Endocrine week 4 pt

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 DISEASE Lets 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 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 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 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 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 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 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 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 SYNDROME Lets 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 SYNDROME
Adrenal hyperfunction; opposite of Addison’s disease
3x more common in women.
Excess amounts of glucocorticoids, mineralocorticoids and sex homone
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

S/S- buffalo hump, thin extremities, weight gain, weakness, delayed wound healing, osteoporosis, female hirsutism, deepened voice, susceptible to infection.
Moonface
Buffalo hump
Thin arms and legs
Hypokalemia; proteinuria
Increased urinary calcium excretion
Susceptible to infections
Depression
Loss of libido

Ecchymoses and petechiae
Weight gain
Abdominal enlargement
Hirsutism in women
Menstrual irregularities
Deepening of the voice
Diagnosis
Physical exam, plasma cortisol level, skull x-ray, 24- hr. urine, CT scan, MRI, ultrasound
Hypokalemia, hyperglycemia, elevated ACTH, hypernatremia

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

Nanda
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

PHEOCHROMOCYTOMA Lets watch this

pheochromocytoma
A pheochromocytoma or phaeochromocytoma ( PCC )
Chromaffin cell tumor; usually found in the adrenal medulla
Causes excessive secretion of epinephrine and norepinephrine
Hypertension, kidney damage, tachycardia, polyuria, hyperglycemia, headache, intolerance to heat, tremors, nausea
Diagnosis
24 hr urine, MRI, ultrasound, CT scan, IVP
Surgical removal of tumor

PHEOCHROMOCYTOMA
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 (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 (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

ADRENALECTOMY
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 MELLITUS Lets watch this

DIABETES 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 MELLITUS
Diabetes mellitus
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 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 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.
Type I and type II
“ 3 Ps”
Polyuria
Polydipsia
Polyphagia

DIABETES MELLITUS
Type I
Sudden onset
Weight loss
Hyperglycemia
Under 40 years old
Type II
Slow onset
May go undetected for years
“ 3 Ps” are usually mild
If untreated, may have skin infections and arteriosclerotic conditions

DIABETES MELLITUS
Diagnostic tests
Urine glucose and acetone
Blood glucose
Oral glucose tolerance test
2-hour postprandial blood sugar
Glycohemoglobin (A1C)

DIABETES MELLITUS
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 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

Endocrine week 4 pt

by iothman

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Endocrine week 4 pt Presentation Transcript