w7 quiz - endocrine Flashcards

1
Q

Chemical structure: steroid

A

lipids that enter the cell nucleus to initiate transcription directly

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2
Q

chemical structure: nonsteroid

A

needs secondary messanger system to activate transcription in nucleus

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3
Q

What do the endocrine and nervous systems do?

A

regulate metabolic activites

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4
Q

positive feedback system

A

g

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5
Q

negative feedback system

A

g

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6
Q

what is an antogonist to calcitonin

A

parathyroid hormone

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7
Q

what is an antagonist for insulin

A

glucagon

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8
Q

Describe how hormone release is most often controlled by negative feedback mechanisms

A

Endocrine and nervous system work together to regulate metabolic activities

  • complex system for some hormones
  • secretion of hormones may be controlled by more than one mechanism
  • rate and timing of secretion may vary (cyclic patterns)
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9
Q

endocrine disorders reflect what

A

impaired control or feedback

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10
Q

excess hormone levels are caused by what

A

a. tumor producing high levels
b. excretion by liver or kidney impaired
c. congenital condition produces excess hormones

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11
Q

Deficit of hormone or reduced effects are due to what

A

a. Tumor produced too little hormone caused by inadequate tissue receptors present
- antagonist hormone production is increased
- malnutrition
- atrophy, surgical removal of gland
- congential deficit

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12
Q

Endocrine system: diagnostic test

A

Blood tests (check hormone levels, radioimmunoassay, immunochemical methods)

urine tests

stimulation or suppression tests

scanning, ultrasound, MRI

Biopsy

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13
Q

Endocrine system treatments

A

Replacement therapy (hormone deficit)

medication, surgery, radiation (hormone excess)

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14
Q

diabetes mellitus results in

A

abnormal carb, protein and fat metabolism

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15
Q

some tissue can transport glucose in the absense of insulin such as

A

CNS, kidney, mycardium, gut, skeletal muscle

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16
Q

Type 1 diabetes

A

Autoimmune destruction of beta cells in pancreas

  • insulin replacement requires
  • not linked to obesity
  • genetic factors
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17
Q

what type of diabetes has acute onset in children and adolescents

A

type 1

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18
Q

type 1 diabetes: metabolic changes

A

Catabolism of fats and proteins

    • excess fatty acids and metabolites
    • ketones in blood
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19
Q

What type of diabetes has decompensated metabolic acidosis

A

type 1

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20
Q

Type 2 diabetes

A

non-insulin dependent; caused by decrease production of insulin / decreased resistance by body cells to insulin

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21
Q

type 2 diabetes onset

A

slow and insideoous, unsually in those older than 50

- associated with obesity

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22
Q

what diabetes is associated with a component of metabolic syndrome?

A

2

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23
Q

Control of type 2 diabetes

A

diet, increase bodys use of glucose by exercise, reducing insulin resistance, stimulate beta cells of pancreas to produce more insulin

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24
Q

initial stage of diabetes

A

Insulin deficit
BG rise
excess glucose in urine (large urine vol.)
dehydration –> thirst

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25
Q

manifestations of diabetes

A

polyphagia, fatigue, hyperglycemia, glucosuria, dehydration, polyuria, polydipsia

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26
Q

diabetes diagnostics

A
fasting BG level
glucose tolerance test
glycosylated hemoglobin test 
-- clinical and subclinincal diabetes
-- monitor glucose levels over several months
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27
Q

Diabetes treatment

A

Keep BG in normal range

diet and exercise (exercise lowers BG as skeletal muscle uses glucose)

oral medications (incurease insulin secretions, reduce BG levels)

insulin replacement

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28
Q

Complications of diabetes

A

Directly related to duration and extent of abnormal BG levels

Complications can be acute or chronic

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29
Q

What factors may lead to fluctuations in serum glucose levels

A

Variations in diet and alcohol use
Change in PA
Infection
Vomiting

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30
Q

Acute complication of diabetes: hypoglycemia (insulin shock)

A

more common with insulin replacement treatment; can occur because excess oral hypoglycemic drugs

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31
Q

What may cause an excess of insulin in ciruclation

A
Glucose deficit in blood
strenuous exercise
dosage error
vomiting
skipping meal after taking insulin
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32
Q

Hypoglycemic shock: s/s

A
disoriented / behavior change
anxiety / decrease responsiveness
decreased BP, increase HR 
may appear impaired
decreased BG level
Decrease level of consciousness

IMMIDIATE ADMIN. OF GLUCOSE IS REQUIRED TO PREVENT BRAIN DAMAGE

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33
Q

hypoglycemic shock: emergency treatment

A

If conscious, immidiately give sweet fruit juice, honey, candy, sugar

If unconscious, give nothing PO; IV glucose 50% required

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34
Q

Emergent treatment for diabetic ketoacidosis:

A

Insulin, fluid, and sodium bicarbonate.

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35
Q

Diabetic ketoacidosis (DKA)

A

Occurs in insulin dependent clients; more commonly in type 1

results of insufficient insulin in blood

high BG levels

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36
Q

What results in the production of ketoacids

A

Mobilization and use of lipids to meet cellular needs

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37
Q

what may DKA be initiated by?

A

infection or stress

38
Q

what might DKA result from

A

dose error, infection, change in diet, alcohol, exercise

39
Q

DKA s/s

A
Thirst
Dry, rough oral mucosa
Rapid pulse, but weak and thready
BP low
Oliguria 
Rapid, deep respirations 
Acetone breath (fruity)
Lethargy and decreased responsiveness indicates depression of CNS, owing to acidosis and decreased blood flow
40
Q

Metabolic acidosis

A

decrease serum bicarbonate levels and decreased serum pH

41
Q

Metabolic acidosis s.s

A

dehydration progresses, renal compensation reduced, acidosis becomes decompensated

LOC

42
Q

Hyperosmolar Hypoglycemic Nonketotic Coma (HHNK)

A

Type 2
Diagnosis often missed
Occurs in older pt. and assumed to be cognitive impairment
results in severe dehydration and electrolye imbalances

43
Q

Manifestations of Hyperosmolar HypoglycemicNonketotic Coma (HHNK)

A

hyperglycemia
severe dehydration
- increased hemotocrit, loss of turgor, increase HR and resp.

44
Q

Hyperosmolar HypoglycemicNonketotic Coma (HHNK) - electrolyte imbalances result in what

A

neurological deficits, muscle weakness, difficulties with speech, abnormal reflexes

45
Q

Chronic complications of diabetes: vascular

A

atherosclerosis in small and large arteries

46
Q

Chronic complications of diabetes: microangiopathy (changes in microcirculation)

A

Obstruction/rupture of small capillaries and arteries

  • tissue necrosis and loss of function
  • neuropathy and loss of sensation
  • retinopathy (leading cause of blindness)
  • chronic renal failure (degeneration of glomeruli in kidney)
47
Q

Chronic complications of diabetes: macroangiopathy - affects large arteries

A

Result of abnormal lipid levels

  • high incidence of MI, strokes, PVD
  • may result in ulcers on legs and feet (slow healing)
  • frequent infections and gangrenous ulcers
  • amputation may be necessary
48
Q

chronic complications of diabetes - peripheral neuropathy

A

Caused by ischemis and microcirculation to peripheral nerves

impair sensations, numbness, tingling, weakness, muscle wasting

49
Q

Neuropathy leads to

A

impaired sensation, numbness, tingling, weakness, muscle weakness

50
Q

chronic complications of diabetes: infections

A

infection in feet and legs caused by neurologic impairment

fungal infections common (candidica)

UTI

dental caries

gingivitis and periodontitis

51
Q

chronic complications of diabetes: cataracts

A

Related to abnormal metabolism of glucose

52
Q

chronic complications of diabetes - pregnancy

A

Both mother and fetus may experience complications

- spontaneous abortions

53
Q

Infants born to diabetic mothers can experience what

A

increase size and weigh

hypoglycemia in first hours after birth

54
Q

Hypoparathyroidism leads to

A

hypocalcemia

  • weak cardiac muscle contractions
  • increased excitability of nerves (spontaneous contraction of skeletal muscle)
55
Q

causes of hypoparathyroidism

A

Congenital lack of parathyroid
Surgery or radiation in neck area
Autoimmune disease

56
Q

hyperparathyroidism results in what

A

hypercalcemia

  • forceful cardiac contractions
  • osteoporosis
  • predisposition to kidney stones
57
Q

caused of hyperparathyroidism

A

tumor
secondary to renal failure
enlargement (hyperplasia) of glands

58
Q

What are the most common cause of pituitary hormones

A

adenomas

59
Q

Pituitary adenomas: effect of mass

A

May cause pressure in skull

– headaches, siezures, drowsiness, visual deficits

60
Q

How to adenomas effect pituitary hormone secretion

A

Dependent on cells and location involved

May cause excessive or decreased release of hormones

61
Q

Growth hormone (GH): Dwarfism

A

Deficit in growth hormone production and release

62
Q

GH: gigantism

A

excess GH prior to puberty anf fusion of epiphysis

63
Q

GH: Acromegaly

A

Excess GH secretion in adults

  • associtated with adenoma
  • bones: broader and heavy
  • soft tissue grows (hands and feet, change in facial features)
64
Q

How does diabetes insipidus is what

A

Deficit of ADH

65
Q

What is Diabetes insipidus often associated with

A

adenoma

66
Q

Diabetes insipidus may originate in the neurohypopysis, meaning what

A

Head injury or surgery
Possible genetic problem
Replacement treatment required

67
Q

Inappropriate AHD syndrome

A

Excess ADH (temporary from stress, secreted from ectopic source such as tumor)

68
Q

Innappropriate ADH syndrome Treatment

A

diuretics

Na supplements

69
Q

Goiter: Endemic goiter

A

Hypothyroid condition in regions with low iodine levels in soil and food

70
Q

Goiter: goitrogens

A

Foods that contain elements to block synthesis of T3 and T4

71
Q

What are T3 and T4 (names)

A

triiodothyronine (t3) and thyroxine (t4)

72
Q

goiter: toxic goiter

A

results from hyperactivity of thyroid glans

73
Q

hyperthyroidism

A

Related to autoimmune factor

Hypermetabolism and increased stimulation of SNS

toxic goiter

Exophthalamos

74
Q

Exophthalamos

A

Presense of protruding, staring eyes, decreased blind and eye movement

result of increased tissue mass in orbit

may result in visual impairment

75
Q

Hypothyroidism

A

Iodine deficit

76
Q

Hypothyroidism: hasmimoto thyroiditis

A

autoimmune disorder

77
Q

hypothyroidism: tumor

A

surgical removal or treatment of gland

78
Q

hypothyroidism: cretinism

A

Results in short statue and severe cognitive deficits

Untreated congenital hypothyroidism

May be related to iodine deficiency during pregnancy

79
Q

Hypothyroidism manifestations

A

Goiter (if caused by iodine deficit)

intolerance to cold

increased BMI

lethargy and fatige

decrease appetite

Myxedema

80
Q

myxedema

A

nonpitting edema in face, thickened tongue

81
Q

myxedema coma

A

acute hypotension, hypoglycemia, and hypothermia result in loss of consciousness; life threatening if untreated

82
Q

diseases of adrenal medulla

A

Pheochromocytoma

83
Q

diseases of adrenal cortex

A

cushing syndrome

addisons disease

84
Q

Pheochromocytoma

A

Benign tumor of adrenal medulla - secretes epinephrine, norepinephrine and possible other substances

occassionally many tumors

85
Q

Pheochromocytoma s/s

A

HA, palpitation, sweating, intermittent or constant anxiety

86
Q

Cushing syndrome

A

caused by excessive level of glucocorticoids

87
Q

Cushing syndrome is a possible result of what

A

adrenal adenoma, pituitary adenoma, ectopic carcinoma, iatrogenic conditions, substance abuse

88
Q

changes assiciated with Cushing syndrome (appearance)

A

round face with ruddy color, truncal obesity with fat between scalpulae, thin limbs, think hair, fragile skin, striae

89
Q

What are systemic changes with Cushing disease

A

a. retention of Na and H2O
b. suppression of immune system
c. erythrocyte production
d. emotional lability and euphoria
e. increase catabolism of bone and protein
f. slowed healing
g. increase insulin resistance and possible glucose intolerance

90
Q

Addison’s disease

A

Deficiency of adrenocorticoid secretions; autoimmune reason is a common cause

adrenal gland may be destroyed by hemorrhage or infection

91
Q

Addisons disease s.s

A
decreased BG levels
inadequate stress response
fatigue
weight loss
infections 
lower serum Na concetration
decrease BV
hypotension
high K+ levels