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Metabolic Endocrinology > Final Exam (after midterm) > Flashcards

Final Exam (after midterm) Flashcards

1
Q

The adrenal gland is…

A

Paired
8-10g
Above, medial, & back to the kidneys

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2
Q

Components of adrenal gland

A

Surrounded by fibrous capsule

Divided into functional layers: capsule, adrenal cortex (90%), & adrenal medulla (10-15%)

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3
Q

Cortex of adrenal gland

A 
Is ~90% of adrenal mass
Has 3 zones: 
- zona glomerusa
- zona fasciculata (thickest; ~80%)
- zona reticularis
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4
Q

Hormones of adrenal gland

A

Aldosterone: synthesized in zona glomerulosa
Cortisol, corticosterone: synthesized in zona fasciculata
Sex steroids: synthesized in zona reticularis
Catecholamines (epinephrine & norepinephrine): synthesized in medulla

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5
Q

Initiation of steroidogenesis

A

Formation of pregnenolone from cholesterol (occurs in mitochondria): this is the beginning of all hormones of adrenal gland

  1. Regulated by steroid acute regulatory (StAR) protein
    - A cAMP-inducible gene that increases in response to tropic hormones
  2. P450scc (side-chain cleavase) cleaves side chain of cholesterol to produce pregnenolone (on inner mitochondrial membrane)
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6
Q

Synthesis of steroid hormones

A
  1. All are derived from cholesterol (mostly LDL)
    - HDL can be synthesized from acetyl-CoA
  2. Zone specific expression of enzymes determines steroid production
    - Enzymes in mitochondria or ER (Steroid intermediates shuttle back & forth)
  3. Most steroids differ by minor modification of side groups (often hydroxyl groups): lead to enormous differences
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7
Q

Function of zona fasciculata

A

Produce cortisol

  • no storage
  • half-life is 70-120 mins
  • converted to inactive cortisone & other metabolites by liver & other target cells (can be reconverted)
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8
Q

Secretion of cortisol

A
  1. Cortisol production activated by ACTH
    - Begins G-protein/cAMP signaling pathway
  2. Stimulates formation of pregnenolone from cholesterol
  3. ACTH secretion is pulsatile (circadian rhythm): highest in morning)
    - Rapid inc/dec. in response to ACTH pulse (can change due to stress)
    * if synthesis of ACTH is suppressed for long time, a months may be needed to resume (this could be due to exogenous administration of cortisol)
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9
Q

Transport of circulating cortisol

A

Use: corticosteroid-binding globulin

  • Synthesized by liver
  • has high affinity for cortisol
  • Binds ~ 75% of all cortisol (10% is free, 15% is bound to serum albumin)
  • bound cortisol is protected from liver inactivating it (due to delay of metabolic clearance)
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10
Q

Cortisol inactivation by liver…

A

Is due to inc. H2O solubility (HSD11B2 (90% of this is secreted by kidneys))
*HSD11B1 can reactivate cortisol

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11
Q

Significance of converting cortisol to cortisone

A

Changes depends on need of cortisol and aldosterone
Cortisol can bind to mineralocorticod receptor (MR)
- High conc. can lead to aldosterone-like symptoms (hypertension, hypokalemia, low renin, low aldosterone levels)
Cortisol conc. is 100-1000x higher than aldosterone conc.
- Aldosterone responsive cells need to inactivate cortisol to respond specifically to aldosterone
* Enzyme deficiency of HSD11B2 inc. cortisol; leading to apparent mineralocorticoid excess (AME) syndrome

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12
Q

Cortisol receptor

A

Glucocorticoid receptor (NR3C1)

  • Functions of cortisol depend on GR
  • GR-beta inhibits GR-alpha
  • Uses ligand binding to translocate GR into nucleus
  • GR response element (GRE) is located on promoters of target genes (binds GR)
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13
Q

Metabolic effects of cortisol

A

Inc. transcription of specific genes
Effects: opposite of insulin, similar to GH
- at expense of protein & fat
Action depends on target cells
- muscle cells, adipocytes, & lymphocytes = inc. catabolism
- liver cells = glycogen synthesis
Overall effects: anabolic effect on liver
- inc of blood glucose

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14
Q

Anti-inflammatory effects of cortisol

A

Inhibits immune response
Dec. number of lymphocytes & antibody production
Become susceptible to infections
Ex. hydrocortisone cream
Uses 3 mechanisms:
1. Activated inhibitor (IkB) of immune response transcription factor NFkB
- Coactivator w/ C-fos/C-jun
2. GR-cortisol binds & inhibits nuclear migration of NFkB
3. GR competes w/ NFkB for other interacting transcription factors

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15
Q

Other effects of cortisol

A
  • Hypertension: sensitizes arterioles to action of norepinephrine
  • Glycogneolysis -> hyperglycemia: Inc. effect of norepinephrine on carbohydrate metabolism
  • Euphoria: inc. activity of CNS
  • Inc of extracellular fluid: act as mineralocorticoid b/c it interacts with MR
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16
Q

Function of zona glomerulosa

A

Recovery of Na+ in kidney & enhanced K+ secretion into urine (balances charge difference)
Adjustment of ECF

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17
Q

Sodium appetite

A

Triggered by negative sodium balance

Not strongly manifested in normal conditions (suppressed)

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18
Q

Renin-angiotensin-aldosterone system (secretion of aldosterone)

A
  1. renin from kidneys converts angiotensinogen (from liver) to angiotensin I (found in lungs)
  2. Angiotensin-converting enzyme (ACE) converts angiotensin I to angiotensin II (in lungs)
    - Comes from endothelial cells of lungs
  3. Angiotensin II stimulates aldosterone secretion (in adrenal cortex) or angiotensin III (degradation product)
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19
Q

Renin-angiotensin-aldosterone system (kidney)

A

Macula densa cells: line distal tubule & detect Na+ levels in kidney tubule
Juxtaglomerular cells: line afferent arterioles & detect blood pressure
Pericytes: near afferent arterioles; produce renin based on macula densa & juxtaglomerular cell detections

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20
Q

The juxtaglomerular apparatus

A

Consists of pericytes
Source of renin
Found in kidneys

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21
Q

Effects of angiotensin II

A

Change in peripheral resistance: rapid pressure response (water retention (higher blood pressure)
Change in renal function: slow pressure response (inc. Na+ absorption/K+ excretion)
Structural changes remodeling: vascular and cardiac hypertrophy & remodeling (stimulates water reabsorption into kidneys)

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22
Q

Function of aldosterone

A

Regulate fluid volume
Water absorption
Sodium/potassium homeostasis
- Na+ transport in: distal tubules of kidney, colon, salivary & sweat glands

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23
Q

Effects of aldosterone

A

Lag period of response: 1 hr Distal tubules & collecting ducts of kidney
Promotes retention of Na+ and excretion of K+ & H+
Sensitizes arterioles to vasoconstrictor agents
Rise in plasma volume & blood pressure

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24
Q

Natriuretic peptides (general)

A 
Two main types: ANP & BNP 
Produced in the heart muscle cells & stored in granules
Receptors are present in glomeruli, medullary collecting ducts of kidney, zona glomerulosa of adrenal cortex, & peripheral arterioles
Function:
- Dec. renin production
- Inc. excretion of H2O & Na+
- Inc. glomerular filtration
- Reduces blood volume/pressure
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25
Q

Production of sex steroids

A

Mainly synthesized in gonads
- Synthesis is regulated by gonadotrophins
Adrenal cortex contributes to production of DHEA & androstenedione
- Regulated by ACTH & hypothalamic CRH
Converted to testosterone in peripheral tissues

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26
Q

Adrenal medulla (general)

A

Total mass = 1g
15% of adrenal gland weight
Creates fight/flight response by inc. blood pressure & cardiac output and dilating pupils

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27
Q

What are the adrenal medulla & chromaffin cells part of?

A

Sympathetic nervous system

*Chromaffin cells are modified neurons

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28
Q

Adrenal medulla releases catecholamines via…

A

Pre-ganglionic neurons releasing acetylcholine to stimulate adrenal medulla
Steps:
1. Tyrosine is translated into dopa via tyrosine hydroxylase (rate limiting step)
2. Dopa is translated into dopamine via dopa decarboxylase
3. Dopamine is translated into norepinephrine via dopamine beta-hydroxylase
4. Norepinephrine is translated into epinephrine via Phenylethanolamine N-methyltransferase (PNMT)
*PNMT is stimulated from cortisol
*stored in granules

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29
Q

Hormones of the adrenal medulla

A

Catecholamines (20% norepinephrine & 80% epinephrine)
Met-enkephalin & leu-enkephalin
- co-secreted with catecholamines
- Can block neurotransmitters (endogenous analgesics)
Released due to stimuli

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30
Q

Fight or flight response

A

From adrenal medulla nervous system
Major hormones: catecholamines
Occurs at expense of other organs
Epinephrine: rapidly mobilizes fatty acids as primary fuel for muscles
Norepinephrine: elicits responses for cardiovascular system (inc. blood flow; dec. insulin secretion)
Also uses ACTH to release about 30 other hormones

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31
Q

Acute fight/flight response is…

A

Integrated adjustment of many complex processes in organs vital to response

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32
Q

Adrenergic receptors (general)

A

alpha & beta 1 bind to epinephrine (E) & norepinephrine (NE)
beta 2 binds to epinephrine mostly
Different target tissues = different responses
- Drugs specific to receptors have different effects

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33
Q

Alpha 1 adrenergic receptor

A

Target: smooth muscle
Potency: NE>/=E
Action: Gq

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34
Q

Alpha 2 adrenergic receptor

A

Target: nerve terminals
Potency: E>NE
Action: Gi

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35
Q

Beta 1 adrenergic receptor

A

Target: heart, cerebral cortex
Potency: NE>E
Action: Gs

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36
Q

Beta 2 adrenergic receptor

A

Target: lung, smooth muscle, cerebellum
Potency: E>NE
Action: Gs

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37
Q

Cardiac stimulation leading to greater cardiac output: which is greater (E or NE)?

A

Epinephrine&raquo_space; norepinephrine

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38
Q

Constriction of blood vessels; leading to inc. peripheral resistance; to inc. arterial pressure: which is greater (E or NE)?

A

Norepinephrine > epinephrine

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39
Q

Increasing metabolism: which is greater (E or NE)?

A

Epinephrine&raquo_space; norepinephrine

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40
Q

Disorders of the adrenomedullary

A 
Adrenomedullary deficiency
Epinephrine deficiency
Hypotension
Hypoglycemia
Adrenal catecholamines
Pheochromocytoma
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41
Q

Cells of the exocrine pancreas

A

Acinar cells: secretion of digestive enzymes (proteases, amylase, lipase)
Duct cells: secretion of NaHCO3
Secrete into duodenum

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42
Q

Cells of endocrine pancreas

A

alpha-cells: glucagon
beta-cells: insulin
delta-cells: somatostatin
epsilon-cell: ghrelin
F-cells: pancreatic polypeptide
All hormones that are secreted into blood (veing capillaries)
*glucagon, somatostatin, pancreatic polypeptide, & ghrelin also produced by cells of the gastrointestinal mucosa

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43
Q

What are the islets of Langerhans also called?

A

The endocrine pancreas
2% of total mass
Consists of 3 mill. islets

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44
Q

The blood supply of the pancreas

A

Aortic artery: hepatic artery branching

Portal vein: splenic and mesenteric veins

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45
Q

The islets of Langerhans are…

A

highly vascularized
Blood supplies beta-cells first -> alpha- & delta-cells
Heterogenous (variable)

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46
Q

Beta-cells of islets

A

Function together
Proliferation is minimal after 5 years
Avg lifespan = 25 years
Immature beta-cells are called neogenic niches (surround the beta-cell islets)
Alpha- & delta-cells transdifferentiate under extreme beta-cell loss

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47
Q

Insulin granules

A

Each is made by 51 a.a.
Metabolized in the liver (C-peptide (part of proinsulin) is metabolized in kidney)
beta-cells contain 5,000-8,000 granules
Half-life: 5 days
Young granules = deeper in cytoplasm; more mobile (faster)
Older granules: degrade intracellularly
Each contain insulin hexamer stabilized by calcium & zinc

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48
Q

Steps of insulin release from beta-cells

A

Glucose is main stimulator

  • hexokinase is glucose sensors
    1. Glucose is taken into beta cells by GLUT2
    2. Aerobic glycolysis + inc. of ATP/ADP ratio
    3. Inhibition of ATP-sensitive K+ channels (reduce K+ efflux)
    4. Voltage-gated Ca2+ channels open
    5. Inc. Ca2+ triggers exocytosis of insulin-containing granules
    6. Ca2+ activated potassium channels opens; leads to repolarization of membrane
    7. Metabolic coupling factors are generated during glucose metabolism; facilitate exocytosis and/or proinsulin synthesis
    8. GLP-1/related peptides bind GLP-1 receptors & trigger cAMP production. Amplifies pathway, ion channels, & exocytosis (allows insulin to leave cells)
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49
Q

Regulation of insulin secretion

A

Vagus nerve: acts as sensory neuron & motor neuron (main neuronal coordinator of appetite control, digestion, & metabolism)
- Release of acetylcholine in pancreas stimulates insulin release

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50
Q

Homeostasis of glucose

A

Regulated by hormones that affect appetite & cell metabolism

51
Q

Hormones effecting blood glucose levels

A 
Major:
- Insulin (only hormone that lowers blood glucose)
- Glucagon (inc. blood glucose)
Minor:
- Epinephrine
- Cortisol
- Growth hormone
- Thyroid hormone
- Secretin
- Cholecystokinin
Act together to form integrated control system
52
Q

Regulation of blood glucose

A

Serum glucose during fasting: 3-5mM (normal is below 6.1)
- Glucose from liver is tightly regulated at this time
Serum glucose after meal: 7mM (bad is above 11)
Insulin: synthesizes protein, lipid, & glycogen and inhibits their degradation (use glucose)
- Targets: liver, muscle, adipose tissue
Glucagon inc. catabolic processes (mostly in liver) & fatty acid mobilization

53
Q

Liver vs muscle glucose metabolism

A

Liver:

  • Has glucagon receptor
  • Produces F26BP
  • Pyruvate kinase is phosphorylated by PKA
54
Q

how insulin promotes glucose uptake/organ

A

Insulin promotes glucose uptake in muscle & adipose tissue
- Inc. GLUT4 transporters on cell surface
Insulin promotes glucose uptake in liver
- stimulates glucokinase & promotes phosphorylation of glucose to form glucose 6-phosphate

55
Q

Steps of fuel metabolism during prolonged fasting

A
  1. Protein degradation yields glucogenic amino acids
  2. Urea is exported to kidney & excreted in urine
  3. Citric acid cycle intermediate is diverted to gluconeogenesis
  4. Glucose is exported via bloodstream to brain
  5. Fatty acids are oxidized as fuel (producing acetyl-CoA)
  6. Lack of oxaloacetate prevents acetyl-CoA entry into citric acid cycle (acetyl-CoA accumulates)
  7. Acetyl-Coa accumulation favors ketone body synthesis
  8. Ketone bodies are exported via bloodstream to brain for fuel
  9. Excess ketone bodies go to urine
56
Q

Hormonal regulation of food intake

A

alpha-MSH & NPY neurons receive hormonal input from peripheral organs

  • alpha-MSH neurons regulate neurons that stimulate anorexia & catabolism (less eating)
  • NPY neurons stimulate orexia & anabolism (more eating)
57
Q

Type 1 diabetes mellitus

A 
5-10% of cases
Insufficient production of insulin
Mostly due to autoimmune destruction of beta-cells
Usually develops early in life
Idiopathic
58
Q

Type 2 diabetes mellitus

A 
80-95% of cases 
Insulin resistance
Usually develops in late adulthood
Associated with obesity
Cells don't respond correctly to insulin
59
Q

Insulin resistance is due to:

A 
Pre-receptor
- antibodies against insulin
- mutant insulin
Receptor
- reduced INSR expression
- reduced affinity for insulin
- impaired tyrosine-kinase activity
- INSR antibodies
60
Q

Symptoms of diabetes

A 
Blood sugar elevated
- Body tries to dilute glucose; leads to excess urination/thirst
Type 1: high production of ketone bodies
- Fat breakdown is accelerated
Type 1: dramatic weight loss
61
Q

What are the long-term effects of elevated blood sugar?

A

Proteins are glycosylated
Excessive glucose causes glycation
Hemoglobin is glycated b/c entry of glucose into erythrocytes is not regulated
- compromises O2 delivery
- impaired injury repair
Inc. risk of cardiovascular disease, renal failure, & small blood vessels & nerve damage

62
Q

Symptoms of prolonged type 2 diabetes

A 
Abdominal obesity
High triglycerides
Low HDL
High blood pressure
Elevated blood glucose
63
Q

The pathway from obesity to type 2 diabetes

A

Called the “lipid burden” hypothesis

  1. Adipocytes become packed
    - Can’t accomodate TAG
  2. No TAG deposit leads to FA in blood
  3. Excess FA enters muscle & liver
    - Create TAG lipid droplets
    - Cause these organs to lose sensitivity to insulin (interferes with GLUT4 movement)
  4. Blood glucose levels rise
64
Q

Ways to treat diabetes

A

Weight loss
- reduces insulin resistance, hepatic glucose production, & fasting hyperinsulinemia
- less calorie intake = adipose tissue-derived NEFA provides fuel for muscle, liver, & myocardium
Metformin & Thiazolidinediones
- inc. insulin sensitivity
- dec. glucose output by liver
Sulfonylureas & Meglitinides
- promote insulin secretion from pancreas
GLP-1 receptor agonists
- inc. insulin secretion
Alpha-glucosidase inhibitors
- dec. the absorption of carbohydrates from intestine

65
Q

Wolffian ducts

A

Male
Epididymis & vas deferens
Occurs if antimullerian hormone exists (regresses Mullerian duct)

66
Q

Mullerian ducts

A

Female
Uterus & oviduct
Occurs if NR2F2 (orphan nuclear receptor) exists (regresses Wolffian duct by stopping FGF)

67
Q

Steps of sexual differentiation

A
  1. Establishment of genetic sex
  2. Translation of genetic sex to gonadal sex
  3. Translation of gonadal sex to phenotypic sex
68
Q

Human sex chromosome

A

Either X or Y chromosome (number 23)

69
Q

X chromosome statistics

A

About 160 megabases (Mb) long
Represents 5% of genome
Encodes about 850 proteins
- Regulate gametogenesis & hypothalamus-pituitary functions
- Most regulate non-reproductive functions

70
Q

Y chromosome statistics

A

About 60 Mb long
Represents 2% of genome
Encode about 57 proteins
- Most regulate reproductive functions

71
Q

Sex chromosome aneuploidy is…

A

Nondisjunction of sister chromatids during meiosis

72
Q

Sex chromosome mosaicism is…

A

Nondisjunction of sister chromatids in zygote

73
Q

What did Alfred Jost determine about sexual differentiation?

A

Testes are needed for male sexual differentiation

Ovaries are not necessary for female differentiation (are not hormone dependent)

74
Q

What is needed for normal sex differentiation?

A
  • Normal intact chromosome complement
  • Fully functioning sex determination genes
  • Intact steroidogenic pathway and receptors
75
Q

XX male occurs…

A

When SRY gene is on an X chromosome

76
Q

XY female occurs…

A

When there is a deleted or mutated SRY gene on a Y chromosome

77
Q

Purpose of SRY gene

A

Only on Y chromosome

Binds to DNA to induce transcription of other genes

78
Q

Germ cell development to gonadal cells

A
  1. Primordial germ cells differentiate in allantoic ectoderm
  2. Migrate to endoderm & along hindgut to genital ridges
  3. Are polar during migration
    - Migration involves cell protrusion & adhesion in leading edge/retraction in lagging edge
  4. Guiding cells biochemically direct the migration
79
Q

Defects in testosterone synthesis or actions cause…

A 
Phenotypic female (XY)
No ovaries
Undescended testes
Infertility
Blind ending vagina
80
Q

Defects in testosterone synthesis or actions are caused by…

A

Translation doesn’t occur at any stage between cholesterol and androgen synthesis

81
Q

Congenital adrenal hyperplasia (CAH) causes…

A

Hyperplasia of adrenal glands before birth ->
Excessive androgen production ->
Masculinization of genitalia

82
Q

Congenital adrenal hyperplasia is caused by…

A

Addition of testosterone during development

- Causes DHT (an androgen)

83
Q

Sexual differentiation of the brain is…

A

A marked difference between the sexes in the structure and behaviour of the brain
*Occurs during a critial time period (different for each species)

84
Q

Sexual differentiation of the hypothalamus (male)

A

Testosterone freely enters brain & converts to estradiol

Has tonic center: controls LH/FSH post-puberty

85
Q

Sexual differentiation of the hypothalamus (female)

A

Estradiol produced by fetal ovary can’t cross blood-brain barrier
Retains surge center + tonic center: control LH/FSH after puberty

86
Q

Puberty includes…

A

All physiological, morphological, & behavioral changes that occur in the growing animal as gonads/brain/phenotype change from adolescent to adult
Begins:
- Female: frist cycle
- Male: first ejaculation

87
Q

Control of puberty

A

By pulsatility of GnRH release (regulated from neural mechanism in hypothalamus)

  • LH and FSH present in pituitary and hypothalamus before puberty, but not released
  • Pulsatile administration of GnRH induced menstrual cycle in prepubertal monkeys
88
Q

What are the endocrine mechanisms of puberty?

A

Levels of GnRH rise (in amplitude & frequency)
- Caused by dec. sensitivity of tonic center to negative feedback from gonadal steroids
Surge center (females only) does not change sensitivity
- Before puberty, E2 levels aren’t high enough to stimulate surge release
- After puberty, has E2 has positive feedback on surge center & release of GnRH
Result in pulses of LH/FSH increasing and levels of steroids increasing
- Inhibin is able to stop FSH secretion if E2 levels are too high

89
Q

Regulation of GnRH

A

Kisspeptin (KISS1) neurons are located in anteroventral periventricular & arcuate nuclei of the hypothalamus
- Express estrogen and androgen receptors
- Signal through its receptor (KISS1R) in GnRH neurons to regulate pulsatile secretion of GnRH
There are two types of KISS1 neurons
- They respond differently to steroid feedback

90
Q

GnRH (general)

A

Small peptide (10aa) cleaved from larger precursor
Released with gonadotrophin associated peptide (GAP)
Synthesized by 1-3K neurons in hypothalamus
- Axons terminate in either hypophyseal portal capillaries to release GnRH or other brain areas to affect sexual behavior
GnRH is also synthesized in placenta, gonads, breasts, lymphocytes, & pituitary (the function of these is unknown)

91
Q

Actions of LH and FSH

A

Similar to ACTH
Inc. intracellular cholesterol
Transport cholesterol to inner mitochondrial membrane (using StAR)
- Rate limiting step
Convert pregnenolone by side-chain cleavage
Target cells: male & female reproductive
- Testis: LH acts on Leydig cells (testosterone)& FSH on Sertoli cells (estradiol)
- Ovaries: Both LH & FSH are steroidogenic; act on theca interna (testosterone) & granulosa cells (estradiol). LH also acts on luteal cells (progesterone)

92
Q

During spermatogenesis there are three different important cell types. These are?

A

Spermatogonia: cells that become sperm (main)
Sertoli cells: physically support differentiation process
Leydig cells: produce testosterone

93
Q

Androgen synthesis & secretion (males)

A

Most important androgens secreted by testes: DHEA, testosterone (over 95%)
- 4-10mg/day
- 98% is bounds to albumin & sex-hormone-binding globulin
Testosterone: acts on internal genitalia development & muscle cells
Testosterone (not DHT) can be converted to estradiol

94
Q

Action of androgens (males)

A

Powerful anabolic hormone
In young children: occasional pulses (nocturnal) of LH & FSH -> production of steroid hormones -> high enough level to produce secondary sex characteristics

95
Q

Oocyte of female

A

Mitosis of oogonia occurs before 1st meiotic division
Millions of oocytes remain in prophase I until ovulated
Primordial follicles: single cell layer surrounding oocyte

96
Q

Loss of oocytes

A

Highest number of oocytes (~7mill) at 5th month in womb
At birth: ~1.5mill oocytes
Progressive loss of oocytes after birth
About 400-500 ovulations occur in lifetime

97
Q

Formation of corpus luteum

A

Called luteinization
Tonic center produces GnRH
CL maintains basal levels of LH
LH stimulates the CL to secrete P4

98
Q

Hormones of estrous cycle

A

Progesterone (P4): highest during luteal phase; declines during follicular phase
Estradiol (E2): peaks during middle of luteal & middle of follicular phase
FSH: Peaks at beginning & end of luteal phase and end of follicular phase
LH: Peaks at end of follicular phase

99
Q

Steps of conception & implantation

A

Fertilization of ovum occurs in oviduct

  1. Hydrolytic enzymes in acrosome of sperm loosen expanded cumulus cells & zona pellucida around ovum
  2. One sperm penetrates & fertilizes oocyte
  3. Causes cortical reaction & exocytosis of Ca outside plasma membrane
    - Zona becomes impermeable to other sperm
  4. Ciliated cells move the zygote along the oviduct to uterus
  5. Zygote begins to divide & derives energy from oviductal & uterine secretions until implantation
100
Q

What are the changes that occur in the uterine endometrium during the menstrual cycle?

A

Days 1-3: breakdown
Days 3-14: estrogenic proliferative phase
Days 14-28: Progestational secretory phase

101
Q

Ways to prevent conception (female)

A

Intrauterine device: molded plastic devices that disrupt normal uterine environment (sperm can’t get to oocytes)
Tubal ligation: tying the tubes
Oral (every day) & transdermal (3 patches): stop P4 & E2 synthesis
Injection (once a month) & implant (once a month): stops P4 synthesis

102
Q

Ways to prevent conception (male)

A

Very little ideas on hormonal contraceptives
Condoms
Vasectomy: tying the tubes

103
Q

Types of anti-progesterones

A

RU486: receptor complex binds but genes do not activate
ONA: receptor complex does not bind

104
Q

Secretion of placental hormones

A

Human chorionic gonadotropin (hCG) is secreted by placenta
- Maintains the CL
- Serves as an indicator of pregnancy
Progesterone (P4) production is taken over by placenta at around 2.5 months into pregnancy

105
Q

What are the changes in the breast during pregnancy?

A

Normal estrogen levels: stimulate duct formation & accumulation of fat
- Inc. during pregnancy
Glucocorticoids, prolactin, & placental lactogen: induce enzymes for milk production
- During nursing, prolactin levels stay high: inhibit normal cycling of GnRH (prevent ovulation)
Estrogen & progesterone: high concentrations prevent milk production
- After parturition, E2 & P4 levels fall: milk production begins

106
Q

How to reduce symptoms associated with menopause:

A

Symptoms: vasomotor, osteoporosis, short-term memory change, depression…
Hormonal replacement therapy (HRT): estrogen or estrogen + progesterone
- Almost 75% of women don’t need HRT

107
Q

What happens to GH in adults?

A

Deficiency
Symptoms:
- Cardiovascular risk
- Reduced bone health

108
Q

What happens to thyroid hormone in adults?

A 
Hypothyroidism
Presents multiple clinical symptoms:
- Myxedema
- Coma
Treatment: L-T4 replacement
109
Q

Statistics of menopause

A

At age 51: affects ~90% of women
At age 37.5: oocyte pool is reduced to ~25K
- Increased rate of follicular atresia after this

110
Q

Advantages & disadvantages of HRT

A

Estrogen can inc. risk of endometrial & breast cancer
- Progesterone promotes conversion of estradiol to estrone. Estrone has low affinity to estrogen receptors so can reduce cancer risk
- Long-term effects of progesterone are unknown
Without treatment: bone loss = 1-2% each year (inc. risk of bone fractures)
Estrogen is used to decrease depression due to menopause

111
Q

Prevalence of doping

A

High school, college, & professional athletes ~ 11%

Hollywood actors above 40 years = 50%

112
Q

How caffeine is considered doping

A 
A methylxanthine (purine metabolites)
Exerts effects by:
- Inc. cAMP by inhibition of phosphodiesterase
- Translocation of Ca for inc. neuro-muscular availability
Sport beneficial causes:
- Enhanced nervous function
- Inc. cardiovascular function
Banned in large doses for sports
Most beneficial: in endurance events
Legal limit: 15ug/ml (6-8 cups coffee)
113
Q

How beta blockers are considered doping

A 
Uses:
- Reduce blood pressure
- For migraine headaches
- Reduces heart arrhythmia
- For alcohol withdrawal & anxiety
Function:
- Block beta receptor in cardiac muscles (reduce anxiety, jitters, & slows heart rate
Most beneficial: in sports needing steady hands
114
Q

How erythropoietin (EPO) is considered doping

A 
Uses:
- Stimulates RBC production
- Inc. hematocrit
- Inc. oxygen carrying capacity
Most beneficial: in heavy working sports
115
Q

What do steroidogenic enzymes depend on?

A 
Electron transfer proteins
Mitochondrial electron transporters:
- ADR
- ADX
Microsomal electron transporters:
- POR
- B5
116
Q

What is the function of CYP21A2?

A

Drives production of aldosterone & cortisol of steroidogenesis

117
Q

Inactivation of catecholamines

A

Done via COMT or MAO

- Develop pathways to VMA, which is excreted

118
Q

What occurs when there is high blood glucose?

A

Dec. glucogen breakdown
Inc. glucogen synthesis
Inc. glycolysis

119
Q

Ways to diagnosis diabetes:

A

Check blood glucose levels
- Normal: 6.1mmol/L; 110mg/dl
Check hemoglobin
- Normal: Less than 5.7%

120
Q

What is the normal peak concentration of testosterone during male development?

A

10nmol/L

121
Q

Two types of cells surround a follicle; they are:

A

Theca interna cells: CYP17A1 (capable of synthesizing own androgens)
- Uses LH
Granulosa cells: CYP19A1 (need androgens from theca cells)
- Uses FSH

122
Q

Causes of ovulation

A
  • Elevated blood flow
  • Breakdown of connective tissue
  • Ovarian contractions
    All lead to rupture of follicular wall
123
Q

What are phytoestrogens?

A 
Outside sources (food)
Are not steroids
- Are able to interact with steroid hormones
124
Q

Function of phytoestrogens on hormones

A 
Inhibit TPO
- Result in hypothyroidism
Inc. SHBG (sex hormone)
- Inc half-life of sex steroids
Can bind to estrogen receptors
Induce IGF-1
- Positive effect on bone physiology
Inhibit GnRH
Inc. insulin sensitivity
Induce Adiponectin
Inhibit PSA
* Positive & negative effects

Metabolic Endocrinology (1 decks)

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