Midterm Flashcards
1
Q
progesterone converts to
A
aldosterone
2
Q
endocrine
A
cells secrete hormones that interact with hormone receptors
3
Q
when in the menstrual cycle does progesterone drop? what happens then?
A
luteal phase–behavior PMS correlates with cyclee
4
Q
endocrine glands
A
glands of endocrine system that secrete their products (hormones) into the blood
5
Q
exocrine
A
cells secrete hormones via duct/tube into internal or external environment (ie outside of bloodstream) (eg into lumen in intestines)
6
Q
ectocrine
A
substances released outside the individual that impact another animal
7
Q
paracrine
A
cells secrete products that affect other cells
8
Q
intracrine
A
chemical mediation of intracellular events
9
Q
chemical messenger
A
substance produced by a cell that affects function of another cell (e.g. NT; homrone)
10
Q
cytokine
A
chemical messenger that evokes proliferation of other cells (esp in immune system)
11
Q
hormone
A
chemical messenger released into bloodstream or tissue fluid system that affects function of target cells distant from source
12
Q
neurohormone
A
hormone produced by a neuron
13
Q
neuromodulator
A
hormone that modulates response of a neuron to other factors
14
Q
neuropeptide
A
peptide hormone produced by neuron
15
Q
neurosteroid
A
steroid hormone produced by neuron
16
Q
neurotransmitter
A
chemical messenger that acts across neural synapse
17
Q
hormones produced by hypothalamus
A
thyrotropin releasing hormone
dopamine
growth hormone releasing hormone
somatostatin
gonadotropin releasing hormone
corticotropin releasing hormone
oxytocin
vasopressin
18
Q
hormone produced by pineal gland
A
melatonin
19
Q
hormones produced by thyroid
A
triiodothyronine
thyroxine
20
Q
hormones produced by anterior pituitary
A
growth hormone
thyroid stimulating hormone
adrenocorticotropic hormone
follicle stimulating hormone
luteinizing hormone
prolactin
21
Q
hormones produced by posterior pituitary
A
oxytocin, vasopressin, (stored oxytocin,) (stored anti diuretic hormone)
22
Q
hormones produced by intermediate pituitary
A
melanocyte stimulating hormone
23
Q
basic function: hypothalamus
A
control of hormone secretions–>basic drives; regulates pituitary
24
Q
basic function: pineal
A
reproductive maturation; body rhythms
25
basic function: anterior pituitary
hormone secretion by thyroid + adrenal cortex + gonads; growth
26
basic function: posterior pituitary
water balance, salt balance
27
basic function: thyroid
growth, development, metabolic rate
28
basic function: adrenal cortex
salt/water and carbohydrate metabolism; inflammatory reactions
29
basic function: adrenal medulla
emotional arousal, stress response
30
basic function: pancreas
sugar metabolism
31
basic function: gut
digestion, appetite control
32
basic function: gonads
body development and maintenance of reproductive organs in adults
33
neural transmission (as opposed to hormonal)
chemical, rapid onset, synaptic cleft, more voluntary control, travels 20-30nm
34
hormonal transmission (as opposed to neural)
chemical, slower with longer term effects, blood stream/extracellular space, less voluntary control, 1mm-2m
35
pituitary gland hormones w/ tropic effects only
FSH
LH--luteinizing hormone (targets gonads)
TSH--thyroid stimulating hormone (targets thyroid)
ACTH--adrenocorticotropic hormone (targets adrenal cortex to produce cortisol, androgens)
36
pituitary gland hormones w/ nontropic effects only
prolactin (targets mammary glands)
MSH (targets melanocytes) (melanocyte stimulating hormone)
37
pituitary gland hormone with nontropic and tropic effects
Growth hormone (targets liver, bones, other tissues)
38
tropic
stimulates indirectly (ie triggers release of another hormone)
39
nontropic
direct stimulation
40
hypothalamic communication to anterior pituitary
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.
41
portal system
special closed blood system that connects the hypothalamus to anterior pituitary
42
hypothalamic communication to posterior pituitary
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
43
follicule stimulating hormone
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
44
corticotropin releasing hormone
stimulating adrenocorticotropin (which will trigger cortisol release) and beta endorphins from anterior pituitary
45
melanocyte stimulating hormone
memory and skin color
46
neuropeptide Y
regulation of energy balance and appetite
47
gonadotropin releasing hormone
stimulates FSH and LH from anterior pituitary
48
substance P
transmits pain, increases smooth muscle contractions of GI tract
49
luteinizing hormone
stimulates leydig cell development and testosterone production. stimulates corpora lutea development and production of progesterone
50
growth hormone
mediates somatic cell growth; produced by anterior pituitary; important for childhood/adolescent growth and metabolic rate throughout life
51
thyroid stimulating hormone
primary stimulus for thyroid hormone production by thyroid gland
52
anterior pituitary's release of acth/lh/fsh targets what to produces what
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
53
Mineralocorticoids
Mineralocorticoids are a class of steroid hormones that regulate salt and water balances. Aldosterone is the primary mineralocorticoid.
54
side effects of gonadotroph adenoma of pituitary gland
vision loss, hypopituitarism, high prolactin
55
hypopituitarism
deficiency in GH, TSH, or LH/FSH
56
GH deficiency
short stature, fatigue, weakness, lack of ambition
57
LH and FSH deficiency
decreases gametes and estrogen or testosterone production
lower sex drive, infertility, fatigue
58
TSH deficiency
fatigue, weight gain, dry skin, constipation, sensitivity to cold/difficulty staying warm
59
ACTH deficiency
severe fatigue, low blood pressure, nausea/vomiting/abdominal pain, confusion
60
ADH deficiency
excessive urination, thirst, and electrolyte imbalances
61
pineal gland tumor side effects
fucked up sleep cycle
62
thyroid and parathyroid glands release what
release calcitonin, parathyroid hormone, thyroxine, triiodothyronine, parathyroid related peptide
63
calcitonin
lowers serum calcium levels
64
parathyroid hormone
stimulates bone resorption, increases serum calcium levels
65
thyroxine
t4. increases oxidation rate in tissue
66
triiodothyronine
t3. increases oxidation rate in tissues
67
parathyroid related peptide
regulation of bone and skin development
68
pancreas hormones
glucagon, insulin, stomatostatin, pancreatic polypeptide
69
glucagon
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
70
insulin
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
71
stomatostatin
inhibits insulin and glucagon secretion. product of pancreas
72
pancreatic polypeptide
feedback inhibitor of p;ancreatic secretion
73
glycogenolysis
breakdown of glycogen
74
gluconeogenesis
creation of glucose
75
glycogen
stored form of glucose in liver
76
pancreas location
under liver
77
thyroid location
surrounding trachea
78
adrenal glands
located on kidneys, made of outer cortex and inner medulla. releases aldosterone, 11-deoxycorticosterone, cortisol, corticosterone, DHEA, adrenaline, noradrenaline
79
steroid
product of cholesterol
80
aldosterone
sodium and water retention, product of progesterone, secreted by adrenal glands
81
11-deoxycorticosterone
sodium and water retention
82
cortisol
carb metabolism, stress modulation
83
corticosterone
carb metabolism, stress modulation
84
DHEA
dehydroepiandrosterone; weak sex hormone plays role in reproductive health
85
adrenaline
aka epinephrine. fight/flight response
86
noradrenaline
norepinephrine. responsible for tonic + reflexive changes in cardiovascular tone
87
addison's disease
adrenal gland insufficiency. no stress response. low blood pressure, low blood sugar, weight loss
88
cushing syndrome
excessive cortisol--weight gain, diabetes, high blood pressure (adrenal gland condition)
89
hyperaldosteronism
high aldosterone, sodium retention, high blood pressure (adrenal gland condition)
90
pheochromocytoma
tumor-->excess adrenaline and noradrenaline. high blood pressure, anxiety, tremors, sweating. (adrenal gland condition)
91
adipose tissue
fat tissue. releases leptin, adiponectin, plasminogen activator inhibitor 1
92
leptin
regulates energy balance, reduces appetite
93
adiponectin
modulates endothelial adhesion molecules, protective
94
plasminogen activator inhibitor 1
regulation of vascular homeostatis
95
desensitized receptors for insulin and leptin
receptors for insulin and leptin in hypothalamus may become desensitized, leads to aberrant eating, inflammation, reduced synaptic plasticity, cognitive decline, depression
96
testes hormones
androstenedione, dihydrotestosterone, testosterone
97
androstenedione
male sex characteristics
98
dihydrotestosterone
male secondary sex characteristics
99
testosterone
spermatogenesis; male secondary sex characteristics
100
testicular cancer
interestingly does not influence testicular hormones, symptoms are more so physical: pain swelling lump
101
ovaries hormones
estradiol, estrone, estriol, estrogen, progesterone
102
chemosignal
a type of ectocrine signal
103
how does the pill work
suppress the production of endogenous (estrogen, estradiol, progesterone) hormones by producing synthetic, nonconvertable versions (of estrogen and progesterone)
104
what hormonally differs based on sex
levels, not receptors
105
monoamine hormones
produced from single amino acids like melatonin (product of serotonin, product of tryptophan)
106
hormones that guide eating behavior
insulin, glucagon, cortisol
107
which areas of the brain guide eating behavior
visual cortex, gustatory cortex, prefrontal cortex, striatum, amygdala, nucleus of tractus solitarius, gut vagus nerve connection
108
gustatory cortex
prompts taste and smell of food
109
striatum
reward/pleasure--dopamine circuits, reward, motivation, guided by repetitive movement
110
liking and wanting system
liking=taste receptors on tongue, instantaneous
wanting system is delayed, nutrient sensing, intestines say "where's sugar, amino acids, etc"-gut brain axis
111
artificial sweeteners
dont act on walking system
112
amygdala's relationship to eating behavior
emotions/stress
113
nucleus of tractus solitarius relationship to eating behavior
satiety/chewing
114
gut/vagus nerve relationship to eating behavior
sensing nutrients
115
catabolic
stimulates breakdown of fats/amino acids
116
gluconeogenesis
production of glucose from triglycerides, fats
117
which organs does glucagon target
brain, pancreas, liver, brown adipose tissue, heart
118
what does glucagon promote in brain
less food intake/appetite, more satiety
119
what does glucagon promote in pancreas
insulin secretion; (due to mobilization of lipids and amino acids)
inhibits secretion from exocrine cells
120
what does glucagon promote in liver
glucose production from amino acids and lipid breakdown; less glucose breakdown and creation of glycogen; uptake of amino acids, glycogenolysis
121
what does glucagon promote in brown adipose tissue
prevents food from being too thermogenic bc adipose tissue is highly thermogenic. increases resting energy expenditure
122
what does glucagon promote in heart
raised heart rate, contractility
123
glycolysis
glucose breakdown
124
glycogenolysis
breakdown of glycogen into glucose
125
what does glucagon do in adipose tissue
adipose is site of lipolysis or lipogenesis. glucagon causes lipolysis there
126
what does glucagon do in kidney
increases glomerular filtration rate/urin flow rate
127
glomerular filtration rate
hang on maybe we need this we're fasting
128
what stimulates glucagon secretion
hypoglycemia, epinephrine, amino acids, ach, cAMP, GIP, Bombesin, gastrin, cholecystokinin, neurotensin
129
what inhibits glucagon secretion
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
effect of insulin on adipose
lipogenesis
131
GLP-1
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
effect of proglucagon
glucagon, grpp, ip2 in pancreas
glp-1, glp-2, ip-2 in gut/brain
133
key features of glp-1 in eating behavior
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
how does glp 1 induce satiation
central and peripheral pathways which mediate diff GI stimuli
135
how does glp1 activate hindbrain neurons
vagal afferent sensory nerve fibers
136
glp1 classified as an incretin why
potentiates nutrient induced insulin secretion
137
glp-1 analog effects
effective in normalizing blood glucose levels in diabetics/reducing body weight in obese individuals
138
glp 1 impact in muscle
increases glycogen synthesis and glucose oxidation
139
glp 1 impact in brain
decrease appetite, increase satiety
140
glp 1 impact in heart
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
glp 1 impact in GI tract
decreased gastric emptying and acid secretion
142
glp 1 impact in kidney
increased natriuresis (execretion of sodium)
143
glp 1 impact in adipose
INCREASED lipolysis and glucose uptake
144
glp 1 impact on pancreas
increased insulin secretion, decreased glucagon secretion, increased beta cell proliferation
145
GLP1 receptors expressed in which brain regions
paraventricular nucleus, dorsal medial nucleus of hypothalamus, arcuate nucleus, nucleus of tractus solitarius
146
exendin-9
blocks glp-1 and increases food intake
147
GLP1 signaling steps
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
insulin release from beta cells
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
where are insulin receptors in the brain
concentrated in olfactory bulb, hypothalamus, retina, choroid plexus vessels, striatum, cerebral cortex
150
how does glucose enter the brain
blood brain barrier and GLUT 1. might be locally synthesized or actively transported from bloodstream
151
glycogenesis
formation of glycogen
152
effect of insulin in brain
neuropeptide, involved in satiety, appetite regulation, olfaction, memory and cognition
153
GLUT1
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
GLUT2
both insulin dependent and independent glucose transporter expressed in brain (limited, hypothalamic neurons, glia, and tanycytes), liver, kidneys
155
GLUT3
sodium dependent glucose transporter expressed in neurons, glia, and endothelial cells in the cerebellum, striatum, cortex, and hippocampus--also , placenta, fetus
156
GLUT4
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
GLUT5
insulin dependent glucose transporter expressed in small intestines, testes
158
GLUT8
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
what stimulates insulin release
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
insulin impact on appetite
stimulates appetite, therefore used to treat anorexia (generalized appetite loss)
161
blood sugar and insulin curves over time after administered
rises and then drops
162
insulin release is higher in evening: one possible outcome
no breakfast=obesity
163
why do people use food as coping mechanism
insulin acts on striatum
164
people living with obesity brain differences
greater recruitment in insula, putamen, inferior frontal gyrus, middle temporal gyrus during food cues and stressful stimuli
165
why might the fed hormone increase appetite but the fasting hormone decrease appetite
metabolism slows down to compensate for the nonavailability of food
166
leptin
produced from adipose tissue to signal satiety and fullness. amount in blood directly proportional to amoujnt of adipose tissue
167
where is leptin active
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
without a functional ob gene....
ob gene=leptin gene. eating abnormalities=never satiated.
169
what hormone release does leptin influence
thytropin releasing hormone, growth hormone releasing hormone, adrenocorticotropic releasing hormone
170
insulin impact on ventral tegmental area
increases reward threshold=more needed to elicit same reward response
171
leptin impact on ventral tegmental area
reduced food intake
172
history of nicotine exposure
-->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
endocannabinoids
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
cb1 receptor
cannabinoid receptor found in cns--cortex, basal ganglia, hippocampus, cerebellum
175
Bardet Biedl syndrome
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
cilia in brain
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
prader willi syndrome
dysfunction of hypothalamus leading to widespread issues
178
prader willi syndrome brain symptoms
intellectual + learning disability, mood lability/anxiety, deficit in theory of mind and empathy, poor social skills, sleep diksorder
179
nuclei of the hypothalamus
dorsomedial nucleus, ventromedial nucleus, arcuate nucleus, tuber cinereum, mammilariy bodies, paraventricular nucleus, lateral and medial preoptic nuclei, anterior nucleus, suprachiasmatic nucleus, supraoptic nucleus,
180
primary hormone deficiency in prader willi (other than ghrelin)
decreased spontaneous growth hormone secretion after growth
181
how does growth hormone impact metabolism
primarily by upregulating production of insulin like growth factor 1.
182
possible reason for GH deficiencyh in obesity
damage to anterior pituitary
183
lifestyle choices that stimulate GH secretion
fasting, exercise
184
how menstruation affects GH stimulation
increase from exercise higher during ovulation unless on oral birth control. fasting not impacted by cycle
185
ketogenic diet is popular bc
Ketogenic popular bc fat doesn’t stimulate insulin release
186
anorexia nervosa
psychiatric illn ess w/ highest mortality rate in women (10%)
low intake of food-->hormonal imbalance
distinct from anorexia
187
anorexia
general loss of appetite
188
treatment for anorexia nervosa
insulin will stimulate appetite but worsen psychiatric symptoms. family based treatment best, cbt. antidepressants/antipsychotics not effective
189
ghrelin
gut--hunger hormone. inhibits insulin release and stimulates hunger.
190
bulimia nervosa hormonal imbalance
higher ghrelin, higher insulin post binge, lower leptin post binge-->less satiety, more craving
191
how to rebalance hormones, reduce cravings-->lower insulin
eat early in day, exercise, lower carb intake, avoid binging,
192
effect of exercise on eating hormones
reduced insulin and increased glucagon
193
mood disorder
chronic condition with marked disruptions in emotions, including depression, pmdd, bipolar disorder
194
BPI
A syndrome in which a complete set of mania
symptoms has occurred lasting for at least one week
or required hospitalization.
195
mania
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
diagnostic criteria bulimia
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
diagnostic criteria anorexia nervosa
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
bipolar ii
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
hypomania
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
genetics of bipolar disorder
fill in
201
neurobio of bipolar disorder
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
endocrinology of anorexia nervosa
fill in
203
symptoms anorexia nervosa
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
main difference betwn anorexia nervosa and bulimia nervosa
body weight--anorexia low, bulimia normal or high
205
major depressive disorder prevalence
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
Hamilton Depression rating scale
common depression scale
207
DMDD
disruptive mood dysregulation disorder--frequent outbursts, out of proportion, irritability
208
PDD
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
PMDD
severe PMS with psychological and physiological symptoms.
210
PMDD symptoms
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
etiology of PMDD
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
neuroimaging findings PMDD
increased amygdala response during luteal phase, altered GABA levels in left basal ganglia, anterior cingulate cortex, medial prefrontal cortex, lower gaba:glutamate
213
etiology of PMDD factors
genetics, progesterone and allo, estrogen/serotonin/bdnf, functional/structual differences, hpa axis
214
primary risk factor for depression
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
treatment options pmdd
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
ovulation behaviors
high estrogen/risk taking. after ovulation high progesterone/safe behavior regardless of whether or not pregnancy
217
ptsd
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
GAD
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
diagnostic criteria GAD
fill in
220
other psychiatric criteria w depression as primary symptom
schizophrenia, GAD, PTSD, personality disorder
221
Neurobiology of Major
Depressive Disorder
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
tbi cytokine response
new, higher baseline-->reduced sensitivity to anti inflammatorys
223
inflammation impact on neuronal function
fill in
224
chronic stress
reduced sensitivity of negative feedback hpa system due to increased circulating glucocorticoids.
225
brain risks chronic stress
increased risk for cognitive, behavioral, emotional dysfunction; mdd, anxiety disorders, memory problems.
226
immune risks chronic stress
increased risk for autoimmune syndromes, levels of cytokines, and chronic/low grade inflammation throughout the body
227
cardiovascular risks chronic stress
hypertension, vascular damage
228
disease risks chronic stress
cancer, diabetes, cushing's, obesity
229
cushing's
high cortisol levels
230
relationships of inputs of adrenal and gonadal steroid hormone receptors to HPA circuitry
all these nuclei acting on each other, androgen receptors, estrogen alpha and betas, glucocorticoid receptor, mineralcorticoid, PVN and nts at center
231
sleep deprivation effects
transient help with depressive symptoms short term, long term chronic sleep deprivation negative effect
232
glutamate signaling, ketamine depression
fill in
233
The hypothalamus-pituitary-thyroid (HPT) axis
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
Tyrosine products
T4 (-->T3) and norepinephrine (-->epinephrine)
235
effects of thyroid hormone signaling on liver
increases metabolic rate
236
effects of thyroid hormone signaling on muscle and bone
promotes growth
237
effects of thyroid hormone signaling on brain
increases neuron growth, neurotransmitters, development
238
effects of thyroid hormone signaling on heart
increases cardiac output
239
effects of thyroid hormone signaling on adipose tissue
lipolysis
240
effects of thyroid hormone signaling on proteins
promotes production, turnover
241
T3 function/thyroid hormone signaling
D1/2/3 deiodinases T4 to produce T3, which attaches to TR (attached to RXR and coactivator) -> triggers TRE to produce mRNA -> proteins
242
RXR
retinoic acid receptor
243
TR
thyroid hormone receptor
244
TRE
thyroid hormon e response eliment
245
TRa1 expression
widespread, cardiac and skeletal muscles, brown fat, bone
246
TRa2 + TRa3 expression
widespread, skeletal muscle, brain, kidney
247
TRß1 expression
widespread, brain liver kidney
248
TRß2 expression
retina hypothalamus anterior pituitary cochlea
249
HPT conserved in whom
vertebrates
250
thyroid critical for developmental transitions
251
goiter
enlargement of thyroid generally due to iodine deficiency, now treated thru iodine supplements
252
other causes of goiter
hashimoto's, grave's, cancer
253
hashimoto's
hypothyroidism, autoimmune destruction of thyroid gland
254
grave's disease
autoantibody activation of TSH receptor -->hyperthyroidism
255
congenital hypothyroidism
caused by prenatal insufficient thyroid hormone signaling, prob iodine deficiency, goiter, intellectual disability etc, rare today
256
hypothyroidism symptoms
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
hyperthyroidism
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
autoimmune hashimoto encephalopathy
personality changes, memory loss, delusions, dementia, seizures, ataxia, hallucinations, coma
259
tbi
new baseline of inflammation/cytokines, depression, dementia
decreased cortisol-->increased inflammation
260
thyroid hormone role in cerebral cortex development
cortical progenitor proliferation, excitatory neuronal migration, layer specification, synaptogenesis
261
thyroid hormone role in general brain development
establishment of connectivity, oligodendrocyte differentiation, myelination; inhibitory interneuron abundance in CC and hippocampus
262
thyroid hormone role in retinal development
M cone differentiation, M opsin expression
263
thyroid hormone role in hippocampal development
neuronal migration, neuron and glia maturation, synaptogenesis
264
thyroid hormone role in cerebellum development
precursor proliferation (nec compounds for growth(, granule cell migration, bergman glia and purkinje cell maturation and arborization, inhibitory interneuron generation, cell survival (expand!)
265
thyroid hormone role in motor neuron development
production, establishment of corticospinal projections
266
thyroid hormone role in cochlea development
inner hair cell maturation, vestibulocochlear nerve myelination
267
thyroid hormone role in striatum development
rhes gene expression regulation, motor control, anxiety, gender specific behaviors
268
thyroid hormone role in basal forebrain development
cholinergic neuron maturation and arborization, glia maturation
269
thyroid hormone role in hypothalamus and pituitary development
establishment of the HPT axis
270
function of cerebellum
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
purkinje cells
principal neurons of cerebellar cortex, dendritic development of which induced by thyroid
272
thyroid hormone regulates...
metabolism, growth of most tissues, and developmental transitions
273
list of endo glands, hormones, main effect, added pathology
ok
274
prader willi syndrome hypothalamic/pituitary symptoms
GH deficiency, hypogonadism, hypothyroidism, corticotropin deficiency, dysautonomia, abnorbal oxytocin neurons, hydroelectrolytic disorders
275
prader willi syndrome respiratory/cardio symptoms
sleep related breathing disorders, impaired central chemoreceptors, cardiomyopathy, impaired sympathetic/parasympathetic control
276
prader willi syndrome opthamological issues
strabismus, hypermetropia, myopia
277
prader willi syndrome oral symptoms
thick saliva, dental, orthodontic issues
278
prader willi syndrome metabolic symptoms
diabetes, dyslipidemia, increased fat mass/decreased lean mass, severe obesity, liver steatosis
279
prader willi syndrome GI symptoms
dysphagia, gastric emptying deficit, constipation, bowel distention/risk of Gi rupture
280
prader willi syndrome orthopedic symptoms
early scoliosis, kyphosis, hip dysplasia, joint hypermobility
281
prader willi syndrome urogenital symptoms
enuresis, delayed sphincter control, cryptorchidism
282
prader willi syndrome skin symptoms
skin picking, frequent lymphedema, risk of erysipelas, capillary fragility/increased hematomas
283
prader willi syndrome hormonal symptoms
increased ghrelin
284
name endocrine glands
Hypothalamus
* Pituitary Gland
* Pineal Gland
* Thyroid Gland
* Pancreas
* Ovaries
* Testes
* Adrenal glands
* Adipose tissue
285
Hypothalamus related pathology
prader willi syndrome
286
* Pituitary Gland related pathology
*
adenoma-->GH deficiency
287
Pineal Gland related pathology
pineal tumor--fucked up sleep cycle
288
* Thyroid Gland related pathology
*
hashimoto's - hypopituitarism
289
Pancreas related pathology
diabetes
290
* Ovaries related pathology
high androgens -- PCOS
291
* Testes related pathology
testicular cancer--no hormonal signs
292
* Adrenal glands
*related pathology
cushing's
293
Adipose tissue related
leptin desensitization--see above
294
gonadotropin
FSH, LH
295
glucocorticoid
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
impacted brain regions bipolar disorder
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
Using CBT for patients : bipolar disorder
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
MDD diagnosis
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.
