Exam 4 Flashcards

1
Q

Endocrinology

A

Study of intra and extracellular communication by hormones

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2
Q

Hormone

A

Chemical substance produced and secreted into the blood by an endocrinological organ or tissue

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3
Q

Endocrine hormone

A

Synthesized in 1 location and released into blood circulation, binds to specific receptor in cells at a distant site to elicit response

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4
Q

Paracrine hormone

A

Synthesized in endocrine cells and released into interstitial space, binds to specific receptor of nearby cell and affects it function

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5
Q

Autocrine hormone

A

Synthesized in endocrine cells and sometimes released into interstitial space, binds to specific receptor on the cell of origin autoregulating its function

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6
Q

Exocrine hormone

A

Synthesized in endocrine cells and released into lumen of GI, binds to cells lining the GI at varying distances from the endocrine cells affecting their functions

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7
Q

Function of hormones

A

Maintain homeostasis for efficient function, influence growth and development, part of overall control of bodily function, linked to CNS through hypothalamus and pituitary to regulate and respond to target organs

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8
Q

Mechanism of action of hormones

A

Binding of a hormone to its receptor on the surface of the cell membrane through cAMP or Phospholipase C pathway

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9
Q

Bioassay

A

Based on observations of physiological responses that are specific for the hormone being measured

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10
Q

Immunoassay

A

ELISA. RIA, EMIT, fluorescence polarization and chemiluminescent immunoassay

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11
Q

Radioreceptor assay

A

An in vitro assay which allows interaction of hormone with its biological receptor

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12
Q

Hypothalamic-pituitary axis location

A

The portion of the brain located in the walls and floor of the third ventricle, which is connected to the posterior pituitary by the pituitary stalk

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13
Q

Hypothalamic-pituitary axis purpose

A

Control over pituitary function by direct neurostimulation and neurosecretion events of the hypothalamus, direct relationship with posterior pituitary, indirect relationship with anterior pituitary through the portal system

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14
Q

Pituitary location

A

Below the hypothalamus anatomically

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15
Q

Pituitary function

A

Releases hormone such as ADH, oxytocin, ACTH, GH, prolactin, LH, FSH and TSH

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16
Q

General features of over-secretion of pituitary hormones

A

Overproduction of only 1 hormone, deficient in more than 1 and eventually all the anterior pituitary hormones, sequentially loss of hormones, GH - FSH - LH - TSH - ACTH and prolactin, delayed diagnosis due to slow development of symptoms

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17
Q

Growth hormone physical actions

A

Promotes growth in soft tissues, cartilage and bone, causes positive nitrogen and phosphorous balance, stimulates hepatic glycogenolysis and antagonizes the effect of insulin on glucose uptake by peripheral cells, promotes linear growth through other hormone factors

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18
Q

Insulin-like growth factors

A

Polypeptides structurally related to insulin, exhibit metabolic and growth promoting effects similar to insulin

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19
Q

IGF I

A

One of the major regulators of cell growth and differentiation, synthesis mainly in liver, dependent on GH

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20
Q

Regulation of GH

A

Stimulated by GHRH, inhibited by somatostatin

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21
Q

Over-secretion of GH

A

By adenomas of pituitary, impairment of glucose tolerance

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22
Q

Pituitary giant

A

If overproduction occurs before long-bone growth is complete

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23
Q

Acromegaly

A

If overproduction occurs after long-bone growth is complete, prior to closure of epiphyseal plates

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24
Q

GH deficiency as an isolated disorder

A

Pituitary dwarfism in children, no clinical symptoms in adult

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25
Q

GH deficiency as part of panhypopituitarism

A

Pituitary dwarfism plus symptoms resulted from other hormone deficiency in children, symptoms related from other hormone deficiency (without symptoms caused by GH deficiency) in adults

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26
Q

Prolactin

A

Initiation and maintenance of lactation through induction of ductal growth, development of the lobular alveolar system and synthesis of specific milk protein, secretion initiated by dopamine and stimulated by TRH and by sucking

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27
Q

Hyperprolactinemia

A

Caused by a decrease in PIF or autonomous production of prolactin by a pituitary tumor, certain medicine or renal failure, presented with amenorrhea and/or galactorrhea in women and oligospermia or impotence or both in men, diagnosis is radiology and prolactin levels

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28
Q

ADH and oxytocin

A

Released from posterior lobe of pituitary gland, synthesized in 2 nuclei of hypothalamus, transported through neuronal axons in pituitary stalk to posterior lobe of pituitary, released when stimulation of hypothalamus by ADH or oxytocin, regulated by baroreceptors that respond to alteration in blood volume

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29
Q

Physiological actions of ADH

A

Regulate water permeability of the collecting tubules, generalized vasoconstriction to increase BP when released in sufficient amount

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30
Q

Physiological actions of ADH

A

Regulate water permeability of the collecting tubules, generalized vasoconstriction to increase BP when released in sufficient amount

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31
Q

Physiological actions of oxytocin

A

Stimulate the contraction of the uterus in the estrogen-primed uterus

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32
Q

Diabetes insipidus

A

Decreased secretion of ADH upon osmoregulatory stimulation, unresponsive to ADH due to nephrogenic problems, failure of the renal tubule to reabsorb water manifested by polyuria, sense of thirst, Hypernatremia and high plasma osmolality

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33
Q

Water deprivation test

A

Used to diagnose type of diabetes insipidus, measures plasma and urine osmolality before and after DDVAP

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34
Q

Normal Water deprivation results

A

Plasma: 280-300 (before)
<5% increase (after

Urine: >600 (before)
>700 (after)

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35
Q

Neurogenic diabetes insipidus water deprivation results

A

Plasma: >300 (before)
Decreased (after)

Urine: <300 (before)
>600 after

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36
Q

Nephrogenic diabetes insipidus water deprivation results

A

Plasma: >300 (before)
No change (after)

Urine: <300 (before)
<300 (after)

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37
Q

Hypersecretion of ADH

A

ADH levels inappropriately increased relative to a low plasma osmolality, ADH overproduction due to CNS disorders, pulmonary diseases or malignancy, manifested by low serum Na+, high urine Na+ and urine osmolality > serum osmolality

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38
Q

Thyroid gland

A

Made of follicular cells, synthesizes thyroid hormone (T3 and T4), parafollicular cells make calcitonin

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39
Q

Metabolism of T3 and T4

A

> 99.9% are protein bound, TBG, TBPA, TBA, metabolized through successive deiodination (80%) and nondeiodinative mechanisms, formation of T3 by monodeiodination of T4 (80%) in peripheral tissue synthesis of T3 (20%), conversion of T4 -> T3 (30%) T4 -> rT3 (60%), potency of T3 greater than T4 but less concentrated in blood

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40
Q

Growth and development with thyroid hormones

A

Regulates optimal growth and development of all body tissue, stimulates protein synthesis

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41
Q

Cretinism

A

Caused by deficiency in iodine, failure of thyroid to develop, present with dwarfism, mental retardation, pale skin, slow heart rate, low body temperature

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42
Q

Calorigenic effect with thyroid hormones

A

Increase resting or basal metabolic rate of whole organism, increase body temperature

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43
Q

Cardiovascular effects with thyroid hormones

A

Increase adrenergic activity and sensitivity, increase heart rate, increase force of contraction, increase cardiac output, decrease peripheral vascular resistance

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44
Q

metabolic effects with thyroid hormones

A

Increase calorigenesis and O2 consumption, increase heat dissipation, increase protein catabolism, increase glucose production, increase glucose uptake

45
Q

GI effects with thyroid hormones

A

increase motility, hyperthyroidism with hyperdefecation, hypothyroidism with constipation

46
Q

Hypothyroidism

A

Deficiency of thyroid activity, occurs in mild or severe forms, affects women more than men and increases with age, may have obvious or subtle symptoms, commonly caused by diseases or treatments that destroy thyroid tissues or interefere with thyroid biosynthesis and less often by disorders of the pituitary or hypothalamus

47
Q

Primary hypothyroidism

A

An impaired synthesis of T4 and T3 due to intrinsic factor or inherited defect in thyroid hormone biosynthesis, hypersecretion of TSH with decreased T4, may be goitrous or nongoitrous, most frequently caused by Hashimoto’s in developed countries and iodine deficiency most common in goitrous worldwide

48
Q

Primary hypothyroidism symptoms

A

Weakness, cold intolerance, constipation, weight change, depression, menorrhagia and hoarseness, dry skin, bradycardia

49
Q

Hashimoto’s disease

A

Primary hypothyroidism, aka chronic lymphocytic thyroiditis, goiytous, associated with antithyroid antibodies and may coexist with other autoimmune diseases

50
Q

Iodine deficiency

A

Primary hypothyroidism, goitrous

51
Q

Congenital hypothyroidism

A

May be due to absence of the thyroid gland or defects of thyroid hormone synthesis, is reversible if treated early, can be detected by screening in neonate

52
Q

Hyperthyroidism

A

Excessive quantities of thyroid hormone, increased secretion of thyroid hormones by TSA, autonomous production by solitary or multiple thyroid nodules, excessive TSH secretion by pituitary tumors or by increased or leakage of stored T3 or T4

53
Q

Grave’s disease

A

most common cause of hyperthyroidism, diffuse goiter, ophthalmopathy and pretibial edema, caused by immunological disorder where serum antibodies bind to thyroid cell membrane at or near TSH receptor, diagnosed by a decreased TSH and in increased free T4 and presence of TSI

54
Q

Assays for thyroid function

A

TSH, total and free T4, total and free T3, rT3, T3 uptake, FT4 index, FT3 index, TRH stimulation, TBG, antithyroglobulin antibodies, antimicrosomal antibodies, TSH receptor antibodies

55
Q

Tests to use if sensitive serum TSH assay is undetectable

A

Hyperthyroid suspect, Free T4, T3 if free T4 normal

56
Q

Tests to use if sensitive serum TSH assay is subnormal

A

Borderline thyroid status, Free T4 and T3, TRH test

57
Q

Tests to use if sensitive serum TSH assay is normal

A

No hyperthyroid dysfunction

58
Q

Tests to use if sensitive serum TSH assay is elevated

A

Hypothyroid suspect, Free T4

59
Q

Increased TBG

A

Caused by pregnancy or oral contraceptives, increased TBG level, decreased saturation, increased binding of T4 and T3, decreased free T4 and T3

60
Q

Decreased TBG

A

Caused by androgens, malnutrition and lover disease, decreases TBG and saturation, decreased binding of T4 and T3. increase free T4 and T3

61
Q

Adrenal glands

A

On upper pole of each kidney

62
Q

3 layers of adrenal gland cortex

A

zona glomerulosa, zona fasciculata, and zona reticularis

63
Q

Aldosterone

A

regulation of potassium metabolism, regulation of extracellular fluid volume, and is controlled by the renin-angiotensin system and ACTH

64
Q

Renin

A

Produced by the juxtaglomerular apparatus of the kidney in response to decreased renal perfusion pressure and/or decreased serum sodium levels, acts on angiotensinogen to produce angiotensin I which is converted to angiotensin II by angiotensin-converting enzyme present mainly in the lungs

65
Q

Angiotensin II

A

constricts blood vessels, stimulates secretion of aldosterone by the zona glomerulosa

66
Q

physiological function of cortisol

A

Anti-insulin effects on carbohydrate, stimulate protein catabolism, cause a central distribution of fat in the face, neck and trunk when present in excess, anti-inflammatory, immunosuppressive effects, effects on water and electrolyte balance

67
Q

Biosynthesis of corticosteroids

A

the conversion of cholesterol to pregnenolone which is stimulated by ACTH (the rate-limiting step), hydroxylation of progesterone at the 17, 21, and 11 positions in the zona reticularis and zona fasciculata leads to the formation of cortisol, hydroxylation of progesterone at the 21, 11, and 18 in the zona glomerulosa forms aldosterone

68
Q

Biosynthesis of adrenal androgens

A

12 alpha-hydroxypregnenolone is the main precursor for adrenal androgens, DHEA-S and DHEA are the most abundant adrenal androgens which can be converted to testosterone which can then be converted to estrogen peripherally, estrogen is largely derived from the gonads and from peripheral conversion of testosterone and androstenedione

69
Q

Regulation of cortisol

A

ACTH, stimulated by CRH, positively regulates cortisol secretion, the free circulating cortisol acts in a negative-feedback manner to control the release of ACTH

70
Q

Characteristics of serum cortisol levels

A

Diurnal variation with the highest levels present in the morning around 8 AM and the lowest levels present in the late afternoon, mainly bound to carrier protein, increased urine free cortisol levels = a sensitive indicator of adrenal hyper-function

71
Q

Hypercortisolism

A

Caused by excessive production of ACTH by a pituitary adenoma (Cushing’s disease), ectopic ACTH by a tumor of non-endocrine tissue, excessive production of cortisol by an adrenal tumor or carcinoma (Cushing’s syndrome), exogenous administration of cortisol

72
Q

Signs and symptoms of hypercortisolism

A

Truncal obesity with gain predominantly in the face, neck, shoulders, and abdomen with relatively thin extremities, abnormal glucose metabolism, protein wasting, with thinning of the skin and development of striae, easy bruising, muscle wasting and hypertension

73
Q

Screening tests for hypercortisolism

A

overnight low-dose dexamethasone suppression test, 24-h urine free cortisol level, the morning and afternoon serum cortisol determination

74
Q

Differentiation tests for hypercortisolism

A

high-dose dexamethasone suppression test, metyrapone stimulation test, plasma ACTH, and bilateral inferior petrosal sinus sampling after CRH administration to differentiate pituitary tumor from ectopic ACTH

75
Q

Hypoadrenalism causes

A

primary adrenal disease, secondary to pituitary abnormalities

76
Q

Addison’s disease

A

Results from idiopathic atrophy of the gland, characterized by weight loss, weakness, and a variety of GI complaints plus dehydration with hypotension, hyponatremia and hyperkalemia, may show hyperpigmentation of the skin and mucous membranes due to excess pituitary synthesis of ACTH

77
Q

Studies for Addison’s disease

A

low serum sodium, high serum potassium, low glucose level, decreased of normal cortisol level, increased ACTH with blunted cortisol response to ACTH stimulation test

78
Q

Adrenal androgen

A

Adrenal glands synthesize DHEA-S, DHEA, androstenedione and small amount to testosterone and DHT, regulated or partially regulated by ACTH not by FSH or LH, major source of testosterone in females

79
Q

Male hormone production in the testis

A

Part of the hypothalamus-pituitary-gonadal axis, primary site of androgen production in the male, regulated by FSH and LH

80
Q

Testosterone

A

Mainly produced by the testis under the control of LHH, converted to dihydrotestosterone by enzyme found in prostate, skin and seminal vesicle, major circulating androgen and responsible for male differentiation of the fetal genital tract and development and maintenance of male secondary sex characteristics and spermatogenesis, bind to SHBG and albumin with free testosterone being biologically active, serum level is used to evaluate hirsutism and virilization

81
Q

Sex hormone binding proteins

A

Testosterone and dihydrotestosterone circulate mainly bound to SHBG in men, estradiol, DHEA-S and DHEA are bound to albumin

82
Q

Primary hypergonadism

A

Testicular tumor or adrenal disorder, no clinical abnormality in males, early onset of the pubertal changes in the prepubertal male or children, noted high serum androgen levels, low serum gonadotropins and high urinary 17-ketosteroids

83
Q

Secondary hypergonadism

A

Secondary to altered pituitary-hypothalamic axis function, resulting in elevation of gonadotropins, characterized by elevated androgens and elevated gonadotropins

84
Q

Primary hypogonadism

A

Caused by genetic defect, infection, trauma, radiation, or tumor, show delayed puberty in children and impotence and loss of secondary sex characteristics in adults, manifested by increased serum and urine gonadotropin and by decreased serum androgen levels and decreased urinary 17-ketosteroid levels

85
Q

Secondary hypogonadism

A

Results from failure of the pituitary-hypothalamic axis, resulting in a decreased production of FSH and LH, accompanied by other pituitary hormone deficiencies, show delayed puberty in children and impotence and loss of secondary sex characteristics in adults, characterized by decreased serum and urinary gonadotropins with diminished gonadal function after adolescence

86
Q

The ovary

A

Made of the basic reproductive unit, primordial follicle which consists of a small oocyte arrested in the diplotene stage of meiotic prophase, function as both producers of ova and secretors of the sex hormones

87
Q

Functions of estrogen

A

Growth of the uterus, fallopian tubes and vagina, promotion of breast development, deposition of body fat into the lobules of the breast for lactation, affect calcium homeostasis and plasma proteins

88
Q

Regulation of estrogens

A

Regulated by FSH and LH, undergoes changes characteristics of the female reproductive system

89
Q

Biosynthesis of estrogens

A

Conversion of androgens to estrogens by aromatase system in ovary, production of estrogens by peripheral aromatization of androgens in adipose tissue, generation of estriol in the placenta

90
Q

Clinical synthesis of testing estrogen

A

Evaluate ovarian function, diagnose postmenopausal bleeding, evaluate the fetoplacental unit for fetal distress, intrauterine growth retardation, affect plasma proteins

91
Q

Primary ovarian hyperfunction

A

Caused mainly by estrogen-secreting tumors, can occur before puberty, during the period of reproductive life or after menopause, characterized by precocious puberty and intermittent uterine bleeding in the premenarchal years, irregular uterine bleeding and amenorrhea during the active reproduction life or uterine bleeding during the postmenopausal years, associated with low serum FSH and LH levels and elevated or normal estrogen levels

92
Q

Ovarian hypofunction

A

Primary amenorrhea during the prepubertal period, secondary amenorrhea during the post-pubertal period

93
Q

Primary hypofunction

A

Result from premature ovarian failure, resistant ovary syndrome, ovarian tumors, gonadal agenesis, Turner’s syndrome and 17 a-hydroxylase deficiency, characterized by increased gonadotropins and decreased estrogen levels

94
Q

Secondary ovarian hypofunction

A

Characterized by decreased estrogen and progesterone levels associated with decreased gonadotropin levels

95
Q

Progesterone

A

Maintain the endometrium, inhibit uterine contractions, stimulate the lobar unit of the breast, used for the synthesis of cortisol and sex hormone precursors

96
Q

Estriol

A

Produced in the placenta, major product of estrogen in pregnant women, can be used to predict fetoplacental function

97
Q

Chorionic gonadotropin

A

Maintains progesterone production by the corpus luteum in the early pregnancy, stimulates development of fetal gonads and synthesis of androgen by the fetal testes, measured for diagnosis of pregnancy, prediction of spontaneous abortion, detection of multiple pregnancies, and detection and follow-up of HCG-producing tumors

98
Q

Placental lactogen

A

Similar to GH and prolactin structurally, immunologically and functionally, act in concert with HCG to stimulate estrogen and progesterone synthesis by the corpus luteum, stimulates development of the mammary gland, used for monitoring conditions associated with a decrease in functioning placental tissue and in diagnosis of intrauterine growth retardation

99
Q

Catecholamines

A

Consists of monoamines attached to a benzene ring bearing 2 hydroxyl groups

100
Q

Norepinephrine

A

Major substance released by the postganglionic sympathetic nerves

101
Q

Epinephrine

A

Most important substance produced by the adrenal medullar

102
Q

Dopamine

A

Present in dopaminadenic neurons

103
Q

Physiological actions of the catecholamines

A

Influence the vascular system and affect metabolic processes such as carbohydrate metabolism

104
Q

A-adrenergic (epinephrine and norepinephrine)

A

Vasoconstriction, decrease in insulin secretion, sweating, stimulation of glycogenolysis in the liver and skeletal muscle

105
Q

B-adrenergic

A

Vasodilation, stimulation of insulin release, increase of cardiac contraction rate, relaxation of smooth muscle in the intestinal tract, bronchodilation by relaxation of smooth muscles in bronchi, stimulation of renin release

106
Q

Pheochromocytoma

A

Occur in the adrenal medulla (90%) and extra-adrenal sites (10%, paragangliomas), arise from ANS or adrenal medulla, produce excessive amounts of catecholamines or catecholamine metabolites, found in 0.1 to 0.3% of the population

107
Q

Pheochromocytoma appearance

A

Sustained or paroxysmal hypertension, weight loss, spells of sweating, headache, palpitation, anxiety

108
Q

Lab studies for Pheochromocytoma

A

Increased urinary metanephrines (24 hour urine) and elevated urinary VMA and free catecholamines

109
Q

Neuroblastoma

A

One of most common malignant tumors in pediatric patients, manifests as a lump or mass in the abdomen or around the spinal cord in chest, neck, or pelvis, a cancer of the SNS, characterized by rapid growth and widespread metastasis, associated with excessive production of catecholamines and catecholamine metabolites, characterized by increased urinary norepinephrine, VMA, HVA and dopamine