Endocrine: Advanced patho

posterior lobe hormones **know what each lobe secretes

-ADH -Oxytocin

ADH

-ADH acts on the vasopressin receptors of the renal tubular cells to increase their permeability which leads to increased water reabsorption into the blood, thus concentrating the urine and reducing serum osmolality -This can be inhibited by Hypercalcemia, prostaglandin E, and hypokalemia -Secretion is primarily regulated by osmoreceptors of the hypothalamus -ADH secretion is also increased by baroreceptors in left atrium when there are changes in intravascular volume

Chronic complications of DM: irreversibility of glucose

-AGE/RAGE -Glucose binds to collagen and other RBC -Traps protein (albumin, LDL) -Thickening of basement membranes and increases permeability of vessels

Hypoparathyroid

-Abnormally low PTH levels -Depressed serum calcium level -Calcium clots our blood and is an important secondary messenger (helps with cardiac contractions) -Increased serum phosphate level -Usual causes: parathyroid damage in thyroid surgery, autoimmunity, or genetic mechanisms

obesity pathophysiology

-Adipocyte: cellular basis of obesity ("fat cells") -Its function is lost during obesity related to adipocyte hypertrophy -Major role is storage of energy in form of fat -From white adipose tissue -Manages A LOT of things in body (energy, immune responses, thermoregulation, fibrinolysis, fertility, blood pressure regulation) -Molecules that stimulate eating: orexins (hypocretins [from the hypothalamus], a peptide family that act as neurotransmitters for stimulating eating)

Mechanisms related to type 2 diabetes mellitus

-Alteration in the production of adipokines by adipose tissue: leptin resistance -Elevated serum free fatty acids and intracellular lipid deposits -Release of inflammatory cytokines from adipose tissue -Reduced insulin-stimulated mitochondrial activity -Obesity-associated insulin resistance

Diabetic ketoacidosis

-An absolute or relative deficiency of insulin and an increase in insulin counter-regulatory hormones -Most common in type 1 diabetes mellitus -Often what children show -Precipitating factors: infection, trauma, surgery, or myocardial infarction -Increased fat mobilization with the release of fatty acids, leading to DKA

Adrenal Medulla Hyperfunction: Pheochromocytomas

-Are caused by tumors derived from the chromaffin cells of the adrenal medulla (don't have to be in the adrenal medulla, can be growing on the outside of adrenal medulla) -This condition is very rare -The tumors secrete catecholamines (norepinephrine, epinephrine) EXAMPLE: Patient comes in and has a labile high blood pressure (120 /80 then next time you take it its 180/120). They state they are taking their medications. Ask if they have palpitations, diaphoretic, or anxiety when blood pressure is high. This is a sign of a pheochromocytoma. Will test urine to see if they have a lot of catecholamines. You have to catch them during a crisis to diagnosis this. The pheochromocytomas do not constantly pump out these catecholamines. Can see this with MRI and CAT scan if the tumor is big enough

Beta cell dysfunction type 2 DM

-Beta cell mass is decreased. -Inflammation and changes occur in adipokines -Insulin starts to decrease -Hypoglycemia with beta cell dysfunciton

Acromegaly

-Cardiac hypertrophy; hypertension; atherosclerosis; type 2 diabetes mellitus, leading to coronary artery disease; other malignancies -Can have a lot of sleep disorder issues (breathing, apnea) -A lot of growth hormone

Treatment of type 1 diabetes mellitus

-Combination of insulin, meal planning, exercise, and self-monitoring of blood glucose -Transplant: islet cells and the whole pancreas

Identify the functions of the endocrine system

-Composed of various glands located throughout the body which synthesize and release special chemical messengers called hormones -Numerous hormones are synthesized and released form endocrine cells within the upper and lower GI tract -The endocrine system has five general functions: 1. Differentiation of the reproductive and central nervous systems in the developing fetus 2. Stimulation of sequential growth and development during childhood and adolescence 3. Coordination of the male and female reproductive systems, which makes sexual reproduction possible 4. Maintenance of an optimal internal environment throughout the life span 5. Initiation of corrective and adaptive responses when emergency demands occur

Ghrelin and DM

-Decreased in type 2 -Peptide that also increases food intake -A little lower in obesity and changes with weight loss

Amylin and DM (type 1 and 2)

-Decreased in types 1 and 2 -If you bock it, you have a physiological drive to increase food intake -If activated, can decrease food intake

Dawn phenomenon

-Early morning glucose elevation without nocturnal hypoglycemia -Related to nocturnal growth hormone elevation -Treatment: alter timing and dose of insulin

increased gherkin and endocannabinoids in obesity

-Endocannabinoids are derived from arachidonic acid in brain and peripheral nerve tissues -Have effect on endocannabinoid receptors in orexigenic pathways by increasing appetite, enhancing nutrient absorption, stimulating lipogenesis, and increasing white adipose tissue accumulation -Increase appetite -Ghrelin is produced by stomach gastric mucosa in response to hunger -Stimulates food intake through activation of ghrelin receptor GHS-R on NPY/AgRP neurons in hypothalamus -Stimulates release of GH from anterior pituitary cells -Releases gastric acid, increases GI motility, and increases pancreatic secretion of insulin

autoimmune type 1 diabetes mellitus

-Environmental and genetic factors are thought to trigger cell-mediated destruction of pancreatic beta cells (type 1A). -Autoantibody, T-cell, and macrophage destruction of pancreatic beta cells occur with a loss of insulin production and a relative excess of glucagon.

chronic complications of DM: hyperglycemia and the polyol pathway

-Excessive accumulation of sorbitol (sugar alcohol) -Increases osmotic pressure, attracts water in the tissue which leads to swelling -Predisposition got cataracts, damage to schwann cells around nerves -Activation of polyol pathway which leads to destruction of antioxidants

Manifestations and treatment of DM

-Fatigue, pruritus, recurrent infections (due to sugar), visual changes, or symptoms of neuropathy (paresthesia or weakness) -Treatment -Exercise, diet, treatment of obesity, oral hypoglycemics, bariatric surgery

Genetic susceptibility to diabetes mellitus type 1

-First-degree relative (parent or sibling) with type 1 diabetes -Strongest association with major histocompatibility complex (MHC)

SIADH diagnosis and manifestations

-For diagnosis, normal renal, adrenal, and thyroid function must exist. -Will see: Hyponatremia (due to water rentention), Hypoosmolality, Urine hyperosmolality, Hypervolemia, Weight gain

decreased peptide YY and glucagon-like peptide 1 (GLP-1) in obesity

-Glucagon-like peptide 1 is an incretin secreted rom intestinal endocrine cells when nutrients enter small intestines -Stimulates pancreatic glucose-dependent insulin secretion -Suppresses appetite and delays gastric emptying -Used to treat obesity and type II diabetes -Peptide YY is released from intestinal endocrine cells in response to nutrients entering intestines -Inhibits gastric motility and decreases appetite

How do we diagnose diabetes mellitus?

-Glycosylated hemoglobin (HgA1C) levels -Permanent attachment of glucose to hemoglobin molecules; reflects average glucose exposure over life of a red blood cell (RBC) (approximately 120 days) -Fasting plasma glucose (FPG) levels -Two-hour plasma glucose during oral glucose tolerance testing (OGTT) using a 75-g oral glucose load -Random glucose levels in an individual with symptoms

Prolactinoma pathophysiology

-Hallmark is increase in prolactin serum concentration -Adenoma can become an increasingly space-occupying lesion, hypopituitarism may occur because of compression of surrounding hormone-secreting cells -CNS s/s may develop because of growth and pressure of adenoma within the sella turcica -Amenorrhea, infertility, nonpeurperal milk production (galactorrhea), hirsutism

Polycystic ovarian syndrome pathophysiology

-High insulin stimulates androgen secretion by ovaries causing higher amount of free testosterone levels -There is a high level of androgens ("male hormone") secreted by ovaries that causes premature follicular failure and persistent anovulation leading to enlarged polycystic ovaries = hyperandrogenism -Have excess adrenal production of androgen -Androgen is produced by testes (large amount in men), ovaries, and adrenal cortex (small amount) -Androgen is important precursor for estrogen production and it cannot be produced without androgen -Androgen is a sex steroid that activates androgen receptors within cells -Testosterone is type of androgen -Androgens are secreted in higher amounts in men than women -There is a high level of insulin causing a higher than normal insulin blood level, which leads to insulin resistance (body's cells do not respond normally to insulin leading to high glucose levels in blood) -50% have insulin resistance -Hyperinsulinemia = insulin resistance -Muscles resist to insulin; although adipose keeps making androgens (hirsutism) -The more insulin, the harder it is to lose weight because get fat accumulation (most common in trunk) -Starts with the mature gonadotropin levels achieved during puberty -Gonadotropins are released from anterior pituitary gland of hypothalamus that acts on ovaries and testes -Known as the gonadotropin-releasing hormone (GnRH or LH-releasing hormone) -They secrete two primary gonadotropins: luteinizing hormone (LH) and follicle-stimulating hormone (FSH) -LH stimulates secretion of sex steroids from gonads -Stimulates secretion of testosterone by binding to receptors on Leydig cells in men in testes -Theca cells in ovaries respond to LH stimulation by secreting testosterone, which is converted to estrogen by adjacent cells -Stimulates production of progesterone and estradiol by corpus luteum (formed from residual cells of ovulation) -FSH stimulates maturation of ovarian follicles; causes ovaries to secrete estrogen -FSH secretes large amounts of estrogen during pregnancy -Androgen is converted to estrogen in females -Levels are low before puberty and during menstruation there is a dramatic increase in both hormones at ovulation -In women, human chorionic gonadotropin (HCG) is produced by the placenta during pregnancy

Hyperosmolar Hyperglycemic Nonketotic syndrome

-Hyperglycemic hyperosmolar state (HHS) -Get very high glucose, fluid deficiencies, very elevated glucose readings with it -Life-threatening emergency -Precipitated by -Infections, medications, nonadherence to diabetes treatment, or coexisting disease Usually associated with type 2 -Some insulin deficiency: more profound in DKA -Fluid deficiency: more marked than in DKA -Elevated glucose levels: more marked than in DKA

Prolactinoma

-Hypersecretion of prolactin -Most common of the hormonally active pituitary adenomas

Pehochromocytoma manifestations and treatment

-Hypertension, diaphoresis, tachycardia, palpitations, and severe headache -Treatment -Alpha- and beta-adrenergic blockers for hypertension -Laparoscopic surgical excision of the tumor with adjunctive radiopharmaceutical agents or chemotherapy

acute complication of DM

-Hypoglycemia (Too low of blood sugar, could be due to over treatment) -Diabetic ketoacidosis (DKA) -Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS) -Somogyi effect -Dawn phenomenon

Somogyi Effect

-Hypoglycemia over the night with rebound hyperglycemia in the morning (gluconeogenesis leads to hyperglycemia in morning) -Counter-regulatory hormones cause gluconeogenesis -Most common in persons with type 1 diabetes mellitus and in children

type 1 diabetes mellitus pathophysiology

-Immunologically mediated destruction of beta cells -Lymphocyte and macrophage infiltrate islets, resulting in inflammation (insulinitis) and islet beta cell death. -Autoantibodies are produced against islet cells, insulin, glutamic acid decarboxylase (GAD), and other cytoplasmic proteins. -Hyperglycemia, glucagon, and hyperketonemia -Both alpha and beta cell functions are abnormal, and both lack insulin and amylin and have a relative excess of glucagon, contributing to hyperglycemia.

Prolactinemia

-In women: amenorrhea, galactorrhea, hirsutism (male hair distribution), infertility -In men: erectile dysfunction, infertility, osteopenia

Peripheral artery disease and DM

-Incidence increases in those with diabetes (especially type 2), for peripheral arterial disease (PAD), neuropathy, ulcers, gangrene, and amputation. -Age, duration of diabetes, glycemic control, genetics, and other factors are risk factors. -Occlusions of small arteries/arterioles (especially below the knee) cause gangrenous changes of lower extremities. -Lesions begin as ulcers -Progress to osteomyelitis or gangrene -Amputation

secondary hyperparathyroidism

-Increase in PTH but it cannot achieve normal calcium levels because of insufficient levels of activated vitamin D, secondary to chronic disease (common in chronic kidney disease); CKD or Dietary deficiency of Vitamin D and calcium -Hypercalcemia does not occur; secondary hyperparathyroidism is a compensatory response of the parathyroid glands to chronic hypocalcemia which is a common complication of CKD or vitamin D deficiency

obesity

-Increase in body fat mass -BMI of 30 or more -Body fat mass of 25% or more -Major cause of morbidity, death, and increased health care costs

Prolactin

-Induce milk production during pregnancy and lactation -Has immune stimulatory effects and modulates immune and inflammatory responses with both physiologic and pathologic reactions -Vasoactive intestinal polypeptide, serotonin, and growth factor stimulate the synthesis of prolactin, while its release is inhibited by dopamine

chronic complication of DM: microvascular disease

-Is a disease in the capillaries caused by diabetes -Characteristics -Thickening of the capillary basement membrane, endothelial cell hyperplasia, thrombosis, and pericyte degeneration -Hyperglycemia (must be present) -Hypoxia and ischemia

Diabetes Mellitus

-Is a dysfunction of the endocrine pancreas -Affects metabolism of fat, protein, and carbohydrates -Is characterized by hyperglycemia, resulting from defects in insulin secretion, insulin action, or both

Gestational diabetes mellitus

-Is any degree of glucose intolerance with the onset or first recognition occurring during pregnancy -Recommendation: high-risk women who are found to have diabetes at their initial prenatal visit receive a diagnosis of overt diabetes -Contributing factors -Insulin resistance and inadequate insulin secretion -If gestational diabetes mellitus develops, then the risk for type 2 diabetes increases. -Babies get really large due to increased amount of sugar -Worry about afterbirth hypoglycemia -Less than SS of 30 for a newborn -Less than SS of 60 for an adult

Type 2 diabetes mellitus

-Is more common than type 1 diabetes mellitus -Risk factors -Age, obesity, hypertension, physical inactivity, and family history; metabolic syndrome -Affects both adults and children -Genetic, epigenetic, and environmental interactions: must be genetically predisposed -Insulin resistance and decreased insulin secretion by beta cells: are major mechanisms

Diabetic retinopathy

-Is the leading cause of blindness worldwide; microvascular disease leads to this -Develops more rapidly in type 2 diabetes -Maculopathy -Progressive process that accompanies retinal capillary permeability, vessel occlusion, ischemia -Macular edema -Fluid accumulation and retinal thickening -Treatment -Laser treatment, vitrectomy, intravitreal steroids, antivascular endothelial growth factor, and renin-angiotensin system inhibitors

Diabetic neuropathies

-Is the most common complication of diabetes -Sensory deficits generally precede motor involvement -Peripheral neuropathy: distal portions of the neurons are initially and eventually more severely affected -Axonal and Schwann cell degeneration b/c it cannot protect itself for excess sugar -Distal symmetrical polyneuropathy: includes large and small nerve fibers -Small: neuropathic pain, loss of sensation -Large: sensory loss of proprioception

Stroke and DM

-Is twice as common in those with diabetes (especially, type 2). -Survival rate for people with diabetes after a massive stroke is typically shorter than for a person without diabetes. -Hypertension, hyperglycemia, hyperlipidemia, thrombosis, sleep apnea are risk factors. -Treatment -Aggressive management of blood pressure, hyperglycemia, and lipidemia

Cardiovascular disease and DM

-Is ultimate cause of death in up to 68% of people with diabetes -Increases with the duration but not the severity of diabetes -Is a consequence of accelerated atherosclerosis, HTN, and increased risk for thrombus formation -Can result in coronary artery disease (CAD), congestive heart failure, and myocardial infarction -Cardiomyopathy is higher in people with diabetes

Macrovascular disease and DM

-Lesions that develop in large and medium-sized arteries from hyperglycemia -Advanced glycation end products (AGE) attach to their receptor for AGE (RAGE) in the walls of blood vessels -Promote oxidative stress, inflammation, endothelial and vascular smooth muscle dysfunction, and hyperlipidemia

SIADH

-Levels of antidiuretic hormone (ADH) are abnormally high. -Ectopic secretion of ADH is the most common cause; is also common after surgery and some cancers. -Water retention: action of ADH on renal collecting ducts increases their permeability to water, thus increasing water reabsorption by the kidneys.

Manifestations of type 1 diabetes mellitus

-Long preclinical period with gradual beta-cell destruction, leading to insulin deficiency and hyperglycemia -Loss of function of the insulin-secreting beta cells in the islet of Langerhans occurs before hyperglycemia develops. -Polydipsia, polyuria, polyphagia (the 3 P's), weight loss, and fatigue -Polyuria—glucose accumulates in blood and can't accumulate in cells so appears in urine; get this osmotic diuresis as the renal threshold cannot handle all that glucose

Hypoglycemia

-Lowered plasma glucose level -Newborns: less than 47 mg/dL -Children and adults: less than 70 mg/dL -Called insulin shock, insulin reaction -Shock/reaction: people feel palpitations, tachycardia, diaphoretic tremors, arousal anxiety

infection and DM

-Morbidity and mortality from infectious agents increase in those with diabetes -Risk for infection increases for several reasons -Impaired senses -Hypoxia -Rapid replication of pathogens from increased glucose -Decreased blood supply -Suppressed immune response -Delayed wound healing

Diabetic kidney disease

-Most common cause of end-stage kidney disease -Glomerular enlargement, glomerular basement membrane thickening -Will hurt the glomerular cells -Microalbuminuria -The first sign that we have damaged the glomerulus -Treatment -Has decreased from tight glucose control and angiotensin- converting enzyme (ACE) inhibitors or angiotensin II receptor blockers -ACE and ARBs lower glomerular pressure -Aggressive treatment of hypertension

Primary adenoma

-Most commonly adenoma if you have hyperfunction -Visual changes, temporary blindness, headache, fatigue, neck pain/stiffness, seizures if the tumor enlarges

Hormone transport

-Once released in the circulatory system, hormones are distributed throughout the body -Protein (peptide) hormones are water soluble and generally circulate in free forms -Water soluble hormones have a short half-life of seconds to minutes because they are catabolized by circulating enzymes -EX: insulin has a half life of 3 to 5 minutes and is catabolized by insulinases -Lipid soluble hormones such as cortisol and adrenal androgens, are transported bound to a carrier protein and can remain in the blood for hours to days -Only free hormones (those not bound to the carrier protein) can initiate changes within a target cell -At cell membrane, lipid-soluble hormones dissociate from their carrier protein and diffuse into the cell

hormone receptors

-Only target cells with specific receptors for that hormone are affected -Target cell response depends on blood levels of the hormone, the concentration of target cell receptors, and affinity of the receptor for the hormone -Hormone receptors of the target cell have two main functions -To recognize and bind with high affinity to their particular hormones -Initiate a signal to appropriate intracellular effectors

Prolactinoma can be caused by

-Other conditions or medications can elevate prolactin level in the absence of pituitary pathologic condition -Renal failure, polycystic ovarian disease, breast stimulation, stress of venipuncture can increase prolactin levels -Medications that block the secretion of dopamine form the hypothalamus to the lactotropes also result in hyperprolactinemia -Elevated with hypothyroidism

glucagon and type 2 DM

-Pancreatic alpha cells are less responsive to glucose inhibition; hyperglycemia— abnormally high levels of glucagon increase hepatic production of glucose. -Glucagon tells the liver to produce more glucose in order to maintain homeostasis -Hyperglycemia with glucagon increase

Type 1 diabetes mellitus

-Pancreatic atrophy and loss of beta cells (make our insulin) -Maybe due to a viral phenomenon or genetic abnormality that kills off these beta cells -autoimmune and non-immune

Type 2 diabetes mellitus and metabolic syndrome

-People refer to it as pre-diabetic but that term is NOT correct -Also called resistance syndrome or syndrome X -Cluster of conditions that occur together increasing risk of heart disease, stroke, and diabetes: -prehypertension -central obesity -elevated fasting blood glucose -dyslipidemia/high triglycerides -Abdominal obesity: defined as a waist circumference in men ≥102 cm (40 in) and in women ≥88 cm (35 in) -Serum triglycerides ≥150 mg/dL (1.7 mmol/L) or drug treatment for elevated triglycerides -Serum high-density lipoprotein (HDL) cholesterol <40 mg/dL (1 mmol/L) in men and <50 mg/dL (1.3 mmol/L) in women or drug treatment for low HDL cholesterol -Blood pressure ≥130/85 mmHg or drug treatment for elevated blood pressure -Fasting plasma glucose (FPG) ≥100 mg/dL (5.6 mmol/L) or drug treatment for elevated blood glucose -Two-fold increase in CV Disease over 10-year period and 5-fold increase of developing diabetes over 10-year period -Higher rates of sedentary lifestyle

polycystic ovarian syndrome

-Polycystic ovaries do not have to be present; their presence alone does not establish the diagnosis -Result of strong genetic and environmental factors -Defined by having two of three features: -Irregular ovulation -Elevated levels of androgens (testosterone) -Appearance of polycystic ovaries on ultrasound

diabetic ketoacidosis manifestations and treatment

-Polyuria; dehydration; Kussmaul respirations; acetone breath odor -Serum glucose >250 mg/dL; serum bicarbonate <18 mg/dL; serum pH <7.30; anion gap; serum and uringe ketones -**Low serum pH, High serum glucose -Treatment -Administration of insulin to decrease glucose levels -Fluids -Replacement of electrolytes

growth hormone (somatotropin)

-Produced by somatotropes in the anterior pituitary -Necessary for linear bone growth in children -Stimulates cells to increase in size and divide more rapidly -Enhances amino acid transport across cell membranes -Increases the rate at which cells use fatty acids -Decreases the rate at which cells use carbohydrates -Secretion is increased during sleep, stress, puberty, exercise, and hypoglycemia -Secretion is decreased by somatostatin, obesity, and hyperglycemia

decreased adiponectin in obesity

-Produced by visceral adipose tissue, cardiomyocytes, and skeletal muscle -Anti-inflammatory and antiatherogenic plasma protein -When decreased, there is an increase in hepatic gluconeogenesis and decreased skeletal muscle uptake, which increase risk for CAD

Increased angiotensinogen (AGT) in obesity

-Produced from liver and fat cells (adipocytes) -Before conversion of angiotensin I to angiotensin II -Vasoconstrictor (at risk for hypertension); increased vascular resistance -Causes renal retention of water and sodium and release of aldosterone -Release of angiotensin II causes inflammation, lipogenesis, and insulin resistance, which all increase risk for CAD and HTN

macrophage infiltration of adipocytes

-Release of inflammatory mediators -Increased adipocyte lipolysis -Increased leptin (leptin resistance) and retinol-binding protein 4 (RBP4) in obesity -Retinol-binding protein 4 binds vitamin A and contributes to inflammation and insulin resistance in liver and muscle -Produced by liver and adipocytes -Increased in visceral adiposity -Decreased adiponectin in obesity -Possible insulin resistance -Increased ghrelin and endocannabinoids in obesity -Increased angiotensinogen (AGT) in obesity -Decreased peptide YY (PYY) and glucagon-like peptide 1 (GLP-1) in obesity -Alterations in the expression of these hormones and neurotransmitters, affecting appetite and metabolic rate at the level of the hypothalamus -Reduced cholecystokinin (CCK) in obesity

Insulin resistance and type 2 DM

-Response of insulin-sensitive tissues (especially liver, muscle, and adipose tissue) to insulin is suboptimal -Obesity makes one prone to insulin resistance.

Oxytocin

-Responsible for contraction of the uterus and milk ejection in lactating women and may affect sperm motility in men -Has an antidiuretic effect similar to that of ADH -In women, oxytocin is secreted in response to suckling and mechanical distention of female reproductive tract -Oxytocin binds to receptors on myoepithelial cells in mammary tissues and causes contraction of those cells which increase intramammary pressure and milk expression (let down effect)

anterior pituitary lobe hormones **know what each lobe secretes

-TSH, LH, and FSH -ACTH -Growth hormone (somatotropin) -Prolactin

Hypoglycemia manifestations and treatment

-Tachycardia, palpitations, diaphoresis, tremors, pallor, and arousal anxiety -Treatment -Oral or IV glucose -Glucagon: prescribed for emergency use

polycystic ovarian syndrome manifestations and treatment

-Those with this syndrome have a three times greater chance of uterine cancer later in life. -Dysfunction in ovarian follicle development -Leading cause of infertility in the United States -Associated with metabolic disorder -Clinical manifestations -Dysfunctional bleeding or amenorrhea, hirsutism (excessive hair growth), acne, acanthosis nigricans, male pattern baldness, and infertility -Treatment -Combined oral contraceptives (COCs), antiandrogens, fertility agents, insulin sensitizers -Weight loss

regions of anterior pituitary

-Three regions (pars distalis, pars tuberalis, and pars intermedia) -Pars distalis is the major component of the anterior pituitary and the source of the anterior pituitary hormones

Type 1 vs type 2 diabetes mellitus

-Type1—pancreas is not functioning -Type2 -pancreas is functioning, cannot synthesize insulin

Diabetes insipidus manifestations

-Will have COPIOUS amounts of urine -Neurogenic (Insufficient amounts of ADH) -Nephrogenic (Insensitivity of the renal collecting tubules to ADH) -Dipsogenic (Excessive fluid intake, lowering plasma osmolarity to the point that it falls below the threshold for ADH secretion) -Polyuria and polydipsia; excretion of large volumes of urine; Hypernatremia (don't have enough water to concentrate urine); Urine hypoosmolality

growth hormone in children: GH excess

-gigantism -results in increased linear bone growth

Growth hormone in children: GH deficiency

-interferes with linear bone growth -results in short stature or dwarfism

Hyper function of pituitary can cause...

-primary adenoma -acromegaly -prolactinemia -thin hair; exophthlamos; nomral or enlarged thyroid; heart failure (tachycardia); weight loss; diarrhea; warm skin, sweaty palms; hyperreflexia; pretrial myxedema

Hormone release is regulated by what mechanisms?

1. chemical factors (blood glucose or Ca levels) 2. Endocrine facts (a hormone from one endocrine glad controlling another endocrine gland) 3. neural control

chronic complications of DM: hyperglycemia and the hexosamine pathway

Another enzyme that occurs and creates more insulin resistance and oxidative stress

Hypofunction of pituitary

Can be related to hypothalamus not working, damaged to pituitary gland, surgery to remove part of it (had a hyperfunction, now have Hypofunction) *will see deficiency in all anterior pituitary hormones -loss of hair; coarse, brittle hair; periorbital edema; puffy face; normal, enlarged, or small thyroid; heart failure (brady); constipation; cold intolerance; muscle weakness; decreased bone mineral density (osteoporosis); edema of extremities

primary hyperparathyroidism

Excess secretion of PTH from one or more parathyroid glands and Hypercalcemia; 80%-85% caused by parathyroid adenomas

down-regulation

High concentrations of hormone decrease the number or affinity of receptors

manifestations of hyperparathyroidism

Hypercalcemia and hypophosphatemia, possible kidney stones from hypercalciuria, alkaline urine, pathologic fractures

Manifestations of hypoparathyroidism

Hypocalcemia, lowers threshold for nerve and muscle excitation, muscle spasms, Chvostek (elicited by tapping the cheek, resulting in twitching of the upper lip) and Trousseau (elicited by sustained inflation of the sphygmomanometer placed on the upper arm to a level above the systolic BP with resultant painful carpal spasm) signs, Phosphate retention

Chronic complications of DM: hyperglycemia and protein kinase C

Inappropriately activated intracellular signaling proteins

Diabetes insipidus

Insufficiency of ADH; Is characterized by the inability of the kidney to increase permeability to water; Partial or total inability to concentrate the urine

Tertiary hyperparathyroidism

Long, excessive secretion of PTH that is not dealt with and Hypercalcemia from long-standing secondary hyperparathyroidism

up-regulation

Low concentrations of hormone increase the number of receptors per cell

non-immune type 1 diabetes mellitus

Occurs secondary to other diseases, such as pancreatitis, or secondary to a more fulminant disorder termed idiopathic diabetes (type 1B)

Chronic complications of diabetes mellitus: oxidative stress

Production of reactive oxygen species (ROS), which damage large and small vessels

Thyroid-stimulating hormone (TSH)

Regulates activity of the thyroid gland -Immediate increase in release of stored thyroid hormone -Increase in iodide uptake and oxidation -Increase in thyroid hormone synthesis -Increase in synthesis and secretion of prostaglandins by thyroid -control production of T4 (thyroxine) and T3 triiodothyronine/thyronine

Adrenocorticotropic hormone (ACTH)

Regulates the release of cortisol from the adrenal cortex

T3 and T4

Thyroxine and triiodothyronine are essential for maintaining body's metabolic rate, heart and digestive functions, muscle control, brain development, and maintenance of bones

pituitary function

anterior lobe linked to hypothalamus (hypothalamic hormones act on anterior lobe); posterior lobe is driven from neural tissue (synthesized by nerve cells bodies)

the release of ADH an oxytocin is mediated by

cholinergic and adrenergic neurotransmitters; major stimulus is glutamate and the major inhibitor is GABA

obesogens

exogenous chemicals related to development of obesity (plastics, pesticides, food products) -Stimulate adipogenesis and fat storage -Some can cross placenta and be transmitted through breastmilk -Can provide epigenetic changes and gene regulation and expression, which increases risk for diseases secondary to obesity (CV, diabetes)

ARC (arcuate nucleus)

in hypothalamus regulates food intake and energy metabolism by balancing opposing effects of two sets of neurons -One set of neurons produces agouti-related protein (AgRP) and neuropeptide Y (NPY) -They promote appetite, stimulate eating, and decrease metabolism (orexins) -Known as AgRP/NPY neurons -Other set of neurons synthesize pro-opiomelanocortin-producing peptide (POMC-producing) and cocaine-and-amphetamine-regulated transcript (CART) -Known as POMC/CART neurons -They suppress appetite, inhibit eating, and increase metabolism (anorexins)

Luteinizing hormone (LH) and follicle-stimulating hormone (term-100FSH)

influence reproductive function

anorexins

molecules that inhibit eating

Negative feedback system

most common and occurs when a changing chemical, neural, or endocrine response decreases the subsequent synthesis and secretion of a hormone

Positive feedback

occurs when a neural, chemical, or endocrine response increases the synthesis and secretion of a hormone. Also occurs when an increased hormone level further increases the synthesis and secretion of that same hormone -EX: female reproductive system when the rise of estradiol levels provides positive feedback on the anterior pituitary and hypothalamus, causing a subsequent increase in gonadotropin-releasing hormone and follicle-stimulating hormone -Page 646 show image of negative and positive feedback loop

letpin

regulates hepatic gluconeogenesis, insulin sensitivity, and glucose -Also regulates lipid metabolism in liver, muscle, and adipose tissue -Inhibit or increase orexigenic neurons and anorexigenic neurons by acting on hypothalamus depending on leptin levels -Increased leptin levels equal increased number of adipocytes -Expressed by adipocytes -Retinol-binding protein 4 binds vitamin A and contributes to inflammation and insulin resistance in liver and muscle -Produced by liver and adipocytes -Increased in visceral adiposity

posterior lobe parts

the median eminence, the pituitary stalk, and the infundibular process