Final Exam Study Guide

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HORMONES:
- Endocrine glands/cells = secrete chemical messengers directly into blood
- Can be transported to distant targets
- ([RFULQHJODQGVGRQWVHFUHWHKRUPRQHV± e.g. salivary, sweat, mammary glands
- Effect over time ± sec, min, hour, day, week, month
- Low concentration effects
HORMONE EFFECTS:
- Growth and development, metabolism, regulates temp, pH, water balance, hunger, reproduction
- Bind to receptor for response
- Acts on multiple tissues
- Hormone effect depends on tissue type and development stage
- Enzymes degrade it into inactive metabolites ± liver, kidneys
- Excreted in urine and bile
- Half life = time needed to decrease hormone concentration in blood by half
HORMONE TYPES:
1. Amine hormone
- Small molecule
- ½ life = seconds
- E.g. melatonin, thyroid hormone
2. Peptide hormone
- Most common = made all over body
- Lipophobic ± b/c binding to membrane receptor
- Fast acting ± ½ life = minutes
- Hydrophilic ± transported easily thru body
- E.g. pituitary hormones, pancreas hormones ± insulin, glucagen
Preprohormone
- 1+ copies of peptide hormone
- Large and inactive ± from ribosomes
- Have signal sequence that directs it to RER
PEPTIDE HORMONE SYNTHESIS:
1. ULERVRPHVP51$ELQGVSUHSURKRUPRQH± directed into ER by signal sequence on preprohormone
2. Enzymes in ER chop signal sequences = inactive prohormone
3. Prohormone passes from ER to golgi complex
4. Secretory vesicles w/ enzymes and prohormone buds of golgi ± prohormone chopped into 1+ peptide hormones
5. Secretory vesicle releases contents by exocytosis into extracellular fluid
6. Hormone moves into circulation for transport to target
7. Peptide hormone = lipophilic
8. Binds to surface membrane receptor
9. Hormone-receptor complex initiates cell responses
10. Activates 2nd messenger cascade ± e.g. cAMP
11. Causes opening/closing of ion channels, metabolic enzymes and transport proteins, protein synthesis
3. Steroid hormone - cholesterol
- All similar structure
- Lipohilic ± receptor w/in target cell [cytoplasm/nucleus]
- Bind DNA to activate/turn off protein synthesis
- Slow acting ± ½ life long
- Not soluble in plasma/body fluids = hydrophobic ± need carrier protein for circulation [sometimes specific =
corticosteroid binding protein or are general plasma proteins = albumin]
- Made in adrenal glands, gonads, placenta
- Synthesized in SER
- E.g. cortisol, sex hormones
STEROID HORMONE ACTION
1. Steroid binds to plasma protein carriers in blood ± only unbound hormones diffuse into targets
2. steroid hormone receptors in cytosol/nucleus ± some steroid hormones bind to membrane receptors a nd use 2nd
messenger systems for rapid cell responses
3. Receptor-hormone complex binds to DNA ± activates/represses 1+ genes
4. Activated genes create new mRNA that moves into cytoplasm
5. Translation produces new proteins for cell processes
ADRENAL GLAND
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- Specialized neuroendocrine tissye of SNS
- Secretes 3 steroid hormones:
- Aldosterone = mineralocorticoid ± controls water/sodium retention in kidneys
- Glucocorticoids = cortisol
- Sex hormones = androgens, estrogen, progesterone
PANCREAS
- Controls digestion/absorption of nutrients
- Secretes insulin and glucagon
- Female gonads secrete estrodiol and progesterone
- Male gonads secrete adrogens = testosterone and androsrenedione
THYROID
- Secretes thyroid hormones = triiiodthyronin T3 and tetraiodothyronin T4
- Controls metabolic rate, growth, development
- Calcitonin = controls calcium levels
PARATHYROID
- PTH = parathyroid hormone ± controls calcium levels
THYMUS GLAND
- Secretes thymosin = maintains levels of cytoplasmic G-actin
- Controls IS
- Secretes T lymphocytes = T cells
- Pineal gland releases melatonin
- Influence circadian rhythms
- Inhibits sexual behavior
- Stimulates IS
- Endocrine cell senses stimulus and responds by secreting hormone
- Endocrine cell acts as sensor/receptor and integration system
- E.g. insulin and glucagon secreted from pancreas to modulate blood glucose
PTH
- Monitors plasma calcium
- Parathyroid cells linked to GPCR that binds calcium
- When calcium bound to GPCR, PTH secretion inhibited
- When plasma calcium falls, less calcium bound to GPCR and PTH inhibition stops
- PTH secreted into blood stream ± act on bone, kidney, intestine to increase calcium
ANTERIOR PITUITARY GLAND
- True endocrine gland of epithelial origin
- Synthesizes/secretes 6 hormones
POSTERIOR PITUITARY GLAND
- Extension of neural tissue
- Stores/secretes hormones synthesized in hypothalamus ± trafficked by infundibulum
- Posterior pituitary gland secretes hormones synthesized in hypothalamus
- Vasopressin = antidiuretic hormone, controls water balance
- Oxytocin = ejection of milk, contraction of uterus in labor
ANTERIOR PITUITARY GLAND
- w/out it, die in 2-3 days
- Secretes: prolactin, thyroid stimulating hormone = thyrotropin, adenocorticotrophin, growth hormone, follicle
stimulating hormone, lutenizing hormone
- Secretion of ANTPIT hormones controlled by hypothalamus
- All ANTPIT hormones regulate secretion of another hormone in endocrine target cell
- Antpit hormones = trophic hormones ± µWRQRXULVK
- Antpit hormones named by target
HHPS = hypothalamic-hypophyseal portal system
- Specialized region of circulation ± connects antpit and hypothalamus to closed circuit of blood vessels
- Transports hypothalamic trophic neurons to antpit ± regulates antpit hormone secretion
- Portal allows smaller amounts of hormone to be released to elicit given response compare dot hormones released into
general circulation
- Complex feedback look regulates secretion of hypothalamic/pituitary hormones
- More complex than simple feedback loop
- 3 integrating centers:
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- Hypothalamus
- Pituitary gland
- Endocrine gland
- Hormones act as negative feedback ± NOT response
- Hormone suppresses hormone secretion
- Change in secretion of 1 hormone in complex reflex pathway causes secretion of other hormones in loop to change
- Trophic hormone = controls release of another hormone
- 'RQWDIIHFWWDUJHWRUJDQV
ENDOCRINE PATHOLOGIES
- Hyposecretion = when not enough hormone secreted
- Exogenous medication = replaces/exceeds normal, cause atrophy of gland
PRIMARY AND SECONDARY PATHOLOGIES
- Diagnosis of endocrine pathologies depend on complexity of reflex
- When pathology arises in last endocrine gland in reflex = PRIMARY PATHOLOGY
- E.g. tumor in adrenal cortex producing excessive cortisol causes primary hypersecretion
- If pathology arises in tissue producing trophic hormones = SECONDARY PATHOLOGY
- E.g. pituitary damaged due to head trauma, corticotrophin secretion decreased, results in cortisol deficiency ±
secondary hyposecretion
CORTISOL
- hypothalamic-pituitrary-adrenal cortex axis = HPA ± controls cortisol secretion
- Cortisol releasing hormone CRH = released from hypothalamus into HHPS = hypothalamic-hypophyseal portal system
- Causes secretion of adenocorticotrophin hormone ACTH from pituitary
- Acts on adrenal cortex causing release of cortisol
- Cortisol controls negative feedback
- Transported cortico-steroid binding globulin ± receptors located in nucleus/cytosol
- Cortisol released continuously ± release highest in morning, lowest at night
- Removal or adrenal glands causes death w/in days when exposed to stress
- Cortisol release increased in response to stress ± fight/flight ± protects body from hypoglyycemia
- Brain function = mood, learning, memory
- Cortisol = cataboilic [fig 23.3]
- Breaks down glycogen to glucose = glycogenolysis ± in liver, released into blood
- Breaks down protein in muscle to form glucose = gluconeogenesis
- Lipolysis = increased fat breakdown to form fatty acids for energy
- Decreased blood plasma calcium ± decreased bone density
- Suppression of IS:
- Decrease WBC, antibodies, inflammation
- Immunosuppressant for bee sting, poison ivy, organ transplant rejection
- Hypercortisolism = excess cortisol [fig 7.20]
- When pathology arises in primary endocrine gland in reflex = PRIMARY PATHOLOGY
- E.g. tumor in adrenal cortex produces excess cortisol, causes primary hypersecretion
- If pathology arises in tissue producing trophic hormones = SECONDARY PATHOLOGY
- +\SHUFRUWLFROLVP&86+,1*66<1'520(
- - excess gluconeogenesis causes hyperglycemia
- Muscle and tissue wasting ± thin arms/legs
- Increase appetite ± causes increased fat deposition in trunk/waist ± µPRRQIDFH
- Mood elevation followed by depression
- +\SRFRUWLVROLVP$'',6216',6($6(
- Hyposecretion of all adrenal steroid hormones
- Fatigue, nausea, vomiting, hyperpigmentation, generalized weakness
- Hypoglycemia
- Caused by autoimmune destruction of adrenal cortex and defects in enzymes needed for adrenal hormone production
TH - TRH = thyroid releasing hormone
- TSH = thyroid stimulation hormone = thyrotrophin
- Promotes synthesis of thyroid hormones = T3 / T4 ± targets tissues
- Negative feedback controlled by T3 / T4
HYPERTHYROIDISM
- Increased thyroid hormone
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Document Summary

Endocrine glands/cells = secrete chemical messengers directly into blood. Effect over time sec, min, hour, day, week, month. Growth and development, metabolism, regulates temp, ph, water balance, hunger, reproduction. Hormone effect depends on tissue type and development stage. Enzymes degrade it into inactive metabolites liver, kidneys. Half life = time needed to decrease hormone concentration in blood by half. E. g. melatonin, thyroid hormone: peptide hormone. Most common = made all over body. Lipophobic b/c binding to membrane receptor. Fast acting life = minutes. E. g. pituitary hormones, pancreas hormones insulin, glucagen. Have signal sequence that directs it to rer. Lipohilic receptor w/in target cell [cytoplasm/nucleus] Bind dna to activate/turn off protein synthesis. Not soluble in plasma/body fluids = hydrophobic need carrier protein for circulation [sometimes specific = corticosteroid binding protein or are general plasma proteins = albumin] Aldosterone = mineralocorticoid controls water/sodium retention in kidneys. Male gonads secrete adrogens = testosterone and androsrenedione.

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