Question

• Describe alzheimer's disease as well as associated alterations. Explain the pathophysiology of the alterations, including changes that occur in at least two body systems.
• Explain how genetics, gender, ethnicity, age, and behavior might impact the pathophysiology of the alterations you identified, as well as diagnosis and treatment of your selected disorder.
• Construct a mind map for the disorder you selected. Include the epidemiology, pathophysiology of alterations, risk factors, and clinical presentation, as well as the diagnosis and treatment of the disorder.

Answer 1

A Alzeimer's disease is a specific degenerative brain disease characterised by senile plaques, neuritic tangles, and progressive loss of neurons, the presumptive cause of Alzheimer's disease. (A

disease. Epidemiology • About 3% of men of women aged 65-74 have algheimas. & nearly half of those aged 85 a older may have the Risto fuelors (a) Down's syndrome (b) Fancily history (e) Chronic high BP. (d) Head injuries (e) Cender - women (f) Sonoking & drinking

Pathophysiology and Alzheimer's disease is characterised by the loss of neurons and synapses in the

cerebral cortex and certain subcortical regions. This loss results in gross atrophy y of of the the affected regions, including degeneration in the temporal lobe and parietal lobe and parts of frontal cortex and angulated ggrus. • Gross pathophysiological changes: - cortical atrophy - enlarged ventricles - basal ganglia wasting. Microscopically: changes in the proteins of the nerve cells of the cerebral cortex. I accumulation of neuro fibrillary tangles and neuritic plaques. - granulovas cular degeneration - loss of cholinergic nerve cells important in memory, function, cognition) The main pathological hallmarks of Alzheimer's disease: - extracellular deposition of B-amyloid. (AB) plaques. - intaneuronal neurofibrillary tangles .

Newritic Plaques : cleared by B-secretare - Secretase mutation of amylou o precursor protein on gen Chromosome no. 21ris s Increased production of amyloid precursor protein x-secretase has a genesy 142, when these undergoes mutation, they lead to increased clearing of a se xerase. These increased clearing of APP results in increased production of ß-amyloid protein I Produces amybid protein Accumulation of in B-amyloid protein Directly neurotoxin Algheimer's disease Neuro fibrillary tangles :- • Neurons have an internal support structure partly made up of microtubules. A protein called tau helps stabilize microtubules. In AD, tau changes, causing microtubules, to collapse, a tau proteins clump together to form neuro fibrillary tangles. s an Further research, particularly in the genetic domain, led to identification of APP and Presenilin genes (APP, PSENI & PEN & mutations in these genes as cause of rare forms of early-onset familial AD.

on other hand, Eu allele of apolipoprotein E gene CAPOE) has been recognised as a major risk factor for late - onset AD. Clinical manifestations : signs: memory loss Difficulty to performing familiar tasks • Problems with language. Pis orientation to time and place poor or decreased judgement Problems with abstract thinking Misplacing things changes in mood or behavior changes in personality. loss of initiatire. Symptoms : Confusion disturbance in short-taim memory problems with attention and spatial personality change. Orientation. language difficulties. an explained mood swings. gs: Evaluation: and neuro- • Psychiatric assessments. mental status examination psychological assessment laboratory test.

Brain imaging - CT scan - MRI - PET - SPECT CSF examination Electro-encephalo gram (EEG) • Electromyogram ns . treatment : 1. Caregiving! Since Alzheimer's has no cure and it gradually renders people in capable of tending for their own needs, care giving essentially is the treatment and must be carefully managed over the course of the disease. 2. Pharmacological intervention! (4) Acetylcholinesterase inhibitors prevent the break down of acetyl choline, a chemical messenger important for learning and memory. eg: Donepezil Rivastigmine Galantamine (B) N-methyl a-aspartate Receptor Antagonis (NADA) eg! Methr Memantine rotta. CC) Ann-depressants (d) Anxiolytics (e) Antipsychotics (f) Anticonvulsants.

3. Psychosocial intervention :- • Behavioral approach Emotional oriented approach - Remnisence therapy - validation therapy loft - Supportive psychotherapy - sensory integration - Stimulated presence therapy nition oriented approach Stimulation oriented approach

Mind-mapi Due to the chological factors the neure Changes occur in the cells of the cerebral proteins of cortex accaimulation of neurofibrillary tangles 4 I plaques granulo vascular degeneration los of Cholinergic nerve cells. loss of memory function & congnition