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HB2 Final > Week 9 -Endo > Flashcards

Week 9 -Endo Flashcards

1
Q

What are each of these hormones made from:
Peptide?
Steroids?
Amines?

A

peptides- amino acids
steroids- cholesterol
amines- tyrosine

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2
Q

What are steroid hormones synthesized and secreted by?

A
  • adrenal cortex
  • gonads
  • corpus luteum
  • placenta
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3
Q

What are the steroid hormones?

A
  • cortisol
  • aldosterone
  • estradiol and estriol
  • progesterone
  • testosterone
  • 1,25-dihydroxycholecalciferol
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4
Q

What are the amine hormones?

A
  • catecholamines (epi, norepi, dopamine)

- thyroid hormones

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5
Q

Define long loop feedback inhibition.

A

the hormone feeds all the way back to inhibit the hypothalamus

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6
Q

What is the pituitary gland aka?

A

the hypophysis

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7
Q

What functions does the anterior pituitary carry out?

The posterior pituitary?

A
  • anterior: endocrine function

- posterior: neurologic function

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8
Q

What connects the pituitary gland to the hypothalamus?

A

the infundibulum

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9
Q

What does the posterior pituitary secrete?

A
  1. ADH

2. oxytocin

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10
Q

What does the anterior pituitary secrete?

A
  1. TSH (thyroid stimulating hormone)
  2. FSH (follicle stimulating hormone)
  3. LH (lutenizing hormone)
  4. GH (growth hormone)
  5. prolactin
  6. ACTH (adrenocorticotropic hormone)
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11
Q

Why is the blood supply to the hypothalamus unique?

A

most of the blood supply is venous, supplied by long and short hypophysial portal vessels

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12
Q

What cell type secretes TSH?

Where are they located?

A
  • thyrotrophs

- the anterior pituitary

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13
Q

What cell type secretes FSH?

Where are they located?

A
  • gonadotrophs (also makes LH)

- the anterior pituitary

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14
Q

What cell type secretes LH?

Where are they located?

A
  • gonadotrophs (also makes FSH)

- the anterior pituitary

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15
Q

What cell type secretes ACTH?

Where are they located?

A
  • corticotrophs

- the anterior pituitary

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16
Q

What cell type secretes growth hormone?

Where are they located?

A
  • somatotrophs

- the anterior pituitary

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17
Q

What cell type secretes prolactin?

Where are they located?

A
  • lactotrophs

- the anterior pituitary

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18
Q

What is unique about the secretory pattern of growth hormone?

A

secretion occurs in a pulsatile pattern, especially during sleep

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19
Q

What are potent stimulators for growth hormone secretion?

A

hypoglycemia and starvation

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20
Q

What molecule stimulates release of growth hormone?

A

GHRH (growth hormone releasing hormone)

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21
Q

What molecule inhibits release of growth hormone?
What is it released by?
How does it work?

A
  • somatostatin
  • the hypothalamus and pancreas delta cells
  • acts by blocking the action of GHRH on the somatotroph
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22
Q

Why is prolactin usually inactive in non-lactating individuals?

A

prolactin secretion is tonically inhibited by dopamine from the hypothalamus, which overrides the stimulatory effect of TRH/PRH

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23
Q

How does prolactin participate in negative feedback?

A

it inhibits its own secretion by increasing synthesis/secretion of dopamine from the hypothalamus

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24
Q

What is the major hormone concerned with regulation of body fluid osmolarity?

A

ADH

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25
Q

What is ADH aka?

A

vasopressin

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26
Q

What stimulates release of ADH?
Where does it act?
What does it do?

A
  • an increase in serum osmolarity sensed by osmoreceptors in the anterior hypothalamus
  • distal tubules of the kidney
  • increases water absorption
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27
Q

What does the adrenal medulla secrete?

A

catecholamines epinephrine (80%) and norepinephrine (20%)

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28
Q

What is each zone of the adrenal cortex called?

What does each layer make?

A
  1. zona glomerulosa, mineralocorticoids
  2. zona fasciculata, glucocorticoids
  3. zona reticularis, sex hormones (androgens)
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29
Q

What is the basis for the specialization of the layers of the adrenal cortex?

A

the presence or absence of the enzymes that catalyze various modifications of the steroid nucleus

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30
Q

What is the precursor molecule for all things made in the adrenal cortex?

A

cholesterol

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31
Q

What is a primary endocrine disorder a problem with?

A

secretion by the target gland

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32
Q

What is a secondary endocrine disorder a problem with?

A

secretion by the pituitary gland

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33
Q

What is a tertiary endocrine disorder a problem with?

A

secretion by the hypothalamus

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34
Q

What is the metabolic clearance rate of a hormone?

A

the volume of plasma cleared of a hormone per minute

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35
Q

How can hormones be removed from plasma?

A
  1. metabolism or binding in the tissues
  2. hepatic excretion
  3. renal excretion
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36
Q

What is the relative time of onset of action for protein-bound hormones?
What is their relative length of action?

A
  • slower onset

- longer duration of action

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37
Q

Peptide hormones:
Onset fast or slow?
Duration long or short?
Method of action?

A
  • fast
  • short
  • surface binding to activate second messengers or ion channels
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38
Q

Steroid/thyroid hormones:
Onset fast or slow?
Duration long or short?
Method of action?

A
  • slow
  • long
  • alter gene transcription or translation
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39
Q

What class of hormones does the anterior pituitary secrete- peptide, steroid, or amine?

A

peptide

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40
Q

What molecule stimulates the release of TSH?

Any notable negative control?

A
  • TRH (thyrotropin-releasing hormone)

- none

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41
Q

What molecule stimulates the release of ACTH?

Any notable negative control?

A
  • CRH (corticotropin-releasing hormone)

- none

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42
Q

What molecule stimulates the release of FSH?

Any notable negative control?

A
  • GnRH (gonadotropin-releasing hormone)

- none

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43
Q

What molecule stimulates the release of LH?

Any notable negative control?

A
  • GnRH (gonadotropin-releasing hormone)

- none

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44
Q

What molecule stimulates the release of GH?

Any notable negative control?

A
  • GHRH (growth hormone-releasing hormone) (dominant)

- somatostatin

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45
Q

What molecule stimulates the release of prolactin?

Any notable negative control?

A
  • PRH and TSH, but not really

- dopamine/PIF (dominant)

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46
Q

What is dopamine aka?

A

PIF (prolactin inhibiting factor)

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47
Q

What pattern of release do all hypothalamic-pituitary axis hormones exhibit?

A

pulsatile release superimposed on a circadian rhythm

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48
Q

What are the effects of GH?

A
  1. most important endocrine regulator of final body size by stimulating linear growth through stimulation if IGF-1 secretion
  2. opposes the effects of insulin by causing lipolysis in adipose, reducing glucose uptake in muscle, and stimulating gluconeogenesis in the liver
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49
Q

When is the largest release of GH?

What are some other triggers for release?

A
  1. during the first 2 hours of deep sleep

2. stress, hypoglycemia, starvation

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50
Q

What is the largest source of plasma IGF-1?

A

the liver

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51
Q

How is GH secretion turned off?

A

negative feedback from IGF-1

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52
Q

Why is binding hormones to proteins a good thing?

A
  1. increases the half life of the hormone

2. provides a stable reservoir in the blood

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53
Q

What is the primary hormone that controls water balance in the body?

A

ADH

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54
Q

What causes release of ADH?
How much of a change is needed to produce release of ADH?
What receptor does each use?

A
  1. changes in body fluid osmolarity, V2 receptors; increase of only 1%
  2. drops in blood volume, V1 receptors; drop in 15%
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55
Q

How does ADH respond to a drop in blood volume?

A

V1 receptors caused generalized arteriolar vasoconstriction in vascular smooth muscle

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56
Q

What are the major functions of oxytocin?

A
  1. uterine contraction
  2. milk let-down
  3. promotion of maternal behavior
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57
Q

What do thyroid follicles contain?
What, then, is that?
What is it produced by?

A
  • thyroid colloid
  • a protein-rich extracellular material
  • by follicular cells, endocrine cells around each follicle
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58
Q

What is the major protein in thyroid colloid?

What does it contain as part of its primary structure?

A
  • thyroglobulin

- T3 and T4

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59
Q

What must happen before thyroid hormone can be secreted into the blood?

A

follicular cells must uptake and hydrolyze the thyroglobulin-linked T3 and T4 to free them

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60
Q

What are the steps in thyroid hormone synthesis?

A
  1. iodine trapping by follicular cells
  2. thyroglobulin made in follicular cells and secreted into the colloid, and iodonation
  3. conjugation of 2 iodinated tyrosyl gropus to make T3/T4 linked to thyroglobulin
  4. endocytosis back into the follicular cells, hydrolysis of the T3/T4-thyroglobulin to make free T3/4, as well as DIT and MIT (incomplete molecules that are recycled)
  5. T3/4 secreted
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61
Q

How much of the secreted thyroid hormones is T3?

T4?

A

10% is T3

90% is T4

62
Q

Are T3/T4 found free or bound in blood?

Why?

A
  • bound to plasma proteins

- poorly soluble in water

63
Q

What are the T3/T4 binding proteins?

A
  • thyroid binding globulin
  • transthyretin
  • albumin
64
Q

Which has a greater biological activity, T3 or T4?

A

T3

65
Q

How do you get more T3 in tissues if so little is secreted?

How does this happen?

A
  • 75% of circulating T3 is derived from deiodination of T4 in tissues
  • types one and two 5’-deiodinase (type three makes an inactive version of T3)
66
Q

What is the difference between types one, two, and three 5’-deiodinase?

A

type 1- produces T3 in most target tissues (can be regulated)
type 2- expressed in pituitary gland, where locally made T3 augments the negative feedback inhibition of TSH secretion (does not get turned down, really)
type 3- produces reverse T3, which is inactive

67
Q

What changes in the T4/T3 system during starvation that allows homeostasis?

A

type 1 5’-deiodinase production is reduced, allowing a low rate of thyroid hormone secretion, decrease in circulating T3, reducing BMR, and conserving energy stores

68
Q

What are the primary effects of thyroid hormone?

A

Increasing metabolism
Beta adrenergic drive
GI smooth muscle activity

  1. increasing BMR
  2. induce gluconeogenesis
  3. coordinate normal growth and development
69
Q

How do thyroid hormones affect BMR?

A
  • stimulates ‘futile cycles’ that generate body heat
  • increases heat production in brown adipose (neonates only) by uncoupling ox/phos
  • increases expression of B-adrenergic receptors to indirectly increase metabolic rate
70
Q

Will increase in thyroid hormone cause hyperglycemia?

A

No. Even though thyroid hormone causes increased gluconeogenesis, this will be balanced by insulin if the pancreas is properly functional

71
Q

What does TSH do?

A

it stimulates all of the steps in thyroid hormone synthesis and secretion by thyroid follicular cells

72
Q

What can a sustained excess of TSH in the blood cause?

Why?

A
  • hyperplasia of the thyroid

- TSH has a trophic effect

73
Q

How can you tell the difference between primary and secondary hypothyroidism from a blood test?

A
  • primary: low T3/4, high TSH

- secondary: low T3/4 and low TSH

74
Q

How can you tell the difference between primary and secondary hyperthyroidism from a blood test?

A
  • primary: high T3/4, low TSH

- secondary: high T3/4 and high TSH

75
Q

What are symptoms commonly associated with hyperthyroidism?

A

high metabolic rate, weight loss, heat intolerance, sweating, muscle weakness, tachycardia, tremor

76
Q

What are the most common causes of hypothyroidism?

Hyperthyroidism?

A

Hypo- dietary iodine deficiency (most common) or Hashimoto’s thyroiditis
Hyper- secretory tumor or Grave’s disease

77
Q

What type of cells make up the adrenal medulla?

A

chromaffin cells

78
Q

What do chromaffin cells mainly (and minorly) secrete?

What is the stimulus for secretion?

A
  • 80% epi, 20% norepi

- acetylcholine from sympathetic stimulation

79
Q

What do high levels of cortisol in the adrenal glands stimulate?
Why is this important?

A
  • production of epi

- aids in coordination of the stress response

80
Q

What hormone is a mineralocorticoid?

What does it do?

A
  • aldosterone

- regulates electrolyte balance in several organs, particularly the kidney by conserving Na and secreting K

81
Q

What hormone is a glucocorticoid?

What does it do?

A
  • cortisol

- increases blood glucose concentration

82
Q

What is the rate-limiting step in steroid synthesis?

A

conversion of cholesterol to pregnenolone by 20,22 desmolase

83
Q

What enzyme is uniquely required for aldosterone synthesis?

A

aldosterone synthase

84
Q

What enzyme is uniquely required for cortisol synthesis?

A

17a-hydroxylase

85
Q

Which zone of the adrenal cortex is the largest?

A

the zona fasciculata

86
Q

What is the function of cortisol?

A
  • mobilizes glucose via gluconeogenesis
  • reduces cellular metabolism of glucose
  • reduces sensitivity to insulin
  • mobilizes amino acids from muscle
  • mobilizes fatty acids
  • resists the inflammatory/immune responses
87
Q

What stimulates cortisol release?

A

CRH stimulates ACTH stimulates cortisol release

88
Q

How is ACTH made?

What else is made in the process?

A
  • processing of POMC

- MSH (melanin, hunger), Y-lipotropin, and B-endorophin (prior 2 important in reward systems and addiction)

89
Q

What is aldosterone secretion controlled by?

A

angiotensin II, some by K, and weakly by ACTH

90
Q

What does aldosterone do?

A

it maintains fluid balance by conserving Na and excreting K

91
Q

Where is renin produced?

Where is angiotensinogen produced?

A
  • renin made in the kidney

- angiotensinogen is made in the liver

92
Q

What is a secondary stimulus for aldosterone secretion?

How does it work?

A
  • an increase in plasma K

- depolarizes the glomerulosa cell membrane potentials, causing urinary K excretion

93
Q

What is Addison’s disease?

What are the major signs and symptoms?

A
  • adrenocortical insufficiency
  • cortisol deficiency: hypoglycemia, low rates of gluconeogenesis, hypotension (lack of catecholamines), weakness, fatigue, no cortisol in response to stress
  • aldosterone deficiency: hypovolemia and hyponatremia (urinary loss of NaCl and water), and hyperkalemia and metabolic acidosis (from reduced urinary excretion of K and H)
  • androgen deficiency: reduced libido and thinning of pubic hair in females (no effects in males)
94
Q

How can you test the hypothalamic-pituitary-adrenal axis if you suspect adrenocortical insufficiency?

A

using an ACTH stimulation test, where you administer an ACTH analog and see if the serum cortisol levels increase appropriately

95
Q

What is hypercortisolism aka?
What produces the signs/symptoms?
What are the signs/symptoms?

A
  • Cushing’s syndrome (secondary only)
  • excess glucocorticoid
  • hyperglycemia (increased gluconeogenesis)
  • muscle wasting and weakness (protein catabolism)
  • truncal obesity and moon face (redistribution of body fat)
  • hypertension (mineralocorticoid effects of excess glucocorticoids)
96
Q

What is the cause of primary hypercortisolism?

A

adenoma of the adrenal cortex (secretory tumor)

97
Q

What is the cause of secondary hypercortisolism?

A

maybe a pituitary adenoma, or from excess ACTH, or from an ectopic source of ACTH secretion (small cell lung carcinoma)

98
Q

What is the cause of tertiary hypercortisolism?

A

excess CRH

99
Q

What is Conn’s syndrome?
What causes it?
What are the associated symptoms?

A
  • primary hyperaldosteronism
  • an aldosterone-producing adrenal adenoma, causing excessive mineralocorticoids
  • hypertension (excessive retention of Na and fluids by kidney)
  • hypokalemia (increased urinary K excretion)
  • metabolic alkalosis (increased urinary H excretion)
100
Q

Which is more common, primary or secondary hyperaldosteronism?
Why?

A
  • secondary
  • conditions that activate the RAS system (renal artery stenosis, cirrhosis, CHF) are more common than an adrenal adenoma (Conn’s)
101
Q

What is the most common congenital error in adrenal steroid metabolism?
What does it cause?

A
  • 21a-hydroxylase deficiency
  • symptoms of primary adrenal insufficiency (can’t make cortisol or aldosterone)
  • accumulation of adrenal androgens (pathway shunting)
  • adrenal hyperplasia (high levels of ACTH from loss of negative feedback from cortisol)
102
Q

What are epi and norepi derived from?
What is the rate-limiting step in their synthesis?
Where does the final step occur?

A
  • tyrosine
  • conversion of tyrosine to L-dopa by tyrosine hydroxylase
  • only in chromaffin cells
103
Q

What is release of catecholamines controlled by?

A

CNS via sympathetic neurons releasing acetylcholine

104
Q

What stimulates the steps for norepi synthesis?

What stimulates the final enzyme to convert norepi to epi?

A
  • ACTH and sympathetic nerve stimulation

- cortisol delivered via portal blood from the adrenal cortex

105
Q

What is the major product released by the adrenal medulla?

What is the major sympathetic neurotransmitter released?

A
  • epi

- norepi

106
Q

What type of receptors does epi have a greater affinity for?

A

B1 and B2 (although still binds to alpha receptors like norepi)

107
Q

In the stress response, what are catecholamines responsible for?
What is cortisol responsible for?

A
  • catecholamines = short term response: increased cardiac output, bronchodilation, and elevated blood glucose
  • cortisol = long term response: mobilization of glucose, fatty acids, and amino acids, and suppression of the immune system
108
Q

How are catecholamines broken down?

What is the end product, and how is it disposed of?

A
  • COMT and MAO

- vanillymandelic acid (VMA), excreted in the urine

109
Q

How do you assess catecholamine synthesis by the adrenal medulla?

A

measure the levels of catecholamines, metanephrines (intermediate), and VMA in the urine

110
Q

What is the issue with pheochromocytoma?

Associated symptoms?

A
  • a secretory tumor of the adrenal medulla that hypersecretes catecholamines in episodes
  • transient hypertension, palpitations, sweating, increased body temperature, and increase blood glucose
111
Q

Where are endocrine cells located in the pancreas?

What are the major cell types located there, where are they located, and what do they make?

A
  • islets of Langerhans
  • a cells: periphery of islets, secrete glucagon
  • B cells: center of islets (majority), secrete insulin, proinsulin, and C peptide
  • delta cells: in the middle (few), secrete somatostatin
112
Q

How can you tell the difference between too much endogenous insulin (insulinoma) vs overdose of exogenous insulin?

A

Measure C peptide. C peptide and insulin levels will match if the issue is with endogenous secretion.

113
Q

Why is the arrangement of cells in the islets of Langerhans important?

A

Blood flows from the center (B cells) to the periphery (a cells). This allows the insulin to bathe the a cells, thereby suppressing glucagon secretion.

114
Q

When you cleave proinsulin, what are the products?

A

1 insulin and 1 C peptide

115
Q

What effect does insulin have on the liver?

A
  • increases metabolism of glucose as fuel
  • increases storage of glucose as glycogen
  • converts glucose to triglycerides
  • stimulates hepatic protein synthesis (and inhibits breakdown)
116
Q

What effect does insulin have on skeletal muscle?

A
  • increases glucose uptake by stimulating GLUT4
  • increases usage of glucose as fuel
  • increases glycogen synthesis
  • reduces use of circulating triglycerides as fuel (allowing storage in adipose)
117
Q

Which GLUT transporter is insulin sensitive?

Where is it found?

A
  • GLUT4

- skeletal muscle and adipose tissue

118
Q

What effect does insulin have on adipose tissue?

A
  • stimulates glucose uptake via GLUT4
  • increases glucose storage as triglycerides
  • increases expression of lipoprotein lipase, which releases fatty acids from circulating CM and LDL, so they can be stored as triglycerides
119
Q

What effect does insulin have on ion balance?

A

insulin increases cellular uptake of K

120
Q

How would you rapidly treat a patient with hyperkalemia?

A

insulin infusion (to bring K down) with glucose infusion (to prevent hypoglycemia)

121
Q

What is an important determinant of the cellular response to insulin?
In what population is this in jeopardy?

A
  • the number of available insulin receptors, the receptor tyrosine kinase
  • obesity can reduce expression of insulin receptors
122
Q

What is the primary regulator of insulin secretion?

A

blood glucose concentration

123
Q

What are the steps in the stimulation of insulin secretion in B cells?

A
  1. glucose taken up via GLUT2 to make ATP
  2. increases in cellular ATP/ADP ratio inhibits ATP-sensitive K channels, depolarizing the membrane
  3. this activates voltage-sensitive Ca channels, causing influx of Ca
  4. Ca-induced Ca release from ER triggers exocytosis of granules containing insulin
124
Q

What do sulfonylureas do?
How do they work?
What is a limitation?

A
  • stimulate release of stored insulin, reducing blood glucose
  • bind and inhibit the ATP-sensitive K channels (artificially starting the process)
  • they do NOT cause increase in insulin synthesis
125
Q

What things stimulate insulin release?

A
  1. blood glucose rise
  2. increase in arginine, leucine, or lysine
  3. GIP and GLP-1 (from small intestinal response to glucose)
126
Q

What are the major incretins?

What is their role?

A
  • GIP and GLP1

- minimize spikes in blood sugar

127
Q

What can be made from preproglucagon?

What cells makes them?

A
  • alpha cells make glucagon

- intestinal L cells make GLP-1

128
Q

What organ is the main target for glucagon?
What is its primary effect?
What can glucagon do during starvation (high concentrations)?

A
  • the liver
  • to increase hepatic production of glucose (stimulated via gluconeogenesis and glycogenolysis) and ketones
  • stimulate lipolysis in adipose and proteolysis in muscle to maintain substrate supply
129
Q

What are the major ketones?

How do you make them?

A
  • B-hydroxybutyrate and acetoacetic acid

- The breakdown of fatty acids gives off lots of acetyl CoA’s. Put 2 together to make a ketone.

130
Q

What is glucagon secretion stimulated by?

Inhibited by?

A
  • hypoglycemia, protein (especially arginine and alanine)

- hyperglycemia and insulin

131
Q

If you eat only protein, how do insulin and glucagon levels change?

A

both increase, keeping the ratio comparable

132
Q

What things rapidly counter hypoglycemia?

What things support a sustained response to hypoglycemia?

A
  • rapid: glucagon and catecholamines

- sustained: cortisol and GH

133
Q

Why are Ca and phosphate homeostasis linked?

A

they are both present in hydroxyapatite crystals, which form the major mineral component of bone

134
Q

Why is Ca important?

A

it is necessary for bone structure, muscle contraction, exocytosis, intracellular signaling, and nerve conduction

135
Q

What processes put Ca and phosphate into the circulation?

What processes take them out?

A
  • IN: GI inputs and resorption of bone

- OUT: renal excretion and bone formation

136
Q

In what forms does Ca exist in plasma?

A
  • 45% as free ionized Ca (tightly regulated levels)
  • 45% bound to plasma proteins, especially albumin
  • 10% complexed with low molec weight ions, like citrate and oxalate
137
Q

How does the acid/base status of a patient affect free Ca in the blood?

A

by changing the Ca’s ability to bind to protein, as H competes with Ca to bind to albumin in acidic states

138
Q

Metabolic acidosis can cause hyper- or hypo-calcemia?

A

hypercalcemia

139
Q

In what forms does phosphate exist in plasma?

A
  • 80% as alkaline phosphate (HPO₄²⁻) at normal pH

- 20% as acid phosphate (H₂PO₄⁻)

140
Q

Which concentration is more tightly regulated in the plasma, Ca or phsophate?

A

Ca

141
Q

What exerts dominant control of Ca and phosphate homeostasis?
Secondary control?
Minor control?

A
  • PTH
  • vitamin D
  • calcitonin
142
Q

What produces PTH?

A

chief cells of the parathyroid gland

143
Q

What does PTH do?

What is the net effect?

A
  1. stimulates bone resorption, adding Ca and phosphate to plasma
  2. decreases renal Ca excretion
  3. increases renal phosphate excretion
    (4. stimulates the final step in vit D synthesis in the kidney)
    - increase plasma Ca and decrease plasma phosphate
144
Q

How is PTH secretion controlled?

A
  • decrease in plasma free Ca (sensed by CaSR) is the most potent stimulus for PTH secretion
  • prolonged increase in plasma phosphate stimulates PTH secretion
  • vit D has a negative feedback action on PTH secretion
145
Q

Where does activation of vitamin D take place?

What stimulates the activation?

A
  • in the kidney by 1-hydroxylation

- strongly by PTH, somewhat by low plasma phosphate concentration

146
Q

What is the activated form of vitamin D called?

What is its function?

A
  • calcitrol

- simulation of dietary Ca and phosphate absorption in the small intestine (and kidney)

147
Q

What makes calcitonin?
What stimulates its production?
What does it do?

A
  • parafollicular cells in the thyroid
  • hypercalcemia
  • probably nothing in humans, as it has a weak effect on Ca and phosphate homeostasis
148
Q

What are the general signs and symptoms associated with hypercalcemia?

A

“bones, stones, moans, groans, and psychiatric overtones”

  • bones: bone pain
  • stones: kidney stones
  • moans: abdominal pains from constipation or pancreatitis
  • groans: general malaise and weakness
  • psychiatric overtones: depression, delirium, and coma
149
Q

What is Metabolic Syndrome?

What does it put you at a higher risk for?

A
  • type 2 diabetes, hypertension, and hyperlipidemia

- cardiovascular disease and stroke

150
Q

What do acidophils secrete?

Where are they located?

A
  • GH and prolactin

- the anterior pituitary

151
Q

What do basophils secrete?

Where are they located?

A
  • FSH, LH, ACTH, TSH (FLAT Back)

- the anterior pituitary

HB2 Final (5 decks)

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