Physio Midterm Flashcards

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1
Q

Brain Protection

A
  • Skull/Cranium
  • Meninges
  • Cerebrospinal Fluid (CSF)
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2
Q

Spinal Cord

A
  • Connected to the brain by the brain stem
  • Long bundle of nerves
  • Sends motor commands from the brain to the body, sends sensory information from the body to the brain, and coordinates reflexes
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3
Q

3 Main Sections of the Spinal Cord

A
  • Cervical Spinal Cord: sends nerves to the face and neck
  • Thoracic Spinal Cord: sends nerves to the arms, chest, and abdomen
  • Lumbar-Sacral Spinal Cord: sends nerves to the lower body
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4
Q

Cauda Equina

A
  • A bunch of nerves at the bottom of the spinal cord
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5
Q

Types of Neurons in the Somatic Nervous System

A
  • Sensory Neurons: carry signals from the outer parts of your body (periphery) into the central nervous system
  • Motor Neurons: carry signals from the central nervous system to the outer parts (muscles, skin, glands) of the body
  • Interneurons: connect various neurons within the body and spinal cord
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6
Q

The Somatic Nervous System is made up of:

A
  • Spinal Nerves: mixed nerves that carry sensory information into and motor commands out of the spinal cord
  • Cranial Nerves: they are the nerve fibers that carry information into and out of the brain stem
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7
Q

ASIA Impairment Scale

A
  • A: complete; no motor, no sensory, no sacral sparing
  • B: incomplete; no motor, sensory only
  • C: incomplete; 50% of muscles LESS than grade 3 (can’t raise arms or legs off bed)
  • D: incomplete; 50% of muscles MORE than grade 3 (can raise arms or legs off bed)
  • E: normal; motor and sensory function are normal
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8
Q

Amygdala

A
  • Happiness and enjoyment
  • Anxiety, irritability, and unease - withdrawal feelings = rewarding or aversive
  • PTSD = HIGHER AMYGDALA AND LOWER VMPFC ACTIVATION
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9
Q

Amygdala with Hippocampus

A
  • Long term memories
  • Episodic Memory: long-term memory that involves conscious recollection of previous experiences
  • Long-term Potentiation: a process involving persistent strengthening of synapses that leads to a long-lasting increase in signal transmission between neurons
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10
Q

Amygdala with Hypothalamus

A
  • Sympathetic nervous response (fight or flight)
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11
Q

Amygdala with Thalamus

A
  • Unconscious fear processing
  • Conditioned emotional response (classical conditioning)
  • Unconscious response
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12
Q

Structures of the Amygdala

A
  • Lateral Nucleus: regarded as the sensory input gateway; located in dorso-lateral part of the amygdala
  • Central Nucleus: key role in emotional response to aversive stimuli –> stress; damage = less stress hormones, ulcers, and stress-induced illnesses; stimulation = higher fear, agitation, gastric ulcers
  • Basal Nucleus: major output pathways to cerebral cortex; projects to the VMPFC –> extinction of conditioned fear
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13
Q

Ventral Tegmental Area

A
  • Dopamine-rich nucleus that mediates reward system
  • Located in midbrain, next to substantia nigra
  • Sends dopamine to the nucleus accumbens, amygdala, hippocampus, and prefrontal cortex
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14
Q

Ventromedial Prefrontal Cortex (VMPFC)

A
  • Impulse control, courage, moral decision making
  • Interface between emotional responses and control of complex behaviors
  • Using emotional reasons to guide behaviors
  • Courage = higher VMPFC activation
  • Impulsive/emotional murderers = lower VMPFC activation vs. calculating/careful - typical brain patterns
  • Antisocial personality disorder = 11% less gray matter in VMPFC
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15
Q

Patient E.R.

A
  • Bilateral damage of the VMPFC
  • Excellent social judgement in verbal responses to hypothetical situations, expansive reasoning shared
  • Real life situations = unable to prioritize between trivial and important decisions
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16
Q

Neuron Structures

A
  • Cell body (Soma)
  • Dendrites
  • Axons
  • Myelin Sheath
  • Terminal Buttons/Axon Terminals
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17
Q

Cell Body (Soma)

A
  • Contains the nucleus
  • Shape varies in different kinds of neurons
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18
Q

Dendrites

A
  • A branched, treelike structure attached to the soma of a neuron
  • Receives information transmitted across synapse
  • Neurons converse with one another, and dendrites are recipients of these messages
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19
Q

Axons

A
  • Long, thin. cylindrical structures
  • Axon Hillock: gate keeper of whether an action potential is strong enough
  • Carries information from cell body to terminal buttons/axon terminal
  • Action potential is basic message
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20
Q

Terminal Buttons/Axon Terminals

A
  • Buds at the end of a branch of an axon
  • Forms synapses with another neuron
  • Secretes chemicals called neurotransmitters
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21
Q

Types of Glial Cells

A
  • Microglia
  • Astrocytes
  • Oligodendrocytes
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22
Q

Microglia

A
  • Smallest glial cells
  • Clean up dead cells
  • Protect the brain from invading microorganisms/toxins
  • Damage/toxins = microglial cells produce inflammatory mediators to call other cells to the injury –> promote and perpetuate the inflammatory response –> can worsen neurodegeneration
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23
Q

Astrocytes

A
  • Star shaped
  • Neuron “glue” - holds them in place
  • Engulf debris (phagocytosis)
  • Provide nourishment via transfer of fuel - neurons use a lot of energy but cannot store it
  • Provide electric insulation for unmyelinated neurons
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24
Q

Oligodendrocytes

A
  • Produces myelin in the form of a tube by wrapping itself around the axon
  • Forms sheath in segments
  • Episodic gaps = Nodes of Ranvier
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25
Q

Action Potential

A
  • Rapid burst of depolarization followed by hyperpolarization
  • All or none law
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26
Q

Depolarization

A
  • Reduction of membrane potential (less negative inside)
  • Lower in electrical charge = lower membrane potential
  • Threshold of Excitation = set point to produce an action potential = -55mV
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27
Q

Hyperpolarization

A
  • Increase in membrane potential
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28
Q

Post-synaptic Potential Types

A
  • Determined by characteristics of postsynaptic receptors; type of ion channel they open
  • Excitatory (EPSP): Sodium channel opened; depolarizing
  • Inhibitory (IPSP): Potassium channel opened; Hyperpolarizing
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29
Q

Glutamate

A
  • “Go”
  • Main excitatory neurotransmitter in brain and spinal cord
  • Stored in vesicles and released from presynaptic neuron following an action potential
  • Removed from synapse by excitatory AA transporters
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30
Q

GABA

A
  • “Stop”
  • Inhibitory in the brain
  • Stored in presynaptic vesicles
  • GABA transporters re-uptake; aminotransferase deactivates
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31
Q

GABAA Receptor

A
  • 5 binding sites
  • Indirect agonists that bind the GABAA = benzos, some sleep meds, barbiturates, steroid hormones = sedating effects
  • indirect antagonists at high doses = seizures
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32
Q

Glycine

A
  • Inhibitory in the spinal cord and lower brain stem
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33
Q

NMDA Receptors

A
  • 6 binding sites (4 on exterior and 2 located deep in the channel)
  • Requirements for Glutamate to bind: Glycine must be attached; Mg must not be attached –> depolarized
  • When channel is opened NMDA receptor allows sodium and calcium into cell –> depolarization
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34
Q

Dopamine Primary Effect

A
  • Movement, attention, learning, and the reinforcing effects of substances
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35
Q

Serotonin Primary Effects

A
  • Involved in mood and pain regulation, and the control of eating, sleep, arousal, and dreaming
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36
Q

Norepinephrine Primary Effects

A
  • Vigilance/Attentiveness
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37
Q

Oxytocin

A
  • Post-Orgasm: in women, higher oxytocin = feelings of attachment and bonding
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38
Q

Vasopressin

A
  • Post-Orgasm: in men, higher vasopressin = vigilance and need to guard/protect partner
39
Q

Key Structures of the Brain’s Reward System

A
  • Ventral Tegmental Area
  • Nucleus Accumbens
  • Amygdala
  • Hippocampus
  • Prefrontal Cortex
40
Q

Nucleus Accumbens

A
  • Involved in all motivationally relevant stimuli = rewarding or aversive
  • Interface between motivation and action
41
Q

Hippocampus

A
  • Memory and learning
42
Q

Prefrontal Cortex

A
  • Reasoning, problem-solving, impulse control, creativity, perseverance
43
Q

Positive Reinforcement

A
  • Add something to the environment to increase behavior
44
Q

Positive Punishment

A
  • Add something to the environment to decrease the behavior
45
Q

Negative Reinforcement

A

Remove something from the environment to increase the behavior

46
Q

Negative Punishment

A

Remove something from the environment to decrease the behavior

47
Q

Role of Stress

A
  • Stress = higher corticotropin-releasing hormone (CRH)
  • Strengthens amygdala
  • Weakens the hippocampus and prefrontal cortex
  • Results in: Negative emotional state, Lack of executive control (higher risk of relapse), Memory of relief/cravings
48
Q

Studies of Stress

A
  • 1/3 adolescents with reported abuse/neglect will develop SUD before 18
  • 2-4x of those with PTSD developing chemical dependencies
  • COVID-19 = 23% increase in AUD
49
Q

Ethanol Absoprtion

A
  • 20% stomach and 80% small intestine (several variables)
  • Food inhibits absorption causing oxidation of alcohol
  • 20-30% BAC absorbed fastest
  • > 30% irritates gastric mucosa –> slowed absorption
  • IMPAIRED THIAMINE ABSORPTION
50
Q

Ethanol Metabolism

A
  • Primarily hepatic (90%)
  • Alcohol dehydrogenase (ADH) oxidation (requires B vitamins)
  • Metabolized to form acetaldehyde (carcinogenic, prevents, absorption of nutrients)
51
Q

Ethanol Excretion

A
  • Urine
  • Diuretic properties –> decreased nutrients and dehydration
52
Q

Ethanol Intoxication

A
  • Consuming ETOH faster than liver can break it down
  • 1 standard drink per hour
  • 80% of individuals with AUD = thiamine deficiency due to lower vitamin absorption and higher thiamine use by ADH
53
Q

Stimulant Pharmacokinetics

A
  • Stimulants impact the brain’s level of epinephrine/norepinephrine, dopamine, and serotonin
  • Primary risk factors: Reduced seizure threshold; Higher BP, HR, HTB = higher risk of stroke, MI; Poor appetite, mood swings, anxiety, insomnia; Toxic levels = paranoia, psychosis
54
Q

Nicotine Absorption

A
  • Tobacco smoke - enters blood stream via lungs
  • Smokeless tobacco - mucosal membrane of mouth, nose, or skin
  • Reaches the brain in 7 seconds
  • Mimics Ach = arousal, learning, memory, and emotions
55
Q

Nicotine Effects

A
  • Binds to nicotinic receptors –> changes cerebral metabolism
  • Stimulates adrenal glands –> higher BP, HR, respiration, alertness and epinephrine
56
Q

Nicotine Metabolism and Excretion

A
  • Higher metabolism
  • Metabolized by liver, kidneys, lungs = cotinine
  • Excreted via urine
57
Q

Cannabis Absorption

A
  • Inhalation: peak plasma conc. 3-10 minutes; bioavailability = 10-35%
  • Oral: peak plasma conc. ~ 120 minutes, bioavailability = 6-20%
58
Q

Cannabis Distribution

A
  • Rapidly to well-vascularized organs
  • Accumulates in adipose tissue
59
Q

Cannabis Metabolism

A
  • Predominately hepatic
  • Able to cross the placenta; released in breast milk
  • Excreted through urine, feces, and sweat
60
Q

Neural Effects of Ethanol

A
  • OVERALL CNS DEPRESSANT
  • Higher GABA and lower glutamate = slowed/inhibited NT firing –> sedation
  • Higher serotonin and dopamine = relaxation and good mood
  • Cerebellum –> loss of coordination and consciousness
  • PFC –> decreased inhibition
  • Blocks vasopressin = more urination and dehydration
61
Q

Functions of Sleep

A
  • To stay away from predators
  • Conserve energy
  • Allow body time to rest and regenerate
  • Waste clearance
  • Memory consolidation
62
Q

Sleep Waves

A
  • Synchronous Delta Activity: if the cells are active at about the same time their electrical messages are synchronized and appear as a large, clear wave in EEG data
  • Desynchronous Beta Waves Activity: if neurons are active at different times, their electrical messages are desynchronized and appear as small, chaotic waveforms without a clear pattern in the EEG data
63
Q

Roles of Slow-Wave Sleep in Learning/Memory

A
  • Slow-wave sleep facilitates consolidation of declarative memories
  • The brain rehearses newly learned information during slow-wave sleep
64
Q

Roles of REM Sleep in Learning/Memory

A
  • REM is important for early neurological development
  • REM sleep facilitates consolidation of nondeclarative memories
65
Q

Neural Chemicals Involved in Sleep

A
  • Adenosine
  • Histamines
  • Acetylcholine
  • Serotonin
  • Norepinephrine
  • Orexin
66
Q

Adenosine

A
  • Inhibitory
  • Sleep deprivation = lower glycogen stores and higher adenosine = sleepiness
  • Increases steadily during day producing sleepy feeling at night
67
Q

Histamines

A
  • keeps us awake
  • antihistamines make us drowsy
68
Q

Acetylcholine

A
  • High during wakefulness and REM
69
Q

Serotonin

A
  • Low during REM sleep = limited movement
70
Q

Norepinephrine

A
  • Higher locus coeruleus firing = higher vigilance/focus
71
Q

Orexin

A

High during alert or active waking, especially exploratory activity

72
Q

Insomnia

A
  • Effects 30% of adults
  • Primary insomnia: difficulty falling asleep after going to bed or after awakening during the night
  • Secondary insomnia: inability to sleep due to another mental or physical condition (e.g., pain, medication)
73
Q

Narcolepsy

A
  • Orexin-related neurological disorder
  • Sleep attacks = overwhelming urge to sleep
  • Cataplexy = sudden muscle weakness/paralysis
  • Sleep paralysis = inability to move before onset of sleep or waking
  • Treatment = modafinil, methylphenidate, SSRIs
74
Q

REM Sleep Behavior Disorder

A
  • Lack of muscle paralysis during REM –> acting out of dreams
  • Can be comorbid with narcolepsy
  • Typical onset 60 years+
  • Believed to be neurodegenerative
  • Treatment = clonazepam
75
Q

Sleep Apnea

A
  • 18 million Americans
  • Difficulties sleeping and breathing at the same time
  • Wake up gasping for airway and decreased slow wave activity
  • Obstructive sleep apnea: due to narrowing of airway
  • Central sleep apnea: brain does not signal need to breath
  • Untreated: sig. deficits in attention, memory, and executive functions; increase risk of stroke, MI; in kids 2.5x risk of behavioral problems
76
Q

Melatonin

A
  • Produced by the Pineal Gland in response to evening/darkness about 2 hours before normal sleep time
  • Serotonin is converted into melatonin
  • Exogenous melatonin = take 1-2mg 30 to 1 hour before bedtime
  • Light (especially blue light) negates melatonin effects
  • Contraindicated in older adults with dementia and those with dementia
77
Q

Emotional Response Components

A

Behavioral –> Emotional Response –> Hormonal; Autonomic

78
Q

Kluver-Bucy Syndrome

A
  • Can be caused by stroke, encephalitis, tumors, TBI, and even a lobotomy
  • Damage to the bilateral amygdaloid nuclei (anterior temporal lobes) and hippocampus
  • Results in: Absence of fear and anger response; psychic blindness/visual agnosia; hyper-orality; hyper-sexuality without sexual desire; binge eating disorder/bulimia; memory disorders
79
Q

Urbach-Weithe Disease

A
  • Rare genetic disorder
  • Progressive damaging of neural tissue (via calcification)
  • In the brain is confined to the amygdala complex
  • 400 people worldwide (1/4 in South Africa)
  • First symptom = weak cry/hoarse voice
  • typical cognition across all domains
  • Patient SM = lack of fear response
  • Lack of pathway to VMPFC = no inhibition from typical fear inducing stimuli
80
Q

Relationship between Heredity, Serotonin, and Aggression

A
  • Higher correlations between monozygotic twins in antisocial and unemotional behavior
  • 50-65% heritability –> believed to be due to gene modifications impacting serotonin synthesis/signaling
  • Aggressive child-parent interactions = higher amygdala activation and aggression
  • Serotonin inhibits aggression and risky behavior
  • SSRIs = lower irritability and aggression
81
Q

Emotional Expressions

A
  • No differences between the expressions of congenitally blind, noncongenitally blind, and sighted athletes when expressing happiness
  • Namibians and European-English = matched the same vocalizations with the correct story
82
Q

Affective Blindness

A
  • Those with damage to the visual cortex, can recognize facial expressions of emotions without conscious awareness of looking at a person’s face
  • “I can’t see it” –> while matching it
83
Q

Wernicke-Korsakoff Syndrome

A
  • Wernicke’s Encephalopathy (WE): ACUTE phase = confusion, incoordination, ataxia, decreased consciousness, memory deficits, abnormal gait
  • Korsakoff Psychosis: can develop after WE or without - CHRONIC phase = severe short term memory loss, poor coordination
  • Caused by chronic ETOH use and/or Thiamine deficiency
84
Q

Alcoholic Neuropathy

A
  • Peripheral nerve damage
85
Q

Alcoholic Cerebellar Damage

A
  • Deterioration or cerebellar neurons
  • Chronic incoordination, slurred speech, jerky movements, tremor, nystagmus
86
Q

Blood Brain Barrier

A
  • Selectively permeable
  • Area Postrema = weakest region (vomiting); has an additional barrier
  • Blocks all molecules except those with: lipid soluble, specialized sugars and amino acids via facilitated diffusion, water molecules
87
Q

Saltatory Conduction

A
  • In myelinated fibers, depolarization and repolarization processes occur from one node of ranvier to the next instead of the entire area of the membrane
  • Economic and speedy
88
Q

Sleep Stages (5)

A
  1. Waking
  2. NREM: Stage 1
  3. NREM: Stage 2
  4. NREM: Stage 3
  5. REM
89
Q

NREM: Stage 1 (N1)

A
  • Transition between wakefulness and sleep
  • Lightest stage of sleep
  • Theta waves (4/7Hz)
  • 2-5% of total sleep time
  • Hypnic jerks
  • Increased proportion suggests sleep fragmentation
90
Q

NREM: Stage 2

A
  • About half the night
  • Slowed HR, breathing, muscle activity, eye movements
  • Reduced body temp
  • Characterized by sleep spindles and K complexes
91
Q

NREM: Stage 3

A
  • Slow-wave sleep
  • Low frequency, high amplitude delta waves
  • 20% TST
  • Thought to be the most restorative sleep stage: memory consolidation, waste clearance
  • Predominates first half of the night
92
Q

REM

A
  • Rapid eye movement sleep
  • Muscle paralysis
  • Dreams
  • Easily awoken from this stage
  • Desynchronized EEG
  • Absence of movement on EMG
93
Q

Sleep Cycles

A
  • Each cycle lasts ~ 90 minutes
  • Alternates from REM to NREM
  • SWS predominates first half of the night
  • REM predominates second half