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Endocrine Flashcards

(42 cards)

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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

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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

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

How does PTH induce bone resorption

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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

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A

Intermittent PTH release can also stimulate bone formation

21
Q

How do thyroid hormones increase BMR

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A

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

22
Q

When are thyroxine-binding globulin levels increased and decreased

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

- ↓ TBG in hepatic failure, steroid use

23
Q

Wolff-Chaikoff effect

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A

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

24
Q

Metyrapone stimulation test

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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
Addison disease
- 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
What type of adrenal insufficiency is seen in patients with chronic exogenous steroid use
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
In which types of adrenal insufficiency is aldosterone synthesis preserved
Secondary and tertiary adrenal insufficiency
28
What type of cells do neuroendocrine tumors arise from
Kulchitsky and enterochromaffin-like cells. They contain amine precursor uptake decarboxylase (APUD).
29
Compare physical presentations of neuroblastoma and Wilms tumor
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
Jod-Basedow phenomenon
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
Pseudohypoparathyroidism type 1A and pseudopseudohypoparathyroidism
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
Familial hypocalciuric hypercalcemia
- 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
Osteitis fibrosa cystica
- 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
Renal osteodystrophy
Renal disease → secondary or tertiary hyperparathyroidism → bone lesions
35
Nelson syndrome
- 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
Pituitary apoplexy
- 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
Compare the histological appearance of TIDM and TIIDM
- TI: islet leukocytic infiltrate | - TII: islet amyloid polypeptide (IAPP) deposits
38
Hyperosmolar hyperglycemia nonketotic syndrome
- 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
Glucagonoma
- Tumor of pancreatic alpha cells → overproduction of glucagon - Presents with dermatitis (necrolytic migratory erythema), diabetes (hyperglycemia), DVT, declining weight, depression - Treatment: octreotide, surgery
40
Insulinoma
- 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
Somatostatinoma
- 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
Zollinger-Ellison syndrome
- 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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