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Endo II - Path (Tobin) > Lecture 1: Endocrinology Review > Flashcards

Lecture 1: Endocrinology Review Flashcards

1
Q

Which endocrine hormones utilize the PLC mechanism? (GOAT HAG mnemonic)

A

GnRH + Oxytocin + ADH + TRH + Histamine + Angiotensin II + GHRH

GOAT HAG

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2
Q

Which enzyme is responsible for the degradation of intracellular cAMP to inactive 5’ AMP in the adenylyl cyclase/cAMP pathway?

A

Phosphodiesterase

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3
Q

What are the 2 classes of homrones which are amines?

A
  • Catecholamines (epinephrine, NE, and dopamine)
  • Thyroid hormones
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4
Q

When a steroid hormone binds its receptor what occurs to the hormone-receptor complex?

A

Dimerizes and binds via zinc fingers to specific DNA sequences, called steroid-responsive elements (SREs)

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5
Q

Once the steroid hormone-receptor complex dimerizes and binds to the SREs of the target gene, what has this complex now become and what does it regulate?

A

A transcription factor that regulates the rate of gene transcription

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6
Q

What is the epithelial and neural portion of the pituitary gland?

A
  • Anterior pituitary (adenohypophysis) = epithelial portion
  • Posterior pituitary (neurohypophysis) = neural portion
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7
Q

Generally cancers of the pituitary expand where and compress what?

A

Up into the brain and compress the optic nerves

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8
Q

The posterior pituitary is a collection of axons whose cell bodies are located in the hypothalamus; what are these 2 cell bodies and which neuropeptides is each cell body associated with?

A
  • Supraoptic nucleus (SON) –> mainly ADH
  • Paraventricular nucleus (PVN) –> mainly oxytocin
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9
Q

Which 6 hormones are secreted by the anterior pituitary?

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

*FLAT PiG*

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10
Q

How is the anterior pituitary connected to the hypothalamus?

A

Hypothalamic-hypophysial portal vessels

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11
Q

Which portion of the pituitary gland has both neural and endocrine connections with the hypothalamus; which has exclusively neural?

A
  • Anterior pituitary = BOTH endocrine and neural
  • Posterior pituitary = only neural
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12
Q

Contrast primary endocrine disorder, secondary endocrine disorder, and tertiary endocrine disorder.

A
  • 1° disorder = due to defect in the peripheral endocrine gland
  • 2° disorder = due to defect in the pituitary gland
  • 3° disorder = due to defect in the hypothalamus
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13
Q

Gonadotrophs release what hormone(s)?

A

FSH and LH

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14
Q

Somatotrophs release what hormone?

A

GH

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15
Q

What is the most important somatomedin mediating the indirect effects of GH?

A

IGF-1

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16
Q

What is the effect of GH on insulin, blood glucose levels, and adipose tissues?

A
  • Causes insulin resistance –> ↑ blood insulin
  • Effects are diabetogenic –> ↑ in blood glucose levels
  • ↑ lipolysis in adipose tissue
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17
Q

What are 2 metabolic effects of GH which are mediated by somatomedins (IGF-1)?

A
  • ↑ protein synthesis and organ growth (↑uptake of AA’s)
  • ↑ linear growth (↑ metabolism in cartilage-forming cells and chondrocytes proliferation)
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18
Q

What are 2 of the most potent stimuli for GH secretion?

A

Hypoglycemia and starvation

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19
Q

Conditions with excess secretion of GH are treated with what?

A

Somatostatin analogs –> ocreotide

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20
Q

What are 4 ways that GH deficiency can result?

A
  • ↓ secretion of GHRH (hypothalamic dysf.)
  • ↓ GH secretion (pituitary dysf.)
  • Failure to generate somatomedins in the liver
  • GH or somatomedin resistance (deficiency of receptors)
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21
Q

GH excess causes what if before puberty or what if after puberty?

A
  • Before puberty = gigantism
  • After puberty = acromegaly
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22
Q

Where does prolactin released from the anterior pituitary act and what is its function?

A

Acts on the hypothalamus to ↓ GnRH secretion —-> ↓ FSH and LH

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23
Q

What is the inhibitory and stimulatory pathway from the hypothalamus regulating prolactin release from the anterior pituitary?

A
  • Inhibitory = Dopamine (aka PIF)
  • Stimulatory = TRH
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24
Q

How does prolactin inhibit its own secretion?

A

By increasing the synthesis and secretion of dopamine from the hypothalamus (negative feedback)

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25
Q

What are the 2 most important stimuli for prolactin secretion?

A
  • Breast feeding
  • Pregnancy
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26
Q

Secretion of ADH is most sensitive to changes in what?

A

Plasma osmolarity

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27
Q

What are 6 triggers for the secretion of ADH from the posterior pituitary?

A
  • ↑ plasma osmolarity = most important stimulus
  • ↓ BP
  • ↓ blood volume
  • ↑ Angiotensin II
  • Sympathetic stimulation
  • Dehydration
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28
Q

In volume expansion (aka hypervolemia) what occurs with ADH secretion even in the presence of increased plasma osmolarity?

A

ADH secretion is inhibited

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29
Q

What is the major action of ADH and via what receptor?

A
  • ↑ water permeability of principal cells in the late distal tubule and collecting duct
  • Via the V2 receptor on principal cells
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30
Q

What is the effect of ADH on vascular smooth muscle and via which receptor?

A

Contraction of vascular smooth m. (aka vasoconstriction) via the V1 receptor

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31
Q

Central diabetes insipidus is caused by what; what are ADH levels like?

A
  • Caused by: damage to posterior pituitary or destruction of hypothalamus
  • LACK of ADH so will see ↓ plasma ADH
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32
Q

What will be seen in terms of urine production and serum osmolarity in patient with central DI?

A
  • Large volumes of dilute urine
  • Bodily fluids are concentrated i.e., ↑ serum osmolarity and ↑ serum [Na+]
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33
Q

What is occuring in nephrogenic DI; what are plasma levels of ADH like?

A

Kidneys are unable to respond to ADH (↑ plasma ADH)

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34
Q

What are 2 major causes of nephrogenic DI?

A
  • Drugs like lithium
  • Chronic disorders i.e., polycystic kidney disease, sickle cell anemia
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35
Q

What is the Tx of Central DI vs. Nephrogenic DI?

A
  • Central DI is treated with desmopressin (ADH analogue)
  • Nephrogenic DI is treated with thiazide diuretics (desmopressin does NOT work)
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36
Q

What is the serum and urine osmolarity like in SIADH?

A
  • Serum osmolarity is decreased due to excess water reabsorption by collecting ducts —> HYPOosmolarity fails to inhibit ADH release
  • Urine is inappropriately concentrated (i.e., too concentrated for the serum osmolarity)
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37
Q

What are the 3 layers of the adrenal cortex and what are the main hormones produced by each layer?

A
  • Zona Glomerulosa –> mineralocorticoids (aldosterone)
  • Zona Fasciculata –> glucocorticoids (cortisol)
  • Zona Reticularis –> androgens (DHEA)
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38
Q

Which hormones are produced by the adrenal medulla?

A

Catecholamines (epinephrine and NE)

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39
Q

What is the precursor for all adrenal cortex hormones?

A

Cholesterol

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40
Q

Which pathway(s) of hormone synthesis in the adrenal cortex does the enzyme 17α-hydroxylase play a role in?

A
  • Cortisol synthesis
  • Androgen synthesis
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41
Q

Which pathway(s) of hormone synthesis in the adrenal cortex does the enzyme 21β-hydroxylase play a role in?

A
  • Aldosterone synthesis
  • Cortisol synthesis
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42
Q

Which pathway(s) of hormone synthesis in the adrenal cortex does the enzyme 11β-hydroxylase play a role in?

A
  • Aldosterone synthesis
  • Cortisol synthesis
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43
Q

For each indicate if the levels will be ↑ or ↓ in 17α-hydroxylase deficiency: mineralocorticoids, cortisol, sex hormones, BP, and [K+]

A
  • ↑ mineralocorticoids
  • ↓ cortisol
  • ↓ sex hormones
  • ↑ BP
  • ↓ [K+]
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44
Q

Which enzyme deficiency is associated with ↓ androstenedione levels?

A

17α-hydroxylase

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45
Q

For each indicate if the levels will be ↑ or ↓ in 21β-hydroxylase deficiency: mineralocorticoids, cortisol, sex hormones, BP, and [K+]

A
  • ↓ mineralocorticoids
  • ↓ cortisol
  • ↑ sex hormones
  • ↓ BP
  • ↑ [K+]
46
Q

Which enzyme deficiency of the adrenal cortex is associated with ↑ renin and ↑ 17-hydroxy-progesterone?

A

21β-hydroxylase

47
Q

For each indicate if the levels will be ↑ or ↓ in 11β-hydroxylase deficiency: mineralocorticoids, cortisol, sex hormones, BP, and [K+]

A
  • ↓ aldosterone and ↑ 11-deoxycorticosterone (DOC) = ↑ BP
  • ↓ cortisol
  • ↑ sex hormones
  • ↑ BP
  • ↓ [K+]
48
Q

Which enzyme deficiency of the adrenal cortex is associated with ↓ renin activity?

A

11β-hydroxylase

49
Q

What will the presentation in a male vs. female child be with 17α-hydroxylase deficiency?

A
  • Male = undescended testes; ambiguous genitalia
  • Female = lack of 2° sexual development
50
Q

When does 21β-hydroxylase deficiency most commonly present and how?

A
  • In infancy w/ salt wasting or childhood (precocious puberty)
  • In females = virilization
51
Q

How does 11β-hydroxylase deficiency present in females?

A

Virilization = dev. of male physical characteristics

52
Q

Which endocrine hormones utilize the AC/cAMP pathway (mnemonic from FA)

A

FSH + LH + ACTH + TSH + CRH + hCG + ADH + MSH + PTH

FLAT ChAMP

53
Q

What is the effect of cortisol on the liver, muscle, and adipose tissue?

A
  • Liver = gluconeogenesis
  • Muscle = protein catabolism
  • Adipose tissue = lipolysis
54
Q

Describe the regulation of cortisol secretion (aka axis)

A

CRH (hypothalamus) stimulates ACTH (pituitary) –> cortisol production (adrenal fasciculata)

55
Q

What is the cause of Cushing’s Syndrome; what changes are seen in CRH, ACTH and cortisol?

A
  • Adrenal tumor
  • ↓ CRH
  • ↓ ACTH
  • ↑ Cortisol
56
Q

What is the cause of Cushing’s Disease; what changes are seen in CRH, ACTH and cortisol?

A
  • Pituitary tumor
  • ↓ CRH
  • ↑ ACTH
  • ↑ Cortisol
57
Q

What is the cause of Addison’s Disease; what changes are seen in CRH, ACTH and cortisol?

A
  • Caused by autoimmune disease of the adrenal gland
  • ↑ CRH
  • ↑ ACTH
  • ↓ Cortisol
58
Q

What is the cause of Secondary Adrenal Insufficiency; what changes are seen in CRH, ACTH and cortisol?

A
  • Glucocorticoid drugs suppressing H-P axis
  • ↓ CRH
  • ↓ ACTH
  • ↓ Cortisol
59
Q

Which 2 diseases affecting cortisol secretion will have hyperpigmentation?

A
  • Secondary (pituitary) excess
  • Primary deficiency

*Processes where ACTH is elevated

60
Q

What is responsible for the increased synthesis and secretion of aldosterone by stimulating cholesterol desmolase and aldosterone synthase?

A

Angiotensin II

61
Q

How does levels of K+ affect aldosterone secretion?

A
  • ↑ [K+] —> ↑ aldosterone
  • ↓ [K+] —> ↓ aldosterone
62
Q

What are the 3 main actions of aldosterone on the late distal tubule an collecting duct of the kidney?

A
  • ↑ Na+ reabsorption
  • ↑ K+ secretion
  • ↑ H+ secretion
63
Q

What is secreted by the α cells of the endocrine pancreas and where are these cells located?

A
  • Secrete glucαgon
  • Located near periphery of islet
64
Q

Describe the paracrine mechanism of communication between the alpha, delta, and beta cells of the pancreatic islets.

A
  • Delta cells (somatostatin) inhibit secretion from both beta and alpha cells
  • Beta cells (insulin) inhibit secretion from alpha cells
  • Alpha cells (glucagon) stimulate secretion from beta cells
65
Q

Describe the downstream effects upon glucose binding its receptor and increasing the intracellular [ATP] for the synthesis of insulin

A

↑ ATP –> K+ channels close —> cell depolarizes, which opens voltage-sensitivie Ca2+ channels —> ↑ intracellular Ca2+ leads to exocytosis of insulin

66
Q

Explain the mechanism which makes sulfonylurea drugs (i.e., tolbutamide and glyburide) useful in the tx of T2DM

A

Sulfonylurea receptor (SUR) promotes the closing of ATP-dependent K+ channels –> depolarization and ↑ release of insulin

67
Q

Why is C peptide useful as a diagnostic tool in the screening of endogenous B cell function?

A

Is secreted in equimolar amounts with insulin and excreted unchanged in the urine

68
Q

Which glucose transporter on pancreatic beta cells does glucose use to enter and promote the secretion of insulin?

A

GLUT2

69
Q

What is responsible for down-regulation of the insulin receptor by decreasing the rate of synthesis and increasing the rate of degradation?

A

Insulin down-regulates its own receptor

70
Q

What is the effect of insulin on [K+]?

A

↑ K+ uptake into cells

71
Q

List 10 factors which stimulate insulin secretion

A
  • ↑ [glucose] + ↑ [AA’s] + ↑ [fatty acids] and [ketoacid]
  • Glucagon
  • Cortisol
  • GIP
  • Vagal stimulation; ACh
  • K+
  • Sulfonylurea drugs
  • Obesity
72
Q

List 6 factors which inhibit the release of insulin

A
  • ↓ blood glucose
  • Fasting
  • Exercise (don’t want glucose entering cell!)
  • Somatostatin
  • α-adrenergic agonists
  • Diazoxide
73
Q

Insulin receptor signaling causes the translocation of which receptor to the cell membrane for the transport of glucose into the cell?

A

GLUT4

74
Q

What is the incretin effect and list incretins.

A
  • Oral glucose has a greater effect on the secretion of insulin compared to glucose given via IV
  • Incretins = GLP-1 and GIP which are secreted in response to GI glucose and fat
75
Q

What are 3 factors that inhibit the secretion of glucagon?

A
  • Insulin
  • Somatostatin
  • ↑ fatty acid and ketoacid concentration
76
Q

What is the the major factor stimulating the secretion of glucagon?

A

Decreased blood [glucose]

77
Q

Which 2 amino acids stimulate the secretion of glucagon?

A

Arginine and alanine

78
Q

Which hormone released from the GI tract stimulates the secretion of glucagon?

A

CCK

79
Q

What are the 4 major actions of glucagon?

A
  • ↑ glycogenolysis
  • ↑ gluconeogenesis
  • ↑ lipolysis
  • ↑ ketoacid formation
80
Q

What effect does ↑ phosphate concentration have on ionized Ca2+ concentration?

A

↑ phosphate concentration –> ↓ ionized Ca2+ concentration

81
Q

Which 2 hormones stimulate an increase in bone resorption to ↑ Ca2+ concentration?

A

PTH and Vit D (1,25-dihydroxy)

82
Q

The extracellular concentration of what ion is regulated by the same hormone that regulate Ca2+ concentration?

A

Phosphate (Pi)

83
Q

Which hormone can cross the cell membrane in the parathyroid gland and downregulate PTH gene transcription and upregulate CaSR gene transcription?

A

1,25-Vitamin D

84
Q

What is responsible for inhibiting the synthesis and secretion of PTH?

A

↑ extracellular Ca2+

85
Q

What can you look for in the urine to assess the action of PTH on the kidney?

A

Urinary cAMP levels will be ↑ with ↑ PTH

86
Q

What levels of [Ca2+], PTH and [Phosphate] stimulate 1α-hydroxylase in the renal proximal tubule to ↑ 1,25-(OH)2-cholecalciferol production?

A
  • ↓ [Ca2+}
  • ↓ [Phosphate]
  • ↑ PTH
87
Q

Which 2 hormones act synergistically to stimulate osteoclast activity and bone resorption?

A

PTH and 1,25-(OH)2-cholecalciferol

88
Q

How does the short-term vs. long-term action of PTH on bone differ?

A
  • Short-term = bone formation (via direct action on osteoblasts)
  • Long-term = ↑ bone resorption (indirect action on osteoclasts mediated by cytokines released from osteoblasts)
89
Q

What is the effect of vitamin D on the kidney in terms of Pi and Ca2+?

A
  • Promotes Pi reabsorption by proximal nephrons (stimulates NPT2a expression)
  • Minimal actions on Ca2+
90
Q

Which type of hyperparathyroidism does this represent?

A

Primary Hyperparathyroidism

91
Q

In terms of secondary hyperparathyroidism, blood levels of what can help you determine if the underlying cause is renal failure vs. vitamine D deficiency?

A
  • Renal failure —> ↑ Pi
  • Vitamin D deficiency —> ↓ Pi
92
Q

What are the levels of PTH, Ca2+, Pi, and Vitamin D like in hypoparathyroidism?

A
  • ↓ PTH
  • ↓ Ca2+
  • ↑ Pi
  • ↓ Vitamin D
93
Q

What are the levels of PTH, Ca2+, Pi, and Vitamin D like in albright hereditary osteodystrophy (pseudohypoparathyroidism type 1a)?

A
  • ↑ PTH
  • ↓ Ca2+
  • ↑ Pi
  • ↓ Vitamin D
94
Q

What are the levels of PTH, Ca2+, Pi, and Vitamin D like in humoral hypercalcemia of malignancy?

A
  • ↓ PTH
  • ↑ Ca2+
  • ↓ Pi
  • ↓ Vitamin D
95
Q

How does the congenital disorder pseudovitamin D-deficient rickets type I differ from type II?

A
  • Type I = ↓ 1α-hydroxylase
  • Type II = ↓ vitamin D receptor
96
Q

How does rickets differ from osteomalacia?

A
  • Rickets is due to vitamin D deficiency in children; insufficient Ca2+ and phosphate are available to mineralize the growing bone.
  • Osteomalacia is vitamin D deficiency in adults; new bone fails to mineralize, resulting in bendng and softening of weight-bearing bones
97
Q

How does outer ring deiodination vs. inner ring deiodination of T4 in the peripheral conversion to T3 affect its activity?

A
  • Outer ring deiodination —> active T3
  • Inner ring deiodination —> inactive T3
98
Q

The “Iodide-trap” for thyroid hormone biosynthesis utilizes which pump on the basolateral membrane of thryoid follicular cells?

A

Na+-I-cotransport (symporter)

99
Q

What 3 steps of thyroid hormone synthesis utilize thyroid peroxidase?

A
  • Oxidation of I- —> I2; moves iodine through pendrin channel into the follicular lumen
  • Organification of I2 w/ TG to form MIT and DIT
  • Coupling reaction of MIT and DIT into T3 and T4
100
Q

What are 2 competitive inhibitors of Na+-I- contransport, blocking the uptake of I- into follicular cells?

A

Thiocyanate and Perchlorate

101
Q

Why is the administration of propylthiouracil (PTU) an effective treatment for hyperthyroidism?

A

Blocks all steps of thyroid hormone synthesis catalzyed by thyroid peroxidase

102
Q

Which enzyme found inside follicular epithelial cells is responsible for deiodination of residual MIT and DIT in turn “salvaging” both I- and tyrosine for another cycle of thyroid hormone synthesis?

A

Thyroid deiodinase

103
Q

Deficiency of which enzyme mimics dietary I- deficiency?

A

Thyroid deiodinase

104
Q

What is the Wolff-Chaikoff effect in regards to thyroid hormone synthesis?

A

High levels of I- inhibit organification and synthesis of thyroid hormones

105
Q

Thyroxine-binding protein (TBG) has a higher affinity for what type of thyroid hormone?

A

T4

106
Q

In hepatic failure there is decreased production of thyroxine-binding protein (TBG) and what effect does this have on levels of free T3 and T4 and the synthesis of thyroid hormones?

A
  • Causes an ↑ in the level of free T3 and T4 because less is bound to TBG
  • This ↑ in free thyroid will negatively feedback to thyroid to inhibit synthesis of thyroid hormones
107
Q

What is the effect of pregnancy of levels of TBG, free T3,T4 and the synthesis of thyroid hormone?

A
  • ↑ levels TBG —> ↑ bound T3, T4 —> ↓ free T3, T4
  • Transient ↓ T3, T4 causes ↑ in the synthesis and secretion of T3, T4 by the thyroid
  • Overall = ↑ total T3, T4, but levels of free, physiologically active, thyroid hormone are normal = clinically euthyroid
108
Q

Release of TSH from the anteror pituitary is positively and negatively regulated by what?

A
  • (+) regulated by TRH from the hypothalamus
  • (-) regulated by free T3
109
Q

What is the effect of hyper- and hypothyroidism on bone?

A
  • Hyperthyroidism = osteoporosis
  • Hypothyroidism = stunted growth
110
Q

Explain how thyroid-stimulating immunoglobulins which underlie the pathophysiology of Graves Disease affect the HPT axis and effect levels of TSH and thyroid hormones?

A
  • TSI’s stimulate the TSH receptor without TSH hormone
  • Leads to an ↑ in circulating thyroid hormones which inhibit the secretion of TSH

Endo II - Path (Tobin) (6 decks)

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