dementia and Parkinson's disease

Question 1

what is agnosia?

Answer 1

is a defect of pattern recognition—a failure to recognize the form and nature of objects. Agnosia can be tactile, visual, or auditory, but only one sense is generally affected.
-ex may be unable to identify a safety pin by touching it with a hand but able to name it when looking at it

Question 2

what is aphasia?

Answer 2

is impairment of comprehension or production of language with impaired written or verbal communication.

Question 3

what is acute confusional state and delirium?

Answer 3

(also may be known as acute organic brain syndromes) are transient disorders of awareness and may have either a sudden or a gradual onset.
-most commonly occurs in critical care units, following surgery, or during withdrawal from central nervous system depressants (i.e., w/drawl alcohol or narcotic agents). Hospitalized older individuals are at greatest risk for delirium
Delirium is associated with autonomic nervous system hyperactivity and typically develops over 2 to 3 days.

Question 4

manifestations of delirium

Answer 4

Delirium initially manifests as difficulty in concentrating and focusing attention, restlessness, irritability, insomnia, tremulousness, and poor appetite. Some persons experience seizures. Unpleasant, even terrifying dreams, hallucinations or delusions may occur.
-the person appears distressed and often perplexed; conversation is incoherent.
Violent behavior
-pt cannot sleep, is flushed, and has dilated pupils, a rapid pulse rate (tachycardia), elevated temperature, and profuse sweating (diaphoresis).

Question 5

what is dementia?

Answer 5

Dementia is an acquired deterioration and a progressive failure of many cerebral functions that includes impairment of intellectual processes with a decrease in orienting, memory, language, judgment, and decision making. Because of declining intellectual ability, the individual may exhibit alterations in behavior, for example, agitation, wandering, and aggression
Classified according to etiologic factors (e.g., trauma, tumors, vascular disorders, infections)
-Age is the greatest risk factor.

Question 6

patho of dementia

Answer 6

Mechanisms leading to dementia include neuron degeneration, compression of brain tissue, atherosclerosis of cerebral vessels, and brain trauma.

• Genetic predisposition is associated with the neurodegenerative diseases, including Alzheimer, and Parkinson diseases
• . CNS infections, including the human immunodeficiency virus (HIV) can also lead to nerve cell degeneration and brain atrophy.

Question 7

what is alzhemiers disease?

Answer 7

Dementia of the Alzheimer type (DAT): A chronic, progressive disease that foundly diminishes memory, reasoning ability, and thinking skills
-Specific diagnosis can only be made by postmortem examination.
Clinical history, cognitive testing, course of the illness, laboratory tests, and brain imaging are used for diagnostic evaluation
-leading cause of dementia
-irreversible
-age and family hx is the greatest risk factors

Question 8

what are other risk factors of Alzheimer’s?

Answer 8

• Diabetes, hyperlipidemia, midlife hypertension
• Physical inactivity, midlife obesity
• Smoking, depression
• Female sex, estrogen deficit during menopause
• Elevated serum homocysteine, oxidative stress, -neuroinflammation

Question 9

what are the proposed protective factors of Alzheimers?

Answer 9

• Lifelong activity
• Presence of apoE2 and antioxidant substances
• Omega-3 fatty acids
• Low-calorie diet
• Use of NSAIDs (but causes HTN in the elders)

Question 10

early onset of familial Alzhemiers?

Answer 10

Early-onset FAD is autosomal dominant (familial)

-Linked to 3 gene mutations on chromosome 21

Question 11

late onset of AD?

Answer 11

• Related to gene on chromosome 19 which interferes with amyloid beta clearance from brain
• Amyloid can be processed into neurotoxic fragments found in plaques and tangles
• Sporadic late-onset AD is most common and does not have a specific genetic association

Question 12

amyloid

Answer 12

• Failure to clear amyloid precursor protein–> accumulation toxic fragments of amyloid beta protein –> formation of diffuse neuritic plaques, disruption of nerve impulse transmission and neuronal death
• Deposited in cerebral arteries impairing blood

Question 13

Tau protein (a microtubule-binding protein)

Answer 13

• Forms an insoluble filament called a neurofibrillary tangle, contributing to neuronal death
• Tangles are flame shaped
• Degeneration of basal forebrain cholinergic neurons with loss of acetylcholine

Question 14

clinical manifestations of AD

Answer 14

• Progresses from mild short-term memory deficits and culminates in a total loss of cognition and executive functions; exhibits different stages
• Includes forgetfulness; emotional upset; disorientation; confusion; lack of concentration; and declines in abstraction, problem solving, and judgment
• Dyspraxia may appear (stiff muscles- affects movement and coordination
• Mental status changes induce behavioral changes, including irritability, agitation, and restlessness

Question 15

Genetic susceptibility testing consist of?

Answer 15

-PSEN1 (presenilin 1), PSEN2 (presenilin 2), and APP (amyloid-_ precursor protein) are used to screen for early-onset AD

Question 16

goal of therapy for AD?

Answer 16

Treatment focused on using devices to compensate for the impaired cognitive function, such as memory aids and maintaining or improving the general state of hygiene, nutrition, and health

Question 17

what is the goal- drug therapy for Alzhemiers disease

Answer 17

Goal of pharmacotherapy is to improve function in ADLs, behaviour, and cognition

• slow progression of disease
• therapy is initiated as soon as diagnosis of AD is confirmed
• mainstay treatment of AD dementia is acetylcholinesterase inhibitors

Question 18

what is Parkinson’s disease?

Answer 18

-Is a complex debilitating motor disorder accompanied by systemic nonmotor and neurologic symptoms
Classification: Primary parkinsonism & Secondary parkinsonism
-Primary: Onset after 40 years of age

Question 19

what is Primary Parkinsonism

Answer 19

• Sporadic (idiopathic); most common form
• Genetic: autosomal dominant; autosomal recessive
• Phenotype may be influenced by gene-environment interactions

Question 20

what is Secondary Parkinsonism?

Answer 20

• Neurodegenerative disorders
• Genetically mediated disorders with occasional parkinsonian features
• Miscellaneous acquired conditions
• Repeated head trauma
• Infectious and postinfectious diseases
• Metabolic conditions
• Multiple sclerosis
• Neoplastic disease
• Drugs
• Toxins

Question 21

what is Substantia nigra?

Answer 21

• region in the brain where dopamine (inhibitory neurotransmitter) is synthesized that is responsible for regulation of unconscious muscle movement
• Neurons in substantia nigra supply dopamine to corpus striatum

Question 22

what is Corpus striatum?

Answer 22

• area of the brain responsible for unconscious muscle movement
• Dopamine –> normal flow of impulses in striatum–> coordinated, unconscious muscle movement

Question 23

patho of Parkinson’s disease

Answer 23

-Primary PD pathogenesis is unknown
Severe degeneration of the basal ganglia (corpus striatum) involving the dopaminergic nigrostriatal pathway
Loss of dopaminergic-pigmented neurons in the substantia nigra
Dopaminergic deficiency in putamen portion of striatum (striatum includes putamen and caudate nucleus)
-Degeneration of locus coeruleus (norepinephrine neurons) also occurs

Question 24

norepinephrine neurons

Answer 24

it is neuroprotective but degnentrates w/ parikson’s disease

Question 25

locus coeruleus

Answer 25

loss of locus coreuleus –> may be associated with worsening of disease progression and behavioural symptoms

Question 26

patho of PD (cont)

Answer 26

Molecular events associated with neurodegeneration in PD:
-Mitochondrial dysfunction (where we get o2)
-Oxidative stress
-Abnormal folding and accumulation of alpha-synuclein
-Abnormal phosphorylation
-Dysfunction of the ubiquitin proteasome system (which regulates intracellular protein processing)
↓ dopamine (inhibitory) & ↑cholinergic (excitatory) in feedback circuit
-Hypertonia (tremor and rigidity) &
-Akinesia → syndrome of abnormal movement called parkinsonism

Question 27

clinical manifestations of Parkison’s disease

Answer 27

-Onset of symptoms insidious and appear after 60-70% loss of striatal dopamine
Classic manifestations of PD
-Resting tremor
-Rigidity: cogwheel, plastic
-Bradykinesia/akinesia (slow and sluggishness movement)
-Masklife facies
-Postural disturbance (flexed, forward learning), disorders of equilibrium
-Shuffling gait, weakness
-Unable to make the appropriate postural adjustment to tilting or falling and falls like a post when starting to tilt
-Dysarthria (slurred speech)
-Dysphagia
-Nonmotor symptoms (sleep disorders, sensory disturbances)
-Autonomic-neuroendocrine symptoms
-Cognitive-affective symptoms and dementia

Question 28

goal for drug therapy for Parkinson’s disease

Answer 28

• Does not cure disorder
• Goal of pharmacotherapy is to ↑client’s ability to perform normal ADLs such as eating, walking, dressing, and bathing
• Aim is to decrease symptoms and improve quality of life
• Aim is to restore functional balance of dopamine and acetylcholine in the brain (corpus striatum)
• Loss of drug effect
• Symptoms worsen because the concentration of the drug has fallen below the therapeutic level
• On-off syndrome
• Alternation between symptom-free periods (on) and times when the drugs stop working and symptoms abruptly reappear (off)

Question 29

apraxia

Answer 29

-inability to perform motor activités, despite intact motor function

Question 30

stages and major characteristics of Alzheimer’s disease

Answer 30

stage 1 (mild) forgetfulness 
stage 2 (moderate) confusion 
stage 3 (moderate to severe) ambulatory dementia 
stage 4 (late) end stage -pt is bed ridden