endocrine system Flashcards

1
Q

compare the differences between endocrine system and nervous system

A

endocrine system - slow, releases hormones, regulate activities that require duration rather than speed like growth and reproduction, maintains homeostasis, long distance signalling where the hormone travels in the bloodstream to target cells

nervous system - fast, releases neurotransmitters, regulate activities of muscles and glands, local signalling through paracrine and synapse signalling

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2
Q

what is paracrine signalling

A

secreting cells act on nearby target cell by discharging molecules from a local regulator into ecf

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3
Q

what is synapse signalling

A

nerve cells release neurotransmitter molecules into a synapse, stimulating the target cell

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4
Q

what is hormonal signalling

A

specialised endocrine cells that secrete hormones into body fluids

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5
Q

what is a hormone

A

substances released by endocrine glands that travel in the bloodstream to target tissues where they act to regulate specific functions by binding to hormone receptors on target cells

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6
Q

how do you classify hormones

A

central and peripheral

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7
Q

what are examples of central glands

A

pineal, hypothalamus, pituitary

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8
Q

what are examples of peripheral glands

A

thyroid, parathyroid, thymus, adrenal, pancreas, ovary/testis

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9
Q

what hormone does hypothalamus secrete

A

releasing and inhibiting hormones

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10
Q

what hormone does thyroid gland secrete

A

T4, T3, calcitonin

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11
Q

what hormone does parathyroid gland secrete

A

PTH

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12
Q

what does adrenal gland secrete

A

cortex - aldosterone, cortisol, androgens

medulla - epinephrine, norepinephrine

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13
Q

what does the gonads secrete

A

testis - testosterone, estradiol, inhibin, mullerian-inhibiting hormone (MIH)

ovary - progesterone, estradiol, inhibin

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14
Q

what does the placenta secrete

A

human chorionic gonadotropin (hCG), progesterone, estrogen

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15
Q

what does the pancreas secrete

A

insulin, glucagon, somatostatin

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16
Q

what does the pineal secrete

A

melatonin

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17
Q

what does the kidney secrete

A

calcitriol (vitD)

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18
Q

which of the hormones are proteins and peptides

A

LH, FSH, GH, ACTH, PTH, inhibin, calcitonin, ADH, vasopressin oxytocin, hCG, insulin, glucagon

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19
Q

which of the hormones are amines

A

T4, T3, epinephrine, norepinephrine, melatonin

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20
Q

which of the hormones are steroids

A

cortisol, aldosterone, testosterone, progesterone, estradiol, estrogen, calcitriol

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21
Q

compare the difference between an endocrine gland and an exocrine gland

A

endocrine glands produce hormones and are ductless glands that releases hormones into surrounding tissue fluid

exocrine glands produce nonhormonal substances and have ducts that carry substances to a membrane surface

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22
Q

what hormones does the pituitary secrete

A

anterior - LH, FSH, GH, adrenocorticotropin (ACTH), TSH, prolactin (PRL)

posterior - antidiuretic hormone (ADH), vasopressin oxytocin

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23
Q

are protein and peptide hormones hydrophilic or lipophillic

A

all hydrophilic

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24
Q

are steroid hormones hydrophilic or lipophilic

A

all lipophilic

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25
Q

are amine hormones hydrophilic or lipophilic

A

hydrophilic - T3, T4

lipophilic - NE, E

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26
Q

what does it mean for a hormone to be hydrophilic

A

dissolved and transported freely in blood

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27
Q

what does it mean for a hormone to be lipophilic

A

bound to plasma protein, bind to intracellular receptors

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28
Q

what is the moa of hormones

A

signal amplification and alteration of functional and structural proteins, enzyme activation and transcription

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29
Q

what happens during signal amplification

A

hormones bind to receptor which activate G proteins (guanine), subsequently activate adenylyl cyclase to trigger formation of cAMP

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30
Q

what happens during alteration

A

alteration occurs in channel permeability by acting on pre existing channel forming proteins, second messenger systems to alter activity of pre existing proteins and activate specific genes to form new proteins

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31
Q

how to measure hormone levels

A

radio immunoassays (RIA), enzyme linked immunosorbent assays (ELISA), measurement sites (blood, urine, saliva, tissue)

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32
Q

what are the two types of hormone receptors

A

cell membrane receptors and intracellular receptors

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33
Q

what type of hormones are cell membrane receptors for

A

lipophilic

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34
Q

what type of hormones are intracellular receptors for

A

hydrophilic

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35
Q

what AA is amine hormones

A

tyrosine derivatives

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36
Q

where is the thyroid located

A

in the neck, anterior surface of trachea, immediately below the larynx

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37
Q

what are some characteristics of the thyroid

A

two lobes connected by isthmus, extensive blood supply for hormones produced to go into circulation

38
Q

what are the components of the thyroid

A

follicular cells, thyroid follicles, colloid, parafollicular/ C cells

39
Q

what is the function of the follicular cells

A

generate a globular protein called thyroglobulin and secrete into colloid of thyroid follicles

40
Q

what is the function of the thyroid follicle

A

functional unit for thyroid hormone production

41
Q

what is the function of the colloid

A

extracellular space where storage of thyroglobulin that is attached with iodine atoms

42
Q

what is the function of the parafollicular cells

A

cells in between the follicles that secrete calcitonin to regulate Ca homeostasis

43
Q

how is thyroid hormone synthesised

A

thyroglobulin produced by ER/ golgi complex in the follicular cells and Tyr is attached during its production which is then exported in vesicles from follicular cells into colloid by exocytosis

I- is picked up by thyroid from blood stream and is transferred into the colloid by Na/K pump whre Na+ enters the cell down its concentration gradient and I- enters the cell against its concentration gradient

I- oxidised to active iodine by thyroperoxidase (TPO) which is a membrane bound enzyme and active iodide enters the colloid through a channel

TPO attaches the active iodide to Tyr within the Tg molecule to produce mono-iodotyrosine (MIT) and di-iodotyrosine (DIT)

coupling of MIT and DIT produces tri-iodothyronine and coupling of DIT and DIT produces tetraiodothyronine/ thyroxine

when there is stimulation of production of TH, the follicular cells internalises a part of the Tg-hormone complex by phagocytosing a part of the colloid such that it shuttles the colloid into the follicular cells

lysosomes attack engulfed vesicles and split the iodinated products from Tg

lipophilic T3 and T4 diffuse freely through the outer membranes of the follicular cells into the blood

iodinase enzymes in follicular cells removes iodide frm MIT and DIT since it is of no endocrine value such that it allows freed iodide to be recycled for hormone synthesis

when T3 and T4 enters the blood, since it is lipophilic it will quickly bind to plasma proteins

44
Q

how is T3 and T4 metabolised and excreted

A

they are metabolised by conjugation with glucoronic acid in the liver which is then secreted in the bile and largely eliminated in the feces with small amounts in the urine

45
Q

is T3 or T4 the active form

A

T3, primarily makes T4 first then 80% of T3 derived from secreted T4

46
Q

how is T3 and T4 released

A

hypothalamus uses precursor thyrotropin releasing hormone (TRH) to stimulate the anterior pituitary to release TSH which stimulates thyroid glands to release T3 and T4

47
Q

how is the level of TH managed

A

by negative feedback

if there is sufficient T3, negative feedback to anterior pituitary to stop releasing TSH and hence causes hypothalamus to stop releasing TRH

if insufficient T3, positive feedback to hypothalamus to make TRH and to pituitary to release TSH, TSH will form peptide bonds with TSH receptors to cause signal amplification which causes release of T3 and T4

48
Q

what are the physiological effects of T3 and T4

A

increases BMR
sympathomimetic effects
cvs effect
essential for normal bone growth and development
for cns development
increase synthesis and metabolism of protein, lipids and carbs

49
Q

which tissues does not have BMR

A

brain, skin, spleen, gonads, thymus

50
Q

how does T3 and T4 increase BMR

A

increase in number and size of mitochondria and increase in enzymes that regulate oxidative phosphorylation thus resulting in increase in O2 consumption and energy use under resting condition

51
Q

what happens when there is increase in BMR

A

heat production

52
Q

how does T3 and T4 cause sympathomimetic effects

A

TH increases proliferation of catecholamines target cell receptors hence increases target cell responsiveness to catecholamines

53
Q

what happens when there is sympathomimetic effects

A

increase heart responsiveness to cathecolamines which increases HR and force of contraction and thus increase CO

54
Q

why is TH essential for bone growth

A

TH stimulates secretion of GH and increases IGF-1 production by liver and promote effects of GH and IGF-1 on synthesis of new structural proteins on skeletal growth

55
Q

what are the causes of hypothyroidism

A

primary failure of thyroid gland itself, cannot make TH
secondary to deficiency of TRH, TSH/ both
inadequate supply of iodine

56
Q

what are the clinical symptoms of hypothyroidism

A

dull blank expression, extreme fatigue, brittle hair and nails, constipation, intolerance to cold

57
Q

what are the late manifestations of hypothyroidism

A

subnormal temperature, bradycardia, weight gain, cardiac complications, thickened skin

58
Q

what are the causes of hyperthyroidism

A

production of TSI (an immunoglobulin)
secondary to excess TSH, TRH or both
hypersecreting thyroid tumor which causes excess secretion of TH

59
Q

what are the clinical symptoms of hyperthyroidism

A

bulging eyes, intolerance to heat, diarrhoea, weight loss, increase systolic BP, enlarged thyroid, muscle wasting, fatigue, restlessness, oligomenorrhea and amenorrhea, irritability, sweating

60
Q

what are the treatment options for hyperthyroidism

A

antithyroid drugs that interfere with TH synthesis by either blocking uptake of I- or inhibition of TPO, surgical removal of hypersecreting thyroid gland, administration of radioactive iodine to destroy thyroid glands

61
Q

what is grave’s disease

A

an autoimmune disease that leads to hyperthyroidism

62
Q

what is the cause of grave’s disease

A

production of TSI which is an Ab that competes with TSH for binding to TSH receptors and is not susceptible to negative feedback thus leading to hypersecretion and growth of the thyroid

63
Q

what is goiter

A

enlarged thyroid gland and develops when thyroid gland is overstimulated by increase in TSH or increase in TSI

64
Q

how does hypothyroidism cause goiter

A

due to inability to make TH, there is increase in TSH production by anterior pituitary
if there is lack of iodine, there is also low TH which causes negative feedback and cause high TSH

65
Q

how does hyperthyroidism cause goiter

A

excessive TSI-TSH receptor activation

66
Q

how does growth of thyroid tissue occur

A

increase follicle formation, increase number and size of cells, increase DNA, RNA, protein and phospholipid synthesis

67
Q

where is the pancreas located

A

in the abdomen, behind the stomach

68
Q

what are the two parts of the pancreas

A

exocrine portion and endocrine portion

69
Q

what are the components in the exocrine portion

A

acinar and duct cells

70
Q

what are the components in the endocrine portion

A

islets of langerhans

71
Q

what do acinar and duct cells secrete

A

acinar cells secrete digestive enzymes, duct cells secrete NaHCO3 solution

72
Q

what do islets of langerhans secrete

A

hormones into blood stream

73
Q

what are the cell types in islets of langerhans

A

beta cell, alpha cell, D cell, capillaries

74
Q

what do beta, alpha and D cell secrete

A

beta cells secrete insulin and amylin, alpha cell secrete glucagon, D cell secrete somatostatin

75
Q

what is the importance of insulin and glucagon

A

to regulate fuel metabolism

76
Q

how is insulin produced

A

result from excitation-secretion coupling

foods rich in carbohydrates causes beta cell to uptake glucose via transporter GLUT2

glucose undergoes phosphorylation to form glucose-6-phosphate which feeds into the Krebs cycle in the mitochondria

G-6-P undergoes oxidation which releases ATP as a product and acts on ATP sensitive K channel which causes depolarisation such that there is more K+ in the cell as less leaves

this causes increase in Ca2+ entering the beta cell through the voltage gated Ca channel and thus beta cell produces and releases insulin from the insulin vesicle

77
Q

what is glucose phosphorylation

A

trapping of glucose inside the cell and keep plain glucose levels low to maintain diffusion gradient

78
Q

what are the actions of insulin

A

glucose uptake through GLUT4 and increase glycogenesis, lipogenesis and proteogenesis

79
Q

where are the different GLUT transporters located

A

GLUT1 - endothelial cells in bbb
GLUT2 - kidney, liver, beta cells in pancreas
GLUT3 - neurons
GLUT4 - insulin sensitive in adipose and muscle tissues

80
Q

what is the process of glycogenesis

A

carbohydrates (metabolic fuel) -> glucose (circulating) -> glycogen (stored form)

81
Q

what is the process of lipogenesis

A

fats -> FFA -> TGL in adipose tissues

82
Q

what is the process of proteogenesis

A

protein -> AA -> protein in muscles

83
Q

how is blood glucose regulated

A

by uptake for cellular and brain function, storage of excess glucose for later use (in liver and muscles as glycogen and as TGL in adipose tissues)

84
Q

what is the function of glucagon

A

mobilise energy rich molecules from their stores, opposes action of insulin and overall increases blood glucose levels

85
Q

what is the difference between type 1 and type 2 DM

A

type 1 diabetes occurs as a result of an autoimmune process where the beta cells in pancreas is destroyed and thus insulin cannot be produced, is affected by genetic and/or environmental factors

type 2 diabetes occurs as the insulin produced is insufficient or not well utilised due to insulin resistance, is affected by lifestyle and genetics

86
Q

what is insulin resistance

A

cells with receptors cannot be activated by insulin for gate to open and uptake

87
Q

what is glucogenesis

A

glucose formation from non carb sources (eg. from protein)

88
Q

draw flow chart of effects of insulin deficiency

A

carbs metabolism (increased hepatic output, decreased uptake by cells)

fat metabolism (decrease TG synthesis, increased lipolysis)

protein metabolism (decrease AA uptake by cells, increased protein degradation)

89
Q

what are the chronic complications of DM

A

microvascular (nerve damage, retinopathy due to damage to eye blood vessels, kidney failure)

macrovascular (stroke due to damage of blood vessels in brain, heart attack due to damage and blockage of heart blood vessels, reduced blood circulation)

90
Q

what is the balance equation for ketosis

A

H2O + CO2 -> H2CO3 -> H+ + CO3-