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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
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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
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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)
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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
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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
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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)
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Prl disorders - Hyper
- Prolactinoma: Prl secreting pituitary tumor
- *HOOK EFFECT IS VERY COMMON
- more obvious in females (lactation)
- anti-dopaminergic drugs
- hypothyroidism
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Prl testing
- Immunoassay
- HOOK EFFECT IS VERY COMMON
- Macroprolactin: (IgG-bound, physiologically inactive)
- Not synthesized in excess, but not excreted appropriately
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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
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define adrenarche and menarche
- Andrenarche: onset of adrenal androgen synthesis
- Menarche: onset of menstrual cycles
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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)
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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)
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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?)
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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
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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
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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
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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)
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Osteoclast vs osteoblast
- clast: induce bone resorption (serum Ca increase)
- blast: induce bone formation (serum Ca decrease)
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Osteoporosis vs osteopenia
- Osteoporosis: loss of bone mass (asymp until inappropriate fracture)
- Osteopenia: loss of bone mass <osteoporosis
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What causes most bone disease (decreased mineralization?)
Vitamin D deficiency (formation, or intake)
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What is Paget's disease
- Increased osteoclastic bone resorption plus DISORDERED osteoblastic bone formation
- weak, thickened, painful bones
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