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36 Cards in this Set
- Front
- Back
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Major Human Endocrine Glands
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Hypothalamus
Pituitary (Hypophysis) Thyroid and parafollicular (“C”) cells Parathyroids Adrenal cortices Adrenal medulla Pancreatic islets of Langerhans Gonads Many other endocrine tissues, e.g., atrial myocardium, kidney (juxtaglomerular cells, erythropoietin, calcitriol), enteroendocrine hormones, neuroendocrine factors (e.g., hypothalamic releasing and inhibiting hormones) |
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hypothalamus
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The hypothalamic supraoptic and paraventricular nuclei produce oxytocin (OCT) and vasopressin (antidiuretic hormone-ADH) and store them in the posterior pituitary (neurohypophysis).
The hypothalamus also directly stimulates and may directly inhibit production of trophic hormones by the anterior pituitary (adenohypophysis). Includes GH-releasing hormone; GH-inhibitory hormone; several others. |
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Pituitary (aka hypophysis
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In response to hypothalamus releasing hormones..
Anterior pituitary (adenohypophysis) produces trophic hormones: Growth Hormone(GH), Adrenocorticotropic hormone (ACTH), gonadotropins (Luteinizing Hormone (LH) and Follicle Stimulating hormone(FSH)). Posterior pituitary (neurohypophysis) stores and releases antidiuretic hormone(ADH) and oxytocin (OCT). For example: low conc of circulating cortisol is sensed by hypothalamic receptors ->> release of corticotrophin releasing hormone from the hypothalamus into portal veins to act on ant pit gland ->> this stimulation leads ant pit to release ACTH into venous system->>adrenal glands then synthesize and release cortisol into blood circulation system, as cortisol increases hypothalamus reduces amt of corticotrophin releasing hormone= negative feedback loop. ENDOCRINE ALL ABOUT FEEDBACK LOOPS |
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Related Diseases (pituitary)
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Pituitary hypofunction (Hypopitiutaryism)
Partial or complete loss of anterior pituitary hormone secretion Generally permanent condition Complicated treatment regimes: replace cortisol 1st, then T4, then sex steriods when stable, last to be replaced is GH PT precautions: decreased bone density, slipped capital femoral epiphysis possible |
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ACTH (adrenorcorticotropic hormone)
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Replace diagnostically to determine Addisons disease versus secondary adrenal insufficiency
Addisons: no effect Insufficiency: increased gluticosteriod production in adrenals. ACTH: stimulates adrenocorticosteriod pathway thus converting cholesterol to cortisol in adrenal cortex. Cortisol provides needed glucose for brain function. Addison's disease is a disorder that occurs when your body produces insufficient amounts of certain hormones produced by your adrenal glands. In Addison's disease, your adrenal glands produce too little cortisol and often insufficient levels of aldosterone as well. Also called adrenal insufficiency or hypocortisolism, Addison's disease occurs in all age groups and affects both sexes. Addison's disease can be life-threatening. Treatment for Addison's disease involves taking hormones to replace the insufficient amounts being made by your adrenal glands, in order to mimic the beneficial effects those naturally made hormones would normally produce. Symptoms Addison's disease symptoms usually develop slowly, often over several months, and may include: Muscle weakness and fatigue Weight loss and decreased appetite Darkening of your skin (hyperpigmentation) Low blood pressure, even fainting Salt craving Low blood sugar (hypoglycemia) Nausea, diarrhea or vomiting Muscle or joint pains Irritability Depression |
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ADH (antidiuretic Hormone)
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a.k.a. arginine vasopressin
Maintains proper body fluid balance in body Release of ADH may increase blood volume. This plus vasoconstrictive action may raise BP (elevated levels of ADH). Inc in plasma osmolality or decrease in blood volume is main stimuli for ADH release. Receptors in cardiovascular system sense dec in BP=release of ADH from post. Pit. |
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ADH may be used in Rx
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Desmopressin (Stimate):Metered dose nasal spray for diabetes insipidus or to stop bleeding of esophageal varices.
Treatment of nocturnal enuresis Treatment of hemophilia to prevent bleeding Overuse dangers= water intoxication or hyponatremia or headache and tremors. esophageal varices (or oesophageal varices) are extremely dilated sub-mucosal veins in the lower third [1] of the esophagus. They are most often a consequence of portal hypertension, commonly due to cirrhosis; patients with esophageal varices have a strong tendency to develop bleeding Hyponatremia is a condition that occurs when the level of sodium in your blood is abnormally low |
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Growth Hormone
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GH located in anterior pituitary, naturally high levels during deep sleep and early morning
Anabolic effects on several tissues including skeletal mm and epiphyseal cartilage= growth Deficiency: Pituitary dwarfism-RX: replacement human GH (somatropin or somatrem) Idiopathic: kids 2.25 SD below growth curve Adult administration: reduces central obesity, improves lipid levels, increases bone density and lean mm mass, increase isokinetic strength with exercise Offset long term steroid use effects GH: stimulates protien synthesis and uptake of amino acids into cells. Stimulates the production of IGFa which activates receptors on bone and mm to promote growth. |
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Excessive GH
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Acromegaly
Excessive production of GH in adults Skin thickening Thyroid enlargement Excessive sweating Enlarged heart Enlargement of the hands, feet, facial features Treatment drug of choice: decreases GH levels Somatostatin analogs (Somatostatin, Lanreotide acetate, Octreotide (synthetic somatostatin), Pegvisomat: GH receptor antagonist. Non surgical candidates or failed surgical candidates |
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Thyroid Hormones - function
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Control basal metabolic activity of all tissues
Stimulate tissue oxygen consumption Compliment the sympathetic nervous system Enhance gluconeogenesis Increase metabolism of carbs, fats, and proteins Regulate body temp, increasing HR and contractility, enhance red blood cell mass and circulatory volume Need good levels for bone growth 1-4:Tissue wasted in order to supply glycogen. 5: by influencing insulin, glucagon, glucocorticoids and catecholamines by influencing carbohydrate metabolism 7; pts with hyperthyroidism= net effect on bone cells is bone reapsorption=osteoporosis and risk of fx. |
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Thyroid Gland
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Follicular cells form T4 (tetraiodothyronine) and T3 (triiodothyronine) under control of adenohypophyseal TSH (thyrotropin).
Parafollicular (“C”) cells secrete calcitonin in response to hypercalcemia, without influence from hypothalamus or adenohypophysis. Thyroid gland secretes 3 main hormones. Rich blood flow into thyroid gland thus t3 and t4 are secreted into circulation. Thyroid function regulated by a negative feedback effect from T3 and T4. Thyroid glands requires uptake of 70mg of iodine daily. Decreased plasma iodine level=reduction in hormone production=increase in TSH. Elevated plasma iodine level=increase in hormone production and decrease in TSH |
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Related Diseases (thyroid)
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Hyperthyroidism
Symptoms: nervousness, weight loss, heat intolerance, fatigue. tremor, tachycardia, hyperhidrosis (excessive sweating), occular stare (intense), and enhanced reflexes Could be Graves disease: proptosis, diplopia (double vision), corneal inflammation Treatment: antithyroid drugs: Thionamides (requires 6 weeks), radioactive iodine, surgery Secondary to overproduction TH or excessive ingestion of TH. Hyperhidrosis=excessive sweating. Exopthalmos/proptosis=bulging of the eye anteriorly out of the orbit. Serious side effects to thionamides: skin rash, fever, achy, abnormal taste, liver dysfunction, bone marrow depression. Maybe precursor to radioactive iodine administration Rad iodine: administered in : to reduce levels of TH until surgery can be performed or use to destroy thyroid gland. Takes 2-4 months to complete. Pt radioactive for a while after thyroid is destroyed. Pts need to take supplemental TH once gland is destroyed. Need to take beta blockers until redioisotope treatment is effective: thse help to reduce tremors and tachycardia. Complication: thyroid storm=severe form of thyrotoxocosis and is a medical emergency: need IV fluids, cortisol, oral postassiom iodide to block TH release and beta blockers to lower HR |
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Related Diseases (hypothyroidism again)
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Hypothyroidism
TH deficiency cause by destruction of the gland Symptoms include: bradycardia, lethargy, weight gain, cold intolerance, myxedema (generalized nonpitting edema) Treatment: replacement drug therapy with synthetic oral levothyroxine Risks: males= femur fractures; effects of hyperthyroidism Primary hypothyroidism=Hashimotos thyroiditis from antibody mediated destruction of the thyroid gland. Secondary hypothyroidism+ dec secretion of TSH from pit gland or TRH hypothalamus |
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summary of thyroid meds
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Thyroid hormones orally for hypothyroidism:
T4 levothyroxine (Trade name: Synthroid.) T3 liothyronine (Trade name: Cytomel.) Combination (Trade name: Thyroid USP). Actions to increase metabolic rate of all cells, thus also O2 consumption, heart rate, pulse pressure. Monitor dose with TSH levels, watching for signs of hyperthyroidism. Hyperthyroidism: nervousness, weightloss, heat intolerance, tremor, tachycardia, excessive sweating, enhanced reflexes, bulging eyes |
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Adrenal Cortex
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Formation of 3 types of steroid hormones:
glucocorticoids (e.g. cortisol, hydrocortisone) affect carb and protein metabolism, mineralocorticoids (e.g., aldosterone, DOCA) responsible for water and electrolyte balance, sex hormones precursors (DHEA, androstenedione) which are converted in the gonads to active estrogens, testosterone. |
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Steroids
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Direct effects on target cells without need for surface receptors.
Glucocorticoids (anti-inflammatory potency): Cortisone, hydrocortisone, prednisone, prednisolone, methylprednisolone, betamethasone Mineralocorticoids (Na, K, Cl, water): |
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Glucocorticoids
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Elevation of levels in early morning, reduction in late evening/replacement therapy trys to mimic this
Cortisol: stress response hormone Gluconeogenesis and lipolysis = fuel for brain and physical activity Anti-inflammatory and immune suppressive Cushings Syndrome: excess levels. weakness, osteoporosis, moon face, fragile skin, ect. Treat with surgery and some drug intervention Addisons Disease: low levels. weight loss, fatigue, reduced cardiovasc function, arthralgia. Treat with replacement therapy |
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N.B. (Nota Bene)
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After about three weeks of continuous glucocorticoid therapy by any route, medication may not be stopped abruptly without potentially life-threatening consequences.
Must be tapered down slowly over weeks. |
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Mineralocorticoids
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Aldosterone primary.
Increase permeability of kidney tubules to sodium. Water then passivle reabsorbed. Stimulates the Na+/K+-ATPase pump= sodium reabsorption and excretion of potassium and hydrogen Deficiency: orthostatic hypotension, dehydration, oliguris, poor skin turgor. Treat with replacement therapy (Fludrocortisone) Excess: Conns syndrome. Treat with surgery |
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Gonads (ovaries and testes)
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In addition to producing, maturing and releasing gametes, they produce estrogens, progesterone, and testosterone.
Controlled by anterior pituitary (adenohypophyseal) gonadotropins (LH, FSH), themselves released by GnRH from hypothalamus. |
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Hormones and Reproduction
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General indications for Rx sex hormones:
Male: Stimulators of anabolism Replacement therapy Female Replacement therapy OCs Infertility treatment Treatment of metastatic endometrial carcinoma and, rarely now, of metastatic prostate carcinoma. |
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Androgens
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Testosterone analogs or derivatives
Types include: injectable aqueous testosterone. testosterone cyprionate fluoxymestrone methyltosterone Adverse effects of androgens are multiple and may include jaundice and testicular atrophy. |
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Oral Contraceptives
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OCs have effects by altering the hypothalamic-pituitary-gonadal cycling
Alteration in cervical mucus consistency Inhibition of endometrial implantation NEVER use in pts w/ past hx of stroke, venous thromboembolism, hypertension or even current smokers. Levels may be increased by concomitant benzodiazepines administration. Levels may be decreased by penicillin and TCNs |
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Clomiphene
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A SERM which blocks negative feedback inhibition of estrogens on hypothalamus, leading to secretion of large amounts of GnRH
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Sildenafil (Viagra)
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Initially evaluated as a possible treatment for arterial hypertension, and is sometimes used in pulmonary hypertension.
Inhibits a phosphodiesterase isoenzyme leading to accumulation in the corpora cavernosa of NO and consequent vasodilation. Adverse effects include priapism, hypotension and MI mostly in patients also on nitrates, rare blue vision and sudden hearing loss. |
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Diabetes Mellitus
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Cornerstone of optimal anti-diabetic therapy is diet and exercise!!
Great majority of adult diabetics are Type II (a.k.a., maturity-onset, obesity-related, non-ketosis-prone). Characterized by age, obesity, insulin insufficiency with peripheral “insulin resistance.” Type I (formerly called “juvenile”) DM, less than 10% of all 19 million U.S. diabetics; noted for absent insulin and prone to ketoacidosis. Polyuria and severe dehydration. Total diabetics worldwide is expected to be 220 million. |
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Pancreatic islets of Langerhans
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ß cells produce insulin in response to hyperglycemia.
Alpha cells produce glucagon in hypoglycemia. Δ cells release somatostatin (GHIH). |
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Diabetus Mellitus Drugs
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Type I diabetics dependent on exogenous insulin. Body attacks beta cells, and insulin isnt produced in response to meal, blood sugar rises. Autoimmune disease.
In type II DM, oral antiglycemic agents which increase output of already normal insulin amounts may increase peripheral effectiveness. Liver and muscles don’t respond to insulin. Pancreas burns out trying to supply more insulin. Connected to obesity. Continuing efforts must be made to maximize diet and exercise, and to thus minimize drug dosage. |
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Oral Antiglycemic Agents
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These should NEVER be used in pregnancy or in women who may become pregnant! ?Teratogenic.
Classes of drugs: Sulfonylureas MOA: stimulate ß cells to secrete more insulin 1st generation: Acetohexamide chlorpropamide (Diabinese) tolbutamide (Orinase) tolazamide (Tolinase) Next slide for 2nd generation sulfonylureas |
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Oral Antiglycemic Agents (2)
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2nd generation sulfonylureas
glipizide glyburide 3rd generation sulfonylurea glimepiride All sulfonylureas are prone to cause hypoglycemia, and individual agents may be teratogenic or increase incidence of acute MI. |
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Oral Antiglycemic Agents (3)
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Biguanides such as metformin
Reduce hepatic gluconeogenesis Peripheral insulin resistance inhibitors Avandia, Actos Drugs inhibiting luminal CHO catabolism acarbose |
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Types of Exogenous Insulins
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Types you’ll most likely encounter, their peaks of action and durations:
Ultra Short acting: (5 min onset, peak at 1 hour; duration of 3-5h) Lispro, Aspart Short-acting (30 min onset, peak 2-5h; duration 5-8h) Regular insulin, Humulin R Intermediate-acting (1-4h onset,p 6-12h; duration 14-24 h) NPH, Humulin N, Lente, Humulin L Long acting: (onset 4-6 hours, peak 8-20 hours, duration up to 36 hours Ultralente |
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Exercise and Diabetes
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Skeletal mm use stores of glycogen and triglycerides to meet energy requirements during exercise.
Diabetic pts may have ill effect of not having enough insulin= ketoacidosis and increase high levels of glucose. Or may also get hypoglycemia induced as a result of high plasma insulin level with injection of insulin. Pt needs to adjust medication dosage in response to exercise and meal. Pt must be able to self monitor blood glucose levels. |
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General Guidelines for blood/glucose levels rising or dropping
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Blood glucose should be between 100-250 mg/dL. Give snack if under 100 mg/dL. No exercising if > 300 mg/dL, caution at 250mg/dL
Monitor blood glucose levels before, during and after exercise. Consume carbs to avoid hypoglycemia. May need snack every 30 min during activity Measure blood glucose levels after activity for 6-12 hours. Know the persons typical response. Consult p 233 for more details and guidelines |
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Osteoporosis
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Loss of bone mass which reduces strength of bone.
Influenced by age, smoking, ETOH, immobility Prevention with healthy diet and adequate intake of Vitamin D and calcium. May need drug therapy to combat bone loss (osteopenia) Lots of antiresorptive agents used but need to continue using forever May use anabolic therapy which stimulate increases in BMD. Investigating statins, GH, PTH related peptides, flourides. |
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PT guidelines
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Drug therapies don’t typically impact PT directly.
Drugs are injections, so site may be sore. Don’t exercise or use modalities near injection sites. For pts using bisphosphonates: exercise that inc abd pressure in supine should be avoided because drugs may cause reflux or esophagitis. |
