Unit 3 Flashcards
1
Q
Hormones
A
Chemicals that send signals to different parts of the body, either to or from the body to or from the brain. Required to produce Gender.
2
Q
Steroid Hormone
A
Body -> Brain. Hydrophobic, thus bypasses the hydrophobic blood-brain barrier. In utero: causes physical differences btw genders (genitalia/musculoskeletal). Puberty: activates expression of sexual physiology and gamete formation. All steroid based on cholesterol.
3
Q
Peptide Hormone
A
Brain -> Body. Hydrophilic. Not restricted by blood brain barrier. Produced by proteolysis from precursor proteins. IE vasopressin, oxytocin.
4
Q
Proteolysis
A
Process by which peptides are produced by being broken off from larger “precursor” proteins. Can lead to multiples effects and reactions to stress (ACTH [stress] is cleaved off of POMC precursor, but so is enkephalin [pain relief]).
5
Q
Anterior Pituitary
A
Contains endocrine cells controlled by cells in the hypothalamus. Hypothalamus cells release neurotransmitters into the blood to start up endocrine cells in AP (pituicytes) to release hormones into brain. Contains larger variety of cells and peptides than posterior.
6
Q
Posterior Pituitary
A
Contains pre-synaptic terminals from cells in the hypothalamus. Offers a direct connection between the brain and body as peptides are directly released into the blood.
7
Q
Pituitary Gland
A
Master gland. Controls release of peptide hormones into the bloodstream. Essentially is a portal system through which the brain interacts with the body chemically.
8
Q
Hypothalamus
A
Site of synthesis of peptide hormones. Releases hormones into blood via terminals in the posterior pituitary.
9
Q
Vasopressin
A
ADH (anti-diurectic hormone). Controls water retention. Stops bed-wetting. Influence sex behavior in males and maternal behavior in females.
10
Q
Oxytocin
A
Controls uterine contractions during labor and milk letdown from breasts. Influence sex behavior in males and maternal behavior in females.
11
Q
Corticotrophs
A
A pituicyte in the ant. pituitary. Synthesizes POMC (precursor protein), and thus secretes ACTH (stress) into the blood stream. Hormone release from the AP is stimulated by Thyrotropin (Corticotropin Releasing Thyroid Hormone) producing cells.
12
Q
Gonadotrophs
A
A pituicyte in the ant. pituitary. Synthesizes and secretes Follical Stimulating Hormone (FSH) and Lutenizing Hormone (LH) into blood supply. Release from AP is stimulated by Gonadotropin Releasing Hormone (GnRH) cells in the hypthalamus.
13
Q
Negative Feedback in the Pituitary Gland
A
Body must maintain homeostasis, thus some hormones have actions that prevent further production of the hormone. EG: HPA Axis: Hypothalamus releases CRH -> AP releasing ACTH -> Adrenal Cortex releasing cortisol -> cortisol inhibits CRH and ACTH release.
14
Q
Genomic vs. Non-Genomic Effects of Steroid Hormone
A
Genomic: Passes through membrane onto a nuclear receptor on the nucleus where it activates the relevant genes (SLOW).
Non-Genomic: Lands on a membrane receptor which activates 2nd messengers (FAST).
15
Q
Progesterone/Estradiol
A
Steroid Hormones responsible for female reproduction. High concentration in breasts, vagina, uterus, and assoc brain regions.
16
Q
Testosterone
A
Steroid hormone with organization and activational role in male reproduction. High concentration in male genitalia, hair follices, muscle groups, and assoc. brain regions.
17
Q
Cortisol
A
Steroid hormone related to stress in males and females.
18
Q
Steroid Conversion
A
Aromatase turns testosterone carbon ring into estrogen by aromatization. Causes gynoclymastia
Reductase turns testosterone carbon into ditestosterone by adding a Carbon ring. Causes male baldness
19
Q
Steroids and Gender
A
Men and women both have testosterone and estrogen (among others), just in different levels. Steroid responsiveness is determine by presence and concentration of receptor, not hormone.
20
Q
Primary Sexual Characteristics
A
Determined by genotype in the developmental state of the primordial gonad. Y chromosome: gene for the testosterone-sensitive Testes Determination Factor, which signals formation of testes instead of ovaries. If no testosterone, no testes.
21
Q
Secondary Sexual Characteristics
A
More visible expressions of gender. Determined by the presence or absence of estrogen/testosterone activity.
22
Q
Castration
A
Produces a feminizing effect before puberty.
23
Q
Testicular Feminization Syndrome
A
XY genotype but unresponsive to androgen, thus develops as the default female phenotype.
24
Q
Homosexuality
A
No natural equivalent for exclusive homosexuality in animal kingdom, and no evolutionary pressures for non-reproductive behaviors. Early theory by LeVay: smaller hypothalamus. Debunked b/c subjects were HIV+.
25
Testosterone Levels
Rises rapidly after puberty, peaks around mid-20s, and slowly declines thereafter, dropping after 60. Link between blood testosterone, aging, and sex activity
26
Female Receptivity
Passive females accepts male sexual activity. Early theory of all sexuality.
27
Female Selectivity
Females are discriminate, only accepting advances from dominant males.
28
Female Proceptivity
Females are aggressive and actively seek sexual contact. Driven behavior: Alpha has sex -> overthrown by others -> new alpha having sex = Genetic Variability.
29
Female Menstrual Cycle
CONSULT DIAGRAMS
30
Estrus Sex Behavior
Sex only at certain times, usually peri-ovulatory. Males very interested at only this time, otherwise are hunting/foraging/etc. Largely in animals
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Menstrual Sex Behavior
Sexual behavior throughout cycle with increased frequency and constant male attendance necessary. Leads to tribal groups as females cannot be left alone. Human behavior
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Lutenizing-hormone Releasing Hormone
Produces sexual behavior in female mammals.
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Fixed Action Patterns
Discrete stages of mating.
Ultimate Fixed Action Patterns: responsible for initiating causal event (attraction, arousal) [Lordosis: female arching of spine].
Proximate Fixed Action Patterns: direct cause and effect (copulation) [erection, intromission, ejaculation in males]
34
SEXY BRAIN STUFF
CONSULT OTHERS' NOTES
35
Pharmacology
Study of the action of drugs on living organisms.
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Neuropharmacology
Drug-induced changes in functioning of nerve cells.
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Psychopharmacology
Drug-induced changes in behavior
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Neuropsychopharmacology
Drug-induced changes in the function of select neurons that influence specific behaviors
39
Drug Action
Molecular changes produced by drug binding to target site or receptor
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Drug Effects
Molecular changes that alter physiological/psychological function
41
Therapeutic Drug Effects
Drug/receptor interactions that produce the desired effect
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Drug Side Effects
All non-desired drug effects varying from annoying to dangerous
43
Depressants
Produce general decrease in cognitive and behavior processes. Ex: marijuana, barbituates, benzos
44
Stimulants
Produce general increase in behavior and thought. Ex: nicotine, caffeine, amphetamines, cocaine
45
Hallucinogens/Opiates
Alter perception of reality. Ex: LSD, opium
46
Pharmacokinetic Factors Determining Drug Action
Discrete Factors: 1) route of administration 2) absorption/distribution 3) Binding characteristics 4) Inactivation 5) Elimination. Influenced by chemical structure of the drug (how it interacts w/ body), dosage, and bioavailability (amount of drug in blood available to bind to target)
47
Drug Administration
Determines how quickly and how much is liberated and absorbed into the blood and how quickly it reaches its target and induces drug effect.
48
Liberation
Release of a drug into a biological system from an administered form. Drugs are mixed with excipients that allow drug to exist in different forms. Also different formulations: time or sustained release.
49
Time vs. Sustained Release
Time release: drug released slowly -> longer active time, more need to be taken to keep peak.
Sustained release: drug released in layers -> more peaks in less time.
50
Oral Administration (PO)
Most common and convenient. Is difficult route as the drug must survive the harsh stomach environment and reach blood capillaries which makes it an inefficient method. Also, majority of PO drugs not fully absorbed until they reach small intestine. Absorption influenced by: food in stomach (large amounts/fatty foods slow drug movement, absorption), and First Pass Effect (absorbed PO drugs go straight to liver which lowers bioavailability of drug -> slow, unpredictable levels)
51
Intravenous Administration (IV)
Directly into blood stream. Most common in medicine as it is an effective, easy, and rapid route as it circumvents stomach and first pass effect. Complication with high doses. Quick onset = immediate brain effect = little room for correction. Requires sterile environment. Dissolving of drugs in fillers may pose hazard.
52
Subcutaneous Administration (SC)
Beneath the skin. Easy route w/ slow and prolonged absorption, though is subject to variable absorption depending on blood flow
53
Intramuscular Administration (IM)
Into muscle tissue. Easy route w/ slow and even absorption. Often localized irritation at site of injection, needs sterile equipment.
54
Rectal Administration
Via rectum. Easy route and has the advantage of circumventing the intestinal tract.
55
Intraperitoneal Administration (IP)
In gut. Most commonly used in animal experimentation (larger area).
56
Gaseous/Inhalation Administration
Inhaled. Easy and speedy route with large absorption surface and no necessary injection equipment, though can be difficult to measure dosage and drug may irritate or damage nasal passages/lungs
57
Distribution
Movement of drug from site of administration to the blood circulation to the body. Influenced by route of administration and liberation factors.
58
Topical Administration
On skin. Localized action of effects and ease of self-administration. However, may be absorbed into general circulation.
59
Transdermal Administration
Through skin. Produces controlled and prolonged absorption, but is useful only for lipid soluble drugs and may cause local irritation.
60
Epidural Administration
Around epidural area at base of spinal cord. Very effective as it bypasses the blood-brain barrier with a rapid effect on the CNS, but is irreversible and requires a trained anesthesiologist to avoid possible nerve damage.
61
Elimination
Duration of effectiveness before a drug is broken down and inactivated, measured by half-life and drug metabolism (biotransformation) in liver. Most drugs only meant to have a temporary action.
62
Biotransformation
Drug metabolism wherein drug broken down in liver into metabolite. Two phases/types that inactive drugs and make them water soluble so they are easier to excrete.
63
Phase 1 of Biotransformation
Phase 1: modification of parent structure by oxydiation or hydrolysis, producing a polar metabolite that can be excrete through urine.
64
Phase 2 of Biotransformation
Phase 2: Conjugation with a salt/amino acid, producing an ionized, biologically inactive molecule.
65
Tolerance
More drug is required to produce a desired effect. Due to DA receptor downregulation.
66
Withdrawal
Physical and psychological symptoms opposite from those the drug induces. Upon removal of A-Process, body is left with a strengthened but unopposed B-Process -> strong opposite effects.
67
Opponent-Process Theory of Addiction
The body strives to maintain homeostasis, thus when drug produces change from homeostasis (A-Process), body tries to reduce changes by producing opposite effects (B-Process).
68
Addiction
Physiological and psychological need for drug. Increases the strength of a body's B-Processes, requiring stronger or more frequent A-processes.
69
Alcohol
Naturally occurring byproduct of distilling and fermenting sugar.
Administration: beverage.
Distribution: small intestine (rapid).
Elimination: liver metabolization.
Long-term effects: Korsakoff's disease (memory loss due to thiamine deficiency), Liver Cirrhosis, Fetal Alcohol Syndrome in children of drinking mothers (low birth weight, IQ)
70
Marijuana
Active ingredient: THC. Low doses: sedative/hypnotic. High doses: euphoria, hallucination.
Administration: Inhalation, ingestion
Distribution: Through lungs. Peak concentration in 30 mins, behavioral peak 2-3 hours.
Elimination: 30 hours half-life to leave bodyfat.
CNS effects: short term: mood alterations, increased appetite (disinhibition of hunger control), distortion of time. Long term: lung pathologies, immunosuppression.
Used for reduction of pain for glaucoma, nausea relief for chemotherapy/AIDs patients
71
Membrane Theories of CNS Depressants
Alcohol: causes neuronal membrane to become more flexible, reduces efficiency of neuronal transmission, disrupts activity of membrane receptors.
Marijuana: THC affects membrane surrounding certain receptor site.
72
Receptor Theories of CNS Depressants
Alcohol: Binds to and influences the activity of GABA receptor (results in inhibition by increasing Cl- influx), Glutamate receptor (inhibition by decreasing Ca++ influx). [Increase inhibition, decrease excitation]
Marijuana: Specific cannabinoid receptor concentrated in BG and CB (motor effects), and front cortex (euphoria, relaxation, temporal distortion). Also endogenous ligand for cannabinoid receptors (anandamide).
73
Sedatives and Tranquilizers
Decrease anxiety by producing global depression of CNS. Super-addictive effects: combination of different types can lead to potentially lethal combinations.
74
Barbituates
Class of synthetic compounds, usually taken orally, though differ in length of action. Currently used as sleep aids and anticonvulsants.
Low dose effects: euphoria, loss of behavioral inhibition by acting as a GABA allosteric agonist.
Risks: addiction, tolerance, insomnia on withdrawal
75
Benzodiazapines
Synthetic compounds used as one of the most widely prescribed (anti-anxiety) drugs. Taken orally. GABA allosteric agonist. Used to treat anxiety disorders. Side effects: lethargy, drowsiness. Great hazard of overdose if combined with alcohol. Ex: Valium, Xanax, Librium. High addictive potential.
76
GABA Channels and Sedatives
Benzos/Barbs are allosteric GABA agonists, thus activate Cl- influx (inhibition). Mixing with alcohol (also Cl- increasing and Ca++ reducing) leads to supra inhibition which may inhibit neural centers involved in respiration, heart rate, blood pressure, etc -> DEATH
77
Nicotine
Stimulant (alertness, irritability, hunger suppression, increased blood pressure/heart rate). Primary active ingredient in tobacco products.
Administration: inhalation, chewing
Distribution: absorption through lungs
Elimination: metabolized into inactive compounds within 2 hours.
Risks: long-term toxicities due to tar/chemicals from burning -> cancers/heart disease.
78
Caffeine
Most widely used drug in the world (stimulant).
Effects: adenosine (sedation, bronchospasm) receptor antagonist, increase in alertness, decrease in fatigue, ease in breathing
Administration: 80% of adults drink 3 cups of coffee (200-300 mg) a day.
Distribution: Rapid stomach/small intestine absorption. Significant blood levels within 30 minutes, peak after 2 hours.
Elimination: half-life of 3-5 hours
Risk: Nervousness, hyperventilation, possibility of panic attacks, insomnia, irritability
79
Amphetamines
Synthetic compound with a chemical structure similar to catecholamines.
Administration: oral, nasal, IV
Distribution: blood stream
Elimination: half-life of 18-24 hours (liver metabolization)
Effects: increase in blood pressure, motor activity, libido, pain threshold, decrease in bronchial muscle tone, fatigue, appetite, euphoria. High doses lead to paranoia
Risks: fatal overdose due to cerebral hemorrhage.
Related to Ritalin
80
Cocaine
Derived from coca plant.
Administration: nasal, smoked (crack)
Distribution: nasal (mucosal membrane). inhaled (absorbed directly into blood)
Elimination: half life of 15-30 minutes. Metabolized by specific esterase enzyme in brain.
Effects: increased heart rate, blood pressure, body temp, euphoria.
Risks: cardiovascular, cerebrovascular problems
Genetic variant of esterase can predispose users to death.
81
Dopamine Re-Uptake Mechanism of Action
Catecholamines usually inactivated by reuptake at synapse. Cocaine/amphetamines block reuptake process amplifying DA effects. Amphs also increase DA release extending activity time.
82
Peyote
Active ingredient: mescaline.
Taken orally in the form of dried cactus tops (buttons). Absorbed rapidly by gut, producing significant levels in the brain at 30-60 minutes, physiological effects can last for 10 hours.
Effects: small doses: increase blood pressure, heart rate, and pupil dilation. Larger doses: hallucinations.
Risks: Neuronal cell death as it is a potent neuronal excitotoxin.
83
Ecstasy
Synthetic of mescaline (MDMA). Dangerous and potent toxin of serotonin cells.
84
LSD
Best known hallucinogenic. Acts by inhibiting inhibitory (serotonin) neurons to produce excitation. Taken orally as blots/sugar cubes. onset 30-60 minutes, halflife of 3 hours, can last 10-12 hours.
Effects: increased heart rate, pupil dilation, perceptual alterations, occasional psychotic episodes and synesthesia. Not addictive, though tolerance may form.
Risk: psychotic break leading to suicide.
85
Psilocybin
"Magic Mushrooms". Oral ingestion, body converts mushroom to psilocin (200x less powerful than LSD). Produces distortions of thought, perception.
86
Morphine
Opiate. Typically taking IV or orally. Eliminated by liver. CNS effects include analgesia, euphoria, sedation.
Risk: respiratory depression (stop breathing as respiratory systems are inhibited)
87
Heroin
Synthetic derivative of morphine (10x more powerful. Very dangerous)
88
Heterogeneity of Opiate Receptors
```
4 different receptors for endogenous opiates
Mu opiate receptor: pain analgesia
kappa: pain analgesia
delta: altering affect and euphoria
sigma: dysphoria, feelings of discomfort
```
89
Natural Agonists and Synthetic Opiate Antagonists
Endogenous Opiates: enkephalins, beta-endorphins, dynorphins.
Pharmaceutical Antagonists: naloxene, naltrexone: bind receptors more tightly = emergency treatment as competitors for drug overdose victims
90
Diagnostic and Statistical Manual
Attempts to draw contrast between disorders that are biological in nature and those that are psychological in nature.
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Senility
Previously thought to be single disease. Now known to be collection of specific disease states including Alzheimer's and Multi-Infarct Dementia.
92
Alzheimer's Disease
Progressive mental deterioration with memory loss, confusion, and disorientation in mid- to late-life.
93
Multi-Infarct Dementia
Step-like deterioration in intellectual function resulting from decreased blood flow to the hemispheres due to strokes.
94
Division of Psychiatric Problems
Psychological complaints (treated by therapy) and brain disorders (treated by drugs)
95
Schizophrenia
Group of disorders comprising 6-month period of disturbances in communication, perception, and thought. Not a mood disorder, but disorder of perception and comprehension of reality with sensory abnormality (false realities [hallucinations, synesthesia] that conflict with cognition)
96
Symptoms of Schizophrenia
Florid Symptoms: disorganized thinking, paranoia, delusions of grandeur, bizarre ideation.
Negative Symptoms: neglect of personal hygiene, odd behavior and ideas, social isolation, withdrawal, catatonia. (Negative often precede Florid symptoms)
97
Rule of Thirds of Schizophrenia
1/3 recover, 1/3 remiss and relapse, 1/3 chronically ill.
98
Treatment of Schizophrenia
Neuroleptics (Atypical Antipsychotics like Thorazine) reduce florid symptoms, do not affect negative symptoms and leave sedative effect.
Hospitalization climbed through the 1900's before dropping off with new drug therapies.
99
Neuroleptic Drugs
Dopamine receptor antagonists, blocking D2. Suggests that underlying problem in schizophrenia is excess DA transmission in certain areas of the brain, notably the thalamus (DA Hypothesis)
100
Genetic Factors and Schizophrenia
Twin studies show a correlation between shared genes and development of schizophrenia
101
Brain Differences in Schizophrenia
PET scans show that schizophrenics have larger cerebral ventricles than normal
102
Viral Causes and Schizophrenia
Dramatic increase in the birthrate of schizophrenics among women who developed flu in the 2nd trimester
103
Affective Disorders
Person perceives reality normally, but feelings and affect about that reality are distorted. Include Mania, unipolar/bipolar illness
104
Mania
Symptoms include accelerated thought process, euphoria, exaggerated sexual or physical appetite, illusions of invincibility, and grandiose ambitions. Treated by Lithium (Li+Cl-)
105
Unipolar and Bipolar Illness
Mania often relapses, resulting in periods of depression. Symptoms of depression: Expressions of Helplessness, Hopelessness, and Worthelessness. Also, suicidal thoughts, anhedonia, psychomotor retardation, sleep disturbances resulting in lost REM sleep. Unipolar illness: depression w/o mania. Bipolar illness: brief periods of depression/mania interspersed with normalcy.
106
Depression on a Diagnostic Continuum
Most experience transcient depression. Traumatic events lead to short-term depression (Reactive Depression). Drug therapy helps all along the continuum.
107
Monoamine Hypothesis and Depression
Monoamine Hypothesis: abnormality in monaminergic transmission underlies almost all mental illnesses. Depression hypothesis: too little catecholamines (DA/NE). Thus, 1st drugs designed to increase extracellular catecholamines.
108
MAO Inibitors
Block the breakdown of catecholamines, increasing their levels. Alleviates depression. Similar effect as amphetamines. Side effects: accelerated heart rate, hypertension
109
Tricyclics
Block monoamine reuptake by binding to the pump, elevating extracellular monoamine levels. Structure resembles neuroleptics. Developed as a drug affecting only depression-related sites of the brain. Less cardiovascular effects than MAOIs.
110
Atypical Antidepressants
Selective Serotonin Reuptake Inhibitors: selectively block serotonin reuptake thus raising extracellular levels of serotonin. Therapeutic effects take weeks, though biochemical effects are immediate. Increase 5HT in all parts of brain, leading to loss of some pleasure drives
111
Anxiety Disorders
Symptoms include intense dread and generalized avoidance.
| Treated by anxiolytics (benzo family) which act as tranquilizers
112
Hazards of Medication
Poor understanding of modes of action -> unknown side effects. Addictive prescription drugs with withdrawal effects. Meds may exacerbate pre-existing conditions. Drugs in combination may be lethal. Developmental use produces unknown brain changes. Long-term maintenance leads to poorly understood brain changes.
