CLSChem - 06 - Endocrinology

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  1. Endocrine vs exocrine vs paracrine
    • Endocrine: secrete hormone into blood stream
    • acts at distant tissue site
    • Exocrine: secrete non-hormone into ductal system
    • acts at distant OR adjacent site
    • Paracrine: secrete hormone that acts DIRECTLY on nearby cells
  2. Diff in function (tport, method of action) of hormones (protein, steroid, thyroid hormones, catecholamines)
    • Protein: usually circulate WITHOUT carrier protein
    • interact w/ cell memb receptors
    • Steroid: transported bound to protein
    • enter cell, modulate gene transcription
    • Thyroid: transported bound to protein
    • enter cell, modulate gene transcription
    • Catecholamines: circulate unbound
    • interact w/ cell memb receptors
  3. What is the "axis concept" in endocrinology?
    • Hypothalamic releasing hormones stimulate pituitary secretion of trophic hormones
    • Trophic hormones stimulate endocrine gland synthesis/secretion of primary hormone
    • Endocrine hormone effects action at target tissue
    • *NOTE - endocrine hormone usually has negative feedback to hypothalamus and/or pituitary
    • *NOTE - Estradiol has positive feedback (unique)
  4. anterior vs posterior pituitary (activation + types)
    • Anterior (adenohypophysis): hypothalamic neurons secrete releasing factors into ciruclation which directly feeds pituitary
    • Direct effectors - GH, hGH, Prl
    • Trophic - ACTH, FSH, LH, TSH, GH
    • Posterior (neurohypophysis): hypothalamic neurons extend INTO neurohypophysis and secrete hormones there
    • AVP/ADH, Oxytocin
  5. GH disorders - hyper and hypo
    • Gigantism: excess during growth phase
    • Acromegaly: excess after growth is complete
    • *NOTE - both common from pituitary tumor
    • Pituitary dwarfism: lack of secretion in growth phase
    • Adult hypo: mental issues, osteoporosis
  6. GH testing
    • IGF-1 preferred (random GH not reliable due to pulse)
    • Hyper secretion test: Oral GGT should suppress GH to <1 ng/mL
    • Hypo secretion test: Insulin tolerance test, Arginine infusion (promotes GHRH)
  7. Prl disorders - Hyper
    • Prolactinoma: Prl secreting pituitary tumor
    • more obvious in females (lactation)
    • anti-dopaminergic drugs
    • hypothyroidism
  8. Prl testing
    • Immunoassay
    • Macroprolactin: (IgG-bound, physiologically inactive)
    • Not synthesized in excess, but not excreted appropriately
  9. What are some causes of panhypopituitarism?
    • Pituitary tumors
    • Hypothalamic tumors
    • Trauma, radiation, infarction
    • *NOTE - loss of direct effector hormones is less apparent, but trophic hormones are CRITICAL and will be obvious
    • Will require hormone replacement
  10. define adrenarche and menarche
    • Andrenarche: onset of adrenal androgen synthesis
    • Menarche: onset of menstrual cycles
  11. Describe hormone development during menstruation during the follicular phase, ovulatory phase, and luteal phase
    • Follicular: E2 and P4 decline from previous cycle
    • FSH increases (no negative feedback)
    • FSH stimulates follicular proliferation -> E2 synth
    • Several follicles -> dominant follicle -> E2 simulates endometrium/suppresses FSH
    • Ovulatory: Rising E2 stimulates LH surge ~d12
    • LH at peak stimulates ovulation
    • LH stimulates P4 synthesis by follicle
    • Ovum captured by fallopean tubes
    • Luteal phase: follicle -> corpus lutem
    • CL synth P4 and E2
    • P4 suppress LH and FSH
    • fertilization = hCG synth by trophoblast -> CL maintained -> CL maintains endometrium
    • no fertilization = no hCG -> CL regression -> sloughing (menses)
  12. What is menopause and what happens hormonally?
    • 12 months of amenorrhea (no menses)
    • Primary depletion of ovarion follicles -> decreased E2 -> increased FSH LH (no neg feedback)
  13. How to determine primary or secondary problem in primary amenorrhea?
    • primary: elevated FSH = ovarian non-response
    • proceed with genetic testing (Turner's? 45, X0)
    • secondary/tertiary: low FSH/LH (decreased synth?)
  14. Primary amenorrhea vs secondary amenorrhea
    • Primary: no menses by age 16
    • Turner's (45, X0), CAH, etc
    • Secondary: loss of menses for >6 mo
    • Preggo, PCOS, Cushing's, drugs, stress
    • no genetic testing
  15. Hyperandrogenism vs hyperandrogenemia.  What symptom are they related to?
    • Related to PCOS
    • ism: symptoms
    • hirstuism (male hair pattern), virilization (muscle mass, deep voice)
    • emia: increased andro hormones
    • ASD, DHEA, testosterone
    • DHEA-S normal
  16. How does testosterone travel in blood?  Describe it's activity
    • sex-hormone binding globulin (SHBG): low capacity, high affinity 
    • ~60% bound
    • not available to tissue
    • *also binds E2
    • Albumin: high capacity, low affinity
    • ~35% bound
    • considered available to tissue
    • Free: 2-3%
    • controversy if free or both free and weak are biologically active
  17. hypogonadtorophic hypogonadism vs hypergonadtrophic hypogonadism
    • hypo: decreased testosterone, and LH/FSH
    • secondary and tertiary (gonad not being stim)
    • hyper: decreased testosterone, increased LH/FSH
    • primary (gonad not responding)
    • Androgen insensitivity syndrome: genotyped XY, but NO external male development (appears as female)
    • testosterone normal/high (no response)
  18. Osteoclast vs osteoblast
    • clast: induce bone resorption (serum Ca increase)
    • blast: induce bone formation (serum Ca decrease)
  19. Osteoporosis vs osteopenia
    • Osteoporosis: loss of bone mass (asymp until inappropriate fracture)
    • Osteopenia: loss of bone mass <osteoporosis
  20. What causes most bone disease (decreased mineralization?)
    Vitamin D deficiency (formation, or intake)
  21. What is Paget's disease
    • Increased osteoclastic bone resorption plus DISORDERED osteoblastic bone formation
    • weak, thickened, painful bones
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CLSChem - 06 - Endocrinology
2016-10-17 05:58:39
CLSChem 06 Endocrinology
CLSChem - 06 - Endocrinology
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