SCIE 231 - Module 11 .docx

• Define dementia. Dementia is the impairment of memory, abstract thinking, judgment, and personality, and other higher cognitive functions, resulting in changes in personality and significant interference in work or social activities. 3 Questions = Brain Confusion • Define confusion. A pe...

• Define dementia. Dementia is the impairment of memory, abstract thinking, judgment, and personality, and other higher cognitive functions, resulting in changes in personality and significant interference in work or social activities. 3 Questions = Brain Confusion • Define confusion. A person experiences an altered level of consciousness, disorientated to time, person, or place; disturbed mental status. • Differentiate dementia from confusion. Dementia is more permanent and irreversible, all have confusion. Confusion is more reversible and helps correct the situation that has resulted in confusion since not all cases of confusion have dementia. • Discuss the work up for acute confusion. Hypothyroidism: Side effect drugs Heart Failure: Myocardial infarction: Depression: Dehydration & electrolyte imbalance Alcohol abuse Infections in the elderly: Anemia: Renal failure: Liver disease: Malnutrition Intracranial pathos • Describe etiologies for dementia/chronic confusion. 60% Alzheimer’s Disease 15% Lewy Body Dementia 10% Mixed 10% Other 5% Vascular (Atherosclerosis) 1 Questions = Lewy Body Dementia • Describe the etiology for Lewy Body Dementia. Lewy Body Dementia (LBD) is a progressive brain disorder. The neuron has trouble processing alpha-synuclein protein fragments. Lewy bodies build up in the Brain tissues. There is a ↓ in the neurotransmitter Acetylcholine. Bottom Line: problems in areas of the brain that regulate behavior, cognition, and movement. Result of misfolded proteins that collect in cytoplasm of neurons destroy neurons levels of acetylcholine and dopamine communication dementia Can exist as a single disease[affects cerebral cortex], or as a component of Alzheimer’s [_Decrease_] or Parkinson’s [_Decrease_] 8 Questions = Alzheimer’s Disease • Compare memory issues of normal aging with Alzheimer’s Disease. Memory issues: Forget whole experiences Rarely remember things later Gradually unstable to follow written or spoken directions and make choices. Often get lost in familiar places. • Identify the number one risk factor. Age Genetic defect: Chromosome 19 • Describe plaque formation. Amyloid precursor protein on our brain. If that is cut, it activates beta amyloid, which increases plaque. • Describe the impact of plaque formation on the brain. Beta amyloids clump together and form neurotoxic plaque. • Describe the development of tangles. Sitting in the cytoplasm of the neuron. Tau should hold the microtubules together to keep cell healthy, however something stops that from happening and they cells get tangled. • Describe the impact of tangles on the cells of the brain. Tau is abnormal - can't hold cells together - microtubules destroyed - tangles - neuron cell death. • Describe the impact of AD on acetylcholine and nerve conduction in the brain. Terminal axons do not produce acetylcholine. No neurotransmitter- cells can't “talk” to each other. Impact on normal brain function. • Describe the altered anatomy, where it starts and how it progresses. Starts: Hippocampus - (Memory) Impairment is an early symptoms. Up over and around the brain. Goes to the frontal lobe - problem solving, judgment. Limbic systemic - emotions - angry. • Arrange steps in order ending with cerebral atrophy. (Already in Order) Amyloid precursor (membrane) protein on brain cell surface. Enzymes cut APP in abnormal location Beta amyloid fragments clump and form plaques. Brain toxicity → nerve cells apoptosis. Cerebral atrophy. • Tau: Arrange steps in order. (Already in Order) Tau are defective, not able to hold microtubules together. Defective tau forms tangles. Tangles in cytoplasm of brain neurons → nerve cell apoptosis cerebral atrophy. • Recognize AD as a diagnosis by exclusion. Excludes all other etiologies or other reasons for confusion or forgetfulness. General physician Exam and workup Mini Mental State Examination • Identify cerebral changes evident on an MRI or CT Scan. Might show cerebral atrophy and enlarged ventricles with AD. • Identify the definitive diagnostic test for AD. Autopsy - rarely done • Provide an overview of pharmacologic Treatment. Cholinesterase inhibitors increase acetylcholine neurotransmitter → improve memory. Donepezil • Arrange steps in order: Loss acetylcholine to cognitive changes of AD. (Already in Order) Plaques and tangles destroy neurons. Fewer vesicles are present in axon foot plates. Less acetylcholine is available at synapse. Strength of impulse transmission is lessened. Lessened ability to send messages to various parts of the brain. Problems with memory and making sense of the world. • Arrange steps in order: Rationale for cholinesterase inhibitors. (Already in Order) AD means neuron cell death. Less acetylcholine is available at the synapse. Give a drug to block cholinesterase. More acetylcholine at neuron synapse. Strength of impulse transmission is improved. Increase ability to send messages to various parts of the brain. May slow the cognitive decline of the disease. • Recognize the fatal complications of AD. Decrease glutamate- Increased release-neurotoxic • Identify interventions that can promote brain health. Heart Healthy life choices Quality sleep Move your body Eat well Be social Try new things 2 Questions = VCI • Define vascular cognitive impairment. Vascular cognitive impairment (VCI) - is a decline in thinking skills caused by a condition that blocks or reduce arterial blood flow to the brain, which deprives the brain cells from O2 and other nutrients. • Describe the underlying vascular problem. Progressive narrowing - sluggish blood clots Atherosclerosis • Arrange the steps in order … atherosclerosis (Already in Order) Vessel injury or tear. Neutrophils are attracted to the area. Monocytes leaves vessel. Monocytes becomes macrophage and combines with LDL. Foam cell forms Growth factors → intimal thickening. Foam cell ruptures Plaque laid down below endothelium Vessel (artery) narrows Ischemic tissues → In this case ischemic brain tissue progressing to necrosis. Atherosclerosis → Altered perfusion → Vascular cognitive impairment. • Identify an early symptom. Memory loss is the early symptom. • Explain the role of MRI in the diagnosis of VCI. Dementia R/T multiple small cerebral infarctions. MRI Lacunar infarction - subcortical (below cerebral infarction). 2 Questions = Huntington Disease • Provides an overview of Huntington’s Disease. Is an inherited disorder that causes nerve cells in parts of the brain to gradually break down and die. Worsens over time Attack motor control regions of the brain primarily. • Identify the genetic basis for the disease. Chromosome 4 Genetics - autosomal dominant. Fetal Breakdown of nerve cells in the brain Deterioration of physical ability - Basal ganglia affect and mental capabilities. Onset often between the ages of 30 and 50. • Explain the rationale for signs and symptoms. Difficulty concentrating Memory lapses Depression Stumbling and clumsiness Mood swings