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Med/Surg 1 > Endocrine System > Flashcards

Endocrine System Flashcards

1
Q

What is Addision’s Disease?

A

disorder caused by damaged adrenal glands that cant produce enough cortical hormones

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2
Q

What does Addison’s disease result in?

A

Deficiency of:

  1. Cortisol
  2. Aldosterone
  3. Adrenal Androgens
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3
Q

Manifestations of Cortisol Insufficiency

A
  1. Decreased Liver Fx
  2. Decreased stomach enzymes
  3. Hyperpigmentation
  4. Hypoglycemia
  5. N/V/D
  6. Lethargy/Weakness
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4
Q

Manifestations of Aldosterone Insufficiency

A
  1. Dehydration
  2. Hyponatremia
  3. Orthostatic hypotension
  4. Hypovolemic shock
  5. Hyperkalemia (arrhythmias)
  6. Syncope
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5
Q

Adrenal Gland Disorders

A

Cushing’s syndrome

Addison’s disease

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6
Q

Pituitary Gland Disorders

A

SIADH

Diabetes Insipidus

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7
Q

What are functions of thyroid gland?

A
  1. Produce/stores/release TH
  2. Increase metabolism
  3. Promote growth
  4. Very vascular
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8
Q

An increase of ACTH causes

A

hyperpigmentation

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9
Q

What are androgens (Sex Hormones) and what do they do?

A
  1. Testosterone, Estrogen, Progesterone

2. Aid in growth & development

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10
Q

Over-secretion of androgens lead to

A

masculinization/male features

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11
Q

What happens when cortisol/glucocorticoids are increased?

A
  1. Glucose increase
  2. Fatty acid production is increased
  3. Increase protein breakdown
  4. Anti-inflammatory effects
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12
Q

What is Grave’s disease? (pathophysiology)

A
  1. Autoimmune disorder

2. Antibodies bind to TSH which cause over stimulation of TH (T3 & T4)

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13
Q

What is the relationship between hyperthyroidism and the clinical manifestations?

A

Everything is sped up

HYPERthyroidism

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14
Q

Clinical Manifestations of Hyperthyroidsim

A
  1. Hypertension
  2. Increased appetite,
  3. Tachycardia
  4. Increased Metabolism –> weight loss
  5. Angina/HF
  6. Hyperactive bowels and Diarrhea
  7. Nervousness
  8. Exophthalmos*
  9. Goiter
  10. Amneorrhea (no period)
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15
Q

What is exophthalmos? How is it caused? Characteristics?

A
  1. Edema & inflammation behind eyes; pressure pushes eyes outward
  2. Too much TH forces eye out
  3. Permanent symptom even with hyperthyroid treatment
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16
Q

Major concern if patient has a goiter

A

Airway!!

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17
Q

How is hypothyroidism treated?

A
  1. Meds (Methimazole & Propylthiouracil)

2. Radioactive Iodine

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18
Q

Why is radioactive iodine given preop?

A

to make thyroid gland less vascular to decrease risk of hemorrhaging/bleeding

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19
Q

Why is thyroid replacement needed after RAI?

A

RAI destroys thyroid-producing cells which reduces TH production

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20
Q

Nursing Interventions for RAI Therapy

A
  1. Patient must be isolated for 2-3wk
  2. Set time frame for being in room
  3. Everything remains in room because considered radioactive
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21
Q

Why is propranolol administered with anti-thyroid meds?

A

Hyperthyroidism inc BP/HR.

Betablockers used to decrease BP & HR

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22
Q

Why is iodine solution given 10 days prior to thyroidectomy?

A

To put patient in euthyroid state to decrease risk for thyroid storm

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23
Q

What is thyroidectomy used for? What is needed following thyroidectomy?

A

To treat thyroid cancer

Lifelong hormone replacement since removing thyroid gland

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24
Q

Nursing Interventions for Post Op Thyroidectomy

A
  1. Support Head/Neck (prevents hemorrhaging that can cause airway block)
  2. Voice checks (want to rest voice but need to ensure no vocal cord damage)
  3. Perform eye care (expothalmos = high risk for infection)
  4. Monitor for infection/BP/HR/RR
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25
Q

What are complications of thyroidectomy?

A
  1. Hemorrhaging
  2. Respiratory Obstruction
  3. Hypocalcemia
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26
Q

Why is hypocalcemia a complication of thyroidectomy?

A
  1. Parathyroid is on thyroid glands
  2. Parathyroid regulates calcium
  3. Remove thyroid gland, may remove parathyroid, thus causing hypocalcemia
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27
Q

Signs of Hypocalcemia

A
  1. Positve Chvostek (twitching)
  2. Positive Trousseau (flexion of wrist and elbow, extension of finger)
  3. CATS
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28
Q

How is hypocalcemia treated?

A

Calcium glucaonate via IV if severe

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29
Q

How is calcium gluconate given and why?

A

Via central line to prevent vasospasm

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30
Q

What is the most common cause of hypothyroidism?

A

Hashimoto’s thyroiditis

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31
Q

Primary causes of hypothyroidism

A
  1. Defect in thyroid gland
  2. Thyroidectomy
  3. Hyperthyroidism treatment
  4. Hashimito disease (autoimmune)
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32
Q

Secondary causes of hypothyroidism

A
  1. TSH deficiency

2. resistance to TH

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33
Q

If hypothyroidism is caused by thyroid issue, what hormone levels would you expect?

A
  1. Decreased T3 & T4

2. Increased TSH

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34
Q

If hypothyroidism is caused by pituitary/hypothalamus issue, what hormone levels would you expect?

A

Decreased TSH

35
Q

What is the relationship between hypothyroidism and the clinical manifestations?

A

Everything is slow like a hippo

1. Bradychardia, decreased cardiac output, hypotension, slow metabolism (weight gain)

36
Q

Other clinical manifestations of Hypothyroidism

A
  1. Increased atherosclerosis (elevated lipid and plaque build up)
  2. Low serum iron and folate
  3. intolerance to cold
  4. Dry/coarse hair
  5. Depression
37
Q

What causes myxedema coma?

A

No production of thyroid hormone

38
Q

Manifestations of Myxedema Coma

A
  1. Metabolic rate is severely decreased (alot of weight gain)
  2. LOC decrease
  3. Hypoventilaiton
  4. Hypothermia (low body temp)
  5. Hypotension
  6. CV collapse, shock
39
Q

How is myxedema treated?

A
  1. Life support
  2. IV thyroxine/glucose/corticosteroids
  3. Fluids to increase BP
40
Q

Nursing Interventions for Myxedema Coma

A
  1. Monitor for increasing severity
  2. Reposition patient
  3. Ventilator support
  4. Avoid hypnotic/sedative
  5. Give thyroxine with extreme caution can cause angina
41
Q

How is hypothyroidism treated?

A

Low dose levothyroxine

42
Q

Pearls for Levothyroxine

A
  1. Too much can cause hypertension/tachycardia
  2. Use cautiously with anticoags (inc bleeding risks)
  3. NEVER substitute for generic form, not bioequivalent
43
Q

Hormones released by Adrenal Gland Medulla

A
  1. Androgens (Estrogen/Testosterone)
  2. Catecholamines (Epi & Norepi)
  3. Peptiedes (Somatostatin & Sub P)
44
Q

Hormones released by Adrenal Gland Cortex

A

Glucocorticoids (Cortisol/Cortisone)

Mineralocorticoids (Aldosterone/Corticosterone)

45
Q

What causes Cushing’s syndrome?

A

Adrenal gland produces too much glucocorticoids and androgens because there is an excess ACTH release by pituitary

46
Q

What causes Cushing’s syndrome?

A
  1. Chronic use of steroid meds
  2. Pituitary Tumors (cause excess ACTH)
  3. Adrenal tumors
  4. Lung cancer (can produce ACTH)
47
Q

Most common cause of Cushing’s syndrome?

A

Stopping medications abruptly

48
Q

Relationship between pituitary gland and Cushing’s syndrom

A
  1. Pituitary releases ACTH that triggers the adrenal gland to release corticosteroids
  2. Hyperfunction of ACTH = excess corticosteroids
49
Q

Clincal Manifestations of Cushing’s syndrome

A
  1. Impaired carb metabolism –> increased glucose production
  2. Increased protein catabolism (muscle weakness, poor wound healing, easily bruised skin)
  3. Reduced inflammatory response (increase risk for infection)
  4. Obesity/Moon face/buffalo bump
  5. Increased stomach acid (more risk for GERD)
  6. Sodium retention
50
Q

How would a HCP confirm Cushing’s syndrome?

A
  1. Elevated cortisol levels
  2. 24 hour unrinary free cortisol levels would be elevated
  3. ACTH suppression/48h dexamethasone test results would be elevated
  4. Cortisol levels would remain elevated in the evening
51
Q

How is Cushing’s treated?

A
  1. Mitotane
  2. Aminiogluthemide
  3. Adrenalectomy
52
Q

Mechanism of action for Mitotane and Aminogluthemide

A
  1. Mitotane: destroys cancerous cells
  2. Aminogluthemide: blocks production of adrenal steroids (neg feedback –> pituitary cant release ACTH then ACTH cant trigger release of corticosteroids)
53
Q

When would Adrenalectomy be treatment of choice?

A

If Cushing’s is caused by adrenal cortex tumor

54
Q

Nursing Interventions for Adrenalectomy

A
  1. Monitor electrolytes (K & Na)
  2. Increase Na intake b/c removing adrenal gland
  3. Monitor for infection (at high risk)
  4. Monitor cortisol levels (will need lifelong replacement if adrenal glands are removed)
55
Q

Nursing Interventions for Cushing’s syndrome

A

Monitor blood glucose (Insulin therapy to keep glucose down)
Monitor daily weight ( may be elevated due to fluid retention)
Monitor BP and HR
Watch for signs of infection
Avoid injury
Administer calcium, vitamin D per orders (risk for ostreoporosis

56
Q

What is pheochromocytoma and what does it cause?

A
  1. Tumor of the adrenal medulla

2. Excessive production of catecholamines (epinephrine/norepinephrine)

57
Q

What are the S/S of Pheochromocytoma?

A

5 H’s

  1. Hypertension
  2. Headache
  3. Hyperhydrosis,
  4. Hypermetabolism
  5. Hyperglycemia
58
Q

Effect of catecholamines on the body

A
  1. Norepinephrine (inc BP and peripheral resistance)

2. Epinephrine ( inc HR, BP, CO and pupil/bronchi dilation)

59
Q

How is Pheochromocytoma diagnosed?

A
  1. Family Hx
  2. CT/MRI to show tumor location
  3. Catecholamines in urine & plasma
  4. Clonidine suppression test (clonidine not surpassed and epi/norepi remains elevated)
  5. Hyperglycemia/glucosuria (high epic = inc conversion of glycogen to glucose)
60
Q

Nursing Management for Pheochromyctoma

A
  1. Control HTN with prazosin/nifedipine
  2. Propranol to control HR
  3. Adrenalectomy
  4. Monitor BP closely
  5. Monitor for Addisonian crisis
  6. Restrict coffee/tea/chocolate/alcohol/bananas prior to catecholamine test
61
Q

Why is adrenalectomy a high surgical risk for pheochromayctoma patients?

A

Tumor manipulation can cause overproduction of catcecholimines which leads to hypertensive crisis

62
Q

What causes Addison’s disease?

A
  1. Autoimmune
  2. HIV & TB (pathogens attack)
  3. Hemorrhage
  4. Tumor
  5. Adrenelectomy
63
Q

How soon can Addisonian Crisis develop?

A

24-48h

64
Q

What triggers Addisonian Crisis?

A
  1. Stress (biggest trigger)
  2. Infection
  3. Trauma
  4. Sudden withdrawal of replacement hormones
65
Q

S/S of Addisonian Crisis

A
  1. Sudden Pain (low back, leg, abdominal)
  2. Severe N/V/D
  3. Confusion, Fever, Cyanosis
  4. Volume depletion –> Hypotension
  5. Can lead to shock
66
Q

Long Term treatment of Addisoninan Crisis

A

Fludrocortisone (corticoid replacement)

67
Q

Acute Treatment of Addisonian Crisis

A
  1. Monitor BP/Pulse/Weight/Fatigue
  2. Administer/Encourage fluids to help with hypotension
  3. Administer Hydrocortisone IV?IM then IV fluids, vasopressors and sodium
  4. Administer dextrose IV for sever hypoglycemia
  5. Correct electrolytes (Na will be decreases and K would be elevated)
  6. Administer antibiotics prophalytically
68
Q

What hormones are released by posterior pituitary gland?

A
  1. ADH, Vasopressin

2. Oxytocin

69
Q

What hormones are released by anterior pituitary gland?

A
  1. GH
  2. ACTH
  3. TSH
  4. FSH & LH
  5. Prolactin
70
Q

What is the function of ADH?

A

stimulate reabsorption of water from urine in kidneys when serum osmolality is concentrated/high

71
Q

High serum osmolality leads to

A
  1. ADH release

2. Urine output decreases

72
Q

Low serum osmolality leads to

A
  1. ADH withheld

2. Urine output will increase

73
Q

What occurs with too much ADH? Too little ADH?

A
  1. Too Much = SIADH

2. Too Little = DI

74
Q

Manifestations of SIADH

A

Occur as result of water retention

  1. Hyponatremia (leads to water intoxication)
  2. Serum Hypo-osmolality
  3. Confusion/Nausea/Irritabilty if Na <125
  4. Seizures/Coma if Na <115
75
Q

What causes SIADH

A
  1. Tumors that release ADH
  2. TB infection
  3. Head injury
  4. Diuretics
76
Q

What lab values would you expect for an SIADH patient? And why?

A

> 1.030

SIADH have concentrated urine specific gravity because retaining fluid will be high

77
Q

How is SIADH treated?

A
  1. Restrict fluids (1L/day)
  2. Monitor Na levels/Na replacement
  3. Hypertonic Saline Solution if severe hyponatremia
  4. Diuretics (furosemide) to correct hypo-osmolality
  5. Demeclocycline (antibiotic with polyuria side effect)
78
Q

What causes Diabetes Insipidus?

A
  1. Brain tumors/onfection
  2. Closed head trauma with increased ICP
  3. Secondary to medications (phenytoin/lithium)
79
Q

How soon will DI appear following head injury?

A

3-6 days

80
Q

Manifestations of Diabetes Insipidus

A
  1. Polyuria
  2. Polydipsia
  3. Dehydration
  4. Hypernatremia
  5. Decreased BP
  6. Increased HR
81
Q

What trends would you expect to see in lab values for a DI patient?

A

Decreased:

  1. Urine specific gravity
  2. Urine Osmolality
  3. Urine sodium

Increased:

  1. Serum Osmolality
  2. Serum Sodium
82
Q

Treatment/Intervention of Diabetes Insipidus

A
  1. Administer IV hypotonic solutions
  2. Encourage fluids
  3. Replace ADH hormones with desmopressin
  4. Monitor serum and urine labs
    5 Monitor weight and I&Os (determines if dehydration has been corrected)
83
Q

Normal Values for ADH; Specific Gravity (urine); Urine Osmolality ; Urine Sodium ; Serum Osmolality; Serum Sodium

A
  1. ADH: 1-5
  2. Urine Specific Gravity: 1.005-1.030
  3. Urine Osmolality: 200-800
  4. Urine sodium: 75-200
  5. Serum Osmolality: 275 - 290
  6. Serum Sodium: 135 - 145

Med/Surg 1 (3 decks)

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