Effects
Hypoglycemia at night, rebound hyperglycemia in the morning. More common in type 1 children, rarley in type 2. May wake up in the middle of the night sweating.
What is Somogyi Effect?
lack of insulin > hyperglycemia > breakdown of fat (lipolysis) > fatty acids converted to ketones > acidosis
What is DKA?
SICK DAY TEACHING:
-Take meds even if not eating, -May need to increase insulin, -Drink fluids 4-6 oz every 30 mins, -50 g of carbs (CHO) fluids or foods, Type 1 needs to test for ketones.
Which type of insulin is used for IV administration?
What is Regular insulin?
A patient with suspected DKA presents with the following findings: glucose 520 mg/dL, K+ 3.0, BP 88/54, and deep rapid respirations. What is the nurse’s priority action?
Begin rapid IV fluids
Suar begins to rise after it levels out around 2 am. Morning hyperglycemia without an episode of hypoglycemia at night.
What is Dawn Phenomenon?
polyuria, polydipsia, polyphagia, blurred vision, hypotension, altered mental status, seizures, paralysis (reversible), weight loss, weakness, headaches, no ketones, mild GI symptoms
What is HHNKS (HHS)?
When should a SICK diabetic go to the ER?
If ketones are in urine, not eating normal diet > 24 hrs, unable to drink for >4 hrs, v/d for >6 hrs, sugar <60 OR >300, trouble breathing, confusion, AMS.
A patient taking this class of oral antidiabetic medication is at increased risk for lactic acidosis when consuming alcohol and must temporarily discontinue the drug before and after contrast dye procedures to prevent renal complications. NAME THE CLASS AND NAME THE DRUG ITSELF.
What are biguanides (metformin/Glucophage)?
A DKA patient’s glucose is now 240 mg/dL. What is the next nursing action?
Add dextrose to IV fluids
Not enough insulin to control sugar, peaks too soon (desensitized) OR the effect of insulin decreases during the night. Insulin is used up too rapidly or has shorter duration in some people peaks sooner. A person also has hyperglycemia in the morning.
What is Waning Effect?
What are the 3 main features with DKA and explain s/s with them:
Hyperglycemia: Fruity breath, ketones in urine/blood, polydipsia, polyuria, polyphagia, headache, abdominal pain, blurry vision, fatigue, confusion, lethargic. Dehydration: Thirsty, fatigue, sodium hemodiluted, urine concentrated, dark urine, low BP, tachycardia, high RR, low grade fever, high BUN/creatinine, dizziness, skin tenting, dry mucous membranes. Acidosis: pH <7.35, kussmaul respirations (deep/rapid), GI distress, high potassium
A patient diagnosed with diabetic ketoacidosis is treated with rapid IV fluid resuscitation using 1–2 liters of normal saline followed by 0.45% saline, continuous IV insulin to reduce hyperglycemia and stop ketone production, and management of the underlying illness or infection. As blood glucose approaches 250 mg/dL, potassium and dextrose are added to IV fluids to prevent hypoglycemia and correct electrolyte shifts caused by insulin therapy.
What is the management/treatment of diabetic ketoacidosis (DKA)?
Stimulates insulin release from beta-cells of pancreatic islets. Best given 30 mins before breakfast. Name the drug class and drug names.
What is glipizide, glucorol, and glyburide? What is sulfonylureas?
Why should sulfonylureas be taken before meals?
Stimulate insulin release before glucose rises
What can someone do to help not have the somogyi effect?
reduce evening dose of NPH or eat larger bedtime snack
What are the diagnostic findings with Hyperosmolar hyperglycemic nonketotic syndrome?
Glucose 600-1200, hyponatremia (from diuresis), and hypo, normal, or hyperkalemia.
A patient with severe hyperglycemia is managed with aggressive fluid replacement prioritizing perfusion, including isotonic fluids for vascular dehydration followed by hypotonic fluids for cellular dehydration, along with IV insulin therapy, correction of electrolyte imbalances, and frequent neurological assessments due to sodium shifts and risk for altered mental status.
What is the management/treatment of hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)?
Patient teaching for sufonylureas?
May cause hypoglycemia, GI upset/abdominal pain, dizziness, weight gain, heartburn/epigastric fullness, possible disulafiram-like reaction with alcohol (mainly with glyburide).
Why does DKA cause acidosis?
Fat breakdown produces ketones
1. Treatment for Dawn Phenomenon? 2. Treatment for waning effect?
1. What is increasing or adding evening (PM) insulin, such as NPH or a basal insulin like Lantus? 2. What is increasing the evening dose of insulin or switching to a longer-acting (basal) insulin?
What are the diagnostic findings with DKA?
Glucose 300-800, pH <7.35, positive urine ketones, hyperkalemia (from cells shrinking, pushing K+ into bloodstream), and hyponatremia (from diuresis).
What is the ratio for IV insulin? Do we piggy back or have a Y site?
1:1 ratio so 1 unit- 1 mL, NO piggy back, NO Y site.
Patient teaching for biguanides?
-Can NOT take before contrast dye studies- must be off of med for at least 48 hrs before or after, must have food on stomach before taking, alcohol may increase likelihood of lactic acidosis, does not typically cause hypoglycemia.
Why are neuro checks critical in HHNKS?
Risk of sodium shifts affecting brain function