1. Water Soluble Hormones
Fast acting hormones – affect depends on 2nd messenger, not hormone
Signal amplification – hormones that stimulate synthesis of 2nd messengers can produce an almost instantaneous response because they influence existing enzymes; each receptor produces 1000s of 2nd messengers, leading to a cascade effect & ultimately amplification of hormonal signal
Signal Amplification

2. Lipid Soluble Hormones
Slow acting hormones – requires intracellular receptor
Increases or decreases synthesis…

3. Heads Up
I am obviously not Steve

4. The Pea Sized Pituitary a.k.a. ‘Hypophysis’
TWO lobes
Anterior pituitary (Adenohypophysis) – 7 hormones
Glandular tissue – produces hormones in situ (by specific cell)
Posterior pituitary (Neurohypophysis) – 2 hormones
Hormones produced in hypothalamus  transported via nerve cell to pituitary
diencephalon  ‘infundibulum’  pituitary

5. Pro-opiomelanocortin - The Prohormone
POMC – large precursor molecule of anterior pituitary
Enzymatic Breakdown Products Include
Adrenocorticotropic hormone (ACTH)
2 natural opiates – enkephaline & beta endorphin
Melanocyte-stimulating hormone (MSH)

6. Anterior Pituitary Hormones
Hormones – 6 distinct but two of prohormone origin
Growth hormone (GH)
Thyroid-stimulating hormone (TSH) or thyrotropin – tropic
Adrenocorticotropic hormone (ACTH) – prohormone origin tropic
Follicle-stimulating hormone (FSH) – tropic
Luteinizing hormone (LH) - tropic
Prolactin (PRL)
Melanocyte stimulating hormone (MSH) – prohormone origin
TROPIC =
affects activity of other endocrine glands

7. Hypothalamus & Anterior Pituitary Relationship
A.K.A. Adenohypophysis
‘glandular undergrowth’
Hypothalamus hormones travel through delivery system to anterior pituitary
‘portal system’
Negative feedback allows control…

8. Understanding The Endocrine System Health VS Disease
Hormones are ‘Just’ chemicals…
The Goldie Locks Rule!!!
Too Much Hormone
Just Right Hormone Level
Too Little Hormone

9. Growth Hormone (GH)
Stimulates most cells, but esp. bone & skeletal muscle
Promotes protein synthesis & fat mobilization
Most effects are mediated indirectly by insulin-like growth factors (IGFs)
Hypothalamus has regulatory role over A.P. hormone release!!!
IGFs are a family of growth-promoting proteins produced by liver, skeletal muscle, bone & other tissues. IGFs from liver act as hormones, others act locally within those tissues. IGFs stimulate uptake of nutrients from blood & incorporation into proteins & DNA allowing growth by cell division. They also act to form collagen & deposition of bone matrix.
GHIH – growth hormone-inhibiting hormone (somatostatin)

10. Homeostatic Imbalances of Growth Hormone
Hypersecretion
Children – gigantism
Adults – acromegaly
Hyposecretion
Children – pituitary dwarfism
Adults – Simmond’s disease

11. Thyroid-Stimulating Hormone (Thyrotropin)
Basic Function
Summary of Regulation
Stimulates the normal development and secretory activity of the thyroid
Regulation of TSH release
Stimulation = thyrotropin-releasing hormone (TRH)
Inhibition = thyroid hormones  2 impacts
Packet calls it ‘thyroid releasing factor’ – TRF
‘Endocrine’ pg 11

12. Adrenocorticotropic Hormone (Corticotropin)
Stimulates the adrenal cortex to release corticosteroids
Regulation of ACTH release
Hypothalamus releases corticotropin-releasing hormone (CRH) in a daily rhythm
Fever, hypoglycemia, and stress can alter the release of CRH

13. Gonadotropins – ‘Stimulate Gonads’
FSH – follicle stimulating hormone
LH – lutenizing hormone
Regulation of Gonadotropin Release
FSH stimulates gamete (egg or sperm) production
LH stimulates ovulation & corpus luteum formation in women, & production of sperm in men
Both absent in blood prepuberty…

14. Prolactin PRL PRL primarily controlled via inhibitory hormone
Stimulates milk production
Blood levels rise toward the end of pregnancy
Suckling stimulates PRL release and promotes continued milk production
Secreted in men, no apparent function
PRL primarily controlled via inhibitory hormone

15. Melanocyte Stimulating Hormone
MSH
Hormonal Control of Energy Balance
Stimulates melanocytes to synthesize & deposit melanin
NOT important in humans
Agouti-related peptide (AgRT), CRH, corticotropin releasing hormone, MCH – melanin-concentrating hormone, alpha MSH = melanocyte-stimulating hormone, NPY – neuropeptide Y, orexins, orexigenic peptides, POMC – pro-opiomelanocortin, PYY peptide YY, TRH – thryotropin releasing hormone
Acts as CNS neurotransmitter involved in control of appetite

16. Posterior Pituitary – A Different Breed
Hormones are produced in neurons of hypothalamus
Stored in axon terminals that extend into pituitary
Release is stimulated with nerve impulses not chemical signals
Rely on 2nd messengers
A.K.A. Neurohypophysis
‘neural undergrowth’

17. Posterior Pituitary Hormones
Antidiuretic Hormone (ADH) a.k.a. vasopressin
Increases water retention at kidneys & arteriole vasoconstriction
Hyposecretion  ‘diabetes insipidus’ (cause - head trauma)
Symptoms include???
Hypothalamus – measures blood [solute]
Alters kidney function – maintain water balance

18. Posterior Pituitary Hormones
Oxytocin
Stimulates uterine contractions during labor
Triggers milk ejection (“letdown” reflex) during nursing
Synthetic form used to induce labor or stop postpartum bleeding

19. Thyroid & Parathyroid Glands
Below larynx
2 Lobes & Isthmus
Produces 2 hormone types
Metabolic & [Ca2+] regulation
4-8 tiny glands - posterior aspect of the thyroid
Produces 1 hormone
[Ca2+] regulation

20. Thyroid Gland Follicles produce glycoprotein thyroglobulin
(Thyroglobulin + iodine) fills follicles is precursor of thyroid hormone
Parafollicular cells produce the hormone calcitonin

21. Thyroid Hormone (TH) TH = 2 Hormones Actually two related compounds
T4 (thyroxin); has 2 tyrosine molecules + 4 bound iodine atoms
T3 (triiodothyronine); has 2 tyrosines + 3 bound iodine atoms

22. Thyroid Hormone (TH) Functions Increases metabolic rate
Regulates tissue growth & development
Especially nervous system
Increases reactivity of mature nerve cells
Heart rate, digestive motility
Guess ‘who’ regulates it’s release???
Catecholamines – epinephrine, norepinephrine, dopamine etc.

23. Transport and Regulation of TH
Negative feedback regulation of TH release

24. Synthesis of Thyroid Hormone
Follow the 7 Steps
Iodide enters & converted to iodine &…
binds with thyroglobulin
(tyrosine + iodized thryoglobulin) enters lysosome
thyroglobulin removed & T3 & T4 go to blood
T3 10x more active than T4
- T4 converted to T3 by peripheral tissues enzymes

25. Homeostatic Imbalances of TH
Hyposecretion in adults— endemic goiter if due to lack of iodine ; myxedema
Hyposecretion in infants—cretinism
Hypersecretion—Graves’ disease
Myxedema = ‘mucous swelling’ – low BMR, chills, constipation, thick dry skin & puffy eyes, edema, lethargy & mental sluggishness
Goiter = enlarged thyroid occurs if myxedema results from lack of iodine. Follicular cells produce colloid but cannot iodinate it and make functional hormones. Pituitary gland secretes increasing TSH, but only causes increase size of follicles as more colloid accumulates.
Cretinism =
Graves = autoimmune disease where production of antibodies that mimic TSH cause continuous release of TH.
excessive thyroxin – high metabolic rate, exopthalamia, weight loss (autoimmune)
insufficient thyroxin – small stature, mental retardation, low body T, fat buildup
insufficient thyroxin – lethargy, low body T., swollen face, edema, leathery skin

26. Thyroid & Parathyroid Balancing Act
- Osteoblast activity
- Ca2+ uptake in bone
FEEDBACK
- Ca2+ absorption
- Osteoclast activity
- Ca2+ reabsorption

27. Homeostatic Imbalances of PTH
Hyperparathyroidism due to tumor
Bones soften and deform
Elevated Ca2+ depresses the nervous system and contributes to formation of kidney stones
Hypoparathyroidism following gland trauma or removal
Results in tetany, respiratory paralysis, and death

28. Another More Holistic View

29. Adrenal (Suprarenal) Glands
Structurally and functionally, they are 2 glands in 1
Adrenal medulla—nervous tissue; part of the sympathetic nervous system (NE, E)
Adrenal cortex—glandular tissue that synthesize & secrete 3 corticosteroids from 3 layers

30. Mineralocorticoids – Outer Cortex
Mineralcorticoids
Important - Aldosterone
Regulate ECF electrolytes esp. Na+ and K+
Na+  affects ECF volume, BV, BP, other [ions]
K+  sets RMP of cells
Aldosterone increases reabsorption of Na+, H2O retention, & secretion of K+

31. Glucocorticoids – Middle Cortex Cortisol & Cortisone
General Function
Function to regulate carb. metabolism
Released in response to ACTH, eating patterns, activity & stress
Maintain BP by increasing vasoconstriction & suppress inflammation
When someone experiences a stressful event, the level of glucocorticoids in their blood rises. Via specific receptors in the hippocampus, this activates the hypothalamus, which then secretes corticotropin-releasing hormone (CRH). The CRH in turn causes the pituitary gland to release adrenocorticotropic hormone (ACTH) into the bloodstream, from which it enters the adrenal glands and causes them to secrete cortisol. This process creates a negative feedback loop in which the excess cortisol activates the brain's glucocorticoid receptors and suppresses the production of CRH. In depressed patients, however, this loop no longer works, resulting in excess production of CRH and hence of cortisol. Many seriously depressed patients have high blood levels of cortisol, caused by chronic stress.

32. Glucocorticoids – Middle Cortex Cortisol & Cortisone
How it Works
#1 metabolic effect is ‘gluconeogenesis’
protein  AA  glucose (in liver)
Promotes rises in blood glucose, fatty acids, and amino acids
Gluconeogenesis – synthesis of glucose from a noncarbohydrate precursor

33. Homeostatic Imbalances of Glucocorticoids
Hypersecretion—Cushing’s syndrome
Hyperglycemia
Redistribution of body fat
Easy bruising, poor wound healing
Loss of body protein
Tx – remove pituitary OR adrenals…why???
Cushing’s syndrome – glucocorticoid excess VS Cushing’s disease - caused by an ACTH-releasing pituitary tumor
Suppresses inflammation, immune function & causes gluconeogenesis which harvests nutrients such as fat & protein breakdown products to produce more glucose

34. Homeostatic Imbalances of Glucocorticoids
Hyposecretion—Addison’s disease
Weight loss
High K+, low Na+
Hypoglycemia
Bronzing of the skin
Fatal if untreated
ACTH activates MSH receptors on melanocytes
Usually involves both deficit of glucocorticoids & mineralcorticoids  which is why patients experience high K+ & low Na+ because of deficiency of aldosterone
Leading to hypotension & dehydration due to inappropriate fluid & electrolyte balance
Alpha MSH is identical to ACTH in the 1st 13 AA  due to this similarity it is thought that ACTH is able to stimulate melanocytes to produce melanin.

35. Gonadocorticoids (Sex Hormones) – Inner Cortex
Primary function – supplement hormones released in ovaries & testes
May contribute to
The onset of puberty
The appearance of secondary sex characteristics
Sex drive
Nothing to do with anything

36. Adrenal Medulla NS controlled  80% E & 20% NE
Remember ‘sympathomimetic’
2 hormones exert ‘same’ effects
E. metabolic activities, bronchial dilation, & BF to skeletal muscles & heart
N peripheral vasoconstriction & BP, heart rate & stroke volume

37. Thymus 2 lobed organ – high in chest, anterior to aorta
Fetal development & 2 yrs post-birth  atrophy
Produces thymosin (& others)  stimulate lymphocyte production
Autoimmune diseases often associated with enlarged thymus

38. Pineal Gland Produces melatonin, derived from serotonin
Melatonin may affect
Timing of sexual maturation and puberty
Day/night cycles
Physiological processes that show rhythmic variations (body temperature, sleep, appetite)
3rd ventricle – part of epithalamus

39. Stress & Adaptation – Hans Selye
Physical or psychological – response varies
Hypothalamus - monitors & can set homeostasis to new values
Eustress VS Distress

40. Stress & Adaptation – Hans Selye
General Adaptation Syndrome (GAS)
Alarm Stage
Resistance Stage
Exhaustion Stage

41. Fight or Flight – Plateau – Failure
Alarm - immediate
Hypothalamus, symp. NS & adrenal medulla
What is the reaction? HR BP
vessels
respiration
RBC #
glyc/gluc
sweat
digestion
Resistance – long-term modification
Hypothalamus  pituitary
Angiotensin
ACTH  glucocorticoids
TSH  thyroxin GH
ADH
Inc. E. availability!!!
Build
Circulate
i.e. Physical Fitness
Exhaustion – loss of battle (possibly death)
Continual K+ loss
Glucocorticoid depletion
Cell starvation
Immune failure

42. Pancreas Exocrine cells  enzyme-rich digestive juices Endocrine cells
Long, flat organ behind the stomach
Exocrine cells  enzyme-rich digestive juices
Endocrine cells
Alpha ()  Glucagon
Beta ()  Insulin

43. Diabetes mellitus

44. Homeostatic Imbalances of Insulin
Diabetes mellitus (DM) – I & II
Alternative Table
‘Endocrine’ 16