Chapters 74, 78, 75 Flashcards Preview

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Flashcards in Chapters 74, 78, 75 Deck (185)
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0
Q

What are endocrines secreted by?

A

Ductless glands

1
Q

What are endocrines?

A

Chemical messengers that coordinate activities at cell, tissue, organ, and systemic levels

2
Q

What is classic endocrine signaling?

A

Hormones travel to distant organs to regulate target organs function

3
Q

What is an intracrine?

A

Endocrine that has effect on cell that produces it WITHOUT secretion

4
Q

What is an autocrine?

A

Endocrine has effect on cell that secretes it

5
Q

What is a paracrine?

A

Endocrine that has effect on neighboring cells

6
Q

What is a hormone?

A

Endocrine that has effect on cell in different location

7
Q

What is a neuroendocrine?

A

Endocrine secreted by neuron and delivered to another location

8
Q

What makes an endocrine a cytokine?

A

If it is secreted into ECF and establishes a gradient - can act as paracrine, autocrine, or hormone

9
Q

How do chemical messengers maintain homeostasis?

A

Change in environment -> hormone secretion -> action on target cell -> restoration of normal environment

10
Q

What are the three general classes of endocrines?

A
  1. Proteins/polypeptides
  2. Steroids (cholesterol backbone)
  3. Amine derivatives (tyrosine, tryptophan)
11
Q

What is the solubility of protein hormones?

A

Water soluble

12
Q

What is the precursor and production of protein hormones?

A

Synthesized as larger precursors, undergo proteolytic cleavage into a pro hormone, then are cleaved again into biologically active hormone

13
Q

How are protein hormones stored?

A

In secretory vesicles in cells

14
Q

Examples of protein hormones?

A

TSH, ADH, insulin, PTH

15
Q

What is the solubility of steroid hormones?

A

Lipid soluble

16
Q

What is the precursor/production of steroid hormones?

A

All synthesized from cholesterol - differ in ring structure and side chains

17
Q

How are steroid hormones stored?

A

Usually not - large stores of cholesterol in cytoplasmic vacuoles, stimulus causes them to be synthesized into steroid

18
Q

What are some types of steroid hormones?

A
Glucocorticoids (cortisol)
Mineralcorticoids (aldosterone)
Androgens (testosterone, DHEA)
Estrogens (estradiol, estrone)
Progestins (progesterone)
19
Q

When are steroid hormones synthesized?

A

On an as needed basis for immediate release

20
Q

Where are steroid producing enzymes located?

A

Mitochondria and ER

21
Q

What is a secosteroid?

A

Cholesterols with a broken ring

22
Q

What is solubility of a secosteroid?

A

Lipid soluble

23
Q

Example of secosteroid?

A

Vitamin D

24
Q

What are the two groups of hormones derived from tyrosine?

A

Thyroid hormones and catecholamines

25
Q

What is the solubility of thyroid hormones?

A

Lipid soluble

26
Q

What is the structure of thyroid hormones?

A

“Double” tyrosine with incorporation of 3 or 4 iodine atoms

27
Q

What is the structure of catecholamines?

A

“Single” tyrosine

28
Q

What is the solubility of catecholamines?

A

Water soluble

29
Q

What are examples of catecholamines?

A

Neurohormones (epinephrine, norepinephrine)

Neurotransmitters

30
Q

What hormones are synthesized from tryptophan?

A

Serotonin and melatonin

31
Q

What hormone is synthesized from glutamic acid?

A

Histamine

32
Q

What other hormone is synthesized from tyrosine?

A

Dopamine

33
Q

What are eicosanoids?

A

Signaling molecules derived from polyunsaturated fatty acids (omega 3 or omega 6 fats)

34
Q

Which eicosanoids are pro-inflammatory?

A

Omega 6 derivatives

35
Q

Which eicosanoids are anti-inflammatory?

A

Omega 3 derivatives

36
Q

What is the most abundant eicosanoid precursor?

A

Arachidonic acid

37
Q

How long are eicosanoids active?

A

Only a few seconds

38
Q

What are the 4 main eicosanoids?

A

Prostaglandins, prostacyclins, leukotrienes, thromboxanes

39
Q

What do anti inflammatory drugs do to eicosanoid synthesis?

A

Down regulate

40
Q

Why is a cell called a target?

A

It has a specific receptor for a particular hormone

41
Q

How are endocrines regulated using receptors?

A

Target cell receptors decrease in number if there is an excess of hormone in blood

42
Q

What do physiologic effects of hormones depend on?

A

Their concentration in blood and ECF and number of receptors present on target cells

43
Q

Why is precise control over hormone circulation crucial?

A

Hormone concentrations that are too high or too low can lead to disease

44
Q

How is hormone secretion regulated?

A

Most commonly: Negative feedback loop

Less commonly: positive feedback loop

45
Q

What is the most highly regulated aspect of endocrine control?

A

Synthesis/secretion of hormones

46
Q

What are 4 ways hormones are metabolized and excreted?

A
  1. Metabolic destruction by tissues
  2. Binding to tissue and subsequently “recycled”
  3. Excretion by liver into bile
  4. Excretion by kidney into urine
47
Q

What is the link between nervous system and endocrine system?

A

Hypothalamus

48
Q

How does chronotropic control work?

A

Works in conjunction with neural control

Superimposed on negative/positive feedback control systems

49
Q

What is circadian rhythm?

A

Hormones released at set interval everyday

50
Q

What are diurnal rhythms?

A

Biological circadian rhythms that synchronize with day/night cycle

51
Q

What is the sleep-wake cycle?

A

Can be different than diurnal rhythm in people with sleep problems or who work late night shifts

52
Q

What is circhoral release of hormones?

A

Release frequency of about 1 hour

53
Q

What is ultradian release of hormones?

A

Episodic release of longer than an hour but less than 24 hours

54
Q

When is episodic secretion of hormones considered circadian?

A

If the periodicity is approximately 24 hours

55
Q

What controls the circadian rhythm?

A

Suprachiasmatic nucleus in hypothalamus

56
Q

Why is pulsatile release of GnRH important?

A

Slower frequency will not maintain gonadal function, faster or continuous release will inhibit gonadotropin secretion and block gonadal steroid production

57
Q

Down regulation: What does an increased hormone concentration and receptor engagement lead to

  1. Functionally?
  2. Structurally?
A
  1. Decreased sensitivity of target tissue (inactivation of Receptor molecules, inactivation of intercellular signaling)
  2. Decrease in number of receptor sites (temporary removal of receptor or receptor destruction)
58
Q

What is hormone up regulation?

A

Decreased hormone concentration and receptor engagement leads to increased sensitivity of target tissue to stimulating effects of hormone - same mechanisms as down regulation

59
Q

Where are receptors for water soluble hormones found?

A

Surface of target cell

60
Q

What are water soluble hormone receptors coupled to?

A

Second messenger systems

61
Q

Where are receptors for fat soluble hormones located?

A

In the nucleus of target cell

62
Q

What happens when a hormone binds an enzyme linked receptor?

A

Conformational change, usually involving phosphorylation of a tyrosine

63
Q

What does phosphorylation of a tyrosine do?

A

May activate/inactivate intercellular enzymes, may catalyze second messenger, may generate new protein => change cell function

64
Q

How do G protein linked receptors work?

A

Hormone binds to receptors -> conformational change in receptor -> intracellular G protein recruited to receptor -> alpha subunit has GTPase activity -> cellular change (open/close ion channels, activate adenyl Cyclase, change other enzyme activity)

65
Q

What do second messengers do?

A

Amplify hormone signal

66
Q

What does generation of second messengers and activation of specific protein kinases result in?

A

Changes in activity of target cell

67
Q

How fast are changes invoked by second messengers?

A

Rapid

68
Q

Three examples of second messenger systems?

A
  1. Cyclic nucleotides (cAMP)
  2. Calcium and calmodulin
  3. Phospholipase C
69
Q

What does activated G protein complex recruit?

A

Adenyl Cyclase

70
Q

What does adenyl Cyclase do?

A

Converts ATP to cAMP

71
Q

What does cAMP do?

A

Activates protein kinase

72
Q

What does activated protein kinase do?

A

Phosphorylates specific proteins that trigger cellular response to hormone

73
Q

Hormones using adenyl Cyclase/cAMP system?

A

ACTH, angiotensin II, calcitonin, catecholamines, CRH, FSH, glucagon, HCG, LH, PTH, secretin, somatostatin, TSH, vasopressin

74
Q

What does phospholipase C do?

A

Breaks down membrane phospholipids into IP3 and DAG

75
Q

What does IP3 do?

A

Mobilizes mitochondrial/ER calcium to cause smooth muscle contraction and cell secretion

76
Q

What does DAG do?

A

Activates protein kinase C that promotes protein phosphorylation and arachidonic acid conversion to prostaglandins

77
Q

Hormones using phospholipase C system?

A

Angiotensin II, catecholamines, GnRH, GHRH, oxytocin, TRH, vasopressin

78
Q

What does calcium entry into cells cause?

A

Binds calmodulin -> activation/inhibition of protein kinases

79
Q

How do lipid soluble hormone receptors work?

A

Hormones diffuse through lipid bilayer, bind to receptor (in cytoplasm or nucleus), undergoes conformational change -> binds specific DNA sequence called “response elements in the nucleus”

80
Q

What do steroid hormones cause in target cells?

A

Protein synthesis (enzymes, transport proteins, structural proteins)

81
Q

How fast are responses evoked by lipid soluble hormones?

A

SLOW due to transcription/translation mechanism

82
Q

What is an agonist ligand?

A

Binds to receptor -> hormone response

83
Q

What is an antagonist ligand?

A

Binds to receptor and inhibits hormone response

84
Q

What is a partial agonist/partial antagonist?

A

Binds receptor -> hormone response < full agonist

If concentration high enough can act as antagonist

85
Q

What is a mixed agonist-antagonist?

A

Compounds that act in different ways through same receptor depending on context

86
Q

What is hormone deficiency usually due to?

A

Destructive process at gland where hormone produced

87
Q

What are two other ways to cause hormone deficiency?

A

Genetic defects in hormone production, inactivating mutations of receptors

88
Q

How does hormone excess happen?

A

May be overproduced by gland, or by tissue that is not endocrine organ
Endocrine gland tumors

89
Q

What does overproduction of tropic hormones lead to?

A

Overstimulation of target gland

90
Q

Example of overstimulated target gland disease?

A

Cushing’s

91
Q

What does activating mutations of cell surface receptors cause?

A

Aberrant stimulation of hormone production by endocrine gland

92
Q

Example of activating mutation disease?

A

McCune-Albright syndrome

93
Q

What does malignant transformation of non-endocrine tissue cause?

A

Lack of differentiation -> ectopic production of hormones

94
Q

What do anti-receptor antibodies do?

A

Stimulate receptor instead of block it

95
Q

What do alterations in receptor number and function result in?

A

Endocrine disorders

96
Q

What will an aberrant increase in level of specific hormones most commonly cause?

A

Decrease in available receptors => down regulation (eg type II diabetes)

97
Q

What can ingestion of exogenous hormone cause?

A

Hormone excess

98
Q

Which hormones does the pancreas secrete?

A

Insulin, glucagon, amylin, somatostatin, pancreatic polypeptide

99
Q

Which hormones are secreted by beta cells?

A

Insulin and amylin

100
Q

Which hormone is secreted by alpha cells?

A

Glucagon

101
Q

Which hormone is secreted by delta cells?

A

Somatostatin

102
Q

What is insulin?

A
  1. Energy abundance hormone
  2. Energy storage hormone
  3. Hypoglycemic hormone
103
Q

What is the dominant hormone in regulation of blood sugar?

A

Insulin

104
Q

How is insulin synthesized?

A

As preprohormone after translation of insulin RNA

Cleaved in ER to proinsulin

105
Q

What happens to proinsulin?

A

Cleaved in Golgi to insulin

-packaged in secretory granules and secreted into blood

106
Q

How long does insulin circulate in blood?

A

Cleared in 10-15 minutes

107
Q

How is insulin degraded?

A

By insulinase to allow rapid “turn off”

108
Q

What happens with a lack of C peptide?

A

Neuropathy, cardiovascular disease, kidney issues

109
Q

What does C peptide do in nervous system?

A

Promotes axonal repair

110
Q

What does C peptide do in cardiovascular system?

A

Promotes micro vascular blood flow by stimulating Na+/K+ pump and release of NO

111
Q

What does C peptide do in urinary system?

A

Promotes glomerular filtration

112
Q

What happens with too much C peptide?

A

C peptide deposits on endothelia cause inflammation

  • macrophages become foam cells
  • T cell mediated inflammation
  • smooth muscle proliferation
113
Q

What is the primary factor that stimulates beta cells?

A

Increased blood glucose

114
Q

Which transporter is on beta cells?

A

GLUT2

115
Q

How does glucose get into beta cell?

A

Diffusion using GLUT2 transporter

116
Q

How is insulin secreted?

A

Glucose uptake into beta cells using GLUT2
Glucokinase makes G6P
Glycolysis products NADH and ATP close K+ channels
Ca2+ channels open
Preformed vesicles bind Ca2+ and release insulin to blood

117
Q

What other factors increase Ca2+ influx and therefore insulin secretion in the presence of glucose?

A
Glucagon
Arginine
Lysine
GI hormones
Acetylcholine 
Sulfonurea drugs
118
Q

What is the effect of insulin on carbohydrates?

A

Increased glucose uptake
Increases glycogenesis
Decreased gluconeogenesis

119
Q

What is the effect of insulin on fat?

A

Increased triglyceride synthesis

Decreased triglyceride breakdown

120
Q

What is the effect of insulin on protein?

A

Increased synthesis

Decreased breakdown

121
Q

What type of receptor does insulin bind to?

A

Enzyme linked receptor

122
Q

What are the end effects of insulin binding?

A
  1. Within seconds, 80% of body’s cells increase glucose uptake by mobilizing GLUT4
  2. Phosphorylation of glucose allows it to be substrate for CHO metabolic functions
123
Q

What happens to cell membrane under influence of insulin?

A

Becomes permeable to amino acids, K+ and phosphate

124
Q

What does insulin do to Na/K pump activity?

A

Increases activity

125
Q

What happens after a high CHO meal?

A

Increased glucose -> increased insulin -> rapid uptake, storage and use

126
Q

Why is it important To have low serum insulin between meals?

A

So glucose can go preferentially to brain

127
Q

What does insulin do in liver?

A

Stimulates glycogen synthetase and inhibits glycogen phosphorylase

128
Q

What happens to most glucose after a meal?

A

Stored immediately in liver as glycogen

129
Q

What enzyme does insulin increase to promote glucose uptake by liver?

A

Glucokinase

130
Q

What does decreased glucose between meals lead to?

A

Less insulin

- activates phosphorylase and induces glycogenolysis

131
Q

What is insulin’s effect on

  • glucose storage/utilization enzymes?
  • glucose mobilization/synthesis enzymes?
A
  • activates

- inactivates

132
Q

What does resting muscle preferentially use for energy?

A

Fatty acids

133
Q

Two conditions where muscle uses glucose?

A
  1. Exercise

2. After meal - blood glucose high, insulin is high= rapid transport of glucose into muscle

134
Q

What happens to glucose transported into muscle cell after a meal if not exercising?

A

Store as glycogen

135
Q

What does insulin do to muscle amino acids?

A

Inhibits release so not available for gluconeogenesis

136
Q

What does insulin do to fat?

A

Increase fat synthesis, decrease fat breakdown

137
Q

What happens when liver glucose storage reaches limit?

A

Conversion of excess sugar into fatty acid by liver

138
Q

What is insulin’s action on adipose?

A

Inhibits hydrolysis of TG, preventing free fatty acids from getting to blood. Increases use of glucose for energy and decreased use of fat

139
Q

When insulin is low, what is preferentially used for energy?

A

Fat

140
Q

What is the signal for switching from fat to CHO for energy use?

A

Blood glucose

  • low BG = low insulin = FAT use
  • high BG = high insulin = CHO use
141
Q

Other hormones that play a role in switching from fat to CHO use?

A

Growth hormone, cortisol, glucagon

142
Q

What effect does insulin have on amino acid uptake?

A

Promotes it

143
Q

What effect does insulin have on protein catabolism?

A

Inhibits catabolism via inhibition of normal degradation

144
Q

What is insulin’s effect on potassium?

A

Promotes K+ uptake to decrease serum [K+]

Inhibits K+ efflux

145
Q

What effect does insulin have on phosphate?

A

Promotes phosphate uptake

146
Q

What happens if insulin or growth hormone is absent?

A

Leads to decreased growth

147
Q

What type of hormone is glucagon considered?

A

Hyperglycemic

148
Q

What is the most important action of glucagon?

A

To increase blood glucose

149
Q

What are the two main effects of glucagon on glucose metabolism?

A
  1. Glycogenolysis

2. Gluconeogenesis

150
Q

What increases secretion of glucagon?

A
  1. Low blood glucose
  2. Exercise
  3. High serum amino acids
151
Q

What decreases glucagon secretion?

A

High blood glucose, somatostatin

152
Q

What is the solubility of amylin?

A

Can be chemically modified to be water soluble or insoluble

153
Q

What does amylin do if insoluble?

A

Forms fibrils, induces apoptosis of pancreatic beta cells, therefore inhibiting insulin secretion

154
Q

What does amylin do if water soluble?

A

Decreases blood glucose

  • synergizes with insulin
  • decrease glucagon
155
Q

What does somatostatin do?

A

Inhibits glucagon and insulin

156
Q

What increases somatostatin secretion?

A

Ingestion of food

157
Q

What is the main goal of somatostatin?

A

Extend period of time over which food/nutrients are assimilated, decreases use of absorbed nutrients by tissues

158
Q

What does somatostatin secreted by the hypothalamus do?

A

Suppress secretion of GH by anterior pituitary

159
Q

What happens to proteins with lack of insulin?

A

Protein storage and synthesis slows down dramatically, increased catabolism of protein in muscle

160
Q

What happens with use of fat for energy with lack of insulin?

A

Increased use by all tissues except brain - causes lipolysis
Increased FFA in blood leads to liver conversion of FA into phospholipids, TG, and cholesterol => atherosclerosis

161
Q

What is diabetes mellitus?

A

Syndrome of impaired CHO, PRO, FAT metabolism

162
Q

Two causes of DM?

A
  1. Lack of insulin secretion

2. Decreased insulin sensitivity of tissues

163
Q

What are the 2 main types of DM?

A

Type I - overt beta cell failure

Type II - loss of insulin sensitivity

164
Q

What is insulin dependent DM?

A

Type I
Genetic predisposition
Pancreatic beta cells fail

165
Q

What is non-insulin dependent DM?

A

Type II
Body responds poorly to insulin
Pancreatic beta cells begin to fail

166
Q

When does type I generally onset?

A

Childhood to early adolescence

167
Q

How quickly does type I DM develop?

A

Abruptly

  • increased BG
  • increased use of fats for energy
  • depletion of protein
168
Q

What are symptoms of type I DM?

A

High BG
Polyuria/increased thirst => dehydration
Osmotic diuresis causes decreased electrolytes
Polyol pathway is stimulated - “sugar coated proteins”

169
Q

What effect does chronic high blood glucose have on

  • vascular system?
  • nerves?
A
  1. Arteriosclerosis, renal disease, retinopathy, blindness, ischemia, gangrene, hypertension, atherosclerosis
  2. Peripheral neuropathy, impaired CV reflexes, impaired bladder function
170
Q

What happens to metabolism in type I DM?

A

Shift from CHO to fat metabolism

171
Q

What are the effects of fat metabolism?

A

Hyperventilation increased for expiration of co2
Increased cholesterol in circulation cause arteriosclerosis
Depletion of protein stores causes weight loss, fatigue, polyphagia, severe wasting, death

172
Q

When is typical onset of type II DM?

A

Usually >30

173
Q

How fast does type 2 DM develop?

A

Gradually

174
Q

What is the greatest risk factor for type 2 DM?

A

Obesity

175
Q

What happens in type II DM?

A

Decreased sensitivity to insulin so beta cells increase insulin secretion
=> impaired CHO use, increased BG, increased insulin secretion

176
Q

Warning signs of type II DM?

A
Obesity
Reactive hypoglycemia
Insulin resistance
Fasting hyperglycemia 
Lipid abnormalities 
Hypertension
177
Q

Causes of insulin resistance?

A
Chronic insulin exposure
Obesity 
Excess cortisol 
Excess GH 
Pregnancy/ gestational DM 
Polycystic ovarian syndrome 
Hemochromatosis 
Genetic causes of obesity
178
Q

What happens in the later stages of insulin resistance?

A

Pancreatic beta cells burn out, no longer able to produce insulin => IDDM

179
Q

Testing for DM - what will be found in UA?
Type I
Type II

A

Type I - high glucose, high ketones

Type II - high glucose, low ketones

180
Q

Testing for DM - what will be seen on oral glucose/ tolerance test?
Type I vs type II

A

Both DM types - BG does not return to normal for 4-6 hrs
Type I - insulin low or undetectable
Type II - insulin high in early stage (low in late stage)

181
Q

What does insulinoma cause?

A

Hypersecretion of insulin

182
Q

What can happen if insulinoma untreated?

A

Can lead to insulin shock due to hypoglycemia

183
Q

Causes of fasting hypoglycemia?

A

Drugs
Hormone deficiencies (hyperglycemic hormones)
Liver failure
Critical illness
Endogenous hyperinsulinisn (insulinoma)
Autoimmune - insulin or insulin receptor antibodies

184
Q

Causes of postprandial hypoglycemia?

A

Congenital deficiency of enzyme of CHO metabolism

Gastrointestinal