Download Free Medical Alterations in the Endocrine System PowerPoint Presentation

Alterations in the Endocrine System PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : pituitary

Tags : endocrine, pituitary

Published on : May 25, 2019 | Views : 1873 | Downloads : 8

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Advanced Medical Surgical Nursing Unit 2 Alterations in the Endocrine System
Slide 2-

Endocrine System The endocrine system is all the organs of the body that are endocrine glands. An endocrine gland secretes hormones. Hormones are molecules that are secreted into the blood. Hormones are substances that are secreted by one group of cells that affects the physiology of another group of cells (organs). The endocrine system is controlled by the pituitary gland and the hypothalamus. Compared to most other organs in the body, endocrine organs are well vascularized. VIDEO http://www.youtube.com/watch?v=HrMi4GikWwQ
Slide 3-

Endocrine System A system of ductless glands Secrete messenger molecules called hormones Interacts closely with the nervous system Endocrinology – study of hormones and endocrine glands
Slide 4-

Major Endocrine Glands Hypothalamus Pituitary Gland Thyroid Gland Parathyroid Glands Thymus Gland Adrenal Glands Pancreas Ovaries Testes Pineal Gland
Slide 5-

Scattered throughout the body Pure endocrine organs Pituitary, pineal, thyroid, parathyroid, and adrenal glands Organs containing endocrine cells Pancreas, thymus, gonads, and the hypothalamus Richly vascularized
Slide 6-

Hormones Hormones generally are thought of as chemical messengers that are transported in body fluids. They are highly specialized organic molecules produced by endocrine organs that exert their action on specific target cells. Hormones do not initiate reactions; they are modulators of systemic and cellular responses. Most hormones are pre- sent in body fluids at all times, but in greater or lesser amounts depending on the needs of the body.
Slide 7-

Hormones can be synergistic; aldosterone and antidiuretic hormone (ADH) both help increase volume of fluid in body to raise blood pressure. Some hormones are antagonists; Atrial natriuretic peptide (ANP, produced by heart cells) is released when you have high blood pressure. It causes the kidney to secrete more water, so blood pressure can decrease. That is the opposite of ADH, which makes you urinate less. Some hormones are permissive; you need one in order for a second to do its job well. Thyroid hormone is permissive for growth hormone (you need thyroid hormone in order for GH to work). Not enough thyroid hormone can cause stunted growth, even if enough growth hormone is present.
Slide 8-

Endocrine versus Nervous system NEURO Nervous System Nervous system performs short term crisis management The nervous system sends electrical messages to control and coordinate the body Nerve impulse is delivered by the axon of a nerve cell called neuron ENDOCRINE Endocrine System Endocrine system regulates long term ongoing metabolic activity The endocrine system uses chemicals messenger called hormones to “communicate”. Hormones alter metabolic activities of tissues A hormone is secreted by a group of specialized cells called gland Hormones are transported by the blood vessels Paracrine communication involves chemical messengers between cells within one tissue
Slide 9-

Quiz: Introduction to Endocrine System The endocrine system acts through neurotransmitters called hormones that influence growth, development, and metabolic activities. True False Endocrine glands have ducts that carry their secretory product to a surface. True False Since the endocrine glands are scattered throughout the body, they are regarded as different systems. True False
Slide 10-

The specific cells that respond to a given hormone have receptor sites for that hormone. True False A negative feedback system causes a reversal of increases and decreases in body conditions in order to maintain a state of stability or homeostasis. True False
Slide 11-

Some glands have endocrine and non-endocrine regions, which function differently. True False Growth hormone is a protein that stimulates the growth of bones, muscles, and other organs by promoting protein synthesis. This hormone is produced by the pituitary gland. True False
Slide 12-

The Endocrine System
Slide 13-

ppt slide no 13 content not found
Slide 14-

MAJOR ACTIONS AND SOURCES OF SELECTED HORMONES
Slide 15-

ppt slide no 15 content not found
Slide 16-

The adrenal cortex consists of two regions, with each region producing a different group or type of hormones. True False The gonads, the primary reproductive organs, are only responsible for secreting hormones and are considered to be endocrine glands. True False
Slide 17-

Parts of the Endocrine System The major glands that make up the human endocrine system are the hypothalamus, pituitary, thyroid, parathyroids, adrenals, pineal body, and the reproductive glands, which include the ovaries and testes. Although the endocrine glands are the body's main hormone producers, some non-endocrine organs — such as the brain, heart, lungs, kidneys, liver, thymus, skin, also produce and release hormones.
Slide 18-

The Hypothalamus This is located at the base of the brain. It is part of the limbic system, which controls the autonomic nervous system and the endocrine systems. The hypothalamus controls the endocrine system by controlling the pituitary gland. Secretes releasing hormones to cause the pituitary to release hormones Secretes inhibiting hormones to turn off secretion of pituitary hormones
Slide 19-

The Hypothalamus The hypothalamus, a collection of specialized cells that is located in the lower central part of the brain, is the primary link between the endocrine and nervous systems. Nerve cells in the hypothalamus control the pituitary gland by producing chemicals that either stimulate or suppress hormone secretions from the pituitary. Although it is no bigger than a pea, the pituitary gland, located at the base of the brain just beneath the hypothalamus, is considered the most important part of the endocrine system. It's often called the "master gland" because it makes hormones that control several other endocrine glands.
Slide 20-

The production and secretion of pituitary hormones can be influenced by factors such as emotions and seasonal changes. To accomplish this, the hypothalamus relays information sensed by the brain (such as environmental temperature, light exposure patterns, and feelings) to the pituitary.
Slide 21-

The Pituitary Gland This is located in the sella tursica (totally encased in bone), which gives you a clue as to how important this gland is. The adenohypophysis portion of the pituitary gland (anterior lobe) actually develops from an embryonic pouch that grows upward from the ectoderm of the pharynx! One type of diabetes (insipidus) can be caused by trauma to the pituitary gland. A tumor of the pituitary gland can lead to blindness because it is so close to the optic chiasma.
Slide 22-

The Pituitary Gland The tiny pituitary gland is divided into two parts: the anterior lobe and the posterior lobe. The anterior lobe regulates the activity of the thyroid, adrenals, and reproductive glands. Among the hormones it produces are: growth hormone, which stimulates the growth of bone and other body tissues and plays a role in the body's handling of nutrients and minerals
Slide 23-

prolactin, which activates milk production in women who are breastfeeding thyrotropin, which stimulates the thyroid gland to produce thyroid hormones corticotropin, which stimulates the adrenal gland to produce certain hormones
Slide 24-

The pituitary also secretes endorphins, chemicals that act on the nervous system to reduce sensitivity to pain. In addition, the pituitary secretes hormones that signal the ovaries and testes to make sex hormones. The pituitary gland also controls ovulation and the menstrual cycle in women. The posterior lobe of the pituitary releases antidiuretic hormone, which helps control body water balance through its effect on the kidneys and urine output; and oxytocin, which triggers the contractions of the uterus that occur during labor.
Slide 25-

The Thyroid and Parathyroids The thyroid, located in the front part of the lower neck, is shaped like a bow tie or butterfly and produces the thyroid hormones thyroxine and triiodothyronine. These hormones control the rate at which cells burn fuels from food to produce energy. As the level of thyroid hormones increases in the bloodstream, so does the speed at which chemical reactions occur in the body.
Slide 26-

Thyroid hormones also play a key role in bone growth and the development of the brain and nervous system in children. The production and release of thyroid hormones is controlled by thyrotropin, which is secreted by the pituitary gland. Attached to the thyroid are four tiny glands that function together called the parathyroids. They release parathyroid hormone, which regulates the level of calcium in the blood with the help of calcitonin, which is produced in the thyroid.
Slide 27-

The Adrenal Glands The body has two triangular adrenal glands, one on top of each kidney. The adrenal glands have two parts, each of which produces a set of hormones and has a different function. The outer part, the adrenal cortex, produces hormones called corticosteroids that influence or regulate salt and water balance in the body, the body's response to stress, metabolism, the immune system, and sexual development and function.
Slide 28-

The inner part, the adrenal medulla, produces catecholamines, such as epinephrine. Also called adrenaline, epinephrine increases blood pressure and heart rate when the body experiences stress. (Epinephrine injections are often used to counteract a severe allergic reaction.)
Slide 29-

ppt slide no 29 content not found
Slide 30-

ppt slide no 30 content not found
Slide 31-

ppt slide no 31 content not found
Slide 32-

The control of hormonal secretion is “homeostatic feedback” Another name for this is: “negative feedback” Remember negative feedback reverses the direction of change back to physiologic normal if hormone level too high----- the gland is shut down if hormone level too low ------the gland is stimulated Positive feedback augments the direction of change if hormone level high ----- the gland is stimulated if hormone level too low---- the gland is shut down, even further Most endocrine diseases are centered around: TOO MUCH = hypersecretion--- from glandular hyperplasia or a functional tumor (adenoma or carcinoma) TOO LITTLE = hyposecretion – from glandular atrophy or a destructive carcinoma
Slide 33-

Endocrine System Disorders Topical Outline Pituitary Gigantism /Achromegly Diabetes Insipidus / SIADH Thyroid/Parathyroid Hyper/Hypo; Grave’s Disease; Hyperparathyroidism Adrenal Addison’s Disease; Cushing’s Syndrome
Slide 34-

Diseases of the Pituitary TSH hypersecretion = hyperthyroidism hyposecretion = hypothyroisism ACTH hyposecretion = Addison’s disease hypersecretion = Cushing’s disease FSH hyposecretion M = poor sperm production F = low estrogen, amenorrhea hypersecretion F = menopause LH hyposecretion F = no ovulation M = low testosterone MSH hypersecretion = excess pigment GH hypersecretion during growth = giantism after growth = acromegaly hyposecretion = dwarfism PRL hypersecretion = galactorrhea, infertility hyposecretion = poor milk production ADH Hypersecretion = SIADH hyposecretion = diabetes insipidus
Slide 35-

Endocrine System Disorders Categories of Endocrine dysfunction 1. Hypofunction 2. Hyperfunction Causes of Endocrine Dysfunction 1. Hypofunction congenital defects; gland destruction; receptor deficits 2. Hyperfunction excessive stimulation; hormone-producing tumors; hyperplasia of gland
Slide 36-

Endocrine System Disorders Categories of Endocrine disorders Primary – originates with target gland that is responsible for producing hormone Secondary – target gland may be normal; function altered by defective levels of stimulating hormone or releasing factors for hypothalamic-pituitary systems
Slide 37-

Endocrine System Disorders Diagnostic Evaluation Tools Measurement of effect of hormone on body function (Ex: Blood glucose levels) Measurement of actual hormone levels (Ex: plasmaphoresis levels) Measurement of urinary hormones or metabolite excretion (Ex: 24 Hr Ua.) Hormone suppression testing – usually indicated for diagnosing hyperfunction Hormone stimulation tests – usually indicated for diagnosing hypofunction
Slide 38-

Endocrine System Disorders Effects of Aging Many endocrine disorders are most common in persons 40 – 50 years old Most clinical findings associated with endocrine pathophysiology are very nonspecific Almost all of the early clinical findings associated with endocrine disorders can be attributed to “old age” Very important to assess older adults for correctable causes before assuming it is an Endocrine disorder
Slide 39-

Endocrine System Disorders Common Nursing Diagnoses Activity intollerance r/t … Impaired verbal communication r/t … Fluid volume deficit: Potential r/t … Potential for infection r/t … Knowledge deficit r/t … Noncompliance r/t … Impaired skin integrity r/t …
Slide 40-

Endocrine System Disorders Summary Endocrine disorders are the result of hypo or hyperfunction of a specific gland They can occur as a primary or secondary deficit Diagnostic tests are designed to measure hormone levels and their effects on the body systems Natural aging process slows down the functioning of the endocrine system and clinical s/s should not be mistaken for disorders
Slide 41-

Pituitary Gland Disorders Pituitary Gland – considered the “Master” gland Anterior Pituitary Hormones: ACTH; MSH; TSH; FSH; LH; GH; PRL Functions under the control of the hypothalmic center of the brain Posterior Pituitary Hormone: concerned with the regulation of fluid balance: ADH
Slide 42-

Anterior Pituitary Disorders Gigantism / Acromegly Pathophysiology: excessive secretion of Growth Hormone (GH) Genetic; Tumor Produces rapid longitudinal growth of long bones (Gigantism) After somatic growth is completed, GH hypersecretion produces thickening of bones & tissues resulting in Achromegly
Slide 43-

The Pituitary Gland The pituitary gland (hypophysis) is composed of two lobes: the anterior pituitary (adenohypophysis) and posterior pituitary (neurohypophysis).
Slide 44-

The Pituitary Gland The anterior lobe is larger, and its secretory activities are controlled by tropic hormones produced by and transmitted from the hypothalamus in response to negative feedback mechanisms. It secretes seven of the nine pituitary hormones
Slide 45-

PITUITARY HORMONES Adrenocorticotropic hormone (ACTH), which stimulates adrenocortical growth and secretion of adrenocortical hormones. Thyroid-stimulating hormone (TSH), or thyrotropic hormone, which stimulates thyroid growth and secretion of thyroid hormones Follicle-stimulating hormone (FSH), which stimulates ovulation in females and sperm production in males.
Slide 46-

PITUITARY HORMONES Luteinizing hormone (LH), called the interstitial cell stimulating hormone (ICSH) in males,' in whom it stimulates production of testosterone; in females it stimulates ovulation and development of ovarian follicles. Melanocyte stimulating hormone (MSH), which causes pigmentation.
Slide 47-

PITUITARY HORMONES Luteotropic hormone (LTH), also called prolactin, which stimulates secretion of milk in females. Growth hormone (GH), or somatotropic hormone (STH), which accelerates body growth.
Slide 48-

Posterior pituitary glands Posterior pituitary secretion is regulated by nerves impulses originating in the hypothalamus in response to stimuli from other parts of the body. It produces two hormones: 1. Antidiuretic hormone (ADH), or vasopressin, which acts on the renal tubules to increase reabsorption of water. 2. Oxytocin, which stimulates milk "letdown" and contraction of the uterus
Slide 49-

POSTERIOR PITUITARY HORMONES These hormones are synthesized in the hypothalamus and stored in secretory granules located in the nerve terminals of the posterior pituitary.
Slide 50-

In children, excessive secretion of GH results in gigantism. When the onset of GH excess occurs before closure of the epiphyses, the long bones are still capable of longitudinal growth. The excessive growth is usually proportional. These children may grow as tall as 8 feet (240 cm) and weigh more than 300 lb (136 kg).
Slide 51-

In adults, excessive secretion of GH results in acromegaly. Acromegaly is characterized by an overgrowth of the bones and soft tissues. Because the problem develops after epiphyseal closure in adults, the bones are unable to grow longer. Instead, the bones increase in thickness and width. Acromegaly is relatively rare. Only three out of every 1 million adults in the United States is diagnosed with this disease each year, with a prevalence of 40 to 60 out of every 1 million individuals.1 Both genders are affected equally.
Slide 52-

Progressive development of facial features of acromegaly
Slide 53-

Collaborative care in acromegaly The therapeutic goal in acromegaly is to return GH levels to normal. This is accomplished by surgery, radiation, drug therapy, or a combination of these therapies. The prognosis depends on age at onset, age when treatment is initiated, and tumor size. Usually bone growth can be arrested and soft tissue hypertrophy can be reversed. However, sleep apnea and diabetic and cardiac complications may persist in spite of treatment
Slide 54-

Assessment Clinical Manifestations Enlargement of hands and feet Changes in facial features Enlargement of Para nasal & frontal sinuses Enlargement of mandible, tongue & vocal cords Deformities of the spine, inc. curvature of the spine; frequent episodes of back pain
Slide 55-

Planning & Implementation Collaborative Management Medical – Pituitary irradiation Pharmacology – somatostatin analog ( to induce sustained suppression of GH) Surgical – resection of pituitary tumor Nursing Care: Supportative; Patient Teaching; Postoperative / Post radiation Management; Discharge Planning
Slide 56-

Surgical management Surgery (hypophysectomy) is the treatment of choice and offers the best hope for a cure, especially for smaller tumors (microadenomas smaller than 10 mm). More than 97% of surgeries done to remove pituitary tumors associated with acromegaly are accomplished with the transsphenoidal approach. With this procedure, an incision is made in the inner aspect of the upper lip and gingiva. The sella turcica is entered through the floor of the nose and sphenoid sinuses
Slide 57-

Surgery on the pituitary gland is most commonly performed with the transsphenoidal approach. An incision is made in the inner aspect of the upper lip and gingiva. The sella turcica is entered through the floor of the nose and sphenoid sinuses
Slide 58-

Nursing diagnosis Nursing diagnoses for the patient with GH excess include, but are not limited to, the following: ▪ Disturbed body image related to enlargement of the hands, feet, jaw, and soft body tissue ▪ Deficient fluid volume related to polyuria ▪ Disturbed sleep pattern related to soft tissue swelling ▪ Disturbed sensory perception (visual) related to enlarged pituitary gland
Slide 59-

Post op care The patient should be instructed to avoid vigorous coughing, sneezing, and straining at stool (Valsalva maneuver) to prevent cerebrospinal fluid leakage from the point at which the sella turcica was entered. After surgery in which a transsphenoidal approach has been used, the head of the patient's bed should be elevated at a 30-degree angle at all times. This elevation avoids pressure on the sella turcica and decreases headaches, a frequent postoperative problem. Monitoring neurologic status, including pupillary response, should be done in order to detect neurologic complicat
Slide 60-

Post op care cont Any clear nasal drainage should be sent to the laboratory to be tested for glucose. A glucose level greater than 30 mg/dl (1.67 mmol/L) indicates cerebrospinal fluid leakage from an open connection to the brain. If this happens, the patient is at an increased risk for meningitis. Complaints of persistent and severe generalized or supraorbital headache may indicate cerebrospinal fluid leakage into the sinuses. A cerebrospinal fluid leak usually resolves within 72 hours when treated with head elevation and bed rest. If the leak persists, daily spinal taps may be done to reduce pressure to below-normal levels and allow the fossa to heal..
Slide 61-

Post op care cont Intravenous (IV) antibiotics are usually administered when there is a cerebrospinal fluid leak to prevent meningitis. If the leak does not respond to treatment in 72 hours, surgical intervention may be required. Mild analgesia is given for headaches. The nurse should perform mouth care every 4 hours to keep the surgical area clean and free of debris and to promote patient comfort. Toothbrushing should be avoided for at least 10 days to prevent disrupting the suture line and to avoid discomfort
Slide 62-

Posterior Pituitary Disorders Two conditions of abnormal secretion of the antidiuretic hormone (ADH) Diabetes Insipidus (DI):A H2O metabolism problem caused by an ADH deficiency(either a decrease in ADH synthesis or an inability of the kidneys to respond to ADH) which result in theproduction of large volume of diluted urine. Syndrome of Inappropriate ADH secretion (SIADH): occurs when vasopresin is secreted even when plasma osmolarity is low or normal which result in dilutional hyponatremia
Slide 63-

Diabetes Insipidus Symptoms = polyuria & polydipsia Get large amounts of dilute urine & dehydration Etiol: head injury or surgery = temporary condition Nephrogenic tubular insensitivity to ADH = permanent condition Tx = replacement therapy with ADH SIADH Get too much ADH secretion & get retention of fluid Etiol : Some cancers especially oat cell lung cancer (very common cancer) Post op (temporary, only last 1 week) Stress Psychiatric diseases Pathophysiology = hypoosolarity & hyponatremia Symptoms related to low serum sodium First = fatigue & weakness Then G-I sx Then twitchings, convulsions, & coma
Slide 64-

Diabetes insipidus Diabetes insipidus (DI) is a condition that can result from one of several problems: primary (neurogenic) DI: is caused by a defect in the synthesis of ADH by the hypothalamus or release from the posterior pituitary. Nephrogenic DI: is an inherited disorder whereby the renal tubules did not respond to ADH actions that result in poor H2O reabsorption. Secondary DI: can result from tumor within the hypothalamus or pituitary glands, head trauma or surgical procedures such as hypophysectomy drug induced DI: usually caused by lithium, democleocycline which interfere with the response of the kidney to ADH.
Slide 65-

Disorders of the Pituitary Gland Except for when it follows infection or trauma, DI is usually insidious, with progressively increasing polydipsia and polyuria. DI Following Trauma or infection has three phases: Phase 1: Polydipsia and polyuria immediately follow injury and last 4-5 days Phase 2: Which last about 6 days the symptoms disappear Phase 3: The patient experiences continued polydipsia and polyuria.
Slide 66-

Diabetes Insipidus Description: Production of large quantities of “bland” urine resulting from the kidney’s inability to concentrate urine. Major Gland Dysfunction: 1. Hyposecreation of ADH (Prinary) 2. Inability to respond to ADH (Neurogenic DI)
Slide 67-

Diabetes Insipidus Pathophysiology: Primary (central) DI: cranial surgery, head trauma, brain tumors, encephalitis or meningitis Additional causes: adverse effects of medications (Dilantin, Reserpine, Lithium) and alcohol Causes of neurogenic DI: adverse drug effects, CRF, chronic hypokalemia
Slide 68-

Diabetes Insipidus Prognosis / Complications Major: Hyperosmolarity; Chronic Hypernatremia; Hypovolemia Result: Hypertonic encephalopathy with permanent CNS injury or death Hypervolemia = H20 Intoxication Life expectancy: closely related to the cause and tissue damage / involvement
Slide 69-

DI is characterized by increased thirst (polydipsia) and increased urination (polyuria). The primary characteristic of DI is the excretion of large quantities of urine (5 to 20 L per day) with a very low specific gravity (less than 1.005) and urine osmolality of <100 mOsm/kg (<100 mmol/kg). Serum osmolality is elevated (usually greater than 295 mOsm/kg [295 mmol/kg]) as a result of hypernatremia due to pure water loss in the kidney. In partial central DI, urinary output may be lower (2 to 4 L per day). Most patients compensate for fluid loss by drinking great amounts of water so that serum osmolality is normal or only moderately elevated. The patient with central DI particularly favors cold or iced drinks. The patient may be fatigued from nocturia and may experience generalized weakness.
Slide 70-

Assessment Clinical Manifestations: MOSTLY R/T DEHYDRATION Most prominent: Polyuria (24 hr urine volume up to 15 L) & Polydipsia Nocturia; bladder distention Hydronephrosis Polydipsia; Weight loss; loss of appetite; constipation; possibly sleep deprivation
Slide 71-

Assessment Diagnostic Evaluation Tools Plasma Osmolarity (greater than 290mOsm/kg of water) Water deprivation Test Urinalysis (Urine Osmolarity; 24 Hr Ua) Hematological; Biochemistry; I & O
Slide 72-

Assessment Signs and symptoms: Polydipsia, polyuria (2-20 L/day) with dilute urine (specific gravity <1.007). Physical assessment: Signs of dehydration if fluid intake is inadequate. Impairment of neurologic status, including altered LOC and sensory or motor deficits. History of: Cranial injury, especially basilar skull fracture; meningitis; primary or metastatic brain tumor; surgery in the pituitary area; cerebal hemorrhage; encephalitis; syphilis; or tuberculosis (TB). Familial incidence rarely is a factor.
Slide 73-

Diagnostic Tests Vasopressin challenge test: One serious side effect of this test is precipitation of heart failure in susceptible individuals. Hypertonic saline infusions: 3% sodium chloride (NaCL) solution is infused IV to assess for subsequent water conservation. Water deprivation test
Slide 74-

Plan & Implementation Collaborative Management Treatment is according to type of DI Medical: Pharmacological: Diabenese; Thiazide Diuretics; desmopressin acetate (dDAVP) Fluid Restrictions; I & O Drug-induced DI is almost always reversible and treated by D/C the causative agent
Slide 75-

Collaborative Management For central or neurogenic DI Rehydration: Lost water is replaced with IV hypotonic (e.g., 0.45% NaCI) solution. The initial replacement is rapid, necessitating close monitoring of BP, HR, and UO
Slide 76-

Collaborative Management Administration of exogenous vasopressin (Pitressin): Potential side effects include: a. Hypertension b. Myocardial infarction c. Uterine cramps d. Increased peristalsis
Slide 77-

Collaborative Management Achieving mild antidiuretic effect with hydrochlorothiazide, clofibrate, chlorpropamide, carbamazepine or any medication which increases action or release of ADH.
Slide 78-

For nephrogenic DI: Indomethacin therapy: Therapy with thiazide diuretics (e.g., hydrochlorothiazide, 50-100 mg daily, or chlorthalidone, 50 mg daily): Although it may seem antithetical, they block the ability of kidneys to excrete free water, which is the problem with DI. For psychogenic DI Psychotherapy: Necessary for patients with compulsive water drinking. Thioridazine and lithium should be avoided because they cause polyuria.
Slide 79-

Nursing Management Desired Outcomes Maintenance of stable body weight with appropriate balance of I & O Ability to maintain F & E balance Return to normal ADL with a satisfying life-style Monitor I & O; Electrolytes Observe for changes in mentation; LOC Monitor VS; Daily weights Discharge Planning / Patient Teaching
Slide 80-

Nursing Diagnoses and Interventions Deficient fluid volume related to active fluid loss secondary to polyuria Decreased CO R/Tdecrease plasma volume Ineffective protection related to potential for side effects of vasopressin
Slide 81-

Education Patient-Family Teaching and Discharge planning Importance of continued medical follow-up Medications
Slide 82-

Education Indicators that necessitate medical attention (e.g., signs of dehydration or water intoxication) Recommendation for fluid replacement
Slide 83-

Evaluation Evaluation of therapy is reflected in Patient Outcome Goals.
Slide 84-

SIADH Description: Occurs when ADH secretion continues without regard to the serum osmolarity. Result: inappropriate reabsorption of water in the renal tubules = hypervolemia w/ dilutional hyponatremia
Slide 85-

Syndrome of Inappropriate Antidiuretic Hormone Syndrome of inappropriate antidiuretic hormone (SIADH) is caused by release of ADH from the pituitary gland without regard to serum osmolarity, plasma volume or BP, resulting in excessive water retention and hyponatremia.
Slide 86-

SIADH The action of ADH increases reabsorption of water in the last segment of the distal tubules and collecting ducts of the kidney. SIADH is seen in postoperative and oncology patients, and in individuals with multiorgan dysfunction syndrome.
Slide 87-

SIADH Pathophysiology Non-Endocrine Organ/System Dysfunction Pulmonary disease; malignant tumors; CNS infections; CND dysfunction Development of dilutional hyponatremia differentiates from dysfunction of ADH caused by CV disease; Hepatic Cirrhosis w/ Acites; over aggressive IV Therapy; Antineoplastic drugs, anticonvulsant drugs and Diuretic Therapy
Slide 88-

PATHOPHYSIOLOGY Normally water which would be excreted is reabsorbed into the circulation, resulting in water retention and eventually causing serum osmolarity and Na+ to decrease because of dilutional effects. Decreased serum osmolarity causes movement of water into cells, which can result in cerebral edema. Further water retention results in increased glomerular filtration rate and decreased aldosterone secretion, and more Na+ filtered out into urine. Water intoxication, cerebral edema and severe hyponatremia if left untreated, lead to death.
Slide 89-

SIADH Prognosis / Complications Most Prominent: problems associated with hyponatremia Prognosis most often determined by the dysfunction causing ADH excess
Slide 90-

Assessment Clinical Manifestations S/S will vary in patients withy acute & chronic Hyponatremia Acute: rapid reduction of Na.; reduced LOC; reduced deep tendon reflexes (DTR); hypothermia; seizures; coma; death Chronic: Weight gain; lethargy; weakness; confusion; anorexia; N/V; abnormal muscle cramps
Slide 91-

Assessment Signs and symptoms: Decreased urine output with concentrated urine Signs of water intoxication may appear Altered LOC Fatigue Headache
Slide 92-

Assessment Diarrhea Anorexia Nausea Vomiting
Slide 93-

Assessmemt Seizures Weight gain without edema Elevated BP Altered mental status
Slide 94-

Assessment Diagnostic Evaluation Tools Measurement of serum Na. levels; Measurement of serum/Ua. Osmolarity levels Hematology; Biochemistry Diagnosis (Dx) is made if no other factors are causing Hyponatremia
Slide 95-

Diagnostic Tests Serum Na+ level: Decreased to <137 mEq/L Plasma osmolality: Decreased to <275 mOsm/kg Urine osmolality: Elevated disproportionately relative to plasma osmolality Urine Na+ level: Increased to >200 mEq/L Urine specific gravity: >1.030 Plasma ADH level: Elevated
Slide 96-

management In cases of severe hyponatremia (less than 120 mEq/L), especially in the presence of neurologic symptoms such as seizures, intravenous hypertonic saline solution (3% to 5%) may be administered. Hypertonic saline requires a very slow infusion rate on an infusion pump to avoid too rapid a rise in sodium. A diuretic such as furosemide (Lasix) may be used to promote diuresis, but only if the serum sodium is at least 125 mEq/L (125 mmol/L), because it may promote further loss of sodium. Because furosemide increases potassium excretion, potassium supplements may be needed. A fluid restriction of 500 ml per day is also indicated for those with severe hyponatremia.
Slide 97-

In chronic SIADH, water restriction of 800 to 1000 ml per day is recommended. Because this degree of restriction may not be tolerated, demeclocycline (Declomycin) and lithium may be administered. These agents block the effect of ADH on the renal tubules, thereby allowing a more dilute urine.
Slide 98-

ppt slide no 98 content not found
Slide 99-

Plan / Implementation Collaborative Management Medical: Acute Hyponatremia (serum Na < 120mEq.L) accompanied by CNS symptoms requires emergency treatment before permanent damage can occur Treatment (Tx) may include: administration of large amounts of Saline & Lasix based on patient’s Na. deficit
Slide 100-

Plan / Implementation Collaborative Management Chronic Hyponatremia Fluid restrictions (800-1,000mL/24hr) administration of drugs known to inhibit activity of ADH: (Lasix; demeclocycline)
Slide 101-

Collaborative Management Fluid restriction Isotonic (0.9%) or hypertonic (3%) NaCl, Lithium or demeclocycline Treatment of underlying cause
Slide 102-

Plan / Implementation Nursing Management Vital Signs; Cardiac status IV Therapy/Meds ( normal or hypertonic saline w/ IV Lasix) Neuro Checks Monitor IV therapy; I & O; Electrolytes; Fluid restrictions Discharge Planning / Patient Education
Slide 103-

Nursing Diagnoses and Interventions Excess fluid volume related to compromised regulatory mechanisms resulting in increased serum ADH level
Slide 104-

Patient-Family Teaching and Discharge Planning Importance of fluid restriction How to safely enrich the diet with Na+ and K+ salts Teach daily weights and indicators of water intoxication and hyponatremia Medications Importance of continued medical follow-up Importance of obtaining a MedicAlert bracelet
Slide 105-

Evaluation Patient is able to recognize s/s of hyper/hyponatremia and take appropriate actions Patient understands medication regime and how to properly administer medications Patient will adapt to dietary restrictions (low or high Na. depending on medications prescribed
Slide 106-

ppt slide no 106 content not found