Lesson 11 Endocrine system Flashcards

1
Q

This is the coordinating center of the endocrine system, consolidates signals derived from thoughts, feelings, autonomic function, environmental cues, and peripheral endocrine feedback.

A

Hypothalamus

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2
Q

This is a pea-sized organ located in the center of the brain, is called the master gland because it regulates all the body’s endocrine glands. It can be compared to a dispatcher because, in response to a signal from the hypothalamus, it releases one of its many tropic hormones

A

pituitary

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3
Q

this secretes growth hormone (GH), prolactin (PRL), ACTH, thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH), and luteinizing hormone (LH).

A

Anterior pituitary

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4
Q

This synthesizes ADH and oxytocin (OXT), which are stored and released by the posterior pituitary. ADH is also called arginine vasopressin (AVP), and GH is also called somatotropin.

A

hypothalamus

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5
Q

This stores and releases ADH and oxytocin (OXT)

A

posterior pituitary

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6
Q

this regulates each of the hypothalamic-pituitary-hormone axes, a process that maintains hormone levels within a narrow range.

A

Negative feedback

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7
Q

When an individual is running in a marathon, the hypothalamus receives signals from the body that the muscles and organs have extra metabolic needs. The hypothalamus secretes _________1________. which stimulates the ____2______ gland. This then secretes ______3______, which stimulates the adrenal gland to secrete the hormone _____4_____. These levels in the blood rise, the pituitary senses increased level and shuts off stimulus to ___5____. this is an example of _____6____.

A
  1. corticotrophin-releasing factor (CRF)
  2. pituitary
  3. ACTH
  4. cortisol
  5. adrenal gland
  6. endocrine negative feedback system
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8
Q

For instance, prolonged, excessive stimulation of an endocrine gland often results in receptor insensitivity and may decrease its number of receptors in a process known as what?

A

Downregulation of receptors (caused by excessive, prolonged dose of glucocorticoid drugs)

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9
Q

What is the most common reason for upregulation of receptors?

A

a reduction in the receptor stimulation by hormones.

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10
Q

what are the 2 categories of endocrine gland dysfunction?

A

hypofunction and hyperfunction

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11
Q

This dysfunction caused by the endocrine gland itself

A

Primary endocrine disorder

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12
Q

This dysfunction caused by abnormal pituitary activity

A

secondary endocrine disorder

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13
Q

This dysfunction caused by a hypothalamic origin

A

tertiary endocrine disorder

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14
Q

These tumors can cause such problems as growth disturbances, electrolyte imbalances, and infertility. They classically cause visual disturbances because of their proximity to the optic chiasm in the brain.

A

pituitary tumors

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15
Q

These are the etiologies for what?
tumors, cranial radiation, traumatic brain injury, subarachnoid hemorrhage, infectious and inflammatory disorders, and postpartum pituitary necrosis (Sheehan’s syndrome). The pituitary adenoma, a benign, epithelial neoplasm, is the most common tumor of the pituitary gland.

A

hypopituitarism

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16
Q

These hormones are secreted by which part of the pituitary gland?
*Thyrotropin, or TSH
* Gonadotropins, or FSH and LH
* Somatotropin, or GH
* Corticotropin, or ACTH
* Prolactin, or PRL

A

Anterior pituitary

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17
Q

What is unique about the posterior pituitary? (how is it different from the anterior?)

A

does not produce its own hormones; it stores hormones. The hypothalamus produces ADH (also referred to as AVP) and OXT. These two hormones are released into the hypothalamic–hypophyseal tract to the posterior pituitary, where they are stored.

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18
Q

How is the endocrine system impacted by hypopituitarism?

A

results in secondary failure of the target endocrine glands

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19
Q

What are the most serious concerns for hypopituitarism?

A

drenal insufficiency, hypothyroidism, and diabetes insipidus (DI), the last of which occurs because of a lack of posterior pituitary secretion of ADH.

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20
Q

What are the clinical presentations in the neonate and infant?

A

dwarfism, developmental delay, various visual and neurological symptoms, seizure disorder, and a number of congenital malformations.

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21
Q

How do adults present for hypopituitarism

A

radual symptoms of hypothyroidism, adrenal insufficiency, and ADH deficiency. The clinical presentation may be weakness, weight loss, and hypotension caused by adrenal insufficiency, or weight gain, sluggishness, and depression caused by hypothyroidism. Lack of ADH causes excessive urination and dehydration, a syndrome known as DI.

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22
Q

What are the clinical presentations when hypopituitarism is acute

A

a rapidly deteriorating state of hypotension; severe dehydration; neurological deficits; and abnormalities in electrolyte levels, glucose levels, body temperature, and heart rate.

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23
Q

What are the diagnostic findings for someone with hypopituitarism

A

low serum levels of pituitary tropic hormones, such as TSH, ACTH, FSH, LH, GH, PRL, and ADH, and low corresponding endocrine organ hormones, such as thyroxine (T4), cortisol, and estrogen.

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24
Q

How is hypopituitarism treated?

A

varies depending on which tropic hormones are lacking. Hormone replacement and surgical excision of the tumor, if present, are the treatment measures.

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25
Q

This is a disorder of hypopituitarism that originates in the posterior pituitary, also called the neurohypophysis. The disorder involves ADH, and there are two categories of disease: either a lack of secretion of ADH from the posterior pituitary, or the kidney fails to respond to ADH.

A

Diabetes Insipidus

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26
Q

This occurs because of a lack of secretion of ADH from the posterior pituitary

A

central diabetes insipidus

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27
Q

This occurs when the kidney fails to respond to ADH.

A

nephrogenic diabetes insipidus

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28
Q

What can cause Central Diabetes Insipidus?

A

tumors such as craniopharyngiomas or head trauma that causes injury of the posterior pituitary or the hypothalamic–hypophyseal tract. Other causes include pituitary surgery, inflammatory disorders, infection, or exposure to chemical toxins.

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29
Q

What can cause nephrogenic diabetes insipidus

A

nephrotoxic drugs such as lithium, obstructive uropathy, ischemia of the kidney, hypokalemia, or hypocalcemia.

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30
Q

True or False, the same pathophysiological process occurs in both nephrogenic DI and central DI.

A

True: The nephron does not perform antidiuresis, meaning that the nephron does not reabsorb water from the tubule fluid. As a consequence, the body loses high amounts of water in the urine, causing polyuria and highly dilute urine. The bloodstream loses water, which concentrates its sodium content, causing hypernatremia, polyuria, dilute urine, and dehydration.

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31
Q

What syndrome can present similarly to DI?

A

psychogenic polydipsia: the patient drinks excessive amounts of water and therefore has excessive, very dilute urine.

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32
Q

Name the disorder for the following symptoms: frequent urination (polyuria) and thirst (polydipsia). In addition, because of dehydration, neurological problems can occur, including confusion, disorientation, myoclonus, seizures, and, in severe cases, coma.

A

DI: Diabetes Insipidus

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33
Q

What is the differentiating factor between DM and DI?

A

serum glucose: Serum glucose is elevated in DM, but not in DI.

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34
Q

The following treatment is used for what disorder?
administration of desmopressin or synthetic vasopressin. Chlorpropamide, thiazides, or carbamazepine can also be used. Surgical treatment

A

DI

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35
Q

This is the most common cause of hyperpituitarism.

A

A PRL-producing adenoma, also called prolactinoma

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36
Q

In children, a GH-secreting tumor causes ___1___, whereas in adults, it causes ____2___

A
  1. Gigantism
  2. Acromegaly (bones increase in size, limited to the bones of your hands, feet and face)
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37
Q

What are the symptoms for females of prolactinoma (most common pituitary adenoma)?

A

menstrual abnormalities, amenorrhea, galactorrhea, vaginal dryness, and osteopenia occur.

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38
Q

What are the symptoms for males of prolactinoma (most common pituitary adenoma)?

A

hypogonadism, decreased libido, erectile dysfunction, and infertility occur.

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39
Q

What type of adenoma stimulates the adrenal gland to produce excess cortisol, and the presentation is called Cushingoid appearance. The signs include obesity; stunted growth; swollen face, called moon facies; acne; ruddy complexion; hirsutism; fat in the posterior neck area, called buffalo hump; and striae, also known as stretch marks.

A

ACTH-secreting adenoma

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40
Q

These adenomas are rare but can present with signs and symptoms of hyperthyroidism, including nervousness, tremulousness, palpitations, weight loss, visual disturbances, headaches, and hypersensitivity to heat.

A

TSH-secreting adenomas

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41
Q

What is the treatment for Hyperpituitarism?

A

medications that block GH and surgical excision of any pituitary tumor.

42
Q

This is a common condition in patients who sustain brain injury or those who undergo neurosurgery for brain disorders. The syndrome is characterized by hyponatremia and hypo-osmolality of the blood that result from excessive secretion or action of ADH.

A

Syndrome of inappropriate antidiuretic hormone (SIADH)

43
Q

What can SIADH be secreted by, in particular?

A

tumors; particularly lung cancer

44
Q

What does SIADH cause?

A

excess water reabsorption into the bloodstream. This excess water creates hypervolemia, dilutional hyponatremia, and highly concentrated urine.

45
Q

What do the following signs/symptoms indicate?
symptoms related to fluid volume overload and dilutional hyponatremia, including fatigue, weakness, confusion, and headache.
if hyponatremia is severe or rapid in onset, findings include myoclonus, slowed reflexes, seizures, problems with gait and balance, nystagmus, dysarthria, dysphagia, and coma.

A

SIADH

46
Q

How is SIADH diagnosed?

A

measurements of sodium, electrolytes, and water of the blood and urine are most important. Diagnostic tests include urine-specific gravity, urine osmolality, hematocrit, and plasma osmolality. Results in SIADH will demonstrate dilutional hyponatremia, elevated urine osmolality, excessive urine sodium, and decreased serum osmolality.

47
Q

The follow treatment is for what disorder?
Fluid restriction is a first-line treatment that can resolve hyponatremia.
Slow correction of hyponatremia by 6 mEq/L over 24 hours using 3% hypertonic saline is recommended if fluid restriction does not raise sodium
ADH receptor antagonists
furosemide
Urea or IV mannitol

A

SIADH

48
Q

This is a 2-inch, butterfly-shaped gland located in the neck.

A

Thyroid gland

49
Q

This is the regulator of body metabolism, which influences almost every body system.

A

Thyroxine

50
Q

Is thyroid more common in men or women?

A

women

51
Q

What does an enlarged thyroid indiicate?

A

hypofunction or hyperfunction

52
Q

This is an enlargement of the thyroid gland with or without symptoms of thyroid dysfunction.

A

goiter

53
Q

When there are no symptoms of thyroid disease, the enlargement is referred to as a ?

A

nontoxic goiter

54
Q

Excess what can stimulate enlargement of the thyroid gland and cause goiter formation?

A

pituitary TSH

55
Q

If what levels are decreased in the body, thyroid hormone synthesis is diminished, causing the pituitary to compensate by increasing TSH causing goiter formation?

A

iodine levels

56
Q

What are the risk factors for hypothyroidism?

A

age older than 50 years; female gender; pregnancy; autoimmune disease; radiation to the neck; family history; and certain drugs, including radioactive iodine, amiodarone, interferon alpha, interleukin, and lithium.

57
Q

What is the hallmark of Hashimoto’s thyroiditis?

A

Anti-TPO antibodies
(anti-thyroperoxidase)

58
Q

In Hashimoto’s thyroiditis, biopsy of thyroid tissue reveals a high number of _________ in the thyroid gland.

A

lymphocytes

59
Q

What is a significant physical sign of hypothyroidism?

A

Reduction in the conversion of carotene to vitamin A causes hypercarotenemia, which gives skin a yellow-orange tint.

60
Q

What are other signs symptoms of Hypothyroidism?

A

puffy face
characteristic hoarse voice
yellow-orange tint to skin
hypercapnia and hypoxia
cold intolerance
weight gain
lethargy
fatigue
memory deficit
poor attention span
muscle cramps
constipation
decreased fertility
hair loss
brittle nails

61
Q

This is is the result of thyroid hormone deficiency during embryonic development and early neonatal life. The child exhibits short stature, intellectual disability, and other metabolic disorders.

A

Cretinism

62
Q

This results from defective iodine incorporation into thyroid hormone. It is associated with sensorineural hearing loss and an enlarged thyroid gland.

A

Pendred’s syndrome

63
Q

This is a rare disorder where the body develops antibodies against a number of endocrine organs. It is associated with Addison’s disease, hypoparathyroidism, mucocutaneous candidiasis, and hypothyroidism.

A

Autoimmune Polyendocrinopathy

64
Q

This is a disorder in which thyroid function is only mildly low, so that the blood level of thyroxine (T4) remains within the normal range, but the blood level of TSH is elevated, indicating mild thyroid failure. Individuals can suffer mild symptoms of hypothyroidism, such as fatigue, difficulty losing weight, and depression.

A

Subclinical hypothyroidism

65
Q

What is the following treatment for?
includes replacement hormone therapy with levothyroxine and surgical intervention, if necessary.

A

primary hypothyroidism

66
Q

What can happen if hypothyroidism is untreated?

A

it can progress to myxedema coma, a serious illness with a high mortality rate. There are severe hypothyroid symptoms, as well as susceptibility to SIADH, hypoglycemia, and hyponatremia. If left untreated, the symptoms will progress to confusion and coma.

67
Q

What is another term for hyperthyroidism?

A

thyrotoxicosis

68
Q

This is an autoimmune stimulation of the thyroid gland, causing an excessive secretion of thyroid hormone and is the most common cause of hyperthyroidism

A

Graves’ disease

69
Q

This is the second most common cause of hyperthyroidism, an inflammation of the thyroid gland that causes release of excessive thyroid hormone. It occurs in approximately 15% to 20% of cases of hyperthyroidism, often following extreme stress or infection.

A

subacute thyroiditis

70
Q

This is a form of primary hyperthyroidism where the thyroid contains autonomously hyperfunctioning nodules. It occurs more commonly in older individuals, especially in patients with a long-standing goiter.

A

Toxic multinodular goiter, also called Plummer’s disease

71
Q

This is caused by a single hyperfunctioning thyroid tumor.

A

toxic thyroid adenoma

72
Q

This occurs in patients with excessive iodine intake, such as after an iodinated radiocontrast study. Patients can also endure hyperthyroidism secondary to administration of amiodarone, a cardiac antiarrhythmic agent. Amiodarone contains iodine and is structurally similar to thyroid hormone.

A

Iodide-induced thyrotoxicosis, also known as Jod-Basedow syndrome

73
Q

Why can pregnancy cause hyperthyroidism?

A

Placental human chorionic gonadotropin (HCG) is structurally similar to TSH, and the increase in HCG during pregnancy can stimulate TSH receptors.

74
Q

a wide-eyed stare that is often present, is associated with increased sympathetic tone and infiltration of the extraocular area with deposits, push the eyes forward and produce periorbital edema and bulging of the eyes: associated with Graves disease

A

Exophthalmos

75
Q

refers to skin changes in the lower legs. Because of accumulation of glycosaminoglycans, the skin becomes thickened and develops a nonpitting edema. can be seen in hypo or hyperthyroidism

A

myxedema

76
Q

This is an intense, overwhelming release of thyroid hormones that exerts an intense stimulus on the metabolism. This is a life-threatening condition most commonly precipitated by surgery, trauma, or infection.

A

Thyrotoxic crisis, also called a thyroid storm

77
Q

The patient presents with the following symptoms: high fever, tachycardia, nausea and vomiting, tremulousness, agitation, and psychosis. Late in the progression of the disease, patients may become stuporous or comatose with hypotension.
Heart failure and pulmonary edema can develop rapidly and cause death.

A

Thyrotoxic crisis, also called a thyroid storm

78
Q

Most of these are asymptomatic, but they can cause hypothyroidism or hyperthyroidism, pts will occasionally report complaints of dysphagia, dysphonia, and pain caused by the structural pressure created by the nodule.

A

thyroid nodules

79
Q

Which is more often associated with malignancy a single thyroid nodule or multiple nodules?

A

single thyroid nodule
multiple nodules are often benign, though the presence of any nodule must be carefully evaluated to rule out neoplastic disease

80
Q

What can rule out a malignant thyroid nodule?

A

Ultrasound-guided fine needle aspiration biopsy

81
Q

What is the treatment for a thyroid nodule that is malignant or obstructive?

A

surgical intervention

82
Q

These are four pea-sized glands nestled within the thyroid tissue of the neck. The glands produce and secrete PTH in response to a low serum calcium level

A

parathyroid glands

83
Q

This promotes calcium reabsorption in the renal tubules and the release of calcium from bone. It also promotes vitamin D production by the kidney, which helps maintain normal calcium levels within the body

A

Parathyroid hormone

84
Q

What are factors suggesting a malignant thyroid nodule?

A
  • Age younger than 20 years or older than 70 years
  • Male sex
  • Associated symptoms of dysphagia or dysphonia
  • History of neck irradiation
  • Firm, hard, or immobile nodule
  • Presence of cervical lymphadenopathy
85
Q

This is a very rare disorder, and is most often because of trauma or inadvertent damage or removal of the specific glands during thyroid surgery.

A

Hypoparathyroidism

86
Q

What are some additional causes for hypoparathyroidism besides inadvertent damage?

A

neck irradiation, autoimmune disease, many different genetic disorders, and metal toxicity, fetal alcohol syndrome

87
Q

Why can secondary hypoparathyroidism occur?

A

lack of pituitary parathyroid-stimulating hormone, can occur because of any primary disease that causes hypercalcemia. The high calcium levels send feedback to the pituitary gland to diminish parathyroid-stimulating hormone.

88
Q

If a patient has hypoparathyroidism what ion will increase in the blood/body because of it’s concomitant relationship with calcium?

A

Phosphate levels with increase, low PTH lessens phosphate excretion by the kidney

89
Q

What symptoms do the following indicate?
muscle cramps, irritability, tetany, and convulsions, carpal spasm known as Trousseau’s sign and facial muscle twitch called Chvostek’s sign.

A

Hypoparathyroidism: hypocalcemia

90
Q

This is excessive secretion of PTH that affects calcium homeostasis in the body and affects women more than men

A

Hyperparathyroidism

91
Q

In 85% of cases hyperparathyroidism is caused by what?

A

an adenoma: growth in the parathyroid gland causes excessive secretion of PTH with resulting high levels of calcium in the blood. Any disorder that causes hypocalcemia can cause stimulation of the parathyroid gland and resultant hyperparathyroidism.

92
Q

What do the following symptoms indicate?
muscle weakness, poor concentration, neuropathies, hypertension, kidney stones, metabolic acidosis, osteopenia, pathological fractures, and constipation.
may include depression, confusion, or subtle cognitive deficits
can increase gastric acid secretion, may have a higher prevalence of peptic ulcer disease.

A

Hyperparathyroidism: hypercalcemia

93
Q

What is the diagnostic testing indicated for hyperparathyroidism

A

Blood testing for PTH levels:
elevated PTH level with an elevated ionized serum calcium level is diagnostic of primary hyperparathyroidism. A radiolabeled sestamibi scan and ultrasound are also used to detect parathyroid tumors.

94
Q

The treatment for this disease includes: reducing elevated serum calcium levels through the use of diuretics, calcitonin, and bisphosphonates. Vitamin D should also be administered. Surgical intervention is also frequently needed.

A

hyperparathyroidism

95
Q

What are the 2 parts of the adrenal gland?

A

cortex and medulla

96
Q

This part of the adrenal gland secretes corticosteroids (also called glucocorticoids), androgens and mineralcorticoids, mainly aldosterone

A

cortex

97
Q

This part of the adrenal gland secretes epinephrine and norepi (referred to as catecholamines)

A

medulla

98
Q

This assists the body in dealing with stress; they stimulate gluconeogenesis to increase blood sugar, mobilize fat stores, and break down proteins. during stress it gives the body great strength and vigor for a temporary period.

A

cortisol

99
Q

What are the negative long-term effects of the secretion of corticosteroids like cortisol?

A

suppression of the immune system and breakdown of bone. White blood cells (WBCs) do not function well in the presence of prolonged elevated blood cortisol levels, so immune defenses diminish.

100
Q

These hormones from the adrenal gland assist in fluid and electrolyte balance. (the main one increases sodium and water reabsorption into the blood at the nephron. It also causes secretion of K+ into the nephron tubule, which eventually causes loss of K+ in the urine)

A

Mineralocorticoids: mainly aldosterone

101
Q

How is the adrenal gland stimulated to release its hormones: cortisol, epinephrine, norepinephrine, androgens, and aldosterone?

A

the hypothalamus secretes CRF, which stimulates the pituitary gland to release ACTH, which stim the adrenal gland

102
Q
A