embryology-final-review

Start Studying!

Terms

undefined, object

copy deck

theca produces what/why?: androgen- substrate for granulosa-prod. estrogen
ovulation releases from ovary?: 2ndary oocy. w/ 1st polar body, zona pell., corona rad.
cumulus oophorus becomes?: corona radiata
sperm binds with egg how? species-specific: sperm cell zona binding sites w/ ZP3 zona sperm receptor on oocyte
sperm-oocyte membrane binders?: integrin receptor on oocyte
what occurs during the 2nd week following fertilization?: embryo implants. amniotic cavity/primitive yolk sac form
trophoblast produces what 5 days after fertilization?: enzymes: disrupt zona pellucida Â– causes hatching
after hatching?: trophoblast can make contact with endometrium.
What is hCG? (basis for pregnancy test): Human Chorionic Gonadotropin: essential hormone for pregnancy: maintains proliferation of corpus luteum, secretes hormones - keeps uterine lining:receptive state
inner cell mass during process of implantation?: two layered structure:bilaminar embryonic disc Â– hypoblast facing the blastocyst cavity Â– becomes yolk sac w/in cytotrophoblast . inner cell mass cavitiesÂ‡ form amniotic cavity: floor is single cell layer: epiblast.
main developmental task during the third week?: gastrulation Â– third tissue layer appears
primitive streak forms when?: 13 Â– 14 days after fertilization until 5th week
primitive streak later in gastrulation?: becomes smaller, more caudal as embryo grows. disappears in 5th week from sacrococcygeal trunk
ectoderm contribute to?: nervous system, epidermis body surface tissues (epidermis, hair, nails), glands connected by ducts to body surface (sweat glands, sebaceous glands)
timing of closure of anterior and posterior neuropores?: 23 days +/-
endoderm form: lining of the GI tract, ducts that open to tract, and secretory cells (parenchyma) and glands
causes embryo to fold during 4th week of development?: different rates in the growth of tissue neurotube/notoch
when are most structures complete?: end of 8th week after fertilization
gonadal factors which may cause infertility?: sex chromosomes aneuploidy; space occupying lesions Â– cysts, tumours, scars; environmental agents Â– lead, alcohol, nicotine; testicular dysfunction
Kleinfelters karyotype: 47XXY (male with extra X chromosome)
Kleinfelters: have breasts, small testes, no spermatogenesis
Turners Syndrome karyotype: 45X0 Â– most donÂ’t survive.female, req. hormone repl.
post gonadal factors may include?: obstruction of accessory reproductive ducts
what % of female infertility due to obstruction?: 50%
tightly structured mucin glycoprotein cervical mucous: type GÂ– may be barrier to microorganisms and sperm
loosely structured mucous: Type EÂ– sperm can get through-in cervix: periovulatory
what causes Type G Â– E mucous change: rising estrogen levels in periovulatory period
woman/men developing antibodies to sperm cells: isoimmunity (woman) autoimmunity (man)
placenta: apposition of fetal and parental tissues for purposes of physiological exchange and hormonal production
main components that form placenta?: syncytiotrophoblast/cytotrophoblast (forms villous chorion)-disappears 4th month
layers of placental Â“barrierÂ”: maternal blood, syncytiotrophoblast, cytotropoblast, extracellular space, endothelium of fetal blood vessels, fetal blood
before placenta formation Â– fetus survives how?: uterine secretions from uterine glands Â– until day 13
chorion/chorionic sac def.: extra-embryonic mesoderm + two layers of trophoblast
contained within the chorion?: embryo/amniotic+yolk sacs susp. via conn. stalk in chorionic cavity
only single artery in placenta - % and type of problems: 16%premature, 17%abnormal, 34% small baby
what might cause cessation of pregnancies?: combinations & unknowns 60 Â– 70% chromosome abnormality/mutation 25%, radiation 1%, infections 2 Â– 3%, drugs and chemicals 4 Â– 5%,
60 Â– 70% of early abortions due to: chromosomal disorders: trisomy 50%, polyploidy 25%, 45 + X 25%
terathanasia: monster death: tera= monster, thanatos=death
Of spina bifida cases, what % dies?: 90%
Retinoids cause defects of: CNS, face, ears, heart, kindey, esophagus, thymus. Cause spontaneous abortions.
Cardiovascular system derived mainly from: splanchnic mesoderm (forms primordium of heart), paraxial and lateral mesoderm midway along hindbrain, & neural crest cells from between otic vessicles (primitive ears) and 3rd pair of somites
in the primitive heart, future site of Semilunar valves?: bulbo-truncal junction
what does the right vitelline vein become: inferior vena cava
how does left atrium form: first sign of left atrium: primary pulmonary vein FROM LEFT ATRIUM (Not SV). grows toward/ Â‘cannibalizesÂ’ pulmonary vein walls, absorbing them to create its walls
divides the truncus into the aorta & pulm. trunk: aorticopulmonary septum: (truncal bulbar cushions)
fallotÂ’s teratology?: pulmonary stenosis, overriding aorta (destropositioning) interventricular communication, hypertrophy of R ventricle
cyanosis: venous blood in systemic system
lung formed by: endoderm and mesoderm. endoderm=lung epithelium. splanchnic mesoderm:cartilage, musc., blood vess
two types of fistula in lung development: tracheoesophageal fistula, and esophageal atresia
stimuli for breathing at birth: temp., pain, hypoxia Â– chg in chemoreceptor sensitivity
hyaline membrane disease also known as: respiratory distress syndrome Â– not enough surfactant
connects only foregut to anterior body wall: ventral mesentery
primitive gut lined with, and supported by Â– tissues?: lined with endoderm, supp. by splanchnic mesoderm
endoderm forms what in GI tract: tissue lining GI tract and its outgrowths (including lungs, airways) and parenchyma
if laryngotracheal diverticulum forms incorrectly, result?: fistula (causes polyhydramnios)
stomach rot. 90 deg. clockwise around long.axis when: during 7th week
in umbilicus, which direction does the herniation of the midgut loop rotate?: counterclockwise
what does the final rotation accomplish?: duodenal-jejunal junction to adult location
failure of midgut to return to gut Â– name?: omphalocele Â– intestines within umbilical cord
tear of abdominal wall near umbilicus: gastroschisis Â– tissue becomes rigid and brittle Â– amniotic fluid bad for tissue
divides cloacal membrane into urogenital and anal membranes?: urorectal septum
if anal membrane doesnÂ’t break down Â– condition?: congenital membranous atresia
if urorectal septum fuses with posterior cloaca rather than cloacal membrane Â– result?: complete anal atresia: VERY difficult to correct (no anal opening, no sphincters, etc.)
if incomplete fusion of urorectal septum and cloacal membrane Â– result?: because urorectal septum is bifid, incomplete fusion can mean fistulas connect urogenital and rectoanal organs
tissue type: liver and gallbladder: outgrowth of endoderm near distal foregut
what does ventral pancreatic bud become?: uncinate process with MAIN pancreatic duct
embryonic tissue becomes: diaphragm central tendon?: cranial part of septum transversum
rest of diaphragm: from dorsal mesentery assoc. w/ esophagus + projections of tissue: pleuroperitoneal folds from body wall
pancreatic cause of obstruction: annular pancreas: ring of pancreatic tissue, surrounds duodenum like a collar
if bowel becomes twisted: congenital volvulus: can block both lumen and blood supply Â– can become gangrenous
condition where bowel telescopes on itself: intussusception
condition where anus is stenosed by incorrect chamber division: imperforate anus
intestine of newborn contains: meconium: secretions, cells, detritis swallowed with amniotic fluid
why might intestinal contents not pass? suspect what?: if too viscous (too much mucous) meconium wonÂ’t pass. common in kids with cystic fibrosus
kidney development: 3 stage, with which structure: nephrogenic cords of intermediate mesoderm from cervical Â– sacral segments
1st stage kidney development begins when: 3rd week
stage name, & what develops: proenephric phase Â– proenephric vessicles near cervical segments form proenephric duct into cloaca
during 4th week, what happens to duct?: proenephros and cervical proenephric duct degenerate
second phase of kidney development: mesonephric Â– remaining proenephric duct now called mesonephric, is opposite thoracic/lumbar segment
what develops in second stage: mesonephric tubules, which open into mesonephric duct
what do remnants of the second stage contribute to: male reproductive system
where and when does third stage develop: beginning in 5th week, at caudal mesonephric duct with appearance of ureteric bud
ureteric bud becomes: ureter, renal pelvis, calyces, collecting ducts/tubules
metenephric mass becomes what: glomerulus, nephrons (creating urine)
metanephric mass forms what around ureteric bud: metanephric mass forms condensation of masses of mesoderm cells around branches of the ureteric bud, called a TISSUE CAP
tissue cap forms what: metanephric vessicles: twist and elongate
twisting, elongation of tissue cap forms: loop of henle, convoluted tubules
if metanephric mass doesnÂ’t link up with collecting syst?: will make urine, but nowhere for it to go: kidney cyst
recessive polycystic kidney disease: autosomal recessive, effects both kidneys, massive kidneys, filled with vessicles:take up normal healthy tissue space. collecting tubules are widely dilated. Children usually die. treatment: dialysis or transplant.
ureteric bud triggers?: sends out survival signals to metanephric mesoderm mass so that kidney tubules and tissue cap survive, nephrons form (condensation of metanephric mass, and tubologenesis)
nephrons form but donÂ’t join ureteric bud branches Â– result?: nephrons canÂ’t drain, may form cysts
if nephrogenic cords fuse, results?: kidneys will fuse, probably wonÂ’t be able to ascent
name four abnormalities that ureteric bud-metanephric mass interaction difficulties may cause: bifid ureter, supernumary kidneys, crossed renal ectopia, renal agenesis
causes of oligohydramnios: bilateral polycystic kidney disease, bilateral renal agenesis, premature rupture of amniotic membrane (leakage of fluid), posterior urethral valve (remnant of urogenital membrane) Â–causes blockage
which ducts and tubes join the urogenital sinus: ureters, and mesonephric ducts (common excretory ducts)
allantois forms?: uracus (when involutes) umbilicus-bladder remnant
uracus forms?: fibrous median umbilical ligament
problem with bladder development: extrophy Â– mesoderm doesnÂ’t separate bladder from sinus, body wall tears, or ureter opens to body surface: result is similar Â– bladder open to body wall
phenotypic sex is what?: structural gender. develops over first 3 months
genital ridge tissue structure: intermediate mesoderm core, with covering of epithelial lining of body cavity (coelom)
what are sex cords?: cord-like extensions of coelomic epithelium penetrating mesoderm of genital ridge
what is between the sex cords?: intermediate mesoderm
stimulates further development of gonad?: epiblast primordial germ cells appear near origin of allantois, migrate to genital ridges, arrive and enter sex cords -appear at 4th week, arrive at 6th week
if no Y chromosome, what happens to sex cords?: begin to fragment
what do germ cells become if no Y chromosome: oogonia (primary oocytes)
what do sex cord cells become if no Y chromosome: follicular cells around oocytes
If Y chromosome (and SRY gene) germ cells become: spermatogonia
if Y chromosome, sex cords do what?: elongate to form seminiferous tubules
if Y chromosome, sex cord cells become: sertoli cells - secrete antimuellerian hormone
if Y chromosome, what do intermediate mesoderm cells between the sex cords of genital ridge become?: Leydig cells, which secrete testosterone
describe the 2nd phase of test. descent: trans-inguinal: during 7th month, happens over two days, active process
where are ductus and testicular vessels after descent: within spermatic cord
gubernaculum between ovary and uterus becomes: ligament of the ovary
gubernaculum between uterus- labium majus becomes: round ligament of the uterus
mass of endoderm created between urogenital sinus and uterovaginal primordium called: vaginal plate or sinovaginal bulb
If testicle present, what is induced?: antimuellerian from sertoli cells induces paramesonephric ducts and uterovaginal primordium to undergo regression
after regression, remnants of uterovaginal primordium?: prostatic utricle and appendix of testes
androgens from leydig cells diffuse into adjacent tissues, inducing what three processes?: mesonephric excretory tubules link with rete testes, forming efferent ductules, mesonephric duct develops into epididymis, vas deferens and ejaculatory duct, and seminal vessicles grow out of mesonephric ducts
If no testicle present, paramesonephric ducts become: uterine tubes
If no testicle, uterovaginal primordium develops into: uterus
if no testosterone present (i.e. no testicle) mesonephric ducts: regress and degenerate
mesonephric duct remnants are called: epoophoron and paroopharon in broad ligament, gartners cyst near uterus
vagina develops from what two structures: uterovaginal primordium, plus endoderm of urogenital sinus area called vaginal plate
condition if hymen not perforated?: hydrocolpos
problems caused if hymen not perforated: fills with fluid, compresses urethra, urine backs up, can cause hydronephrosis
how is fissure created on ventral surface of glans: ingrowth of epithelium(ectoderm) forms glandular plate, which breaks down, creating the fissure
direction of fusion of male urethral folds, and result: posteriorÂ– anterior bringing urethral meatus out to glans
condition where body canÂ’t create cortisol: congenital virulizing adrenal hyperplasia :genotypic females, phenotypic males: no breasts, small penis, chest hair, male pattern baldness XX (female) masculinizes due to androgen
gonadal dysgenesis: 46XX or 46 XY Â– usually only streak ovary, with uterus/uterine tubes. No testicle, leydig/testosterone, no male duct development: remain pre-pubertal female, with no functioning gonad
Androgen resistance syndrome (or androgen insensitivity syndrome): canÂ’t take up androgens, so no masculinizing takes place. Genetically male 46XY, but otherwise female: external genitalia, short vagina to nowhere, no pubic or axillary hair, ample breasts. no male ducts, no descent of testes.
what is a somite: visibly segmented mesoderm
skull and facial bones derived from: neural crest cells: ectoderm from area (more headwards than somites)
vault of skull created from: unsegmented mesoderm
bifid abnormality of notochord means: two brains, two faces
portion of somite which forms bones Â– which bones?: ventromedial somite: sclerotome: ribs and vertebrae
face created from: brain (neuroectoderm), neural crest cells + mesoderm
mesoderm (neural crest cells) forms which part of face: facial bones Â– proliferate & migrate -> face bones
placode: ectodermal thickenings: naso, optic, otic
forms sides of roof of mouth: secondary palatal shelves
Cyclops: holoprosencephaly, non-hemispheric brain, nose in forehead(or absent), 1 eye, upper lip=maxillary processes (no nasal tissue), no incisor teeth, canines in midline Â– mentally retarded
median cleft face syndrome: hyperteloric, mentally normal, variety: facial abnorm.
cleft lip causes: genetic + environmental (pollution?): MUTATION
cleft lip may or may not occur with: cleft palate
Treacher Collins syndrome:: Autosomal dominant with mutations (GENETIC) small mandible/maxillae, cleft palate, no zygomas, anti-mongoloid eyeslant, no lower eyelashes, notched lid, DEAF: abnormal incus/malleus, malformed ears, NORMAL MENTALLY
Lateral facial displasia: due to bleeding in utero: toxic. Normal mentally, asymmetry Â– can involve all structures
endocrine glands (3): thyroid, parathyroid, pituitary
thyroid derivation: endoderm of tongue
thyroid created from: foramen cecum tunnel at back of tongue Â– buds off, foramen atrophies, becomes fibrous
hormones of thyroid produced by: endodermal cells
thyroid has components of what germ layers: all Â– neural crest which migrate to thyroid, vessels from mesoderm, epithelial layer
thyroid cells produce: calcitonin
thyrotoxicosis: HUNGRY, anxious, panicky Â– high heart rate, heart may fail: beats too fast to fill, staring bulging eyes, jumpy fast metabolic rate
Thyroid deficiency: Myxedema in adults, cretinism in children: mentally retarded dwarfs, sleep a lot, donÂ’t want to eat, tongue hangs out, if neo-natal, MUST give thyroid hormone, or will have developmental problems
if too much parathyroid, condition?: hyperparathyroidism: high calcium level in blood, stones in urinary tract, less calcium in bones = fractures, paranoia: stones bones moans groans
parathyroid glands develop where: pouches 3 & 4
anterior pituitary origin: stomadeal placode Â–> rathkes pouch -> anterior pit.
posterior pituitary origin: downgrowth of diencephalons infundibulum Â– posterior pituitary + stalk
anterior pituitary produces: hGH
Posterior pituitary produces: antidieuretic hormone
Anterior pituitary stalk connection: blood vessels
Posterior pituitary stalk connection: nerves
benign tumour of Rathkes pouch -where ant. pit. devel: Craniopharyngioma
rathkes pouch tumour will effect: hormone & cranial nerve problems, esp. CNII, compressed by tumour growth
craniopharyngeoma symptoms: bitemporal hemianopia (canÂ’t see out to sides or may go blind if enough nerves damaged) hormonal problems (kids with pubic hair, breasts, pigmented nipples, that are also BLIND) SURGICAL TRTMNT.

Start Studying!

Deck Info

Number of cards 164