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Endocrine > EXAM #1: REVIEW > Flashcards

EXAM #1: REVIEW Flashcards

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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
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

Endocrine (34 decks)

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