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A & P final > Endocrine Anatomy and Physiology > Flashcards

Endocrine Anatomy and Physiology Flashcards

1
Q

what type of feedback regulation is endocrine function

A

most is negative and btwn many different points
-self limiting
ex. ant pituitary inhibits hypothalamus
horomes inhibit ant pituitary or hypothal

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2
Q

what is an example of positive feedback

A

LH induction of estrogen from ovaries which induces explosive LH surge
-estrogen or estradiol act on ant pituitary to promote more estrogen or estradiol

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3
Q

what does the hypothalamus release

A

releasing factors (vs inhibiting factors) which go into circulation to have an effect elsewhere

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4
Q

what is another name for the putuitary

where does it sit

A

aka hypophysis
master gland
sits in the hypophyseal fossa/sella turcica/ sphenoid

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5
Q

what kind of innervation does the pineal gland receive

what can happen if it englarges

A

sympathetic NS innervation
-it can compress the cerebral aqueduct if englarge=>leads to hydrocephaly which may effect eye movements
=>pretectal nuclei (upward gaze) and insterstituial nuclei (CN3) downward gaze

  • goes through superchiasmic nucleus
  • releases melatonin =>circadian rhythm
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6
Q

what does the thyroid gland release

C cells release what here

A

thyroid hormone

c cells here release calcitonin

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7
Q

what is the thymus gland involved in the production of

A

involved in the production of mature T-lymphocytes

-produces various growth factors

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8
Q

what hormone does the heart release

what does this promote

A

releases atrial natriuretic factor hormone
ANF promotes Na loss
-released when the atrium senses increased blood volume
-imp in bedridden people

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9
Q

in the lungs, what does ACE concert antiotensin to

A

angiotension 2

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10
Q

what do the adrenal glands release

A

aldosterone

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11
Q

what do the kidneys release

A

erythropoeitin and renin

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12
Q

what does the stomach release

A

gastrin

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13
Q

what do neuroendocrine cells in the small intestine release

A

neuroendocrine cells release gastric inhibitory peptide

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14
Q

what are the types of secretion here

A
  1. endocrine -acting on distant cells
    ex. hormones
  2. paracrine-acting on neighboring cells
    ex. nitric oxide
  3. autocrine-cells acting on themselves
    - most notably in the immune system
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15
Q

what are the types of hormones in the endocrine system

A

aa
polypeptides
steroid

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16
Q

aa: what are norepinephrine and thyroxine derived from

what is melatonin derived from

A
  • norepinephrine and thyroxine derived from tyrosine

- melatonin from tryptophan

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17
Q

polypeptides:
what are examples of glycoproteins
what are examples of growth hormones
what are examples of the secretin family

A

glyco: LH, FSH, TSH, hCG
growth hormones: GH, PRL, hPL
secretin: secretin, VIP, glucagon, GIP

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18
Q

what are steroids derived from

A

cholesterol

-aldosterone, cortisol, androgens estrogens

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19
Q

what are plasma transport proteins bound to

what are generally not

A

steroid and thyroid hormones

-aa and polypeptide hormones generally are not

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20
Q

what are polypeptide and protein hormone production synthesized as?

  • what is signal peptide then cleaved to form?
  • when is this proteolytically cleaved
A

preprohormone

  • may contain sequences for several diff molec depending on where it is cleaved
  • signal peptide is then cleaved to form prohormone
  • prohormone proteolytically cleaved when its packaged into vesicles
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21
Q

what can POMC become

A 
ACTH (adrenocorticotropic hormne) 
alpha MSH (melanocyte stim hormone) 
CLIP (corticotropin-like intermediate prot)
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22
Q

POMC is cleaved to ACTH
what does ACTH stimulate
what is an exmpale of a negative feedback here

A

ACTH stimulates the adrenal cortex to release its hormones
ex: if the adrenal cortex isn’t producing hormones properly, ACTH lvls may rise bc the end-product isn’t available to shut down ACTH production

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23
Q

ACTH cleaved to a-MSH and CLIP

A

a-MSH controls skin pigmentation, so an excess of ACTH (=>excess of a-MSH) has a symptom of skin darkness

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24
Q

what are the 2 parts of the anterior pituitary and what are they

A
  1. pars tuberalsis
    - outer covering of pituitary stalk
  2. pars distalis
    - anterior lobe
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25
Q

what are the parts to the posterior pituitary

A
  1. median eminence of hypothalamus
  2. infundibular stalk
  3. infundibular process (post lobe)
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26
Q

what synthesize posterior pituitary hormones

A

hypothalamic neurons whose axons terminate in the posterior lobe synthesize post pituitary hormones

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27
Q

what are anterior pituitary hormones synthesized and secreted in reponse to

A

hypothalamic releasing hormones carried in the hypophyseal portal circulation

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28
Q

what does CRH (corticotropin-releasing hormone) stimulate

A

ACTH secretion by the ant pituitary

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29
Q

what does TRH (thyrotropin-releasing horm) stimulate

A

TSH secretion by the AP

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30
Q

what does GHRH (growth horm-releasing hormone) stimulate

A

stimulates GH secretion by the AP

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31
Q

what does LHRH (luteinizing hormone-releasing hormone) stimulte

A

stimulates LH and FSH secretion by the AP

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32
Q

what does ADH do

A

increases water reabsorption by collecting ducts in kidneys
-release induced by catecholamines, angiotension 2, reduced blood volume

increases aquaporin gene transcription and incorporation into kidney collecting duct membrane

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33
Q

what does oxytocin do

-what is this release induced by

A

stimulates smooth muscle contraction in breasts and uterus
-release induced by:
- sensory neurons in nipples
=> oxytocin stimulates myoepithelial cells in alveoli of mammary land
-stretch receptors in cervix during chidbirth

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34
Q

how do the monogamous prairie vole and promiscuous meadow vole differ in their distribution of oxytocin and vasopressin

A

monogamous have a higher density and distribution of oxytocin and vasopressin receptors in the brain
-the promiscuous ones have a much diff receptor distribution

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35
Q

what are the tropic hormones (basophils) of the anterior pituitary

A

ACTH: glucocorticoids, cortisol and corticosterone
TSH: T3 and T4 (thyroxine)
Gonadotropins: FSH-ovarian follicle development and spermatogenesis
LH-ovulation and luteinization of ovulated graafian follicle; stimulates estrogen and progesterone production by ovary and testosterone by leydig cells in testes

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36
Q

what are examples of non tropic hormones (acidophils) from the anterior pituitary

A

GH: stimulates growth during childhood
PRL: synthesis of milk during lactation

37
Q

what does ACTH (adrenocorticotropic hormone) do

what is it a feedback regulator of

A

diurnal secretion regulated by corticotropin releasing hormone (CRH) and increased during stress
-feedback regulator of synthesis and secretion of glucocorticoids by zona fasciculata and reticularis of adrenal cortex
=>not a regulator of aldosterone secretion from zona glomerulosa

38
Q

what is TR (thyrotropin releasing hormone) released w/

A

dirunal rythym

39
Q

what is growth hormone secretion stimulated by

what is it inhibited by

A
  • secretion stimulated by GHRH and thyroid hormones

- inhibited by somatostatin (SRIF)

40
Q

what does GH stimulate

A

IGF-I, a mitogenic factor that mediates growth-promoting effects of GH

41
Q

how is GH secreted

A

in short, pulsatile bursts day and night, but GF secretion is maximal at night

42
Q

how does GF mediate effects

A

through JAK2 tyrosine kinase, which phosphorylates cytoplasmic and nuclear proteins

43
Q

what happens when there is too much GH? too little?

A

too much: acromegaly

too ligght: pituitary dwarfism

44
Q

what are some other functions of GF

A
  1. mobilizes triglycerides
  2. decrease glucose use by muscle and fat cells
  3. increases liver glucose production (anti-insultin actions, like glucocorticoids)
  4. increases protein synthesis in most organs
45
Q

what does the thyroid gland produce

what does it regulate

A

T3 (triiodothyronin-4x more potent than T4) and T4 (thyroxine)
-regulates development and metabolic rate

46
Q

what is colloid composed of

A

thyroglobulin (Tg), the storage form of thyroid hormones

47
Q
  • Tg where is forced into
  • what occurs here
  • what are the cells here entered through and exported by
  • what is dietary iodide essential for
A
  • Tg extruded into apical space where iodination occurs; iodine enters cells through sodium iodide symporter and is exported apically by pendrin
  • dietary iodide essential for hormone synthesis
48
Q

how many T4 and T3 do Tg contain

A

up to 30 T4 and a few T3s

-Tg is the storage form of T3/T4

49
Q

how does the thyroid gland produce T3 and T4

A
  1. iodide symported (with Na) into follicular cells from blood
  2. pendrin exports iodide into lumen
  3. in the lumen Tg binds MIT, DIT, T3 and T4
    - all the same molec, but with 1,2,3,4 iodides
  4. macrophocytosis: a pseudopod form follicular cells grabs grab some Tg from thyroid colloid in the lumen when needed
  5. proteolysis occurs, liberating T3 and T4
50
Q

what is thyroid hormone metabolism

A

reverse T3-an inactive metabolic byproduct

  • T3 and T4 are active products
  • a clinical measure of thyroid functions
51
Q

what are the functions of thyroid hormone

A

critical role in CNS development, growth, and basal energy metabolism

52
Q

what is a goiter

A

a diffuse or nodular enlargement of the thyroid gland

53
Q
  • what kind of receptors mediate thyroid effects
  • what does thyroid hormore increase production of? what does this directly increase?
  • what does TH promote?
  • what rate does TH increase?
  • what does TH stimulate
A
  • type 2 receptors mediate by nuclear receptors that modulate gene transcriptions
  • increases GH production
  • directly increases synthesis of structural and enzymatic proteins in many tissues
  • promotes growth/calcification of bone
  • increases basal metabolic rate (BMR) by stimulating oxidative phosphorylation
  • stimulates synthetic and degradative pathways of carb, lipid, and protein metabolism
54
Q

what are the 3 zones that the cortex in the adrenal gland has?
what do they produce?

A
  1. zona glomerulosa
    - produces aldosterone
  2. zona fasciculata and 3. zona reticularis
    - produce glucocorticoids, cortisol, corticosterone, androgen dehydroepiandrosterone
55
Q

which zone of the cortex produces most of the androgen

A

reticularis

56
Q

what is the medulla of the adrenal gland

what is it derived from

A

modified sympathetic ganglion

derived from neural crest

57
Q

what is steroid hormone synthesis driven by

A

the availability of cholesterol

58
Q

what is addison’s disease

A

glucocoritcoid and aldosterone deficiency due to infection or autoimmunity

59
Q

what will generate free cholesterol

A

cholesterol esterases will generate free cholesterol (liberating it from cellular membranes)

60
Q

what do StAR (steroidogenic acute regulatory protein) do?

A

moves cholesterol from the outer to inner mitochondrial membrane
-the rate-limiting step

61
Q

what does ACTH promote

A

promotes activity of enzymes which cleave cholesterol and promote one of 3 interconnected pathways (mostly in smooth ER some in mit)

62
Q

what are the 3 pathways that ACTH can promote

what are the end products of each

A 
1. miteralocorticoid 
end product: aldosterone 
2. glucocorticoid
end product: cortisol 
3. androgen
end product: DHEA, A'Dione 
enzyme: 17 alpha-hydroxylase/17,20 lyase
63
Q

what is the production of aldosterone stimulated by

what does it stimulate and increase?

A
  • production stimulated by low bp, andiotension 2, and high extracellular potassium
  • stimulates sodium reabsorption by distal convulted kidney tubles,
  • increases water retention, increaes blood pressure, and increases secretion of potassium
64
Q 
what do glucocorticoids bind to?
what do they stimulate? 
what do they inhibit? 
-what do they act as
what do they protect the body during
A
  • bind to glucocorticoid response elements in DNA
  • stimulates gluconeogenesis
  • stimualtes fat breakdown in adipose tissue
  • inhibits glucose uptake
  • acts an anti-inflammatory and immunosuppressive
  • protects body in times of stress (keeps energy availble for the brain)
65
Q

how do glucocorticoids stimulate gluconeogensise particularlyin the liver

A

-stimulates gluconeogenesis, (liver)

=> mobilizes aa from extrahepatic tissues to serve as substrates

66
Q

how do glucocorticoids stimulate fat breakdown in adipose tissue

A

by using hormone-sensitive lipase
-the fatty acids released by lipolysis are used for production of energy in tissues like muscle, and the released glycerol provides another substrate for gluconeogenesis

67
Q

how do glucocorticoids inhibit glucose uptake

A

by muscle and adipose tissue to converse glucose

68
Q

what are the adrenal medullary hormones

what do they mediate

A

norepinephrine and epinephrine

  • MORE EPINE released
  • mediate fight or flight and metabolic response to hyperglycemia
69
Q

what do the glucocorticoids in cortex catalyze

A

glucocorticoids in cortex catalyze methylatin of norepinephrine to produce epinephrine

70
Q

how is norepinephrine changed to epinephrine

A

by methyl transferase (methylation of norepinephrine)
-in the cortex, glucocorticoids catalyze the conversion of norep to rep
L-tyrosine => L-DOPA => domapine => norepinephrine => ephinephrine

71
Q

what are the cells in the islets of langerhans

what do they produce

A 
alpha cells: produce glucagon 
-glucagon promotes glucose in the blood
beta cells: produce insulin and amylin
-amylin reduces glucagon release
delta cells: produce somatostatin
-somatostatin inhibits insulin, glucagon, GH and pancreatic polypeptide
Fcells: produce pancreatic polypeptide
-PP slows absorption of food, blunting the glucose response
72
Q

what is the primary regulator of insulin secretion

A

glucose

73
Q

is insulin response greater after oral of IV glusose

A

oral: factors (glucagon-like peptide, incretin-like gastin inhibitory polypeptide) are released by gut lining cells and promote insulin release
- enhance the effect of insulin for an equiv quantitiy of glucose

74
Q

what is glucokinase
how does it act as a glucose sensory?
what causes the blockade of the ATP-dependent K channels

A

glucose sensor on beta cells which triggers insulin release
-by determining rate of glycolysis
-increase in cytosolic ATP causes blockade of ATP-dependent K channel
=> inhibits K efflex
=> target of sulfonylurea drugs
=>promotes depolarization (bc K efflux promotes repolarizatoin) and Ca influx
=>cells release insulin

75
Q

what kind of Km does glucokinase have

A

low Km

lower than hexokinase

76
Q

what uptake does insulin increase in cells
what does this reduce
what can this lead to

A

insulin increases K uptake into cells

  • this reduces circulatory K levels (hypokalemia)
  • severe hypokalemia can lead to fibrillation/death
77
Q 
what do insulin and glucagon do to...
glucose 
fatty acids
ketoacid 
amino acids
K
A 
glucose: insulin decrease, gluc increase
fatty acids: insul decrease, gluc incr
keotacid: insulin decre, gluc incr
aa: insulcin decreases, gluc NO EFFECT
K: insulin decreases, gluc NO EFFECT
78
Q

how does insulin promote glucose updake in muscles and fat

A

by increasing GLUT4 on membrane

79
Q

what is calcium and phosphate regulated by?

A

hormones of the kidneys and liver

80
Q

what is calcium and phosphate obtained from? what determines their fate
-what are they absorbed by? how are they absorbed

A

diet: Gi tract, kidnys, and bones determine ultimate fate of each
- absorbed by small intestine by active transoprt and diffusion by active transport and diffusion

81
Q

wehre is most calcium and phosphorus stored

A

99% ca stored in bones and teeth

86% phosphorus stored in bones nd teeth

82
Q

what regulates calcium and phosphate

A 
parathyroid hormone (PTH) 
calcitonin
vit D3 (cholecalciferol)
83
Q

what is PTH released from
what is it stimulated by?
what does this increase and decrease
what does this upregulate

A

PTH released from 3 paris of parathyroid glands
-stimulated by low plasma calcium
=> increases plasma calcium and decreases phosphate
-upregulates osteroCLAST activity (degrades bone)

84
Q 
what does calcitonin have the opp effect of? 
what is calcitonin released by
what is it stimulated by
what does this decrease 
what does it stimulate
A

opposite effect of PTH
released by parafollicular cells in thyroid
stimuated by high plasma calcium
decreases plasma calcium and phosphate
stimulates osteoBLAST activity (builds bone)

85
Q

how do we obtain vit D?
what is this converted to?
what does this increase?

A

-from diet or sunlight effect on 7-dehydrocholesterol
=>converted in liver and kidneys to 1,25-dihydroxyvitamin D3 (calcitriol)
-1 is by liver enzymes
-25 is by kidney enzymes
-increases plasma calcium and phosphate

86
Q

why is PTH involved in vit D3 processing?

what is PTH then inhitibed by

A

to increase Ca uptake

PTH is then inhibited by increased plasma levels of Ca

87
Q

what is osteoporosis

A

reduction in total bone mass; equal loss of both mineral and ORGANIC MATRIX (collagen)

88
Q

what are the causes of osteoporosis

A
  1. long term ca deficiency
  2. vit c deficiency; needed for collagen synthesis
  3. reduction in mechanical stress on bone-too much bed rest
  4. decline in estrogen at menopause
89
Q

a decline in estrogen following menopause leads to osteoporosis, what are the 2 major reasons this happens

A
  1. estrogen inhibits osteoclastic factors (those promoting bone breakdown) released by T cells
  2. estrogen causes PTH effects on bone and enhances PTH effects on the kidneys
    - active PTH => breakdown of bone

A & P final (8 decks)

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