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15 Endocrine > Endocrine physiology review, mnemonics > Flashcards

Endocrine physiology review, mnemonics Flashcards

1
Q

Hypercalcemia symptoms:

A

“stones, bones, groans, and psychiatric overtones”

  1. stones–renal
  2. Bones–bone pain
  3. Groans–weakness, constipation
  4. psychiatric overontes–depression
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1
Q

What blocks the Na-I transporter in the thyroid? (2)

A
  1. Thiocyanate (cyanide)
    - can be side effect of nitroprusside for HTN emergency
  2. Perchlorate
    - byproduct in rocket propellants. can be in contaminated drinking water.

Both cause decreased I uptake, so hypothyroidism

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1
Q

why does oral glucose induce a stronger insulin response than injected glucose?

A

Oral glucose also stimulates the secretion of GIP (glucose-dependent insulinotropic peptide) from the GI tract

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2
Q

Why is there no lactation during pregnancy, even though prolactin levels are high?

A

Estrogen and progesterone down-regulate prolactin receptors. After parturition, both E and P decrease, releasing inhibition.

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3
Q

Anterior pituitary:

  • secretes what
  • what do Ant Pit basophils secrete?
A

FLAT PeG:

FSH, LH, ACTH, TSH, Prolactin, GnRH

B-FLAT:

FSH, LH, ACTH, TSH

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3
Q

How does chronic renal failure affect Ca levels?

A

2 mechanisms:

  1. Decreased resorption of Ca
  2. decreased 1 OHlation of 25 Vit D, so decreased Ca intake.
    - Note: in secondary hyperparathyroidism, Ca levels may be normal instead of low because the PTH has compensated for the low Ca
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4
Q

Why is there hyperkalemia in T1 DM?

A

Insulin promotes K uptake into cells (protects body from transient hyperkalemia after a meal).

No insulin means hyperkalemia

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5
Q

starvation effect on thyroid hormones/metabolism

A

Starvation inhibits 5’ iodinase in TH target tissues, except in brain. 5’ iodinase is required to convert T4 to T3, so this effect is beneficial in reducing basal metabolic rate during starvation.

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6
Q

17A OHlase deficiency:

-are aldosterone levels increased or decreased?

A
  • Aldo is decreased, although it would seem to increase at first thought.
  • The excess mineralocorticoid symptoms act on the RAAS to reduce Aldosterone synthase. (HTN reduces renin, reduces Angio II, reduces Aldo synthase. Hypokalemia directly reduces Aldo synthase)
  • So, excess 11-DOC and Corticosterone are formed, which cause the mineralocorticoid symptoms.
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7
Q

Calcitonin

-function

A

“calcitonin TONES down Ca levels”

-decrease Ca blood levels by decreasing bone resorption

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7
Q

ADH:

2 major stimulators. which one overrides the other in case of conflict?

A
  1. increased osmolarity (person deprived of water)
  2. hypovolemia (eg bleeding)

Blood volume overrides. Eg: person has hypervolemia but increased osmolarrity–no ADH

Eg: person has hypovolemia but decreased osmolarity–yes ADH secretion

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8
Q

what happens to thryoid hormone levels during pregnancy and why?

A

High estrogen during pregnancy inhibits liver’s breakdown of TBG (thyroid binding globulin). Therefore, more T4/T3 is bound to TBG and free T4/T3 goes down.

In response, the thryroid gland produces more TBG in response to low free T4/T3. Final result: Increased TBG and normal free T4/T3 levels.

Pt is ‘clinically euthyroid’ meaning thyroid function is normal despite increased TBG levels.

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9
Q

Ant vs Post pituitary:

-how are the connections from hypothalamus different?

A

Ant: hormone, by blod

post: neural

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10
Q

Which organs uptake glucose independent of insulin’s effect?

A

‘BRICK L’

Brain, RBCs, Intestine, Cornea, Kidney, Liver

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11
Q

Signaling pathways of endocrine hormones:

steroid receptor

A

‘VETTT CAP’

VitD, Estrogen, Testosterone, T3, T4

Cortisol, Aldosterone, Progesterone

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13
Q

Anterior and posterior pituitary:

-derived from what tissues?

A
  1. ant–oral ectoderm (rathke’s pouch)
  2. post–neuroectoderm
14
Q

Adrenal cortex and medulla:

divided in what parts, and what do they secrete?

A

“GFR,” “Salt, sugar, and sex”

Zona glomerulosa–Aldosterone

fasciculata–Cortisol, also androgens

reticularis–androgens

Medulla–catecholamines

15
Q

dexamethasone suppression test:

  • what is it used for
  • how does it work
A
  • Used in pts with hypercortisolism to dx primary or secondary.
  • If there is an ACTH-secreting tumor in the AP, low lose of dexamethasone will have no effect, but high dose will lower ACTH and therefore cortisol level. (tumor tissue is less sensitive to glucocorticoid negative feedback).
  • If there is a cortisol-secreting tumor in the adrenal gland, no amount of dexamethasone will affect cortisol level (tumor has no negative feedback from glucocorticoid)
17
Q

Signaling pathways of endocrine hormones:

cAMP

A

“FLAT ChAMP”

FSH, LH, ACTH, TSH

CRH, hCG, ADH, MSH, PTH,

calcitonin, GHRH, glucagon

18
Q

How do these affect calcium blood levels?

  1. changes in plasma protein concentration
  2. changes in anion concentration
  3. acid-base abnormalities
A

Remember, 40% of total blood Ca is bound to proteins, mainly albumin. 60% is free, ionized Ca.

  1. decreased albumin will decrease total blood Ca. Free Ca levels are usu not increased b/c this process happens slowly
  2. Increased PO4 will complex with free Ca, lowering free Ca.
  3. H+ competes with Ca for space on albumin, so in acidosis, free Ca increases. in alkalosis, free Ca decreases.

(thus, in acute respiratory alkalosis, free Ca decreases and you see signs of hypocalcemia)

20
Q

How does cortisol inhibit inflamm/immune response? (5 mechs)

A

Inflammatory, Immune responses–decreases.

  1. inhibits production of LTs, prostaglandins.
  2. inhibits leukocyte adhesion–neutrophilia
  3. blocks histamine release from mast cells
  4. reduces eosinophils
  5. blocks IL-2 production
21
Q

Posterior pituitary:

-secretes what?

A

ADH, Oxytocin

23
Q

T3 functions

A

“4 B’s”

  1. Brain maturation
  2. Bone growth
  3. Beta-adrenergic effects
  4. Basal metabolic rate, increases
24
Q

Signaling pathways of endocrine hormones:

IP3

A

“GOAT HAG”

GnRH, Oxytocin, ADH, TRH

Histamine, Angio II, Gastin

25
Q

Cortisol:

all physiology effects:

A

cortisol is a “BIG FIB”

Blood pressure–increases by increasing NE, Epi sensitivity (upregulate A1 receptors on arterioles)

Insulin resistance–increases (diabetogenic)

Gluconeogenesis, lipolysis, proteolysis–decreases

Fibroblast activity–decreases (causes striae)

Inflammatory, Immune responses–decreases.

  1. inhibits production of LTs, prostaglandins.
  2. inhibits leukocyte adhesion–neutrophilia
  3. blocks histamine release from mast cells
  4. reduces eosinophils
  5. blocks IL-2 production

Bone formation–decreases (reduce osteoblast activity)

26
Q

ADH:

effects (2)

A
  1. increased water permeability–aquaporins in collecting duct (cAMP)

V2 receptor

  1. contraction of vascular smooth m (IP3)

V1 receptor

27
Q

PTH:

functions, mnemonic

A

‘Phosphate Trashing Hormone’

Bone: resorbs Ca and PO4

Kidney: -increases reabsorption of Ca in DCT

  • decrease reabsorption of PO4 from PCT
  • increase 1,25 Vit D prduction by stimulating 1A-OHlase
28
Q

Signaling pathways of endocrine hormones:

Receptor-associated tyrosine kinase

A

“PIG”

Prolactin, Immunomodulators (cytokines IL2, etc), GH

15 Endocrine (7 decks)

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