Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
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 |