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Endocrinology

Francisco Sacadura Physiology Englisch 50 Karten

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  1. 1What is major difference between hydrophilic & hydrophobic H?Molecular structure: hydrophilic have polar/charged chemical groups, majority peptide/protein (polar peptide bonds+ polar/charged aa side-chains) whereas hydrophobic r non polar often w/cyclic C structures (derivatives of cholesterol, tyrosine or fat-soluble vitamins A & D)
  2. 2Name major classes hydrophilic H & what renders them H2O solublePeptides/proteins H: polar peptide bonds & polar/charged aa side-chains
    Glycoprotein H: H2O solubility ↑ by N-linked+/O-linked carbohydrate chains
    Catecholamines: several polar OH groups
    Prostaglandins: lipid derivatives but COOH group(remnant origin arachidonic acid) renders them H2O soluble
  3. 3Name major classes hydrophobic H & give examples 4 each 1Cholesterol derivatives: steroid H (progesterone, testosterone, cortisol, aldosterone, oestradiol)
    Tyrosine derivatives: thyroid H (MIT, DIT, thyroxine/T4, triiodothyronine/T3)
    Fat soluble vitamins (A & D) derivatives
  4. 4Contrast mechanism of action of hydrophilic & hydrophobic HHydrophilic: unable cross PM, must bind cell surface R 2 initiate TM signaling pathway involving 2nd messengers & PK/phosphatase enzymes
    Hydrophobic: can diffuse across PM 2 interact directly w/ INC R, in unbound state R in cytoplasm/nucleus, ligand-activated R go 2 nucleus & dimerise 2 bind DNA & act as ligand-dependent TF (↑/↓ transcription target genes)
  5. 5When cells produce either hydrophilic/ hydrophobic H how is H secretion affected?Hydrophilic: unable cross PM, packaged in vesicles that fuse w/PM b4 secretion=> distinction synthesis/release=>plasma [H] controlled both level synthesis & secretion
    Hydrophobic: cross freely PM, rate secretion directly ∝ rate synthesis
  6. 6Explain structure simplest endocrine axisH X controls & responds 2 [metabolite Y] (H, nutrient, ion). If [Y] departs from normal physiological range, homeostatic chain of events initiated whereby [X] alters so that [Y] returns 2 normal range
  7. 7What is homeostatic negative feedback? Give examplesSignal produces response which feeds back on the signal generator 2 ↓level signal
    If X increased [Y], increase in Y would act opposite direction 2 suppress synthesis/ secretion X (e.g. insulin/glucose, aldosterone/K+, calcitriol/Ca2+)
  8. 8How doe we maintain plasma glucose c w/in normal physiological range (3-5mM)?Insulin & glucagon act antagonistically (in opposition): if [glucose]↓, not only stimulus insulin secretion↓, but also ↑secretion glucagon=>decelerate glucose uptake/ metabolism+mobilize body glucose stores
  9. 9What can endocrine disorders reflect?1. defects synthesis appropriate H
    2. defects H secretion
    3. defects cellular response 2 H
    4. defects response endocrine gland 2 appropriate solute/ion
  10. 10Explain typical complex endocrine axisH A stimulates synthesis+/secretion 2nd H B that stimulates production 3rd H C that exerts homeostatic action on c solute/ion S. W/in endocrine axis, C exerts negative feedback on production stimulatory H A+/B (B may exert negative feedback A)
  11. 11Explain structure of endocrine axes driven by hypothalamo-pituitary complex?Releasing H A synthetized hypothalamus acts anterior pituitary stimulate secretion tropic H B stimulates synthesis+/secretion active H C. C effect physiological/metabolic process+negative feedback hypothalamus +anterior pituitary (2 control drive A+/B)
  12. 12Explain 4 hypothalamo-pituitary axesHPG: GnRH>LH>gonadal steroids (testosterone/progesterone/oestradiol)> germ cell maturation (gonadal steroids< LH+GnRH, LHACTH>cortisol(+DHEA)> glucose (cortisolTSH>thyroid H>metabolism (thyroid HGH>IGF-I >growth (IGF-I
  13. 13What normally leads 2 endocrine disorders involving HP axes?Loss of negative feedback between relevant H C & endocrine drive 2 relevant endocrine gland. Failure of negative feedback can be due 2:
    1) defects synthesis H C
    2) defects secretion H C
    3) defects cellular response 2 H C (defect expression/activation of R 4 H C)
    4) ectopic production of endocrine stimulus 2 production H C (synthesis H A +/B outside HP complex)
  14. 14How can negative feedback HPA axis b defective?1. Failure synthesis cortisol
    2. R HPT+/anterior PG 2 cortisol
    3.ectopic synthesis ACTH(small lung tumor)
  15. 15What is positive feedback? Give examplesH X exerts positive action on physiological process Y & that process exerts positive feedback on production H X (e.g. posterior PG H oxytocin, preovulatory LH surge)
  16. 16Describe OXT positive feedback in parturition. Why is it important?OXT (& prostaglandins)=>contraction myometrium=>expel infant uterus=> passage across cervix =>distension vaginal walls=>further secretion OXT (Fergusson reflex). Positive feedback loop normal physiological mechanism 4 expulsion infant w/ min delay & risk foetal distress
  17. 17How is OXT involved in lactation?Months following birth: auditory input from crying infant=>secretion OXT=> contraction lobulo-alveolar ducts of breast=>ejection milk from nipple
    Suckling reflex: neural reflex input from suckling=>OXT secretion=>milk ejection=> further suckling
  18. 18Which factors influence [H]?[H] balance between increase c active H (rate H synthesis & secretion) & decrease c free active H (interaction binding proteins, metabolic inactivation - liver/kidneys - & clearance from bloodstream)
  19. 19Which factors influencing [H] r + important 4 either hydrophilic/hydrophobic H?Hydrophilic: control rate of secretion
    Hydrophobic: hepatic metabolism of H
  20. 20What is the endocrine system?Collection glands that secrete chemical messages (H). Signals passed through blood 2 arrive at target organ which has cells possessing appropriate R
  21. 21Why is endocrine system important?1. Maintains homeostasis & long-term control using chemical signals
    2. Works in // w/ NS 2 control homeostasis
    3. >50 human H identified (all bind R)
  22. 22What r 3 classes of H based on biochemical structure?Peptides: short aa chains; majority; secreted by PG, parathyroid, heart, stomach, liver, kidneys
    Amines: derived from tyrosine, secreted by thyroid & adrenal medulla
    Steroids: lipids derived from cholesterol; testosterone is male sex H; estradiol (similar 2 testosterone) responsible 4 many female sex characters; secreted by gonads, adrenal cortex, placenta
  23. 23What is difference between endocrine, paracrine & autocrine signaling?Endocrine: circulating H (blood), distant target cells
    Paracrine: local H, nearby target cell
    Autocrine: local H, same cell
  24. 24Describe non-steroidal signaling mechanismsNon-steroid H (hydrophilic) don't enter cell but bind PM R generating chemical signal (2nd messenger) inside target cell
  25. 25What r the 5 different 2nd messengers?cAMP, cGMP, IP3, DAG, Ca2+
  26. 26Describe steroid signaling mechanismsSteroid H pass through PM, bind nuclear membrane R producing activated H-R complex that binds DNA & activates specific genes, ↑ production of protein
  27. 27What r possible endocrine-related problems?Overproduction H, underproduction H, non-functional R=>insensitive target cells,
  28. 28How do endocrine glands arise during development?They arise from all 3 germ layers. Type of endocrine product determined by germ layer origin. Glands of ectodermal & endodermal origin produce peptide & amine H, mesodermal-origin glands secrete lipid-derived H
  29. 29How does PG develop?From Rathke's pouch (mesoderm) & diencephalon below 3rd ventricle (ectoderm) forming adenohypophysis (from mesoderm) & neurohypophysis (ectoderm) just below optic chiasm
  30. 30Contrast posterior & anterior PGPosterior PG: H (OXT, ADH) synthesized soma magnocellular neurons (PVN, SON) & transported down axon in vesicles from HPT 2 posterior PG (hypothalamo-hypophyseal tract)
    Anterior PG: HPT releasing/ inhibitory factors secreted by parvocellular neurons in2 blood (hypohyseal portal veins) 2 stimulate/inhibit secretion H by neuroendocrine cells in anterior PG
  31. 31What r anterior pituitary H?TSH, LH & FSH: heterodimeric glycoproteins (common α-subunit, specific β-subunit: TSHβ, LHβ, FSHβ)
    ACTH: 39aa fragment of POMC
    GH & PRL: 190aa peptides - internal di-S bonds, homologous R)
  32. 32What is intermediate lobe of the PG? What is its function?Closely associated posterior PG & separated anterior lobe by hypophyseal cleft. Considerable variation in size among species. Small in humans, much larger in amphibians. MSH predominant H secreted
  33. 33How does HPT control synthesis & secretion of anterior PG H?HPT releasing H & HPT inhibitory factors synthesised by parvocellular neuro-secretory cells in the PVN & secreted median eminence 3rd ventricle
  34. 34Name all HPT releasing H & HPT inhibitory factors (IF)HPT releasing H:
    TRH (3aa)=>stimulates thyrotropin (TSH)
    GnRH (10aa)=> || gonadotropins (LH, FSH)
    CRH (41aa)=> || corticotropin (ACTH)
    GHRH (44aa)=>stimulates GH
    HPT IF: SRIF (somatostatin)=>inhibits GH
  35. 35What is the rule and the exception of HPT control of anterior PG?Rule: anterior PG stimulated by HPT RH (& may b suppressed by HPT IF)
    Exception: no stimulus identified 4 PRL synthesis/secretion, appears 2 b under dominant negative control by DA (from arcuate nucleus)=> stimulus=less inhibition
  36. 36Summarise HPT, HPG & HPA axesHPT: TRH=>TSH=>Thyroid H (T4+T3)
    HPG: GnRH=>LH(+FSH)=>progesterone, testosterone, oestradiol
    HPA: CRH=>ACTH=>cortisol
    (all tropins exert negative feedback on HPT RH & all active H inhibit tropins & HPT RH)
  37. 37How r OXT & ADH similar?OXT & ADH r 9aa peptides synthsised in magnocellular neurons in PVN of HPT & differ in 2 of the 9 aa. Both H packaged in2 granules & secreted along w/ carrier proteins (neurophysins)
  38. 38What r effects of ADH in kidney?↑H2O permeability of collecting duct
    ↑urea permeability in inner medullary region of collecting duct
    ↑NaCl reabsorption in thick ascending limb
    Net effect=>H2O reabsorption in kidney
  39. 39What r cellular actions of OXT?1.Stimulation milk ejection (milk letdown) -milk initially secreted small sacs mammary gland (alveoli), OXT stimulates contraction myoepithelial cells, milk ejected ducts & cisterns
    2. Stimulation uterine SM contraction at birth: uterus must contract vigorously & 4 prolonged period t 2 deliver foetus
    3. Establishment maternal behaviour: successful reproduction in mammals demands mothers attached 2 & nourish offspring immediately after birth
  40. 40How is OXT secretion stimulated?Positive feedback mediated by neural reflexes: suckling reflex (act of nursing/ suckling relayed w/in few ms 2 brain via spinal reflex arc, signals stimulate OXT-secreting neurons 2 release OXT), Fergusson reflex (stretch vaginal wall stimulates OXT secretion at birth)
  41. 41Give examples H & function produced in: 1. Pancreas 2. Kidneys 3. Liver 4. Heart 5. Fat cells 6. GI tract1.Insulin, glucagon=>glucose metabolism
    2. renin, erythropoeitin, vit D3=>BP, RBC production, plasma Ca2+
    3. IGF-I, IGF-II=>growth
    4. ANF=>Na+ excretion by kidneys
    5. Leptin=>regulates appetite
    6. gastrin, secretin, CCK=>digestion
  42. 42What is half-life of H? What does it depend on?t required 2 reduce circulating [H] by half
    Depends how quickly H can b metabolised
  43. 43What r the principle endocrine glands? And other non-classical endocrine glands?Principal endocrine glands: pituitary, thyroid, parathyroid, adrenals, gonads
    Non classical endocrine glands: heart, liver, kidney, brain, GI tract, islets of Langerhans
  44. 44What r endocrine, paracrine, autocrine & neuroendocrine cells?Endocrine: secrete H in2 blood vessel & H transported 2 (distant) target cells
    Paracrine: secrete local H that acts neighbouring cells
    Autocrine: secrete H that acts same cell
    Neuroendocrine: secrete from neural axon terminals straight in2 bloodstream
  45. 45Name & give examples different classes H1. proteins/polypeptides (insulin)
    2. glycoproteins (LH, FSH, TSH)
    3. derivatives aa Tyr (A, thyroid H: T3 & T4)
    4. steroids derived from cholesterol
    5. lipid-derived molecules (prostaglandins)
  46. 46How r hormones transported in blood? What r the consequences?peptides & protein H hydrophilic=> circulate freely in blood; steroid & thyroid H (T4) hydrophobic=>transported in blood bound serum proteins (T4 binds T4 binding globulin, cortisol binds cortisol BP); each globulin specific 2 H; only free circulating H active (remainder reservoir) =>H levels altered by changing levels BP
  47. 47How do hydrophilic H act?interact w/specific cell surface R on target cells generating 2nd messengers or by Tyr phosphorylation of specific target proteins
  48. 48Explain mechanisms of action of 2 most used 2nd messenger systems (cAMP, DAG)1. R interacts GTP-BP Gs=>activates AC=> conversion ATP 2 cAMP=>interacts PKA=> phosphorylates target proteins
    2. R interacts GTP-BP Gq=>activates PLC=> hydrolysis PIP2 2 release IP3+DAG=>IP3 ↑ [Ca2+] cytosol & DAG(+Ca2+) activate PKC
  49. 49Give examples of Tyr phosphorylation as a signal transducer eventR 4 insulin & PDGF r TYK themselves=> cause Tyr phosphorylation target proteins
    GH & PRL R single membrane spanning proteins & activate STATS
  50. 50—

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Physiology Karteikarten am Endocrinology , erstellt von Francisco Sacadura am 08/04/2017.
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Francisco Sacadura
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