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Bio 472 > The Endocrine System > Flashcards

The Endocrine System Flashcards

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1
Q

Endocrine System

A

communication system where cells release messenger substances into blood stream that have actions on specific target tissues

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2
Q

Messagers of the Endocrine System

A

Hormones
Neurohormones
Prostaglandins(Arachadonic Acid Cascade)

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3
Q

Classes of Hormones

A
  1. Protein(peptide) hormones
  2. Amines (neurohormones + thyroxine)
  3. Steroid hormones
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4
Q

Peptide + Amine Hormone Action

cAMP Mechanism

A
  1. Peptide/Amine hormone binds to membrane receptor
  2. activates G protein
  3. activates adenylate cyclase
  4. activates cAMP
  5. activates cAMP dependent Protein Kinases
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5
Q

Peptide + Amine Hormone Action

IP3/DAG Mechanism

A
  1. membrane receptor recieves signalfrom Peptide/Amine hormone
  2. G protein activation
  3. Phospholipase C cleaves PIP2 into IP3 and DAG
  4. Calcium release
  5. cell membrane ion channel alteration
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6
Q

Peptide + Amine Hormone Action

A
  1. cAMP Mechnanism
  2. IP3/DAG Mechanism
  3. Direct membrane Calcium Channel activation
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7
Q

Steroid Hormone action

A

activates cycoplasmic and nucleus receptors, activates genes (transcription, translation), triggers protein synthesis

can activate membrane receptors

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8
Q

Pituitary Gland

Anterior

A

synthesis of releasing factors and growth factors

derived from Rathke’s Pouch(mouth lining), contains blood portal system

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9
Q

Pituitary Gland

Posterior

A

secretes hormones that are stored in the posterior pituitary(ADH, Oxytocin)

derived from brain tissue

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10
Q

ADH

A

anti diuretic hormone,

small peptide (9AA)

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11
Q

ADH Modes of Action

A
  1. water reabsorbtion by DCT, collecting duct of nephron, and action on sweat glands and GI tract
  2. binding to receptors on smooth muscle, stimulating calcium entry and contraction, vasocontriction
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12
Q

Causes for ADH Release

A
  1. Changes is body osmolality (osmoreceptors shrinking-low bp)
  2. Drop in plasma volume (hemorrhage) detects 7-15% change
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13
Q

Diabetes Insipidis

A

not sugar diabetes, large amount of dilute urine produced,

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14
Q

Diabetes Insipidis

Neurogenic cause

A

no ADH release

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15
Q

Diabetes Insipidis

Nephrogenic cause

A

failure of tubules to respond to ADH,

similar to results when consuming alcohol

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16
Q

Oxytocin in Females

A

stimulates uterine contraction, released by milk ejection by mammary glands

does not induce labor naturally, but will trigger contractions if administered

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17
Q

Oxytocin

Function in Males

A

uncertain, but oxytocin levels are high in people who have longtime partners

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18
Q

Anterior Pituitary Cells

A

true endocrine cells, each cell produces their own hormones,

each cell can produce more that one hormone

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19
Q

Anterior Pituitary Regulation

A

Anterior Pituitary hormone release is regulated by hypothalmus regulatory hormones

CRH, GnRH

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20
Q

Anterior Pituitary Hormone

FSH, LH

A

stimulate gonads, Tropic Hormone

Follicle Stimulating hormone and Luteinizing hormone

Tropic Hormone - stimulates other glands

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21
Q

Anterior Pituitary Hormone

TSH

A

stimulates thyroid, Tropic Hormone

Thyroid Stimulating hormone

Tropic Hormone - stimulates other glands

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22
Q

Anterior Pituitary Hormone

ACTH

A

stimulates adrenal cortex, Tropic Hormone

Adrenocorticotropic Hormone

Tropic Hormone - stimulates other glands

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23
Q

Growth Hormone

A

growth of body tissues, shifts body metabolism to anabolic paths, main target is liver,

triggers somatomedin(IGF-1, IGF-2) release from liver

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24
Q

Prolactin

A

induces milk production in mature mammary glands

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25
Q

Growth Hormone

Insulin-like Actions

A

Muscle: increase AA uptake, protein synthesis (increases muscle mass)
Liver: increase protein synthesis

storage, increased protein synthesis

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26
Q

Growth Homrone

Anti-insulin Actions

A

Muscle: decrease glucose uptake
Liver: increase gluconeogenisis
Adipose: increase lipolysis, decrease glucose uptake

increases plasma glucose

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27
Q

Bone Somatomedins

A

increase protein and collagen synthesis, increase cell proliferation

linear increase (growth)

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28
Q

Tissue Somatomedins

A

increase cell proliferation, increase DNA, RNA, and protein synthesis

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29
Q

Acromegaly

A

too much growth hormone

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30
Q

Growth Hormone System

A

Hypothalamus
1. increase GHRH
2. Decrease Somatostatin
Anterior Pituitary
3. GH release
Liver
4. GH stimulates somatomedins
5. inhibit Anterior Pituitary GH release
6. Stimulates somatostatin release by hypothalmus
7. further inhibits GH release

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31
Q

MSH

A

no function in humans, secreted by the Intermediate Lobe of Pituitary

melanocyte stimulating hormone

oversecretion causes skin bronzing

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32
Q

Thyroid Gland

A

metabolic rate regulator, calcium homeostasis, bilobed gland, below larynx, linked at center by isthmus

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33
Q

Thyroxine

A

growth, development, and metabolism regulator, causes increased oxygen consumption,

causes brown fat thermogenesis

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34
Q

Glycogenolysis

A

glycogen breakdown

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35
Q

Gluconeogenesis

A

glucose synthesis from fat

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36
Q

Lypolysis

A

mobilizes free fatty acids

mobilizes stored energy

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37
Q

Follicular Cells

A

control the release of Thryoxine Hormone (TH)

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38
Q

Colloid

A

Thyroglobulin, protein storage complex for Iodine, T3, T4 synthesis

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39
Q

Parafollicular Cells

A

synthesizes Calcitonin, lowers plasma Ca++

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40
Q

Parathyroid Gland

A

synthesizes Parathyroid Hormone, increases plasma Ca++, essential for life

4 pea sized glands on the Thyroid surface

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41
Q

Hormonal Regulation Process

A
  1. TRH from hypothalamus stimlates TSH from ant. pit.
  2. active transport of Iodine into follicular cells
  3. thyroglobulin synthesis
  4. increased production of Thyroxine by colloid
  5. increased pinocytosis of T3, T4
  6. increased release of T3, T4 by follicular cell into blood

is a loop somehow

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42
Q

*

TH assembly

A

T4 = DIT + DIT
T3 = MIT + DIT

tyrosine iodination

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43
Q

DIT

A

diiodotyrosine

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44
Q

MIT

A

monoiodotyrosine

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45
Q

T4

A

4 iodines, high production, high plamsa concentration, prehormone

deiodinated to form T3

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46
Q

T3

A

3 iodines, low plasma concentration, biologically active,

product of deiodination of T4

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47
Q

RT3

A

biologically inactive, product of deiodination

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48
Q

T3 and T4 in Plasma

A

they are bound to carrier proteins, inactive when bound

Thyroxine Bindng Globulin and Albumin, unbound is active, but there is less unbound so there is always a large reserve for a contant supply if needed

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49
Q

Hypothyroidism

A

underactive thyroid state

In children: Cretinism
In adults: Myxedema

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50
Q

Hypothyroidism

Causes

A
  1. Iodine Deficiency
  2. Hypothalamus problem (decrease TRH)
  3. Ant. Pit. problem (decrease in TSH or no response to TRH)
  4. Hashimoto’s Disease
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51
Q

Hashimoto’s Disease

A

autoimmune disease, antibodies attack thyroid gland and diminish its output

52
Q

Hypothyroidism

Symptoms

A
  1. decreased metabolsm (weight and water gain)
  2. decreased HR, SV, CO
  3. cold, clammy, lethargic, decreased mental capability
  4. depressed nail, bone, and hear growth
  5. raspy voice (mucopolysaccharide accumilation in larynx)
53
Q

Hyperthyroidism

Symptoms

A
  1. increased metabolism (weight loss, water loss)
  2. increased HR, SV, CO
  3. increased temp
  4. exopthalmos
54
Q

Hyperthyroidism

Graves Disease

A

autoimmune disease whos antibodies resemble TSH and stimulate the thyroid

basically no TRH, but high T3 and T4 levels

55
Q

Hyperthyroidism

Exopthalmos

A

swelling of eye muscles and fat, protruding eyes, autoimmune attack

common in Graves disease

56
Q

Hyperthyroidism

Treatment

A

drugs that block iodine uptake by follicular cells, drugs that block iodination, destruction of the thyroid gland

57
Q

Destruction of the Thyroid Gland

A

done using surgery or radiation, treatment for hyperthyroidism

TH replacement is required after Thyroid removal

58
Q

Goiters

A

enlarged thyroid glands, caused by hyperthyroidism(overstimulation), and hypothyroidism

59
Q

Hypothyroid Goiters

A

due to iodine deficiency, little T3, T4 for inhibition, high TSH stimulates glands

60
Q

Where is Calcium located?

A

99% of body calcium is found in bones(calcium hydroxyapatite), 1% is in plasma

61
Q

Plasma Calcium

A

narrow range of 10mg/dl, 45% is bound to albumin, 10% in phosphate/citrate complexes, 45% free and subject to hormonal control

62
Q

Osteoblasts

A

Calcium deposition on bone(calcitonin)

63
Q

Osteoclasts

A

bone reabsorbtion (Ca++ uptake)(PTH)

64
Q

Major Regulators of Body Ca++

A
  1. Parathyroid Homrone (PTH)
  2. Calcitonin (calcium regulating)
  3. Vitamin D3 (allows calcium to be absorbed in diet)
65
Q

Parathyroid Hormone (PTH)

A

release caused by low plasma Ca++, increases bone reabsorbtion, increased plasma Ca++, increases Ca++ reabsorbtion in PCT, stimulates Vit D3 production

66
Q

Body Without PTH

A
  1. low plasma Ca++ increases Na+ permeability
  2. causes hyperexcitable nerves
  3. leads to hypocalcemic tetany, Trousseau’s sign
67
Q

Trousseau’s Sign

A

praying mantis arms, thumbs under pointer and middle fingers

68
Q

PTH

Estrogen Effects

A
  1. Estrogen decreases PTH release
  2. Menopause decreases estrogen and therefore increases PTH
  3. Bone reabsorbtion increases
  4. Osteoporosis can result

treatable with estrogen replacement therapy

69
Q

Calcitonin

A

from Parafollicular “C” cells of thyroid, decreases plasma Ca++, decreases bone reabsorbtion, decreases kidney reabsorbion of Ca++

70
Q

Vitamin D

A

allows Ca++ uptake by intestines, stimulate Ca++ reabsorbtion in kidneys, shuts down PTH release

1,25 dihydroxycholecalciferol

71
Q

Vitamin D3 Synthesis

A
  1. Synthesized with sunlight from dehydrocholesterol
  2. in the liver, Vit D converted to 25 hydroxycholecalciferol
  3. in the kidney, converted to 1,25 dihydroxycholecalciferol
72
Q

Body without Vitamin D3

A

poor intestinal Ca++ reabsorbtion, rickets or osteomalacia

73
Q

Osteomalacia

A

softening of bones due to lack of vitmain D

74
Q

Islets of Langerhans

A

endocrine Pancreas cells, A, B, D, F cells

75
Q

Islets of Langerhans

Alpha cells

A

glucagon, increases plasma glucose, catabolic

body tissue breakdown

76
Q

Islets of Langerhans

Beta cells

A

insulin, decrease in plasma glucose, anabolic

body tissue buildup

77
Q

Islets of Langerhans

Delta cells

A

somatostatin, inhibits A, B, and F cells

78
Q

F cell

A

amylin, slows gastric emptying, slows nutrient absorbtion, slows post-prandial glucose spike

promotes satiety in concert with insulin

79
Q

Liver

Endocrine Functions

A

stores glucose, generates glucose through action of glucose 6 phosphate

80
Q

Insulin structure

A

produced by B cells, short arm of chromosome 11, 5 minute half life, broken down by insulin protease in liver or kidney

proinsulin C chain is used to assay B cell funciton when exogenous insulin is administered

81
Q

Insulin Function

A
  1. increased transport of glucose, AA, and K+ into insulin sensitive tissues,
  2. synthesis of glycogen synthase
  3. stimulation of protein synthesis
  4. increases lipogenic enzymes
  5. inhibits protein breakdown
  6. inhibits gluconeogenic enzymes
82
Q

Insulin Sensitive Tissues

A

muscle, fat, liver

83
Q

Insulin Modes of Action

A
  1. Tyrosine Kinase Receptor signal pathway
  2. Adds GLUT transporters to cell membrane
84
Q

GLUT receptors

A

7 different types, allow for glucose to enter a cell

85
Q

GLUT 4

A

most important for insulin action, found in muscle, heart and adipose tissue

86
Q

GLUT 1, 3

A

found in brain, not insulin dependent

87
Q

GLUT 2

A

found in liver, not insulin dependent

88
Q

Diabetes Mellitus

A

sweet urine, lack of or inneffective use of insulin,

“sugar diabetes”

89
Q

Diabetes Mellitus Symptoms

A

Polyurea
Polydipsea
Polyphagia

90
Q

Experimental Causes of Diabetes Mellitus

A
  1. Pancreatectomy (removal of part of or entire pancreas)
  2. Streptozocin (B cell toxin, kills B cells)
91
Q

Normal Blood Glucose

A

resting at 80 mg/dl
peak between 150-180 mg/dl

92
Q

Diabetic Blood Glucose

A

resting above 120 mg/dl
peak above 200 mg/dl

93
Q

Type 1 Diabetes

A

body does not produce insulin, observed in young ages, no strong genetic link, 10% of diabetics, caused by antibodies destroying B cells, triggered by viral infections

treated with insulin

94
Q

Untreated Type 1 Diabetes

A

high BG, body burns fats and proteins, ketoacidosis,

acid + dehydration leads to coma and death

95
Q

Hyperglycemic Coma

A

acid + dehydration leading to coma, caused by high BG

96
Q

Insulin Shock

A

patient administed insulin without eating, results in Hypoglycemic Coma, glucose cures

97
Q

Type 2 Diabetes

A

usually ages 35+, obesity component, genetic component, peripheral tissues (muscle, liver, fat) becomes insulin resistant, reduced insulin output by B cells

98
Q

Type 2 Diabetes Treatment

A

low cal + low fat diet, exercise, Sulfonylurea drugs

99
Q

Sulfonylurea Drugs

A
  1. depolarize B cells,
  2. elevate intracellular Ca++,
  3. enhance insulin release by B cells
100
Q

HbA1C or A1C test

A

tests for glycated hemoglobin, long term average for blood sugar levels

Normal Person - 5%
Diabetic Target - 7%
Diabetic Uncontrolled - 25%

101
Q

Metformins

A

enhances insulin sensitivity in peripheral tissues(muscles, liver, fat), suppresses gluconeogenesis by liver

102
Q

GLP-1

Glucagon Like Peptide

A

enhances insulin output by Beta cells when used with sulfonylurea drugs, suppresses glucagon release and slows gastric emptying

103
Q

GLP -1 + GIP

A

enhance insulin secretion, reduce glucagon levels, delay gastic emptying, decrease food intake, discourages alchohol use

gives a greater feeling of satiety

marketed as a weight loss drug

104
Q

SLGT2 Inhibitors

A

blocks glucose reabsorbion in the PCT, excretes more glucose in urine

lowers HbA1C, can lead to UTIs, Type 2 Diabetics Only

105
Q

Insulin Pumps

A

deliver various forms of insulin with a computer programmable pump

pump can change insulin levels with regards to diet, exercise, and time of day

106
Q

Artificial Pancreas

A

pump delivery of insulin and glucagon, manages blood glucose in real time

107
Q

Stem Cell Treatments for Diabetes

A

pancreatic stem cells injected or transplanted to make a new pancreas

not approved in the US

108
Q

BMI Formula’s

A

mass in Kg/height in m squared
703 x weight in lbs/height in inches squared

109
Q

Potentially Underweight BMI

A

18-19

110
Q

Healthy BMI

A

20-24

111
Q

Overweight BMI

A

25-29

55% of Americans

increased risk of diabetes, stroke, heart disease, and cancer when over 27

112
Q

Clinically Obese BMI

A

30+

even greater risk for medical conditions

113
Q

Orexins

A

compounds released by Hypothalmus in response to low BG, increases appetite

114
Q

Adrenal Gland

A

made of the cortex and medulla

115
Q

Adrenal Gland Cortex

A

produces mineralocorticoids, glucocortoroids,
and sex steroid hormones

116
Q

Adrenal Gland Medulla

A

extension of sympathetic nervous system

epinephrine and norepinephrine production/release

117
Q

Regulation and Secretory Control of Adrenal Cortex

A
  1. CRH release from hypothalmus
  2. stimulates ACTH release from pituitary
  3. stimulates secretion of hormones from adrenal cortex (cortisols and androgens)
  4. adrenal hormones provide negative feedback to hypothalmus and anterior pituitary to shut down ACTH production
118
Q

3 Zones of the Adrenal Cortex

A
  1. Zona Glomerulosa
  2. Zona Fasiculata
  3. Zona Reticularis
119
Q

Adrenal Cortex

Zona Glomerulosa

A

produces aldosterone, a mineralocorticoid

causes body to retain water

120
Q

Adrenal Cortex

Zona Fasiculata

A

produces glucocorticoids and cortisol compounds

121
Q

cortisol effects

A
  1. immune system inhibition
  2. decrease in muscle, bone, and connective tissue mass
  3. glycogenolysis, gluconeogenesis, FFA release
  4. increase BP
  5. increase GFR

useful as anti-inflammatory and anti-rejection drugs

122
Q

Zona Reticularis

A

produces androgens and sex hormone precursors

123
Q

Cushing’s Syndrome

A

Excessive Cortisol Production leading to:
1. muscle atrophy
2. osteoporosis
3. thin skin w/visible blood vessels
4. accumulation of fat in the abdomen
5. capillary rupture and striae

124
Q

Addisons Disease

A

Lack of Adrenocortical Function leading to:
1. anorexia, fatigue, hypoglycemia
2. poor stress tolerance
3. lack of negative feedback from adrenal hormones on pituitary
4. 3 causes hypersecretion of ACTH
5. 4 stimulates melanocytes causes localized dark pigmentation on the body

125
Q

Conn’s Syndrome

Primary Hyperaldosteronism

A

adrenal tumor or hypersecretion of aldosterone from Zona Glomerulosa results in elevated BP and K+ depletion and muscle weakness

126
Q

Androgenital Syndrome

A

excessive output of androgens causes masulization of the female body, can cause ambiguous genital development in infants

Bio 472 (23 decks)

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