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Madsen Triad EPPP > Physio > Flashcards

Physio Flashcards

1
Q

Terms

loss of color vision due to an acquired brain disorder

A

Achromatopsia

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2
Q

Terms

inability to interpret sensations and hence to recognize things, typically as a result of brain damage

A

agnosia

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3
Q

Terms

achromotopsia damage area

A

ventral medial region of the occipital lobe

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4
Q

Terms

posterior parietal cortex and occipitotemporal regions

A

agnosia damage area

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5
Q

Terms

a life-threatening condition that involves having severely low levels of white blood cells called neutrophils.

A

agranulocytosis

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6
Q

Terms

akathisia

A

is a movement disorder characterized by a subjective feeling of inner restlessness accompanied by mental distress and an inability to sit still

dopamine

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7
Q

Terms

Inability to initiate voluntary movement

A

akinesia

Parkinsons symptom

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8
Q

Terms

anomia

A

a mild, fluent type of aphasia where individuals have word retrieval failures and cannot express the words they want to say (particularly nouns and verbs

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9
Q

Terms

damage to the left parietal lobe

A

anomia location

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10
Q

Terms

a person with a disability is cognitively unaware of having it due to an underlying physical or psychological condition

A

anosognosia

damage to parietal lobe

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11
Q

Terms

anticholinergic effects

A

block the action of ACh

delirium, extrapyramidal symptoms, GI, insomnia

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12
Q

Terms

aphasia

A

unable to comprehend or unable to formulate language because of damage to specific brain regions

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13
Q

Terms

apraxia

A

difficulty with motor planning to perform tasks or movements

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14
Q

Terms

loss of recognition or awareness of part of the body

A

asomatognosia

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15
Q

Terms

lack of voluntary coordination of muscle movements that can include gait abnormality, speech changes, and abnormalities in eye movements, that indicates dysfunction of parts of the nervous system that coordinate movement, such as the cerebellum

A

ataxia

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16
Q

Terms

variations in melody, intonation, pauses, stresses, intensity, vocal quality, and accents of speech

A

dysprosydy

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17
Q

Terms

constellation of symptoms[1] that suggests the presence of a lesion usually near the junction of the temporal and parietal lobes at or near the angular gyrus

A

Gerstmann’s syndrome

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18
Q

Terms

Gerstmann’s syndrome symptoms

A
  • dysgraphia/agraphia
  • dyscalculia
  • finger agnosia
  • left-right orientation
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19
Q

Terms

[ ] a rare, but potentially fatal side effect of the antipsychotic drugs.

A

Neuroleptic Malignant Syndrome

It involves a rapid onset of motor, mental, and autonomic symptoms including muscle rigidity, tachycardia, hyperthermia, and altered consciousness. To avoid a potentially fatal outcome, the drug must be stopped as soon as symptoms of NMS develop.

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20
Q

Terms

abnormal sensation of the skin (tingling, pricking, chilling, burning, numbness) with no apparent physical cause

A

paresthesia

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21
Q

Terms

involuntary repetitive body movements, which may include grimacing, sticking out the tongue or smacking the lips

A

tardive dyskinesia

long-term use of antipsychotics

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22
Q

Terms

face-blindness

A

prosopagnosia

occipito-temporal lobe damage

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23
Q

Terms

perceptual phenomenon in which stimulation of one sensory or cognitive pathway leads to involuntary experiences in a second sensory or cognitive pathway

A

synestheisa

reason unknown

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24
Q

Terms

impairment in recognition of visually presented objects

A

visual agnosia

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25
Q

Nervous System Overview

golgi complex

Neuron Cell Body

A

system of membranes that prepare neurotransmitters for secretion

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26
Q

Nervous System Overview

collaterals

A

most neurons have a single axon that divides into numerous branches (called collaterals)

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27
Q

Nervous System Overview

myelin sheath

A

covers the axon, acts as an insulator and speeds up the conduction of nerve impulses

made up of glial cells

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28
Q

Nervous System Overview

  • holding neurons together
  • providing neurons with nutrients
  • removing cellular debris
A

functions of glial cells

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29
Q

Nervous System Overview

messages transmitted from neurons dendrites to the end of the axon through a [ ] called [ ]

A

electrical process called conduction

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30
Q

Nervous System Overview

[ ] charged sodium ions enter the cell to create a state of [ ]

A

positively charged; depolarization

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31
Q

Nervous System Overview

action potential

A

With sufficient stimulation from other cells, a cell becomes depolarized (the interior of the cell becomes less negative), which triggers an action potential - i.e., an electrical impulse that travels quickly through the cell.

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32
Q

Nervous System Overview

The [ ] principle predicts that an action potential will always be of the same magnitude regardless of the amount of stimulation received by a neuron as long as the minimal level of stimulation (the threshold) has been reached.

A

all-or-none

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33
Q

Nervous System Overview

[ ] mediates neuromuscular transmission, parasympathetic arousal, and memory (e.g., memory loss in Alzheimer’s dementia).

A

Acetylcholine

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34
Q

Nervous System Overview

involved in inhibitory motor regulation and motivational/emotional functions.

A

Dopamine

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35
Q

Nervous System Overview

insufficient dopamine in basal ganglia

A

parkinsons

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36
Q

Nervous System Overview

too much dopamine

A

schizophrenia and tourettes

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37
Q

Nervous System Overview

ordinarily inhibits behavior and is involved in the regulation of mood, hunger, arousal, sleep, temperature, and pain and in the Bipolar and Depressive Disorders, Schizophrenia, and OCD

A

Serotonin

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38
Q

Nervous System Overview

[ ] is the most common inhibitory neurotransmitter and is believed to be involved in anxiety, sleep, and seizures.

A

GABA

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39
Q

Nervous System Overview

not enough GABA

A

Huntingtons

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40
Q

Nervous System Overview

mood, attention, dreamining, learning, autonomic functions

A

norepinephrine

according to the catecholamine hypothesis, low levels of norepinephrine are linked to depression

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41
Q

Nervous System Overview

excitatory neurotransmitter, plays a role in learning and memory, Long-Term-Potentiation

A

glutamate

excess can lead to excitotoxicity, seizures, stroke

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42
Q

Nervous System Overview

endorphins

A

endogenous morphines, pain relief, substance P

also involved in memory, learning, sexual behavior

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43
Q

Nervous System Overview

31 segments, 5 parts

A

spinal cord

cervical, thoracic, lumbar, sacral, coccygeal

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44
Q

Nervous System Overview

Damage at the cervical level ordinarily results in [ ] (loss of sensory and voluntary motor functioning in the arms and legs),

A

quadriplegia

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45
Q

Nervous System Overview

damage at the [ ] level causes paraplegia (loss of functioning in the legs).

A

thoracic

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46
Q

Nervous System Overview

The [ ] are the four cavities of the brain that contain cerebrospinal fluid. Blockage of the ventricles and a resulting build-up of fluid can cause [ ] .

A

ventricles; hydrocephalus

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47
Q

Nervous System Overview

12 pairs of cranial nerves and 31 sets of sensory and motor nerves

A

PNS (peripheral nervous system)

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48
Q

Nervous System Overview

SNS

A

somatic nervous system: from the sense receptors to the CNS, and from the CNS to the skeletal muscles

controls voluntary activity

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49
Q

Nervous System Overview

autonomic nervous system (ANS)

A

is a division of the peripheral nervous system and is involved in the control of visceral functions (e.g., heart rate, blood pressure, respiration, digestion, and sweating).

contains parasympathetic and sympathetic branches

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50
Q

Nervous System Overview

sympathetic branch

of the ANS

A

The sympathetic branch is involved in the mediation of flight or fight (emergency) reactions.

Activation of the sympathetic branch produces increased heart rate, pupil dilation, increased blood sugar, and inhibition of the digestive processes.

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51
Q

Nervous System Overview

parasympathetic branch

of the ANS

A

The parasympathetic branch regulates energy conservation and relaxation.

Activation is associated with slowing of heart rate, lowered blood pressure, contraction of pupils, reduction of sweat gland output, and increased activity of the digestive system.

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52
Q

Nervous System Overview

proliferation

CNS Development

A

new cells produced in neural tube

starts at 2.5 weeks

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53
Q

Nervous System Overview

migration

CNS Development

A

cells migrate to their final destination

8 weeks

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54
Q

Nervous System Overview

differentiation

CNS Development

A

start off looking like other cells, neurons then turn into neurons with axons and dendrites

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55
Q

Nervous System Overview

myelination

CNS Development

A

glial cells form a sheath around cells axon

occurs post-natally

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56
Q

Nervous System Overview

synaptogenesis

CNS Development

A

formation of synapses, influenced by endogenous and exogenous factors

occurs post-natally

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57
Q

Nervous System Overview

apoptosis

CNS Development

A

pruning, cell death, “fine-tunes” brain development

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58
Q

Nervous System Overview

structural techniques

Neuroimaging

A

Computed tomography (CT) and magnetic resonance imaging (MRI) are structural techniques.

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59
Q

Nervous System Overview

Functional techniques

Neuroimaging

A

Positron-emission tomography (PET), single proton emission computed tomography (SPECT), and functional magnetic resonance imaging (fMRI) provide information on the functional activities of the brain.

(spect is lower resolution than PET)

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60
Q

Brain Anatomy and Physiology

[ ] is a hindbrain structure that controls the flow of information between the spinal cord and brain and regulates a number of vital functions including breathing, heartbeat, and blood pressure.

A

The medulla

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61
Q

Brain Anatomy and Physiology

The [ ] is a large structure on the dorsal aspect of the hindbrain. It is involved in the extrapyramidal control of motor activities (e.g., coordination, balance, posture).

A

cerebellum

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62
Q

Brain Anatomy and Physiology

Damage to the cerebellum can result in

A

ataxia, which is characterized by slurred speech, severe tremors, and a loss of balance.

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63
Q

Brain Anatomy and Physiology

midbrain contains

A
  • superior and inferior colliculi
  • substantia nigra
  • reticular formation
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64
Q

Brain Anatomy and Physiology

hypothalamus

A

The hypothalamus consists of a cluster of nuclei that control the autonomic nervous system and endocrine glands, mediate basic drives, and regulate emotional expression.

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65
Q

Brain Anatomy and Physiology

SCN

A

The suprachiasmatic nucleus (SCN), which is located in the hypothalamus, is involved in regulation of the body’s circadian rhythms.

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66
Q

Brain Anatomy and Physiology

thalamus

A

The thalamus is a “relay station” for all of the senses except olfaction and is also involved in language and memory.

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67
Q

Brain Anatomy and Physiology

Wernicke-Korsakoff definition

A

Wernicke-Korsakoff syndrome is due to a thiamine deficiency that causes atrophy of neurons in certain areas of the thalamus and the mammillary bodies of the hypothalamus and is usually the result of chronic alcoholism.

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68
Q

Brain Anatomy and Physiology

Wernicke Korsakoff course

A

It begins with Wernicke’s encephalopathy, which is characterized by mental confusion, abnormal eye movements, and ataxia; and is then followed by Korsakoff’s syndrome, which involves severe anterograde amnesia, retrograde amnesia, and confabulation.

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69
Q

Brain Anatomy and Physiology

The [ ] is a network of nerve fibers involved in wakefulness, arousal, and consciousness.

A

reticular activating system (RAS)

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70
Q

Brain Anatomy and Physiology

reticular formation

A

contains 90 nuclei, extends from the spinal cord through the hindbrain and midbrain into the hypothalamus and forebrain

damage disrupts sleep/wake cycle

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71
Q

Brain Anatomy and Physiology

The [ ] are subcortical structures (caudate nucleus, putamen, globus pallidus, and substantia nigra) that are involved in planning, organizing, and coordinating voluntary movements

A

basal ganglia

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72
Q

Brain Anatomy and Physiology

basal ganglia parts

A

caudate nucleus, putamen, globus pallidus, and substantia nigra

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73
Q

Brain Anatomy and Physiology

Basal ganglia pathology has been linked to

A

Huntington’s disease, Parkinson’s disease, Tourette’s Disorder, OCD, and ADHD

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74
Q

Brain Anatomy and Physiology

amygdala

A

motivational, emotional, attaches emotions to memories, recall of emotionally charged experiences

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75
Q

Brain Anatomy and Physiology

lesions in the amygdala leads to

A

reduction of fear and aggression, called Kluver-Bucy syndrome

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76
Q

Brain Anatomy and Physiology

The [ ] is a limbic system structure that is important for spatial and explicit memory and the consolidation of declarative memories.

A

hippocampus

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77
Q

Brain Anatomy and Physiology

cingulate cortex

A
  • surrounds the corpus callosum
  • involved in attention, emotion, and perception and subjective experience of pain
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78
Q

Brain Anatomy and Physiology

The right and left hemispheres are connected by several bundles of fibers, the largest of which is the [ ]

Forebrain

A

corpus callosum.

If the corpus callosum is severed, the two hemispheres operate essentially as separate, independent brains.

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79
Q

Brain Anatomy and Physiology

contralateral representation

A

For most sensory and motor functions, the cortex exhibits contralateral representation, which means that the left hemisphere controls the functions of the right side of the body and vice-versa.

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80
Q

Brain Anatomy and Physiology

brain lateralization

A

Though the left and right hemispheres are both involved to some degree in most functions, they tend to specialize.

This specialization is referred to as brain lateralization and was initially studied in split-brain patients, whose corpus callosums had been severed to control severe epilepsy.

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81
Q

Brain Anatomy and Physiology

right hemisphere dominates in

A
  • visual-spatial activities such as facial recognition
  • spatial interpretation and memory for shapes
  • negative emotions.
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82
Q

Brain Anatomy and Physiology

left hemisphere dominates in

A
  • verbal activities spontaneous speaking and writing
  • word recognitio
  • memory for words and numbers
  • analytical, logical thought
  • positive emotional states
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83
Q

Brain Anatomy and Physiology

frontal lobe parts

A
  • primary motor cortex, * supplementary motor area,
  • premotor cortex
  • Broca’s area
  • prefrontal cortex
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84
Q

Brain Anatomy and Physiology

frontal lobe involved in

A
  • initiative
  • planning ability
  • abstract thinking
  • other executive functions * personality and mood
  • motor functions.
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85
Q

Brain Anatomy and Physiology

Damage to Broca’s area

A

produces Broca’s (expressive) aphasia

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86
Q

Brain Anatomy and Physiology

Damage to the prefrontal cortex produces

A

personality changes and deficits in higher-level cognitive abilities

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87
Q

Brain Anatomy and Physiology

damage to dorsolateral area

prefrontal cortex

A

impaired judgement, insight, planning

individuals become perseverative, poor hygiene

88
Q

Brain Anatomy and Physiology

damage to orbitofrontal area

prefrontal cortex

A

pseudopsychopathy

89
Q

Brain Anatomy and Physiology

damage to mediofrontal area

prefrontal cortex

A

frontal apathetic symdrome, pseudodepression

90
Q

Brain Anatomy and Physiology

parietal lobe contains

A

somatosensory cortex

91
Q

Brain Anatomy and Physiology

apraxia

parietal lobe

A

tactile agnosia, asomatognosia, anosognosia

parietal lobe damage

92
Q

Brain Anatomy and Physiology

Wernicke’s area

parietal lobe

A

comprehension, lesions produce receptive aphasia

when you’re inwvolved with something you comprehend it

93
Q

Brain Anatomy and Physiology

The occipital lobe contains the

A

visual cortex

94
Q

Brain Anatomy and Physiology

Damage to the [ ] lobe can result in visual agnosia (inability to recognize familiar objects), color agnosia, word blindness, and/or scotomas (blind spots).

A

occipital

95
Q

Brain Anatomy and Physiology

Lesions at the junction of the occipital, temporal, and parietal lobes can produce [ ]

A

prosopagnosia (inability to recognize familiar faces).

96
Q

Sensation and Perception

According to the [ ], there are three types of color receptors that are each receptive to a different primary color (red, blue, or green). All other colors are produced by variations in the activity of these three receptors.

A

trichromatic theory

97
Q

Sensation and Perception

opponent-process theory

A
  • postulates three bipolar receptors: red-green, yellow-blue, and white-black.
  • some cells are excited by red and inhibited by green, and so on; and the overall pattern of stimulation of these cells produces the various colors that we perceive.
98
Q

Sensation and Perception

  • usually caused by a gene on the x crhomosome
  • 8-10% of male population
A

color-blindness

99
Q

Sensation and Perception

congenital achromatopsia

A

inherited form of total colorblindness

100
Q

Sensation and Perception

olfaction process

A

olfactory receptors → olfactory bulb → primary olfactory cortex, orbitofrontal cortex, amygdala

101
Q

Sensation and Perception

area of the body that is innvervated by the dorsal root of a given segment of the spinal cord

A

dermatome

102
Q

Sensation and Perception

older adults with chronic pain report

A
  • lower pain than younger adults
  • fewer symptoms of depression dealing with the pain
103
Q

Sensation and Perception

According to [ ], there are mechanisms in the spinal cord that mediate (block) the perception of pain.

A

gate-control theory

104
Q

Sensation and Perception

a rare condition in which the stimulation of one sensory modality triggers a sensation in another sensory modality. For example, a person with synesthesia might hear a color or taste a shape.

A

synesthesia

105
Q

Sensation and Perception

just noticeable differences (JNDs) are measured by

A

psychophysical laws (Webers, Fechners, Steven’s Power)

106
Q

Sensation and Perception

difference between

  • Webers
  • Fechner’s
  • Steven’s Power
A
  • Webers- W for WEIGHT- if if 1 gram has to be added to ten grams for a difference to be detected, then 10 grams would have to be added to 100 grams
  • Fechners LawGarithm - logarithmic change
  • Steven’s Power Law- “the the power of” meaning it has to be exponential
107
Q

Physio: Learning and Memory

The [ ] which encode, store, and retrieve of long-term declarative memories.

A

temporal lobes

108
Q

Physio: Learning and Memory

The [ ] consolidates of long-term declarative memories (transferring information from short-term to long-term memory).

A

hippocampus

109
Q

Physio: Learning and Memory

The [ ] plays a key role in fear conditioning, learning about rewards and punishments, and adding emotional significance to memories.

A

amygdala

110
Q

Physio: Learning and Memory

The [ ] is associated with short-term memory, episodic memory, and prospective memory.

A

prefrontal cortex

issues linked with schizophrenia

111
Q

Physio: Learning and Memory

The [ ] is involved in processing information and transferring it to the neocortex.

A

thalamus

112
Q

Physio: Learning and Memory

Neural mechanisms that are believed to mediate long-term memory include [ ] and [ ]

A

long-term potentiation and protein/RNA synthesis

113
Q

Physio: Learning and Memory

is a physiological process involving the modification of nerve synapses, especially at glutamate receptors in the hippocampus

A

Long-term potentiation (LTP)

114
Q

Physio: Learning and Memory

Inhibiting the synthesis of protein or RNA at the time of learning prevents the formation of [ ]

A

long-term memories

115
Q

Physio: Language

difficulty producing written or spoken language with little or no comprehension issues;

A
  • Broca’s aphasia is caused by damage to Broca’s area and involves
  • it often includes anomia and impaired repetition.
116
Q

Physio: Language

damage to Wernicke’s area

A

Wernicke’s aphasia

  • involves an inability to comprehend written or spoken language along with the production of rapid
  • seemingly effortless speech that is lacking in content; it may include anomia, paraphasia, and impaired repetition.

WEEKEND at bernie’s- acting like you make sense but actually gibberish

117
Q

Physio: Language

damage to the arcuate fasciculus

A

Conduction aphasia

  • comprehension intact
  • anomia, paraphasia, impaired repetition
118
Q

Physio: Language

Transcortical aphasia types

A
  • transcortical motor aphasia
  • transcortical sensory aphasia
  • mixed transcortical aphasia

caused by lesions outside of broca’s and wernicke’s area

119
Q

Physio: Language

widespread brain injury aphasia type

A

global aphasia

  • few words
  • automatic speech (exclamations)
120
Q

Physio: Emotion and Stress

“you are afraid because your knees are shaking and your heart is pounding”

A

James-Lange theory focuses on peripheral factors, proposing that emotions represent perceptions of bodily reactions to sensory stimuli.

J comes before L just like Body comes before Emotion

121
Q

Physio: Emotion and Stress

[ ] theory focuses on the brain mechanisms that mediate emotion, proposing that emotional and bodily reactions to stimuli occur simultaneously due to thalamic stimulation of the cortex and the peripheral nervous system.

A

Cannon-Bard

CB are close to each other, simultaneous reaction

122
Q

Physio: Emotion and Stress

[ ] theory says that emotions are universal but differences in how emotion-arousing events are appraised.

A

Lazarus’s cognitive appraisal

  • It distinguishes between three types of cognitive appraisal: primary, secondary, and re-appraisal.
123
Q

Physio: Emotion and Stress

Two-Factor Theory

Schachter and Singer

A

emotional experiences are a combination of physiological arousal and cognitive interpretation

epinephrine study- explaining arousal based on the behavior of a confed

124
Q

Physio: Emotion and Stress

[ ] was proposed as a brain mechanism (circuit) that mediates the experience and expression of emotion.

A

Papez’s circuit

It includes the hippocampus, mammillary bodies, anterior nuclei of the thalamus, and cingulate gyrus.

125
Q

Physio: Emotion and Stress

General Adaptation Syndrome

Selye

A

response to stress is mediated by adrenal-pituitary secretions (e.g., cortisol) and involves three stages:

  • alarm reaction
  • resistance
  • exhaustion

The model predicts that prolonged stress can result in illness or death.

126
Q

Physio: Emotion and Stress

Type A Behavior Pattern

A

People exhibiting the Type A behavior pattern are highly competitive and achievement-oriented, have a sense of time urgency, and tend to be hostile, easily irritated, and impatient.

127
Q

Physio: Emotion and Stress

A number of studies have confirmed that, of the Type A characteristics, [ ] is most strongly associated with health problems, especially coronary heart disease in males.

A

cynical or antagonistic hostility

128
Q

Physio: Sex, Sleep, Dreaming

sexual dimorphism in brain development

A

differences in size of

  • corpus callosum
  • hippocampus
  • SCN

differential exposure to androgens

129
Q

Physio: Sex, Sleep, Dreaming

when the hypothalamus secretes chemicals that stimulate the anterior pituitary gland, which then releases the gonadotropic hormones that stimulate testosterone and sperm production by the testes or ovulation and estrogen production by the ovaries. This system is referred to as the [ ]

A

hypothalamic-pituitary-gonadal axis

130
Q

Physio: Sex, Sleep, Dreaming

female sex drive and androgen

A

androgen more effective than estrogen for restoring sexual arousal, but there is a plateau effect

131
Q

Physio: Sex, Sleep, Dreaming

sleep stages

A

alpha, beta, theta, delta

132
Q

Physio: Sex, Sleep, Dreaming

beta waves

A

alert, fully awake

133
Q

Physio: Sex, Sleep, Dreaming

alpha waves

A

awake, rested, relaxed

134
Q

Physio: Sex, Sleep, Dreaming

theta waves

A

deep relaxation, light sleep

135
Q

Physio: Sex, Sleep, Dreaming

Stage 1 sleep

A

alpha replaced by theta

136
Q

Physio: Sex, Sleep, Dreaming

Stage 2 sleep

A

theta predominates, interrupted by spindles, and k complexes

137
Q

Physio: Sex, Sleep, Dreaming

Stage 3 sleep

A

large slow delta waves appear

138
Q

Physio: Sex, Sleep, Dreaming

Stage 4 sleep

A

deep sleep, delta waves

139
Q

Physio: Sex, Sleep, Dreaming

Stage 5 sleep

A

REM

140
Q

Physio: Sex, Sleep, Dreaming

sleep stages are on a cycle every

A

90-100 minutes

141
Q

Physio: Sex, Sleep, Dreaming

effects of age on sleep

A
  • REM is 50% of newborn’s total sleep, drops to 30% @ 6mo
  • less REM
  • bed earlier, waking up earlier
  • do not require less sleep than younger adults
142
Q

Physio: Neurobehavioral

close-head injuries have two sites of impact: the [ ] and the [ ]

A
  • coup (point of impact)
  • contrecoup (other side where the brain hit the skull)
143
Q

Physio: Neurobehavioral

closed head injuries are often accompanied by

A
  • loss of consciousness
  • anterograde/retrograde amnesia
144
Q

Physio: Neurobehavioral

TBI severity determined by

A
  • GCS (glasgow coma score)
  • PTA (posttraumatic amnesia)
  • duration of LOC (loss of consciousness)
145
Q

Physio: Neurobehavioral

TBI retrograde amnesia

A

recent memories (pre-injury) more affected than remote memories

146
Q

Physio: Neurobehavioral

CVA refers to a

A

stroke

cerebrovascular event

147
Q

Physio: Neurobehavioral

CVA types

stroke

A

thombosis, embolism, hemorrhage

148
Q

Physio: Neurobehavioral

CVA risk factors

A

hypertension and atherosclerosis

149
Q

Physio: Neurobehavioral

Huntington’s

genetics

A

Huntington’s disease is an inherited degenerative disease that is transmitted by a single autosomal dominant gene

150
Q

Physio: Neurobehavioral

Huntington’s

Emotional and Cognitive Symptoms

A

For many patients, emotional and cognitive symptoms appear first and include depression, apathy, anxiety, antisocial tendencies, and forgetfulness.

151
Q

Physio: Neurobehavioral

Huntington’s

Motor Symptoms

A

Early motor symptoms include fidgeting, and clumsiness, which are followed by facial grimaces and “piano-playing” movements of the fingers.

152
Q

Physio: Neurobehavioral

Huntington’s

etiology

A

Huntington’s disease is believed to be due to a loss of GABA-secreting neurons and glutamate excitotoxicity in the basal ganglia, especially in the caudate nucleus, putamen, and globus pallidus.

153
Q

Physio: Neurobehavioral

Parkinson’s

symptoms

A

Parkinson’s disease is a progressive degenerative disease characterized by tremor, muscular rigidity, akathisia, akinesia, and speech difficulties; and it may eventually include dementia.

154
Q

Physio: Neurobehavioral

Parkinson’s

treatment

A

Symptoms are temporarily relieved by L-dopa, a dopamine agonist.

155
Q

Physio: Neurobehavioral

Parkinson’s

etiology

A

due to degeneration of dopamine-containing cells, especially in the substantia nigra.

156
Q

Physio: Neurobehavioral

Parkinson’s

Positive Symptoms

A
  • tremor at rest
  • muscle rigidity
  • akathisia
157
Q

Physio: Neurobehavioral

Parkinson’s

negative symptoms

A
  • postural disturbances
  • speech difficulties
  • bradykinesia (slowed movement)
158
Q

Physio: Neurobehavioral

grand mal seizures include a [ ] stage wherein the muscles contract and the body stiffens; a [ ] stage with rhythmic shaking of the limbs; and postseizure depression or confusion with amnesia for the ictal event.

A

tonic; clonic

159
Q

Physio: Neurobehavioral

[ ] seizures are brief attacks involving a loss of consciousness without prominent motor symptoms.

A

Absence (petit mal)

160
Q

Physio: Neurobehavioral

[ ] seizures begin in one side of the brain and affect one side of the body, at least initially but can spread into generalized seizures.

A

Partial

161
Q

Physio: Neurobehavioral

[ ] is a progressive disease of the nervous system that involves a degeneration of the myelin that surrounds nerve fibers in the central nervous system.

A

Multiple sclerosis (MS)

162
Q

Physio: Neurobehavioral

MS symptoms

A
  • optic neuritis
  • motor impairments
  • sensory abnormalities
  • fatigue

Additional symptoms that arise as the disease progresses include tremors, speech problems, mood symptoms, and cognitive impairment.

163
Q

Physio: Neurobehavioral

types of MS

A
  • relapsing-remitting type
  • secondary progressive type
164
Q

Physio: Neurobehavioral

Primary (essential) hypertension occurs when there is [ ]

Secondary hypertension occurs when elevated blood pressure is related to a known disease.

A

no known physiological cause (85-90% of cases)

165
Q

Physio: Neurobehavioral

hypertension prevalence by race and age

A

Older adults have higher rates than younger adults, and African Americans have higher rates than Whites. Rates are generally higher for men; however, for older adults and African Americans, rates are higher for women.

166
Q

Physio: Neurobehavioral

migraine types

A
  • common
  • classic (starts with an aura) (12% of migraine sufferers)
167
Q

Physio: Neurobehavioral

headache types

A
  • cluster headache (many a day)
  • tension headache (non-throbbing, bilateral, band of pressure)
  • Sinus headache (first thing in the morning, over the eyes)
168
Q

Physio: Neurobehavioral

PMS prevalence

A
  • 30-80% of women of reproductive age
169
Q

Physio: Neurobehavioral

hyposecretion of ADH

antidiuretic hormone

A

diabetes insipidus

170
Q

Physio: Neurobehavioral

hypo/hyper-secretion of ADH

in childhood

A

dwarfism/giantism

171
Q

Physio: Neurobehavioral

hyperthyroidism

A

Grave’s disease

over-secretion of thyroxine

172
Q

Psychopharmacology

A

Agonists produce effects similar to those produced by a neurotransmitter

173
Q

Psychopharmacology

[ ] produce an effect opposite the effect produced by a neurotransmitter or an agonist.

A

Inverse agonists

174
Q

Psychopharmacology

[ ] produce effects that are similar to (but less than) the effects produced by a neurotransmitter or an agonist.

A

Partial agonists

175
Q

Psychopharmacology

[ ] produce no activity in the cell on their own but, instead, reduce or block the effects of a neurotransmitter or agonist.

A

Antagonists

176
Q

Psychopharmacology

dosing older adults

A

“start low and go slow”

same with asians and african americans

177
Q

Psychopharmacology

direct antagonists

A

attach to receptor site

178
Q

Psychopharmacology

indirect antagonists

A

attach to a binding site on a receptor cell and interfere

179
Q

Psychopharmacology

Antipsychotic

Use

A

The traditional antipsychotic drugs (e.g., phenothiazines) are used for the management of Schizophrenia and other psychoses. They are most effective for positive symptoms (delusions, hallucinations, agitation, thought disorders).

180
Q

Psychopharmacology

Antipsychotic

Side Effects

A

Side effects include anticholinergic, extrapyramidal effects, and neuroleptic malignant syndrome.

181
Q

Psychopharmacology

Antipsychotic

Mode of Action

A

These drugs exert their beneficial effects primarily by blocking dopamine receptors, and their effectiveness provides support for the dopamine hypothesis which attributes schizophrenia to overactivity at dopamine receptors.

182
Q

Psychopharmacology

[ ] is a potentially irreversible extrapyramidal side effect associated with long-term use of traditional antipsychotic drugs.

A

Tardive dyskinesia

Symptoms include rhythmical, stereotyped movements of the muscles of the face, limbs, and trunk (similar to Huntington’s chorea).

183
Q

Psychopharmacology

Tardive Dyskenisia treated by

A

In some cases, symptoms are alleviated by a GABA agonist or by gradual withdrawal of the drug.

184
Q

Psychopharmacology

Atypical Antipsychotics

names, uses

A

clozapine, resperidone, olanzapine, quetiapine

Schizophrenia, Bipolar, Huntingtons, Parkinsons

185
Q

Psychopharmacology

Atypical Antipsychotics

use in schizophrenia

A

alleviates both positive and negative symptoms of Schizophrenia

186
Q

Psychopharmacology

Atypical Antipsychotics

method of action

A

D4 and other dopamine receptors

also serotonin and glutamate

187
Q

Psychopharmacology

Tricyclics

names

A

amitriptyline, nortitriptyline, doxepin, imipramine, clomipramine

188
Q

Psychopharmacology

Tricyclics

Use

A

Depression that involves decreased appetite/weight loss

Panic Disorder, Agoraphobia, Bulimia, OCD

189
Q

Psychopharmacology

Tricyclics

Method of Action

A

block the reuptake of norepinephrine, serotonin, dopamine

190
Q

Psychopharmacology

Tricyclics

problems

A
  • cardiotoxic
  • ataxia, agitation, hypotension
  • overdose can be lethal
191
Q

Psychopharmacology

SSRIs

names, uses

A

fluoxetine, fluvoxamine, paroxetine, sertraline

melancholic depression, Bulimia, Panic Disorder, PTSD

192
Q

Psychopharmacology

SSRIs

differences from TCAs

A
  • less cardiotoxic
  • safer in overdose
  • less likely to produce cognitive impairment
193
Q

Psychopharmacology

MAOIs

names/uses

A
  • isocarboxazid
  • phenelzine
  • tranylcypromine

non-endogenous and atypical depressions

194
Q

Psychopharmacology

MAOIs

method of action

A

inhibits the enzyme monoamine oxidase, which is involved in deactivating dopamine, norepinephrine, and serotonin

195
Q

Psychopharmacology

NRDIs

norepinephrine dopamine reuptake inhibitor

A
  • Buproprion (Wellbutrin)
  • used to treat MDD and depressive Bipolar
  • less cardiotoxic, fewer anticholinergic effects
  • may aggravate pre-existing psychosis
196
Q

Psychopharmacology

SNRIs

serotonin norepinephrine reuptake inhibitor

A
  • Effexor
  • MDD, GAD, Social Anxiety Disorder, OCD
  • faster onset, increase in blood pressure
197
Q

Psychopharmacology

Lithium

A

used for classic Bipolar, reduces mania and suppresses mood swings

198
Q

Psychopharmacology

Lithium

method of action

A
  • not well understood
  • related to the reuptake of serotonin and norepinephrine
199
Q

Psychopharmacology

Lithium

side effects

A
  • nausea
  • metallic taste
  • weight gain
  • fine hand tremor
  • polyuria/polydipsia
200
Q

Psychopharmacology

Lithium

Lifestyle considerations

A

must be careful to avoid fluctuations in salt intake and avoid caffeine, alcohol, other diuretics

201
Q

Psychopharmacology

Carbamazepine

anticonvulsant

A

used to control mania, used for non-responders to Lithium

better for “rapid cyclers”

202
Q

Psychopharmacology: sedative-hypnotics

Barbiturates

amobarbital, pentobarbital, secobarbital, phenobarbital

A
  • sedatives and analgesics
  • infrequently used, deadly
203
Q

Psychopharmacology: sedative-hypnotics

Barbiturates

method of action

A

interrupting impulses to the reticular activating system

204
Q

Psychopharmacology: sedative-hypnotics

Benzodiazepines

anxiolytics

A

diazepam, alprazolam, oxazepam, lorazepam

anxiety, sleep disturbances, cerebral palsy

205
Q

Psychopharmacology: sedative-hypnotics

Benzodiazepines

method of action

A

simulates the inhibitory action of neurotransmitter GABA

206
Q

Psychopharmacology: sedative-hypnotics

Azapirone

Buspirone

A
  • reduces anxiety without sedation
  • non-addictive, non-habit-forming
207
Q

Psychopharmacology: beta-blockers

Propranolol

Inderal

A

used for blood pressure, angina, and physical symptoms of anxiety

208
Q

Psychopharmacology: beta-blockers

Propranolol

Method of Action

A

blocks beta-adrenergic receptors, which respond to epinephrine and norepinephrine

209
Q

Psychopharmacology: beta-blockers

Propranolol

Side Effects

A

bradycardia, shortness of breath, arterial insufficiency, sexual dysfunction

fatal for people with obstructive pulmonary disease

210
Q

Psychopharmacology: beta-blockers

Propranolol

should not be stopped suddenly b/c:

A

it will cause sweating, palpitations, headache, tremulousness, arrhythmia

211
Q

Psychopharmacology: Narcotic Analgesics

Opioids

uses/method of action

A
  • analgesics, cough suppressants
  • acts on opioid receptors in the spinal cord
212
Q

Psychopharmacology

Naltrexone

A
  • disulfaram inhibits alcohol metabolism
  • prevents craving and reinforcing effects of alcohol
213
Q

Psychopharmacology

Therapeutic Drug Monitoring

A

optimizing medication by measuring specific drugs at designated intervals to maintain a constant concentration in bloodstream

214
Q

Psychopharmacology

genetic testing types

A
  • cytogenic
  • biochemical
  • molecular testing
215
Q

Psychopharmacology

cytogenic

genetic testing types

A

examination of chromosomes and their abnormalities

216
Q

Psychopharmacology

biochemical

genetic testing types

A

examining the protein instead of the gene

Madsen Triad EPPP (9 decks)

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