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First Aid > Endocrine 2 > Flashcards

Endocrine 2 Flashcards

1
Q

What is the most common steroidogenic enzyme deficiency?

A

21-hydroxylase deficiency

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2
Q

What is the effect of 21-hydroxylase deficiency on mineralocorticoids?

A

Decreased

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3
Q

What is the effect of 21-hydroxylase deficiency on cortisol?

A

Decreased

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4
Q

What is the effect of 21-hydroxylase deficiency on sex hormones?

A

Increased

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5
Q

What is the effect of 21-hydroxylase deficiency on blood pressure (BP)?

A

Low

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6
Q

What is the effect of 21-hydroxylase deficiency on potassium levels ([K+])?

A

High

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7
Q

What are the lab findings in 21-hydroxylase deficiency?

A

Increased renin activity & 17-hydroxyprogesterone

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8
Q

What is the presentation of 21-hydroxylase deficiency?

A

Presents in infancy (salt wasting) or childhood (precocious puberty); XX: virilization

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9
Q

What is the effect of 11-hydroxylase deficiency on mineralocorticoids?

A

Decreased aldosterone, increased 11-deoxycorticosterone

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10
Q

What is the effect of 11-hydroxylase deficiency on cortisol?

A

Decreased

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11
Q

What is the effect of 11-hydroxylase deficiency on sex hormones?

A

Increased

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12
Q

What is the effect of 11-hydroxylase deficiency on blood pressure (BP)?

A

Increased (due to increased 11-deoxycorticosterone)

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13
Q

What is the effect of 11-hydroxylase deficiency on potassium levels ([K+])?

A

High

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14
Q

What are the lab findings in 11-hydroxylase deficiency?

A

Increased renin activity

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15
Q

What is the presentation of 11-hydroxylase deficiency?

A

XX: virilization

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16
Q

What is the source of cortisol?

A

Adrenal zona fasciculata

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17
Q

What is cortisol bound to?

A

Corticosteroid-binding globulin

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18
Q

What are the functions of cortisol?

A

A BIG FIB: Appetite, BP, Insulin resistance, Gluconeogenesis, lipolysis & proteolysis, Fibroblast activity, Inflammatory & Immune response, Bone formation

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19
Q

How does cortisol increase blood pressure?

A

Upregulates alpha-1 receptors on arterioles, increasing sensitivity to NE & Epi

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20
Q

At high concentrations, which receptors can cortisol bind?

A

Mineralocorticoid (aldosterone) receptors

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21
Q

How does cortisol decrease inflammatory/immune responses?

A

Inhibits production of leukotrienes & prostaglandins, WBC adhesion, blocks histamine release, causes eosinopenia, lymphopenia, and blocks IL-2 production

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22
Q

What can exogenous corticosteroids cause reactivation of?

A

TB & candidiasis

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23
Q

What regulates cortisol secretion?

A

CRH stimulates ACTH release, leading to cortisol production in adrenal zona fasciculata

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24
Q

In what forms does Ca2+ exist?

A

Ionized/free (~45%), Bound to albumin (~40%), Bound to anions (~15%)

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25
Q

What is the effect of pH on Ca2+ levels?

A

Decreased pH decreases affinity of albumin to bind Ca2+, leading to hypocalcemia

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26
Q

What is the primary regulator of PTH?

A

Ionized/free Ca2+

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27
Q

What is the source of parathyroid hormone (PTH)?

A

Chief cells of parathyroid

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28
Q

What are the functions of PTH?

A

Bone resorption of Ca2+, kidney reabsorption of Ca2+ in DCT, reabsorption of PO43- in PCT, 1,25-(OH)2 D3 production in PCT

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29
Q

How does PTH affect 1,25-(OH)2 D3 production?

A

By stimulating kidney 1-alpha-hydroxylase in PCT

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30
Q

How does PTH affect serum Ca2+, serum PO43-, urine PO43- & urine cAMP?

A

Serum Ca2+: increased, serum PO43-: decreased, urine PO43-: increased, urine cAMP: increased

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31
Q

What is PTH known as?

A

Phosphate-Trashing Hormone

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32
Q

How does PTH trigger bone resorption?

A

By secreting RANK-L which stimulates osteoclasts

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33
Q

What is PTH-related peptide (PTHrP)?

A

Functions like PTH, commonly found in malignancies

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34
Q

How does Ca2+ regulate PTH?

A

Increased serum Ca2+ decreases PTH secretion

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35
Q

How does PO43- regulate PTH?

A

Increased serum PO43- increases PTH secretion

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36
Q

How does Mg2+ regulate PTH?

A

Increased serum Mg2+ decreases PTH secretion

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37
Q

What are common causes of decreased Mg2+?

A

Diarrhea, aminoglycosides, diuretics, alcohol abuse

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38
Q

What is the source of calcitonin?

A

Parafollicular cells (C cells) of thyroid

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39
Q

What is the function of calcitonin?

A

Decreases bone resorption of Ca2+

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40
Q

What regulates calcitonin secretion?

A

Increased serum Ca2+ increases calcitonin secretion

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41
Q

What are thyroid hormones?

A

Iodine-containing hormones that control body’s metabolic rate

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42
Q

What is the source of thyroid hormones?

A

Follicles of thyroid

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43
Q

What converts T4 to T3 in peripheral tissue?

A

5’-deiodinase

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44
Q

What inhibits the conversion of T4 to T3?

A

Glucocorticoids, beta-blockers, propylthiouracil (PTU)

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45
Q

What are the functions of thyroid peroxidase?

A

Oxidation, organification of iodide, coupling of MIT & DIT

46
Q

What are inhibitors of thyroid peroxidase?

A

PTU and methimazole

47
Q

What is the Wolff-Chaikoff effect?

A

Excess iodine temporarily decreases thyroid peroxidase activity and T3/T4 production

48
Q

What are the functions of T3?

A

Brain maturation, Bone growth, Beta-adrenergic effects, Basal metabolic rate, Blood sugar, Breakdown of lipids

49
Q

How does T3 increase basal metabolic rate?

A

Increases Na+/K+-ATPase activity, increasing O2 consumption, respiratory rate, body temperature

50
Q

How are thyroid hormones regulated?

A

TRH stimulates TSH release, primarily regulated by free T3/T4

51
Q

What increases thyroid-binding globulin (TBG) levels?

A

Pregnancy, OCP use

52
Q

What decreases TBG levels?

A

Hepatic failure, steroids, nephrotic syndrome

53
Q

What hormones use cAMP as a second messenger?

A

FLAT ChAMP: FSH, LH, ACTH, TSH, CRH, hCG, ADH (V2-receptor), MSH, PTH

54
Q

What hormones use cGMP as a second messenger?

A

BAD GraMPa: BNP, ANP, EDRF (NO)

55
Q

What hormones use IP3 as a second messenger?

A

GOAT HAG: GnRH, Oxytocin, ADH (V1-receptor), TRH, Histamine (H1-receptor), Angiotensin II, Gastrin

56
Q

What hormones have intracellular receptors?

A

PET CAT on TV: Progesterone, Estrogen, Testosterone, Cortisol, Aldosterone, T3/T4, Vitamin D

57
Q

What hormones have a receptor tyrosine kinase?

A

Insulin, IGF-1, FGF, PDGF, EGF

58
Q

What hormones utilize a nonreceptor tyrosine kinase?

A

PIGGLET: Prolactin, Immunomodulators, GH, G-CSF, Erythropoietin, Thrombopoietin

59
Q

What increases the solubility of steroid hormones?

A

Steroid hormones are lipophilic and must circulate bound to specific binding globulins

60
Q

What is the impact of increased SHBG in men?

A

Increased SHBG decreases free testosterone, leading to gynecomastia

61
Q

What is the impact of decreased SHBG in women?

A

Decreased SHBG raises free testosterone, leading to hirsutism

62
Q

What is the impact of OCPs/pregnancy on SHBG levels?

A

OCPs and pregnancy increase SHBG

63
Q

What is the most common cause of Cushing syndrome?

A

Exogenous corticosteroids

64
Q

What is responsible for the majority of endogenous cases of Cushing syndrome?

A

Cushing disease (ACTH-secreting pituitary adenoma)

65
Q

What are the etiologies of Cushing syndrome?

A

Exogenous corticosteroids, adrenal adenoma, hyperplasia, or carcinoma, ACTH-secreting pituitary adenoma, paraneoplastic ACTH secretion

66
Q

What are the clinical findings in Cushing syndrome?

A

HTN, weight gain, moon facies, abdominal striae, truncal obesity, buffalo hump, skin changes, hirsutism, osteoporosis, hyperglycemia, amenorrhea, immunosuppression

67
Q

What are the screening tests for Cushing syndrome?

A

Free cortisol on 24-hr urinalysis, midnight salivary cortisol, no suppression with overnight low-dose dexamethasone test

68
Q

What should be the next step if a patient presents with increased free cortisol on 24hr urinalysis, increased midnight salivary cortisol, no suppression with overnight low-dose dexamethasone & increased serum ACTH?

A

Measure serum ACTH

69
Q

What is the next step if a patient presents with increased free cortisol on 24hr urinalysis, increased midnight salivary cortisol, no suppression with overnight low-dose dexamethasone & increased serum ACTH?

A

Distinguish between Cushing disease & ectopic ACTH secretion

70
Q

How to interpret results of high-dose dexamethasone suppression test?

A

Determines etiology of ACTH-dependent Cushing syndrome: No suppression indicates ectopic ACTH secretion; Adequate suppression indicates Cushing disease

71
Q

How to interpret results of CRH stimulation test?

A

Determines etiology of ACTH-dependent Cushing syndrome: Increased ACTH & cortisol indicates Cushing disease; No increase indicates ectopic ACTH secretion

72
Q

What is adrenal insufficiency?

A

Inability of adrenal glands to generate enough glucocorticoids and/or mineralocorticoids for the body’s needs

73
Q

What are the symptoms & treatment for adrenal insufficiency?

A

Symptoms: weakness, fatigue, orthostatic hypotension, muscle aches, weight loss, GI disturbances, sugar &/or salt cravings. Treatment: glucocorticoid/mineralocorticoid replacement

74
Q

How to diagnose adrenal insufficiency?

A

Measurement of serum electrolytes & morning/random serum cortisol, ACTH response to ACTH stimulation test, metyrapone stimulation test

75
Q

What are cortisol & ACTH levels in primary adrenal insufficiency?

A

Decreased cortisol, increased ACTH

76
Q

What are cortisol & ACTH levels in secondary/tertiary adrenal insufficiency due to pituitary/hypothalamic disease?

A

Decreased cortisol, decreased ACTH

77
Q

What is the metyrapone stimulation test?

A

Metyrapone blocks last step of cortisol synthesis; normal response is decreased cortisol & compensatory increased ACTH & 11-deoxycortisol

78
Q

What are the results of metyrapone stimulation test in primary adrenal insufficiency?

A

ACTH is increased but 11-deoxycortisol remains decreased after test

79
Q

What are the results of metyrapone stimulation test in secondary/tertiary adrenal insufficiency?

A

Both ACTH & 11-deoxycortisol remain decreased after test

80
Q

What is oxycortisol used for?

A

Used to diagnose adrenal insufficiency.

81
Q

What are the results of the metyrapone stimulation test in primary adrenal insufficiency?

A

ACTH is increased, but 11-deoxycortisol remains low after the test.

82
Q

What are the results of the metyrapone stimulation test in secondary/tertiary adrenal insufficiency?

A

Both ACTH and 11-deoxycortisol remain low after the test.

83
Q

What is primary adrenal insufficiency?

A

Deficiency of aldosterone and cortisol production due to loss of gland function.

84
Q

What are the symptoms of primary adrenal insufficiency?

A

> Hypotension (hyponatremic volume contraction)
Hyperkalemia
Metabolic acidosis
Skin/mucosal hyperpigmentation (due to MSH, a byproduct of ACTH production from POMC)
Associated with autoimmune polyglandular syndromes.

85
Q

What is acute primary adrenal insufficiency?

A

> Sudden onset (e.g., due to massive hemorrhage)
May present with shock in acute adrenal crisis.

86
Q

What is chronic primary adrenal insufficiency?

A

Addison disease due to adrenal atrophy or destruction by disease.

87
Q

What is the most common cause of Addison disease in the Western world?

A

Autoimmune destruction.

88
Q

What is the most common cause of Addison disease in the developing world?

A

Tuberculosis (TB).

89
Q

What is Waterhouse-Friderichsen syndrome?

A

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

90
Q

What characterizes secondary adrenal insufficiency?

A

> Seen with decreased pituitary ACTH production.
No skin/mucosal hyperpigmentation.
No hyperkalemia (aldosterone synthesis preserved due to intact RAAS).

91
Q

What characterizes tertiary adrenal insufficiency?

A

> Seen in patients with chronic exogenous steroid use, precipitated by abrupt withdrawal.
Aldosterone synthesis unaffected.

92
Q

What are the clinical features of hyperaldosteronism?

A

> Increased secretion of aldosterone from the adrenal gland.
Clinical features include hypertension, hypokalemia or normal potassium levels, and metabolic alkalosis.

93
Q

How does primary vs secondary hyperaldosteronism affect edema?

A

> Primary hyperaldosteronism does not directly cause edema due to aldosterone escape mechanism.
Certain secondary causes of hyperaldosteronism (e.g., heart failure) may impair aldosterone escape mechanism, worsening edema.

94
Q

What is primary hyperaldosteronism associated with?

A

> Seen with adrenal adenoma (Conn’s syndrome) or bilateral adrenal hyperplasia.
Increased aldosterone, decreased renin.
Causes resistant hypertension.

95
Q

What is secondary hyperaldosteronism associated with?

A

> Seen in patients with renovascular hypertension, juxtaglomerular cell tumors (renin-producing), and edema (e.g., cirrhosis, heart failure, nephrotic syndrome).

96
Q

What are neuroendocrine tumors?

A

A heterogeneous group of neoplasms that begin in neuroendocrine cells, which have traits similar to nerve cells and hormone-producing cells.

97
Q

What do neuroendocrine tumor cells contain and secrete?

A

> Contain amine precursor uptake decarboxylase (APUD).
Secrete different hormones (e.g., serotonin, histamine, calcitonin, neuron-specific enolase [NSE], chromogranin A).

98
Q

Where do most neuroendocrine tumors arise?

A

Most tumors arise in the GI system, pancreas, and lungs.

99
Q

What neuroendocrine tumors arise from the GI system?

A

> Carcinoid
Gastrinoma.

100
Q

What neuroendocrine tumors arise from the pancreas?

A

> Insulinoma
Glucagonoma.

101
Q

What neuroendocrine tumor arises from the lungs?

A

Small cell carcinoma.

102
Q

What is the most common tumor of the adrenal medulla in children?

A

Neuroblastoma, usually occurring in kids under 4 years old.

103
Q

Where does neuroblastoma originate and occur?

A

> Originates from neural crest cells.
Occurs anywhere along the sympathetic chain.

104
Q

What is the presentation of neuroblastoma?

A

> Abdominal distension.
Firm, irregular mass that can cross midline (vs Wilms tumor: smooth/unilateral).
Less likely to develop hypertension than with pheochromocytoma (neuroblastoma is normotensive).
Can also present with opsoclonus-myoclonus syndrome (‘dancing eyes-dancing feet’).

105
Q

What will you see in the urine of a neuroblastoma patient?

A

Increased HVA and VMA (homovanillic acid and vanillylmandelic acid, catecholamine metabolites).

106
Q

What are the histological characteristics of neuroblastoma?

A

> Homer-Wright rosettes (characteristic of neuroblastoma and medulloblastoma).
Bombesin and NSE (neuron-specific enolase).

107
Q

How is neuroblastoma classified and what oncogene is it associated with?

A

> Classified as an APUD tumor (amine precursor uptake decarboxylase, common to neuroendocrine cells).
Associated with overexpression of N-myc oncogene.

108
Q

What is the most common tumor of the adrenal medulla in adults?

A

Pheochromocytoma.

109
Q

What is pheochromocytoma derived from and associated with?

A

> Derived from chromaffin cells (arise from neural crest).
Associated with germline mutations (e.g., NF-1, VHL, RET [MEN 2A, 2B]).

110
Q

What is the ‘rule of 10s’ for pheochromocytoma?

A

> 10% malignant.
10% bilateral.
10% extra-adrenal (e.g., bladder wall, organ of Zuckerkandl).
10% calcify.
10% in kids.

111
Q

What is the organ of Zuckerkandl?

A

> Chromaffin body derived from neural crest.
Located at the bifurcation of the aorta or at the origin of the inferior mesenteric artery.
Can be a source of a paraganglioma (extra-adrenal pheochromocytoma).

112
Q

What are the symptoms of pheochromocytoma?

A

> Most tumors secrete epinephrine, norepinephrine, and dopamine, which can cause episodic hypertension.
May also secrete EPO, leading to polycythemia.
Symptoms occur in ‘spells’ (relapse and remit).

First Aid (18 decks)

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