Exam 2: Endocrine & Reproductive Flashcards
What are types of muscle are there and characteristics
Cardiac - striated, involuntary
Skeletal - striated, voluntary, hundred of nuclei
Smooth - involuntary
Explain the properties of muscles
Contractility: ability to generate force by contracting
Excitability: ability to respond to a stimulus
Extensibility: Stretch beyond resting length without being damaged
Elasticity: ability to return to resting length after being stretched
Function of skeletal muscle
Primary: generate force through locomotion
Secondary: maintain posture, stabilize joints, generate heat
Skeletal muscles attach to bone via tendons
Muscle tension on tendon causes joint movement
Primary function of cardiac muscle
generate force and blood flow
Primary function of smooth muscle
generate force as in move substance within the body (blood, urine, food)
what is origin in skeletal muscle
Origin: remains immobile during the action of the
muscle; more proximal/closer to midline of the body
what is insertion in skeletal muscle
the place on the bone
that moves during the action of the muscle; more distal/further to midline of the body
Function of agonist and antagonist muscle
Agonist: prime mover of the action
Antagonist: act on the same joint to produce opposite actions
Structural organization of the muscle (muscle fiber to tendon)
Explain parallel fascicles
Involved in range of motion
arranged in the same direction as the long axis of the muscle
Explain pennate fascicles
Involved in power
Can fit more muscle fibers in the space
Type of fascicles
Explain a muscle cell and the structure
Known as a myofiber
Striated appearance, multi-nucleated
Explain the sarcomere
Function unit of muscle contraction
I band: thin filament
A band: thick filament
Explain contraction in terms of the sarcomere shortening
Thin filaments slide between thick filaments
Distance between z discs shorten and they get closer together
I-bands (actin only) shorten
H-bands (myosin only shorten)
A bands (actin/myosin overlap) do NOT shorten
Explain the sliding mechanism/sliding filament mechanism
Sliding is the contraction of muscle
Explain the biochemistry of contraction
How cross bridge cycling is regulated
Tropomyosin
- Lies in groove along actin filament
- blocks actin active site during relaxation
Troponin
- Attached to tropomyosin
- Ca2+ binding alters troponin configuration
- displaces tropomyosin
- exposes actin active site
- allows crossbridge attachment
Concept of a motor unit
Motor unit: each motor neuron plus the muscle fibers it innervates
each axon branches to innervate multiple fibers
each muscle fiber receives a single axon terminal from its motor neuron
Characteristic:
- all-or-none meaning when a neuron is activated, all fibers it innervates depolarize
- innervation ration is ration of motor neuron : muscle fibers
- muscle fibers are spread throughout the muscle
- fibers of a motor unit are all the same fiber-type
The steps in excitation-contraction coupling
different types of muscle contraction
Twitch:
- muscle stimulated by a single AP
- quickly contracts and relaxes
Tetanus:
- muscle stimulated repetitively
- relaxation incomplete between APs
- force exceeds twitch force (temporal summation)
- tetanic force increases with AP frequency
Summation:
- accumulating contractile force resulting from sequential activations
explain muscle relaxation
APs must stop
Ach-esterase degrades Ach
Ca2+ release channels close
Ca2+ pumped back into sarcoplasmic reticulum
through Ca2+ATPase pump
Describe length-tension relationship
Difference between isometric and isotonic muscle contractions
Isometric:
- muscle length remains constant
- the load is greater than the force of contraction (i.e. if person is not moving)
Concentric:
- active shortening
- muscle shortens with contraction
- force of contraction exceeds the load (i.e. bicep curling a 5lb dumbell)
Eccentric:
- active lengthening
- muscle lengthens with contraction
- load may exceed force of contraction
Different energy systems used to generate ATP
Phosphagen:
- resynthesizes ATP (fastest)
- sprinter (8-10 seconds)
Glycolytic (fast):
- swimmer (1.3-1.6 minutes)
Aerobic:
- lower intensity but much longer
- marathon runner
Describe force-velocity curve
Explain the phosphogenic system
Explain the glycolytic system
Explain the aerobic metablosim
Mitochondria converts glucose and fats to ATP
Consumes O2
By-product of aerobic metabolism is CO2, H2O and heat
Produces more energy (ATP) but at a slower rate
Slow twitch fibers (type I)
Fibers have red appearance
Many capillaries, much myoglobin (carries oxygen)
Many mitochondria (aerobic)
High oxidative capacity
Resistance to fatigue
Common in endurance muscles
Fast twitch fibers (type 2a)
Fast contraction
Highly aerobic (many mitochondria)
fatigue resistance
Fast twitch fibers (type 2x)
Fibers have a white appearance
anaerobic adaption
large stores of glycogen
Few capillaries, mitochondria
Adapted for sprint tasks
Fiber type characteristics
Muscle stem cells and function
Satellite cell: skeletal muscle stem cell
Cell has potential for:
- self-renew
- differentiate (become) a mature cell
Types:
- totipotent (whole organism; extra-embryonic)
- pluripotent (all cells of the body)
- multipotent (tissue restricted)
Duchenne muscular dystrophy
Most common form of muscular dystrophy
Recessive, X-linked (primarily affects boys)
Mutation in the dystrophin gene
Dystrophin: provides structural stability to cell membrane
Symptoms:
- first appear between ages of 2-3 years old
- progressive proximal muscle weakness of legs and pelvis associated with muscle mass loss
- Pseudo-hypertrophy (calf and deltoid muscles)
- muscle replaced by fat fibrotic tissue
- paralysis (life expectancy is about 30 yrs old)
Differences between skeletal and cardiac muscles
Cardiac:
- myocardial cells bifurcated
- cell joined by gap junctions
- AP spreads among cells via gap junction
- cells behave as one unit (syncitium)
- sarcomeres contain actin and myosin
- contract via sliding filament
activated by calcium transient
Smooth:
- no sarcomeres
- higher actin:myosin ration (16:1)
- actin filaments attached to dense bodies
Regulation of smooth muscle contraction
Stimulated by rise in intracellular Ca2+
Ca2+ binds calmodulin
Ca2+-calmodulin complex activates myosin light chain kinase
Myosin heads are phosphorylated
Myosin heads bind actin
Relaxation when Ca2+ decreases
Explain skeletal muscle repair (regeneration)
The endocrine glands
- pancreas
- hypothalamic-pituitary
- thyroid-parathyroids
- adrenals
- male gonads (testes)
- female gonads (ovaries)
Explain how the endocrine system controls bodily functions: comparison to the nervous system
Nervous system:
- point to point
- min to min
- rapid but short lived controls using neurotransmitters
Endocrine system:
broadcasting (blood reaches every corner of the body) and slow but sustained control using hormones
Members, and their synthesis, storage, and secretion of hydrophilic hormones (peptides and amines)
Polar hormones
They are stored in secretory vesicles and released only after the cell is stimulated
Almost all of hydrophilic hormones travel free of proteins in plasma
Bind and activate their specific trans-membrane (integral) receptor protein
Catecholamine hormones:
- secreted by sympathetic neurons and adrenal medulla (DA, NE, and Epi)
- synthesized via enzymatic reactions, from amino acid tyrosine
- tyrosine -> DOPA -> DA -> NE -> Epi
- tyrosine hydroxylase (rate limiting protein)
- bind to G protein couple receptor then activates adenylyl cyclase then more 2nd messengers activate cAMP
Peptide/protein hormones
- insulin and prolactin
- chains of amino acids
- stored in secretory vesicles and secreted in response to stimuli
- specific trans-membrane receptors (GPCR, TKR, JAK) and evoke rapid response
Members, and their synthesis, storage, and secretion of hydrophobic hormones (thyroid hormones, steroid hormones, vitamin D)
Non-polar hormones
Thyroid hormones:
- synthesis involves enzymatic incorporation of iodide onto tyrosine
- not stored- made on demand
- bind intracellular receptors, ligand-induced transcription factors
- slow cellular response involving changes at transcription-translation
- metabolized for increased solubility and excreted
Steroid hormones
- secreted by adrenal glands, ovaries, and testes
- synthesis involves enzymatic reactions from cholesterol
- not stored- made on demand
- bind intracellular receptors, ligand-induced transcription factors
- slow cellular response involving changes at transcription-translation
- metabolized for increased solubility and excreted
Vitamin D:
- synthesis involves enzymatic activation to 1,25-dihydroxy-vitamin D
- not stored- made on demand
- bind intracellular receptors, ligand-induced transcription factors
- slow cellular response involving changes at transcription-translation
- metabolized for increased solubility and excreted
Describe what contributes to plasma concentration of a hormone
Metabolism & degradation
Binding to their receptors in target cells
Excretion by kidneys
Explain how hormones circulate in plasma: Free vs.
protein-bound
Free - these hormones freely float in the blood stream and they can bind to target cells to get a response; they can diffuse into the cells
Protein Bound - transport lipid soluble hormones through the blood
Explain how a target cell responds to hydrophilic and hydrophobic hormones: transmembrane vs. intracellular receptors
Hydrophilic - diffuse into cells and bind their specific intracellular receptor proteins and modulate the rate f transcription
Hydrophobic - bind and activate their specific intracellular receptor proteins and alter/change the rate of transcription of the target genes (these are slower acting hormones)
Compare and contrast the modes of cellular responsiveness: up- and down-regulation, sensitivity, synergism, and permissiveness
Max response: related to the number of functionality available receptors
- Up-regulation: can be caused by prolonged exposure to low levels of hormone
- Down-regulation: can be caused by prolonged exposure to high levels of hormones
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Sensitivity: [H] that elicits the half-maximal response… the sensitivity is linked to genetics, inhibitors, or activators - insensitivity: could be caused by the low number of the receptor or de-sensitized receptors -> requiring MORE [H] for the same response
- hypersensitivity: could be caused by the high number of the receptors or hyper-sensitized receptors -> requiring LESS [H] for the same response
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1) Permissiveness: hormone A cannot exert its full effects in the absence of hormone B (i.e. has no effect by itself)
2) Synergism: Hormones A and B individually exert effects
effects of together > effects of A + effects of B
3) Antagonism: A hormone opposes the effect of another
Describe hormones
Hormones - chemical messengers from DUCTLESS glands
Explain how peptide hormones bind their specific transmembrane receptors
Know the hormones in the hydrophilic and hydrophobic categories
What is a prohormone and what are they
Precursor to a hormone
1) Catecholamines: NE -> Epi
2) Peptide hormones: a polypeptide hormone (pro-insulin) -> a shorter hormone (insulin) + a copeptide (C-peptide)
3) Steroid hormones:
- testosterone -> estradiol
- testosterone -> 5-dihydrotestosterone
4) Thyroid hormone: thyroxine (T4) -> T3
5) 25-(OH)-Vitamin D -> 1,25-(OH)2-vitD
Explain pancreatic hormones and their functions during an absorptive phase
Absorptive phase (< 4 hrs: FED)
Low glucagon & elevated insulin, and insulin stimulates anabolism and inhibits catabolism
↑ glucose -> ↑ insulin & ↓ glucagon
Insulin promotes glucose consumption for energy by all cells
- energy storage in liver (glycogen), skeletal (glycogen & protein), fat tissue (TG/FAT)
Explain pancreatic hormones and functions during fasting state (post-absorptive)
Post-Absorptive phase (> 4 hrs: FASTING)
Low insulin: elevated glucagon
Mobilize the stored energy from liver, fat, and skeletal muscle
All cells must use energy substrates resulting from catabolism
Glucose for CNS cells: FFA and Ketones for non-CNS cells
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↓ glucose -> ↓ insulin & ↑ glucagon
Low insulin and high glucagon promote catabolism
Liver (glycogen -> glucose)
Skeletal (glycogen -> pyruvate/lactic acid & protein -> a.a. for long-term fasting)
Fat tissue (fat/TG -> glycerol & FFA)
Causes of diabetes (type I and type II), symptoms and treatments
Diabetes mellitus
- when glucose homeostasis is not maintained
- symptoms: polyphagia, polyuria, polydipsia (hunger, fatigue and weight loss)
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Type I
- insulin dependent diabetes mellitus due to insulin deficiency (beta cell destruction)
- autoimmune genetic (most whites)
- rapid onset
- associated with ketoacidosis (can be fatal)
- insulin therapy
- treated with pancreas transplant, beta cells in a bag, stem cell-derived pancreas, artificial pancreas
Symptoms:
- tired and sleepy
- blurred vision
- confusion/passing out
- thirsty, sweet breath smell
- needing to pee
- high blood sugar levels
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Type II
- Insulin-independent diabetes mellitus due to impaired cellular response to insulin
- majority of people have this type
- strong genetic component
- associated with obesity
- slow onset
- body tries to overcome by secreting more insulin -> beta cell exhaustion
- treated with metformin
can be reversed with weight loss
Symptoms:
- peripheral neuropathy
- tingling
- tiredness
- drowsiness
- frequent infections
- darkening in skin folds
End-results of Insulin-stimulated E-storing intermediary metabolism
How does insulin promote glucose removal from blood
Anatomical differences between posterior and anterior pituitaries
Posterior:
- has arterial blood supply
- neurons send axons through the pituitary stalk and terminates at the posterior pituitary
Anterior
- No arterial blood supply (arterial supply -> median eminence -> primary capillary plexus -> hypothalamic-pituitary portal vessel -> secondary capillary plexus in anterior pituitary
- neuron terminates at the median eminence, releases factors carried to the A.P. in the portal blood
Explain the hypothalamic-pituitary-target axis with a focus on regulation of 6 anterior pituitary hormones (FSH, LH, GH, PRL, ACTH, TSH)
LH: luteinizing hormone
FSH: follicle-stimulating hormone
TSH: thyroid-stimulating hormone ACTH: adrenocorticotropic hormone
GH: growth hormone
PRL: prolactin
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The hypothalamic pituitary target axis is controlled by negative feedback
Define panhypopituitarism and explain the changes at the level of the hypothalamic- pituitary target axis using a blood clot in the hypothalamic-pituitary portal vessel (example 1) and Kalmann’s syndrome (example 2)
Panhypopituitarism:
- Loss of all anterior pituitary function
- Destruction of the gland (hemorrage of a large adenoma -> systemic plasma levels of all anterior pituitary hormones decrease to nothing -> hypothalamic RH ↑ or IH ↓
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Blood clots in the portal vessel leading to a total loss of blood supply to the anterior pituitary and all anterior pituitary hormone levels will ↓
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Kallmann’s syndrom:
- fetal GnRH neurons fail to migrate due to defective KAL1; no GnRH -> deficiency of LH and FSH -> hypogonadism
- treatment is lifelong replacement therapy of hormones or sex steroids
Define Acromegaly and explain the changes at the level of the hypothalamic-pituitary target axis
Case of post-pubertal GH-secreting tumor (excess secretion)
Explain the hypothalamic-pituitary-target axis with a focus on regulation of 2 posterior pituitary hormones (ADH and Oxytocin)
- Antidiuretic hormone (ADH and Oxytocin) are synthesized in the soma/cell body in the hypothalamus -> to being stored in the posterior pituitary
for secretion stimuli -> A.P. generated in hypothalamus -> A.P. propagated to posterior pituitary(PP) -> secretion of stored neurohormones (ADH or OT) from the PP
- ASH stimulates water re-absorption by the kidney
too little ADH -> diabetes insipidus (a lot of urine with no taste)
- Oxytocin stimulates smooth muscle contraction and modulates the neuronal activities
Explain how hormones of anterior and posterior pituitaries are involved in milk production
and milk ejection as a part of nursing
List hormones secreted by the thyroid gland and the parathyroid glands
Triiodothyroine (T3), Thyroxine (T4), and parathyroid hormone
TRH -> TSH -> T3 & T4
T3 & T4 inhibit TRH & TSH secretion (anterior pituitary) via negative feedback
Explain why the total removal of the thyroid by an unskilled physician seems to
affect calcium balance
PTH hormones from parathyroid glands target bones and kidneys directly and gut indirectly, in order to maintain plasma calcium levels -> critical for life
If unskilled, then they may take the parathyroids out all together which can be life threatening
Explain the differences between T3 and T4: secretion, half-life, and
bioactivity
Secretion level:
T4»_space; T3
Half-life in the plasma: bound to thyroxine-binding globulins:
T4 (7 day)»_space; T3 (1-2 day)
Potency (bioactivity):
T3»_space;> T4
T4 -> T3 by deiodinase in peripheral tissues
Briefly explain thyroid hormone synthesis and secretion by focusing on the
role of the thyroid follicular cell and colloid.
Define the negative feedback for the hypothalamic (TRH)- pituitary (TSH)-
thyroid (thyroid hormones) axis.
Explain systemic physiological effects of thyroid hormones.
Free T3 goes into target cells and activates nuclear T3R (TR) and the following occurs:
- Increasing BMR (calorigenic effects)
- Potentiating sympathetic responses (beta-adrenergic responses)
- Mediating complex bodily processes
- neuron function
- nerve/muscle reflexes
- GH secretion /action
- normal reproduction in adults
- normal recognition
- cretinism of the fetus/infant
Explain the causes and symptoms of hyperthyroidism, with a focus on (a) a
TSH-secreting tumor and (b) Grave’s disease.
Explain the causes and symptoms of hypothyroidism, with a focus on chronic
iodine deficiency (a) and Hashimoto’s disease (b).
Explain the relationship between PTH and plasma calcium. Explain the cause and symptoms of the primary hypoparathyroidism vs. the primary
hyperthyroidism.
PTH:
- Bones: stimulates bone reabsorption
- Kidneys: stimulates reabsorption of Ca2+(increase) & PO4-2 excretion (decrease)
- kidneys increases 1-hydroxylase -> synthesizes calcitrol [1.25-(OH02-vitD]
- calcitrol stimulates Ca2+ & PO4-2 absorption by the gut
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Hypoparathyroidism:
↓ PTH, ↓Ca, ↑ PO4
Symptoms:
- weak bones, tetany, tingling, muscle cramps, muscle twitching, carpopedal spasms in hands (Trousseaus) or on the cheek (Chvostek - tapping on facial muscle), seizures, decreased myocardial contractility
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Hyperparathyroidism:
↑ PTH, ↑Ca, ↓PO4
Symptoms:
- kidney stones, muscle weakness, fatigue, lethargy, depression, EEG abnormalities, memory impairment, personality changes, bone weakness, pain, fractures, calcification of joint, blood vessels, possible cardiac arrest)
Define the site of calcitonin secretion and its function.
Explain the fight-or-flight response. List the adrenal medullary hormones mediating the fight-or-flight response and explain how they synthesized and secreted.
Secretion of catecholamines:
- NE and Epi are derived from tyrosine
- Tyrosine hydroxylase is the rate-limiting enzyme for either NE or Epi
- Major product is Epi, although some NE is also made and secreted
Tyrosine -> DOPA-> DA -> NE -> Epi
Between tyrosine to DOPA, there is tyrosine hydroxylase
Explain the steroid hormones secreted by the adrenal cortex.
Mineralocorticoids - aldosterone
Glucocorticoids- cortisol
Adrenal androgens- DHEA and androstenedione
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Angiotensin simulates secretion of aldosterone
Aldosterone controls homeostasis of ECF volume
- targets kidneys
- increases Na+ reabsorption -> increasing blood pressure & K+ excretion
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ACTH stimulates glucocorticoid secretion (cortisol)
Cortisol inhibits ACTH via negative feedback
increases blood glucose and BP; increases bone resorption; controlled by circadian rythm
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ACTH stimulates secretion of adrenal androgens
NO negative feedback loop; decreases during aging
androstenedione & DHEA are weal androgens (work like testosterone but weakly)
List the major hormone that controls the secretion of aldosterone, cortisol, and adrenal androgens.
Angiotensin simulates secretion of aldosterone
ACTH stimulates glucocorticoid secretion (cortisol)
ACTH stimulates secretion of adrenal androgens
Explain the causes and symptoms of Addison’s disease; changes in the plasma levels of aldosterone,
cortisol, adrenal androgens, and ACTH
Explain the causes and symptoms of Cushing’s: changes in the plasma levels of aldosterone, cortisol, adrenal androgens and ACTH
Explain the differences between mitosis vs. meiosis (# of daughter cells, formation and
separation of sister chromatids, and separation of homologous chromosomes)
Mitosis:
- 1 diploid parent cell (2n) creates 2 diploid daughter cells(2n)
- somatic cells used during DUPLICATION
- cells differentiate to perform specific function
Meiosis:
- formation of gametes in gonads
- 1 diploid parent (2n) creates 4 haploid daughter cells (n)
- used by germ cells for gametogenesis
- Homologous chromosomes are separated in meiosis 1
- sister chromatids are separated in meiosis 2
List primary sex characteristics (46 XY male vs. 46 XX female) (gonads, internal genitalia,
and external genitalia)
Explain in utero sex differentiation of a 46 XY male embryo (roles of SRY, MIH, T, and
DHT)
- an early embryo (4 wks) is at an indifferent stage and has a potential to develop female or male primary sex characteristics
- An 46, XX embryo follows the default pathway during 4-12 weeks
- bipotentials gonads -> ovaries
- mullerian ducts -> female internal genitalia
- wolffian ducts regress
- female external genitalia and urethra - XY embryo develop male primary sex characteristics during 4-12 wks
(4 wks):
- SRY gene causes bipotential gonads to become testes
- Testes secrete MIH (regression of mullerian ducts) and T (wolffian ducts become male genitalia)
(8 wks):
- T converted to DHT
- DHT causes male external genitalia & prostate along with urethra
(3rd trimester-brith):
- T causes testis descent into scrotum
List puberty-induced changes (secondary sex characteristics) in a 46 XY male vs. 46 XX
female. Define precocious puberty and explain the possible cause(s) of precocious
puberty.
Precocious Puberty:
A child’s body begins changing into that of an adult too soon before age 8 in girls and before age 9 in boys
- due to elevation of gonadal steroids
- possible causes are earlier onset of hyper secretion of gonadotropins (LH and FSH) due to genetic mutations
Explain the biological basis of androgen-insensitivity syndrome in a 46 XY subject. List
gonads, internal genitalia, and external genitalia in a 46 XY subject with complete
androgen-insensitivity syndrome, and puberty-induced secondary sex characteristics.
Person considered girl at birth
No menstruation at puberty
Testes are in body cavity (cryptorchidism)
Has testosterone secretion but no T action on LH secretion
More LH secretion
More testosterone secretion
Elevated estradiol female secondary sex characteristics
Spermatogonia
Explain erectile reflex and the mechanism of action for Viagra in treating impotence.
Explain some bodily effects of testosterone, and list desired an undesired effects of exogenous androgenic anabolic steroids.
Testosterone effects:
- strong bone, more RBCs, lean muscle, sex-drive & fertility, development of puberty-related secondary sex characteristics
Lack of testosterone:
- hypogonadism Kleinefelter syndrome (47, XXY)
- abnormal secondary sex characteristics
Long term effects of synthetic anabolic steroids:
- Lean muscle, strong bone, aggression and infertility in males, facial hair growth and masculine body in females
- decrease LH levels, decreases GnRH levels; decrease FSH levels, decrease Endogenous T secretion, decrease in spermatogenesis
- testicular atrophy
Explain when oogenesis begins and ends in the human ovaries. Explain the meiotic stage of
oocytes of new born girls, the cause of the resumption of meiosis of these oocytes, the
meiotic stage of the ovulated egg, and the cause of the resumption of meiosis in the ovulated egg toward meiotic completion
List some bodily effects of estrogen with a focus on uterus and cervical mucus
Explain the fertile period in a woman and list some examples of plan A and plan B
contraceptives
Plan A: Use effective birth control correctly and consistently
Plan B: An emergency contraception: morning after pill, synthetic progestin, levonorgestrel
Condom = only thing protecting against an STD
List some conditions associated with infertility in women.
Infertility = associated with follicular depletion, turners syndrome, PCOS, endometriosis
- Follicular depletion
- ovarian failure (menopause)
- can be natural or due to genetics or chemo or radiation
- decrease in estrogen and progesterone, increase in FSH & LH - Turners syndrome
- Lack of estrogen
- streaked ovaries (no follicles)
- no puberty-related growth due to lack of estrogen and progesterone
- no breast growth, no menstruation
- short statue and less feminine
- heart defects
- hormone replacement - Endometriosis
- endometrial tissues grow outside the uterine cavity and cause scar tissues preventing egg transport and infertility - PCOS
- hormonal imbalance leading to lack of ovulation and infertility
- irregular periods(excess body/facial hair), excess androgen, insulin insensitivity
List two types of cells of a blastocyst and their fate. Define a teratogen and explain when during the pregnancy it is most detrimental. List some examples of abortifacient?
Blastocyst:
1. Trophoblast
- outer cell layer later becomes part of placenta -> when implanted, they secrete hCG which is detected on pregnancy test
2. Inner cell mass (ICM)
- embryonic stem cells, can become all cell types, tissues, or organs of the fetus (pluripotent stem cells)
Teratogen:
- substances that can cause damage to the embryo/fetus (alcohol, drugs, certain medications)
Abortifacient:
- substance that induces miscarriage or abortion
- physical removal of fetus
- medical abortion with synthetic drugs for myometrial contraction
