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Endocrine Flashcards

1
Q

Thyroglossal duct cyst

A

Presents as an anterior midline neck mass that moves with swallowing or protrusion of the tongue (vs persistent cervical sinus leading to branchial cyst in lateral neck)

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2
Q

Thyroid tissue is derived from

A

Endoderm

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3
Q

Parafollicular C cells are derived from

A

Neural crest

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4
Q

Anabolic effects of insulin

A
  • ↑ glucose transport in skeletal muscle and adipose tissue
  • ↑ glycogen synthesis and storage
  • ↑ triglyceride synthesis
  • ↑ NA+ RETENTION (KIDNEYS)
  • ↑ protein synthesis in muscle
  • ↑ CELLULAR UPTAKE OF K+ AND AMINO ACIDS
  • ↓ glucagon release
  • ↓ lipolysis in adipose tissue
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5
Q

Does insulin cross the placenta

A

Unlike glucose, insulin does not cross the placenta

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6
Q

GLUT-1

A
  • Insulin independent

- RBCs, brain, cornea, placenta

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7
Q

GLUT-2

A
  • Insulin independent
  • Bidirectional
  • Beta islet cells, liver, kidney, small intestine
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8
Q

GLUT-3

A
  • Insulin independent

- Brain, placenta

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9
Q

GLUT-4

A
  • Insulin dependent
  • Adipose tissue, striated muscle
  • Exercise can also increase GLUT-4 expression
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10
Q

GLUT-5

A
  • Fructose
  • Insulin independent
  • Spermatocytes, GI tract
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11
Q

Regulation of prolactin

A
  • Tonically inhibited by dopamine from hypothalamus
  • Can also inhibit its own secretion by ↑ dopamine synthesis and secretion from hypothalamus
  • TRH ↑ prolactin secretion (eg primary or secondary hypothyroidism)
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12
Q

How does GH release to insulin

A

↑ insulin resistance (diabetogenic)

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13
Q

Describe the roles of the V1 and V2 receptors of ADH

A
  • V1 regulates blood pressure
  • V2 regulates serum osmolarity
  • Nephrogenic DI can be caused by a mutation in V2 receptor
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14
Q

How does cortisol work to increase blood pressure

A

Upregulates alpha-1 receptors on arterioles and increases sensitivity to norepinephrine and epinephrine

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15
Q

At high concentrations, what receptors can cortisol bind to

A

At high concentrations, cortisol can bind to mineralocorticoid (aldosterone) receptors

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16
Q

How can exogenous corticosteroids cause reactivation of TB and candidiasis

A

Exogenous corticosteroids can cause reactivation of TB and candidiasis by blocking IL-2 production

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17
Q

At increased pH, does the affinity of albumin for Ca2+ increase or decrease

A

It increases, as albumin has a more negative charge at higher pH, leading to hypocalcemia (cramps, pain, parasthesias, carpopedal spasm)

18
Q

What urinary changes are seen as a result of PTH action

A
  • ↓ Ca2+
  • ↑ PO43-
  • ↑ cAMP
19
Q

How does PTH induce bone resorption

A

↑ RANK-L (receptor activator of NH-KB ligand) secreted by osteoblasts and osteocytes → binds RANK receptor on osteoclasts and their precursors to stimulate osteoclasts and ↑ Ca2+ → bone resorption

20
Q

How can PTH stimulate bone formation

A

Intermittent PTH release can also stimulate bone formation

21
Q

How do thyroid hormones increase BMR

A

Increase BMR via ↑ Na+/K+ ATPase activity → ↑ O2 consumption, RR, body temperature

22
Q

When are thyroxine-binding globulin levels increased and decreased

A
  • ↑ TBG in pregnancy or OCP use (estrogen)

- ↓ TBG in hepatic failure, steroid use

23
Q

Wolff-Chaikoff effect

A

Excess iodine temporarily inhibits thyroid peroxidase → ↓ iodine organification → ↓ T3/T4 production

24
Q

Metyrapone stimulation test

A
  • To test for adrenal insufficiency
  • Metyrapone blocks the last step of cortisol synthesis (11- deoxycortisol → cortisol)
  • Normal response is ↓ cortisol and compensatory ↑ ACTH and 11-deoxycortisol
  • PRIMARY ADRENAL INSUFFICIENCY: ACTH is ↑ but 11-deoxycortisol remains ↓ after the test
  • SECONDARY AND TERTIARY INSUFFICIENCY: both ACTH and 11-deoxycortisol remain ↓ after test
25
Q

Addison disease

A
  • Chronic primary adrenal insufficiency
  • Due to adrenal atrophy or destruction by disease
  • Autoimmune destruction most common cause in Western world
  • TB most common cause in developing world
26
Q

What type of adrenal insufficiency is seen in patients with chronic exogenous steroid use

A

Tertiary adrenal insufficiency is seen in patients with chronic exogenous steroid use and is precipitated by abrupt withdrawal. Aldosterone synthesis is unaffected in these patients.

27
Q

In which types of adrenal insufficiency is aldosterone synthesis preserved

A

Secondary and tertiary adrenal insufficiency

28
Q

What type of cells do neuroendocrine tumors arise from

A

Kulchitsky and enterochromaffin-like cells. They contain amine precursor uptake decarboxylase (APUD).

29
Q

Compare physical presentations of neuroblastoma and Wilms tumor

A

Neuroblastomas most commonly present with abdominal distention and a firm, irregular mass that can cross the midline (vs Wilms tumor, which is smooth and unilateral). Neuroblastomas can also present with opsoclonus-myoclonus syndrome.

30
Q

Jod-Basedow phenomenon

A

Thyrotoxicosis if a patient with iodine deficiency and partially autonomous thyroid tissue (eg autonomous nodule) is made iodine replete. Opposite of Wolff-Chaikoff effect.

31
Q

Pseudohypoparathyroidism type 1A and pseudopseudohypoparathyroidism

A

Pseudohypoparathyroidism type 1A:

  • Albright hereditary osteodystrophy
  • Unresponsiveness of kidney to PTH → hypocalcemia despite ↑ PTH levels
  • Characterized by shortened 4th/5th digits, short stature
  • AD
  • Due to defective Gs protein alpha subunit causing end-organ resistance to PTH
  • Defect must be inherited from mother due to imprinting

Pseudopseudohypoparathyroidism:

  • Physical exam features of Albright hereditary osteodystrophy but without end-organ PTH resistance
  • Occurs when defective Gs protein alpha subunit is inherited from father
32
Q

Familial hypocalciuric hypercalcemia

A
  • Defective Ca2+-sensing receptor (CaSR) in multiple tissues (eg parathyroids, kidneys)
  • Higher than normal Ca2+ levels required to suppress PTH
  • Excessive renal Ca2+ reuptake → mild hypercalcemia and hypcalciuria with normal to ↑ PTH levels
33
Q

Osteitis fibrosa cystica

A
  • Causes by hyperparathyroidism
  • Cystic bone spaces filled with brown fibrous tumor (“brown tumor” consisting of osteoclasts and deposited hemosiderin from hemorrhages)
  • Causes bone pain
34
Q

Renal osteodystrophy

A

Renal disease → secondary or tertiary hyperparathyroidism → bone lesions

35
Q

Nelson syndrome

A
  • Enlargement of existing ACTH-secreting pituitary adenoma after bilateral adrenalectomy for refractory Cushing disease (due to removal of cortisol feedback mechanism)
  • Presents with hyperpigmentation, headaches and bitemporal hemianopia
  • Treatment: pituitary irradiation or surgical resection
36
Q

Pituitary apoplexy

A
  • Cause of hypopituitarism
  • Sudden hemorrhage of pituitary gland, often in the presence of an existing pituitary adenoma
  • Usually presents with sudden onset severe headache, visual impairement (eg bitemporal hemianopia due to CNIII palsy) and features of hypopituitarism
37
Q

Compare the histological appearance of TIDM and TIIDM

A
  • TI: islet leukocytic infiltrate

- TII: islet amyloid polypeptide (IAPP) deposits

38
Q

Hyperosmolar hyperglycemia nonketotic syndrome

A
  • State of profound hyperglycemia-induced dehydration and ↑ serum osmolarity, classically seen in elderly TIIDM with limited ability to drink
  • Hyperglycemia → excessive osmotic diuresis → dehydration → eventual onset of HHNS
  • Symptoms: thirst, polyuria, lethargy, focal neurological deficits (eg seizures), can progress to coma and death if left untreated
  • Labs: hyperglycemia ( > 600 mg/dL), ↑ serum osmolarity ( > 320 mOsm/kg), NO ACIDOSIS (pH > 7.3, ketone production is inhibited by presence of insulin)
  • Treatment: aggressive IV fluids, insulin therapy
39
Q

Glucagonoma

A
  • Tumor of pancreatic alpha cells → overproduction of glucagon
  • Presents with dermatitis (necrolytic migratory erythema), diabetes (hyperglycemia), DVT, declining weight, depression
  • Treatment: octreotide, surgery
40
Q

Insulinoma

A
  • Tumor of pancreatic beta cells → overproduction of insulin → hypoglycemia
  • May see Whipple triad: low blood glucose, symptoms of hypoglycemia (eg lethargy, syncope, diplopia), and resolution of symptoms after normalization of glucose levels
  • Symptomatic patients have ↓ blood glucose and ↑ C peptide levels
  • 10% of cases associated with MEN1 syndrome
  • Treatment: surgical resection
41
Q

Somatostatinoma

A
  • Tumor of pancreatic delta cells → overproduction of somatostatin → ↓ secretion of secretin, cholecystokinin, glucagon, insulin, gastrin
  • May present with diabetes/glucose intolerance, steatorrhea, gallstones
  • Treatment: surgical resection, somatostatin analogues (eg octreotide) for symptom control
42
Q

Zollinger-Ellison syndrome

A
  • Gastrin secreting tumor (gastrinoma) of pancreas or duodenum
  • Acid hypersecretion causes recurrent ulcers in duodenum and jejunum
  • Presents with abdominal pain (peptic ulcer disease, distal ulcers), diarrhea (malabsorption)
  • Positive secretin stimulation test: gastrin levels remain elevated after administration of secretin, which normally inhibits gastrin release
  • May be associated with MEN1

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