Endocrinology Flashcards
1
Q
Homeostasis
A
- Process of maintaining a constant internal environment despite changes in condition
- Homeostasis isn’t equilibrium
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)
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
4
Q
Reflexes
A
- Simple reflexes mediated by nervous or endocrine system
- Complex reflexes mediated by both systems and go through several integrating systems
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
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
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
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
9
Q
Three types of hormones
A
- Peptide/protein(eg. insulin)
- Steroid(eg. cortisol)
- Amine(single amino acids)(eg. catecholamines)
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)
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
12
Q
Synthesis of catecholamines
A
- Synthesized in adrenal medulla
- Stored in vesicles prior to release
- Released by exocytsosi
- Lipophobic
- Bind to membrane receptors
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
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
15
Q
Anterior Pituitary
A
- Hypothalamic releasing and inhibiting hormones
- Does not create hormones
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
