Endocrinology Flashcards

1
Q

Homeostasis

A
  • Process of maintaining a constant internal environment despite changes in condition
  • Homeostasis isn’t equilibrium
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2
Q

Feedback Control

A
  • Negative Feedback: Initial Stimulus -> Response -> Stimulus that inhibits initial stimulus from generating response(eg. regulation of cortisol secretion)
  • Positive Feedback: Initial Stimulus -> Response -> Stimulus that reinforces response, turned off by outside factors(eg. Oxytocin secretion during birth)
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3
Q

Intercellular Communication

A
  • Gap Junctions: Form direct connections between adjacent cells. Small ions and molecules move through gap junctions(eg. cardiac)
  • Contact Dependent: Require interaction between membrane molecules of two cells. Membrane protein binds to membrane protein(eg. immune system)
  • Autocrine: Autocrine acts on same cell that secreted them. Paracrine are secreted by one cell and diffuse to adjacent cells. Molecules move through interstitial fluid
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4
Q

Reflexes

A
  • Simple reflexes mediated by nervous or endocrine system
  • Complex reflexes mediated by both systems and go through several integrating systems
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5
Q

Why different control systems?

A
  • Specificity: Neural terminates on a single target cell. Endocrine effects most of cell in body
  • Nature of signal: Electrical signal passes through neuron, and chemical neurotransmitters carry signal. For endocrine, chemical signals secreted in blood for distribution throughout the body
  • Speed: Very rapid for neural. Much slower for endrocrine
  • Duration: very short for neural. Endocrine lasts much longer
  • Coding for stimulus intensity: Signal identical in strength for neural. Endocrine is correlated with amount of hormone secreted
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6
Q

Features of hormones

A
  • Can be made by different places in the body
    -Chemicals made by cells in specific endocrine gland
  • Transported in blood to different targets
  • Binds to specific receptors
  • Alter activity in cells
  • Action must be terminated
  • Maintain homeostasis
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7
Q

Hydrophilic Hormones

A
  • Water soluble
  • Not lipid soluble(lipophobic), cannot cross plasma membrane
  • Synthesized in advance
  • Dissolved in blood
  • Peptide hormones, protein hormones, catecholamines
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8
Q

Hydrophobic Hormones

A
  • Not water soluble, does not dissolve in plasma
  • Synthesized on demand
  • Lipid soluble(lipophilic), readily cross plasma membrane
    -Bound to carrier proteins in blood
  • Steroid and thyroid hormones
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9
Q

Three types of hormones

A
  • Peptide/protein(eg. insulin)
  • Steroid(eg. cortisol)
  • Amine(single amino acids)(eg. catecholamines)
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10
Q

Peptide Hormones

A
  • Linked amino acids
  • Made in advance
  • Synthesized like secreted proteins
  • Stored in vesicles, released by exocytosis upon signal
  • Water soluble
  • Bind to membrane receptors
  • C-peptide cleaved after release(proinsulin example)
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11
Q

Steroid Hormones

A
  • Synthesized from cholesterol
  • Made on demand
  • Not stored in vesicles
  • Released by simple diffusion
  • Water insoluble
  • Long half-life
  • Diffuse into target cells
  • Cytoplasm or nucleus receptors
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12
Q

Synthesis of catecholamines

A
  • Synthesized in adrenal medulla
  • Stored in vesicles prior to release
  • Released by exocytsosi
  • Lipophobic
  • Bind to membrane receptors
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13
Q

How do stimuli trigger hormone release

A
  • Chane in membrane potential
  • Increase free cytosolic Ca++
  • Change enzymatic activity
  • Alter transcription of genes coding for hormones
  • Promote survival of endocrine cell
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14
Q

Glucose stimulation of insulin release

A
  • Glucose goes into cell(increase blood sugar)
  • ATP inhibits K+ channel
  • Depolarizes cell
  • Opens voltage gated Ca++ channel
  • Triggers exocytosis insulin release
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15
Q

Anterior Pituitary

A
  • Hypothalamic releasing and inhibiting hormones
  • Does not create hormones
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16
Q

Hormone Interactions

A
  • Synergistic: Multiple hormones act together for greater effect
  • Permissive effects: One hormone enhances the target organ’s response to a second later hormone
  • Antagonistic: One hormone opposes the action of another
17
Q

Calcium Balance

A
  • RANK/RANKL to increase osteoclast differentiation
  • OPG blocks RANK/RANKL
  • PTH hormone increase RANK/RANKL and decrease OPG to increase calcium levels -> stimulate calcitriol
  • Calcitonin activated in high calcium -> used to decrease calcium levels
18
Q

Fluid Balance

A
  • Vasopressin(ADH): used to conserve body water and increase blood volume/pressure -> cAMP release send aquaporin-2 pores to collecting duct lumen -> increase permeability of water -> water flow to bloodstream
  • Aldosterone: Na reabsorption(retain water) and K secretion -> stimulated by angiotensin 2(RAAS) -> aldosterone signaling cause transcription/translation of new channels/pumps -> balances Na/K(Na reabsorb and K out) -> Na pump back into bloodstream
  • Atrial Natriuretic Peptide(ANP): increase K reabsorption and decrease Na and water reabsorption(lowers blood pressure) -> causes decrease renin and aldosterone
19
Q

Adrenal Medulla

A
  • Cortisol: Secreted by adrenal cortex, mediates long term stress -> CRH in hypothalamus stimulate ACTH to release cortisol
  • Addison’s Disease: hyposecretion of adrenal steroid hormones -> hypoglycemia
  • Cushing’s Syndrome: Cortisol excess -> hyperglycemia or tumors
  • Zona glomerulosa: Aldosterone
  • Zona fasciulata: Glycocorticoids
  • Zona reticularis: Sex hormones
  • Adrenal medulla: catecholamines
20
Q

Growth and Thyroid Hormone

A
  • Hypothalamus stimulate GHRH -> release GH -> acts on liver to secrete IGF-1 -> growth promoting effects on cells on the body -> chondrocyte recruitment. GH inhibited by GHIH(somatostatin)
  • Gigantism: too much GH in childhood, Acromegaly: too much GH in adulthood
  • Thyroid hormone: TRH stimulate TSH -> make and release T3, T4
  • Hyperthyroidism: Too much thyroid hormone, cause goiter, high heart rate(eg. Grave’s disease)
  • Hypothyroidism: Thyroid hormone deficiency, slowed heart rate
21
Q

Male reproductive

A
  • Spermiogenesis: Spermatids mature into spermatozoa, lose cytoplasm and gain tail
  • Sertoli cells: Sperm development
  • Leydig cells: Secrete testosterone
  • GnRH stimulates LH and FSH -> FSH stimulates Sertoli cells(sperm development) and LH stimulate Leydig cells(secrete testosterone)
  • Hypogonadism: Decreased functional activity of testes -> decreased androgen production
22
Q

Female Reproductive

A
  • Granulosa cells: Support oocyte development
  • Theca cells: Secrete steroid hormone precursors
  • Menstrual cycle:
    - Ovarian cycle: Follicular phase(oocyte development) and luteal phase(corpus luteum forms)
    - Uterine cycle: Menstrual and Proliferative phase(Days 1-14) and Secretory phase(Days 4-28)
  • Early to mid follicular phase: LH stimulates androgen release from theca cells, FSH stimulates conversion to estrogen by granulosa cells, Granulosa cells secrete AMH. Estrogens exert negative feedback
  • Late follicular to ovulation: Inhibit inhibits FSH, high estrogen increase frequency of GnRH pulses -> LH surge(completion of meiosis 1 and cause ovulation)
  • Early to mid luteal phase: Secretion of inhibin, progesterone and estrogen -> negative feedback to turn off FSH and LH
  • Late luteal phase: If no fertilization, corpus luteum undergoes apoptosis
23
Q

Pregnancy

A
  • Human chorionic gonadotropic(hCG) maintains corpus luteum
  • Labour triggered by increase in estrogen/oxytocin receptors, fetal cortisol, CRH, prostaglandins
  • Estrogen and progesterone inhibit milk production
  • Decrease in dopamine cause prolactin and oxytocin increase -> Milk secretion and smooth muscle contraction
24
Q

Sex Determination

A
  • Males have SRY gene that promotes testes development -> SOX9 transcription -> repress female structures via AMH and initiate sertoli cell differentiation
  • Beta-catenin suppress SOX9 expression -> female organs