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endocrine Flashcards

1
Q

Feedback regulation

Negative

A

Sensors detect a decrease in hormone levels, they increase hormone production. When hormone levels rise above the set point of system, sensors decrease hormone production.

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2
Q

Feedback regulation

Positive

A

Rising levels of a hormone cause another gland to release a hormone that is stimulating the first.
Ex: estradiol production causes increased gonadotropin (FSH) production. this stimulates further increases in estradiol levels until demise of follicle.

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3
Q

Hypofunction

A

Altered endocrine function.
Can occur due to absence or impaired development of a gland or a deficiency of an enzyme needed for hormone synthesis. Gland could be destroyed .

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4
Q

Hyperfunction

A

Altered endocrine function.
Excessive hormone production. Can result from excessive stimulation and hyperplasia of the endocrine gland of from a hormone-producing tumor.

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5
Q

Hormone Resistance

A

Altered endocrine function.
May be associated with receptor defects at the target cells. Hormone receptors may be absent or the receptor binding of hormones may be defective.

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6
Q

Hypopituitarism

A

Altered endocrine function.
Characterized by a decreased secretion of pituitary hormones and is associated with increased morbidity and mortality. May be congenital or acquired.

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7
Q

Growth hormone
(also called somatotropin)
ANTERIOR PITUITARY

A

necessary for growth and contributes to the regulation of metabolic functions.
GHRH- increases GH release-
somatostatin- inhibits GH

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8
Q

Short stature in children (GH)

A

condition in which height is less than the third percentile on the app. growth curve.

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9
Q

causes of short stature in children (GH)

A

endocrine causes- GH deficiency, hypothyroidism, and panhypopituitarism (deficiency of all pituitary-derived hormones)
genetic or chromosomal- Turner syndrome, Noonan syndrome, achondroplasia, & skeletal dysplasias.

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10
Q

Familial and constitutional short stature (GH)

A

not a disease. but variation from population norms. requires monitoring but not treatment.

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11
Q

Psychosocial dwarfism (psychosocial short stature) (GH)

A

Involves functional hypopituitarism and is seen in some emotionally deprived children.
Present with poor growth, potbelly, and poor eating and drinking habits.
Severely neglected or disciplined.
GH returns to normal when removed from environment.

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12
Q

Growth hormone deficiency in adults (GH)

A

2 categories:

  1. present in childhood.
  2. developed during adulthood.
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13
Q

Diagnosis of GH deficiency in adults

A

Low IGF-1 level in the presence of low levels of 3 or more pituitary hormones indicated GH deficiency

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14
Q

Treatment of GH deficiency in adults

A

recombinant GH replacement

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15
Q

Growth hormone deficiency in children (GH)

A

present with short stature (pituitary dwarfism). increased fat in abdomen, immature facial features with frontal bossing, delayed dentition, and an underdeveloped nasal bridge.

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16
Q

GH deficiency in children (GH) causes

A

genetic mutations. some are idiopathic. can occur as pituitary tumors

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17
Q

Tall stature (GH)

A

height is greater than the 97th percentile.

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18
Q

Tall stature (GH) causes

A

genetic or chromosomal (Marfan syndrome, Klinefelter syndrome, fragile X sydrome, and Beckwith-Wiedemann syndrome). other causes is normal familial stature and advancement of growth

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19
Q

GH excess in children

A

occurring before puberty and the fusion of the epiphyses of the long bones result in pituitary gigantism. All tissues and bones grow rapidly.

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20
Q

GH excess in children causes

A

Excessive secretion of GH by somatotrope adenomas causes gigantism in the prepubertal child. Epiphyses are not fused and high levels of IGF-1 stimulate excessive skeletal growth.

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21
Q

Acromegaly (GH excess in adults)

A

occurs in adulthood or after the epiphyses of the long bones have been fused.

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22
Q

Acromegaly causes

A

excess circulating blood levels of GH and IGF-1. most common cause is a GH-secreting somatotrope adenoma in the pituitary gland.

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23
Q

Acromegaly manifestations

A

Soft tissue growth (person does NOT get taller).
- enlarged small bones of the hands and feet, broad bulbous nose, protruding lower jaw, and a slanting forehead, deepened voice, kyphosis (hunchback), cardiomegaly (hypertension), barrel chest, glucose tolerance/insulin resistance, male sexual dysfunction/menstrual in women, degenerative arthritis, thickened skin (sweaty and smelly)

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24
Q

Precocious puberty

A

early activation of the hypothalamic-pituitary-gonadal axis, resulting in the early development of sexual characteristics and fertility.
pubertal changes noted before 8 for girls and 9 for boys.

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25
Q

Precocious puberty causes

A

idiopathic or by gonadal, adrenal, or hypothalamic disease.

CNS malignant tumors

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26
Q

precocious puberty signs

A

girls- early thelarche (breast development), adrenarche (early sexual maturation), and menarche.
boys- genital enlargement.

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27
Q

Hypothyroidism

A

Can be congenital or acquired.

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28
Q

Congenital Hypothyroidism

A

Common cause of preventable intellectual disability. In the infant it may result from a congenital lack of thyroid gland or from abnormal biosynthesis of thyroid hormone deficient TSH secretion.
Manifestation are referred to as cretinism.

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29
Q

Transient hypothyroidism (congenital)

A

Caused by maternal or infant exposure to substances such as povidone-iodine used as a disinfectant (vaginal douche or skin disinfectant)

30
Q

Congenital hypothyroidism treatment

A

Hormone replacement.

31
Q

Acquired Hypothyroidism & Myxedema

A

Hypothyroidism in older children and adults causes a general slowing down of metabolic processes and myxedema.
Myxedema implies nonpitting mucus type of edema caused by an accumulation of a hydrophilic mucopolysaccharide substance in the connective tissues throughout the body. May progress to angioedema (life-threatening).

32
Q

Acquired hypothyroidism causes

A

Destruction or dysfunction of the thyroid gland (primary hypothyroidism), or it can be a secondary disorder caused by impaired pituitary function or as a tertiary disorder caused by hypothalamic dysfunction.

33
Q

Primary hypothyroidism

A

More common. May result from thyroidectomy (surgical removal) or ablation of the gland with radiation for treatment of hyperthyroidism. Large amounts of iodine can block thyroid production and cause hypothyroidism.

34
Q

Hashimoto thyroiditis

A

Most common cause of acquired hypothyroidism. It is an autoimmune disorder in which the thyroid gland may be totally destroyed by an immunologic process. Major cause of acquired hypothyroidism in children and adults. Predominantly a disease of women. At onset, a goiter may be present.

35
Q

Acquired hypothyroidism manifestations

A

Hypermetabolic state: gradual onset of weakness and fatigue, weight gain despite lack of appetite, and cold intolerance. As it progresses, the skin becomes dry and rough and the hair becomes coarse and brittle. Puffy face, edematous eyelids, and thinning of outer eyebrow.
CNS involvement is manifested in mental dullness, lethargy, and impaired memory.
Myxedamatous involvement: fluid is most obvious in face but can also spread to interstitial spaces. Tongue is often enlarged and voice becomes hoarse and husky. Cardiac dilation & bradycardia.

36
Q

Diagnosis of hypothyroidism

A

Low serum T4 and elevated TSH levels are characteristic.

37
Q

Treatment for hypothyroidism

A

replacement therapy with synthetic preparations of T3 or T4.
“go low and go slow” approach is done for older people.
People must remain on their hormone therapy to have consistent levels.

38
Q

Myxedematous coma

A

Life-threatening, end-stage expression of hypothyroidism.
long-standing hypothyroidism leads to a crisis state with severely reduced cellular metabolism that affects all organ systems throughout the body.
- Hypothermia also develops and is a strong predictor of mortality.

39
Q

Hyperthyroidism

A

Thyrotoxicosis is the clinical syndrome that results when tissues are exposed to high levels of circulating thyroid hormone.

40
Q

Etiology/pathogenesis of hyperthyroidism

A

Thyrotoxicosis is due to hyperactivity of the thyroid gland, or hyperthyroidism. Most common cause is Graves diseases, which is accompanied by ophthalmopathy, dermopathy, and diffuses goiter.

41
Q

manifestations of hyperthyroidism

A

Nervousness, irritability, fatigability; weight loss is common despite large appetite; tachycardia, palpitations, shortness of breath, excessive sweating, muscle cramps, and heat intolerance; may appear restless and have a fine muscle tremor; abnormal retraction of the eyelids and infrequent blinking; hair and skin are thin and silky.

42
Q

Treatment of hyperthyroidism

A

directed toward reducing the level of thyroid hormone.
- Done by eradication of the thyroid gland with radioactive iodine, surgical removal, or drugs that decrease thyroid function.

43
Q

Graves Disease

A

state of hyperthyroidism, goiter, and ophthalmopathy.. Affects those under 40 years.
It is an autoimmune disease characterized by abnormal stimulation of the thyroid gland by thyroid-stimulating antibodies (TSH receptor antibodies) that act through the normal TSH receptors.

44
Q

Thyroid storm

A

Thyrotoxic crisis. It is an extreme and life-threatening form of thyrotoxicosis rarely seen today. Seen most often in undiagnosed or those who have not been adequately treated for hyperthyroidism.

45
Q

Thyroid storm manifestations

A

Very high fever, extreme cardiovascular effects (tachycardia, congestive failure, and angina), and severe CNS effects (agitation, restlessness, and delirium). Mortality rate is high.

46
Q

Congenital Adrenal Hyperplasia (CAH)

A

congenital disorder caused by an autosomal recessive trait in which a deficiency exists in any of the enzymes necessary for the synthesis of cortisol.

47
Q

Characteristics of CAH

A

defect in the synthesis of cortisol that results in increased levels of ACTH and adrenal hyperplasia. Increased levels of ACTH overstimulate the pathways for production of adrenal androgens.

48
Q

CAH manifestations

A

Female infants: virilization syndrome of ambiguous genitalia with an enlarged clitoris, fused labia, and urogenital sinus.
Male infants: seldom diagnosed at birth unless they have enlarged genitalia or lose salt and manifest adrenal crisis.

49
Q

CAH treatment

A

oral or parenteral glucocorticoid replacement.

50
Q

Addison disease (primary adrenal cortical insufficiency)

A

Adrenal cortical hormones are deficient (cortisol & aldosterone) and ACTH levels are elevated because of lack of feedback inhibitors.

51
Q

Manifestations of Addison Disease

A

Manifestations do not become apparent until 90% of the gland is destroyed. Hyperkalemia, hyponatremia, decreased cardiac output, loss of extracellular fluid; salt appetite; orthostatic hypotension, dehydration, weakness, and fatigue are common early symptoms; poor tolerance to stress; hypoglycemia, lethargy, weakness, fever, and GI symptoms such as anorexia, nausea, vomiting, and weight loss; hyperpigmented skin (appears bronzed); gums and oral mucous membranes may become bluish black.

52
Q

Addison Disease treatment

A

Requires lifetime hormone replacement therapy. Hydrocortisone is usually the drug of choice. Fludrocortisone (a mineralocorticoid) is used for people who do not obtain a sufficient salt-retaining effect from hydrocortisone.

53
Q

Secondary adrenal cortisol insufficiency

A

Can occur as the result of hypopituitarism or because the pituitary gland has been surgically removed.
- More common is either the rapid withdrawal of glucocorticoids that have been administered therapeutically for asthma or an exacerbation of MS.

54
Q

Acute adrenal crisis

A

Life-threatening situation.
If Addison disease is the problem, exposure to a minor illness or stress can precipitate nausea, vomiting, muscular weakness, hypotension, dehydration, and vascular collapse.

55
Q

Acute adrenal insufficiency treatment

A

Five Ss:

  1. Salt replacement.
  2. Sugar (dextrose) replacement.
  3. Steroid replacement.
  4. Support of physiologic functioning.
  5. Search for and treat the underlying cause (infection)
56
Q

Cushing Syndrome

Glucocorticoid hormone excess

A

Can result from an adrenal tumor.
It is al exaggeration of the many actions of cortisol. Cushing Syndrome refers to the manifestations of hypercortisolism.

57
Q

Cushing Syndrome manifestations

A

altered fat metabolism- protruding abdomen; buffalo hump; moon face; muscle weakness, think extremities due to muscle wasting; advanced stages: skin over forearms and legs become thin; purple striae develop over breasts, thighs, and abdomen; osteoporosis; renal calculi; increased susceptibility to infection; increased androgen levels causes hirsutism, mild acne, and menstrual irregularities in women.

58
Q

Cushing Syndrome diagnosis

A

2 step process: 1. diagnosis of hypercortisolism 2. testing to determine the cause of cortisol hypersecretion.
Most common tests are the 24hr urinary free cortisol level, midnight plasma and late-night salivary cortisol measurements and the low-dose dexamethasone suppression test.

59
Q

Cushing Syndrome treatment

A

If untreated it can cause serious morbidity and death. Transsphenoidal removal of a pituitary adenoma or a hemihypophysectomy is the preferred method of treatment.

60
Q

Incidental Adrenal Mass

A

Mass found unexpectedly in an adrenal gland by an imaging procedure.

61
Q

Beta cells, alpha cells, and delta cells

A

Beta- secrete insulin
Alpha- secrete glucagon
Delta- secrete somatostatin

62
Q

Insulin (glucose-regulating hormone)

A

only hormone that acts to lower blood glucose levels.

63
Q

Actions of insulin include:

A
  1. promoting glucose uptake by target cells and storage glucose as glucagon (liver) or fat (adipose tissue)
  2. inhibit fat and glycogen breakdown
  3. inhibit gluconeogenesis and increase protein synthesis
64
Q

Glucagon (glucose-regulating hormone)

A

Produced in the pancreas in response to a decrease in blood glucose. Maintains blood glucose levels between meals and during periods of fasting. Also increased during strenuous exercise to prevent a decrease in blood glucose.

65
Q

Somatostatin

A

Acts locally to decrease secretion of insulin

66
Q

Type 1 Diabetes

A

Characterized by insufficient insulin production. It is an autoimmune destruction of pancreatic beta cells and lead to absolute insulin deficiency. Idiopathic.

67
Q

Type 2 Diabetes

A

Characterized by a state of insulin resistance and progressive decline in pancreatic beta-cell secretion of insulin. Commonly accompanied by metabolic syndrome.

68
Q

Type 2 abnormalities:

A
  1. Insulin resistance
  2. Deranged secretion of insulin by the pancreatic beta cells.
  3. Increased glucose production by the liver.
69
Q

Signs and Symptoms of Diabetes:

A
  1. Polyuria (excessive urination)
  2. Polydipsia (excessive thirst)
  3. Polyphagia (excessive hunger)
70
Q

Metabolic Syndrome

A

Constellation of abnormalities from insulin resistance:
obesity, high levels of plasma triglycerides and low levels of high-density lipoproteins, hypertension, systemic inflammation, macrovascular disease (coronary artery, cerebrovascular, and peripheral arterial disease

71
Q

Clinical signs of metabolic syndrome

A

obesity and hyperpigmented skin changes

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