The beeties class slides Flashcards
Glycogenolysis
Triglycerides and proteins will break down to fatty acids and amino acids which form glucose, however this glucose cannot be utilized therefore hyperglycemia develops
DKA
Insulin deficiency and counter regulatory or catabolic hormone excess
Fatty acids not directly used by cells go to liver, convert to acetoacetic acid, too much accumulates along with B-hydroxibutryic acid terms ketones
DKA acidosis
Ketones along with lactic acid from decreased perfusion and a by product of cell resp w/o glucose drop pH (metabolic acidosis)
Shift in DKA
Increased glucose in vasculature causes osmotic extracellular shift
Kidneys DKA
Increased glucose in kidneys will not be reabsorbed if systemic is above 10mM/L causing osmotic shifting into kidneys and urine, which shifts fluid from cells to vasculature to urine causing profound dehydration
K+ DKA
K+ shifts extracellular because of acidosis, causing spike in serum K but as diuresis continues and pH is raised due to treatment levels will drop dramatically
Sodium is also of concern because by the time serum glucose levels drop cerebral edema will occur as a result of fluid therapy
6 I’s of DKA
Infection, infarction, ignorance, ischemia, intoxication, implantation (preggo)
Sympathomimetics, glucagon, cortisol, gH also cause hyperglycemia
S&S
Polydipsia, uria, phagia
Kussmaul resps, fruity odor, postural hypotension
Anorexia/weight loss, abd pain
CNS depression, weakness/lethargy/cramping/N/V, warm/dry skin, dry mucous membranes, visual disturbances
Tachycardia and hypotension late signs
TX
12 lead, ABG (pH, bicarb) serum lytes, urinalysis
1ml/kg/hr if dehydrated
BGL >14 mmol/L pH <7.35 Bicarb<15mM, Anion Gap>20mM, Ketones 3+
Clinical triad
Hyperglycemia, metabolic acidosis, ketonuria
More TX
Insulin continued after BGL drops below 14mM/L as glucose is cleared faster.
5-10% dextrose infusion begun at this point to avoid hypoglycemia
Insulin can be stopped at 15mEq/L of bicarb (combats acidosis without insulin)
Bicarb only in pre-hospital setting if there are ECG changes indicative of hyperkalemia. In hospital used when pH measured AND bicarb is low
Bicarb dose in hospital
50-100mEq in 1L NS over 30-60 minutes if pH is measured
TX order for DKA
Fluid replacement
Electrolyte replacement
Hypergylecmia TX
Acidosis tx
Fluid in DKA
20mL/kg bolus (they may need massive amounts) use with antiemetic
K+ with ECG changes in preshospital
KCL in hospital if K+ drops below upper range of normal as this indicates it will continue to drop
Bicarb dangers in DKA
It is hypertonic and hyperosmolar which will cause a further increase in intravascular volume
Hyperglycemic Hyperosmolar Nonketotic Coma
Type 2 diabetics still capable of producing insulin to partially nourish cells so no acidosis
Otherwise same conditions apply as in DKA, increased glucose in vasculature causes osmotic shift, increased glucose in urine causes osmotic diuresis along with lytes
More on HHNC
Longer onset than DKA, lack of early signs/symptoms (likely in coma by the time issue is found)
Primarily in the elderly, BGL generally higher in DKA
HHNC precipitating factors
Endogenous insulin failure, insulin agonists (glucagon, catecholamines, cortisol, growth hormones) sympathomimetics, infection, 6 I’s, supplemental parenteral/enteral feedings (increased carb intake)
Dialysis
Stress/burns/pancreatits
Difference in S&S of HHNC to DKA
No kussmaul, no fruity odor to breath
Difference in tx of HHNC to DKA
No bicarb, decreased insulin doses
Diabetes insipidus
Decreased ADH due to hypothalmic pituitary disorder, causes increased diuresis leading to polydipsia/polyuria which leads to dehydration and hypovolemia
ADH
Vasopressin, retains solute free water and constricts arterioles.
From posterior pituitary
Wernicke-Korsakoff syndrome
ETOH abuse and malnutrition causes B1 (thiamine) deficit which is a major cofactor in metabolism
Anything which increases glucose metabolism will exacerbate thiamine deficiency (giving D50)
Wernicke’s encephalopathy
Acute thiamine deficiency and is reversible.
Triad of opthalmoplegia, confusion and ataxia
Opthalmoplegia
Paralysis of the eye
Korsakoff’s
Due to chronic thiamine deficiency, non reversible.
Characterized by memory problems, decreased cognition, disorientation, hallucinations and in some cases painful extremities
IF ETOH or malnourishment suggested in hypoglycemic pt pre treat with 100mg thiamine IV, consider if pt unresponsive to glucose administration
Somogyi effect
Over reaction to hypoglycemia caused by counter-regulatory hormones causes hyperglycemia
Most likely from untreated hypoglycemia during sleep
Pts will wake up with high BGL in morning and not understand why
Dawn Phenomenon
Sometime between 0400-1100 body releases counter-regulatory hormones causing an increase in insulin resistance as well as glycogenolysis/gluconeogenesis causing increased BGL in the morning
Fun facts!
7 types on insulin, 1 is natural
3 of modified are faster acting with a shorter duration than reg insulin
3 slower acting with longer duration
All are clear except NPH (bound to protamine)
Two process can be used to prolong insulin - add a protein or alter the molecule
All can only be given subq except regular insulin
Insulin
Reg is the only on given IV
Short/rapid slin
Humalog, novolog
Regular: slin
Humulin R, Novolin R
Intermediate slin
Humulin N, Novolin N
Long slin
Lantus
Sulfonylureas
Increased insulin secretion by pancrease and increased tissue response to insulin
Meglitinides
Increased insulin secretion by pancreas
Biguanide
(Metforin, glucophage) decreased glucose production by liver and increased glucose uptake by muscle
Thiazolidineodiones
Decreased slin resisitance and decreased glucose production by liver
Alpha-glucosidase inhibitors
Inhibits carb digestion/absorption
