By MD, PhD, Associate Professor

CONTENTPituitary gland. Hyperfunction and hypofunction, Etiology, pathogenesis, and manifestations. Adrenal gland, etiology, pathogenesis, manifestations of hyperfunction and hypofunction.Thyroid gland. Hyperfunction and hypofunction, Etiology, pathogenesis, and clinical manifestations.Parathyroid glands.

Actuality of the lecture.The endocrine system is involved in all of the integrative aspects of life, including growth, sex differentiation, metabolism, and adaptation to an ever-changing environment. This chapter focuses on general aspects of endocrine function, organization of the endocrine system, hormone receptors and hormone actions, and regulation of hormone levels.The endocrine system uses chemical substances called hormones as a means of regulating and integrating body functions. The endocrine system participates in the regulation of digestion, use, and storage of nutrients; growth and development; electrolyte and water metabolism; and reproductive functions. Although the endocrine system once was thought to consist solely of discrete endocrine glands, it is now known that a number of other tissues release chemical messengers that modulate body processes. The functions of the endocrine system are closely linked with those of the nervous system and the immune system.

*Major human endocrine glands

Hormones chemical nature:) steroid hormones (mineral and glucocorticoids, female and male sexual hormones); b) derivatives of aminoacids (thyreoid hormones, catecholamines, melatonine); c) protein peptide hormones (releasing-hormones, vasopressin, oxytocin, hormones of adenohypophysis, insuline,glucagone, parathyrin, calcitonine).

Somatostatin

Lipid-soluble hormones (steroid hormones) pass easily through cell membranes, while water-soluble hormones (polypeptides and amines) do notThe solubility of a hormone correlates with the location of receptors inside or on the surface of target cells

Water-soluble hormones are secreted by exocytosis, travel freely in the bloodstream, and bind to cell-surface receptors Lipid-soluble hormones diffuse across cell membranes, travel in the bloodstream bound to transport proteins, and diffuse through the membrane of target cells

SignalreceptorTARGETCELLSignal receptorTransportproteinWater-solublehormoneFat-solublehormoneGeneregulationCytoplasmicresponseGeneregulationCytoplasmicresponseORSignal receptorWater-solublehormoneFat-solublehormoneTARGETCELLNUCLEUS(a)(b)TransportproteinSignalreceptor(a)NUCLEUS(b)

*Receptor location varies with hormone type

Glycogendeposits receptorVesseldilates.Epinephrine(a) Liver cellEpinephrine receptorGlycogenbreaks downand glucoseis released.(b) Skeletal muscle blood vesselSame receptors but differentintracellular proteins (not shown)

Epinephrine receptor

Different receptorsEpinephrine receptorVesselconstricts.(c) Intestinal blood vessel

*One hormone, different effects

Etiology of endocrine disordersReasons and kinds of endocrine disorders. Among numerous ethiological factors of endocrine disorderss it is possible to select the following main ones: a mental trauma, necrosis, tumour, inflamatory process, bacterial and viral infections, intoxications, local disorders of blood circulation (hemorrhage, thrombosis), alimentary disorders (deficiency of iodine and cobalt in food and drinking water, redundant consumption of carbohydrates),ionising radiation,inherent chromosome and gene defects.

There are three variants of endocrine functions disorders:

1. Hyperfunction of endocrine glands2. Hypofunction of endocrine glands3. Disfunction of endocrine glandsDisfunction is characterized by different changes of hormonal production and production physiologic active precursors of their biosynthesis in the same endocrine gland or synthesis and enteringin blood of atypical hormonal products.

Pathogenesis of endocrine disordersThe mechanisms of function disorders of an endocrine gland can be various depending on localization and character of process. In pathogenesis of endocrine disorders it is possible to select three main mechanisms:

1) Disorders of regulation of endocrine glands disregulatory disorders; 2) Disorders of biosynthesis of hormones and their secretion glandular disorders;3) Disorders of the transport, reception and metabolism of hormones peripheral disorders.

Control of hormone release1. Negative feedback ["stimulatory-inhibitory"]2. Positive feedback ["stimulatory-stimulatory"]3. Endocrine gland stimuli: humoral stimuli, neural stimuli, hormonal stimuli

This gland makes me wake up in the morning and ready to go!Pineal Gland

melatonin"The 3rd Eye" Midline location above the quadrigeminal plate

*The pineal gland (also called the pineal body, epiphysis cerebri, epiphysis or the "third eye") is a small endocrine gland. It produces melatonin, a hormone that affects the modulation of wake/sleep patterns and photoperiodic (seasonal) functions. It is located near to the center of the brain between the two hemispheres, tucked in a groove where the two rounded thalamic bodies join. Unlike much of the rest of the brain, the pineal gland is not isolated from the body by the blood-brain barrier system. It is reddish-gray and about the size of a pea (8 mm in humans).

This gland is called the master gland because it secretes nine hormones many of which control other endocrine glands by feedback control.Pituitary Gland

*Anterior pituitary lobe = adenohypophysis = Rathkes pouch = pars distalis. Hormones released here are also made here. Anterior lobe is WiFi.Posterior pituitary lobe = neurohypophysis = infundibulum = pars nervosa. Hormones released here are made in the hypothalamus. Posterior lobe is Hard-Wired.

Tropic effects only:FSHLHTSHACTHNontropic effects only:ProlactinMSH

Nontropic and tropic effects:GH

*Hormones from basophils go to other endocrine glands, thyroid, adrenal cortex, ovary, testis. Cells from acidophils do NOT.Acidophils make GROWTH related hormones.Basophils make hormones which stimulate other endocrine glands.Chromophobes make NOTHING.The posterior pituitary (aka, pars nervosa or neurohypophysis) looks like typical brain tissue. Why? Ans: It IS typical brain tissue. The pituicytes are glial cells. Herring bodies are massively dilated terminal axons from the hypothalamus.The posterior pituitary does not make these hormones, it just releases them. The hypothalamus actually makes the hormones and transfers it down the stalk to the neurohypophysis.

Anterior PituitaryPosterior pituitary

*A tropic hormone regulates the function of endocrine cells or glandsThe four strictly tropic hormones areThyroid-stimulating hormone (TSH) Follicle-stimulating hormone (FSH)Luteinizing hormone (LH)Adrenocorticotropic hormone (ACTH)

Type of AdenomaSecretionStainingPathologyCorticotrophic adenomasSecrete adrenocotrophic hormone (ACTH) and Proopiomelanocortin (POCM)BasophilicCushings diseaseSomatotrophic adenomasSecrete growth hormone (GH)AcidophilicAcromegaly (Gigantism)Thyrotrophic adenomas (rare)Secret thyroid stimulating hormone (TSH)BasophilicOccasionally hyperthyroidism usually does not cause symptomsGonadotrophic adenomasSecrete luteinizing hormone (LH), follicle stimulating hormone (FSH)BasophilicUsually does not cause symptomsProlactinomasSecret prolactinAcidophilicGalactorrhea, hypogonadism, amenorrhea, infertility and impotenceNull cells adenomasDo not secrete hormonesMay stain positive for synaptophysin

Disturbances of functions of hypophysis.Hypofunction of adenohypophysis (hypopituitaritism)There arepanhypopituitarity and partial hypopituitarity

*Anterior pituitary hormones:1. Pro-opiomelanocortin [POMC]: a prohormone which is the source of adrenocorticotropic hormone (ACTH), some enkephalins and endorphins and melanocyte-stimulating hormone (MSH)2. Growth hormone [GH] or somatotropin 3. Thyroid-stimulating hormone [TSH] [a hormone that has as its primary function the regulation of hormone secretion by another endocrine gland is classified functionally as a "tropic" ("nourishing") hormone]a.Thyroid gland: metabolism, growth & development; secretes calcitonin 4. Adrenocorticotropic hormone [ACTH] [tropic]a. The adrenal cortex, the outer layer of the adrenal gland, secretes aldosterone [Na+ & K+ balance], cortisol [glucose, protein & lipid metabolism; the "stress hormone"] & sex hormones [including dehydroepiandrosterone]5. Gonadotropins [tropic]a. Follicle-stimulating hormone [FSH] & Luteinizing hormone [LH] [also called Interstitial cell- stimulating hormone [ICSH] in males6. Prolactin The posterior pituitary & hypothalamic hormonesOxytocin [the drug pitocin induces labor]

Satisfactional Hormone? [Active in both sexes; helps orchestrate many of life's more pleasurable social & sexual interactions. Affects relationships between males & females, parents & offspring, neighbor & neighbor. Major role in human sexuality & happiness (high levels in males moments before orgasm and during ejaculation (The New York Times 1-22-91)]2. Antidiuretic hormone [ADH] [vasopressin]Rakish Rodents Reformed Vasopressin modulates male social behavior in a wide variety of mammals. In pair-bonding prairie voles the brain receptor for vasopressin is abundant, while in promiscuous meadow voles, males have much less of the receptor. Its a story of Wow, this feels good, and Im with her vs. This is a female, and I want to do this again (Discover, 1/2005)]

Panhypopituitarity is the decrease of formation of all adenohypophysis hormonesThe following clinical forms of panhypopituitarity are known:

1) Hypophysar cachecsia of Simonds; 2) Afterbearing necrosis of hypophysis syndrome of Schegan; 3) Chromophobe hypophysis adenomas, i.e. tumors, which grow from chromophobe cells. For want of it the tumour squeezes and damages glandular cells of adenohypophysis.The clinical manifestations of panhypopituitarity are connected with deficiency of adenohypophysis hormones and disorders of activity of peripheral endocrine glands (thyroid gland, cortex of adrenal, sexual glands). The first symptoms of lesion of adenohypophysis occur in damage of 70-75% of gland tissue, and for development of complete picture of panhypopituitarity destruction of 90-95 %of adenohypophysis is necessary. Vessels disorders in hypophysis and hypothalamus (most frequently afterbearing longtime spasm of vessels of brain and hypophysis owing of haemorrhage), trauma of the skull basis, tumour of hypophysis and hypothalamus, inflammatory damage (tuberculosis,sepsis) of hypophysis, inherent aplasia and hypoplasia can lead to development of panhypopituitarity. The most frequently gonadotropic function of hypophysis and secretion of STH is damaged with the consequent connection of nonsufficient secretion of H, ACTH and prolactine.

Hypophyseal Simonds cachexia

Causes of HypopituitarismTumors and mass lesions pituitary adenomas, cysts,

metastatic cancer, and other lesions: association with multiple endocrine neoplasia (MEN) I syndrome (include pituitary adenoma, hyperparathyroidism, pancreatic tumor (Zollinger-Ellison syndrome or insulinoma);Pituitary surgery or radiationInfiltrative lesions and infections hemochromatosis,

lymphocytic hypophysitisPituitary infarction infarction of the pituitary gland after

substantial blood loss during childbirth (Sheehans syndrome)Pituitary apoplexy sudden hemorrhage into the pituitary glandGenetic diseases rare congenital defects of one or more

pituitary hormonesEmpty sella syndrome an enlarged sella turcica that is not entirely filled with pituitary tissueHypothalamic disorders tumors and mass lesions

(e.g., craniopharyngiomas and metastatic malignancies),hypothalamic radiation, infiltrative lesions (e.g., sarcoidosis),trauma, infections

Partial hypopituitarity is the disorder of formation of separate hormones ofadenohypophysis (not all). The following variants of partial hypopituitarity are described: Hypophysar nanism1) Hypophysar nanism (dwarfishness) - deficiency of STH;2) Secondary hypohonadism - deficiency of FSH and LH;3) Secondary hypothyrosis - deficiency of TTH;4) Secondary hypocorticism - deficiency of ACTH.

The insufficiency of STH results to

development of hypophysar dwarfishness, or nanism and appears by such disorders:1) decrease of intensity of protein synthesis

that leads to delay and stop of growth (more than 30% from average) and development of bones, internal organs, muscles. The disorders of protein synthesis in connective tissue results in loss of its elasticity; 2) decrease of inhibiting action of STH on an absorption of glucose with predominance of insulinic effect and development of hypoglycemia; 3) fallout of fat mobilizing action and tendency to obesity.

Children have delayed puberty;Adult females have secondary amenorrhea; produces osteoporosis, hot flashes (lack of estrogen), decreased libido;Males have impotence, due to decreased libido from decreased testosterone;Gonadotropin stimulation test:No significant increase of FSH/LH in hypopituitarismEventual increase of FSH/LH in hypothalamic diseaseMetyrapone test: stimulation test of pituitary ACTH reserve; metyrapone inhibits adrenal11-hydroxylase, which causes a decrease in cortisol and a corresponding increase in plasma ACTH (pituitary) and 11-deoxycortisol (adrenal), which is proximal to the enzyme block; in hypopituitarism, neither ACTH or 11-deoxycortisol are increased

Insufficiency of gonadotropic hormones results in decrease of ability of Sertoli cells to accumulate androgens and oppression of spermatogenesis and ability to impregnation in men. In case of defect of LG (Luteinizing) hormone the function of Leidigs cells is infringed, the formation of androgens ceases and develops eunuchoidism with preservation of partial ability to impregnation, as the process of spermatozoids maturing does not stop.

Decreased GH decreases synthesis and release of IGF-1Children have growth delay; delayed fusion of epiphyses; bone growth does not match the age of the childAdults have hypoglycemia; decreased gluconeogenesis; loss of muscle mass; increased adipose around waist

Arginine and sleep stimulation tests: no increase in GH or IGF-1; normally, GH and IGF-1 are released at 5 a.m. Secondary hypothyroidism: decreased serum T4 and TSH Cold intolerance, constipation, weakness No increase in TSH after thyrotropin-releasing factor (TRF) stimulation

Secondary hypocortisolism: decreased ACTH and cortisolHypoglycemia: decreased gluconeogenesisHyponatremia: mild syndrome of inappropriate antidiuretic hormone (SIADH) loss of inhibitory effect of cortisol on ADH;Weakness, fatigue

Short ACTH stimulation test: no increase in serum cortisol over decreased baseline levelsProlonged ACTH stimulation test: eventual increase in cortisol over the decreased baseline value once the adrenal gland is restimulatedMetyrapone test: no increase in ACTH or 11-deoxycorticosterone

By producing too much of one or more hormones

Adrenocorticotropic hormone:causes weight gain (particularly in the bodys trunk, not the legs or arms)high blood pressurehigh blood sugarbrittle bonesemotional changesstretch marks on the skineasy bruising.

The insufficiency of ACTH leads to secondary partial insufficiency of adrenal cortex. The glucocorticoid function suffers mainly. Mineralocorticoid function practically does not vary

Hyperfunction of adenohypophysis (hyperpituitarism)

The main reasons of

hyperpituitarism development are the benign tumours adenomas of endocrine cells.There are two groups of adenomas.1. Eosinophilic adenoma, develops from acidophilic cells of adenohypophysis forming STH. Clinically hyperproduction of STH appears by giantism (if adenoma develops in children and young people before closing of epiphysar cartilages) and acromegalia (in adult). Giantism is characterized by the proportional increase of all body components.

Gigantism

Jane Bunford 2.41mZeng Jinlian 249 smYao Defen 2.34

By producing too much of one or more hormonesGrowth hormone: causes ACROMEGALYa syndrome that includes:excessive growth of soft tissues and boneshigh blood sugarhigh blood pressureheart diseasesleep apneaexcess snoringcarpal tunnel syndromepain symptoms (including headache).

Acromegaly appears by increased growth of hands, legs, chin, nose, tongue, liver, kyphoscoliosis. Besides thatincreased metabolic activity of STH -hyperglycemia, insulin resistanse, even to development of metahypophysar diabetes, fatty infiltration ofliver develop.

*What kind of cells of the pituitary might be proliferating here? (acidophil or basophil)

BITEMPORALHEMIANOPSIA

**What part of the optic nerves/chiasm/tracts would have to be injured to produce this?

Usually the bitemporal hemianopsia is NOT perfectly symmeetrical. Why? Because pituitary tumors are under no law to grow perfectly midline.

**Usually the bitemporal hemianopsia is NOT perfectly symmeetrical. Why? Because pituitary tumors are under no law to grow perfectly midline.

2. Basophilic adenoma, grows from basophilic cells of adenohypophysis which more often produce ACTH. During this the Itsenko-Cushing disease develops. It is characterized by: ) secondary hypercorticism; b) strengthened pigmentation of skin. There are tumors which produce other hormones of adenohypophysis less often: TTH, gonadotropic hormones, prolactin, MSH.The increased level of ACTH during this disease is combined with increase of level of other products of proopiomelanocortin.

BASOPHILIC ADENOMA OF HYPOPHYSIS

Hyperfunction of neurohypophysis

Leads to redundant production vasopressin and oxytocin. Their main effects:Vasopressine (antidiuretic hormone) renders the following influence through V1 and V2 receptors:

1) Acting on tubulus contortus distalis and collective tubules of kidneys, strengthens reabsorption of water; 2) Causes contraction of smooth muscles of blood vessels; 3) Strengthens glycogenolysis and gluconeogenesis in liver; 4) Stimulates consolidation of memory traces and mobilization of saved information (hormone of memory); 5) Endogenic analgetic (depresses pain).

Oxytocin renders the following functional influences:

1) Stimulates secretion of milk (lactation) causing contraction of myoepithelial cells of small-sized ducts of mammary glands; 2) Initiates and strengthens contractions of uterus of pregnant woman; 3) Worsens storing and mobilization of information (amnestic hormone).Redundant secretion of vasopressin arises in tumors of different tissues forming vasopressin, and also in disorders of hypothalamic endocrine function regulation. Its main manifestation is hypervolemia leading to development of constant arterial hypertension.

GALACTORRHEAProlactinomas are the most common type of pituitary adenoma.Lactotroph cells secrete prolactin, which results in hyperprolactinemia.Clinical features include galactorrhea, amenorrhea, and infertility, ordecreased libido and impotence.

**Galactorrhea in a young woman (non pregnant of course) is often the expression of an acidophil tumor of the adenohypophysis.Hyperprolactinemia is the most common anterior pituitary disorder and has many causes. Pathologic hyperprolactinemia, caused by prolactin-secreting adenomas (prolactinomas) or other clinical states that result in elevated prolactin levels such as primary hypothyroidism or dopamine-receptor blocking drug therapy, must be distinguished from the physiologic hyperprolactinemia of pregnancy and lactation. Roughly 40% of tumors found in autopsies are prolactinomas. Most of the patients had no symptoms from microadenomas and died of unrelated causes.

Hypofunction of neurohypophysisInsufficient production of vasopressin results to development of diabetes insipidus.

There are two pathogenetic variants: central (neurogenic) during which will a little quantity of vasopressine, is formed and nephrogenic during which the sensitivity of epithelial cells receptors of distal nephron parts and collective tubules to vasopressin action (absence or a little quantity receptors) is reduced. The decreasing of water reabsorption in kidneys results to poliuria and decreasing of circulatting blood volume (hypovolemia), fallingof arterial pressure and hypoxia.The decreasing of oxytocin production appears by disorders of lactation, weakness of labor activity.

Adrenal cortex - secretes several classes of steroid hormones (glucocorticoids and mineralocorticoids) - with three concentric zones of cells that differ in the major steroid hormones they secrete.

Adrenal medulla - source of the catecholamines epinephrine and norepinephrine. - chromaffin cell is the principle cell type. - The medulla is richly innervated by preganglionic sympathetic fibers and is, in essence, an extension of the sympathetic nervous system.

*1. The Adrenal CortexCorticosteroids [adrenocortical hormones]

* Mineralocorticoids: regulation of extracellular electrolytes [e.g., Na+, K+]* Aldosterone * Glucocorticoids: energy metabolism and stress responses* Cortisol [raises blood glucose, promotes "glucose sparing", suppresses inflammation]* Gonadocorticoids [sex hormones]* Testosterone, estrogen2. Adrenal Medullaa. Sympathetic "ganglia" [ANS fight or flight]* Epinephrine [E] and norepinehrine [NE]

*Figure 45.21b Stress and the adrenal gland

Actions of Cortisol

Major InfluenceEffect on BodyGlucose metabolismStimulates gluconeogenesisDecreases glucose use by the tissuesProtein metabolismIncreases breakdown of proteinsIncreases plasma protein levelsFat metabolismIncreases mobilization of fatty acidsIncreases use of fatty acidsAnti-inflammatory action (pharmacologic levels)Stabilizes lysosomal membranes of the inflammatory cells, preventing the release of inflammatory mediatorsDecreases capillary permeability to prevent inflammatory edemaDepresses phagocytosis by white blood cells to reduce the release of inflammatory mediatorsSuppresses the immune responseCauses atrophy of lymphoid tissueDecreases eosinophilsDecreases antibody formationDecreases the development of cell-mediated immunityReduces feverInhibits fibroblast activityPsychic effectMay contribute to emotional instabilityPermissive effectFacilitates the response of the tissues to humoral and neural influences, such as that of the catecholamines, during trauma and extreme stress

Disorders of adrenal gland function

The most frequently there are following manifestations:

1) Hypofunction of adrenal cortex - hypocorticism Addison disease;2) Hyperfunction of fascicular zone - syndrome of Itsenko-Cushing Hypersecretion of cortisol;3) Hyperfunction of glomerulose zone hyperaldosteronism Hyperfunction of adrenal cortex resulting in excess secretion of aldosterone;4) Dysfunction of adrenal cortex - adrenogenital syndrome

Insufficiency of adrenal cortex

According to etiology there are primary and secondary kinds of adrenal cortex insufficiency. Primary insufficiency arises as a result of adrenals injury,secondary is connected with the defeat of hypotalamus (deficiency of corticoliberin), or with hypofunction of adenohypophysis (deficiency of ACTH). Insufficiency of corticosteroids can be total when the operation of all hormones drops out, and partial fallout of activity of one adrenal hormone. Insufficiency of adrenal cortex can be acute and chronic.Examples of acute insufficiency are:

) state after removal of adrenals; b) hemorrhage in adrenals which arises during sepsis, meningococci infection (syndrome Waterhouse-Friderixan); c) syndrome of cancellation of glucocorticoides preparations.Fast falling of the adrenals function causes development of collaps and the patients can die during the first day.

The chronic insufficiency of adrenals cortex is characterized for Addisons disease (bronzed disease). The most often reasons of it are:

) tuberculose destruction of adrenals; b) autoimmune process. Tuberculose of adrenal gland. Adisons disease

Skin hyperpigmentation at case of Adisons disease

. Manifestation, connected with the falling of mineralocorticoids functions of adrenal cortex:

1) dehydration develops owing to loss of sodium ions (decreases rearbsortion) with the loss of water (poliuria); 2) arterial hypotension is stipulated by decrease of circulating blood volume; 3) hemoconcentration (condensation of blood) is connected with liquid loss, results to disorders of microcirculation and hypoxia; 4) decreasing of kidney blood circulation is stipulated by increase of arterialpressure with disturbances of glomerular filtration and development of intoxication (nitrogenemia); 5) hyperpotassiumemia is stipulated by decrease of canales secretion of potassium ions and their outputfrom the damaged cells. It causes disorders offunction of arousing tissues; 6) distal canales acidosis. It is connected with disorders of acidogenesis in distal nephron canales; 7) gastro-intestinal disorders (nausea, vomiting, diarrhea). Loss of sodium (osmotic diarrhea) and intoxication have significant meaning. This disorders without appropriate correction result to death.

. Manifestations stipulated by disorders of glucocorticoid function of adrenals. To such manifestations concern:

1) hypoglycemia which results to starvation; 2) arterial hypotension (permissive reaction on catecholamines); 3) decrease reaction of fat tissue on lipotrophic stimules; 4) decrease resistance of an organism on action of different pathogenic factors; 5) decrease of ability to remove water during water load (water poisoning); 6) muscular weakness and fast tiredness; 7) emotional disorders (depression); 8) delay of growth and development of children; 9) sensor disorders - loss of ability to distinguish separate shades gustatory osmotic acoustical sensations; 10) distress-syndrome of a newborn (hyalinic membranosis). It is stipulated by disorders of surfactant formation in lungs owing to what lungs are not straightened after birth of a child.

Increase of adrenals cortex function

Hyperaldosteronism. Arises during hyperfunction of glomerular zone of adrenals cortex, which produce mineralcorticoides.

There are primary and secondary hyperaldosteronism.Primary hyperaldosteronism (Conn syndrome) arises in adenoma of zone glomerular, which secretes high quantity of aldosteron. Main manifestations of this disease:

1) arterial hypertension. It is connected with increase of sodium contents in blood and in wall of blood vessels, after what the sensitivity of their smooth muscles to action of pressore factors, particularly catecholamines increases. 2) hypopotassiumaemia (result of hypersecretion of potassium ions in canaliculas of kidneys). It causes disorders of arousing organs and tissues (disorders of heart activity, miostenia, pareses); 3) ungas alcalosis. It is connected with amplification of acidogenesis in distall nephron canaliculas; 4) polyuria arises as a consequence sensitivity of kineys canales epithelium loss to action of vasopressin. It explains absence of volume increase of circulatting blood and edema.Secondary hyperaldosteronism is a result of renin-angiotensin system activation. This state appears by:

a) arterial hypertension; b) edemas; c) hypopotassiumaemia; d) ungas alcalosis.

There are two clinical forms of hypercorticism with hyperproduction of glucocorticoides:

1. Cushings disease basophil adenoma of anterior hypophysis part.2. Cushings syndrome: ) tumoral adenoma of zona fasticulata of adrenal cortex; b) ectopic production of CH by some malignant tumors (pulmonar cancer); c) iatrogenic introduction of glucocorticoides in an organism with the medical purpose.

MOON FACIESBUFFALO HUMPSTRIAE

**What kind of cells of the pituitary might be proliferating here? (acidophil or basophil)

Glucocorticoid hypercorticism appears by:1) arterial hypertension;2) hyperglycaemia metasteroid diabetes mellitus; 3) obesity; 4) development of infectious diseases without signs of an inflammation; 5) gastric hypersecretion and formation of ulcers in stomach and duodenum; 6) osteoporosis; 7) muscular weakness; 8) slow of wounds healing.

Adrenogenitalsyndrome results from the hereditary stipulated blockade of cortisole synthesis and amplified formation of androgens from general intermediate products.Depending on thelevel of blockade of cortisole synthesis there are three variants of adrogenital syndrome.. Disorders of early stages of synthesis deficiency of glucocorticoides, mineralcorticoides and androgens hyperproduction. Manifestations: signs of insufficiency of gluco- and mineralocorticoidal functions of adrenal cortex features of early sexual maturing inmales, virilization in women (appearance of man's sexual features).. Disorders of intermediate stages deficiency of glucocorticoides, surplus of androgens,formation of mineralocorticoides is not infringed (classical androgenic syndrome). Manifestations are the same, as in the first case, only without signs of insufficiency of mineralocorticoidal function.. Disorders at final stages of cortisol synthesis deficiency of glucocorticoides, hyperproduction of androgens and mineralocorticoide.Features of hyperaldosteronism are connected with manifestations of classical androgenital syndrome.

Adrenogenital syndrome

Disorders of adrenal medulla functionHyperfunction of adrenal medullaarises during tumors of chromaphine cells pheochromocytome. Appears by arterial hypertension, tachycardia, extrasystole, flatering of atriums, hyperglycaemia, hyperlipidaemia, hyperthermia.Development of moderately expressed diabetus, thyreotoxicosis is possible. In time of paroxizmvertigo, headache, hallucinations, increased excitability of the nervous system, cramps appear.

Hypofunction of adrenal medullahappens seldom because of the fact that these functions can be accepted by other chromaphine cell.

HYPOADRENALISMCaused by any anatomic or metabolic lesion of the adrenal cortex that impairs output of the cortical steroids.Primary Acute Adrenal Insufficiency

- Waterhouse Friderichsen Syndrome due to overwhelming septicemic infection caused by meningococci, but occasionally other virulent organism such as gonococci, pneumococi and staphylococci. morphology: massive bilateral adrenal hemorrhage

Acute adrenal insufficiency is a potentially fatal bilateral hemorrhagic infarction of the adrenal glands associated with a Neisseria meningitidis infection in children. It is clinically characterized by disseminated intravascular coagulation (DIC), acute respiratory distress syndrome, hypotension and shock, and acute adrenal insufficiency. Treatment is with antibiotics and steroid replacement.

ADRENAL MEDULLA PHEOCHROMOCYTOMA: "dark/dusky-colored tumor, is an uncommon benign tumor of the adrenal medulla, which produces catecholamines (norepinephrine and epinephrine) . It can present with severe headache, tachycardia and palpitations, diaphoresis and anxiety, or hypertensive episodes.Note the Rule of 10s:10% occur in children 10% are bilateral10% are malignant 10% are familial (MEN II and III)10% occur outside the adrenal glandDiagnosis is by demonstrating elevated urinary vanillylmandelic acid (VMA) and catecholamines. Treatment involves controlling the patient's blood pressure and surgical removal of the tumor.

- occassionally, this tumor produces other biogenic steroids or peptides associated with Cushings Syndrome. -morphology: - ave . weight of 100 gms - Zellballen appearance

This large adrenal neoplasm has been sectioned in half. Note the grey-tan color of the tumor compared to the yellow cortex stretched around it and a small remnant of remaining adrenal at the lower right. This patient had episodic hypertension. This is a tumor arising in the adrenal medulla - a pheochromocytoma.

MULTIPLE ENDOCRINE NEOPLASIA (MEN) SYNDROMES1 . Multiple endocrine neoplasia (MEN) syndromes are autosomal dominant conditions with

incomplete penetrance that are characterized by hyperplasia and tumors of endocrine glands.2. MEN I (Werner syndrome) features tumors of the pituitary gland, parathyroids, and

pancreas. It is associated with peptic ulcers and the ZollingerEllison syndrome. The affected gene is MEN I, a tumor suppressor gene that encodes a nuclear protein called menin.3. MEN II (Ila or Sipple syndrome) features medullary carcinoma of the thyroid,

pheochromocytoma, and parathyroid hyperplasia or adenoma. The genetic mutation involves RET proto-oncogene, which is a receptor tyrosine kinase for members of the glial cell line-derived neurotrophic factor family of extracellular signaling molecules.4. MEN III (IIb) features medullary carcinoma of the thyroid, pheochromocytoma, and

mucocutaneous neuromas. There is a genetic mutation of RET ("rearranged during transfection") proto-oncogene.

Cardiovascular: Coronary artery

disease, hypertension, stroke, arrhythmia. Muscles: Tension headaches, backacheConnective tissues: Rheumatoid arthritisPulmonary: Asthma.Immune: Immunosuppression, deficiency, autoimmunityGastrointestinal: Ulcer, irritable bowel syndrome, diarrhea, nausea and vomiting, ulcerative colitisIntegumetary: Eczema, neurodermatitis, acneEndocrine: Diabetes mellitus, amenorrheaCentral nervous: Fatigue and lethargy, type A behavior, overeating, depression, insomnia.

The thyroid gland and the follicular structure

*The thyroid glandThe thyroid gland maintains the metabolic level of almost all cells in the body by producing, in its follicular cells, two thyroid hormones: triiodothyronine (T3), and tetraiodothyronine (T4) or thyroxine. Iodine (I2) has an atomic weight of 127 and a molecular weight of 254; T4 has a molecular weight of 777 Daltons of which 508 is iodide.Thyroid hormones are essential for normal neural development, linear bone growth, and proper sexual maturation.Parafollicular cells called C-cells are located close to the follicular cells. C-cells produce the polypeptide hormone, calcitonin.

Hormones of the Thyroid Gland

Thyroxine (T4)Principle hormoneIncreases energy and protein metabolism rateTriiodothyronine (T3)Increases energy and protein metabolism rateCalcitoninRegulates calcium metabolismWorks with parathyroid hormone and vitamin D

*Actions of Thyroid HormoneAll the major organs in the body are affected by altered levels of thyroid hormone. Thyroid hormone has two major functions: it increases metabolism and protein synthesis, and it is necessary for growth and development in children, including mental development and attainment of sexual maturity.Metabolic Rate. Thyroid hormone increases the metabolism of all body tissues except the retina, spleen, testes, and lungs. The basal metabolic rate can increase by 60% to 100% above normal when large amounts of T4 are present. As a result of this higher metabolism, the rate of glucose, fat, and protein use increases. Lipids are mobilized from adipose tissue, and the catabolism of cholesterol by the liver is increased. Blood levels of cholesterol are decreased in hyperthyroidism and increased in hypothyroidism. Muscle proteins are broken down and used as fuel, probably accounting for some of the muscle fatigue that occurs with hyperthyroidism. The absorption of glucose from the gastrointestinal tract is increased. Because vitamins are essential parts of metabolic enzymes and coenzymes, an increase in the metabolic rate speeds up the use of vitamins and tends to cause vitamin deficiency.Cardiovascular Function. Cardiovascular and respiratory functions are strongly affected by thyroid function. With an increase in metabolism, there is an increase in oxygen consumption and production of metabolic end-products, with an accompanying increase in vasodilatation. Blood flow to the skin, in particular, is augmented as a means of dissipating the body heat that results from the higher metabolism. Blood volume, cardiac output, and ventilation all are increased as a means of maintaining blood flow and oxygen delivery to body tissues. Heart rate and cardiac contractility are enhanced as a means of maintaining the needed cardiac output. However, blood pressure is likely to change little because the increase in vasodilatation tends to offset the increase in cardiac output.Gastrointestinal Function. Thyroid hormone enhances gastrointestinal function, causing an increase in motility and production of gastrointestinal secretions that often results in diarrhea. An increase in appetite and food intake accompanies the higher metabolic rate that occurs with increased thyroid hormone levels. At the same time, weight loss occurs because of the increased use of calories.Neuromuscular Effects. Thyroid hormone has marked effects on neural control of muscle function and tone. Slight elevations in hormone levels cause skeletal muscles to react more vigorously, and a drop in hormone levels causes muscles to react more sluggishly. In the hyperthyroid state, a fine muscle tremor is present. The cause of this tremor is unknown, but it may represent an increased sensitivity of the neural synapses in the spinal cord that control muscle tone.In the infant, thyroid hormone is necessary for normal brain development. The hormone enhances cerebration; in the hyperthyroid state, it causes extreme nervousness, anxiety, and difficulty in sleeping.Evidence suggests a strong interaction between thyroid hormone and the sympathetic nervous system. Many of the signs and symptoms of hyperthyroidism suggest overactivity of the sympathetic division of the autonomic nervous system, such as tachycardia, palpitations, and sweating. Tremor, restlessness, anxiety, and diarrhea also may reflect autonomic nervous system imbalances. Drugs that block sympathetic activity have proved to be valuable adjuncts in the treatment of hyperthyroidism because of their ability to relieve some of these undesirable symptoms.

Disorders of the Thyroid Gland

Goiter is enlargement of thyroid glandSimple goiterAdenomatous or nodular goiterHypothyroidismInfantile hypothyroidism (cretinism)MyxedemaHyperthyroidismGraves diseaseThyroid stormThyroiditisHashimoto disease

Hypothyroidism (Hashimotos disease, Goiter) and Hyperthyroidism (Graves disease)

Multinodular goiter (nontoxic goiter) refers to an enlarged thyroid gland with multiple colloid nodules. Females are affected more frequently than males. Multinodular goiter is frequently asymptomatic, and the patient is typically euthyroid, with normal T4, T3, and TSH. Plummer syndrome is the development of hyperthyroidism (toxic multinodular goiter) late in the course.Microscopically, the tissue shows nodules of varying sizes composed of colloid follicles. Calcification, hemorrhage, cystic degeneration, and fibrosis can also be present.

HYPERTHYROIDISM1. The term hyperthyroidism is used when the mean metabolic rate of allcells is increased due to increased T4 or T3. Clinical features include: tachycardia and palpitations; nervousness and diaphoresis; heat intolerance; weakness and tremors; diarrhea; and weight loss despite a good appetite.Laboratory studies show elevated free T4. In primary hyperthyroidism,TSH is decreased, while in secondary and teritiary hyperthyroidism, TSHis elevated.2. Graves disease is an autoimmune disease characterized by production of IgG autoantibodies to the TSH receptor. Females are affected more frequently than males, with peak age 20 to 40 years. Clinical features include hyperthyroidism, diffuse goiter, ophthalmopathy (exophthalmus) , and dermopathy (pretibial myxedema). Microscopically, the thyroid has hyperplastic follicles with scalloped colloid.3. Other causes of hyperthyroidism include toxic multinodular goiter;toxic adenoma (functioning adenoma producing thyroid hormone); andHashimoto and subacute thyroiditis (transient hyperthyroidism) .

Hyperthyroidism (Graves Disease)

Thyroid eye disease (with exophtalmus) is not confined to Gravess hyperthyroidism only. Some exophtalmus patients are euthyroid or hypothyroid. Common to all types of thyroid eye diseases are specific antibodies that cause inflammation of the retro-orbital tissue with swelling of the extraocular eye muscles, so they cannot move the eyes normally. Proptosis and lid lags are typical signs, and conjunctivitis and scars on the cornea follow due to lack of protective cover. The oedematous retro-orbital tissue may force the eye balls forward and press on the optic nerve to such an extent that vision is impaired or blindness results. The best treatment is to normalise the accompanying thyrotoxicosis. Other therapeutic measures are palliative.

Lid lag in Graves diseaseThe lids appear congested and edematous congestive ophtalmopathy.

Lid lag occurs when the sclera B/W upper eyelid and cornea becomes visible as the patient gaze follows the examiner fingers down ward from position of maximum elevation.The eye moves not in close contact with eyelid as a delay in lid movement.

Exophthalmos protrusion of the eye ballAppearance of sclera B/W the lower lid and limbus of cornea.Symmetrical in Graves disease with hyperthyroidism.Caused by increased bulk of orbital contents.The fat is increased and the muscles enlarged, infiltrated with lymphocytes and contain increased amounts of water and mucopolysccharides.Usually alters little with treatment and may be remarkably persistent.In some, it is progressive and may cause loss of vision if effective treatment not given (malignant exophthalmos).

Unilateral exophthalmos causes:

**

1. The term hypothyroidism is used when the mean metabolic rate of all cells is decreased due to decreased T4 or T3.a. Clinical features include fatigue and lethargy; sensitivity to cold temperatures;

decreased cardiac output; myxedema (accumulation of proteoglycans and water); facial and periorbital edema; peripheral edema of the hands and feet; deep voice; macroglossia; constipation; and anovulatory cycles.b. Laboratory studies show decreased free T4. In primary hypothyroidism, TSH

is elevated, while in secondary and tertiary hypothyroidism, TSH is decreased.

2. Iatrogenic hypothyroidism is the most common cause of hypothyroidism in the

United States, and is secondary to thyroidectomy or radioactive iodine treatment. Treatment is with thyroid hormone replacement.

3. Congenital hypothyroidism (cretinism) in endemic regions is due to iodine

deficiency during intrauterine and neonatal life, and in nonendemic regions is due to thyroid dysgenesis. Aff ected individuals present with failure to thrive, stunted bone growth and dwarfism, spasticity and motor incoordination, and mental retardation. Goiter is present in endemic cretinism.

4. Endemic goiter is due to dietary deficiency of iodine and is uncommon in the United States and Ukraine.

HYPO-THYROIDISMCretinism

Severe retardationCNS/Musc-skelShort statureProtruding tongueUmbilical herniaMaternal iodine defic.Myxedema (coma)

SluggishnessCold skinStructural or functional derangement that interfere with the production of adequate levels of thyroid hormonePrimary, secondary, or tertiary

CretinismHypothyroidism that occurs in infancy or early childhoodImpaired development of the skeletal system and CNSManifests as severe mental retardation, short stature, coarse facial features, protruding tongue and umbilical hernia

Cretinism, also known as Neonatal hypothyroidism is decreased thyroid hormone production in a newborn.

**

MyxedemaHypothyroidism developing in the older child or adultGull diseaseCharacterized by slowing of physical and mental activity Accumulation of matrix substances (glycosaminoglycans and hyaluronic acid) in the skin, subcutaneous tissues, and visceral sites edema, broadening and coarsening of facial features, enlargement of the tongue, and deepening of the voiceMeasurement of serum TSH level is the most sensitive screening test

**

Primary hypotyrioidismMyxedema

Myxedematous Coma.Myxedematous coma is a lifethreatening, end-stage expression of hypothyroidism. It is characterized by coma, hypothermia, cardiovascular collapse, hypoventilation, and severe metabolic disorders that include hyponatremia, hypoglycemia, and lactic acidosis. It occurs most often in elderly women who have chronic hypothyroidism from a spectrum of causes. It occurs more frequently in the winter months, which suggests that cold exposure may be a precipitating factor. The severely hypothyroid person is unable to metabolize sedatives, analgesics, and anesthetic drugs, and buildup of these agents may precipitate coma.Treatment includes aggressive management of precipitating factors; supportive therapy such as management of cardiorespiratory status, hyponatremia, and hypoglycemia; and thyroid replacement therapy. Prevention is preferable to treatment and entails special attention to high-risk populations, such as women with a history of Hashimotos thyroiditis. These persons should be informed about the signs and symptoms of severe hypothyroidism and the need for early medical treatment.

1. Hashimoto thyroiditis is a chronic autoimmune disease characterized by immune destruction of the thyroid gland and hypothyroidism. It is the most common noniatrogenic/nonidiopathic cause of hypothyroidism in the United States; it most commonly causes painless goiter in females more than males, and has peak age 40 to 65 years.Clinically, Hashimoto thyroiditis most commonly causes hypothyroidism (due to destruction of thyroid tissue), but the initial inflammation may cause transient hyperthyroidism (hashitoxicosis).Hashimoto thyroiditis may b e associated with other autoimmune diseases (SLE, rheumatoid arthritis, Sjogren syndrome, etc.), and it has an increased risk of non-Hodgkin B-cell lymphoma.Pathology. Hashimoto thyroiditis grossly produces a pale, enlarged thyroid gland, which microscopically shows lymphocytic inflammation with germinal centers and epithelial Hrthle cell" changes.

2. Subacute thyroiditis (also called de Quervain thyroiditis and granulomatous thyroiditis) is the second most common form of thyroiditis; it affects females more than males and has peak age 30 to 50 years. The condition is typically preceded by a viral illness, produces a tender, firm, enlarged thyroid gland, and may be accompanied by transient hyperthyroidism.Microscopy shows granulomatous thyroiditis. The disease typically followsa self-limited course.

Hashimoto ThyroiditisChronic lymphocytic thyroiditisStruma lymphomatosaMost common cause of hypothyroidism in areas of the world where iodine levels are sufficientPathogenesis:CD8+ cytotoxic T-cell mediated cell deathCytokine mediated cell deathBinding of anti-thyroid Abs ADCCAnti-TSH receptor Abs, antithyroglobulin, antithyroid peroxidase Abs

A woman presenting with an enlarged thyroid who has Hashimoto's thyroiditis

**

Females are affected more frequently than males, with most patients being middle-aged. Riedel thyroiditis causes an irregular, hard thyroid that is adherent to adjacent structures.The condition may clinically mimic carcinoma and present with stridor, dyspnea, or dysphagia. Microscopic examination shows dense fibrous replacement of the thyroid gland with chronic inflammation. Reidel thyroiditis is associated with retroperitoneal and mediastinal fibrosis.3. Riedel thyroiditis is a rare disease of unknown etiology, characterized by destruction of the thyroid gland by dense fibrosis and fibrosis of surrounding structures (trachea and esophagus).

THYROI D NEOPLASIA1. Adenomas. Follicular adenomas are the most common. Clinically, adenomas are usually painless, solitary nodules that appear "cold" on thyroid scans. They may be functional and cause hyperthyroidism (toxic adenoma).2. Papillary carcinoma accounts for 80% of malignant thyroid tumors. Females are affected more than males, with peak age 20 to 50 years. Radiation exposure is a risk factor. Resection is curative in most cases. Radiotherapy with iodine 1 3 1 is effective for metastases. The prognosis is excellent, with 20-year survival of 90% due to slow growth and metastasis to regional cervical lymph nodes.Microscopically, the tumor typically exhibits a papillary pattern. Occasional psammoma bodies may be seen. Characteristic nuclear features include clear "Orphan Annie eye" nuclei; nuclear grooves; and intranuclear cytoplasmic inclusions. Lymphatic spread to cervical nodes is common.3. Follicular carcinoma accounts for 1 5% of malignant thyroid tumors. Females are affected more often than males, with peak age 40 to 60 years. Hematogenous metastasis to the bones or lungs is common.4. Medullary carcinoma accounts for 5% of malignant thyroid tumors. This tumor arises from C cells (parafollicular cells) and secretes calcitonin. Microscopic examination shows nests of polygonal cells in an amyloid stroma. A minority (25%) of cases are associated with MEN II and MEN III syndromes.5. Anaplastic carcinoma affects females more than males, with peak age greater than 60 years. Anaplastic carcinoma can present with a firm, enlarging, and bulky mass; or with dyspnea and dysphagia. The tumor has a tendency for early widespread metastasis and invasion of the trachea and esophagus. Microscopically, the tumor is composed of undifferentiated, anaplastic, and pleomorphic cells. This very aggressive tumor is often rapidly fatal.

The Parathyroid Glands Four glands in posterior capsule of thyroidSecrete parathyroid hormone (PTH)Works with calcitonin to regulate calcium metabolism

If this gland is not working properly, your nerves and muscles will not function properly either due to calcium deficiency.

Calcium MetabolismCalcium balance requiresCalcitriol (dihydroxycholecalciferol)Produced by modifying vitamin D in liver then in kidneyParathyroid hormoneCalcitonin

Disorders of the Parathyroid GlandsTetanyInadequate production of parathyroid hormone (PTH)Fragile bones and kidney stonesExcess production of parathyroid hormone (PTH)

Etiology. Adenomas are the most common cause of primary hyperparathyroidism(80%), and they may be associated with MEN I.Parathyroid hyperplasia accounts for 15% of cases and is characterized by diffuse enlargement of all four glands. The enlarged glands are usually composed of chief cells. Parathyroid carcinoma is very rare.Hyperparathyroidism can also occur as a paraneoplastic syndrome of lung and renal cell carcinomas.Clinical features. The excess production of parathyroid hormone (PTH) leads to hypercalcemia, with laboratory studies showing elevated serum calcium and PTH. Primary hyperparathyroidism is often asymptomatic, but may cause kidney stones; osteoporosis and osteitis fibrosa cystica, metastatic calcifications, or neurologic changes.

Caused by any disease that results in hypocalcemia, leading to increased secretion of PTH by the parathyroid glands. The condition can result from chronic renal failure, vitamin D deficiency, or malabsorption.

Hypoparathyroidism can result from surgical removal of glands during thyroidectomy, DiGeorge syndrome, or idiopathic cause.

Clinical features. Laboratory studies show hypocalcemia. Treatment is with vitamin D and calcium. Chvostek sign demonstrates twitching of the ipsilateral facial muscles after tapping the muscles, suggestive of neuromuscular excitability caused by hypocalcemia. Trousseau sign is performed by inflating a sphygmornanometer cuff above systolic blood pressure for several minutes so that if hypocalcemia is present, then muscular contractions, including flexion of the wrist and metacarpophalangeal joints, hyperextension of the fingers, and flexion of the thumb on the palm occur, suggesting neuromuscular excitability. Clinical problems related to hypocalcemia. The hypocalcemia may also cause psychiatric disturbances and cardiac conduction defects (ECG: prolonged QT interval) . Treatment is with vitamin D and calcium.

**

*Major human endocrine glands*Receptor location varies with hormone type*One hormone, different effects*The pineal gland (also called the pineal body, epiphysis cerebri, epiphysis or the "third eye") is a small endocrine gland. It produces melatonin, a hormone that affects the modulation of wake/sleep patterns and photoperiodic (seasonal) functions. It is located near to the center of the brain between the two hemispheres, tucked in a groove where the two rounded thalamic bodies join. Unlike much of the rest of the brain, the pineal gland is not isolated from the body by the blood-brain barrier system. It is reddish-gray and about the size of a pea (8 mm in humans). *Anterior pituitary lobe = adenohypophysis = Rathkes pouch = pars distalis. Hormones released here are also made here. Anterior lobe is WiFi.Posterior pituitary lobe = neurohypophysis = infundibulum = pars nervosa. Hormones released here are made in the hypothalamus. Posterior lobe is Hard-Wired.*Hormones from basophils go to other endocrine glands, thyroid, adrenal cortex, ovary, testis. Cells from acidophils do NOT.Acidophils make GROWTH related hormones.Basophils make hormones which stimulate other endocrine glands.Chromophobes make NOTHING.The posterior pituitary (aka, pars nervosa or neurohypophysis) looks like typical brain tissue. Why? Ans: It IS typical brain tissue. The pituicytes are glial cells. Herring bodies are massively dilated terminal axons from the hypothalamus.The posterior pituitary does not make these hormones, it just releases them. The hypothalamus actually makes the hormones and transfers it down the stalk to the neurohypophysis.*A tropic hormone regulates the function of endocrine cells or glandsThe four strictly tropic hormones areThyroid-stimulating hormone (TSH) Follicle-stimulating hormone (FSH)Luteinizing hormone (LH)Adrenocorticotropic hormone (ACTH)*Anterior pituitary hormones:1. Pro-opiomelanocortin [POMC]: a prohormone which is the source of adrenocorticotropic hormone (ACTH), some enkephalins and endorphins and melanocyte-stimulating hormone (MSH)2. Growth hormone [GH] or somatotropin 3. Thyroid-stimulating hormone [TSH] [a hormone that has as its primary function the regulation of hormone secretion by another endocrine gland is classified functionally as a "tropic" ("nourishing") hormone]a.Thyroid gland: metabolism, growth & development; secretes calcitonin 4. Adrenocorticotropic hormone [ACTH] [tropic]a. The adrenal cortex, the outer layer of the adrenal gland, secretes aldosterone [Na+ & K+ balance], cortisol [glucose, protein & lipid metabolism; the "stress hormone"] & sex hormones [including dehydroepiandrosterone]5. Gonadotropins [tropic]a. Follicle-stimulating hormone [FSH] & Luteinizing hormone [LH] [also called Interstitial cell- stimulating hormone [ICSH] in males6. Prolactin The posterior pituitary & hypothalamic hormonesOxytocin [the drug pitocin induces labor]

Satisfactional Hormone? [Active in both sexes; helps orchestrate many of life's more pleasurable social & sexual interactions. Affects relationships between males & females, parents & offspring, neighbor & neighbor. Major role in human sexuality & happiness (high levels in males moments before orgasm and during ejaculation (The New York Times 1-22-91)]2. Antidiuretic hormone [ADH] [vasopressin]Rakish Rodents Reformed Vasopressin modulates male social behavior in a wide variety of mammals. In pair-bonding prairie voles the brain receptor for vasopressin is abundant, while in promiscuous meadow voles, males have much less of the receptor. Its a story of Wow, this feels good, and Im with her vs. This is a female, and I want to do this again (Discover, 1/2005)]*What kind of cells of the pituitary might be proliferating here? (acidophil or basophil)

**What part of the optic nerves/chiasm/tracts would have to be injured to produce this?**Usually the bitemporal hemianopsia is NOT perfectly symmeetrical. Why? Because pituitary tumors are under no law to grow perfectly midline.**Galactorrhea in a young woman (non pregnant of course) is often the expression of an acidophil tumor of the adenohypophysis.Hyperprolactinemia is the most common anterior pituitary disorder and has many causes. Pathologic hyperprolactinemia, caused by prolactin-secreting adenomas (prolactinomas) or other clinical states that result in elevated prolactin levels such as primary hypothyroidism or dopamine-receptor blocking drug therapy, must be distinguished from the physiologic hyperprolactinemia of pregnancy and lactation. Roughly 40% of tumors found in autopsies are prolactinomas. Most of the patients had no symptoms from microadenomas and died of unrelated causes.*1. The Adrenal CortexCorticosteroids [adrenocortical hormones]

* Mineralocorticoids: regulation of extracellular electrolytes [e.g., Na+, K+]* Aldosterone * Glucocorticoids: energy metabolism and stress responses* Cortisol [raises blood glucose, promotes "glucose sparing", suppresses inflammation]* Gonadocorticoids [sex hormones]* Testosterone, estrogen2. Adrenal Medullaa. Sympathetic "ganglia" [ANS fight or flight]* Epinephrine [E] and norepinehrine [NE]*Figure 45.21b Stress and the adrenal gland**What kind of cells of the pituitary might be proliferating here? (acidophil or basophil)*The thyroid glandThe thyroid gland maintains the metabolic level of almost all cells in the body by producing, in its follicular cells, two thyroid hormones: triiodothyronine (T3), and tetraiodothyronine (T4) or thyroxine. Iodine (I2) has an atomic weight of 127 and a molecular weight of 254; T4 has a molecular weight of 777 Daltons of which 508 is iodide.Thyroid hormones are essential for normal neural development, linear bone growth, and proper sexual maturation.Parafollicular cells called C-cells are located close to the follicular cells. C-cells produce the polypeptide hormone, calcitonin.*Actions of Thyroid HormoneAll the major organs in the body are affected by altered levels of thyroid hormone. Thyroid hormone has two major functions: it increases metabolism and protein synthesis, and it is necessary for growth and development in children, including mental development and attainment of sexual maturity.Metabolic Rate. Thyroid hormone increases the metabolism of all body tissues except the retina, spleen, testes, and lungs. The basal metabolic rate can increase by 60% to 100% above normal when large amounts of T4 are present. As a result of this higher metabolism, the rate of glucose, fat, and protein use increases. Lipids are mobilized from adipose tissue, and the catabolism of cholesterol by the liver is increased. Blood levels of cholesterol are decreased in hyperthyroidism and increased in hypothyroidism. Muscle proteins are broken down and used as fuel, probably accounting for some of the muscle fatigue that occurs with hyperthyroidism. The absorption of glucose from the gastrointestinal tract is increased. Because vitamins are essential parts of metabolic enzymes and coenzymes, an increase in the metabolic rate speeds up the use of vitamins and tends to cause vitamin deficiency.Cardiovascular Function. Cardiovascular and respiratory functions are strongly affected by thyroid function. With an increase in metabolism, there is an increase in oxygen consumption and production of metabolic end-products, with an accompanying increase in vasodilatation. Blood flow to the skin, in particular, is augmented as a means of dissipating the body heat that results from the higher metabolism. Blood volume, cardiac output, and ventilation all are increased as a means of maintaining blood flow and oxygen delivery to body tissues. Heart rate and cardiac contractility are enhanced as a means of maintaining the needed cardiac output. However, blood pressure is likely to change little because the increase in vasodilatation tends to offset the increase in cardiac output.Gastrointestinal Function. Thyroid hormone enhances gastrointestinal function, causing an increase in motility and production of gastrointestinal secretions that often results in diarrhea. An increase in appetite and food intake accompanies the higher metabolic rate that occurs with increased thyroid hormone levels. At the same time, weight loss occurs because of the increased use of calories.Neuromuscular Effects. Thyroid hormone has marked effects on neural control of muscle function and tone. Slight elevations in hormone levels cause skeletal muscles to react more vigorously, and a drop in hormone levels causes muscles to react more sluggishly. In the hyperthyroid state, a fine muscle tremor is present. The cause of this tremor is unknown, but it may represent an increased sensitivity of the neural synapses in the spinal cord that control muscle tone.In the infant, thyroid hormone is necessary for normal brain development. The hormone enhances cerebration; in the hyperthyroid state, it causes extreme nervousness, anxiety, and difficulty in sleeping.Evidence suggests a strong interaction between thyroid hormone and the sympathetic nervous system. Many of the signs and symptoms of hyperthyroidism suggest overactivity of the sympathetic division of the autonomic nervous system, such as tachycardia, palpitations, and sweating. Tremor, restlessness, anxiety, and diarrhea also may reflect autonomic nervous system imbalances. Drugs that block sympathetic activity have proved to be valuable adjuncts in the treatment of hyperthyroidism because of their ability to relieve some of these undesirable symptoms.**

**

**

**

**