Flashcards in Lecture 31: Urea Cycle, Metabolic Priorities, and Diabetes Deck (81)
What is ammonium?
What are levels of acetyl-CoA in the mitochondria representative of?
Pretty much nothing
What are the 2 ways in which adipose tissue regulates itself?
1. Decrease appetite
2. Increase fatty acid beta oxidation by increasing uncoupling proteins
What are the 2 ways in which AMPK can be activated in diabetics?
2. Thiazolidinediones drugs (Avandia and Actos) which increase adiponectin in adipose tissue
What are the 3 side effects of thiazolidinediones?
Increased risk of:
2. Heart attacks
3. Bladder cancer
On what hypothalamic nucleus does leptin act?
Where does the hyperglycemia come from in ketoacidosis?
Why does DKA not cause the same symptoms as lactic acidosis?
Lactic acid will be converted to glucose again in the liver or lactic acid will fill up the TCA cycle and be used to catabolize fatty acids in the liver, so it does not cause as many problems
What causes lactic acidosis?
Exercise and being out of breath most of the time
What often causes DKA in diabetics?
Stress which increases energy needs and cortisol and cathecholamines powerfully stimulate gluconeogenesis causing excess ketogenesis
Why could it be dangerous to only inject insulin in a patient with diabetic DKA? What else should be injected with insulin?
As we inject insulin, the blood pH will begin to rise. This will then lead to potassium being transported back into the cells causing an extremely low levels of potassium in the extracellular matrix.
K+ should also be injected
What organ regulates Kussmaul breathing?
What is the normal range of blood bicarbonate?
What is the normal blood [K+]?
3.5-5.0 mEq/L = 50 mEq/kg
What is the normal BUN range?
What is the normal BUN range?
What is pancreatitis? Symptom? Patients at risk?
Pancreatic enzymes get processed too soon and start digesting the pancreas
Upper abdominal pain that extends through the back
Happens in diabetes and digestive disorders
What is alcohol ketoacidosis?
Alcohol consumption => liver needs to oxidize ethanol to detoxify it generating a lot of NADH => not enough NAD+ to drive gluconeogenesis nor convert alpha-ketoglutarate to glutamate so glucoenogenesis using AAs is inhibited => not enough energy fuel after a night of binge drinking => high levels of ketones
Why can heavy drinking cause hyperglycemia?
Many alcoholic beverages have a lot of sugar
What are the symptoms of DKA? Explain each.
• Hyperglycemia: Over 300 mg/dL glucose (this is very elevated glucose) due to gluconeogenesis lack of insulin
• Low bicarbonate: Less than 15 mEq/L: used in gluconeogenesis and to buffer low blood pH
• Acidosis: pH is less than 7.30: low bicarbonate and high ketone bodies
• Ketonemia and Ketonuria: high blood and urine levels of ketone bodies. Ketone bodies are not just metabolic fuel but a mechanism of getting rid of excess levels of Acetyl-CoA in the liver.
• Water deficit: increased urine output with high spill off of glucose and ketones + lots of hydrolyses reactions H2O is being consumed rapidly by the cells.
• Total body potassium deficit (deficit of 3-5 mEq/kg body weight with normal being 55
mEq/kg): K+ used to counter balance the low pH of blood (the potassium levels in the blood are normal or can even be elevated, but the total body potassium is low because excreted in urine)
• High blood urea nitrogen: the body is in starvation mode, thus fat and protein breakdown leads
to urea build up