Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Anatomy and Phyisology > HLTH 2501: chronic degenerative disorders > Flashcards

HLTH 2501: chronic degenerative disorders Flashcards

1
Q

multiple sclerosis

A

involves a progressive demyelination of the neurons of the brain, spinal cord, and cranial nerves; there are multiple types

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is the result of multiple sclerosis

A

the loss of myelin interferes with conduction of impulses in the affected fibres (motor, sensory, or autonomic); this causes neural degeneration that varies in its severity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how does multiple sclerosis develop?

A

an inflammatory response creates a lesion that results from cells that do not normally enter the brain, but attack neurons, causing a loss of myelin in the white matter of the brain; this develops into larger areas of inflammation and demyelination termed plaques

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what might be responsible for the development of multiple sclerosis?

A

a protein in the body’s blood-clotting mechanism that triggers the immune response; it is also believed to be an autoimmune disorder and linked to genetic and environment conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

where do plaques commonly develop in multiple sclerosis?

A

in the lateral ventricles, the brainstem and the optic nerves; these appear pinkish and swollen, but later become grey and firm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

who does multiple sclerosis affect more?

A

women between the ages of 20 and 40 and often those of European descent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

signs of multiple sclerosis

A

blurred vision is the common early sign, weakness in the legs, diplopia (double vision), scotoma (spot in the visual field), dysarthria (poor articulation), paresthesias, and as it progresses, loss of coordination of the bladder and bowel may occur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

complications arising from multiple sclerosis

A

those related to immobility like respiratory infection, decubitus ulcers, and contractures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

diagnosis for multiple sclerosis

A

no definitive test but includes a history of exacerbations and remissions, involvement of multiple focal areas, and absence of other disorders; MRI’s can be used, CSF analysis, and optical coherence tomography

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are CSF serum levels like in those with multiple sclerosis?

A

elevated protein, gamma globulin, and lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

treatment for multiple sclerosis

A

interferon beta-1b can reduce frequency of exacerbations, glucocorticoids, muscle relaxants, avoiding fatigue, stress, injury, or infection, PT, OT, and speech therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

parkinson disease other name

A

paralysis agitans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

parkinson’s disease

A

is a progressive degenerative disorder that affects motor function through loss of extrapyramidal activity due to changes in the basal nuclei and substantia nigra, leading to decreased dopamine release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what does the lack of dopamine release in Parkinson’s disease cause?

A

leads to an imbalance between excitation and inhibition of the basal nuclei; this causes affected movement and posture by increasing muscle tone, restless tremors, muscle rigidity, difficulty in initiating movement, and instability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what neurons are lacking in Parkinson’s disease?

A

cortical neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

toxins that may cause parkinson’s disease

A

manganese, carbon monoxide, carbon disulfide, and some pesticides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

primary parkinson’s disease

A

usually develops after age 60 and is associated with genes, toxins, mitochondrial damage, and lewy bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

mitochondrial damage in Parkinson’s patients

A

changes in the mitochondria due to oxidative stress lead to the accumulation of free radicals within the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

lewy bodies and parkinson’s disease

A

these are clumps of specific substances in the affected brain cells that contain a protein called alpha-synuclein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

secondary parkinsonism

A

may follow encephalitis, trauma, or vascular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

drug-induced parkinson’s disease

A

is linked to the use of phenothiazines (antipsychotic’s)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

signs of parkinson’s disease

A

fatigue, muscle weakness, muscle aching, decreasing flexibility, less spontaneous change in facial expression, hand tremors that progress to feet, face, tongue, and lip tremors, muscle rigidity, difficulty initiating movement, lack of associated involuntary movements, propulsive gait, bradykinesia, low voice, drolling, reduced linking, and increased risk for falls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

bradykinesia

A

slow movements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

propulsive gait

A

short, shuffling steps with increasing acceleration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

treatment for parkinson’s disease

A

dopamine replacement (Levodopa), monoamine oxidase B inhibitors, anticholinergic drugs, catechol-O-methyltransferase inhibitors, antidepressant drugs, speech therapy, PT, and OT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

levodopa

A

is a precursor of dopamine and used for parkinson’s treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

monoamine oxidase B inhibitors

A

selegiline and rasagiline; these block the breakdown of L-dopa in the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

anticholinergic drugs

A

include benztropine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

catechol-O-methyltransferase inhibitors

A

include entacapone that mildly prolong the effect of L-dopa therapy by blocking an enzyme that breaks down dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

ALS

A

amyotrophic lateral sclerosis

30
Q

2 other names for ALS

A

Lou Gehrig disease and motor neuron disease

31
Q

amyotrophic meaning

A

muscle wasting

32
Q

sclerosis means

A

hardening; for ALS it refers to the degenerative hardening of the lateral corticospinal tracts

33
Q

ALS

A

is a progressive degenerative disease affecting both UMNs in the cerebral cortex and LMNs in the brainstem and spinal cord; sensory neurons are not affected; this is a fatal disease

34
Q

how does ALS develop?

A

supportive glial cells called astrocytes secrete a neurotoxin, leading to the death of motor neurons

35
Q

what does damage to the UMNs result in?

A

spastic paralysis and hyperreflexia

36
Q

what does damage to the LMNs result in?

A

flaccid paralysis, with decreased muscle tone and reflexes

37
Q

what does the progressive muscle weakness in ALS lead to?

A

affected respiratory function

38
Q

signs of ALS

A

the upper extremities, particular the hands manifest weakness and muscle atrophy, with a loss of fine motor coordination; stumbling and falls are common, along with muscle cramping and twitching, speech loss, impaired respiration, and swallowing difficulties

39
Q

treatment for ALS

A

to treatment to reverse the course; Rulutrek slows damage to neurons, allowing for swallowing and ventilation to remain; exercise and rest is also helpful, along with respiratory therapist, nutritionist, speech pathologist, OT, PT, psychologist, and social workers

40
Q

myasthenia gravis

A

is an autoimmune disorder that impairs the receptors for ACh at the neuromuscular junction; cause is not known but is related to thymus disorders like hyperplasia or benign tumors

41
Q

what happens in mysasthenia gravis

A

immunoglobulin G autoantibodies to ACh receptors form, blocking and ultimately destroying the receptor site, thus preventing any further stimulation of the the muscle; this leads to skeletal muscle weakness and rapid fatigue of the affected muscles

42
Q

what muscles are often affected in myasthenia gravis

A

the facial and ocular muscles, followed by the arm and trunk muscles

43
Q

tests for myasthenia gravis

A

EMG to test muscle fatigue, looking at serum antibodies, and a test that uses edrophonium chloride (Tensilon) which is a shorter-acting anticholinesterase inhibitor to prolong the action of ACh at the myoneural junction

44
Q

signs of myasthenia gravis

A

noticeable muscle weakness, fatigue, diplopia and ptosis impairs vision, speech becomes monotone, spontaneous facial expressions are lost (droopy face), difficulty chewing and swallowing, head droops, upper respiratory infections are common and myasthenic crisis

45
Q

myasthenic crisis

A

occurs when there is added stress such as an infection, trauma, or alcohol intake and involves an increase in weakness and fatigue, and respiratory impairment may develop

46
Q

treatment for myasthenia gravis

A

anticholinesterase agents, glucocorticoids (prednisone) for suppressing the immune system, other immunosuppressants, plasmapheresis, and thymectomy

47
Q

anticholinesterase agents for myasthenia gravis

A

can be neostigmine and this temporarily improves neuromuscular transmission through prolonging the action of Ach

48
Q

plasmapheresis

A

is a process that removes antibodies from the blood and can be treatment for myasthenia gravis

49
Q

huntington disease

A

is an inherited disorder that does not manifest until midlife and is characterized by progressive atrophy of the brain, including degeneration of neurons, particular of the basal ganglia of the frontal cortex, and dilation of the ventricles

50
Q

genetic factors for huntington’s disease

A

is a genetic disorder via an autosomal-dominant trait carried on chromosome 4 (50% probability) and maternal inheritance delays the onset compose to paretrnal

51
Q

what neurotransmitters are reduced in huntington’s disease

A

GABA (inhibitory neurotransmitter) and Ach

52
Q

signs of huntington’s disease

A

mood swings, personality changes, restlessness and choreiform (rapid, jerky) movements in the arms, and possibly early signs on intellectual impairment like loss of problem-solving skills, difficulty learning, and poor judgement

53
Q

how is huntington’s disease diagnosed?

A

DNA analysis

54
Q

treatment for huntington’s disease

A

no therapy but the drug tetrabenazine is used to maintain mobility and other drugs for behavioral changes, as well as PT

55
Q

dementia

A

is a progressive chronic disease in which cortical function is decreased, there are impaired cognitive skills, decreased motor coordination, loss of memory, and behavioural changes

56
Q

how is normal forgetfulness distinguished from dementia

A

those with dementia cannot recall after being given clues, the day cannot be identified, calculations are difficult, and reminders are needed for meals and hygiene

57
Q

causes of dementia

A

vascular disease (ex. atherosclerosis), infections, toxins, and genetic disorders

58
Q

most common dementia disorder

A

Alzheimer’s disease

59
Q

alzheimer’s disease

A

is characterized by a loss of intellectual function, and includes personality changes, lack of initiative, repetitive behaviours, judgement impairment, abstract-thinking, and problem-solving abilities

60
Q

how does Alzheimer’s disease develop?

A

progressive cortical atrophy leads to dilated ventricles and widening of the sulci; neurofibrillary tangles and senile plaques are present, and these disrupt neural conduction; there is also a deficit of Ach

61
Q

what is contained in the plaques in those with Alzheimer’s disease?

A

beta-amyloid precursor protein

62
Q

causes of Alzheimer’s

A

unknown but is genetic, as at least four defective genes are located on different chromosomes (1, 14, and 21 are autosomal dominant traits and 21 in those with down’s syndrome); there is another late-onset AD that is associated with chromosome 19

63
Q

early stage of Alzheimer’s

A

gradual loss of memory and lack of concentration; the ability to learn new information and to reason is impaired, along with behavioural changes; this progresses and ADL become impaired, along with wandering

64
Q

late stage of Alzheimer’s disease

A

the person does not recognize his or her family, lacks awareness or interest, it incontinent, cannot function and motor function degenerate

65
Q

treatment for Alzheimer’s disease

A

OT, depression and anxiety medication, anticholinesterase drugs, and providing a safe space, with a daily routine and some light exercise

66
Q

4 types of dementia

A

Alzheimer’s disease, vascular dementia, Creutzfeldt-Jakob disease, and acquired immunodeficiency syndrome dementia

67
Q

vascular dementia

A

is caused by cerebrovascular disease and frequently is a result of multiple small brain infarctions; common in those with hypertension

68
Q

Creutzfeldt-Jakob disease

A

is rare, but progresses rapidly; can be cause by infection by a prion, which is an altered, infectious form of the prion protein that has a preference for nervous tissue

69
Q

how does the prion protein cause Creutzfeldt-Jakob disease

A

it alters the shape of normal host PrPs which has a long incubation period and then is followed by rapid destruction of neurons and the formation of plaques and vacuoles in the neurons

70
Q

how it Creutzfeldt-Jakob disease acquired?

A

can be genetic (a defect in the human prion protein gene) or have be through surgeries, corneal transplants, or other invasive procedures

71
Q

how is Creutzfeldt-Jakob disease diagnosed?

A

MRI and EEG

72
Q

treatment for Creutzfeldt-Jakob disease

A

no treatment but amantadine, steroids, interferon, acyclovir, antiviral agents, and antibiotics may help to alleviate symptoms

73
Q

acquired immunodeficiency syndrome dementia

A

dementia may develop in later stages on acquired immunodeficiency syndrome and occurs when the virus itself invades brain tissue and may be exacerbated by other infectious agents like Candida, toxoplasma species, and tumors such as lymphoma

Anatomy and Phyisology (71 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions