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25 Cards in this Set
- Front
- Back
Local Hormones
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AcH, secretin, CCK, NE
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General hormones
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Epi, NE, thyroid hormones, GH
Effects: fight or flight, inc met rate, hypermetabolism, disproportionate grwoth, work via blood stream |
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Pineal gland
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circadian rhythm, modulates peaks and trophs in hormonal levels
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Pituitary
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Master gland
Anatomy: sits in sella turcia, blood supply, near optic chiasm (visual disturbances), relationship to cavernous sinus Regions: Anterior (adenohypophysis) --> GH, ACTH, LH, TSH, FSH, Prolactin Posterior (neurohypophsis) --> ADH, Oxytocin |
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Thyroid
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T4, T3, calcitonin
Needs iodine |
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Pancreas
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insulin (beta cells)
glucagon (alpha cells) |
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Adrenals
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coritsol, aldosterone
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Ovaries and testes
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progesterone, estrogen, testosterone
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Placenta
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hCG, estrogen, progesterone, somatotrophin
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Tyrosine derivatives
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thyroxine, triiodothyronine, epi/ne
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Proteins, peptide, E/NE
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target = cell membrane and surface
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Steroids
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target = cellular cytoplasm
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Thyroid hormones bind to chromosomes and associate with proteins
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Target = cellular nucleus
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Hormone MOA
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1. change in membrane permeability
2. intracellular enzyme activation 3. gene activation (intracellular binding) |
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Second Messengers: cAMP
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MOA: R + cAMP (enzyme activator): hormones stim adenyl cyclase to form cyclic AMP which stims and produces via amplificaiton
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Second messengers: Calmodulin
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other second messenger
4 Ca2+ binding sites conformational steric effects different pathways from cAMP secondary back up pathway |
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Steroid hormones
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source: adrenal cortex
MOA: mRNA diffuses out to cytoplasm for translation on ribosomes to SPECIFIC PROTEINS ex. Aldosterone (zona glomerulosa): enters renal tubular cytoplasm --> induces Na+ protein absorption synthesis |
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Growth hormone
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Increase protein synthesis**
Stimulation for release: STARVATION, protein deficiency, trauma, hypoglycemia, low FFA in blood, deep sleep, exercise, excitment |
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Diabetic emergencies/pancreas
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hypoglycemia
hyperglycemia (DKA, HHNC/HHNK) |
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Thryoid endocrine emergencies
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thyrotoxicosis, thyroid storm, myxedema coma
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DM type I
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juvenile onset
insulin dependent IMMUNOLOGIC DESTRUCTION OF PANCREATIC ISLET CELLS LEADING TO LITTLE OR NO INSULIN PRODUCTION tx = insulin |
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DM type II
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adult onset
NON insulin dependent DEC RESPONSE TO INSULIN: obesity, age >40 Tx: oral hypoglycemics, dietary modification |
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Hypoglycemia
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serum glucose <50mg/dl
CAN CAUSE DEATH Etiology: inc insluin, inc oral hypoglycemia dosing/intake, change in oral intake, change in activity, dz processes, med change, surgery, pentamide, aspirin, haloperidol, age extremes, insulinoma, renal failure, adrenal insufficiency, sepsis, ETOH, heart failure Presenting sx: sweating, light headedness, irritability, confusion, seizure, trembling, palpitations, lack of focus, neuro deficiency Tx: glucose IV; glucagon IM |
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Hyperglycemia
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serum glucose >80-120 mg/dl
consequences of hyperglycemia: ostmotic diuresis, electrolyte imbalance, neuropathy (stocking glove), opthalomic, mononeuropathy multiplex, cranial mononeuropathy, AI insufficiency, impairment of WBC fnx/sepsis, retinopathy, PVD, ketoacidosis in type I, vascular changes, gastroparesis, urinary retention DM impact on other diseases: heart dz, stroke, kidney dz, nerve dz, eye dz |
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DKA
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Etiology: insulin deficiency; inc stress hormone levels in body (glucagon, NE/E, cortisol, GH)
Signs & Sx: n/v, change in mental status, K+ derangement, abd pain, tachypnea, Na+ derangement, RUQ pain (liver capsule), Fruity odr Changes/shifts in: Cl-, Ca2+, Mg2+, phosphorous Clinical/Lab findings of DKA with hyperglycemia: osmotic diuresis, dehydration, polyuria, polydipsia, wt loss, gluconeogenesis/glycolsysis, metabolic acidosis/lipolysis (acetoacetate, beta hydroxylbutyrate) |