Alterations Of Neuron Functions

Question 1

Dementia

Answer 1

Progressive determination of cerebral function including a decline in orientation, memory, language, executive attentional functioning and behavior alterations

Question 2

Ischemia (dementia)

Answer 2

Cardiovascular disease leads to ischemia of CNS neurons and neuronal dysfunction and degeneration

Question 3

Dementia with levy bodies (dementia)

Answer 3

Accumulation of proteins within neuron cytoplasm disrupts synaptic function

Question 4

Alzheimer disease (dementia)

Answer 4

Dementia characterized by progressive failure of cerebral function not associated with an impaired level of consciousness

Question 5

Mental impairments of (AD)

Answer 5

Orientation 
Recent memory 
Remote memory 
language 
Executive attention all function 
behavior

Question 6

Early onset (rare) (AD)

Answer 6

Occurs in people age 30-60
Accounts for <5% of AD cases
Caused by single-gene mutations that cause abnormal proteins to be formed

Question 7

Late onset (most commmon) (AD)

Answer 7

Develops after age 60
Most common form of AD
Combination of genetic susceptibility, environment and immunological factors

Question 8

Non-modifiable (AD)

Answer 8

Age
Family history/genetics
Females mainly
Blacks, hispanics mainly

Question 9

Modifiable (AD)

Answer 9

Cardiovascular disease
Social and cognitive engagement
Traumatic brain injury

Question 10

Moderate TBI (AD)

Answer 10

Increases risk of dementia by 2.3

Question 11

Severe TBI (AD)

Answer 11

increase risk of dementia by 4.5

Question 12

Protective factors (AD)

Answer 12

Physical activity
Antioxidants
Low calorie diet
Statins and NSAIDs (ibuprofen)

Question 13

Pathophysiology (AD)

Answer 13

Characterized by the accumulation of amyloid plagues and neurofibrillary tangles spread by the brain causing neuronal dysfunction and cell death

Question 14

Amyloid plagues (AD)

Answer 14

Accumulation of amyloid beta peptides in the extracellular matrix surrounding the CNS neurons- accumulation are called amyloid plaques

Form clusters that block neurotransmitter release and also cause cell injury

Question 15

Neurofibrillary tangles (AD)

Answer 15

Caused by deposits of tau protein that accumulate in the cytoplasm of the neurons

Question 16

Tau protein (AD)

Answer 16

Accumulates inside the cells and destroy the microtubule system, therefore nutrients and other molecules are unable to move throughout the cell
Leads to cell death

Question 17

Clinical manifestations
Early signs (AD)

Answer 17

Alzheimer disease starts with a gradual onset of vague problems such as forgetfulness, emotional upset and fatigue
Short term memory becomes progressively worse and the individual often becomes disoriented or disinhibition during these episodes

Question 18

Clinical manifestations 
Later signs (AD)

Answer 18

Cognitive decline
Mood disturbances
Motor changes
Function decline

Question 19

Cognitive decline (AD)

Answer 19

In addition to the progressive of short and eventually long term memory, alzheimer disease causes a wide variety of other cognitive changes

Question 20

Mood disturbances (AD)

Answer 20

AD leads to many mood disturbances including irritability, depression, anxiety.

Question 21

Motor changes (AD)

Answer 21

If the disease process affects the frontal lobe, motor problems such as muscle rigidity, flexion posturing, propulsion, and repulsion are common

Question 22

Function decline (AD)

Answer 22

Later stages of alzheimer disease present with bowel and urinary incontinence

Question 23

Parkinson’s Disease

Answer 23

A complex motor disorder caused by neurological in the basal ganglia. 2nd most common neurodegenerative disease

Question 24

Causes (PD)

Answer 24

Idiopathic
Genetic
Gene

Question 25

Idiopathic (PD)

Answer 25

Most common

Question 26

Genetic (PD)

Answer 26

Autosomal dominant and recessive traits have been identified

Question 27

Gene (PD)

Answer 27

environment interaction

Question 28

Risk factors (PD)

Answer 28

Age, family history, male, environmental exposure, whites mainly, traumatic brain injury

Question 29

Pathophysiology (PD)

Answer 29

Disorder of sequential progression | Degeneration neurons that release dopamine in the substantial Nigeria of the basal ganglia

Question 30

Degeneration neurons released caused by (PD)

Answer 30

Free-radical injury Toxins Age related changes

Question 31

Normal role of dopamine (PD)

Answer 31

Fine-tune coordination of movement | Acetylcholine works in conjunction with dopamine to produce smooth movement

Question 32

Progressive loss of dopamine (PD)

Answer 32

Activity and relative excess of acetylcholine activity in the basal ganglia leads to loss of smooth motor movements and other changes

Question 33

Clinical consequences | Abnormal motor movements (PD)

Answer 33

Resting tremor Muscle rigidity Bradykinesia Postural instability

Question 34

Resting tremor (PD)

Answer 34

Usually asymmetric at first and most evident in one hand

Question 35

Muscle rigidity (PD)

Answer 35

Muscle tone increased in both flexor and extensor muscles providing a constant resistance to passive movements of the joints

Question 36

Bradykinesia (PD)

Answer 36

Generalized slowness of movement and difficulty with ADL's

Question 37

Postural instability (PD)

Answer 37

Postural fixation with PD is involuntary flexion of neck and head Balance and righting abnormalities common

Question 38

``` Clinical consequences (PD) Dysfunction of the autonomic nervous system ```

Answer 38

Impaired gastrointestinal motility Bladder dysfunction Orthostatic hypotension

Question 39

``` Clinical consequences (PD) Depression ```

Answer 39

Mild to moderate

Question 40

``` Clinical consequences (PD) Cognitive impairment ```

Answer 40

Mild cognitive decline including impaired visual-spatial perception, slowness in execution of motor tasks

Question 41

Multiple sclerosis

Answer 41

``` An auto immune demyelinating disorder resulting in damage to the yelping sheath of CNS neurons Age of onset is 20-40 years Females Caucasian s Lasts more that 30 years ```

Question 42

Etiologies (MS)

Answer 42

Combinations of genetics and environment factors

Question 43

Genetic risk factors for (MS)

Answer 43

Pattern of inheritance is unclear Over 50 genetic loci Interleukin receptor mutations

Question 44

Environmental risk factors (MS)

Answer 44

Vitamin D deficiency EBV infection Cigarette smoking

Question 45

Myelin sheath structure and function

Answer 45

Formed from glial cells | Main function is to speed up the conduction of the nervous impulse

Question 46

Pathophysiology (MS)

Answer 46

Characterized by degeneration of the myelin sheath of CNS neurons, leading to inflammation, scarring, and loss of axons

Question 47

Autoimmune destruction of myelin (MS)

Answer 47

Activation of Tc cells, cross blood barrier to attack oligodendrocytes (glial cells forming myelin) in the CNS Activation of B lymphocytes that produce antibodies that damage myelin sheath

Question 48

Inflammation (MS)

Answer 48

Infiltration by neutrophil, macrophages and eosinophils Phagocytes release of oxygen free radicals and glutamate Scarring and formations of plaques

Question 49

Consequences of demyelination (MS)

Answer 49

Slowing down and halting of nervous impulse transmission | Disruption of ion channels in neuronal membranes

Question 50

Axonal destruction (MS)

Answer 50

Firing of action potentials no longer if axons destructed

Question 51

Clinical consequences (MS)

Answer 51

Sensory loss of paresthesias Motor consequences Autonomic consequences Cerebellar dysfunction