Endo General Flashcards

1
Q

What are steroids derived from

A

cholesterol

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2
Q

What are amines/AA derived from?

A

tyrosine

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3
Q

peptide hormone receptor location at target cell

A

plasma mem

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4
Q

steroid hormone receptor location at target cell

A

intracellular

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5
Q

peptide hormone speed of action

A

fast onset

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6
Q

steroid hormone speed of action

A

slow onset

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7
Q

Corticotropin-releasing hormone (CRH) is released from what gland?

fn?

A

hypothalamus

Fn: Stimulates adrenocorticotropic hormone (ACTH)

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8
Q

ACTH is released from what gland?

fn?

A

Anterior pituitary

Fn: Stimulates synthesis and secretion of cortisol, aldosterone, and androgens

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9
Q

Antidiuretic hormone (ADH) (also called arginine vasopressin, or AVP) is released from what gland?

fn?

A

Posterior pituitary

Fn: Increases water retention at kidney, vasoconstricts arterioles

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10
Q

Oxytocin is released from what gland?

fn?

A

Posterior pituitary

fn: Stimulates uterine contractions during labor, milk ejection in lactation

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11
Q

Aldosterone is released from what gland?

fn?

A

Adrenal cortex

Fn: Decreases urinary Na+ excretion, Increases urinary K+ and H+ excretion

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12
Q

Cortisol is released from what gland?

fn?

A

Adrenal cortex

Fn: Released in response to stress, Multiple metabolic actions

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13
Q

Insulin (β cell) is released from what gland?

fn?

A

Pancreas

Fn: Promotes storage of glucose as glycogen in liver and muscle
Promotes uptake of glucose and storage as triglyceride in adipose tissue and liver

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14
Q

Hormones circulate at (low/high) levels and bind to receptors with (low/high) affinity

A

Hormones circulate at LOW levels and bind to receptors with HIGH affinity

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15
Q

Hormone generally (can/cannot) cross cell membrane via diffusion

A

Hormone generally CANNOT cross cell membrane via diffusion

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16
Q

↑ receptor number when hormone level is low

A

Upregulation

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17
Q

when hormone level is high and/or continuous

A

Downregulation or desensitization

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18
Q

The plasma free hormone concentration is affected by:

A
  1. The rate of hormone secretion
  2. The rate of hormone elimination
  3. The extent of hormone binding to plasma proteins
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19
Q

What are the Trophic hormones?

A
GH: Growth Hormone
ACTH: Adrenocorticotropic Hormone
LH: Luteinizing Hormone
FSH: Follicle Stimulating Hormone
TSH: Thyroid Stimulating Hormone
PRL: Prolactin
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20
Q

What hormone stimulates release of pancreatic enzymes and where is it released from?

A

Cholecystokinin (CCK) from Small Intestine

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21
Q

Where is GH produced & released?

A

anterior pituitary

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22
Q

What are the most abundant cells in the anterior pituitary?

A

somatotrophs

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23
Q

What is the MC pituitary cell to become malignant

A

somatotrophs

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24
Q

What do malignant somatotrophs produce?

A

GH & PRL

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25
Q

What occurs due to growth of a pituitary adenoma?

A

compresses infundibulum decreasing hypothalamic hormonal stimulation of anterior pituitary hormone release but also decreasing anterior pituitary hormones due to inability to suppress

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26
Q

How do GHRH neurons regulate GH production?

A

Positive feed-forward regulation

GHRH is released into hypo-physeal portal system and transported to somatotrophs causing GH release to secondary capillary plexus and to the body of the anterior pituitary

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27
Q

How is GH regulated by hypothalamic somatostain neurons?

A

Negative feed-forward regulation

Somatostain is released into hypophyseal portal system goes to somatotrophs and inhibits GH release

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28
Q

Fn of GH

A
Linear growth (soft tissue, visceral organ, muscle & bone) in growing ages
Maintains lean body mass in adulthood
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29
Q

What is fetal growth mediated by?

A

IGF1 and IGF-2

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30
Q

How does GH work?

A

utilizes fat as main energy source
maximizes protein deposition for lean body mass
marks glucose for use by the brain

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31
Q

What contains the greatest number of GH receptors?

A

liver and cartilage

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32
Q

What is the effect on insulin when GH acts on fat and causes lipolysis and increased FA release?

A

antagonistic to insulin

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33
Q

GH action on AA

A

maximize AA and protein for lean body mass production

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34
Q

What is GH action on glucose metabolism?

A

antagonistic (so blood glucose levels increase)

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35
Q

What happens when there is excessive chronic GH release?

A

there is sustained increase in plasma glucose causing an increase in insulin and eventually insulin resistance and diabetogenesis

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36
Q

What causes GH excess?

A

pituitary adenoma
extrapituitary GH excess
excess GHRH

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37
Q

What hormones are secreted from the adrenal cortex?

A

corticosteroids
mineralocorticoids
androgens

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38
Q

What hormones are secreted from the adrenal medulla?

A

epinephrine

NE

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39
Q

What regulates glucocorticoid synthesis?

A

episodic secretion and circadian rhythm of ACTH
stress responsiveness of HPA axis
FB inhibition by cortisol on ACTH sectretion

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40
Q

When are ACTH burst most frequent?

A

in the AM

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41
Q

What are the physiological actions of glucocorticoids?

A

maintain blood glucose levels during fasting (increase during stress) by increasing liver synthesis of glucose and glycogen deposition

calcium homeostasis by slowing bone growth and inducing bone demineralization

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42
Q
What is the effect of glucocorticoids on:
CV system
Skeletal muscls
CNS
Immune system
A

CV: HEN with prolonged levels

Skeletal muscle: wasting with prolonged high levels

CNS: either excess fo insufficiency will cause alterations in mood, behavior and excitability

Immune: secreted in response to stress

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43
Q

What prevents glucocorticoids from interacting with the mineralocorticoid receptor?

A

11β-HSD2 will turn cortisol into cortisone so only the aldosterone can interact witht the MR

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44
Q

MR binds to cortisol with (high/low) affinity. MR target tissues express 11-betaHSD2 which (inactivates/activates) cortisol.

A

HIGH

INACTIVATES

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45
Q

What is the most active androgen?

A

testosterone

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46
Q

What is the consequence of 21-Hydroxylase deficiency?

A

Decreased cortisol and aldosterone

Hypoglycemia because of low cortisol

Loss of sodium because of mineralocorticoid deficiency Virilization because of excess androgen production

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47
Q

What is the consequence of 11β-Hydroxylase deficiency?

A

Excess mineralocorticoid activity

Hypoglycemia because of low cortisol

Salt and water retention

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48
Q

What is the consequence of 11β-HSD2 deficiency?

A

Decrease in glucocorticoid inactivation in mineralocorticoid- sensitive cells leading to excess mineralocorticoid activity

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49
Q

ACTH dependent causes of cushings

A

ACTH secreting tumors

CRH secreting tumors

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50
Q

ACTH independent causes of cushings

A

glucocorticoid secreting tumors

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51
Q

Causes of addison’s disease

A

primary adrenal insufficiency due to destruction of adrenal cortex

both mineralocorticoid and glucocorticoid deficiency

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52
Q

What is effect of Mifepristone at high doses on Glucocorticoid Function?

A

blocks the glucocorticoid receptor, blocks feedback regulation of HPA, increases ACTH and cortisol but blocks the action of cortisol at the receptor

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53
Q

What is effect of Spironolactone and Eplenerone at on Mineralocorticoid Function?

A

Inhibits binding of aldosterone to the MR

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54
Q

What is secreted from zona glomerulosa layer of adrenal cortex?

A

Mineralocorticoids

Aldosterone, deoxycorticosterone

55
Q

What is secreted from zona fasiculata layer of adrenal cortex?

A

Glucocorticoids

Cortisol, corticosterone

56
Q

What is secreted from zona reticularis layer of adrenal cortex?

A

Sex Steroids

Androgen

57
Q

What is the precursor for adrenal steroidogenesis?

A

cholesterol

58
Q

What is the principal hormone that stimulates adrenal glucocorticoid synthesis and secretion and where is it syntehsized?

A

ACTH synthesized in the anterior pituitary

59
Q

What controls POMC secretion which leads to the production of ACTH?

A

CRH
Argininevasopressin
Endogenouscircadianrhythm

60
Q

What causes hyperpigmentation in primary AI?

A

increased production of POMC which produces melanocyte stimulating hormone in addition to ACTH

61
Q

What does TH do?

A

Maintains level of metabolism in tissues optimal for normal function

62
Q

What happens if fetus/neonate has thyroid hypofn?

A

results in mental retardation and dwarfism

63
Q

What happens if adult has thyroid hypofn?

A

mental and physical slowing, poor resistance to cold; adult hyperthyroidism-body wasting, nervousness, tachycardia, tremor, excess heat production

64
Q

Effect of TH on heart

A

Increased number of beta-adrenergic receptors

65
Q

Effect of TH on adipose tissue

A

Stimulated lipolysis

66
Q

Effect of TH on muscle

A

Increased protein breakdown

67
Q

Effect of TH on bone

A

Promote normal growth and skeletal development

68
Q

Effect of TH on nervous system

A

Promote normal brain development

69
Q

Effect of TH on gut

A

Increased rate of carbohydrate absorption

70
Q

Effect of TH on lipoprotein

A

Formation of LDL receptors

71
Q

What cells secrete thyroid hormones, which are critical to development, growth and metabolism?

A

Follicle cells

72
Q

What cells secrete calcitonin, which regulates circulating levels of calcium

A

Parafollicular cells

73
Q

What is minimum daily intake of iodine recommended for normal adult thyroid fn?

A

150 ug/d

74
Q

Deiodination is dependent on what?

A

P450

75
Q

What is conserved with a decline in T3?

A

calories and protein

76
Q

What happens to the thyroid if you remove the pituitary?

A

gland atrophies

77
Q

What happens to the thyroid if you administer TSH?

A

thyroid fn is stimulated

if prolonged will become a goiter

78
Q

What is Wolff-Chaikoff effect?

A

large doses of iodine inhibit organification and metabolic activity of the thyroid gland is decreased

79
Q

What is NIS?

A

sodium iodide symporter

80
Q

What happens to TH receptors during starvation?

A

decreased number of receptors

81
Q

Thyrotoxicosis

A

thyroid hormone excess

82
Q

Hyperthyroidism

A

excessive thyroid function

83
Q

What is the MC thyroid abnormality?

A

goiter

84
Q

Causes of goiter

A

Iodide deficiency

Hashimoto’s (aka chronic lymphocytic thyroiditis or autoimmune thyroiditis)

Grave’s disease

85
Q

When do sx of hypoglycemia develop in healthy individuals?

A

<55 mg/dl

86
Q

Name the only endogenous steroid inhibiting ACTH

A

Cortisol (synthetics also suppress)

87
Q

What do Extraadrenal ganglia produce?

A

NE

88
Q

What does adrenal medulla produce?

A

epi

89
Q

Innermost concept of self as

male, female, a blend of both or neither

A

Gender Identity

90
Q

External appearance of one’s gender expressed through behavior, clothing etc.

A

Gender Expression

91
Q

Who you like, desire, are attracted to

A

Sexual Orientation

92
Q

What cells make up the majority of the islets of langerhans?

A

Beta cells (which secrete insulin)

93
Q

What do alpha cells in islets of langerhans secrete?

A

glucagon

94
Q

What do beta cells in islets of langerhans secrete?

A

insulin

95
Q

What do delta cells in islets of langerhans secrete?

A

somatostatin

96
Q

What do F(PP) cells in islets of langerhans secrete?

A

pancreatic polypeptide

97
Q

Fn of insulin

A

energy conservation-directs fuel metabolism to CHO use

DECREASES blood glucose concentration

98
Q

Fn of glucagon

A

energy use

INCREASES BG concentration

99
Q

What is insulin’s halflife?

A

5 min

100
Q

What stimulates insulin release?

A

glucose, GLP1 and GIP

parasym stimulation

Beta 2 adrenergic receptor agonists

101
Q

Biphasic effect of sympathetic stil

A

inhibition via alpha 2 and stimulation via beta2

Overall effect is INHIBITORY

102
Q

What occurs as a result of insulin signaling?

A

cell growth, differentiation, survival, protein synthesis, glycogen syntehsis, metabolic pathways

103
Q

What occurs in muscle and fat tht lowers blood glucose?

A

insulin promotes relocalization of GLUT4 transporter to cell mem

104
Q

GLUT 2 Fn

A

Regulation of insulin release

105
Q

GLUT 4 Fn

A

Insulin-mediated glucose uptake

found primarily in adipose tissues and striated muscle (skeletal and cardiac)

106
Q

What occurs as a result of chronic activation of insulin receptor?

A

causes receptor internalization & down- regulation of response

107
Q

Glycolysis

A

breakdown of glucose

108
Q

Gluconeogenesis

A

generation of glucose

109
Q

Glycogenolysis

A

breakdown of glycogen into glucose

110
Q

Glycogenesis

A

formation of glycogen

111
Q

What does somatostatin do?

A

inhibits everything

112
Q

Effect of glucagon on:

glucose
FA
ketoacids

A

Increases them all

113
Q

What hormones increase BG besides glucagon?

A

catecholamines- fast when SEVERELY hypoglycemic or stress

glucocorticoids- slow when stress, prolonged fasting or hypoglycemia

GH- slow when fsating, sleep or stress

114
Q

epi, NE and dopamine

A

catecholamines

115
Q

Effect of catecholamines on:
insulin secretion
glycogenolysis
gluconeogenesis

A

Inhibits insulin secretion

Stimulates glycogenolysis

Stimulates gluconeogenesis

116
Q

Effect of glucocorticoids on:
insulin secretion
glycogenolysis
gluconeogenesis

A

Reduces insulin sensitivity

Does NOT stimulate glycogenolysis

Stimulates gluconeogenesis

117
Q

Effect of GH on:
insulin secretion
gluconeogenesis

A

Reduces insulin sensitivity (decreases glucose uptake)

Stimulates gluconeogenesis

118
Q

What stimulates somatostatin release and what is its effect?

A

stimulated by glucose; amino acids; fatty acids

Inhibitory effect on virtually all gastrointestinal and pancreatic exocrine and endocrine functions.

119
Q

Why is somatostatin’s effect on insulin and glucose limited?

A

it is produced in delta cells which are in the periphery of islet and the blood flows from the center first then to the periphery

120
Q

What is the effect of pancreatic polypeptide?

A

antagonizes CCK and inhibits gallbladder contraction and decreases GI motility

121
Q

Why does insulin resistance occur as fat increases?

A

fat cells synthesize and release hormone signals (adipokines) that antagonize insulins effects on target cells

122
Q

What adipose signal can aid in insulins effects?

A

Leptin

123
Q

Fn of leptin

A

Acts in brain to lower appetite

124
Q

What is the effect of exercise on glucose and insulin?

A

↑ glucose entry into skeletal muscle

insulin-independent ↑ in the number of GLUT-4
transporters

Can precipitate hypoglycemia in diabetics

125
Q

What does a 1% change in HbA1c do to plasma glucose

A

29 mg/dl change in average plasma glucose

126
Q

What is a strong predictor of cardiovascular disease in patients with type 2 diabetes?

A

Microalbuminuria

127
Q

Effect of PTH

A

increase bone reabsorption, inc ca and Cl and decrease PO4 and HCO3-

128
Q

Effect of calcitriol (1,25-OH)2 vit D

A

increase Ca, PO4 abs

129
Q

What is recommended daily vit D intake?

A

Children, adults, pregnancy, lactation- 600 IU

> 70- 800 IU

130
Q

What is optimal vit D levels?

A

20-60 ng/ml

131
Q

What is the active form Vit D?

A

1,25 (OH) vitamin D

132
Q

What cells produce T4 and T3?

A

Follicular cells

133
Q

Colloid represents

A

stored thyroid hormone