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level 1 Pathophysiology Exam 1 > Alterations Of Neuron Functions > Flashcards

Alterations Of Neuron Functions Flashcards

1
Q

Dementia

A

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

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2
Q

Ischemia (dementia)

A

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

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3
Q

Dementia with levy bodies (dementia)

A

Accumulation of proteins within neuron cytoplasm disrupts synaptic function

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4
Q

Alzheimer disease (dementia)

A

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

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5
Q

Mental impairments of (AD)

A 
Orientation 
Recent memory 
Remote memory 
language 
Executive attention all function 
behavior
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6
Q

Early onset (rare) (AD)

A

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

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7
Q

Late onset (most commmon) (AD)

A

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

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8
Q

Non-modifiable (AD)

A

Age
Family history/genetics
Females mainly
Blacks, hispanics mainly

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9
Q

Modifiable (AD)

A

Cardiovascular disease
Social and cognitive engagement
Traumatic brain injury

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10
Q

Moderate TBI (AD)

A

Increases risk of dementia by 2.3

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11
Q

Severe TBI (AD)

A

increase risk of dementia by 4.5

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12
Q

Protective factors (AD)

A

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

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13
Q

Pathophysiology (AD)

A

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

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14
Q

Amyloid plagues (AD)

A

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

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15
Q

Neurofibrillary tangles (AD)

A

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

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16
Q

Tau protein (AD)

A

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

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17
Q 
Clinical manifestations
Early signs (AD)
A

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

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18
Q 
Clinical manifestations 
Later signs (AD)
A

Cognitive decline
Mood disturbances
Motor changes
Function decline

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19
Q

Cognitive decline (AD)

A

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

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20
Q

Mood disturbances (AD)

A

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

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21
Q

Motor changes (AD)

A

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

22
Q

Function decline (AD)

A

Later stages of alzheimer disease present with bowel and urinary incontinence

23
Q

Parkinson’s Disease

A

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

24
Q

Causes (PD)

A

Idiopathic
Genetic
Gene

25
Q

Idiopathic (PD)

A

Most common

26
Q

Genetic (PD)

A

Autosomal dominant and recessive traits have been identified

27
Q

Gene (PD)

A

environment interaction

28
Q

Risk factors (PD)

A

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

29
Q

Pathophysiology (PD)

A

Disorder of sequential progression

Degeneration neurons that release dopamine in the substantial Nigeria of the basal ganglia

30
Q

Degeneration neurons released caused by (PD)

A

Free-radical injury
Toxins
Age related changes

31
Q

Normal role of dopamine (PD)

A

Fine-tune coordination of movement

Acetylcholine works in conjunction with dopamine to produce smooth movement

32
Q

Progressive loss of dopamine (PD)

A

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

33
Q

Clinical consequences

Abnormal motor movements (PD)

A

Resting tremor
Muscle rigidity
Bradykinesia
Postural instability

34
Q

Resting tremor (PD)

A

Usually asymmetric at first and most evident in one hand

35
Q

Muscle rigidity (PD)

A

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

36
Q

Bradykinesia (PD)

A

Generalized slowness of movement and difficulty with ADL’s

37
Q

Postural instability (PD)

A

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

38
Q 
Clinical consequences (PD)
Dysfunction of the autonomic nervous system
A

Impaired gastrointestinal motility
Bladder dysfunction
Orthostatic hypotension

39
Q 
Clinical consequences (PD)
Depression
A

Mild to moderate

40
Q 
Clinical consequences (PD)
Cognitive impairment
A

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

41
Q

Multiple sclerosis

A 
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
42
Q

Etiologies (MS)

A

Combinations of genetics and environment factors

43
Q

Genetic risk factors for (MS)

A

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

44
Q

Environmental risk factors (MS)

A

Vitamin D deficiency
EBV infection
Cigarette smoking

45
Q

Myelin sheath structure and function

A

Formed from glial cells

Main function is to speed up the conduction of the nervous impulse

46
Q

Pathophysiology (MS)

A

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

47
Q

Autoimmune destruction of myelin (MS)

A

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

48
Q

Inflammation (MS)

A

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

49
Q

Consequences of demyelination (MS)

A

Slowing down and halting of nervous impulse transmission

Disruption of ion channels in neuronal membranes

50
Q

Axonal destruction (MS)

A

Firing of action potentials no longer if axons destructed

51
Q

Clinical consequences (MS)

A

Sensory loss of paresthesias
Motor consequences
Autonomic consequences
Cerebellar dysfunction

level 1 Pathophysiology Exam 1 (10 decks)

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