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Pathopharm 326 > Neuro > Flashcards

Neuro Flashcards

1
Q

nervous system is divided into two sections:

A

central nervous system: brain and spinal cord

peripheral nervous system: cranial/spinal nerves and the autonomic nervous system

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2
Q

two basic types of cells in nervous system

A

neuron: primary functional unit; doesn’t divide (generally) or replace themselves
neuroglia: more numerous and supportive to neuron; can replicate

when neurons are destroyed, generally replaced by neuroglia cells

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3
Q

types of neuroglia and function

A

oligodendrocytes: produce the myelin sheath in the CNS and make up white matter of brain

Shwann cells: myelinate the nerve fibers in the periphery

Astrocytes: provide structural support to neurons and form BBB; found in gray matter of brain

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4
Q

migraines

A

an episodic neurologic disorder that’s characterized by a HA that lasts between 4-72 hrs

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5
Q

diagnosis of migraine

A

two features must occur:

  • unilateral head pain
  • throbbing pain
  • worsens with activity
  • moderate/severe pain

AND one of these:

  • N/V
  • photophobia
  • phonophobia
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6
Q

classification of migraines

A

aura present - visual, sensory, or motor sxs
aura not present
chronic - 15 days/month for 3 months

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7
Q

risk factors of migraines

A

family hx
estrogen and progesterone
genetic and env. factors (triggers)

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8
Q

migraine triggers

A 
fatigue
oversleeping
missed meals
overexertion
weather change
stress
hormonal changes
bright lights or strong smells
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9
Q

patho of migraines

A

change in neurotransmitter levels in CNS
blood vessel tone

not completely understood; changes in brain metabolism and blood flow, dilation of blood vessels

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10
Q

clinical phases of migraines

A

premonitory phase
- 1/3 have fatigue, irritability, loss of concentration, stiff neck, food cravings

Migraine aura
- up to 1/3 have aura sxs lasting up to an hr

Headache phase

  • throbbing pain
  • fatigue, N/V, dizziness, hypersensitivity to touch on head
  • lasts 4-72 hrs

Recovery phase

  • irritability, fatigue, or depression
  • this phase can linger b/t hrs to days
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11
Q

sumatriptan

Imitrex

A

serotonin 1B/1D receptor agonists

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12
Q

sumatriptan

MOA

A

constrict intracranial blood vessels
suppress release of inflammatory neuropeptides
block brain pathways for pain

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13
Q

sumatriptan

SE

A

injection site rx, *chest pressure, *flushing, *weakness, HA, bad taste (nasal)

  • more frequent with subcut route
    contra: ischemic stroke, heart disease, angina
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14
Q

rimegepant

Nurtec

A

Calcitonin Gene-related peptide (CGRP)

this class is used when pts can’t take triptan due to contraindications, etc.

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15
Q

rimegepant

A

CGRP antagonist

used to treat acute migraines

mediates pain transmission

SE: GI upset (dyspepsia, abd. pain, N)

CYP substrate

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16
Q

migraine preventive therapy

A

beta blockers
tricyclic antidepressants
antiepileptic drugs
estrogens

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17
Q

multiple sclerosis

A

chronic, inflammatory, autoimmune disorder

potentially disabling; loss of myelin sheath

characteristics:
- inflammation (white matter of brain and spinal cord)
- demyelination
- scar development (gliosis)

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18
Q

MS etiology

A

unknown
may be triggered by infection
genetic predisposition

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19
Q

MS risk factors

A

age: 20-40
gender: women
location: moderately cool climate (northern US)
race: caucasian
genetics: family hx

men may have a more, severe progressive form

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20
Q

possible MS risk factors

A

smoking
vitamin d deficiency
obesity
infection (incl. epstein barr)

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21
Q

MS patho

A

autoimmune attack against the myelin sheath ending in axon destruction

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22
Q

types of progression of MS

A

benign: no disability with a return to baseline b/t attacks

relapsing-remitting: 80-90% of cases; always end of up a little weaker after each exacerbation

primary-progressive: steady increase in disability w/o attacks

secondary-progressive: initial RRMS that suddenly begins to decline w/o pds of remission

progressive-relapsing: steady decline; still declining even during remissions

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23
Q

clinical manifestations of MS

dependent on what nerves are impacted

A 
numbness, tingling
fatigue
walking difficulty (increases risk for falls)
pain
muscle spasms
emotional changes
urinary incontinence
cog fog
sexual issues
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24
Q

interferon beta-1a/b
varying trade names
(Avonex) 1a

A

used to treat MS

naturally occurring substance

MOA: inhibit pro-inflammatory WBCs from crossing BBB

decrease relapse by up to 30%

AE: flu-like rx, liver toxicity, bone marrow suppression (monitor blood counts), depression, drug interactions

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25
Q

glatiramer acetate

Copaxone

A

treat MS

MOA: increased production of anti-inflammatory T-cells which cross BBB and suppress inflammation

similar efficacy as interferons

AE:

  • injection site rxs
  • post-injection rxs: flushing, palpitations, chest pain, rash laryngeal constriction (all are transient and no treatment is necessary unless severe constriction)
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26
Q

fingolimod

Gilenya

A

oral agent

retain lymphocytes in the lymph nodes, preventing them from crossing BBB therefore decreasing inflammation

RRMS

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27
Q

dimethyl fumarate

Tecfidera

A

oral agent

developed specifically for MS

thought to inhibit immune cells and may have antioxidant properties

28
Q

natalizumab
(Tysabri)
infusion

A

MOA: prevents circulating T cells from leaving the vasculature and crossing BBB

treats MS and Crohn’s

monotherapy only; relapsing form of MS

29
Q

natalizumab

AEs

A

HA, fatigue (these most common)

Black Box: progressive multifocal leukoencephalopathy; risk increased when combined with other immunosuppresants

drug only available through the TOUCH program

hepatotoxic (monitor LFTs), hypersensitivity

30
Q

other infusion meds used to treat MS

A

alemtuzumab (Lemtrada)
- reserved for pts with poor response to 2 or more MS meds

mitoxantrone (Novantrone)

  • secondary progressive
  • progressive-relapsing
  • worsening RRMS (w/o complete remission)
31
Q

treating an acute relapse of MS

A

preferred
- high dose glucocorticoid

IV gamma globulin
- pts intolerant to glucocorticoids

ACTH (H.P. Acthar Gel)
- unable to tolerate steroids or have not been effective

32
Q

managing MS sxs

A 
urinary frequency - anticholinergics
urinary retention - cholinergics
constipation - bulk-forming laxative, stay hydrated
fatigue - amantadine, need more rest
muscle spasms - muscle relaxants
cognitive dysfx - donepezil (Aricept)
33
Q

myasthenia gravis (MG)

A

autoimmune disease; almost the opposite of parkinson’s except it’s autoimmune mediated by antibodies at the Ach receptors at the neuromuscular junction

characterized by fluctuating weakness of certain muscle groups

course of disease is variable

34
Q

MG risk factors

A

age: 10-65
gender: women

35
Q

MG patho

A

antibodies attack Ach receptors

this prevents Ach molecules from attaching and stimulating muscle contraction

36
Q

myasthenia gravis clinical manifestations

A

often first appear during pregnancy, post-partum or after anesthesia

  • insidious onset
  • fluctuating weakness of skeletal muscle
  • strength comes back after resting
  • muscles involved:
    eyes/eyelids, facial, speaking, breathing

at risk for impaired nutrition, aspiration and impaired ventilation

37
Q

myasthenic crisis

A

can develop as disease progresses

acute exacerbation of muscle weakness

triggered by a stressor:
infection, surgery, emotional distress, pregnancy, menses, inadequate pharmocotherapy (or noncompliant)

major complication:
- breathing muscle weakness leading to possible resp. arrest

38
Q

MG pharmacotherapy

A

immunosuppressants (steroids)

cholinesterase inhibitors - prevent inactivation of ACh by cholinesterase; give 30-45 minutes prior to eating to strengthen swallowing muscles

39
Q

neostigmine

Prostigmin

A

cholinesterase inhibitor

uses: MG and profound constipation

MOA: enhances cholinergic action by facilitating transmission of impulses across neuromuscular junctions; affects both muscarinic and nicotinic receptors

40
Q

nicorinic receptors

A

adrenal

skeletal muscles

41
Q

muscarinic receptors

A

glands

sweat

42
Q

neostigmine

AEs

A

muscarinic:

  • increased secretions, GI motility
  • urinary urgency
  • bradycardia
  • bronchial constriction
  • miosis (pupil constriction), near-sightedness

nicotinic (neuromuscular):

  • increased muscle contraction
  • toxic doses - reduced contraction

toxicity could lead to cholinergic crisis

43
Q

cholinergic crisis

A 
extreme muscle weakness or paralysis
s/s of excessive muscarinic stimulation
treatment: mechanical ventilation
antidote: atropine
pt should wear med alert bracel AAT
44
Q

MG crisis v. cholinergic crisis

A

ends are the same

MG - not enough ACh, muscle weakness, resp failure

cholinergic - too much ACh or nystigmine, overstimulation of muscles, wear out, resp failure

45
Q

differentiating between MG and cholinergic crisis

A

Give endrophonium which is a short acting cholinesterase inhibitor

will improve if MG crisis
worsen if cholinergic

46
Q

amyotrophic lateral sclerosis (ALS) aka Lou Gehrig’s disease

A

rare, progressive neuro disorder characterized by the loss of motor neurons (upper and lower)

death usually occurs around 3 years after diagnosis

unknown etiology

47
Q

ALS risk factors

A

age: 40-70
gender: male
genetics: 10%
smoking

48
Q

ALS patho

A

motor neurons in the brainstem and spinal cord gradually degenerate

49
Q

excitotoxicity hypothesis

A

excessive levels of glutamate intitiate a cascade of events that lead to neuron death

50
Q

ALS clinical manifestations

A

weakness of upper extremities (sometimes begins in legs), muscle wasting, spasticity

dysarthria, dysphagia, drooling

cognitive and behavioral changes

constipation

sleep problems

breathing - most common cause of death is resp. failure

51
Q

riluzole

Rilutek

A

glutamate inhibitor

only drug approved for ALS

MOA: glutamate antagonist; reduces damage to motor neurons

SE: dizziness, GI upset, hepatotoxic

increases life expectancy 3-6 months

52
Q

Guillain-Barre Syndrome (GBS)

A

autoimmune disorder that causes demyelination

myelin sheath is damaged by autoantibodies

onset: days to weeks following a viral infection

53
Q

GBS clinical manifestations

A

weakness/tingling in lower extremities that ascends up the body

severity of sxs increases over hrs or weeks

potentially life threatening if resp muscles are involved

recovery: descends down the body

54
Q

GBS clinical manifestations

A 
uncoordinated movements
 - loss of strength
 - difficulty walking
 - increased risk of falling
numbness and decreased sensations
 - as it ascends
loss of bladder/bowel control
blurred vision
 - often presents early, doesn't follow ascending pattern
difficulty breathing, swallowing, chewing
55
Q

GBS pharm

A

no known cure
some only get once, others have reoccurences
Goal of Rx: reduce severity & accelerate recovery
high dose steroid therapy, then taper
high-dose immunoglobulin therapy

56
Q

meningitis

A

acute inflammation of the meningeal tissues of the brain and spinal cord

etiology: infection (lungs or bloodstream) or penetrating wounds

Streptococcus pneumoniae and Neisseria meningitidis
Enteroviruses
fungi, parasites and toxins

57
Q

meningitis risk factors

A

older adults > 40
college students, military bases, prisoners
spread through resp. droplet, contaminated saliva
often follows an ear or sinus infection or in the immunocompromised

some people are carriers

occurs in the pia mater and the subarachnoid space with CSF

58
Q

meningitis classic triad

A

fever
headache
stiff neck

59
Q

meningitis other clinical manifestations

A 
N/V
photophobia
altered mental status (d/t increased ICP)
 -drowsiness - coma
 - seizures 
meningococcus
 - skin rash
 - petechiae or purpuric rash
60
Q

Positive Kernig sign

A

indicative of meningitis

flex knee and hip and then begin to extend leg toward ceiling, will cause pain in neck

61
Q

Positive Brudzinski sign

A

indicative of meningitis

pt lying supine, begin to flex chin towards chest, this will cause pt to flex the knees and hips

62
Q

bacterial meningitis

A

more deadly than viral

can cause long term effects such as hearing loss, seizure, brain damage, emboli causing loss of digits and limbs

63
Q

treatment for bacterial meningitis

A 
start abx immediately
aggressive antibiotics
IV, often multiple drugs
ceftriaxone, vancomycin
acyclovir (just in case it's viral)
steroid therapy
prophylaxis vaccines
64
Q

encephalitis

A

acute inflammation of the brain
almost always viral
west nile encephalitis, measles, chicken pox, mumps, HSV

65
Q

encephalitis clinical manifestations

A 
signs appear on day 2 or 3 of infection
range from mild changes in mental status to coma
other sxs:
 - fever
 - HA
 - N/V
 - other CNS changes
66
Q

encephalitis pharm

A 
acyclovir is used for HSV infection only
seizure disorders d/t increase in ICP
 - antiseizure meds
Supportive care
 - fluids
 - acetominophen
 - antiemetics
67
Q

brain abscess

A

accumulation of pus within the brain tissue

etiology: local or systemic infection
most common: ear, tooth, mastoid, or sinus infection
strep or staph usually

Pathopharm 326 (16 decks)

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