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Brain and the hypothalamus have osmorecptors that continual sample the blood. When blood osmoality is hypertonic (which means high particle low water )water will be pulled out of the osmorecpetors causing them to crenate . Which causes osmorecptors to trigger release of ADH to retain Na and water, this then triggers thirst mechanism, so we drink water to dilute blood and take osmoality back to normal ranges 285-300 mosm ADH released in response to blood osmoality,and also low bp, and pain and some drugs such as nicotine, morphine and barbituites

Greater than 300 Mosm hypertonic, dehydration Less than 285 Mosm hypotonic overhydrated
Source ADH- post pituitary Target- kidneys Effect- save water control osmoality casoconsriction of abdominal visera By doubling Na conc in blood find body osmoality with tests Na value 135 *2=osmality 270 =overhydrated DIABETES INSEPIDOUS- problems making ADH From tumor or radiation , polyuria and excessive thirst but unable to reabsorb water Maybe due to infection tumor of post pituitary, head trauma radiation damage kidney do not respond to ADH

TH Thyroid Hormone
Target- all body cells except brain spleen testes and uterus Effect- accelerate Basal Metabolism of target cells increase # of kilocalories burned 2nd effect- increase adrenerfic receptors NE on BV makes BP rise
Cells use more ATP producing more heat raises temp

Sympathetic nercous system will vasoconstict at skin and abdominal not at skeletal muscle and brain Hypothyroidism- decrease in amount of TH low production Goiter disease. Iodine is a essential component of TH must have iodine to make T3 and T4 wihtout iodine body sends messages saying we need TH, so synthesizes Colloid precursor to TH but no iodine is there so no Th is made then body sends more signals saying we need TH so synthesizes Colloid Precursor but no iodine so no TH is made and Colloid Precursor builds up and enlares thyroid gland Goiters Disease Hyperthyrodism- producing to much TH---Graves diseaseautoimmune disorder Antibodies on blood mimic TSH which causes and overstimulated thyroid S/S--- increase metabolism ,Weight loss, sweating , irregular hrt rate , and sometimes exopthalamus(protruding eye balls) Treat with radioactive iodine

PTH parathyroid hormone: Ca control in ECF

Targets--- bone, kidney, small intestine Effect raise bld calcium
Small intestines help absorb Ca better Kidney retain more Ca and put back into blood Calcium is needed for muscle contractions nerve impulses and blood clotting Stimulated bylow bld ca

Sourceadrenal cortex Target kidneys Effect aintains proper amounts of Na and K and BV and BP (kidney absorbs Na and secretes K)
Water reabsorption causes blood volume to increase and this causes bld pressure to increase

Na is regulated by aldosterone so if K is high Na is low there are K receptors on adrenal cortex 3 triggers for release of aldosterone Low blood pressure High K levels hyperkalemia Prolonged stress

Regulation of blood glucose = Glucocorticoid Source- Adrenal Cortex Effectskeeps blood sugar stable between meals using gluconeogenesis (new glucose form fat/proteins) Accelerates lipolysis (break down of triglycerides into FA and Glycerol) Enhances vasoconstriction(raise BP by EPI) To much cortisol will weaken immunity and be sicker Target- many cells widespread effect

DISEASES Cushings Disease too much cortisol

Tumor of ant pituitary/ cancer of lungs pancreas and kidneys S/Shigh blood sugar/ muscle protein loss/ Increased BP/ swelling and puffines

Source- Pancreas Target- Mainly muscle, fat and possibly liver Effects- Reduce blood sugar by taking glucose in cells Lowers BS Insulin aids facilitated of glucose into cells Diseases Diabetes Mellitus insuli dependentdo not make insulin at all Pancreatic insulin receptors are destroyed ny immune system

Without insulin blood glucose is high causing problems and muscle and fat cells can not take in glucose High blood sugar damages--- BV- poor supply more likely to bind and cause gangrene --- Damages nerves --- Causes Lipidema- body cant use available sugar so breaks down lipids for fuel bow elevated cholesterol in blood causing grater risk of heart attack stroke and kidney damageat INSULIN SHOCK- overdose of insulin leaving no glucose for brain b/c fat and muscles take it all in

DIABETES MELLITUS- Non insulin dependent= Hyperglycemia Most common form Fatty tissues produce mimcing chemicals that interfere with reaction of target cell to insulin. Body must have physical activity to regulate insulin insulin production and for insulin re-uptake Insulin increases uptake of glucose by 10 times Number of insulin receptors is low/ insulin receptors have less response

GlucoseIn brain and liver cells by simple diffusion no assistance brain only uses glucose as a means of fuel Pancreas monitors glucose in response to these levels insulin or glucagon are released Muscle Cells and take glucose and insulin for fuel/ Liver converts it into glycogen/ fat cells transform it into triglycerides Muscles never give up glucose Fats turn glucose into triglycerides Liver ony one to store G


Generic Effects of Hormones

Alter membrane permeability and therefore RMP Alter synthesis of protein and Enzymes

Alter activity of existing enzyme Stimulates Mitosis

Magnatiude of response depends upon

Concentration of hormone in blood Number receptor sites present on target cells Affinity of hormone for receptor Up-Regulation- increase in receptors due to another hormone Down-Regulation- receptors decline after binding with that hormone

Secretion of Hormones Triggered BY

NEURAL- Nerve impulses directly to gland EPI,NE HUMORAL-change in blood concentration of calcium potassium sodium and glucose HORMONAL- Blood concentration of one hormone effect antoher TSH,FSH,ACTH Hormone Specificity- hormones only bind to certain receptors

4 ways to rid body of hormones

Excrete them in urine or bile By metabolism by enzymes degradation of enzymes in blood/ISF/ICF Active transport into a cell taking out of blood Conjugation by liver changing hormone to no longer a hormone-non functional easier to excrete

Varibles of hormones that can and will change

Concentration of hormone in blood influences concentration in ISF, the more hormone in ISF the more hormone receptor complex formed= greater response Receptors for hormones are short lived, fluctuates based on usage, other hormones

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