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Endocrine Flashcards

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1
Q

what is hypopituitarism

A

under activity of the pituitary gland

most often caused by a benign pituitary tumor

other causes:
brain surgery
head trauma
infections of the brain
radiation
stroke
subarachnoid hemorrhage
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2
Q

hypopituitarism manifestations

A

hypogonadism

  • failure of the gonads
  • testes in males
  • ovaries in females

amenorrhea
infertility
breast and uterine atrophy
vaginal dryness

loss of libido
sexual dysfunction
loss of armpit and pubic hair

hypothyroidism
hypoadrenism
SIADH
diltuional hyponatremia

decreased GH

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3
Q

hypopituitarism diagnostic studies

A

history and physical exam
neuro-opthalmaological exam

X-ray of pituitary fossa and radio immunoassays of anterior pituiary hormones

CT scan or MRI
lab test:
serum ACTH
cortisol
estradiol
FSH
LH
TSH, T4
testosterone
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4
Q

hypopituitarism pharmacological care

A

hormone replacement therapy
steroid therapy

endocrine problems often amnifest differently in an older adult than a younger person

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5
Q

what is hyperpituitarism

A

anterior pituitary gland secretes too much GH

acromegaly occurs when growth plates are closed

gigantism occurs when growth plactes are still open

acromegaly: enlargement of hands, feet, face

overproductions of ACTH leads adrenal gland to overproduce cortison –> Cushings disease

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6
Q

hyperpituitarism manifestations

A

excess prolactin

  • headache
  • visual disturbances
  • growth failure
  • pubertal arrest with menstrual abnomralities in girl

excess ACTH
- weight gain with concurrent growth failure

excess GH causes:
- mild to moderate obestiy
-gigantism
- macrocephaly: overly large head
- cardiovascular disease
- coarse facila features
- tumors
0 endocrinopathies

physical changes of acromegaly are irreversible

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7
Q

hyperpituitarism diagnostic studies

A

hx and physical exam
CT
plasma homrone levels

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8
Q

hyperpituitarism care

A

microsurgery to remove tumor
- common treatment surgery for patient with pituitary tumors but can cause infertility

pituitary radiation
gamma knife radiation

growth hormone suppressant
- bromocriptine or octreotide

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9
Q

hyperpituitarism management

A

restrict soidum intake
assess signs for diabetes inspidus

treatment usually produces hypopituitiarism

lifelong hormone replacement therapy with regular check ups

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10
Q

what is diabetes insipidus

A

occurs when posterior pituitary fland makes TOO LITTLE antidiuretic hormone
- causing failure of tubular reabsorption of water in kidney

you being to pee a lot and often feel thirsty
- it fails to reabsorb so it just comes out

central DI is the most common form
- usually caused by damage to hypothalamus or pituitary gland

nephrogenic DI: defect in tubular reabsorption of water back into bloodstream

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11
Q

diabetes inspisidus manifestations

A 
polydipsia
polyuria
nocturia
dehydration
conspitation
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12
Q

diabetes inspidus diagnostic studies

A

water deprivation tests
- measures body’s inability to concentrate urine

osmotic stimulation
CT scan or MRI

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13
Q

diabetes inspidius pharmacological care

A 
pharmacological interventions:
desmopressin and vasopressin
chlorpropamide
carbamazepine
diuretics
surgical removal of a tumor

nephrogenic DI: if cause is due to lithium then discontinue or damage may become permanent

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14
Q

diabetes insipidius management

A

monitor findings of dehydration
measure urine and specific gravity

administer meds
monitor fluids and give IV fluids

intake and output
weigh daily

monitor and care for clients with increased intracranial pressure

health promotion:
- teach how record intake and output
- about prescribed medications and side effects
- avoid fluids with diuretic effects
(caffeinated beverages)
- check urine specific gravity
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15
Q

what is SIADH

A

too much ADH with water intoxification and a decrease in sodium concentration

you have too much water in your body

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16
Q

SIADH manifestations

A

changes in level of consciousness and mental status
tachycardia
hyponatremia
weight gain
urinary specific gravity will be greater than 1.030
hypertension

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17
Q

SIADH pharmacological care

A

diuretics:
furosemide
bumetanide

careful administration of hyperteonic 3% NaCl Iv solution
- too rapid of an infusion rate can cause permanent neurologic defects

osmotic diuretics - mannitol

vasopressor receptor antagonists

  • conivaptan
  • tolvaptan
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18
Q

SIADH management

A

monitor intake and output
sxs for fluid overload and hyponatremia

weigh daily
electrolytes and enruologic strokes

restrict fluid intake as ordered
sodium replacement therapy

seizure precautions

SIADH can be chronic and clients will need to learn to manage the condition at home
- should weigh themselves daily and adhere to prescribed fluid restriction typically 800-1000mL/ day

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19
Q

what is hypothyroidism

A

thyroid gland does not make enough thyroid hormones

myxedema crisis or come = loss of brain function
- happens as a result of severe, lnogstanding hypothyroidism

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20
Q

hypothyroidism causes

A

hashimotos thyroditis
atrophic thyroiditis

lithium
amiodarone
interferon alpha
genetics
radiation treatments to the neck or brain
radioactive iodine
surgical removal of all or part of thyroid gland

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21
Q

hypothyroidism manifestations

A 
early symptoms;
constipation
increased sensitivity to cold
fatigue
heavy menstrual period
joint and muscle pain
pale dry skin
depression
brittle hair and nails
weight gain
if left untreated:
decrease in taste and smell
hoarseness
puffy face
puffy hands and feet
slow speech
thickening of skin
thinning of eyebrows
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22
Q

hypothyroidism pharmacological care

A

most accurate and sensitive test to measure thyroid function is TSH level
- often first test done to evaluate thyroid function and monitor effectivenss of homrone replacement therapy

pharamacologic interventions:
levothyroixine
liothyronine

myxedema crisis/coma management will include:

  • mechanical ventilation
  • treatment of associated infection
  • correct hypothermia
  • IV thyroid hormone replacement therapy
  • conserve energy
  • avoid stress
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23
Q

hypothyroidism diagnostic studies

A

hx and physical exma

labs:
INCREASED:
- TSH
- cholesterol and triglycerides
- liver enzymes
- prolactin

DECREAED:

  • T3 and T4
  • serum sodium
  • serum glucose

CBC anemia

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24
Q

hypothyroidism management

A

meds
signs for myxedema
restful environment
protect client from cold

levothyroxine life threatening side effects: cardiac dysrhythmias
- check with HCP to switch to a different brand

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25
Q

what is hyperthyroidism

A

overactive thyroid makes too much thyroid

thyroitoxic crisis (thyroid storm) rare but potentially fatal

causes:
Graes disease
too much iodine
thyroditis
non-cancerous growth of thyroid gland
 over dosage of thyroid hormone
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26
Q

hyperthyroidism manifestation

A

difficuly concentrating
fatigue
hyperphagia - excessive or extreme hunger

weight loss
diarrhea
goiter

heat intolerance
exopthalamos

tachycardia
palpitation
restlessness

thing, brittle hair
pliable “plummers” nails
irregular menstrual priods
insomnia

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27
Q

hyperthyroidism diagnostic studies

A

hx and physical exam
goiter
hyperactive reflexes

labs:
increased T3 and T4
increased radioactive iodine uptake
presence of thyroid nodules
decreased TSH levesl
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28
Q

hyperthyroidism pharmacological care

A 
pharamcologic:
radioactivie iodin
methimazole
antithyroid (propylthiouracil)
beta adrenergic blocking agents (propanolol)

surgical intervention: thyroidectomy

exopthalamos: classic finding of graves disease
- cornea can become dry, irritated and devleop ulcerations

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29
Q

hyperthyroidism management

A

vital
Hr
quiet restful, cool environment

diet therapy, extra fluids

diet high in calories, protein and carbs

stress avoidance

energy conservation

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30
Q

what is hypoparathyroidism

A

parathyroid hormone produces too little parathyroid hormone

results in hypocalcemia

most common cause: injury to parathyroid glands during thyroid surgery

other causes;
low serum amgnesium levels
metabolic alkalosis

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31
Q

hypoparathyroidism manifestations

A

neuromuscular irritability
muscle weakness or cramping
personality changes

numbness of fingers and caropedal spams

tetany - muscular spasms

seizures
laryngospasm

dry, scaly skin and hair loss
abdominal cramping

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32
Q

hypoparathyroidism diagnostic studies

A

hx and physical exma
positive chvosteks facial signs - cheek
positive trousseaus signs - BP cuff

ECG shows abdnormal heart rhythms

labs:
decreased:
- calcium
- magnesium
- PTH levels
- urine

increased: phosphate

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33
Q

hypoparathyroidism pharmacological care

A

calcium replacement therapy

Vit D preparations
calcium rich, low phosphorus diet

34
Q

hypoparathyroidism management

A

monitor signs of tetany
place an oral airway, suction equipment and tracheostomy tray at clients bedisde

seizure precautions
monitor vitals

have calcium gluconate available if signs of low calcium

reduce phosphrous intake, no:

  • fish
  • eggs
  • cheese
  • cereals
35
Q

what is hyperparathyroidism

A

parathyroid secretes too much parathyroid hormone

results in hypercalcemia

36
Q

primary hyperparathyroidism

A

enlargement of one or more of the parathyroid glands

no known causes

37
Q

secondary hyperparathyroidism

A

body produces extra parathyroid hormones because calcium levels are too low

38
Q

tertiary hyperparathyroidism

A

parathyroid continues to produce too much even though calcium levels are back to normal

occurs with kidney disease

39
Q

hyperparathyroidism manifestations

A

constipation
nausea and vomiting
anorexia

bone pain
deminieralization
deformities

kdieny stones
blurred vision
muscle weakness and fatigue

depression

40
Q

hyparathyroidism diagnostic studies

A

hx and physical exam

increase calcium
decrease phosphorus

x-rays and DEXA revel bone demineralization

CT scan
MRI
ultrasound of the neck

41
Q

hyparathyroidism pharmacological care

A

drink more fluids
avoid thiazide type diuretics

surgical interventions to remove parathyroid glands

42
Q

hyperparathyroidism management

A

postoperatively, observe signs of hypocalcemia

monitor laryngeal damage
monitor renal involvement

increase their fluid intake to dilue calcium levels in blood and urine

consume a diet rich in calcium and vitamin D

43
Q

what is addisons disease

A

decreased production of cortisol and aldosterone

symptoms of addison disease do not become apparent until around 90% of the adrenal cortex is destroyed

44
Q

addison diseae manifestation

A 
fatigue
weakness
dehydrartion
low BP
decreased resistance to stress

hyperpigmentation and alopecia

weight loss
pathological fractures
depression
lethargy
emotional lability
45
Q

addison crisis clinical manifestation

A 
nausea and vomiting
abdominal pain
fever
extreme weakness
severe hypoglycemia, hyperkalemia and dehydration

BP falls which can lead to shock and coma

death if not treated

46
Q

addison diseasee diagnostic studies

A

hx and physical exam

labs:
ACTH stimulation test - low cortisol level
hypoglycemia
electrolytes - low sodium and high potassium
24 hour urine output

47
Q

addison disease pharmacgologial care

A

hydrocortison
fludrocortison acetate

diet high in protein, carbs and sodium
low in potassium

48
Q

addisonian crisis interventions

A

emergency management
IV hydrocortisone

carefully monitor IV infusion of 0.9% NaCl or D5W/NaCl

Iv glucose or glucagon
insulin with dextrose in normal saline

potassium-binding and excreting resin
vitals

49
Q

addison disease management

A

weigh daily

monitor electrolytes
preserve clients energy by assisting with ADLs

collaborate with dietician
measure intake and output
monitor blood sugar levels

health promotion;
lifelong hormone replacement therapy
avoid or manage stress
add more sodium to diet

avoid extra potassium
have quick acting sugar
increasing fluid intake to 2,000-3,000 ml/day

    • clients with addison disease will require lifelong hormone therapy with glucocorticoids and mineral corticoids
  • taking these with an extended periods of time can lead to serous complication and side effects
50
Q

what is cushings syndrome

A

occurs when adrenal galnd secrete too much cortisol

overproduction can be due to:

  1. cushings disease
  2. tumors of the pituitary gland
  3. tumors in other organs and glands in the body that produce cortisol or ACTH
51
Q

cushings syndrome manifestation

A

upper body obesity with thin arms or legs
buffalo hump
moon face

acne
striae (purple marks) on abdomen, thighs, breasts
easy bruising

backache
bone pain or tenderness

excess hair growth on face, neck, chest, abdomen, thighs for women

for men, impotent or have decreased libido
personality changes
fatigue

52
Q

cushings syndrome diagnostic studies

A

hx and physical exam

labs:
3 standard tests
- 24 hour urinary free cortisol
- late night salivary cortisol
- overnight dexmethasone suppression test

labs will include an increase in cortisol, sodium, and glucose
a decrease in potassium

if underlying cause for cushings syndrome is pituitary adenoma surgical removal of pituitary gland will most likely be required

53
Q

cushings syndrome pharmacological care

A

if cause is by corticosteroid use, slowly decrease medication under medical supervision

if cause is by pituitary tumor or tumor that release ACTH, the tumor will be removed (transphenoidal surgery)

if cause if due to an adrenal tumor or other tumors, the tumor will be removed
- if tumor cannot be removed then medicatioin will be needed to block the release of cortisol

pharmacological interventions:

  • agents that inhibit steroidogenesis:
  • metyrapone
  • mitotane
  • ketocoriazole

diet including sufficient calcium and vitamin D

54
Q

cushings syndrome management

A

monitor signs of hypokalemia and vit

health promotion:
need for lifelong treatment
medication management
need to increase activities, slowly and gradually

body changes from disease may reverse but can take months to years to see changes

monitor signs of depression or difficulty coping

55
Q

what is pheochromocytoma

A

benign tumor of the adrenal medulla

causes the adrenal medulla to secrete too much epinephrine and norepinephrine

56
Q

pheochromocytoma manifestations

A 
abdominal pain
chet pain
irritabiltiy
nervousness 
severe stress response
unusual skin pallor
palpitations with tachycardia
severe headache
diaphoresis
weight loss
tremors
hypertension
difficulty coping
57
Q

pheochromocytoma diagnostic studies

A

adrenal biopsy
abdominal CT scan
MRI

MIBG scintiscan
- tet that uses injected radioactive material and special scanner to locate or confirm pheochromocytoma

labs:
-24 hour urine collection
- increase catecholamines
serum glucose levels

a client with hypertension, especially if it severe and reffractory to medication should be evaluated

58
Q

pheochromocytoma pharmacological care

A

pharamcological intervention:
pre-operatively:
- antihypertensives
- antidysrhythmic

beta adrenergic blocking: propanolol and nadolol
tyrosin inhibitors
alpha adrenergic blocking agents: post-operatively
- phenoxybenzamine

59
Q

pheochromocytoma management

A

vitals
meds
keep phentolamine available for treatment of a hypertensive crisis

DO NOT palpate the abdomen

if bilateral adrenalectomy is performed, lifelong steroid therapy will be required

60
Q

what is diabetes mellitus

A

pancreas produced too little insulin or cells to stop responding to insuline

results in hyperglycemia

type 1: thought to be genetic autoimmune response
type 2: lifestyle factors

61
Q

diabetes mellitus manifestations

A

hyperglycemia
fatigue
weight loss with type 1 only

blurred vision
possible vaginal infections

slow wound healing
polydipsia
polyuria
polyphagia

62
Q

diabetes mellitus diagnostic exams

A

hx and physical

labs;
fasting blood sugar
oral glucose tolerance test
glycosylated hemoglobin test

63
Q

diabetes mellitus pharmacological care

A

eat foods high in nutrition and low in fat and calories

exercise to lower glucose levels

64
Q

meds for type 1 diabetes mellitus

A

insulin
hypertensive meds:
- ACE inhibitors
- ARBs

cholesterol-lowering drugs
- statins

Pramlinitide

65
Q

meds for type 2 diabetes mellitus

A

oral hypoglycemic meds

  • sulfonylureas
  • meglitinides
  • biguanides
  • thiazolidinediones

metofmrin is the first line therapy for most clients

66
Q

diabetes mellitus management

A

teach about med interactions with insulin and oral hypoglycemic meds

teach client to maintain:
balanced diet
eat carbohydrate shake with protein before strenuous exercise

self monitor blood glucose
carry rapid absorbing carbs
self monitor blood glucose

perform appropriate foot care
wear a med alert bracelet

receive regular eye exams

67
Q

meds that can increase blood glucose levels

A
  • glucocorticoids
  • thiazide diuretics
  • thyroid agents
  • oral contraceptive
  • estrogen
68
Q

meds that can decrease blood glucose levels

A 
aspirin
alcohol
oral anticoagulants
beta blockers
tricyclic antidepressants
tetracyclines
MAOIs
69
Q

proper foot care for diabetes mellitus

A

wash feet daily with soap and water

do not soak feet
pat to dry, not rub

attend to corn, calluses but never cut on your own

lotion, but not in between toes

cotton socks and can change if seaty

no heating pads, electric blankets on feet

do not wear circular garters

70
Q

hypoglycemia manifestations

A

diaphoresis
cold, clammy skin

anxiety
tremors
headache

slurred speech
client will be weak
nausea and experience mental confusion

71
Q

hypoglycemia management

A 
if client is conscious and able to swallow;
give at least 15 g of carbs
- 4 oz of orange juice
- regular soda
- 2 tbsp of raisins
- 4-5 saltine cracklers
- 4 tsp of sugar
- 1 tbsp of honey or corn syrup

check blood sugar 15 min after intervention

if still less than 70, then repeat the intervention

72
Q

retinopathy

A

cause blindness

73
Q

nephropathy

A

progressive decrease in kidney function

eventually leading to end stage renal disease

74
Q

neuropathy

A

deterioration of nervous system

75
Q

what is diabetic ketoacidosis

A

acute complication of DM
severe insulin deficiency and has sudden onset

typically caused by undiagnose diabetes or the inadequacy of prescribed therapy

76
Q

DKA manifestations

A

blood sugar greater than 300
pH less than 7.35

fruity sweet odor in breath
Kussmauls rrespirations

flushed appearance
dry skin
metabolic acidosis

thirst
polyuria
anorexia
vomiting

can lead to shock and coma if not treted properly

77
Q

DKA care

A

correct fluid depletion - IV fluids
correct electrolyte depletion
- potassium

correct metbolic acidosis

  • by lowering the blood sugar with short acting insulin
  • given continuous infusion

when blood sugar levels fall below 250, IV should be changed to dextrose containing solution

  • 0.9% NaCl
  • 5% dextrose
78
Q

what is hyperosmolar hyperglycemic state (HHS)

A

complication of diabetes mellitus type 2

untreated high blood sugar levels in high serum osmolality without ketoacidosis

has a gradual onset

79
Q

HHS manifestations

A

severe hyperglycemia
usually greater than 600

pH less than 7.4
negative ketones

prfound dehydration
altered level of consciousness

usually precipitated by physcial stress, such as an infection

in non-diabetics, HHS can occur due to tube feedings without supplemental water or because of a too rapid rate of infusion for parenteral nutrition

80
Q

HHS pharmacological care

A

aggressive IV rehydration with normal saline or LR

lowering the blood sugar with short-acting insulin (regular)

when blood sugar levels falls below 250 –> IV solution should be changed to dextrose containing solution

  • 0.9% NaCl
  • 55 dextrose

NCLEX (21 decks)

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