Nursing Care of Patients with Endocrine Disorders PDF
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This document is a lecture on nursing care of patients with endocrine disorders. It details the various components of the endocrine system, including the glands and their functions. The lecture also covers different disorders of the endocrine system.
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NCM 3116 (Care of Clients with Problems in Nutrition and Gastro-intestinal metabolism and Endocrine Function, Perception and Coordination-Acute and Chronic – LECTURE) NURSING CARE OF PATIENTS WITH...
NCM 3116 (Care of Clients with Problems in Nutrition and Gastro-intestinal metabolism and Endocrine Function, Perception and Coordination-Acute and Chronic – LECTURE) NURSING CARE OF PATIENTS WITH The Thyroid secretes: o Thyroxine (T4) DISTURBANCES IN ENDOCRINE o Triiodothyronine (T3) o Thyrocalcitonin I. THE ENDOCRINE SYSTEM The Parathyroid secretes: Is made of hormone secreting glands that helps maintain and o Parathormone (PTH) regulate vital functions such as: o Response to stress and injury THE ADRENAL GLANDS o Growth and development The two adrenal glands are located o Reproduction immediately anterior to the kidneys o Ionic homeostasis o Energy metabolism TWO REGIONS Inner Medulla, which is a source of the catecholamines epinephrine and norepinephrine. Outer Cortex, which secretes several classes of steroid hormone, glucocorticoids and mineralocorticoids. The Adrenal Cortex: o Glucocorticoids THE PITUITARY GLAND o Mineralocorticoids o Androgens The Pituitary Gland, also The Adrenal Medulla: known as the hypophysis, and o Epinephrine (adrenaline) master gland THE PANCREAS An elongated organ nestled next to the first part of the small intestine. The endocrine pancreas refers to those cells within the pancreas that TWO PARTS synthesize and secrete hormones. The endocrine portion of the pancreas takes the form of many small clusters of cells called islets of Langerhans. THREE MAJOR CELL TYPES: Alpha cells (A cells) secrete the hormone glucagon, Beta cells (B cells) produce insulin and cells Anterior Pituitary (adenohypophysis) secretes: Delta cells (D cells) secrete the hormone o Growth Hormones (GH) or Somatotropin somatostatin, which is also produced by a o Prolactin (Mammotropic, Lactotropic, Luteotropic) number of other endocrine cells in the o Gonadotropic hormones (LH & FSH) body o Thyrotropic hormone (TSH) o Andrenocorticotropic hormones (ACTH) THE OVARIES & TESTES Posterior pituitary (neurohypophysis) secretes: The gonads, the primary reproductive organs, are the testes in o Antidiuretic hormone (ADH) the male and the ovaries in the female. These organs are o Oxytocin responsible for producing the sperm and ova, but they also o Melanocyte-stimulating hormone (MSH) secrete hormones and are considered to be endocrine glands. THE THYROID & PARATHYROID Thyroid gland is located in the neck, in close approximation to the first part of the trachea. In humans, the thyroid gland has a “butterfly” shape Close examination of a thyroid gland will reveal one or more small, light-colored nodules on or protruding from its surface – these are parathyroid glands (meaning “beside the thyroid”). 1 TESTES HYPERPITUITARISM Male sex hormones, as a group, are called androgens. Over secretion of one or more of the hormones secreted by the The principal androgen is testosterone, which is secreted by the pituitary gland caused by a secreting pituitary tumor, typically testes. benign adenoma. This steroid hormone is responsible for: THREE TYPES OF PITUITARY TUMORS The growth and development of the male reproductive structures a. Eosinophilic Tumor Increased skeletal and muscular growth - Enlargement involves all tissues and organs (gigantism) Enlargement of the larynx accompanied by voice changes - Many of these patients suffer from headaches and visual Growth and distribution of body hair disturbances because the tumors exert pressure on the optic Increased male sexual drive nerves b. Basophilic Tumor OVARIES - Give rise to Cushing’s syndrome with features largely attributable to hyperadrenalism, including masculinization Two groups of female sex hormones are produced in the ovaries, and amenorrhea in females, truncal obesity, hypertension, the estrogens and progesterone. osteoporosis, and polycythemia Theses steroid hormones contribute to the development and c. Chromophobic Tumor function of the female reproductive organs and sex - Represent 90% of pituitary tumors characteristics. - Produce no hormones but destroy the pituitary gland causing hypopituitarism At the onset of puberty, estrogens promote: - Patient with this disease are often obese and somnolent and The development of the breasts exhibit fine, scanty hair, dry, soft skin, a pasty complexion Distribution of fat evidenced in the hips, legs, and breast and small bones Maturation of reproductive organs such as the uterus and vagina - They also experience headache, loss of libido and visual Repair endometrium after menstruation defects progressing to blindness - Other signs and symptoms include polyuria, polyphagia, Progesterone causes: lowering of the basal metabolic rate and a subnormal body The uterine lining to thicken in preparation for pregnancy temperature. Regulation of Hormones SIGNS AND SYMPTOMS The secretion of many hormones is initiated by a negative-feedback Systemic system Excessive or abnormal growth patterns Abnormal milk secretion (galactorrhea) Overstimulation of one or more of the target glands, resulting in the release of excessive thyroid, sex, or Adrenocortical hormones Local Blindness due to pressure in the optic nerve Headaches Somnolence (state of being drowsy) DIAGNOSTIC EVALUATION 1. Radiologic 2. Laboratory testing a. Sensitive and specific immunologic staining methods that help determine the nature of the hormones synthesized and secreted by pituitary tumors. b. Plasma levels of GH, LTH, FSH, and LH 3. Metrizamide – accentuated CT scan Gigantism, which is an overgrowth of the long bones, develops in DISORDERS children before the age at which the epiphyses of the bones close. - Individual suffering from gigantism may grow as tall as 8 or 9 PITUITARY feet. Pituitary Gland Dysfunction Acromegaly is a disease of adult that develops following closure of the epiphyses of the long bones. HORMONE HYPERPITUITARISM HYPOPITUITARISM - Marked by both increases in bone thickness and hypertrophy of Growth Gigantism (child) Short stature and the soft tissues hormone Acromegaly (adult) dwarfism (child) (Somatotropin) Silent (adult) Robert Wadlow Prolactin Infertility and Postpartum Lactation galactorrhea (female) failure ACTH Cushing’s disease Adrenocortical insufficiency TSH Hyperthyroidism Hypothyroidism LH and FSH Gonadal dysfunction Hypogonadism II. DISORDERS OF THE PITUITARY GLAND 2 Report output greater than 900ml/2hrs. (DI) Cushing’s Disease Oversecretion of ACTH by a basophilic tumor, which in turn results in oversecretion of adrenocortical hormones Sexual Disturbance Excess secretion of gonadotrophic hormones from pituitary tumors produces sexual precocity in children. Excess prolactin secretion causes amenorrhea or galactorrhea (excessive flow of milk) in women. NURSING INTERVENTIONS Help the client accept the altered body image that is irreversible Assist family to understand what the client is experiencing Help the client recognize that medical supervision will be required for life Help the client understand the basis for the change in sexual functioning Assist the client in expressing feelings Care for the client following a hypophysectomy: o Protect from stress situations o Protect from infection o Follow and maintain an established schedule for hormone INTERVENTION replacement Drug: Bromocriptine (Parlodel) lower GH level and prolactin Follow a nursing care for the client undergoing intracranial level surgery: a. Perform neurologic assessments Octreotide and Lanreotide (somastatin analog) used b. Measure specific gravity of urine, MIO, and check daily preoperatively to improve patient condition and shrink the tumor weight to identify complication of DI Hypophysectomy treatment of choice c. Check nasal drainage for glucose to determine presence of CSF Hypophysectomy d. Encourage deep breathing but not coughing Partial or complete removal of pituitary gland e. Institute measures to prevent constipation o Indications ▪ Pituitary tumors HYPOPITUITARISM ▪ Diabetic retinopathy Deficiency of one or more of the hormones produced by the ▪ Metastatic cancer of breast or prostate anterior lobe of the pituitary When both the anterior and posterior lobes fail to secrete Surgical approaches: hormones, the condition is called panhypopituitarism o Craniotomy – transfrontal o Transsphenoidal – incision via inner aspect of upper lip and Causes gingiva 1. Hypophysectomy 2. Non-secreting pituitary tumors TRANSPHENOIDAL APPROACH 3. Pituitary dwarfism 4. Post-partum pituitary necrosis 5. Functional disorders Specific Disorder resulting to Hypopituitarism 1. Dwarfism 2. Secondary Adrenocortical insufficiency 3. Myxedema (severe hypothyroidism) 4. Sexual and reproductive disorders INTERVENTION NURSING INTERVENTIONS AFTER TRANSPHENOIDAL 1. Removal HYPOPHYSECTOMY 2. Permanent replacement of the hormones secreted by the target Keep head elevated to promote venous drainage for 2 weeks organ Maintain nasal pack as per doctor’s order 3. Medication Provide good oral care a. Corticosteroids for correction of secondary Adrenocortical Avoid blowing of nose and other activities that increase ICP insufficiency 3 b. Thyroid hormone for treatment of myxedema c. Sex hormone to correct hypogonadism NURSING MANAGEMENT Physical assessment and continue monitoring of F and E imbalance status: I and O, daily weight, skin turgor, electrolyte levels Replace fluid by mouth or parenterally Monitor response to ADH replacement Teach client on long term vasopressin therapy the need for daily weight records, recognition of polyuria Advised wearing of medical identification bracelet SIADH (SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE) NURSING INTERVENTIONS Excessive ADH secretion from the pituitary gland Monitor effects of hormone replacement Opposite of diabetes insipidus Discuss the importance of adhering medical regimen on a long- Patient cannot excrete a dilute urine term basis Retain fluids Allow client ample time to verbalize feelings regarding the long- Develop sodium deficiency term nature of the disease and impact on daily life May occur in pt. with Bronchogenic CA, severe pneumonia, Provide adequate rest periods pneumothorax and other disorders of the lungs DIABETES INSIPIDUS (ADH DEFICIENCY) CLINICAL MANIFESTATIONS Disorder of the posterior lobe of the pituitary gland characterized Headache by a deficiency of ADH (vassopresin) Nausea/vomiting Muscle cramps Causes of ADH insufficiency Restlessness 1. Vasopressin deficiency (ADH deficiency) due to Lethargy - Abnormalities in the hypothalamus and primary gland from Confusion familial or idiopathic causes primarily diabetes insipidus Decreased reflexes - Destruction of the gland by tumors in the Seizure hypothalamopituitary region, trauma, infectious process, Coma vascular accidents or metastatic tumors from breast or lung (secondary diabetes insipidus) Death - Medications such as phenytoin (Dilantin), alcohol, and lithium carbonate MEDICAL MANAGEMENT 2. Nephrogenic diabetes insipidus Eliminating underlying cause - Owing to an inherited defect, the kidney tubules cannot Establish airway reabsorb water Restricting fluid intake as per doctor’s order - This condition also may develop secondary to potassium Hypertonic solution depletion or pyelonephritis. Diuretic drugs Mannitol (hypertonic solution) ASSESSMENT Lasix Major Manifestations Bumex (loop diuretic) 1. Polyuria – urine output greater than 250ml per hour Corticosteroids 2. Polydipsia – drinks 2L-20L of fluid daily and craves for cold Barbiturates water Positioning 3. Urine specific gravity of 1.001 to 1.005 Hyperventilation Control temperature DIAGNOSTIC EXAMS 1. Water deprivation test – is carried out by withholding fluids for NURSING MANAGEMENT 8-12 hours or until 3%-5% of the body weight is lost close monitoring of fluid and intake, daily weight, urine and - The patient is weighed frequently during the test blood chemistries and neurologic status - Plasma and osmolality studies are performed at the monitoring and regulating IVF accurately beginning and end of the test - The inability to increase the specific gravity and osmolality administer medications as per doctor’s order of the urine is characteristic of diabetes insipidus assessment of patients for side effects of treatment of SIADH 2. Does not respond to ADH injection (only for Nephrogenic D.I.) asses for pain, anxiety, and depression; and provide interventions 3. Plasma level of ADH to improve pain management and coping ability monitor signs and symptoms of complications INTERVENTION 1. Desmopressin (DDAVP) a synthetic vasopressin given III. DISORDERS OF THE THYROID GLAND intranasally 2. Surgical resection of tumor Thyroid Enlargement (simple goiter, non-toxic goiter, nodular goiter) 3. Vasopressin injection (aqueous Pitressin) or vasopressin tannate the thyroid gland needs iodine in order to synthesize and secrete (Pitressin Tannate) its hormones - Pitressin typically alleviates polyuria, and usually polydipsia for 24-72 hours. 4. Synthetic polypeptide DDAVP (desmopressin acetate) can be insufflated through the nose. Largely replaced vasopressin for long term treatment of person with severe D.I. 5. Chlorpropamide (diabenese) and thiazide are used in mild forms 4 GOITER SYMPTOMS Types of Goiter Weight loss 1. Endemic (iodine deficient) Goiter Polyphagia - Is principally caused by nutritional iodine deficiency - It is twice as prevalent in women as in men Diaphoresis - Commonly develops in adolescents, pregnant women and Nervousness nursing mothers residing in iodine deficient regions Restlessness 2. Sporadic Goiter Heat intolerance - Is not restricted to any geographic area Increased sweating Causes include: Fatigue a. Genetic defects resulting in faulty iodine metabolism Insomnia b. Ingestion of large amounts of nutritional goitrogens (e.g., Frequent bowel movements cabbage, soybeans, peanuts, peaches, peas, strawberries, spinach, Menstrual irregularities in women and radishes) c. Ingestion of medical goitrogens, e.g., thiouracil ASSESSMENT (prohylthiouracil), thiocarbamides (aminothiazole, tolbutamide) Increased heart rate and iodine in large doses. Systolic blood pressure may be elevated Thyroid enlargement or goiter DIAGNOSIS AND ASSESSMENT The goiter grows large enough to distort the appearance of the LABORATORY EXAMS neck Serum TSH is usually decreased They may also experience respiratory distress and difficulty T3 and free T4 are usually elevated swallowing if the goiter is very large Triglycerides T3RU MEDICAL MANAGEMENT Radioactive iodine uptake Pharmaceutical Management Glucose test Strong iodine solution (Lugol’s solution) or saturated solution of Cholesterol test potassium iodine (SSKI drops) Antithyroglobulin antibody Thyroid hormone replacement with sodium levothyroxine (Synthroid), Desiccated thyroid (thyroid USP) and sodium THYROID SCAN liothyronine (Cytomel) Measures the affinity of the thyroid gland for radioactive iodine When administering thyroid preparations, assess the individual carefully (Normal 15-40%) for symptoms of thyrotoxicosis, (tachycardia, increased appetite, Preparation diarrhea, sweating, agitation, tremors, palpitation) No diagnostic test with contrast medium in the past 3 mos. No foods or drugs with iodine for 2 weeks prior to test Surgical Management Discontinue contraceptive pills Subtotal thyroidectomy NPO 6-8hrs if 131 is used IV No fasting HYPERTHYROIDISM (THYROTOXICOSIS; OVERACTIVE THYROID) TREATMENT Excessive synthesis and secretion of endogenous or exogenous Antithyroid medications (Thyroid Inhibitors) thyroid hormones by the thyroid o Examples: iodine (Lugol’s Solution), Methimazole (Tapazole), PTU (Propylthiouracil) CAUSES, INCIDENCE, AND RISK FACTORS o Major S/E: Graves disease ▪ Agranulocytosis (decreased WBC) Toxic multinodular goiter ▪ Skin disturbances (hypersensitivity) Toxic adenoma ▪ N/V (irritation of gastric mucosa) Thyroiditis ▪ Decreased metabolism ▪ Iodine: bitter taste; stains teeth (local oral effect on Tumors of the testes or ovaries teeth and mucosa) Inflammation (irritation and swelling) of the thyroid due to viral infections or other causes NURSING INTERVENTIONS Ingestion of excessive amount of thyroid hormone Report the occurrence of any S/E to physician especially sore Ingestion of excessive iodine throat and fever Avoid crowded places and potentially infectious situations Administer liquid iodine prep dilute in beverage of choice through a straw Assess client for signs of hypothyroidism Radioactive iodine therapy 5 Thyroidectomy (If the thyroid must be removes with radiation or surgery, replacement thyroid hormones must be taken for the rest GRAVE’S DISEASE (TOXIC DIFFUSE GOITER, of the person’s life) EXOPHTALMIC GOITER) Beta-blockers (propranolol and atenolol) It is predominantly a disorder of females It affects women four times as often as it does men, especially young women between the ages of 20 and 40 Causes 1. Over functioning of the entire gland 2. Single or multiple functioning adenomas of thyroid cancer 3. Over treatment of myxedema with thyroid hormone HALLMARKS OF GRAVE’S DISEASE 1. Hyperthyroidism Thyroid gland enlargement 2. Exophthalmos (abnormal protrusion of the eyes) 3. Dermopathy (skin lesions) Complications of Thyroidectomy Rapid heart rate, congestive heart failure, and atrial fibrillation Thyroid crisis or “storm” Fever Decreased mental alertness Abdominal pain may occur Increases the risk for osteoporosis NURSING INTERVENTIONS Monitor V/S, I&O Provide cool, quiet environment Provide adequate rest; promote normal though processes ETIOLOGY (minimize sleep disruption); use safety measures to reduce risk of Grave’s disease is an autoimmune disorder trauma or fall Have circulating autoantibodies that react against thyroglobulin Provide high caloric, protein, CHO, vitamin diet without Thyroid-stimulating immunoglobulins (TSI) are present in the stimulants, extra fluid; restrict stimulants (tea, coffee, alcohol) serum of 80 to 90 percent of hyperthyroid individuals IVF therapy as prescribed Weigh client daily ASSESSMENT AND DIAGNOSIS Provide eye protection: ophthalmic medicine Extremely agitated and irritable, with a hand tremor at rest Provide emotional support Weight loss occurs owing to the quickened metabolism Be alert for complications: corneal abrasion, heart disease, The person’s bodily processes literally “speed up” thyroid storm Maintain skin integrity SIGNS AND SYMPTOMS Explain procedures to client and encourage verbalization of Loose bowel movements feelings Heat intolerance Thyroidectomy: Preoperative care Profuse diaphoresis Administer prescribed antithyroid drugs to achieve euthyroid Tachycardia state Tremors Teach coughing, DBE, and use of hands to support neck and to Skin become warm and smooth avoid strain on suture lines Hair appears thin and soft Pre-Operative Emotions are adversely may be cyclic, ranging from mild Achieve euthyroid state by Lugol’s administration and any euphoria to extreme fatigue and depression, again followed by antithyroid drug as per doctor’s order episodes of over activity Takes 2-3 weeks to decrease the vascularity of the thyroid and ASSESSMENT prevent post operative hemorrhage Grave’s disease is diagnosed on the basis of a. The person’s often striking physical appearance (enlarged neck, Postoperative Care protruding eyes, agitated expression) Semi-fowler’s position without pillows b. The symptoms of agitation, restlessness, and weight loss; and Limit head movement c. The serum thyroid hormone levels, 24-hour radio-iodine uptake, Avoid tension on suture line and T3 resin uptake are usually all elevated Check dressing esp. back of neck Observe for respiratory distress caused by tracheal edema The Three Major Forms of Therapy Be alert for signs of hemorrhage 1. Antithyroid medication e.g., Propylthiouracil and Methimazole Instruct patient: talking limited, note any hoarseness – may 2. Radioiodine e.g., 131 Iodine (1311) therapy indicate injury in laryngeal nerve 3. Surgery NURSING INTERVENTIONS (CONT...) NURSING INTERVENTION Observe for signs of tetany: Chvostek’s sign, Trousseau’s sign Provide an environment that is restful both mentally and Calcium gluconate IV at bedside physically Have tracheostomy set and suction machine ready at bedside Explain to significant others that any bizarre, difficult behavior is Observe for signs of thyroid storm (high fever, tachycardia, likely to be temporary and should steadily improve with irritability, delirium, coma) intervention Gradual increase ROM of neck Maintain a quiet, understanding manner when caring 6 Accept their irritation and emotional outburst as normal LATE SYMPTOMS: expressions of the disease Slow speech Incorporate occupational therapy into care planning Dry flaky skin Provide a well-balanced diet Thickening of the skin Provide cool environment Puffy face, hands and feet Decreased taste and smell THYROID STORM Thinning of eyebrows Uncontrolled and potentially life-threatening hyperthyroidism Hoarseness due to sudden and excessive release of thyroid hormone into the Abnormal menstrual periods bloodstream Note: patient with hypothyroidism are hypersensitive to narcotics and PRECIPITATING FACTORS barbiturates - Stress - Infection - Unprepared thyroid surgery CLINICAL MANIFESTATIONS Hyperpyrexia, diarrhea, dehydration, extreme tachycardia, arrythmias, extreme irritation, delirium, coma, shock and death if not adequately treated MANAGEMENT Drug therapy: antithyroid drugs Propylthoiuracil (PTU), Hydrocortisone, sedatives, cardiac drugs, oxygen administration, LABORATORY EXAMINATIONS Iodine to lower output of T4 T4 test (low) Immediate management of hyperthermia, tachycardia and Serum TSH (high in primary hypothyroidism, low or low-normal prevention of vascular collapse in secondary hypothyroidism Increased cholesterol levels NURSING INTERVENTION Increased liver enzymes Administer IV therapy as ordered Increased serum prolactin Low serum sodium Complete blood count (CBC) that shows anemia HYPOTHYROIDISM Myxedema – Adult Hypothyroidism TREATMENT Cretinism – hypothyroidism in infants and children Replace the deficient thyroid hormone (Synthetic levothyroxine) Examples: Levothyroxine Sodium (Synthroid), Liothyronine Definition sodium (Cytomel), Liothrix (Euthroid, Thyrolar) The thyroid gland fails to produce enough thyroid hormones Administration of high dose glucocorticoids every 8 to 12 hrs for 24 hrs. followed by low dose therapy as per doctor’s advised Causes Hashimoto’s thyroiditis (the most common, an autoimmune MAJOR S/E: disease) – chronic progressive disease of thyroid gland caused by Increased metabolism infiltration of lymphocyte Hyperactivity Progressive destruction of the parenchyma and hypothyroidism if Cardiac stimulation untreated Medications: lithium, iodine compounds, antithyroid medications NURSING CARE Radiation to the neck and head Take the medication as scheduled at the same each day Congenital defects Take radial pulse; notify physician if greater than 100 beats/min Surgical removal of the thyroid gland Monitor V/S to detect changes in CV status and ability to Inflammatory conditions respond to stress Monitor ECG tracings to detect arrythmias Risk Factors Provide warm environment and prevent chilling Age over 50 years Administer fluids and all prescribed drugs with caution Female gender WOF and teach patients signs of complications Obesity a. Angina pectoris Thyroid surgery b. Cardiac failure: dyspnea, palpitations Exposure of the neck to X-ray or radiation treatments c. Myxedema coma: weakness, syncope, slow pulse rate, subnormal temperature, slow respirations, lethargy SYMPTOMS Adequate hydration and roughage in diet (high fiber) EARLY SYPMTOMS Control of dietary intake to limit calories and reduce weight Weakness Low calorie, high protein, increase fiber and fluids Fatigue Patient teaching on continued HRT through life; regular medical Cold intolerance check-up; energy conservation techniques and the need to Constipation increase activity gradually; how and when to take medications Weight gain (unintentional) Depression COMPLICATIONS Joint or muscle pain Myxedema coma, the most severe form of hypothyroidism Thin, brittle fingernails Thin and brittle hair Symptoms and signs of myxedema coma include: Paleness o Unresponsiveness o Decreased breathing 7 o Low blood pressure Reduced bone mineral density on bone densitometry (DEXA) o Low blood sugar Urinary calcium may be increased o Below normal temperature TREATMENT Other complications: Treatment depends upon the severity and cause of the condition. o Heart disease o Increased risk of infection In primary hyperparathyroidism, if the calcium level is very high o Infertility or symptoms are present, surgery may be necessary to take out o Miscarriage the gland that is overproducing the hormone. Secondary hyperparathyroidism is treated by restoring the calcium back into the normal range, usually by giving calcium and vitamin D alone or in combination, depending on the underlying disorder NURSING INTERVENTION Strain the urine, observing for stones Encourage fluid intake, especially fluids such as cranberry juice to acidify the urine Assist the client in ambulating to help prevent demineralization MIO Combat constipation Limit intake of foods high in calcium especially milk/dairy products IV. DISORDERS OF THE PARATHYROID GLAND COMPLICATIONS HYPERPARATHYROIDISM Complications that result from excess calcium deposits within the body is excessive production of parathyroid hormone by the Skeletal damage parathyroid glands Urinary tract infection due to kidney stones and obstruction Peptic ulcer disease TYPES OF HYPERPARATHYROIDISM Pancreatitis 1. Primary hyperparathyroidism Pseudogout - Parathyroid hormone is produced without regard to the calcium levels HYPOPARATHYROIDISM - It is caused by enlargement of one or more of the is having insufficient parathyroid hormone, which causes parathyroid glands. abnormal low blood levels of calcium and phosphorous 2. Secondary hyperparathyroidism - When the body produces extra parathyroid hormone Causes because the calcium levels are too low 3. Tertiary hyperparathyroidism lack of PTH - If the parathyroid glands continue to produce too much blood calcium levels fall, and phosphorous rise parathyroid hormone even though the calcium level is back injury to the parathyroid glands during head and neck surgery to normal side effect of radioactive iodine treatment for hyperthyroidism PTH secretion also may be impaired when blood levels of SYMPTOMS magnesium are low Fatigue When blood pH is too high, a condition called metabolic Back pain alkalosis Joint pain Fracture of long bones SYMTPOMS Decreased height Tingling lips, hands and feet Increased urine output Muscle cramps Increased thirst Pain in the face, legs, and feet Upper abdominal pain Abdominal pain Loss of appetite Dry hair Nausea Brittle nails Muscular weakness Dry, scaly skin Muscle pain Cataracts Depression Weakened tooth enamel in children Personality changes Muscle spasms called tetany (can lead to spasms of the larynx, Stupor and possibly coma causing breathing difficulties) Itching of the skin Convulsion (seizures) Blurred vision (because of cataracts) LABORATORY EXAMINATIONS Bone pain or tenderness Low serum calcium level LABORATORY EXAMINATION High serum phosphorous level Serum calcium is increased Low serum parathyroid hormone level Serum phosphorus is decreased Low serum magnesium level (possible) Serum alkaline phosphatase may be increased Abnormal heart rhythms on ECG Intact parathyroid hormone (PTH) in the blood is increased Urine calcium Bone X-ray shows bone reabsorption or fractures TREATMENT Imaging of the kidneys or ureters may show calcification or Goal to increase serum Ca level to 9 to 10 mg/dl and eliminate obstruction the symptoms 8 Ca Chloride or Ca gluconate given IV for emergency treatment Calciferol (vit D) to help raise serum calcium levels Parathormone injections High calcium diet Aluminum hydroxide to decrease absorption of phosphorous from the GI tract NURSING INTERVENTIONS Observe for respiratory distress and have emergency equipment available to perform a tracheostomy Maintain seizure precautions Monitor serum Ca and phosphate levels Check V/S frequently Provide a calm environment free of harsh stimuli Provide a drug and dietary instruction including elimination of milk, cheese and egg yolks because of high phosphorous content V. DISORDERS OF THE ADRENAL GLANDS ADDISON’S DISEASE Alternative Names ASSESSMENT AND LABORATORY EXAMINATIONS o Adrenocortical hypofunction Blood pressure is low o Chronic adrenocortical insufficiency Cortisol level is low o Adrenal insufficiency Serum sodium is low Increased potassium Definition An abdominal x-ray may show adrenal calcification o Adrenal hormone deficiency caused by damage to the outer An abdominal CT scan may show adrenal calcification, layer of the adrenal gland (adrenal cortex) enlargement or atrophy Causes MEDICAL MANAGEMENT Damage to the adrenal cortex caused by the following: Immediate treatment for combating circulatory shock o Autoimmune disease Restoring blood circulation o Infections such as tuberculosis, HIV, or fungal Administering fluids and corticosteroids infections Monitoring V/S o Hemorrhage, blood loss Placing pt in a recumbent position with legs elevates o Tumors Hydrocortisone (Solu-Cortef) via IV o Use of blood-thinning drugs, (anticoagulants), anticonvulsants and rifampicin D5NSS Vasopressor amines maybe required if hypotension persist RISK FACTORS NURSING INTERVENTIONS Type 1 diabetes Monitor V/S, be alert for elevation of temperature (infxn, DHN), Hypoparathyroidism alterations in PR and rhythm and alteration in BP Hypopituitarism Observe for signs of Na and K imbalance Pernicious anemia MIO and weigh daily Testicular dysfunction Administer steroids as ordered Grave’s disease Administer steroids with antacid to limit ulcerogenic factor of the Chronic thyroiditis drug Candidiasis Put the client in a private room to prevent contact with clients Dermatitis herpetiformis – eruption of itching papules, vesicles, having infectious diseases and lesion resembling hives typically in clusters Limit the number of visitors Vitiligo – skin disorder manifested by smooth white spots to various parts of the body CUSHING’S DISEASE Myasthenia gravis – progressive weakness of voluntary muscles EXCESSIVE CORTICOSTEROIDS Additional symptoms that may be associated with this disease: SYMPTOMS o Weight gain (unintentional) Extreme weakness o Buffalo hump Fatigue o Skin spots, red Emaciation o Skin blushing/flushing Nausea and vomiting o Muscle atrophy or thin extremities Chronic diarrhea o Fatigue Loss of appetite o Bone pain or tenderness Darkening of the skin – patchy skin color o High blood pressure o Unnaturally dark color in some locations o Paleness may also occur ASSESSMENT AND LABORATORY EXAMINATION Mouth lesions on the inside of a cheek Serum cortisol, urinary cortisol and low dose dexamethasone Slow, sluggish, lethargic movement suppression test Changes in the blood pressure or heart rate Cranial MRI or cranial CT scan may show pituitary tumor Abdominal CT may show adrenal mass 9 Glucose test is elevated EXERCISE GUIDE for DIABETES FITNESS: Potassium test may be low Frequency – 3x a week Increase serum Na Intensity – 60-80% of Maximal Heart Rate White blood cell count may be elevated Time – AEROBIC ACTIVITY 20-30mins. With 5-10 mins. Warm Up TREATMENT Cushing’s syndrome caused by drug therapy with corticosteroid, the drug must be slowly decreased under medical supervision Cushing’s disease caused by a tumor, surgery to remove the ORAL HYPOGLYCEMIC AGENTS tumor is recommended. (HYPOPHYSECTOMY) Sulfonylureas Radiations is needed as well o Chlorpropamide (Diabinase) Hydrocortisone (cortisol) replacement therapy is needed after o Tolbutamide (Orinase) surgery, and sometimes forever o Glimepinide (Solosa) o Acetohexamide (Dymelor) NURSING INTERVENTIONS Prandial Glucose Regulator Monitor vital signs, MIO, daily weight, blood glucose and o Repaglinide (Novonorm) electrolytes o Rosiglitazone (Avandia) Protect the client from exposure to infections Non- Sulfonylureas Minimize stress in the environment by limiting visitors and o Metformin (Glucophage) explaining procedures carefully o Precose (Acarbose) Instruct the client regarding diet and supplementation; encourage o Rosiglitazone (Avandia) diet rich in nutrient dense foods such as fruits and vegetables, whole grains and legumes to improve and maintain nutritional MAJOR S/E OF ANTIDIABETICS status and prevent any possible drug-induced nutrient Irritability deficiencies Confusion Tachycardia OTHER MANAGEMENT Tremor Increased protein and potassium but decrease calories and Moist skin sodium Headache Medication: Hunger o Aminoglutethimide (Cytadren) Oral hypoglycemics o Mitotane (Lysodren) Skin rash o Ketoconazole (Nizoral) Jaundice o Trilostane (Modastane) Pruritis Surgery: adrenalectomy Allergic reactions NURSING CARE FOR PATIENTS TAKING ANTIDIABETICS VI. DISORDERS OF PANCREATIC GLAND - Assess clients for signs of hypoglycemia - Instruct client to DIABETES MELLITUS ❖ Use proper medication procedure A group of metabolic diseases characterized by increased levels ❖ Comply with dietary program of glucose in the blood resulting from defects in insulin secretion, ❖ Avoid alcohol insulin action or both (American Diabetes Association 2016) ❖ Be prepared for hypoglycemic incidents (rapid acting glucose solution, hard candy, orange juice) MAJOR TYPES 1. Insulin-Dependent Diabetes – formerly called juvenile type; has Insulin Administration rapid onset and requires insulin administration ❖ Administer all form of insulin subcutaneously 2. Non-Insulin Dependent Diabetes – formerly called adult onset ❖ Use only regular insulin for IV administration type, often can be controlled with diet ❖ When mixing insulin, draw regular insulin into the syringe first 3. Gestational Diabetes – occurs during pregnancy usually during ❖ Rotate sites of administration 2nd and 3rd trimester MAJOR COMPLICATIONS OF DIABETES MELLITUS ASSESSMENT Hypoglycemia Polyphagia Diabetic ketoacidosis (DKA) Polydipsia Hyperglycemic hyperosmolar nonketotic syndrome (HHNS) Polyuria Hyperglycemia CAUSES OF HYPOGLYCEMIA Wight loss Too much insulin Blurred vision Excessive intake of antidiabetic agents Slow wound healing Unusually high levels of exercise Vaginal infections Insulin potentiating drugs Weakness & paresthesias Signs of inadequate feet circulation SIGNS OF HYPOGLYCEMIA Sweating Approach to Diabetes Mellitus: Tremor Nutritional Therapy Low glycemic index Tachycardia Exercise Palpitations Oral Hypoglycemic Agents/Insulin Nervousness Education Hunger Monitoring SIMPLE CARBOHYDRATE TO TREAT HYPOGLYCEMIA 10 3 or 4 commercially prepared glucose tablets o CHILD: 2-3 glucose tabs 4-6 ounces of fruit juice or regular soda o CHILD: ½ cup or 120ml or orange juice or sugar-sweetened juice 6-10 Life Savers or hard candy o CHILD: 3-4 hard candies or 1 candy bar 2-3 teaspoons of sugar or honey o CHILD: 1 small box of raisins 10-15g of simple carbohydrate DIABETIC KETOACIDOSIS Assessment: 3 main clinical features: o Hyperglycemia o DHN and electrolyte loss o Acidosis 3Ps Blurred vision Marked fatigue Headache Hypotension Weak, rapid pulse Anorexia, nausea, vomiting & abdominal pain Acetone breath (fruity odor) Kussmaul respirations Mental status changes MANAGEMENT FOR DKA Treating hyperglycemia correcting dehydration thru rehydration, electrolyte loss and acidosis HYPERGLYCEMIC HYPEROSMOLAR NONKETOTIC COMA A metabolic disorder of type 2 resulting from a relative deficiency initiated by an illness that raises the demand for insulin Management same with DKA CHRONIC COMPLICATIONS OF DM 1. Peripheral Neuropathies - Result from thickening of vessel walls that supply peripheral nerves causing alteration in sensory perception 2. Retinopathy - Microangiopathy of the retina leading to retinal microvascular occlusion, eventually leading to blindness 3. Nephropathy - Thickening of glomerular basement membrane resulting in hardening and thickening of the glomeruli 4. Macrovascular disease - Atherosclerosis 11