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196 Cards in this Set

  • Front
  • Back
primary sex organs
produce germ cells (sperm, ova)
endocrine fxn (test, est)
secondary sex organs
duct work: vas def, oviduct
assoc glands: prostate,cervix
leydig cells location and job
between tubules, caps and cell clumps
-make testosterone
x =
gymnosperm
y =
androsperm
axoneme
9 pairs of tubules + middle
=10, shorten and whip the tail
basic requirements for fertility
1. sufficient #/conc (20 mill/ml)
2. motility (>50% progressive)
3. ability to penetrate ovum (acrosomal enzymes)
4. complete and fxnal genetic material
how many sperm made a day
approx 100-200 million
how does spermatogenesis synchronize
via cytoplasmic bridges
how does spermatogenesis occur> how often
in cycles
16 days apart
how long does the entire spermatogenesis process take
70 days
2-4 wks in the epididymis
how does sperm get the tail to whiop
dependent on envt
uses CHO to make ATP
sertoli cells have tight jxns bc
blood testes barrier
-WBCs could attack sperm
fxns of sertoli cells
1. blood testis barrier
2. nourish spermatozoa
3. secrete luminal fluid
4. site of hormonal (FSH,testosterone) control
5. produce and secrete inhibin
6. produce adn secrete ABP
inhibin fxn
regulate FSH
ABP does what
inside tubule
-soaks up testosterone, can release it and follow sperm
composition derived from seminal secretions is
1. prostate-30%
2. seminal vesicles - 60%
3. bulbourethral -5%
4. sperm cells 5%
properties of seminal plasma
nutritive-fructose, AA's
buffering
clotting-form gel to protect sperm
antibiotic-vagina isn't antiseptic
capacitation
can fertilize in female reproductive tract
prostaglandins fxn
ocntractions of urethra and uterus
countercurrent flow occurs where in men describe
pampinform plexus
-veins wrap around artery to cool and pick up the heat and go to testes and back up to body
-muscles raise and drop testes to control temp
lipids on head of sperm do what to the membrane and then the vag
stabilize
vag washes them off
testes veins are prone to? explain
varicose
-drain to left renal vein harder time getitng into circ
epididymis and lumen size
changes for different secretions
-duct work for sperm to exit testes
erectile tissue is what type of NS and describe
3 tubes
-parasymp
-neurovascular bc of BVs and nerves
what type of function is sperm production
endocrine
neurotransmitter in penis
Ach
sympathetic in penis
NorEpi
gonadotropins fxn for testes
maintain size and function
8 impt androgen actions
1. development of male reproductive tract in utero
2. modulation of spermatogensis
3. growth and differentiation of accessory organs
4. expression of secondary sex characteristics
5. protein anabolism and bone growth
6. sex drive and aggressive behavior
7. erythropoiesis
8. increase BMR
how viagra works
inhibits breakdown of cGMP
-levels don't go down and you get erect
how you can be impotent
1. neurogenic
2. endocrinologic
3. psychogenic
4. vasculogenic
5. drug induced
6. misc
cardiovasc and resp changes in the mother
1. increased plasma vol
2. increased RBC vol
3. increased CO
4. decreased or unchanged BP
5. activation of renin-angiotensin system
6. increased minute volume
non specific defenses
1. physical barriers
2. phagocytes and NKC's
3. interferons
4. inflammation
5. complement proteins
6. fever
causes of sperm damage
1. radiation
2. motility defects
3. acrosomal defects
4. genetic defects
5. envt toxins
6. hyperthermia
how many oogonia in utero by 20-24 wks
7 million
how many primary oocytes at birth
1-2 million
how many oocytes by puberty
400,000
after puberty how many oocytes may be ovulated
500
attrition ultimately leads to
menopause
steps after in utero for oogonia to oocytes
transform into primary oocytes and attrition
-enter first meiotic division and arrest in prophase
primordial follicles, inactive
in cortex
-single layer of squamous cells surround primary oocyte
primary follicles (developing)
each menstrual cycle
-some primordial follicles begin to develop with squamous cells transforming into a cuboidal appearance and eventually forming granulosa cells
-primary oocyte completes its first meiotic division
secondary follicles, developing
6-12 layers
oocyte eccentric
paused in metaphase of second meiotic division
remains until fertilized
graafian follicle,mature
pedestal begins to soften and to form granulos acells that adhere to the oocyte and will be attached to it following ovulation
1st half of ovarian cycle
follicular phase...estrogen
2nd half of menstrual/ovary
luteal, progesterone
hypothalamo-pituitary axiss
-cyclic and pulsatile nature of hormone secretion
-mechanism for encoding/effecting
ovarian phases
1. follicular
2. ovulatory
3. luteal
uterine phases
1. menstrual
2. proliferative
3. secretory
what is the LH surge triggered by
high estrogen levels
the LH surge triggers
ovulation
what type of mechanism is the LH surge
positive feedback
importance of estrogen derived from dominant follicle
1. inhibit growth of cohort follicles
2. prime GnRH action on LH secretion to evoke ovulatory surge
3. prepare endometrium for progesterone to evoke secretory response
4. affect fallopian tube to favor transport of ovum and zygote
5. alter cervical mucus to enhance sperm transport
theca cells fxn
synthesisze androgens, influenced by LH and convert to estrogen, influenced by FSH (granulosa cells)
midcyle LH surge is released how and does what
in pulses, not steady pattern
-promotes ovulation
high levels of estrogen from almost mature ovarian follices does what
stimulates release of GnRH
how can you determine ovulation
elevation of body temp after
endometrial changes during uterine cycle
1. destruction of fxnal zone
2. repair and regeneration of functional zone
3. secretion of endometrial glands
1st half of cycle under influence of? describe endometrium
egg
endometrium
clear mucus
2nd half of cycle under influence of? describe endometrium
progesterone
-corpus
-thick mucus
-thick endometrium
what forms during menstruation
corpus albicans
8 impt actions of estrogen
1. stimuation of growth of ovaries and follicles
2. maintenance of smooth muscle and epithelium
3. growth of external genitalia
4. growth of breasts
5. development of female appearance
6. stimulation of watery sebaceious gland secretions
7. retention of fluid
8. closure of epiphyses of bone
what are the two types of receptors for estrogen? what do they do?>
alpha and beta
do diff things, similar
7 impt actions of progesterone
1. stimulation of secretions by endometrial glands
2. induction of thick, sticky cervical secretions
3. stimulation of myometrial growth (pregnancy)
4. decrease in motillity of uterine smooth muscle
5. stimulation of breast growth
6. inhibition of prolactin effects during pregnancy
7. feedback effects on hypothalamus and pituitary
common reproductive disorders
1. PMS
2. amenorrhea
3. endometriosis...grow into fallop tube
4. benign tumors
5. PID
phases of human sexual response
1. desire
2. excitement
3. plateau
4. orgasmic
5. resolution
steps in human fertilization
1. gametogenesis
2. sperm and oocyte transport through the reproductive tract
3. sperm capacitation
4. sperm penetration through the cumulus
5. acrosome rxn, zona binding
6. penetration of teh zona
7. sperm-oocyte membrane fusion
8. cortical + zona rxns
9. pronucleu formation/polar body formation
oocyte enters fallopian tube within
15 min of ovulation
fimbria fxn
find oocyte-granulosa complex adherent to ovarian surface
what is not required for fertilization
fallopian tube, can take egg out w/o ever entering tube
sperm ascend into what
mucous microstructure
sperm are found in tube within
5 minutes
non-capacitated sperm stored where?
cervical crypts
fertilizable lifespan for sperm
80 hours
what starts the sperm transport in teh female reprod tract
capacitation
sperm capacitation definition
-ability to undergo acrosome rxn
-ability to bind the zona pellucida
-hypermotility
what allows egg penetration
removal of lipids from teh sperm head
with capacitation what happens to teh sperm membrane
less stable
what does the sperm lose with capacitation
epididymally derived coating factors
what can sperm respond to with capacitation
to oocyte chemotactic factors
with capacitation the sperms lifespan...
finite and shortened
zona pellucida contains
3 glycoproteins in a porous 3D matrix
name the 3 layers of the zona pellucida and what they do
1. ZP-1: structural
2. ZP-2: sperm binding, block to polysperma
3. ZP-3: sperm binding
what allow receptor binding and activation or inactivation
SERM's and naturally occuring estrogen
3 hours after fertilization
meiosis II completed-second polar body
10 hrs after fertilization
protein synthesis begin
maternal legacy
maternal mRNA involved in early embryo protein synthesis
acrosome rxn
once one get in all others are blocked
-it releases something and the granules fuse around zone of pellucida and make the 3 pro's crosslink and form hard shell
morula
solid balls of cells
fertilization goes to...what implants in the wall
blasocyst
parts of the blastocyst
trophoblast
inner cell mass
blastocoele
zona pellucida
chorionic plate
top of placenta
basoplate
bottom of placenta
chorionic plate contains
fetal villi
basal plate contains
maternal vessels
placenta exchange
o2 from mom co2 from fetus
water, e from mom, water,urea fetus
-CHO, lipids, etc fetus waste
-hormones, antibodides drugs, viruses from mom
-hormones from fetus
placenta as an endocrine organ
1. hCG
2. estrogen
3. progesterone
4. hPL
5. prolactin
6. relaxin
luteoplacental shift
CL to placenta
3 stages of labor
1. longest: most painful
2. expulsion: uterus contracts
3. placenta expulsion
milk's immunobeneficial effects
1. immunoglobulins
2. antibacterial/antiviral factors
3. cytokines
4. immune cells
benefits of breast feeding to infant
1. immunologic
2. better GI health
3. reduced incidence of diabetes and obesity later
4. reduced incidence of SIDS
5. possible cognitive benefits
breast feeding benefits to mothers
1. promotes uterine involution
2. reduces risk of postpartum hemorrhage
3. lowers risk of ovarian and breast cancer
4. facilitates earlier return to pre-preg weight
5. may decrease risk of postmenopausal osteoporosis
6. bondign with infant
where is oxytocin produced
post pit
oxytocin binds to
a G-protein coupled receptor
oxytocin mediates
milk letdown reflex
oxytocin stimulats
uterine contraction
what plays a role in mother/infant bonding
oxytocin
where in the body do we fight against disease
body surfaces
loose CT's
unique organs and structures...lymphatic system
tiniest of white blood cells
lymphocyte
where are b lympocytes formed
bone marrow
where do t lymphocytes mature
thymus
lymph vessels do what to cardiovasc system
return ECF
lymphatic caps can open and permit uptake of
large pros
cell debris
pathogens...cancer cells
lymph caps fxn
carry lymph into larger lymphatic vessels and eventually back ot blood...passes through nodes on the way
where are lymph nodes
along lymphatic vessels
largest colelctions of lymph nodes are where
1. groin
2. armpit
3. neck
does all lymph pass through at least one node before returning to blood
yes
explain flow in lymph nodes
1 way
-lymph passes over cells and remoes things, immune system cells activated and lymph is collected back into lympatic vessel at other side
hwo to test for metastatic cancer
remove lymph nodes
downside to removing nodes
edema
what is used to spare lymph nodes
sentinel lymph node biopsy
-eject dye into region
tonsils are
swelling sof the lining of the throat that contain lymphatic tissue
how tonsils get inflamed
bacteria gets in crypts
lymphatic nodules aka? fxn?where?
protect!
MALT cells
-under epithelial surfaces, GI and respiratory
spleen job
filter blood
arteries of spleen fxn
branch out through the spleen, discharge blood at sinusoidal caps
loose meshwork w/ macrophages of sleep fxn
pick out worm RBC's and collections of lymphocytes to detect pathogens
blood in spleen fxn
collected back into venules and returned to circulation
damage to teh spleen can cause
internal bleeding
what protects spleen
rib cage
how are body defenses classified
specific or non-specific
non specific defenses do what
respond regardless of the type of invading agent
specific defenses
protect against particular invading agents
-provide immunity
-have a memory
non specific defenses ex
phys barriers
phagocytes
interferons
inflammation
complement proteins
fever
first line of defense
physical barriers
pathogens must do what to penetrate body tissues
must cross an epithelium
epidermis
expose surface
strat squam epi
dermis
mixed loose and dense CT with BV's, glands, nerves, hairs
hypodermis
CT with variable amts of fat
epidermis layer is hard to..
live on and invade
what are often secreted onto exposed epithelial surfaces
protective fluids
-acidic pH
what impedes movement of pathogens in the body
one way movement of secretions
moving aroudn in what skin layer is easy
dermis
loose CT under epi...what happens why?
lots of space between cells, BV's
-infections spread easily
-internal defenses take action
most internal defenses relate to
BV's in CT
-wbc
blood pro
chemical signals released in damaged tissue trigger
vascular responses
how phagocytes get to site of injury or infection
diapedesis
chemotaxis
chemotaxis
chemicals released to signal and slow down neutrophils to sit next to endo
phagocytes are relased when and how
on demand out of bloodstream
neutrophils
first line of defense, most abundant wbc
eosinophils
involved in allergic rxns and parasitic infections
types of phagocytes
1. neutrophils
2. macrophages
3. eosinophils
special class of lymphocytes
nat kill cells
immunological surveillance
process by which NKCs look for foreign material
-adhere to target cell and release perforins onto target
perforin proteins fxn
create holes in target cell, cause it to rupture
interferons
some celsl release chem signals to other cells telling them to build up their defenses
-viruses may infect adjacent cell but might not replicate
-slows spread of infection
how do some interferons work
as hormones
mast cells release
histamine
mast cells effect is
local
inflammation big 4
1. local swelling
2. redness
3. heat
4. pain
complement protein system
attacks and breaks down cell walls
-attracts phagocytes, activated by pathogen
-stimulates inflammation
complement proteins,s ome bind to pathogen membrane and?
create pores to rupture cell
-enhance histamine release...enhance inflammatory response
fever
mobilizes defenses
accelerates repairs
inhibits pathogens
fever defined
maintained body temp about 99F
fever rises bc of pyrogens, what are they
pathogens, toxins, wbc's etc
-circ in blood, stimulate temp-reg center in hypothalamus
fever increases?
rate of metab, faster recovery
nonspecific bc
each process works no matter what the prob is
specific resistance
protection against particular threat
what provide resistance against specific viral and bacterial infections...IMMUNITy
B and T lymphocytes
antigens
any factors capable of stimulating an immune response, part of surface pro a lot
b and t with immunity job
look for specific antigens, ignore your own self antigens
-responsible for immunity
self antigens
marker proteins on your normal body cells
non self
pathogens have markers that say this
when pathogens are recognized by phaogcytes...
engulf and digest pathogen
when pathogens are recognized by t and b lymphocytres
immune response
maturation of b and t involved
leaning of self from non self
immunity
coordinated attack of b and t against specific antigen
4 characteristics of immunity
1. specific: each T or B cell has receptors for only ONE antigen
2. versatile: millions of diff popn's of lymphocytes in body, prepared to find antigens
3. tolerance: lymphocytes will ignore normal tissues and recognize only foreign
4. memory: lymphocytes will remember antigens they have found, and will be able to attack more quickly next time
how would the rest of the body know about phagocytes invasion
t lymphocytes recognize display
cell-mediated immunity
-display pieces of digested pathogens on their cell surface
helper t cells
use chemical signals to activate other T cells and B cells
cytotoxic t cells
can directly attack and kill cells displaying antigens
both classes of t cells produce
clones including memory t cells
how do b cells resond to antigens
antigen binds to receptor
2. activation of b cell
3. cell division
4. differentiation into plasma cells
5. plasma cells produce antibodies
b cells that find their antigen become
plasma cells that produce antiboides-immunoglobulins
plasma cells produce how many anitbodies per second
2000
antibodies are like floating receptors, how?
bind to antigens
-flag them for phags to destroy
-antigens stick together
-turn on nonsepcific resistance partners
-body mobilizes quickly
what cells are responsible for humoral immunity
b cells, (antibody-mediated)
2 ways to gain immunity
naturally and artificially
2 natural immunity ways
active, infection
passive-mom etc
2 artifically immunity ways
active-vaccine
passive-injection of immune serum
HIV virus does what
destroys t helper cells, shuts down immune system
autoimmune diseases
immuen cells fail to recognize self antigens and attack the body's own cells
atherosclerosis is what type of disease
inflammatory
3 steps of athero
1. high levels of LDL lead to accum of LDL in tun int
2. chem fxn of LDL in int leads to lympocyte and monocyte attraction from blood, LDL=foreign
3. chemicals relased from lymphocytes and macros induce inflamm, causes thickening of wall
result of athero
narrowing of opening
-calcification over time, increased workload for heart