Endocrine Conditions Flashcards

1
Q

growth hormone

A

too high = acromegaly

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2
Q

ADH

A

If low = diabetes insidious
if high = syndrome of inappropriate anti-diuretic hormone

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3
Q

Thyroid Hormone (T3, T4)

A

high = grave’s disease, hyperthyroidms
low = hypothyroidism

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4
Q

thyroid stimulating hormone (TSH)

A

low = hyperthyroidism
high = hypothyroidsm

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5
Q

parathyroid hormone (PTH)

A

high = hyperparathyroidism
low = hypoparathyroidism

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6
Q

cortisol

A

high = Cushing’s syndrome

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7
Q

adrenal corticosteroids (glucocorticoids, mineralocorticoids, androgens)

A

low = Addison’s disease

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8
Q

aldosterone

A

high = hyperaldosteronism

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9
Q

catecholamines (epi, norepinephrine)

A

high = pheochromocytoma

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10
Q

what are hormones of the anterior pituitary gland?

A

1) thyroid stimulating hormone (TSH)
2) adrenocorticotrophic hormone (ACTH)
3) Growth hormone (GH)
4) prolactin
5) gonadotropic hormone (FSH and LH)

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11
Q

what hormones are secreted by the posterior pituitary gland?

A

ADH and oxytocin

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12
Q

what is acromegaly

A

hypersecretion of growth hormone but the anterior pituitary

  • usually occurs because of a benign pituitary tumour
  • hypersecretion of growth hormone leads to secondary elevation of insulin-like growth factor (IGF-1) leading to an overgrowth of the bones and soft tissues in hands, feet and face
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13
Q

what are the physical appearance in acromegaly?

A

1) increased size of mandible causes the jaw to jut forward

2) enlargement of the tongue results in speech difficulties

3) thick, leathery, oily skin

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14
Q

what are some inter professional care for acromegaly?

A

1) return serum GH and circulating IGF-1 levels to normal

2) surgery
- trans-sphenoidal surgery aka remove the tumour
- hypophysectomy aka remove the entire pituitary gland which means losing all the hormones

3) radiation

4) medications
- to reduce GH levels

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15
Q

what are nursing managements for acromegaly?

A
  • assess for signs and symptoms for abnormal tissue growth. take photos too
  • if receiving surgery, post op finding: clear nasal drainage should be sent to lab to test for glucose because if its higher than 1.67, it indicates cerebral spinal fluid risk which means the pt is high risk for meningitis
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16
Q

discuss hypopituitarism

A

a decrease in one or more of the pituitary hormones

  • the most common aetiology you should know is comes from pituitary tumour
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17
Q

what are some clinical manifestations of hypopituitarism?

A

headaches, visual changes, loss of smell, nausea and vomiting, seizers basically the basic stuff

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18
Q

discuss syndrome of inappropriate antidiuretic hormone ( SIAH)

A

impaired water excretion from abnormal production or sustained secretion of ADH

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19
Q

what are characteristics of SIAH

A
  • Fluid retention
  • serum hypo-osmolality
    -dilution hyponatremia, hypocholermia
    -concentrated urine in the presence of normal renal function
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20
Q

what causes SIAH?

A

head trauma, psychosis, medications

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21
Q

what are the clinical manifestations of SIAH?

A

1) ECF volume expands

2) sodium increases

3) plasma osmolality decreases

4)GFR increases

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22
Q

what are the diagnostic values?

A

serum sodium < 134mmol/L (muscle twitch, low urine out, weight gain, seizures)

serum osmolality < 280mmol/kg

urine specific gravity > 1.005

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23
Q

how to treat SIAH?

A

remove meds that stimulate ADH

restore fluid by restriction and SLOW administration of HYPERTONIC saline (3% NaCl)

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24
Q

discuss diabetes insipidus (DI)

A

group of conditions associates with either

1) deficiency of ADH production or secretion

2) decreased renal response to ADH caused by injury

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25
Q

if ADH decreases what happens?

A

fluid and electrolyte imbalances caused by increased urinary output and increased plasma osmolality

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26
Q

what are the 3 types of diabetes insipidus and their causes?

A

1) central (neurogenic) : results from delay in ADH production or release
- cause: tumour, head injury, CNS infection

2) nephrogenic : results from inadequate renal response to ADH despite presence in adequate levels
- cause : drug therapy especially LITHIUM, renal damage or disease

3) Primary : results from excessive water intake
- cause: structural lesion in the thirst centre

27
Q

what are clinical manifestations of DI?

A
  • Increased polydipsia (thirst)
  • nocturnia
  • polyuria (increase urination)
  • CNS manifestations (irritability, mental dullness, coma)
28
Q

what test is given for DI?

A

water deprivation test watch YouTube video

  • baseline vital, weight, urine/plasma osmolality etc taken and all fluid withheld for 8-16 hours

these values are assessed q1h test continues until
1) urine osmolality stabilizes
2) body weight declines by 3%
3) orthostatic hypotension develops

then ADH is given and urine osmolality measured an hour later
1) If pts urinary osmolality increases significantly = central DI
2) No response to urinary osmolality = nephrogenic DI

29
Q

what are interprofessional care for central and nephrogenic DI

A

central:
- hormonal replacement with desmopressin acetate or vasopressin
- hypotonic solution saline (0.45%) titrated to replace urinary output

Nephrogenic:
- hormone replacement has little effect as kidneys are unable to respond to ADH
- DIETARY MEASURES (LOW SODIUM)
- thiazide diuretics (slow GFR and allow kidneys to increase sodium and water reabsorption)

30
Q

what are the 2 thyroid hormones and what do thyroid hormones do?

A

thyroid hormones regulate energy metabolism, growth and development

1) thyroxine (T4)
2) Tri-iodothyronine (T3)

31
Q

Discuss goitre

A

abnormal growth of the thyroid gland

  • happens in pt with hyperthyroidism such as Grave’s disease
    -over or under production of thyroid hormones
  • also lack of idodine in diet can cause this
32
Q

what is thyroiditis? 5 things

A

inflammation of thyroid gland caused by either

1) subacute granulomatous thyroiditis : caused by viral infection (ex: mumps, measles, adenovirus, URI)

2) acute thyroiditis : caused by bacterial or fungal infection

3) chronic autoimmune thyroiditis (Hashimoto’s thyroiditis) : can lead to hypothyroidism. also Hashimoto is where thyroid tissue is replaced by lymphocytes and fibrous tissue

4)Silent thyroiditis : a form of lymphocytic thyroiditis and has no apparent symptoms. Resembles hashimoto’s

5) Post party thyroiditis - occurs in women w/history of thyroid disease who have recently given birth. this also resembles hashimotos

33
Q

discuss hyperthyroidism/Grave’s disease

A

Hyperactivity or thyroid gland with sustained increase in synthesis and release of thyroid hormones

basically thyroid getting big an the excess thyroid hormone secretion = Grave’s disease

they develop abnormal antibodies that mimic TSH and send false signals to TSH receptors that stimulate release of T3, T4, or both

34
Q

what are clinical manifestations of hyperthyroidism/Grave’s disease

A
  • increase metabolism = weight loss
  • increase tissue sensitivity to SNS stimulation
  • Goitre
  • Bruits
  • Exophthalmos - redness in eye
35
Q

what are some complications of hyperthyroidism/Grave’s disease

A
  • thyrotoxic crisis (aka thyroid storm) meaning all symptoms are intensified
  • heart and nerve tissues become more sensitive to SNS activation (so severe tachycardia, hyperthermia etc)
36
Q

differentiate primary and secondary hypothyroidism

A

primary - from destruction of thyroid tissue or defective hormone synthesis

secondary - related to pituitary disease (decreased secretion of TSH) or hypothalamic dysfunction (decreased secretion of thyrotropin-releasing hormone - TRH)

37
Q

what is the most common cause of hypothyroidsm in general and Canada?

A

general - iodine deficiency

Canada- hashimotos disease

38
Q

what are symptoms of hypothyroidms

A
  • insidious and non specific SLOWING of body processes
  • myxoedema : accumulation of hydrophilic mucopolysaccharides in the dermis and other tissues
39
Q

what are complications of hypothyroidism

A

think SLOW symptoms

  • mental sluggish and drowsiness
  • Myxedema coma
40
Q

what are inter professional care for hypothyroidism

A

levothyroxine medication of choice for hormone replacement

41
Q

discuss parathyroid gland and its role

A

secretes parathormone (PTH)

major role is to regulate calcium and encourage release of calcium and phosphate in blood and hold when not needed.

1) when calcium or magnesium levels are low, PTH INCREASES

2) when calcium or magnesium levels are high, PTH decreases

42
Q

discuss hyperparathyroidism

A

increased secretion of parathyroid hormone (PTH)

caused by:
1) benign neoplasm/single adenoma (primary)

2) compensatory process to hypocalcémie (secondary)

3) kidney transplant for CRF (tertiary)

43
Q

what does over secretion of PTH mean?

A

hypercalcemia and hypophosphatemia

44
Q

what are symptoms of hyperparathyroidism?

A

check youtube

45
Q

what are some inter professional care?

A

surgical therapy - parathyroidectomy

non surgical therapy such as annual lab testing, bone density testing

46
Q

discuss hypoparathyroidism

A

uncommon and often related to accidental removal or destruction of vascular supply of parathyroid glands

47
Q

what does under stimulation of PTH mean?

A

hypocalcemia

48
Q

what are the clinical manifestations of hypoparathyroidism?

A

watch YouTube

49
Q

what are nursing managements?

A

1) treat acute complications (ex: tetany)

2) correct magnesium imbalance

50
Q

discuss adrenal cortex

A

3 main classifications of adrenal steroid hormones

1) glucocorticoids - regulate metabolism and stress (cortisol)

2) mineralocorticoids - regulate sodium and potassium (aldosterone)

3) androgens - contribute to growth and develop of both genders

51
Q

when someone says corticosteroid what do they mean?

A

they are referring to any of the 3 types of adrenal steroid hormones

52
Q

discuss Cushing’s syndrome

A

hypercortisolism

  • most often from ACTH secreting pituitary tumour but can also be caused by exogenous corticosteroids over long periods of time
53
Q

what is the most common symptom of bushings disease?

A

weight gain

but can also have unexplained hypokalemia, purplish striae

54
Q

why do we not do surgery for cushing’s?

A

surgery to adrenal glans is risky due to vascularity thus risk for hemorrhage

55
Q

discuss adrenocortical insufficiency

A

2 causes

1) primary cause (Addisons disease)
- supply of all 3 adrenal steroid hormones is reduced
- mostly bc of autoimmune

2) secondary cause (lack of ACTH secretion)
- mineralocorticoids is normal BUT corticosteroids and androgens are defecient

56
Q

how do we catch adrenocortical insufficiency

A

unfortunately, it is a slow onset issue

when it is caught, 90% of adrenal cortex is destroyed

57
Q

what’s a unique symptom to Addison’s disease?

A

skin hyperpigmentation

58
Q

what is a complication to adrenocortical insufficiency

A
  • adrenal crisis aka addisonian crisis : acute adrenal insufficiency

triggered by stress, sudden withdrawal of corticosteroid hormones

59
Q

what are manifestations of glucocorticoid and mineralocorticoid deficiencies?

A

hypotension, hyperkalemia, hyponatremia

60
Q

what is corticosteroid therapy used for?

A

1) anti-inflammatory

2) immunosuppresion

3) maintain BP

4) carbohydrate and protein metabolism

61
Q

discuss hyperaldesteronism

A

mostly caused by small solitary adrenocortical adenoma

62
Q

what are symptoms of hyperaldosteronism

A
  • sodium retention and elimination of potassium
    BUT be careful edema doesnt occurs became the rate of its excretion is higher than retention
63
Q

where would you see hyperaldosteronism

A

in pt’s with hypokalemia that are not being treated with diuretics