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Critical Care > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What 3 hormones does the thyroid gland produce?

A

T3, T4, and Calcitonin

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2
Q

What does calcitonin do?

A

Decreases serum calcium by taking calcium out of the blood and pushing it back into the bones.

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3
Q

T4 is increased and TSH decreased in what disorder?

A

Hyperthyroidism

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4
Q

What disorder causes an enlarged thyroid?

A

Hyperthyroidism, goiter

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5
Q

Which cardiac drug contains high levels of iodine and may affect thyroid function?

A

Amiodarone

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6
Q

Treatment for hyperthyroid?

A

methimazole (Tapazole), propylthiouracil (PTU) which stops the thyroid from making thyroid hormone. Used preoperatively to stun thyroid. Beta blockers, iodine compounds and radioactive iodine therapy.

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7
Q

What iodine compounds are given for hyperthyroid and why?

A

potassium iodine (SSKI and Lugol’s) to decrease size and vascularity of thyroid. Give in milk or juice and use a straw because it stains teeth!

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8
Q

What BP meds are used as supportive therapy for hyperthyroidism?

A

Beta blockers. These block epinephrine and norepinephrine (fight or flight) and decreases HR/BP/anxiety

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9
Q

Who should NOT receive beta blockers?

A

Asthmatics and diabetics. Beta blockers can hide symptoms of hypoglycemia.

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10
Q

What are important assessments after a thyroidectomy?

A

Bleeding! Report feelings of pressure, check behind neck for pooled blood.
Assess for laryngeal nerve damage by listening for hoarse/weak voice. This can lead to vocal cord paralysis and obstruction requiring trach.
Assess for parathyroid removal (hypocalcemia)

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11
Q

What causes increased TSH and decreased T4?

A

Hypothyroidism

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12
Q

What disease are people with hypothyroid at increased risk of developing?

A

Coronary Artery Disease (CAD)

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13
Q

What is tetany?

A

A medical sign consisting of involuntary contraction of muscles.

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14
Q

What two electrolyte disorders result from hyperparathyroidism?

A

hypercalcemia and hypophosphatemia

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15
Q

Signs and symptoms of hyperparathyroidism?

A

sedation/fatigue

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16
Q

What two electrolyte disorders result from hypoparathyroidism?

A

hypocalcemia and hyperphosphatemia

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17
Q

What is pheochromocytoma?

A

Benign tumors of the adrenal medulla that secrete epinephrine and norepinephrine in boluses causing episodes of increased BP/HR/palpitations/flushing/sweating/headache. Tends to run in families.

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18
Q

What tests diagnose pheochromocytoma?

A

Vanillylmandelic acid test (VMA) and metanephrine (MN) test. These tests are altered by anything with vanilla in it, vitamin B, fruit juice, bananas and caffeine.
Avoid stress prior to test!

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19
Q

How to take a 24 hour urine?

A

Throw away the first void and keep the last!

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20
Q

Avoid doing what assessment on patients suspected of pheochromocytoma?

A

Avoid palpating the abdomen as this can cause a sudden release of catecholamines (epi/norepi) and severe HTN.

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21
Q

What are glucocorticoids?

A

A steroid produced by the adrenal cortex that affects mood, can alter defense mechanisms (immunosuppression), helps to break down fats and proteins (which both regulate glucose metabolism), inhibits insulin.

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22
Q

What is Aldosterone?

A

A mineralocorticoid (steroid) produced by the adrenal cortex that causes you to retain sodium and water and lose potassium.

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23
Q

What are adrenocorticotropin hormones? ACTH

A

Hormones made in the pituitary that stimulate the adrenal cortex to make cortisol. If ACTH increases, cortisol increases.

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24
Q

What are the 4 biggest concerns with adrenal cortex problems?

A

1) Not enough steroids
2) shock
3) hyperkalemia
4) hypoglycemia

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25
Q

What is Addison’s disease?

A

Adrenocortical insufficiency. Not enough steroids!

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26
Q

What are signs and symptoms of Addison’s disease?

A

Extreme fatigue, nausea/vomiting/diarrhea, anorexia/weight loss, hypotension, confusion, decreased sodium, increased potassium, hypoglycemia, hyper-pigmentation (bronzing) of skin and mucous membranes vitiligo

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27
Q

What are treatments for Addison’s disease?

A

Combat shock caused by loss of sodium and water, increase sodium in the diet, I/O and daily weight, treat fluid volume deficit, monitor BP, give corticosteroids

*think: ADD steroids! Add fluids!

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28
Q

What is Addisonian crisis?

A

Severe hypotension and vascular collapse caused by infection/emotional stress/physical exertion/sudden stopping of steroids. Can cause hypoglycemia and hyperkalemia. LIFE THREATENING!

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29
Q

What is Cushing’s disease?

A

Too many steroids!

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30
Q

Signs and symptoms of Cushing’s?

A

Thin extremities, truncal obesity, buffalo hump, hyperglycemia, increased risk of infection, moon face, oily skin/acne, women with male traits, high BP, CHF, weight gain, fluid volume excess, low potassium

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31
Q

What is the treatment for Cushing’s?

A

Adrenalectomy. Will need lifetime steroid replacement. Provide a quiet environment (lessen stress), avoid exposure to infections
hint long term steroid use can lead to osteoporosis

32
Q

How do steroids decrease Ca?

A

By excreting it through the GI tract.

33
Q

What values are altered in the client on long term steroid therapy?

A

glucose and ketones

34
Q

Why are diabetics prone to infection?

A

The high levels of serum glucose provide an ideal environment for bacteria.

35
Q

When should diabetics exercise?

A

When blood sugar is highest.

36
Q

What drug should be discontinued before any procedure involving dye contrast?

A

Metformin

37
Q

Which insulin is clear?

A

Regular

38
Q

Which insulin is cloudy?

A

NPH

39
Q

Which insulin is drawn first?

A

Clear (reg)

40
Q

What is the standard insulin given IV?

A

regular

41
Q

Clients must eat before what kind of insulin?

A

rapid acting

42
Q

When should diabetics eat?

A

When insulin is at its peak.

43
Q

In diabetes, what is the concerning complication of illness?

A

DKA

44
Q

What is the only insulin type used in insulin pumps?

A

Rapid acting

45
Q

What delays glucose absorption?

A

Fat

46
Q

What is the 15-15-15 rule for hypoglycemia?

A

Eat or drink 15 grams of carbs, recheck in 15 mins, if needed repeat another 15 grams

47
Q

Avoid what when eating to combat hypoglycemia?

A

Fat - it slows absorption of glucose.

48
Q

What causes the presence of ketones in the urine?

A

Fat breakdown

49
Q

What are the 2 “hypo”’s to watch for during administration of insulin?

A

hypoglycemia and hypokalemia

50
Q

What do you anticipate the primary healthcare provider will add to the IV solution for a patient with DKA?

A

potassium

51
Q

What type of diabetes is at risk for DKA?

A

Type 1

52
Q

What is Hyperosmolar Hyperlycemic Nonketosis (HHNK)?

A

Similar to DKA but there is no acidosis. Seen in Type 2 diabetics. It is a hyperglycemic state with profound dehydration. There is no fat breakdown so there will be no ketones in the urine, no fruity breath and no Kussmaul respirations.

53
Q

What type of diabetes is at risk for HHNK?

A

Type 2

54
Q

Insulin decreases both sugar and ____?

A

Potassium

55
Q

Hourly _____ and _____ are important when treating both DKA and HHNK.

A

Outputs and sugar/potassium levels

56
Q

Will patients with DKA and HHNK need cardiac monitoring?

A

Yes, because of potassium fluctuations.

57
Q

What is a major concern with polyuria?

A

Shock (hemovolemic)

58
Q

What fluid will be given FIRST to diabetics with DKA or HHNK?

A

Normal Saline

59
Q

After blood sugar stabilizes to 250-300 mg/dL, what solution is used to replace NS and why?

A

D5W, another isotonic solution that helps prevent hypoglycemia.

60
Q

What are 2 major complications of diabetes?

A

Diabetic retinopathy (blindness) and nephropathy (leading to dialysis).

61
Q

What are some types of neuropathy (nerve damage) experienced by diabetics?

A

Sexual problems (decreased sensation), foot/leg problems, decreased sensation and paresthesias, neurogenic bladder, gastroparesis (delayed emptying, risk for aspiration)

62
Q

What is more dangerous, hypo or hyper glycemic?

A

Hypoglycemia

63
Q

What are S/S of hypoglycemia?

A

cold/clammy, confusion, shaky, headache, increased HR, nervousness, nausea, hunger

64
Q

What should a hypoglycemic client do?

A

Eat/drink a simple carb (soda, honey, etc)

65
Q

What is given when a client is unconscious and hypoglycemia is suspected?

A

D50W. This is hard to push and requires a large bore IV.

66
Q

If there is no IV access to push D50W, what is given IM?

A

Glucagon (GlucaGen)

67
Q

When is rapid-acting insulin given?

A

Before meals, to cover the food eaten,

68
Q

What is the most widely used oral anti-diabetic medication?

A

Metformin (Glucophage)

69
Q

What is the role of insulin?

A

It carries glucose out of the blood and into the cell.

70
Q

In Type 1 diabetes, what is destroyed?

A

Beta cells in the pancreas. Type 1 diabetics have little or no insulin.

71
Q

What are the 3 “P”s of diabetes?

A

polyuria (diuresis), polyphagia (hunger), polydipsia (thirst)

72
Q

What is the difference between Type 1A and Type 1B?

A

Type 1A is autoimmune response, Type 1B is idiopathic.

73
Q

What happens to the blood when glucose builds up in Type 1 diabetes?

A

It becomes hypertonic, pulling fluid into the vascular space. The cells begin to starve as the kidneys excrete excess glucose and fluid (causing diuresis and glucose in urine). Starving cells turn to protein and fat, which releases ketones (acid) leading to metabolic acidosis. Kussmaul respirations are a response by the lungs to correct the acidosis.

74
Q

What type of diabetics are oral anti-diabetics and non-insulin injectables prescribed for?

A

Type 2

75
Q

Will oral anti-diabetic medication work for Type 1?

A

No, they must have insulin.

76
Q

What do extremes in blood sugar do?

A

Cause vascular damage

Critical Care (10 decks)

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