ND 3 Worksheet - N/A PDF

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Neurological Disorders Part III Worksheet 1) Multiple Sclerosis (MS) a. Major Signs and Symptoms - They have attacks where their MS is really bad. The more in remission they are the better. ฀ cycles of exacerbation and remission - Effects women more than men - Involves different areas of the CNS b. Area of the CNS affected and type of neuron - Autoimmune disorder - Progressive demyelinating disease of the CNS - PNS is spared c. Pathophysiology - Most common source of neurological disability in young adults - Familial predisposition - Nerve fibers of brain, spinal cord, and optic nerve are effected - Inflammation and scarring are usually present - Decreasing the speed of neurotransmission - Exposed nerve, first myelin is degraded and then the nerve - Scarring takes the form of plaques d. Type of NT affected and how - Antibody mediated damage against myelin oligodendroglial protein – degrading myelin and then neuron e. Theory of Etiology - Familial predisposition to human leukocyte antigen (HLA)-DR2 haplotype – cell surface antigen that allows you to tell self from non-self gives you an increased risk for different conditions f. Prognosis - No cure symptoms can only be controlled g. Hallmark features - Depending on the location and extent of the lesions: o Visual disturbances o Fatigue o Muscle weakness o Speech disturbance o Swallowing difficulty o Spasticity o Bladder and bowel problems o Numbness, tingling or pain o Tremor o Vertigo h. General treatment strategies - No cure - Treatments include: o Drugs used to treat acute symptoms ฀ corticosteroids suppresses the immune system (glucocorticoids like prednisone o Drugs to modify the course of the disease and treat chronic symptoms (ex. Increasing time in remission) ฀ interferon-beta immunosuppressants such as methotrexate, baclofen 2) Amyotrophic Lateral Sclerosis (ALS)

a) Major Signs and Symptoms - Without factors providing support and sustenance Lou Gehrigs disease – steve Hawkins - Progressively effects motor function - Onset between 40-60 years - Effects men more than women - Mean survival 2-5 years b) Area of the CNS affected and type of neuron - PNS is effected c) Pathophysiology - Destruction of upper motor neurons in the cerebral cortex and the lower motor neurons in the brain stem and spinal cord - Spares cognitive function, pt doesn’t lose their ability to function coherently - Paralyzed cant function on their own – lose ability to breathe on their own - Lacks stimulation to motor system skeletal muscle and muscle atrophy d) Type of NT affected and how - Doesn’t have astrocytes in the joint ฀ picking up excess glutamate in the synapse the transmitters are called EAAT2, doesn’t bind to NMDA receptors causing too much damage - Too much excitotoxicity - Too much glutamate - To much activation of NMDA receptors - Excitatory amino acid transfer 2 - Lots of calcium coming in leading to free oxygen radical production and inappropriate activation of enzymes and neurons die - Makes less SOD because of problems with the gene that encodes for this enzyme, so oxygen free radicals go unchecked - Cant neutralize them as well - Neurons die e) Theory of Etiology - Unknown - May be genetic o Linked to malfunctioning genes for glutamate transporter ฀ excitotoxicity o And/or malfunctioning genes for SOD f) Prognosis - Progressive and pt eventually dies g) Hallmark features - Symptoms: o Muscle weakness/atrophy o Difficulty speaking o Trouble chewing and swallowing ฀ Increased risk of choking ฀Trouble breathing needing a ventilator o Bladder and bowel control are usually preserved in ALS – these nerves aren’t expected ▪ In SNS muscle atrophies ▪ Doesn’t effect sympathetic or parasympathetic h) General treatment strategies - No cure - Respiratory/speech/physical therapy - Riluzole: anti-glutamate drugs o Blocks excitotoxicity – slowing down effects of this disease o Physical therapy helps them to maintain muscle tone

3) Parkinson’s Disease (PD) *multifactorial a. Major Signs and Symptoms - Progressive ND disease - Around 60 yrs - Incidence increases with age - Too much or too little dopamine ฀ causes problems and generates jerky and/or unwanted muscle movements b. Area of the CNS affected and type of neuron Less dopamine released in striatum – part of the CNS c. Pathophysiology - Rhotenone is a pesticide – that is used in order to induce PD in mice - Symptoms don’t start until there is 80% of structural deficit in the brain – pt has a lot of damage before symptoms occur d. Type of NT affected and how - Hypodopaminergic disorder - Results from destruction of dopamine neurons of the nigrostriatal pathway in the midbrain - SCALE: little of dopamine (inhibitory) and normal amt of acetylcholine (excitatory) e. Theory of Etiology - Unknown etiology - A small % of PD cases are familial, resulting from a genetic mutation in the alpha syn nuclein aggregation gene ฀ it misfolds - Protein misfolding and aggregation - Idiopathic PD may be multifactorial with several intrinsic and extrinsic factors contributing to its development - Viral encephalitis patients afterwards had symptoms like PD f. Prognosis - Onset of symptoms is gradual g. Hallmark features Main symptoms: o Rigidity (cogwheel) – the pt is v stiff o Bradykinesia – slow movement o Resting tremor ฀ cease w voluntary movement and during sleep ▪ Starts off with one hand during resting shakes o Postural abnormalities – leaned forward gait, shuttles, small steps o Loses sense of smell o Insomnia o Drooling and difficulty swallowing o “pill rolling” rhythmic tremor o Difficulty initiating and stopping movements o Has trouble moving facial muscles o They can aspirate on their food o Hard time movement – they freeze and cant make themselves move o Dementia o Lack of arm swing o Occasional freezing episodes o Mask like face and seborrhea o Micrographia – their hand writing gets small, microphasia – soft voice h. General treatment strategies - No cure, treatment alleviates symptoms

o Increases dopamine levels, stimulates dopamine receptors, decreases dopamine breakdown 4) Alzheimer’s Disease (AD) a. Major Signs and Symptoms - Causes dementia - Characterized by cortical atrophy, loss of neurons (esp. in the parietal and temporal lobes), and enlargement of the ventricles - Cognitive regions effected are language and memory b. Area of the CNS affected and type of neuron - Effects CNS c. Pathophysiology - Neuritic senile plaques o Hallmark features of AD o Patches of degenerating nerve terminals surrounding a core of amyloid beta peptide o Toxic ฀ may induce inflammatory responses, activation of microglia, and releases of free radicals d. Type of NT affected and how - Increased levels of acetylcholine - Neurons that release acetylcholine are dying - Loss of cortical neurons results in a deficit of choline transferase ฀ Ach - Gyri shrink and ventricles expand - Microscopic findings: neurofibrillary tangles: made form tau which becomes hyperphorphorylated – aggregating around the nucleus of these neurons – leads to neuronal death o Which displaces the nucleus - Amyloid precursor protein o Alpha – the body can clear this o Beta/gamma – B cuts it once and g cuts it again and the body cant clear this protein o Amyloid beta protein when it aggregates you have oxidation, excitotoxicity, tau phosphorylation causing senile plaques and inflammation e. Theory of Etiology - Exact etiology is unknown - Diagnosis o Based on symptoms o Definitive diagnosis = post-mortem histology of the brain o MRI serves to exclude other disease states, and may show cortical atrophy ▪ Bacteria from gingivitis that could contribute to AD f. Prognosis No cure, treatment alleviates symptoms g. Hallmark features - Symptoms o Short term memory loss and inability to acquire new info o Pt may get lost o Has trouble handling money and paying bills o Daily tasks take longer to complete o Starts effecting long term memory - As it progresses: o LTM becomes compromised o Changes in mood and personality o Cognition is impaired ฀ dementia

o Difficulty in performing learned motor tasks o Psychosis h. General treatment strategies - Cholinesterase inhibitors Ex. Aricept – better on early in the diagnosis - NMDA receptors (Namenda) o Doesn’t help everyone 5) Huntington’s Disease (HD) a. Major Signs and Symptoms - Called huntingtons chorea - Progressive ND disorder effecting 1/10,000 get effected - Offspring has a 50/50 chance of developing the disease - Gradual loss of cognitive function b. Area of the CNS affected and type of neuron - Massive neuronal loss in caudate and putamen = striatum - Also secondary loss of neurons from the frontal cortex c. Pathophysiology - Hyperdopaminergic ฀ more dopamine - Considered a hyperdopaminergic condition because less GABA is released in the striatum ฀ increased dopamine release d. Type of NT affected and how hyperdopaminergic e. Theory of Etiology - Has definitive gene that causes the mutation leading to protein aggregation – a mutation in the gene for a protein called huntingtin f. Prognosis - No cure g. Hallmark features - Causes constant involuntary writhing or dance-like movements o Involving extremities at first and then the entire bods h. General treatment strategies - Treatment helps with symptoms o Antipsychotics ฀ blocks dopamine receptors o Helps alleviate symptoms, block rxn of dopamine, blocks actions of dopamine...