1. ADRENAL GLANDS
Zelne Zamora, DNP, RN

2. LAUGHTER IS THE BEST MEDICINE

3. PHYSIOLOGY Adrenal medulla secretes catecholamines
Adrenal cortex secretes steroid hormones

4. ADRENAL MEDULLA ANS Epinephrine, Norepinephrine
Regulate metabolic pathways
Release free fatty acids
↑ basal metabolic rate
↑ blood glucose level

5. HYPOTHALAMIC PITUITARY ADRENAL AXIS
Hypothalamus secretes corticotropin-releasing hormone (CRH)
Pituitary gland stimulated, secretes adrenocortiotropic hormone (ACTH)

6. HYPOTHALAMIC PITUITARY ADRENAL AXIS
Stimulates adrenal cortex to secrete glucocorticoids
Increased levels of adrenal hormone inhibit production or secretion of CRH and ACTH

7. NEGATIVE FEEDBACK

8. ADRENAL CORTEX Glucocorticoids Mineralocorticoids Sex hormones
(Sugar hormone)
Hydrocortisone
Mineralocorticoids
(Salt hormone)
Aldosterone
Sex hormones
Androgens

9. GLUCOCORTICOIDS Affect glucose metabolism
↑ hydrocortisone causes ↑ blood glucose levels
Secreted in response to the release of ACTH
Negative feedback
Glucocorticoids in the blood inhibit the release of CRH from the hypothalamus and also inhibits ACTH secretion from the pituitary resulting in decrease ACTH secretion and decrease release of glucocorticoids from the adrenal cortex

10. GLUCOCORTICOIDS Corticosteroids Exogenous glucocorticoids
Inhibit the inflammatory response
Suppress allergic reactions
Side effects
Diabetes mellitus
Osteoporosis
Peptic ulcer
Increased protein breakdown
Muscle wasting
Poor wound healing
Redistribution of body fat

11. GLUCOCORTIOIDS Exogenous glucocorticoids
Large amounts inhibit release of ACTH and endogenous glucocorticoids
Adrenal cortex atrophy
Adrenal insufficiency

12. MINERALOCORTICOIDS Electrolyte metabolism
Renal tubular and GI epithelium
Increased sodium absorption, excretion of potassium or hydrogen
Secreted in response to angiotensin II

13. MINEARLOCORTICOIDS Increase aldosterone promotes sodium reabsorption
Increased by hyperkalemia
Primary hormone for long-term regulation of sodium balance

14. ANDROGENS (Sex hormones) Effects similar to male sex hormone
Secrete small amount of estrogen
Controlled by ACTH

15. ADRENOCORTICAL INSUFFICIENCY
Primary
Autoimmune
Idiopathic
Surgical Removal
Infection
Tuberculosis
Histoplasmosis
Cancer
Secondary
Inadequate secretion of ACTH from pituitary gland
Hypothalamic dysfunction

16. ADDISON’S DISEASE Chronic primary adrenocortical insufficiency
Deficiency of all 3 hormones
Glucocorticoids
Mineralocorticoids: Aldosterone
Sex hormones: Androgens

17. CLINICAL MANIFESTATIONS
Onset is insidious
Progresses over weeks to months
Hyponatremia
Dehydration
Hypotension
Hyperkalemia

18. CLINICAL MANIFESTATIONS
Hypoglycemia
Weakness
Fatigue
Weight loss
Dark pigmentation of oral mucosa and skin
Decreased axillary and pubic hair

19. CLINICAL MANIFESTATIONS
Depression
Emotionally labile
Apathy
Confusion

20. ASSESSMENT AND DIAGNOSTIC FINDINGS
Primary insufficiency
↓ Aldosterone level
↓ Cortisol level
Hypoglycemia
Hyponatremia
Hyperkalemia
↑ BUN
↑ Hematocrit
ACTH Stimulation Test
Primary
↑ ACTH
↓ Cortisol
Secondary
↓ or normal ACTH
Gradual ↑ in Cortisol
Early morning serum cortisol and plasma ACTH are performed to differentiate primary adrenal insufficiency from secondary adrenal insufficiency from normal adrenal function

21. MEDICAL MANAGEMENT Mineralocorticoid
Fludrocortisone acetate (Florinef)
Correct fluid and electrolyte imbalance
Glucocorticoids
Corticosteroids
Hydrocortisone (Solu-Cortef) IV
Check blood glucose

22. SIDE EFFECTS ↑ Blood glucose Delayed wound healing Infection
Ulcers or gastritis
Weight gain
Hypertension
Insomnia
Avoid abrupt withdrawal

23. ADDISONIAN CRISIS Most common cause
Sudden cessation or withdrawal of corticosteroids
Infection
Surgery
Trauma

24. CLINICAL MANIFESTATIONS
Cyanosis
Pallor
Apprehension
Rapid and weak pulse
Rapid respirations
Hypotension
Disease progression and acute hypotension
Circulatory shock
Overexertion can put a patient into addisonian crisis: exposure to cold, acute infection, decrease in salt intake

25. ADDISONIAN CRISIS Headache Nausea Abdominal pain Diarrhea Confusion
Restlessness

26. MEDICAL MANAGEMENT Steroids Fluid replacement Vasopressors Antibiotics
Hydrocortisone IV then Prednisone PO
Fluid replacement
NS or plasma
Vasopressors
Antibiotics
Oxygen
Monitor BP
Electrolytes
Blood glucose
EKG
I & O

27. PREVENTION Do not stop steroids abruptly Take medication as prescribed
Notify physician if anticipating stressful situation
Cortisone IM
Medic-alert bracelet

28. CUSHING’S SYNDROME Hyperfunction Primary Secondary Iatrogenic
Glucocorticoid oversecretion
Primary
Cortisol-secreting adrenal tumors
Benign or malignant
Secondary
ACTH secreting tumor
Pituitary or hypothalamus
Iatrogenic
Overdosage of glucocorticoids

29. CLINICAL MANIFESTATIONS
Hyperglycemia
Protein tissue wasting
Muscle weakness and wasting
Thin extremities
Bruising
Osteoporosis
Delayed wound healing

30. CLINICAL MANIFESTATIONS
Abnormal fat distribution
Truncal obesity
Striae
Cervical fat pad
Moon face

31. CLINICAL MANIFESTATIONS
Hypokalemia
Cardiac arrhythmias
Muscle weakness
Edema
Weight gain
Increased susceptibility to infection

32. ASSESSMENT AND DIAGNOSTIC FINDINGS
Laboratory Values
↑ plasma cortisol and urinary cortisol excretion
↑ blood glucose
↑ Sodium
↓ Potassium
Plasma ACTH
ACTH Suppression Test
Administer dexamethasone
Check cortisol levels
Positive for Cushing’s syndrome if cortisol levels rise

33. MEDICAL MANAGEMENT Adrenalectomy Medications Mitotane (Lysodren)
Aminogluethimide (Cytadren)
Metyrapone (Metopirone)

34. NURSING MANAGEMENT Pre-operative Administer glucocorticoid Operative
Hydrocortisone or cortisol continuous IV
Post-operative
Bleeding
Addisonian Crisis
Prevent infection
NPO
Replacement hormones

35. HYPERALDOSTERONISM Primary Conn’s syndrome Adrenal tumor
Typically benign
Secondary
Alteration in RAAS
Renal artery disease
Cardiac failure

36. ASSESSMENT AND DIAGNOSTIC FINDINGS
↑ sodium and water
↓ potassium
Polyuria
Polydipsia
Metabolic alkalosis
No overt edema
↑ plasma and urine aldosterone level
Plasma renin level
CT Scan: Adrenal gland
Variable causes
Increased salt intake
ACE-inhibitor ingestion

37. MEDICAL MANAGEMENT Surgical Adrenalectomy Medical
Potassium Sparing Diuretic
Spironolactone (Aldactone)
Amiloride (Amiloride)
ACE-inhibitor
Enalapril (Vasotec)

38. CONGENITAL ADRENAL HYPERPLASIA
Adrenogential syndrome
Excessive androgen secretion
Defective negative feedback mechanism
Adrenal tumor that secretes androgens

39. CLINICAL MANIFESTATION
Adult females
Hirsutism
Balding
Breast atrophy
Masculine body build
Female infants
Masculinization of external genitalia

40. CLINICAL MANIFESTATIONS
Adult males
Not so dramatic
Boys may develop secondary sex characteristics early

41. MEDICAL MANAGEMENT Tumor Congenital
Medications to restore negative feedback mechanism
Decrease ACTH
Reverse overproduction of androgens

42. ADRENAL MEDULLA Controlled by sympathetic nervous system
Secretes catecholamines
Increase of vitals
Increase BMR
Increase blood sugar
Epinephrine and norepinephrine

43. MEDULLA HYPOFUNCTION Rarely causes problems
Sympathetic nervous system produces similar effects

44. MEDULLA HYPERFUNCTION
Caused by a pheochromocytoma
Benign tumor
Chromaffin cells of the adrenal medulla
40-50 years old
Cause of high blood pressure in 0.1% of patients with HTN

45. CLINICAL MANIFESTATIONS
Triad of Symptoms
Headache
Diaphoresis
Palpitations
Other Symptoms
Tremor
Flushing
Anxiety
Polyuria
Nausea and vomiting
Diarrhea
Abdominal pain
Impending doom

46. PAROXYSMAL PHEOCHROMOCYTOMA
Characteristics
Acute, unpredictable
Seconds to hours
Symptoms are abrupt and subside slowly
Signs & Symptoms
Extremely anxious
Tremulous
Weakness
Vertigo
Blurring of vision
Tinnitus
Air hunger
Dyspnea

47. COMPLICATIONS Cardiac dysrhythmias Dissecting aneurysm Stroke
Acute renal failure

48. ASSESSMENT Marked elevation of blood pressure Hypertension Headache
Hyperhidrosis
Hypermetabolism
Hyperglycemia

49. DIAGNOSTIC FINDINGS Plasma and urine catecholamine and metanephrine
24-hour urine sample
Free catecholamines
Metanephrine
Vanillymandelic acid
Clonidine suppression test
CT, MRI, and ultrasonography
Most direct and conclusive tests for overactivity of the adrenal medulla
Test results can be altered by medications, food (coffee, tea, chocolate)
Total plasma catecholamine concentration is measured with the patient supine and at rest for 30 minutes
Factors that elevate catecholamine concentration: tobacco use, emotional and physical stress, amphetamines, nose drops or sprays, decongestants, bronchodilators
Clonidine suppression test: clonidine is a centrally acting antiadrenergic medication that suppresses the release of neurogenically mediated catecholamines. Pheochromocytoma, increased catecholamine levels result from the diffusion of excess catecholamines into the circulation, bypassing normal storage and release mechanism. Patients with pheochromocytoma, clonidine does not suppress the release of catecholamines.
Imaging studies localize the pheochromocytoma and determine whether more than one tumor is present

50. PHARMACOLOGIC MANAGEMENT
Alpha-adrenergic blockers
Phentolamine (Regitinel)
Smooth muscle relaxants
Nitroprusside (Nipride)
Long acting alpha-adrenergic blockers
Phenoxybenzamine (Dibenzyline)
Calcium channel blockers
Nifedipine (Procardia)
Beta blockers
Propanolol (Inderal)
Lower the blood pressure quickly

51. SURGICAL MANAGEMENT Adrenalectomy Surgical removal of the tumor
Definitive treatment for pheochromocytoma

52. NURSING MANAGEMENT Pre-operative Stabilize blood pressure
Nifedipine (Procardia)
Nicardipine (Cardene)
IV corticosteroids
Methylprednisolone (Solu-Medrol)
Post-operative
IV corticosteroid replacement
Methylprednisolone (Solu-Medrol)
Oral corticosteriod replacement
Prednisone

53. NURSING MANAGEMENT Blood pressure Blood glucose ECG changes
Fluid and electrolyte balance

54. QUESTIONS