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Endocrine II midterm > Lopez: Endocrine Review > Flashcards

Lopez: Endocrine Review Flashcards

1
Q

What correlates with plasma half-life and metabolic clearance of hormones?

A
  • the degree of protein binding

- the thyroid hormones do this a lot

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2
Q

What kind of mechanism does ACTH, LH, FSH, TSH, and glucagon use?

A 
the adenylyl cyclase mechanism
-Gs ptn
-ATP to cAMP
-activation of PKA
...
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3
Q

What mechanism does GnRH, TRH, GHRH, and oxytocin use?

A

PLC mechanism

  • Gq ptn
  • activates PLC
  • makes DAG and IP3
  • DAG gets PKC
  • IP3 releases Ca2+ from ER
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4
Q

What mechanism do Thyroid hormones, glucocorticoids, aldosterone, estrogen, and testerone use?

A

the steroid hormone MOA

  • binds cytoplasmic receptor
  • dimerizes
  • goes to nucleus
  • gets the SRE… gene transcription
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5
Q

What is the connection between the hypothalamus and the posterior pit?

A

-just neural

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6
Q

connection b/w hypothalamus and ant pit

A
  • neural and endocrine

- via the hypothalamic-hypophysial portal vessels

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7
Q

What is a primary endocrine disorder

A

-low or high levels of hormone due to defect in the peripheral endocrine gland

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8
Q

What is a secondary endocrine disorder?

A

-low or high levels of hormone due to defect in the pituitary gland

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9
Q

What is a tertiary endocrine disorder

A

low or high levels of hormone due to defect in the hypothalamus

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10
Q

Ant pit hormones

A
  • TSH
  • FSH
  • LH
  • ACTH
  • GH
  • Prolactin
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11
Q

What will PRL excess give us clinically?

A
  • galactorrhea and hypogonadism

- it inhibits LH and FSH as well

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12
Q

Where does somatostatin and PIF (dopamine) come from?

A

the hypothalamus

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13
Q

difference between a functioning and non functioning pituitary adenoma?

A
  • functional: releases active hormone…. lots of it

- non functional: doesn’t

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14
Q

Prolactinoma

A

-hypogonadism and galactorhea

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15
Q

excess GH symptoms

A

Acromegaly in adults and gigantism in children

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16
Q

Cushing’s disease

A

-pituitary tumor w/ an overproduction of cortisol

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17
Q

What syndrome do pituitary adenomas show up in?

A

MEN1 patients (25% of the time)

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18
Q

What does PRL excess do to LH ad FSH?

A

lowers them both

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19
Q

What are the two hormones released from the post pit?

A

ADH and oxytocin

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20
Q

Which hypothalamic nucleus releases ADH?

A

-Supraoptic nuclei

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21
Q

Which nucleus releases oxytocin?

A

paraventricular nuclei

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22
Q

What kind of hormones are ADH and oxytocin

A

neuropeptides

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23
Q

What is secretion of ADH most sensitive to?

A

plasma osmolarity changes

-gets V1 and V2 receptors

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24
Q

What are the triggers of ADH release?

A
  • high plasma osm
  • low BP
  • low BV
  • high ANGII
  • sympathetic stimulation
  • dehydration
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25
Q

What is Diabetes insipidus?

A
  • lack of an effect of ADH on the renal collecting duct
  • fequent urination
  • large volume of urine is dilutes
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26
Q

Central DI

A
  • lack of ADH… so low ADH

- results from damage to pituitary or destruction of hypothalamus

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27
Q

Tx of Central DI?

A
  • desmopressin

- drug that prevents water excretion

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28
Q

NEphrogenic DI

A

-kidneys are unable to respond to ADH… so high plasma ADH

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29
Q

Causes of Nephrogenic DI?

A
  • drugs like lithium
  • Chronic disorders (PCKD, SSA)
  • desmopression tx does not work
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30
Q

What is the water deprivation test for DI?

A
  • cut off fluids
  • weigh pt every 1-2 hrs for 8 hrs
  • measure plasma osmolarity and urine
  • if looks like DI, allow pt to drink, administer desmopressin
  • then measure plasma and urine osmolality again
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31
Q

SIADH

A
  • excessive secretion of ADH
  • excessive water retention
  • hypoosmolarity fails to inhibit ADH release
  • wathc for sodium below 120…. hyponatremic encephalopathy
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32
Q

What does the adrenal cortex secrete?

A
  • Aldosterone
  • Cortisol
  • Androgens
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33
Q

What does the adrenal medulla secrete?

A

E and NE

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34
Q

From outside to inside, name the layers of the adrenal gland and the hormones they secrete

A
  • GFRM
  • Glomerulosa: Mineralocorticoid (aldosterone)
  • Fasciculata: Glucocorticoids(cortisol), androgens
  • Reticularis: Glucocorticoids and androgens again
  • Medulla: E and NE (catecholamines)
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35
Q

What is the first step in synthesis of steroid hormones?

A
  • Cholesterol to pregnenolone
  • mediated by cholesterol desmolase
  • then we split three ways to make Aldosterone, cortisol, or androstenedione
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36
Q

how is Aldosterone made?

A
  • Pregenolone, progesteron, Deoxycorticosterone (DOC), Corticosterone, Aldosterone!
  • 3B, 21, 11, aldosterone synthase
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37
Q

How is cortisol made?

A
  • Pregnenolone, 17-OH Pregnenolone, “ “ progesterone, 11-deoxycortisol, cortisol!
  • 17, 3B, 21, 11
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38
Q

How are androgens made?

A
  • pregnenolone, 17-OH pregnenolone, DHEA, Androstenedione (androgens!)
  • 17, 17+20, 3B
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39
Q

How can you tell a 21 vs and 11 deficiency?

A
  • in 11 deficiency, there will be increased BP due to the mineralocorticoid effect of DOC that builds up
  • that doesn’t happen with 21 deficiency because we never get to the DOC point
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40
Q

What does Aldosterone do?

A
  • increases sodium concentration in the blood

- raises BP

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41
Q

What will we have a lot of if there is a 17 alpha deficiency?

A
  • mineralocorticoids
  • they will be totally fine because we don’t need 17 for aldosterone synthesis
  • that is 3B, 21, 11, aldosterone synthase
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42
Q

What will we have a lot of if there is a 21B deficiency?

A
  • Sex hormones!
  • they don’t need 21
  • they are just 17, 17+20, 3B
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43
Q

What will we have a lot of in 11B deficiency?

A
  • Sex hormones again!
  • again, they don’t need 11
  • remember though, there will be high BP b/c of DOC creation
  • 21 still works well :)
44
Q

Which one is the most common deficiency?

A
  • 21B
  • high Renin activity for some reason
  • also high 17-hydroxyprogesterone
45
Q

What is Cushing’s syndrome

A
  • high cortisol due to an ADRENAL tumor

- there is just high cortisol… lower down the chain

46
Q

What is Cushing’s disease?

A
  • high ACTH which leads to high cortisol

- caused by a PITUTARY tumor

47
Q

What is Addison’s disease?

A
  • caused by autoimmune disease of the adrenal gland

- so… low cortisol, high ADH and high CRH… the adrenal gland is where the problem is at

48
Q

What is Secondary adrenal insufficiency?

A
  • caused by glucocorticoid drugs suppressing H and P

- everything is low

49
Q

If we have high ACTH, what else will we have besides high plasma cortisol?

A

-hyperpigmentation

50
Q

If we have a primary excess, where is the problem?

A

the adrenals… so high cortisol, low everything else

51
Q

If we have a secondary excess, where is the problem?

A

the pituitary, so high ACTH, pigmentation, and cortisol elevated
-these same things go for deficiency

52
Q

What is ANGII’s effect on the adrenal cortex?

A

-makes it secrete aldosterone

53
Q

Which zone makes aldosterone?

A

Glomerulosa

54
Q

What do pancreatic B cells secrete?

A

insulin

-located more toward the center of the islets of Langerhans

55
Q

What do alpha cells make?

A

glucagon

56
Q

What do the delta cells secrete?

A

-somatostatin

57
Q

What is glucagon’s effect on insulin secretion?

A

increases it

-weird because insulin from B cells will decrease the glucagon from delta cells

58
Q

What can be use as a long-term marker of endogenous insulin secretion?

A

C peptide

-it’s secreted in equimolar amounts with insulin

59
Q

What do the sulfonylurea do the the ATP-dependent K+ channels?

A

closes them… K+ is stuck in the cell now

  • makes the cell depolarize
  • Ca2+ channels open
  • Ca2+ comes in
  • Exocytosis of insulin… yay
  • hypokalemia
60
Q

What kind of receptor does insulin bind?

A

RTK

  • autophosphorylates itself
  • insulin down-regulates its own receptor
61
Q

What are the effects of insulin?

A
  • we start storing stuff
  • increased glycogen/lipid/protein synthesis
  • decreased lipolysis
  • cell growth and differentiation
  • decreased gluconeogenesis
62
Q

When in doubt, what does insulin do to things in the blood?

A

lowers them!

  • increased glucose uptake… low glucose
  • increased Ptn synth…. low aa’s
  • Increased fat deposition…. low FA;s
  • decreased lipolysis…. low ketoacids
  • increased K uptake into cells… low K+
63
Q

What is Type 1 DM?

A

-inadequate insulin secretion
-destruction of B cells, often as the result of autoimmune disease
-no symptoms until 80% of symptoms are gone
-kids
-ketosis
-

64
Q

What is Type 2 DM?

A
  • Insulin resistance
  • more common type
  • progressive exhaustion of active B cells
  • pts can make insulin, but no enough to overcome insulin resistance
  • adults
  • family Hx
  • fat ppl
65
Q

If we are given the mmol/L of glc, how do we get the concentration of glucose in mg/dL?

A

multiply by 18

66
Q

What does Glucagon do?

A

-increases lipolysis and inhibits GA synthesis , which shunts substrates towards gluconeogenesis

67
Q

What are produced from FA?

A

Ketoacids!

68
Q

Where is the vast majority of calcium stored in our body?

A

-bones and teeth

69
Q

What does PTH and Vit D do to bone resorption?

A

increases it

  • gives us more Ca2+ in blood
  • PTH also helps us reabsorb the Ca2+ from the kidneys
70
Q

What must the kidneys do to maintain Ca2+?

A

excrete the same amount of Ca2+ that is absorbed by the GI tract

71
Q

How is extracellular Pi related to Ca2+ levels?

A
  • inversely related!

- extracellular concentration of Pi is regulated by the same hormones that regulate Ca2+ concentration

72
Q

What wil PTH do to Pi?

A
  • decrease its reabsorption from the kidney
  • so we get phophaturia
  • we will also have very high cAMP urine levels for some reason
73
Q

So, if we have a high serum Ca2+ level, what will that do to our PTH?

A

inhibit it

74
Q

What does Vit D do genetically?

A
  • goes in and stops PTH gene and upregulates CaSR gene

- the CaSR will respond to the high calcium levels and also inhibit PTH

75
Q

What is the active form of Vit D

A

1,25 cholecalciferol

-24,25 is the inactive form

76
Q

Where does Vit D get converted into its active form?

A

the renal prosimal tubule

-by 1 alpha hydroxylase… makes sense

77
Q

Where does Vit D (cholecalciferol) get the 25 hydroxyl group slapped onto it?

A

the liver

  • that happens first
  • so that is the main circulating form of Vit D
78
Q

Where are the PTH receptors located?

A
  • on the OsteoBLASTS… not clasts
  • so, short term, it will increase bone formation via direct action on osteoblast
  • basis for use of intermittent synthetic PTH administration in osteoporosis tx
79
Q

What is the long term actions of PTH?

A
  • high bone resorption
  • indirect action on osteoclasts mediated by cytokines released from osteoblast
  • Vit D acts synergistically with PTH to stimulate osteoclast activity and bone resorption
80
Q

At what part of the renal tubule is Ca2+ reabsorbed because of PTH?

A
  • Thick ascending limb

- PTH also gets the 1 alpha hydroxylase… activates Vit D

81
Q

Vit D effects on Small intestine?

A

-increase Ca2+ and Pi absorption by increasing calbindin expression

82
Q

Vit D effects on bone

A
  • sensitizes osteoblasts to PTH

- regulates osteoid production and calcification

83
Q

Vit d effects on kidney

A
  • promotes Pi reabsorption by proximal nephrons (PTH does opposite)
  • minimal actions on Ca2+
84
Q

Vit D effects on parathyroid gland?

A
  • Directly inhibits PTH gene expression

- Directly stimulates CaSR gene expresion

85
Q

Primary hyperparathyroidism?

A

-lots of Pi, cAMP, Ca2+ excretion
-Stone, bones, and groans
-hypercalciuria… stones
-high bone resorption…
-constipation… groans
tx usually requires parathyroidectomy
-HYPERCALCEMIA/HYPOPHOSPHATEMIA

86
Q

Lab values for hyperparathyroidism?

A
  • PTH: high
  • Ca2+: high
  • Pi: low
  • Vit D: high
87
Q

Secondary hyperthyroidism?

A
  • increase in PTH levels secondary to low Ca2+ in blood

- causes: renal failure, Vit D deficiency

88
Q

lab values for Secondary hyperparathyroidism due to renal failure?

A
  • PTH: high
  • Ca2+: low
  • Pi: high
  • Vit D: low
89
Q

lab values for secondary hyperparathyroidism due to Vitamin D deficiency?

A

-PTH: high
-Ca2+: low
Pi: low
-Vit D: low

90
Q

Hypoparathyroidism?

A
  • PTH isn’t made anymore!
  • no Vit D
  • No Ca2+
  • no Pi excretion
  • Hypocalcemia/Hyperphosphatemia
91
Q

lab values for hypoparathyroidism?

A
  • PTH: low
  • Ca2+: low
  • Pi: high (PTH normally promotes Pi excretion)
  • Vit D: low
92
Q

What is Albright hereditary osteodystrophy?

A
  • inherited autosomal dominant disorder, Gs for PTH in bone and kidney is defective
  • Hypocalcemia and hyperphosphatemia develop
  • high PTH levels….. so it’s a psuedohypoparathyroidism
  • administration of exogenous PTH won’t do shit
93
Q

lab values for Pseudohypoparathyroidism?

A
  • PTH: high
  • Ca2+: low
  • Pi: high
  • Vit D: low
94
Q

what is the phenotype for albright hereditary osteodystorphy?

A

-short stature, short neck, obesity, subcutaneous calcification, shortened metatarsal and metacarpals

95
Q

What is PTHrP

A

-secreted by tumor cells…. acts like PTH

96
Q

lab values for humoral hypercalcemia of malignancy

A
  • PTH: low
  • Ca2+: high
  • Pi: low
  • VitD: low (apparently doesn’t activate that one enzyme…)
97
Q

Familial hypocalciuric hypercalcemia (FHH)

A
  • auto dominant
  • Mutations inactivate CaSR in PT glands
  • decreased urinary Ca2+ excretion and increased serum Ca2+
98
Q

Rickets type 1 and 2

A
  • congenital disorders
  • Vit-D deficiency (kinda)
  • type 1: no 1 alpha hydroxylase
  • type 2: no vitamin D receptor
  • lots of Pi and cAMP in the urine
99
Q

how long does the body have enough Thyroglobulin for if everything were to shut down?

A

-2 to 3 months

100
Q

What enzyme is involved with the peripheral conversion of T4 to T3?

A

-deiodinase

101
Q

When the availability of iodide is restricted, what is favored more? T3 of T4?

A

T3

-makes sense because that takes less iodine >

102
Q

What drugs will inhibit the sodium idodide symporter?

A
  • perchlorate
  • thiocynate
  • PTU is an effective treatment for hyperthyroidism
103
Q

What will oddly inhibit organification and synthesis of thyroid hormones?

A

high levels of Iodide

  • this is called the Wolff-Chaikoff effect
  • it’s wierd because either too much or too little Iodine will inhibit Thyroid hormone
104
Q

How are thyroid hormones transported?

A

in the bloodstream either bound to plasma proteins or free

-mostly bound to ptns (TBG)

105
Q

What is TSH regulated by?

A
  • TRH

- Free T3

106
Q

What is something that makes TSH secretion different from GH secretion?

A

-TSH secretion occurs at a steady rate

107
Q

Most common cause of thyrotoxicosis?

A

Graves disease

  • Thyroid stimulating Ig’s (TSI) stimulate TSH receptor without TSH hormone
  • TSH levels are low because of high circulating levels of thyroid hormones inhibits TSH secretion!
  • exophthalmos

Endocrine II midterm (13 decks)

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