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The Endocrine System.

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Presentation on theme: "The Endocrine System."— Presentation transcript:

1 The Endocrine System

2 Relevance of the Endocrine System
Recall nervous system: Control is largely “instant” and “transient” Only exerts control over target organ while action potentials & neurotransmitter is released Must directly innnervate that organ (must have synapses within the target organ) Once neurotransmitter release has halted, organ usually returns to “normal” or “unstimulated” state

3 Relevance of the Endocrine System
Endocrine system allows nervous system to control over longer periods Endocrine effects usually long-lasting Normally requires less of the “signal compound” or hormone to stimulate compared to neurotransmission Allows 1 endocrine organ in a central location to influence/stimulate many other organs without direct contact Endocrine system uses BLOOD to deliver the signal Can have a very DIVERSE target (broad delivery pattern) Nervous system is very specific…uses neurons to deliver the signal…very precise targeting

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5 Endocrine System Features
Endocrine glands vs. exocrine glands: Endocrine = no ducts, secrete directly into the bloodstream Hormones are rarely secreted into sweat or ear wax Exocrine = ducts, secrete to the exterior of the body Mucus, sweat, oil, ear wax etc. Endocrine signals (hormones) are generally proteins or modified “lipids” Recall neurotransmitters: single modified amino acids or small peptides Hormones generally larger: Proteins ( amino acids long) Modified lipids (cholesterol)

6 Endocrine System Features
Recall nervous system = very quick effects Stimulus-CNS-response Effects are only during neurotransmitter release Endocrine effects usually much slower Stimulus-CNS-response-hormone release…. Effects much longer-lasting due to the method by which hormones influence their target cells

7 Endocrine System Features
Hormones require the presence of a specific hormone receptor Similar to a neurotransmitter receptor (binds a specific protein rather than neurotransmitter) Receptor does not act as an ion channel (unlike neurotransmitter receptor) Instead, hormone receptors use chemical modifications within the cytoplasm “second messenger” Phosphorylation “dimerization” All of these chemical modifications require time, energy etc.

8 Endocrine System Features
Key point: Like neurotransmitter receptors, unless the target cell expresses the specific hormone receptor, it will not “sense” anything, and will not respond Without the specific hormone receptor, target cells cannot respond to the presence of a hormone Recall that hormones are secreted into blood: Not very much “specific targeting” when it comes to delivery (practically every cell in your body will have access to the hormone once it enters the blood) Specificity requires the target cell to have already expressed the particular receptor for that hormone

9 Endocrine System Features
Recall the types of hormones: Protein: requires a cell-surface receptor Once bound to a hormone, these receptors undergo chemical changes that result in changes within the cytoplasm “second messenger” in your book Modified lipids (cholesterol…steroid hormones) Fat-soluble (lipds) hormones can cross the plasma membrane without an external receptor Bind to cytoplasmic receptors INSIDE the cell rather than on the surface Trigger similar “second messenger” signal “pathway” within the cell

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11 Endocrine System Features
Confusion: from the schematic, you’d think that ALL hormones trigger cyclic adenosine monophosphate (cAMP) production. cAMP is only 1 of many “second messengers” within a cell If cAMP were the ONLY second messenger, ALL hormones would elicit the SAME effects Other second messengers = cGMP, chemical alterations of plasma membrane lipids, phosphorylation of various proteins within the cell etc.

12 Endocrine System Features
Confusion: in this schematic for steroid hormones (modified lipid hormones), it would appear that no second messengers are utilized (in this case, no indication of cAMP) This is also too “simplified”: the cytoplasmic receptors can trigger chemical changes within the cell similar to “second messengers”

13 First & Second Messengers
The “First messenger” = hormone itself Usually doesn’t have to enter the cytoplasm Receptor-hormone binding triggers chemical changes within the cell These chemical changes (cytoplasmic signals through chemical modifications) = “second messenger” Hormone does not have to enter the cytoplasm in order to elicit these effects

14 Second Messengers Whole field of biochemistry & molecular biology devoted studying “signal transduction” What signals are used for particular receptors Endocrine, stress etc. all use signal transduction pathways Series of chemical reactions within the cell that are SPECIFIC for each receptor These different signal transduction pathways are what give hormones their “specificity” WITHIN the cell

15 Second Messengers ?????? Example: 4 different hormones
3 are proteins (water soluble) 1 is a modified lipid (steroid) All 4 have different receptors However, all 4 receptors can elicit cAMP activity (for argument’s sake) HOW do these 4 different receptors stimulate the cell to do completely different things? Different signal transduction pathways AFTER receptor-ligand binding…the cAMP activity might stimulate completely different effects, despite using the same second messenger Imagine trying to chase down all the possible chemical pathways!!!! (it can get overwhelming)

16 Second Messengers ?????? Remember how acetylcholine (neurotransmitter) and epinephrine (neurotransmitter) can have opposite effects in some tissues? Both are generally “stimulatory”, however, in some tissues, these neurotransmitters are inhibitory (reduce activity) Similar concept to different hormone receptors 1 hormone can elicit different effects in different cells if their “second messenger” signal transduction pathways are different

17 Feedback Control Many hormones rely on feedback for secretory control
Once they elicit their effects, the target cells can feed back signals to the origin and reduce hormone secretion Alternatively, once hormone levels reach a particular concentration in the blood, the endocrine organ halts secretion “Negative feedback” (acts to limit; most common feedback control mechanism) “Positive feedback” = stimulation of the target organ/cell triggers MORE hormone release Often seen during parturition & breast feeding

18 Endocrine organs Can be divided into 2 groups: Cranial Extracranial
Within the skull Hypothalamus Pituitary gland Pineal gland Extracranial Outside the skull Thyroid gland Parathyroid gland Thymus Pancreas Adrenals Gonads

19 Hypothalamus Recall regions of the brain
Hypothalamus = below the thalamus Very small region, forms the “third ventricle” Controls the pituitary gland

20 Hypothalamus Secretes number of hormones that control pituitary gland:
“releasing” and “inhibiting” hormones that act on the pituitary gland Tell the gland to “release” a hormone, or “stop releasing” Also produces a number of hormones that are transported into the pituitary to other specialized “storage” cells These cells will release the hypothalamus-produced hormones upon neural commands from the hypothalamus itself

21 Green = hormones produced in the hypothalamus that are transported into the posterior pituitary gland Purple= hormones produced in the anterior pituitary that are only released upon the correct hormone signal from the hypothalamus

22 Pituitary gland Sometimes mistakenly called “master endocrine gland”
Remember that the pituitary gland will NOT release anything unless it receives input from the hypothalamus Two distinct regions of the pituitary gland: Posterior (neurohypophysis) Under neural control Anterior (adenohypophysis) Under hormone control

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24 Pituitary gland Two distinct regions of the pituitary gland:
Posterior (neurohypophysis) Anterior (adenohypophysis) Remember the hypothalamus: Releases “control” hormones to the anterior pituitary gland Anterior pituitary then releases or stops releasing the corresponding hormone This system relies on a distinct blood flow/vessel system = portal blood system

25 Portal System In order to directly control the pituitary, the hypothalamus blood vessels are joined to the pituitary blood vessels in a “portal system” Veins from the hypothalamus (where the hypothalamic hormones are released into) merge with capillaries that feed into the anterior pituitary Carries oxygen-rich blood to pituitary, along with the “control” hormones from the hypothalamus Normally artery-capillary-vein-heart Portal system = artery-capillaryA-vein-capillaryB-vein-heart

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27 Pituitary hormones Anterior lobe (adenohypophysis) hormones
Growth hormone Thyrotrophin (stimulates thyroid…another endocrine organ) Adrenocorticotrophic hormone (stimulates adrenals…another endocrine hormone) Follicle stimulating hormone (FSH…stimulates gonads) Lutenizing hormone (with FSH, triggers ovulation & sperm production) Prolactin (for breastmilk production) Melanocyte stimulating hormone (skin tone)

28 Pituitary Hormones Posterior lobe (neurohypophysis)
Oxytocin: actually made in hypothalamus, transported down to posterior pituitary Triggers labor contractions Stimulates mammary glands to produce milk Anti-diuretic hormone (vasopressin) Also made in hypothalamus & stored in posterior pituitary Reduces H2O loss from renals (reduces water loss)

29 Pineal Gland Located behind/posterior to the thalamus, above cerebellum Larger in children than adults Secretes melatonin: involved in circadian rhythm

30 Thyroid Located in neck (surrounds trachea) Largest endocrine gland
Heavily reliant on iodine Thyroxine: increase protein synthesis, increase carbohydrate metabolism Tri-iodo-thyronine: more potent than thyroxine Calcitonin: decrease blood calcium through inhibition of osteoclast activity

31 Parathyroid Parathyroid gland(s)
Behind/posterior to the thyroid gland (para = around) 4 distinct glands Secretes parathyroid hormone: increase blood calcium concentration Increase osteoclast activity Antagonizes calcitonin

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33 Adrenal Glands On superior edge of both kidneys 2 portions:
Outer cortex (adrenal cortex) bulk of the adrenal gland Inner medulla (adrenal medulla) Produce adrenaline & norepinephrine (catecholamines) Increase cardiac output, dilate blood vessels, increase mental alertness, increase metabolic rate

34 Adrenal Glands Outer cortex (bulk of the adrenal gland)
Mineralcorticoids (mineral-targeting hormones from the cortex) Controls electrolyte homeostasis (influences aldosterone…works on kidneys to control sodium and potassium losses) Glucocorticoids (glucose-metabolism hormones from the cortex) Controls metabolic rate, inflammation, vasoconstrictoin Gonadocorticoids (gonad-targeting hormones from the cortex) Estrogen & testosterone

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36 Pancreas Has BOTH endocrine & exocrine functions
Endocrine = blood-glucose regulation Glucagon: acts to increase blood glucose through gluconeolysis (liver digestion of glycogen stores) From alpha cells of the endocrine pancreas Insulin: acts to decrease blood glucose through gluconeogenesis (liver & skeletal muscle polymerization of glycogen from glucose) From beta cells of the endocrine pancreas

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38 Gonads (sex/reproductive organs)
Testes & ovaries “mixed glands” (make both sex hormones & sex cells) Testes: testosterone made by interstitial cells Controls sex organ development Ovaries: follicles produce estrogens Corpus luteum also produces progesterone (for pregnancy)

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40 Thymus Larger in children than adults
Associated heavily with the lymphatic system (“T-cell” = thymus-dependent cell) Produces thymosin: influences T-cells following exit from the thymus

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42 Endocrine pathophysiology
Endocrinology often quite challenging Hormones are very specific (target specific receptors on specific cells) Responses are often linked (often 4-5 hormones can elicit similar “whole body” effects) Often linked to metabolic disorders Have to treat metabolic condition first, endocrine issue follows Often diagnosed via blood tests Radioimmunoassays (check for hormone concentration) Cholesterol tests (assess metabolic function) Iodine (assess thyroid function)

43 Endocrine pathophysiology
Pituitary pathophysiology Panhypopituitarism: reduced pituitary activity or total loss of pituitary function Decreased sex organ function Supplement with exogenous hormones Abnormal growth hormone: Inadequate during childhood = pituitary dwarfism Inadequate during adulthood = Simmond’s disease Premature aging Oversecretion during childhood = gigantism Oversecretion during adulthood = acromegaly Bones thicken, soft tissues grow inappropriately

44 Acromegaly Gigantism Occurs during adulthood Begins during childhood

45 Endocrine pathophysiology
Pituitary pathophysiology Inadequate anti-diuretic hormone secretion Diabetes insipidus (polyurea…excess urination; ionic imbalances secondary to excess urine production)

46 Endocrine pathophysiology
Thyroid & parathyroid pathophysiology Hypothyroidism During childhood = cretinism (“cretins”) Child starts normally due to thyroxine from mother Treat with exogenous thyroxine During adulthood = myxedema Edema throughout the body, increased blood pressure Goiter (abnormal thyroid growth) Endemic = inadequate iodine intake Grave’s disease = autoimmune disease; antibodies act as thyroid stimulating hormone to stimulate inappropriate thyroid growth

47 Cretinism Myxedema Endemic goiter Grave’s disease

48 Endocrine pathophysiology
Pancreatic pathophysiology Diabetes mellitus Type I diabetes: insulin dependent due to autoimmune destruction of pancreatic beta cells (loss of insulin production) Type II diabetes: insulin insensitive due to reduced responsiveness to insulin (metabolic obesity) Reactive hypoglycemia (usually coupled with Type II diabetes) Carbohydrates trigger excessive insulin response = post-prandial hypoglycemia

49 Endocrine pathophysiology
Adrenal pathophysiology Pheochromatocytomas: chromaffin cell tumor Excessive norepinephrine secretion = resembles ANS overstimulation Addison’s disease: decreased mineralcorticoid & glucocorticoid secretion Constant hypoglycemia, electrolyte imbalances Cushing’s syndrome: increased glucocorticoid secretion (Zona fasciculata) Altered metabolism and physical changes indicative of edema

50 Pediatric Cushing’s syndrome


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