10/15- Acute Complications of Diabetes Flashcards
What are some acute complications of diabetes?
- Insulin-induced hypoglycemia
- Diabetic ketoacidosis
- Hyperosmolar hyperglycemic nonketotic state (HONK)
- Lactic acidosis
What are some hypoglycemic reactions?
- Neurogenic
- Neuroglycopenic
Neurogenic (responses of S/PS systems):
- Sweaty
- Hungry
- Tingling
- Shaky/tremulous
- Heart Pounding
- Nervous/anxious
Neuroglycopenic (responses of central NS):
- Warm
- Weak
- Difficulty thinking/confused
- Tired/drowsy, faint, dizzy
- Difficulty speaking
- Blurred vision
What are counterregulatory responses (substances) to hypoglycemia?
- Glucagon* (fastest)
- Cortisol
- Growth hormone (slowest)
*(Normally low insulin levels correspond to higher glucagon, which would seem to be protective about hypoglycemia in diabetes… but for some reason, not the case. No surge; it’s an acute response)
What is Diabetic Ketoacidosis?
Uncontrolled diabetes leading to:
1. Hyperglycemia:
- Osmotic diuresis
- Volume depletion
- Dehydration
2. Ketogenesis: anion-gap acidosis
3. Other metabolic changes
Difference between volume depletion and dehydration?
- Volume depletion: loss of isotonic fluid
- Gauged pretty much only clinically: blood pressure, urine production, orthostatic hypotension, mental status, skin turgor…
- Dehydration: loss of water; hypertonic serum
- Measured by serum sodium or serum osmolarity
Describe the liver and adipocyte collaborate to produce ketoacidosis?
- Insulin fails to restrain storage of fatty acids in adipocyte
- FAs released and go to liver
- Liver has high oxidation and ketone production (faster than ability to esterify fatty acids)
Depends on 2 things:
- Complete lack of insulin
- Excess of glucagon
What 2 things are necessary for the regulation of ketogenesis?
1. Insulin deficiency
- Activates lipolysis (fat cells)
- Increased plasma FFA concentration
- Increased liver fatty acids
- Accelerated ketogenesis
2. Glucagon excess
- Increased hepatic carnitine content with decreased malonyl CoA content (removes inhibition from –)
- Activation of CPT-1
- Accelerated ketogenesis
T/F: Massive excess of glucagon, cortisol, GH, and catecholamines (due to increased stress) can also push pt into DKA despite normal (not low) insulin levels
False- really never happens
- If someone comes in with DKA, suspect sudden drop in insulin rather than acute rise in other factors
What are etiologies of DKA?
86% of DKA episodes have an identifiable precipitating factor:
- Alcohol
- Drugs
- Infection
- MI/stroke
- Trauma
- Pregnancy
- Treatment errors
How do trauma, stroke, and pregnancy contribute to DKA?
Stress levels (?)
Do people with Type I or Type II DM get DKA more commonly?
- Type I are morel likely to get DKA in black and white populations
- Type II more commonly get DKA in Hispanic and Asian
What is the cause of hyperglycemia in DKA?
Insulin deficiency leading to:
- Increased hepatic glucose production
- Decreased peripheral glucose utilization
What are the effects of hyperglycemia in DKA?
Osmotic effects
- H20 from ICF to ECF
- Osmotic diuresis ECF volume
Renal loss of water > electrolytes
- Volume depletion
- Some degree of dehydration
What causes metabolic acidosis in DKA?
- Excess acetoacetic acid and β-OH butyric acid production (ketones)
- Diminished renal excretion of H+
What are effects of metabolic acidosis in DKA?
Buffer of protons and bicarb increases CO2 and H2O production, but ultimate correction of H excess depends on:
- Oxidation of AAA + βOHB - Renal excretion of H+
- Exchange of H+ for Na+
- Ammonia -> ammonium
- Loss of electrolytes in urine
What causes water and electrolyte imbalance in DKA?
- Osmotic diuresis
- Vomiting
- Increased aldosterone
- ICF – ECF shift (K+3PO4)
What are the effects of water and electrolyte imbalance in DKA?
10% body weight lost as fluid
- 50% extracellular
- 50% intracellular
Significant loss of extra- and intracellular electrolytes
- K
- Na
- PO4
What are symptoms of DKA? Signs?
Symptoms:
- Nausea/vomiting
- Polyuria/polydipsia
- Abdominal pains
- Mental changes (lethargy to near-coma)
Signs:
- “Fruity” breath (due to acetone)
- Kussmaul’s respirations (rapid, deep breaths)
- pH of less than 7.2 (sharp inflection point)
- Signs of volume depletion (tachycardia, orthostatic hypotension)
- Signs related to precipitating factors (infection, MI, trauma, etc.)
What are lab tests that may be done for the diagnosis of DKA?
- Elevated blood glucose
- pH < 7.35
- Low HCO3-
- High anion gap
- Positive serum ketones!
How to calculate corrected serum sodium concentration? Why do you want this?
- Corresponds to initial state of sodium depletion/volume depletion (?)
How to calculate anion gap?
What is normal?
Why do you want this?
AG = Na - (Cl + HCO3)
Normal value = 8-12 (+/-2)
- This can tell you if something else is going on (simple or complex acid-base disorder)
What is the treatment for DKA?
- Mainly isotonic fluid!!
- Insulin!!
- Reverses ketosis and acidosis
- Potassium
- HyperK due to lack of insulin, but overall body is actually K-depleted (will be seen when volume corrected)
- MONITOR
- very rapidly; don’t stop insulin when glucose is approaching normal, just add glucose drip (takes longer to correct ketogenesis and acidosis)
- Normalization is marked by disappearance of ketones or normalization of pH
- Treat precipitating cause(s)
What is “HONK”
- Characteristics
Aka HHNS
- Hyperosmolar hyperglycemic nonketotic state
Characteristics:
- Extreme hyperglycemia
- Poorly treated/undetected diabetes
- Renal insufficiency
- Age/mental obtundation -> decreased oral fluids
- Absence of ketosis:
- Insulin is not totally deficient
- Severe dehydration and volume depletion
- Coexisting chronic illnesses
- High mortality
What is the critical calculation that should be done if you suspect HONK? Why?
- How to calculate
- Normal values
- HONK values
Serum osmolality
- Grade of consciousness of patient is quite related to serum osmolality
- Mortality is in turn related to the grade of consciousness
Calculation: 2Na + glucose/18 + BUN/2.8
- Normal is 290-300 mOsm
- HONK is >> 300 mOsm
