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physiology except 10 times harder thanks to my stupid fucking depression > midterms again except this time cymbalta is kicking my ass even more > Flashcards

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!!!!!!!!!!!!!!!!

1
Q

Where is GnRH made

A

hypothalamus

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2
Q

What does LH do where is it made

A

anterior pituitary, it acts on endocrine cells to make steroid and peptide hormones. ONLY IN FEMALE it contributes to gamete production

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3
Q

What does FSH do where is it made

A

Gamete production made in anterior pituitary

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4
Q

What does high GnRH pulses do, opposite?

A

LH secretion for high. FSH for low

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5
Q

Sertoli cells

A

gie sperm nutrients and remove waste. are packed close to the spermatids and shit

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6
Q

leydig cells

A

make t

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7
Q

spermatogenesis

A

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)

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8
Q

blood testis barrier

A

weird shit on sperm surface makes it look wonky so you need a barrier by tight junctions so its not attacked

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9
Q

Acrosome

A

comes from golgi, has hyalyronsidase and acrosin which breaks down the zona pellucida (glycoprotein that covers oocyte)

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10
Q

semen composition

A

water, lubricant (mucus), buffers to neutralize acid, nutrients, enzymes, zinc, prostaglandins

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11
Q

FSH regulation

A

makes inhibin that make cell products which makes inhibin that negatively regulates FSH.

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12
Q

LH regulation

A

LH acts on leydig cells which make T, which negatively regulates GnRH

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13
Q

FSH purposes for XY

A

sperm deveopment, secrete androgen binding protein to bring more androgens to testis

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14
Q

LH purposes for XY

A

stimulates leydig cells which make T

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15
Q

LH and FSH cycle throughout XY life

A

go up and down prenatally, low during childhood, increases in puberty (basically like T)

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16
Q

AMH (anti mullerian not malarian!) cycle throughout XY life

A

high to low from childhood to puberty

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17
Q

XY hypogonadism symptoms (for both types)

A

decreased activity of testes, low androgens inhibin B, low AMH, low sperm production

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18
Q

primary hypogonadism

A

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)

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19
Q

secondary hypogonadism

A

hypothalamus/anterior pituitary gland damaged. LOW EVERYTHING BITCH. treatment include gonadotropin therapy

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20
Q

DHT (di hydro T)

A

male pattern balding and prostate growth 5- a reductase inhibitors can treat prostate enlargement and baldness

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21
Q

testosterone effects

A

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

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22
Q

oogenesis

A

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.

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23
Q

ovulation

A

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.

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24
Q

Thecal cells

A

make steroid hormone precursors (i.e. androgens)

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25
Q

ovarian cycle: follicular phase

A

days 1-14. one dominant follical matures. antrums form in secondary. antral fluids have estrogen and enzymes

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26
Q

ovarian cycle: luteal phase

A

left behind follicular cells from follicular phase become corpus luteum. releases progesterone and estrogen. when no fertilization, corpus luteum degenerates to form corpus albicans.

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27
Q

corpus luteum when fertilization does what

A

makes progesterone + estrogen until end of first trimester.

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28
Q

uterine cycle: menses

A

menses (days 1-5) decreases progesterone, estrogen. causes endometrium blood vessel constriction, shedding of endometrium lining.

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29
Q

uterine cycle: proliferative

A

5-14 tissue of endometrium grow, high estrogen

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30
Q

uterine cycle: secretory phase

A

14-28 glands in endometrium makes more viscous fluid endometrial cells deposit lipid and glycogen in cytoplasm due to progesterone and estrogen

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31
Q

LH ovarian cycle effects early follicular

A

LH make theca cells release androgens.

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32
Q

FSH ovarian cycle effects early follicular

A

FSH makes granulosa cells convert androgens into estrogens

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33
Q

AMH ovarian cycle effects early follicular

A

granulosa cells secrete AMH so you don’t recruit more follicles

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34
Q

early follicular phase estrogen

A

positive loop around granulosa cells, makes more and more E. shuts doen FSH LH GnRH

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35
Q

late follicular phase and ovulation follicles

A

you now have a tertiary follicle

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36
Q

late follicular and ovulation hormones secreted

A

inhibin (inhibits FSH), progesterone (increases sensitivity to GnRH) and estrogen

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37
Q

high estrogen effect on GnRH

A

pulses every 65 min (positive feedback), causing LH surge to trigger ovulation

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38
Q

corpus luteum when LH and FSH

A

progesterone, inhibin, estrogen (negative on hypothalamus, pituitary)

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39
Q

progesterone and estrogen on GnRH pulses

A

now one every 3-4 hr

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40
Q

corpus luteum late luteal phase

A

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)

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41
Q

what do pregnancy tests detect

A

hCG

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42
Q

Estrogen effects

A

follicular development, ovulation, growth of endometrium, reproductive tract. negative on the H gang. boobs, ass thighsa

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43
Q

androgens on adult female

A

hairy n horny???

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44
Q

menopause hormone

A

low estradiol and progestrone. high FSH, LH, but ovaries cannot respond to it

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45
Q

capacitation

A

sperm becomes hyperactive, albumin, enzymes, lipoproteins bind to sperm remove glycoprotein coat, cuase intracellular changes to get the jizz through muc lmfao

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46
Q

what helps jizz gets where it needs to go

A

uterine and oviduct contractions, estrogens and prostaglandins in semen.

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47
Q

oocyte viability

A

1 day

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48
Q

spermatozoa viability

A

4-6 days

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49
Q

fertilization

A

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

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50
Q

why is joker x batman good

A

because evil green man. insanity, murder, blood everywhere yipeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeeee

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51
Q

after fertilization timeline

A

day 1: fertilization
2-4: cell division
4-5: blastocyst reaches uterus
5-9: blastocyst implants (blastocyst eventually becomes embryo)

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52
Q

hCG

A

takes from pituitary to maintain corpus luteum, prevent menstruation. similar to LH. muy importante!!!!!!! stimulates fetal testis (helps it get a pp)

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53
Q

placenta

A

digestive, respiratory, renal systems for fetus. waste, nutrients, O2, CO2, proteins/chemicals

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54
Q

placenta circulation

A

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

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55
Q

progesterone for placental hormone

A

supresses cervical contractions, cervical plug, mammary gland development. first 2 so you don’t squish the baby lmfaooooooo

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56
Q

estrogen for placental hormone

A

uterine development (growth of placenta, blood supply, oxytocin receptor), breast duct development

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57
Q

human placental lactogen

A

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

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58
Q

terms of pregnancy

A

first trimester: first week after last period. preterm: born >28 weeks, usually don’t need invervention, early need ICU because lungs not developed

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59
Q

maternal adaptations for pregnancy

A

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.

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60
Q

triggering labor

A

relaxin released from ovary. placenta loosens ligaments in pelvic bone, softens cervix. cervical stretch has positive feedback

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61
Q

before parturition

A

estrogens and progesterone needed for mammary glands but inhibit milk production just yet

62
Q

after parturition

A

oxytocin goes to myoepithelial cells, squeezes the epithelial milk making cells which are activated by prolactin.

63
Q

child crying does what

A

decreases PIH (prolactin inhibiting hormone), increases prolactin and oxytocin

64
Q

bipotential primordium

A

6 weeks. mullerian duct can become fallopian tube, uterus, upper vagina. wolffian duct can become epididymis, vas deferens, seminal vesicle

65
Q

fetal develop of XX

A

gonadal cortex becomes ovary when there is no SRY gene. wolffian duct gone cuz no T. mullerian duct becomes fallopian tube, uterus, upper vagin

66
Q

SF1 and SRY

A

SF1 is a transcription factor that activates SRY gene which makes AMH to supress female characteristics.

67
Q

SOX9 in fetus

A

initiate Sertoli cell differentiation. cellular events downstream form testis structure

68
Q

Development of XY in fetus

A

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.

69
Q

common XX hormones in fetus

A

B catenin stops SOX-9 cuz no Sertoli. No AMH/T

70
Q

Xy with complete androgen insensitivty

A

undescended testes not visible at birth. external closed vagina. high androgens converted to estrogens. breasts but no hair. high in LH

71
Q

metabolism

A

sum of chem rxns in body

72
Q

anabolic

A

small molecules become bigger ones. like using glucose for energy, building bigger molecules

73
Q

catabolic

A

large molecules become small ones. fasted states 3-4 hrs after eating. using glucose and fat for energy

74
Q

glut2

A

kent is pathetic liar: kidney, intestines, pancreas liver. glucose transport, secrete insulin. glut 2 always there regardless of insulin

75
Q

glut4

A

adipose and skeletal. insulin dependent, transporters exocytosed when fed, or working out, letting glucose in

76
Q

insulin

A

dominant hormone of fed state, synthesized as typical peptide. binds to tyrosine kinase. forms glycogen, fat, protein

77
Q

glut 2 regulation

A

insulin activates hexokinase, phosphorylating glucose. more glucose in

78
Q

GIP-1

A

released by K cells in small intestine when nutrients are in lumen. B pancrea cells bind to GIP 1 release insulin

79
Q

GLP-1

A

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

80
Q

glucagon

A

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

81
Q

cortisol on glucagon and einephrine

A

permissive effect

82
Q

glucacon secretion

A

low plasma glucose, high plasma amino acid so insulin doesn’t yoink too much glucose

83
Q

proglucagon

A

in a pancrea cells, mostly makes glucagon. in L intestine/brain cells, mostly makes GLP 1 and 2

84
Q

type 1 diabetes

A

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)

85
Q

type 2 diabetes

A

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

86
Q

Posterior pituitary

A

neural tissue, secretes 2 neurohormones (ADH and oxytocin). hypothalamus sends shit down. not actually endocrine

87
Q

anterior pituitary

A

endocrine tissue. makes prolactin, thyrotropin, adrenocorticotropin, GH, FSH, LH. hypothalamus sends neurohormones (like GnRH) into portal system, endocrine then send second set.

88
Q

Ossification

A

need osteoblasts. when cartilage gets turned to bone (osteoblasts replace chondrocytes, laying new bone, causing bone growth)

89
Q

GH (growth hormone)

A

from AP, stimulated by GHRH (growth hormone releasing hormone) from hypothalamus and somatostatin, IGF (insulin like growth factors) which MAKES EVERYTHING FUCKING GROW BITTTTTTTTTTTTCH

90
Q

growth hormone catabolic shit

A

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)

91
Q

things that affect growth

A

diet, genetics, hormones, GH and IGFs, thyroid hormones, insulin (more glucose for growth), sex hormones, cortisol (catabolize tissue for growth)

92
Q

TSH

A

from anterior pituitary, after TRH

93
Q

T3 and T4

A

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

94
Q

hyperthyroidism

A

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

95
Q

grave’s disease

A

antibodies that pretend to be TSH, making a shit ton of thyroid hormones. most common cause of thyroid enlargement in developed countries

96
Q

hypothyroidism

A

lack of iodine or underactive thyroid gland. goiter, slow heart rate, slow speech, fatigue, cold intolerance, cretinism, stunted growth. treated with exogenous T4.

97
Q

iodine deficiency

A

stops T3 and T4 from being made so high TSH TRH

98
Q

Brain, spinal cord, enteric nervous sys. neuron number

A

brain 86 bil, spinal cord 1 bil. enteric nervous system 100-600 mil

99
Q

grey matter

A

nerve cell bodies, unmyelinated axons, dendrites. in layers or clusters called nuclei

100
Q

white matter

A

myelinated axons running in bundles called tracts

101
Q

(PNS) ganglia

A

clusters of neurons

102
Q

(PNS) nerves

A

bundles of axons

103
Q

why is brain greedy asf

A

2% mass, 15% blood, half of body’s glucose. only support 4% neurons working

104
Q

Dorsal root of spinal cord

A

incoming sensory info, close to somatic sensory nuclei (skin) and visceral sensory nuclei (heart, stomach)

105
Q

Ventral root of spinal cord

A

leaving motor info. close to autonomic efferent nuclei (glands, smooth). somatic motor nuclei (skeletal)

106
Q

ascending tracts, descending tracts

A

ascending: sensory to brain, mostly dorsal. vice versa

107
Q

propriospinal tracts

A

stay in spinal cord

108
Q

brainstem

A

medulla, pons, midbrain. breathing, swallowing, vomiting, blood pressure

109
Q

cranial nerves

A

nerves that leave/enter brain but aren’t brainstem

110
Q

diencephalon

A

thalamus, hypothalamus, pituitary, pineal.

111
Q

cerebral grey matter

A

contains cortex, limbic, basal ganglia (movement)

112
Q

left hemi

A

speech, writing, language, math

113
Q

right hemi

A

analysis by touch, spatial analysis

114
Q

limbic system

A

cingulate gyrus, amygdala, hippocampus. motivation, emotion, memory.

115
Q

4 somatic senses

A

touch, temp, proprioception, nociception

116
Q

Receptors

A

sometimes neurons sometimes non-neuronal epithelial cells. graded potentials usually, unless it’s a neuron, then it can fire APs

117
Q

types of receptors

A

chemo, mechano, thermo, photo

118
Q

receptor potential

A

photoreceptors can see a single photon of light

119
Q

perceptual threashold

A

how much you need to actually consciously notice

120
Q

phasic

A

respond to change, then stop firing (e.g. retinal cels)

121
Q

tonic

A

signal present level

122
Q

spatial change

A

create edges. for example wih pressure, lateral inhibition uses tertiary neurons to block each other and shit uhhh

123
Q

what doesn’t go through thalamus

A

olfactory

124
Q

zonules

A

shit that holds lens in place

125
Q

vitreous body

A

jelly of eyeball

126
Q

cornea

A

bulge at front of eyeball continuous with schlera

127
Q

ring shaped pupillary constrictor muscle

A

responds to parasympathetic signals from brain in bright light, shrinking pupil. vice versa when it is dark, except its dilator muscle

128
Q

can you focus with pupils no lens

A

yeah

129
Q

constricted pupils means what depth of field

A

full depth of field. see everything. dilated pupils means see stuff at given distance

130
Q

how to focus when dilated pupil

A

bigger hole means brighter and blurrier. use refraction.

131
Q

lens role in refraction

A

1/3 of refraction but can change shape. made of clear cells and packed with crystallin proteins in concentric layers.

132
Q

angle of incidence

A

angle at which the light gets in.

133
Q

rounder lens means focus what

A

focus closer. parasympathetic nerve signals contract ring shaped siliary and reduces tension, lens becomes round

134
Q

nearest point of accomodation

A

cloest point a person can focus

135
Q

presbyopia

A

lens stiffening as you get old. fucks with accomodation

136
Q

hyperopia

A

focal point falls behind retina. solved by convex lens

137
Q

myopia

A

nearsightedness, vice versa of hyperopia

138
Q

Outer segment of rods and cones

A

disc like with pigments that respond to light

139
Q

Inner segment and basal segment

A

inner: nucleus and organelles for protein synth. basal: glutamate.

140
Q

What happens when light hits photoreceptors

A

hyperpolarizes due to pigments, decreases glutamate release. photoreceptors most active in dark

141
Q

macula

A

central disc with shit ton of photoreceptors

142
Q

cones

A

color vision, less sens. in fovea

143
Q

rods

A

low light, dark adapt 30 min. rhodopsin.

144
Q

bipolar cells

A

may connect 45 photoreceptors. need contrast. 126 mil photoreceptors to 1 mil ganglion.

145
Q

centre surround

A

receptive field that is excited when it is lit in the middle

146
Q

retinal ganglion cells

A

also detect contrast with center surround receptive fields. find contrast, do fire action potentials

147
Q

importance of ganglion location

A

near fovea, gets input from few photoreceptors, but very clear. vice versa.

148
Q

M cells

A

large, magnocellular. movement of objects, phasic, 10% of ganglion cells

149
Q

P cells

A

parvocellular, small. fine detail and texture, 70% of ganglion

150
Q

melanopsin

A

photoreceptors with own pigment, melanopsin. projects onto suprechiasmatic nucleus for circadian rhythsm. IS A PHOTORECEPTOR

151
Q

2LGN has how many neurons

A

2 mil neuron. about same as 2 retinas ganglion cells

152
Q

draw the optic nerve and where it projects

A

check your notes you idiot

physiology except 10 times harder thanks to my stupid fucking depression (2 decks)

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