useful for ug and pg medical surgical nursing students

1. Adrenocortical
disorders
Presented by :
Blessy Susan Babu
First Year Msc Nsng.
KINS, KARAD

2. ANATOMY & PHYSIOLOGY OF
ADRENAL GLAND
• Either of two small, dissimilarly shaped
endocrine glands, one located above each
kidney, consisting of the cortex, which
secrets several steroid hormones and the
medulla which secretes epinephrine.
• Also called suprarenal gland.
• The adrenal glands, located on the
cephalad portion of each kidney, consists
of a cortex and medulla, each with
separate endocrine functions.

4. • The adrenal gland consist of an outer
yellowish part, the cortex, which
produces cortisol (hydrocortisone), a
close relation of cortisone and an inner
medullary portion producing both
epinephrine (adrenalin) and
norepinephrine (noradrenalin)

5. • The important hormones secreted by
the adrenal cortex are hydrocortisone,
aldosterone and corticosterone, which
are intimately concerned with
metabolism, growth, renal function and
muscle tone. These functions are
essential to life.

6. • The adrenal cortex
produces
glucocorticoids
(primarily cortisol),
mineralocorticoids
(primarily aldosterone)
and androgens
(primarily
dehydroepiandrosteron
e and androstenedione).

8. PHEOCHROMACYTOMA
DEFINITION:
Pheochromacytoma is a
catecholamine secreting tumour of
the cromaffin cells of the
sympathetic nervous system it is
usually found in the adrenal medulla.

10. ETIOLOGY
• The cause of most cases of
pheochromocytoma is unknown.
• About one-third of cases are
hereditary.

11. PATHOPHYSIOLOGY
Neuroendocrine tumour of the medulla of
the adrenal glands.
Originates from the cromaffin cells along
the paravertebral sympathetic chain
extending from pelvis to base of the skull.
The tumors produce, store, and release
epinephrine and norepinephrine

12. CLINICAL MANIFESTATIONS
• Abdominal pain
• Chest pain
• Irritability
• Nervousness
• Pallor
• Palpitations
• Tachycardia
• Severe headache
• Sweating
• Weight loss

13. “PHEochromocytoma”
• Palpitations
• Headache
• Episodic sweating (diaphoresis)
Pheochromocytoma: 3 most
common symptoms

15. “FIVE H’s”
Hypertension
Headache
Hyperhidrosis
Hyper Metabolism
Hyperglycaemia

16. Diagnostic tests
• 24-hour urine test for
metanephrines and
vanillylmandelic acid
(VMA)
• urine and plasma levels of
catecholamines and
metanephrine (MN)
• plasma values of
epinephrine
• clonidine suppression test

17. Imaging studies
• Abdominal CT
• MRI
• ultrasonography
• 131I
metaiodobenzylguani
dine (MIBG)
scintigraphy

19. Pharmacologic Therapy
• Administering alpha-adrenergic
blocking agents and smooth muscle
relaxants to lower the blood
pressure quickly.

20. Surgical Management
• The definitive treatment of
pheochromocytoma is surgical removal
of the tumour, usually with
adrenalectomy.
• Bilateral adrenalectomy may be
necessary if tumours are present in
both adrenal glands.

21. Contd..
• Use of alpha-adrenergic blocking agents
may be required during and after
surgery to control the BP and HR
• Corticosteroid replacement is required
for bilateral adrenalectomy.
• Close monitoring of BP and HR.

22. NURSING MANAGEMENT
• Risk for Injury related to
hypertensive crisis.
• Anxiety related to prognosis and
treatment

23. Implementations
• Monitor vital signs and report elevated pulse and
blood pressure promptly. Prompt treatment helps
prevent complications.
• Approach the patient calmly and maintain a quiet
environment. Stress may precipitate a
hypertensive episode.
• Administer medications as ordered to control
symptoms.
• Teach the patient how the medications will
reduce symptoms, and the importance of avoiding
foods and beverages containing caffeine, so that
the patient can participate in self-care.
• If patient has surgery, continue careful
monitoring because manipulation of tumor can
increase catecholamine release.

25. Introduction
• Cushing’s syndrome (hypercortisolism) is
a hormonal disorder caused by prolonged
exposure to high levels of steroid
hormones called glucocorticoids.
• Exogenous Cushing’s syndrome caused by
taking excessive amounts of medications.
• Endogenous Cushing’s syndrome caused
by excess cortisol produced by the
adrenal glands.

26. • Cushing’s disease: Cushing’s syndrome
when caused by a tumour of the pituitary
gland.
• Cushing’s syndrome: Caused by
overproduction of cortisol for any
reason. Cushing’s syndrome is a result of
excessive circulating free
corticosteroids, caused by unnecessary
adrenocortical activity.

27. Disease vs. Syndrome
• Cushing’s disease is the result of the
pituitary tumour secreting inappropriate
ACTH.
• Cushing’s syndrome causes the same
symptoms, but is caused by
overproduction of adrenal hormones.
Basically;
Disease = increased cortisol from pituitary
Syndrome = all other sources

28. ETIOLOGY
• Adrenal hyperplasia: which means
there is increased number and
growth of the cells in the adrenal
glands. These cells then make too
much cortisol.
• pituitary Cushing’s disease
• adrenal Cushing’s disease

30. PATHOPHYSIOLOGY
When stimulated by ACTH, the adrenal gland
secretes cortisol and other steroid hormones.
The switch that controls the feedback mechanism
is cortisol
When the levels are low the systems turns on and
when high the systems turns off
Excessive use of steroids leads to excess free
circulation of cortisol in the body.

31. PATHOPHYSIOLOGY (cont..
Excess cortisol in the body will cause the liver to
release more sugar, increased breakdown of muscle and
fat for energy and also lowers the body amount of
energy used by the cells of the body
It will also decrease the anti-inflammatory effects and
lowers the body’s ability to protect itself.

32. Lipid mobilization
Lipid catabolism
Lipid redistribution
Moon face
Buffalo hump
Truncal obesity
Violaceous striae
Hypercortisolism
Hepatic glucose
production
insulin resistance
glucose intolerance
• protein metabolism
• Negative nitrogen balance
• Disruption of water and
electrolytes metabolism
Proximal muscle weakness
dependent edema
Hypertension
Hypokalemic metabolic alkalosis

33. CLINICAL MANIFESTATIONS
• Arrest of growth
• Obesity
• Glucose intolerance
• Buffalo hump
• Heavy trunk
• Thin extremities
• Fragile skin
• Weight gain
• hirsutism
• breasts atrophy
• Libido
• clitoris enlarges
• voice deepens
• menses cease
• Purple striae
• Weakness

34. • Sleep is disturbed
• Osteoporosis.
• Backache
• Vertebrae fractures
• Hypertension
• Heart failure
• Hypokalaemia
• Moon-faced
• Increased susceptibility to infection
• Hyperglycaemia
• Ecchymoses (bruises)

37. History
• History of glucocorticoid therapy
• significant weight gain
• increased appetite
• activity or sleep patterns
• Menstrual history

38. Physical examination
• Body fat :
o weight gain
o central obesity
o moon face
o buffalo hump
• Skin :
o Purple abdominal
striae
o Easy bruising
o hirsutism
• Bone :
o Osteopenia
o Osteoporosis (vertebral
fracture)
• Muscle: Proximal
myopathy
• CVS:
o Diastolic hypertension
o Hypokalemia
o Oedema
o atherosclerosis

39. • Reproductive
system:
o Amenorrhea
o Decreased libido
• CNS:
o Irritability
o Emotional liability
o Paranoid psychosis
• Blood:
o Increased
susceptibility to
infections
o Increased WBC
o Hyper
coagulations
• Metabolism:
o Impaired glucose
tolerance
o dyslipidaemia

40. Laboratory Assessment
• Serum cortisol level
• Salivary cortisol level
• Urine cortisol level
• ACTH levels
• Dexamethasone suppression test

41. Imaging Assessment
• X-rays
• CT scans
• MRI
• Arteriography

43. MEDICAL MANAGEMENT
• Adrenal enzyme inhibitors
• Tapering the corticosteroid
therapy

44. SURGICAL MANAGEMENT
• Cushing’s syndrome is caused by
pituitary tumours rather than tumours
of the adrenal cortex, treatment is
directed at the pituitary gland.
• Surgical removal of the tumour by
transsphenoidal hypophysectomy is the
treatment of choice.
• Adrenalectomy is the treatment of
choice in patients with primary adrenal
hypertrophy.

45. NURSING MANAGEMENT
• Risk for injury related to weakness
• Risk for infection related to altered protein
metabolism and inflammatory response
• Self-care deficit related to weakness, fatigue,
muscle wasting, and altered sleep patterns
• Impaired skin integrity related to edema,
impaired healing, and thin and fragile skin
• Disturbed body image related to altered
physical appearance, impaired sexual
functioning, and decreased activity level
Disturbed thought processes related to mood
swings, irritability, and depression

46. Nursing Interventions
• Decreasing Risk of Injury
• Decreasing Risk of Infection
• Preparing the Patient for Surgery
• Encouraging Rest and Activity
• Promoting Skin Integrity
• Improving Body Image
• Improving Thought Processes
• Nutrition therapy

47. COLLABORATIVE PROBLEMS/
POTENTIAL COMPLICATIONS
Potential complications may include the
following:
Addisonian crisis
Adverse effects of adrenocortical
activity

49. ADDISON’S DISEASE
• Inadequate secretion of ACTH
from pituitary glands results
adrenal insufficiency. Primary
adrenal insufficiency results from
idiopathic atrophy or destruction of
adrenal glands by autoimmune
process.

50. ETHIOLOGY
Primary adrenal
insufficiency
• Idiopathic
autoimmune
dysfunction
• Tuberculosis
• HIV, Cancer
• Adrenalectomy
• Fungal infection
Secondary adrenal
insufficiency
• Steroid
withdrawal
• Hypophysectomy
• Pituitary neoplasm

51. PATHOPHYSIOLOGY
Destruction of adrenal cortex
Low production of aldosterone & cortisone
Kidney sodium and water loss with potassium
retention
Chloride will follow sodium level
Decreased blood volume (hypovolemia)
Increase of urea in blood (hyperuremia)

52. CLINICAL MANIFESTATIONS
• General weakness
• Darkened areas of skin (pigmentation)
• Low blood pressure
• Anorexia & weight loss
• Nausea & vomiting
• Abdominal pain
• Diarrhoea or constipation
• Muscle cramps
• Depression& emotional liability

53. Addison’s disease
• Hyponatremia hypotension
• hyperkalaemia & hypoglycaemia muscular weakness
• Vomiting dehydration hypotension
renal blood flow & GFRoliguria
urea retention
• capacity to withstand stresses
e.g. hemorrhage

56. Diagnostic tests
• serum cortisol concentration
• plasma ACTH level
• Serum electrolyte levels
• CBC
• Urinary 17-hydroxycorticosteroids
• ACTH stimulation test

57. Imaging Assessment
• Skull x-rays
• CT
• MRI
• arteriography

59. MEDICAL MANAGEMENT
• Restoring blood circulation
• Administering fluids and
corticosteroids
• Monitoring vital signs
• Placing the patient in a recumbent
position with the legs elevated

60. Treatment
• Immediate treatment must be started
if patient displays features of adrenal
insufficiency.
• IV Hydrocortisone 100mg every 6hrs,
3L of saline given in 6hrs under careful
cardiac monitoring
• Chronic adrenal insufficiency =
replacement therapy with daily oral
hydrocortisone (10mg) and
fludrocortisone (0.1mg)

61. Nursing management
• Deficient Fluid Volume related to
deficient adrenal cortical hormones
• Risk for Ineffective Self Health
Management related to deficient
knowledge about self-care of Addison’s
disease
• Activity intolerance weakness
• Altered nutrition less than body
requirement related to anorexia

63. REVIEW OF ANATOMY AND
PHYSIOLOGY
• PANCREAS
HORMONES:
INSULIN BY BETA CELLS
GLUCAGON BY ALPHA CELLS

64. • Pancreas secretes 40-50 units of
insulin daily in two steps:
- secreted at low levels during fasting
(basal insulin secretion)
- Increased levels after eating
(prandial)
- an early burst of insulin occurs within
10 minutes of eating
- Then proceeds with increasing release
as long as hyperglycemia is present.

65. Insulin
• Insulin allows glucose to
move into cells to make
energy.
• Inhibits glucagon activity

66. Insulin (normal values)
CPG <200 mg/Dl
FPG <100 mg/Dl
OGTT <140 mg/Dl
HbA1C <5.7%

67. Physiology

68. DIABETES MELLITUS
• Is a chronic
disorder of
carbohydrate,
protein, and fat
metabolism
resulting from
insulin deficiency
or abnormality in
the use of insulin

69. Who are at risk..???

70. Risk factors
• Family history of diabetes (i.e., parents or siblings
with diabetes)
• Obesity (i.e., >20% over desired body weight or BMI
27 kg/m2)
• Race/ethnicity (e.g., African Americans, Hispanic
Americans, Native Americans, Asian Americans,
Pacific Islanders)
• Age >45 y
• Previously identified impaired fasting glucose or
impaired glucose tolerance
• Hypertension (>140/90 mm Hg)
• HDL cholesterol level >35 mg/dL (0.90 mmol/L)
and/or triglyceride level >250 mg/dL (2.8 mmol/L)
• History of gestational diabetes or delivery of babies
over 9 lb

71. Types
• Type 1 – Insulin Dependent
Diabetes Mellitus (IDDM)
Beta-cell destruction leading to
absolute insulin deficiency (Little or
no insulin production)
Autoimmune (Islet cell antibodies)
Idiopathic

73. • Type 2 – Non Insulin Dependent
Diabetes Mellitus (NIDDM)
• Ranges from insulin resistance with
relative insulin deficiency to
secretory deficit with insulin
resistance.
•

74. CLINICAL MANIFESTATIONS
• Classic Symptoms of DM
Polydipsia (excessive thirst)
Polyuria (excessive urination)
Polyphagia (excessive hunger)

75. CLINICAL MANIFESTATIONS
• Weight loss
• Nausea/vomiting
• Weakness
• Fatigue
• Increased blood sugar/ glucose
level
• (+) glucose in urine (glycosuria)
• Nocturia

77. Cardinal Symptoms of Diabetes
Mellitus

78. ASSESSMENT AND
DIAGNOSTIC FINDINGS
• Fasting Plasma Glucose Level
• Random Plasma Glucose
• Oral glucose tolerance test
• Glycohemoglobin

79. MANAGEMENT
Goal of Treatment
Is
To control the blood glucose
levels

80. MANAGEMENT
• Nutritional therapy
• Exercise
• Oral anti-diabetic agents
• Insulin
• Pancreas transplantation
• Islet cell transplantation

81. Dietary Management
• Follow individualized meal plan and snacks
as scheduled.
• Patient must have adequate CHO intake to
correspond to the time when insulin is most
effective
• Routine blood glucose testing before each
meal and at bedtime is necessary during
initial control, during illness and in unstable
patients.
• Do not skip meals
• Less added fat, fewer fatty foods and low
cholesterol

82. Exercise
Purpose
• Controls blood glucose and
lowers blood glucose.
• Reduce the amount of insulin
needed.

83. Insulin Therapy
• Insulin in current use may be stored at
room temperature, all others in
refrigerator or cool area.
• Avoid injecting cold insulin – lead to
tissue reaction
• Roll insulin vial to mix, do not shake,
remove air bubbles from syringe
• Press the site after injection (rubbing
may alter the rate of absorption of
insulin)

84. Insulin Therapy
• Rotate the site

85. MICROVASCULAR
COMPLICATIONS
• Diabetic Neuropathy
• Diabetic Retinopathy
• Diabetic Nephropathy

86. Nursing Management
• Assessment : Medicines,
Allergies, Symptoms, Family
History
• Nursing Diagnosis : Unstable
Blood Glucose Level
• Implementation
• Evaluation

88. Summary

89. Conclusion

90. Assignment
• Write nursing care plan for
patients on different endocrine
disorders.

91. Bibliography
• Joyce M Black, Jane Hokanson Hawks; “Medical
Surgical Nursing”, Volume 2, 8th Edition,
Published By Elsevier, Page No.1040-1054
• Linda S Williams, Paula D Hopper; “Understanding
Medical Surgical Nursing”, 5th Edition, Published
by F.A.Davis Company, Philadelphia, Page No.
877-879, 907-914
• Suzanne C. Smelter, Brenda Bare, “Brunner and
Suddarth’s Textbook of Medical Surgical
Nursing”, 12th edition, published by Lippincott
Williams and Wilkins, page no. 1276-1288

92. Bibliography
• Anne-Marie Brady, Catherine McCabe,
Margaret McCann; “Fundamentals of
Medical Surgical Nursing, A System
Approach”, First Edition 2014, Published
by John Wileys & Sons Ltd., Page no.
331-337
• Ignatavicius, Workman; “Medical
Surgical Nursing, Patient Centered
Collaborative Care”, 7th Edition,
Published By Elsevier, Page No.1381-
1391