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FHB - Endocrinology (by Richie) > Review Session "Must Knows" > Flashcards

Review Session "Must Knows" Flashcards

1
Q

TH functions like

A

steroid hormone

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2
Q

Steroid hormones act via

A

transcriptional effects

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3
Q

GHRH produced in what nuclei?

A

Arcuate nucleus

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4
Q

GnRH produced in what nuclei?

A

POA

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5
Q

CRH produced in what nuclei?

A

PVN (parvocellular division)

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6
Q

TRH produced in what nuclei?

A

PVN

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7
Q

Somatostatin produced in what nuclei?

A

PeVN

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8
Q

Name 2 hypothalamic releasing hormones manufactured in the PVN

A

CRH and TRH

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9
Q

Does prolactin have a hypothalamic releasing factor?

A

No. It’s under tonic inhibitory control of dopamine.

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10
Q

Under pathological conditions, excessive TRH can stimulate

A

Prolactin

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11
Q

Prolactin is a potent inhibitor of

A

GnRH

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12
Q

SS inhibits GH release at the

A

anterior pituitary

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13
Q

SS inhibits GHRH pulsatility at the

A

hypothalamus

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14
Q

Name 2 hormones produced by acidophiles

A

Prolactin, Growth Hormone

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15
Q

Name 4 hormones produced by basophiles

A

FSH
LH
ACTH
TSH

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16
Q

AVP-secreting magnocellular neurons are derived from what brain nuclei?

A

SON and PVN

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17
Q

AVP-secreting parvocellular neurons are derived from what brain nucleus?

A

PVN

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18
Q

What are the two divisions of the PVN?

A

Magnocellular and parvocellular

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19
Q

AVP-secreting magnocellular neurons regulate

A

Water balance

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20
Q

AVP-secreting parvocellular neurons regulate

A

stress

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21
Q

What happens to the zona fasciulata under exogenous corticosteroid treatment (long-term)

A

atrophy

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22
Q

What’s the precursor gene for ACTH and alpha-MSH

A

POMC

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23
Q

Small cell lung carcinomas can secrete

A

excess ACTH

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24
Q

Kd refers to hormone affinity or specificity to receptor?

A

Affinity

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25
Q

Receptor kinases versus receptor linked kinases

A

Receptor kinases have intrinsic kinase activity; linked don’t.

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26
Q

Name hormones that bind receptor-linked kinases (3)

A

GH
Prolactin
EPO

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27
Q

Name hormones that bind regular receptor kinases (3)

A

Insulin
IGF-1
ANP

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28
Q

Recite the melatonin synthesis pathway

A

Tryptophan to 5-HTP via tryptophan hydroxylase (RLS). 5-HTP to 5HT. 5HT to melatonin through N-acetyltransferase (RLS for melatonin, in PINEAL gland).

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29
Q

Recite the dopamine synthesis pathway

A
  1. Tyrosine

…tyrosine hydroxylase (RLS)….

  1. X-Dopa (L-Dopa is active)
  2. Dopamine

…dopamine B-hydroxylase (ACTH promotes)…

  1. Norepinephrine

…PMNT (cortisol promotes)…

  1. Epinephrine
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30
Q

Where is melatonin synthesized

A

pineal gland

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31
Q

PRIMARY lesion in thyroid gland will show up as…

A

High basal TSH, since no T3/4 to negatively feedback on a. pit

Responsive to TRH challenge

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32
Q

SECONDARY lesion in pituitary gland will show up as what, on the TRH test?

A

Low baseline TSH, unresponsive to TRH challenge

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33
Q

High GnRH pulse releases

A

LH at ant. pit

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34
Q

Low GnRH pulse releases

A

FSH at ant. pit

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35
Q

Where is the hypophyseal portal system? Whats the blood supply?

A

Ant. pit, superior hypophysial artery.

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36
Q

Kallman’s

A

GnRH can’t migrate

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37
Q

Lesion to adenohypophysis. What kind of hormones impaired?

A

FLAT (basophile 10%) PiG (acidophile 40%)

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38
Q

2 main causes of central diabetes insipidus?

A

Etiology: 2 main causes

  1. Decreased AVP release – most common defect
    Hypothalamic or pituitary defect due to trauma, cancer, or infectious disease.
  2. Decreased renal responsiveness to AVP
    Genetic: X-linked mutation in AVP type-2 receptor – 90% males Acquired: lithium treatment, hypokalemia AVP levels are normal in these cases.
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39
Q

The secretion of which hormones is suppressed by somatostatin?

A

GH and TSH!

Note: TH promotes GH release. They’re connected.

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40
Q

SS14 is made where?

A

Brain. This is the one that suppresses GH and TSH.

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41
Q

SS28 is made where?

A

Intestines.

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42
Q

What are burin, PC1, PC2?

A

The endopeptidases Furin, PC1, and PC2 aid in processing of the mature SS28 and SS14.

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43
Q

GH acts on effectors cells through what pathway?

A

JAK-STAT

44
Q

Name 4 inhibitors of GH release

A

SS28, IGF1, Free fatty acids, Glucose

45
Q

Name 4 promoters of GH release

A 
GHRH
Hypoglycemia
Catecholamines (exercise)
Amino acids 
Thyroid hormone
46
Q

GH effect on adipose?

A

Via Jak/STAT:

Decrease glucose uptake (keeps GLUT4 intracellular), increase lipolysis

47
Q

GH effect on muscle cells?

A

Via Jak/STAT:

Decrease glucose uptake (keeps GLUT4 intracellular)

48
Q

GH effect on liver?

A

Via JAK/STAT:

Increase RNA synthesis
Increase protein synthesis
Increase gluconeogenesis
Increase IGF BP
Increase IGF
49
Q

IGF-1 effect on bone, heart, lung, chondrocytes?

A

Increase protein synthesis
Increase RNA/DNA synthesis
Increase cell size/number
GROWTH

50
Q

IGF-1 effect on muscle? **

A

Increase amino acid uptake
Increase protein synthesis

(it acts like insulin at muscle)….but it is INSULIN DEPENDENT…glut 4…need energy to power the growth of muscle!

51
Q

Diabetes type 1 eats a steak. What will happen?

A

GH is released (free AA’s) but no insulin, so no IGF-1. So starvation amidst plenty.

52
Q

What is the rate limiting step of steroid hormone synthesis? What hormone regulates this step?

A

Steroidogenic regulatory protein (StAR), which transfers the free cholesterol from the outer to the inner mitochondria. This is RLS. This is promoted by ACTH.

53
Q

What does does p450cc catalyze?

A

p450cc is desmolase.

Free cholesterol to pregnenalone.

54
Q

Prednisone

A

More potent GC effect, than MR effect.

55
Q

Why does prednisone not increase blood pressure?

A

Because it acts on GC receptors not MR.

56
Q

Cortisol: MR or GR potency?

A

1:1

Equal potency for both! That’s why we need 11-Beta-HSD2 to convert it to cortisone, lest it activates the MR receptor!

57
Q

Which has a stronger GR activity: prednisone or methylprednisone?

A

Methylprednisone

58
Q

What drug has zero MR relative potency?

A

Dexamethasone

59
Q

What drug has more MR potency than GC potency?

A

Fludrocortisone

60
Q

Fludrocortisone. 1st thought?

A

MR»»»GR

61
Q

Dexamethasone. 1st thought?

A

No MR potency! All MR!

62
Q

Prednisone and methylprednisone. 1st thought?

A

GR»»MR. Methylprednisone is stronger than regular prednisone.

63
Q 
Which of the following will raise your BP the most?
A. Cortisol
B. Prednisone
C. Methylprednisone
D. Dexamethasone
E. Flurdocortisone
A

E

64
Q

11BHSD2 is blocked by carbenoxolone. Or too much licorice. Effect?

A

Excess MR activation. High BP, high Na and H20 retention.

65
Q

Local cortisol production by what enzyme?

A

11-beta-HSD1

Novel DMT2 target

66
Q

Blood from capsular artery sees steroid hormones in what order?

A

Mineralocorticoids, glucocorticoids, androgens, catecholamines (not a steroid hormone)

67
Q

What are the direct and indirect ways that cortisol suppresses inflammation?

A

Direct: cortisol-GR directly sequesters NFK-B so it can’t transcribe TNF-alpha

Indirect: Cortisol-GR increases transcription of IkB, which then sequesters NFK-B so it can’t enter nucleus

68
Q

Cortisol increases transcription of proteolysis via what factors?

A

E3 ubiquitin ligase

MuRF-1

69
Q

How do BOTH hypo and hyperthyroidism lead to goiter?

A

Hypothyroidism: low T3/T4 due to lack of iodine, or TPO defect, or hashimotos. Results in lack of negative feedback on TSH secretion from basophils in ant. pituitary, thus lots of TSH.

Hyperthyroidism: high T3/T4 due to too much stimulation by TSH or autoantibodies to TSH-R (grave’s disease).

70
Q

Why don’t you want to use aspirin for thyroid storm?

A

Aspirin suppresses thyroid binding globulin, increasing T3/4 levels

71
Q

2 types of parathyroid cells

A

Chief cells - make PTH

Oxyphil cells - unknown function

72
Q

Hashimoto’s

A

Auto-antibodies destructive to thyroid tissue

73
Q

KEY OBESITY STATISTICS

A

BMI>30 (at least 20% of population)
Waist:hip > 0.95 in men
Waist:hip > 0.85 in women

74
Q

Metabolic syndrome X statistics

A

4 requirements

  1. Dyslipidemia (TG>150mg/dl, HDL135/80)
  2. Visceral obesity
    (waist>40in in men, >35in women)
  3. Insulin resistance (fasting glucose > 100mg/dl)
75
Q

PPAR-gamma agonists

A

TZD - used for insulin resistance and T2DM

(aka avandia)

Induces differentiation of adipocytes, increase fat storage, and weight gain side effect.

76
Q

Hypothalamic appetite modulators

A

Stimulators: Neuropeptide Y, AGRP

Inhibitors: aMSH, CART

77
Q

Best measure for diabetes

A

HbA1C (glycosylated RBC)

78
Q

In the follicular phase, what two hormones are inhibiting anterior pituitary release of FSH/LH?

A

Inhibin and estrogen from ovary

79
Q

In the ovulatory phase, something special happens with estrogen

A

Surpasses threshold amount and switches from negative to positive feedback to ant. pituitary, promoting LH/FSH surge.

80
Q

In the Luteal phase, the follicle reorganizes into the corpus luteum, which begins making…

A

E2 and progesterone. Strong negative feedback to anterior pituitary (LH/FSH) and hypothalamus (GnRH)

81
Q

What marks the beginning of a new menstrual cycle?

A

absent hCG, and LH, E2, and progesterone, promotes sloughing of endometrium (bleeding/menses)

82
Q

Theca cells (female) come from same progenitor as their male counterpart….

A

Leydig cells (spermeogenesis support)

Theca cells don’t have aromatase…they help granulosa cells make estrogen.

83
Q

Granulosa cells (female) come from the same progenitor as their male counterpart…

A

Sertoli cells

Granulosa cells make the estradiol because they have aromatase.

84
Q

Female phenotype, no uterus

A

XXY klinefelters.

MIF from sertoli cells degraded mullein ducts.

85
Q

Give an example of male pseudohermaphroditism

A

Phenotypically female, with testes.

86
Q

If T too low in development

A

excess gonoadotropic signalling promotes scar tissue formation on testes

87
Q

Larynx enlargement is due to action of

A

Testosterone

88
Q

Where does in the seminiferous tubule does spermatogenesis occur, anatomically?

A

BASAL COMPARTMENT of seminiferous tubule –> blood testes barrier –> inner seminiferous tubule –> lumen of tubules

89
Q

Are spermatogonia inside or outside the blood-testes barrier?

A

Outside! Once the first meiotic division starts, the spermatogonium turns into a “primary spermatocyte” that crosses the blood-testes barrier!

90
Q

Leading cause of female infertility

A

Female infertility quadruples between 20 and 40 years old. Also:

PCOS (polycystic ovarian syndrome). Root cause of PCOS is insulin resistance and androgen production (causing infertility)…and increased conversion to estrogens (weight gain)….sleep apnea, hirsuitism…

91
Q

Leading cause of male infertility

A

androgen deficiency: inadequate production or action of T, promotes poor spermatogenesis. Or defects in seminal tract. Idiopathic oligospermia.

Note: infertility doesn’t mean impotence (erectile dysfunction)

92
Q

What is the role of CRH during parturition?

A

CRH potentiates contracture response to prostaglandins and oxytocin.

93
Q

Decrease in Progesterone/E2 ratio

A

promotes contractions

94
Q

Increase in E2/Progesterone ratio

A

promotes contractions

95
Q

Increase in Progesterone/E2 ratio

A

promotes quiescence

96
Q

Decrease in E2/progesterone ratio

A

promotes quiescence

97
Q

Inhibin B

A

secreted by follicular cells. negative regulation of LH/FSH

98
Q

Inhibin A

A

secreted by corpus luteum. negative regulation of LH/FSH

99
Q

Paracrine effect of inhibin, on theca cells

A

PROMOTES androgen production in inhibin cells. remember that inhibin lacks aromatase, which is why it makes androgens (androstenedione) for later aromatization at the granulosa cell

100
Q

What is TCF72?

A

most highly associated genetic polymorphism…T2DM

101
Q

what does insulin do to serum K and Pi levels?

A

Decreases K and Pi (increases uptake into the cell; indirect stimulation of Na/K pump)

102
Q

Effect of insulin on HCO3- and pH?

A

increases HCO3-

Increases pH

103
Q

Effect of insulin on lipolysis and ketone bodies

A

Stops lipolysis, so no more substrates for ketone body synthesis, so no ketoacidosis and thus no left shift in equilibrium towards CO2,

104
Q

AVP potentiates the effect of

A

CRH (think AVP pertains to stress)

105
Q

Insulin counter-regulatory hormones

A

GH
Cortisol
Glucagon
Catecholamines

106
Q

PCB

A

competes with thyroid hormone binding to TBG. Increases TH production

107
Q

DES

A

Non-steroidal estrogen

DES daughter tragedy

FHB - Endocrinology (by Richie) (24 decks)

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