeated exacerbations of autoimmune activity and oligodendrocyte injury; Gliosis, permanent placques with scarring |
|
Definition
|
|
Term
| permanent plaques of sharply defined areas of gray discoloration of white matter, and permenent disruption in conducton |
|
Definition
| Gliosis (glial scarring) glisa=neurolgia |
|
|
Term
| clinical: episodes of neurologic deficit followed by gradual, partial remission; as progresses, less improvement between exacerbations/increased neurological dysfunction |
|
Definition
|
|
Term
| Plaque in optic nerve causing visual disturbances; plaque in spinal cord and brain stem-causing paraesthesia, numbness, less proprioception, thermal sense, pain |
|
Definition
| Sensory clinical manifestations of MS |
|
|
Term
Plaque in brain stem causing ataxia, nystagmus, paralysis, hyperreflexia, less coordination,
plaque in spinal cord causing motor impairment of trunk and limbs |
|
Definition
| Motor clinical manifestations of MS |
|
|
Term
| Bladder incontinence, impotence |
|
Definition
|
|
Term
| What type of disorders is Alzheimer's Disease, |
|
Definition
| Degenerative disorder of the cerebral cortex |
|
|
Term
| Proposed patho: Neuritic plaques, Amyloid beta peptid production, neurofibrillary tangles, loss of neurons/transmission, Inflamm response to AB deposits |
|
Definition
|
|
Term
| patho: collection of neuritic processes around a central amyloid AB peptide core, interferes with synaptic transmission of Acetylcholine, tends to occure in hippocampus, amygdala, and cortex |
|
Definition
| Neuritic plaques in Alzheimer's Disease |
|
|
Term
| Formed from abnormal breakdown of Amyloid Precursor Protein (APP),and breakdown products do not produce the AB peptide that is usually cleared from the brain |
|
Definition
| Amyloid Beta Peptid Production (major protein in neuritic plaques) patho of alzheimer's |
|
|
Term
| usually synthesized by neuronal membrane and expressed on cell surface, neurons use this to support the growth of neurites |
|
Definition
| Amyloid Precursor Protein (APP) When abnormally broken down the products form plaques in Alzheimer's Disease |
|
|
Term
| microtubular proteins in the neuron become distorted, twisted, displace or encircle nucleus and interfere with funcition,get neuronal loss; Insoluable and persist in tissue after cell death |
|
Definition
| Neurofibrillary tangles (patho of alzheimers) |
|
|
Term
| Neurofibrillary tangles--what disease |
|
Definition
| Alzheimers, microtubular proteins become tangled causing neuronal dysfunction/loss, are insoluble so cell death |
|
|
Term
| patho: Loss of neurons and interference with normal transmission |
|
Definition
|
|
Term
| What is the inflammatory response to AB deposits (amyloid beta peptid-protein in neuritic plaques) |
|
Definition
| oxidative damage, alteration in Calcium homeostasis (Alzheimer's patho) |
|
|
Term
| Progressive dementia from progressive neuronal loss and reductions in brain acetylcholine and other neurotransmitters |
|
Definition
|
|
Term
| what phase? impairment of higher intellectual function and alteration in mood and behavior |
|
Definition
|
|
Term
| Progressive disorientation, memory loss, aphasia and functional decline |
|
Definition
|
|
Term
| profoundly disabled, mute and immobile |
|
Definition
|
|
Term
| What does neuronal loss in AD lead to in the brain |
|
Definition
|
|
Term
| Two types of degenerative diseases of basal ganglia and brain stem |
|
Definition
Huntington's Disease
Parkinson's Disease |
|
|
Term
| Huntinton's Disease, Parkinson's Disease: what types of disease? |
|
Definition
| degenerative disease of brain stem and ganglia |
|
|
Term
| Etiology: idiopathic (most common), gene mutations, exposure to toxins/heavy metal, herbicides causing free radical damage to dopamine secreting neurons; Drugs that are dopamine depleters; trauma/other disease |
|
Definition
|
|
Term
| What type of drugs are dopamine depleters? |
|
Definition
| Anti-psychotic drugs, can be a cause of Parkinson's Disease |
|
|
Term
| Designer drugs MPTP-cause free radical damage to dopaminergic neurons |
|
Definition
|
|
Term
Patho: loss of dopaminergic neurons in substantia nigra and nigrostriatial pathway, decreased dopamine, loss of normal dopamine/acetylcholine balance in striatum:
All result in increased inhibitory output from striatum |
|
Definition
|
|
Term
| Pale substantia nigra; LEWY bodies--neuronal filaments around a protein core |
|
Definition
| Histology of Parkinson's Disease |
|
|
Term
| clinical: Increases striatal inhibitory output causes: diminished facial expression, akinesia/bradykinesia (slowness of voluntary movement); rigidity, pill rolling tremor; postural instability caused by loss in speed of normal postural reflexes; depression, slow thinking |
|
Definition
|
|
Term
| Hereditary disease with progressive movement disorders, dementia, and neuronal degeneration in the corpus striatum and frontal cerebral cortex |
|
Definition
|
|
Term
| disorder of corpus striatum and frontal cerebral cortex |
|
Definition
|
|
Term
| disorder of substantial nigra or nigrostriatal pathway |
|
Definition
|
|
Term
| disorder of cerebral cortex |
|
Definition
|
|
Term
| Etiology:genetic-autosomal dominant mutation to chromosome 4, encodes a protein, mutatin increases the number of CAG repeats, inversely R/T age of onset, increasing repeats earlier disease |
|
Definition
|
|
Term
| Patho: mutant protein damages brain neurons, proposed: causes functinal abnormalities in mitochondria, mutant protein is degraded and forms aggregates; mutant protein fails to fold properly; loss of neurons of corpus striatum (caudate nucleus and putamen): results of above decreased striatal inhibitory control, less modulation of movement |
|
Definition
|
|
Term
| Insufficient supply of energy for cell function and interferes with manufacture and packaging of neurotransmitters, interferes with manufacture of antioxidants leading to ROS damage |
|
Definition
| Mutant protein in Huntington's disease causing these functional abnormalities in mitochondria |
|
|
Term
| In Huntington's, what happens when the mutant protein is degraded and form aggregates? |
|
Definition
| interferes with normal neuronal function |
|
|
Term
| In Huntington's, what happens when the mutant protein fails to fold properly? |
|
Definition
| Accumulation of misfolded protein triggers apoptosis |
|
|
Term
clinical: involuntary, rapid jerky movements (chorea), slow writhering movements of limbs and trunk (athetosis);
cognitive impairment, dementia, depression;
dopamine antagonists reduce involuntary movement: block inhibition of remaining striatal neurons |
|
Definition
|
|
Term
| involuntary, rapid, jerky movements |
|
Definition
|
|
Term
| slow writhering movements of limbs and trunk |
|
Definition
|
|
Term
| types of disease: Amyotrophic Lateral Sclerosis |
|
Definition
| Degenerative disease of upper and lower motor neurons |
|
|
Term
| progressive neuromuscular disorder that is caused by the degeneration of upper and lower motor neurons |
|
Definition
| Amyotrophic Lateral Sclerosis |
|
|
Term
| upper and lower motor neuron disorder |
|
Definition
|
|
Term
| Patho: defect (gene encoding SOD1)interferes with enzymes that produce SOD1(superoxide dismutase); genetic mutation may cause misfolding of the protein (apoptosis); clutamate toxicity can also contribute to neuronal loss; results: degen and loss of upper and lower motor neurons, so skeletal myo denervatin and atrophy |
|
Definition
| Amyotrophic lateral sclerosis |
|
|
Term
| What happens in ALS when the defect interferes with enzymes that produce SOD 1 (anti-oxidant)? |
|
Definition
| free radical damage to upper and lower motor neuron and neuronal degeneration and loss |
|
|
Term
| When genetic mutation causes misfolding in ALS, what happens to the protein? |
|
Definition
|
|
Term
| What does glutamate toxicity result in? |
|
Definition
neuronal loss.
ALS patients have raised levels of glutamate in the fluid that surrounds the brain and spinal cord) |
|
|
Term
| Loss of upper motor neurons in ALS includes what? |
|
Definition
| degeneration and loss including corticobulbar tracts |
|
|
Term
| Loss of lower motor neurons in ALS includes what? |
|
Definition
| degeneration and loss in corticospinal tracts in the lateral portion of the spinal cord and loss of anterior horn cells |
|
|
Term
| Skeletal muscle denervation and skeletal muscle atrophy is a result of ??? in what disease? |
|
Definition
| degeneration and loss of upper and lower motor neurons in ALS |
|
|
Term
| Clinical: muscle weakness, atrophy, loss of use; hyperreflexia and spasticity of arms and legs; cramping and fasciculations; bulbar myo cause speech, swallowing, breathing, coughing; preservation of INTELLECT; fatal in 3-5 years |
|
Definition
|
|
Term
| Early manifestations of muscle weakness and atrophy in ALS |
|
Definition
| asymmetric weakness of hands and difficulty in fine motor |
|
|
Term
This results in what in ALS?
degeneration of corticospinal tract neurons>release of reflexes from inhibition |
|
Definition
| Hyperreflexia and spasticity of arms and legs |
|
|
Term
| Involvement of bulbar muscles in ALS result |
|
Definition
| difficulty with speech, swallowing, breathing, coughing (no involvement of III, IV, or VI |
|
|
Term
| Reason ALS is fatal in 3-5 years |
|
Definition
| involvement of respiratory muscles and pulmonary infectin |
|
|
Term
|
Definition
|
|
Term
Etiology:
neonate B strep, E. Coli;
infants, children, adults: H-influenze, Neissseria meningitides (meningococcal meningitis) and strep pneumonia |
|
Definition
|
|
Term
| Patho: entry into CNS through choroid plexus or altered blood brain barrier; multiply in subarachnoid space, followed by inflamm response with damage, and final scar tissue formation and neuron loss |
|
Definition
|
|
Term
| Why do bacteria multiply in the subarachnoid space in the brain? |
|
Definition
| Host defenses are inadequate to control infection here |
|
|
Term
| In inflamm response of bacterial meningitis: what does the cytokine release result in? |
|
Definition
| TNFa, IL-1, and other proinflamm cause neuronal injury |
|
|
Term
| In inflamm response of bacterial meningitis: what does the increased permeability of blood-brain barrier cause? |
|
Definition
|
|
Term
| In inflamm response of bacterial meningitis: what does vasodilation cause? |
|
Definition
| ruptures in small vessels causing bleeding |
|
|
Term
| In inflamm response of bacterial meningitis: what does the stimulation of the clotting cascade cause? |
|
Definition
|
|
Term
| In inflamm response of bacterial meningitis: what does neutrophil migration into the subarachnoid space cause? |
|
Definition
| Thick exudate, interferes with normal CSF drainage causing hydrocephalus |
|
|
Term
Clinical: meningeal irritation and inc ICP (HA, photophobis, nuchal rigidity, altered mentation, irritable, fever);
CSF-cloudy, WBC's, hi protein, low sugar;
meningococcal meningitis will cause a petechial rash;
Complications: septicemia, secondary brain infection or abscess, herniation |
|
Definition
|
|
Term
| Disorders of the Visual System |
|
Definition
Common visual field defects
Glaucoma
Retinal disorders |
|
|
Term
prechiasmal lesions
lesions that compress central portion of chiasm
retrochiasmal lesions (behind chiasm) |
|
Definition
| Common Visual Field Defects |
|
|
Term
complete lesions of the optic nerve
partial lesion of the optic nerve |
|
Definition
|
|
Term
| What does complete lesions of the optic nerve cause? |
|
Definition
| Blindness in eye affected |
|
|
Term
|
Definition
| partial lesion of optic nerve, impaired vision in the ipsilateral side (same side) |
|
|
Term
| What type of vision loss would you see in hemianopia |
|
Definition
| one half of vision blocked outer vertical half |
|
|
Term
| What type of vision loss would lesions that compress the central portion of the chiasm result in? and what could this be? |
|
Definition
| Bitemporal hemianopia: loss of temporal half of each eye. loss of outer vertical both eyes: Pituitary tumors |
|
|
Term
| What type of vision loss would retrochiasmal lesions produce (behind the chiasm) |
|
Definition
| Lesions on the optic tract and optic radiation: visual loss in the contralateral field of both eyes. vertical loss, both left side or right side of each eye. (Homonymous hemianopia) |
|
|
Term
| What type of vision loss would retrochiasmal lesions produce (behind the chiasm) Partial lesions across optic tract or optic radiation |
|
Definition
| superior quadrantanopia: quarter vision loss, same quad each eye. Superior upper, or inferior quadrantanopia |
|
|
Term
| Most common form of glaucoma |
|
Definition
|
|
Term
| Abnormality/blockage in the trabecular meshwork slowing drainage of aqueous humor that increases intraocular pressure. |
|
Definition
|
|
Term
| What controls the flow of aqueous humor into the Canal of Schlemm? |
|
Definition
| trabelular mesh; abnormalities or blockage causes increased intraocular pressure: glaucoma |
|
|
Term
| angle formed by the cornea and iris narrows preventing aqueous humor from draining out of the eye |
|
Definition
| Angle-closure glaucoma: with aging, lens gets larger |
|
|
Term
| With aging lens grows larger, what results? |
|
Definition
| Ability of aqueous humor to pass between iris and lens on its way to the anterior chamber decreases, causing fluid pressure to build behind iris, makes arrow more narrow: ANGLE CLOSED glaucoma |
|
|
Term
|
Definition
|
|
Term
|
Definition
| types of macular degeneration |
|
|
Term
| Most common type of macular degeneration |
|
Definition
|
|
Term
| waste products from photoreceptors accumulate under retinal pigment epithelium-drusen; atrophy and degen of rod and cone photoreceptors/retimal pigment epithelium |
|
Definition
| Dry type of macular degeneration |
|
|
Term
| Subretinal neovascularization, bleeding, and scar tissue formation |
|
Definition
|
|
Term
| hearing loss due to external or middle ear problems |
|
Definition
|
|
Term
| hearing loss due to diseases of the cochlea or 8th cranial nerve |
|
Definition
|
|
Term
| hearing loss due to diseases affecting cochlear nuclei or auditory pathways in the CNS |
|
Definition
|
|
Term
| fluctuating endolymph pressure of the inner ear; dilation of membranous labyrinth (hydrops) from increased pressure, may be from decreased absorption of endolymph, blockage of endolymphatic paths, or incr productn of endolymph |
|
Definition
|
|
Term
| Possible causes of increased pressure causing dilation of membranous labyrinth (hydrops) in Meniere's |
|
Definition
decreased absorption of endolymph
blockage of endolymphatic pathways
increased production of endolymph |
|
|
Term
PATHO: trigger phase,
aura with expanding area of reduced cortical electrical activity, decreae in blood flow
activation of area in brain stem
release of pro-inflamm peptides |
|
Definition
|
|
Term
| Cause of aura in migraines |
|
Definition
| slowly expanding area of reduced cortical electrical activity and decrease in blood flow |
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Term
| patho of? activation of area in brain stem responsible for what? |
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Definition
| Migraines: physiological responses to stress and panic (locus ceruleus) and excitation of trigeminal nuclei |
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Term
1. trigeminal ganlion
2. nucleus caudalis
3. thalamus |
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Definition
| Trigeminal nerve activation in migraine |
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Term
| Patho of migraines release pro-inflamm peptides where? |
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Definition
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Term
| Platelet release of 5-HT, degranulation of mast cells, pro-inflamm peptides in meninges and vessels |
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Definition
| Patho of migraines: Neurogenic inflammation |
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Term
| VD, plasma protein extravasation, edema of meninges and dura; blood brain barrier disturbance cause N/V |
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Definition
| Result of neurogenic inflammation in migraines |
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Term
| 1/5th aura; pain, N/V, photophobia, irritability, malaise, nasal congestion, rhinorrhea, lacrimation |
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Definition
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Term
| Cause of pain in migraines |
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Definition
| Activation of trigeminal nerve anteriorly and upper cervical nerves (C2 and C3) posteriorly; |
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Term
| Why is neck pain, neck muscle tenderness and spasms a part of migraine headaches? |
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Definition
| Trigeminal nerve activation anteriorly and upper cervical nerves, C2, C3 posteriorly |
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Term
| Alterations in PAG (periaquaductal grey matter) and brain stem nuclei: causes loss of natural anti-nociceptive function |
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Definition
| Cause of pain in migraines. |
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Term
Patho: proposed
Monoamine hypothesis: deficit in norepinephrine, dopamine or serotonin |
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Definition
Depression
decreased levels in synaptic cleft due to decreased presynaptic release or decreased postsynaptic sensitivity, decrease in serotonin receptor binding in serotonin system |
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Term
Patho: proposed
Classic Stress Pathway hypothesism disturbance in function of HPA axis |
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Definition
| Depression: first part: impaired feedback inhibition of CRH by endogenous glucocorticoids, hypersecretion of CRH. hi corticol levels in morning and evening, cortisol levels spike erratically over 24 hour day |
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Term
Patho: proposed
Classic Stress Pathway hypothesism disturbance in function of HPA axis
Second part |
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Definition
| Depression: Decreased glucocorticoid function of CNS: Possible Down regulation of glucocorticoid receptors.decreased glucose metab; prolonged hi levels of CRH: down regulate CRH receptors in the pituitary; and can alter DNA expression changing function of neurons |
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Term
Patho: proposed
Classic Stress Pathway hypothesism disturbance in function of HPA axis
Third part |
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Definition
| Depression: antidepressants may upregulate glucocorticoid receptor function |
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Term
Patho: proposed
decreased frontal lobe volumes and temporal lobe volumes
-decreased blood flow to frontal cortex
-increased blood flow/O2 use in cortical areas connected to amygdala: negative affect |
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Definition
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Term
| Part of brain important in helping a person relate to surrounding environment and then pattern appropriate behavior, emotional function, regulation and modulation |
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Definition
| Amygdala. In depression, a negative affect may be influenced by increaed blood flow and O2 use to cortical areas connected to amygdala |
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Term
| Decreased glucocorticoid function in the CNS can cause depression how? |
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Definition
down regulates glucocorticoid receptors (less glucose metab)
-hi levels of CRH secretion cn down regulate CRH receptors in pituitary and alter DNA expression to change function of neurons |
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Term
| The release of a neurotransmitter at a chemical synapse in the CNS is dependent on what? |
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Definition
| Influx of Calcium into the synaptic terminal(causes synaptic vesicles to fuse with presynaptic membrane and release transmitter agent into synaptic cleft |
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Term
| Lesion of the optic chiasm will lead to? |
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Definition
| bitemporal hemianopsia : temporal half eof each field. will affect both retinas from red book |
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