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Endocrine > Lopez Review > Flashcards

Lopez Review Flashcards

1
Q

Adenylyl cyclase mechanism

A

E.g. ACTH, LH, FSH, TSH, glucagon

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2
Q

Phospholipase C mechanism

A

E.g. GnRH, TRH, GHRH,

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3
Q

hormone-receptor complex works as a transcription factor that regulates the rate of transcription of a gene

A

E.g. thyroid hormones, glucocorticoids, aldosterone, estrogen, testosterone bind to receptor intracellularly and then bind to the SRE site on the DNA

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4
Q

The connections between the hypothalamus & anterior lobe are

A

The connections between the hypothalamus & anterior lobe are both neural & endocrine!

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5
Q

The connections between the hypothalamus and the posterior pituitary is

A

neural

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6
Q

1° endocrine disorder:

A

1° endocrine disorder: low or high levels of hormone due to defect in the peripheral endocrine gland

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7
Q

2° endocrine disorder:

A

.2° endocrine disorder: low or high levels of hormone due to defect in the pituitary gland

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8
Q

3° endocrine disorder:

A

3° endocrine disorder: low or high levels of hormone due to defect in the hypothalamus

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9
Q
A
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10
Q

what is the target of somatostatin?

A

somatotrophs in the AP, inhibits GH release

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11
Q

what is the target of GHRH?

A

somatrophs in the AP–> causes release of GH

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12
Q

what is the target of PIF?

A

lactotrophs. dopamine (PIF) decreases prolactin release

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13
Q

what is the target of TRH?

A

thyrotrophs in the AP normally; thyrotrophs AND lactotrophs when it is abnormally elevated

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14
Q

when is growth hormone highest and lowest?

A

adolescence it is highest; adulthood it is lowest

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15
Q

Somatomedins

A

insulin like growth factor (IGF-1): secreted by target tissues in response to growth hormone: negatively inhibits AP release of GR and positively stimulate hypothalamus to release the somatostatin to inhibit GH release from the AP

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16
Q

Growth hormone effects

A
  1. Diabetogenic effects
    1. increase in blood glucose concentration) • C
    2. insulin resistance by decreasing glucose uptake & utilization by target tissues
    3. increases lipolysis in adipose tissue
    4. Results in an increase of blood insulin
    5. increased protein synthesis & organ growth
    6. increased uptake of a.a •
    7. Stimulates synthesis of DNA, RNA, & protein
    8. Mediated by somatomedins (IGF-1)
    9. linear growth
    10. Stimulates synthesis of DNA, RNA, & protein
    11. Mediated by somatomedins (IGF-1)
    12. increases metabolism in cartilage-forming cells & chondrocytes proliferation
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17
Q

…..an important of determinant of GH, IGF-1, & insulin levels

A

nutritional status: fasting DECREASES somatomedin

18
Q
A
  1. GH deficiency occurs with
    1. decreased secretion of GHRH due to hypothalamic dysfunction
    2. decreased growth hormone secretion 1° deficiency (lack of somatomedin feedback)
    3. GH or somatomedin resistance caused by deficiency of receptors
19
Q

hyperprolactinemia: feedback system

A

prolactin negative feedbacks to the hypothalamus and suppresses GnRH (no LH or FSH), inhibits itself by stimulating dopamine release.

20
Q

……neurons have cell bodies primarily in the supraoptic nuclei of the hypothalamus

A

ADH neurons have cell bodies primarily in the supraoptic nuclei of the hypothalamus

21
Q

….. neurons have cell bodies primarily in the paraventricular nuclei of the hypothalamus

A

oxytocin neurons have cell bodies primarily in the paraventricular nuclei of the hypothalamus

22
Q

Secretion of ADH is most sensitive to

A

Secretion of ADH is most sensitive to plasma osmolarity changes! An increase of only 1% in the osmolarity will increase ADH secretion

23
Q

ADH triggers and receptors

what receptors do they act on in the body?

A

V1 receptors in blood vessels; V2 receptors in the kidneys

triggers: think the “big 3” one for each letter in ADH

  1. decreased blood pressure on barroreceptors in the cardiac and aortic receptors
  2. decreased stretch receptors stimulation in the atria
  3. increased osmolarity
  4. increased Plasma osmolarity (above 280 mOsm)
  5. DECREASED Blood pressure
  6. DECREASED Blood volume
  7. increased Angiotensin II
  8. Sympathetic stimulation
  9. Dehydration
24
Q

three common trigger points for ADH

A

1) cardiac and aortic baroreceptors
2) aortic stretch receptors
3) mOsm receptors via interneurons

25
Q

causes of decreased ADH

A
  1. primary polydipsia: Hypothalamus
    * Primary stimulation of thirst osmoreceptors (Primary polydipsia)
  2. Central DI
    * decreased ADH from a problem in the hypothalamus or pituitary
  3. Nephrogenic DI
    * resistance to ADH caused by renal damage, sickle cell anemia, or drugs such as lithium
26
Q

botton line: if ADH increases after administration of desmopressin

A

if ADH increases with desmopressin, it is either normal or nephrogenic

27
Q

Hypoosmolarity fails to inhibit ADH release

A

SIADH

28
Q

causes of SIADH

A
  1. SCC –> ADH secretion
  2. Lymphoma
  3. adrenal insufficiency
  4. CNS tumor
  5. brain damage
29
Q

SIADH symptoms: above Na 120 and below Na 120

A

above is asymptomatic; below –> vomiting, lethargy, anorexia, confusion, headach, extensor plantar response

30
Q

17 alpha deficiency

A

substrates shunted away from cortisol and androgen production and into mineralcorticoid production –> increased aldosterone

31
Q

CRH regulation

A
  1. stress + FB, circadian rhythm +/-
  2. cortisol NFB on both pit and hyptothal
32
Q

whenever ACTH is high, what do you get

A

high cortisol and hyperpigmentation

33
Q

what is the substrate directly responsible for stimualting aldosterone release?

A

angiotensin II

34
Q

alpha, beta, delta cells: secretory products and location

A

alpha- glucagon, peripheries

beta- insulin, central

delta- somatostatin, between alpha and beta cells

35
Q

+ and - feedback between insulin, glucagon, and somatostatin

A

glucagon +fb –> insulin released

insulin -fb–> decreases glucagon release

somatostatin -fb–> decreases insulin and glucagon

36
Q

Sulfonylurea drugs (e.g. tolbutamide, glyburide)

A

Sulfonylurea drugs (e.g. tolbutamide, glyburide)

  1. promotes the closing of ATP-dependent K (potassium inward rectifier)
    1. increases insulin secretion; used in the treatment of type II diabetes mellitus
37
Q

accumulation of what molecule closes the inward rectifier K channel, triggering depolarization and inward Ca2+ influx–> releasing insulin?

A

ATP

38
Q

+ stimulus for insulin; - fb decreasing insulin release

A

FF, aa’s, glucose, glucagon, K+, cotisol, GIP, vegal stim (ACh), sulfonylurea drugs, obesity

decreasing blood glucose, fasting exercise, somatostatin, alpha adreneric agonist, diazoxide

39
Q

adipocytes as an endocrine tissue: what does it secrete, and how does it contribute to DM?

A

adipokines, FFs (increase insulin release, inflammation –> insulin resistance

40
Q

convert mmol/l blood glucose into mg/dl

A

multiple mmol/L x 18 –> mg/dl

41
Q

CaSR how it works

A

Gq and Gi inhibit PTH hormone and PTH gene in the presence of high calcium stimulation; when not stimulated the inhibition is released (i think); when inhibition is released, PTH is produced and released. Vit D (1, 25) also inhibits PTH production but stimulated CaSR synthesis and release

42
Q
A

Endocrine (20 decks)

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