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25 Cards in this Set

  • Front
  • Back
Local Hormones
AcH, secretin, CCK, NE
General hormones
Epi, NE, thyroid hormones, GH

Effects: fight or flight, inc met rate, hypermetabolism, disproportionate grwoth, work via blood stream
Pineal gland
circadian rhythm, modulates peaks and trophs in hormonal levels
Pituitary
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
Thyroid
T4, T3, calcitonin

Needs iodine
Pancreas
insulin (beta cells)
glucagon (alpha cells)
Adrenals
coritsol, aldosterone
Ovaries and testes
progesterone, estrogen, testosterone
Placenta
hCG, estrogen, progesterone, somatotrophin
Tyrosine derivatives
thyroxine, triiodothyronine, epi/ne
Proteins, peptide, E/NE
target = cell membrane and surface
Steroids
target = cellular cytoplasm
Thyroid hormones bind to chromosomes and associate with proteins
Target = cellular nucleus
Hormone MOA
1. change in membrane permeability
2. intracellular enzyme activation
3. gene activation (intracellular binding)
Second Messengers: cAMP
MOA: R + cAMP (enzyme activator): hormones stim adenyl cyclase to form cyclic AMP which stims and produces via amplificaiton
Second messengers: Calmodulin
other second messenger
4 Ca2+ binding sites
conformational steric effects
different pathways from cAMP
secondary back up pathway
Steroid hormones
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
Growth hormone
Increase protein synthesis**

Stimulation for release: STARVATION, protein deficiency, trauma, hypoglycemia, low FFA in blood, deep sleep, exercise, excitment
Diabetic emergencies/pancreas
hypoglycemia
hyperglycemia (DKA, HHNC/HHNK)
Thryoid endocrine emergencies
thyrotoxicosis, thyroid storm, myxedema coma
DM type I
juvenile onset
insulin dependent
IMMUNOLOGIC DESTRUCTION OF PANCREATIC ISLET CELLS LEADING TO LITTLE OR NO INSULIN PRODUCTION

tx = insulin
DM type II
adult onset
NON insulin dependent
DEC RESPONSE TO INSULIN: obesity, age >40

Tx: oral hypoglycemics, dietary modification
Hypoglycemia
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
Hyperglycemia
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
DKA
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)