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Physiology > Lecture 7 Endocrine Part 2 > Flashcards

Lecture 7 Endocrine Part 2 Flashcards

1
Q

4 hormone structural classification groups

A

amines, polypeptides, glycoproteins, and steroids

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2
Q

which 2 amines are hormones made from

A

tyrosine and tryptophan

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3
Q

list the 4 steroid hormones and what they are made from

A

cholestrol –> estrogen, progesterone, testosterone, and cortisol

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4
Q

hydrophobic hormones - which are they, what type of mechanism and why

A

steroids and T3/T4, genomic mechanism, they are lipophilic/hydrophobic and can enter the cell plasma membrane and bind to receptors in the cytoplasm/nucleus

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5
Q

hydrophilic hormones - which are they and what mechanism and why

A
  • all other hormones except steroid and T3/T4
  • bind to surface receptors and use secondary messengers
  • hydrophilic aka lipophobic and cannot pass through plasma membrane
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6
Q

series of events of genomic effect of a hormone

A

hormone dissociates from carrier protein –> enters cell –> binds to cytoplasmic/nuclear receptor –> hormone receptor complex binds to promoter regions and acts as a transcription factor –> transcription / gene expression turned on

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7
Q

how is progesterone produced and what function does it have

A

FSH –> follicle matures and ovulation releases egg –> follicle becomes corpus luteum –> progresteroen released –> causes vascularization and thickening of endometrium in preparation for implantation

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8
Q

how is testosterone produced

A

LH –> interstitial cells of Lyedig –> produce testosterone

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9
Q

how is estrogen produced

A

FSH –> follicle matures and releases estrogen

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10
Q

explain what could happen when hormone levels are at pharmacological doses

A

pharmacological concentration –> hormone binds to other receptors and causes side effects

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11
Q

prohormone vs prehormones and example

A
  • prohormone = precursor to a hormone ex: proinsulin

- prehormone = precursor to a prohormone ex preproinsulin

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12
Q

synergistic hormones and example

A
  • 2 hormone with similar effect together have effect that is greater than their sum - ex: glucagon and cortisol to raise blood glucose
  • glucagon and epi to raise blood glucose
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13
Q

permissive hormone and example if permissive hormone not present

A
  • permissive = necessary for other hormones to function, allows other hormones to function
  • ex: testosterone and estrogen may be present in boy and girl but if not thyroid hormone development will not occur
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14
Q

antagonistic hormone and example

A
  • hormones have opposite effect
  • glucagon and insulin
  • calcitonin and parathyroid hormone
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15
Q

half life meaning

A
  • amount of time for the concentration to decrease by half
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16
Q

priming effect aka upregulation

A

hormone causes cell to increase receptors for itself

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17
Q

densenitization and down regulation - how does this relate to diabetes and insulin secretion

A
  • hormone causes cells to decrease receptors for itself
  • diabetes: constant insulin –> downregulation of insulin receptors –>. insulin resistance
  • can be reversed by exercise
  • insulin secretion is supposed to be pulsatile
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18
Q

3 characteristics of hormone receptors

A
  • high affinity to the hormone
  • specificity to the hormone
  • low capacity = not a lot of hormone is needed
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19
Q

time for genomic action vs non genomic action

A
  • genomic = slow, 30 minutes because transcription and translation
  • nongenomic = fast, a few minutes
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20
Q

albumin

A

most abundant blood protein, a carrier protein

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21
Q

amount of free vs bond hormones

A
  • free hormones are very low, 99% are bound to carrier proteins
  • amount of free hormone depends on interaction between receptor and hormone and concentration of hromone
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22
Q

nuclear hormone receptor and 2 domains

A
  • receptor for hormone located inside cell, travels into nucleus
  • ligand binding and DNA binding domain
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23
Q

another name for promoter region

A

hormone response element

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24
Q

explain dimerization and how it differs for steroid vs T3/T4

A 
steroid = homodimerziation 
T3/T4 = heterodimerzation with cis retinoic acid from vitamin A
25
Q

list 3 nongenomic hormone mechanisms

A

adenylate cyclase, phospholipase C, and tyrosine kinase

26
Q

adenylate cyclase cAMP workflow

A

hormone binds to receptor –> G protein activation –> adenylate cyclase activated and converts ATP to cAMP –> cAMP activates kinases –> activates other enzymes and protein kinases

27
Q

phospholipase C work flow

A

hormone binds to receptor –> G protein activated –> binds to phospholipase C which uses phospholipid from membrane to make DAG and IP3 –> Ca2+ released from ER –> Ca2+ calmodulin complex –> complex phosphorylates protein kinases –> activation of other enzymes and protein kinases

28
Q

tyrosine kinase work flow

A

dimerization –> insulin or IGF binds –> autophosphorylation on tyrosine amino acids –> activation of protein kinases and other enzymes

29
Q

liver cell as an example of having 2 receptors

A
  • alpha adrenergic uses phosphlipase C
  • beta adrenergic uses adenylate cyclase
  • both result in activation of protein kinases ultimately causing glycogen break down
30
Q

3 zones of adrenal gland what they produce and general effect of products

A
  • GFR
  • glomerolsa = aldosterone and mineralcorticoid, Na+ and water reabsorption and K+ excretion
  • fasiculata = glucocorticoid, stress steroid hormones which increase blood glucose - cortisol and corticosterone
  • reticularis - androgens which are masculinizing
31
Q

congenital adrenal hyperplasia cause and effect on hormone levels

A
  • cause is lack of any enzyme that plays a role in conversion of cholestrol to cortisol
  • low cortisol –> high CRH and ACTH
  • intermediates build up and result in lots of androgens
32
Q

symptoms for onset iin utero/infants

A
  • female = ambiguous genitalia

- male = large and hairy penis

33
Q

symptoms for childhood onset

A
  • male = early puberty

- female = infertility

34
Q

symptoms for adult onset

A
  • salt wasting in male and female
  • female = hirsutism
  • male = salt wasting
35
Q

hirsutism

A
  • facial hair, acne
36
Q

salt wasting

A
  • cortisol is a weak mineralcorticoid so without cortisol Na+ and water are NOT reabsorbed and K+ is not excreted –> lots of urine and low sodium leading to chronic hypotension and hyperkalemia
37
Q

thyroid follicles

A

make up the thyroid - single layer of follicle cells with hollow inside filled with protein solution of thyroglobulin

38
Q

colloid

A

= solution where solute is a protein - in this case thyroglobulin

39
Q

process of T3/T4 production

A

iodide enters follicle cells –> follicle cells release iodide and thyroglobulin into inside of follicle –> iodide converted to iodine –> iodine binds to tyrosine amino acids on thyroglobulin forming DIT and MIT –> MIT and DIT bind together to form T3/T4

40
Q

process of T3/T4 release

A

TSH –> receptors on thyroid follicle cells –> follicle cells bring in T3/T4 still connected to thyroglobulin –> T3/T4 cleaved from thryoglobulin and released into blood after attaching to carrier protein and thyroglobulin is recycled

41
Q

endemic goiter and cause

A

enlarged thyroid caused by hypothyroidism

- low T3/T4 –> lots of TRH and TSH –> thryoid swells

42
Q

graves disease and cause

A

autoimmune disease - autoantibodies that mimic TSH accidentally created (thyroid stimulating immunoglobulin TSI) –> bind to thyroid –> lots of T3/T4 –> low TSH and TRH

43
Q

expohtalmos

A

clear sign of graves = protruding of eyes

44
Q

hypothyroidism symptoms

A

fatigure, lethargy, lack of appetite, weight gain, depression and moodiness, low pulse rate, always cold
MYXEDEMA

45
Q

hyperthyroidism symptoms

A

insomnia, excited, weight loss, always hot, nervous, sweating constantly high heart rate

46
Q

myxedema

A
  • advanced hyPOthryoidism

puffiness of face, hands, and feet

47
Q

parathyroid hormone effects - 3

A

increases blood calcium by increasing reabsorption of calcium in kidneys, increasing resorption of bone (bone break down) and activation

48
Q

pancreas - acinar cell function

A
  • most cells are acinar cells that secrete pancreatic juices into duodenum of small intestine
49
Q

islet of langherhans 2 types of cells and differing functions

A
  • beta cells, adenylate cyclase release insulin

- alpha cells use phospholipase C and release glucagon

50
Q

autocrine vs paracrine signaling

A
  • autocrine = hormones go to the same cell type
  • paracrine = molecules go ot a different cell type
  • both are local
51
Q

cytokines

A
  • regulate immune system
52
Q

growth factors

A
  • cause cell growth and division
53
Q

insulin like growth factors

A
  • tyrosine kinase, release by cartilage and liver causing cell growth and division
54
Q

NO

A
  • paracrine, made in epithelial cells but effect smooth vascular muscle to cause vasodilation
55
Q

interluekins

A
  • cytokines between WBC
56
Q

prostaglandin production

A
  • omega 3/6 –> COX or LOX –> prostaglandins
57
Q

NSAID effect and side effect

A
  • inhibits COX1 and COX2
  • COX1 used by stomach and kidney to produce protective proteins
  • COX2 causes inflammation
  • binding is non specific
58
Q

tylenol / acetaminophen effect

A
  • COX3 inhibition, reduces fever and pain but not inflammation

Physiology (25 decks)

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