Brainscape's Knowledge GenomeTM

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


See full index

PATHO/PHARM II > Conditions Effecting the Nervous System and PharmacotherapyPart Five: Neurodegenerative DX- Multiple Sclerosis MS > Flashcards

Conditions Effecting the Nervous System and PharmacotherapyPart Five: Neurodegenerative DX- Multiple Sclerosis MS Flashcards

Exam 4 (Final)

1
Q

Multiple Sclerosis: What is it?

A

Chronic inflammatory autoimmune disorder damages myelin sheath of CNS neurons

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

Multiple Sclerosis:

What happens in MS?

A

Immune system (lymphocytes & macrophages) attack myelin sheath (insulation) surrounding nerve fibers

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

Multiple Sclerosis:

What gets interrupted?

A

Electrical impulse conduction gets interrupted

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

Multiple Sclerosis:

What may stimulate an abnormal immune response?

A

Viruses may stimulate abnormal immune response

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

Multiple Sclerosis

What does it result in?

A

Results in inflammation, loss of myelin, scarring producing plaques (sclerosis)

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

Multiple Sclerosis

What are there periods of?

A

Initial periods of exacerbation (relapses/flares) & alternating periods of partial/complete recovery (remission) but sometimes unrelenting

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

Multiple Sclerosis

What happens to symptoms overtime?

A

Over time sx –> progressive worse – NO CURE!

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

Multiple Sclerosis:

How is the disease pattern?

A

Unpredictable disease pattern

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

Multiple Sclerosis:

What is the etiology?

A

Etiology unknown

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

Multiple Sclerosis:

When is onset? Who is it more common in?

A

Onset between 20-40 yrs of age, more common in women, but men have more progressive course

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

Multiple Sclerosis:

Where is there a higher prevalence?

A

Prevalence higher in northern latitudes

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

Multiple Sclerosis:

What are inconclusive risk factors?

A

Inconclusive risk factors:

smoking,

vitamin D deficiency,

obesity,

infection,

genetics,

autoimmune reactions,

environmental toxins

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

Patho of MS

What is the hallmark?

A

Hallmark is multifocal regions of inflammation & myelin destruction in brain, spinal cord, optic nerve.

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

Patho of MS:

What is mistaken by immune system?

A

Immune system mistakes myelin components of the CNS (not PNS) as foreign & attacks!!!

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

Patho of MS:

What is Oligodendrocytes?

A

Oligodendrocytes produce myelin, which insulates the axons and allows nerve signals to be transmitted.

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

Patho of MS:

What triggers release of inflammatory mediators & oligodendrocyte loss?

A

Autoreactive T & B cells, & macrophages cross BBB, attack myelin, trigger release of inflammatory mediators & oligodendrocyte loss

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

Patho of MS

What contributes to inflammation and injury?

A

Resident brain macrophages (glial cells) get activated, contribute to inflammation & injury

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

Patho of MS

What happens to myelin and oligodendrocytes?

A

Myelin destroyed and oligodendrocytes injured and die.

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

Patho of MS cont.

What occurs throughout the whole central nervous system?

A

Demyelination throughout the central nervous system.

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

Patho of MS cont.

What happens to destroyed myelin?

A

The destroyed myelin is replaced by hard lesions from the damage

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

Patho of MS cont.

What can inflammation do?

A

Inflammation can damage axons & oligodendrocytes

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

Patho of MS cont.

What happens as more myelin is destroyed?

A

As more myelin is destroyed, nerve conduction is slowed, resulting in weakness, coordination difficulties, visual impairment, and speech disturbances.

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

Progression of Multiple Sclerosis

Damage to Myelin

In the initial stages: What do attacks lead to?

A

Attacks lead to damage to the myelin sheaths in the brain and spinal cord.

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

Progression of Multiple Sclerosis

Damage to Myelin

In the initial stages: What is not yet impacted?

A

Nerve fiber is not yet impacted.

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

Progression of Multiple Sclerosis

Damage to Myelin

In the initial stages: What is not yet impacted?

A

Nerve impulses continue to be transmitted but are slowed.

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

Progression of Multiple Sclerosis

Damage to Myelin

In the initial stages: How is patient?

A

Patients become aware of impaired function (weakness).

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

Progression of Multiple Sclerosis

Damage to Myelin

In the initial stages: How is the myelin?

A

Myelin is capable of regenerating, and as it regenerates, the symptoms disappear.

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

Progression of Multiple Sclerosis

Damage to Myelin

In the initial stages: What do patients experience?

A

Patients experience remission.

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

Progression of Multiple Sclerosis

Damage to Myelin

What may eventually form due to myelin loss?

A

Eventually plaque development from myelin loss:

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Progression of Multiple Sclerosis

Damage to Myelin

Eventually plaque development from myelin loss:

How are initial plaques?

A

Initial plaques are pink and swollen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Progression of Multiple Sclerosis

Damage to Myelin

Eventually plaque development from myelin loss:

How do they become progressively?

A

They progressively become gray and firm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Progression of Multiple Sclerosis

Damage to Myelin

Eventually plaque development from myelin loss:

What size are the plaques? How may they become?

A

They vary in size.

They may merge into a single patch.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

When acute attack is over:

A

Inflammation subsides

Some degree of recovery at least in the early stages

Recurrent episodes ~ less and less complete recovery/remyelination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

When acute attack is over:

Inflammation subsides: What happens to damaged tissue?

A

Damaged tissue replaced.

Astrocytes contribute to the repair & scarring process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

When acute attack is over:

Inflammation subsides: What forms?

A

Formation of scars ~ scleroses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

When acute attack is over:

Some degree of recovery at least in the early stages due to:

A

Partial remyelination

Axonal compensation ~ redistribution of Na channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

When acute attack is over:

Some degree of recovery at least in the early stages:

Due to what developing?

A

Development of alternative neuronal circuits, bypassing damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

When acute attack is over:

Recurrent episodes ~ less and less complete recovery/remyelination

What develops? What happens to neurons and oligodendrocytes?

A

Mounting astrocytic scarring

Irreversible axonal injury

Death of neurons and oligodendrocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Progression of Multiple Sclerosis:

What occurs?

A

Loss of Axon Function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Progression of Multiple Sclerosis:

Loss of Axon Function: With disease progression

What continues?

A

Inflammation continues.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Progression of Multiple Sclerosis:

Loss of Axon Function: With disease progression

What happens to myelin?

A

Myelin loses its regeneration capability.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Progression of Multiple Sclerosis:

Loss of Axon Function: With disease progression

What gets impacted by the inflammation occurring?

A

Adjacent oligodendrocytes are impacted.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Progression of Multiple Sclerosis:

Loss of Axon Function: With disease progression

How is axon impacted?

A

Damage occurs to the axon.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Progression of Multiple Sclerosis:

Loss of Axon Function: With disease progression

What happens to nerve transmission? What does this lead to?

A

Nerve transmission is disrupted in all types of nerve fibers (motor, sensory, autonomic) leading to permanent loss of nerve function.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Progression of Multiple Sclerosis

Loss of Axon Function:

What each relapse involve?

A

Each relapse involves additional areas of the CNS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Progression of Multiple Sclerosis

As the inflammatory process diminishes:

What happens to damaged tissue?

A

Damaged tissue is replaced with glial scar tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Progression of Multiple Sclerosis

Loss of Axon Function:

How does severity of the disease occur?

A

Severity of the disease progression varies from a slow progression in some patients and a rapid progression in others.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Progression of Multiple Sclerosis

As the inflammatory process diminishes:

What is created?

A

It results in the creation of hard, sclerotic plaques.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Progression of Multiple Sclerosis

As the inflammatory process diminishes:

It results in the creation of hard, sclerotic plaques. Where is this found?

A

It is found in the CNS white matter.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Clinical Manifestations

A

Damage to cerebellum

Emotional & behavioral changes

Damage to cranial nerves

Damage to motor nerve tracts

Damage to sensory nerve tracts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Clinical Manifestations:

Damage to cerebellum causes what?

A

Loss of balance

Ataxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Clinical Manifestations:

Damage to cranial nerves causes what?

A

Visual disturbances

Diplopia (double vision)

Loss of vision

Scotoma (spot in the visual field)

Disturbances with verbalization

Dysarthria (poor articulation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Clinical Manifestations:

Damage to motor nerve tracts causes what?

A

Weakness

Paralysis

Spasticity

Urinary incontinence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Clinical Manifestations:

Damage to sensory nerve tracts causes what?

A

Paresthesia of face, trunk, limbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

MS subtypes:

What are they?

A

Clinical Isolated Syndrome

Relapsing-Remitting (RRMS)

Secondary-Progressive (SPMS)

Primary-Progressive (PPMS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

MS subtypes:

What is the worst subtype?

A

Primary-Progressive (PPMS)

The worst

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

MS subtypes:

Clinical Isolated Syndrome: What are neuro symptoms caused by?

What is this subtype considered?

A

Neuro symptoms caused by demyelination & inflammation last for at least 24 hours

1st episode of MS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

MS subtypes:

What is the most common category of MS experienced? What percent of patients are in this category?

A

Relapsing-Remitting (RRMS)

Most common category of MS experienced (85% of diagnosed patients are in this category).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

MS subtypes:

Relapsing-Remitting (RRMS):

What is it characterized by?

A

Defined periods of deteriorating neurologic function (relapses).

Followed by partial or complete recovery (remission).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

MS subtypes:

Relapsing-Remitting (RRMS):

How do symptoms develop? How do symptoms vary?

A

Sx develop over several days, resolve within weeks

S/sx vary based on size/location of lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

MS subtypes:

Relapsing-Remitting (RRMS):

On average, how many relapses?

A

Avg: 2 relapses every 3 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

MS subtypes:

Secondary-Progressive (SPMS): What characterizes the initial course?

A

Relapses and remissions characterize initial course.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

MS subtypes:

Secondary-Progressive (SPMS):

What is this?

A

When a pt with RRMS develops steadily worsening dysfunction & followed by chronic progression.

64
Q

MS subtypes:

Secondary-Progressive (SPMS):

How do Remission/relapse/plateau occur?

A

Remission/relapse/plateau may occur infrequently.

65
Q

MS subtypes:

Secondary-Progressive (SPMS):

What do new treatments do for this?

A

New treatments may slow down progression.

66
Q

MS subtypes:

Secondary-Progressive (SPMS):

What eventually progresses in this category?

A

Most relapsing-remitting eventually progress to this category.

67
Q

MS subtypes:

Secondary-Progressive (SPMS):

How many people will develop this subtype?

A

Within 10 to 20 years of onset, about 50% of patients with MS will develop this type

68
Q

MS subtypes:

Primary-Progressive (PPMS)
The worst

How many MS patients is this seen in ?

A

It is seen in 10% of MS patients.

69
Q

MS subtypes:

Primary-Progressive (PPMS)
The worst

What occurs in this?

A

There is a steady deterioration of neurologic function from outset.

Minor improvements/ plateaus may occur.

70
Q

MS subtypes:

Primary-Progressive (PPMS)
The worst

What does not occur in this?

A

No distinct remission or relapse occurs.

71
Q

Diagnosis of MS

How is diagnosis ? What is the definite test?

A

Delayed DX

⍉ definitive test

72
Q

Diagnosis of MS

What can symptoms occur with or without?

A

Sx can occur with or without lesions

73
Q

Diagnosis of MS

Diagnostics

A

PMH

PE

MRI – most sensitive test

Lumbar puncture with CSF analysis

Nerve conduction studies

74
Q

Diagnosis of MS

MRI – most sensitive test
When do the first lesions begin?

A

The first lesions begin in conjunction with the inflammatory response.

75
Q

Diagnosis of MS

MRI – most sensitive test

What is seen in the MRI?

A

large areas of inflammation and demyelination plaques typically seen next to the lateral ventricles, brain stem, and optic nerve.

76
Q

Diagnosis of MS

Lumbar puncture with CSF analysis

What is measured?

A

Levels of protein, gamma globulin, lymphocytes

77
Q

Diagnosis of MS

Nerve conduction studies

What does it measure?

A

Decreased conduction velocity in visual, auditory, sensory pathways

78
Q

Management Overview for MS:

What is the purpose of management?

A

Slow progression, prevent exacerbations, tx relapse & permanent damage

Minimizing symptoms & modify disease process, maximizing QOL

79
Q

Management Overview for MS:

How to treat chronic fatigue?

A

Chronic fatigue – overwhelming, rest

80
Q

Management Overview for MS:

How to treat sexual dysfunction ?

A

Sexual dysfunction – Sildenafil (Viagra)

81
Q

Management Overview for MS:

How to treat Depression/Cognitive dysfunction?

A

SSRIS, Donezepril

Referrals – PT/OT/VNS, support groups, local MS chapter, counseling

82
Q

Management Overview for MS:

How to decrease core body temp?

A

Use AC, cooling blankets to decrease core body temp

83
Q

Management Overview for MS:

Mobility issues:

A

Respiratory infections

Decubitus ulcer formation - Skin care – pressure relief, moisturize

Contractures – PT/OT

Spasticity

84
Q

Management Overview for MS:

Mobility issues: Spasticity- how treat?

A

Spasticity – anti-spasmodics, PT for strengthening

85
Q

Management Overview for MS

Due to development of plaques along the spinal tract

What develops?

A

Bowel disorders

UTI/Bladder dysfxn:

Sexual dysfunction

86
Q

Management Overview for MS

Due to development of plaques along the spinal tract

Bowel disorders - How to treat?

A

bulk-forming lax, stool softeners, fiber, fluids

87
Q

Management Overview for MS

Due to development of plaques along the spinal tract

UTI/Bladder dysfxn: - How to treat?

A

OAB, intermittent cath, antibiotics

88
Q

Management Overview for MS

Due to development of plaques along the spinal tract

Sexual dysfunction - How to treat?

A

Sexual dysfunction – meds for ED

89
Q

Management Overview for MS

How to treat pain and other abnormal sensations?

A

Pain (neuropathic) & other abnormal sensations –

Gabapentin,

muscle relaxants,

NSAIDs,

antiepileptic drugs

90
Q

Management Overview for MS

Dysphagia- How to treat?

A

Dysphagia – thick fluids, soft foods, aspiration precautions, PEG tube

91
Q

Management Overview for MS

TX strategies: What meds?

A

GC ~ acute episodes (relapses)

92
Q

Management Overview for MS

TX for Acute Episode (Relapse): What is it?

A

High-dose IV GC ~ methylprednisolone

93
Q

Management Overview for MS

TX for Acute Episode (Relapse):

High-dose IV GC ~ methylprednisolone

What is it for? How long is course?

A

Suppress inflammation
Reduce attack severity
Short course ~ 3-5d

94
Q

Management Overview for MS

Disease-modifying agents: What are they?

A

Immunomodulators

95
Q

Management Overview for MS

Plasmapheresis: What are they?

A

Unresponsive exacerbations

96
Q

Management Overview for MS

Gamma globulin (immune globulin): What are they for? What are they reserved for?

A

Acute episodes

Reserved for TX failure or GC-intolerance or contraindicated

97
Q

MS Pharmacotherapy AKA

A

AKA “Disease-modifying drugs”

98
Q

MS Pharmacotherapy AKA “Disease-modifying drugs”

What do they decrease?

A

Decrease frequency & severity of relapse

99
Q

MS Pharmacotherapy AKA “Disease-modifying drugs”

Decrease frequency & severity of relapse how?

A

↓ development of brain lesions & disability, frequency & severity of relapses, future disability

Slow axon damage

Maintain quality of life

100
Q

MS Pharmacotherapy AKA “Disease-modifying drugs”

Decrease frequency & severity of relapse:

What does it prevent?

A

May prevent damage to axons

101
Q

MS Pharmacotherapy AKA “Disease-modifying drugs”

Decrease frequency & severity of relapse: Is it effective in everyone? Who does it benefit the most?

A

⍉ efficacy in all patients

Relapsing-remitting benefit most

$$$

102
Q

MS Pharmacotherapy

2 main groups: What are they?

A

Immunomodulators, safer & preferred

Immunosuppressants

103
Q

MS Pharmacotherapy

2 main groups:

Immunomodulators, safer & preferred

What are the names?

A

Interferon beta 1a & 1b

104
Q

MS Pharmacotherapy

2 main groups:

Immunomodulators, safer & preferred

Interferon beta 1a & 1b: When do you start this drug? How long does treatment continue?

A

Begin soon after dx to prevent permanent neuro deficits & axonal injury

Tx continues indefinitely

105
Q

MS Pharmacotherapy

2 main groups:

Immunosuppressants: When is this used?

A

If tx with immunomodulator fails

106
Q

MS Pharmacotherapy

2 main groups:

Immunosuppressants: What is the example drug?

A

Mitoxantrone

107
Q

MS Pharmacotherapy

2 main groups:

Immunosuppressants:

Mitoxantrone: What is a serious problem with this drug?

A

Can cause serious toxicity

Myelosuppression, heart damage

108
Q

Interferon Beta (Disease Modifying Drug I: Immunomodulator):

What kind of actions do they have?

A

Antiviral, antiproliferative, and immunomodulatory actions

109
Q

Interferon Beta (Disease Modifying Drug I: Immunomodulator):

How is natural interferon beta produced?

A

Natural interferon beta produced in response to viruses

110
Q

Interferon Beta (Disease Modifying Drug I: Immunomodulator):

What does this inhibit?

A

Inhibits migration of proinflammatory leukocytes across BBB, preventing these cells from reaching CNS neurons

111
Q

Interferon Beta (Disease Modifying Drug I: Immunomodulator)

What does it suppress?

A

Suppresses T-helper cell activity

112
Q

Interferon Beta (Disease Modifying Drug I: Immunomodulator)

What is it manufactured using?

A

Different preparations, given by injection, manufactured using recombinant DNA technology

113
Q

Interferon Beta (Disease Modifying Drug I: Immunomodulator)

What shouldn’t be administered while doing this med?

A

Live vaccines shouldn’t be administered during therapy to avoid risk of virus transmission

114
Q

Interferon Beta (Disease Modifying Drug I: Immunomodulator)

Live vaccines shouldn’t be administered during therapy to avoid risk of virus transmission.

When should live vaccines be given if needed?

A

Give 4-6 wks before therapy

115
Q

Interferon Beta (Disease Modifying Drug I: Immunomodulator)

What are the therapeutic uses of this drug?

A

Reduces the frequency and severity of attacks

Reduces the number and size of lesions detectable with MRI

Delays progression of disability

116
Q

Interferon Beta (Disease Modifying Drug I: Immunomodulator):

How often should this drug be given?

A

Given once a week, QOD, 3x a week by IM/Sq injection – depends on preparation

117
Q

Interferon Beta (Disease Modifying Drug I: Immunomodulator):

Adverse effects and drug interactions

A

Flu-like reactions

Hepatotoxicity

Myelosuppression

Injection-site reactions

Depression

Suicidal thoughts

Neutralizing antibodies

Drug interactions

118
Q

Interferon Beta (Disease Modifying Drug I: Immunomodulator):

Adverse effects and drug interactions: Flu-like reactions

How to minimize symptoms? What can also be used for these symptoms?

A

Minimize sx by starting with low dose, titrating up

Acetaminophen, ibuprofen

119
Q

Interferon Beta (Disease Modifying Drug I: Immunomodulator):

Adverse effects and drug interactions: Hepatotoxicity

What should be done to prevent?

A

Monitor? Baseline, 1 mo, 3 mo x 1 yr, every 6 mos after

120
Q

Interferon Beta (Disease Modifying Drug I: Immunomodulator):

Adverse effects and drug interactions: Myelosuppression

What should be done to prevent?

A

Monitor?

121
Q

Interferon Beta (Disease Modifying Drug I: Immunomodulator):

Adverse effects and drug interactions: Injection-site reactions

What occurs in injection site reactions? What should be done?

A

pain, redness, rash itch

Rotate sites, ice, warm compress

122
Q

Interferon Beta (Disease Modifying Drug I: Immunomodulator):

Adverse effects and drug interactions: Depression

What occurs that has to do with depression?

A

May promote or exacerbate

123
Q

Interferon Beta (Disease Modifying Drug I: Immunomodulator):

Adverse effects and drug interactions: Neutralizing antibodies

How does this happen with the meds?

A

Med can stimulate Abs against itself because its immunogenic/foreign protein

124
Q

Interferon Beta (Disease Modifying Drug I: Immunomodulator):

Adverse effects and drug interactions: Drug interactions

A

Other drugs that suppress bone marrow, cause liver injury

125
Q

Interferon Beta (Disease Modifying Drug I: Immunomodulator):

Preparation, dosage, and administration

How is it dispensed? What do you educate patient about?

A

Dispensed as single-use syringes and vials

Pt ed: How to self-inject, store in fridge

126
Q

Disease-Modifying Drugs II: Immunosuppressants:

Mitoxantrone
How should this drug be handled?

A

Hazardous agent requiring special handling

127
Q

Disease-Modifying Drugs II: Immunosuppressants:

What is the prototype?

A

Mitoxantrone

128
Q

Disease-Modifying Drugs II: Immunosuppressants

How do they compare to immunomodulators?

A

More toxic than immunomodulators

Produce greater suppression of immune function

129
Q

Disease-Modifying Drugs II: Immunosuppressants

What were they originally developed for?

A

Developed to treat cancer & later approved for MS

130
Q

Disease-Modifying Drugs II: Immunosuppressants

What is there a significant risk for?

A

Significant risk for toxicity

131
Q

Disease-Modifying Drugs II: Immunosuppressants

What is the therapeutic use?

A

Decreases neurologic disability and clinical relapses in pts with MS (RRMS & SPMS)

May delay the time to relapse, time to disability progression & new MRI-detectable lesions

132
Q

Mitoxantrone

Mechanism of action: How are they to all cells?

A

Cytotoxic to all cells, whether dividing or not

133
Q

Mitoxantrone

Mechanism of action:
What does it bind with?

A

Binds with DNA and inhibits DNA & RNA synthesis

134
Q

Mitoxantrone

Mechanism of action:

What does it suppress? What does this lead to?

A

Suppresses B&T lymphocyte & macrophage production –> decreased autoimmune destruction of myelin

Reduced cytokines (eg TNF, IL-2) that participate in immune response

135
Q

Mitoxantrone

Mechanism of action:

What is this drug especially toxic to? Like what tissues?

A

Especially toxic to tissues with high % of actively dividing cells

Bone marrow, hair follicles, GI mucosa

136
Q

Mitoxantrone:

How is it administered?

A

Given by infusion - 12mg/m^2 every 3 months (max dose 140mg/ m^2 due to cardiotoxicity)

137
Q

ADRs Mitoxantrone include:

A

Myelosuppression

Cardiotoxicity

Fetal harm

Tissue injury with extravasation

Reversible hair loss, injury to GI mucosa, n/v, amenorrhea, allergy symptoms, and blue-green tint to urine, skin, and sclera

138
Q

ADRs Mitoxantrone include:

Myelosuppression: What occurs?

A

Loss of neutrophils 10-14d after dosing (check cbc @ baseline, before tx, 10-14d after)

139
Q

ADRs Mitoxantrone include:

Myelosuppression:

When should you hold the dose?

A

Hold if neutrophil count falls below 1500 cells/mm3 (norm 2500-7000)

140
Q

ADRs Mitoxantrone include:

Myelosuppression:

What should be done to avoid myelosuppression?

A

Avoid sick contacts, report s/sx of infection, no live virus vaccines

141
Q

ADRs Mitoxantrone include:

Cardiotoxicity:

How does it appear?

A

Irreversible injury, LVEF reduced or HF, may present months/years after drug use ceases,

142
Q

ADRs Mitoxantrone include:

Cardiotoxicity:

What should be done to avoid this?

A

measure LVEF before 1st dose, every dose, if <50% & - hold or if HF s/sx develop

143
Q

ADRs Mitoxantrone include:

Cardiotoxicity:

Who is this med NOT given to? What is this med related to?

A

Not to be given if cardiac impairment

Related to cumulative lifetime dose

144
Q

ADRs Mitoxantrone include:

Tissue injury with extravasation:

What occurs, what must be done to avoid this?

A

– severe local injury, dilute with at least 50cc NS

145
Q

ADRs Mitoxantrone include:

Reversible hair loss, injury to GI mucosa, n/v, amenorrhea, allergy symptoms, and blue-green tint to urine, skin, and sclera

What do patients rarely develop?

A

Rarely pts develop leukemia

146
Q

Common Immunomodulator/Suppressant Concerns

What shouldn’t be given with Immunomodulator/Suppressants? But if needed, when should it be given?

A

Live vaccines should not be administered during tx

If needed, give 4-6 wks prior to tx

147
Q

Common Immunomodulator/Suppressant Concerns

What shouldn’t be given with Immunomodulator/Suppressants due to additive effect?

A

Avoid other immunosuppressants because of additive effects

148
Q

Common Immunomodulator/Suppressant Concerns

Because it requires special handling, who does it present a danger to?

A

Special handling required for certain immunomodulators

Presents hazards for pregnant nurses

149
Q

Common Immunomodulator/Suppressant Concerns

How are Immunomodulators recognized by body?

A

Immunomodulators recognized by body as foreign proteins

150
Q

Common Immunomodulator/Suppressant Concerns

Immunomodulators recognized by body as foreign proteins

What does this do?

A

Immunogenic, can stimulate production of Abs against itself, decreasing clinical benefits

151
Q

Common Immunomodulator/Suppressant Concerns

What other changes can occur?

A

Hypersensitivity reactions

Hematologic changes

152
Q

Common Immunomodulator/Suppressant Concerns

Vaccine risks: What response if there to vaccines?

A

Decreased response to vaccines d/t immunosuppressant effects

153
Q

Common Immunomodulator/Suppressant Concerns

Why are infections common?

A

Infections are common due to immunosuppressant effects

154
Q

Common Immunomodulator/Suppressant Concerns

Infections are common due to immunosuppressant effects- What does this lead to?

A

Opportunistic- Progressive multifocal leukoencephalopathy (PML)

155
Q

Common Immunomodulator/Suppressant Concerns

Infections are common due to immunosuppressant effects

Opportunistic
Progressive multifocal leukoencephalopathy (PML)

What is this? What kind of symptoms occur? How many people are effected?

A

Fatal CNS infection

Unilateral weakness, limb clumsiness, disturbed vision, changes in thinking & memory

80-90% left disabled

PATHO/PHARM II (27 decks)

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