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316 Pharmacology > Exam 3: Endocrine disorders > Flashcards

Exam 3: Endocrine disorders Flashcards

1
Q

Endocrine glans are

A

Ductless glands that affect bodily activities

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2
Q

Endocrine glands release chemical messengers called

A

Hormones

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3
Q

Hormones are released directly into the extracellular space to go into

A

Capillaries, then the blood, then into the target organ

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4
Q

Hormones exert specific effects on

A

Target organs or tissues that have specific receptors for the hormone

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5
Q

Receptors for lipid-soluble hormones

A

Inside the cell

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6
Q

Receptors for water soluble hormones

A

Outside cell

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7
Q

Hormones are released

A
  • In response to altered cellular environment

- In order to maintain a regulated level of certain substance

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8
Q

Hormone secretions are typically regulated by

A

Negative feedback control

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9
Q

Negative feedback

A

Information about the effects of the hormone are fed back to the gland, which ten decreases secretion of the hormone

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10
Q

Master gland

A

Pituitary gland

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11
Q

Pituitary gland to attached to

A

Hypothalamus

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12
Q

Anterior lobe is also called

A

Adenohypophysis

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13
Q

Anterior lobe is connected to the hypothalamus via

A

blood vessels

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14
Q

Posterior lobe is also called

A

Neurohypophysis

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15
Q

Posterior lobe it ____ to the hypothalamus

A

Neurally connected

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16
Q

Anterior and posterior lobe is separated by

A

Pars intermedia

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17
Q

Regulating hormones form the hypothalamus stimulate or inhibit

A

release of hormones from adenohypophysis

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18
Q

Does the posterior lobe synthesis hormones?

A

No, instead it stores and releases two hormones

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19
Q

Hormones that posterior lobe stores and releases

A

ADH

Oxytocin

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20
Q

Posterior lobe is connected to hypothalamus via

A

Hypothalamic-hypophyseal tract

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21
Q

Hypothalamic axons terminate in the

A

Neurohypophysis

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22
Q

ADH

A

Anti-diuretic hormone; vasopressin

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23
Q

Major stimuli for ADH secretion

A

Under normal conditions ADH is the primary endocrine factor regulating urinary H2O balance

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24
Q

Changes in plasma osmolarity sensed by osmoreceptors in hypothalamus –>

A

Stimulate or inhibit ADH -> target tissue -> fluid volume changes -> changes in osmolarity

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25
Q

Increased osmolarity =

A

stimulation of thirst

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26
Q

ADH also excreted via RAAS ->

A

Vasoconstriction & H2O retention, leading to increased BP

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27
Q

Diabetes insipidus

A 
Diabetes = overflow 
insipidus = tasteless
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28
Q

Diabetes insipidus

A

Disorder associated with dysfunction of neurohypophysis or interruption go the pituitary stalk

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29
Q

Hyposecretion of ADH leads to

A

Inability to concentrate urine, leading to increased excretion of dilute urine, dehydration, thirst, hypotension, hypernatremia

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30
Q

Normal urine output

A

1200 - 1500 mL/ 24 hours

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31
Q

Polyuria in diabetes insipidus

A

Output may be as much as 20 liters/day

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32
Q

urine specific gravity with diabetes insipidus

A

Decrease urine specific gravity

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33
Q

Normal urine specific gravity

A

1.005 - 1.030

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34
Q

Desmopressin (DDAVP)

A

Vasopressin analog, synthetic ADH replacement

- Hormone replacement for Diabetes insipidus

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35
Q

Desmopressin administration

A

PO, IM, IV, IM, intranasal

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36
Q

Desmopressin moA

A

Increase permeability of renal tubular cells to water, leading to increase absorption of water INTO plasma, leading
-Decreased UP and increased uric osmolality

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37
Q

Desmopressin nursing considerations

A
  • Monitor UO/ I&O
  • Monitor urine specific gravity
  • Vital signs
  • Serum electrolytes
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38
Q

High levels of ADH WITHOUT normal physiologic stimuli for its release leads to

A

Increased renal water retention leading to dilutional hyponatremia
– decreased UO
– increased specific gravity
Possibly water intoxication, edema, hypertension, headache, confusion, nausea, and vomiting

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39
Q

Various causes of inappropriate ADH secretion

A

tumors
post-pituitary surgery
brain trauma
meningitis

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40
Q

Treatment of inappropriate ADH secretion

A
  • Treatment of underlying medical conditions
  • Diuretics
  • Infuse 3% saline cautiously
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41
Q

If 3% saline is given too fast, it can cause

A

Neurologic issues including seizures

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42
Q

Thyroid gland

A

Butterfly shaped gland

Anterior to trachea

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43
Q

Thyroid gland requires ___ for function

A

Iodine

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44
Q

Thyroid gland rich blood supply

A

80-100 mL/min

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45
Q

Thyroid gland is able to deliver

A

high levels or hormones if necessary

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46
Q

Thyroid gland histology

A

Thyroid follicles
Filled with colloid
Walls of follicles

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47
Q

Thyroid gland is filled with

A

colloid: glycoprotein-iodine complex

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48
Q

Walls of follicles:

A

Follicular cells

Parafollicular cells produce calcitonin

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49
Q

Follicular cells

A

triiodothyronine (T3)

thyroxine (T4)

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50
Q

Calcitonin

A

calcium hemostasis, along with actions of parathyroid

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51
Q

Key actions of thyroid glands

A
  • Main determinant of basal metabolic rate
  • Influences synthesis & degradation of carbohydrate, fat, & protein metabolism (e.g. mobilization of glycogen, gluconeogenesis)
  • Increases target-cell responsiveness to catecholamines
  • Increases heart rate & force of contraction
  • Essential for normal growth (deficiency of thyroid hormones during fetal development, infancy, or childhood causes stunted bone growth & severe mental disability)
  • Plays crucial role in normal development of nervous system
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52
Q

TSH (thyroid stimulating hormone) is regulated by

A

Hypothalamic pituitary thyroid feedback system

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53
Q

Decreased blood level of thyroid hormones –>

A

Decreased metabolic rate and body temperature, leading to

  • TRH
  • TSH
  • –> thyroid hormones
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54
Q

Hypothyroidism

A

Deficient production of thyroid hormones

55
Q

Primary hypothyroidism

A

Problems with thyroid gland

56
Q

Secondary hypothyroidism

A

problems with pituitary or hypothalamus

57
Q

Deficient thyroid hormone affects

A

ALL body systems

58
Q

Clinical manifestations of hypothyroidism

A 
Decreased BMR (basal metabolic rate) 
Increased TSH levels (primary hypothyroidism)
Goiter ***
Lethargy
Fatigue
Cold intolerance
Weight gain
--> Myxedema 
---> myxedema coma
59
Q

Myxedema

A

is a characteristic sign of severe or long-standing hypothyroidism
—non-pitting, boggy edema

60
Q

Myxedema coma is due to

A

Prolonged hypothyroidism

61
Q

Myxedema coma:

A 
medical emergency
Decreased LOC
Hypothermia
Hypoventilation
Hypotension
Hypoglycemia
62
Q

Levothyroxine

A

Thyroid hormone replacement; synthetic T4

63
Q

Levothyroxine indications

A

Hypothyroidism, myxedema, myxedema coma

64
Q

Levothyroxine moA

A

T4 binds to thyroid receptors in cell nucleus, leading to metabolic effects via DNA transcription & protein synthesis

65
Q

Levothyroxine administration

A

PO for replacement

IV for emergencies

66
Q

Signs and symptoms of too much Levothyroxine

A

S/S of hyperthyroidism

67
Q

Levothyroxine black box warning

A

Do not use for weight reduction, ineffective & potentially life-threatening

68
Q

Diseases of hyperthyroidism

A

Thyrotoxicosis
Graves disease
Thyrotoxic crisis (thyroid storm)

69
Q

Thyrotoxicosis

A

tissues are exposed to high levels of thyroid hormone

70
Q

Causes of thyrotoxicosis

A 
Hyperactivity of thyroid gland
Graves disease
Thyroid cancer
Adenoma of thyroid
Multinodular goiter
Ingestion of excessive thyroid hormone
71
Q

Clinical manifestations are related to the hypermetabolic state of thyrotoxicosis

A

Increase…

  • oxygen consumption
  • use of metabolic fuels
  • sympathetic nervous system activity
Weight loss
Nervousness/irritability
Palpitations
SOB
Excessive sweating
72
Q

Most common cause of hyperthyroidism; thyrotoxicosis

A

Graves disease

73
Q

Graves disease is autoimmune caused by

A

Antibodies against the TSH receptor

74
Q

in graves disease, TSI stimulates

A

TSH receptors but is NOT subject to negative feedback like TSH

75
Q

in graves disease, antibodies stimulate thyroid cells to

A

Make high levels of thyroid hormone

76
Q

Thyrotoxic crisis (Thyroid storm)

A
  • Extreme, life-threatening form of thyrotoxicosis
  • Death may occur within 48 hours without treatment
  • Often present to ED as undiagnosed hyperthyoridism, or partially treated Graves disease; precipitated by stress, trauma, infection
77
Q

Clinical manifestions of thyrotoxic crisis

A 
Hyperthermia
Tachycardia
Tachydysrhythmias
High-output heart failure
Agitation
Delirium
N/V
Diarrhea
Dehydration
78
Q

propylthiouracil drug class

A

Antithyroid agent

79
Q

propylthiouracil drug class

A

Antithyroid agent

80
Q

Antithyroid agent indication

A

Hyperthyroidism

Thyroid storm

81
Q

propylthiouracil moA

A

MOA: inhibits synthesis of thyroid hormones by blocking oxidation of iodine in thyroid gland; also prevents conversion of T4 to T3 at target tissues which decreases S/S hyperthyroidism

82
Q

propylthiouracil black box warning

A

severe liver injury (some fatal) & acute liver injury have been reported

83
Q

Adrenal glands located superior to each kidney

A

2 regions:

(1) adrenal cortex
(2) adrenal medulla

84
Q

Adrenal cortex: 3 regions that have different cells that secrete different groups of steroid hormones:

A

(1) zona glomerulosa
(2) zona fasciculata
(3) zona reticularis

85
Q

Adrenal medulla is innervated directly by

A

the sympathetic division of the ANS

86
Q

Adrenal medulla secretes

A

epinephrine & norepinephrine

87
Q

Sympathomimetic: fight or flight response

A 
vasoconstriction
Increase:
-BP
-HR/force of contraction
-RR, dilate bronchioles 
-Blood glucose levels
88
Q

Zona glomerulosa:

A

mineralocorticoids

89
Q

Zona glomerulosa: mineralocorticoids control

A

water & electrolyte homeostasis; primarily sodium & potassium ions

90
Q

Primary mineralocorticoid

A

Aldosterone

91
Q

Aldosterone acts on the kidneys causing

A

Increase reabsorption of Na

  • Increase excretion of k
  • Increase H2O retention
92
Q

ACTH has

A

Minimal effect on aldosterone

primarily secreted in presence of angiotensin II

93
Q

Zona fasciculata:

A

Glucocorticoids

94
Q

Zona fasciculata: Glucocorticoids

A

A group of hormones concerned with normal metabolism & response to stress

95
Q

3 glucocorticoids

A

(1) cortisol (hydrocortisone); most abundant
(2) corticosterone
(3) cortisone

96
Q

CRH ->

A

ACTH -> Cortisol

97
Q

Functions of glucocorticoids:

A
  • Ensure enough energy is available for metabolic needs (catabolic: mobilization of proteins & fatty acids for glucose production)
  • Provide resistance to stress: glucose gives body energy to combat stresses such as fright, temperature extremes, infection, trauma, surgery
  • Antiinflammatory function
98
Q

Anti-inflammatory function of glucocorticoids

A

inhibit cell-mediated & humoral immunity

99
Q

Zona reticularis

A

gonadocorticoids

100
Q

Zona reticularis: gonadocorticoids hormones

A

Estrogens & androgens

101
Q

Zona reticularis: gonadocorticoids;

tumors of the adrenal glands

A
  • virilizing adenomas in women

- feminizing adenomas in males

102
Q

Adrenal insufficiency Primary:

A

Addison’s disease

destruction of the adrenal gland (usually autoimmune)

103
Q

Adrenal insufficiency: Secondary

A

Pituitary disease

104
Q

Adrenal insufficiency tertiary

A

hypothalamic dysfunction

105
Q

Secondary adrenal insufficiency is caused by

A

dysfunction of the hypothalamic-pituitary axis

106
Q

Addison’s disease is an example of ____ adrenal insufficiency

A

Primary

107
Q

In addition’s disease, pituitary will continue to secrete

A

ACTH via negative feedback, BUT NO glucocorticoids are excreted by the adrenals

108
Q

Addisons disease is a chronic metabolic disorder that requires lifelong management:

A 
replacement therapy of missing hormones
regular dietary schedule
stress management
avoidance of infection
medical ID bracelet
109
Q

Addisons disease clinical manifestations

A
  • Mental lethargy
  • Anorexia
  • N/V
  • Weight loss
  • Hypoglycemia
  • Decrease BP
  • Decrease CO
  • Hyperpigmentation (ACTH has intrinsic MSH activity)
  • hypoglycemia (decrease gluconeogenesis)
  • Mineralcorticoid deficiency: hypotension (SBP < 110), orthostatic hypotension, hyperkalemia, hyponatremia, hypovolemia, salt cravings
  • Other: weakness, irritability, emotional lability; ♀: amenorrhea, decrease libido, sparse axillary & pubic hair
110
Q

Adrenal crisis =

A

“Addisonian Crisis”

111
Q

“Addisonian Crisis” is

A

Life-threatening

112
Q

“Addisonian Crisis” is caused by

A

Acute lack of glucocorticoids & mineralcorticoids

113
Q

Precipitating events (for a person with Addision’s disease or a slowly developing, previously recognized adrenal insufficiency):

A
  • Severe infection
  • Trauma
  • Surgery
  • Dehydration
  • Profound hypoglycemia
  • Shock: hypotension & vascular collapse; shock often unresponsive to vasopressors
  • Coma
  • Fatal if not recognized & treated promptly (0.9% NS, hydrocortisone, epinephrine, dextrose)
114
Q

Hydrocortisone

A

Systemic corticosteroid

115
Q

hydrocortisone administration

A

PO, IM, IV, topical

116
Q

hydrocortisone indication

A

Adrenal insufficiency
Anti-inflammatory
Immunosuppressive

117
Q

hydrocortisone cautions

A
  • Increase incidence of secondary infections
  • GI irritation
  • May cause suppression of HPA axis
  • may cause increase glucose; - may cause iatragenic Cushing syndrome with high doses; withdraw therapy with gradual tapering of dose
118
Q

Hydrocortisone is used caution with patients with

A

renal impairment

119
Q

Hydrocortisone can cause

A

iatragenic Cushing syndrome with high doses; withdraw therapy with gradual tapering of dose

120
Q

Hydrocortisone nursing considerations

A

Serum glucose
Presence of infection
Gradual tapering of dose

121
Q

Cushing Syndrome

A

Clinical condition resulting from chronic exposure to excessive circulating levels of glucocorticoids

122
Q

Cushing syndrome causes

A

(1) excess secretion of ACTH from anterior pituitary
(2) excess secretion of glucocorticoids due to adrenal disease
(3) iatrogenic: chronic administration of glucocorticoids (e.g. hydrocortisone, prednisone)

123
Q

Cushing syndrome; hyper secretion of adrenal glucocorticoids clinical manifestations

A 
Truncal obesity
Spindly legs
Moon face
Buffalo hump
Pendulous abdomen
Poor wound healing
Hyperglycemia
Osteoporosis
Hypertension
Mood alterations
- Poor wound healing, thinning of skin, wound dehiscence following surgery 
-Easy bruising
-Diabetogenic effect of glucocorticoids
124
Q

Cushing syndrome can lead to

A
  • Poor wound healing, thinning of skin, wound dehiscence following surgery (inhibition of fibroblasts & mediators of inflammation; loss of collagen by high steroid levels)
  • Easy bruising (inhibition of mediators of clotting)
  • Diabetogenic effect of glucocorticoids
125
Q

Hyperthyroidism left untreated or undetected can lead to

A

Thyorotoxic crisis –> Thyroid storm

126
Q

Graves disease is more common in

A

Women

127
Q

T3 is known as the

A

Biologically active thyroid hormone

128
Q

T4 is known as the `

A

Prohormone that must be converted to T3

129
Q

Zona glomerulosa; aldosterone controls

A

Water and electrolyte homeostasis; primarily sodium Ions

130
Q

Cortisol levels are influences by

A

Stress; acute and chronic

Time of day

131
Q

Alterations in adrenal function

A

HYPO-cortical Function (Addison Disease)

HYPER-cortical Function (Cushing Disease, Cushing Syndrome)

132
Q

Treatment options for Cushing syndrome

A
  • Decrease use of corticosteroids
  • Surgical removal of pituitary tumor
  • Radiation to site of tumor
133
Q

Pharmacotherapeutic options for Cushing syndrome

A
  • Ketoconazole (Nizoral) – to control excessive production of cortisol at the adrenal gland; PO
  • Pasireotide (Signifor) – works by decreasing ACTH production from a pituitary tumor; injection, BID

316 Pharmacology (19 decks)

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