Endocrine Emergencies Flashcards
what is the causal difference in type 1 and type 2 diabetes?
Diabetic Emergencies
Type 1; an absolute insulin deficiency
Type 2; impaired glucose secretion, peripheral insulin resistance, and increased hepatic glucose production
Diabetic Ketoacidosis has a __-__% mortality rate
3-10%
DKA; Infection, illness, pregnancy, or situational stressors can lead to ____. This creates insulin ____. In some patients, excess circulating glucose due to poor dietary management can overwhelm an already stressed system.
gluconeogenesis
insulin deficiency
Name four things that can lead to gluconeogenesis.
Infection, illness, pregnancy, or situational stressors
Insulin deficiency leads to the release of counterregulatory hormones (such as ____ and ____), which can lead to gluconeogenesis
glycogen and cortisol
After a prolonged insulin deficiency, the patient can present with four acute concurrent problems, what are they?
Hyperglycemia, dehydration, electrolyte depletion, and metabolic acidosis
Hyperglycemia increases serum ____ and leads to osmotic ____, which causes significant dehydration from urinary loses of water, and these five electrolytes
osmolarity
osmotic diuresis, which causes significant dehydration from urinary loses of water, sodium, potassium, magnesium, calcium, and phosphorus
With DKA, Hyperosmolarity further impairs ____ secretion and promotes insulin ____. Without insulin, the newly liberated ____ cannot be used, further increasing the blood glucose level, urine glucose concentration, and osmotic diuresis
insulin
resistance
glucose
With DKA, The body burns ____ and ____ ____ for energy. The ensuing lipolysis causes a buildup of fatty acids, which overcomes the body’s natural buffering system and leads to ____
fats and muscle proteins
ketoacidosis
Diabetic Ketoacidosis develops over this timeframe
2 to 3 days
The presenting signs of hyperglycemia include what? (5)
polydipsia, polyuria, fatigue, weakness, and weight loss in new diabetics
Ketoacidosis can cause additional signs and symptoms including
(8)
Nausea, vomiting,
hypotension and dehydration
Sinus tachycardia (most common) and possibly dysrhythmias caused by electrolyte disturbances,
Decreased appetite, abdominal cramping
Decreased LOC
Hyperthermia
Kussmaul respirations as the respiratory system compensates for metabolic acidosis
Fruity odor on the breath, which indicates worsening acidosis
Lab tests for DKA involve:
Blood glucose usually exceeds __,
Serum osmolarity greater than __ mOsm/kg
Serum acetone titrations that are ____
Serum ____ level that is increased
For diagnosis and monitoring, expect to use serum ketone testing based on the measurement of
____-____ (the main ketoacid in acidosis), which is recommended. A level greater than __ mmol/L is considered positive
ABG analysis with a decreased PCO2 and metabolic ____
UA with increased ketone and glucose levels
250 310 positive ketone Beta-hydroxybutyrate 1.5 acidosis
____-____ is the main ketoacid in acidosis, which is recommended. A level greater than __ mmol/L is considered positive
Beta-hydroxybutyrate (the main ketoacid in acidosis), which is recommended. A level greater than 1.5 mmol/L is considered positive
what are the steps in treating DKA?
- Monitor mental status, VS, and urine output every ____ until it has improved, and then monitor q 2 to 4 hours
- Monitor ____ q 1 to 2 hours while the patient is on an insulin drip
- Check ___ q 2 to 4 hours
- Bolus 1 to 2 L of NSS over the first __ to __ hours
hour
potassium
BMP
1 to 2
When treating DKA, after initiating the intravenous fluid replacement, be prepared to administer an initial loading IV bolus of __ units/kg regular insulin followed by a continuous infusion rate of __ units/kg/hr. To prevent life threatening hypokalemia, insulin replacement should generally not be started until serum ____ is greater than greater than __ mEq/L
0.1
0.1
potassium
3.3
In treating DKA, why is it important to decrease the blood glucose level gradually?
If the blood glucose level falls too rapidly, the resulting fluid shift can lead to cerebral edema, which is associated with a higher mortality rate.
How does insulin therapy correct metabolic acidosis?
Insulin therapy generally corrects metabolic acidosis because the energy is allowed into the cells leading to decreased protein lysis and lipolysis and ultimately resolving ketoacidosis.
When treating DKA, Continue with the insulin infusion until the ___ or serum ____ level returns to normal.
pH
bicarbonate
Potassium in DKA treatment; fluid replacement dilutes the serum potassium and promotes ____. In addition, ____ ____ exacerbates total body hypokalemia. Begin potassium replacement after infusing ____ ____ ____ of IV fluid, even when the initial electrolyte levels are ____. In the first few hours after treatment starts, expect the potassium level to ____ precipitously, why?
diuresis metabolic acidosis the initial liter normal because potassium moves back to the intracellular space along with the insulin and existing glucose.
HHS stands for what?
HHS; Hyperosmolar Hyperglycemic State
10-60% mortality rate
HHS; Hyperosmolar Hyperglycemic State has a __-__% mortality rate
10 - 60
HHS; Hyperosmolar Hyperglycemic State can result from
8
An underlying infection, acute MI, CVA, certain medications, medication and treatment noncompliance, undiagnosed diabetes, substance abuse, coexisting disease
what is the pathophysiology of Hyperosmolar Hyperglycemic State?
How does it cause dehydration?
How does Underlying renal disease increase the glucose level even further?
The loss of more water than sodium leads to ____
The metabolism of fat and muscle tissues as energy sources, which increases circulating fatty acid and amino acid levels
The resulting hepatic ____ compounds existing hyperglycemia
-Osmotic diuresis and an osmotic shift of fluids from the intravascular space can contribute to severe dehydration. The condition worsens because the patient cannot replace the lost fluids
-Underlying renal disease or decreased intravascular volume reduces the glomerular filtration rate and increases the glucose level even further.
hyperosmolarity
gluconeogenesis