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insulin is released from the pancreatic ____ cells. what effect does it have on blood glucose, blood fatty acid and ketoacid concentration, protein synthesis, and potassium uptake?
beta cells; decreases blood glucose, decreases blood fatty acid and ketoacid concentrations, increases protein synthesis, and promotes uptake of potassium by the cells by activation of the Na/K ATPase
glucagon is released from the pancreatic ___ cells; what effect does it have on lipolysis, glycogenolysis, and gluconeogenesis, and ketoacid formation?
alpha cells; stimulates glycogenolysis and gluconeogenesis, increases lipolysis, and increases ketoacid formation
explain type 1 vs type 2 DM
1: autoimmune t cell mediated destruction of beta cells
2: increased insulin resistance and progressive pancreatic beta cell failure
What is the mechanism of DKA?
insulin deficiency and glucagon excess→ hyperglycemia
briefly explain how stress triggers DKA
stressful event → increase in glucagon, epi, and cortisol → increased glycogenolysis and gluconeogenesis and decreased insulin production and sensitivity → increased blood glucose
increased glucagon with insulin deficiency in diabetes causes what?
hyperglycemia and increased lipolysis (fatty acids shunted towards ketone synthesis)
What are 4 main things we see in DKA?
hyperglycemia, volume depletion, polyuria, and polydipsia
What electrolyte imbalances do we see with DKA?
hyponatremia (high serum osmo causes water to rush into serum), hyperkalemia (K shifts extracellular and no insulin activation of Na/k ATPase), and decreased total body K
what acid base disorder do we see with DKA?
primary anion gap metabolic acidosis with compensatory respiratory alkalosis
What is the anion gap in DKA and how do we calculate it?
high anion gap (>12)
calculation: Na - (Cl + HCO3)
What are some clinical features of DKA? (5)
delirium/psychosis/coma, kussmaul respirations, abdominal pain/n/v, dehydration, fruity odor in breath
What do we expect with DKA: K, Na, glucose, ketones
hyperkalemia, hyponatremia, and serum and urine ketones, and hyperglycemia (250+)
How can we detect serum ketones and urine ketones?
serum: assay of beta-hydroxybutyrate
urine: positive nitroprusside stick test
With what condition do we expect ECG changes? what are the changes and why?
DKA: peaked T waves on ECG from hyperkalemia
What do we expect to see with DKA for BUN/Creatinine?
increased ratio
What do we expect to see on anion gap for DKA?
>12 (normal is 8-12)
How do we treat DKA? (2)
IV normal saline (fixes hypovolemia and electrolyte imbalance) and insulin (only is K 3.3+, if less than 3.3 then fix that first)
Explain bicarb in treating DKA
it is usually not given, but can consider giving bicarb if pH 6.9 or less
What are some complications of DKA? (6)
cerebral edema, cardiogenic shock, cardiac arrythmias, hypokalemia, hypoglycemia, and mucormycosis
What condition is commonly found in type 1 dm vs type 2?
1: DKA
2: HHS
What is the mechanism of HHS?
insulin deficiency and inadequate water intake → hyperglycemia and hyperosmolarity
Explain the slight difference in the pathophysiology of HHS vs DKA
in HHS some insulin is present with enough insulin activity to prevent the pt from going into ketoacidosis
What condition has more neurologic symptoms and what has more GI symptoms?
neuro: HHS
GI: DKA
What are some clinical features of HHS? (6)
polyuria, polydipsia, lethargy, seizures, focal neuro deficits, possible progression to coma
note: no n/v/abdominal pain or kussmaul respirations
If we see Kussmaul respirations what condition should we think?
DKA
if we see abdominal pain, nausea, and vomiting what condition should we think?
DKA
what do we expect with HHS: serum glucose, serum and urine ketones, ABG, ECG
high serum glucose (600+), no/mild serum and urine ketones, normal pH, and normal ECG
What do we expect with HHS: BUN/creatinine, potassium, sodium, anion gap
increased BUN/Creatinine, normal potassium, normal sodium, normal anion gap
How do we treat HHS?
IV fluids and IV insulin
treatment of HHS is carried out until when?
plasma osmolality is less than 315
If we see ECG changes and ABG changes what should we suspect?
DKA
What is the bottom line difference between the pathophysiology of DKA and HHS?
DKA: absolute insulin deficiency
HHS: relative insulin deficiency