MS/Pituitary Flashcards

1
Q

MS

A
  • chronic, inflammatory disease of CNS, demyelination disease (myelin, neurons, axons are destroyed)
  • when myelin is lost in multiple areas, plaques occur
  • results in periodic loss of neurological function (relapse) and often progressive disability
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2
Q

Uhthoff’s phenomena

A

-MS symptoms worsen in the heat

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3
Q

Relapse

A
  • new neurologic disability that lasts greater than 24 hrs
  • may be recurrence of old symptom or a new one
  • onset usually subacute
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4
Q

Clinical definition of MS

A

-disease that is separated by time & space

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5
Q

MS tests

A
  • spinal fluid (inflammatory profile): lymphocytes, IgG, oligoclonal bands (NEVER neutrophils in classic MS)
  • MRI: plaques are hyperintense (can be enhanced with gadolinium)-inflammation & breakdown of BBB to let it enter
  • Visual Evoked Response: P100, measures how quickly the cortex detects light input from retina (normal is 100msec)
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6
Q

Classical Diagnostic Criteria for MS

A
  • clinical evidence for lesions that reflect white matter dysfunction disseminated in time & space in age 18-50
  • objective abnormalities on neurological exam
  • at least 2 clear cut episodes of functionally sig. symptoms each lasting over 24 hrs separated by at least 1 month
  • slow progressive deterioration of the same disseminated pattern evolving over at least 6 months
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7
Q

MS Plaque

A
  • damage to white matter which contains myelin
  • many present in regions adjacent to cortical gray matter
  • located in deep white matter and periventricular areas
  • Juxtacortical
  • demyelination (luxo fast blue stain stains normal myelin blue)
  • inflammatory )Perivascular “cuff”, T & B cells, macrophages & microglia
  • damage of nerve cells & axons
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8
Q

Pathogenesis of MS

A
  • cause uncertain
  • immune-mediated inflammatory disease of central nervous system
  • may develop in genetically susceptible individuals who are exposed to undefined environmental “triggers”
  • leukocytes penetrate BBB, secrete inflammatory cytokines
  • T-cells, B-cells, & macs orchestrate autoimmune attack against myelin antigens
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9
Q

MS Epidemiology

A
  • 350,000 in US affected (1 million worldwide)
  • diagnosed 20-40
  • 2/3 are women (RRMS)
  • equal for PPMS
  • incidence inc. with distance from equator
  • 8,500 to 10,000 new cases per year
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10
Q

Clinical Types of MS

A
  1. Relapsing

2. Progressive

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11
Q

Relapsing MS

A

-exacerbations followed by complete or incomplete recovery
-slow, inconsistent accumulation of disability occurs in the majority of patients
~85% of patients

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12
Q

Progressive MS

A
  • steady progression of disability with few or no exacerbations
  • develop spastic paraparesis over a period of years
  • corticospinal dysfunction (spasticity, weakness), sensory disturbance & urinary symptoms
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13
Q

Benign MS

A
  • few relapses, never progress

- rare

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14
Q

Secondary Progressive MS

A

-# of plaques increases within the CNS, patient worsen when relapses stop

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15
Q

Primary Progressive MS

A
  • patients worsen without relapses
  • usually lose ability to ambulate due to spastic paraparesis & other symptoms referable to CNS systems that affect gait (balance, sensory input)
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16
Q

Natural History of ALS

A
  • 1 relapse per year (fewer over time)
  • 25% of patients never lose ability to perform daily activities
  • 15% become severely disabled within short time
  • median time to reach moderate disability is 15 yrs, severe is 46 yrs
  • mortality from MS as primary cause is low
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17
Q

How is MS diagnosed?

A
  • Clinical signs & symptoms
  • MRI
  • Spinal tap
  • Evoked Potentials
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18
Q

Symptoms of MS

A
  • weakness
  • numbness
  • fatigue
  • vision problems
  • slurred speech
  • poor coordination
  • short-term memory loss
  • depression
  • bladder & bowel dysfunction
  • partial or complete paralysis (severe)
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19
Q

Optic Neuritis

A

demyelinating syndrome

  • unilateral, retrobulbar, pain
  • no retinal exudates, disc hemorrhage infrequent, some recovery
20
Q

Myelitis

A

demyelinating syndrome

  • partial sensory > motor (assymetrical)
  • band-like pressure
  • Lhermitte’s sign
  • Bowel & bladder sx are common
  • Acute dystonias
21
Q

Brainstem demyelinating syndrome

A
  • ocular motor (INO, nystagmus)
  • trigeminal neuralgia, hemifacial spasm, Bell’s palsy
  • vestibulopathy & other cranial neuropathies
22
Q

Cerebellum demyelinating syndrome

A

-acute ataxia, tremor, eye movement problems

23
Q

Afferent Pupillary defects

A

-consistent with a demyelination & axon damage on side of lesion

24
Q

Clinically Isolated Syndrome

A

-a clinical episode suggestive of a MS patients first relapse

  • optic nerves, brainstem, spinal cord (partial transverse myelitis)
  • lasts at least 24 hrs
  • typically ages 20-45
  • no evidence of infection, fever or encephalopathy
25
Q

Lesion

A

-plaque

26
Q

Attack

A

-relapse

27
Q

Treatments for MS

A

-Drugs for MS related symptoms
(steroids, baclofen, tizanidine, amantadine, modafinal, antidepressnats)
-Treat underlying cause: reduce risk of relapse, new plaque formation & neurological progression
(INF-beta, glatiramer acetate, mitoxantrone, natalizumab, teriflunomide, fingolimod)

28
Q

Transverse Myelitis

A
  • acute neurologic condition that reflects focal inflammation of spinal cord
  • acute or subacutely developing motor, sensory & sphincter disturbance (usually asymmetrical)
  • spinal segmental level of sensory disturbance with well defined upper limit
  • no evidence of spinal cord compression
  • absence of other neuro disease
  • may be first sign of MS (30%)
  • treat: IV steroids
29
Q
Neuromyelitis Optica (NMO)
-
A
  • severe thoracic pain, bouts of optic neuritis, acute paraparesis with urinary retention
  • demyelination of grey & white matter
  • infiltration of macrophages
  • thickened, hyalinized blood vessels
  • mech: ab mediated demyelination & axonal injury & necrosis
30
Q

Internuclear Ophthalmoplegia (INO)

A
  • damage to medial longitudinal fasciculus

- lesion is on the side of the adduction deficit

31
Q

ADH

A

-kidney water retention

32
Q

Oxytocin

A
  • uterine contractions

- milk let down

33
Q

Prolactin

A

-milk production

34
Q

FSH & LH

A

-estrogen, progesterone, testosterone production

35
Q

ACTH

A

-corticosteroids

36
Q

THS

A

-thyroid T3 & T4

37
Q

GH

A

long bone growth

38
Q

Adenamatous Growths of Pituitary

A

-benign neoplasma that present as endocrine hyperactivity disorders dependent upon what cell type & what hormone is over secreted
-size determines therapeutic approach
1. Microademomas (10mm) surgery
80% of pit tumors

39
Q

Craniopharyngioma

A
  • rare tumor derived from remnants of Rathke’s pouch along a line from the nasopharynx to diencephalon
  • located intrasellar or suprasellar
  • 1/2 present clinically during childhood or adolescence other after 2nd/3rd decade
  • present with growth retardation in kids (interfere with GH), adults (visual defects) compress optic chiasm/nerve or diabetes insipidus
40
Q

Meningioma

A
  • benign tumors derived from meningeal membranes

- arise anywhere within calvaria and those that occur near sella cause visual impairment & hormonal deficiencies `

41
Q

Pituicytoma

A
  • rare, low-grade gliomas derived from the pituicytes of the posterior pituitary
  • present as mass lesion with signs/symptoms similar to meningioma
  • non-secreting tumors
42
Q

Somatotroph Adenomas

A

-secrete GH (acromegaly)

43
Q

Corticotroph adenomas

A

-secrete ACTH (cushing disease)

44
Q

Thyrothroh adenomas

A

-may secrete or not (TSH)

present as pit mass or hyperthyroidism

45
Q

Gonadotroph adenomas

A

-usually nonsecreting but may cause infertility