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Physiology Exam #2 > Endocrine Physiology > Flashcards

Endocrine Physiology Flashcards

1
Q

what are the two types of glands?

A

endocrine and exocrine

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2
Q

what do exocrine glands secrete?

A

substances to the outside (e.g digestive glands, sweat glands)

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3
Q

Do ducts allow secretion?

A

YEAH

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4
Q

what do endocrine glands secrete?

A

hormones to the blood (e.g thyroid, gonads, pituitary

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5
Q

Are ducts required in endocrine glands?

A

no

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6
Q

nonpolar hormones?

A
  • cant dissolve in plasma -> carrier proteins
  • pass through PM DIRECTLY into cell
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7
Q

what are examples of nonpolar hormones?

A

steroids and thyroid hormones

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8
Q

where are steroids derived from?

A

cholestorol

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9
Q

where are thyroid hormones derived from?

A

tyrosine

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10
Q

polar hormones?

A
  • dissolve easily in plasma
  • can’t pass through PM, must use receptor
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11
Q

What are examples of polar hormones?

A

amines (melatonin), polypeptides (insulin), proteins (growth hormones)and glycoproteins (LH)

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12
Q

what is a pituitary gland also called?

A

hypophysis

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13
Q

where is the pituitary gland located?

A

directly below hypothalamus (connected by infundibulum)

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14
Q

how many glands are in the pituitary gland?

A

2

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15
Q

what are the names of the 2 pituitary glands?

A

anterior and posterior

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16
Q

what is AP (or adenohypophysis) derived from?

A

oral epithelium

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17
Q

what is the connection between AP and the hypothalamus?

A

there is no neural connection between them

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18
Q

what is PP (or neurohypophysis) derived from?

A

brain

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19
Q

what is the connection between PP and the hypothalamus?

A

axons extend from the hypothalamus

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20
Q

are hormones from PP secreted or produced?

A

secreted

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21
Q

what is an example of an antidiuretic hormone (ADH)?

A

vasopressin

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22
Q

what does the stimulus equal in an ADH?

A

high osmolality (dehydration), increased blood pressure

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23
Q

what is the target of ADH?

A

kidney, arterioles

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24
Q

what is the action of ADH?

A

H2O retention, vasocontriction

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25
Q

what is an example of a stimulus for Oxytocin?

A

baby sickling

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26
Q

what is the target for oxytocin?

A
  • uterine smooth muscle -> contraction at parturition
  • mammary alveoli -> milk ejection (let down)
  • brain -> maternal bonding
  • men = sperm transport
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27
Q

what are the two hormones secreted by PP?

A

antidiuretic hormone and oxytocin

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28
Q

what does the AP do?

A

produces and releases hormones

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29
Q

what kind of hormones does the AP produce/release?

A

growth hormones, thyroid stimulation hormone, and adrenocorticotropic hormone

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30
Q

growth hormones (GH)

A
  • i.e somatotropin
  • promotes tissue and organ growth, synthesis
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31
Q

thyroid stimulating hormone (TSH)

A
  • i.e thyrotropin
  • stimulates the thyroid to secrete thyroxine (T4) and triiodothyronine (T3)
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32
Q

adrenocorticotropic hormone (ACTH)

A
  • i.e corticotropin
  • stimulates the adrenal gland to release steroids (e.g cortisol)
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33
Q

follicle-stimulating hormone (FSH)

A
  • i.e. folliculotropin
  • women -> stimulates growth of ovarian follicles
  • males -> stimulates production of sperm in testes
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34
Q

Luteinizing hormone (LH)

A
  • i.e. luteotropin
  • women -> stimulates ovulation and formation of corpus luteum in ovaries
  • men -> stimulates interstitial Leydig cells of testes to secrete testosterone
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35
Q

prolactin (PRL)

A
  • women -> stimulates milk production by mammary glands
  • roles in reproduction and kidneys of men and women
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36
Q

what is the system that controls the AP?

A

hypothalamo- hypophyseal portal system

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37
Q

what does the hypothalamus secrete?

A

releasing hormones

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38
Q

corticotropin-releasing hormone (CRH)

A

AP-> ACTH

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39
Q

thyrotropin-releasing hormone (TRH)

A

AP -> TSH

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40
Q

gonadotropin-releasing hormone (GnRH)

A

AP -> FSH & LH

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41
Q

growth hormone-releasing hormone (GHRH)

A

AP -> GH

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42
Q

do all or some hypothalamic hormones inhibit AP?

A

some

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43
Q

what does hypothalamic control of AP apply to?

A

AP hormones that DON’T stimulate hormone production by other glands

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44
Q

somatostatin of hypothalamic control of AP

A

AP blocks production of GH

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45
Q

prolactin-inhibiting hormone (hypothalamic control of AP) (PIH)

A

AP blocks production of PRL

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46
Q

control of AP hormone secretion

A
  • negative feedback inhibition
  • eventually, reach hypothalamus and AP
    • inhibit the production of releasing and stimulating hormones
  • anabolic steroid abuse
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47
Q

what are hormones produced in control of AP hormone secretion?

A

by target organ circulating in the blood

48
Q

what kind of disorders can be found in endocrine?

A

primary and secondary

49
Q

primary endocrine disorders

A
  • the dysfunction is at all the levels of the final gland (e.g. thyroid and adrenal)
  • negative feedback functions on AP
50
Q

secondary endocrine disorders

A
  • the dysfunction is at the level of the AP (tumor is the most likely cause)
  • negative feedback does NOT function
51
Q

what are the two parts of an adrenal gland?

A

adrenal medulla and adrenal cortex

52
Q

adrenal medulla has what type of control?

A

sympathetic

53
Q

what does the adrenal medulla produce?

A

epinephrine (& norepinephrine)

54
Q

what does the adrenal medulla promote?

A

fight or flight

55
Q

what kind of stress response does the adrenal medulla have?

A

a quick response

56
Q

what does the adrenal medulla dilate?

A

airways

57
Q

what does the adrenal medulla stimulate?

A

glycogenolysis

58
Q

what is the adrenal cortex controlled by?

A

ACTH from AP

59
Q

what are glucocorticoids in the adrenal cortex?

A
  • high blood glucose (glycogenolysis & gluconeogenesis)
  • promote breakdown of AA
60
Q

what weakness does the adrenal cortex have?

A

weak androgens

61
Q

what type of response does the adrenal cortex have?

A

slow response

62
Q

what is the first stage of the general syndrome (GAS)?

A

alarm reaction -> adrenal gland activated

63
Q

what is the second stage of GAS?

A

stage of resistance -> readjustment occurs

64
Q

what is the possible third stage of GAS?

A

stage of exhaustion -> sickness or death (readjustment didn’t work)

65
Q

what are two common adrenal gland disorders?

A

cushing’s syndrome and addison’s disease

66
Q

what is Cushing’s syndrome?

A

excessively high corticosteroids in blood

67
Q

what is the cause of CS?

A

tumor of anterior pituitary or adrenal cortex

68
Q

what are the symptoms of CS?

A

changes in carb & protein metabolism, hyperglycemia, hypertension, muscular weakness, pully appearance (buffalo hump or moon face)

69
Q

what is the treatment of CS?

A

tumor removal

70
Q

what is Addison’s disease?

A

inadequate secretion of glucocorticoids and mineralocorticoids

71
Q

what is the cause of Addison’s disease?

A

damage to adrenal cortex due to autoimmune disease, infection, use of anticoagulants, tumor

72
Q

what are the symptoms of AD?

A

hypoglycemia, Na+ & K+ imbalance, dehydration, hypotension, weight loss, weakness

73
Q

what is the treatment for AD?

A

corticosteriods

74
Q

what does the thyroid gland produce and secrete?

A

two nonpolar hormones
- thyroxine (T4) (carrier protein = thyroxine binding globulin TBG)
- triiodothyronine

75
Q

what does T4 lose at the target cell through the membrane?

A

TBG

76
Q

what does the target cell convert T4 into?

A

T3

77
Q

when T3 uses cytoplasmic protein “stepping stones” what happens next?

A

nuclear receptor into gene transcription

78
Q

what is required for proper growth/development of infants?

A

T3/T4

79
Q

what is T3/T4 particularly important to?

A

CNS

80
Q

what is cretinism?

A

severe mental disability caused by inadequate T4

81
Q

what is cretinism treated with?

A

thyroxine

82
Q

what does T3/T4 stimulate?

A

cell respiration

83
Q

effects of T3/T4 in cell respiration?

A
  • helps set the BMR
  • extremely important for metabolism
84
Q

what are two thyroid disorders?

A

hypothyroidism and hyperthyroidism

85
Q

what is hypothyroidism?

A

low T3/T4 levels

86
Q

what happens when T4/T3 levels are low?

A

high TSH levels giving no feedback which raises the stimulation of thyroid and that causes enlargement of thyroid (goiter)

87
Q

what are the possible causes of hypothyroidism?

A
  • low dietary iodine (iodized salt)
  • autoimmune attack (Hashimoto’s thyroiditis)
88
Q

what are symptoms of hypothyroidism?

A
  • lethargy
  • intolerance to cold
  • absent perspiration
  • slow pulse
  • coarse, dry skin
  • increased body weight
89
Q

what is the treatment to hypothyroidism?

A

oral thyroxine (levothyroxin)

90
Q

what is hyperthyroidism?

A

high/excessive T4/T3

91
Q

what is the most common hyperthyroidism disease?

A

grave’s disease

92
Q

what is grave’s disease?

A

an autoimmune disease where the immune system produces antibodies to the thyroid that cause it to grow, and when the thyroid tissue increase so does the T3/T4 levels

93
Q

does negative feedback work in grave’s disease?

A

no, the antibodies are continuously stimulating

94
Q

what are the symptoms of grave’s disease?

A
  • impaired sleep
  • intolerance to heat
  • excessive perspiration
  • rapid pulse
  • loss of body weight
95
Q

what are treatments for grave’s disease?

A
  • anti-thyroid drug
  • radioactive iodine
  • thyroidectomy
96
Q

what do parathyroid glands produce & secrete?

A

parathyroid hormone (PTH)

97
Q

how do parathyroid glands regulate BLOOD CALCIUM?

A

reflects absorption from diet, deposition in bone and resorption from bone

98
Q

what are three parts of endocrine pancreas?

A

islets of Langerhans, glucagon, and insulin

99
Q

what is glucagon produced by?

A

alpha cells

100
Q

what is glucagon stimulated by?

A

low blood glucose (inhibited by high blood glucose)

101
Q

what does glucagon promote?

A
  • glycogenolysis (liver
  • gluconeogensis (liver)
  • lipolysis (adipose)
  • ketogenesis (multiple tissues)
102
Q

what is insulin produced by?

A

beta cells

103
Q

what is insulin stimulated by?

A

high blood glucose (inhibited by low blood glucose)

104
Q

what promotes insulin?

A

movement of glucose into liver, muscles (glycogen), adipose tissue (triglycerides)

105
Q

type I diabetes

A
  • “childhood-onset diabetes”
  • autoimmune disease
106
Q

type II diabetes caused by?

A

“adult-onset diabetes”
- generally caused by poor diet (high fat & sugar) and lack of exercise

107
Q

what is insulin resistance in type II diabetes?

A

decreased response to insulin in tissue, which means more insulin is required (also called insulin insensitivity, glucose tolerance)

108
Q

what is treatment for type I diabetes?

A

insulin injections

109
Q

what is treatment for type II diabetes?

A

diet and exercise, oral drugs

110
Q

what does the pineal gland secrete?

A

melatonin upon stimulation by SCN of the hypothalamus

111
Q

what does the pineal gland regulate?

A

circadian rhythms

112
Q

what does adipose tissue a huge producer of?

A

hormones and adipokines

113
Q

what is adipose tissue a major player in?

A

satiety, hunger, obesity

114
Q

what is Leptin?

A

hormone that induces satiety (feeling full)

115
Q

what happens if you have more adipose?

A

you have more leptin and feel less hungry

116
Q

what is resistin?

A

hormone involved in development of insulin resistance

Physiology Exam #2 (4 decks)

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