Exam 2: Endocrine & Reproductive Flashcards

1
Q

What are types of muscle are there and characteristics

A

Cardiac - striated, involuntary

Skeletal - striated, voluntary, hundred of nuclei

Smooth - involuntary

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2
Q

Explain the properties of muscles

A

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

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3
Q

Function of skeletal muscle

A

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

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4
Q

Primary function of cardiac muscle

A

generate force and blood flow

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5
Q

Primary function of smooth muscle

A

generate force as in move substance within the body (blood, urine, food)

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6
Q

what is origin in skeletal muscle

A

Origin: remains immobile during the action of the
muscle; more proximal/closer to midline of the body

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7
Q

what is insertion in skeletal muscle

A

the place on the bone
that moves during the action of the muscle; more distal/further to midline of the body

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8
Q

Function of agonist and antagonist muscle

A

Agonist: prime mover of the action

Antagonist: act on the same joint to produce opposite actions

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9
Q

Structural organization of the muscle (muscle fiber to tendon)

A
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10
Q

Explain parallel fascicles

A

Involved in range of motion

arranged in the same direction as the long axis of the muscle

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11
Q

Explain pennate fascicles

A

Involved in power

Can fit more muscle fibers in the space

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12
Q

Type of fascicles

A
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13
Q

Explain a muscle cell and the structure

A

Known as a myofiber

Striated appearance, multi-nucleated

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14
Q

Explain the sarcomere

A

Function unit of muscle contraction

I band: thin filament

A band: thick filament

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15
Q

Explain contraction in terms of the sarcomere shortening

A

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

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16
Q

Explain the sliding mechanism/sliding filament mechanism

A

Sliding is the contraction of muscle

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17
Q

Explain the biochemistry of contraction

A
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18
Q

How cross bridge cycling is regulated

A

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

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19
Q

Concept of a motor unit

A

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

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20
Q

The steps in excitation-contraction coupling

A
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21
Q

different types of muscle contraction

A

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

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22
Q

explain muscle relaxation

A

APs must stop

Ach-esterase degrades Ach

Ca2+ release channels close

Ca2+ pumped back into sarcoplasmic reticulum
through Ca2+ATPase pump

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23
Q

Describe length-tension relationship

A
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24
Q

Difference between isometric and isotonic muscle contractions

A

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

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25
Q

Different energy systems used to generate ATP

A

Phosphagen:
- resynthesizes ATP (fastest)
- sprinter (8-10 seconds)

Glycolytic (fast):
- swimmer (1.3-1.6 minutes)

Aerobic:
- lower intensity but much longer
- marathon runner

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26
Q

Describe force-velocity curve

A
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27
Q

Explain the phosphogenic system

A
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28
Q

Explain the glycolytic system

A
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29
Q

Explain the aerobic metablosim

A

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

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30
Q

Slow twitch fibers (type I)

A

Fibers have red appearance

Many capillaries, much myoglobin (carries oxygen)

Many mitochondria (aerobic)

High oxidative capacity

Resistance to fatigue

Common in endurance muscles

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31
Q

Fast twitch fibers (type 2a)

A

Fast contraction

Highly aerobic (many mitochondria)

fatigue resistance

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32
Q

Fast twitch fibers (type 2x)

A

Fibers have a white appearance

anaerobic adaption

large stores of glycogen

Few capillaries, mitochondria

Adapted for sprint tasks

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33
Q

Fiber type characteristics

A
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34
Q

Muscle stem cells and function

A

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)

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35
Q

Duchenne muscular dystrophy

A

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)

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36
Q

Differences between skeletal and cardiac muscles

A

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

37
Q

Regulation of smooth muscle contraction

A

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

38
Q

Explain skeletal muscle repair (regeneration)

A
39
Q

The endocrine glands

A
  • pancreas
  • hypothalamic-pituitary
  • thyroid-parathyroids
  • adrenals
  • male gonads (testes)
  • female gonads (ovaries)
40
Q

Explain how the endocrine system controls bodily functions: comparison to the nervous system

A

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

41
Q

Members, and their synthesis, storage, and secretion of hydrophilic hormones (peptides and amines)

A

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

42
Q

Members, and their synthesis, storage, and secretion of hydrophobic hormones (thyroid hormones, steroid hormones, vitamin D)

A

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

43
Q

Describe what contributes to plasma concentration of a hormone

A

Metabolism & degradation

Binding to their receptors in target cells

Excretion by kidneys

44
Q

Explain how hormones circulate in plasma: Free vs.
protein-bound

A

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

45
Q

Explain how a target cell responds to hydrophilic and hydrophobic hormones: transmembrane vs. intracellular receptors

A

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)

46
Q

Compare and contrast the modes of cellular responsiveness: up- and down-regulation, sensitivity, synergism, and permissiveness

A

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
    _________________________
    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

_________________________
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

47
Q

Describe hormones

A

Hormones - chemical messengers from DUCTLESS glands

48
Q

Explain how peptide hormones bind their specific transmembrane receptors

A
49
Q

Know the hormones in the hydrophilic and hydrophobic categories

A
50
Q

What is a prohormone and what are they

A

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

51
Q

Explain pancreatic hormones and their functions during an absorptive phase

A

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)

52
Q

Explain pancreatic hormones and functions during fasting state (post-absorptive)

A

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
________________________

↓ 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)

53
Q

Causes of diabetes (type I and type II), symptoms and treatments

A

Diabetes mellitus
- when glucose homeostasis is not maintained
- symptoms: polyphagia, polyuria, polydipsia (hunger, fatigue and weight loss)
________________________

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
________________________

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

54
Q

End-results of Insulin-stimulated E-storing intermediary metabolism

A
55
Q

How does insulin promote glucose removal from blood

A
56
Q

Anatomical differences between posterior and anterior pituitaries

A

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

57
Q

Explain the hypothalamic-pituitary-target axis with a focus on regulation of 6 anterior pituitary hormones (FSH, LH, GH, PRL, ACTH, TSH)

A

LH: luteinizing hormone
FSH: follicle-stimulating hormone
TSH: thyroid-stimulating hormone ACTH: adrenocorticotropic hormone
GH: growth hormone
PRL: prolactin
________________________

The hypothalamic pituitary target axis is controlled by negative feedback

58
Q

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)

A

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 ↓
________________________

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 ↓
________________________

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

59
Q

Define Acromegaly and explain the changes at the level of the hypothalamic-pituitary target axis

A

Case of post-pubertal GH-secreting tumor (excess secretion)

60
Q

Explain the hypothalamic-pituitary-target axis with a focus on regulation of 2 posterior pituitary hormones (ADH and Oxytocin)

A
  1. 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

  1. ASH stimulates water re-absorption by the kidney

too little ADH -> diabetes insipidus (a lot of urine with no taste)

  1. Oxytocin stimulates smooth muscle contraction and modulates the neuronal activities
61
Q

Explain how hormones of anterior and posterior pituitaries are involved in milk production
and milk ejection as a part of nursing

A
62
Q

List hormones secreted by the thyroid gland and the parathyroid glands

A

Triiodothyroine (T3), Thyroxine (T4), and parathyroid hormone

TRH -> TSH -> T3 & T4

T3 & T4 inhibit TRH & TSH secretion (anterior pituitary) via negative feedback

63
Q

Explain why the total removal of the thyroid by an unskilled physician seems to
affect calcium balance

A

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

64
Q

Explain the differences between T3 and T4: secretion, half-life, and
bioactivity

A

Secretion level:
T4&raquo_space; T3

Half-life in the plasma: bound to thyroxine-binding globulins:
T4 (7 day)&raquo_space; T3 (1-2 day)

Potency (bioactivity):
T3&raquo_space;> T4

T4 -> T3 by deiodinase in peripheral tissues

65
Q

Briefly explain thyroid hormone synthesis and secretion by focusing on the
role of the thyroid follicular cell and colloid.

A
66
Q

Define the negative feedback for the hypothalamic (TRH)- pituitary (TSH)-
thyroid (thyroid hormones) axis.

A
67
Q

Explain systemic physiological effects of thyroid hormones.

A

Free T3 goes into target cells and activates nuclear T3R (TR) and the following occurs:

  1. Increasing BMR (calorigenic effects)
  2. Potentiating sympathetic responses (beta-adrenergic responses)
  3. Mediating complex bodily processes
    - neuron function
    - nerve/muscle reflexes
    - GH secretion /action
    - normal reproduction in adults
    - normal recognition
    - cretinism of the fetus/infant
68
Q

Explain the causes and symptoms of hyperthyroidism, with a focus on (a) a
TSH-secreting tumor and (b) Grave’s disease.

A
69
Q

Explain the causes and symptoms of hypothyroidism, with a focus on chronic
iodine deficiency (a) and Hashimoto’s disease (b).

A
70
Q

Explain the relationship between PTH and plasma calcium. Explain the cause and symptoms of the primary hypoparathyroidism vs. the primary
hyperthyroidism.

A

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
_________________________

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
_________________________

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)

71
Q

Define the site of calcitonin secretion and its function.

A
72
Q

Explain the fight-or-flight response. List the adrenal medullary hormones mediating the fight-or-flight response and explain how they synthesized and secreted.

A

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

73
Q

Explain the steroid hormones secreted by the adrenal cortex.

A

Mineralocorticoids - aldosterone
Glucocorticoids- cortisol
Adrenal androgens- DHEA and androstenedione
___________________

Angiotensin simulates secretion of aldosterone

Aldosterone controls homeostasis of ECF volume
- targets kidneys
- increases Na+ reabsorption -> increasing blood pressure & K+ excretion
___________________

ACTH stimulates glucocorticoid secretion (cortisol)

Cortisol inhibits ACTH via negative feedback

increases blood glucose and BP; increases bone resorption; controlled by circadian rythm
___________________

ACTH stimulates secretion of adrenal androgens

NO negative feedback loop; decreases during aging

androstenedione & DHEA are weal androgens (work like testosterone but weakly)

74
Q

List the major hormone that controls the secretion of aldosterone, cortisol, and adrenal androgens.

A

Angiotensin simulates secretion of aldosterone

ACTH stimulates glucocorticoid secretion (cortisol)

ACTH stimulates secretion of adrenal androgens

75
Q

Explain the causes and symptoms of Addison’s disease; changes in the plasma levels of aldosterone,
cortisol, adrenal androgens, and ACTH

A
76
Q

Explain the causes and symptoms of Cushing’s: changes in the plasma levels of aldosterone, cortisol, adrenal androgens and ACTH

A
77
Q

Explain the differences between mitosis vs. meiosis (# of daughter cells, formation and
separation of sister chromatids, and separation of homologous chromosomes)

A

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

78
Q

List primary sex characteristics (46 XY male vs. 46 XX female) (gonads, internal genitalia,
and external genitalia)

A
79
Q

Explain in utero sex differentiation of a 46 XY male embryo (roles of SRY, MIH, T, and
DHT)

A
  1. an early embryo (4 wks) is at an indifferent stage and has a potential to develop female or male primary sex characteristics
  2. 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
  3. 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
80
Q

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.

A

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

81
Q

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.

A

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

82
Q

Spermatogonia

A
83
Q

Explain erectile reflex and the mechanism of action for Viagra in treating impotence.

A
84
Q

Explain some bodily effects of testosterone, and list desired an undesired effects of exogenous androgenic anabolic steroids.

A

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

85
Q

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

A
86
Q

List some bodily effects of estrogen with a focus on uterus and cervical mucus

A
87
Q

Explain the fertile period in a woman and list some examples of plan A and plan B
contraceptives

A

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

88
Q

List some conditions associated with infertility in women.

A

Infertility = associated with follicular depletion, turners syndrome, PCOS, endometriosis

  1. 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
  2. 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
  3. Endometriosis
    - endometrial tissues grow outside the uterine cavity and cause scar tissues preventing egg transport and infertility
  4. PCOS
    - hormonal imbalance leading to lack of ovulation and infertility
    - irregular periods(excess body/facial hair), excess androgen, insulin insensitivity
89
Q

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?

A

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