Gland: Hormone: Main Targets: Effect

1. Posterior Pituitary Gland: ADH (made by the hypothalmus): Kidneys: conserve water by concentrating the urine and reducing urine volume. Another target is Vasopression: causes vasocontriction and raises b/p and increases water retention,reduces urine output. osmolarity gradiant.

hypothalmus>Infundibulum>Posterior Pituitary Gland

Disorders:

diabetes insipidus : Central DI (CDI):

Tumor or head trauma at the Infudibulum : No ADH goes to the Pituitary Gland.

ADH Deficiency: Central DI (CDI): we have no ADH: damage head trauma or tumor: Produces massive amounts of urine: Cannot retain water: 8-10 liters of urine a day. Blood volume goes: Hypertonic ECF: Fluid shift: Cells are going to shrink: Plasma hydrostatic pressure is down:

ADH is low: Thirsty! : Tx:

Pharmacologic: Vasopressin(ADH) and fluid replacement

                    Nephrogenic DI(NDI): Receptor problem and kidney do not respond to it. ADH is produced but Problem with renal response: Blood Volume Drop: urine output goes up pure water: ECF: Hypertonic:

ADH level is normal or high. Specific gravity: be pure water: Draw a ADH level. Would not response to vasopresson. Hypovolemic.

It is not lack of hormone: non response problem: Associated with certain drugs:

Lithium, tetracycline. What to do withdrawal the drug and fluid replacement.

Compulsive water drinking ODC disorder. I am peeing like crazy: 10 L a day: polyuria:

Measure ADH: Stop producing ADH and ADH will be really low and body stops making ADH. CDI. How much water drinking two or three gallons. Restrict water: but a quicker way to determine:  Electrolytes: ECFosmolarity: Hypotonic ECF and sodium 108 low.

Anterior Pituitary gland:

Productions and reduced of 7 hormones. Made and release in the anterior pituitary. 12 different disorders.

GH( growth homone): Target: Most Cell of body

Effects: raises blood sugar: growth: carb

TSH (Thyroid Stimulating hormone):Target: Thyroid Gland:

Effect: Stimulate: T3 T4 (Thyroid Hormone)

ACTH(Adrenocorticotropic Hormone): Targets: Adrenal Cortex: Effect: Increase cortisol release

FSH (follicle stimulating hormone): Target: Gonads 

Effects: Stimulate produce eggs, sperms, estrogen, testostrone.

      LH(Luteinizing hormone) : Target: Gonads: Effects:

Stimulate produce eggs, sperms, estrogen, testostrone.

MSH( Melanocyte stimulating hormone ) : Not going to deal with.

Prolactin( Mammary Glands) : Target: Mammary glands: Effect: Milk production : Most common Prolactoma: beign stimulate more hormone.

Thyroid Gland: Thyroid Hormone:Calcatone Target: Most Cells: Effect: Increase Basic Metabolism Rate and Increase body of sympathetic system. Increase more Hyperthyroid gland: B/p up, heart rate up, weight loss.

Excess TH: Thyroidtoxicosis from any source:synthoid took more in. Include hyerthyroidism: Measure the blood level.

Hyperthyroid:

Primary: Abnormal in thyroid gland to much.

TH^^^^^ Broad TSHLLLLL Then TH will drop.

Thyroid is behaving abnormally if it is still elevated. Radiation ablation.

Secondary: Cause to outside the thyroid

Symptoms: wired, weight loss: ^mbr, heat intolerant:^mbr, increased to sympathetics, elevated b/P, heart rate: elevated: increased to hemmorahagic stroke. Thyroid is producing to much hormone. Anterior Pituitary: TSH   Thyroid: TH

Thyroid function tests: show high TH

TSH^^^ inappropiate response (problem is in APG)

TH^^^^^ Secondary to (may be a tumor in the APG) Remove the tumor: the TH should decrease.

Hypothyroid: Children: cental nervous sytstem:

Dwarf: Cretinism

Hypothyroid: cold intolerance: weight gain:

Parathyroid Gland: Hormone: PTH: Target: bone, Kidney, gut. Effect: Blood calcium raises: bone is broken down calcium goes to blood calcium. Less calcium excreted by the kidney, GI absorbtion of the calcium into the blood system. Raises blood calcium.

Hyper Parathyroid: Pathological fx.

 Hypercalcemia

^^^PTH  hypercalcium: increase threshold: Muscle weakness: see exam I: bone density: less dense:fractures develop.

Hypo Parathyroid: HypoCalcium levels stay low. decrease threshold: neuromuscular excitability:

The parathyroid is by the thyroid: Thyroidectomy becareful no destroy: can no regulate calcium and causes death.

Adrenal Glands: On top of each Kidney

Adrenal Medula: Hormone: Catecholamines: Epi(adrenal) and Neoepi(  Noralepid): flight and fight. 80/20% but not in hyperfuntion 20/80

Hyperfunction: Pheochromocytomas caused by tumor

Hyper: Neoepi secretion^, Hr: ^: contractitility^: ^ cardiac output: b/p goes up. Lot of SVR^ net effect of vasoconstiction. More synpathetic affect. In abnormal: Vasoconstriction: ^^^^Hypertension!

Normal fight and fight: Lung dilate: eye dilate: slow digestion: GU:slow: ventilation: increase: skin and visceral organs:decrease: blood sugar: increase

Abnormal:

Pheochromocytomas: tumor of cell epi/norepi

20/80: Adrenal response: sympathetics:

Severe life threating Hypertension.

Lower the pressure: take month:

IV in hospital: Later remove the tumor from the medula.

Secondary form of hypertension.

Adrenal Cortex: Hormone: Aldosterone Target: Kidney Effects: Na retention(ecf osmalarity and blood volume) and K excretion(: resting membrane potential and neuromuscular excitability.

Can have increase or decrease of Aldosterone

Adrenal Cortex:Hormone:Cortisol: effect: increases glucose by stimulate glucogensis: fat and protein to amino acid to glucose:

effects: antinflammatory effects: steriods: cortiosteroid: stress hormone increases more.

Can have increase or decrease of cortisol.

Abnormal: cortisol or aldostrone

Excess

deficeincy

Hypercortisolism:High circulating cortisol levels:

Primary: steriod effects: Cortisol

^^^^Cortisol   ACTHLLLLLL

Secondary:cushings symptoms:

Symptoms: moon face, hump, tunk obesity, stretch stria

Caused excess ACTH by the APG: to much cortisol

Give Cortisol Medication:

LLLLCortisol LLLLACTH

Takes along time for the adrenal to act again: There is no aldosterone.

Give Prednisone: ^^ Cortisol for anti-inflammatory properties. ACTHLLLLL      LLLLLLCortisol  and aldostrone: secretion Level in the blood is up!!!!

Stop taking the tablet circulating LLLL in blood: ACTH and Cortisol are sleep: no adrenal function: No Cortisol and Aldosterone.  No aldosterone will not be able to regulate Hyperkalemia and threshold: 48 hours: tapered off. Addison crises: JFK had Addison dx.

Hyperantremia: blood volume

K Hypokalemia: lower rest mm potiential   See exam one:

Deficiency in aldosterone: K sparing diuretic: spirodonoli

Aldosterone K excrestion and k falls: spare it the the : spiron:

What is going on: Cortisol blood levels:

ACTH     High (normal)

Cortisol   Low   Primary: Hypocortisolism   That is what Addison dx looks like : Primary adrenal insufficiency

Gland: Pancreas: Hormone: Alpha cells and beta Cells:

Alpha: glucogan

Beta Cells: insulin

Hormone: insulin: effect on blood sugar: Lowers it: anabolic hormone: built synthesis of glycogen synthesis: storage form of glucose :skeletal mm or liver

Goes down in the blood. Direct up take of glucose into the cells to use. Protein and lipid metabolism: Insulin does to these protein synthesis. Bluilding protein. Effect on fat increase synethsis of fat and storage. For a time of protential time of fasting phase later on. To fold affect and breakdown of all glycogen, fat, lipids.

Diabete type I: no insulin: glucose goes up and build protein , lipids: Keto acids form. Lost weight. Lost muscle. Loss the anabolic effect.

Alpha: glucogan:Hormone: Glucogan: catabolic: breakdown of glucogon and breakdown of lipids: low carb fatigue:Glucogan raises glucose

Diabetes Mellitus: sweet with honey

Type I: Absolute deficiency: Do not produce Beta cells have been destroyed! Autoimmune reaction. Juvnile:  Low insulin level: Thin: cannot store fat or prevent the breakdown: Cannot build protein: muscle wasting. Hypoglycemia:

Type II: beta cell impairment: Resistant to insulin: relative insulin deficiency: anabolic synthesize 90%

Obese: causes type II: resistances: obesity : resistant hormone: genetic factors:

Makes more resistance to the effect insulin. Decrease

Blood sugar, protein metabolism, lipid metabolism

Long term effects:

Poor circulation, Plaque, independent risk factor for CAD,tight control of blood glucose

Stroke, Macro and Micro: ESR: Neuropathy: Limb amputation:

Classic presented: polyuria, Polydipsia, Polyphsia: Water is going to follow the glucose out the kidney: Osmolarity ^ECF: Cells are starving for fuel!!!!

Thyrotoxicosis:any source

Hyperthyroidism: primary or secondary

To much synthoid medication:

To much TH^^^^TSHLLLLLL

Thyroid ablation and on synthoid from hx.

Child took the synthoid:

THLLLLL TSHLLLLL : blood serum will be elevated

Most common cause hyperthyroidism: Graves Dx

Thyroid: TSantibodies stimulating the thyroid gland:

TH:^^^^^ THSLLLLLLLL going to look like primary hyperthyroidism. Test to detect the THantibodies.

Th:^^^^  THS.......normal check AP

Hypothyroidism:

Symptoms: weight gain, LLBMR, lethagic, fatigue, constipation, LLLHR, LLL b/p

Primary:Thyroid: LLLL TH

^^^^THS

Secondary: Thyroid: LLLLTH

LLLLLLTHS problem with APG