midterms again except this time cymbalta is kicking my ass even more Flashcards
GRABBING CYMBALTA BY THE FUCKING NECK BECAUSE I MIGHT HAVE BRAIN ZAPS AND A SHITTY MEMORY BUT THE ASIAN IN ME NEEDS THE 4. FUCKNG 0!!!!!!!!!!!!!!!!
Where is GnRH made
hypothalamus
What does LH do where is it made
anterior pituitary, it acts on endocrine cells to make steroid and peptide hormones. ONLY IN FEMALE it contributes to gamete production
What does FSH do where is it made
Gamete production made in anterior pituitary
What does high GnRH pulses do, opposite?
LH secretion for high. FSH for low. pulses needed for reproductive function.
Sertoli cells
gie sperm nutrients and remove waste. are packed close to the spermatids and shit
leydig cells
make t
spermatogenesis
spermatogonia form during fetal development. 2n spermatogonia split to make primary spermatocytes which are also 2n. secondary spermatocytes also 2n. Spermatids are n and so are spermatozoa (they are the mfs with the tails)
blood testis barrier
weird shit on sperm surface makes it look wonky so you need a barrier by tight junctions so its not attacked
Acrosome
comes from golgi, has hyalyronsidase and acrosin which breaks down the zona pellucida (glycoprotein that covers oocyte)
semen composition
water, lubricant (mucus), buffers to neutralize acid, nutrients, enzymes, zinc, prostaglandins
FSH regulation
makes inhibin that make cell products which makes inhibin that negatively regulates FSH.
LH regulation
LH acts on leydig cells which make T, which negatively regulates GnRH
FSH purposes for XY
sperm deveopment, secrete androgen binding protein to bring more androgens to testis
LH purposes for XY
stimulates leydig cells which make T
LH and FSH cycle throughout XY life
go up and down prenatally, low during childhood, increases in puberty (basically like T)
AMH (anti mullerian not malarian!) cycle throughout XY life
high to low from childhood to puberty
XY hypogonadism symptoms (for both types)
decreased activity of testes, low androgens inhibin B, low AMH, low sperm production
primary hypogonadism
high GnRH, LH, FSH, low T due to genetics injury, inflammation in testes. Solution exogenous testosterone (not me pretending to have this to get my fucking T)
secondary hypogonadism
hypothalamus/anterior pituitary gland damaged. LOW EVERYTHING BITCH. treatment include gonadotropin therapy
DHT (di hydro T)
male pattern balding and prostate growth 5- a reductase inhibitors can treat prostate enlargement and baldness
testosterone effects
more sperm. prostate and seminal vesicle secretion. maintains reproductive tract, increases sex drive, negative feedback on GnRH, LH, FSH, male pattern hair growth, muscle, sebaceous gland secretion, protein making, aggression, more blood
oogenesis
oogonium go through mitosis to make diploid oogonia. before birth, oogonia enter meiosis I. you are born with primary oocyte and stuck with it until you get ur period.
ovulation
release primary oocyte from meiosis 1 and put it into meiosis II. now secondary oocyte. THIS IS THE FIRST INSTANCE OF HAPLOIDY. increase LH. increase progesterone (smooth muscle contraction). increase collagenase (to dissolve connective tissue). oocyte and cumulus cells yeeted into gap, picked up by fimbria.
Thecal cells
make steroid hormone precursors (i.e. androgens)
ovarian cycle: follicular phase
days 1-14. one dominant follical matures. antrums form in secondary. antral fluids have estrogen and enzymes
ovarian cycle: luteal phase
left behind follicular cells from follicular phase become corpus luteum. releases progesterone and estrogen. when no fertilization, corpus luteum degenerates to form corpus albicans.
corpus luteum when fertilization does what
makes progesterone + estrogen until end of first trimester.
uterine cycle: menses
menses (days 1-5) decreases progesterone, estrogen. causes endometrium blood vessel constriction, shedding of endometrium lining.
uterine cycle: proliferative
5-14 tissue of endometrium grow, high estrogen
uterine cycle: secretory phase
14-28 glands in endometrium makes more viscous fluid endometrial cells deposit lipid and glycogen in cytoplasm due to progesterone and estrogen
LH ovarian cycle effects early follicular
LH make theca cells release androgens.
FSH ovarian cycle effects early follicular
FSH makes granulosa cells convert androgens into estrogens
AMH ovarian cycle effects early follicular
granulosa cells secrete AMH so you don’t recruit more follicles
early follicular phase estrogen
positive loop around granulosa cells, makes more and more E. shuts doen FSH LH GnRH
late follicular phase and ovulation follicles
you now have a tertiary follicle
late follicular and ovulation hormones secreted
inhibin (inhibits FSH), progesterone (increases sensitivity to GnRH) and estrogen
high estrogen effect on GnRH
pulses every 65 min (positive feedback), causing LH surge to trigger ovulation
corpus luteum when LH and FSH
progesterone, inhibin, estrogen (negative on hypothalamus, pituitary)
progesterone and estrogen on GnRH pulses
now one every 3-4 hr
corpus luteum late luteal phase
gets fertilized or dies (12 days lifespan). if dies, progesterone and estrogen levels fall, so GnRH returns to one every 1.5 hr (LH and FSH release)
what do pregnancy tests detect
hCG
Estrogen effects
follicular development, ovulation, growth of endometrium, reproductive tract. negative on the H gang. boobs, ass thighsa
androgens on adult female
hairy n horny???
menopause hormone
low estradiol and progestrone. high FSH, LH, but ovaries cannot respond to it
capacitation
sperm becomes hyperactive, albumin, enzymes, lipoproteins bind to sperm remove glycoprotein coat, cuase intracellular changes to get the jizz through muc lmfao
what helps jizz gets where it needs to go
uterine and oviduct contractions, estrogens and prostaglandins in semen.
oocyte viability
1 day
spermatozoa viability
4-6 days
fertilization
about 100 sperm get there, guided by chemotaxis (progesterone from cumulus cells). sperm tunnel through barriers w/ acrosomal enzymes, dock w/ sperm binding proteins. oocyte depolarizes, oocyte then blocks other sperm
why is joker x batman good
because evil green man. insanity, murder, blood everywhere yipeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeee
after fertilization timeline
day 1: fertilization
2-4: cell division
4-5: blastocyst reaches uterus
5-9: blastocyst implants (blastocyst eventually becomes embryo)
hCG
takes from pituitary to maintain corpus luteum, prevent menstruation. similar to LH. muy importante!!!!!!! stimulates fetal testis (helps it get a pp)
placenta
digestive, respiratory, renal systems for fetus. waste, nutrients, O2, CO2, proteins/chemicals
placenta circulation
mother’s blood not directly connected to fetus, mother’s blood forms a lake. fetal chorionic villi transfer gases and solutes between mother and fetus
progesterone for placental hormone
supresses cervical contractions, cervical plug, mammary gland development. first 2 so you don’t squish the baby lmfaooooooo
estrogen for placental hormone
uterine development (growth of placenta, blood supply, oxytocin receptor), breast duct development
human placental lactogen
high in mother, lower in fetus. similar to growth hormone and prolactin. lowers maternal cellular uptake of glucose and maternal lipolysis to give baby energy from mother’s reserve
terms of pregnancy
first trimester: first week after last period. preterm: born >28 weeks, usually don’t need invervention, early need ICU because lungs not developed
maternal adaptations for pregnancy
increased vasopressin levels increase blood volume, increase fluid retention for more blood. boost cardiovascular system, lower immune system (something new, don’t want it to be attacked). increase PTH to move calcium to fetus. calcitonin to prevent too much bone loss.
triggering labor
relaxin released from ovary. placenta loosens ligaments in pelvic bone, softens cervix. cervical stretch has positive feedback
before parturition
estrogens and progesterone needed for mammary glands but inhibit milk production just yet
after parturition
oxytocin goes to myoepithelial cells, squeezes the epithelial milk making cells which are activated by prolactin.
child crying does what
decreases PIH (prolactin inhibiting hormone), increases prolactin and oxytocin
bipotential primordium
6 weeks. mullerian duct can become fallopian tube, uterus, upper vagina. wolffian duct can become epididymis, vas deferens, seminal vesicle
fetal develop of XX
gonadal cortex becomes ovary when there is no SRY gene. wolffian duct gone cuz no T. mullerian duct becomes fallopian tube, uterus, upper vagin
SF1 and SRY
SF1 is a transcription factor that activates SRY gene which makes AMH to supress female characteristics.
SOX9 in fetus
initiate Sertoli cell differentiation. cellular events downstream form testis structure
Development of XY in fetus
sry protein causes gonadal medulla to form testis, gonadal cortex regresses. AMH makes Mullerian ducts go away, T turns Wolffian duct. With testis, Leydig cells make T, some converted to DHT for male genitalia.
common XX hormones in fetus
B catenin stops SOX-9 cuz no Sertoli. No AMH/T
Xy with complete androgen insensitivty
undescended testes not visible at birth. external closed vagina. high androgens converted to estrogens. breasts but no hair. high in LH
metabolism
sum of chem rxns in body
anabolic
small molecules become bigger ones. like using glucose for energy, building bigger molecules
catabolic
large molecules become small ones. fasted states 3-4 hrs after eating. using glucose and fat for energy
glut2
kent is pathetic liar: kidney, intestines, pancreas liver. glucose transport, secrete insulin. glut 2 always there regardless of insulin
glut4
adipose and skeletal. insulin dependent, transporters exocytosed when fed, or working out, letting glucose in
insulin
dominant hormone of fed state, synthesized as typical peptide. binds to tyrosine kinase. forms glycogen, fat, protein
glut 2 regulation
insulin activates hexokinase, phosphorylating glucose. more glucose in
GIP-1
released by K cells in small intestine when nutrients are in lumen. B pancrea cells bind to GIP 1 release insulin
GLP-1
same as GIP, except its by L cells and can be in large intestine. stay full longer. glucose release lowered, slower gastric emptying. more beta cells, increase insulin. cardioprotective
glucagon
pancreatic a cells. prevent 低血糖. large peptide protein. in response to starvation, glucagon binds to receptor and makes shit ton of glucose in liver. glucose diffuses into blood by passive diffusion
cortisol on glucagon and einephrine
permissive effect
glucacon secretion
low plasma glucose, high plasma amino acid so insulin doesn’t yoink too much glucose
proglucagon
in a pancrea cells, mostly makes glucagon. in L intestine/brain cells, mostly makes GLP 1 and 2
type 1 diabetes
low/no insulin secretion, 10% of all diabetes. starts young, need insulin injections/pumps. body thinks its starving. breaks glycogen stores to increas eblood sugar, urinate lots of glucose, low blood volume, increasing ADH. pissing a lot. high osmolarity. fat/protein breakdown because no usable glucose, causing acidosis (which causes hyperventilation and ab pain)
type 2 diabetes
90% mature onset, chronic high sugar, insensitivity to insulin. treated by diet and exercise, oral hypoglycemics. sulfonylureases close Katp which cause cell depolarization, meaning shit ton of Ca2+ in, exocytoses insulin
Posterior pituitary
neural tissue, secretes 2 neurohormones (ADH and oxytocin). hypothalamus sends shit down. not actually endocrine
anterior pituitary
endocrine tissue. makes prolactin, thyrotropin, adrenocorticotropin, GH, FSH, LH. hypothalamus sends neurohormones (like GnRH) into portal system, endocrine then send second set.
Ossification
need osteoblasts. when cartilage gets turned to bone (osteoblasts replace chondrocytes, laying new bone, causing bone growth)
GH (growth hormone)
from AP, stimulated by GHRH (growth hormone releasing hormone) from hypothalamus and somatostatin, IGF (insulin like growth factors) which MAKES EVERYTHING FUCKING GROW BITTTTTTTTTTTTCH
growth hormone catabolic shit
stimulates adipose cells to break down stored fat. increases uptake of amino acids from blood, decreases cell death. targets bone, muscle, nervous, immune. stimulates liver to break glycogen into glucose (gluconeogenesis)
things that affect growth
diet, genetics, hormones, GH and IGFs, thyroid hormones, insulin (more glucose for growth), sex hormones, cortisol (catabolize tissue for growth)
TSH
from anterior pituitary, after TRH
T3 and T4
T3 3-5x more potent. in blood bound to plasma proteins. both bound to nuclear thyroud receptors. increase metabolic rate, O2 consumption, heat production, protein degradation, lipolysis. boosts speech, thinking reflexes. works with GH in kids. increases heart rate, heart contraction, peripheral blood flow, beta adrenogenic receptors. too much causes muscular weakness
hyperthyroidism
caued by tumors, thyroid-stimulating immunoglobulins (grave’s disease). symptoms include goiter, nervousness, insomnia, anxiety, bulging eyes, high heart rate, weight loss. treated by blocking part of thyroid, blocking synthesis of T3/T4 or conversion of T4 to T3
grave’s disease
antibodies that pretend to be TSH, making a shit ton of thyroid hormones. most common cause of thyroid enlargement in developed countries
hypothyroidism
lack of iodine or underactive thyroid gland. goiter, slow heart rate, slow speech, fatigue, cold intolerance, cretinism, stunted growth. treated with exogenous T4.
iodine deficiency
stops T3 and T4 from being made so high TSH TRH
Brain, spinal cord, enteric nervous sys. neuron number
brain 86 bil, spinal cord 1 bil. enteric nervous system 100-600 mil
grey matter
nerve cell bodies, unmyelinated axons, dendrites. in layers or clusters called nuclei
white matter
myelinated axons running in bundles called tracts
(PNS) ganglia
clusters of neurons
(PNS) nerves
bundles of axons
why is brain greedy asf
2% mass, 15% blood, half of body’s glucose. only support 4% neurons working
Dorsal root of spinal cord
incoming sensory info, close to somatic sensory nuclei (skin) and visceral sensory nuclei (heart, stomach)
Ventral root of spinal cord
leaving motor info. close to autonomic efferent nuclei (glands, smooth). somatic motor nuclei (skeletal)
ascending tracts, descending tracts
ascending: sensory to brain, mostly dorsal. vice versa
propriospinal tracts
stay in spinal cord
brainstem
medulla, pons, midbrain. breathing, swallowing, vomiting, blood pressure
cranial nerves
nerves that leave/enter brain but aren’t brainstem
diencephalon
thalamus, hypothalamus, pituitary, pineal.
cerebral grey matter
contains cortex, limbic, basal ganglia (movement)
left hemi
speech, writing, language, math
right hemi
analysis by touch, spatial analysis
limbic system
cingulate gyrus, amygdala, hippocampus. motivation, emotion, memory.
4 somatic senses
touch, temp, proprioception, nociception
Receptors
sometimes neurons sometimes non-neuronal epithelial cells. graded potentials usually, unless it’s a neuron, then it can fire APs
types of receptors
chemo, mechano, thermo, photo
receptor potential
photoreceptors can see a single photon of light
perceptual threashold
how much you need to actually consciously notice
phasic
respond to change, then stop firing (e.g. retinal cels)
tonic
signal present level
spatial change
create edges. for example wih pressure, lateral inhibition uses tertiary neurons to block each other and shit uhhh
what doesn’t go through thalamus
olfactory
zonules
shit that holds lens in place
vitreous body
jelly of eyeball
cornea
bulge at front of eyeball continuous with schlera
ring shaped pupillary constrictor muscle
responds to parasympathetic signals from brain in bright light, shrinking pupil. vice versa when it is dark, except its dilator muscle
can you focus with pupils no lens
yeah
constricted pupils means what depth of field
full depth of field. see everything. dilated pupils means see stuff at given distance
how to focus when dilated pupil
bigger hole means brighter and blurrier. use refraction.
lens role in refraction
1/3 of refraction but can change shape. made of clear cells and packed with crystallin proteins in concentric layers.
angle of incidence
angle at which the light gets in.
rounder lens means focus what
focus closer. parasympathetic nerve signals contract ring shaped siliary and reduces tension, lens becomes round
nearest point of accomodation
cloest point a person can focus
presbyopia
lens stiffening as you get old. fucks with accomodation
hyperopia
focal point falls behind retina. solved by convex lens
myopia
nearsightedness, vice versa of hyperopia
Outer segment of rods and cones
disc like with pigments that respond to light
Inner segment and basal segment
inner: nucleus and organelles for protein synth. basal: glutamate.
What happens when light hits photoreceptors
hyperpolarizes due to pigments, decreases glutamate release. photoreceptors most active in dark
macula
central disc with shit ton of photoreceptors
cones
color vision, less sens. in fovea
rods
low light, dark adapt 30 min. rhodopsin.
bipolar cells
may connect 45 photoreceptors. need contrast. 126 mil photoreceptors to 1 mil ganglion.
centre surround
receptive field that is excited when it is lit in the middle
retinal ganglion cells
also detect contrast with center surround receptive fields. find contrast, do fire action potentials
importance of ganglion location
near fovea, gets input from few photoreceptors, but very clear. vice versa.
M cells
large, magnocellular. movement of objects, phasic, 10% of ganglion cells
P cells
parvocellular, small. fine detail and texture, 70% of ganglion
melanopsin
photoreceptors with own pigment, melanopsin. projects onto suprechiasmatic nucleus for circadian rhythsm. IS A PHOTORECEPTOR
2LGN has how many neurons
2 mil neuron. about same as 2 retinas ganglion cells
draw the optic nerve and where it projects
check your notes you idiot
sperm production
in testis, optimal at 2-3 degrees below body temp, about 64 days, 200 million a day, mature in epididymis
how many vas deferens
2
how many seminal vesicles
2
