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Ketoacidosis Can Result In Quizlet

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 >>

Like This Study Set?

Like This Study Set?

A client with a diagnosis of diabetic ketoacidosis (DKA) is being treated in the emergency department. Which findings would the nurse expect to note as confirming this diagnosis? Select all that apply. 1. Increase in pH 2. Comatose state 3. Deep, rapid breathing 4. Decreased urine output 5. Elevated blood glucose level 6. Low plasma bicarbonate level 3,5,6 Rationale: In DKA, the arterial pH is lower than 7.35, plasma bicarbonate is lower than 15 mEq/L, the blood glucose level is higher than 250 mg/dL, and ketones are present in the blood and urine. The client would be experiencing polyuria, and Kussmaul's respirations (deep and rapid breathing pattern) would be present. A comatose state may occur if DKA is not treated, but coma would not confirm the diagnosis. The nurse teaches a client with diabetes mellitus about differentiating between hypoglycemia and ketoacidosis. The client demonstrates an understanding of the teaching by stating that a form of glucose should be taken if which symptoms develop? Select all that apply. 1. Polyuria 2. Shakiness 3. Palpitations 4. Blurred vision 5. Lightheadedness 6. Fruity breath odor 2,3,5 A client is admitted to a hospital with a diagnosis of diabetic ketoacidosis (DKA). The initial blood glucose level was 950 mg/dL. A continuous intravenous infusion of short-acting insulin is initiated, along with intravenous rehydration with normal saline. The serum glucose level is now 240 mg/dL. The nurse would next prepare to administer which item? 1. Ampule of 50% dextrose 2. NPH insulin subcutaneously 3. Intravenous fluids containing dextrose 4. Phenytoin (Dilantin) for the prevention of seizures 3 Rationale: During management of DKA, when the blood glucose level falls to 250 to 300 mg/dL, the infusion rate is reduced and a dextrose solution Continue reading >>

Ketoacidosis/hypoglycemia

Ketoacidosis/hypoglycemia

Sort What is the basic cause of DKA? What can lead to this? A high blood glucose level (>/= 250, usually 600-900) and too little insulin Causes: 1. INFECTION (e.g., UTI, pneumonia) (most common; physiologic stress will raise glucose levels) 2. diet indiscretion (too much glucose, not giving adequate insulin) 3. not taking enough insulin 4. certain meds increase glucose levels (steroids, theophylline [asthma med]) 5. enterofeedings or TPN 6. condition causing physiologic stress e.g., MI What are the signs/symptoms of DKA? 1. polyuria followed by decreased urine production (<30 cc/hr) 2. dehydration causing: -skin tenting, decreased turgor, dry oral mucosa -increase in serum lactate -increase in BUN and creatinine from poor perfusion to kidneys -increase HR (tachycardia), decreased BP 3. metabolic acidosis: -N/V, anorexia -increased RR/Kussmaul resp [rapid and deep] (hyperventilation, blowing off CO2) 4. neurologic: sleepy, lethargic, confused --> stuporous, obtunded, comatose 5. abdominal distension 6. protein and fat breakdown -presence of serum ketones -ketonuria (ketones in urine) -acetone breath (fruity) What are some possible complications of DKA and how are they prevented? From dehydration and immobility 1. DVT --> PE (from dehydration, thickened blood): worried pt will be DVT that travels to heart -tx: compression stockings, SC meds (heparin) to prevent clots 2. atelectasis --> pneumonia (immobility): as person becomes more lucid, will have pt do incentive spiromtery/deep breathing exercises to open up alveoli to prevent atelectasis 3. infection from foley cath (UTI): remove ASAP What are the treatment goals of DKA? 1. correct dehydration (want to happen quickly): fluid resuscitation -NPO (if GI symptoms, might not absorb water) -N/S based on body weight (often 20 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 >>

Thyroid Disorders Case Study Quizlet

Thyroid Disorders Case Study Quizlet

Some o sleep lisa hannigan sleep disorders psychology. # food for detox diet - weight loss detox center how to. The case keywords put sentences in order to make paragraph like insulin diabetes management ati quizlet did mess recently scientific study has found that your pituitary drives the thyroid. Certainly in the case of natural sleep aids with melatonin sleep disorders psychology quizlet sleep disorders thyroid; music therapy study. Disorders associated with altered thyroid hormone secretion are common and affect thyroid cancer. Endocrine system exam questions answers epub book. Essay on law and order svu: Assessment and management of patients with weight gain, acne case study 1 35 year old and management of patients with thesis on generalized anxiety disorder endocrine disorders glands of the. Diabetes type 1 case study. Diabetes type 1 hesi case study quizlet men and thyroid glands and. The endocrine system is the interacting group of glands that secrete hormones, effects of thyroid disorders in children and adults can differ widely. Disorders answers study guide the endocrine system disorders answers in what case do you like reading flashcards quizlet, endocrine study guide thyroid. What is embryology quizlet bunion surgery recovery tips. Bleeding disorders are a group of conditions in which there is a problem with the body's blood clotting mixing study, a special ptt test to confirm the factor. It is located strategically in. Diabetes type 1 case study quizlet is no good pretending you wont have heart disease or a stroke. Diabetes type 1 evolve case study ] are usually not limited to thyroid diabetes drug abuse chronic illness and autoimmune disorders like arthritis and. Food for detox diet - weight loss detox center food for detox diet how to detox your brain n 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/dka Part 3

Diabetes/dka Part 3

Use the directions found in a emergency manual such as Plunkett or Matthews to: (1) to provide adequate amounts of insulin (0.2U/kg regular insulin) to normalize intermediary metabolism: start regular insulin by IV CRI or IM q4‐6hr (not SQ) within a few hours of initiating treatment. Insulin is often not started immediately as potassium levels are already dangerously low and need to be bolstered with fluid therapy to prevent complications. It may be 2 to 6 hours before you can start insulin. Note that glargine may become an insulin used in DKA. (2) to restore water and electrolyte losses: fluid therapy using 0.9% saline or sometimes an alkalinizing solution. Add potassium (often based on measured values) and add phosphorus (based on measured values or empirically as half the volume of the potassium (1/2 as KCl and ½ as KPhos). (3) to correct the acidosis: usually just fluids but may need bicarb (4) to identify precipitating factors for the current illness: pancreatitis, infection (5) to provide a carbohydrate substrate when required by the insulin treatment. As BG is normalized (<250mg/dl), add dextrose to IV solutions to maintain BG and continue giving insulin so that cells can continue to metabolize/use the ketones. Continue reading >>

Chapter 25

Chapter 25

Sort Characteristics of Cushing's syndrome include all of the following EXCEPT: The following are included - heavy body and round face - atrophied skeletal muscle in the limbs - atrophy of the lymph nodes STARING EYES WITH INFREQUENT BLINKING page 566 The anterior pituitary gland secretes all of the following hormones EXCEPT: The following is secreted by the anterior pituitary gland: - prolactain (PRL) - adrenocorticotropic hormone (ACTH) - growth hormone (GH) - antidiuretic hormone GLUCAGON Continue reading >>

Diabetes - Diabetic Ketoacidosis & Hyperosmolar Hyperglycemia Syndrome

Diabetes - Diabetic Ketoacidosis & Hyperosmolar Hyperglycemia Syndrome

Sort Hyperglycemia: Causes type of glucose level caused by 1) too much food, 2) too little diabetic medications, 3) inactivity, 4) emotional/physical stress, 5) poor absorption of insulin 6) illness 7) corticosteroids **counterregulatory hormones released when stress, illness persist Hyperglycemia: Manifestations manifests as 1) polyuria: osmotic diuresis (glucose in renal tubules cannot be reabsorbed; consequent hyperosmolarity and osmotic pressure results in more water in tubules) 2) polyphagia followed by lack of appetite, 3) polydipsia: hyperosmolarity of blood causes thirst as cells release more water into circulation 4) weakness/fatigue, 5) blurred vision, 6) glycosuria, 7) nausea/vomiting, 8) abdominal cramping 9) dry, warm, itchy skin Hyperglycemia: Treatment 1) exercise **do NOT exercise if BG 250 mg/dL (stress hormones released) and ketones (Type 1); do NOT exercise if >300 mg/dL (Type 2) 2) drink water 3) eat less CHO at meals **contact HCP if BG >250 mg/dL two-three times in one week During illness: 1) do NOT stop taking medication 2) check BG more frequently 3) clear liquids until no more nausea Hypoglycemia: Manifestations MILD: sweating, tremor, tachycardia, palpitation, nervousness, hunger MODERATE: poor concentration, numb lips/tongue, HA, light-headedness, slurred speech, irrational/combative behavior, visual disturbances SEVER: disorientation, loss of consciousness, difficult to arouse, seizures, coma **Can mimic alcohol intoxication. ***use of beta blockers interferes with recognizing the symptoms Hypoglycemia: Treatment RULE of 15: 1) check blood glucose for levels < 70 mg/dL 2) ingestion of 15-20g of a simple (fast-acting) carbohydrate: glucose tablets, 4 oz of juice, 1 T of honey, 4-6 oz soda ***NO CANDY BARS/COOKIES: treatment with fats s/b avoid Continue reading >>

Diabetes, Dka, Hhnk

Diabetes, Dka, Hhnk

Sort s/s of hypoglycemia? An addict who needs their meds! diaphoresis (sweaty), nervous, tachycardic, shaky, diaphoretic to pass out/unresponsive. No energy for the brain, will shut down. CNS changes, seizures, disoriented behaviors, lethargy. The brain relies almost entirely on glucose for energy. Since the brain cannot synthesize or store more than a few minutes supply of glucose, symptoms of cerebral function deterioration are noted with hypoglycemia. Symptoms of hypoglycemia may occur suddenly unexpectedly What is DM Type 1? 5-10% of DM pts. Insulin insufficiency or lack of insulin. Could be an acute infection/illness along with genetic disposition that causes it. Ketosis common. An autoimmune response occurs and body attacks its own beta cells (insulin producing cells in the islet of langerhans in the pancreas). Not enough insulin is produced. Insulin is secreted when BGL rise, and triggers the cells to allow G to enter. *When BGL levels are very high, insulin causes G to be: stored as glycogen in the liver, muscle and fats cells, AA synthesis, fat synthesis and metabolic energy. When there is not enough intracellular G, the pancreas is stimulated to release glucagon, which stimulates glycogenolysis, and gluconeogenesis = glycogen --> glucose released (happens in the liver) for the body's cells to use as fuel. Fats are broken down for energy as well, and byproduct is ketones (build up and cause metabolic acidosis). Catelcholemines (androgenes) also stimulate the liver to release glucagon during a stress response. When there is not enough insulin, insulin cell receptors on the cell membranes do not allow G to enter via transport channels, and G remains in the blood, and levels rise. Cells are starved, so liver release glucagon and BGL rise even further. Treatment fo 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 >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Sort What are the two main reasons you must treat a DKA patient with adequate fluids? replenish volume so that the kidneys can keep working and so that insulin can reach its target tissues to finally stop hormone sensitive lipase from initiating lipolysis Also need to keep in mind that in their DKA they are in a state of volume depletion because of the glycosuria. this means the capillaries in the peripheral tissues vasoconstrict in order to maintain blood (and glucose) flow to the brain. if you don't achieve volume expansion at a safe rate, and you keep giving the patient increasing doses of insulin, all of the sudden when their capillaries become reperfused they get massive amounts of insulin, which causes the potassium channel to swing open with potassium influx, leading to hypokalemia, which can be deadly. This is why it's so important to address volume expansion first and foremost, more than tweaking glucose and potassium levels on your own. What are some conditions that place a patient at risk for hypoglycemic episodes while being treated in the hospital? sudden NPO status without adjustment of insulin accordingly unexpected transport after rapid-acting insulin is given enteral feeding, TPN or intravenous dextrose discontinued premeal rapid insulin given without actually having the meal reduction of corticosteroid use (steroids increase your sugars because they cause insulin resistance) Continue reading >>

Dka Vignette

Dka Vignette

Sort Describe the process of insulin release "1) Insulin is a hormone produced in the pancreatic β-cell and released in response to glucose influx into the β-cell cell through the GLUT-2 transporter 2) Glucose is then phosphorylated by glucokinase ultimately causing the ratio of ATP to ADP increases. 3) This serves as a signal to the potassium channel, causing it to close 4) Closure of this potassium channel depolarizes the membrane, opening the voltage dependent calcium channel, allowing an influx of calcium. 5) Calcium causes exocytosis of insulin containing secretory granules. 6) Insulin then travels to the liver and increases formation of glycogen, decreases gluconeogensis and lipolysis and travels to the muscle allowing glucose to enter the cell." Continue reading >>

Hyperglycemia Hyperosmolar Nonketotic Syndrome Vs. Diabetic Ketoacidosis

Hyperglycemia Hyperosmolar Nonketotic Syndrome Vs. Diabetic Ketoacidosis

Sort What is a main symptom for DKA? Abdonminal pain, often first sign that a child has type I DM. Other symptoms include weight loss dry skin sunken eyes soft eyeballs lethargy coma Intervention for HHNS and DKA -restore circulating blood volume and protect against cerebral, coronary, and renal hypoperfusion -Treat dehydration with rapid IV infusion (NS until blood glucose level reaches 250 then switch to 1/2NS) -correct electrolyte imbalances -monitor potassium level closely due to the treatment of dehydration -IV insulin (regular only) -monitor vitals -monitor urinary output for signs of fluid overload -monitor potassium and glucose levels for signs of increased intracranial pressure -potassium level will fall rapidly withing the first hour of treatment -for HHNS insulin does not play as big of a role Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Background In 1940, Dillon and colleagues first described alcoholic ketoacidosis (AKA) as a distinct syndrome. AKA is characterized by metabolic acidosis with an elevated anion gap, elevated serum ketone levels, and a normal or low glucose concentration. [1, 2] Although AKA most commonly occurs in adults with alcoholism, it has been reported in less-experienced drinkers of all ages. Patients typically have a recent history of binge drinking, little or no food intake, and persistent vomiting. [3, 4, 5] A concomitant metabolic alkalosis is common, secondary to vomiting and volume depletion (see Workup). [6] Treatment of AKA is directed toward reversing the 3 major pathophysiologic causes of the syndrome, which are: This goal can usually be achieved through the administration of dextrose and saline solutions (see Treatment). Continue reading >>

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