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NUR 326 Exam 3 > Endocrine Disorders > Flashcards

Endocrine Disorders Flashcards

1
Q

anterior pituitary

A

secretes 6 different hormones, including TSH and adrenocorticotropic hormone (ACTH)

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2
Q

posterior pituitary

A

secretes 2 hormones –> antidiuretic hormone, oxytocin

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3
Q

where are adrenal glands situated?

A

sit on top of kidneys

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4
Q

anatomical components of adrenal glands

A

composed of inner medulla and outer cortex

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5
Q

what does the adrenal medulla secrete?

A

epi and norepi

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6
Q

what does the adrenal cortex secrete?

A

–glucocorticoids (Cortisol)
–mineralcorticoids (Aldosterone)
–sex steroids (Androgens)

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7
Q

definition of Cushing Syndrome

A

a collection of signs and symptoms associated with hypercortisolism

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8
Q

Primary hyperfunction cause

A

disease of adrenal cortex (Cushing’s syndrome)

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9
Q

Secondary hyperfunction cause

A

disease of anterior pituitary (Cushing’s disease)

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10
Q

what do exogenous steroids cause?

A

Cushing’s syndrome

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11
Q

Cortisol functions

A

–raises blood sugar (opposes insulin)
–protects against the physiologic effects of stress
–suppresses immune and inflammatory processes
–breaks down protein and fat

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12
Q

increased cortisol effect on glucose availability

A

–glucose intolerance
–hyperglycemia

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13
Q

increased cortisol effect on maintenance of vascular system

A

–hypertension
–capillary friability

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14
Q

increased cortisol effect on protein breakdown

A

–muscle wasting
–muscle weakness
–thinning of skin
–osteoporosis and bone pain

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15
Q

increased cortisol effect on fat breakdown

A

–redistribution of fat to abdomen, shoulders, and face

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16
Q

increased cortisol effect on suppression of immune and inflammatory responses

A

–impaired wound healing and immune response
–risk for infection

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17
Q

increased cortisol effect on CNS excitability

A

–mood swings
–insomnia

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18
Q

clinical manifestations of Cushing’s

A

–red cheeks
–abdominal stretch marks
–pendulous abdomen
–fat pads (Buffalo hump)
–bruise easily
–thin arms and legs

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19
Q

treatment for Cushing’s

A

treatment depends on cause
–pituitary or adrenal tumor: surgery or radiation

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20
Q

drugs used with Cushing’s

A

–aminoglutethimide
–ketoconazole

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21
Q

MOA of aminoglutethimide

A

blocks synthesis of all adrenal steroids

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22
Q

indication of aminoglutethimide (Cytadren)

A

temporary therapy to decrease cortisol production

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23
Q

effects of aminoglutethimide (Cytadren)

A

–reduces cortisol levels by 50%
–does not affect the underlying disease process

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24
Q

adverse effects of aminoglutethimide (Cytadren)

A

–drowsiness
–nausea
–anorexia
–rash

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25
Q

MOA of ketoconazole (Nizoral)

A

antifungal drug that also inhibits glucocorticoid synthesis

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26
Q

indication for ketoconazole (Nizoral)

A

adjunct therapy to surgery or radiation for Cushing syndrome

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27
Q

main adverse effect of ketoconazole (Nizoral)

A

severe liver damage

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28
Q

safety issues with ketoconazole (Nizoral)

A

–do not take with ETOH or other drugs that harm liver
–do not give during pregnancy (fetal thyroid damage)

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29
Q

definition of Addison disease

A

disease of the adrenal cortex that causes hyposecretion of all 3 adrenocortical hormones

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30
Q

cortisol = ?

A

sugar

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31
Q

salt = ?

A

aldosteron

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32
Q

sex = ?

A

androgens

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33
Q

etiology of Addison disease

A

idiopathic, autoimmune, or other

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34
Q

patho of Addison disease

A

–adrenal gland destroyed
–symptoms when 90% non-functional
–adrenocorticotropin hormone (ACTH) and melanocyte-stimulating hormone (MSH) are secreted in large amounts

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35
Q

early clinical manifestations of Addison disease

A

–anorexia
–weight loss
–weakness
–malaise
–apathy
–electrolyte imbalances
–skin hyperpigmentation

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36
Q

symptoms of hypoaldosteronism

A

–hypotension (decreased vascular tone, decreased CO, decreased circulating blood volume)
–salt craving (decreased serum NA levels, decreased serum K levels, dehydration)

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37
Q

symptoms of hypocortisolism

A

–hypoglycemia
–weakness and fatigue
–unsuppressed ACTH production
–hyperpigmentation

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38
Q

pharmacology for Addison Disease

A

–lifelong corticosteroid replacement therapy (adrenal insufficiency)
–glucocorticoid
–hydrocortisone (drug of choice)
–prednisone
–dexamethasone
–some require mineralcorticoid
–fludrocortisone

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39
Q

important issues with pharmacotherapy

A

–dosing mimics natural release of hormones
–never abruptly stop therapy
–dose will need to be increased during stress
–always maintain emergency supply
–wear Medic Alert bracelet

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40
Q

adrenal medulla disorder

A

pheochromocytoma

41
Q

pheochromocytoma

A

rare tumor of the adrenal medulla that produces excessive catecholamines

42
Q

risk factor for pheochromocytoma

A

young-middle age

43
Q

What does a pheochromocytoma trigger in the body?

A

SNS stimulation –> excessive release of epi, norepi

44
Q

symptoms of pheochromocytoma

A

–HA
–hypertension
–diaphoresis
–tachycardia

45
Q

drug therapy for pheochromocytoma

A

–principal cause of hypertension = activation of alpha 1 receptors on blood vessels
–treatment = surgery
–alpha-adrenergic blockers for inoperable tumors, pre-op to reduce risk of HTN

46
Q

example of alpha-blockers for pheochromocytoma

A

phenoxybenzamine HCl (Dibenzyline)

47
Q

indication for phenoxybenzamine HCl (Dibenzyline)

A

pheochromocytoma

48
Q

MOA for phenoxybenzamine HCl (Dibenzyline)

A

long-lasting, irreversible blockage of alpha-adrenergic receptors

49
Q

drug effects of phenoxybenzamine HCl (Dibenzyline)

A

lowers BP

50
Q

adverse effects of phenoxybenzamine HCl (Dibenzyline)

A

–orthostatic hypotension
–reflex tachycardia
–nasal congestion
–sexual side effects in men

51
Q

antidiuretic hormone (ADH)

A

released in response to high serum osmolality and/or hypotension

52
Q

function of ADH

A

causes water retention via action in the kidneys

53
Q

way to remember function of ADH

A

“ADH–this hormone stops the pee pee”

54
Q

SIADH

A

syndrome of inappropriate antidiuretic hormone

55
Q

SIADH definition

A

an abnormal production or sustained secretion of ADH

56
Q

what is SIADH characterized by?

A

–fluid retention
–serum hypoosmolality and hyponatremia
–concentrated urine

57
Q

etiology of SIADH

A

–malignant tumors
–CNS disorders
–drug therapy
–miscellaneous (hypothyroidism, infection)

58
Q

malignant tumors associated with SIADH

A

small cell carcinoma of the lung

59
Q

CNS disorders associated with SIADH

A

–head trauma
–stroke
–brain tumors

60
Q

patho of SIADH

A

increased antidiuretic hormone –> increased water reabsorption in renal tubules –> increased intravascular fluid volume –> dilutional hyponatremia and decreased serum osmolality

61
Q

serum osmolality in SIADH

A

low

62
Q

urine osmolality and specific gravity in SIADH

A

high

63
Q

serum sodium in SIADH

A

low

64
Q

urine output in SIADH

A

low

65
Q

weight in SIADH

A

gain

66
Q

water retention in SIADH

A

retaining pure water without salt

67
Q

what do symptoms depend on with SIADH?

A

depend on severity and rate of onset of hyponatremia

68
Q

symptoms of hyponatremia

A

–dyspnea
–fatigue
–lethargy
–confusion
–dulled sensorium
–musical twitching
–convulsions
–impaired taste
–anorexia
–vomiting
–cramps

69
Q

severe symptoms of SIADH

A

sodium = 100-115 –> irreversible neuro damage

70
Q

water intoxication

A

when serum levels of sodium become lower than what is INSIDE the cells
–cells swell

71
Q

symptoms of water intoxication

A

–neurologic: confusion, lethargy, coma, death

72
Q

pharm with SIADH

A

–not first line of defense
–treatment –> underlying cause
–chronic SIADH = demeclocycline

73
Q

classification of demeclocycline (Declomycin)

A

tetracycline broad-spectrum antibiotic

74
Q

MOA of demeclocycline

A

interferes with renal response to ADH

75
Q

adverse effects of demeclocycline

A

–photosensitivity
–teeth staining
–nephrotoxic

76
Q

definition of diabetes insipidus

A

a deficiency of ADH or a decreased renal response to ADH

77
Q

what is DI characterized by?

A

excessive loss of water in the urine

78
Q

two forms of DI

A

–neurogenic (central)
–nephrogenic

79
Q

cause of neurogenic DI

A

hypothalamus or pituitary gland damage

80
Q

associated disorders with neurogenic DI

A

–stroke, TBI
–brain surgery
–cerebral infections

81
Q

etiology of neurogenic DI

A

–sudden onset
–usually permanent
–neuro origin

82
Q

etiology of nephrogenic DI

A

–renal origin
–slow onset
–progressive

83
Q

cause of nephrogenic DI

A

–loss of kidney function
–often drug-related

84
Q

associated disorders of nephrogenic DI

A

CKD

85
Q

patho of DI

A

decreased antidiuretic hormone –> decreased water reabsorption in renal tubules –> decreased intravascular fluid volume –> increased serum osmolality/excessive urine output

86
Q

serum osmolality in DI

A

high

87
Q

urine osmolality and specific gravity in DI

A

low

88
Q

serum sodium in DI

A

high

89
Q

urine output in DI

A

high

90
Q

weight in DI

A

loss

91
Q

symptoms of DI

A

–polyuria
–polydipsia
–dehydration
–electrolyte imbalances
–hypovolemic shock –> death

92
Q

pharm for neurogenic DI

A

–synthetic ADH replacement

93
Q

pharm for nephrogenic DI

A

–thiazide diuretics

94
Q

why are diuretics used in someone who is peeing constantly?

A

paradoxical effect decreases polyuria and increases urine osmolality

95
Q

desmopressin (DDAVP)

A

treatment for neurogenic DI

96
Q

MOA for desmopressin

A

–synthetic ADH replacement
–anti-diuretic effects

97
Q

route for desmopressin

A

–nasal spray
–PO
–IV
–SQ

98
Q

adverse effects for desmopressin

A

small doses: none
nasal spray: nasal irritation
large doses: hyponatremia, water intoxication

99
Q

DI acronym

A

D: dry
I: I&O, daily weight
L: low specific gravity
U: urinates lots
T: treat=desmopressin
E: rEhydrate

NUR 326 Exam 3 (11 decks)

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