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Physiological Psychology And Psychopharmacology > Video Summaries > Flashcards

Video Summaries Flashcards

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1
Q

The nervous system

A
  • consists of two types of cells: neurons and glial cells
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2
Q

Neurons

A
  • communicate info within the nervous system
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3
Q

Glial cells

A
  • provide neurons with structural support, insulation, And nutrients
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4
Q

Structure of a neuron

A
  • May vary in size and shape, but I’ll have one or more dendrites a cell body( soma) and an axon
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5
Q

Dendrites

A
  • receive information from a presematic neuron
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6
Q

Cell body

A
  • contains nucleus, mitochondria, and other elements essential for cell survival
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7
Q

Axon

A
  • transmits info to a postsynaptic cell
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8
Q

Synapse

A
  • Small space between presynaptic cells axon and receptor on a postsynaptic cell
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9
Q

Mylien

A
  • some axons are insulated by this

+ Speeds up conduction

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10
Q

Multiple sclerosis

A
  • destruction of mylien that insulates axons in the brain and spinal cord caused by a malfunctioning immune system
  • symptoms very depending on location of damage
  • impaired coordination and vision, pain, fatigue, slurred, speech, tremor
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11
Q

Neurotransmitters

A

+ chemicals that transmit information from presynaptic neurons to the adjacent Post-Synaptic neuron

+ Many have excitatory or inhibitory effects depending on the type of a post-synaptic cell and others are primarily one or the other

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12
Q

Excitatory

A
  • released into the synapse is likely that an action potential will occur in a post- synaptic cell
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13
Q

Inhibitory

A

+ release into synapse decreases the likelihood that an AP will occur in a postsynaptic cell

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14
Q

Inhibitory

A

+ release into synapse decreases the likelihood that an AP will occur in a postsynaptic cell

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15
Q

Action potential

A
  • electrical impulse that travel the length of cells axon and is responsible for the release of neurotransmitters into the synapse
  • occurs when there is sufficient stimulation from a pre-synaptic neuron

-All or nothing

+ Always occurs at the same frequency

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16
Q

Dopamine

A

+ movement, learning, mood, sleep, and the reinforcement effects of drugs

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17
Q

Abnormal levels of dopamine

A
  • Parkinson’s disease, Huntington’s disease, tourette’s disorder, ADHD, depression, and schizophrenia
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18
Q

Dopamine hypothesis

A

+ original: schizophrenia is due to excessive or hyperactivity of dopamine receptors

+ Revision: positive symptoms are due to dopamine hyperactivity in the subcortical regions of the brain

  • negative symptoms are due to hypoactivity and cortical regions of the brain, especially the prefrontal cortex
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19
Q

Acetylcholine

A
  • voluntary movements: controls contractions of the skeletal muscles
  • regulate smooth and cardiac muscles
  • arousal, attention, and memory
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20
Q

Low acetylcholine

A
  • in hippocampus linked to early memory loss associated with Alzheimer’s
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21
Q

Cholinetarse inhibitors

A
  • reduce the breakdown of ACH
  • temporarily reverse or slow down memory loss or other cognitive impairments associated with people who have mild to moderate Alzheimer’s
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22
Q

Glutamate

A
  • primarily excitatory
  • movement, emotions, learning, and memory
  • involved in long-term potentiation which is essential for the formation of long-term memory
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23
Q

Long-Term potentiation

A

,- essential for the formation of long-term memories

  • rapid and or high frequency stimulation cause an increase in efficiency and strength of a synaptic transmission
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24
Q

Excessive glutamate

A
  • glutamate induced excitotoxicity causes cell damage or death believed to contribute to brain damage associated with stroke, seizures, TBI, or several neurogenitive disorders like Alzheimer’s and Huntington’s disease
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25
Q

Norepinephrine

A
  • arousal, sleep, learning, attention, mood and memory
  • abnormal levels equal ADHD, mania and depression
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26
Q

Catecholamine hypothesis

A
  • some forms of depression are caused by a deficiency
  • mania is caused by excessive norepinephrine
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27
Q

Catecholamine hypothesis

A
  • some forms of depression are caused by a deficiency
  • mania is caused by excessive norepinephrine
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28
Q

Serotonin

A

Inhibitory

asleep, sex, aggression, mood, hunger, pain, and body temp

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29
Q

Low levels of serotonin

A

in certain areas of the brain have been linked to depression, increased risk for suicide, bulimia nervosa, obsessive-compulsive disorder, and migraine headaches.

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30
Q

Excessive serotonin

A
  • anorexia nervosa have higher-than-normal brain levels of serotonin that cause anxiety and obsessive thinking and that food restriction lowers serotonin levels which alleviates these symptoms

Pplhigher-than-normal blood levels of serotonin have been found in individuals with autism spectrum disorder and individuals with chronic schizophrenia who also have enlarged cerebral ventricles and/or cerebral atrophy.

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31
Q

Gaba

A
  • primarily inhibitory
  • memory, mood, sleep, and motor control
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32
Q

Low levels of gaba

A
  • anxiety, mania, insomnia, seizures, Parkinson’s and Huntington’s disease
  • benzos enhance the effects of gaba
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33
Q

Endorphins

A

Inhibitory

  • contribute to the feelings of pleasure and well-being

Help relieve pain

  • produced by the pituitary gland and hypothalamus during strenuous exercise and produce the runner’s high
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34
Q

Agonist

A
  • mimics or increases the effects of the neurotransmitter at receptors
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35
Q

Partial agonist

A

+ produces effects similar but weaker than the effects of the neurotransmitter at receptors

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36
Q

Inverse agonist

A
  • produce effects that are opposite of the neurotransmitter at receptors
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37
Q

Antagonist

A
  • produce no effects on their own, but block or reduce the effects of a neurotransmitter or agonist at receptor
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38
Q

Dopamine agonist

A

Used to treat Parkinson’s disease and exert their effects by mimicking the effects of dopamine at dopamine receptors

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39
Q

Buspirone

A

+ partial agonist serotonin receptors and is useful for treating anxiety

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40
Q

Some atypical antipsychotic

A
  • act as inverse agonist at serotonin receptors
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41
Q

Psychotic drugs that blocked dopamine receptors

A

Antagonists

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42
Q

Myasthenia gravis

A
  • autoimmune disorder in which antibodies destroy receptors for acetylcholine that neuromuscular junctions and thereby cause skeletal muscle fatigue and weakness
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43
Q

Naloxone

A
  • has no response on its own but blocks receptors for heroin

Antagonist

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44
Q

Central nervous system

A
  • Brain and spinal cord
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45
Q

Hindbrain

A

located directly above the spinal cord

+The most primitive part of the brain. It

medulla, pons and cerebellum

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46
Q

Mid brain

A

Connects the hind brain with forebrain and includes the reticular activating system and substantia nigra

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47
Q

Brain stem

A
  • midbrain
  • pons
  • medulla
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48
Q

Forebrain

A

Aka cerebrum

It’s the largest and most complex region of the human brain and consists of subcortical and cortical structures

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49
Q

Spinal cord

A
  • Comsists of 31 Pairs of spinal nerve that consist of bundles of axons, dendrites and cell bodies
  • transmits sensory and motor information between the brain and the peripheral nervous system

+8 cervical, 12 thoracic, five lumbar, five sacral and one coccygeal

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50
Q

Effects of spinal cord injury

A
  • depend on its location, whether an injury is complete or incomplete and whether It affects sensory or motor nerves motor nerves
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51
Q

Damage at the cervical level

A
  • causes quadriplegia which is also known as tetraplegia and involves partial or complete loss of movement and or sensation in the arms, trunk and legs
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52
Q

Injury at thoracic or lumbar level

A
  • paraplegia: partial or complete loss of movement and or sensation in the legs and all are part of the trunk
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53
Q

Peripheral nervous system

A
  • translates transmits information between the central nervous system and the rest of the body and includes the somatic and autonomic nervous systems.
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54
Q

somatic nervous system

A

-transmits information from the body’s sensory receptors to the central nervous system and from the central nervous system to the skeletal muscles and it’s responsible for actions that are usually considered voluntary

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55
Q

Autonomic nervous system

A
  • transmits information between the body’s smooth muscles of the organs and glands and the central nervous system. It’s responsible for activities that are usually considered involuntary, although some activities can be brought under voluntary control using biofeedback
  • consists of the sympathetic and parasympathetic branches
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56
Q

Autonomic nervous system

A
  • transmits information between the body’s smooth muscles of the organs and glands and the central nervous system. It’s responsible for activities that are usually considered involuntary, although some activities can be brought under voluntary control using biofeedback
  • consists of the sympathetic and parasympathetic branches
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57
Q

Sympathetic branch

A
  • mediates fight or flight response and energy output

Causes pupil dilation,Sweating and increase heart and respiration rates and inhibits digestion and sexual activity

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58
Q

Parasympathetic branch

A
  • responsible for rest and relaxation and energy conservation
  • And it causes the body to return to its pre-emergency state after a fight-or-flight response
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59
Q

Sympathetic and parasympathetic branches

A
  • both active to some degree o some degree most of the time and work together cooperatively for some functions
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60
Q

General adoption syndrome

A
  • frequently cited model regarding the body’s reaction to stress

-proposes that the body’s response to all types of stress is the same is mediated by the sympathetic and parasympathetic nervous systems and involves three stages

Alarm reaction stage
Resistance stage
Exhaustion stage

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61
Q

Alarm reaction stage

A

-the hypothalamus stimulates the pituitary gland to release ACTH, which in turn stimulates the adrenal medulla to release epinephrine and norepinephrine in the adrenal cortex to release cortisol.

These hormones cause an increase in heart and respiration rates, a rise in glucose levels, and other physical changes that provide the body with the energy. It needs to respond to the stressor with a fight or flight reaction

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62
Q

Resistance stage

A
  • If the stressor continues, this stage begins

+ During this stage, the parasympathetic nervous system attempts to return some physiological functions to their normal level, but the stress hormone cortisol continues to circulate in an elevated level which helps the body maintain a high level of energy

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63
Q

Exhaustion stage

A
  • If the stress starts effects are not resolved this stage begins

-The pituitary and adrenal glands lose their ability to maintain elevated hormone levels in physiological processes begin to break down.

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64
Q

Prolonged exposure to stress

A

suppression o is the hybrid which is located just above the spinal cord f the body’s immune system which causes an increase in the body’s susceptibility to infection

Partially due to chronically elevated levels of cortisol and other stress hormones

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65
Q

Medulla

A

Regulates vital autonomic nervous system, functions: respiration, heart rate, blood pressure and digestive processes as well as coughing, swallowing, sneezing and other reflexes

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66
Q

Damage to the medulla

A
  • Brain injury, certain diseases and opioids and other drugs can disrupt the functioning of the medulla and result in death
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67
Q

Pons

A

+ connects the two halves of the cerebellum and the cerebellum to the forebrain

  • helps coordinate movements on two sides of the body
  • raousal sleep and the regulation of respiration by coordinating the transition between inhalation and exhalation
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68
Q

Cerebellum

A
  • coordinates and sequences complex voluntary movements that are initiated in the motor cortex

+ Involved in posture and balance

  • responsible for processing and storing procedural memories
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69
Q

Procedural memories

A
  • walking, riding a bicycle and driving a car as well as other types of automatic behaviors such as reciting, the alphabet and multiplication tables
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70
Q

Damage to the cerebellum

A
  • can cause ataxialack of muscle control, impaired balance and coordination, slurred speech and blurred or double vision
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71
Q

Reticular activating system

A

+ also known as the ascending reticular activating system

The network of neurons that extend from the medulla into the midbrain

  • mediates behavioral arousal and consciousness control the sleep wake cycle and alerts the cerebral cortex to incoming sensory signals
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72
Q

Lesions on the Ras

A

Can cause a comatose state while directs electrical stimulation or stimulation by sensory input. Can awaken a sleeping person and cause an awake person to become more alert

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73
Q

Substantial niagra

A
  • plays a role in reward seeking behaviors, drug addiction and through its connection to the basal ganglia motor control
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74
Q

Degeneration of dopamine producing cells in the substantia nigra

A
  • contribute to the motor symptoms associated with Parkinson’s disease
  • contribute to the slow movement, tremors,muscle rigidity and other motor symptoms
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75
Q

Subcortical structures

A
  • hypothalamus
  • thalamus
  • Basil ganglia
  • amygdala
    -Hippocampus
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76
Q

Hypothalamus

A
  • regulates the body’s homeostasis. (HR, BP, appetite, and thirst) Through effects on ANS and endocrine glands
  • influence is development of secondary sex characteristics and sexual /reproductive behaviors by stimulating pituitary gland to release sex hormones
  • regulates body’s response to stress by stimulating pituitary gland to release ACH
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77
Q

Suprachiasmatic nucleus

A
  • Located in the hypothalamus
  • control circadian rhythms (sleep wake cycle, body temperature, and hormones)

+ Bodies biological clock

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78
Q

Mammillary bodies

A
  • attached to the hypothalamus
  • memory
  • damage interferes with ability to form new declarative memories
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79
Q

Declarative memories

A
  • semantic memory
    -Episotic memory
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80
Q

Thalamus

A
  • The railway station for all senses but smell
  • receives and transmits sensory information to appropriate areas of the cortex
  • coordinates incoming sensory info with motor functions regulated by a basal ganglia, cerebellum, and motor cortex

Involved in memory

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81
Q

Damage to the thalamus and mammillary bodies

A
  • korsakoff syndrome
  • caused by a thiamine deficiency, drinking
  • anterior grade amnesia, retrograde amnesia and confabulation
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82
Q

Basal ganglia

A
  • caudate nucleus, putamen,and globus pallidus
  • important role in initiating/coordinating voluntary movements, emotional processing and responses, procedural memory and habit forming, other aspects of cognition including attention, insight, planning, and prioritizing

+ Sensitive to rewards involved in reward-based associative learning

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83
Q

Damage to the basal ganglia

A

+ Huntington’s disease
+ Parkinson’s disease
+Tourette’s
+ Ocd
+ Adhd
+ Schizophrenia

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84
Q

Limbic system

A
  • several structures involved in memory and emotion

+ Amigdala
Hippocampus

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85
Q

Amygdala

A
  • emotional reactions, (especially fair and anger)

+ Attaches emotions to memory

  • responsible for recognizing emotions in facial expressions
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86
Q

Damage the amygdala

A
  • bilateral lesions and amygdala and temporal lobe in monkeys produces Kluver bucy syndrome
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87
Q

Kluver Bucy syndrome

A
  • hyperphagia
  • hyperperiority
  • reduced fear and aggression
  • hypersexuality.
  • psychic blindness- inability to recognize familiar objects
88
Q

Damage to amygdala

A
  • ptsd
    +Depression
    +anxiety disorders
89
Q

Hippocampus

A

+ implicated more in learning and memory

  • consolidation of declarative memories (transferring declarative info from short-term to long-term memory)
  • spatial memory
90
Q

Damage to the hippocampus

A
  • trouble storing new memories in long-term memory but can recall memories formed before damage
  • degeneration of cells in hippocampus and intrahenial cortex impairment of episodic memory and spatial reasoning connected with Alzheimer’s
91
Q

Cerebral cortex

A

-+ two hemispheres r&L

+ Each hemisphere has a frontal, peripheral, temporal, and occipital lobe

  • corpus callosum: bundle of nerves that connects the two hemispheres allows for communication between two hemispheres
92
Q

Frontal lobe

A

+ prefrontal cortex
+ Primary motor cortex
+ Broca’s area

93
Q

Prefrontal cortex

A
  • important for executive (higher order) cognitive functions: planning, insight, problem solving, decision making, behavioral inhibition, and social judgment
  • contributes to motivation, emotion, regulation, working memory, and prospective memory
94
Q

Damage to the dorsolateral prefrontal cortex

A

Produces a disexecutive syndrome

  • impaired attention, working memory, judgment and abstract, thinking, depression and a decreased range of emotion and perseveration,
95
Q

Perseveration

A

-inappropriate repetition of a response

Ex person keeps using the same problem solving strategy even when it’s clear that it’s not working

96
Q

Damage to the orbital frontal area of the pfc

A
  • disinhibited syndrome

-behavioral disinhibition, distractibility emotional ability, inappropriate euphoria and acquired sociopathy

97
Q

Acquired sociopathy

A

+Risk-taking behavior

+A lack of empathy and insight

+A persistent need for immediate gratification

98
Q

Damage to the medial frontal area of the PFC

A
  • apathetic- a kinetic syndrome
  • decrease motor behavior and verbal output.
  • A lack of motivation and goal-directed activities

-apathy and indifference

99
Q

Primary motor cortex

A

+ executes voluntary movements based on info receives from other areas of the cortex

  • sends signals to muscles
100
Q

Damage to the primary motor cortex

A
  • can range from weakness to muscle paralysis and opposite side of the body
101
Q

Broca’s area

A
  • Major language area
  • Located in the dominant( usually left) hemisphere
102
Q

Damage to Broca’s area

A
  • broca’s aphasia( expressive aphasia)
  • slow labored speech, impaired repetition, anomia, with relatively intact comprehension
  • Just have difficulty expressing language, not comprehending
103
Q

Parietal lobe

A

+ contains the somatosensory cortex

104
Q

Somatosensory cortex

A
  • processes sensory information related to touch, pressure, temperature, pain, and body position
105
Q

Damage to the parietal lobe

A
  • depends on location
  • tactile agnosia, asomatognosia, anosognosia,contralateral neglect, And gerstamin syndrome
106
Q

Tactile agnosia

A
  • inability to recognize objects by touch
107
Q

Asomatognosia

A
  • flack of interest in or recognition of one or more parts of one’s body
108
Q

Anosognosia

A
  • denial of one’s illness or disability
109
Q

Contralateral neglect

A

+ A result of damage to the non-dominant (r) parietal lobe

  • inattention to one side of the body and visual field

Example make room left side of face only and eat only from the left side of the plate

110
Q

Gerstman syndrome

A
  • caused by damage to the dominant (left) hemisphere
  • finger agnosia, right left disorientation, a graphia, and acalculia
111
Q

Temporal lobe

A

+ auditory cortex
+ Wernicke’s area

112
Q

Auditory cortex

A

+ responsible for processing sound

113
Q

Damage to the auditory cortex/ temporal lobe

A

+ auditory agnosia, auditory hallucinations, or cortical deafness

114
Q

Wernicke’s area

A
  • Major language area
115
Q

Damage to wernicke’s area

A

+ Wernicke’s( receptive) aphasia

  • impaired comprehension of written and spoken language, impaired repetition and anomia
  • speech is fluent but contains many word substitutions and other errors and is incoherent and meaningless
116
Q

Articulate fasciculus

A
  • bundle of axons that connects warnickies to Broca’s area
117
Q

Damage to articulate fasciculus

A
  • conduction aphasia

+ Relatively intact comprehension with fluent speech that contains many errors, impaired repetition and anomia

118
Q

Occipital lobe

A
  • contains the visual cortex+ processes visual information
119
Q

Damage to the visual cortex

A
  • visual agnosia
  • visual hallucinations
  • Achromatopsia
  • cortical blindness
  • prosopagnosia
120
Q

Achromatopsia

A

,- loss of color vision

121
Q

Prosopagnosia

A
  • caused by damage to the occipitotemporal junction

+ Inability to recognize the faces of familiar people

122
Q

Neuroimaging techniques

A
  • two types used to diagnose neurological disorders
  • structural
    Functional
123
Q

Structural neuroimaging techniques

A
  • is to identify structural changes due to strokes, tumors, blood clots, degenerative diseases, or infections
  • computerized axial tomography and magnetic resonance imaging
124
Q

Computerized axial tomography (CAT)

A

-aka computed axial tomography or computed tomography

  • uses x-rays to obtain images of horizontal slices of the brain
125
Q

Magnetic resonance imaging (MRI)

A
  • use a strong magnetic fields and radio waves to obtain cross-sectional images of the brain
126
Q

Advantages of CAT

A
  • costs Less then an MRI
  • doesn’t require the patient to remain motionless for a long period of time
  • provides images more rapidly

+ Can be used with patients that have medical in their bodies

127
Q

Advantages of MRIs

A

+ produces three-dimensional and more detailed images

  • doesn’t require the use of radiation

mri is frequently used not only to obtain structural information about the brain and spinal cord but also other internal structures of the body

128
Q

Functional neuroimaging techniques

A
  • provide information about brain structure And neuronal activity by assessing regional cerebral blood flow, oxygen consumption, and glucose metabolism

positron emission tomography (pet)

  • single proton emission computed tomography (SPECT)
  • functional magnetic resonance imaging (fmri))
129
Q

Positron emission tomography (PET)

A

+- person is injected with a radioactive tracer that is taken up by the active brain cells

130
Q

Single proton emission computed tomography (SPECT)

A
  • similar to pet but is easier and less expensive to use
  • produces less detailed images
131
Q

Functional magnetic resonance imaging (fmri)

A
  • similar to MRI but provides information on changes in blood oxygenation and flow
132
Q

Traumatic brain injury

A

+ result of a blow, jolt, or injury to the Head

  • can be open or closed?
133
Q

Open (penetrating) injury

A
  • consequences depend on the location and severity
134
Q

Closed injury

A
  • share several characteristics
  • cause more widespread damage and loss of or alteration of consciousness that varies in duration depending on severity of injury
  • people experience a combination of emotional, cognitive, behavioral, and physical symptoms that vary in severity from mild to severe
135
Q

Cognitive symptoms of TBI

A
  • some degree of anteriorate in retrograde amnesia
  • duration of anterior grade amnesia is a good predictor of recovery
  • used to determine severity of injury
136
Q

Retrograde, amnesia and TBI

A
  • More recent long-term memories are affected then remote
  • More distant memories recover first
137
Q

Recovery and TBI

A
  • mild significant recovery the first 3 months
  • continued recovery into the first year
  • most continue to have symptoms indefinitely, especially for moderate to severe injury
138
Q

Mdd and TBI

A
  • most common diagnosis regardless of injury severity
139
Q

Cerebrovascular accident

A
  • aka stroke
  • caused by a non-traumatic injury that causes a sudden disruption of blood flow to the brain
  • symptoms depend on artery involved
140
Q

Leading risk factor of stroke

A
  • hypertension
141
Q

Risk factors of stroke

A
  • Atribular fibrillation
    + Asterosclerosis
  • diabetes
  • cigarette smoking
  • alcohol use
  • High cholesterol
142
Q

Middle cerebral artery

A
  • supplies blood to the frontal lobe, lateral parietal and temporal lobes
  • most often involved in strokes
143
Q

Middle cerebral artery stroke

A
  • produces contralateral sensory loss, weakness or paralysis, especially in the arm or face
  • impaired vision
  • aphasia if the dominant hemisphere is affected
  • contralateral neglect or aphasia if the non-dominant hemisphere is neglected
144
Q

Anterior cerebral artery

A
  • supplies blood to the frontal and parietal lobes
145
Q

Anterior cerebral artery stroke

A
  • produces contralateral sensory loss, weakness or paralysis, especially in the leg
  • impaired insight and attention
  • impaired speech, confusion, and apathy
146
Q

Posterior cerebral artery

A
  • supplies blood to the temporal and occipital lobes
147
Q

Posterior cerebral artery stroke

A
  • memory deficits
  • unilateral cortical blindness
  • color agnosia
  • other visual impairments
148
Q

Diseases caused by degeneration of cells and motor areas of the brain

A
  • Huntington’s disease
  • Parkinson’s disease
149
Q

Huntington’s disease

A
  • caused by an autosomal dominant Gene
  • Link abnormal levels of gaba, glutamate, and dopamine in the basal ganglia
150
Q

Onset of Huntington’s disease

A

30 to 50 years old

151
Q

Symptoms of Huntington’s disease

A
  • initially depression, apathy or other effective symptoms
  • followed by short-term memory loss, impaired concentration, impaired judgment, and other cognitive symptoms
  • then fidgeting, facial, twitches, and motor symptoms

+ As disease progresses, athyosclerosis and cholera may occur later. Stages motor symptoms are more severe difficulty speaking and swallowing and may develop major mild neurocognitive disorder

152
Q

Cholera

A
  • involuntary rapper jerky movements in the limbs and trunk
153
Q

Athetosis

A
  • non rhythmic slow writhing movements
154
Q

Parkinson’s disease

A
  • caused by loss of dopamine producing cells and the substantia nigra which affects functioning in the basal ganglia and motor cortex
155
Q

Cause of Parkinson’s disease

A
  • unknown but evidence supports exposure to toxins or certain chemicals
156
Q

Symptoms of Parkinson’s disease

A
  • impaired balance and equilibrium
  • muscle rigidity
  • slowed voluntary movements
  • tremors that begin in the hands and involve pill rolling
  • up to 50% experience depression
  • 40% experience anxiety
  • many experience hallucinations and delusions and later stages of the disorder
  • some go on to develop major mild neurocognitive disorder
157
Q

Treatment of Parkinson’s disease

A
  • No cure
  • symptoms treated in early stages and temporarily alleviated with l-dopa
158
Q

Seizure disorders

A
  • caused by abnormal electrical activity of the brain
  • focal onset seizures
  • generalized onset seizures
159
Q

Focal onset seizures

A
  • began in one area of the brain and on one side of the body
  • affect only one side of the body
  • May spread and become generalized seizures
160
Q

Types of focal onset seizures

A
  • focal onset aware Seizures( (simple, partial seizures)
  • focal onset impaired awareness seizures (complex, partial seizures)
161
Q

Focal onset aware seizures

A
  • Don’t affect consciousness
  • last for less than 2 minutes
162
Q

Focal onset impaired awareness seizures

A
  • cause changing consciousness
  • May begin with Aura
  • last 1 to 2 minutes
163
Q

Symptoms of both types of focal onset seizures

A
  • abnormal sensations
  • hallucinations
  • Sense of deja vu
  • automatisms: repeated movements of body, repeated sounds, and walking in circles

-

164
Q

Generalized onset seizures

A

+ Don’t have a focal onset

  • affect both sides of the brain
  • generalized onset motor seizures
  • generalized onset non-motor seizures
165
Q

Generalized onset motor seizures

A

+ tonic clonic or Grand mal seizures

  • change in consciousness
  • tonic phase: stiffening in muscles of face and limbs followed by colonic phase: jerky rhythmic movements in the arms and legs
  • One person regains consciousness may be depressed, confused, and have no memory of events that occurred during seizure
166
Q

Generalize onset and non-motor seizures

A
  • absent or petite Mal seizures
  • involve loss of consciousness that last 10 to 20 seconds
  • blank/absinthe stare head nodding eye fluttering or hand movements
  • after seizure resume pre-seize your activities
167
Q

First generation antipsychotics

A
  • aka traditional or conventional antipsychotics
  • used to treat schizophrenia and other disorders with psychotic symptoms
  • most effective for positive symptoms
168
Q

What are the first generation? Antipsychotics

A

Chlorpromazine (thorazine)

Haloperidol( (haldol)

Thioridazine (mellaril)

Fluphenazine (proloxin)

169
Q

How do first generation antipsychotics work?

A
  • dopamine antagonist: blocks the dopamine receptors
170
Q

Side effects of fga’s

A
  • anticholinergic effects: dry mouth, blurred vision, constipation, confusion , urine retention tachycardia, impaired attention and concentration
  • extra pyramidal effect. S: parkinsonisms, dystonia, akathisia, and tachycardia
171
Q

Parkinsonisms

A
  • resting tremor, muscle rigidity, and slow movement
172
Q

Dystonia

A
  • uncontrollable muscle rigidity, especially in the head and neck
173
Q

Akathisia

A
  • restlessness and pacing
174
Q

Tardive dyskinesia

A
  • potentially life-threatening
  • occurs after prolonged use
  • And voluntary repetitive movements of the tongue, face, and jaw May then affect the trunk over time
  • irreversible for some
175
Q

Treatment of tardive dyskinesia

A
  • gradually withdraw drug then switch to a second generation antipsychotic or administer dopamine depleting or gaba enhancing drug
  • for some symptoms may get worse or not reduce when switched to a second generation antipsychotic
176
Q

Neuroleptic malignments syndrome

A
  • rare, life-threatening
  • muscle rigidity, autonomic dysfunction: unstable blood pressure tachycardia and rapid breathing
  • altered mental state: confusion agitation, and disorientation

Hyperthermia

177
Q

Treatment of neuroleptic malignant syndrome

A
  • Have person stop taking drug at first sign of symptoms
  • medical and supportive treatment for symptoms
178
Q

Second generation antipsychotics

A
  • aka aypical antipsychotics
  • used to treat schizophrenia or other disorders with psychotic symptoms or monotherapy/adjunctive therapy for MDD and bipolar disorder
  • as effective or more effective than first generation, antipsychotics for positive symptoms and some are effective for negative symptoms, especially clozapine
  • clonazepine (clozaril)
  • risperidone( risperdal)
  • olanzapine( zyprexa)
179
Q

How do second generation antipsychotics work?

A
  • dopamine and serotonin antagonists or inverse agonist, reduce effects of dopamine and serotonin

alleviate positive symptoms primarily by blocking dopamine (especially D3 and D4) receptors

alleviate negative and cognitive symptoms primarily by blocking serotonin receptors

180
Q

Advantages of second generation antipsychotics

A
  • less likely to cause extra pyramidal side effects especially clonazepine

effective for patients whodo not respond to or cannot tolerate FGAs.

clozapine is the only FDA-approved antipsychotic for treatment-resistant schizophrenia.

181
Q

Side effects of second generation antipsychotics

A
  • antichlorinergic effect
    -neurocleptic malignant syndrome
  • metabolic syndrome
  • agranocytosis
182
Q

Metabolic syndrome

A

substantial weight gain,
high blood pressure
insulin resistance
hyperglycemia

increased risk for diabetes mellitus and heart disease.

183
Q

Neurogleptic malignment syndrome

A
  • restless severity less for second generation drugs
184
Q

Netropenia & Agraniocytosis and atypical antipsychotics

A

agranulocytosis: severe form of neutropenia.

Both potentially life-threatening and involve dangerously low levels of neutrophils, which are a type of white blood cell that is an essential part of the body’s immune system.

Patients taking clozapine must have regular blood tests and, when neutrophil levels are too low, treatment may include discontinuing the drug and prescribing an antibiotic for infections and medications to improve the body’s ability to produce neutrophils more quickly.

-

185
Q

Ssris

A
  • first line for pharmacological treatment for depression, persistent depression disorders
  • used to treat several other disorders: PMDD, OCD, panic disorder, generalized anxiety disorder, PTSD, bulimia versa, and premature ejaculation
186
Q

How do ssris work?

A
  • block the re-up ticket serotonin into presynaptic cells
187
Q

Side effects of ssris

A
  • mild anticholinergic fx, gastrointestinal disturbance, insomnia, anxiety, headaches and sexual dysfunction
188
Q

Discontinuation syndrome

A
  • caused by abrupt cessation of ssris
  • dizziness, mood liability, impaired concentration, sleep disturbances, and flu-like symptoms
189
Q

Serotonin syndrome

A
  • combinings SSR or maois
  • potentially fatal
  • extreme agitation, confusion, autonomic instability, hyperthermia, tremor, seizure and delirium
190
Q

Treatment of serotonin syndrome

A
  • immediate withdrawal of drug and medical treatment for symptoms
191
Q

SNRIs

A
  • used to treat MDD, anxiety, chronic pain, and several other disorders
  • similar to ssris for a treatment of depression
  • maybe more effective for severe depression
192
Q

Snri drugs

A
  • venlafaxine (effexor,)
  • duloxetine. (Cymbalta)
    -desvenlafaxine (pristique)
193
Q

How do SNRIs work?

A
  • block the re-uptake of serotonin and norepinephrine
194
Q

Side effects of SNRIs

A
  • mild anticolonergic effects, insomnia, headache, and sexual dysfunction
195
Q

Types of patients SNRS or contraindicated for

A
  • hypertension and heart issues due to norepinephrine equals can elevate blood pressure
196
Q

Discontinuation syndrome and serotonin syndrome and snris

A
  • can cause these
197
Q

Tcas

A
  • traceyclic antidepressants
  • used to treat major depressive disorder, panic disorder, anxiety, OCD and neuropathic pain
198
Q

Tca drugs

A
  • amitriptyline(Elavil)
    -imipramine (Tofranil)
  • clomipramine (Anafranil)
  • nortriptyline (Pamelor)
    -doxepin (sinequon)
199
Q

How do tcas work?

A
  • inhibit the reuptake of norepinephrine, serotonin, and dopamine in presynaptic cells
200
Q

Side effects of TCAs

A
  • anticholinergic effects, hypertension, orthostatic hypotension, other cardiovascular effects, tachycardia, and sexual dysfunction, sedation and weight gain
201
Q

What patients are tca’s contraindicated for ?

A
  • toxic
  • can be lethal and overdose
  • describe with caution for patients with heart disease or who are suicidal
202
Q

Maois drugs

A

-Phenelzine (Nordil)
-isocarboxazid (Morplan)
-tranyicypromine (pamate)

203
Q

What are MAOI is used to treat?

A
  • A typical depression
204
Q

A typical depression

A
  • hypersomnia
  • increased appetite
  • leaden paralysis
  • mood reactivity
  • rejection sensitivity
205
Q

How do maois work?

A
  • increase norepinephrine, serotonin, and dopamine by inhibiting the activity of the mono oxidase enzyme
206
Q

Side effects of MAOI inhibitors

A
  • anticholoneergenic effects, orthostatic hypotension, daytime sleepiness, insomnia, and sexual dysfunction
  • can cause a fatal hypotensive crisis
207
Q

Hypertensive crisis

A
  • can a corwin taken with amphetamines or antihistamines or foods with tyramine?
  • throbbing headache, stiff neck, rapid heart rate, nausea, vomiting, sweating, photosensitivity, confusion and dizziness
208
Q

Mood stabilizers

A
  • lithium
  • Anti-Convulsant drugs
209
Q

Anti-Convulsant drugs

A
  • carbamazepine (tegritol)
  • valporic acid (depokene)
210
Q

Lithium

A
  • line for acute mania and classic bipolar disorder
211
Q

Classic bipolar disorder

A
  • acute mania with rapid non-rapid cycling
212
Q

Effectiveness of anti-convulsants

A

,- maybe more effective when lithium doesn’t work
- better for a cute Maine India, bipolar disorder with manicure mixed episodes, or bipolar disorder with rapid cycling

213
Q

How do mood stabilizers work?

A
  • well understood how but linked two alterations in dopamine, glutamate, norepinephrine and serotonin
214
Q

Side effects of lithium

A
  • nausea and vomiting
  • metallic taste
  • hand tremor
  • impaired memory and concentration
  • increase thirst
  • weight gain
215
Q

Lithium toxicity

A
  • must be monitored
  • vomiting, diarrhea, ataxia, seizures, , and death?
216
Q

Side effects of anti-convulsants

A
  • nausea
    ,- dizziness
  • lethargy
  • sleepiness
  • ataxia
  • tremor
  • visual disturbance
  • impaired concentration
217
Q

Monitoring of anti-convulsants

A
  • carbamazepine and vaporic acid for liver failure
  • carbamazepine equal agraniocytosis and aplastic anemia

Physiological Psychology And Psychopharmacology (6 decks)

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