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Final Exam Study Guide

Biological Sciences
Course Code
Ingrid L.Stefanovic
Study Guide

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- 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
- 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
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
- 1+ copies of peptide hormone
- Large and inactive ± from ribosomes
- Have signal sequence that directs it to RER
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
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

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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
- Controls digestion/absorption of nutrients
- Secretes insulin and glucagon
- Female gonads secrete estrodiol and progesterone
- Male gonads secrete adrogens = testosterone and androsrenedione
- Secretes thyroid hormones = triiiodthyronin T3 and tetraiodothyronin T4
- Controls metabolic rate, growth, development
- Calcitonin = controls calcium levels
- PTH = parathyroid hormone ± controls calcium levels
- 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
- 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
- True endocrine gland of epithelial origin
- Synthesizes/secretes 6 hormones
- 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
- 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
- Hyposecretion = when not enough hormone secreted
- Exogenous medication = replaces/exceeds normal, cause atrophy of gland
- 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
- 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
- Increased thyroid hormone
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