EXAM #1: REVIEW Flashcards Preview

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Flashcards in EXAM #1: REVIEW Deck (89):
1

What is the embryonic origin of the posterior pituitary?

Neuroectoderm

2

What two major hormones are secreted by corticotropes?

ACTH and β-lipotrophic hormone

3

What function is associated with the VMN of the hypothalamus?

Satiety

4

What function is associated with the lateral hypothalamus?

Hunger

5

What function is associated with the posterior hypothalamus?

Thermoregulation--heating

6

List two functions of ACTH.

1) Increase cortisol
2) Increase melanin synthesis

7

List three functions of TSH.

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

8

What is the function of LH in males?

Stimulation of Testosterone synthesis

9

What are the functions of LH in females?

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

10

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

Inhibition of ovulation and spermatogenesis respectively

11

What is the function of the anterior hypothalamus?

1) Thirst
2) Thermoregulation--cooling

12

What is the hallmark symptom of hypoprolactinemia?

Failure to lactate

13

List six major causes of hypopituitarism.

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

14

What is the treatment for a macro-prolactinoma?

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

15

What are two basic manifestations of excess prolactin?

1) Galactorrhea
2) Hypogonadism

16

How is excess GH diagnosed?

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

17

List five drugs that most commonly cause hyperprolactinemia.

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

18

How is GH excess treated?

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

19

What is the differential diagnosis for hyperprolactinemia?

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

20

What tests can be done to provoke high ATCH?

1) Metyrapone
2) Insulin induced hypoglycemia

21

List the symptoms of gonadotropin deficiency.

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

22

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

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

23

What are the expected hormones levels in secondary hypogonadism?

Low Estradiol/ Testosterone AND low LH/FSH

24

What are the symptoms of ATCH deficiency?

- Weakness
- Anorexia
- Abdominal pain
- Weight loss

25

What are the signs of ATCH deficiency?

- Postural hypotension/ reflex tachycardia
- Vascular collapse
- Pallor
- Hypoglycemia

26

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

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

27

What are the clinical manifestations of central DI?

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

28

How is adrenal insufficiency treated?

Hydrocortisone

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

29

How is adrenal insufficiency diagnosed?

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

30

What medication is indicated for severe central DI?

Desmopression (ddAVP), a synthetic vasopressin analog

31

What is the embryological origin of the parafollicular C cells?

Neural crest cells

32

What type of epithelium normally surrounds the thyroid follicle?

Simple cuboidal

33

What is the embryological origin of the parathyroid glands?

Superior= 4th pharyngeal pouch
Inferior= 3rd pharyngeal pouch

34

What thyroid hormone is Type II deiodinase active against?

Outer ring of T4

35

What three things are specifically increased by TSH?

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

36

What thyroid hormones is Type III deiodinase active against?

T3 and inner ring T4

37

What thyroid hormone is Type I deiodinase active against?

Both outer and inner ring T4

38

What are the metabolic effects of thyroid hormone?

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

39

Where is Type I deiodinase located?

Liver, kidney, and thyroid

40

Outline the MOA of the thyroid hormones in the nucleus.

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

What are five clinical manifestations of hyperthyroid?

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

42

What is the histological appearance of a goiter?

Colloid rich follicles with FLATTENED epithelium

43

What will biopsy of a medullary carcinoma reveal?

Sheets of malignant cells in an amyloid stroma

44

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

Hurtle cell

45

Describe the histologic appearance of Graves' Disease.

- Pale colloid with resporption vacuoles i.e. "scalloping"
- Hyperplastic follicles with papillary infoldings

46

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

Goiter with a Bossillated feel

47

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

Heterogenous appearance

48

List six etiologies of primary hypothyroidism.

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

49

List four etiologies of secondary hypothyroidism.

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

50

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

1) Proptosis
2) Ophthalmoplegia
3) Periorbital edema

51

List the six major etiologies of hyperthyroidism.

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

52

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

1) Hyperthyroidism
2) Goiter
3) Visual field defect

53

How is Amioadarone Induced Hyperthyroid treated?

1) Prednisone
2) Surgery

54

How is a TSH-producing pituitary adenoma treated?

1) Octreotide
2) Transsphenodial resection

55

What is the specific treatment algorithm for thyroid storm?

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

56

What information can be discerned from a thyroid US?

1) Solid vs. cystic
2) Homogenous vs. heterogenous

57

Where can follicular carcinoma of the thyroid spread?

Hematogenous spread=
- Bone
- Brain
- Lung
- Liver

58

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

1) Calcitonin
2) CEA

59

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

- Rapidly enlarging
- Symptomatic
- Painful
- Poor prognosis

60

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

Lobectomy

61

What is a common location of ectopic parathyroid tissue?

Superior mediastinum

62

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

Majority= proximal tubule
PTH= distal nephron

63

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

Impaired reabsorption leading to hyperchloremic metabolic acidosis

64

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

Normal iPTH

65

What type of bone is most affected by hyperparathyroidism?

Cortical i.e. the wrist

66

What are the NIH indications for surgery in hyperparathyroidism?

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

67

What are the complications of surgery in hyperparathyrodisim?

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

68

What are the medical therapies for primary hyperparathyroidism?

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

69

What are the two most common causes of secondary hyperparathyroidism?

1) Vitamin D deficiency
2) Renal failure

70

What is FHH?

Familial Hypocalciuric Hypercalcemia which is characterized by:
- Inactivating mutation of Ca++ receptor
- Mild hypercalcemia/ iPTH
- Low urinary Ca++

71

What cancer is associated with hypocalcemia?

Prostate and any cancer that induces "osteoblastic metastasis"

72

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

Serum Ca++ is lower

73

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

Serum Ca++ is high

74

How is hypocalcemia treated?

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

75

What labs are seen in both forms of pseudohypoparathyroidism?

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

76

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

MIRP, Minimally-Invasive Radioguided Parathyroidectomy

77

How will a parathyroid adenoma appear histologically?

- 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

What causes secondary hyperparathyroidism?

Parathyroid hyperplasia due to HYPOCALCEMIA from other causes

79

What is the surgical procedure used to treat parathyroid carcinoma?

En bloc resection

80

Grossly, how does a parathyroid carcinoma appear?

Gray-white irregular mass

81

What are the three most common causes of hypoparathyroidism?

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

82

What labs will confirm a diagnosis of hypoparathyroidism?

- Decreased Ca++
- Increased Phosphate

83

What is the treatment for hypoparathyroidism?

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

84

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

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

85

What were the subjects in the NEJM study?

45 y/o+ patients with recent ACS

86

What were the treatment groups in the NEJM study?

1) Patients that got CETP inhibitor, DALCETRAPIB
2) Patients that got placebo (and best evidence based care)

87

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

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

88

What was the conclusion of the NEJM study?

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

89

What is the function of CETP?

Transfers cholestryl ester from HDL to atherogenic particles