Hyperglycemic Crises Flashcards Preview

Endocrine Week 1 > Hyperglycemic Crises > Flashcards

Flashcards in Hyperglycemic Crises Deck (21):

Why is ketoacidosis more assoicated with type I diabetes than type II?

Because the amount of insulin needed to prevent ketone body formation is very low so even in those type II patients with just a little insulin, it can be prevented


Effects of insulin?

Stimulate glucose uptake primarily in skeletal muscle -75%- (via GLUT4 receptors) and some fat (some GLUT4 receptors), inhibits lipolysis and proteolysis, and stimulates glucose use by the liver

Promotes Na renal retention, and K+ cellular uptake


How does insulin work?

Insulin binds to a membrane receptor with tyrosine kinase activtiy to transport GLUT4 receptors to the surface to internalize glucose 


What happens when glucose enters a peripheral cell via a GLUT4 receptor?

It enters the Krebs cycle to produce ATP for energy and eventually end sup as acetyl CoA which is transformed to malonyl CoA via the enzyme acetyl CoA carboxylase (ACC). Malonyl CoA is the first building block of fat synthesis. Malonyl CoA inhibits fatty acids entering the mitochondria via CPT 1/2 channels for fatty acid oxidation. 

Thus, the presence of insulin promotes acetyl CoA being transformed into triglycerides while the lack of insulin opens the CPT channels and allows for fatty acid oxidation to occur which can lead to ketone body formation (acetoacetate and B-hydroxybutyrate). 


How much insulin is lost per yea with type II diabetes?

5% per year


How are alpha cells affected by type II diabetes?

There are more, producing more glucagon 


Describe the ketogenesis pathway

Acetyl CoA converted to acetoacetyl CoA via ACAT 1/2

acetoacetyl CoA converted to hydroxy-B-methylglutaryl CoA via HMG-CoA synthase

hydroxy-B-methylglutaryl CoA converted to either cholesterol via HMG CoA reductase or acetoacetate via HMG-COA lyase

and finally, acetoacetate converted to acetone or D-B hydroxybutyrate via D-B hydroxybutyrate dehydrogenase

These are permitted to be formed by a lack of insulin


Overview of DKA pathogenesis

In situations of insulin deficiency there is increased glucose production by the liver and decreased peripheral glucose uptake leading to hyperglycemia which causes osmotic diuresis and volume depletion, while 


adipose tissue increases release of FFA from lipid breakdown and the liver increases ketogenesis leading to ketoacidosis 


What are the main precipitating factors for DKA?

Infection, especially pneumonia, is the number one factor

New-onset diabetes or Discontinued insulin

Idiopathic (15%)


What causes Hyperglycemic Hyperosmolar Syndrome (HHS)?

The liver increases glucose production and peripheral tissue cannot take up glucose leading the hyperglycemia and severe volume depletion via osmotic diuresis typically triggered by infection, failure to take insulin, etc. 


How does DKA present?

The onset of DKA is relatively quick ranging from hours to 1-2 days and typically presents with symptoms including polydipsia and polyuria, weakness, weight loss, N/V, and SEVERE abdominal pain (dont operate!)


How would you advice a patient in terms of taking insulin if they were sick?

Inflammatory cytokines are anti-insulin so despite their tendency to want to stop taking insulin when they are sick (because they may not be eating as much), you should advise them to take a little more (as well as more fluids)!


What are the signs of DKA?

Hypothermia, tachycardia, and tachypnea, Kussmaul breathing, Ileus, acetone breath, and altered sensorium


How does HHS present?

The onset of HHS is prolonged, ranging from days to weeks and is assoicated with similar symptoms to DKA but may have more signs of altered mental status due to brain swelling 


What labs would you want to get in a DKA patient? What would you see?

complete metabolic profile (glucose, electrolytes, bicarb, etc.), serum ketones, urinalysis 

In a DKA patient, you will see hyperglycemia, decreased pH, decreased bicarb, increased PAG, HYPERKALEMIA and leukocytosis 




How do you calculate plasma anion gap?

PAG= Na- (Cl + HCO3)


How do you measure total serum osmolarity?

2Na+ + glucose (mg/dl)/18 + BUN (mg/dl)/2.8


How are DKA and HHS treated?

-Fluid replacement

-IV Insulin replacement 

Close monitoring of BG, electrolytes, acid-base balance, and clinical status




What are the potential complications of DKA?

Mucormycosis (usually caused by RHizopus infection)

cerebral edema

heart failure and arrhythmias