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Fundamentals Part 2 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What are some examples of the derivative tyrosine

A

epi, norepi, and thyroxine

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2
Q

An increase in functioning of target cell which send which type of feedback to the endocrine gland (positive/negative?)

A

negative

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3
Q

how would negative feedback alter the rate of releasing hormone

A

decrease

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4
Q

What is one example of the positive feedback resulting in increased hormone release

A

Dilation of cervix during labor, stimulates post. pituitary to secrete more oxycotin=more dilation

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5
Q

what receptor type is usually amplifying hormone signal

A

G-protein coupling (cAMP, cGMP, phospholipase C, Ca++, calmodulin)

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6
Q

What type of hormone acts by entering the cell and binding to an intracellular receptor.

A

Steroids

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7
Q

What is the result of a steroid binding with a intracellular receptor?

A

activates a gene, causing transcription, translation of proteins.

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8
Q

Which hormone-receptor system would elicit a faster response between cell surface or intracellular?

A

cell surface (such as G-protein)

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9
Q

Would epinephrine or prednisone cause a more immediate response

A

epi

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10
Q

What is the anterior pituitary also called

A

adenohypophysis

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11
Q

Where is the anterior pituitary or adenohypophysis derived from

A

embryonic cells from the oral cavity(Rathke’s pouch)

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12
Q

Embryonic cells from Rathke’s Pouch is responsible for producing:

A

the anterior pituitary

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13
Q

Neurohypophysis is another name for which component of the endocrine system

A

posterior pituitary gland

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14
Q

How is the posterior pituitary gland produced

A

formed by down growth of cell axons from the 3rd ventricle

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15
Q

Histamine that is released by mast cells diffuse into the ECF to the stomach and influence gastric parietal cells to secrete H+. This is an example of what type of signaling system

A

paracrine

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16
Q

Where are the neuron cell bodies that produce ADH & oxytocin

A

supra optic & paraventricular nuclei of the hypothalamus

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17
Q

How does the hypothalamus link to the anterior pituitary gland

A

through the hypothalamic-hypophysial portal blood vessels

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18
Q

Describe the portal system seen in the anterior pituitary gland

A

capillary beds connected via veins

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19
Q

Why would you pee a lot after drinking alcohol?

A

inhibits ADH release

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20
Q

Pain, nausea, hypoglycemia would cause what to ADH

A

stimulate release of ADH

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21
Q

What does ADH regulate:

A

osmolarity in the body

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22
Q

What cells do ADH act on increasing H2O reabsorption

A

principle cells in the distal renal tubules & collecting ducts

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23
Q

This hormone is responsible for uterine contraction, milk production, and ejection

A

oxytocin

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24
Q

This hormone can help reduce postpartum bleeding

A

ocytocin

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25
Q

HOw many hormones are produced by the Anterior pituitary gland

A

6 GH, TSH, LH, FSH, ACTH, Prolactin

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26
Q

Whats the difference between the anterior and posterior pituitary glands

A

portal vein system

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27
Q

How many cells are responsible for producing the hormones of the anterior pituitary? list them

A

5, somatotrophin(GH) thyrotrophes(TSH), gonadotrophes(FSH & LH) corticotrophs(ACTH) lactotrophs (prolactin)

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28
Q

HOw is prolactin inhibited from being released

A

dopamine

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29
Q

What is pregnancies effect on prolactin (specifically the high levels of estrogen/progesterone?

A

inhibits action of prolactin

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30
Q

What is galactorrhea

A

milk production unassociated with pregnancy/nursing.

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31
Q

what causes galactorrhea

A
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32
Q

How could we treat galactorrhea if it was a result of destructed dopamine

A

dopamine agonist (bromocriptine)

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33
Q

what is the ‘pulsatile release’ refer to in regards to the growth hormone

A

the largest burst occurs within the 1st hour of falling asleep

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34
Q

Why is T3 secreted from the thyroid gland have a “steady-state”

A

highly protein bound (not active when bound), with a long half life

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35
Q

acromegaly would result from a problem in which gland

A

pituitary

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36
Q

what is the mechanism of Grave’s Disease

A

an autoimmune disorder results from antibodies that act against TSH receptors; result in an increased release of T3/T4

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37
Q

describe what you would see in someone who has myxedema

A

puffiness of skin, non-pitting edema, pleural, cardiac effusions

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38
Q

what pathology would myxedema be associated with?

A

Hypothyroidism

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39
Q

Would you expect the T3/T4 levels to be high, low, or the same with someone who is diagnosed with Grave’s Disease

A

Raised

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40
Q

Cretinism causing a look of thick, pale skin with a floppy tongue is caused by what

A

lack of TSH within the thyroid

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41
Q

What is a classic presentation of iodine deficiency

A

Goiter (high TRH, high TSH, low T3/T4)

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42
Q

What are you to see with the TRH, TSH, and T3/T4 levels with a pituitary adenoma

A

Low TRH, high TSH, high T3/T4

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43
Q

What findings would be seen in Grave’s Disease (TRH/TSH/T3/T4) levels

A

Low TRH, low TSH, high T3/T4

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44
Q

The adrenal medulla is responsible for the production of

A

catecholamine

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45
Q

What are the catecholamines produced in the adrenal medulla

A

epinephrine and norepinephrine

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46
Q

the adrenal cortex is responsible for

A

steroid hormones

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47
Q

The three cortical adrenal layers include:

A

zona reticularis, zona fasciculate and zona glomerulosa

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48
Q

What is zona resicularis responsible for

A

androgens

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49
Q

what is zona fasciculate do

A

glucorticoids (cortisol)

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50
Q

what is zona glomerulosa do

A

mineralocorticoids (aldosterone)

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51
Q

what the difference in release of mileralocorticoids (aldosterone) when compared to androgens & glucorticoids (cortisol)

A

it is controlled by the RAAS system whereas the latter two are produced AND released by ACTH

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52
Q

What is one thing to be aware of when reading lab results on hormone levels (hint what does it measure)

A

they measure immunologic amounts NOT biological activity hence the #’s may be normal, but that doesn’t necessarily mean they are functional

53
Q

In terms of concentration- how do the hypothalamic releasing hormones compare with the hormones released into the systemic circulation?

A

They are much more highly concentrated

54
Q

how would alcohol and or ANP affect ADH

A

inhibit the release

55
Q

What controls the pituitary to release ADH

A

osmoreceptors in the hypothalamus, barorecptors in the aortic arch, L atrium, and carotid artery sense hypovolemia/hypervolemia also signaling the hypothalamus via vegas nerve

56
Q

where are the baroreceptors located that are responsible for sensing hypo/hyper volemia

A

aortic arch, L atrium, and carotid artery

57
Q

how do baroreceptors signal the hypothalamus neuronally to increase/decrease ADH secretion

A

via the vegas nerve

58
Q

HOw would you describe nephrogenic DI (diabetes insipidus)

A

loss of osmolar gradient so the loop of Henle can’t concentrate the urine

59
Q

how would you describe Central DI

A

no ADH is released from the brain

60
Q

Oat cell carcinoma of the lung is a condition closely associated with SIADH…. how could you explain these similarities

A

Low Na+ serum

61
Q

this hormones actions are mediated through somatomedins

A

Growth Hormone

62
Q

what acts as a type of negative feedback for growth hormone

A

somatostatins

63
Q

what are 4 actions that growth hormone causes

A

increases linear growth in bones
increases protein synthesis
promotes utilization of fats as energy and this leads to a type of diabetogenic (increase in insulin resistance)

64
Q

How would starvation, fasting, and exercise affect the rate of Growth Hormone secretion

A

it would increase (may utilize fat stores for energy)

65
Q

Which hormone is responsible for lactogenesis

A

prolactin

66
Q

this hormone is responsible for breast development at puberty & pregnancy

A

prolactin

67
Q

This hormone inhibits ovulation by inhibiting gonadotrophin-releasing hormone

A

prolactin

68
Q

Secondary to spermatogenesis, infertility in males can be caused by excess of this hormone

A

prolactin

69
Q

If a patient were to present to you with a headache and galactorrhea, we can assume?

A

pituitary adenoma

70
Q

A failure to lactate or “empty sella syndrome” would cause us to believe what condition

A

prolactin deficient

71
Q

what is empty sella syndrome

A

the pituitary has shrunk so the bony saddle appears partially empty

72
Q

This hormone stimulates development of follicles in the ovary and spermatogenesis

A

follicle stimulating hormone

73
Q

this hormone stimulates development of corpus luteum in the ovaries & testosterone secretion from the Leydig cells of testis

A

Luteinizing hormone

74
Q

luteinizing & FSH are both under control of

A

gonadotrophin releasing hormone

75
Q

Whats the more active form between T3/T4

A

T3

76
Q

the thyroid hormone is contained primarily:

A

thyroglobulin

77
Q

this hormone is comprised of a large number of follicles that are filled with colloid material

A

thyroid

78
Q

This hormone is actually apart of a family including MSH, Beta-endorphin and alpha/beta lipotropin

A

ACTH

79
Q

ACTH produces & stimulates to secrete these two hormones? from these zona’s? in the adrenal cortex

A

cortisol from zona fasciculate & androgens from the zona reticularis

80
Q

What stimulates the secretion of the ACTH from the anterior pituitary

A

the corticotrophin releasing hormone (CRH) from the hypothalamus

81
Q

glucocorticoids/androgens are secreted pulsatile and diurnal, how do you best explain this?

A

Peak release is in early morning. Diurnal=daily

82
Q

this test is a method evaluating the functioning of the pituitary-adrenal axis

A

dexamethasone suppression test (DST) a blood test to measure cortisol levels in the adrenal gland, often diagnose Cushing syndrome

83
Q

This hormone stimulates gleuconeogenesis & glycogen storage

A

cortisol

84
Q

This hormone is an antiinfammatory inhibiting prostaglandins, leukotrienes/histamines/serotonin

A

glucocorticoids (cortisol)

85
Q

this hormone suppresses the immune response & inhibits bone formation

A

cortisol

86
Q

this hormone maintains vascular response to catecholamines & increases GFR

A

cortisol

87
Q

What mechanism of aldosterone’s function would cause metabolic alkadosis

A

increased secretion of H+

88
Q

An abnormal function in the DHEA (dehydro-epiandrosterone) in a female would cause what charecteristic

A

masculinization

89
Q

Addison’s disease is associated with which gland

A

adrenal cortex

90
Q

What is the difference between primary and secondary adrenal insufficiency

A

primary is failure of the gland itself whereas secondary is failure to stimulate the gland

91
Q

How could we have primary destruction of the adrenal gland

A

autoimmune disease, metastatic lung cancer

92
Q

Hyperpigmentation of the nails/hands and gumlines would be associated with this disease

A

Addison’s

93
Q

In a secondary cause of insufficient adrenal hormones, a pituitary hormone would lack this which would also be a sign to rule out primary

A

no hyperpigmentation

94
Q

these symtpoms would be seen in both primary and secondary causes of adrenal insufficiency (Addison’s desease)

A

hypoglycemia, anorexia, and weakness.

95
Q

This one symptom would help determine as to whether Addison’s disease is caused by a primary or secondary failure

A

hyperpigmentation

96
Q

If you had insufficient cortisol secretion with no sign of hyperpigmentation, we could assume the problem is

A

a pituitary tumor

97
Q

What are the hallmark signs of Cushing Syndrome

A

Round Face, Buffalo Bump, abdominal striae, hyperpigmentation, HTN, Hyperglycemia

98
Q

What are some causes of Cushing Syndrome

A

excess cortisol caused by pituitary adenoma, adrenal adenoma, and iatrogenic

99
Q

What is the most common cause of Cushing Syndrome in developed countries?

A

iatrogenic causes

100
Q

In Empty Sella Syndrme ( a secondary hypothyroidism) what are the TRH, TSH and T3/T4 levels

A

High TRH, Low TSH, Low T3/T4

101
Q

If there are low levels of T3/T4, caused by a problem in the hypothalamus. How would you see the TRH & TSH levels

A

low TRH low TSH

102
Q

Estrogen and Progesterone are a negative feedback for what hormones?

A

they act on hypothalamus to inhibit FSH & LH

103
Q

HOw does the FSH & LH act to increase estrogen and progesterone?

A

it acts on ovaries to make it

104
Q

Insulin dependent diabetes mellitus refers to which type

A

Type I

105
Q

What is the mechanism of Type I DM

A

Beta cells are destroyed so u have inadequate insulin secretion

106
Q

Polyuria, polydipsia and polyphagia are hallmark signs of this problem

A

high glucose levels in Type I DM

107
Q

what is ketoacidosis

A

increased use of fatty acids/amino acid for energy particularly in Type I DM

108
Q

Insulin is produced by which type of cells

A

beta cells

109
Q

How can you explain hyperkalemia in a type I diabetic

A

since insulin promotes the uptake of K+ into the cell, Type I diabetics don’t make adequate insulin and hence more K+ is left outside the cells

110
Q

What would u assume is the problem if a patient presets with fruity smelling breath

A

They are experiencing ketoacidosis and may have Type I diabetes

111
Q

What are three things that can increase Insulin secretion

A

GIP (gastric inhibitory peptide) GLP-1 (glucagon like peptide) and sulfonylureas

112
Q

Why would Metformin help treat Type II diabetics (think what their pathophys is)

A

improves tissues usage of insulin…. counteracts the “insulin resistance

113
Q

Which type of diabetes is described as insulin resistance

A

Type II (make enough insulin, but cells don’t utilize it)

114
Q

If you were to treat a hyperkalemic patient with a normal blood glucose level, which pairing of treatment could u use

A

insulin with glucose

115
Q

What opposes insulin and is referred to as the Hormone of Starvation

A

Glucagon

116
Q

What 3 things does Glucagon act on

A

gluceoneogenesis, Glycogenolysis, increased lipolysis

117
Q

Somatostatin

A

acts as a “stop” for growth hormone release produced by hypothalamus; stimulated by ingestion of food

118
Q

What are the hallmark signs of hypocalcemia

A

hyperreflexia, muscle cramping, spontaneous twitching, tingling & numbness, Chvostek sign, and Trosseau sign

119
Q

hallmark signs of hypercalcemia

A

polyuria, polydipsia, hyporeflexia, constipation, lethargy, coma, and death

120
Q

What is the Chvostek sign

A

twitching of facial muscle caused by tapping o facial nerve

121
Q

What is the Trosseau sign

A

carpopedal spasm with inflation of BP cuff

122
Q

How can Chronic Renal failure be caused/linked to problems with parathyroid hormone?

A

It is a secondary form of hyperparathyroidism

123
Q

How can you have a vitamin D deficiency even if you are getting enough from the sun or your diet? (how is it processed)

A

Vitamin D is inactive until it is first synthesized by the liver and modified by the kidney. The kidney can make it active (1,25-dihydroxycholecalciferol) or inactive based on body needs

124
Q

What is the hallmark Vitamin D deficient condition

A

Rickets in children

125
Q

What can you use to treat a mild form of hyperparathyroidism? It also can help treat renal failure

A

Calcitonin

126
Q

How does Calcitonin work to treat hyperparathyroidism?

A

opposes action of PTH, lowering serum Ca++ levels and stimulates deposition of bone when serum Ca++ high.

127
Q

What causes Conn’s Syndrome

A

primary hyperaldosteronism

128
Q

What are some symptoms of Conn’s Syndrome

A

increase in ECF volume HTN, hypokalemia, metabolic alkalosis

129
Q

What is spironolactone’s mechanism if given to treat Conn’s Syndrome

A

an aldosterone antagonist

Fundamentals Part 2 (8 decks)

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