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Physiology of the Endocrine System > Self Test Questions > Flashcards

Self Test Questions Flashcards

1
Q

What are the derivatives of Amine hormones

A

tyrosine

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2
Q

What are the hormones of the hypothalamus?

A

TRH, CRH, GnRH, GHRH, SRIF, PIF,

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3
Q

What are the hormones of the anterior pituitary?

A

TSH, FSH, LH, GH, ACTH, MSH,

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4
Q

What are the hormones of the posterior pituitary?

A

ADH and oxytocin

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5
Q

What hormone is produced by thyroid gland?

A

T3/4

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6
Q

What hormone is produced by adrenal gland?

A

cortisol

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7
Q

What hormone is produced by ovary?

A

estradiol and progesterone

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8
Q

What is the action of TRH?

A

stimulates secretion of TSH (by anterior pituitary) and prolactin

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9
Q

What is the action of CRH?

A

stimulates secretion of ACTH

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10
Q

What is the action of GnRH?

A

stimulates secretion of LH/FSH

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11
Q

What is the action of GHRH?

A

stimulates secretion of GH

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12
Q

What is the action of SRIF?

A

inhibits secretion of GH

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13
Q

What is the action of Dopamie?

A

inhibits secretion of prolactin

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14
Q

What is the action of TSH?

A

stimulates secretion of TH by cAMP mechanism

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15
Q

What is the action of FSH?

A

stimulates growth ovarian follicle and estrogen secretion, and promotes sperm maturation

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16
Q

What is the action of LH?

A

stimulates growth ovarian follicle and estrogen and progesterone secretion, and release of testosterone

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17
Q

What is the action of GH?

A

protein synthesis and growth

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18
Q

What is the role of Prolactin?

A

milk production and bresat growth

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19
Q

What is the action of ACTH?

A

stimulates synthesis of cortisol hormone

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20
Q

What is the action of MSH?

A

melanin synthesis

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21
Q

What is the action of ADH?

A

H2O reabsorption in renal collecting ducts

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22
Q

What is the role of oxytocin?

A

milk ejection, uterine contraction

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23
Q

What is the role of T3/4?

A

skeletal growth, increase O2 consumption, heart production, increase protein/fat/cabs use, and maturation os nervous system in perinatal

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24
Q

What is the role of cortisol?

A

gluconeogenesis, anti-inflammatory and immune suppression

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25
Q

What is the role of esterdiol?

A

growth/development of female reproductive organs, follicular phase of menstrual cycle

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26
Q

What is the role of Progesterone

A

luteal phase of menstrual cycle

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27
Q

What is the role of testesterone?

A

spermatogenesis and development of male secondary sex organs

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28
Q

What is the role of aldosterone?

A

increase renal Na+ reabsorption and H+/K+ secretion

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29
Q

What is the role of insulin?

A

decrease blood glucose/AA/FFA

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30
Q

What is the role of Glucagon?

A

increase blood glucose/AA/FFA

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31
Q

What is the role of HCG?

A

increase estrogen/progesterone synthesis in CL of pregnancy

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32
Q

What is the role of Calcitonin?

A

decrease Ca2+

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33
Q

Where is HCG made

A

placenta

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34
Q

Where is Glucagon made?

A

alpha cells of pancreas

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35
Q

Where is insulin made?

A

beta cells of pancreas

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36
Q

Where is Aldosterone made?

A

adrenal cortex

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37
Q

Which hormone does not have positive feedback?

A

Testerone

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38
Q

What is the commonality of TSH, LH and FSH?

A

they’re glycoproteins with an alpha (identical) and beta subunit (biological activity)

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39
Q

What is the deviated of ACTH, MSH, B-lipotrophin and B-Endorphins?

A

POMC

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40
Q

What is the commonality of GH and Prolactin?

A

somatotrophin and prolactin single chain peptide are homologous

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41
Q

What is the release pattern of GH

A

pulseatile fashion that increased by sleep, stress, puberty, starvation, exercise and hypoglycemia

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42
Q

How does Somatostatin inhibit GHRH?

A

it inhibit secretion of GH by blocking response o anterior pituitary to GHRH (negative feedback)

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43
Q

What is the action of GH in the liver?

A

production of IGF-1 which has tyrosine kinase activity similar to insulin

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44
Q

What are the direct actions of GH?

A

decrease glucose uptake, increase lipolysis/protienpolysis and IGF

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45
Q

What is the role of GH via IGF-1?

A

increase protein synthesis in chondrocytes leading to increase growth of organ, and muscle

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46
Q

What are the consequences of GHRH insufficiency?

A

lack of ant.pit GH, decrease GHRH (no neg. feedback), decrease IGH

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47
Q

What are the consequences of GHRH excess?

A

can be treated by somatostatin analogs, acromegaly can occur after puberty and gigantism if before puberty

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48
Q

What hormone inhibits prolactin?

A

Dopamine and TRH

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49
Q

What is the role of prolactin?

A

works in conjunction w/estrogen for breast development, lactogenesis, and inhibits ovulation by decreasing synthesis of GnRH

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50
Q

What is the consequence of excess prolactin?

A

galactorrhea (decrease libido), amenorrhea (failure to ovulate); can be treated by dopamine agonist

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51
Q

What nucleus does ADH originate?

A

supraoptic nucleus of the hypothalamus

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52
Q

What nucleus does oxytocin originate?

A

paraventicular nuclei of hypothalamus

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53
Q

What triggers release of oxytocin?

A

suckling sends impulses of afferent nerve fiber nipple from the spinal cord, and dilation of the cervix and orgasm

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54
Q

What is the difference between I1/2 of TH?

A

I1 is when iodine is transported into thyroid follicular cells, and I2 is the reactive form of TH that can be combined with tyrosine and thyroglobulin to synthesis T3/4

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55
Q

What is the result of the coupling of MIT/DIT

A

2 DIT = T4 (more commonly synthesized)

1 DIT + 1 MIT = T3 (active form)

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56
Q

What occurs from the stimulation of thyroid cells by TSH?

A

Iodinated thyroglobulin is taken back into follicular cells and endocytose, lysosomal enzymes then digest thyroglobulin, releasing T3/4 int o circulation

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57
Q

What is the result of chronic elevation of TSH?

A

hyperthyroidism

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58
Q

What is the inhibitory role of T3?

A

it down-regulates TRH receptors in anterior pituitary, thereby inhibiting TSH secretion

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59
Q

What is the role of IgG?

A

antibody of TSH receptors on thyroid gland that acts like TSH to stimulate thyroid to secrete T3/

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60
Q

What causes GRave’s disease?

A

high concentration of IgG/TH, and low TSH concentration caused by feedback of inhibition of TH on ant. pituitary

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61
Q

What is the role of TH?

A

works with GH and somatostatin to promote bone formation, vital in perinatal period to prevent Cretinism (from hypothyroidism), prevents hypo/hyperthyroidism , up-regulate B1-Adrenergic receptors in heart, increase O2 (increase Na+K+ ATPase activity) consumption and BMR in tissues (except spleen, brain, gonads), increase cardiac output and ventilation, increase glucose absorption in GI, lipolysis and proteolysis

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62
Q

What hormones are produced in the zona glomerulosa of the adrenal cortex?

A

aldosterone

63
Q

What hormones are produced in the zona fasciculata of the adrenal cortex?

A

cortisol

64
Q

What hormones are produced in the zona reticularis of the adrenal cortex?

A

sex hormones

65
Q

What are the symptoms of hyperthyroidism?

A

increase HR/heart/cardia output, dyspnea, tremor, goiter, weight loss,

66
Q

What are the symptoms of hypothyroidism?

A

decrease HR/heart/cardiac output, goiter, weight gain, mental retardation, myxedema, hypoventilation, drooping eyelids

67
Q

What are the caused of hypothyroidism?

A

decrease TRH/TSH, cretinism, removal of thyroids

68
Q

What are the caused of hyperthyroidism?

A

Grave’s disease, thyroid neoplasm

69
Q

How is Hyper/Hypothyroidism treated?

A

hypo - TH replacement

hyper - B-Blockers, thyroidectomy

70
Q

When is cortisol levels the high/lowest?

A

highest - 8am when first awoken

lowest - 12p when going to bed

71
Q

What nucleus are CRH located?

A

paraventricular nuclei of hypothalamus; secreted into anterior pituitary

72
Q

What happens after CRH is released?

A

it binds on corticotrophin receptors on the anterior pituitary and synthesize POMC to secrete ACTH to initiate change via cAMP

73
Q

How is CRH inhibited?

A

elevated levels of Cortisol cause negative feedback

74
Q

What part of the cortex does Angiotensin II act on?

A

Angiotensin II acts on zona glomerulosa to increase Aldosterone secretion

75
Q

What is the mechanism by which cortisol stimulates gluconeogenesis?

A

increase protein catabolism in muscles, decrease glucose utilization, increase lipolysis to provide more glycerol to liver

76
Q

What are the effects cortisol?

A

induced anti-inflammatory response, inhibit proliferation of T lymphocytes to suppress immune response, inhibit release of histamine and serotonin from mast cells and platelets, up-regulates aplha1 receptors on arterioles increasing vasoconstrictor effect or norepi to decrease aterial pressure

77
Q

What is Addison disease?

A

adrenocrotical insufficiency caused by destruction of adrenal cortex; characterized by decrease androgen (decrease pubic and armpit hair), increase ACTH, hypoglycemia, hyper-pigmentation, hypotension, hyerkalemia, and metabolic acidosis (due to aldosterone deficiceny)

78
Q

What are the effects of Cushing’s syndrome?

A

caused by primary hyperplasia of adrenal glands, causing increased cortisol and decrease ATCH

79
Q

What is Cushing’s disease

A

tumor of the anterior pituitary leading to increased ATCH and Cortisol

80
Q

What are the symptoms of Cushing’s disease/syndrome

A

hyperglycemia, increase protein catabolism/muscle wasting, central obesity of the face and neck due to fat deposition, virilization in woman, hypertension, edema, osteoporosis, striae due to excess proteolysis of collagen and connective tissue

81
Q

How is Cushing’s disease treated?

A

ketoconzaole steroid inhibitor

82
Q

What is the cause of 21-Beta-Hydorxylase deficiency?

A

increase adrenal androgens and progesterone, decrease aldosterne and cortisol

83
Q

What are the symptoms of 21-Beta-Hydorxylase deficiency?

A

virilization of woman, early acceleration of linear growth, early appearance of pubic and axillary hair, enlarged clitoris/decrease gonadal function, congenital adrenal hyperplasia of zona fasciculata and reticularis (b/c oh high ATCH), increased ATCH producing more androgens (b/c of decreased negative feedback of cortisol)

84
Q

What are the actions of insulin?

A

increase glucose and K+ uptake. protein and fat synthesis, decrease glycogenolysis/gluconeogenesis,

85
Q

What stimulates beta cells to secrete insulin?

A

increase blood glucose/FFA/AA/GH/Cortisol

86
Q

What stimulates alpha cells to secrete Glucagon?

A

decrease blood glucose, increase AA/epi/norepi

87
Q

What are the actions of Glucagon?

A

increase glycogenolysis/gluconeogenesis, lipolysis, ketoacid, and urine production

88
Q

How is active insulin made?

A

from the cleavage of c-peptide separating A and B chais

89
Q

How insulin down regulate its own receptors in target tissues?

A

starvation - increase insulin receptors

obesity - decrease insulin receptors

90
Q

What pathophysiological diseases result from insulin deifciency?

A

hyperglycemia, hypotensions, metabolic acidosis, hyperkalemia

91
Q

What is the major androgen synthesized and secreted by the Leydig cells?

A

testerone

92
Q

What hormones stimulates increase testosterone production?

A

LH reinforced FSH mechanism on spermatogenesis and stimulates theca cells to produce testosterone

93
Q

What nuclei is GnRH from?

A

arcuate nuclei of the hypothalamus

94
Q

What is the role of FSH in males?

A

Acts on sertoli cells to maintain spermatogenesis

95
Q

What hormones do sertoli cells secrete

A

FSH and Inhibin (inhibits FSH)

96
Q

What are the actions of testosterone?

A

differentiation and growth of epididymis, vas deferens, seminal vesicles, puberty growth spurt, cessation of epiphyseal closure, libo, deepening of voice, growth of penis, increase muscle mass, negative feedback of LH in anterior pituitary

97
Q

What are the actions of DHT?

A

differentiation and growth of penis, scrotum, prostate, sebaceous gland activity

98
Q

What initiated\s puberty?

A

onset of pulsatile GnRH from hypothalamus

99
Q

What are the variations of FSH/LH in males overtime?

A

childhood - lowest sex hormones FSH>LH
puberty - highest sex hormones LH> FSH
old age - declining sex hormones FSH>LH

100
Q

What happens when testosterone is diffused?

A

it goes to nearby granulosa cells which contains aromatase and converts testosterone to 17b-estradiol

101
Q

What does FSH/LH stimulate in the ovaries?

A

steriodogeneis in follicle and CL, follicular development beyond antral stage, ovulation, luteinization

102
Q

Estrogen causes negative feedback in each phase of mensuration except?

A

mid-cycle phase

103
Q

What is the action of estrogen?

A

maturation and maintenance of FT, uterus, cervix and vagina, development of secondary female sex characteristics, up-regulates LH and progesterone receptors, causes proliferation and development of ovarian granulosa cells, maintains pregnancy, stimulate prolactin secretion, pos. feedback of FSH/LH

104
Q

What are the actions of progesterone?

A

neg. feedback of FSH/LH during Luteal phase, maintains pregnancy, helps in breast development

105
Q

What occurs in the follicular phase of mensuration?

A

primordial follicle -> Graafian, LH/FSH receptors up-regulate theca and granulosa cells, esterdiol levels increase -> cause proliferation of uterus, progesterone levels are low

106
Q

What occurs in the ovulation phase of mensuration?

A

burst of estradiol synthesis at end of follicular phase positively feedbacks effect LH (surge) /FSH secretion, ovulation occurs due to estrogen induced LH surge, cervical mucous increase s making it more permeable to sperm, estrogen levels decline

107
Q

What occurs in the luetal phase of mensuration?

A

CL begins to develop and it synthesizes estrogen and progesterone, secretory and vascularity activity of endometrium increase to prepare to receive fertilize egg, basal body temp increases b/c of effect of progesterone on hypothalamic thermoregulatory center, CL regress is no fertilization and estradiol/progesterone levels decrease abruptly

108
Q

What occurs in the menses phase of mensuration?

A

endometrium is sloughed b/c of abrupt withdrawal of estradiol and progesterone

109
Q

What is the characteristics of pregnancy?

A

steady increasing levels of estrogen and progesterone to maintain endometrium for fetus, suppress ovarian follicular function by inhibiting FSH/LH secretion, and stimulation of breast development

110
Q

What happens to the CL if fertilization occurs?

A

its rescued by HCG produced by the placenta

111
Q

What happens in the first trimester of pregnancy?

A

CL stimulated by HCG to produce estradiol and progesterone

112
Q

What happens in the second and third trimester of pregnancy?

A

progesterone induced by placenta, estrogen by fetal adrenal gland and placenta to synthesize DHEA thats hydroxylated by fetal liver

113
Q

What is parturition of pregnancy?

A

progesterone increase threshold of uterine contraction, in preparation of birth

114
Q

When does lactation occur?

A

after parturition/birth because of abrupt decrease in estrogen/Progesterone levels

115
Q

How is lactation maintained?

A

from suckling and oxytocin and prolactin secretion

116
Q

Why is ovulation suppressed during lactation?

A

b/c prolactin inhibits GnRH secretion of LH/FSH in anterior pituitary, and it also antagonized the actions of Lh and FSH on the ovaries

117
Q

What is the order of neurohormonal flow?

A

High brain centers to hippocampus (attaches memories) to amygdala (attached emotions) to hypothalamus (cortisol and crh will interpret and provide response)

118
Q

What nucleus is GH produced?

A

arcuate nucleus hypothalamus

119
Q

What nucleus is GH produced?

A

Preoptic nucleus of hypothalamus

120
Q

What is the difference between active and resting thyroid follicle?

A

resting - storage of T3/4

active - TSH bind to thyroid cells to allow endocytose of thyroglobulin to liberate T3/4

121
Q

What are the anabolic and effects of TH?

A

Anabolic (low levels) - TH can stimulate synthesis of GH, protein maturation, and enzymes for cell function

122
Q

What are the catabolic and effects of TH?

A

Catabolic (high levels) - increase glucose generating more heat thus increase O2 demands which is satisfied by increasing B-adrenergic receptors on the cardio and pulm tissues creating more CO and increase ventilation.

123
Q

What causes increase of TH?

A
  1. Increase CO and ventillation
  2. increase apetite
  3. liplyosis, proteolysis (AA), and glycoeolysis
  4. and oxidize glucose to generate more cellular energy
124
Q

What are the symptoms of Grave’s disease?

A

Excess TH can cause exophthalmus due to excess proliferation of fibroblasts behind the ocular orbits. Excess TH accelerates visceral organ activity and raises the BMR. High TH also induces more beta adrenergic receptors on cardiovascular tissues, making them more sensitive to catecholamines, heat intolerant (sweating, gittery and nervous at all times), increase contractility of GI tract to burn metabolites/very skinny and increase diarrhea, deeper and faster breathing

125
Q

What are the symptoms of Grave’s disease?

A

Excess TH can cause exophthalmus due to excess proliferation of fibroblasts behind the ocular orbits. Excess TH accelerates visceral organ activity and raises the BMR. High TH also induces more beta adrenergic receptors on cardiovascular tissues, making them more sensitive to catecholamines, heat intolerant (sweating, gittery and nervous at all times), increase contractility of GI tract to burn metabolites/very skinny and increase diarrhea, deeper and faster breathing

126
Q

What do TSH/LH/FSH and GH have in common

A

they all have the same alpha subunit

127
Q

How is hypothyroidism caused?

A

Insufficient availability of iodine in ingested foods causes under production of TH. Loss of TH negative feedback results in excessive TSH secretion that stimulates the growth of the thyroid gland in an attempt to produce more TH. This caused the gland to enlarge into a goiter. The hypothyroidism causes a decreased BMR and slows visceral organ activity. This person would also be cold intolerant

128
Q

What is myxedema?

A

There is an accumulation of mucopolysaccharides in the interstitial spaces that causes an osmotic attraction of water into those spaces, hence the swollen appearance. Fat accumulation will also occur. Symptoms include fatigue, slow mental processing, high cholesterol, cold intolerance, and dry skin

129
Q

How is Cretinism caused?

A

characterized by intellectual and developmental
disabilities. The problem arises due to a perinatal deficiency of thyroid hormone. This lack of TH results in a slowing of mentation due to failure of dendritic branching of neurons, a reduction in synapse formation, and reduced myelin formation on neurons.The condition is easily avoided by the
administration of TH to the newborn if TH is found to be low, or with radioactive Iodine.

130
Q

How is Thyroid storm occured?

A

can occur due to physical and hormonal changes in individuals with hypothyroid (increase B-adernergic receptors). Surgery can be complicated because it can increase cathecolomins (which will bind to B-adernergic receptors) causing increase HR to the extent of ventricular fibrillation. You can use B-blockers or Colon Iodine solution weeks prior to surgery which can cause the Wolftriphall effect

131
Q

What is Wolftriphall effect?

A

acts on negative feedback to suppress overactive TH overwhelm gland with iodine, shutting it down temporality, and it reduced its manufacture of TH and decrease vascularization of the thyroid tissue (doesn’t act on receptor).

132
Q

What do delta produce?

A

somatostatin

133
Q

What happens at the resting state?

A

We a base line output of glucagon and insulin
insulin is used on resting muscles to make glucose in ciruclation
the brain does not require insulin for the uptake of glucose

134
Q

What happens at fight or flight?

A

Activated resting skeletal muscles start to uptake glucose in absence of insulin. The physical movement of the sliding muscle filaments recruits glucose molecules which increase the muscles ability to take up glucose in absence of insulin

135
Q

How many AA is proinsluin

A

21 alpha and 30 beta

136
Q

How does insulin facilitate the diffusion of glucose into target cells?

A

by stimulating the translocation of Glucose Transporter (GLUT1-14) molecules stored inside the cell to be inserted into the plasma membrane to accomplish the facilitated diffusion of glucose uptake into the cell interior.

137
Q

How does insulin facilitate the diffusion of glucose into target cells?

A

by stimulating the translocation of Glucose Transporter (GLUT1-14) molecules stored inside the cell to be inserted into the plasma membrane to accomplish the facilitated diffusion of glucose uptake into the cell interior.

138
Q

What happens during famine?

A

Alpha cells targets liver to increase glucagon production b/c theirs no glucose signal to the beta cells, and this causes the liver to take FFA and convert them to ketone bodies, you get a creation of beta hydroxic buteric acid that lower the pH. In prolong starvation, muscles are metabolize in order to abstract AA from the protein to be converted into glucose for fuel

139
Q

What happens during anticipatory rise of insulin or over ingestion?

A

due to the presence of food and food substrate in the GI tract even before the substrate arrives into the circulation. Increase in parasympathetic inputs to pancreas due to feeding and digestion also stimulate
insulin secretion. All these actions insure the quick and efficient storage of newly arriving glucose

140
Q

What can still occur in type 2 diabetes?

A

The pancreas is still capable of producing insulin, especially with constant eating and increase glucose levels, which can cause desensitization of the insulin receptors, but they still function to a certain extent to prevent ketoacidosis

141
Q

What is type 1 diabetes?

A

a viral disease in which the virus has AA sequence on its coat that mimicks the B-cells, and your immune system attacks the virus and beta cells causeing the complete destruction of beta cells and thus the absence of insulin.
An uncontrolled secretion of glucagon ensues driving up glucose levels with no mechanism to take it up by cells and tissues.glucagon secretion is no longer inhibited, and its uncontrolled levels causes liver to do more gluconeogenesis (since there’s no more insulin) and creating more glucose accumilation leading to hypoglycemia
kidneys can excrete extra glucose to keep the levels from rising too high, but its membrane will eventually become damage, and lead to kidney failure

142
Q

What is the difference between untreated type1 and 2 diabetes?

A

Type 1 will develop a major ketoacidosis whereas the Type 2 will develop little or no ketoacidosis due to the ongoing presence of insulin that prevents it

143
Q

What happens to kidneys when there insufficient insulin?

A

added glucose to the blood draws additional water to the blood and kidneys will excrete more water (osmtomic direusis)
Absence of insulin causes K+ and phosphate into circulation that will go to kidney and end up being excreted, and thus reducing BV (Hypvoluemia), and thus less CO which then leads to hypotension that can impair renal Q

144
Q

What is glycosylation?

A

non-covanetly attachment of glucose to proteins that impaires protein function leading to disease

145
Q

What results from HB A1C?

A

HB overly glycosylated and cannot release O2 to tissue, and theres a glycosylation on surface of RBC’s, causing RBC to become stiffen and cannot easily pass through capillary lumen

146
Q

What is the role of renin-angiotensin?

A

angiotensin stimulates aldosterone from the adrenal cortex

147
Q

What can high levels of ACTH do?

A

ACTH is a 39 amino acid molecule. It can be further processed into the 13 aa alpha-melanocyte stimulating hormone, alpha-MSH produce melanin. Since the first 13 aa of ACTH are the same as MSH, ACTH at high concentrations can bind to MSH receptors on melanocytes and cause increased skin pigmentation by increasing melanin production.

148
Q

What is the dironal rhythm of cortisol?

A

cortisol levels are highest at 8a when we first wake up. Cortisol acts as a glucocorotroid by raising blood glucose when stimulated by light since you were fasting while asleep. Rise in CRH can drive anxiety and depression

149
Q

What occurs at high Cortisol concentrations??

A

Higher concentrations of cortisol drive catabolic processes, resulting in the breakdown of tissues through proteolysis (more AA in circulation to be converted to glucose) and lipolysis (more FFA to make ketones), and Glycogenolysis (liberation of glucose)

150
Q

What occurs at low Cortisol concentrations??

A

Low physiological concentrations of cortisol are anabolic and favor the processes of gluconeogenesis and storage of glucose as glycogen, and protein synthesis.

151
Q

What is congenital adrenal hyperplasia?

A

21-alpha-hydroxylase deficiency -> cortisol and aldosterone pathways blocked -> excess androgens produced -> excess ACTH because low cortisol (main regulator) -> enlarged clitoris and other virilizing effects
Treatment: exogenous cortisol

152
Q

How is testosterone converted to DHT?

A

5a-reductase that Converts testosterone to DHT; they bind to same receptor

153
Q

How is testosterone converted to DHT?

A

5a-reductase that Converts testosterone to DHT; they bind to same receptor

154
Q

What is the difference between endo/neurocrine?

A

neurocrine - rapid response and quick degradation

endocrine - slower and longer activity

Physiology of the Endocrine System (1 decks)

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