The beeties class slides

Question 1

Glycogenolysis

Answer 1

Triglycerides and proteins will break down to fatty acids and amino acids which form glucose, however this glucose cannot be utilized therefore hyperglycemia develops

Question 2

DKA

Answer 2

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

Question 3

DKA acidosis

Answer 3

Ketones along with lactic acid from decreased perfusion and a by product of cell resp w/o glucose drop pH (metabolic acidosis)

Question 4

Shift in DKA

Answer 4

Increased glucose in vasculature causes osmotic extracellular shift

Question 5

Kidneys DKA

Answer 5

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

Question 6

K+ DKA

Answer 6

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

Question 7

6 I’s of DKA

Answer 7

Infection, infarction, ignorance, ischemia, intoxication, implantation (preggo)
Sympathomimetics, glucagon, cortisol, gH also cause hyperglycemia

Question 8

S&S

Answer 8

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

Question 9

TX

Answer 9

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+

Question 10

Clinical triad

Answer 10

Hyperglycemia, metabolic acidosis, ketonuria

Question 11

More TX

Answer 11

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

Question 12

Bicarb dose in hospital

Answer 12

50-100mEq in 1L NS over 30-60 minutes if pH is measured

Question 13

TX order for DKA

Answer 13

Fluid replacement
Electrolyte replacement
Hypergylecmia TX
Acidosis tx

Question 14

Fluid in DKA

Answer 14

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

Question 15

Bicarb dangers in DKA

Answer 15

It is hypertonic and hyperosmolar which will cause a further increase in intravascular volume

Question 16

Hyperglycemic Hyperosmolar Nonketotic Coma

Answer 16

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

Question 17

More on HHNC

Answer 17

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

Question 18

HHNC precipitating factors

Answer 18

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

Question 19

Difference in S&S of HHNC to DKA

Answer 19

No kussmaul, no fruity odor to breath

Question 20

Difference in tx of HHNC to DKA

Answer 20

No bicarb, decreased insulin doses

Question 21

Diabetes insipidus

Answer 21

Decreased ADH due to hypothalmic pituitary disorder, causes increased diuresis leading to polydipsia/polyuria which leads to dehydration and hypovolemia

Question 22

ADH

Answer 22

Vasopressin, retains solute free water and constricts arterioles.
From posterior pituitary

Question 23

Wernicke-Korsakoff syndrome

Answer 23

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)

Question 24

Wernicke’s encephalopathy

Answer 24

Acute thiamine deficiency and is reversible.

Triad of opthalmoplegia, confusion and ataxia

Question 25

Opthalmoplegia

Answer 25

Paralysis of the eye

Question 26

Korsakoff’s

Answer 26

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

Question 27

Somogyi effect

Answer 27

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

Question 28

Dawn Phenomenon

Answer 28

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

Question 29

Fun facts!

Answer 29

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

Question 30

Insulin

Answer 30

Reg is the only on given IV

Question 31

Short/rapid slin

Answer 31

Humalog, novolog

Question 32

Regular: slin

Answer 32

Humulin R, Novolin R

Question 33

Intermediate slin

Answer 33

Humulin N, Novolin N

Question 34

Long slin

Answer 34

Lantus

Question 35

Sulfonylureas

Answer 35

Increased insulin secretion by pancrease and increased tissue response to insulin

Question 36

Meglitinides

Answer 36

Increased insulin secretion by pancreas

Question 37

Biguanide

Answer 37

(Metforin, glucophage) decreased glucose production by liver and increased glucose uptake by muscle

Question 38

Thiazolidineodiones

Answer 38

Decreased slin resisitance and decreased glucose production by liver

Question 39

Alpha-glucosidase inhibitors

Answer 39

Inhibits carb digestion/absorption