Endocrine/ diabetes (20 questions)
1. What organs are involved in the endocrine system?
a. Parathyroids; hypothalamus; pituitary; thyroid; adrenals; pancreas;
ovaries; testes
2. What does the hypothalamus do?
a. Regulates temp; sits at base of brain between pituitary and thalamus
3. What does the pituitary gland do?
a. Size of a pea, sits at the base of the brain; anterior and posterior
b. Anterior hormones: TSH, ACTH, GH, FSH, LH, prolactin
c. Posterior hormones: ADH, oxytocin
4. What does the thyroid gland do?
a. Complex feedback; at the base of the neck below the larynx; 2 lobes on
each side; very vascular
b. Produces T4, T3, thyrocalcitonin
5. What do T3 and T4 do?
a. Regulate cellular metabolism as well as growth and development
6. How is iodine involved in the thyroid?
a. Iodine is required to synthesize thyroid hormones = delicate balance
7. What does the parathyroid gland do?
a. Found on the posterior surface of the thyroid?
b. Secretes parathyroid hormone which increases osteoclast activity
(increases Ca release from the bone); also increases absorption of Ca in
the GI tract and kidneys
8. What is PTH?
a. Works opposite of calcitonin to regulate serum calcium levels; secreted
when calcium levels drop
9. What does the adrenal gland do?
a. Complex feedback; found on each kidney
10. What does the adrenal medulla do?
a. Inner portion that produces epinephrine and norepinephrine
11. What does the adrenal cortex do?
a. Outer portion that produces steroids; stimulated by ACTH from anterior
pituitary to release aldosterone (conserves sodium and water), cortisol
(increases glucose levels), sex hormones (secreted in minimal amounts)
12. What is the function of GH?
a. Promotes protein synthesis, mobilized glucose and free fatty acids;
stimulates liver to produce insulin like growth factor (IGF-!) that causes
elevation in blood glucose
13. What is gigantism?
a. Before growth plates close; long and brittle bones
14. What is acromegaly?
, a. After growth plates close; enlarged bones change in soft tissue
thickness, especially in face; unrelated can cause permanent damage to
cardiovascular system
15. What are clinical manifestations of growth hormone excess?
a. Sleep apnea, visual disturbances and headaches if tumor is on pituitary;
irregular menstrual cycles in women; large hands and feet; prominent
jaw and forehead; coarse facial features; excessive sweating
16. How would we diagnose GH excess?
a. Blood work for IGH-1 levels more accurate than GH levels because GH
levels fluctuate; oral glucose challenge test; MRI and CT to identity and
determine the extent of spread of pituitary tumor
17. How would we care for those with GH excess?
a. GOAL: return that patient’s GH levels to normal
b. Surgical (hypophysectomy), radiation (when surgery has failed), drug
therapy (Sandostatin, Octreotide, Lanreotide SR -> antagonize GH,
given in injection form)
18. What is the etiology of Cushing syndrome?
a. An excess of corticosteroids, particularly glucocorticoids
b. Due to a ACTH secreting tumor or is induced by corticosteroid drugs
(prednisone)
19. What are clinical manifestations of Cushing syndrome?
a. Weight gain (from sodium and water retention, also from increase in
adipose tissue); adipose tissue in trunk, face, and cervical spine area
(moon face); protein wasting due to catabolic affects of cortisol;
menstrual disorders and hirsutism
20. How would we diagnose Cushing syndrome?
a. Urine cortisol, plasma cortisol, plasma ACTH
21. How would we care for someone with Cushing Syndrome?
a. Surgery (remove tumor); radiation; adrenalectomy; drug therapy to
inhibit adrenal activity; if on prednisone gradual discontinuance of
meds
22. What are nursing actions for someone with Cushing Syndrome?
a. Prevention of infection (corticosteroids suppress immune system) s/s
of infection (FEVER); Monitor blood glucose; Provide emotional support
for disturbed body image; Post op care (glands are very vascular
monitor for bleeding; administer high doses of IV corticosteroids after
surgery to prevent complications of abrupt discontinuation (acute
adrenal insufficiency); Monitor levels of cortisol to see if treatment was
effective)
23. What is the etiology of adrenocortical insufficiency?
a. Hypofunction of adrenal cortex
24. What is Addison’s disease?
a. Mainly autoimmune, all three corticoids are deficient
,25. What is secondary adrenocortical insufficiency?
a. Corticoids and androgens are reduced (mineralocorticoids rarely are)
26. What are clinical manifestations of adrenocortical insufficiency?
a. Are not evident until 90% of adrenal cortex is destroyed
b. Fatigue; weight loss; anorexia; skin hyperpigmentation (due to increases
secretion of B lipotopin stimulates melanocyte production);
orthostatic hypotension, hyperkalemia, N/V/D
27. What are complications of adrenocortical insufficiency?
a. Addisonian crisis: triggered by stress, infection, sudden withdrawal of
corticosteroid therapy, after adrenal surgery; LIFE THREATENING (at risk
for shock)
28. How could we care for someone with adrenocortical insufficiency?
a. Hormone replacement therapy; Manage shock: IV fluids; treat
stressful events (medic alert bracelet) doses of corticosteroids are
doubled during minor surgery, tripled during major surgery; carry
emergency kit = hydrocortisone 100 mg IM syringe and
instructions for use
29. What is corticosteroid therapy?
a. Glucocorticoids are used not only to treat endocrine problems, but for
many diseases; long term = side effects; not recommended for minor,
chronic conditions
30. What are effects of corticosteroid therapy?
a. Anti-inflammatory action; immunosuppression; maintenance of normal
BP (potentiate the vasoconstrictor effect of norepinephrine and act on
the renal tubules to increase sodium reabsorption); carbohydrate and
protein metabolism
31. What are complications of corticosteroid therapy?
a. HTN; reactivation of latent TB; reduces resistance to infection and
cancer; inhibit the antibody response to vaccines
32. How would we care for someone on corticosteroid therapy?
a. Thorough instruction to promote compliance (tapering); teach patient
about maintaining an exercise plan (to reduce osteoporosis)
33. What is the etiology of Syndrome of Inappropriate Antidiuretic Hormone
(SIADH)?
a. Fluid retention; serum hypoosmolality; dilutional hyponatremia;
hypochloremia; concentrated urine; normal renal function
34. What are clinical manifestations of SIADH?
a. Hyponatremia – muscle cramps, weakness, thirst, fatigue, dulled
sensorium, low UOP, and weight gain
b. Severe hyponatremia – vomiting, abdominal cramps, muscle twitching ,
and seizures, cerebral edema, anorexia, confusion, coma
35. How can we care for someone with SIADH?
, a. Treat underlying cause (head trauma, drugs, malignant tumors);
Restriction of fluids to 800-1000 ml/day; IV hypertonic solutions for
SEVERE hyponatremia; Diuretics, but only if serum sodium is 125mEq/L
36. What are nursing actions for someone with SIADH?
a. Be alert to low urinary output; Assess for a rapid weight gain; Fluid
restriction; Diuretics as ordered; Teaching regarding S/S of electrolyte
imbalances (sodium, potassium, magnesium) and fluid overload
37. What is the etiology of diabetes insipidus?
a. Associated with a deficiency of production or secretion of ADH, or a
decreased response to ADH; tumor, trauma, idiopathic
b. Two types: central and nephrogenic
38. What are clinical manifestations of diabetes insipidus?
a. Polydipsia, polyuria (5-20 L/day), low urine osmolality, high serum
osmolality, shock in severe cases
39. How would we diagnose diabetes insipidus?
a. Water deprivation test to diagnose central DI fluids withheld for 8-16
hours pt observed for thirst weight loss, urine osmolality, signs of
hypovolemia
40. What are some nursing actions for someone with diabetes insipidus?
a. Adequate hydration; assess for s/s of hypovolemia (HYPOTENSION),
hyponatremia, electrolyte imbalances; administration of DDAVP (SQ, PO,
intranasal)
41. What is hyperthyroidism?
a. Graves’ disease: autoimmune, most common
b. Toxic nodular goiters: nodules that excrete excessive T3 and T4,
independent of TSH stimulation
42. What are clinical manifestations of hyperthyroidism?
a. Goiter, thyroid bruits from increased O2 supply, exophthalmos, anorexia,
weight loss, depression, A fib, agitation, pain, nausea, vomiting
43. What are some complications of hyperthyroidism?
a. Thyrotoxic crisis: severe tachycardia, heart failure, shock, hyperthermia,
agitation, pain, nausea, vomiting
b. Diagnosed via T3, T4, TSH levels
44. What is exophthalmos?
a. Does not go away once developed; eyelids don’t close; use eye drops
for dryness; visual changes
45. How type of care for hyperthyroid pts?
a. Drug therapy, radioactive iodine therapy, surgical therapy, nutritional
therapy
46. What nursing actions can we do for hyperthyroid pts?
a. Thyroid surgery: assess pt q2h for 24 hours for s/s of hemorrhage or
tracheal compression; SEMI FOWLER POSITION (avoid flexion of neck);
1. What organs are involved in the endocrine system?
a. Parathyroids; hypothalamus; pituitary; thyroid; adrenals; pancreas;
ovaries; testes
2. What does the hypothalamus do?
a. Regulates temp; sits at base of brain between pituitary and thalamus
3. What does the pituitary gland do?
a. Size of a pea, sits at the base of the brain; anterior and posterior
b. Anterior hormones: TSH, ACTH, GH, FSH, LH, prolactin
c. Posterior hormones: ADH, oxytocin
4. What does the thyroid gland do?
a. Complex feedback; at the base of the neck below the larynx; 2 lobes on
each side; very vascular
b. Produces T4, T3, thyrocalcitonin
5. What do T3 and T4 do?
a. Regulate cellular metabolism as well as growth and development
6. How is iodine involved in the thyroid?
a. Iodine is required to synthesize thyroid hormones = delicate balance
7. What does the parathyroid gland do?
a. Found on the posterior surface of the thyroid?
b. Secretes parathyroid hormone which increases osteoclast activity
(increases Ca release from the bone); also increases absorption of Ca in
the GI tract and kidneys
8. What is PTH?
a. Works opposite of calcitonin to regulate serum calcium levels; secreted
when calcium levels drop
9. What does the adrenal gland do?
a. Complex feedback; found on each kidney
10. What does the adrenal medulla do?
a. Inner portion that produces epinephrine and norepinephrine
11. What does the adrenal cortex do?
a. Outer portion that produces steroids; stimulated by ACTH from anterior
pituitary to release aldosterone (conserves sodium and water), cortisol
(increases glucose levels), sex hormones (secreted in minimal amounts)
12. What is the function of GH?
a. Promotes protein synthesis, mobilized glucose and free fatty acids;
stimulates liver to produce insulin like growth factor (IGF-!) that causes
elevation in blood glucose
13. What is gigantism?
a. Before growth plates close; long and brittle bones
14. What is acromegaly?
, a. After growth plates close; enlarged bones change in soft tissue
thickness, especially in face; unrelated can cause permanent damage to
cardiovascular system
15. What are clinical manifestations of growth hormone excess?
a. Sleep apnea, visual disturbances and headaches if tumor is on pituitary;
irregular menstrual cycles in women; large hands and feet; prominent
jaw and forehead; coarse facial features; excessive sweating
16. How would we diagnose GH excess?
a. Blood work for IGH-1 levels more accurate than GH levels because GH
levels fluctuate; oral glucose challenge test; MRI and CT to identity and
determine the extent of spread of pituitary tumor
17. How would we care for those with GH excess?
a. GOAL: return that patient’s GH levels to normal
b. Surgical (hypophysectomy), radiation (when surgery has failed), drug
therapy (Sandostatin, Octreotide, Lanreotide SR -> antagonize GH,
given in injection form)
18. What is the etiology of Cushing syndrome?
a. An excess of corticosteroids, particularly glucocorticoids
b. Due to a ACTH secreting tumor or is induced by corticosteroid drugs
(prednisone)
19. What are clinical manifestations of Cushing syndrome?
a. Weight gain (from sodium and water retention, also from increase in
adipose tissue); adipose tissue in trunk, face, and cervical spine area
(moon face); protein wasting due to catabolic affects of cortisol;
menstrual disorders and hirsutism
20. How would we diagnose Cushing syndrome?
a. Urine cortisol, plasma cortisol, plasma ACTH
21. How would we care for someone with Cushing Syndrome?
a. Surgery (remove tumor); radiation; adrenalectomy; drug therapy to
inhibit adrenal activity; if on prednisone gradual discontinuance of
meds
22. What are nursing actions for someone with Cushing Syndrome?
a. Prevention of infection (corticosteroids suppress immune system) s/s
of infection (FEVER); Monitor blood glucose; Provide emotional support
for disturbed body image; Post op care (glands are very vascular
monitor for bleeding; administer high doses of IV corticosteroids after
surgery to prevent complications of abrupt discontinuation (acute
adrenal insufficiency); Monitor levels of cortisol to see if treatment was
effective)
23. What is the etiology of adrenocortical insufficiency?
a. Hypofunction of adrenal cortex
24. What is Addison’s disease?
a. Mainly autoimmune, all three corticoids are deficient
,25. What is secondary adrenocortical insufficiency?
a. Corticoids and androgens are reduced (mineralocorticoids rarely are)
26. What are clinical manifestations of adrenocortical insufficiency?
a. Are not evident until 90% of adrenal cortex is destroyed
b. Fatigue; weight loss; anorexia; skin hyperpigmentation (due to increases
secretion of B lipotopin stimulates melanocyte production);
orthostatic hypotension, hyperkalemia, N/V/D
27. What are complications of adrenocortical insufficiency?
a. Addisonian crisis: triggered by stress, infection, sudden withdrawal of
corticosteroid therapy, after adrenal surgery; LIFE THREATENING (at risk
for shock)
28. How could we care for someone with adrenocortical insufficiency?
a. Hormone replacement therapy; Manage shock: IV fluids; treat
stressful events (medic alert bracelet) doses of corticosteroids are
doubled during minor surgery, tripled during major surgery; carry
emergency kit = hydrocortisone 100 mg IM syringe and
instructions for use
29. What is corticosteroid therapy?
a. Glucocorticoids are used not only to treat endocrine problems, but for
many diseases; long term = side effects; not recommended for minor,
chronic conditions
30. What are effects of corticosteroid therapy?
a. Anti-inflammatory action; immunosuppression; maintenance of normal
BP (potentiate the vasoconstrictor effect of norepinephrine and act on
the renal tubules to increase sodium reabsorption); carbohydrate and
protein metabolism
31. What are complications of corticosteroid therapy?
a. HTN; reactivation of latent TB; reduces resistance to infection and
cancer; inhibit the antibody response to vaccines
32. How would we care for someone on corticosteroid therapy?
a. Thorough instruction to promote compliance (tapering); teach patient
about maintaining an exercise plan (to reduce osteoporosis)
33. What is the etiology of Syndrome of Inappropriate Antidiuretic Hormone
(SIADH)?
a. Fluid retention; serum hypoosmolality; dilutional hyponatremia;
hypochloremia; concentrated urine; normal renal function
34. What are clinical manifestations of SIADH?
a. Hyponatremia – muscle cramps, weakness, thirst, fatigue, dulled
sensorium, low UOP, and weight gain
b. Severe hyponatremia – vomiting, abdominal cramps, muscle twitching ,
and seizures, cerebral edema, anorexia, confusion, coma
35. How can we care for someone with SIADH?
, a. Treat underlying cause (head trauma, drugs, malignant tumors);
Restriction of fluids to 800-1000 ml/day; IV hypertonic solutions for
SEVERE hyponatremia; Diuretics, but only if serum sodium is 125mEq/L
36. What are nursing actions for someone with SIADH?
a. Be alert to low urinary output; Assess for a rapid weight gain; Fluid
restriction; Diuretics as ordered; Teaching regarding S/S of electrolyte
imbalances (sodium, potassium, magnesium) and fluid overload
37. What is the etiology of diabetes insipidus?
a. Associated with a deficiency of production or secretion of ADH, or a
decreased response to ADH; tumor, trauma, idiopathic
b. Two types: central and nephrogenic
38. What are clinical manifestations of diabetes insipidus?
a. Polydipsia, polyuria (5-20 L/day), low urine osmolality, high serum
osmolality, shock in severe cases
39. How would we diagnose diabetes insipidus?
a. Water deprivation test to diagnose central DI fluids withheld for 8-16
hours pt observed for thirst weight loss, urine osmolality, signs of
hypovolemia
40. What are some nursing actions for someone with diabetes insipidus?
a. Adequate hydration; assess for s/s of hypovolemia (HYPOTENSION),
hyponatremia, electrolyte imbalances; administration of DDAVP (SQ, PO,
intranasal)
41. What is hyperthyroidism?
a. Graves’ disease: autoimmune, most common
b. Toxic nodular goiters: nodules that excrete excessive T3 and T4,
independent of TSH stimulation
42. What are clinical manifestations of hyperthyroidism?
a. Goiter, thyroid bruits from increased O2 supply, exophthalmos, anorexia,
weight loss, depression, A fib, agitation, pain, nausea, vomiting
43. What are some complications of hyperthyroidism?
a. Thyrotoxic crisis: severe tachycardia, heart failure, shock, hyperthermia,
agitation, pain, nausea, vomiting
b. Diagnosed via T3, T4, TSH levels
44. What is exophthalmos?
a. Does not go away once developed; eyelids don’t close; use eye drops
for dryness; visual changes
45. How type of care for hyperthyroid pts?
a. Drug therapy, radioactive iodine therapy, surgical therapy, nutritional
therapy
46. What nursing actions can we do for hyperthyroid pts?
a. Thyroid surgery: assess pt q2h for 24 hours for s/s of hemorrhage or
tracheal compression; SEMI FOWLER POSITION (avoid flexion of neck);
