Path- Endocrinology

Front 1

What is the most common cause of endocrine gland hypofunction?

Back 1

Autoimmune disease.

Front 2

What are two examples of hypofunctioning endocrine diseases that are the result of autoimmune reactions?

Back 2

Hashimoto's Thyroiditis and Addison's disease.

Front 3

What are two examples of hypofunctioning endocrine diseases that are the result of infarction?

Back 3

Sheehan's postpartum necrosis (pituitary gland necrosis after great blood loss due to pregnancy) and Waterhouse-Friderichen's syndrome (adrenal hemorrhage associated with meningococcal septicemia).

Front 4

What is the most common cause of endocrine gland hyperfunction?

Back 4

The most common cause is a benign adenoma.

Front 5

What are the most common tumors that alter hypothalamic function?

Back 5

Pituitary adenoma (the most common tumor affecting the hypothalamus), Craniopharyngioma, Midline hamartoma (not a neoplasm), and Langerhans histiocytosis.

Front 6

What are two inflammatory disorders that alter hypothalamic function?

Back 6

Sarcoidosis and Meningitis.

Front 7

Describe some of the clinical findings expected to be present in patient with Hypothalamic dysfunction.

Back 7

1) Secondary hypoituitarism
2) Central diabetes insipidus 3) Hyperprolactinemia (loss of dopamine inhibition causes galactorrhea)
4) Precocious puberty (most common cause in boys is a midline hamartoma of the hypothalamus)
5) Visual field disturbances (bilateral hemianopsia)
6) Mass Effects (obstructive hydrocephalus)
7) Growth disorders (dwarfism in children)
8) Kallmann's syndrome (deficiency of GnRH)

Front 8

Which autonomic system is responsible for stimulating the release of Melatonin from the pineal gland? Where is the Melatonin released into?

Back 8

The Superior cervical sympathetic ganglia stimulates receptors on pinealocytes, which causes the release of melatonin into spinal fluid and blood.

Front 9

Is Melatonin released from the Pineal gland in the morning or at night? Where is the Pineal gland located?

Back 9

Melatonin is released from the Pineal gland at night. The Pineal gland is located in the midline above the quadrigeminal plate.

Front 10

What special visual findings might be present in a patient with a Pineal gland tumor?

Back 10

Parinaud's syndrome- paralysis of upward conjugate gaze.

Front 11

What type of hydrocelphalus may come as a result of tumors of the Pineal gland?

Back 11

Obstructive hydrocephalus due to compression of the aqueduct of Sylvius in the Third ventricle.

Front 12

What is the most common cause of Hypopituitarism in adults?

Back 12

The most common cause is a non-functioning adenoma.

Front 13

Which Multiple Endocrine Neoplasia (MEN) syndrome is a Nonfunctioning pituitary adenoma associated with? List the main features of this syndrome.

Back 13

Nonfunctioning (null) pituitary adenomas are associated MEN I. This MEN is associated with 3P's: Pituitary adenoma, Hyperparathyroidism, Pancreatic tumor (Zollinger-Ellison syndrome or insulinoma).

Front 14

Explain the etiology of Sheehan's postpartum necrosis.

Back 14

The Pituitary gland doubles in size during pregnancy due to synthesis of prolactin, without an associated increase in blood supply. Hypovolemic shock during birth can result in infarction and Pituitary necrosis.

Front 15

What is the most common cause of Hypopituitarism in children? How is this disease acquired?

Back 15

The most common cause of hypopiituitarism in children is a Craniopharyngioma. This is a benign pituitary tumor that is derived from the remnants of Rathke's pouch.

Front 16

Describe what a Craniopharyngioma is and where it comes from. Where is it located? What complications can it cause?

Back 16

A Craniopharyngioma is a benign pituitary tumor derived from the remnants of Rathke's pouch. This is located above the Sella Turcica and can extend into the sella turcica and destroy the gland. This is a cystic tumor with hemorrhage and calcification. It commonly causes bitemporal hemianopsia and may produce central diabetes insipidus.

Front 17

What is Rathke's pouch? What structure does it develop into?

Back 17

Rathke's pouch is an ectodermal derivative derived from the oral cavity. It develops into the anterior lobe of the pituitary.

Front 18

What is Lymphocytic hypophysitis? Who does it happen to?

Back 18

Lymphocytic hypophysitis is the femal dominant autoimmune destruction of the pituitary gland. This occurs during or after pregnancy.

Front 19

What time of the day are GH and IGF-1 released?

Back 19

Normally these hormones are released at about 5am.

Front 20

Low levels of which molecules are at the root cause of Secondary Hypothyroidism?

Back 20

Decreased serum T4 and TSH.

Front 21

What are some of the main causes of Central Diabetes Insipidus?

Back 21

Hypothalamic disease, Transection of the pituitary stalk, Posterior Pituitary disease, and Histiocytosis X.

Front 22

What are some of the main causes of Nephrogenic Diabetes Insipidus?

Back 22

Lithium, demeclocycline, Hypokalemia (vacuolar nephropathy of collecting tubules), Nephrocalcinosis (metastatic calcification of the collecting tubule basement membranes)

Front 23

Describe the findings in Central vs. Nephrogenic diabetes insipidus after injection of ADH.

Back 23

In CDI, the UOsm increases more than 50% from baseline. In NDI, the UOsm increases less than 50% from baseline.

Front 24

What type of a tumor is a Prolactinoma? What symptoms does it produce?

Back 24

A Prolactinoma is a benign adenoma (overall the most common pituitary tumor). Secondary symptoms of a Prolactinoma include amenorrhea and galatorrhea?

Front 25

When you hear that a woman has started having amenohrrea with galactorrhea, and she has not recently given birth, what condition do you think of?

Back 25

Prolactinoma.

Front 26

Why do Prolactinomas cause amenorrhea?

Back 26

Prolactinomas cause amenorrhea because Prolactin inhibits GnRH, which leads to decreased FSH and LH. Without stimulation from these hormones, ovulation does not occur.

Front 27

What type of symptoms do Prolactinomas cause in men?

Back 27

Impotence due to a decrease in testosterone, but there is not galactorrhea because men do not have enough breast tissue to produce this feature.

Front 28

How do you treat the symptoms of Prolactinoma? Why does this work?

Back 28

Dopamine analogues are used because dopamine inhibits the Anterior pituitary from releasing Prolactin.

Front 29

What are the main features of Acromegaly?

Back 29

Increased lateral bone growth, organomegaly, and hyperglycemia.

Front 30

What are the normal functions/properties of GH in the body that either cause the symptoms associated with a GH adenoma or are used to test for a GH adenoma?

Back 30

GH stimulates the liver synthesis/release of insulin growth factor (IGF-1). GH also stimulates gluconeogenesis and amino acid uptake in muscle. It also has a negative feedback relationship normally, with IGF-1 and glucose, whereby those molecules inhibit the release of more GH.

Front 31

What is the function of IGF-1? How does it affect bone growth when it is over produced in children as a result of a GH adenoma? In adults?

Back 31

IGF-1 stimulates growth of bone (linear and lateral), cartilage, and soft tissue. Children develop gigantism due to increased linear bone growth. Adults develop increased lateral bone growth (e.g. hands, feet, jaw), but no linear bone growth because epiphyses are fused.

Front 32

Describe some of the features of Acromegaly that develops in adults as a result of GH adenoma.

Back 32

Increased lateral bone growth, Prominent jaw (spacing between teeth), Frontal bossing (enlarge frontal sinus increases the hat size), Macroglossia, and Cardiomyopathy (cause of death), Hyperglycemia (due to increased gluconeogenesis).

Front 33

What suppression test used to detect GH adenoma? What other hormone is checked?

Back 33

A suppression test that is used to test for GH adenoma is a glucose suppression test. Normally after administering glucose, GH and IGF-1 are suppressed. If glucose is administered and these hormones are not subsequently suppressed, the likelihood of a GH adenoma is increased.

Front 34

What is the most common cause of SIADH syndrome? What are other causes?

Back 34

Small cell carcinoma of the lung. Other causes include Central nervous system injury, Chloropropamide (other Sulfonylureas), Lung infections (e.g. tuberculosis)

Front 35

In SIDAH would you expect to find mental status dysfunction due to cerebral edema or cerebral dehydration? Hypo- or hypernatremia? What is a common osmolar value? How do you treat SIADH? Why?

Back 35

Cerebral Edema. Hyponatremia is common with an osmolar value of <120mEq/L. You treat this condition by restricting water, but you can also use Demeclocycline. This is a drug that produces NDI, but can be used in treating ectopic ADH from small cell carcinoma of the lung because the patient does not have to be deprived of water.

Front 36

Describe the components of Thyroid hormone.

Back 36

Thryroid hormone is an iodide attached to tyrosine.

Front 37

Trapping of Iodide in the thyroid gland is mediated by what hormone? What other steps in thyroid hormone synthesis are mediated by this hormone?

Back 37

Trapping of iodide is in the thyroid gland in order to make thyroid hormone is TSH-mediated. The organification of iodide (incorporation into DIT and MIT), as well as the proteolysis of colloid to release stored thyroid hormone are also mediated by TSH hormone.

Front 38

Oxidation of iodides to iodine in order to incorporate it into the production of thyroid hormone is done by what enzyme?

Back 38

This is a Peroxidase mediated step.

Front 39

Explain the Organification step of iodine in Thryoid hormone synthesis. What hormone mediates this step in thryroid synthesis?

Back 39

Organification of iodine is done through incorporating iodine into Tyrosine to form MIT (monoiodotyrosine) and DIT (diiodotyrosine). TSH mediates this step.

Front 40

How is thyroid hormone stored in the thyroid gland? What does it take to release thyroid hormone from the thyroid gland?

Back 40

Hormones T3 and T4 are stored as colloid in the Thyroid gland, and the proteolysis of colloid occurs through lysosomal proteases that are mediated through TSH.

Front 41

What happens to free T4 in the periphery? What are T3 and T4 bound to when they are not free? Which is the active hormone and which is the prohormone?

Back 41

Free T4 (FT4) is converted to free T3 (FT3) in the periphery by an outer ring deiodinase. Normally T4 and T3 are bound to 1/3 of all binding site on Thyroid Binding Globulin (TBG). FT3 is considered to be the active hormone and FT4 is the prohormone.

Front 42

FT4/FT3 have a negative feedback relationship with what hormone?

Back 42

TSH.

Front 43

What are the forms of T4 that total serum T4 takes into account?

Back 43

Total serum T4 represents T4 bound to TBG and free T4.

Front 44

What types of things increase TBG synthesis? If TBG increases in the serum, will total serum T4 increase?

Back 44

Estrogen increases the synthesis of TBG, thus pregnancy, contraceptive pills, and hormone replacement will all increase TBG synthesis. If serum TBG increases, it binds more T4. If there is more T4 in the TBG-bound state, then the thryoid replaces the free T4 that is lost and overall total serum T4 is allowed to increase.

Front 45

What are some causes of increased TBG (Thyroid binding globulin)?

Back 45

Anabolic steroids, nephrotic syndrome (urinary loss).

Front 46

What are the effects of alterations of TBG on FT4 and TSH? What are the effects on total serum T4?

Back 46

Alterations in TBG alter total serum T4, but have no effect on FT4 and TSH.

Front 47

Are hyper- and hypothyroidisms due to increases in TBG (thyroid binding globulin) or FT4?

Back 47

Increases in FT4, and not TBG, must be present in order to have hyper- or hypothyroidism.

Front 48

What is the best overall test for Thyroid function? Will TSH be elevated in hyper- or hypothyroidism? What are some causes for increased TSH? Causes for decreased TSH?

Back 48

The best overall screening test for Thyroid function is TSH. Increased TSH will occur is Primary Hypothyroidism. Decreased TSH will occur in Thyrotoxicosis (e.g. Graves' disease) and in Hypopituitarism (causes secondary hypothyroidism due to lack of TSH).

Front 49

What is the purpose of administering Radioactive Iodine-131?

Back 49

Iodine-131 is used to evaluate the synthetic activity of the thyroid gland and evaluate the functional status of thyroid nodules.

Front 50

What is Thyroglobulin used as a marker for?

Back 50

Thyroglobulin is used as a marker for thyroid cancer.

Front 51

A mass at the base of the tongue should be suspected for what mass? What is it's etiology? Is it a neoplasm?

Back 51

This could be a lingual thyroid. This occurs from the failed descent of thyroid anlage from the base of the tongue, and it usually represents all of the thyroid tissue.

Front 52

How do you test for and locate a lingual thyroid?

Back 52

Iodine-131 scan locates the lesion and also identifies any other thyroid tissue that is present.

Front 53

What is most often the cause of Acute Thyroiditis? Is there hyper- or hypothyroidism involved?

Back 53

Bacterial infection (e.g. Staphylococcus aureus) is the most common cause of acute Thyroiditis. Initial thyrotoxicosis from gland destruction is possible. This leads to transiently increased serum T4 and subsequent decreased serum TSH. Permanent hypothyroidism is uncommon, but decreased Iodine-131 can be an associated feature.

Front 54

What is the most common cause of Subacute granulomatous thyroiditis? What patient population does this most commonly occur in? What type of illness often precedes this condition?

Back 54

The most common cause of Subacute granulomatous thyroiditis is viral infection (e.g. coxsackie virus). This occurs most often in women 40 to 50 years old. This is often preceded by an upper respiratory infection.

Front 55

What is the most common cause of a painful thyroid? Describe some of the clinical findings that are associated. Is there a Thyrotoxicosis that occurs?

Back 55

The most common cause of a painful Thyroid gland is Subacute granulomatous thyroiditis. Microscopically granulomatous inflammation with multinucleated giant cells are observed. Cervical adenopathy is not prominent and initial thyrotoxicosis occurs due to gland destruction. Permanent hypothyroidism is uncommon and there is decreased uptake of Iodine-131.

Front 56

What are the HLA associations that are tied to Hashimoto's thyroiditis? What part of the immune system is responsible for mediating the destruction? What results from this destruction?

Back 56

HLA Dr3 and Dr5. Cytotoxic T-cells destroy the parenchyma, which contributes to thyrotoxicosis initially, and then eventually produces hypothyroidism.

Front 57

What role do IgG autoantibodies play in Hashimoto's thyroiditis?

Back 57

Blocking IgG autoantibodies against the TSH receptors in the anterior pituitary gland leads to decreased hormone synthesis.

Front 58

Do Antimicrosomal and anti-thyroglobulin antibodies cause initial damage in Hashimoto's thyroiditis?

Back 58

NO!!! Antimicrosomal and thyroglobulin antibodies developing as a RESULT of gland injury. They are not the initial cause of gland injury.

Front 59

What is the most common cause of hypothyroidism?

Back 59

Hashimoto's thyroiditis.

Front 60

Lymphocytic infiltrates with prominent germinal follicles describes what type of Thyroiditis?

Back 60

Hashimoto's Thyroiditis.

Front 61

What type of lymphoma is Hashimoto's thyroiditis a risk factor for?

Back 61

Hashimoto's thyroiditis is a risk factor for primary B-cell malignant lymphoma of the thyroid.

Front 62

Describe the pathophysiology associated with Reidel's thyroiditis. What complications can occur as a result of this condition? What other conditions is it associated with?

Back 62

Reidel's thyroiditis involves fibrous tissue replacement of the gland with extension of fibrosis into surrounding tissue. This can produce tracheal obstruction. It is associated with other sclerosing conditions (e.g. sclerosing mediastinitis).

Front 63

Describe the pathophysiology of Subacute Painless Lymphocytic Thyroiditis? How is it can it be differentiated from Hashimoto's thyroiditis?

Back 63

Subacute painless lymphocytic thyroiditis is an autoimmune disease that develops postpartum. The gland lacks germinal follicles which helps set it apart from Hashimoto's thyroiditis.

Front 64

What are some of the clinical findings associated with Subacute Painless Lymphocytic Thyroiditis?

Back 64

Abrupt onset of thyrotoxicosis die to gland destruction, gland is slightly enlarged and painless, progresses to primary hypothyroidism in 40-50% of cases, and lacks Hashimoto's thyroiditis immunologic markers.

Front 65

What key event occurs before the onset of Subacute Painless Lymphocytic Thyroiditis?

Back 65

Subacute Painless Lymphocytic Thyroiditis occurs postpartum.