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Pathophysiology > Neurological Disorders (Exam 1) > Flashcards

Neurological Disorders (Exam 1) Flashcards

1
Q

Three functions of the nervous system

A

Detect, analyze and transmit information

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2
Q

Communicate through electrochemical signals

A

Neurons

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3
Q

Somatic and autonomic

A

Peripheral nervous system

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4
Q

Voluntary movement

A

Somatic

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5
Q

Involuntary movement (parasympathetic and sympathetic)

A

Autonomic

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6
Q

Arrive at CNS

A

Afferent

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7
Q

Exit from CNS (brain and spinal cord)

A

Efferent

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8
Q

Neurons do not

A

Divide

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9
Q

Sensory receptor cells to the brain

A

Sensory neurons

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10
Q

Brain to muscles

A

Motor neurons

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11
Q

Info between neurons

A

Interneurons

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12
Q

Modulate and regulate the electrical activity of a given neuron

A

Neurotransmitter

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13
Q

Electrical signal that travels down the axon and is created using NA and inhibited by K

A

Action potential

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14
Q

Three basic parts of a neuron

A

Soma, branching dendrites and axon

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15
Q

Junction between two neurons; passes info between them

A

Synapse

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16
Q

Open sodium and calcium channels leads to an action potential

A

Excitatory neurotransmitter

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17
Q

Open chloride channels > hyper polarization > resting potential

A

Inhibitory neurotransmitter

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18
Q

Resting potential average

A

-70 mV

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19
Q

Barrier between circulation and the brain (exception: olfactory lobes)

A

Blood brain barrier

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20
Q

Tight junctions from barriers

A

Endothelial cells

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21
Q

Structural support, immune properties

A

Pericytes

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22
Q

Structural support, recruits WBCs

A

Astrocytes

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23
Q

The BBB is a highly

A

Selective semipermeable membrane

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24
Q

Role of p-glycoprotein pumps

A

Remove harmful compounds

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25
Q

Lacks a functioning BBB; contains receptors to detect toxic substances that lead to emesis

A

Chemoreceptor trigger zone

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26
Q

Dysfunction of the BBB can lead to

A

Alzheimer’s or Parkinson’s

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27
Q

Most drugs are transported over the BBB via

A

Passive diffusion

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28
Q

Endogenous substances and amino acid derived drugs cross the BBB via

A

Carrier mediated

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29
Q

Endogenous substances such as hormones and LDL pass the BBB via

A

Receptor mediated

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30
Q

Some proteins pass the BBB via

A

Absorptive transcytosis

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31
Q

Substances pumped out of the BBB via

A

Active efflux

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32
Q

When a neurotransmitter also functions as a hormone

A

Neurohormones

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33
Q

When a neurotransmitter also functions as a hormone

A

Neurohormones

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34
Q

Membrane potential becomes more positive

A

Excitatory post synaptic potentials

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35
Q

Membrane potential becomes more negative

A

Inhibitory post synaptic potential

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36
Q

Depolarization approximately to

A

+35 mV

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37
Q

When potassium gates close slowly

A

Hyper polarization

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38
Q

When sodium channels close and potassium channels open, potassium flows out

A

Repolarization

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39
Q

Dopamine, norepinephrine and epinepherine

A

Catecholamines

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40
Q

Serotonin, dopamine, norepinephrine and epinephrine

A

Monoamines

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41
Q

Unpleasant sensory and emotional experience associated with actual or potential tissue damage

A

Pain (physiological)

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42
Q

Short duration and resolves

A

Acute

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43
Q

Longer than expected of healing; no useful physiological purpose

A

Chronic (pathophysiological pain)

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44
Q

How many people experience chronic pain at some point in their life?

A

1 in 3

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45
Q

From tissue damage due to trauma/inflammation; mechanical/temp/chemical stimuli

A

Nociceptive pain

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46
Q

Pain from musculoskeletal system (skin, bones, muscle, connective tissue)

A

Somatic

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47
Q

Pain from visceral organs (abdominal pain)

A

Visceral pain

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48
Q

Cancer can be from what type of pain

A

ALL TYPES OF PAIN :(

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49
Q

Functional pain

A

pain with no identified origin

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50
Q

Physiology of Pain (5 steps)

A
  1. transduction
  2. conduction
  3. transmission
  4. modulation
  5. perception
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51
Q
  1. Transduction (Pain process)
A

sensory neurons activated to noxious stimuli

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52
Q
  1. Conduction (Pain process)
A

action potential travels along the neuron to the spinal cord (A fibers and C fibers)

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53
Q

what are A fibers? what are C fibers?

A

A fibers - myelinated neurons; first pain
C fibers - unmyelinated fibers; 2nd pain

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54
Q
  1. Transmission (pain process)
A

sensory neurons release substances that activate a 2nd neuron in spinal cord and sends a message to the brain

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55
Q
  1. Modulation (pain process)
A

pain can be facilitated or inhibited depending on which substances are released

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56
Q
  1. Perception
A

complex interaction between ascending and descending pathways and various brain systems

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57
Q

overtime pain pathways become

A

stronger with repeated pain and leads to pain hypersensitivity

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58
Q

allodynia

A

pain caused by stimulus that does not normally provoke pain

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59
Q

hyperalgesia

A

increased response to stimulus that is normally painful

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60
Q

Substances that facilitate pain (3)

A
  1. Substance P
  2. Glutamate
  3. Inflammatory mediators
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61
Q

substances that reduce pain (4)

A
  1. endogenous opioids
  2. endogenous cannabinoids
  3. GABA
  4. serotonin and norepinephrine
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62
Q

Primary headache disorders

A

not due to another cause

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63
Q

primary headache examples (3)

A
  1. tension
  2. migraine
  3. cluster
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64
Q

secondary headaches

A

due to another medical condition

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65
Q

secondary headache examples (3)

A
  1. sinus headache
  2. brain tumor
  3. meningitis
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66
Q

migraine

A

moderate to severe headache interferes with normal functioning

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67
Q

how long do migraines last?

A

4-72 hours

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68
Q

two types of migraines

A

aura (25%)
without aura (75%)

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69
Q

aura

A

neurological symptoms that occur prior to and during a migraine headache; caused by cortical spreading depression

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70
Q

non rapid eye movement

A

not deep sleep, normal muscle tones, dec metabolism, HR,RR,BP

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71
Q

rapid eye movement

A

deep sleep and vivid dreams; inc in metabolism, low muscle tone, variations in VS

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72
Q

insomnia

A

difficulty falling asleep; constant awakening

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73
Q

the difference between primary insomnia and secondary insomnia

A

primary - unknown cause; 10-20%
secondary - stress; 80-90%

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74
Q

two types of sleep problems (insomnia types)

A
  1. onset insomnia (initiating sleep)
  2. maintenance insomnia (staying asleep)
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75
Q

Narcolepsy

A

uncontrollable excessive daytime sleepiness; altered REM/NREM

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76
Q

narcolepsy type 1

A

narcolepsy with cataplexy

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77
Q

cataplexy

A

loss of muscle control from strong emotions

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78
Q

narcolepsy part 2

A

narcolepsy without cataplexy

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79
Q

pathophysiology of narcolepsy

A

loss of orexin containing neurons

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80
Q

restless leg syndrome

A

desire to move limbs during rest

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81
Q

pathophysiology of restless leg syndrome

A

iron deficiency, poor circulation, dysfunction of dopaminergic neurotransmission

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82
Q

sleep apnea

A

repetitive upper airway, closure during sleep, decrease or stops in airflow leads to waking up

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83
Q

pathophysiology of sleep apnea

A

structure in jaw/neck or fatty deposits in neck

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84
Q

parasomnias

A

undesirable physical/behavioral phenomena occurs during sleep

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85
Q

NREM disorders of parasomnias

A

sleepwalking, sleep terrors, sleep talking, etc.

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86
Q

REM behavioral disorders

A

paralysis fails to occur during REM sleep, acting out in their dreams

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87
Q

circadian rhythms disorders

A

misalignment in sleep cycle

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88
Q

Guillain Barre Syndrome (GBS)

A

autoimmune disorder, attacks myelin around PNS neurons leading to schwann cell and neuronal damage

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89
Q

what is GBS triggered by?

A

infection or vaccine. it is typically reversible

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90
Q

symptoms of Guillain Barre Syndrome

A

-tingling sensation in extremities (paresthesia)
-difficulty with eye muscles, vision, swallowing, speaking, chewing
-pins and needles in hands/feet
-severe pain at night

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91
Q

Pathogenesis of GBS

A

molecular mimicry between offending agents and peripheral nerve gangliosides; leads to antiganglioside antibodies

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92
Q

Multiple Sclerosis

A

autoimmune, neurodegenerative disorder; attacks myelin surrounding CNS neurons leads to oligodendrocyte and neuronal damage

93
Q

symptoms of MS are dependent

A

on location of demylenation

94
Q

symptoms of MS in cerebellum

A

different in balance and coordination

95
Q

symptoms of MS in optic nerve

A

loss of vision, eye pain, involuntary eye movements (nystagmus)

96
Q

pathophysiology Outside In for MS

A

trigger activates T cell/B cell outside (PNS) and leads to infiltration of these cells into the CNS via dysfunctional BBB

97
Q

pathophysiology Inside Out for MS

A

disturbance in a metabolic process in the brain, leading to release of inflammatory cytokines/chemokines which compromises the integrity of BBB allowing T and B cells in

98
Q

Symptoms of MS occur based on

A

plaques

99
Q

CIS

A

clinically isolated syndrome of MS; symptoms last 24 hours and may or may not be MS

100
Q

RR

A

relapse remitting MS

101
Q

PP

A

primary progressive MS

102
Q

SP

A

secondary progressive MS

103
Q

85% originally diagnosed with this type of MS

A

relapse remitting

104
Q

Parkinson’s disease

A

movement disorder which occurs due to loss of dopamine producing neurons in the substantia nigra; lewy bodies present

105
Q

non motor symptoms of Parkinsons

A

Inosmia , rapid eye movement disorder, dementia, altered ANS function and REM sleep disorder

106
Q

pathophysiology of Parkinson’s

A

presence of Lewy bodies - abnormal aggregates of alpha synuclein protein in neurons - Lewy bodies in brain stem

loss of dopamine containing substantia nigra neurons lead to depigmentation in sub. nigra leads to motor symptoms

107
Q

dementia

A

collection of symptoms including decline in memory, reasoning and communication skills

108
Q

Alzheimer’s

A

build up of beta amyloid plaques and neurofibrillary tangles

109
Q

vascular dementia

A

damage to cerebral vasculation from conditions like hypertension, smoking, etc.

110
Q

lewy body

A

Abnormal aggregates of alpha-synuclein protein which form inside of neurons

111
Q

initial symptoms of lewy bodies

A

REM, hallucinations, etc.

112
Q

Frontotemporal Dementia (Pick’s Disease)

A

degeneration in frontal/ temporal lobes and abnormal tau accumulation

113
Q

initial symptoms of Pick’s disease

A

changes in personality, difficulty to produce language

114
Q

glutamate is

A

excitatory, tells the neuron to fire

115
Q

GABA is

A

inhibitory, dampens the firing rate

116
Q

Who brings information to the cell body? who takes information away?

A

dendrite bring
axons take away

117
Q

Neurotransmitter synthesis enzymes

A

enzymes responsible for the synthesis of the NT

118
Q

VG Na+ channel

A

responsible for depolarization in neuronal action potential

119
Q

VG Ca2+ channel

A

activated by membrane depolarization, CA influx leads to NT release

120
Q

Postsynaptic receptors

A

activation of these receptors leads to the physiological response of the NT

121
Q

Degrading enzymes

A

responsible for degradation of NT, can be located intra/extracellularly

122
Q

reuptake pump/transporter

A

transporters responsible for uptake of the NT from the synapse back into the presynaptic neuron

123
Q

Presynaptic autoreceptors

A

activation of presynaptic autoreceptors decreases NT release; negative feedback

124
Q

vesicular transporter

A

located presynaptically and responsible for uptake of NT into vesicles for storage

125
Q

Pathophysiology of circadian rhythm disorders

A

Misalignment of light-dark cycle of sleep

126
Q

Oligodendrocytes

A

Myelinating neuronal axons in CNS

127
Q

Schwann cells are the myelinating cells of the

A

PNS

128
Q

Myelin

A

Fatty substance that increases the rate of action potential; protective layer

129
Q

Nodes of Ranvier

A

Spaces between myelin sheaths with high density of VG NA channels; allows action potential to travel quickly

130
Q

GBS attacks what type of neurons leading to what type of damage?

A

PNS neurons; Schwann cell and neuronal damage

131
Q

Pathogenesis of Acute Inflammatory Demyelinating Polyneuropathy

A

Because of T cell mediated cytokine storm; no detectable antibodies

132
Q

Acute Motor Axonal Neuropathy and Acute Motor and Sensory Axonal Neuropathy are associated with

A

Traditional anti ganglioside antibodies

133
Q

In MS what type of neurons are attacked?

A

CNS neurons

134
Q

What is the immune response when T cells encounter myelin in MS?

What do B cells produce?

A

Production of pro inflammatory cytokines, tumor necrosis factor alpha, interferon gamma

B cells produce auto antibodies

135
Q

In MS, regulatory cells may

A

Reduce the immune response leading to periods of remission

136
Q

MS plaques in brain stem lead to

A

Difficulty swallowing, slurred speech

137
Q

MS plaques in the cerebellum lead to

A

Difficulty with balance and coordination

138
Q

MS plaques around the optic nerve lead to

A

Loss of vision, involuntary eye movements (nystagmus)

139
Q

MS plaques along the motor pathways lead to

A

Tremor, muscle weakness, muscle spasm, paralysis

140
Q

MS plaques in sensory pathways lead to

A

Paresthesia, loss of sensation

141
Q

MS plaques in the cerebral cortex lead to

A

Cognitive impairment, fatigue

142
Q

MS plaques on spinal nerves may result in

A

Urinary incontinence, sexual dysfunction and spasticity

143
Q

Parkinson’s diseases may be ___ or ___

A

Familial or sporadic

144
Q

Most of the medications used in PD

A

Enhance dopamine this neurotransmission but does NOT reduce or prevent loss of neurons

145
Q

Essential criteria for diagnosis of PD

A

Bradykinesia with at rest tremor and rigidity

146
Q

PD is characterized by

A

Lewy bodies in the brain stem

147
Q

Alpha- synuclein

A

Endogenous protein found in presynaptic nerve terminals

148
Q

Reduction in dopamine in what pathway leads to motor symptoms of PD?

A

Nigrostriatal pathway

149
Q

Bradykinesia?

Dyskinesia/hyperkinesia?

A

Too little dopamine

Too much dopamine

150
Q

Lewy body dementia

A

Build up of alpha synuclein in the cortex

151
Q

changes in the brain can

A

occur long before symptoms start to show

152
Q

dementia is caused by ___ and nerve cells become ____ and certain parts of the brain ____.

A
  1. physical brain diseases
  2. damaged and start to die
  3. starts to shrink
153
Q

Amyloid plaques pathophysiology in AD

A

extracellular beta amyloid deposition leads to generation of senile plaques

154
Q

Tau pathophysiology in AD

A

Tau becomes abnormally phosphorylated by kinases which leads to aggregation and structural dysfunction of neurons

155
Q

Hyperphosphorylated tau

A

dissembles microtubules and damages the cytoskeleton and signal transduction processes of neurons

156
Q

Other factors that play a role in AD (4)

A

neuroinflammation
cholinergic insufficiency
mitochondrial dysfunction
autophagy dysfunction

157
Q

Alzheimers disease is a

A

neurodegenerative disorder

158
Q

early onset AD

A

due to familial AD
due to mutations that lead to increased pathogenic amyloid beta
5% of cases

159
Q

late onset AD

A

combination of genetic and environmental factors
95% of cases

160
Q

genetic risk factor of Late onset AD

A

APOE4 gene

161
Q

Cholinergic hypothesis of AD

A

loss of cholenerigc activity is associated with AD severity, enhancing cholinergic signaling preserves cognitive function (ex: inhibit AChE)

162
Q

Glutamatergic hypothesis of AD

A

excess activation of NMDARs by glutamate leads to exitotoxicity and neuronal death in AD (block NMDARs to dec exitotoxicity)

163
Q

Amyloid precursor protein

A

transmembrane protein that plays a role in neuronal growth and repair; cleaved by secreatases which leads to AD

164
Q

Tau

A

intracellular protein that usually stabilizes neuronal microtubules

165
Q

Preclinical AD

A

no symptoms but biomarker evidence, can be 20 years before presence

166
Q

MCI due to AD

A

mild cognitive impairment; mild symptoms and biomarker

167
Q

Dementia due to AD

A

impaired daily function and biomarker

168
Q

examples of biomarkers (3)

A

decreased CSF AB42, increased CSF p-tau, decreased brain glucose metabolism

169
Q

Diagnosis of AD is based on

A

clinical assesment

170
Q

what is needed for a definitive diagnosis of AD

A

Histopathological analysis; done during autopsy

171
Q

Image studies to support diagnosis of AD (3)

A
  1. MRI - hippocamal atrophy
  2. FDG-PET and SPET - reduced cerebral flow and metabolic changes
  3. Amyloid PET - beta amyloid plaque density
172
Q

convulsion

A

sudden attack of involuntary muscular contractions/relaxtations

173
Q

seizure

A

abnormal CNS electrical activity

174
Q

epilepsy

A

a group of recurrent disorders of cerebral function characterized by both seizures and convulsions

175
Q

electroencephalogram

A

plays a central role in diagnosis with seizure disorders; can show irregular activity in the brain that indicates seizures

176
Q

causes of epilepsy (7)

A

genetic, vascular, severe head trauma, infections, tumor, drug abuse, unknown

177
Q

greatest cause of epilepsy

A

UNKNOWN!

178
Q

Partial seizures and 2 types

A

excessive electrical activity in one cerebral hemisphere
types: simple and complex

179
Q

Simple partial

A

preservation of consiouness

180
Q

complex partial

A

loss of awareness at seizure onset, originate in frontal or temporal lobes

181
Q

generalized seizures

A

excessive electrical activity in both cerebral hemispheres; loss of consciousness is common

182
Q

generalized seizures originate in the ___

A

thalamus and brainstem

183
Q

tonic seizures

A

sudden stiffening of the body, arms and legs

184
Q

clonic seizures

A

rhythmic jerking movements of the arms and legs without a tonic component

185
Q

does a normal of EEG rule out a seizure? why?

A

it does not rule out epilepsy. it can only show wavelengths during the test and the abnormal brain waves only happen during a seizure

186
Q

other techniques that can help diagnose epilepsy

A

MRI

187
Q

epilepsy

A

two or more unprovoked seizures that can’t be explained by a medical condition

188
Q

seizures are due to

A

an imbalance in excitation and inhibition in the brain

189
Q

pathophysiology of epilepsy

A

neuronal networks are overreactive
can be enhanced excitatory (inc in glutamate)
can be reduced inhibitory ( dec in GABA)
can be enhancement of overall NT (inc in AP)

190
Q

Brain injury

A

alterations in level of consciousness and in cognitive, motor or sensory function

191
Q

focal brain injury

A

injury to one specific area

192
Q

global brain injury

A

injury to entire brain or numerous areas of it

193
Q

mechanisms of brain injury (4)

A

direct damage
ischemia/hypoxia
excitotoxicity
excessive intracranial pressure

194
Q

excitotoxicity

A

due to glutamate buildup and excessive Ca2+ influx through NMDARs

195
Q

Traumatic brain injury is the

A

leading cause of death and disability among people under than 24

196
Q

primary injury of traumatic brain

A

damage caused by impact

197
Q

secondary injury of traumatic brain

A

damage caused by subsequent brain swelling, infection or ischemia

198
Q

concussion

A

mild type of TBI

199
Q

persistent vegetative state

A

loss of all cognitive functions and awareness for at least one month

200
Q

brain death

A

irreversible loss of function of the brain and brain stem

201
Q

Psychological disorders

A

disturbances in mood, thoughts and behaviors

202
Q

most psychiatric disorders have a

A

significant genetic component and environmental factors

203
Q

schizophrenia

A

positive symptoms, negative symptoms and cognitive dysfunction

204
Q

bipolar disorder

A

cyclic mood disorder characterized by episodes of mania and depression

205
Q

major depressive disorder

A

mood disorder characterized by depressive episodes

206
Q

anxiety disorders

A

excessive anxiety

207
Q

ADHD

A

primarily a disorder of the prefrontal cortex; executive function and maintaining attention

208
Q

pathophysiology of ADHD

A

dysregulation of dopaminergic and adrenergic systems

209
Q

Schizophrenia

A

characterized by positive symptoms, negative symptoms and cognitive impairment

210
Q

example of a positive symptom

A

hallucination

211
Q

example of a negative symptom

A

reduced motivation

212
Q

the most disabling disorder

A

schizophrenia

213
Q

dopaminergic hypothesis

A

inc in dopaminergic activity in mesolimbic, decrease in mesocortical, imbalance leads to schizophrenia

214
Q

mood disorders

A

affect a person’s emotional state

215
Q

most common mood disorders

A

depression and bipolar disorder

216
Q

Depression

A

at least one episode of depression (persistent sadness or loss of interest along with other symptoms)

217
Q

monoamine hypothesis

A

normal amount of monoamine NT becomes reduced, depleted, or dysfunctional, depression occurs

218
Q

HPA axis

A

hypothalamic pituitary axis; activated by stress

219
Q

overreactive HPA

A

in states of chronic stress; associated with MDD and anxiety disorders

220
Q

there is an association between elevated cortisol levels and

A

depression

221
Q

spina bifida

A

most common NTD; one or more vertebrae fail to form a complete vertebral arch for enclosure of the spinal cord

222
Q

Neuronal tube defects

A

stop in normal development of the brain and spinal cord during the first month of development

223
Q

why is supplementation of folic acid important?

A

deficiency in B9 could increase risk for NTDs

224
Q

when should folic acid supplementation begin?

A

before conception

225
Q

spina bifida occulata

A

small gap in spine, no protrusion

226
Q

meningocele

A

meninges protrude outward

227
Q

myelomeningocele

A

spinal cord and meninges protrude outward leading to spinal cord damage

228
Q

autism

A

bio-neurological developmental disability, appears before the age of 3

229
Q

individuals with autism also suffer from

A

numerous comorbid medical conditions

Pathophysiology (7 decks)

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