Multiple sclerosis Flashcards

1
Q

Describe the risk factors associated with Multiple Sclerosis.

A

Risk factors for Multiple Sclerosis include genetics (more common in first-degree relatives and monozygotic twins), vitamin D deficiency, cigarette smoking, diet and obesity in early life, latitude, Epstein-Barr virus, female gender, and various relapse triggers like infections, postpartum period, and stress.

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2
Q

Explain the pathophysiology of Multiple Sclerosis.

A

The precise pathogenesis of Multiple Sclerosis is unknown, but it is believed to be autoimmune. Key features include inflammation, demyelination, axonal loss, and gliosis. In the inflammatory phase, activated T-cells breach the blood-brain barrier, leading to demyelination. The degenerative phase involves axonal loss, destabilization of axonal membrane potentials, gliosis, and scarring.

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3
Q

What are the different patterns of disease in Multiple Sclerosis?

A

Multiple Sclerosis can present in different patterns: relapsing-remitting (RR-MS), secondary progressive (SP-MS), and primary progressive (PP-MS). RR-MS involves relapses followed by periods of remission. SP-MS shows a gradual worsening of symptoms over time, while PP-MS has a steady progression of symptoms from the onset.

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4
Q

Define the inflammatory phase of Multiple Sclerosis.

A

In the inflammatory phase of Multiple Sclerosis, lymphocytes are activated in the periphery. Activated T-cells breach the blood-brain barrier, leading to an influx of inflammatory cells. These T-cells produce inflammatory cytokines, causing direct toxicity and attracting macrophages that contribute to demyelination.

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5
Q

How does axonal loss contribute to the pathogenesis of Multiple Sclerosis?

A

Axonal loss in Multiple Sclerosis disrupts axonal support, leading to destabilization of axonal membrane potentials. This loss, along with gliosis and scarring, contributes to tissue damage. The mechanisms leading to axonal loss and tissue damage can vary among patients.

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6
Q

Describe the characteristics of relapsing-remitting MS (RR-MS) and how it differs from secondary-progressive MS (SP-MS)

A

RR-MS is the most common form of MS, characterized by relapses followed by remissions, with clinically stable periods in between. Each relapse can lead to residual disability. In contrast, SP-MS involves progressive neurological deterioration with mild flares of inflammation. About 25% of RR-MS patients progress to SP-MS within 6 years.

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7
Q

What are the key features primary-progressive MS (PP-MS) and who is most commonly affected by it?

A

PP-MS is characterized by insidious progressive neurological deterioration from onset, affecting 10-15% of MS patients. It often presents late and is more common in men over 40 years, with a poor prognosis.

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8
Q

How does optic neuritis typically present and what symptoms are associated with transverse myelitis?

A

Optic neuritis presents with partial or total unilateral visual loss, pain behind the eye, decreased visual acuity, scotoma, and difficulty differentiating colors. Transverse myelitis is associated with sensory or motor symptoms, L’hermitte’s sign, urinary symptoms, and decreased muscle tone.

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9
Q

Describe the initial presentation and common complications of MS.

A

MS can present with symptoms like fatigue, pain, spasticity, ataxia, tremor, genitourinary dysfunction, bowel dysfunction, sexual dysfunction, and mental health problems. Complications may include mobility issues, posture problems, and difficulties with memory, attention, concentration, anxiety, depression, and emotional lability.

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10
Q

How is spasticity typically manifested in MS patients and where is it commonly present?

A

Spasticity in MS varies in severity and often manifests as stiffness, spasms, cramps, and pains, commonly affecting the legs. It can be challenging to manage and significantly impact a patient’s quality of life.

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11
Q

What are the common symptoms of ataxia and tremor in MS patients, and how do they affect mobility?

A

Ataxia and tremor in MS patients can lead to reduced mobility, causing difficulties in coordination, balance, and movement control. These symptoms can significantly impact daily activities and quality of life.

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12
Q

Describe the diagnostic process for a neurological condition, including the neurological history, examination, imaging, and laboratory evaluation. What are the key indicators of poor prognosis in such conditions

A

The diagnostic process for a neurological condition involves taking a detailed neurological history, conducting a thorough examination (e.g., eye movements, reflex testing, gait assessment), using MRI imaging, and performing laboratory tests. Key indicators of poor prognosis include older age of onset, male gender, early cerebellar or motor involvement, progressive course, and frequent exacerbations.

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13
Q

How is the progression and prognosis of neurological conditions typically characterized in terms of life expectancy and predisposition to infections? What are the goals of treatment for these conditions?

A

Neurological conditions often lead to a decrease in life expectancy by 5-10 years and predispose individuals to potentially fatal infections like bronchopneumonia and UTIs. The goals of treatment include managing acute worsening, symptomatic relief, slowing disability accumulation, and improving quality of life.

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14
Q

What is the recommended approach for the acute management of relapses in neurological conditions? Describe the use of oral methylprednisolone, its effects, and potential side effects.

A

In acute relapses of neurological conditions, oral methylprednisolone is often used at 0.5g daily for 5 days. It helps improve symptoms by reducing inflammation. Side effects are usually mild and transient, and significant recovery can be expected within 2-3 months.

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15
Q

How should complications like fatigue and mobility problems be managed in individuals with neurological conditions? What interventions and medications can be considered for these complications?

A

Complications like fatigue in neurological conditions can be managed by addressing sleep hygiene, treating underlying conditions, and incorporating regular exercise. Mobility problems may require referral to specialists, supervised exercise programs, and medications like Fampridine to improve walking speed.

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16
Q

Describe the role of methylprednisolone in the management of relapses in neurological conditions. How does it work, and what impact does it have on disease progression?

A

Methylprednisolone is used to manage relapses in neurological conditions by reducing inflammation. It does not impact disease progression but helps in reducing the severity and duration of relapses. The medication acts through immunosuppression and reducing fluid accumulation around nerve damage sites.

17
Q

What are the key components of the treatment goals for neurological conditions? How do these goals aim to improve the overall well-being of individuals with such conditions?

A

The treatment goals for neurological conditions include managing acute worsening, providing symptomatic relief, slowing disability progression, and enhancing quality of life. These goals aim to improve overall well-being by addressing symptoms, preventing relapses, and promoting functional independence.

18
Q

Describe the treatment options for spasticity in multiple sclerosis patients.

A

The treatment options for spasticity in multiple sclerosis patients include assessing and treating aggravating factors first, using baclofen as the first-line medication or gabapentin as the second-line (off-label), incorporating physiotherapy, and referring to a physiotherapist or occupational therapist for ataxia or tremor. Additionally, for sensory symptoms and neuropathic pain, low doses of anticonvuls or newer carbamazepine derivatives can be prescribed.

19
Q

How are mental health issues managed in multiple sclerosis patients?

A

Mental health issues in multiple sclerosis patients can be managed by using amitriptyline hydrochloride (off-label) for emotional lability, implementing cognitive behavior therapy (CBT), and addressing oscillopsia (visual disturbance) with trials of gabapentin or memantine (off-label).

20
Q

Define disease-modifying treatments for multiple sclerosis.

A

Disease-modifying treatments for multiple sclerosis are indicated for relapsing forms of the disease and aim to reduce relapse rate and MRI lesion accumulation. These treatments are prescribed and monitored by MS specialist neurologists and can have potentially serious adverse reactions. Examples include interferon beta, glatiramer acetate, fingolimod, and natalizumab.

21
Q

What are the characteristics and treatment options for β-interferons in multiple sclerosis?

A

β-interferons are naturally occurring cytokines that reduce blood-brain barrier disruption, modulate immune cells, and decrease inflammatory lesions by 50-80% in trials. Treatment options include interferon beta-1a (IM injection weekly or SC injection 3x/week), interferon beta-1b (SC injections alternate days), and peginterferon beta-1a (SC injection every fortnight). Regular monitoring of liver function and blood counts is necessary due to potential adverse effects.

22
Q

Describe the mechanism of action and administration of glatiramer acetate in multiple sclerosis treatment.

A

Glatiramer acetate is an immunomodulating drug that consists of synthetic peptides derived from four amino acids. It stimulates regulatory T-cells and reduces the number of relapses by approximately 30% compared to placebo. It is administered 3 times a week via subcutaneous injection and does not require ongoing blood monitoring.

23
Q

How does fingolimod work in the treatment of multiple sclerosis, and what are its contraindications?

A

Fingolimod is a sphingosine-1-phosphate (S1P) receptor inhibitor that interferes with lymphocytes’ ability to exit lymph nodes, preventing them from entering the CNS to initiate MS lesions. It is taken orally once daily. Contraindications include known immunodeficiency, severe active infection, active chronic infections, severe liver impairment, and active malignancies. It may cause bradycardia and heart block after the first dose.

24
Q

Describe the mechanism of action of Natalizumab and its impact on immune cells and the central nervous system.

A

Natalizumab is a humanised monoclonal antibody that inhibits the migration of immune cells across the blood-brain barrier into the central system. This action to a decrease in inflammation and demyelination, which are characteristic features of conditions like multiple sclerosis.

25
Q

What are the key considerations for the administration and monitoring of Natalizumab treatment?

A

Natalizumab is administered via intravenous infusion every 4 weeks. It is recommended to discontinue treatment if there is no response after 6 months. Approximately 6% of patients develop neutralising antibodies. There is an increased risk of opportunistic infections and progressive multifocal leukoencephalopathy (PML) with this medication.

26
Q

How does lifestyle advice contribute to the overall management of patients receiving Natalizumab treatment?

A

Lifestyle advice, including regular exercise, smoking cessation, and optimal management of comorbidities, can promote general good health in patients on Natalizumab. Additionally, signposting to patient organizations can provide valuable support and resources.

27
Q

What special considerations should be taken into account for pregnant women or those planning pregnancy while on Natalizumab treatment?

A

For pregnant women or those planning pregnancy, it is important to note that relapse rates may decrease during pregnancy but increase 3-6 months postpartum. Comprehensive reviews should be conducted at least once a year, and the involvement of specialist MS nurses is recommended for optimal care.

28
Q

Define the potential risks associated with Natalizumab treatment, including the development of neutralising antibodies and specific infections.

A

Natalizumab treatment carries risks such as the development of neutralising antibodies in approximately 6% of patients. There is also an increased risk of opportunistic infections and progressive multifocal leukoencephalopathy (PML), a rare but serious brain infection.