Acute Hyperglycemic Complications Exam 2 Flashcards
1
Q
Pathyphysiology for DKA and HHS
A
- Decreased insulin causes hyperglycemia because cells cannot take up glucose
- This causes the body to think that it doesn’t have enough glucose
- Which activates counter-regulatory hormones
- Glucagon, catecholamines, cortisol, growth hormone
2
Q
What is the cause of hyperglycemia?
A
- increased gluconeogenesis
- accelerated glycogenolysis
- impaired glucose utilization
3
Q
Explain the ketoacidosis in DKA
A
- Release of free fatty acids (lipolysis) - Hepatic fatty acid oxidation (ketones) - Metabolic acidosis and Ketonemia
4
Q
What are the ketones?
A
- Beta-hydroxybutyrate - main metabolic product (esp when testing for ketones)
- Acetoacetate
- Acetone
5
Q
Endogenous insulin role in HHS
A
Adequate enough to prevent lipolysis and ketogenesis
6
Q
Clinical presentation of DKA and HHS
A
- Hyperglycemia
- Polyuria
- Polydipsia
- Polyphagia
- Weight loss
- Nausea / Vomiting
- Dehydration
- Poor skin turgor
- Weakness
- Mental status changes
- Tachycardia
- Hypotension
7
Q
Clinical presentation of DKA only
A
- Rapid onset
- High ketones
- Kussmaul respirations
- Fruity breath odor (acetone)
- Abdominal pain
8
Q
Clinical presentation of HHS only
A
- Onset over several days to weeks
- Mild or no ketones
- Seizures
9
Q
Glucose lab findings for DKA
A
> 250 mg/dL
10
Q
Serum bicarbonate lab findings for DKA
A
- Mild: 15-18
- Moderate: 10 - 14
- Severe: < 10
11
Q
pH for DKA
A
- Mild: 7.25 – 7.30
- Moderate: 7.00 - 7.24
- Severe: < 7.00
12
Q
Glucose lab findings for HHS
A
> 600 mg/dL
13
Q
Serum bicarbonatelab findings for HHS
A
> 15
14
Q
Sodium
A
- Correct sodium first and then assess for sodium or water deficit severity
- Typically will be low in DKA
- Normal to high in HHS
- Normal sodium is 135-145 mEq/L
15
Q
Potassium
A
- Most patients will have elevated levels due to the acidotic condition
- Normal 3.5 – 5.2 mEq/L
- Low < 3.3mEq/L
- High > 5.2mEq/L