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1

Hormones of the pancreas

insulin and glucagon

2

Important paracrine in the pancreas

somatostatin

3

acini

glandular tissue that secretes digestive enzymes and buffer into the pancreatic duct

4

Islets of Langerhans

aka pancreatic islands
contain alpha, beta, and delta cells
small and surrounded by capillaries, important for diffusion of nutrients and hormones

5

alpha cells

secrete glucagon into the blood

6

beta cells

secrete insulin into the blood

7

delta cells

secrete somatostatin which has local actions on the alpha and beta cells

8

Paracrine actions of somatostatin

inhibits both insulin and glucagon secretion

9

Paracrine actions of insulin

inhibits glucagon secretion

10

paracrine actions of glucagon

triggers insulin secretion

11

Insulin promotes/supports

anabolic reactions
fat and glycogen storage

12

Insulin synergizes with

Growth hormone and insulin like growth factor to promote growth, development of muscle mass, and bone density

13

Insulin opposes

catabolic reactions
glycogenolysis, glycolysis, proteolysis, lipolysis, and GNG

14

Insulin structure

small protein (5808 MW)

15

Insulin's half life in blood

6 minutes

16

How long before insulin is cleared from circulation

10-15 minutes
allows for short, rapid response of cells but lets leaves then ready to respond to other hormones

17

If longer insulin action is needed

more insulin can be secreted over time

18

Insulin is synthesized as

a large preprohormone known as "big unsulin"

19

Insulin receptor

embedded in the cell membrane
four subunits: two alpha, two beta

20

The subunits of the insulin receptor are held together by

disulfide bonds

21

Alpha subunits of the insulin receptor

outside the cell membrane
bind insulin

22

beta subunits of the insulin receptor

extend through the cell membrane
have tyrosine kinase enzyme activity inside the cell

23

When insulin binds to the alpha subunits of the insulin receptor

triggers autophosphorylation of the beta subunits, activating tyrosine kinase
tyrosine kinase phosphorylates other proteins which carry out insulin's action

24

Examples of Insulin's action

increased glucose uptake by muscle, adipose, and liver
increased amino acid uptake

25

Increased uptake of glucose leads to

insertion of glucose carrier proteins into the cell membrane
phosphorylation of glucose

26

increased amino acid uptake leads to

increased ribosome activity leading to an increased rate of protein synthesis
change in transcription of genes leading to a changed pattern of enzyme activity

27

At times when insulin is naturally low:

muscle, liver, and other tissues use fat for energy

28

With high insulin levels, muscle is stimulated to

actively take up glucose
use glucose for energy
store glucose as glycogen

29

with high insulin levels, the liver is stimulated to

use glucose to synthesize glycogen (from stored carbohydrates)
glycogenolytic enzymes are inhibited

30

When glucose uptake exceeds the liver's ability to synthesize glycogen:

the liver uses excess glucose to synthesize fatty acids

31

with high insulin levels, the adipose tissue is stimulated to:

actively store both glucose and fatty acids to synthesize triglycerides

32

Insulin stimulates the uptake of which ions

K+, PO4--, and Mg++

33

insulin stimulates the kidney to

retain potassium and phosphate

34

If someone experiencing extreme diabetic ketoacidosis is given insulin, they will experience

extreme drops in plasma K+, PO4, and Mg++

need IV infusions to counteract this

35

In an absence of insulin (fasting, starvation, uncontrolled type I diabetes)

lipolysis--> increased FFA and TG's in the blood
use of fatty acids by all cells except neurons
rapid breakdown of fatty acids leading to ketosis
increased LDL cholesterol in blood
decreased uptake/utlization of glucose (increased blood glucose)
decreased protein synthesis
increased AA's in the blood (acidosis)
use of AA"s for GNG

36

Without insulin, the hypothalamus

cannot detect hyperglycemia so elicits a hypoglycemic response and releases cortisol (causes GNG) and epinephrine (glucose release from liver) leading to further hyperglycemia

37

Type 1 Diabetes Mellitus

insulin dependent
inadequate insulin production due to autoimmune destruction of the pancreatic beta cells

38

Development of Type 1 Diabetes often follows

a viral infection by a virus with extracellular proteins similar to those of the beta cells

39

Type 1 diabetes is characterized by

rapid loss of body weight
acidosis

40

Type 2 Diabetes Mellitus

Insulin insensitivity due to target tissue post-receptor defects
insulin independent
obesity related

41

Metabolic syndrome

pre diabetic stage of diabetes mellitus type II
individuals often exhibit hyperinsulinemia, production of resistin, and may lose leptin sensitivity

42

resistin

a hormone produced by enlarged adipose tissue with metabolic syndrome
interferes with insulin function

43

Leptin

thought to help maintain insulin sensitivity in cells

44

Women with hyperinsulinemia may also develop

polycystic ovarian syndrome
hyperinsulinemia stimulates overproduction of androgens by developing follicles

45

PCOS

polycystic ovarian syndrom
follicles develop into cysts instead of maturing and ovulating
excess androgens cause follicles to become cystic

46

Type 3 diabetes mellitus

insulin dependent diabetes for any reason other than autoimmune destruction of beta cells

47

type 4 diabetes mellitus

gestational diabetes
develops during pregnancy due to high levels of pregnancy hormones which oppose insulin action
Similar to type 2 diabetes

48

Overt clinical signs of diabetes

Polyuria
polydipsia
polyphagia
lack of energy

49

Crisis point of uncontrolled diabetes

high blood glucose leads to glucose loss in urine and dehydration as it takes water with it
loss of potassium from cells leading to hyperkalemia and circulatory shock
ketoacidosis leading to nerve malfunction
excretion of ketoacids as sodium salts leading to hyponatremia and further nerve malfunction

50

Untreated diabetic crisis

leads to coma and death

51

Injection of insulin during a diabetic crisis

will reverse all symptoms except death.........

52

Long term effects of poorly controlled diabetes

atherosclerosis leading to cardiovascular problems, impotency, neuropathy, blindness, kidney failure
poor wound healing leading to gangrene

53

High blood glucose evokes

a biphasic response
fast response and second insulin secretion

54

Fast response, insulin release after a meal

occurs within 3-5 minutes
small peak of short duration
readily releasable pool

55

second insulin secretion, after a meal

occurs after 15-20 minutes
rises over 1 hour to a plateau that is maintained for 1-2 hours
storage pool

56

Early insulin peak is important in

satiety control
satiety neurons in the hypothalamus are sensitive to insulin

57

Satiety neurons in the hypothalamus

insulin alone- hunger
insulin plus elevated glucose- satiety

58

Pre-diabetics show what type of insulin release

a poor first peak, leading to continued eating, obesity and insulin resistance

59

high protein meals favor

insulin and growth hormone release
arginine and lysine

60

amino acids synergies with

glucose in provoking insulin release

61

Fat and protein in the stomach stimulate the release of

cholecystokinin which stimulates insulin release

62

glucose in the stomach stimulate the release of

secretin which stimulates insulin release

63

Protein in the stomach also stimulates the release of

gastrin which stimulates insulin release

64

secretin also triggers

glucagon secretion leading to a rise in blood glucose as glucose is released from liver glycogen

65

growth hormone stimulates insulin secretion through

the hypothalamic connection

66

Effect of progesterone and estrogen on insulin release

stimulates
especially during pregnancy but also helps explain female pattern of fat deposition at puberty

67

Neural connection via the parasympathetic nervous system

thought, sight, smell of food can cause insulin secretion and stimulate fat deposition even without eating

68

Physiological effects of glucagon

opposes action of insulin on blood glucose levels
stimulates glycogenolysis and glucose release from the liver
stimulates GNG
at high levels: supports adipose lipolysis
stimulates insulin release to shuttle glucose from the liver into muscle and adipose

69

glucagon secretion is stimulated by

low blood glucose
high blood amino acids
exhaustive exercise (may be response to ANS)

70

intestinal glucagon secretion

secreted in response to carbohydrates in the digestive tract
starts to elevate blood glucose prior to food absorption
also triggers insulin secretion in anticipation of nutrient absorption

71

Pancreatic somatostatin

produces by pancreatic delta cells
very short lived- can only act locally
same molecules as produced by the hypothalamus as a growth hormone inhibiting hormone

72

Actions of pancreatic somatostatin

inhibits glucagon and insulin secretion
slows the post absorptive process
may prevent enzyme systems from being overwhelmed by nutrients by prolonging the time it takes for nutrients to be removed from the blood and stored in the body

73

Gastrointestinal somatostatin

slows the digestive process and rate of nutrient absorption into the blood

74

Pancreatic somatostatin release is stimulated by:

increased blood levels of glucose, amino acids, fatty acids, and GI hormones

75

GI somatostatin release is stimulated by

nutrients in the GI tract
GI hormones

76

Normal calcium concentraions in the blood

9.4 mg/dl
about half is associated with proteins, the rest is as a free ion

77

Abnormal blood calcium levels

6 mg/dl (35% decrease) is hypocalcemia
12 mg/dl is hypercalcemia
at 17 mg/dl calcium precipitates out of solution

78

Ca++ influence on nerves

ion channels
irritability/sensitivity of nerves to stimuli
release of neurotransmitters

79

Effect of hypocalcemia on nerves

increased irritability by increasing Na+ permeability
creates leaky sodium channels leading to spontaneous action potentials

80

effect of hypercalcemia on nerves

makes the sodium channels harder to open leading to depressed nerve function

81

Ca++ influence on muscle

same effect on Na+ ion channels
Cardiac and smooth muscle depend on ECF levels of Ca++

82

effect of hypocalcemia on skeletal muscles

leaky sodium ion channels leading to spontaneous muscle contractions, tetany

83

Effect of hypocalcemia on cardiac and smooth muscle

weak muscular contrations
can result in inadequate uterine contractions during parturition

84

effect of Hypercalcemia on cardiac and smooth muscle

stronger contractions, can be spastic and lead to cardiac arrest during systole (due to failure to relax) and constipation of the GI tract

85

Ca++ has an influence on

nerves
muscles
second messenger systems
acid base balance
blood clotting
bone structure/strength

86

Regulators of Ca++ also regulate levels of

phosphate in ECF and bone

87

phosphate levels in blood

fluctuate much more widely than Ca++ before causing problems

88

Functions of phosphate

important part of high energy molecules like ATP and GTP, important in bone structure, as a buffer in H3PO4-

89

inadequate phosphate leads to

bone demineralization, inadequate ATP

90

Calcitropic hormones

parathormone, calcitonin, calcitriol

91

Parathormone

PTH
raises blood Ca++ levels

92

absence of PTH

tetany of skeletal muscles, and death due to cessation of breathing

93

Calcitonin

CT
lowers blood calcium

94

Calcitriol

aka 1,25 Vitamin D3
works with PTH to increase blood Ca++ and with calcitonin to enhance bone remodeling and Ca++ turnover

95

Parathormone related peptide

PTHrp
Paracrine, cytokine (local growth factor for many tissues)
stimulates Ca++ uptake by mammary tissue during lactation and has many other local actions
shares a receptor with PTH and can mimic PTH action on bone

96

tumors that produce PTHrp

lead to hypercalcemia and local bone degradation

97

Where is PTH produced

parathyroid glands

98

Where is calcitonin produced

thyroid gland

99

Production of calcitriol involves

the skin, liver, and kidneys, as well as sunlight or vitamin D in the diet

100

Vitamin D

actually a pre-prohormone for calcitriol

101

Approximately how much calcium is in a readily exchangeable pool?

1%
as CaHPO4
allows for a rapid response to changes in blood calcium

102

99% of calcium is stored

as hydroxyapatite, a part of bone structure and requires bone remodeling to be released

103

When Ca++ and PO4 concentrations are high

calcium phosphate salts can precipitate out of solution, leading to stones in the blood, liver, kidneys, ect.

104

Calcium phosphate salts dissolve in

acid and precipitate in base

105

PTH secreting cells

have receptors for Ca++ and calcitriol

106

Effect on extracellular Ca++ on PTH secretion

low EFC Ca++ leads to increased secretion
high ECF Ca++ leads to decreased secretion

107

effect of extracellular Mg+ or Phosphate on PTH secretion

high levels of Mg and phosphate lead to low ECF Ca++ causing in increased secretion of PTH

108

Carbonated sodas can lead to

bone demineralization because their high levels of phosphate causes increased PTH and Calcitriol productions

109

effect of calcitriol on PTH secretion

high levels of calcitriol induces a negative feedback suppression of PTH secretion

110

Effect of PTH on calcitriol secretion

increases Calcitriol release

111

effect of serum phosphate on calcitriol secretion

low serum phosphate leads to increased calcitriol

112

effect of calcitonin on calcitriol secretion

decreases secretion due to conversion of 25 D3 to 24,25 D3

113

Effect of estrogen, growth hormone, and prolactin on calcitriol secretion

increases secretion

114

Calcitonin secreting cells

have receptors for Ca++

115

Effect of calcium levels on calcitonin release

high levels leads to increased secretion
low levels leads to decreased secretion

116

Effect of estrogens and androgens on calcitonin release

increased secretion
androgens have a stronger effect then estrogens

117

Calcium in the gut leads to

increased CCK and gastrin which increases calcitonin before ca++ is absorbed

118

effect of secretin and glucagon on calcitonin secretion

increases secretion

119

PTHrp release in the mammary gland is stimulated by

prolactin

120

Individuals without kidneys

need to be given calcitriol in controlled doses or will experience bone degeneration

121

Hypoparathyroidism

inadequate PTH
blood calcium falls, blood PO4 rises
tetany of skeletal muscles
death due to spasm of laryngeal muscles which obstruct respiration
osteoclasts become inactive

122

treatment of hypoparathyroidism

Vitamin D and Calcium therapy

123

Hyperparathyroidism

too much PTH
stones, bones, abdominal groans, psychic moans
due to tumor of parathyroid gland

124

Hyperparathyroidism is more common in

women due to parathyroid gland stimulation during pregnancy and lactation

125

symptoms of Hyperparathyroidism

extreme osteoclast activity leading to elevated blood calcium and decreased blood PO4
depressed nervous system fn, skeletal muscle weakness, inability of the heart to relax, nausea, vomiting, constipation, anorexia

126

With severely elevated levels of PTH

bone decalcification, broken bones with multiple fracture sites
large areas in bone filled with osteoclasts
precipitation of calcium phosphate salts all over the body
polyuria due to increased calcium and phosphate excretion

127

mild Hyperparathyroidism is marked by

increased incidence of kindey stones

128

Rickets

occurrs in children due to inadequate vitamin D3 (leading to inadequate calcitriol)

129

When is rickets most commonly seen?

In the spring when children have spend a lot of time indoors all winter without adequate intake of vitamin D3

130

Mechanism of Rickets

PTH causes release of Ca++ from bones to maintain blood calcium levels, but Ca++ is not laid back down in the bone, just excreted
osteoblasts lay down bone proteins, so weak osteiod replaces the strong bone

131

Long terms rickets will lead to

low blood calcium, tetany, death

132

Osteomalacia

similar to rickets, but seen in adults
usually due to failure to absorb fats (D3 is fat soluble)

133

Artificial fats decrease

absorption of fat soluble vitamins

134

Osteoporosis

degeneration of bone due to decreased production of bone proteins (osteiod) rather than minerals
as osteoid is lost, calcium phosphate salts have nowhere to precipitate

135

Osteoporosis can be the result of

overactive osteoclasts
underactive osteoblasts

136

Causes of osteoporosis

lack of physical stress due to inactivity or lack of gravity
decreased levels of GH, estrogen, or androgens
malnutrition
excess cortisol
excess levels of thyroxin

137

Treatment of osteoporosis

exercise (especially weight training)
increased Ca++ intake
estrogens/selective estrogen receptor modulators
biphosphonates

138

Biphosphonates

inhibit bone resorption
NaGl stimulates osteoblasts

139

Paget's Disease

overactive osteoclasts (10-20 fold increase in activity)
create local regions of bone resorption without compensatory bone remineralization

140

Cause of Paget's disease

unknown but may include viral induction or genetic tendencies
could also be explained by local action of PTHrp secreting tumors

141

Treatment of Paget's disease

with inhibitors of osteoclast activity such as salmon calcitonin or bisphosphonates

142

Types of cells in the testes

leydig cells
sertoli cells
germ cells

143

Leydig cells

located outside the seminiferous tubules
produce testosterone
primarily respond to luteinizing hormone
independent of sperm production

144

Sertoli cells

located inside the seminiferous tubule
regulates spermatogenesis
physically acts as a blood-testis barrier
produces the testicular lumenal fluid (environment for spermatogenesis)
converts testosterone to estrogen

145

What proteins do the sertoli cells produces

Mullerian inhibiting hormone
inhibin
relaxin
androgen binding protein

146

what hormones do sertoli cells respond to?

FSH and testosterone

147

Primordial gonocytes

arise in the yolk sac and migrate to the testis

148

spermatogonia

diploid, go through mitosis
fertile males produce about 50 million a day

149

primary spermatocytes

form after puberty
one yields four spermatocoa

150

secondary spermatocyes

have completed first meiotic division

151

spermatids

haploid
completed second meiotic division
mature into spermatozoa

152

spermatozoa

mature sperm cells
have a different morphology from spermatids, but are essentially the same cell

153

Actions of testosterone

masculinizes body (secondary sex characteristics)
development of male reproductive tract and external genitals
essential for spermatogenesis

154

Behaviors driven by testosterone

libido, aggression, territoriality

155

brain sex

difference between male and female brains is a result of exposure of the brain to different doses of steroid hormones at critical times during embryological development
relatively few differences have been documented in humans

156

anatomical brain sex influenced by steroid hormones

Hypothalamus
corpus callosum

157

how does the hypothalamus differ between males and females

has sexually dimorphic nuclei, different numbers of neurons and degrees of hypertrophy of synapses in specific hypothalamic nuclei

158

how does the corpus callosum differ between males and females

more connections between the cerebral hemispheres in female than male

159

functional brain sex influenced by steriod hormone

hypothalamic hormone secretion patterns (rats, not primates)
differences in sensitivity to stimuli that induce behaviors

160

Organizational brain sex differences influenced by steroid hormones

exposure to hormones and NT's at critical times during development influences retention of neurons and number of synapses formed and retained
leads to different sensitivities of pathways

161

activational influence of steroid hormones

presence of hormones in adult may influence behaviors

162

Psychological aspects of brain differences between the sexes

gender identity
gender role related behavior
sexual orientation

163

Gender identity

what a person thinks they are, thought to be related to exposure of the brain to testosterone in humans or high levels of estrogens (rats and birds)

164

Congenital Adrenal Hyperplasia

females exposed to elevated adrenal androgens during prenatal development
more are born looking male, some female, and some intersex
have functional ovaries/reproductive tract
gender identity usually based on what they were identified as at birth

165

5 Alpha DHT deficiency

XY males born with internal testes and reproductive tracts that cannot convert testosterone to dihydrotestosterone (more potent)
externally look female until puberty when the skeletal muscle begins converting the testosterone to DHT, causing penis to grow and secondary sex characteristics to develop
strongly identify as male

166

Androgen insensitive XY

have functional internal testes but no testosterone receptors
at puberty, increased testosterone is convertd to estrogen by adipose tissue, further feminizing their external appearence

167

Gender role related behavior

strongly influenced by cultural norms

168

Leydig cells produce testosterone in response to

LH

169

short term regulation of testosterone production in the leydig cells

LH acts through cAMP to phosphorylate cytochrome p450 controlling cholesterol side chain cleavage (rate limiting step)

170

Long term regulation of testosterone production in the leydig cells

LH promotes growth and multiplication of leydig cells and synthesis of enzymes in path for testosterone production

171

Testosterone provides negative feedback control of

LH secretion at the level of the anterior pituitary and hypothalamus

172

Testosterone productions is independent of

FSH levels
no FSH receptors on leydig cells

173

testosterone is influenced by

many other hormones which modulate what LH can do

174

Effect of prolactin on testosterone production

increases LH receptor number
stimulates synthesis of enzymes in the testosterone production pathway
overall effect is to increase the ability of the leydig cells to respond to LH with more testosterone production

175

Effect of excess prolactin on testosterone production

loss of LH receptors, loss of response to LH, loss of libido and fertility

176

Effect of growth hormone on testosterone production

stimulates insulin like growth factor production by leydig cells (paracrine)
promotes similar responses as prolactin
fertility not dependent as with prolactin

177

Effect of GnRH on testosterone production

produced by the testes as a paracrine
decreases the ability of the leydig cells to respond to prolactin through loss of receptors

178

Effect of estrogen on testosterone production

suppresses production
negative feedback from sertoli cells

179

Effect of testosterone on testosterone production

suppresses production
direct end product inhibition on enzyme

180

Effect of glucocorticoids on testosterone production

stress response inhibits prolactin secretion leading to decreased testosterone production

181

Variations in testosterone levels

diurnal rhythm (highest in am)
changes with age
high prenatally
highest from 15-26
slow decline after 40
responds to stress

182

Mullerian inhibiting hormone

suppresses embryonic mullerian tract development into the internal female tract

183

inhibin

negative feedback regulation of FSH secretion

184

Relaxin

supports sperm maturation

185

Oxytocin

produced by testes
causes contractions of male reproductive tract smooth muscle for Sperm Transport

186

estrogen in the testes

local negative feedback on testosterone production

187

spermatogenesis

occurs inside the seminiferous tubule
begins after puberty
requires high levels of local testosterone

188

what is required to initiate spermatogenesis

FSH- acts on sertoli cells to stimulate production of androgen binding protein

189

Androgen binding protein

produced by the sertoli cells, traps testosterone inside the lumen to create high enough levels to initiate spermatogenesis

190

during spermatogenesis, testosterone and FSH stimulate

production of IGF's that stimulate mitotic division of spermatogonia

191

Epididymus

site of further sperm maturation
change from non-motile to moving in circles, to moving straight
absorbs lumenal fluid, phagocytizes dead/abnormal sperm
produces inhibitors of sperm activity to prolong life in the reproductive tract

192

vas deferens

tract that transfers sperm from the epididymus to the urethra

193

seminal fluid is produced by

seminal vesicles
prostate

194

seminal vesicle contribution to seminal fluid

fructose
prostaglandins (sperm motility, influence female tract for better transport
fibrinogen

195

prostate contribution to seminal fluid

citrate ion and calcium phosphate (activate sperm)
clotting enzyme to activate fibrinogen
profibrinolysin to dissolve the semen clot
HCO3 to buffer against vaginal secretions

196

GnRH stimulates the release of

LH and FSH by the anterior pituitary

197

How much FSH and LH is released by the anterior pituitary depends on

what the pituitary has synthesized
what is readily releasable vs. in storage

198

Inhibin acts on

the anterior pituitary to suppress FSH release

199

Testosterone acts on

both the hypothalamus to suppress GnRH and anterior pituitary to suppress LH release

200

High levels of prolactin can interfere with

GnRH release

201

Nervous system role in endocrine system: afferent

gathers information for deciding what concentration/ratio of hormones are needed
measures hormone levels in the blood
gathers signals as to whether hormone levels are meeting the body's needs

202

Nervous system role in endocrine system: efferent

produces NT's/NP's to signal neuroendocrine cells of hypothalamus
hypothalamus controls most of the endocrine system through the anterior pituitary

203

Endocrine influences on the nervous sytem

hormones alter brain organization and function
hormones alter the environment for brain fn

204

inappropriate levels of hormones can cause

symptoms common to mental illness

205

the functioning of most of the endocrine system is best described as

homeodynamics

206

Which ions are controlled through homeoSTASIS rather than dynamics

Ca++ K+ Na+ H+

207

a "normal" level of a hormone depends on

life stage
individual sensitivity to a hormone
levels of other primary messengers in the body

208

Compensatory endocine responses when hormone levels become too high:

receptor downregulation
negative feedback to suppress further secretion