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Define Ketoacidosis Quizlet

Diabetes Insipidus

Diabetes Insipidus

What are the types of diabetes insipidus? Central Diabetes Insipidus The most common form of serious diabetes insipidus, central diabetes insipidus, results from damage to the pituitary gland, which disrupts the normal storage and release of ADH. Damage to the pituitary gland can be caused by different diseases as well as by head injuries, neurosurgery, or genetic disorders. To treat the ADH deficiency that results from any kind of damage to the hypothalamus or pituitary, a synthetic hormone called desmopressin can be taken by an injection, a nasal spray, or a pill. While taking desmopressin, a person should drink fluids only when thirsty and not at other times. The drug prevents water excretion, and water can build up now that the kidneys are making less urine and are less responsive to changes in body fluids. Nephrogenic Diabetes Insipidus Nephrogenic diabetes insipidus results when the kidneys are unable to respond to ADH. The kidneys' ability to respond to ADH can be impaired by drugs-like lithium, for example-and by chronic disorders including polycystic kidney disease, sickle cell disease, kidney failure, partial blockage of the ureters, and inherited genetic disorders. Sometimes the cause of nephrogenic diabetes insipidus is never discovered. Desmopressin will not work for this form of diabetes insipidus. Instead, a person with nephrogenic diabetes insipidus may be given hydrochlorothiazide (HCTZ) or indomethacin. HCTZ is sometimes combined with another drug called amiloride. The combination of HCTZ and amiloride is sold under the brand name Moduretic. Again, with this combination of drugs, one should drink fluids only when thirsty and not at other times. Dipsogenic Diabetes insipidus Dipsogenic diabetes insipidus is caused by a defect in or damage to the thirst Continue reading >>

Chapter 16: The Endocrine System (study Modules 16.09-16.11)

Chapter 16: The Endocrine System (study Modules 16.09-16.11)

Sort Match the following hormone with its function: Insulin Increases Na+ reabsorption in the kidneys Facilitates glucose transport into cells Stimulates embryonic cells (stem cells) to undergo mitosis Causes kidneys to conserve water Increases cell reactions during sympathetic response Facilitates glucose transport into cells Match the following hormone with the appropriate category of hormones: Androgens Gonadocorticoids Mineralocorticoids Glucocorticoids Gonadotropins Gonadocorticoids Sympathetic nerve stimuli are responsible for the release of __________. estrogen insulin aldosterone epinephrine thyroid hormone epinephrine Match the following homeostatic imbalance with the hormone deficiency (or overproduction): Diabetes insipidus Hyposecretion of ADH Insulin deficiency Oversecretion of catecholamines Overproduction of GH Hypersecretion of thyroid hormone Hyposecretion of ADH Insulin enhances the membrane transport of glucose in all of the following tissues except __________. the brain the myocardium skeletal muscle adipose tissue the brain Match the following gland with the hormone it produces (or releases): Adrenal medulla Insulin Growth hormone Antidiuretic hormone Aldosterone Epinephrine Epinephrine Match the following hormone with the condition that would be balanced by that hormone: Insulin High levels of blood sugar Dehydration and low blood pressure Decrease in blood Ca2+ levels Decrease in body metabolism Loss of Na+ from extracellular fluids High levels of blood sugar Which of the following homeostatic imbalances usually results from deficits in both glucocorticoids and mineralocorticoids? Cretinism Graves' disease Cushing's syndrome Addison's disease Addison's disease Match the following hormone with the appropriate category of hormones: Cortisol Gonadotr Continue reading >>

Acute Complications Of Diabetes Mellitus

Acute Complications Of Diabetes Mellitus

Sort Diabetic Ketoacidosis: Collaborative Care • Continuous cardiac monitoring • Start a large bore intravenous line • Administer fluid replacement • Place an indwelling urinary catheter • Monitor serum electrolyte and glucose levels • Replace potassium before administering insulin • Administer Regular Insulin infusion starting at 0.1 units/kg/hour • Monitor blood glucose levels frequently (Q 1 hr) - Blood glucose should fall at a rate of 30 to 50 mg/dL per hour • Monitor fluid status Hyperosmolar Hyperglycemic Syndrome: treatments • Treatments - Fluid replacement • IV 0.9% Sodium Chloride followed by 0.45% Sodium Chloride • Dextrose may be added to IV fluids when blood glucose is 250 mg/dl to prevent hypoglycemia - IV Regular insulin via an infusion pump (in dosages similar to those used in DKA) - Monitor fluid and electrolyte status. • Hypokalemia not as significant as with DKA. Continue reading >>

Diabetic Ketoacidosis And Patho

Diabetic Ketoacidosis And Patho

pathophysiology ketogenesis due to insulin deficiency leads to increased serum levels of ketones anad ketonuria acetoacetate, beta-hydroxybutyrate; ketone bodies produced by the liver, organic acids that cause metabolic acidosis respiration partially compensates; reduces pCO2, when pH < 7.2, deep rapid respirations (Kussmaul breathing) acetone; minor product of ketogenesis, can smell fruity on breath of ketoacidosis patients elevated anion gap Methanol intoxication Uremic acidosis Diabetic ketoacidosis Paraldehyde ingestions Intoxicants (salicyclate, ethylene glycol, nipride, epinephrine, norepinephrine) Lactic acidosis (drug induced; didanosine, iron, isoniazid, metformin, zidovudine) Ethanol ketoacidosis Severe renal failure starvation Blood glucose regulation (6) 1. When blood glucose levels rise above a set point, 2. the pancreas secretes insulin into the blood. 3. Insulin stimulates liver and muscle cells to make glycogen, dropping blood glucose levels. 4. When glucose levels drop below a set point, 5. the pancreas secretes glucagon into the blood. 6. Glucagon promotes the breakdown of glycogen and the release of glucose into the blood. (The pancreas signals distant cells to regulate levels in the blood = endocrine function.) Insulin and Glucagon (Regulation) (10) 1. High blood glucose 2. Beta cells 3. Insulin 4. Glucose enters cell 5. Blood glucose lowered 6. Low blood glucose 7. Alpha cells 8. Glucagon 9. Liver releases glucose from glycogen 10. Blood glucose raised What is the manifestations (symptoms) of Type 1? (10) 1. Extreme thirst 2. Frequent urination 3. Drowsiness, lethargy 4. Sugar in urine 5. Sudden vision change 6. Increased appetite 7. Sudden weight loss 8. Fruity, sweet, or wine like odor on breath 9. Heavy, laboured breathing 10. Stupor, unconscious Continue reading >>

Diabetes 1

Diabetes 1

Sort A client with type one diabetes comes to the clinic because of concerns regarding uratic control of blood glucose with the prescribed insulin therapy. The client has been experiencing a sudden fall in the glucose level, followed by a sudden episode of hyperglycemia. Which complication of insulin therapy should the nurse conclude that the client is experiencing? Somogyi effect A nurses caring for a client newly diagnosed with type one diabetes. When the healthcare provider tries to regulate this client's insulin regimen, the client experiences episodes of hypoglycemia and hyperglycemia and 15 G of a simple sugar is prescribed. What is the reason this is administered when a client experiences hypoglycemia? Increases blood glucose levels Continue reading >>

Emt - Chapter 17

Emt - Chapter 17

Sort A 28-year-old female patient is found to be responsive to verbal stimuli only. Her roommate states that she was recently diagnosed with type 1 diabetes and has had difficulty controlling her blood sugar level. She further tells you that the patient has been urinating excessively and has progressively worsened over the last 24 to 36 hours. On the basis of this patient's clinical presentation, you should suspect that she: is significantly hyperglycemic. A 75-year-old male with type 1 diabetes presents with chest pain and a general feeling of weakness. He tells you that he took his insulin today and ate a regular meal approximately 2 hours ago. You should treat this patient as though he is experiencing: a heart attack. A 42-year-old male is found unresponsive on his couch by a neighbor. During your assessment, you find no signs of trauma and the patient's blood glucose level is 75 mg/dL. His blood pressure is 168/98 mm Hg, his heart rate is 45 beats/min and bounding, and his respirations are 8 breaths/min and irregular. The patient is wearing a medical alert bracelet that states he has hemophilia. You should: suspect that he has intracranial bleeding, assist his ventilations, and transport rapidly to an appropriate hospital. A man finds his 59-year-old wife unconscious on the couch. He states that she takes medications for type 2 diabetes. He further tells you that his wife has been ill recently and has not eaten for the past 24 hours. Your primary assessment reveals that the patient is unresponsive and not breathing. You should check for a carotid pulse for no longer than 10 seconds. You are treating a 40-year-old male with a documented blood sugar reading of 300 mg/dL. The patient is semiconscious and breathing shallowly, and is receiving assisted ventilation from y Continue reading >>

Diabetes (hyperglycemia) & Hypoglycemia

Diabetes (hyperglycemia) & Hypoglycemia

Sort Role of Insulin and Plasma/Blood Glucose Produced by beta cells of pancreas Glucose is important fuel for cell - enters bloodstream first before being delivered to the tissues and cells of the body Ingestion increases plasma and blood sugar levels. Brain can ONLY use glucose Glucose cannot enter tissues and cells without insulin Body's need for insulin will fluctuate with body's need Normal Process 1. Eat 2. Glucose in plasma/blood 3. Insulin released 4. Glucose enters cells/tissue 5. Maintain glucose balance Diabetes 1. Eat 2. Glucose in plasma/blood 3. No insulin release 4. Glucose stays in bloodstream 5. Hyperglycemia Diabete Mellitus Higher risk: American Indian/Alaskan Native, Native Americans, Hispanic/Latino American 2x risk of periodontal disease 6th leading cause of death Chronic Complications Damage to larger vessels DM causes thickening and hardening - leads to arteriosclerosis Damage to smaller blood vessels causes blindness, kidney disease, amputations Amputations- damage to the nervous system. Person cannot feel peripheral tissues. Normal sweat recreation and oil production that lubricates the skin of the is impaired. These factors together can lead to abnormal pressure on the skin, bones, and joints of the foot during the walking and can lead to breakdown of the skin of the foot. Sore may develop. Blood supply damage = tissue damage, immunity compromised Type 1 Diabetes Risk factors - autoimmune response, genetic, environmental factors i.e. virus Immune system destroys pancreatic beta cells - the only cells in the body that make insulin and lead to insulin deficiency children and young adults most affected, though it can occur at any age 10% of all diabetes More severe form of diabetes Type 2 Diabetes Previously call non-insulin dependent DM or adult Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Sort pathophysiology ketogenesis due to insulin deficiency leads to increased serum levels of ketones anad ketonuria acetoacetate, beta-hydroxybutyrate; ketone bodies produced by the liver, organic acids that cause metabolic acidosis respiration partially compensates; reduces pCO2, when pH < 7.2, deep rapid respirations (Kussmaul breathing) acetone; minor product of ketogenesis, can smell fruity on breath of ketoacidosis patients elevated anion gap Methanol intoxication Uremic acidosis Diabetic ketoacidosis Paraldehyde ingestions Intoxicants (salicyclate, ethylene glycol, nipride, epinephrine, norepinephrine) Lactic acidosis (drug induced; didanosine, iron, isoniazid, metformin, zidovudine) Ethanol ketoacidosis Severe renal failure starvation Continue reading >>

Diabetes Mellitus

Diabetes Mellitus

Sort List the 6 classes of oral hypoglycaemic mediations 1. sulfonylureas (gliclazide) primary involvement with stimulating the pancreas to secrete insulin 2. biguanides (metformin) enhancing the glucose lower and combined with other oral hypoglycaemic 3. sulfanylureas & biguanide combination (mixed) 4. thiazolidinediones (pioglitazone) enhance insulin action at receptor cite by increasing insulin secretion from beta cells - targets beta cells 5. alpha-glycosidase inhibitors (acarbose) 6. glitinide (novanorm) lowering glucose level agent What is the action of insulin? insulin allows glucose to move into cells to make energy. It does this by: * glycogenisis - promotes production & storage of glycogen * glycogenolysis - inhibits glycogen breakdown into glucose * increases protein and lipid synthesis * inhibits tissue breakdown by inhibiting liver glycogenolysis (ketogenesis - converts fats to acids) and gluconeogenisis (conversion of proteins to glucose) * in muscle, promotes protein and glycogen synthesis * in fat cells, promotes triglyceride storage List the physical signs of DKA * altered mental status without evidence of head trauma * tachycardia * tachypnea or hyperventilation (kussmaul respirations) * normal/low BP Increased capillary refill time - poor perfusion * lethargy and weakness * fever * acetone door of the breath reflecting metabolic acidosis Describe the treatment management of DKA * initial stabilisation: ABCD, 1/2 hourly BP HR urine output, hourly capillary BGL, 2 hourly electrolytes especially potassium * fluids & electrolytes: most pt's have a deficit of several litres (40-80 ml/kg), rapid fluid reuses for hypovolaemia (first 24hrs give 1/3 fluid in the first 5-6 hours of N/saline), potassium replacement (if not above 6mmol/L give 1/2-2g, 6-26mmol/hr Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Sort Diabetic Ketoacidosis lack insulin = effective state of starvation b/c can't get glucose into cells body starts to make ketones out of fat and proteins PROBLEM: no feedback loop and they continue to produce more and more ketones without stopping. By the time ketone levels (specifically, β-hydroxybutyrate) approach 15 to 25 mM, the resulting pH imbalance leads to profound metabolic derangement and the patient is critically ill. DKA clinical definition an increase in the serum concentration of ketones greater than 5 mEq/L, a blood glucose level greater than 250 mg/dL (although it is usually much higher), and a blood (usually arterial) pH less than 7.3. Ketonemia and ketonuria are characteristic, as is a serum bicarbonate level of 18 mEq/L or less (< 5 mEq/L is indicative of severe DKA). Diabetic Person Decreased insulin = decreased signaling in hypothalamus = increased food intake and weight gain = decreased inhibition of hepatic glucose production = reduced efficiency of glucose upatke in muscle = increased lipolysis in adipocyte = increased plasma NEFA (Non-Esterified Fatty Acids = free fatty acids) levels The increase in body weight and NEFAs contribute to insulin resistance, and the increased NEFAs also suppress the cell's adaptive response to insulin resistance. The increased glucose levels together with the elevated NEFA levels can synergize to further adversely affect -cell health and insulin action, often referred to as 'glucolipotoxicity Hyperosmolar Hyperglycemic State (HHS) serious metabolic derangements that occurs in patients with diabetes mellitus (DM) (It is less common than the other acute complication of diabetes, diabetic ketoacidosis (DKA)) HHS most commonly occurs in patients with T2DM who have some concomitant illness that leads to reduced fluid Continue reading >>

Nurs 355 Chapter 33

Nurs 355 Chapter 33

A child with hypopituitarism is being started on growth hormone (GH) therapy. Nursing considerations should be based on which knowledge? Replacement therapy requires daily subcutaneous injections. Additional support is required for children who require hormone replacement therapy, such as preparation for daily subcutaneous injections and education for self-management during the school-age years. Young children, obese children, and those who are severely GH deficient have the best response to therapy. Replacement therapy is not needed after attaining final height. The children are no longer GH deficient. When therapy is successful, children can attain their actual or near-final adult height at a slower rate than their peers. Peripheral precocious puberty (PPP) differs from central precocious puberty (CPP) in which manner? PPP may be viewed as a variation in sexual development PPP may be viewed as a variation in sexual development. PPP results from hormone stimulation other than the hypothalamic Gn-RH. Isolated manifestations of secondary sexual development occur. PPP can be missed if these changes are viewed as variations in pubertal onset. CPP results from CNS insult, occurs more frequently in girls, and results from hormonal stimulation of the hypothalamic Gn-RH. The nurse is planning care for a child recently diagnosed with diabetes insipidus (DI). What intervention should be included? Encourage the child to wear medical identification DI is a potentially life-threatening disorder if the voluntary demand for fluid is suppressed or the child does not have access to fluids. Medical alert identification should be worn. Fluid intake is not restricted in children with DI. The child is unable to concentrate urine and can rapidly become dehydrated. Fluid intake may be limite Continue reading >>

What`s The Difference Between Diabetic And Insulin Comas?

What`s The Difference Between Diabetic And Insulin Comas?

Dear Dr. Johnson: What is the difference between a diabetic coma and an insulin coma? A diabetic coma is the result of hyperglycemia--too much blood sugar --and typically develops slowly over a matter of hours or days as blood sugar and other unwanted blood products build up in the body. Diabetic coma is treated with insulin administered intravenously. This lowers the blood sugar level. Insulin shock is caused by too much insulin, a state that leads to hypoglycemia--too little blood sugar. This condition can come on very rapidly in a person taking insulin for diabetes; therefore, diabetics are instructed to recognize hypoglycemia`s early warning symptoms (mental changes, sweating, etc.) and then to take action to raise their blood sugar levels. When a person with diabetes is found in an unconscious state, it is often difficult to know whether it is the result of a blood sugar level that is too high or too low. Therefore, the usual course of action is to raise the blood sugar level until testing confirms the nature of the problem. There will be little danger in giving added blood sugar to an individual with an already high level, and it might be lifesaving if the problem is low blood sugar. Dear Dr. Johnson: What is your opinion on the current debate on whether restaurants and fast-food joints should list the ingredients of the foods they prepare? I personally favor a simple form of ingredient listing that would give the percentages of fat, carbohydrates and protein as well as the calorie and salt content of foods. I don`t think all ingredients have to be listed, though I do believe the information should be made available if someone requests it. I think we all would be well served by having the major items of nutritional interest for public view. Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

List Clinicopathologic features that might be present with DKA? Elevation in liver enzymes (hepatic lipidosis, pancreatitis) Hyperlipidemia Hyperlipasemia Hyperamylasemia Metabolic Acidosis Serum Hyperosmolality Azotemia (usually pre-renal) Hemeturia, pyuria, bactiuria (always submit cysto for culture an dsensitivity) Ketonuria Continue reading >>

Diabetes

Diabetes

Sort 1. A 54-year-old patient admitted with type 2 diabetes asks the nurse what "type 2" means. What is the most appropriate response by the nurse? A. "With type 2 diabetes, the body of the pancreas becomes inflamed." B. "With type 2 diabetes, insulin secretion is decreased, and insulin resistance is increased." C."With type 2 diabetes, the patient is totally dependent on an outside source of insulin." D. "With type 2 diabetes, the body produces autoantibodies that destroy β-cells in the pancreas." B."With type 2 diabetes, insulin secretion is decreased, and insulin resistance is increased." Rationale: In type 2 diabetes mellitus, the secretion of insulin by the pancreas is reduced, and/or the cells of the body become resistant to insulin. The pancreas becomes inflamed with pancreatitis. The patient is totally dependent on exogenous insulin and may have had autoantibodies destroy the β-cells in the pancreas with type 1 diabetes mellitus. 2. The nurse caring for a patient hospitalized with diabetes mellitus would look for which laboratory test result to obtain information on the patient's past glucose control? A. Prealbumin level B. Urine ketone level C. Fasting glucose level D. Glycosylated hemoglobin level D. Glycosylated hemoglobin level Rationale. A glycosylated hemoglobin level detects the amount of glucose that is bound to red blood cells (RBCs). When circulating glucose levels are high, glucose attaches to the RBCs and remains there for the life of the blood cell, which is approximately 120 days. Thus the test can give an indication of glycemic control over approximately 2 to 3 months. The prealbumin level is used to establish nutritional status and is unrelated to past glucose control. The urine ketone level will only show that hyperglycemia or starvation is pr Continue reading >>

Multiple Choice Quiz

Multiple Choice Quiz

(See related pages) Please answer all questions 1 Cerebrospinal fluid, fluid within the eyes, joints, and body cavities, and fluid secretions of exocrine glands are all classified specifically as ______________ fluid. 2 What are the two major factors that regulate the movement of water and electrolytes from one fluid compartment to the next? B) osmoreceptors in the hypothalamus detect the increase in osmotic pressure of body fluids and signal the posterior pituitary to release ADH C) chemoreceptors in the renal tubule sense the increased viscosity of renal filtrate and signal the hypothalamus which, in turn, signals the posterior pituitary D) the juxtaglomerular apparatus senses the greater osmotic pressure in the blood and triggers the release of ADH 4 How does alcohol function as a diuretic? B) Alcohol receptors in the liver sense its presence and trigger a biochemical pathway that increases urine output to rid the body of alcohol. D) Alcohol prevents the distal convoluted tubule from reabsorbing water from the filtrate. 5 A so-called "salt craving" is primarily the result of _________________. 6 _______________ ions account for nearly 90% of the positively charged ions found in extracellular fluid. 7 The hormone aldosterone regulates the concentrations of _____________ and ______________ in the body. 8 Edema can be caused by all of these factors except ________________. 9 The imbalance known as ____________ can be caused by certain diuretic medications. 10 Which of the following does not occur as a result of a shift in the acid- base balance of the body? 12 The three most important buffer systems in body fluids include the bicarbonate buffer system, the ______________ buffer system, and the protein buffer system. 13 How is it possible for the rate and depth of breath Continue reading >>

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