DISORDERS OF THE ADRENAL

GLANDS

What are adrenal gland disorders?

• What are adrenal gland disorders?

• Adrenal gland disorders occur when the adrenal glands don’t work properly.  Sometimes, the cause is a problem in another gland that helps to regulate the adrenal gland.  In other cases, the adrenal gland itself may have the problem.  The NICHD conducts and supports research on many adrenal gland disorders.  Some examples include

Adrenal gland disorders

• ADDISON’S DISEASE- Inadaquate amounts of glucocorticoids and mineralocorticoids

• Cushing's Syndrome - Cushing’s syndrome happens when a person’s body is exposed to too much of the hormone cortisol

• Congenital Adrenal Hyperplasia - Congenital adrenal hyperplasia is a genetic disorder of adrenal gland deficiency

• Pituitary Tumors - The pituitary gland is located in the brain and helps to regulate the activity of most other glands in the body, including the adrenal glands

ADDISON’S DISEASEADDISON’S DISEASELets watch This

• Adrenal hypofunction (Addison’s disease)

– Etiology/pathophysiology• Adrenal glands do not secrete adequate amounts of

glucocorticoids and mineralocorticoids• May result from

– Adrenalectomy– Pituitary hypofunction– Long-standing steroid therapy

• Addison’s is primary disease- from atrophy, cancer of the adrenal cortex, fungal infection or TB.

• Secondary- adrenalectomy, pituitary hypofunction, long-term steroid therapy

ADDISON’S DISEASEADDISON’S DISEASE– Clinical manifestations/assessment– The symptoms of Addison's disease develop insidiously, and it may take

some time to be recognized. • Related to imbalances of hormones, nutrients, and electrolytes• Nausea; anorexia• Postural hypotension• Headache• Disorientation• Abdominal pain; lower back pain• Anxiety• Darkly pigmented skin and mucous membranes• Weight loss• Vomiting • Diarrhea• Hypoglycemia• Hyponatremia• Hyperkalemia• Assess for adrenal crisis

DX• Routine investigations may show.• Hypercalcemia • Hypoglycemia, low blood sugar (worse in children

due to loss of glucocorticoid's glucogenic effects) • Hyponatraemia (low blood sodium levels), due both

to a deficiency in Aldosterone (a mineralocorticoid) dependant Sodium retention and also the effect of Corticotropin-releasing hormone to stimulate secretion of ADH

• Hyperkalemia (raised blood potassium levels),

ADDISON’S DISEASEADDISON’S DISEASE

Treatment•Restore fluid and electrolyte balance•Replacement of adrenal hormones•Diet high in sodium and low in potassium•In case of Adrenal crisis:IV corticosteroids in a solution of saline and glucose

Treatment• Maintenance• Treatment for Addison's disease involves replacing the missing

cortisol, sometimes in the form of hydrocortisone tablets, or prednisone tablets in a dosing regimen that mimics the physiological concentrations of cortisol. Treatment must usually be continued for life. In addition, many patients require fludrocortisone as replacement for the missing aldosterone. Caution must be exercised when the person with Addison's disease becomes unwell with infection, has surgery or other trauma, or becomes pregnant. In such instances, their replacement glucocorticoids, whether in the form of hydrocortisone, prednisone, prednisolone, or other equivalent, often need to be increased. Inability to take oral medication may prompt hospital attendance to receive steroids intravenously. People with Addison's are often advised to carry information on them (e.g. in the form of a MedicAlert bracelet) for the attention of emergency medical services personnel who might need to attend to their needs.

Adrenal crisis-• Crisis

• 1.Standard therapy involves intravenous injections of glucocorticoids and large volumes of intravenous saline solution with dextrose, a type of sugar. This treatment usually brings rapid improvement.

• 2.When the patient can take fluids and medications by mouth, the amount of glucocorticoids is decreased until a maintenance dose is reached.

ADDISON’S DISEASEADDISON’S DISEASE• Addison crisis- medical emergency-

– fever, cyanosis, shock, pallor, rapid, weak pulse, low BP.

• Primary and secondary forms basically have the same symptoms,Crisis may occur suddenly or gradually

• First sign is darkening of the skin (bronzed skin)• Fatigue, dry skin, n&v, anorexa, tachycardia, salt

craving, postural hypotension, vertigo, severe headache, weight loss, diarrhea, hypoglycemia (may occur 5-6 hrs after eating)

• Dx:• Decreased glucose level, low Na, high K, low

aldosterone,.

ADDISON’S DISEASEADDISON’S DISEASE• Treatment• Adrenal crisis- immediate rx is to combat shock,

restore circulation, give fluids, monitor v/s• Emergency rx- IV corticosteroids and antibiotics

(Florinef- synthetic corticosteroids)• Diet- high Na and CHON, low K• Nursing care: I&O, daily weight, v/s, maintain a quiet

env’t., protect from infection, administer glucocorticoids and mineralocorticoids, increase fluids, 5-6 small meals a day to control hypoglycemia

ADDISON’S DISEASEADDISON’S DISEASE• Teaching- medications,

report any illness to the MD, avoid infection, eliminate stress, medicalert bracelet

• Corticosteroid therapy- anti-inflammatory, anti-stress. Keep BP elevated, maintain glucose level as steroids cause it to increase

ADDISON’S DISEASEADDISON’S DISEASE• May cause pituitary and

adrenal gland suppression and changes in CNS function- such effects maybe disabling or dangerous.

• Dosage frequently altered to avoid untoward effects

• Ardrenal cortex suppression may persist for up to a year after a 2-wk steroid therapy

ADDISON’S DISEASEADDISON’S DISEASE• Adverse effects more likely to occur with long term

therapy: peptic ulcer, osteoporosis, infection, euphoria, mood changes and psychological dependence.

• Nsg. Diagnosis– Infection, risk for– Fluid volume deficit– Altered nutrition, less than body requirements– Activity intolerance– Prognosis- fair with long term therapy

CUSHING’S SYNDROMECUSHING’S SYNDROMELets watch thisLets watch this

Cushing's syndrome• Cushing's syndrome is a hormone disorder

caused by high levels of cortisol in the blood. This can be caused by taking glucocorticoid drugs, or by tumors that produce cortisol or adrenocorticotropic hormone (ACTH) or CRH Cushing's disease refers to one specific cause of the syndrome, a tumor (adenoma) in the pituitary gland that produces large amounts of ACTH, which in turn elevates cortisol. It is the most common cause of Cushing's syndrome, responsible for 70% of cases excluding glucocorticoid related cases

CUSHING’S SYNDROMECUSHING’S SYNDROME• Adrenal hyperfunction; opposite of Addison’s disease• 3x more common in women.• Excess amounts of glucocorticoids, mineralocorticoids and

sex homone• Etiology/pathophysiology

– Plasma levels of adrenocortical hormones are increased– Hyperplasia of adrenal tissue due to overstimulation by

the pituitary gland– Tumor of the adrenal cortex– Adrenocorticotropic hormone (ACTH) secreting tumor

outside the pituitary– Overuse of corticosteroid drugs

CUSHING’S SYNDROMECUSHING’S SYNDROME• S/S- buffalo hump, thin extremities, weight gain, weakness,

delayed wound healing, osteoporosis, female hirsutism, deepened voice, susceptible to infection.

• Clinical manifestations/assessment– Moonface– Buffalo hump– Thin arms and legs– Hypokalemia; proteinuria– Increased urinary calcium excretion– Susceptible to infections– Depression– Loss of libido

CUSHING’S SYNDROMECUSHING’S SYNDROME• Clinical manifestations/assessment

– Ecchymoses and petechiae– Weight gain– Abdominal enlargement– Hirsutism in women– Menstrual irregularities– Deepening of the voice

• DiagnosisDiagnosis• Physical exam, plasma cortisol level, skull x-ray, 24- hr. urine, CT

scan, MRI, ultrasound• Hypokalemia, hyperglycemia, elevated ACTH, hypernatremia

CUSHING’S SYNDROMECUSHING’S SYNDROME• Medical management/nursing interventions

– Treat causative factor• Adrenalectomy for adrenal tumor• Radiation or surgical removal for pituitary tumors

– Lysodren X 3 months- – Low-sodium, high-potassium diet

• DietDiet- • low Na, low calories, low CHO, • high K• Skin care, I&O, diuretics, Nizoral, Cytadern, Mitotane

CUSHING’S SYNDROMECUSHING’S SYNDROME• NandaNanda• Activity intolerance r/t weakness and

immobility• Self-care deficits• Impaired skin integrity• Ineffective individual coping

• Prognosis- depends whether the tumor is benign or malignant

PHEOCHROMOCYTOMAPHEOCHROMOCYTOMALets watch thisLets watch this

pheochromocytoma• A pheochromocytoma or phaeochromocytoma

(PCC)– Etiology/pathophysiology

• Chromaffin cell tumor; usually found in the adrenal medulla• Causes excessive secretion of epinephrine and norepinephrine

– Clinical manifestations/assessment• Hypertension, kidney damage, tachycardia, polyuria,

hyperglycemia, headache, intolerance to heat, tremors, nausea

– Diagnosis• 24 hr urine, MRI, ultrasound, CT scan, IVP

– Medical management/nursing interventions• Surgical removal of tumor

PHEOCHROMOCYTOMAPHEOCHROMOCYTOMA• Tx:• Surgery• Diet without stimulants (coffee, tea)• Vasopressors, corticosteroids replacement

• Nanda:• Activity intolerance• Anxiety and fear

• Prognosis- depends on tumor size and characteristics

Conn's syndrome

HYPERALDOSTERONISM HYPERALDOSTERONISM (CONN’S SYNDROME)(CONN’S SYNDROME)

• Conn's syndrome is an Aldosterone-Producing Adenoma (APA). Conn's syndrome is named after Jerome W. Conn (1907–1994 )

• Hypersecretion of aldosterone by the adrenal cortex; maybe caused by a benign or malignant tumor

• Results to hypernatremia and hypokalemia• Kidneys unable to concentrate or acidify urine• S/S:• Headache, polyuria, polydipsia, HTN, paresthesia, chills,

fever, muscle weakness

HYPERALDOSTERONISM HYPERALDOSTERONISM (CONN’S SYNDROME)(CONN’S SYNDROME)

• Dx:• Low K, high Na, increased urine pH, x-ray, CT, MRI• Tx:• Surgical removal of the tumor• I&O, diet high in K and low in Na• Spinorolactone- K-sparing diuretic • Regular weights, observe for edema

Adrenalectomy

• Adrenalectomy is the surgical removal of one or both (bilateral adrenalectomy) adrenal glands. It is usually advised for patients with tumors of the adrenal glands. The procedure can be performed using an open incision or laparoscopic technique

ADRENALECTOMYADRENALECTOMY• Maybe performed for Cushing’s syndrome,

Conn’s syndrome that’s caused by a tumor, and pheochromocytoma

• Abdominal or side incision under 12th rib• Protect pt. from infection• Corticosteroids replace hormones no longer

supplied by adrenal glands. No replacement needed if surgery is unilateral

• Maintain serum glucose level• Provide rest, reduce stress

DIABETES DIABETES MELLITUSMELLITUS

Lets watch thisLets watch this

DIABETES MELLITUSDIABETES MELLITUS• Normal blood glucose level: 70-110 mg/dl. Insulin,

a hormone produced by the beta cells of islets of Langerhans of the pancreas, regulates it.

• Insulin moves glucose from the blood to the muscles, liver (glycogen) and fat cells.

• Most common endocrine disorder• Lack of insulin results to blood glucose elevation• Insulin converts glucose to glycogen for storage• Glucagon converts glycogen to glucose and send

it to blood, if blood glucose level drops.

DIABETES MELLITUSDIABETES MELLITUS• Diabetes mellitus

– Etiology/pathophysiology• A systemic metabolic disorder that involves improper

metabolism of carbohydrates, fats, and proteins• Insulin deficiency• Risk factors

–Heredity–Environment and lifestyle–Viruses–Malignancy or surgery of pancreas

DIABETES MELLITUSDIABETES MELLITUS

• Type 1• Insulin dependent diabetes mellitus (IDDM)• Less common but more severe, has familial

predisposition. Patient maybe thin.• Cause is unknown but maybe autoimmune. 5-10%

of cases.• Type 2• Non-insulin dependent diabetes mellitus (NIDDM)• 90% of cases. Most common after 40; 80% are

overweight and with family hx.

DIABETES MELLITUSDIABETES MELLITUS• 2 main problems- insulin resistance and impaired insulin

secretion• Most patients with type 2 diabetes have insulin resistance

where the cell receptors no longer recognize the insulin and glucose never gets into cells for metabolism. Impaired insulin secretion is the trademark of type 1 diabetes hence the need for insulin injections.

• Clinical manifestations/assessment– Type I and type II

• “3 Ps”–Polyuria–Polydipsia–Polyphagia

DIABETES MELLITUSDIABETES MELLITUS– Clinical manifestations/assessment

• Type I– Sudden onset– Weight loss– Hyperglycemia– Under 40 years old

– Clinical manifestations/assessment• Type II

– Slow onset– May go undetected for years– “3 Ps” are usually mild– If untreated, may have skin infections and arteriosclerotic conditions

DIABETES MELLITUSDIABETES MELLITUS• Diagnostic tests

–Urine glucose and acetone–Blood glucose–Oral glucose tolerance test–2-hour postprandial blood sugar–Glycohemoglobin (A1C)

DIABETES MELLITUSDIABETES MELLITUS– Medical management/nursing interventions

• Diet– The cornerstone of treatment– Usually based on caloric needs– Type II—may be controlled by diet alone– Type I—diet is calculated and then the amount of

insulin required to metabolize it is established– American Diabetes Association (ADA) diet

» Seven exchanges» Quantitative diet

– Need three regular meals with snacks between meals and at bedtime to maintain constant glucose levels

DIABETES MELLITUSDIABETES MELLITUS– Medical management/nursing interventions (continued)

•Exercise–Promotes movement of glucose into the cell–Lowers blood glucose–Lowers insulin needs

•Stress of acute illness and surgery–Extra insulin may be required–Increased risk of ketoacidosis (hyperglycemia)–Glucose must be monitored closely