DM Obesity Part 1

Question 1

Describe Type I DM

Answer 1

Abrupt onset
Usually onset by adolescence but can be seen in early 20s

Not obese patient

Question 2

What causes DM I?

Answer 2

ABSOLUTE deficiency of insulin

IA: autoimmune destruction of beta islet cells of langerhans

1B: unknown MOA, possibly genetic

Question 3

How do DM 1 patients respond to insulin? what is their requirement?

Answer 3

Normally, 0.3-0.7 u/kg/day

Question 4

What is DM II?

Answer 4

Gradual onset in adulthood
Obese patients

Question 5

What causes DM II?

Answer 5

Insulin RESISTANCE

May still have some insulin production but it is not enough

May have normal to elevated levels of insulin

Strong familial pattern but more related to lifestyle and diet

Question 6

___ units of regular insulin lowers plasma glucose by ___ to ___ mg/dL

Answer 6

1u; 25-30 mg/dL

Question 7

How do you calculate a regular insulin infusion rate?

Answer 7

Plasma glucose/ 150 = u/hr

Question 8

How do you determine a maintenance glucose infusion rate?

Answer 8

1.5 ml/kg/hr

Question 9

What are some of the cellular effects of insulin?

Answer 9

Promotes glucose transport across cell membrane
Promotes glucose oxidation
Increases amino acid and protein synthesis in muscles
Inhibits lypolysis, FA utilization, ketogenesis and gluconeogenesisha

Question 10

Where is insulin metabolized/

Answer 10

liver and kidneys

Question 11

How are carbohydrates effected by insulin?

Answer 11

stimulates increased cellular uptake of glucose in skeletal muscle tissue and cardiac cells

Question 12

Why do DM pts become hyperglycemic?

Answer 12

Inadequate uptake of glucose into the cells due to inadequate insulin or insulin resistance

Question 13

How are proteins effected by insulin?

Answer 13

No insulin = glycogen stores become depleted –> body must use amino acids for energy

No insulin will cause muscles to catabolize resulting in NEGATIVE nitrogen balance

Question 14

How are fats affected by insulin

Answer 14

Suppresses lipolysis –> causes utilization of glucose by cells thus serving as a fat sparer
Promotes glucose transport into fat cells

Glucose –> formed into fatty acids

Question 15

In summary, what does insulin do?

Answer 15

Increase glucose and potassium entry into the adipose and muscle cells
Increases glycogen, protein and fatty acid synthesis
Decreases glyconeogenolysis, gluconeogenesis, ketogenesis, lipolysis and protein catabolism
Stimulates endothelial nitric oxide synthase –> arterial vasodilation

Question 16

What is glyconeolysis?

Answer 16

Breakdown of glycogen in liver into glucose

Question 17

What is gluconeogenesis?

Answer 17

Formation of glucose from non-carbohydrate substrates

Question 18

What are the four counter regulatory hormones that oppose actions of insulin?

Answer 18

Glucagon
Somatostatin
Epinephrine
Cortisol

Question 19

What do all of the four counter regulatory hormones tend to do to the patient?

Answer 19

Make them more insulin resistantW

Question 20

Where is glucagon produced?

Answer 20

Alpha cells of the islet of langerhanha

Question 21

What does glucagon do?

Answer 21

Glycogenolysis in the liver –> increases blood glucose
Gluconeogenesis in the liver
Lipolysis –> KetogenesisWh

Question 22

What is glucagon stimulated by?

Answer 22

Hypoglycemia
Epinephrine
Cortisol

Question 23

What is glucagon suppressed by?

Answer 23

Glucose intake
Insulin secretion

Question 24

What is somatostatin and where is it produced?

Answer 24

Produced in the delta cells of the islet of langerhan, intestines and stomachs,

Somatostatin is a hormone that suppresses HGH

Question 25

What does somatostatin do?

Answer 25

inhibit secretion of insulin AND glucagon Net effect is to impede digestion -- suppress release of GI hormones, decrease rate of gastric emptying, relaxes smooth muscle contractions in intestines, slows the exocrine function in the pancreas

Question 26

When is somatostatin released?

Answer 26

gamma cells secrete a pancreatic polypeptide that INHIBITS the release of somatostatin

Question 27

What is epinephrine and where is it secreted?

Answer 27

Adrenal medulla Catecholamine

Question 28

What does epinephrine do to insulin?

Answer 28

Increases glyconeolysis to increase BG

Question 29

When is epi released in relation to insulin?

Answer 29

released when the patient is under a lot of stress (sick or postop) This is why insulin resistance is so high in surgical patients

Question 30

What is cortisol and where is it released?

Answer 30

secreted from adrenal cortex

Question 31

What does cortisol do?

Answer 31

increases gluconeogenesis Increases protein catabolism Increases mobilization of fatty acids from adipose tissue

Question 32

What are some of the effects of hyperglycemia?

Answer 32

impaired ischemic conditioning (decreases O2 transport and increases infarct size) reduces coronary collateral BF Increases catechols,ines Increases myocyte death Prolongs QT Increases platelet hyperactivity/adhesion Increases vWF --> Clotting increased Increased cellular adhesion Increased cell permeability Increased inflammation Increases TNF Alpha Breaks down collagen --> impairs wound healing Thrombosis Promotes inactivation of nitric oxide --> vasoconstriction Phagocyte destruction --> increased infection risk Neuronal damage --> accumulation of extracellular glutamate and inhibition of nitric oxide decreases Cerebral BF Consider MI for unexplained HoTN Cardiomyopathies are common Retinopathy Neuropathy Impaired gastric emptying Vasulopathy

Question 33

What type of DM gets DKA?

Answer 33

DM I

Question 34

How does DKA happen?

Answer 34

Lack of insulin --> hyperglycemia --> osmotic diuresis --> dehydration and acidosis Lack of insulin --> decreased uptake of glucose, amino acids, and fatty acids into cells --> catabolism of muscle and lipolysis stimulated --> ketones formed

Question 35

What are some s/sx of DKA?

Answer 35

BG >250 Glycosuria Acidosis (pH <7.3) Dehydration Tachypnea Abdominal Pain, N/V mental status chages serum K+ might be slightly elevated

Question 36

What is the treatment for DKA?

Answer 36

Regular insulin 10u IV followed by insulin infusion initiated (BG/150) u/hr Isotonic IVF, anticipate 4-10 L deficit When UOP >0.5 mL/kg/hr --> give K+ 10-40 mEq per hour with continuous EEG monitoring when the rate is >10 When BG <250, start D5 at 100 mL/hr Consider sodium bicarb when pH <6.9

Question 37

What type of DM pts get IHHS?

Answer 37

DM 2, elderly ptsW

Question 38

How does IHHS occur?

Answer 38

Hyperglycemic diuresis --> dehydration and hyperosmolarity Ketoacidosis IS NOT A PROBLEM because there is enough insulin to try and prevent it

Question 39

What are some s/sx of IHHS?

Answer 39

BG >600 Hyperosmolarity >360 mOsmo Hyponatremia Formation of intravascular thrombiWh

Question 40

How do you treat IHHS?

Answer 40

Rehydration therapy with normal saline and small does of insulin For every 100mg/dL increase in plasma glucose, there is a decrease of plasma sodium by 1.6 mEq Usually respond to fluid hydration (1-2L in 1-2H if no contraindication)

Question 41

What is hypoglycemia?

Answer 41

Most feared consequence in the unconscious patient BG <50 mg/dL Sampling device and site can interfere with measurements

Question 42

What is the preferred method of sampling if the patient is thought to be hypoglycemic?

Answer 42

Arterial >> Venous >> Capillary

Question 43

What are some s/sx of hypoglycemia?

Answer 43

Reflex catecholamine release HTN Tachycardia Tearing Diaphoresis LOC +

Question 44

How do you treat hypoglycemia? (Formula)

Answer 44

In a 70 kg pt, 1mL of D50 will increase a patient's BG level by 2 mg/dL