DIT review - Endocrinology 1 Flashcards

1
Q

Which hormones use the cAMP pathway (Gs and Gi)

A
  • Most hormones of anterior pituitary
  • FSH, LH, ACTH, TSH, hCG, MSH, GHRH, CRH, PTH, calcitonin, glucagon, V2 vasopressin receptor
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2
Q

Which hormones use IP3 pathway (Gq)

A
  • Hormones of posterior pituitary minus V2
  • GnRH, TRH, oxytocin, V1 vasopressin receptor, H1 histamine receptor, angiotensin II, gastrin
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3
Q

Which hormones use cGMP pathway

A
  • Vasodilators
  • Nitric oxide (NO), Atrial natriuretic peptide (ANP)
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4
Q

Which hormones use steroid receptors

A

Estrogens, progesterone, testosterone, glucocorticoids, aldosterone, thyroid hormone (T3/T4), vitamin D

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5
Q

Which hormones use tyrosine kinase receptors

A
  • Insulin, insulin-like growth factor (IGF-1), platelet derived growth factor (PDGF), fibroblast growth factor (FGF)
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6
Q

Which hormones use nonreceptor tyrosine kinase (e.g. JAK/STAT)

A
  • Prolactin, cytokines (IL-2, IL-6, IFN), GH, G-CSF, Erythropoietin, Thrombopoeitin
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7
Q

Causes of hyperprolactinemia

A
  • Pregnancy/nipple stimulation
  • Stress
  • Prolactinoma
  • Dopamine antagonists
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8
Q

Presentation of hyperprolactinemia

A
  • Due to prolactin’s inhibitory effects on GnRh
  • Premenopausal women:
    • Hypogonadism, infertility, oligo/amenorrhea, galactorrhea (rare)
  • Postmenopausal women:
    • Asymptomatic
  • Males:
    • Hypogonadism, decreased libido, impotence, infertility, gynecomastia, galactorrhea (rare)
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9
Q

Effects of growth hormone on insuline

A
  • Increases insulin resistance (diabetogenic)
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10
Q

How do you diagnose acromegaly?

A

Increased serum IGF-1

Growth hormone is secreted in a pulsatile fashion and levels fluctuate throughout the day by IGF-1 levels are generally consistent

Confirmatory test - failure to suppress serum GH following oral glucose tolerance test

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11
Q

What disorder is characterized by failure to breast-feed, absent menstruation, and cold intolerance after giving birth

A

Sheehan Syndrome - ischemic infarct of pituitary following postpartum bleeding

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12
Q

Draw out the steroid synthesis pathway, including enzymes

A
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13
Q

Describe the main features of each of the congenital adrenal hyperplasia enzyme deficiencies (21 a-hydroxylase, 17 a-hydroxylase, 11 b-hydroxylase)

A
  • HINTS:
    • If there is a 1 in the first digit of deficient enzyme (11 or 17) – will be HTN
    • If there is a 1 in the second digit of deficient enzyme (11 or 21) – will be masculinization
    • K+ does the opposite of whatever Na+ does
  • 21 a-hydroxylase
    • Hypotension
    • Hyperkalemia
    • Masculinization
  • 11 b-hydroxylase
    • Hypertension
    • Hypokalemia
    • Masculinization
  • 17 a-hydroxylase
    • Hypertension
    • Hypokalemia
    • Ambigious genitalia in XY
    • Lack of secondary sexual development in XX
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14
Q

What are the actions/effects of cortisol

A
  • Increased BP
    • Upregulates a1 receptors in arterioles, thus increasing sensitivity to NE and Epi
  • Increases insulin resistance (diabetogenic)
  • Increases gluconeogenesis, lipolysis, proteolysis
  • Decreases fibroblast activity (skin thinning and striae)
  • Decreases inflammatory and immune response
    • Will initially see neutrophilia due to decreased WBC adhesion
  • Decreases bone formation
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15
Q

Causes of Cushing syndrome

A
  • Exogenous corticosteroids (most common cause)
  • ACTH-secreting pituitary adenoma (Cushing disease)
  • Paraneoplastic ACTH secretion (e.g. small cell lung cancer)
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16
Q

Describe how a Dexamethasone suppression test helps to differentiate between different causes of Cushing syndrome

A
  • First give low-dose dexamethasone (synthetic glucocorticoid)
  • Measure ACTH:
    • If low, suspect adrenal tumor or exogenous glucocorticoids
    • If high, suspect Cushing disease (ACTH-pituitary adenoma) or ectopic ACTH secreting tumor
      • Give high dose Dexamethasone:
        • Cortisol levels will decrease if Cushing Disease
        • Cortisol levels will remain elevated if ectopic tumor
17
Q

What is the effect of glucocorticoids on bones?

A

Osteoporosis

Chronic glucocorticoid use should be supplemented with calcium and/or vitamin D

18
Q

What is the most common cause of primary adrenal insufficiency

A

Aka Addison disease

Most commonly due to autoimmune destruction of adrenal gland

19
Q

Presentation of primary adrenal insufficiency

A

o Lack of cortisol - Weakness, fatigue, weight loss

o Lack of aldosterone - hypotension, hyponatremia, hyperkalemia

o Increased ACTH - skin hyperpigmentation (due to POMC)

20
Q

Cause of acute primary adrenal insufficiency

A

Waterhouse-Friederichsen syndrome

Acute primary adrenal insufficiency due to adrenal hemorrhage associated with septicemia (usually Neisseria meningitides), DIC, endotoxic shock

21
Q

What is the presentation of secondary adrenal insufficiency

A

o Lack of cortisol due to decreased ACTH à weakness, fatigue, weight loss

o Aldosterone synthesis is preserved (controlled by RAAS) à no hypotension or hyperkalemia

o ACTH low à no hyperpigmentation

22
Q

What is the most common cause of tertiary adrenal insufficiency

A

Usually caused by abrupt withdrawal of exogenous steroids after chronic usage

23
Q

What is Conn syndrome

A

Primary hyperaldosteronism due to adrenal adenoma

24
Q

What is the classic presentation of hyperaldosteronism

A

· Hypertension

· Hypokalemia

· Metabolic alkalosis

25
What is the cause of metabolic alkalosis in hyperaldosteronism
o Aldosterone causes increased H+ urinary loss o Decreased K+ causes cells to push out K+ in exchange for taking up H+
26
What is the basic premise behind secondary hyperaldosteronism
Occurs when kidneys perceive low volume and activate RAAS o Will see elevated renin
27
Causes of secondary hyperaldosteronism
o Renal artery stenosis o Congestive heart failure o Low protein states (decreased osmotic pressure leads to low blood volume) - E.g. Cirrhosis or nephrotic syndrome
28
What is the oncogene associated with neuroblastoma
· Overexpression of N-myc oncogene
29
What are the positive serum markers in neuroblastoma
· Bombesin and NSE (+)
30
What is a neuroblastoma
Tumor of the adrenal medulla (usually in children)
31
What is seen on histology of neuroblastoma
· Homer Wright rosettes (also seen in medulloblastoma)
32
What is the rule of 10's (or 90's) associated with pheochromocytoma
o 90% benign o 90% unilateral o 90% adrenal medulla (some can be extra-adrenal) o 90% do not calcify o 90% adults
33
Treatment of pheochromocytoma
o Surgical resection o Alpha blockers (phenoxybenzamine) o Can also add on beta-blockers § Do not give beta-blockers first – will lead to unopposed alpha vasoconstriction and hypertensive crisis
34
MEN 1
Mutation of MEN 1 * Pituitary tumors (prolactin or GH) * Pancreatic endocrine tumors (Zollinger-Ellison syndrome, insulinomas, VIPomas, glucagonomas) * Parathyroid adenomas
35
MEN 2A
Mutation of RET gene * Medullary thyroid carcinoma (neoplasm of parafollicular C cells which secrete calcitonin) * Pheochromocytoma * Parathyroid hyperplasia
36
MEN 2B
Mutation of RET gene * Medullary thyroid carcinoma * Pheochromocytoma * Mucosal neuromas (oral/intestinal ganglioneuromatosis)
37