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Endocrine Flashcards

1
Q

Derivations of the anterior pituitary and posterior pituitary:

A

Anterior = oral ectoderm (Rathke pouch)

Posterior = neuroectoderm

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2
Q

Where is the most common site of ectopic thyroid?

A

Lingual thyroid- due to failed migration

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3
Q

Child presents with a midline anterior neck mass that moves when he swallows or sticks out his tongue

A

thyroglossal duct cyst

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4
Q

Origin of parafollicular cells (C cells) of the thyroid

A

neural crest (remainder of thyroid tissue is derived from endoderm)

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5
Q

How to distinguish between central diabetes insipidus and nephrogenic diabetes insipidus

A

water deprivation test

o Central DI- urine osmolality will inc after administration of ADH
o Nephrogenic DI- urine osmolality doesn’t change after administration of ADH

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6
Q

Adrenal gland derivations

A

Cortex = mesoderm

Medulla = neural crest cells

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7
Q

Adrenal cortex layers and functions

A

GFR corresponds with Salt (Na), Sugar (glucocorticoids), and Sex (Androgens) – the deeper you go the sweeter it gets

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8
Q

Zona Gomerulosa

A

Regulated by: renin angiotensin system

Secretes: aldosterone

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9
Q

Zona Fasciculata

A

Regulated by: ACTH, CRH

Secretes: Cortisol

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10
Q

Zona Reticularis

A

Regulated by: ACTH, CRH

Secretes: sex hormones (androgens)

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11
Q

Medulla (Chromaffin Cells)

A

Regulated by: Preganglionic sympathetics (ACh)

Secretes: catecholamines (epinephrine, norepinephrine)

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12
Q

What amino acid are the thyroid hormones derived from?

A

Tyrosine

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13
Q

Wolff Chaikoff effect

A

excess iodine temporarily inhibits thyroid peroxidase and causes dec iodine organification → dec T3/T4 production

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14
Q

How does a dietary deficiency of iodine cause goiter?

A

The gland enlarges in an attempt to access more blood to inc iodine uptake

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15
Q

Functions of T3

A

Brain maturation
Bone growth
B adrenergic effects (Inc CO, HR, SV, and contractility)
Basal metabolic rate increases (Via inc Na/K ATPase activity)
Inc glycogenolysis, gluconeogenesis, and lipolysis

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16
Q

Graves Disease

A

Hyperthyroidism – autoantibody that stimulates TSH receptor – Thyroid Stimulating Immunoglobulin (TSI) – and causes increased synthesis and release of thyroid hormone

(Type 2 hypersensitivity)

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17
Q

Goiter, exopthalmos, and pretibial myxedema

A

Graves Disease

o Goiter: constant TSH stimulation causes thyroid hyperplasia and hypertrophy
o Exopthalmos and pretibial myxedema fibroblasts behind the orbit and overlying the shin express the TSH receptor → inflammation due to infiltration of T cells that release cytokines and inc fibroblast secretion of glycosaminoglycan

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18
Q

Baby presents with developmental delay, a umbilical hernia, and a protruding tongue. What do you suspect?

A

Congenital hypothyroidism (cretinism)

pot bellied, pale, puffy faced, protruding umbilicus (hernia), protuberant tongue, and poor brain development

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19
Q

What drugs cause hypothyroidism?

A

Lithium and Amiodarone

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20
Q

Hashimoto Thyroiditis

A

autoimmune destruction of the thyroid gland – due to T cell sensitization to thyroid antigen and antibodies against thyroglobulin and thyroid peroxidase

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21
Q

What HLA subtype is Hashimoto thyroiditis associated with? What are patients with Hashimoto thyroiditis at inc risk of?

What other disease is associated with this HLA type?

A

HLA DR5 (Pernicious anemia)

Inc risk of non Hodgkin lymphoma

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22
Q

Patient presents with jaw pain, tender thyroid, and inc ESR after a recent viral infection

A

Subacute Granulomatous (De Quervain) Thyroiditis

Granulomatous thyroiditis- may be hyperthyroid early on and then progresses to hypothyroid

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23
Q

Patient presents with signs of hypothyroidism and a rock hard thyroid

A

Riedel Fibrosing Thyroiditis (hypothyroidism)

Chronic inflammation with extensive fibrosis of the thyroid gland

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24
Q

Thyroid histo: branching papillary structures with interspersed calcified bodies

A

Papillary thyroid cancer

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25
Q

Thyroid histo: tall/crowded follicular cells with scalloped colloid

A

Graves disease

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26
Q

Thyroid histo: Extensive stromal fibrosis that extends beyond the capsule

A

Riedel thyroiditis

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27
Q

Thyroid histo: Mixed cellular infiltration with occasional multinucleated giant cells

A

Subacute granulomatous thyroiditis (de Quervain)

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28
Q

Thyroid histo: Mononuclear parenchymal infiltration with well-developed germinal centers

A

Hashimoto thyroiditis

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29
Q

Thyroid histo: Empty appearing nuclei with central clearing (Orphan Annie eyes), psammoma bodies and nuclear grooves (coffee beans):

A

Papillary carcinoma

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30
Q

Thyroid histo: sheets of cells in an amyloid stroma

A

medullary carcinoma (from parafollicular “C cells” – produces calcitonin

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31
Q

Hypothyroid myopathy

A

Dec tendon refelxes and myoedema

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32
Q

Patient presents with decreased lateral vision. If you suspect a brain lesion, where would it be?

A

The patient appears to have bitemporal hemianopia, which is characteristic of a pituitary adenoma

Patient will likely have inc prolactin levels, as prolactinomas are most common

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33
Q

Which MEN is associated with Pheochromocytomas, Medullary thyroid carcinoma, and parathryoid hyperplasia?

A

MEN2A
(Mutation in RET gene)
2 P’s: parathyroid and pheochromocytoma

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34
Q

Which MEN is associated with pheochromocytomas, medullary thyroid carcinoma, mucosal neuromas, and marfanoid habitus?

A

MEN2B
(Mutation in RET gene)
1 P: pheochromocytoma

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35
Q

Which MEN is associated with pituitary tumors, pancreatic endocrine tumors, and parathyroid adenomas?

A

MEN1
(Mutation in MEN1 tumor suppressor gene)
3 P’s: parathyroid, pancreas, and pituitary

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36
Q

Zollinger Ellison syndrome is associated with which MEN?

A

MEN1

as are insulinomas and VIPomas

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37
Q

Pheochromocytoma is associated with which other disorders?

A

MEN2A/MEN2B, Von Hippel Lindau, and Neurofibromatosis type 1

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38
Q

What cells do pheochromocytomas arise from? What do they secrete?

A

Arise from chromaffin cells of the adrenal medulla – secrete catecholamines (epinephrine, norepinephrine, and dopamine)

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39
Q

Cortisol functions

A 
Catabolic
BIG FIB
Blood pressure inc
Insulin resistance
Gluconeogenesis, lipolysis, and proteolysis inc
Fibroblast activity dec
Inflammatory/immunosuppression
Bone formation decrease
40
Q

What is the most common cause of Cushings syndrome?

A

Exogenous corticosteroid use

causes dec ACTH and bilateral adrenal atrophy

41
Q

Patient presents with HTN, weight gain, moon facies, abdominal striae, truncal obesity, osteoporosis, hyperglycmeia

A

Cushing Syndrome

  1. HTN: cortisol increases BP
  2. Striae: fibroblast inhbition
  3. Osteoporosis: dec in bone formation
42
Q

Cushing Disease vs Cushing Syndrome

A

Disease – pituitary hypersecretion of ACTH usually from a pituitary adenoma
high ACTH –> high cortisol

Syndrome (many causes): low ACTH –> high cortisol

43
Q

Cushing Disease

A

Pituitary hypersecretion of ACTH usually from a pituitary adenoma

Excess ACTH leads to adrenal cortical hyperplasia and excess cortisol secretion

44
Q

How can you distinguish between Cushing syndrome caused by pituitary secretion of ACTH vs ectopic ACTH secretion

A

Both will have inc ACTH

Use dexamethasone suppression test

Pituitary secretion: ACTH will dec
Ectopic: ACTH will not dec

45
Q

17a hydroxylase deficiency

A

Inc mineralocorticoid (aldosterone) production, dec cortisol, and dec sex hormones

Inc BP and dec serum K+

Ambiguous genitalia, undescended testes, lack of secondary sex characterisitcs

46
Q

21 hydroxylase deficiency

A

Inc sex hormones, dec aldosterone and cortisol

Dec BP, inc serum K+

Salt wasting in infants
Precocious puberty in children

47
Q

11B hydroxylase deficiency

A

Dec aldosterone, inc 11-deoxycortisone (causes inc BP), dec cortisol, inc sex hormones

Inc BP, dec serum K, dec renin, virilization

48
Q

Dec renin

Inc Aldosterone

A

Primary hyperaldosteronism: the adrenal is making a lot of aldosterone and renin system shuts off

49
Q

Inc renin

Inc aldosterone

A

Secondary hyperaldosteronism: abnormal activation of the renin-angiotensin system
ex. juxtaglomerular cell tumor

50
Q

Waterhouse-Friedrichsen syndrome

A

Acute adrenal insufficiency due to bilateral adrenal hemorrhage associated with septicemia (N meningitidis)

51
Q

Addison disease

A

Chronic destruction of the adrenal cortex due to autoimmune destruction or TB infection

52
Q

How does diabetes lead to ketoacidosis?

A

Usually only in T1DM

Dec insulin in the blood causes lipolysis to proceed unregulated. Inc FFA are converted to acetyl-CoA and are used for ketogenesis –> ketone body formation!!

53
Q

C-peptide

A

Secreted from secretory granules with endogenous insulin

Do not see C peptide with exogenous peptide administration

54
Q

Insulin: catabolism or anabolism?

A

Anabolism!!

Promotes the storage of protein, glucose, and lipids

Prevents glycogenolysis by activation of protein phosphatase
Prevents gluconeogenesis by increasing F26BP

55
Q

What type of fuel do RBCs utilize and why?

A

ONLY glucose. They lack mitochrondria so they can’t metabolize FFA or ketones

56
Q

What enzyme does insulin activate, which promotes the storage of glucose as glycogen?

A

Protein phosphatase

57
Q

Autonomic nervous system effects on insulin

A

Sympathetics (epinephrine) prevents insulin release: because during fight or flight, the body wants to mobilize glucose

Parasympathetics (ACh) causes insulin release: during rest or digest, the body wants to store glucose as glycogen for future use

58
Q

What is the major regulator of insulin release?

A

Glucose - enters pancreatic B cells via GLUT2 and promotes insulin secretion

59
Q

Insulin receptor

A

Tyrosine kinase (MAP Kinase)

60
Q

Which transporters are insulin dependent and where are they located?

A

GLUT4, on adipose and skeletal muscle tissue

61
Q

Steps of insulin release

A
  1. glucose enters pancreatic B cells via GLUT2
  2. Glucose undergoes glycolysis to produce ATP
  3. ATP binds to K+ channels and shuts them
  4. K+ cannot leave the cell, causing cell depolarization
  5. Voltage gated Ca2+ channels open and Ca2+ enters the cells
  6. Inc Ca2+ in the cell stimulates the exocytosis of insulin granules
62
Q

Glucagon action: catabolism or anabolism?

A

Catabolism

Promotes glycogenolysis, gluconeogenesis, lipolysis, ketogenesis

63
Q

Histology of T1DM vs T2DM

A

Type 1: leukocytic infiltrate (autoimmune destruction)

Type 2: amyloid polypeptide deposition

64
Q

14 year old boy presents with delayed puberty and complaints of anosmia

A

Kallmann syndrome

Defective migration of GnRH cells and formation of the olfactory bulb – leads to dec GnRH synthesis (synthesis)

Dec GnRH, LH, FSH, and testosterone

65
Q

What cancer can cause SIADH

A

Small cell lung cancer

66
Q

Findings on SIADH

A

Euvolemic hyponatremia: no edema or JVD, due to compensatory suppression of the renin-angiotensin system (water is absorbed, inc extracellular volume, dec renin ang system, salt wasting)

Urine osmolality>Serum osmolality

67
Q

Roles of prolactin

A

Stimulates milk production and decreases GnRH secretion

68
Q

Effects of dopamine on prolactin

A

Dopamine inhibits secretion of prolactin – dopamine antagonists cause prolactin levels to rise –> galactorrhea

69
Q

What do you use to treat prolactinomas?

A

Dopamine agonists (Bromocriptine)

70
Q

Corticosteroid effects on WBCs

A

Neutrophilia – induces demargination of neutrophils previously attached to the vessel wall
Neutrophil recruitment to fight infection in tissues is dcreased

71
Q

What is the primary site of PTH action?

A

The kidney -

  1. inc calcium reabsorption in the DCT
  2. dec phosphate reabsorption in the PCT
  3. inc activation of vitamin D
72
Q

PTH effects on bone

A

Stimulates Osteoblasts to secrete RANKL – which increases the number and function of osteoclasts

Bone resorption and inc Ca release

73
Q

PTHrP
Actions?
When do you see it?

A

PTH related peptide – Functions like PTH

Commonly increased in malignancies (squamous cell carcinoma of the lung, renal cell carcinoma)

74
Q

What lung cancer secretes PTHrP?

A

Squamous cell carcinoma of the lung

75
Q

Vitamin D functions

A

Inc Ca and phosphate absorption in the intestines

76
Q

What activates Vitamin D? Where does this occur?

A

Vitamin D is activated in the kidney by 1a hydroxylase to 1,25 OH2 D3

24,25 OH2 D3 is the inactive form

Activated by inc PTH or by dec phosphate

77
Q

What pathology can increase vitamin D and lead to hypercalcemia?

A

Granulomatous disease

Macrophages cause inc activation of vitamin D

78
Q

Signs of hypocalcemia vs hypercalcemia

A

Hypocalcemia:
- neuromuscular excitability
- muscle cramps, perioral paresthesias, hypotension, chvostek sign, trousseau sign
(common cause = parathyroid damage in thyroid surgery)

Hypercalcemia:
- constipation, polyuria/polydipsia, muscle weakness
(thiazides, bones mets, multivitamin overdose)

79
Q

Hypercalcemia is seen in which MEN syndrome(s)?

A

MEN1
MEN2A

Due to parathyroid pathology

80
Q

POMC gives rise to what?

A

ACTH
Beta endorphins (opioids)
MSH

81
Q

Patient presents complaining of recent weight gain, inc bruising, and hyperpigmentation of the skin. He has epigastric abdominal pain that is relieved by over the counter antacids. He has elevated BP and a CXR shows an irregular mass in the right lung field. What is the mass and what is likely responsible for his symptoms?

A

Small cell carcinoma of the lung that is secreting ACTH

excess ACTH leads to adrenal cortical hyperplasia and excess glucocorticoid secretion
o Will see hyperpigmentation of the skin because ACTH directly stimulates melanotropin receptors due to significant sequence homology with a-MSH

82
Q

Laryngeal nerves

A

o Superior laryngeal nerve (branch of CNX) – innervates the cricothyroid muscle – 4th branchial arch

o Recurrent laryngeal nerve (branch of CNX) – innervates the rest of the laryngeal muscles – 6th branchial arch (can be damaged during thyroid surgery)

83
Q

Why is there pigmentation in primary adrenal insufficiency?

A

Increased levels of ACTH (in an attempt to stimulate the adrenal gland) stimulates melanocytes

**ACTH and MSH are both derived from POMC

84
Q

Patient presents with progressive lethargy. She has had a loss of appetite, constipation, muscle weakness, and inc thirst and urination. She admits to taking large doses of vitamin and mineral substances to help boost her health. What do you suspect?

A

Hypercalcemia

Likely due to inc vitamin D intake from multivitamins

85
Q

A patient with a past medical history of pheochromocytoma presents with a thyroid mass and is diagnosed with thyroid cancer. What type of cancer is most likely in this patient and why?

A

Medullary carcinoma

With a past hx of pheochromocytoma, the patient likely has MEN2A/2B.

86
Q

What are neurophysins?

A

carrier proteins for oxytocin and vasopressin (ADH) – act as chaperone molecules and shuttle these hormones from the hypothalamus to the nerve terminals in the posterior pituitary

87
Q

Familial Hypocalciuric Hypercalcemia

A

defective Ca2+ sensing receptor (G coupled proteins) causing higher than normal calcium levels to suppress PTH
o Inc PTH → inc Calcium renal reuptake → mild hypercalcemia with normal to inc PTH levels

88
Q

Pathophysiology of cataracts and peripheral neuropathy in diabetes:

A

during hyperglycemia, excess plasma glucose is converted to sorbitol by aldose reductase. Sorbitol accumulates in some cells (eye lens and schwann cells) and attracts water into these tissues leading to osmotic cellular injury.

89
Q

Patient presents with several month history of diabetes and a month history of a rash that are coalescing erythematous lesions with crusting and scaling at the borders and central areas of bronze colored necrosis. Biopsy shows superficial necrolysis.

A

Glucagonoma

tumor of pancreatic a cells → overproduction of glucagon
o	Presents with the D’s
o	Dermatitis (necrolytic migratory erythema)
o	Diabetes (hyperglycemia)
o	DVT
o	Declining weight
o	Depression
o	Tx: octreotide, surgery
90
Q

How does increased ethanol intake cause hypoglycemia?

A

Ethanol metabolism uses up NAD+ to form NADH, which causes an increase in the NAD+/NADH ratio.

Lack of NAD+ causes inhibition of gluconeogenesis (lactate cannot be converted to pyruvate and the reaction is instead driven from pyruvate to lactate due to excess NADH).

91
Q

Postpartum female presents with cold intolerance and failure to lactate. What should you be concerned about?

A

Sheehan syndrome: ischemic infarct of pituitary following postpartum bleeding

o During pregnancy, the pituitary enlarges due to estrogen-induced hyperplasia of the lactotrophs → more susceptible to ischemia

92
Q

Hormone changes in chronic glucocorticoid use in response to stress?

A

Tertiary adrenal insufficiency

Dec CRH
Dec ACTH
Dec cortisol

93
Q

What should you be concerned about in a patient with Grave’s disease who comes in with fever and sore throat?

A

Agranulocytosis

This is a rare complication of thionamides (propylthiouracil and methimazole)

94
Q

Estrogen effects in TBG

A

o Inc estrogen → Inc TBG → inc total T4 and T3 (normal levels of free T3 and T4)
o They remain Euthyroid!

95
Q

If patient is exposed to radioactive iodide, what is the best medical management?

A

Potassium iodide

96
Q

Child presents with abdominal distention and myoclonus. Parents report that they have noticed spontaneous bursts of non-rhythmic conjugate eye movements in various directions. What is the likely diagnosis?

A

Neuroblastoma - tumor of the adrenal medulla seen in children

Originates from neural crest cells

Child presents with abdominal distention, hypertension, and opsoclonus-myoclonus syndrome (dancing eyes and dancing feet)

Associated with N-myc oncogene

97
Q

Peripheral artery disease:
Pathophys
Risk factors
Treatment

A

Atherosclerotic plaques causing luminal narrowing
Common in diabetes, hyperlipidemia, HTN, smoking, age >70
Intermittent claudication: symptoms occur with exercise and resolve with rest
Cilostazol: reduces platelet activation by inhibiting platelet phosphodiesterase and is a direct arterial vasodilator

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