T3 Pituitary and Adrenal Glands Flashcards

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1
Q

Secrete hormones

Maintain cellular regulation

A

Pituitary and Adrenal Glands

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2
Q

Regulates growth, metabolism, and sexual development

A

Anterior pituitary*

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3
Q

Vasopressin (ADH)

A

Posterior pituitary*

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4
Q

Hormones are life sustaining

A

Adrenal gland

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5
Q

including fluid and electrolyte balance
When too much or too little of one or more hormones is secreted, physical and psychological changes occur

maintains fluid and electrolyte impbalance and is an antidiuretic hormone

A

Cellular regulation

Vasopressin

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6
Q
This hormone Secretes:
Growth hormone (GH)
Thyroid stimulating hormone (TSH)
Corticotropine (adrenocorticotropin hormone ACTH)
Follicle-stimulating hormone (FSH)
Luteinizing hormone (LH)
Melanocyte-stimulating hormone (MSH)
Prolactin (PRL)
A

Anterior pituitary

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7
Q

Deficiency of one or more anterior pituitary hormones
Selective hypopituitarism
Results in metabolic problems, sexual dysfunction

A

Hypopituitarism

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8
Q

—Decreased production of all anterior pituitary hormones and is rare

A

Panhypopituitarism*

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9
Q

Most life-threatening deficiencies

A

—ACTH and TSH*

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10
Q

Deficiency of gonadotropins changes What?

A

sexual function and sterility/infertility

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11
Q

increases rate of bone destruction and leads to osteoporosis

A

Growth hormone deficiency

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12
Q

ACTH, Adrenocorticotropic hormone; TSH, thyroid-stimulating hormone.
Gonadotropins include LH and FSH

Cause of hypo varies?

A

Can be tumors, malnutrition, shock, head trauma, infection, surgery, AIDS, or can be idiopathic

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13
Q

is the most common cause of pituitary infarction

A

Post partum hemorrhage

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14
Q

Hypopituitarism assessment

A
Assessment* (chart 62-1)
Changes in physical appearance
Organ dysfunction
Decreased libido
Changes is secondary sex characteristics
Menstrual cycle changes
Neuro changes
Visual changes

*Chart 62-1 lists each hormone and signs and symtpoms of deficiency

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15
Q

Tx and considerations/risks with Hypopituitarism

A

Lifelong replacement of deficient hormones

Androgen therapy for virilization; gynecomastia can occur

Estrogens and progesterone

Growth hormone

*Note risk of hypertension and thrombus when taking estrogen especially among smokers

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16
Q

Causes of Hyperpituitarism

A
  • Hormone oversecretion occurs with
  • Pituitary adenoma is most common cause
  • Benign tumor
  • Are classified by hormone secreted

*Tumors are most common in cells that produce GH, PRL, and ACTH

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17
Q

Onset of growth hormone hypersecretion before puberty

The clinical features of growth hormone (GH) excess.

Robert Wadlow, the “Alton giant,” weighed 9 pounds at birth but grew to 30 pounds by the time he was 6 months old. By his first birthday, he had reached 62 pounds. At the time of his death at age 22 from cellulitis of the feet, he was 8 feet, 11 inches tall and weighed 475 pounds.

A

Gigantism

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18
Q

Growth hormone hypersecretion after puberty

A

Acromegaly

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19
Q

The progression of acromegaly.
Onset?

S/s?

Reversible?

A

Onset may be gradual with slow progression
Early detection is essential
Signs include enlargement of face, hands, and feet, increased skeletal thickness, enlarged organs.
May be reversible if caught early (skeletal changes are permanent)

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20
Q

Assessment*: Hyperpituitarism: Acrogmegaly/increased hormones

A
Chart 62-2
Ask about changes in hat, glove, shoe size
Headaches
Changes in appearance
MRI is best imaging
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21
Q

Acrogmegaly tx :

Expected outcomes:

A

Expected outcomes: return to normal or near normal hormone levels and reduce symptoms

Nonsurgical management

Drug therapy (Parlodel, Dostinex, Permax, Sandostatin, Somavert)

Radiation -isn’t instant treatment. May take months or years to see benefits

Gamma knife procedure

Drug therapy can be used in combination with surgery and/or radiation

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22
Q

Acromegaly surgical management

A

The transsphenoidal surgical approach to the pituitary gland. Called hypophysectomy

Selective adenomectomy leaves normal pituitary tissue undisturbed.

23
Q

Post op care for hypophysectomy

Patient teaching?

A

Monitor neurologic response

Assess for postnasal drip

Elevate head of bed

Assess nasal drainage
-Halo sign

Assess for meningitis

Numbness in the area of the incision

Decreased sense of smell

Level of consciousness, visual changes
Observe for CSF leak by salty taste to postnasal drip or halo sign

Avoid coughing
Avoid bending
Avoid straining at stool
Avoid toothbrushing
Vasopressin and hormone replacment

Keep HOB elevated
No straws
Drink to thirst

24
Q

Water metabolism problem caused by an ADH deficiency *(either decrease in ADH synthesis or inability of kidneys to respond to ADH)
Results in large volumes of dilute urine *

Distal kidney tubules and collectin ducts do not reabsorb water

Classifications
Nephrogenic
Primary
Secondary
Drug-related
A

DIABETES insipidus

25
Q

Classifications of DI

A
Classifications
Nephrogenic
Primary
Secondary
Drug-related
26
Q

DI Assessment/ s/s

A

Symptoms of dehydration
Increase in frequency of urination and excessive thirst
Urine diluted with low specific gravity (<1.005)
Urine output may be anywhere from 4-30 L/24 hours (up to 1250 ml/hr)

Water loss increases plasma osmolality and increases sodium levels. Thirst mechanism is essential. Must have access to water

27
Q

DI interventions

Lab to monitor?

Pt teaching?

Drugs?

A

Management focuses on managing symptoms with drug therapy.

If weight gain is more than 2.2 lbs along with other symtpoms such as headache, confusion, nausea, vomiting, patient should go to ER

Desmopressin acetate* is preferred drug
Early detection of dehydration and maintenance of adequate hydration*

DDAVP can be given IV, oral, nasal

Lifelong vasopressin therapy with permanent condition

Wear medic alert bracelet

Teach patients to weigh themselves daily to identify weight gain.*

In hospital: monitor spec grav lab

28
Q

Which statements made by a client who has diabetes insipidus indicates to the nurse that more teaching is needed?

A: If I gain more that 2 lb in a day I’ll limit my fluid intake
B: If I become thirstier, I’ll take another dose of the drug
C: I’ll avoid aspirin and aspirin containing substances
D: I’ll stop taking the drug for 24 hours before I have any dental work performed
E: I’ll limit by intake of salt and sodium to no more than 2 g daily
F: I’ll wear my medical alert bracelet at all times

A

A,C,D,E

29
Q

Vasopressin secretes even when plasma osmolarity is low or normal.

Feedback mechanisms do not function properly.

Water is retained, results in hyponatremia (decreased serum sodium level) and fluid overload.*

A

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)*

30
Q

Causes of SIADH

A
Recent head trauma
Cerebrovascular disease
Tuberculosis or other pulmonary disease
Cancer
Drug use
31
Q

S/s of SIADH?

A

Related to water retention and dilution of serum sodium*

Gi disturbances
-Loss of appetite, N/V

With extreme low sodium* (<115 meq/L)
-Lethargy, headaches, decreased level of consciousness, seizures, and coma

Bounding pulse

Hypothermia -caused by central nervous system dysfunction

Increased urine spec grav*

32
Q

SIADH interventions

A

Fluid restriction
-500-1000 mL/24 hr

Drug therapy (diuretics, hypertonic saline, demeclocycline)

Monitor for fluid overload
-Daily weightslllkpc/l/l.

Safe environment

Neurologic assessment

33
Q

Adrenocortical steroids may decrease from inadequate secretion of ACTH*.

Dysfunction of hypothalamic-pituitary control mechanism

Direct dysfunction of adrenal tissue

Addisonian crisis vs. Addison’s disease*

A

Adrenal gland hypofunction

34
Q

One hormone in the pituitary is ???? This stimulates the adrenal glands.

Insufficiency of the hormones leads to ???

A

ACTH (adrenocorticotropic hormone).

loss of aldosterone and cortisol.

35
Q

Adrenal Insufficiency: life threatening*
Need for cortisol and aldosterone is greater than supply*
Response to stress*
Surgery
Trauma
Infection
Unless treated sodium falls and potassium rises rapidly

Problems are the same as with chronic insufficiency but are more sever
Unless intervention is initiated promptly, sodium levels fall and potassium levels rise rapidly. Severe hypotension results

A

Addisons crisis

36
Q

Assesment of Addison’s

A
Muscle weakness
Fatigue
Joint pain
a/n/v
Salt cravings
Hyperpigmentation
Hypotension
Hypoglycemia
Hyponatremia
Hyperkalemia

Decreased cortisol results in hypoglycemia

Gastric acid production decreases

Glomerular filtration rate decreases leading to excessive BUN

Potassium excretion is decreased causing hyperkalemia.

37
Q

Addisons dx/ labs?

A
Lab findings:
Low serum and salivary cortisol*
Low fasting blood sugar
Low sodium
High potassium
High BUN
38
Q

Addisons interventions

A

Promote fluid balance

Monitor for fluid deficit

Prevent hypoglycemia*

Assess cardiac function

Weigh patient daily

Hormone replacement*

  • Prednisone
  • Fludrocortisone (Florinef)
39
Q

Hypersecretion by adrenal cortex results in Cushing’s syndrome/disease, hypercortisolism, or excessive androgen production.*

A

Adrenal gland hyper function

40
Q

Adrenal gland hyper function cause

A

Can be caused by adrenal cortex itself, problems in anterior pituitary, or problem in hypothalamus.
Glucocorticoid use can cause hypercortisolism

41
Q

S/s of Cushing’s syndrome

A

Sign and symptoms*—skin changes, buffalo hump, moon face, acne, striae, hirsutism cardiac changes, musculoskeletal changes, glucose metabolism, immune changes

Increase in body fat, truncal obesity

Muscle wasting and weakness

Cardiac changes from sodium and water retention leading to hypervolemia and edema, high BP, and full and bounding pulses

Glucose is high because liver release glucose and insulin receptors are less sensitive.

Reduced immunity: excess cortisol reduces the number of circulating lymphocytes
Patient may not have fever or redness

Emotional instability, mood swings, irritability, depression

42
Q

Cushing s labs dx

A
Lab Values
Blood, salivary, and urine cortisol levels will be high*
Late night salivary cortisol
Hyperglycemia
Decreased lymphocytes
Increased sodium
Decreased calcium
43
Q

Cushing s disease priority

A

The priority problems for patients with Cushing’s disease or
Cushing’s syndrome are*
-
-Fluid overload due to hormone-induced water and sodium retention
-Potential for injury due to skin thinning, poor wound healing, and bone density loss
-Potential for infection due to hormone-induced reduced immunity
-Potential for acute adrenal insufficiency

44
Q

Tx and nursing interventions for cushings

A

Restore fluid balance

Reduce skin breakdown

Meds to decrease cortisol
-Metyrapone, ketoconazole, periactin

Nutrition: fluid restriction, sodium restriction, -high calorie*

Daily weights*

Surgical: hypophysectomy or adrenalectomy

-Hormone replacement if pituitary or adrenals are removed

45
Q

Catecholamine-producing tumors arising in the adrenal medulla

Usually occur in one adrenal gland but can be bilateral or in the abdomen

Tumors produce, store, and release epinephrine and norepinephrine.*

Usually benign

Cause is unknown

Although they are benign, they must be removed to prevent life threatening complications

A

Pheochromocytoma

46
Q

Pheochromocytoma s/s or assessment

A

Intermittent episodes of hypertension-HTN can range from few minutes to several hours

Severe headaches

Palpitations

Diaphoresis and flushing

Sense of impending doom

Chest pain

N/V

47
Q

What can induce HTN in Pheochromocytoma

A

Increased abdominal pressure, defecation, vigorous abdominal palpation can provoke hypertensive crisis*

Drugs such as tricyclic antidepressants, glucoagon, metoclopramide, naloxone can induce hypertensive crisis

Tyramine (found in aged cheese and wine, etc) can also induce hypertension

48
Q

Interventions for Pheochromocytoma

A

Surgery is the main treatment*

Adrenalectomy

Monitor for blood pressure changes

Monitor for hypovolemia

If inoperable: alpha and beta adrenergic blockers

49
Q

A 56-year-old woman is admitted to the ED with a blood pressure of 168/92 and reports of fatigue and muscle weakness. She has bruising on her arms and 2+ swelling in her ankles. Her weight has gone from 150 to 185 lbs over the past 6 months. Assessment reveals that she has truncal obesity and thin extremities.

Which diagnosis does the nurse suspect?

Hyperpituitarism (acromegaly)
Hypercortisolism (Cushing’s disease)
Hyperaldosteronism (Conn’s syndrome)
Adrenal insufficiency (Addison’s disease)

A

ANS: B

The patient’s manifestations of elevated blood pressure, fatigue, muscle weakness, bruising, dependent edema, weight gain, and truncal obesity with thin extremities are all key features of hypercortisolism, or Cushing’s disease. Other manifestations of Cushing’s disease include “moon face,” “buffalo hump,” osteoporosis, and thinning skin with striae.

50
Q

The patient is admitted to the acute medical care unit for a workup for Cushing’s disease. When she is assessed, she is found sitting at the bedside crying. She states, “I just don’t know what to do. I feel so confused and down in the dumps.”

What is the nurse’s best response?

“Would you like to speak with a pastor or priest?”
“Have you experienced this kind of confusion before?”
“It’s going to be fine. We’ll find out what’s wrong and take care of it.”
“Have you noticed if your mood goes quickly from happy to sad?”

A

ANS: D

Hypercortisolism can result in emotional lability, including mood swings, irritability, confusion, and depression. Asking this question helps in performing a psychosocial assessment of the patient.

51
Q

The student nurse is creating a care plan for the patient. Which priority problems should be the focus of the care plan? (Select all that apply.)

Fatigue
Fluid overload
Sleep deprivation
Potential for infection
Predisposition to injury
A

ANS: B, D ,E

Fluid overload, risk for injury, and inadequate nutrition are common problems in patients with Cushing’s disease. Sleep deprivation and fatigue are additional possible focus areas, but not as essential as the other three.

52
Q

During evening shift, the patient’s MRI reveals the presence of a pituitary adenoma. The following day, surgery is performed to remove the tumor.

What is the nurse’s priority concern for the patient postoperatively?

Airway management
Assessing for systemic infection
Monitoring for neurologic changes
Development of transient diabetes mellitus

A

ANS: C

Removal of a pituitary adenoma is completed by a transsphenoidal hypophysectomy. Postoperatively, it is essential to monitor the patient for neurologic response, documenting changes in vision, mental status, level of consciousness, or decreased strength in the extremities.

53
Q

Which key interventions should be implemented postoperatively for the patient after undergoing a hypophysectomy? (Select all that apply.)

Report any postnasal drip.
Keep the head of the bed elevated.
Have the patient avoid coughing soon after surgery.
Monitor for a light-yellow color at the edge of clear drainage.
Instruct the patient to take thyroid and glucocorticoid replacement for at least 6 months.

A

ANS: A, B, C, D

After hypophysectomy, the patient will need thyroid and glucocorticoid replacement for the rest of her life.