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NURS 503 > Endocrine disorders > Flashcards

Endocrine disorders Flashcards

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1
Q

What are adrenal disorders marked by?

A

Due to changes in the adrenal gland itself, from the hypothalamic, or pituitary gland dysfunction or through exogenous cause

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2
Q

What three main hormone types are secreted from the adrenal gland?

A
  • Glucocorticoid - cortisol
  • Mineralocorticoid - aldosterone
  • Androgen hormones - male hormones
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3
Q

What are the three most prevalent types of adrenal gland disorders?

A
  • Addison’s disease
  • Cushing’s syndrome
  • Pheochromocytoma
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4
Q

What causes Addison’s disease?

A

Low cortisol secretion

  • Due to autoimmune disturbances (70%), physiologic stress, TB
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5
Q

Symptoms of Addison’s disease

A
  • Chronic malaise
  • Dizziness, nausea, chronic abdominal pain
  • Muscle cramps
  • Hyperpigmentation
  • Decreased libido
  • Weight loss, salt craving
  • Decreased axillary and pubic hair with altered menses (low androgens)
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6
Q

What causes Cushing’s syndrome?

A

Overproduction of cortisol or excess ACTH from the pituitary gland

  • Can be caused by exogenous medications
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7
Q

Symptoms of Cushing’s syndrome

A
  • Rapid weight gain
  • Loss of menses
  • Decreased libido
  • Weakness, bruising
  • HTN
  • Glucose intolerance
  • Insomnia
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8
Q

What causes pheochromocytoma?

A

Catecholamine-secreting tumor of chromaffin (pheochromocyte) cells

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9
Q

Symptoms of pheochromocytoma

A
  • Headache
  • Diaphoresis
  • Palpitations
  • Secondary HTN
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10
Q

Findings on physical exam for Addison’s disease

A
  • Appears chronically ill
  • Exhibits weight loss
  • Dehydration
  • Increased skin pigmentation on light exposed skin folds
  • Darkened creases on the palms, elbows, knees, lips
  • People of color have darkened mucous membranes
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11
Q

If a patient has Addison’s disease and has hypothyroidism, what changes need to be made to their levothyroxine dosage?

A

Levothyroxine metabolizes corticosteroids → need to be followed by endocrinologist

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12
Q

Findings on physical exam for patient’s with Cushing’s disease

A
  • Central obesity
  • Moon face
  • Thickening of facial fat
  • Buffalo hump
  • Increased supraclavicular fat pads, HTN, muscle weakness, wasting
  • Hirsutism, red-purple abdominal skin striae
  • Acne
  • Emotional lability or depression, “senile”, purpura on the hands, bruising
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13
Q

Findings on physical exam for patient’s with pheochromocytoma

A
  • New onset moderate to severe HTN (systolic pressures >170 mmHg)
  • Arrhythmias
  • Sinus tachycardia/bradycardia
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14
Q

Adrenal gland diagnostic studies

A
  • Adrenal antibody studies
  • Rule out TB
  • Medication review (screening for precipitant triggers)
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15
Q

Diagnostic studies specific for Addison’s disease

A
  • Will have elevated serum ACTH
  • Suppressed levels of cortisol
  • Hyponatremia
  • Hyperkalemia
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16
Q

Diagnostic studies specific for Cushing syndrome

A

Classically diagnosed by measurement of >100 mcg of cortisol in the urine during a 24 hour period

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17
Q

Diagnostic studies specific for pheochromocytoma

A

Elevated levels of fractionated metanephrines in urine or plasma

  • Collection during symptomatic episodes (e.g. diaphoresis, palpitations)
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18
Q

Addison’s disease management

  • Acute adrenal crisis
A

Hospitalization w/ IV corticosteroids and shock stabilization

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19
Q

Addison’s disease management

  • Chronic adrenal insufficiency
A

Managed outpatient with oral hydrocortisone in divided daily doses (20-30 mg) to allow restoration of a diurnal pattern

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20
Q

Cushing’s syndrome management

A
  • Daily ketoconazole which mitigates the impact of cortisol
  • Primary tumor resection
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21
Q

Pheochromocytoma management

A

Surgical treatment

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22
Q

What is the underlying cause of diabetes?

A

Group of metabolic disease characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both

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23
Q

Difference between type 1 DM vs type 2 DM

A
  • Autoimmune destruction of the beta cells within the islets of Langerhans in the pancreas in a genetically predisposed individual
  • Contributing to insulinopenia and lifelong dependence on exogenous insulin
  • Abrupt onset in infants and children; more gradual in adults
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24
Q

Difference between type 1 DM vs type 2 DM

A
  • Insidious onset
  • Decreased glucose uptake
  • Increased hepatic glucose production
  • Impaired insulin secretion
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25
Type 1 DM clinical presentation * Acute symptoms
* Polyuria, polydipsia, polyphagia * Weight loss * Blurred vision * Fatigue
26
Signs of ketoacidosis
* Glycosuria * N/V * Abdominal pain * Rapid shallow breathing * Hypotension * Dehydration
27
Type 2 DM clinical presentation
* May have no symptoms at first * Polyuria, polydipsia * Blurred vision * Fatigue * Slow healing wounds * Frequent infections or polyphagia * Weight loss * Tingling of hands and feet
28
DM physical exam components
* Neuro * Eyes * Derm * Thyroid * Cardiac * Abdominal
29
True/false: Diagnostic criteria for DM are based on the glucose threshold above which the risk of retinopathy is increased
True
30
Diagnostic studies: lab findings suggestive of DM
* A1c \>6.5% * Fasting plasma glucose \>126 mg/dL * 2 hour plasma glucose level \>200 mg/dL during oral glucose tolerance test
31
If a patient is asymptomatic, had normal blood work, and a normal PE for DM, what is the providers next steps?
Will need second positive test for a definitive diagnosis (can use the same blood sample twice) * Ex: if plasma glucose was 128 and patient was asymptomatic, provider can add A1c test from the same vial of blood
32
What test can be ordered to screen between type 1 DM vs type 2 DM?
C-peptide level
33
DM management
* Comprehensive annual exam → blood glucose, cardiac/BP, renal, endocrine/neuro, vision, derm monitoring * Encourage healthy diet and regular exercise * Review medications * Follow up every 3 months to check blood work
34
Should the provider be concerned about collecting labs with new diagnosis of type 1 DM?
Not as concerned about kidney and eye damage because of sudden onset → can do eye exam and check for micro kidney damage five years after diagnosis
35
Should the provider be concerned about collecting labs with new diagnosis of type 2 DM?
Will need to perform eye exam and assess for kidney damage at time of diagnosis (there is a gradual onset with type 2 DM so damage may have already been done)
36
What should be done for the patient with recurrent hypoglycemia episodes (blood sugars \<50)?
Need hospitalization
37
What is the definition of primary hyperparathyroidism?
Inappropriate secretion of PTH in the setting of hypercalcemia
38
What is the definition of secondary and tertiary hyperparathyroidism?
_Secondary_: increased secretion of PTH in the setting of low or normal serum calcium (can be caused by vitamin D deficiency or renal failure) _Tertiary_: prolonged secondary hyperparathyroidism in which hypercalcemia develops
39
What is the definition of hypoparathyroidism?
Inappropriately low or normal secretion of PTH in the setting of hypocalcemia
40
Primary hyperparathyroidism clinical presentation
Asymptomatic, but will have nonspecific symptom * Weakness * Easy fatiguability * Depression * Intellectual weariness * Cognitive impairment * Loss of initiative * Anxiety * Irritability * Insomnia * HTN, CAD * Kidney stones * Osteoarthritic findings
41
Secondary hyperparathyroidism clinical presentation
Calcium not properly absorbed * CKD * Vitamin D deficiency * Meds: PPI, glucocorticoids
42
Hypoparathyroidism clinical presentation
Perioral and digital paresthesia to life threatening cardiac arrhythmias, seizures, laryngospasm
43
Primary hyperparathyroidism physical exam components
* Band keratopathy on temporal borders of the cornea * Bone tenderness - tibia, sternum * Palpable neck mass
44
Hypoparathyroidism physical exam findings
* Chvostek's sign * Trousseau's sign
45
Parathyroid gland disorder diagnostic studies
* Bone mineral density assessment of a cortical bone site and lumbar spine/hip * Renal ultrasound * ECG
46
Parathyroid gland labs
* PTH - 2nd or 3rd generation assay * Serum calcium, creatinine, albumin, vitamin D, fasting phosphorus
47
Hyperparathyroidism management
ONLY cure for primary hyperparathyroidism → surgery * Refer to parathyroid surgeon
48
Hypoparathyroidism management
* Parenteral PTH * Calcitriol * Thiazides * Vitamin D supplementation * Encourage weight bearing exercises
49
What is the definition of a thyroid nodule?
A distinct lesion within the thyroid that is radiologically different from the rest of the thyroid
50
What is the definition of hyperthyroidism?
Thyroid hormone hyper secretion and increased metabolism * Graves disease is the most common cause
51
What is the definition of hypothyroidism?
Thyroid hormone reduced secretion and decreased metabolism
52
What is the definition of thyromegaly?
Localized nodules or generalized goiter (benign or malignant, solitary or multiple)
53
What lab findings can be seen with subclinical hyperthyroidism?
Decreased TSH and normal T3/T4 (vice versa for hypothyroidism)
54
Thyroid nodule clinical presentation
* Usually asymptomatic * Identified as a lump by patients or by providers during routine thyroid examinations * If toxic, will have symptoms of hyperthyroidism
55
Hyperthyroidism clinical presentation
* Weight loss * Difficulty sleeping * Tremor * Irritability * Menstrual irregularity * Tachycardia/palpitations/Afib * Proptosis, periorbital edema * ***Thyroid gland diffusely enlarged with soft texture/well-delineated border***
56
What levothyroxine changes will have to be made for pregnant patients with hypothyroidism?
Increase levothyroxine dosage by 30%
57
Hypothyroidism clinical presentation
* Cold intolerance * Weight gain * Hoarseness * Puffiness of the face and hands * Heavy and irregular menstrual periods * Dry skin * Dry and brittle hair * Depression * Paresthesia * Muscle aches * ***Thyroid enlarged, firm, pebbly texture***
58
Thyroid gland disorder physical exam components
* Energy level * Mental status and facial affect * Inspect texture, color, general appearance of skin * Inspect and palpate thyroid gland for nodules (size, consistency, mobility) * Check for lymphadenopathy → supraclavicular, anterior cervical, submandibular * Cardiac and neuro assessment
59
Thyroid gland disorder diagnostic studies
* TSH testing - most sensitive marker of thyroid function * Serum T3 and T4 * Ultrasound * Thyroid cytology via FNA biopsy * Anti-TPO antibody levels for Graves
60
Thyroid gland management
* Biopsy for nodules * Thyroidectomy * Surveillance * Specialist consultation for central and severe cases * ED for myxedema coma
61
What is myxedema coma?
Untreated hypothyroidism * IV levothyroxine/glucocorticoid therapy, warming, ventilatory support * Medical emergency
62
Pharmacological therapy for hyperthyroidism
* Beta blockers (for Graves disease) * Thioamides - methimazole and PTU
63
Pharmacological therapy for hypothyroidism
Levothyroxine

NURS 503 (10 decks)

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