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Endo/Repro > Endo > Flashcards

Endo Flashcards

1
Q

Conversion: cortisol to cortisone

A

11B HSD Type 2
Protective!
Found in kidney and aldosterone target tissue to prevent cortisol from acting on the mineralocorticoid receptor

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2
Q

Main effects of cortisol

A

Metabolic: increase blood sugar, muscle breakdown, insulin antagonist, stimulates appetite
Bone: inhibits bone formation by decreasing intestinal and renal reabsorption, and stimulates bone resorption by stimulating osteoclasts; increases apoptosis of osteoblasts and osteocytes
CT: inhibits collagen formation and fibroblast growth
Kidneys: sodium reabsorption and K+ secretion (because acts as a mineralocorticoid receptor agonist)
Anti-inflammatory
Immunosuppressive: decreases number of T cells
Conversion of norepi–>epi

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3
Q

Cushing’s syndrome

A
  • elevated cortisol NOT due to a pituitary tumor
  • could be due to an ectopic tumor
  • signs and symptoms associated with excess cortisol (hyperfunction)
  • cortisol excess causes obesity, hyperglycemia, muscle atrophy, insulin resistance, infection vulnerability, thin skin with bruises, increased BP due to increased water retention, hypokalemia, increased body hair, oligomenorrhea, acne
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4
Q

Cushing’s disease

A
  • CAUSED BY PITUITARY TUMOR THAT IS HYPER-SECRETING ACTH
  • signs and symptoms associated with excess cortisol (hyperfunction)
  • cortisol excess causes obesity, hyperglycemia, muscle atrophy, insulin resistance, infection vulnerability, thin skin with bruises, increased BP due to increased water retention, hypokalemia, increased body hair, oligomenorrhea, acne
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5
Q

Cushing’s disease/syndrome physical appearance

A

-loss of muscle mass
-fat accumulation in face and abdomen
-striae on abdomen
-moon face
-increase hair
-acne
-

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6
Q

Addison’s Disease

A
  • Hypofunction, most commonly caused by auto-immune destruction of the adrenal cortex
  • signs and symptoms associated with low cortisol: weight loss, hyperpigmentation, loss of appetite, fatigue, hypoglycemia, increased insulin sensitivity, low BP because decreased fluid volume, excessive renin production, reduction in hair
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7
Q

Hyperpigmentation

A
  • due to excess ACTH (no negative feedback from cortisol)
  • usually seen in Addison’s but could be seen with hyperfunction
  • occurs b/c ACTH production via a large hormone that is broken down into many hormones, including one that stimulates melanocyte activity
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8
Q

Growth hormone released in response to…

A
  • GHRH
  • hypoglycemia
  • arginine (protein consumption)
  • ghrelin
  • alpha-2 adrenergic response
  • dopamine and serotonin
  • metabolic or physical stress
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9
Q

Growth hormone down regulated by

A
  • somatostatin
  • beta-2 adrenergic response
  • glucocorticoids
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10
Q

Acromegaly

A
  • excess GH/IGF-1
  • delay in diagnosis because presents as headache, visual field defects, sexual dysfunction, resistant HTN (due to an increase in water retention, increased aldosterone, and VSM remodeling)
  • resistant hypertension due to: increased fluid retention because GH increases lean body mass with water, increased aldosterone because there are GH receptors in zona glomerulosa (elevated ratio of PAC:PRA….renin would be lower because of negative feedback)
  • causes thickening on bone especially of face, head, feet, and nose
  • enlargement of organs, glands, and soft tissue
  • causes excess calcium, leading to biventricular hypertrophy
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11
Q

GH deficiency

A
  • in children: small stature, central obesity, high pitched voice
  • in adults: decreased bone density, central obesity, dislipidemia
  • treatment: hormone replacement therapy
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12
Q

Diagnosis of GH excess or deficiency

A
  • Excess: suppression testing-give patient an oral glucose load; monitor GH levels in blood, which should decrease
  • Deficiency: stimulation testing-attempt to drive GH secretion using arginine, exercise, GHRH
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13
Q

Treatment for GH excess

A
  • excess:
    1. dopamine receptor agonist-this is because most hyper-GH caused by a pituitary adenoma that couples secretion of GH with prolactin…PRL is strongly inhibited by dopamine
    2. Somatostatin analogue (octerotide)
    3. GH receptor antagonist
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14
Q

Acute ACTH

A

Stimulates rate limiting step of cholesterol to pregnenolone

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15
Q

Chronic ACTH

A

Selectively stimulates enzymes involved in up-regulation of cortisol and LDL receptors

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16
Q

Enzyme only expressed in the zona fasiculata and zona reticularis

A

CYP17

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17
Q

Enzyme only expressed in zona glomerulosa

A

Aldosterone synthase

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18
Q

Congenital adrenal hyperplasia

A
  • Excess androgen production
  • Due to a mutation in 21-hydroxylase, which normally would allow for production of aldosterone and cortisol
  • causes a buildup of 17alpha-hydroxyprogesterone and therefore increased androgens
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19
Q

Process of Thyroid Hormone synthesis

A
  1. Free floating iodine trapped by Na+/I symporter using ATP
  2. Oxidation of inorganic iodide by TPO and hydrogen peroxide
  3. Iodination of tyrosine residues by TPO
  4. Coupling of tyrosine residues in RER of follicular cells to form thyroglobulin
  5. TG packaged into endocytotic vesicles in lumen
  6. TPO converts TG to T4 and stores it as colloid
  7. Upon TSH release, colloid is engulfed by follicular cells and then it fuses with lysosomes
  8. Colloid degraded in the cell to release T4 into circulation
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20
Q

Conversion of T4 to T3

A

5’ deiodinase

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21
Q

TH binding proteins

A

Major one is TBG
Also albumin
Act as mobile reservoir and increase half life.
T4 binds to TBG stronger than T3

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22
Q

Binding of TSH causes

A
  1. Increased TPO and increased TG
  2. Increase Na+/K+ ATPase to increase iodide influx via the establishment of an Na+ pump
  3. Increase rate of oxidation, iodination, and coupling
  4. Increase uptake of colloid droplets
  5. Intake uptake of and oxidation of glucose needed for hydrogen peroxide and NADPH
  6. Increased fusion of colloid with lysosomes
  7. Tonic maintenance of number and size of follicular cells and vascularity of the gland
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23
Q

Goiter

A

Cause by production of too much TSH

Can be see in hyper or hypo thyroidism

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24
Q

How does TH act at cellular level?

A

Like steroid hormones to act at level of gene expression
Passive diffusion across cell membrane
Binds to receptor on the nucleus
T3 binds to thyroid response elements (more so than T4) to increase transcription

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25
Q

Physiologic effects of TH

A 
Increased metabolic rate
Increased CO
Increased body temp
Increased linear growth
Maturation of CNS (perinatal period)
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26
Q

TH on cardiovascular function and energy use

A

Elevated BMR causes increased demand for O2
TH increases contractility of heart to increase cardiac output
Increase mitochondria expression
Increase number of energy consuming enzymes (such as Na+/K+ ATPase) and futile cycle to use up energy produced

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27
Q

Temperature on TH

A

Cold stimulates release of TSH
Hot inhibits TSH and TRH release
Acts as an internal thermostat

28
Q

TH on bone

A
  • promotes linear bone growth in children and infants
  • GH initially needs TH; TH stimulates IGF-1
  • cretinism: retardation of linear bone growth because of hypothyroidism in children
29
Q

Grave’s disease

A

Hyperthyroidism due to autoimmune stimulation of TSH receptors on follicular cells
See decreased TSH and elevated T4
Increases metabolic rate to cause weight loss, exopthalamos
Systolic hypertension
Weight loss, increased HR, increased heat production, loss of muscle mass, nervous, decreased heat tolerance
TH shifts from anabolic to catabolic

30
Q

Hyperthyroidism

A

Increased TSH and TH

31
Q

Hypothyroidism

A

Decreased TSH and TH

32
Q

Hashimoto’s

A
  • autoimmune disease destroying the thyroid causing hypothyroidism
  • increased TSH and decreased T4, usually causing goiter
  • high diastolic blood pressure
  • weight gain, decreased HR, decreased CO, cold sensitivity, fatigue, myxedema (ECF accumulation)
33
Q

Treatment for hypothyroidism

A

Thyroxine

34
Q

Treatment for hyperthyroidism

A

Propylthiouracil: inhibits TPO

Ablation or removal of the thyroid

35
Q

Effect of estrogen on bone

A
  • ER-alpha at growth plates to stimulate long bone growth and mineralization
  • stimulates osteoprotegerin which inhibits RANKL
  • inhibits osteoclast differentiation
  • stimulates osteoclast apoptosis
36
Q

Acute PTH

A
  • anabolic
  • promotes osteoblast differentiation and mitosis
  • prevents osteoblast apoptosis
37
Q

Chronic PTH

A
  • catabolic
  • stimulates RANKL
  • inhibits osteoprotegerin
38
Q

FGF23 effects

A
  • produced by osteocytes in response to hyperphosphatemia and calcitriol; mediates the inhibitory effects of E2 on PTH
  • decreases calcitriol by decreases CYP27B1 (needed to activate) and upregulating 24-hydroxylase to convert calcitriol into an inactive metabolite
  • prevents PO4 reaborption at the proximal tubule
  • prevents bone reabsorption by preventing PTH
39
Q

Effect of Elevated/Normal Calcium

A
  • bind to CaSR on parathyroid–>increases VDR

- VDR inhibits PTH secretion (negative feedback) and inhibits chief cell proliferation

40
Q

Effect of Low Calcium

A

-binds to CaSR–>increases PTH, proliferation of parathyroid cells, inhibits VDR ONLY AT PARATHYROID CELLS TO PREVENT NEGATIVE FEEDBACK

41
Q

Calcitonin on Ca2+

A
  • secreted by parafollicular/C-cells of thyroid
  • impairs osteoclasts and impairs renal reabsorption of Ca2+
  • approved for osteoporosis but not generally tolerated
42
Q

Glucocorticoids on bone

A
  • enhances bone reabsorption
  • if prolonged, can cause glucocorticoid induced osteoporosis
  • glucocorticoids inhibit osteoblasts
  • glucocorticoids stimulate osteoclasts
  • stimulates RANKL expression
43
Q

Glucocorticoids on load bearing exercises

A
  • stimulate type II muscle fibers for atrophy/muscle breakdown
  • stimulates myostatin synthesis (myostatin lowers muscle mass)
  • inhibits GH and IGF-1
44
Q

Glucocorticoids on the GnRH pulse generator

A

-inhibits by impairing testosterone and E2 synthesis

45
Q

Biphosphates

A
  • Target osteoclasts to preserve BMD
  • Used for osteoporosis
  • Induces osteoclast apoptosis
46
Q

Causes of hyperparathyroidism

A
  • primary hyperparathyroidism due to an adenoma
  • thiazide diuretics
  • Acute renal failure
47
Q

Signs of hypercalcemia

A
  • bone pain
  • kidney stones (nephrolithiasis)
  • shortened QT syndrome
  • can cause diabetes insipitus…elevated Ca2+ signals CaSR which can impair AQP and NKCC
48
Q

Secretions from posterior pituitary

A

Oxytocin
AVP

Stored in herring bodies until

49
Q

Anterior pituitary: Cell types and hormones produced by each type

A

Acidophils: GH and Prolactin
Basophils: ACTH, TSH, FSH, LH
FLAT PEG

50
Q

Primary source of glucorticoids

A

Cortisol

Adrenal cortex

51
Q

Primary sources of Androgens

A

Testosterone: Leydig and theca cells
DHEAS: adrenal cortex
Androstenedione: Leydig cells, theca cells, adrenal cortex
DHT: peripheral target tissue, some testes

52
Q

Primary source of estrogens

A

E2: granulosa cells and Leydig cells
E3: placenta

53
Q

Primary source of progestin

A

Progesterone: corpus luteum, placenta, granulosa cells

54
Q

Congenital adrenal hyperplasia

A
  • 21alpha hydroxylase deficiency

- causes a build up of androgens (can’t make aldosterone or cortisol)

55
Q

GnRH stimulation test

A
  • takes advantage of feed forward mechanism to test for central precocious puberty
  • measure LH levels after giving GnRH; check against reference
56
Q

Dex Suppression test

A
  • used to determine Cushin
  • dex=glucocorticoid
  • if dex is injected, normally negative feedback should cause cause ACTH and cortisol levels to drop
  • Low dose dex: following a low dose dex, those with Cushing’s disease will still show elevated ACTH and cortisol (because of loss of endogenous negative feedback)
  • High dose dex helps to determine if it is Cushing’s disease or syndrome…causes some decrease in ACTH in those with Cushing’s disease but unlikely to affect those with Cushing’s syndrome caused by an ectopic source of ACTH
57
Q

Salt loading test

A
  • give bolus of salt to see BP go up

- if [Na+] is low but total Na+ in urine is high, means high volume of urine

58
Q

GH main effects

A
  1. Increase blood glucose; antagonizes insulin in order for blood glucose levels to remain high
  2. Amino acid uptake and protein synthesis
  3. Bone growth and lengthening; bone deposition
  4. Increases lipolysis (for energy production that isn’t glucose)
  5. Increase in lean body mass (that is water)
  6. Elevates IGF-1 expression in the liver
59
Q

Estrogen at Bone

A
  • stimulates osteoblast to secrete osteoprotegin, to inhibit RANKL
  • Inhibits osteoclast differentiation
  • stimulates osteoclast apoptosis
60
Q

Cause of FGF-23 secretion

A
  • Hyperphosphatemia

- Calcitriol

61
Q

Effect of FGF23

A
  • inhibits PTH secretion by binding on parathyroid cells (which lack E2 receptors)
  • inhibits PO4 reabsorption
  • inhibits calcitriol
  • promotes bone deposition
62
Q

Glucocorticoids on Calcium

A
  • promote bone reabsorption, but prevents Ca2+ reabsorption at level of kidney and intestines
  • DECREASES SERUM CALCIUM
  • Promotes PTH
63
Q

Lab results Primary Hyperparathyroidism

A

Hypercalcemia
Hypercalcuria
Hyperphosphaturia

Can cause DI due to CaSR shutting off AQP and NKCC

64
Q

Findings for hypocalcemia

A
  • Increase in nerve and muscle excitability
  • Trousseu’s sign (carpal spasm due to loss of brachial artery circulation)
  • Prolonged QT

-due to renal failure that decreases calcitriol synthesis

65
Q

Findings for hypercalcemia

A
  • kidney stones
  • shorted QT
  • bone pain
66
Q

Findings hyper and hypo phosphatemia

A

Hyper: metastatic calcifications, impairs calcitriol synthesis, and impairs PTH–>induces hypocalcemia

Hypo: usually due to hyperparathryroidism; skeletal muscle weakness

Endo/Repro (7 decks)

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