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EPPP > Physio and Psychopharm > Flashcards

Physio and Psychopharm Flashcards

1
Q

Creation of new neurons is called

A

Neurogenesis

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2
Q

Where does neurogenesis occur

A

Hippocampus and caudate nucleus

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3
Q

Three parts to a neuron

A

Dendrite - receives info
Soma - nucleus, mitochondria, ribosomes, summate signals
Axon - transmits info from cell body to other cells, myelinated

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4
Q

Purpose of the golgi complex in neurons

A

Prepares neurotransmitters and other substances for secretion

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5
Q

Conduction

A

The travel of a message within a neuron

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6
Q

Electrical charge of a neuron at resting state

A

Negative

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7
Q

Action potential

A

An electrical signal that travels through the neuron once the dendrites receive a threshold amount of energy

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8
Q

All-or-none principle

A

Regardless of the amount of stimuli to a neuron, the action potential will always be the same strength

(It will fire, or it won’t)

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9
Q

Synaptic transmission

A

Transmission of information fo one nerve cell to another

Chemically mediated, involves the release of neurotransmitters into the synapse, and uptake by neighboring neurons

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10
Q

Neurotransmitters

A

Chemical substances that transmit signals from one neuron to another

Seven major: Ach, dopamine, serotonin, glutamate, GABA, norepinephrine, endorphins

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11
Q

Seven major neurotransmitters

A

Acetylcholine - muscle contraction

Dopamine - reward, movement, mood

Serotonin - sleep, arousal, aggression, mood

Norepinephrine - mood, attention, dreaming, learning

GABA - anxiety, mood control, sleep

Glutamate - learning and memory and LTP

Endorphins - analgesic properties

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12
Q

Acetylcholine

A

Found in the PNS - responsible for muscular contraction

Found in the CNS - REM sleep, memory

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13
Q

Acetylcholine is implicated in what major disease

A

Alzheimer’s - memory deficits

Drugs for tx reduce the breakdown of Ach: cognex, aricept, reminyl, exelon

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14
Q

Drugs used to slow the breakdown of Ach

Alzheimer’s

A

Aricept

Reminyl

Exelon

Cognex

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15
Q

Dopamine

A

Catecholamine (along with E and NE)

Personality, mood, memory, sleep, regulation of movement

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16
Q

Dopamine hypothesis

A

Predicts schizophrenia is a result of elevated dopamine levels or oversensitivity of dopamine receptors

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17
Q

Oversensitivity or excessive dopamine in the caudate nucleus causes…

A

Tourette’s

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18
Q

Degeneration of dopamine receptions in the substantia nigra and nearby areas

A

Parkinson’s symptoms

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19
Q

Elevated levels of dopamine in the mesolimbic system have been implicated in…

A

Reinforcement that comes with stimulant drugs

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20
Q

Norepinephrine

A

Mood, attention, dreaming, learning

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21
Q

Catecholamine hypothesis

A

Some forms of depression are due to lower than normal levels of norepinephrine

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22
Q

Serotonin

A

Mood, hunger, temperature, sex, arousal, sleep, aggression

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23
Q

Elevated levels of serotonin are implicated…

A

Schizophrenia

Autism

Food restriction associated with AN

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24
Q

Low levels of serotonin are implicated…

A 
Aggression
Depression
Suicide
Bulimia nervosa 
PTSD
OCD
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25
Q

GABA

A

Eating, seizures, anx, motor control, sleep

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26
Q

Low levels of GABA have been associated with…

A

Anxiety disorders

Benzos and other drugs used to treat anx enhance the effects of GABA

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27
Q

Degeneration of cells that secrete GABA in the basal ganglia contribute to symptoms of…

A

Huntington’s disease

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28
Q

Glutamate

A

Learning, memory, long term potentiation

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29
Q

Excessive glutamate can lead to…

A

Seizures, Huntington’s, Alzheimer’s

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30
Q

The central nervous system consists of…

A

The brain and spinal cord

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31
Q

Five segments of the spinal cord

A 
Cervical
Thoracic
Lumbar
Sacral
Coccygeal
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32
Q

Quadriplegia v paraplegia

A

Paraplegia - damage to the thoracic spinal area
Loss of sensory and voluntary functioning in the legs

Quadriplegia - damage at the cervical spinal area
Loss of sensory and voluntary functioning in the arms and legs

(Incomplete transection means some sensory or motor function may still remain)

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33
Q

Three layers of the meninges

A

Dura matter

Arachnoid space (full of CSF)

Pia matter

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34
Q

Cerebral ventricles

A

Four hollows in the Brian full of CSF

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35
Q

Hydrocephalus

A

Larger than normal cerebral ventricles

Caused by an obstruction in CSF flow

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36
Q

Job of the peripheral nervous system

A

Relay messages between the central nervous system and the body’s sensory organs, muscles, and glands

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37
Q

The divisions of the PNS

A

Somatic
- skeletal muscle control (voluntary)

Autonomic

  • smooth muscle control (involuntary)
    • sympathetic and parasympathetic divisions
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38
Q

Somatic nervous system

A

Part of the PNS

Carry information from body’s sensory receptors to the CNS and our to the skeletal muscles

Voluntary movement

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39
Q

Autonomic nervous system

A

Part of the PNS

Handle signals from the receptors in the body’s viscera, to the CNS, and out to the smooth muscle, cardiac muscle, and glands
(Involuntary stuffs)

Contains sympathetic and parasympathetic divisions

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40
Q

Sympathetic nervous system

A

Part of the autonomic nervous division in the PNS

Associated with arousal and expenditure of energy

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41
Q

Parasympathetic nervous system

A

Part of the autonomic division of the PNS

Involved in conservation of energy and relaxation

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42
Q

Five stages of CNS development

A

Proliferation - new cells produced inside neural tube (2.5wks)

Migration - neurons move to final destination and aggregate (8wks)

Differentiation - neurons develop axons and dendrites

Myelination - glial cells insulate neurons (postnatal)

Synaptogenesis - formation of synapses (postnatal)

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43
Q

Structural neuroimaging techniques

A

CAT - xray of the brain

MRI - uses magnets to display brain structures

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44
Q

CAT v MRI

A

MRI is $$$, CAT is cheaper

MRIs don’t use xrays, better resolution and more detail, can be 3D and provide images at any angle

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45
Q

Functional neuroimaging techniques

A

fMRI - best resolution, info on brain activity (blood oxygenation)

SPECT - similar to PET with lower resolution

PET - activity thru glucose metabolism, oxygen consumption, blood flow

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46
Q

Structures of the hindbrain

A

Medulla - life sustaining

Cerebellum - movement coordination and balance

Pons - integration of movement between left and right sides of the body

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47
Q

Medulla

A

Part of the hindbrain

Swallowing, coughing, life sustaining functions (breathing, heartbeat, blood pressure)

Damage causes death

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48
Q

Damage to the medulla causes

A

Death

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49
Q

Pons

A

Part of the hindbrain

Plays a role in the integration of movements in the left and right sides of the body

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50
Q

Cerebellum

A

Part of the hindbrain

Balance, posture, coordinated movement (when with basal ganglia)

Damage results in ataxia (slurred speech, tremors, loss of balance)

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51
Q

What part of the hindbrain is substantially impacted by alcohol

A

Cerebellum

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52
Q

Structures of the midbrain

A

Inferior and superior colliculi - routes for visual and auditory info

Substantia nigra - motor activity and reward systems

RAS - consciousness, arousal, wakefulness

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53
Q

Interior and superior colliculi

A

Part of the midbrain

Paths for the transmittal of visual and auditory information (respectively)

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54
Q

Substantia nigra

A

Part of the midbrain

Involved in motor activity and reward systems

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55
Q

Reticular activating system

A

Part of the reticular formation in the midbrain

Consciousness, arousal, wakefulness

Damage = coma

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56
Q

Damage to the reticular activating system could result in…

A

Disruption in sleep-wake cycles

Can produce permanent, coma-like sleep

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57
Q

Structures of the forebrain

A 
Thalamus - sensory switchboard
Hypothalamus - homeostasis and 4 Fs
Basal ganglia - planning, organizing, coordinating voluntary movement
Amygdala - emotion and memory 
Hippocampus - learning and memory
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58
Q

Limbic system

A

Located in the forebrain

Contains amygdala and hippocampus

Learning, memory, emotion

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59
Q

Thalamus

A

Located in the forebrain

Acts as a relay station for the processing of sensory information

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60
Q

Wernike-Korsakoff Syndrome and the thalamus

A

Thiamine deficiency causes atrophy in areas of the thalamus
(Usually the result of chronic alcoholism)

Begins with Wernicke’s symptoms - confusion, dysfunctional eye movements, ataxia
End with Korskoff symptoms - amnesias and confabulation

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61
Q

Hypothalamus

A

Structure in the forebrain

Vital functions (4 Fs and homeostasis)

Contains the suprachiasmatic nucleus (SCN) - sleep wake cycles and circadian rhythms

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62
Q

Suprachiasmatic nucleus

A

Located in the hypothalamus of the forebrain

Responsible for regulating sleep-wake cycles and circadian rhythms

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63
Q

Basal ganglia

A

In the forebrain

Planning, coordination, and execution of voluntary movement

Consists of: substantia nigra, caudate nucleus, puts men

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64
Q

Amygdala

A

Located in the limbic system of the forebrain

Takes care of motivational activities, and attaches memory and emotion
Flashbulb memories

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65
Q

Kluver-Bucy Syndrome

A

Damage to the amygdala and temporal lobes

Reduced rear and aggression

Altered eating habits

Hypersexuality

Psychic blindness - inability to recognize meanings of events or objects

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66
Q

Hippocampus

A

Located in the limbic system of the forebrain

Learning and memory

Consolidation of declarative memories into LTM

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67
Q

Corpus callosum

A

Bundle of fibers that connects the right and left hemispheres

(If severed, the two hemispheres operate as separate, independent brains)

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68
Q

Contralateral representation

A

Left hemisphere controls the functions of the right side and vice versa

(Exception of olfaction)

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69
Q

Brain lateralization

A

Each hemisphere of the brain is specialized for a specific function

R - dominant - spatial processing (geometry), neg emos, nonverbal memory, nonlanguage sounds
L - dominant - language, verbal memory, positive emotions, speech, reading, writing

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70
Q

How was the function of each cerebral hemisphere initially discovered and researched?

A

Thru split-brain patients (had corpus callosum removed for seizure control)

Show object in left visual field - right hem - can pick the object out from behind screen with left hand (can’t say item or pick with right hand)
Show object in right visual field - left hem - can name and select image with right hand (can’t select with left hand)

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71
Q

Four lobes of the cerebral cortex

A

Frontal

Parietal

Temporal

Occipital

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72
Q

Important structures of the frontal lobe

A

Primary motor cortex - motor humunculous, execution of movement, damage results in loss of muscle tone

Supplementary motor area - planning and control of movement

Premotor cortex - control of motor movement in response to external sensory stimuli

PFC - executive function, emotion

Broca’s area - expressive language center

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73
Q

Function of the primary motor cortex

A

Involved in the execution of movement

Contains motor homunculous
(Damage is determined by where on the homunculous it is - weakness occurs on the opposite side of the body)

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74
Q

Damage to the primary motor cortex results in…

A

Loss of reflexes and flaccid hemiplegia (loss of muscle tone) in areas of the body that are contralateral to the damage

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75
Q

Purpose of the supplementary motor area

A

Planning and control of movement

Learning new motor sequences, mental representation of movement (includes other areas)

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76
Q

Function of the premotor cortex

A

Control of movement in response to external, sensory stimuli

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77
Q

Broca’s Area

A

Located in inferior left frontal lobe

Major motor speech area - responsible for expressive language

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78
Q

Function of the prefrontal cortex

A

Involved in a variety of complex behaviors - emotion, attention, self-awareness, executive function

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79
Q

Damage to each region of the prefrontal cortex…

A

Dorsolateral area - dorsal convexity dysexecutive syndrome
(Impaired judgement, insight, planning, and organization)

Orbitofrontal area - orbitofrontal disinhibition syndrome
(Pseudopsychopathy, poor impulse control, emo lability, aggression, lewd comments and inappropriate sexual behavior)

Mediofrontal area - mesial frontal apathetic syndrome
(Pseudodepression, reduced emo range, diminished verbal and motor output, extremity weakness, sensory loss, impaired spontaneity)

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80
Q

Damage to the dorsolateral area of the prefrontal cortex

A

Dorsal convexity dysexecutive syndrome

Impaired insight, judgement, planning, and organization
(Concrete, perseverative, trouble learning from experience, neglect hygiene, reduced sexual interest, apathetic)

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81
Q

Damage to the orbitofrontal area of the prefrontal cortex

A

Orbitofrontal disinhibition syndrome
(Pseudopsychopathy)

Emotional lability, distractibility, poor impulse control, impaired social insight
(Explosive aggressive outbursts, inappropriate humor, lewd comments, engage in inappropriate sexual behavior)

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82
Q

Damage to the mediofrontal area of the prefrontal cortex

A

Mesial frontal apathetic syndrome
(Pseudodepression)

Impaired spontaneity, reduced emotional reaction, diminished motor and verbal behavior, lower extremity weakness and sensory loss
(Bored, lack motivation, may seem dep without neg cognitions and dysphoria)

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83
Q

Important structures of the parietal lobe

A

Somatosensory cortex

Governs sensation of temperature, pressure, pain, proprioception, gustation

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84
Q

Common symptoms of parietal lobe damage

A

Apraxia (inability to perform motor movements despite no issues with motor functioning)

Somatosensory agnosia

Anosognosia (inability to recognize ones own symptoms or disorders)

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85
Q

Damage to the right (non-dominant) parietal lobe

A

Contralateral neglect (loss of knowledge or interest in the left side of the body)

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86
Q

Damage to the left (dominant) parietal lobe

A

Ideational apraxia - inability to carry out sequences of actions

Ideomotor apraxia - inability to carry out a single action in response to a command)

Gerstmann’s Syndrome - finger agnosia, right-left confusion, agraphia, acalculia

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87
Q

Agraphia

A

Aka dysgraphia

Inability to write

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88
Q

Acalculia

A

Inability to perform simple calculations

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89
Q

Important structures of the temporal lobe

A

Auditory cortex - processes auditory information

Wernicke’s Area - comprehension of language

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90
Q

Damage to the auditory cortex of the temporal lobe

A

Results in auditory agnosia
Auditory hallucinations
Other disturbances in auditory sensation and perception

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91
Q

Important structures of the occipital lobe

A

Visual cortex - responsible for visual perception, recognition, and memory

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92
Q

Damage to the occipital lobe (generally)

A

Visual agnosia
Visual hallucinations
Cortical blindness

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93
Q

Psosopagnosia

A

Caused by lesions at the junction of occipital, parietal, and temporal lobes

Inability to recognize familiar faces

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94
Q

Left occipital lobe damage

A

Simultagnosia (inability to see more than one aspect of an object at a time)

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95
Q

Two theories of color vision

A

Trichromatic color theory - red, grn, blu receptors that form all other colors

Opponent-process theory - bipolar receptors (r-g, b-y, b-w) stimulated (and inhibited) in different ways produce the colors we see

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96
Q

Trichromatic theory of color vision

A

Young-Helmholtz

There are three types of color receptors (r, b, g) that are activated in different intensities to produce all the colors we perceive

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97
Q

Opponent-process theory of color vision

A

Hering

Three types of bipolar cells are stimulated and inhibited in different ways to account for all the colors we perceive (r-g, b-y, b-w)

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98
Q

What phenomenon supports opponent-process theory

A

Negative after-images

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99
Q

Color blindness

A

Often the result of a genetic deficiency
(Recessive x-linked trait)

Most common in men

Most common type of color blindness is inability to distinguish between red and green

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100
Q

Achromatopsia

A

Color blindness

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101
Q

Binocular depth perception cues

A

Convergence (eyes turn inward the closer an object gets)

Retinal disparity (each eye sees a different, the closer the image the more disparate the two images)

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102
Q

Convergence

A

Binocular cue

Turning inward of the eyes as an object gets closer (and vice versa)

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103
Q

Retinal disparity

A

Binocular cue

Our two eyes see the world from two different views…the closer an object, the greater the disparity of the two images

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104
Q

Monocular depth perception cues

A

Relative size

Interposition of objects (overlap)

Linear perspective

Motion parallax

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105
Q

Purpose of monocular cues

A

See depth perception for objects at greater distances

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106
Q

Location of the primary olfactory cortex

A

Orbitofrontal cortex

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107
Q

Processing of olfactory memory

A

Amygdala

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108
Q

Dermatomes

A

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

109
Q

Damage to nerves (as it relates to dermatomes)

A

Adjacent dermatomes overlap so that damage to a nerve causes diminished sensation, rather than complete loss of sensation in the corresponding dermatome

110
Q

Gate-control theory of pain

A

The nervous system can only process a limited amount of sensory information at any given time

When too much information is being received, cells in the spinal cord act as a gate that blocks some incoming pain signals

Ex. Massaging injured area, applying ice, engaging in distraction mental activities

111
Q

Coping with pain

A

Pain is very susceptible to placebos

Active strategy - exercise, physical therapy, distraction, ignoring pain

Passive strategy - taking it easy, relaxing, wishful thinking, medication, limiting activity

112
Q

Research on active v passive coping strategies

A

Lower levels of reported pain, greater improvement in psychological and physical functioning associated with active strategies

113
Q

Synesthesia

A

Stimulation of one sensory modality triggers a sensation in another sensory modality

114
Q

Absolute threshold to detecting a stimulus

A

The minimum stimulus needed to produce a sensation

115
Q

Difference threshold in stimulus detection

A

Smallest increment of a stimulus intensity needed to recognize the discrepancy between two stimuli (JND)

116
Q

Weber’s Law

A

The more intense a stimulus, the greater the increase in stimulus intensity required for the increase to produce a JND

(JND)

117
Q

Fetchner’s Law

A

Physical stimulus changes are logarithmically related to their psychological sensations

(Logs)

118
Q

Steven’s Power Law

A

Sensation is an exponential function of stimulus intensity

Power and exponents

119
Q

Three primary laws of psychophysics

A

Weber’s law - JND

Fechner’s law - logs

Steven’s power law - exponents

120
Q

Impact of the temporal lobes on learning and memory

A

Encoding, storage, and retrieval of declarative LTMs

121
Q

Damage to the brain as a result of Alzheimer’s

A

Amyloid plaques in hippocampus, amygdala, and entorhinal cortex

122
Q

Relation of learning and memory to the amygdala

A

Responsible for connecting strong emotions to memories
(Flashbulb memories)

Fear conditioning

Implicated in PTSD

123
Q

How the prefrontal cortex assists in learning and memory

A

Episodic memory
Prospective memory
Constructive memory and false recognition

124
Q

Damage to the prefrontal cortex can impact learning and memory in what way…

A

People may incorrectly claim that new information is familiar

125
Q

What part of the brain is response for working memory

A

Dorsolateral prefrontal cortex

126
Q

Role of the thalamus in leaning and memory

A

Processing incoming information and transferring to to the cortex

127
Q

Long-term potentiation

A

Refers to the greater responsivity of a postsynaptic neuron to low-intensity stimuli, after the neuron has been barraged by high-frequency stimuli

(First studied in aplysia)

128
Q

Impact of protein synthesis on learning and memory

A

Learning and memory are dependent on increased protein synthesis and the presence of RNA (which is required for protein synthesis)

Reduced RNA or protein synthesis leads to the prevention of forming long term memories

129
Q

Broca’s aphasia

A

Damage to Broca’s area (left side of frontal lobe)

Dysprosidy - poorly articulated speech, lacks normal intonation and stress
Anomia - inability to name common or familiar objects or people
Difficulty repeating phrases

Typically aware of their impairment, and experience frustration, anx, dep

130
Q

Wernicke’s aphasia

A

Caused by damage to Wernicke’s area in left temporal lobe

Trouble understanding written and spoken language
Difficulty generating meaningful language

Speech is rapid, effortless, fluent, but meaningless

Typically do not realize their speech is meaningless

131
Q

Conduction (associative) aphasia

A

Caused by damage to the arcuate fasciculous (area where Broca’s and Wernicke’s area connect)

Doesn’t impact language comprehension, but does result in anomia, paraphasia, and impaired repetition

132
Q

Transcortical aphasia

A

Occurs when damage disconnects Broca’s and or Wernicke’s areas from the rest of the brain

Transcortical motor (isolates Broca’s), transcortical sensory (isolates Wernicke’s, mixed transcortical (both areas isolated)

133
Q

Transcortical motor aphasia

A

Damage to the brain isolates Broca’s area from the rest of the brain

Nonfluent, effortful speech, lack of spontaneous speech

134
Q

Transcortical sensory aphasia

A

Caused by damage that isolates Wernicke’s area from the rest of the brain

Deficits in comprehension, anomia, fluent and meaningless speech

135
Q

Mixed transcortical aphasia

A

Caused by damage that separates Broca’s and Wernicke’s areas from the rest of the brain

Able to talk but have nothing to say
Unable to understand spoken and written language
Can sing familiar songs, repeat phrases spoken by others

136
Q

Global aphasia

A

Caused by widespread brain injury involving Broca’s area, Wernicke’s area, and other areas of the Brian

Extensive disruption in language comprehension and production
May be able to produce emotional explanations
Often accompanied by right hemisensory loss, right hemiplegia, and right hemianopia

137
Q

Four major theories of emotion

A

James-Lange - physiological sensations lead to emotion

Cannon-Bard - the cortex and PNS receive thalamic stimulation which produce emotion and physiological sensations simultaneously

Two-Factor - physiological arousal plus cognitive interpretation results in specific emotions

Cognitive-appraisal - appraisal of the environment determines the emotion

138
Q

James-Lange theory of emotion

A

Emotions represent perspectives of bodily reactions to sensory to stimuli

Ex. You area afraid because your knees are shaking and your heart is racing

Supported by studies of quadriplegics and paraplegics who receive limited info from their bodies and report feeling fewer emotional sensations after their injuries

139
Q

Cannon-Bard theory of emotion

A

Thalamic stimulation of the cortex and PNS produce simultaneous bodily sensations/reactions and emotions

Supported by research showing that bodily reactions for all emotions are fairly similar (suggests the nature of emotional experience does not just depend on bodily arousal)

140
Q

Schachter-Singer Two-Factor theory of emotion

A

Physiological arousal and cognitive interpretation of that arousal (and the environmental context) produce your subjective emotional experience

Supported by Schachter and Singer’s “epinephrine study”

141
Q

Cognitive-Appraisal theory of emotion

A

Lazarus

Emotions are universal but there are differences in how emotion-arousing events are interpreted or appraised

So the appraisal of a situation leads to the emotion
(Ex. Two people with the same cognitive appraisal will feel the same emotion)

142
Q

Lazarus’s cognitive-appraisal theory of emotion distinguishes between what three types of cognitive appraisal…

A

Primary appraisal - evaluating a situation as irrelevant, benign, or stressful with regard to their OWN WELLBEING

Secondary appraisal - evaluation of the resources they have to cope with a situation that has been identified as stressful

Re-appraisal - monitors a situation and modifies their primary or secondary appraisals

143
Q

Papez’s circuit

A

The neural circuit that mediates the experience and expression of emotion

144
Q

Areas of the brain key for emotion

A

Cerebral cortex

Amygdala

Hypothalamus

145
Q

Emotion and the left hemisphere

A

Governs happiness and other positive emotions

Damage = depression, anxiety, aggression, paranoia

146
Q

Emotion and the right hemisphere

A

Mediates sadness, fear, and other negative emotions

Damage = indifference, apathy, emotional lability, undue cheerfulness or joking

147
Q

The role of the hypothalamus in emotions

A

Involved in the translation of emotions into physical responses

Damage = uncontrollable rage behaviors or laughter

148
Q

General Adaptation Syndrome

Broadly

A

Mediated by the adrenal and pituitary glands

The response everyone experiences to stress

Three stages: alarm reaction, resistance, exhaustion

149
Q

Alarm reaction phase of general adaptation syndrome

A

First phase of GAS - response to stress

Hypothalamus signals the production of adrenaline, which increases energy, heart rate, and respiration

150
Q

Resistance phase of the general adaptation syndrome

A

Second stage of the GAS - reaction to stressful situations

Breathing and heart rate returns to normal

Hypothalamus signals the production of ACTH which activates cortisol production (which maintains high blood glucose levels for energy)

151
Q

Exhaustion state of the general adaptation syndrome

A

Third stage of the GAS - response to stress

Adrenal and pituitary production of stress hormones tires, and physiological processes begin to break down (results in depression, fatigue, and illness)

152
Q

Type A Behavioral Pattern

A

First studied to link emotion and illness

Type A persons are often high-achieving, competitive, easily irritated, urgent, and impatient

Higher incidence of health problems and (in men predominantly) coronary heart disease

153
Q

Sexual dimorphism

A

There are sex-related, structural, physical differences in the brain

Related to differential exposure to androgens during prenatal and early postnatal development

154
Q

Hypothalamic-pituitary-gonadal axis

A

HPGA releases testosterone or estrogen, which signal the onset of puberty and the development of secondary sex characteristics

155
Q

Menopause

A

Cessation of menstruation

Late 40s or early 50s

Reduction of estrogen - vaginal dryness, moodiness, fatigue, hot flashes, nausea, reduced skin elasticity

156
Q

Hormone replacement therapy

A

Used to treat negative effects of menopause

Largely helpful, but may not improve sex drive and may increase risk for blood clots and breast cancer

157
Q

Four types of brainwaves associated with sleep

A

Beta - awake and alert

Alpha - awake and relaxed

Theta - deep relaxation, light sleep

Delta - deep sleep

158
Q

Five stages of sleep

A

Stage 1 - NREM - starts when you fall asleep, alpha become theta

Stage 2 - NREM - theta with sleep spindles and K complexes

Stage 3 - NREM - theta becomes long and slow delta waves

Stage 4 - NREM - delta waves

Stage 5 - REM - beta and theta, physiologically look awake, flaccid paralysis, rapid eye movement

159
Q

Changes in sleep with age

A

Infants begin with REM…the transition to beginning sleep with NREM occurs around three months of age

Total sleep, stage 4, and REM decrease with age

160
Q

Traumatic brain injury

A

Injury to the brain that is caused by external force that involves temporary or permanent impairments to cognitive, emotional, behavioral, and/or physical functioning

May be open or closed head injury

161
Q

Closed-head injury

A

Nonpenetrating blow

Includes the initial blow (coup) and when the brain knocks against the opposite side of the skull (contrecoup) - can also include hemorrhage (bleeding) or edema (swelling)

Typically results in alterations or loss of consciousness and amnesia

162
Q

Open-head injury

A

Penetrating blow through the skill (eg. gunshot)

Does not usually cause loss of consciousness, but results in more localized damage and highly specific symptoms based on where the damage was

163
Q

Three factors for assessing the level of severity in a traumatic brain injury

A

Score on the GCS

Duration of posttraumatic amnesia

Duration of loss of consciousness

164
Q

Classifications for TBI severity

A

Mild (GCS 13-15, less than one hour PTA, less than 30min LOC)

Moderate (GCS 9-12, PTA 1-24 hours, LOC 30min-24 hours)

Severe (GCS 0-8, PTA more than 24 hours, LOC more than 24 hours)

165
Q

Mild classification of TBI

A

GCS: 13-15

PTA: less than one hour

LOC: less than 30 minutes

166
Q

Moderate severity of TBI

A

GCS: 9-12

PTA: 1-24 hours

LOC: 30min-24hr

167
Q

Severe classification of TBI

A

GCS: 0-8

PTA: more than 24 hours

LOC: more than 24 hours

168
Q

Memory impairment s a result of TBI

A

Posttraumatic (anterograde) amnesia is a good predictor of the persistence of the symptoms caused by injury (loss of ability to form new memories after an event/injury)

Retrograde amnesia (forgetting past memories) can also occur, however it’s typically “shrinking retrograde amnesia” where memories gradually return

169
Q

Postconcussional Syndrome

A

Occurs in up to 50% of persons with mild TBI

Initial sx: nausea, drowsiness, headache, dizziness
Then: cognitive impairment in attention, concentration, processing speed
Finally: depression, anxiety, irritability

Most recover within 3 months

170
Q

Cerebrovascular accident

A

Aka stroke

Refers to a sudden or gradual onset of neurological symptoms resulting from a disruption of the blood supply to the brain

171
Q

Three major causes of stroke/CVA

A

Thrombosis (blood clot)

Embolism (sudden blockage of an artery)

Hemorrhage (brain bleed)

172
Q

Symptoms of stroke/CVA

A

Contralateral hemiplegia

Contralateral hemianesthesia (face, arm, leg)

Contralateral visual field loss

173
Q

Neuropsychiatric symptoms that often follow a stroke/CVA

A

Depression! Typically occurs immediately, but can also occur several months later

Anxiety, mania, apathy, psychosis, dementia, pathological crying or laughter

174
Q

Two major disorders of movement

A

Huntington’s - emo and cog sx, fidgeting, facial grimaces, clumsiness, jerky involuntary movements (chorea), eventually dementia

Parkinson’s - positive sx (resting tremor, rigidity), negative sx (slowed movement, speech difficulty, postural disturbance), depression

175
Q

Seizure

A

Abnormal electrical signals in the brain that causes one or more of:

1 - aura that signals the onset of a seizure
2 - loss of consciousness
3 - some type of abnormal movement

176
Q

How to diagnose seizures

A

Medical hx and physical exam

EEG to observe abnormal electrical signals in the brain

MRI/CT to determine if the seizures are due to a lesion or other abnormality in the brain

177
Q

Tonic-clonic (grand mal) seizure

A

Includes tonic stage (muscle contract) and clonic stage (muscle shaking or jerking)

Postictal depression, confusion, or amnesia for the ictal event may occur after the seizure

178
Q

Absence (petit mal) seizures

A

Brief attacks including loss of consciousness (no prominent motor symptoms)

May look like a blank stare, or have fluttering eyes

Thalamus may be indicated in absence seizures

179
Q

Partial seizures

A

Usually have a focal starting point

Affects usually only one side of the body - sx depend on where the seizure activity is in the brain

Simple partial (no loss of consciousness), complex partial seizures (loss of consciousness)

180
Q

Partial seizure sxs by brain lobe

A

Temporal (most common) - stereotyped movements, hallucinations, changes in personality

Frontal - jerky motor sx, inability to talk, olfactory sx

Parietal - unusually physical sensations on the opposite side of the body

Occipital - rapid eyeblinking, unusual visual phenomena

181
Q

Cause of Huntington’s disease

A

Autosomal dominant gene

50% chance of inheriting if if your parent is a carrier

182
Q

Cause of Parkinson’s disease

A

Progressive degeneration of dopamine-containing cells in the substantia nigra

183
Q

Cause of multiple sclerosis

A

Demyelination of the nerve fibers of the brain and spinal cord

Issues may stem from autoimmune response where body attacks its own myelin

184
Q

Two types of MS

A

Relapsing-remitting type - alternating periods of relapse (sx) and remission (partial or complete recovery)
- many relapsing-remitting pts eventually get secondary progressive

Secondary progressive type - gradual worsening periods without periods of relapse and remission

185
Q

Relapsing-remitting type of MS

A

Experiences periods of symptoms (relapse) and periods with complete or partial symptom remission (remission)

Most patients eventually progres to secondary progressive type

186
Q

Secondary progressive type of MS

A

Gradual worsening of symptoms without periods of remission or relapse

187
Q

Symptoms of MS

A

Initial - eye pain or blurred vision, fatigue that worsens in afternoon, motor impairment (weakness, clumsiness, balance issues)

Progressive - tremor, speech and swallowing problems, hearing loss, dep, anx, cog sx

188
Q

Psychophysiological Disorders

A

Used to describe physical symptoms that are caused, maintained or exacerbated my emotional factors

Hyperventilation, hypertension, fibromyalgia, migraines, PMS

189
Q

Hyperventilation

A

A psychophysiological disorder

Panic attack - chest pain, numbness, dizziness, impaired concentration, tinnitus, etc.

190
Q

Hypertension

A

A psychophysiological disorder

Primary - no physical cause
Secondary - related to a known physical cause

191
Q

Treatment for hyperventilation

A

Relaxation

Breathing into a paper bag

Sedation

192
Q

Treatment for hypertension

A

Lifestyle modification

Blood pressure medication

Blood pressure biofeedback

193
Q

Fibromyalgia

A

A psychophysiological disorder

Muscle aches, tenderness, stiffness, fatigue, sleep disturbances

More common in females

194
Q

Treatment of fibromyalgia can include

A

Psychological treatments

Especially behavioral methods

195
Q

Migraines

A

A psychophysiological disorder

Throbbing headache limited to one side of the head, includes nausea, vomiting, diarrhea, sensitive to light/noise/smells

General (no aura) and classic (contains aura)

196
Q

Treatments for migraines

A

NSAIDS

SSRIs

Beta-blockers

197
Q

Precipitates or aggravating factors for migraines

A

Stress

Alcohol

Changes in barometric pressure

Menstruation

Foods

198
Q

Connection between migraines and personality

A

(More common in females)

Perfectionism
Orderliness
Neuroticism
Inflexibility
Ambitious ness
199
Q

Differential dx for migraines

A

Cluster headaches - occur behind one of the eyes, burning

Tension headache - nonthrobbing, one or both sides of neck and head

Sinus headache - occur over the eyes, felt worse when bending over

200
Q

Three major components to the endorcrine system

A

Pituitary gland - master gland - acts in the kidneys and important for growth

Thyroid gland - metabolism (secretes thyroxine)

Pancreas - involved in uptake and use of glucose (releases insulin)

201
Q

Hyposecretion of ADH from pancreas causes…

A

Dwarfism

202
Q

Hyperscreation of ADH from pancreas causes…

A

Gigantism

In adulthood - acromegaly (large hands, feet, facial features)

203
Q

Purpose of pancreas

A

Secrete growth hormones (ADH)

204
Q

Job of the thyroid gland

A

Regulate metabolism thru the release of thyroxine

205
Q

Job of the pancreas

A

Regulate the uptake and use of amino acids and glucose (releases insulin)

206
Q

Hypersecretion of thyroxine…

A

Hyperthyroidism

Sx: weight loss, fast metabolism, increased appetite, high body temperature, heat intolerance, irritability, emotional lability, impaired attention span

207
Q

Hyposecretion of thyroxine results in…

A

Hypothyroidism

Sx: weight gain, decreased appetite, low body temperature, depression, apathy, lethargy, concentration and memory deficits

208
Q

Hyperinsulinism results in

A

Hypoglycemia (low blood glucose)

Hunger, dizziness, headaches, palpitations, anx, dep, confusion

209
Q

Hypoinsulinism results in

A

Diabetes mellitus (excessive blood glucose)

Increased susceptibility to infection, increased appetite, mental dullness

210
Q

Psychoactive drugs

A

Ideals that interact with the CNS in a way that produces a change in mood, consciousness, perception, and/or behavior.

211
Q

Agonist drugs

A

Produce similar effects to those of neurotransmitters

Direct - mimic the NT
Indirect - bind and facilitate NT action

212
Q

Antagonist drugs

A

Reduce or block the effects of a neurotransmitter

Direct - attach to a receptor site and block
Indirect - attach elsewhere and interfere with the action of the NT

213
Q

Inverse agonist

A

Produce an effect that is opposite that of the neurotransmitter

214
Q

Partial agonist

A

Produces effects that are similar but less than the effects of the neurotransmitter

215
Q

Types of agonists

A

(Agonists bind and increase effects of a neurotransmitter)

Direct - bind and mimics the NT
Indirect - bind elsewhere and facilitate action of the NT
Inverse - produces opposite effect of the NT
Partial - binds an produces a similar but less effect than the NT

216
Q

Factors that contribute to medication-related problems in people over age 65

A

The use of multiple medications

Medication noncompliance

Decreased or increased sensitivity to drug effects

Changes in renal fxning (poor functioning means medications process through more slowly, increasing their half-lives and the risk of toxicity)

217
Q

Cross-ethnic differences in responses to psychotropic medication

A

Higher proportions of Asians and African Americans are poorer metabolizers of some psychotropic medications

So start at a lower dose and titrate up to avoid a sudden presentation of harsh side effects that lead to discontinuation or meds

218
Q

What symptoms do traditional (conventional) antipsychotics treat

A

Positive symptoms (delu, halu) associated with psychosis, organic psychosis, or psychotic symptoms associated with MDD

219
Q

Generic names for traditional antipsychotic drugs

A

Chlorpromazine

Fluphenazine

Thiothixene

Haloperidol

220
Q

Traditional antipsychotic mode of action

A

Blocking D2 dopamine receptors

Dopamine hypothesis - schizo sx due to increased sensitivity to DA or overproduction of DA

221
Q

Side effects to traditional antipsychotics

A

Anticholinergic effects - dry mouth, water retention, blurred vision

Extrapyramidal symptoms - tardive dyskinesia

Neuroleptic malignant syndrome - MATH, can be fatal

222
Q

Anticholinergic effects

A

Side effect of antipsychotic medication

Dry mouth, blurry vision, water retention/constipation, tachycardia, delayed ejaculaton

223
Q

Mechanism for extrapyramidal symptoms

A

Result of the antipsychotic drug on DA receptors in the caudate nucleus

224
Q

Most common extrapyramidal side effects

A

Parkinsonism

Akathisia (extreme restlessness)

Acute dystonia (muscle spasms in mouth, face, and neck)

225
Q

Most severe extrapyramidal symptom

A

Tardive dyskinesia

Six similar to Huntington’s, involuntary movements of limbs and face

May be reversible if medication is gradually withdrawn

226
Q

Neuroleptic malignant syndrome

A

MATH

Muscular rigidity
Altered consciousness
Tachycardia
Hyperthermia

Can be fatal if drug is not discontinued right away if these symptoms develop

227
Q

Types of atypical antipsychotic medications

A

Clozapine

Risperidone

Olanzapine

Quetiapine

228
Q

Use for atypical antipsychotics

A

Psychosis and schizophrenia

For psychosis that is not otherwise treated by traditional antipsychotics

Clozapine: Treatment-resistant bipolar, depression and suicidality, hostility

229
Q

Mode of action for atypical antipsychotics

A

Act on D4 and other dopamine receptors

As well as some receptors for serotonin and glutamate

230
Q

Advantages and disadvantages of atypical antipsychotics

A

Adv - much less chance of extrapyramidal symptoms and tardive dyskinesia, can be used when traditional antipsychotics have failed

Disadv - have slower therapeutic effects than transitional antipsychotics (takes longer for them to work)

231
Q

Side effects of atypical antipsychotics

A

Anticholinergic effects - dry mouth, water retention, tachycardia

Neuroleptic malignant syndrome - MATH

Agranulocytosis - decrease of certain white blood cells
(Requires blood monitoring)

232
Q

Agranulocytosis

A

A marked decrease in a certain type of white blood cell

Possible side effect of atypical antipsychotics

233
Q

Why do atypical antipsychotics require blood monitoring

A

To monitor for the presence of agranulocytosis

Marked decrease of a certain type of white blood cell

234
Q

Two types of antipsychotics

A

Traditional (chlorpromazine, haloperidol)

Atypical (clozapine, risperidone)

235
Q

Three major types of antidepressants

A

TCAs - imipramine, amitriptyline

SSRIs - fluoxetine, sertraline, paroxetine

MAOIs - isocarboxazid phenelzine

236
Q

Uses for tricyclic antidepressant medications

A

Depression with a lot of vegetative or somatic symptoms

Weight loss, sleep disturbance, psychomotor retardation, anhedonia

237
Q

Mode of action for TCAs

A

Block reuptake of NE, serotonin, and/or dopamine

Support catecholamine hypothesis that depression is caused in part by low levels of norepinephrine

238
Q

Primary side effects of TCAs

A

Cardiotoxicity (high or low blood pressure, tachycardia, arrhythmia)

Anticholinergic effects

Cognitive impairment

Weight gain

239
Q

Overdose and TCAs

A

Can be lethal

Prescribe in small doses for those at increased risk for suicide

240
Q

Indications for SSRIs

A

Melancholic depression

PTSD

241
Q

Mode of action for SSRIs

A

Blocks reuptake of serotonin specifically

242
Q

Side effects of SSRIs

A

Frequent unrination

Gastrointestinal issues (nausea)

Insomnia

Sexual dysfunction

Dizziness and headache

243
Q

TCAs vs SSRIs

A

SSRIs are less cardiotoxic

Less toxic in overdose

Less likely to produce cognitive impairment

244
Q

Most widely prescribed antidepressant

A

Fluoxetine (Prozac)

SSRI

BUT accompanied with black box warning about increased risk for suicide

245
Q

SSRI combined with MAOI

A

Serotonin syndrome

Neurological effects, changes in mental state, cardiac arrhythmia
Can result in coma and death

246
Q

Use of MAOIs is indicated in what cases…

A

Atypical depression

- hypersomnia, hyperphagia, interpersonal sensitivity

247
Q

Method of action for MAOIs

A

Inhibit monoamine oxidase, which is involved in deactivating DA, serotonin, and norepinephrine

248
Q

Side effects of MAOIs

A

Hypertensive crisis
- taken with barbiturates, certain foods or beverages that contain tyramine

Headache, stiff neck, rapid heart rate, nausea, sensitive to light

Seek emergency treatment

249
Q

Two newer antidepressants

A

SNRI - serotonin norepinephrine reuptake inhibitor (venlafaxine)
(Used for pain, may act more quickly in the body)

NDRI - norepinephrine dopamine reuptake inhibitor (bupropion)
(No sexual dysfunction but could exacerbate psychosis or seizures)

250
Q

Two main mood stabilizing drugs

A

Lithium

Carbamazepine

251
Q

Indications for lithium salts

A

Classic bipolar disorder

  • mania
  • no rapid cycling episodes

Limits mania and reduces mood swings

252
Q

Side effects of lithium salts

A

Gastrointestinal effects (nausea, vomiting, metallic taste) usually subside in a few weeks

Toxicity is the major danger (dose is too high) - slurred speech, tremor, confusion

Also, increases body’s salt - so watch sodium, alcohol, caffeine, and diuretics

253
Q

Anticonvulsant drug indicated for the treatment of mania/mood swings

A

Carbamazepine

254
Q

Indications for carbamazepine

A

Mania

Bipolar disorder that does not respond to lithium

Rapid cycling

255
Q

Side effects of carbamazepine

A

Cardiovascular effects
Dizziness
Rash
Visual disturbance

256
Q

Types of sedative-hypnotic drugs

A

Barbiturates (-barbitals)

Benzodiazepines (diazepam, alprazolam)

Alcohol

257
Q

Barbiturates

A

Suppress activity in the RAS

Initially used for sedative properties but no longer prescribed that often due to the side effects and risk of death

SEs: dizziness, impaired cog fxn, poor REM sleep

258
Q

Effect of low, moderate, and high doses of sedative-hypnotic drugs

A

Low doses - reduce arousal and motor activity

Moderate doses - sedation and sleep

High doses - anesthesia, coma, death

259
Q

Types of benzodiazepines

A

Diazepam

Alprazolam

(Sedative-hypnotics)

260
Q

Mode of action for benzodiazepines

A

Stimulate the inhibitory action of GABA

261
Q

Why are benzodiazepines prescribed

A

Relief of anxiety

Sleep disturbances

262
Q

Side effects of benzodiazepines

A

Drowsiness, dizziness, lethargy, slurred speech, ataxia, impaired psychomotor abilities

Rebound excitability

Psychological dependence, physical dependence

263
Q

The clinical indications of beta-blockers

A

Physical sx of anxiety

Heart conditions

Tremors

High blood pressure

264
Q

Primary beta-blocker used today

A

Propranolol

265
Q

Most common psychostimulant

A

Methylphenidate

266
Q

Purpose of psychostimulants

A

Treatment of ADHD

267
Q

Side effects of psychostimulants

A

Restlessness

Depression/irritability

Tolerance and dependence

Stunted growth (hence “drug holidays”)

268
Q

“Drug holidays”

A

When people (children, most commonly) are temporarily removed form their psychostimulants, usually over summer holidays.

Purpose: determine if drug is still needed, minimize growth suppression and other side effects

269
Q

Naltrexone (fxn and SEs)

A

Used to reduce reinforcing effects and cravings for alcohol

SEs: abdominal cramps, nausea, vomiting, insomnia, joint and muscle pain

EPPP (14 decks)

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