endocrine Flashcards

1
Q

hormones produced by the thyroid gland x3

A

T3
T4
calcitonin

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2
Q

calcitonin action

A

decreases serum Ca by taking Ca out of blood and returning it to bone

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3
Q

iodine purpose

A

hormone creation

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4
Q

thyroid hormone purpose

A

energy

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5
Q

hyperthyroidism

A

aka Graves Disease

too much energy!

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6
Q

hyperthyroidism: s/s

A

nervous, irritable
sweaty, hot
exophthalmos
thyroid hypertrophy

decreased

  • attention span
  • weight

increased

  • appetite, gi motility
  • bp (workload of heart)
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7
Q

hyperthyroidism: dx

A

increased serum T4

thyroid scan

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8
Q

antiarrhythmic drug containing high levels of iodine

A

amiodarone (Cordarone) - may affect thyroid function

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9
Q

prior to thyroid scan…?

A

discontinue iodine-containing medications 1 week prior

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10
Q

hyperthyroidism: tx

A
anti-thyroid medications
iodine compounds
beta blockers
radioactive iodine
surgery
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11
Q

anti-thyroid medications: action

A
  • stops thyroid from making thyroid hormone

- for hyperthyroidism

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12
Q

used prepoperatively to stun thyroid

A

anti-thyroid med

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13
Q

iodine compounds: action

A
  • decreases the size and vascularity of thyroid gland

- for hyperthyroidism

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14
Q

beta blockers for hyperthyroidism: action

A

decreases myocardial contractility

  • decreases HR, BP, anxiety
  • could decrease cardiac output
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15
Q

radioactive iodine: administration

A
  • for hyperthyroidism
  • 1 dose PO (liquid or tablet form)
    • RULE OUT PREGNANCY FIRST
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16
Q

important nursing consideration for radioactive iodine

A

rule out pregnancy before admin!

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17
Q

radioactive iodine: action

A

destroys thyroid cells resulting in hypothyroidism (not ae - expected)

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18
Q

possible rebound effect post-radioactive iodine

A

thyroid storm

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19
Q

thyroid storm

A

thyrotoxicosis, thyrotoxic crisis

  • uncontrollable hyperthyroidism
  • can be caused by thyroid manipulation, severe infection, stress

MEDICAL EMERGENCY

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20
Q

do not give beta blockers to… x2

A

asthmatics or diabetics

- block catecholamine sites (epi, NE)

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21
Q

thyroid gland regulates

A

body metabolism and growth

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22
Q

use straw with iodine compounds because…?

A

stains teeth

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23
Q

radioactive precautions

A

no babies or kisses for 24 hours

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24
Q

thyroidectomy: positioning

A

HOB up to decrease risk of edema

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25
Q

sign of recurrent laryngeal nerve damage post-thyroidectomy

A

hoarseness

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26
Q

why keep a trach set at the bedside post-thyroidectomy?

A
  • swelling
  • recurrent laryngeal nerve damage (vocal cord paralysis)
  • hypocalcemia
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27
Q

why is hypocalcemia a consideration post-thyroidectomy?

A

possible parathyroid removal

s/s hypocalcemia: tight, rigid muscles, seizure possiblity

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28
Q

hyperthyroidism and eyes

A

dry eyes, photosensitivity

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29
Q

hypothyroidism aka

A

myxedema

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30
Q

hypothyroidism: s/s

A
no energy!!, fatigue
increased weight
cold
decreased gi motility, speech
no expression
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31
Q

cretinism

A

hypothyroidism present at birth, can lead to slowed mental and physical development if undetected

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32
Q

hypothyroidism: tx

A

meds (levothyroxine, thyroglobulin, liothyronine): take FOREVER

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33
Q

common hypothyroidism co-morbidity

A

CAD - every aspect of metabolism slows down; basement membranes not proliferating = narrower artery walls = CAD

possible to throw clots!

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34
Q

hyperthyroidism + hypoglycemia

A

do not give beta blockers to diabetics because they block signs of hypoglycemia

beta blockers: decrease HR, BP, clammy (sweaty), nervous/anxious

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35
Q

hypothyroidism + depression

A

tired, weight gain, immobility (in bed)

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36
Q

parathyroid problem think

A

calcium!

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37
Q

parathyroid hormone: action

A

pull Ca from bone and into serum - serum Ca goes up

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38
Q

hyperparathyroidism =

A

hypercalcemia = hypophosphatemia

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39
Q

hypoparathyroidism =

A

hypocalcemia = hyperphosphatemia

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40
Q

hyperparathyroidism: s/s

A

too much PTH
serum Ca up
serum P down
SEDATED!

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41
Q

hyperparathyroidism: tx

A

partial parathyroidectomy

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42
Q

partial parathyroidectomy

A

take out 2 parathyroid glands

PTH secretion goes down, serum Ca goes down

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43
Q

monitor for what post-parathyroidectomy?

A

hypocalcemia: tight, rigid muscles, seizures

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44
Q

hypoparathyroidism: s/s

A

not enough PTH
serum Ca down
serum P up
hypocalcemia s/s

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45
Q

hypoparathyroidism: tx

A

IV calcium - give SLOWLY

phosphorous binding drugs

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46
Q

ESRD patients tend to retain…

A

phosphorous therefore serum Ca is down

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47
Q

adrenal glands for

A

stress

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48
Q

adrenal medulla hormones

A

epinephrine

norepinephrine

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49
Q

pheochromocytoma

A

benign tumors on adrenal medulla that secrete epi and NE in boluses

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50
Q

pheochromocytoma: s/s

A

increased BP, HR

flushing, diaphoretic

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51
Q

vanillylmandelic acid test

A

24 hour urine specimen checking for increased levels of catecholamines (epi, NE) - used for dx of pheochromocytoma

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52
Q

pheochromocytoma: tx

A

surgery to remove tumors

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53
Q

adrenal cortex hormones

A

glucocorticoids
mineralocorticoids
sex hormones

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54
Q

glucocorticoids: actions x4

A
  • mood
  • immunosuppression (decrease inflammation)
  • inhibit insulin = hyperglycemic…
  • fat, protein metabolism
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55
Q

accuchecks + steroids

A

steroids (glucocorticoids) inhibit insulin

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56
Q

major mineralocorticoid

A

aldosterone

57
Q

aldosterone: retain & lose what?

A

retain: Na, H2O
lose: K+ (dilutional hypokalemia + urinary excretion)

58
Q

too much aldosterone

A

fluid volume excess

hypokalemia

59
Q

not enough aldosterone

A

fluid volume deficit

hyperkalemia

60
Q

major glucocorticoid

A

cortisol

61
Q

pituitary + cortisol

A

pituitary secretes adrenocorticotropin hormones (ACTH)

ACTH stimulate adrenal cortex to produce cortisol

ACTH = cortisol

62
Q

adrenocorticotropin hormones (ACTH)

A

stimulate adrenal cortex to produce cortisol

secreted by pituitary

63
Q

addison’s disease

A

adrenocortical insufficiency: not enough steroids (gluco, mineralo, sex)

ADRENAL CORTEX PROBLEM

64
Q

addison’s disease: s/s

A

majority result from hyperkalemia
- progression: muscle twitching - weakness - flaccid paralysis

other:
gi: gut slows down - anorexia, nausea, decreased bowel sounds, gi upset

hyperpigmentation, vitiligo

hypotension

decreased Na, increased K, hypoglycemia

65
Q

hyperpigmentation

A

bronzing color of skin and mucus membranes

sign of addison’s

66
Q

vitiligo

A

white patchy area of depigmented skin

sign of addison’s

67
Q

addison’s + hypoglycemia

A

addison’s = not enough steroids = decreased glucocorticoids

not enough glucocorticoid = not enough glucose
also inhibits insulin

68
Q

addison’s + aldosterone

A

addison’s = not enough steroids = decreased mineralocorticoids (aldosterone)

insufficient aldosterone = lose Na = retain K = hyperkalemia

69
Q

addison’s + hyperkalemia

A

addison’s = not enough steroids = decreased mineralocorticoids (aldosterone)

insufficient aldosterone = lose Na = retain K = hyperkalemia

70
Q

addison’s + shock

A

addison’s = insufficient steroids = insufficient mineralocorticoids (aldosterone)

decreased aldosterone = lose Na and H2O = lose blood volume = SHOCK

71
Q

addison’s tx

A
  • combat shock
  • increase dietary Na
  • i/o + daily weight
72
Q

addison’s + hypotension

A

decreased BP due to loss of Na

73
Q

fludrocortisone (Florinef)

A

mineralocorticoid replacement - aldosterone

  • daily weights very important
  • given for addison’s disease
74
Q

daily weights + florinef

A

crucial for adjustment of florinef dose, similar to insulin for diabetics

75
Q

addisonian crisis

A

severe hypotension and vascular collapse

could result from abrupt d/c of steroids

76
Q

consideration for discontinuation of steroids

A

taper! never stop abruptly - could result in addisonian crisis

77
Q

cushing’s syndrome

A

too many steroids! glucocorticoids, mineralocorticoids, sex hormones

78
Q

cushing’s: s/s due to too many glucocorticoids

A
growth arrest
thin extremities, lypolysis
increased risk of infection
hyperglycemia, hypoinsulinemia
psychosis to depression
moon face
truncal obesity/lipogenesis
buffalo hump (fat redistribution)
79
Q

buffalo hump due to

A

glucocorticoid excess

fat redistribution

80
Q

moon face due to

A

glucocorticoid excess

fat redistribution or fluid retention

81
Q

cushing’s: s/s due to too many sex hormones

A

oily skin/acne
women with male traits
poor libido

82
Q

cushing’s: s/s due to too many mineralocorticoids

A
high BP
CHF
weight gain
fluid volume excess
decreased serum K
83
Q

cushing’s: tx

A

adrenalectomy
quiet environment
avoid infection

pre-treatment diet:
increased K, protein, Ca
decreased Na

84
Q

cushing’s: pre-treatment diet

A

increased K (cushing’s = decreased serum K)

increased protein (too many glucocorticoids = breakdown of fat and protein)

increased Ca (steroids decrease serum Ca through GI excretion)

decreased Na (retaining already(

85
Q

how do steroids decrease serum Ca?

A

via GI excretion

86
Q

cushing’s: may appear in urine

A

glucose and ketones

protein can’t come out of glomerulus unless it is damaged!

87
Q

diabetes: type 1

A

little or no insulin; appears abruptly despite years of beta cell destruction

usually diagnosed in childhood (by age 30)

88
Q

type 1 DM causes

A

auto-immune response (type 1A)

idiopathic (type 1B)

89
Q

first sign of type 1 DM typically

A

DKA

90
Q

type 1 diabetes: pathophys

A

little to no insulin = glucose builds up in vascular space

blood = hypertonic, pulls fluid in

kidneys filter excess glucose and fluids

cells starving and start breaking down protein and fat for energy

breakdown of fat results in ketones

leads to metabolic acidosis (DKA)

91
Q

type 1 diabetes: s/s

A

polyphagia
polyuria
polydipsia

92
Q

do oral hypoglycemics work for type 1 dm clients?

A

NOPE - need insulin

93
Q

type 2 diabetes: pathophys

A

insufficient insulin or bad insulin (usually just enough to prevent fat breakdown, therefore typically overweight)

can’t keep up with the glucose load being taken in

not as abrupt as type 1, usually found by accident or client presents with other problems (ulcers, infections, etc)

evaluate for metabolic syndrome!

94
Q

metabolic syndrome featuers

A
  • insulin resistance
  • waist circumference 40+ m, 35+ f
  • increased triglycerides + decreased HDL
  • increased BP
  • CAD
95
Q

type 2 diabetes: treatment

A

start with diet and exercise
then add oral agents
then insulin (especially in presence of non-compliance)

96
Q

gestational diabetes

A

resembles type 2; mom needs 2-3x more insulin than normal during pregnancy

97
Q

screen all moms when for gestational diabetes?

A

24 - 28 weeks gestation

1st prenatal visit, if risk factors present

98
Q

gestational diabetes: complications for baby

A

increased birth weight

hypoglycemia after birth

99
Q

diabetes diet: majority of calories should come from x3

A

complex carbs
fats
protein (limit 10-20%)

100
Q

why are diabetics prone to CAD?

A

sugar destroys vessels just like fat

101
Q

diabetics + kidney

A

tend to have kidney disease

102
Q

diabetes + high fiber

A
  • keeps blood sugar steady (may have to decrease insulin)
  • slows down glucose absorption in intestines, which eliminates sharp rise/fall in blood sugar
  • sharp rise/fall of blood sugar = vascular damage
103
Q

how do oral hypoglycemics work?

A

only for type 2. they stimulate the pancreas to make insulin (at least, for the NCLEX)

bottomline: all oral hypoglycemics work to decrease the amount of circulating glucose

104
Q

average adult dose of insulin

A

0.4 - 1.0 units / kg / day

105
Q

need more insulin if what are present in urine?

A

glucose, ketones

106
Q

cloudy insulin

A

NPH

107
Q

clear insulin

A

regular

also, Lantus (long-acting)

108
Q

long-acting insulin

A

Lantus

109
Q

what is the only type of insulin you can give IV?

A

regular

110
Q

long-acting insulin peak

A

none!

111
Q

rapid acting insulin peak

A

meal time

112
Q

when insulin is at its peak, blood glucose…

A

is at its lowest

113
Q

client should eat when insulin is at its

A

peak

114
Q

how do you draw up regular and NPH insulin together

A

clear to cloudy

regular then NPH

115
Q

glycosylated hemoglobin HbA1c blood test

A

gives an average of what your blood sugar has been over the past 3 months

116
Q

HbA1c goal for diabetics

A

4-6% or less

117
Q

HbA1c level that is diagnostic for diabetes

A

6.5 - 7%

118
Q

sq infusion pumps are only used for which type of insulin?

A

rapid acting insulin

119
Q

coverage provided by sq insulin infusion pump

A

basal (continuous)
and
bolus (on-demand)

rapid-acting insulin!

120
Q

diabetics: illness =

A

dka

121
Q

s/s hypoglycemia

A
cold
clammy
headache
nervous
confusion
nause
increased HR
glucose less than 70mg/dL
122
Q

hypoglycemic should eat what?

A

4-6 oz of simple sugar

followed by complex carb + protein once BG is up

123
Q

hypoglycemia prevention x4

A
  • eat
  • take insulin regularly
  • know s/s
  • check BG regularly
124
Q

glucose absorption delayed in foods with lots of

A

FATS!

125
Q

D50 W

A

for unconscious diabetic in hospital

requires large bore IV

126
Q

injectable glucagon (GlucaGen)

A

for unconscious diabetic in hospital with no IV access

given IM

127
Q

diabetic ketoacidosis pathophys

A

absent or inadequate insulin = BG sky high = poly(uria, dipsia, phagia) = fat breakdown (acidosis) = kussmaul respirations + more acidotic = LOC decreases

128
Q

kussmaul respirations

A

diabetic client in dka trying to blow off CO2 to compensate for metabolic acidosis

129
Q

diabetic client + polyuria =

A

think shock

130
Q

IV insulin action

A

decreases glucose and K by driving them out of vascular space and into cell

131
Q

dka tx

A
  • find cause
  • IV insulin
  • hourly BG, K levels (d/t insulin), UOP
  • EKG
132
Q

IVF progression for DKA

A

NS (2 a/c IV if possible)

when BG ~300, switch to D5W
- prevents throwing client into hypoglycemia

133
Q

hyperosmolar hyperglycemic nonketosis (HHNK)
aka
hyperglycemic hyperosmolar state (HHS)

A

looks like DKA but no acidosis

making just enough insulin so not breaking down fat
no fat breakdown = no ketones = no acidosis = no kussmaul respirations

134
Q

type 1 diabetes can lead to

type 2 diabetes can lead to

A

dka & HHNK (HHS)

135
Q

diabetic neuropathy issues x4

A

sexual problems (irreversible so SCREEN)
foot/leg problems: pain, paresthesia, numbness
neurogenic bladder
gastroparesis

136
Q

gastroparesis

A

stomach emptying is delayed due to decreased mesenteric perfusion s/t diabetes meaning increased risk for aspiration

137
Q

neurogenic bladder

A

bladder does not empty properly

  • may empty spontaneously (incontinence)
  • may not empty at all (retention)
138
Q

complications of diabetes x5

A
dka
HHNK (HHS)
vascular problems
neuropathy
infection
139
Q

vascular problems in diabetes x2

A

macrovascular (ex: coronary arteries)

microvascular (ex: kidneys)