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Endocrine Disorders

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cenebute's version from 2018-01-27 01:17

Section 1

Question Answer
Adrenal DisordersAddison Disease (Adrenal Insufficiency)
Pituitary Disorder of water metabolismDiabetes Insipidus (resulting from excessive loss of water caused by hyposecretion of ADH or kidney’s inability to respond to ADH)
Pituitary Disorder of water metabolismSyndrome Of Inappropriate Antidiuretic Hormone (SIADH) – excessive amount of serum ADH resulting in water intoxication and hyponatremia
Adrenal DisordersCushing Syndrome (Hyperfunction of the Adrenal Cortex causing elevated ACTH levels)
Pancreatic DisorderDiabetes Mellitus (disorder of the pancreas resulting in a lack of insulin production, causing hyperglycemia and resulting in multisystem changes in health status.
Pancreatic DisorderDiabetic Ketoacidosis (DKA) - metabolic acidosis resulting from a persistence of hyperglycemia and a breakdown of fats into glucose, leading to the presence of ketones in the blood
Thyroid Gland DisorderHypothyroidism(insufficient amount of TH secreted by thyroid gland)
Thyroid Gland DisorderHyperThyroidism(Grave’s Disease due to excessive amount of TH secreted by thyroid gland)
Thyroid Gland DisorderGoiter
principal functions of the endocrine systemThe endocrine glands secrete hormones directly into the blood stream to affect a variety of biological functions to maintain homeostasis.
Why would the posterior pituitary gland stimulate ADH? Because the body experiencing Hypovolemia and hypotension which are the most powerful stimulators of ADH release; It will signal the kidneys to reabsorb water which would result in a decrease in urine output for the purpose of maintaining fluid volume and homeostasis? Although, there are other stimulators like pain, stress, trauma but the other 2 are most powerful.
Why are Hypovolemia and hypotension the most powerful stimulators? Body experiencing low fluid volume; the neurons are signaled to have ADH retain water to balance fluid volume.
What is the purpose of the Thyroid Gland? To determine the rate of cellular metabolism
T3 & T4increase in energy (ATP production); increase in oxygen consumption; needed for growth & development
Calcitonindecrease Ca2 absorption in blood; decrease osteoclast activity in bones; decrease Ca2 & phosphate reabsorption by the kidneys
When is Calcitonin releasedwhen there’s an increase in Calcium in the blood
What’s the purpose of the Adrenal Glands? To produce hormones that help control the heart rate, blood pressure, the way the body uses food, and other vital functions
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Section 2

Question Answer
Clinical manifestations of Addison's DiseaseHyperpigmentation of skin (eternal tan); Delayed wound healing; Hypoglycemia ; Cardiovascular changes (tachycardia, dysrhythmias, postural hypotension); Dehydration and Hypovolemia, weight loss; Hyperkalemia & Hypercalcemia; Muscle weakness
Addisonian crisisA life threatening response to sudden withdrawal of steroids or exposure to any form of stress, manifested by severe hypotension, circulatory collapse, shock and coma.
Clinical Manefistations of Cushing’s Syndrome?Generalized weakness with muscle wasting; Hirsutism; Buffalo hump; Thin skin that bruises easily, striae and hirsutism; Skin infections or poor wound healing ; Fluid overload and weight gain; Abnormal fat deposits (truncal obesity, moon facies, fat pad on back of neck)
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Question Answer
Diabetes MellitusA disease of chronic hyperglycemia due to poor insulin secretion and/or insulin resistance
What other disease processes does Diabetes contribute? Cardiovascular disease, Hypertension Renal failure, Blindness, Stroke
The hallmark symptoms of diabetes are the 3 P’sPolyuria, Polydipsia, Polyphagia
What labs and diagnostic tests are used to diagnose Diabetes? Fasting blood glucose greater than 126 mg/dl; Two hour glucose greater than 200mg/dl with a glucose tolerance test; Elevated glycosylated hemoglobin (HbA1c)
What are nursing measures should be used when caring for a client with Diabetes? Accuchecks before meals and at bedtime ; Monitor serum glucose levels; Maintaining diabetic diet; Monitor for signs/symptoms of hypoglycemia and hyperglycemia
What are the signs/symptoms of hypoglycemia Cool, clammy skin, diaphoresis, anxiety, irritability, confusion, blurred vision, hunger, generalized weakness
What are the signs/symptoms of hyperglycemia Hot, dry skin, nausea, vomiting, abdominal pain, rapid deep respirations with acetone or fruity odor
What are teaching needs for the client with Diabetes? Diabetic foot care; Reducing risk of injury; Nutritional management; Management of hypoglycemic and hyperglycemic episodes; Sick day guidelines; Insulin administration
What are complications of the Diabetes?Heart and blood vessel disease; Diabetic retinopathy can lead to blindness; Diabetic nephropathy can lead to renal failure; Diabetic neuropathy can lead to foot ulcers
What is the goal of Diabetesmanagement? Consistent management of blood glucose levels within the normal range (70-120 mg/dl)
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Question Answer
Diabetic Ketoacidosis is most frequently associated withDiabetes Mellitus, Type 1 –(sometimes referred to as insulin-dependent diabetes)
DKA isan acute, life-threatening condition; characterized by severe hyperglycemia (>300 mg/dL) and by ketones in the blood and urine has an onset that is typically rapid, over a period of hours
1st Causes of DKAAn INCREASED NEED for insulin, related to: Illness (Infection causes most cases of DKA); Stress; Surgery; Trauma
2nd Causes of DKA includeToo LITTLE insulin, related to: New onset (undiagnosed) diabetes; Lack of compliance with the treatment plan (Too much dietary intake or Too little insulin administered)
Early Signs & Symptoms of DKA includePolyuria, polydipsia, polyphagia; Signs of dehydration – dry skin & mucous membranes, weight loss, sunken eyes, soft eyeballs, lethargy
Late Signs of DKA include‘fruity’ breath; nausea, abdominal pain, vomiting; Kussmaul respirations (deep & rapid) ; decreasing mental status leading to coma
Lab Finding for DKA includeSerum glucose level >300 mg/dL; Serum ketones positive; Urine ketones positive; Serum pH <7.35 (metabolic acidosis); Serum HCO3 <22 mEq/L (metabolic acidosis); Serum K+ can be low (with diuresis) or high (with acidosis)
Because of Dehydrations labs will show Increased Na+ (>145 mEq/dL) ; Increased BUN (>20 mg/dL) Increased Creatinine (>1.5 mg/dL)
Nursing Interventions for DKA includeFluid replacement (usually Normal Saline) to correct hypovolemia ; Administration of IV regular insulin; Monitor serum K+ - with insulin therapy K+ will shift into cells and client may require potassium replacement therapy.
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Question Answer
Primary defect of Diabetes Insipidus (DI)TOO LITTLE Anti-diuretic hormone (ADH)
Most frequent cause of DIDefect in hypothalamus or pituitary, such as trauma, irradiation, cranial surgery
Primary defect of SIADH TOO MUCH Anti-diuretic hormone (ADH)
Most frequent cause of SIADH Defect in hypothalamus or pituitary, such as tumor (especially oat cell Lung CA), head injury, meningitis, CVA, increased intrathoracic pressure (usually from positive pressure ventilation)
S/S of DI POLYURIA – urine output of 5-20 liters per day ; Polydipsia – fluid consumption of 4-30 liters per day ; Dehydration – poor skin turgor, dry mucous membranes, hypotension, tachycardia, weight loss, headache, dizziness, constipation; Hypovolemic shock – hypotension, tachycardia, decreased cardiac output, decreased cerebral perfusion
S/S of SIADHOliguria – excretion of Na+, but reabsorption of water ; Fluid volume excess – weight gain without edema, crackles in lungs, distended neck veins, taut skin, tachycardia, hypertension
Early sign of SIADHEarly – headache, weakness, anorexia, muscle cramps, weight gain
Late sign of SIADHpersonality changes, hostility, decreased deep tendon, reflexes, nausea & vomiting, diarrhea, confusion, lethargy, Cheyne-Stokes respirations, seizures, coma, death
Lab Findings for DIUrine Dilute ; Specific gravity <1.005 ; Low osmolality (50-200 mOsm/kg) ; Decreased pH ; Decreased urine sodium ; Decreased urine potassium; SERUM CONCENTRATED: Increased serum osmolality (>295 mOsm/kg); Increased serum sodium & Increased serum potassium
Lab Findings for SIADHURINE CONCENTRATED & Serum Dilute
Nursing Intervention for DIIV therapy to match output and correct electrolytes; Monitor I&O, sp gravity; Weigh daily ; Monitor for hypotension, tachycardia, skin turgor, mucous; membranes, mental status Encourage fluids as tolerated ; Add bulk foods, juices for constipation; Avoid caffeine products that promote diuresis;
Meds for DI replace ADH; desmopressin (DDAVP) & vasopressin (Pitressin)
Nursing Intervention for SIADHRestrict oral fluids to 500-1000 mL/day; Monitor I&O, sp gravity; Weigh daily ; Seizure precautions ; Monitor for HTN, tachycardia, hypothermia, altered mental status ; Mouth care for limited oral intake Quiet environment
Meds for SIADH include[block renal response to ADH]; demeclocycline (Declomycin); o lithium carbonate ; In severe water intoxication, ; hypertonic IV fluid (3-5% NS)
Teaching for DI include
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