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Behavioral Neuroendocrine > Midterm > Flashcards

Midterm Flashcards

1
Q

progesterone converts to

A

aldosterone

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2
Q

endocrine

A

cells secrete hormones that interact with hormone receptors

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3
Q

when in the menstrual cycle does progesterone drop? what happens then?

A

luteal phase–behavior PMS correlates with cyclee

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4
Q

endocrine glands

A

glands of endocrine system that secrete their products (hormones) into the blood

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5
Q

exocrine

A

cells secrete hormones via duct/tube into internal or external environment (ie outside of bloodstream) (eg into lumen in intestines)

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6
Q

ectocrine

A

substances released outside the individual that impact another animal

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7
Q

paracrine

A

cells secrete products that affect other cells

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8
Q

intracrine

A

chemical mediation of intracellular events

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9
Q

chemical messenger

A

substance produced by a cell that affects function of another cell (e.g. NT; homrone)

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10
Q

cytokine

A

chemical messenger that evokes proliferation of other cells (esp in immune system)

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11
Q

hormone

A

chemical messenger released into bloodstream or tissue fluid system that affects function of target cells distant from source

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12
Q

neurohormone

A

hormone produced by a neuron

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13
Q

neuromodulator

A

hormone that modulates response of a neuron to other factors

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14
Q

neuropeptide

A

peptide hormone produced by neuron

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15
Q

neurosteroid

A

steroid hormone produced by neuron

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16
Q

neurotransmitter

A

chemical messenger that acts across neural synapse

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17
Q

hormones produced by hypothalamus

A

thyrotropin releasing hormone
dopamine
growth hormone releasing hormone
somatostatin
gonadotropin releasing hormone
corticotropin releasing hormone
oxytocin
vasopressin

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18
Q

hormone produced by pineal gland

A

melatonin

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19
Q

hormones produced by thyroid

A

triiodothyronine
thyroxine

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20
Q

hormones produced by anterior pituitary

A

growth hormone
thyroid stimulating hormone
adrenocorticotropic hormone
follicle stimulating hormone
luteinizing hormone
prolactin

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21
Q

hormones produced by posterior pituitary

A

oxytocin, vasopressin, (stored oxytocin,) (stored anti diuretic hormone)

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22
Q

hormones produced by intermediate pituitary

A

melanocyte stimulating hormone

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23
Q

basic function: hypothalamus

A

control of hormone secretions–>basic drives; regulates pituitary

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24
Q

basic function: pineal

A

reproductive maturation; body rhythms

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25
Q

basic function: anterior pituitary

A

hormone secretion by thyroid + adrenal cortex + gonads; growth

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26
Q

basic function: posterior pituitary

A

water balance, salt balance

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27
Q

basic function: thyroid

A

growth, development, metabolic rate

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28
Q

basic function: adrenal cortex

A

salt/water and carbohydrate metabolism; inflammatory reactions

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29
Q

basic function: adrenal medulla

A

emotional arousal, stress response

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30
Q

basic function: pancreas

A

sugar metabolism

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31
Q

basic function: gut

A

digestion, appetite control

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32
Q

basic function: gonads

A

body development and maintenance of reproductive organs in adults

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33
Q

neural transmission (as opposed to hormonal)

A

chemical, rapid onset, synaptic cleft, more voluntary control, travels 20-30nm

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34
Q

hormonal transmission (as opposed to neural)

A

chemical, slower with longer term effects, blood stream/extracellular space, less voluntary control, 1mm-2m

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35
Q

pituitary gland hormones w/ tropic effects only

A

FSH
LH–luteinizing hormone (targets gonads)
TSH–thyroid stimulating hormone (targets thyroid)
ACTH–adrenocorticotropic hormone (targets adrenal cortex to produce cortisol, androgens)

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36
Q

pituitary gland hormones w/ nontropic effects only

A

prolactin (targets mammary glands)
MSH (targets melanocytes) (melanocyte stimulating hormone)

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37
Q

pituitary gland hormone with nontropic and tropic effects

A

Growth hormone (targets liver, bones, other tissues)

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38
Q

tropic

A

stimulates indirectly (ie triggers release of another hormone)

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39
Q

nontropic

A

direct stimulation

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40
Q

hypothalamic communication to anterior pituitary

A

hypothalamic cells synapse on primary plexus of portal system, secrete neurohormones near the capillaries that give rise to portal vessels. neurohormones from portal vessels stimulate or inhibit the release of hormones from anterior pituitary cells, which leave the gland via the blood.

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41
Q

portal system

A

special closed blood system that connects the hypothalamus to anterior pituitary

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42
Q

hypothalamic communication to posterior pituitary

A

axons from hypothalamic neurosecretory cells that produce vasopressin and oxytocin extend through the posterior pituitary and synapse on blood vessels there–those hormones go directly to bloodstream

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43
Q

follicule stimulating hormone

A

targets gonads. development of ovarian follicules, secretion of estrogen, stimulates testicular growth and helps produce a protein that aids in the creation of sperm cells and maintains them

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44
Q

corticotropin releasing hormone

A

stimulating adrenocorticotropin (which will trigger cortisol release) and beta endorphins from anterior pituitary

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45
Q

melanocyte stimulating hormone

A

memory and skin color

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46
Q

neuropeptide Y

A

regulation of energy balance and appetite

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47
Q

gonadotropin releasing hormone

A

stimulates FSH and LH from anterior pituitary

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48
Q

substance P

A

transmits pain, increases smooth muscle contractions of GI tract

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49
Q

luteinizing hormone

A

stimulates leydig cell development and testosterone production. stimulates corpora lutea development and production of progesterone

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50
Q

growth hormone

A

mediates somatic cell growth; produced by anterior pituitary; important for childhood/adolescent growth and metabolic rate throughout life

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51
Q

thyroid stimulating hormone

A

primary stimulus for thyroid hormone production by thyroid gland

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52
Q

anterior pituitary’s release of acth/lh/fsh targets what to produces what

A

steroidogenic factories (ie the adrenal cortex and gonads)
these produce

glucocorticoids, mineralocorticoids, androgens, estrogens, progesterone

which then target peripheral tissues, specifically steroid hormone nuclear receptor complexes–>transcriptional regulation

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53
Q

Mineralocorticoids

A

Mineralocorticoids are a class of steroid hormones that regulate salt and water balances. Aldosterone is the primary mineralocorticoid.

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54
Q

side effects of gonadotroph adenoma of pituitary gland

A

vision loss, hypopituitarism, high prolactin

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55
Q

hypopituitarism

A

deficiency in GH, TSH, or LH/FSH

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56
Q

GH deficiency

A

short stature, fatigue, weakness, lack of ambition

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57
Q

LH and FSH deficiency

A

decreases gametes and estrogen or testosterone production
lower sex drive, infertility, fatigue

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58
Q

TSH deficiency

A

fatigue, weight gain, dry skin, constipation, sensitivity to cold/difficulty staying warm

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59
Q

ACTH deficiency

A

severe fatigue, low blood pressure, nausea/vomiting/abdominal pain, confusion

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60
Q

ADH deficiency

A

excessive urination, thirst, and electrolyte imbalances

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61
Q

pineal gland tumor side effects

A

fucked up sleep cycle

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62
Q

thyroid and parathyroid glands release what

A

release calcitonin, parathyroid hormone, thyroxine, triiodothyronine, parathyroid related peptide

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63
Q

calcitonin

A

lowers serum calcium levels

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64
Q

parathyroid hormone

A

stimulates bone resorption, increases serum calcium levels

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65
Q

thyroxine

A

t4. increases oxidation rate in tissue

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66
Q

triiodothyronine

A

t3. increases oxidation rate in tissues

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67
Q

parathyroid related peptide

A

regulation of bone and skin development

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68
Q

pancreas hormones

A

glucagon, insulin, stomatostatin, pancreatic polypeptide

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69
Q

glucagon

A

fasting hormone, catabolic hormone, released by alpha cells of pancreas. triggers glycogenolysis and gluconeogenesis, promotes lipolysis, increases satiety

peptide hormone which spikes after not eating for 12-16hr
released in a metabotropic sort of way, rises in blood with hypoglycemia

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70
Q

insulin

A

fed hormone. facilitates glucose uptake from blood (into muscle mostly via GLUT4) and glycogen into liver. stimulates glycolysis, glycogenesis, lipogenesis. inhibits lipolysis and glycogenolysis metabotropic release.

failure of insulin or low insulin = high glucose in blood. produced by beta cells of pancreas

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71
Q

stomatostatin

A

inhibits insulin and glucagon secretion. product of pancreas

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72
Q

pancreatic polypeptide

A

feedback inhibitor of p;ancreatic secretion

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73
Q

glycogenolysis

A

breakdown of glycogen

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74
Q

gluconeogenesis

A

creation of glucose

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75
Q

glycogen

A

stored form of glucose in liver

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76
Q

pancreas location

A

under liver

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77
Q

thyroid location

A

surrounding trachea

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78
Q

adrenal glands

A

located on kidneys, made of outer cortex and inner medulla. releases aldosterone, 11-deoxycorticosterone, cortisol, corticosterone, DHEA, adrenaline, noradrenaline

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79
Q

steroid

A

product of cholesterol

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80
Q

aldosterone

A

sodium and water retention, product of progesterone, secreted by adrenal glands

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81
Q

11-deoxycorticosterone

A

sodium and water retention

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82
Q

cortisol

A

carb metabolism, stress modulation

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83
Q

corticosterone

A

carb metabolism, stress modulation

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84
Q

DHEA

A

dehydroepiandrosterone; weak sex hormone plays role in reproductive health

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85
Q

adrenaline

A

aka epinephrine. fight/flight response

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86
Q

noradrenaline

A

norepinephrine. responsible for tonic + reflexive changes in cardiovascular tone

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87
Q

addison’s disease

A

adrenal gland insufficiency. no stress response. low blood pressure, low blood sugar, weight loss

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88
Q

cushing syndrome

A

excessive cortisol–weight gain, diabetes, high blood pressure (adrenal gland condition)

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89
Q

hyperaldosteronism

A

high aldosterone, sodium retention, high blood pressure (adrenal gland condition)

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90
Q

pheochromocytoma

A

tumor–>excess adrenaline and noradrenaline. high blood pressure, anxiety, tremors, sweating. (adrenal gland condition)

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91
Q

adipose tissue

A

fat tissue. releases leptin, adiponectin, plasminogen activator inhibitor 1

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92
Q

leptin

A

regulates energy balance, reduces appetite

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93
Q

adiponectin

A

modulates endothelial adhesion molecules, protective

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94
Q

plasminogen activator inhibitor 1

A

regulation of vascular homeostatis

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95
Q

desensitized receptors for insulin and leptin

A

receptors for insulin and leptin in hypothalamus may become desensitized, leads to aberrant eating, inflammation, reduced synaptic plasticity, cognitive decline, depression

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96
Q

testes hormones

A

androstenedione, dihydrotestosterone, testosterone

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97
Q

androstenedione

A

male sex characteristics

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98
Q

dihydrotestosterone

A

male secondary sex characteristics

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99
Q

testosterone

A

spermatogenesis; male secondary sex characteristics

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100
Q

testicular cancer

A

interestingly does not influence testicular hormones, symptoms are more so physical: pain swelling lump

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101
Q

ovaries hormones

A

estradiol, estrone, estriol, estrogen, progesterone

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102
Q

chemosignal

A

a type of ectocrine signal

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103
Q

how does the pill work

A

suppress the production of endogenous (estrogen, estradiol, progesterone) hormones by producing synthetic, nonconvertable versions (of estrogen and progesterone)

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104
Q

what hormonally differs based on sex

A

levels, not receptors

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105
Q

monoamine hormones

A

produced from single amino acids like melatonin (product of serotonin, product of tryptophan)

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106
Q

hormones that guide eating behavior

A

insulin, glucagon, cortisol

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107
Q

which areas of the brain guide eating behavior

A

visual cortex, gustatory cortex, prefrontal cortex, striatum, amygdala, nucleus of tractus solitarius, gut vagus nerve connection

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108
Q

gustatory cortex

A

prompts taste and smell of food

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109
Q

striatum

A

reward/pleasure–dopamine circuits, reward, motivation, guided by repetitive movement

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110
Q

liking and wanting system

A

liking=taste receptors on tongue, instantaneous
wanting system is delayed, nutrient sensing, intestines say “where’s sugar, amino acids, etc”-gut brain axis

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111
Q

artificial sweeteners

A

dont act on walking system

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112
Q

amygdala’s relationship to eating behavior

A

emotions/stress

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113
Q

nucleus of tractus solitarius relationship to eating behavior

A

satiety/chewing

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114
Q

gut/vagus nerve relationship to eating behavior

A

sensing nutrients

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115
Q

catabolic

A

stimulates breakdown of fats/amino acids

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116
Q

gluconeogenesis

A

production of glucose from triglycerides, fats

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117
Q

which organs does glucagon target

A

brain, pancreas, liver, brown adipose tissue, heart

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118
Q

what does glucagon promote in brain

A

less food intake/appetite, more satiety

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119
Q

what does glucagon promote in pancreas

A

insulin secretion; (due to mobilization of lipids and amino acids)
inhibits secretion from exocrine cells

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120
Q

what does glucagon promote in liver

A

glucose production from amino acids and lipid breakdown; less glucose breakdown and creation of glycogen; uptake of amino acids, glycogenolysis

121
Q

what does glucagon promote in brown adipose tissue

A

prevents food from being too thermogenic bc adipose tissue is highly thermogenic. increases resting energy expenditure

122
Q

what does glucagon promote in heart

A

raised heart rate, contractility

123
Q

glycolysis

A

glucose breakdown

124
Q

glycogenolysis

A

breakdown of glycogen into glucose

125
Q

what does glucagon do in adipose tissue

A

adipose is site of lipolysis or lipogenesis. glucagon causes lipolysis there

126
Q

what does glucagon do in kidney

A

increases glomerular filtration rate/urin flow rate

127
Q

glomerular filtration rate

A

hang on maybe we need this we’re fasting

128
Q

what stimulates glucagon secretion

A

hypoglycemia, epinephrine, amino acids, ach, cAMP, GIP, Bombesin, gastrin, cholecystokinin, neurotensin

129
Q

what inhibits glucagon secretion

A

glucose, free fatty acids, ketone bodies, stomatostatin via SST2 receptor, insulin via gaba, stomatostatin, GLP-1!, secretin, PPAR/retinoid x receptor heterodimer, increased urea production

130
Q

effect of insulin on adipose

A

lipogenesis

131
Q

GLP-1

A

Glucagon like peptide 1, important messenger, incretin hormone broadly expressed which potentiates insulin release and suppresses glucagon secretion in response to ingestion of nutrients. also delays gastric emptying and increases satiety

132
Q

effect of proglucagon

A

glucagon, grpp, ip2 in pancreas
glp-1, glp-2, ip-2 in gut/brain

133
Q

key features of glp-1 in eating behavior

A

mainly released from enteroendocrine l cells of ileum and colon, release stimulated by all 3 macronutrient classes, potent regulatory effects on GI functions, induces satiation, activates hindbrain neurons/locally produced by them, potentiates nutrient induced insulin secretion

134
Q

how does glp 1 induce satiation

A

central and peripheral pathways which mediate diff GI stimuli

135
Q

how does glp1 activate hindbrain neurons

A

vagal afferent sensory nerve fibers

136
Q

glp1 classified as an incretin why

A

potentiates nutrient induced insulin secretion

137
Q

glp-1 analog effects

A

effective in normalizing blood glucose levels in diabetics/reducing body weight in obese individuals

138
Q

glp 1 impact in muscle

A

increases glycogen synthesis and glucose oxidation

139
Q

glp 1 impact in brain

A

decrease appetite, increase satiety

140
Q

glp 1 impact in heart

A

lower blood pressure, increased heart rate and myocardial contractility, diastolic function, cardiprotection, and endothelial function
* note that all of this but endothelial measured by GLPRAs

141
Q

glp 1 impact in GI tract

A

decreased gastric emptying and acid secretion

142
Q

glp 1 impact in kidney

A

increased natriuresis (execretion of sodium)

143
Q

glp 1 impact in adipose

A

INCREASED lipolysis and glucose uptake

144
Q

glp 1 impact on pancreas

A

increased insulin secretion, decreased glucagon secretion, increased beta cell proliferation

145
Q

GLP1 receptors expressed in which brain regions

A

paraventricular nucleus, dorsal medial nucleus of hypothalamus, arcuate nucleus, nucleus of tractus solitarius

146
Q

exendin-9

A

blocks glp-1 and increases food intake

147
Q

GLP1 signaling steps

A

binds to postsynaptic gLP-1R, depolarizes in most brain regions (may hyperpolarize elsewhere). also acts on presynaptic GLP1r to modulate both glutamatergic and GABAergic neurotransmission

148
Q

insulin release from beta cells

A

glucose transported into pancreatic ß cells by GLUT2, phosphorylated by glucokinase and metabolized to produce ATP. elevation of ATP:ADP ratio closes K+ ATP channel –>depolarization–>voltage gated Ca2 channel–>insulin secretion

149
Q

where are insulin receptors in the brain

A

concentrated in olfactory bulb, hypothalamus, retina, choroid plexus vessels, striatum, cerebral cortex

150
Q

how does glucose enter the brain

A

blood brain barrier and GLUT 1. might be locally synthesized or actively transported from bloodstream

151
Q

glycogenesis

A

formation of glycogen

152
Q

effect of insulin in brain

A

neuropeptide, involved in satiety, appetite regulation, olfaction, memory and cognition

153
Q

GLUT1

A

insulin independent glucose transporter most widely expressed. present in brain, (ubiquitous in glia, endothelial cells) microvessels, red blood cells, placenta, kidneys. controlled in brain by insulin and hypoglycemia

154
Q

GLUT2

A

both insulin dependent and independent glucose transporter expressed in brain (limited, hypothalamic neurons, glia, and tanycytes), liver, kidneys

155
Q

GLUT3

A

sodium dependent glucose transporter expressed in neurons, glia, and endothelial cells in the cerebellum, striatum, cortex, and hippocampus–also , placenta, fetus

156
Q

GLUT4

A

insulin dependent glucose transporter expressed in muscle, adipose, and heart; also neurons and glia in olfactory bulb, hippocampus, and hypothalamus cerebellum. neurons and glia, selective. controled by glucose, insulin, exercise training

157
Q

GLUT5

A

insulin dependent glucose transporter expressed in small intestines, testes

158
Q

GLUT8

A

located in neuron bodies and proximal apical dendrites (limited) of hypothalamus, cerebellum, brainstem, hippocampus, dentate gyrus, amygdala, and primary olfactory cortex. controlled by glucose

159
Q

what stimulates insulin release

A

carbs, proteins, and potentially addictive components like nicotine and alcohol. (this is why ketogenic diet works–doesnt stimulate insulin release or produce so much glucose, fats only)

160
Q

insulin impact on appetite

A

stimulates appetite, therefore used to treat anorexia (generalized appetite loss)

161
Q

blood sugar and insulin curves over time after administered

A

rises and then drops

162
Q

insulin release is higher in evening: one possible outcome

A

no breakfast=obesity

163
Q

why do people use food as coping mechanism

A

insulin acts on striatum

164
Q

people living with obesity brain differences

A

greater recruitment in insula, putamen, inferior frontal gyrus, middle temporal gyrus during food cues and stressful stimuli

165
Q

why might the fed hormone increase appetite but the fasting hormone decrease appetite

A

metabolism slows down to compensate for the nonavailability of food

166
Q

leptin

A

produced from adipose tissue to signal satiety and fullness. amount in blood directly proportional to amoujnt of adipose tissue

167
Q

where is leptin active

A

receptors in ventral tegmental area and nucleus of tractus solitarius to modulate eating behavior/acts on receptors in hypothalamus to regulate release of tropic hormones

168
Q

without a functional ob gene….

A

ob gene=leptin gene. eating abnormalities=never satiated.

169
Q

what hormone release does leptin influence

A

thytropin releasing hormone, growth hormone releasing hormone, adrenocorticotropic releasing hormone

170
Q

insulin impact on ventral tegmental area

A

increases reward threshold=more needed to elicit same reward response

171
Q

leptin impact on ventral tegmental area

A

reduced food intake

172
Q

history of nicotine exposure

A

–>elevated blood glucose, glucagon, and insulin because stress signal is sent from medial habenula to pancreas, triggers release of more blood glucose for fight/flight respons

173
Q

endocannabinoids

A

2-arachidonoyl glycerol and arachidonoyl ethaloamide are best studied. THC is exogeneous cannabinoid, found in cannabis sativa, and produce bioeffect. most abundant receptor is cb1. stimulate appetite and levels correlate with body composition, leptin, insulin

174
Q

cb1 receptor

A

cannabinoid receptor found in cns–cortex, basal ganglia, hippocampus, cerebellum

175
Q

Bardet Biedl syndrome

A

rare autosomal recessive ciliopathy. associated with 16 genes; immotile cilia function mainly as sensory organelles regulating signal transduction pathways. retinal dystrophy, renal dysfunction, obesity, cognitive deficit, post axial polydactyly and hypogenitalism. bbs mice have increased leptin/leptin resistance

176
Q

cilia in brain

A

primary cilia are tiny microtuble based signaling devices that regulate different physiological functions (metabolism, cell division). defects lead to obesity, cancer. in mature brain neurons and astrocytes contain single primary cilium. not understood how it regulates energy balance but postulated that ac3 functionally couples to melanocortin receptor in hypothalamus

177
Q

prader willi syndrome

A

dysfunction of hypothalamus leading to widespread issues

178
Q

prader willi syndrome brain symptoms

A

intellectual + learning disability, mood lability/anxiety, deficit in theory of mind and empathy, poor social skills, sleep diksorder

179
Q

nuclei of the hypothalamus

A

dorsomedial nucleus, ventromedial nucleus, arcuate nucleus, tuber cinereum, mammilariy bodies, paraventricular nucleus, lateral and medial preoptic nuclei, anterior nucleus, suprachiasmatic nucleus, supraoptic nucleus,

180
Q

primary hormone deficiency in prader willi (other than ghrelin)

A

decreased spontaneous growth hormone secretion after growth

181
Q

how does growth hormone impact metabolism

A

primarily by upregulating production of insulin like growth factor 1.

182
Q

possible reason for GH deficiencyh in obesity

A

damage to anterior pituitary

183
Q

lifestyle choices that stimulate GH secretion

A

fasting, exercise

184
Q

how menstruation affects GH stimulation

A

increase from exercise higher during ovulation unless on oral birth control. fasting not impacted by cycle

185
Q

ketogenic diet is popular bc

A

Ketogenic popular bc fat doesn’t stimulate insulin release

186
Q

anorexia nervosa

A

psychiatric illn ess w/ highest mortality rate in women (10%)
low intake of food–>hormonal imbalance
distinct from anorexia

187
Q

anorexia

A

general loss of appetite

188
Q

treatment for anorexia nervosa

A

insulin will stimulate appetite but worsen psychiatric symptoms. family based treatment best, cbt. antidepressants/antipsychotics not effective

189
Q

ghrelin

A

gut–hunger hormone. inhibits insulin release and stimulates hunger.

190
Q

bulimia nervosa hormonal imbalance

A

higher ghrelin, higher insulin post binge, lower leptin post binge–>less satiety, more craving

191
Q

how to rebalance hormones, reduce cravings–>lower insulin

A

eat early in day, exercise, lower carb intake, avoid binging,

192
Q

effect of exercise on eating hormones

A

reduced insulin and increased glucagon

193
Q

mood disorder

A

chronic condition with marked disruptions in emotions, including depression, pmdd, bipolar disorder

194
Q

BPI

A

A syndrome in which a complete set of mania
symptoms has occurred lasting for at least one week
or required hospitalization.

195
Q

mania

A

Mania symptoms: elevated mood with three or
more of the following symptoms - increased goal-
directed activity, grandiosity, a diminished need for
sleep, distractibility, racing thoughts,
increased/pressured speech, and reckless behaviors

196
Q

diagnostic criteria bulimia

A

Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the following:
Eating, in a discrete period of time (e.g., within a two hour period), an amount of food that is definitely larger than what most people would eat during a similar period of time and under similar circumstances.
Lack of control over eating during the episode (e.g., a feeling that you cannot stop eating, or control what or how much you are eating).
Recurrent inappropriate compensatory behavior to prevent weight gain, such as self-induced vomiting, misuse of laxatives, diuretics, or other medications, fasting, or excessive exercise.
The binge eating and inappropriate compensatory behaviors both occur, on average, at least once a week for three months.
Self-evaluation is unduly influenced by body shape and weight.
Binging or purging does not occur exclusively during episodes of behavior that would be common in those with anorexia nervosa.

197
Q

diagnostic criteria anorexia nervosa

A

Restriction of energy intake relative to requirements leading to a significantly low body weight in the context of age, sex, developmental trajectory, and physical health.

198
Q

bipolar ii

A

Bipolar II disorder consists of
current or past major
depressive episodes
interspersed with current or
past hypomanic periods of at
least four days in duration.

199
Q

hypomania

A

Hypomania is a more mild form of
mania
* Mania may require hospitalization and
the duration is to be at least one week
* Mania can cause significant impact on
work, school, and relationships
* Hypomania does not require
hospitalization and does not influence
work, school, relationships as
significantly as mania

200
Q

genetics of bipolar disorder

A

fill in

201
Q

neurobio of bipolar disorder

A

Astrocytes and microglia seem to be important in onset and progression in mood disorder. They regulate immune response and inflammation, so they are important in studying mood disorder
Left: homeostasis
Right: mood disorder
Microglia send more signals to astrocytes, microglia expand and become inflated, and neurotransmitters are more present
Shows that it’s not just neurons involved

202
Q

endocrinology of anorexia nervosa

A

fill in

203
Q

symptoms anorexia nervosa

A

restricted eating, low body weight/fear of gaining, osteoporosis, anemia, muscle weakness, brittle hair/nails, growth of fine hair over body, constipation, low blood pressure, slow breathing/pulse, heart damage, drop in body temp, lethargy, infertility, organ failure

204
Q

main difference betwn anorexia nervosa and bulimia nervosa

A

body weight–anorexia low, bulimia normal or high

205
Q

major depressive disorder prevalence

A

Major depressive disorder has a lifetime prevalence of about
5% to 17%.
Women have almost twice the prevalence rate vs. Men.
The annual prevalence rate of depression is 7.1% in U.S.
adults, while the annual prevalence rate for bipolar disorder
is 2.8%.
The median age of onset of major depressive disorder is 32
years.

206
Q

Hamilton Depression rating scale

A

common depression scale

207
Q

DMDD

A

disruptive mood dysregulation disorder–frequent outbursts, out of proportion, irritability

208
Q

PDD

A

A mild but long-term form of depression.
Dysthymia is defined as a low mood occurring for at least two years, along with at least two other symptoms of depression.
Examples of symptoms include lost interest in normal activities, hopelessness, low self-esteem, low appetite, low energy, sleep changes, and poor concentration.

209
Q

PMDD

A

severe PMS with psychological and physiological symptoms.

210
Q

PMDD symptoms

A

A) In the majority of menstrual cycles, at least 5 symptoms must be present in the final week before the onset of menses,
start to improve within a few days after the onset of menses, and become minimal or absent in the week post-menses
Symptoms
B) One or more of the following symptoms must be present:
1) Marked affective lability (e.g., mood swings, feeling suddenly sad or tearful, or increased sensitivity to rejection)
2) Marked irritability or anger or increased interpersonal conflicts
3) Markedly depressed mood, feelings of hopelessness, or self-deprecating thoughts
4) Marked anxiety, tension, and/or feelings of being keyed up or on edge
C) One (or more) of the following symptoms must additionally be present to reach a total of 5 symptoms when combined
with symptoms from criterion B above
1) Decreased interest in usual activities
2) Subjective difficulty in concentration
3) Lethargy, easy fatigability, or marked lack of energy
4) Marked change in appetite; overeating or specific food cravings
5) Hypersomnia or insomnia
6) A sense of being overwhelmed or out of control
7) Physical symptoms such as breast tenderness or swelling; joint or muscle pain, a sensation of “bloating” or weight gain

211
Q

etiology of PMDD

A

drop in progesterone/converted to aldosterone and corticosterone. corticosterone–>psych symptoms, aldosterone–>physical symptoms. tends to have some past life trauma.

The luteal phase is associated with increased
production of proinflammatory molecules such as:
soluble interleukin 6R (sIL-6R), tumor necrosis factor
alpha (TNF-α), and C-reactive protein (CRP).

212
Q

neuroimaging findings PMDD

A

increased amygdala response during luteal phase, altered GABA levels in left basal ganglia, anterior cingulate cortex, medial prefrontal cortex, lower gaba:glutamate

213
Q

etiology of PMDD factors

A

genetics, progesterone and allo, estrogen/serotonin/bdnf, functional/structual differences, hpa axis

214
Q

primary risk factor for depression

A

Primary Risk Factor
Chronic stress.
The pathophysiology of constant stress results from overactivation and then reduced sensitivity of
the hypothalamic-pituitary-adrenal (HPA) axis, which results in
glucocorticoid cortisol level increase.

215
Q

treatment options pmdd

A

eating frequency–fasting can make it worse. exercise, cbt (helps, not by itself for past life trauma), ssris increase serotonin, exercise decreases cortisol, oral contraceptives contribute exogenous progesterone, which suppresses endogenous production and wont get converted to aldosterone but will act on progesterone receptors and allow uterine lining to mature,

216
Q

ovulation behaviors

A

high estrogen/risk taking. after ovulation high progesterone/safe behavior regardless of whether or not pregnancy

217
Q

ptsd

A

psychiatric condition w depression as primary symptom. Symptoms include episodes of
reexperiencing the traumatic event or
reexperiencing the emotions attached to the
event; nightmares, exaggerated startle
responses; and social, interpersonal, and
psychological withdrawal. Chronic symptoms
may include anxiety and depression. PTSD is
categorized as an anxiety disorder.

218
Q

GAD

A

Generalized Anxiety Disorder psychiatric condition w depression as primary symptom.
* Symptoms of anxiety disorders are most often
on the anxiety spectrum, but the chronic stress
faced by individuals with anxiety disorders can
produce depressive symptoms including
irritability, hopelessness, despair, emptiness,
and chronic fatigue.

219
Q

diagnostic criteria GAD

A

fill in

220
Q

other psychiatric criteria w depression as primary symptom

A

schizophrenia, GAD, PTSD, personality disorder

221
Q

Neurobiology of Major
Depressive Disorder

A

stress response/overactive HPA axis –> increased circulating glucocorticols/anti inflammatory, reduced sensitivity to cortisol–>low grade inflammatories, and modifications to indoleamine–>causes tryptophan to become kyn instead of 5HT, and causes KYN to become 3HK and QA instead of KYN acid–>oxidative damage and glutamate excitotoxicity

222
Q

tbi cytokine response

A

new, higher baseline–>reduced sensitivity to anti inflammatorys

223
Q

inflammation impact on neuronal function

A

fill in

224
Q

chronic stress

A

reduced sensitivity of negative feedback hpa system due to increased circulating glucocorticoids.

225
Q

brain risks chronic stress

A

increased risk for cognitive, behavioral, emotional dysfunction; mdd, anxiety disorders, memory problems.

226
Q

immune risks chronic stress

A

increased risk for autoimmune syndromes, levels of cytokines, and chronic/low grade inflammation throughout the body

227
Q

cardiovascular risks chronic stress

A

hypertension, vascular damage

228
Q

disease risks chronic stress

A

cancer, diabetes, cushing’s, obesity

229
Q

cushing’s

A

high cortisol levels

230
Q

relationships of inputs of adrenal and gonadal steroid hormone receptors to HPA circuitry

A

all these nuclei acting on each other, androgen receptors, estrogen alpha and betas, glucocorticoid receptor, mineralcorticoid, PVN and nts at center

231
Q

sleep deprivation effects

A

transient help with depressive symptoms short term, long term chronic sleep deprivation negative effect

232
Q

glutamate signaling, ketamine depression

A

fill in

233
Q

The hypothalamus-pituitary-thyroid (HPT) axis

A

hypothalamus releases TRH @ pituitary gland, which releases TSH @ thyroid, which releases T4 and some T3. T4/T3 creates negative feedback loop with hypothalamus and pituitary gland to maintain homeostasis. T4 deiodinases to T3

234
Q

Tyrosine products

A

T4 (–>T3) and norepinephrine (–>epinephrine)

235
Q

effects of thyroid hormone signaling on liver

A

increases metabolic rate

236
Q

effects of thyroid hormone signaling on muscle and bone

A

promotes growth

237
Q

effects of thyroid hormone signaling on brain

A

increases neuron growth, neurotransmitters, development

238
Q

effects of thyroid hormone signaling on heart

A

increases cardiac output

239
Q

effects of thyroid hormone signaling on adipose tissue

A

lipolysis

240
Q

effects of thyroid hormone signaling on proteins

A

promotes production, turnover

241
Q

T3 function/thyroid hormone signaling

A

D1/2/3 deiodinases T4 to produce T3, which attaches to TR (attached to RXR and coactivator) -> triggers TRE to produce mRNA -> proteins

242
Q

RXR

A

retinoic acid receptor

243
Q

TR

A

thyroid hormone receptor

244
Q

TRE

A

thyroid hormon e response eliment

245
Q

TRa1 expression

A

widespread, cardiac and skeletal muscles, brown fat, bone

246
Q

TRa2 + TRa3 expression

A

widespread, skeletal muscle, brain, kidney

247
Q

TRß1 expression

A

widespread, brain liver kidney

248
Q

TRß2 expression

A

retina hypothalamus anterior pituitary cochlea

249
Q

HPT conserved in whom

A

vertebrates

250
Q

thyroid critical for developmental transitions

A
251
Q

goiter

A

enlargement of thyroid generally due to iodine deficiency, now treated thru iodine supplements

252
Q

other causes of goiter

A

hashimoto’s, grave’s, cancer

253
Q

hashimoto’s

A

hypothyroidism, autoimmune destruction of thyroid gland

254
Q

grave’s disease

A

autoantibody activation of TSH receptor –>hyperthyroidism

255
Q

congenital hypothyroidism

A

caused by prenatal insufficient thyroid hormone signaling, prob iodine deficiency, goiter, intellectual disability etc, rare today

256
Q

hypothyroidism symptoms

A

fatigue, memory impairment, shaggy hair/hair loss, depression, enlarged thyroid, swelling face, eyes, rough voice, weight gain, constipation, slowed heart rate, weakness, dry/rough skin, paresthesia muscle cramps, cycle disorders, sexual desire/potency/fertility problems, cognitive decline, memory loss, demen tia, dysphoria, depression, coma

257
Q

hyperthyroidism

A

nervousness, irritability, insomnia, depression, broken hair, hair loss, weight loss, hunger, diarrhea, enlarged thyroid, increased heart rate/blood pressure/arrhhythmia, muscle cramps/weakness, fragile fingernails, shaking hands, increased body temp, warm /moist skin, cycle disorders, agitation, apathy, mania, delusional behavior, hallucinations, psychosis, dementia

258
Q

autoimmune hashimoto encephalopathy

A

personality changes, memory loss, delusions, dementia, seizures, ataxia, hallucinations, coma

259
Q

tbi

A

new baseline of inflammation/cytokines, depression, dementia
decreased cortisol–>increased inflammation

260
Q

thyroid hormone role in cerebral cortex development

A

cortical progenitor proliferation, excitatory neuronal migration, layer specification, synaptogenesis

261
Q

thyroid hormone role in general brain development

A

establishment of connectivity, oligodendrocyte differentiation, myelination; inhibitory interneuron abundance in CC and hippocampus

262
Q

thyroid hormone role in retinal development

A

M cone differentiation, M opsin expression

263
Q

thyroid hormone role in hippocampal development

A

neuronal migration, neuron and glia maturation, synaptogenesis

264
Q

thyroid hormone role in cerebellum development

A

precursor proliferation (nec compounds for growth(, granule cell migration, bergman glia and purkinje cell maturation and arborization, inhibitory interneuron generation, cell survival (expand!)

265
Q

thyroid hormone role in motor neuron development

A

production, establishment of corticospinal projections

266
Q

thyroid hormone role in cochlea development

A

inner hair cell maturation, vestibulocochlear nerve myelination

267
Q

thyroid hormone role in striatum development

A

rhes gene expression regulation, motor control, anxiety, gender specific behaviors

268
Q

thyroid hormone role in basal forebrain development

A

cholinergic neuron maturation and arborization, glia maturation

269
Q

thyroid hormone role in hypothalamus and pituitary development

A

establishment of the HPT axis

270
Q

function of cerebellum

A

highly conserved/neuron dense region which controls motor timing precision coordination learning and a bunch of higher up recently discovered–memory, reward/satiety, fear and anxiety, social interaction, repetitive behaviors, aggression, cerebellar ataxias, schizophrenia, autism, intellectual disability, epilepsy, huntington’s

271
Q

purkinje cells

A

principal neurons of cerebellar cortex, dendritic development of which induced by thyroid

272
Q

thyroid hormone regulates…

A

metabolism, growth of most tissues, and developmental transitions

273
Q

list of endo glands, hormones, main effect, added pathology

A

ok

274
Q

prader willi syndrome hypothalamic/pituitary symptoms

A

GH deficiency, hypogonadism, hypothyroidism, corticotropin deficiency, dysautonomia, abnorbal oxytocin neurons, hydroelectrolytic disorders

275
Q

prader willi syndrome respiratory/cardio symptoms

A

sleep related breathing disorders, impaired central chemoreceptors, cardiomyopathy, impaired sympathetic/parasympathetic control

276
Q

prader willi syndrome opthamological issues

A

strabismus, hypermetropia, myopia

277
Q

prader willi syndrome oral symptoms

A

thick saliva, dental, orthodontic issues

278
Q

prader willi syndrome metabolic symptoms

A

diabetes, dyslipidemia, increased fat mass/decreased lean mass, severe obesity, liver steatosis

279
Q

prader willi syndrome GI symptoms

A

dysphagia, gastric emptying deficit, constipation, bowel distention/risk of Gi rupture

280
Q

prader willi syndrome orthopedic symptoms

A

early scoliosis, kyphosis, hip dysplasia, joint hypermobility

281
Q

prader willi syndrome urogenital symptoms

A

enuresis, delayed sphincter control, cryptorchidism

282
Q

prader willi syndrome skin symptoms

A

skin picking, frequent lymphedema, risk of erysipelas, capillary fragility/increased hematomas

283
Q

prader willi syndrome hormonal symptoms

A

increased ghrelin

284
Q

name endocrine glands

A

Hypothalamus
* Pituitary Gland
* Pineal Gland
* Thyroid Gland
* Pancreas
* Ovaries
* Testes
* Adrenal glands
* Adipose tissue

285
Q

Hypothalamus related pathology

A

prader willi syndrome

286
Q
  • Pituitary Gland related pathology
    *
A

adenoma–>GH deficiency

287
Q

Pineal Gland related pathology

A

pineal tumor–fucked up sleep cycle

288
Q
  • Thyroid Gland related pathology
    *
A

hashimoto’s - hypopituitarism

289
Q

Pancreas related pathology

A

diabetes

290
Q
  • Ovaries related pathology
A

high androgens – PCOS

291
Q
  • Testes related pathology
A

testicular cancer–no hormonal signs

292
Q
  • Adrenal glands
    *related pathology
A

cushing’s

293
Q

Adipose tissue related

A

leptin desensitization–see above

294
Q

gonadotropin

A

FSH, LH

295
Q

glucocorticoid

A

any of a group of corticosteroids (e.g. hydrocortisone) which are involved in the metabolism of carbohydrates, proteins, and fats and have anti-inflammatory activity.

296
Q

impacted brain regions bipolar disorder

A

comprised cognitive control
Dorsal ACC
Dorsolateral prefrontal cortex
Dorsomedial prefrontal cortex
Increased activity in bipolar disorder
Amygdala, Ventrolateral prefrontal cortex,
Ventral ACC (anterior cingulate cortex)

297
Q

Using CBT for patients : bipolar disorder

A

Affect labeling: being able to label the feelings, target why you feel that way
Reduces the recruitment of amygdala, allows the prefrontal cortex to take over and help a patient think clearly and present good decision-making

298
Q

MDD diagnosis

A

It is diagnosed when an individual has a persistently low or depressed mood, anhedonia or decreased interest in pleasurable activities, feelings of guilt or worthlessness, lack of energy, poor concentration, appetite changes, psychomotor retardation or agitation, sleep disturbances, or suicidal thoughts.

Behavioral Neuroendocrine (1 decks)

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