Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

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

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

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

migraines

A

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

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

classification of migraines

A

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

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

risk factors of migraines

A

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

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

migraine triggers

A 
fatigue
oversleeping
missed meals
overexertion
weather change
stress
hormonal changes
bright lights or strong smells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

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

sumatriptan

Imitrex

A

serotonin 1B/1D receptor agonists

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

sumatriptan

MOA

A

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

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

rimegepant

Nurtec

A

Calcitonin Gene-related peptide (CGRP)

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

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

rimegepant

A

CGRP antagonist

used to treat acute migraines

mediates pain transmission

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

CYP substrate

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

migraine preventive therapy

A

beta blockers
tricyclic antidepressants
antiepileptic drugs
estrogens

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

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

MS etiology

A

unknown
may be triggered by infection
genetic predisposition

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

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

possible MS risk factors

A

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

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

MS patho

A

autoimmune attack against the myelin sheath ending in axon destruction

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
glatiramer acetate | Copaxone
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)
26
fingolimod | Gilenya
oral agent retain lymphocytes in the lymph nodes, preventing them from crossing BBB therefore decreasing inflammation RRMS
27
dimethyl fumarate | Tecfidera
oral agent developed specifically for MS thought to inhibit immune cells and may have antioxidant properties
28
natalizumab (Tysabri) infusion
MOA: prevents circulating T cells from leaving the vasculature and crossing BBB treats MS and Crohn's monotherapy only; relapsing form of MS
29
natalizumab | AEs
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
other infusion meds used to treat MS
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
treating an acute relapse of MS
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
managing MS sxs
``` 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
myasthenia gravis (MG)
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
MG risk factors
age: 10-65 gender: women
35
MG patho
antibodies attack Ach receptors | this prevents Ach molecules from attaching and stimulating muscle contraction
36
myasthenia gravis clinical manifestations
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
myasthenic crisis
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
MG pharmacotherapy
immunosuppressants (steroids) cholinesterase inhibitors - prevent inactivation of ACh by cholinesterase; give 30-45 minutes prior to eating to strengthen swallowing muscles
39
neostigmine | Prostigmin
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
nicorinic receptors
adrenal | skeletal muscles
41
muscarinic receptors
glands | sweat
42
neostigmine | AEs
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
cholinergic crisis
``` extreme muscle weakness or paralysis s/s of excessive muscarinic stimulation treatment: mechanical ventilation antidote: atropine pt should wear med alert bracel AAT ```
44
MG crisis v. cholinergic crisis
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
differentiating between MG and cholinergic crisis
Give endrophonium which is a short acting cholinesterase inhibitor will improve if MG crisis worsen if cholinergic
46
amyotrophic lateral sclerosis (ALS) aka Lou Gehrig's disease
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
ALS risk factors
age: 40-70 gender: male genetics: 10% smoking
48
ALS patho
motor neurons in the brainstem and spinal cord gradually degenerate
49
excitotoxicity hypothesis
excessive levels of glutamate intitiate a cascade of events that lead to neuron death
50
ALS clinical manifestations
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
riluzole | Rilutek
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
Guillain-Barre Syndrome (GBS)
autoimmune disorder that causes demyelination myelin sheath is damaged by autoantibodies onset: days to weeks following a viral infection
53
GBS clinical manifestations
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
GBS clinical manifestations
``` 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
GBS pharm
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
meningitis
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
meningitis risk factors
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
meningitis classic triad
fever headache stiff neck
59
meningitis other clinical manifestations
``` N/V photophobia altered mental status (d/t increased ICP) -drowsiness - coma - seizures meningococcus - skin rash - petechiae or purpuric rash ```
60
Positive Kernig sign
indicative of meningitis flex knee and hip and then begin to extend leg toward ceiling, will cause pain in neck
61
Positive Brudzinski sign
indicative of meningitis pt lying supine, begin to flex chin towards chest, this will cause pt to flex the knees and hips
62
bacterial meningitis
more deadly than viral | can cause long term effects such as hearing loss, seizure, brain damage, emboli causing loss of digits and limbs
63
treatment for bacterial meningitis
``` start abx immediately aggressive antibiotics IV, often multiple drugs ceftriaxone, vancomycin acyclovir (just in case it's viral) steroid therapy prophylaxis vaccines ```
64
encephalitis
acute inflammation of the brain almost always viral west nile encephalitis, measles, chicken pox, mumps, HSV
65
encephalitis clinical manifestations
``` 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
encephalitis pharm
``` acyclovir is used for HSV infection only seizure disorders d/t increase in ICP - antiseizure meds Supportive care - fluids - acetominophen - antiemetics ```
67
brain abscess
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions