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List the key symptoms of DKA.
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Acetone breath, Kussmaul respirations, abdominal pain, nausea, vomiting, altered mental status, tachycardia, polyuria, polydipsia, lethargy, stupor, and unconsciousness.
Describe the respiratory compensation observed in DKA.
Increased respiration rate and tidal volume (Kussmaul respirations) to counteract metabolic acidosis.
What are the main components of pathophysiology in DKA?
Fluid volume deficit and electrolyte imbalance, acid-base imbalance, osmotic diuresis, increased ketones, and increased anion gap.
Identify the main differences between DKA and HHS.
DKA involves ketosis and metabolic acidosis, occurs primarily in Type 1 diabetics, and develops rapidly; HHS involves severe hyperglycemia without ketosis, occurs in Type 2 diabetics, and develops over weeks to months.
What are the risks associated with profound dehydration in HHS?
CNS dysfunction, cardiac respiratory center depression, cerebral edema, cardiovascular collapse, renal shutdown, and vascular embolism.
What are the primary physiological triggers for DKA?
Insufficient or absent insulin levels, leading to increased fatty acid metabolism and ketone production, increased liver gluconeogenesis, and secretion of counter-regulatory hormones.
What are the defining lab values for Diabetic Ketoacidosis (DKA)?
Glucose > 300 mg/dL, Bicarb < 15 mEq/L, pH < 7.3, Ketoneemia & Ketonuria.
What are the initial fluid replacement guidelines for both DKA and HHS?
Initial rapid bolus of 0.9% normal saline (1-3 liters in the first hour), continue until volume is restored, then switch to D5 half NS as glucose normalizes.
What signs and symptoms are typically the reason for delayed treatment in HHS?
Less obvious initial symptoms and gradual onset leading to profound dehydration before intervention.
How does the progression timeline of DKA differ from HHS?
DKA develops in less than 24 hours, while HHS progresses over weeks to months.
Why are Type 2 diabetics more likely to develop Hyperosmolar Hyperglycemic State (HHS) rather than DKA?
Because partially functional insulin in Type 2 diabetics prevents lipolysis and ketone production.
Why is potassium monitoring crucial during the treatment of DKA and HHS?
Due to risk of hypokalemia from extracellular to intracellular potassium shift and insulin administration.
What is the goal of hyperglycemia treatment in DKA and HHS?
To decrease glucose levels by 50-70 mg/dL per hour using IV insulin, while continuing until normal pH is restored.
What can cause a higher anion gap in patients with DKA?
Increased ketone acids from fatty acid metabolism and lactic acid production from anaerobic metabolism.
What are the signs of altered mental status in DKA patients?
Paresthesia, paresis, aphasia, lethargy, stupor, and unconsciousness.
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