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Pathopharm II Exam 1 > 3: Hormonal Regulation (Part 1) > Flashcards

3: Hormonal Regulation (Part 1) Flashcards

1
Q

failure of feedback systems may be caused by (2)

A
  • failing to function properly
  • failure to respond to inappropriate signals
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2
Q

Dysfunction of an endocrine gland may cause (3)

A
  • Inability to produce or obtain an adequate quantity of required hormone precursors
  • Inability to convert precursors to the active hormone
  • Excessive or inadequate hormone production
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3
Q

Receptor-associated disorders can be from (5)

A
  • Decrease in the number of receptors
  • Impaired receptor function
  • Presence of antibodies against specific receptors
  • Antibodies that mimic hormone action
  • Unusual expression of receptor function
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4
Q

intracellular disorders are caused by inadequate synthesis of…

A

a second messenger (cAMP)

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5
Q

Failure of the target cell to produce anticipated hormonal response causes

A

Faulty response to hormone-receptor binding

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6
Q

Faulty response to hormone-receptor binding causes (2)

A
  • Failure to generate required second messenger
  • Abnormal response to the second messenger
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7
Q

posterior pituitary hyperfunction causes too (much/little) antidiuretic hormone

A

too much

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8
Q

examples off too much antidiuretic hormone

A

Syndrome of inappropriate antidiuretic hormone (SIADH) secretion

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9
Q

hypofunction of posterior pituitary causes too (much/little) antidiuretic hormone

A

too little

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10
Q

examples of hypofunction of posterior pituitary

A

Diabetes insipidus
- Neurogenic
- Nephrogenic
- Dipsogenic

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11
Q

levels of antidiuretic hormone in SIADH

A

Levels of antidiuretic hormone (ADH) are abnormally high.

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12
Q

most common cause of SIADH

A

Ectopic secretion of ADH is the most common cause; is also common after surgery and some cancers.

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13
Q

patho of water retention in SIADH

A

Action of ADH on renal collecting ducts increases their permeability to water, thus increasing water reabsorption by the kidneys.

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14
Q

for diagnosis of SIADH what must exist

A

normal renal, adrenal, and thyroid function must exist.

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15
Q

SIADH Na level

A

hyponatremia: Na < 135 mEq/L

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16
Q

SIADH osmolality level

A

hypoosmolality: <280 mOsm/kg

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17
Q

urine osmolality in SIADH

A

hyperosmolality: higher than serum osmolality

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18
Q

weight in SIADH secretion

A

weight gain

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19
Q

serum sodium levels in SIADH

A

Serum sodium levels below 110 to 115 mEq/L: Can cause severe and sometimes irreversible neurologic damage

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20
Q

treatment of SIADH

A

Correction of underlying causal problems

Emergency correction of severe hyponatremia by the administration of hypertonic saline
Conivaptan (Vaprisol) – ADH receptor blocker

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21
Q

what kind of drug is Conivaptan (Vaprisol)

A

ADH receptor blocker

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22
Q

fluid restriction in SIADH

A

between 800 and1000 mL/day

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23
Q

treatment for resistant or chronic SIADH

A

Demeclocycline

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24
Q

what is Demeclocycline

A

a tetracycline analog with a known SE of causing nephrogenic diabetes insipidus by blocking normal ADH activity

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25
Q

diabetes insipidus is caused by too (much/little) antidiuretic hormone

A

too little antidiuretic hormone

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26
Q

diabetes insipidus clinical manifestations (3)

A

Polyuria
Polydipsia
Partial or total inability to concentrate the urine

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27
Q

neurogenic diabetes insipidus is caused by

A

Insufficient amounts of ADH

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28
Q

nephrogenic diabetes is caused by

A

Insensitivity of the renal collecting tubules to ADH

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29
Q

dipsogenic diabetes insipidus is caused by

A

Excessive fluid intake, lowering plasma osmolarity to the point that it falls below the threshold for ADH secretion

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30
Q

diabetes insipidus is characterized by

A

the inability of the kidney to increase permeability to water

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31
Q

diabetes insipidus urine excretion

A

Excretion of large volumes of dilute urine

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32
Q

diabetes insipidus plasma osmolality

A

Increase in plasma osmolality: 300 mOsm or more, depending on adequate water intake

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33
Q

diabetes insipidus urine output

A

Urine output: 8 to 12 L/day; normal output: 1 to 2 L/day

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34
Q

clinical manifestations of diabetes insipidus

A
  • Polyuria, nocturia, continual thirst
  • Low urine-specific gravity: <1.010
  • Low urine osmolality (<200 mOsml/kg)
  • Hypernatremia
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35
Q

treatment of neurogenic DI

A

Administration of the synthetic vasopressin analog desmopressin acetate (DDAVP)

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36
Q

treatment of nephrogenic DI

A

Treatment of any reversible underlying disorders, discontinuation of etiologic medications, and correction of associated electrolyte disorders; administration of thiazide diuretic agents

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37
Q

treatment of dipsogenic DI

A

Effective management of water ingestion

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38
Q

hyperfunction of anterior pituitary effects

A
  • Hyperpituitarism
  • Hypersecretion of growth hormone
  • Hypersecretion of prolactin
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39
Q

examples of diseases from hyperfunction of anterior pituitary (3)

A
  • Primary adenoma
  • Acromegaly
  • Prolactinoma
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40
Q

hypofunction of anterior pituitary diseases

A
  • Panhypopituitarism
  • Adrenocorticotropic hormone (ACTH) deficiency
  • Thyroid-stimulating hormone (TSH) deficiency
  • Follicle-stimulating hormone (FSH) and luteinizing hormone (LH) deficiency
  • Growth hormone (GH) deficiency
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41
Q

hypopituitarism is characterized by…

A

the absence of selective pituitary hormones or the complete failure of all pituitary hormone functions.

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42
Q

t/f the pituitary is avascular

A

False! Pituitary is vascular and therefore vulnerable to ischemia and infarction.

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43
Q

causes of hypopituitarism

A
  • Inadequate supply of hypothalamic-releasing hormones
  • Damage to the pituitary stalk
  • Inability of the gland to produce hormones
  • Pituitary infarction
  • Tumor or surgical removal
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44
Q

Adrenocorticotropic hormone (ACTH) deficiency
causes __________

A

cortisol deficiency

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45
Q

Thyroid-stimulating hormone (TSH) deficiency causes __________

A

altered metabolism

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46
Q

FSH and LH deficiency causes ____________

A

Lack of secondary sex characteristics

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47
Q

growth hormone (GH) deficiency causes ____________

A

Lack of growth in children

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48
Q

treatment of hormone deficiency

A

Replacement of deficient hormone(s)

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49
Q

what commonly causes hyperpituitarism

A

Commonly from benign, slow-growing pituitary adenoma

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50
Q

clinical manifestations of hyperpituitarism (4)

A
  • Headache and fatigue
  • Visual changes
  • Hypersecretion of pituitary hormones from tumor
  • Hyposecretion of neighboring anterior pituitary hormones
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51
Q

treatment of hyperpituitarism (4)

A
  • Headache and fatigue
  • Visual changes
  • Hypersecretion of pituitary hormones from tumor
  • Hyposecretion of neighboring anterior pituitary hormones
52
Q

what is giantism caused by

A

GH hypersecretion in children and adolescents

53
Q

acromegaly is caused by

A

Hypersecretion of GH during adulthood

54
Q

what does a pituitary adenoma cause

A

acromegaly

55
Q

mortality associated with pituitary adenoma

A

Cardiac hypertrophy; hypertension; atherosclerosis; type 2 diabetes mellitus, leading to coronary artery disease

56
Q

connective tissue proliferation associated with acromegaly can cause

A

Enlarged tongue, interstitial edema, increase in size and function of sebaceous and sweat glands, coarse skin and body hair

57
Q

bony proliferation associated with acromegaly can cause

A

Large joint arthropathy, kyphosis, enlargement of facial bones and hands and feet, protrusion of the lower jaw and forehead, need for increasingly larger sized shoes, hats, rings, and gloves

58
Q

a patient with acromegaly can have symptoms of what disease?

A

diabetes (polyuria and polydipsia)

59
Q

CNS symptoms associated with acromegaly

A

Headache, seizure activity, visual disturbances, papilledema

60
Q

primary treatment for acromegaly

A

Transsphenoidal surgery or endonasal endoscopic surgery for the removal of the GH-secreting adenoma

61
Q

pharmacologic treatment of acromegaly

A

octreotide, octreotide long-acting, lanreotide, cabergoline, pegvisomant

62
Q

function of octreotide (Sandostatin), octreotide long-acting (Sandostatin LAR), and lanreotide (Somatuline) (somatostatin analogs)

A

to lower GH levels (inhibits secretion)

63
Q

cabergoline class

A

dopaminergic agonist

64
Q

mechanism of action of cabergoline

A

to lower prolactin levels (DA same as PIH)

65
Q

pegvisomant mechanism of action

A

blocks GH receptor

66
Q

hypersecretion of prolactin is causedby

A

prolactinomas

67
Q

most commonly active pituitary tumor

A

prolactinoma

68
Q

in women, prolactinomas cause…

A

Amenorrhea, galactorrhea, hirsutism, and osteoporosis

69
Q

in men, prolactinomas cause…

A

Hypogonadism, erectile dysfunction

70
Q

what is the function of bromocriptine (Parlodel), cabergoline, and pergolide (dopaminergic agonists) ?

A

Rapid reduction in the size of the tumor and a reversal of the gonadal effects (DA same as PIH)

71
Q

if a patient w prolactinoma is resistant or intolerant to medication what is the next treatment ?

A

Transsphenoidal surgery, endonasal endoscopic surgery, and radiotherapy

72
Q

hyperthyroidism disease examples (4)

A
  • Thyrotoxicosis
  • Graves disease
  • Hyperthyroidism resulting from nodular thyroid disease
  • Thyrotoxic crisis (thyroid storm)
73
Q

hypothyroidism disease examples (6)

A
  • Primary hypothyroidism
  • Hashimoto disease
  • Secondary hypothyroidism
  • Subclinical hypothyroidism
  • Congenital hypothyroidism
  • Thyroid carcinoma
74
Q

hypothyroidism vs hyperthyroidism

A
75
Q

primary alterations of thyroid function are caused by…

A

Dysfunction or disease of the thyroid gland

76
Q

secondary alterations of thyroid function are caused by…

A

Conditions that cause alterations in pituitary or hypothalamic functioning

77
Q

primary alterations of thyroid function alters…

A

thyroid hormone (TH) production

78
Q

secondary alterations of thyroid function alters…

A

TSH or thyrotropin-releasing hormone (TRH) production

79
Q

what is thyrotoxicosis

A

A condition that results from any cause of increased level of thyroid hormone.

Excess amounts of thyroid hormone are secreted from the thyroid gland.

80
Q

clinical manifestations of thyrotoxicosis

A

Increased metabolic rate with heat intolerance and increased tissue sensitivity to stimulation by the sympathetic nervous system; enlargement of the thyroid gland (goiter)

81
Q

treatment of thyrotoxicosis (4)

A
  • Methimazole (Tapazole) or propylthiouracil: - - Antithyroid drugs (synthesis blockers)
  • Radioactive iodine therapy
  • Surgery
82
Q

graves disease patho

A

hyperthyroid condition; Is an autoimmune disease; develops autoantibodies
Clinical manifestations

83
Q

Ophthalmopathy associated with graves disease

A

exophthalmos and diplopia

84
Q

exophthalmos with Graves disease is caused by…

A

Increased secretion of hyaluronic acid, orbital fat accumulation, inflammation, and edema of the orbital contents

85
Q

what is pretibial myxedema?

A

Graves dermopathy
Leg swelling due to increased deposition of mucopolysaccharides

86
Q

treatment for Graves disease

A

Antithyroid drugs, radioactive iodine, or surgery

Does not reverse infiltrative ophthalmopathy or pretibial myxedema

87
Q

what 2 kinds of hyperthyroidism can result from nodular thyroid disease

A

Toxic multinodular goiter

Solitary toxic adenoma

88
Q

how does toxic multinodular goiter differ from Solitary toxic adenoma

A

with toxic, severe hyperfunctioning nodules secrete thyroid hormone

solidary- only one nodule becomes hyperfunctioning

89
Q

clinical manifestations of nodular thyroid disease (2)

A

Are the same as hyperthyroidism but occur slowly.

Exophthalmos and pretibial myxedema do not occur

90
Q

treatment of nodular thyroid disease

A

Examination is performed for cancer.

Radioactive iodine, surgery, or antithyroid drugs are administered.

91
Q

Rare but life threatening within 48 hours if not treated.

A

thyrotoxic crisis

92
Q

what causes a thyrotoxic crisis/ thyroid storm

A

Increased action of thyroxine (T4) and triiodothyronine (T3)

93
Q

clinical manifestations of thyroid storm

A

Hyperthermia; tachycardia, especially atrial tachydysrhythmias; high-output heart failure; agitation or delirium; and nausea, vomiting, or diarrhea

94
Q

treatment of thyroid storm

A

Propylthiouracil or methimazole (Tapazole): Blocks thyroid hormone synthesis

Beta-blockers to control cardiovascular symptoms, corticosteroids, potassium iodide (SSKI) (sat’d soln)

Supportive care

95
Q

function of Propylthiouracil or methimazole (Tapazole)

A

Blocks thyroid hormone synthesis

96
Q

hypothyroidism patho

A

Deficient production of thyroid hormone by the thyroid gland

97
Q

primary hypothyroidism is mostly caused by ____________ worldwide

A

iodine deficiency (endemic goiter)

98
Q

primary hypothyroidism is most commonly caused by ____________ in the US

A

autoimmune thyroiditis (Hashimoto disease)

99
Q

congenital hypothyroidism is caused by

A

Thyroid hormone deficiency present at birth

100
Q

if congenital hypothyroidism is not treated, ____________ develops

A

cretinism

101
Q

what is the treatment for congenital hypothyroidism

A

administration of T4

102
Q

most common endocrine malignancy from ionizing radiation

A

thyroid carcinoma

103
Q

Changes in voice and swallowing and difficulty in breathing, related to a tumor growth impinging the trachea or esophagus is related to

A

thyroid carcinoma

104
Q

do patients with thyroid carcinoma have normal T3 and T4 levels?

A

some may

105
Q

secondary hypothyroidism may be caused by

A

Conditions that cause either pituitary or hypothalamic failure with deficiency of thyrotropin-releasing hormone (TRH) and TSH

106
Q

clinical manifestations of hypothyroidism

A

Low basal metabolic rate, cold intolerance, lethargy, tiredness, and slightly lowered basal body temperature; also possible diastolic hypertension

107
Q

what is myxedema

A

Nonpitting, boggy edema, especially around the eyes, hands, and feet; thickening of the tongue

108
Q

what is myxedema coma

A

Medical emergency, diminished level of consciousness; hypothermia without shivering, hypoventilation, hypotension, hypoglycemia, lactic acidosis, and coma

109
Q

treatment of hypothyroidism

A

levothyroxine

110
Q

myxedema coma treatment

A

Thyroid hormone, combined with circulatory and ventilatory support

Management of hyponatremia and hypothermia

111
Q

primary hyperparathyroidism is caused by

A

Excess secretion of PTH from one or more parathyroid glands and hypercalcemia

80% to 85% caused by parathyroid adenomas

112
Q

secondary hyperparathyroidism is caused by…

A

Increase in PTH, secondary to a chronic disease

  • Chronic renal failure
  • Dietary deficiency of vitamin D, calcium
113
Q

does hypercalcemia occur with secondary hyperparathyroidism

A

no

114
Q

Tertiary hyperparathyroidism patho

A

Excessive secretion of PTH and hypercalcemia from long-standing secondary hyperparathyroidism

115
Q

what is pseudohypoparathyroidism

A

Inherited condition, resistance to PTH

actually hyperparathyroidism!!!

116
Q

what is Familial hypocalciuric hypercalcemia associated with?

A

Benign autosomal dominant condition; hyperparathyroidism

117
Q

clinical manifestations of hyperparathyroidism

A
  • Most asymptomatic
  • Hypercalcemia and hypophosphatemia, possible kidney stones from hypercalciuria, alkaline urine, pathologic fractures
  • Secondary: Low serum calcium but elevated PTH
118
Q

treatment of hyperparathyroidism

A

Surgery, bisphosphonates (block osteoclast activity, preserving bone density ex- Alendronate (Fosamax), corticosteroids, and calcimimetics (lower calcium and PTH levels ex- Cinacalcet (Sensipar))

119
Q

hypoparathyroidism

A

abnormally low parathyroid hormone levels

  • Depressed serum calcium level
  • Increased serum phosphate level
120
Q

usual causes of hypoparathyroidism

A

Parathyroid damage in thyroid surgery, autoimmunity, or genetic mechanisms

121
Q

clinical manifestations of hypoparathyroidism

A
  • Hypocalcemia
  • Lowering of the threshold for nerve and muscle excitation
  • Muscle spasms; hyperreflexia; tonic-clonic convulsions; laryngeal spasms; death from asphyxiation
  • Chvostek and Trousseau signs
  • Phosphate retention
122
Q

treatment of hypoparathyroidism

A
  • Calcium and vitamin D
  • Phosphate binders, if needed (ex-Calcium Acetate (PhosLo))
123
Q

diabetes mellitus is a dysfunction of…

A

the endocrine pancreas

124
Q

diabetes mellitus affects metabolism of…

A

fat, protein, and carbohydrates.

125
Q

DM is characterized by…

A

hyperglycemia, resulting from defects in insulin secretion, insulin action, or both.

Pathopharm II Exam 1 (11 decks)

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