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USE THIS ONE Hypoglycemia, DKA, HHNS
Terms in this set (50)
- diaphoresis (cold, clammy skin)
- excess hunger
- anxious but alert
- confusion, vertigo
- behavior changes
- loss of consciousness
- shallow respirations
- medical ER, administer glucose immediately
Symptoms of diabetic ketoacidosis (DKA)
- skin hot, dry, decreased turgor
- increased pulse
- blurred vision
- altered mental status
- confusion to coma
- fruity odor to breath (sympts of ketoacidosis)
- kussmauls respirations (deep,nonlabored)
Symptoms of Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNS)
- skin hot, dry, decreased turgor
- increased pulse
- blurred vision
- altered mental status
- confusion to coma
Positive serum ketones
Absolute lack of available or unusable insulin
Glucose level less than 700mg/dL
Acidotic due to ketone bodies
7). Mental status changes
8). "Fruitty odor" breath
DKA PRECIPITATING FACTORS
1). Infection--UTI, pneumonia
2). Omission of diabetic therapy/inadequate treatment
3). Insulin pump therapy
6). Acute illness--pancreatitis, trauma, renal failure, bowel obstruction
7). Alcohol intoxication/substance abuse
8). Financial issues
9). Drugs/medications--steroids, Ca+ channel blockers, Beta blockers, Dilantin, HCTZ, antidepressents, diuretics
3 major abnormalities of DKA
1). Elevated blood glucose level >350mg/dL
2). High ketones
3). Metabolic acidosis (pH<7.30, low HCO3) with an elevated anion gap
GOAL OF TX DKA
2). Restore and maintain normal glucose metabolism
3). Correct electrolyte deficiencies and acidosis
4). Provide glucose when needed
5). Prevent complications
A significant decrease in serum glucose can be achieved in the absence of any insulin therapy by what method?
Fluid therapy lowers hyperglycemia by dilution and increased glomerular rate.
When blood glucose concentrations reach 250 mg/dL or lower, what is the next step in treatment and what will it prevent?
Add 5% dextrose to maintenance fluids which will help to prevent hypoglycemia and cerebral edema.
How often should the blood glucose be monitored when the patient is unstable?
How often should the blood glucose be monitored in the stable patient?
Every 2 hours
The insulin drip should be continued even in the presence of a normal blood glucose until what has been resolved?
Acidosis (normal anion gap) and ketonemia
SQ insulin is usually given ________ and glucose levels continue to be monitored every 4 hours.
1-2 hrs prior to discontinuation
What is the most common early morning hyperglycemia in diabetics using insulin?
Insufficient Insulin aka Dawn Phenomenon
What is a common cause of early morning hyperglycemia in diabetics using insulin?
Dawn Phenomenon aka Insufficient Insulin
What is insufficient insulin?
Inadequate night time basal insulin dose which leads to blood glucose that continuously rising through the night.
What is the Dawn phenomenon?
It is an early morning physiologic surge in growth hormone and cortisol in which the blood glucose is stable all night till around 2-3 am and then there is a significant increase in blood sugar leading to hyperglycemia.
What is the treatment for insufficient insulin?
Increase night time intermediate or long acting insulin dose
What is the least common cause of early morning hyperglycemia in diabetics using insulin?
Somogyi effect aka rebound hyperglycemia
What is the Somogyi effect?
it is excessive night time basal insulin dose which leads to hypoglycemia in the middle of the night and triggers a release of counter regulatory hormones.
What is the treatment for the Somogyi effect?
Decrease night time intermediate or long acting insulin dose
What test is least indicated to look for a medical event that night have excited an episode of DKA?
Chest and abdominal CT
Serum Osmolarity in DKA
Glucose causes an excess loss of solutes in relation to solvents, therefore less water for the particles in the blood. As osmolarity rises above 300 thirst is stimulated, to compensate the body pulls water from the intracellular fluid.
Serum Osmolarity: 2(Na)+BUN/2.8+BG/18. Normal range 285-295.
Hyperosmolar hyperglycemic state
No positive ketones
Relative resistance to insulin produced
Glucose levels >800-1000mg/dL
Acidosis due to circulatory collapse
Normal blood glucose range
Insulin and glucagon both released by the
Glycogen is stored and broken down into glucose by the
Type 1 Diabetes
Absolute lack of insulin secretion due to destruction of pancreatic beta cells
Type 2 Diabetes
Insulin resistance in target cells, beta cell death
Glucose intolerance with an onset during pregnancy
Women with gestational diabetes at increased risk for developing diabetes with 5-10 years of delivery
Can be an indicator that the pt will become type 2 diabetic later in life
Polyuria, polydipsia, polyphagia
Excess glucose molecules increase osmotic pressure, leading to polyuria and polydipsia
Insufficient nutrient stores become depleted, triggering polyphagia
Other signs and symptoms
blurred vision, fatigue, paresthesias, skin infections, and possible nocturia secondary to polydipsia
Kidneys cannot reabsorb high blood glucose levels, resulting in glucosuria
Type I Diabetes
Absolute lack of insulin due to destruction of pancreatic beta cells in the pancreas
Require insulin therapy; no oral antidiabetics
Accounts for 5-10% of DM cases; most frequent in children and young adults, but may occur at any age
Life-threatening complications include treatment-induced hypoglycemia and diabetic ketoacidosis (DKA)
Occurs primarily in patients with type 1 diabetes
Without insulin to break down glucose, the body begins to break down fatty acids
Fatty acid break down produces ketones, which cause acidosis
Three major disturbances are hyperglycemia, metabolic acidosis, and osmotic diuresis.
Other Signs and Symptoms:
N/V, severe fatigue,
abdominal pain, fruity breath,
stupor, and eventual coma,
Kussmaul's respirations with increased rate and depth.
Hypokalemia may be from loss of K from body stores, and an intracellular to extracellular shift of K.
Rehydration also decreases K levels. Administration of insulin enhances the movement of K from the extracellular fluid into the cells. May be first presenting symptom of DM.
Treatment: Fluid replacement to improve perfusion. Regular insulin to decrease blood glucose gradually, cautions K replacement is vital to avoid dysrhythmias. Correct acidosis; Treat any identified cause
Mortality rate of less than 5% with proper treatment.
Type II Diabetes Mellitus
Target cells become insulin resistant
Pancreas hyper-secretes insulin as blood glucose rises
Hyper-secretion of insulin leads to beta cell death
Insulin resistance AND insufficient insulin production
Life-threatening complications include treatment-induced hypoglycemia and hyperosmolar hyperglycemic state (HHS) (aka Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS))
Hyperosmolar Hyperglycemic State (HHS) AKAHyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS)
Usually seen in Type II DM patients; often elderly, obese, with comorbidities
Characterized by hyperglycemia (>600mg/dL), hyperosmolarity (>310 mOsm/L), dehydration, and absence of ketoacidosis, and CNS dysfunction
Other Signs and Symptoms: Dehydration from osmotic diuresis, tachycardia and hypotension from fluid depletion; confusion, lethargy, may lead to stupor and coma, seizures, hemiparesis, aphasia, visual disturbances
Onset is gradual, and may be mistaken for stroke in elderly patients
Treatment: Fluid replacement, carefully to avoid pulmonary and cerebral edema. Correction of electrolyte abnormalities. IV infusion of low dose insulin, seizure precautions, monitor vital signs, I&O. Find treat any identified cause and treat.
Mortality rate of 20-40%
Exemplar: Human regular insulin (Humulin R, Novolin R)
Short-acting; usually used in combination with longer-lasting insulin
Identical to endogenous insulin
Mechanism of Action
Decrease blood glucose by increasing cellular uptake of glucose
Stimulates storage of glucose as glycogen
Inhibits release of glucagon
Routes of Administration
Routes: SQ, IV,
ONLY regular insulin may be given IV
Rapid absorption after SQ injection; may vary by administration site
Onset of action
SQ: 30-60 minutes
IV: 15 minutes
Duration: 6-10 hours
Monitor patients with hypokalemia (may worsen this condition); use with caution with pregnancy, renal dysfunction, fever, thyroid disease, age extremes
Many drugs may influence glycemic levels; use caution when administering with any other medication (consult drug references)
Additional Nursing Responsibilities
Nursing Application (p. 1194-1196)
Elderly: Increased risk for hypoglycemia; monitor self-administration related to visual or dexterity changes
Carry supply of readily available sugar or quick-acting carbohydrates in case of hypoglycemia
Wear medical alert identification and carry medical alert card
Abnormally low blood glucose in either type 1 or type 2 diabetes.
-Too much insulin
-Too much exercise without enough food
-Some oral antidiabetic drugs such as sulfonalureas
-Skipping meals without reducing medication dose
-Alcohol consumption can decrease gluconeogenesis
**Signs and Symptoms:
Headache, difficulty concentrating, confusion, behavioral changes, tachycardia, anxiety, sweating, cool/clammy skin
Some drugs, such as beta-adrenergic blockers can block tachycardia, mask sympathetic symptoms of hypoglycemia, delaying awareness and treatment. Is medical emergency because if severe or prolonged, can cause brain damage or death.
Exemplar: Glucagon (GlucaGen)
Identical in structure to human glucagon (hormone)
Used for emergency treatment of hypoglycemia when patient cannot consume glucose and no IV access
May be given IM, SQ
Increases glucose levels by stimulating breakdown of stored glycogen (not effective in patients without glycogen reserves)
Increases glycogenolysis, stimulates uptake of amino acids and their conversion to glucose, and promotes lipolysis in the liver (releases fatty acids and glycerol)
If patient can swallow, 15 grams of glucose such as orange juice or sugared soda. Wait 15 minutes and recheck blood glucose again. If still low, repeat treatment.
If IV in place administer IV D50
For unconscious patient and no IV access, administer glucagon (GlucaGen) IM or SC. It stimulates breakdown of glycogen. Be prepared to assist patient with emesis basin
Sensitivity to protein compounds
Depleted glycogen stores or pheochromocytoma
Precautions: Coronary artery disease (may affect blood pressure, heart rate, and myocardial oxygen demand)
Pregnancy category B
Adverse Effects Glucagon
Nausea very common.N/V, hypersensitivity reactions, transient changes in BP (high and/or low), tachycardia, hyperglycemia, and hypokalemia
Drug Interactions Glucagon
Beta-adrenergics inhibit the effect of glucagon and increase cardiac risks
Assess glucose before, during, and after glucagon administration
After client is awake and able to take oral intake consider administering carbohydrates or protein
Educate about signs and symptoms of hypoglycemia
Review family teaching regarding the use of emergency glucagon kit
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