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MS 2 > ADRENAL DYSFUNCTION > Flashcards

ADRENAL DYSFUNCTION Flashcards

1
Q

Located at the top of Kidneys

A

Adrenal Gland

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2
Q

Divided into the adrenal cortex and adrenal medulla

A

Adrenal Gland

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3
Q

Adrenal Cortex is refferred as

A

Adrenocortical hormones

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4
Q

Adrenal Medulla is referred as

A

Adrenomedullary Hormones

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5
Q

The Adrenocortical Hormones

A

Sugar (Glucocorticoids
Salt (Mineralocorticoids
Sex (Sex Hormones)

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6
Q

Adrenomedullary Hormones

A

Catecholamines
-Epinephrine
-Norepinephrine

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7
Q

Glucocorticoids involves mainly cortisol, what is the function of glucocorticoids?

A

-Norepinephrine sensitizer
-Increased bone demineralization
-Secretion of gastric acid
-Immunosuppression (anti-inflammatory)
-Glucose elevation
-Adipose redistribution

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8
Q

Mineralocorticoids involves mainly aldosterone, what is the function of mineralocorticoids?

A

Pro-Sodium, Anti-Potassium

-Retains Sodium
- Excretes potassium and hydrogen

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9
Q

Sex hormones involves mainly androgen, what is the function of sex hormones?

A

-In females, androgen is responsible for androgen-dependent processes (pubertal growth spurt)
-Growth of axillary and pubic hair
-Development and maintenance of sex drive

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10
Q

Epinephrine involves adrenaline, what is the function of epinephrine?

A

-(+) chronotropy and inotropy
- Bronchodilation
- Increased metabolism

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11
Q

Norepinephrine function

A

Vasoconstriction

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12
Q

A tumor of the chromaffin cells of the adrenal medulla (usually benign; 10% malignant)

A

Pheochromocytoma

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13
Q

What age does the Pheochromocytoma peaks?

A

40-50 years old

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14
Q

Pheochromocytoma mostly affects

A

Affects men and women equally

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15
Q

Clinical Manifestations of Pheochromocytoma

A

-Palpitation
- Headache
- Episodic Sweating

-Sustained or Paroxysmal Hypertension

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16
Q

Means persistently high BP even with maintenance and medications of HTN

A

Sustained Hypertension

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17
Q

Means on and off BP or rise and fall of BP even with maintenance or meds

A

Paroxysmal Hypertension

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18
Q

What is the Diagnostic for Pheochromocytoma?

A

Vanillylmandelic Acid (VCMA) Test

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19
Q

Measures urinary excretion of catecholamine metabolite

A

Vanillylmandelic Acid (VCMA) Test

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20
Q

Specimen of Vanillylmandelic Acid (VCMA) Test

A

24-hour urine sample

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21
Q

In Vanillylmandelic Acid (VCMA) Test what foods must be avoided?

A

Avoid coffee and tea, banana, chocolate, vanilla, and aspirin

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22
Q

Normal Level of Vanillylmandelic Acid (VCMA) Test

A

1.4-6.5 mg/24 hours

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23
Q

Instructions for Specimen Collection in Vanillylmandelic Acid (VCMA) Test

A

-Decide with patient on collection start time
- Discard first specimen (collected on start time)
- Collect all subsequent specimens over 24-hour period
- Store collected specimens in refrigerator
-Collect last specimen

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24
Q

Medical Management of Pheochromocytoma

A

Alpha-Adrenergic Blockers

-Phenoxybenzamine (Dibenzyline)
-Given 10 to 14 days prior to surgery
- S/E: orthostasis, nasal stuffiness, fatigue, retrograde ejaculation

Beta-Adrenergic Blockers

  • Propranolol (Inderal)
  • Initiated once alpha-adrenergic control is achieved

Calcium-Channel Blockers

-Nifedipine (Adalat)
- Alternative treatment if blood pressure control is inadequate or patient is unable to tolerate side effects

25
Q

Surgical Management of Pheochromocytoma

A

Adrenalectomy

26
Q

-Removal of one or both adrenal glands
-Definitive treatment of pheochromocytoma

A

Adrenalectomy

27
Q

Complication of Adrenalectomy

A

-Hypertensive Crisis (Intra/Post-Op)
- Results from the manipulation of the tumor during surgical excision

27
Q

What is the pre-operative preparation of adrenalectomy?

A

Control Blood Pressure

28
Q

Management for Adrenalectomy if Complication occurs

A

-Sodium nitroprusside (Nitropress)
- Phentolamine (Oraverse)

28
Q

Nursing Management of Pheochromocytoma

A

-Institute bed rest with HOB elevated to promote orthostatic decrease in BP during episodes of hypertension or tachycardia

29
Q
  • is a clinical condition that results from chronic exposure to excessive cortisol
    -Affects women>men
A

Cushing’s Syndrome

30
Q

What causes of Cushing’s Syndrome?

A

-Steroid Use (Exogenous Source
- Cushing’s Disease (ACTH- producing pituitary adenoma)
- Adrenal Hyperplasia
-Malignancies

31
Q

Clinical Manifestations of Cushing’s Syndrome

A

-“Moon Face”

-Skinny arms and legs
-Amenorrhea
-Depression

-Hypertension and hyperglycemia
-Infections (Often recurrent)
-Purpura and peptic ulcers
-Osteoporosis
-Non-healing wound

32
Q

Diagnostic Test of Cushing’s Syndrome

A

Dexamethasone Suppression Test

33
Q

Assesses adrenal gland function by measuring changes in the body’s ACTH and cortisol level in response to oral doses of dexamethasone

A

Dexamethasone Suppression Test

34
Q

Screening Test for Crushing’s Syndrome

A

Low-Dose Suppression
(Dexamethasone 1 mg)

Procedure
1. Low- dose Dexamethasone PO at 11 PM
2. Plasma cortisol is measured at 9AM of the following day

Interpretation
Low plasma cortisol – Normal
Normal/High plasma cortisol – Cushing’s syndrome

35
Q

Determines Etiology or Causes of Cushing’s Syndrome

A

High-dose Suppression
(Dexamethasone 8 mg)

Procedure

High- dose Dexamethasone PO at 11 PM
Plasma cortisol is measured at 9AM of the following day

Interpretation

Low plasma cortisol – Cushing’s Disease
Normal/High plasma cortisol, check ACTH
ACTH is low – Adrenal Cushing
ACTH is high – Ectopic ACTH source

36
Q

Medical-Surgical Management of Cushing’s Syndrome

A

-Transsphenoidal hypophysectomy
-Done if cause is a pituitary tumor

-Adrenalectomy (Laparoscopic)
-Done if cause is adrenal hyperplasia

Post operative care of Adrenalectomy (Laparoscopic)

         -Symptoms of adrenal insufficiency may appear 12 to 48 hours after surgery
      -Hydrocortisone is given for several months

Dose reduction
-Done if cause of syndrome is the administration of corticosteroids
-Dose is tapered to the minimum dosage needed to treat underlying disease process

37
Q

Key Nursing Interventions of Cushing’s Syndrome

A
  1. Institute safety/fall precautions
  2. Adhere to infection prevention and control measures
  3. Provide meticulous skin and wound care
  4. Encourage verbalization of concerns
  5. Monitor vital signs and blood glucose frequently. Intervene as needed
38
Q

Primary Adrenal Insufficiency

A

Addison’s Disease

39
Q

Occurs when the adrenal glands are damaged and cannot secret adrenocortical hormones

A

Addison’s Disease

40
Q

Causes of Addison’s Disease

A

-Autoimmune
- Adrenal gland destruction (commonly from tuberculosis)

41
Q

Clinical Manifestations of Addison’s Disease

A

-Progressive weakness
-Fatigue
-Anorexia
-Weight loss
-Nausea and vomiting
-Occasional diarrhea
-Salt cravings
-Orthostatic hypotension
-Impotence
-Decreased libido
-Amenorrhea

42
Q

Eternal tan of Addison’s Disease

A

Hyperpigmentation

43
Q

-Usually generalized but commonly affects the sun- exposed areas.
-Involves the skin and mucous membranes
-It is caused by the stimulant effect of excess adrenocorticotrophic hormone (ACTH) on the melanocytes to produce melanin.

A

Hyperpigmentation

44
Q

-white patchy areas
-Commonly associated with Addison’s disease having an autoimmune etiology

A

Vitiligo

45
Q

Diagnostic Test for Addison’s Disease

A

ACTH Stimulation Test

46
Q

assesses the functional capacity of the adrenal cortex to synthesize cortisol.

A

ACTH Stimulation Test

47
Q

ACTH stimulation Test Procedure & Interpretation

A

Procedure:

  1. Baseline cortisol and aldosterone levels are obtained
  2. Synthetic ACTH is administered IM or IV
  3. Cortisol and aldosterone levels are checked 30 or 60 minutes after

Interpretation

-Normal: elevation of cortisol and aldosterone levels to twice the baseline level
-Addison’s disease: little or no response to ACTH stimulation

48
Q

Due to low cortisol levels

A

Hypoglycemia

49
Q

Due to low aldosterone levels

A

Hyponatremia

50
Q

Due to low aldosterone levels

A

Hyperkalemia

51
Q

Medical Management of Addison’s Disease

A

-Hydrocortisone (Solu- cortef)
-Drug of choice for Addisonian crisis and daily maintenance
-Possesses both glucocorticoid and mineralocorticoid properties

-Fludrocortisone (Florinef)
-Has a more potent mineralocorticoid property
-Used when patient needs to be weaned off hydrocortisone

52
Q

Key Nursing Interventions of Addison’s Disease

A
  1. Instruct to increase salt intake during hot weathers
  2. Provide diet that is high in sodium but low in potassium
  3. Caution about condiments that uses potassium citrate as salt substitute
  4. Encourage to increase fluid intake
  5. Provide small, frequent feedings especially if with anorexia
  6. Educate on stress management and avoidance of infection, crowded places, and extremes of temperatures
53
Q

What triggers Addisonian Crisis?

A
  1. Stress (infection, trauma, surgery, emotional turmoil)
  2. Failure to increase steroid during anticipated stress
  3. Bilateral adrenal hemorrhage (Meningococcal/Pseudemona complication, pregnancy)
54
Q

Clinical Manifestations of Addisonian Crisis

A
  1. Nausea and vomiting
  2. Hypotension
  3. Rapid but weak pulse
  4. Decreasing mental status (initially restlessness, confusion)
  5. Cyanosis
    6.vHyperpyrexia (T>38.5)
  6. Abdominal pain, if with adrenal hemorrhage
55
Q

Medical Management of Addisonian Crisis

A

-Priority: restore volume deficit and correct hypotension
-Infuse 0.9% Sodium Chloride (PNSS)
-Glucose supplementation, if hypoglycemic
-D50W via IV Push
-Identify and correct precipitating cause
-Steroid replacement
-Hydrocortisone 100mg continuous infusion
-Tapered down as the condition improves

56
Q

Key Nursing Interventions of Addisonian Crisis

A
  1. Start an IV line using a large- bore IV catheter
  2. Closely monitor vital signs, glucose, and neurologic status
  3. Use an infusion pump to administer hydrocortisone infusion
  4. Provide supportive care

MS 2 (27 decks)

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