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Endocrine > EXAM #1: REVIEW > Flashcards

EXAM #1: REVIEW Flashcards

1
Q

What is the embryonic origin of the posterior pituitary?

A

Neuroectoderm

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2
Q

What two major hormones are secreted by corticotropes?

A

ACTH and β-lipotrophic hormone

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3
Q

What function is associated with the VMN of the hypothalamus?

A

Satiety

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4
Q

What function is associated with the lateral hypothalamus?

A

Hunger

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5
Q

What function is associated with the posterior hypothalamus?

A

Thermoregulation–heating

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6
Q

List two functions of ACTH.

A

1) Increase cortisol

2) Increase melanin synthesis

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7
Q

List three functions of TSH.

A

1) Increased synthesis and release of thyroid hormones
2) Growth of the thyroid
3) Release of prolactin

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8
Q

What is the function of LH in males?

A

Stimulation of Testosterone synthesis

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9
Q

What are the functions of LH in females?

A

1) Stimulation of ovulation
2) Formation of the Corpus Luteum
3) Estrogen and progesterone synthesis

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10
Q

Aside from milk production and breast development, what are two major effects of prolactin in females and males?

A

Inhibition of ovulation and spermatogenesis respectively

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11
Q

What is the function of the anterior hypothalamus?

A

1) Thirst

2) Thermoregulation–cooling

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12
Q

What is the hallmark symptom of hypoprolactinemia?

A

Failure to lactate

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13
Q

List six major causes of hypopituitarism.

A

1) Tumor
2) Pituitary surgery or radiation
3) TBI or subarachnoid hemorrhage
4) Pituitary apoplexy
5) Sheehan Syndrome
6) Empty Sella Syndrome

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14
Q

What is the treatment for a macro-prolactinoma?

A

1) Bromcriptine AND Tamoxifen
2) Radiation
3) Transsphenodial resection

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15
Q

What are two basic manifestations of excess prolactin?

A

1) Galactorrhea

2) Hypogonadism

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16
Q

How is excess GH diagnosed?

A

1) Increased IGF
2) CT/MRI
3) GH suppression test with glucose load

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17
Q

List five drugs that most commonly cause hyperprolactinemia.

A

1) Verapamil
2) Methyldopa
3) Reglan
4) Resperidone
5) Haldol

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18
Q

How is GH excess treated?

A

1) Octreotide–somatostatin (GHIH)
2) Pegvisomant–GH receptor antagonist
3) Radiation/ surgery

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19
Q

What is the differential diagnosis for hyperprolactinemia?

A

1) Pituitary adenoma
2) Decreased dopamine inhibition
3) Decreased renal clearance of prolactin
4) Unknown i.e. cirrhosis and primary amyloidosis

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20
Q

What tests can be done to provoke high ATCH?

A

1) Metyrapone

2) Insulin induced hypoglycemia

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21
Q

List the symptoms of gonadotropin deficiency.

A

1) Infertility
2) Irregular periods
3) Osteopenia or osteoporosis

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22
Q

What are the three basic causes of hypopituitarism? Which is the most common?

A

1) Pituitary disease*
2) Hypothalamic disease
3) Idiopathic

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23
Q

What are the expected hormones levels in secondary hypogonadism?

A

Low Estradiol/ Testosterone AND low LH/FSH

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24
Q

What are the symptoms of ATCH deficiency?

A
  • Weakness
  • Anorexia
  • Abdominal pain
  • Weight loss
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25
Q

What are the signs of ATCH deficiency?

A
  • Postural hypotension/ reflex tachycardia
  • Vascular collapse
  • Pallor
  • Hypoglycemia
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26
Q

List the relative order in which hormone deficiency is most common in panhypopituitarism.

A

1) GH
2) LH/FSH
3) TSH
4) ACTH

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27
Q

What are the clinical manifestations of central DI?

A

1) Hypotonic polyuria
2) Hypernatremia
3) Loss of pituitary bright spot

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28
Q

How is adrenal insufficiency treated?

A

Hydrocortisone

*Note that you’ll need to increase the dose in times of stress

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29
Q

How is adrenal insufficiency diagnosed?

A

1) Morning cortisol
2) Cortrosyn stimulation test
3) Measure ACTH

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30
Q

What medication is indicated for severe central DI?

A

Desmopression (ddAVP), a synthetic vasopressin analog

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31
Q

What is the embryological origin of the parafollicular C cells?

A

Neural crest cells

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32
Q

What type of epithelium normally surrounds the thyroid follicle?

A

Simple cuboidal

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33
Q

What is the embryological origin of the parathyroid glands?

A 
Superior= 4th pharyngeal pouch 
Inferior= 3rd pharyngeal pouch
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34
Q

What thyroid hormone is Type II deiodinase active against?

A

Outer ring of T4

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35
Q

What three things are specifically increased by TSH?

A

1) Iodide transport
2) Transcription of thyroglobulin
3) Transcription of thyroid peroxidase

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36
Q

What thyroid hormones is Type III deiodinase active against?

A

T3 and inner ring T4

37
Q

What thyroid hormone is Type I deiodinase active against?

A

Both outer and inner ring T4

38
Q

What are the metabolic effects of thyroid hormone?

A

1) Increased O2 consumption leading to heat production
2) Increased adipose tissue lipolysis
3) Increased glycogenolysis and gluconeogenesis

39
Q

Where is Type I deiodinase located?

A

Liver, kidney, and thyroid

40
Q

Outline the MOA of the thyroid hormones in the nucleus.

A

1) TR binds DNA with RXR
2) TR/RXR recruits HDAC, repressing transcription
3) Binding of T3 or T4 displaces HDAC for HAT*

HAT complex turns target genes ON

41
Q

What are five clinical manifestations of hyperthyroid?

A

1) Hypermetabolism
2) Enhanced epinephrine effect
3) Lid lag
4) A-fib
5) Thyroid storm

42
Q

What is the histological appearance of a goiter?

A

Colloid rich follicles with FLATTENED epithelium

43
Q

What will biopsy of a medullary carcinoma reveal?

A

Sheets of malignant cells in an amyloid stroma

44
Q

What type of cell is pathognomonic for Hashimoto’s thyroiditis?

A

Hurtle cell

45
Q

Describe the histologic appearance of Graves’ Disease.

A
  • Pale colloid with resporption vacuoles i.e. “scalloping”

- Hyperplastic follicles with papillary infoldings

46
Q

What is the major physical exam feature seen in Hashimoto’s Thyroiditis?

A

Goiter with a Bossillated feel

47
Q

What is the hallmark US finding associated with Hashimoto’s thyroiditis?

A

Heterogenous appearance

48
Q

List six etiologies of primary hypothyroidism.

A

1) Thyroiditis
2) Iodine deficiency
3) Radiation
4) Surgery
5) Infiltrative
6) Drugs

49
Q

List four etiologies of secondary hypothyroidism.

A

1) Surgical
2) Infiltrative/metastatic
3) Radiation therapy
4) Apoplexy

50
Q

List three changes to the eyes that are specific to Grave’s Disease.

A

1) Proptosis
2) Ophthalmoplegia
3) Periorbital edema

51
Q

List the six major etiologies of hyperthyroidism.

A

1) Graves’ Disease
2) Autonomous nodules
3) Subacute thyroiditis
4) Iodine-induced
5) TSH-producing adenoma
6) HCG-mediated i.e. pregnancy

52
Q

What are the clinical features associated with TSH-producing pituitary adenoma?

A

1) Hyperthyroidism
2) Goiter
3) Visual field defect

53
Q

How is Amioadarone Induced Hyperthyroid treated?

A

1) Prednisone

2) Surgery

54
Q

How is a TSH-producing pituitary adenoma treated?

A

1) Octreotide

2) Transsphenodial resection

55
Q

What is the specific treatment algorithm for thyroid storm?

A

1) Beta-blocker
2) Glucocorticoids
3) Antithyroids
4) Iodine

56
Q

What information can be discerned from a thyroid US?

A

1) Solid vs. cystic

2) Homogenous vs. heterogenous

57
Q

Where can follicular carcinoma of the thyroid spread?

A

Hematogenous spread=

  • Bone
  • Brain
  • Lung
  • Liver
58
Q

What are the tumor markers for Medullary Carcinoma of the Thyroid?

A

1) Calcitonin

2) CEA

59
Q

What are the major clinical features associated with Anaplastic Carcinoma of the Thyroid?

A
  • Rapidly enlarging
  • Symptomatic
  • Painful
  • Poor prognosis
60
Q

If a thyroid tumor is less than 1 cm in size, what surgical procedure should be performed?

A

Lobectomy

61
Q

What is a common location of ectopic parathyroid tissue?

A

Superior mediastinum

62
Q

Where does the majority of Ca++ absorption occur in the kidney? Where does PTH fine-tune Ca++ reabsorption?

A 
Majority= proximal tubule 
PTH= distal nephron
63
Q

What effect can PTH have on bicarbonate? What acid/base abnormality will this causes?

A

Impaired reabsorption leading to hyperchloremic metabolic acidosis

64
Q

In the setting of hyperparathyroidism, what is the unusual lab that you would NOT expect?

A

Normal iPTH

65
Q

What type of bone is most affected by hyperparathyroidism?

A

Cortical i.e. the wrist

66
Q

What are the NIH indications for surgery in hyperparathyroidism?

A

1) Symptomatic patient
2) Serum Ca++ over normal limit
3) Creatinine clearance less than 70%
4) Less than 50 y/o

67
Q

What are the complications of surgery in hyperparathyrodisim?

A

1) Recurrent laryngeal nerve damage
2) Hypocalcemia
3) Hungry bone syndrome

68
Q

What are the medical therapies for primary hyperparathyroidism?

A

1) Avoid dehydration
2) Bisphosphonates
3) Calcimimetics
4) Monitor Ca++, creatinine and DEXA scans

69
Q

What are the two most common causes of secondary hyperparathyroidism?

A

1) Vitamin D deficiency

2) Renal failure

70
Q

What is FHH?

A

Familial Hypocalciuric Hypercalcemia which is characterized by:

  • Inactivating mutation of Ca++ receptor
  • Mild hypercalcemia/ iPTH
  • Low urinary Ca++
71
Q

What cancer is associated with hypocalcemia?

A

Prostate and any cancer that induces “osteoblastic metastasis”

72
Q

If serum albumin is greater than 4, how does it affect your serum Ca++?

A

Serum Ca++ is lower

73
Q

If serum albumin is less than 4, how does it affect your serum Ca++?

A

Serum Ca++ is high

74
Q

How is hypocalcemia treated?

A

1) IV or PO Ca++
2) Vitamin D
3) +/- synthetic PTH (NATPARA)

75
Q

What labs are seen in both forms of pseudohypoparathyroidism?

A

1) Low Ca++
2) High Phosphate
3) High iPTH

76
Q

What is the name of the surgical procedure to remove a parathyroid adenoma?

A

MIRP, Minimally-Invasive Radioguided Parathyroidectomy

77
Q

How will a parathyroid adenoma appear histologically?

A
  • Dominance of chief cells with no fat/stromal cells
  • Outlined by a thin rim of normal parathyroid

(Vs. hyperplasia that DOES NOT have a thin rim of normal tissue)

78
Q

What causes secondary hyperparathyroidism?

A

Parathyroid hyperplasia due to HYPOCALCEMIA from other causes

79
Q

What is the surgical procedure used to treat parathyroid carcinoma?

A

En bloc resection

80
Q

Grossly, how does a parathyroid carcinoma appear?

A

Gray-white irregular mass

81
Q

What are the three most common causes of hypoparathyroidism?

A

1) Iatrogenic during thyroidectomy
2) Autoimmune disorder
3) DiGeorge Syndrome

82
Q

What labs will confirm a diagnosis of hypoparathyroidism?

A
  • Decreased Ca++

- Increased Phosphate

83
Q

What is the treatment for hypoparathyroidism?

A

1) Vitamin D
2) Calcium gluconate*
3) Recombinant human PTH

84
Q

What is the main question of the NEJM study on the exam?

A

Will raising HDL cholesterol by inhibiting cholestryl ester transfer protein (CETP) improve cardiovascular outcomes?

85
Q

What were the subjects in the NEJM study?

A

45 y/o+ patients with recent ACS

86
Q

What were the treatment groups in the NEJM study?

A

1) Patients that got CETP inhibitor, DALCETRAPIB

2) Patients that got placebo (and best evidence based care)

87
Q

What was the primary efficacy end-point of the study?

A

1) Death
2) CPR w/ resc.
3) MI or unstable angina
4) CVA

88
Q

What was the conclusion of the NEJM study?

A

Dalcetrapid increased HDL but did NOT reduce the risk of recurrent cardiovascular events

89
Q

What is the function of CETP?

A

Transfers cholestryl ester from HDL to atherogenic particles

Endocrine (34 decks)

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