DM Obesity Part 1 Flashcards
Describe Type I DM
Abrupt onset
Usually onset by adolescence but can be seen in early 20s
Not obese patient
What causes DM I?
ABSOLUTE deficiency of insulin
IA: autoimmune destruction of beta islet cells of langerhans
1B: unknown MOA, possibly genetic
How do DM 1 patients respond to insulin? what is their requirement?
Normally, 0.3-0.7 u/kg/day
What is DM II?
Gradual onset in adulthood
Obese patients
What causes DM II?
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
___ units of regular insulin lowers plasma glucose by ___ to ___ mg/dL
1u; 25-30 mg/dL
How do you calculate a regular insulin infusion rate?
Plasma glucose/ 150 = u/hr
How do you determine a maintenance glucose infusion rate?
1.5 ml/kg/hr
What are some of the cellular effects of insulin?
Promotes glucose transport across cell membrane
Promotes glucose oxidation
Increases amino acid and protein synthesis in muscles
Inhibits lypolysis, FA utilization, ketogenesis and gluconeogenesisha
Where is insulin metabolized/
liver and kidneys
How are carbohydrates effected by insulin?
stimulates increased cellular uptake of glucose in skeletal muscle tissue and cardiac cells
Why do DM pts become hyperglycemic?
Inadequate uptake of glucose into the cells due to inadequate insulin or insulin resistance
How are proteins effected by insulin?
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
How are fats affected by insulin
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
In summary, what does insulin do?
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
What is glyconeolysis?
Breakdown of glycogen in liver into glucose
What is gluconeogenesis?
Formation of glucose from non-carbohydrate substrates
What are the four counter regulatory hormones that oppose actions of insulin?
Glucagon
Somatostatin
Epinephrine
Cortisol
What do all of the four counter regulatory hormones tend to do to the patient?
Make them more insulin resistantW
Where is glucagon produced?
Alpha cells of the islet of langerhanha
What does glucagon do?
Glycogenolysis in the liver –> increases blood glucose
Gluconeogenesis in the liver
Lipolysis –> KetogenesisWh
What is glucagon stimulated by?
Hypoglycemia
Epinephrine
Cortisol
What is glucagon suppressed by?
Glucose intake
Insulin secretion
What is somatostatin and where is it produced?
Produced in the delta cells of the islet of langerhan, intestines and stomachs,
Somatostatin is a hormone that suppresses HGH
What does somatostatin do?
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
When is somatostatin released?
gamma cells secrete a pancreatic polypeptide that INHIBITS the release of somatostatin
What is epinephrine and where is it secreted?
Adrenal medulla
Catecholamine
What does epinephrine do to insulin?
Increases glyconeolysis to increase BG
When is epi released in relation to insulin?
released when the patient is under a lot of stress (sick or postop)
This is why insulin resistance is so high in surgical patients
What is cortisol and where is it released?
secreted from adrenal cortex
What does cortisol do?
increases gluconeogenesis
Increases protein catabolism
Increases mobilization of fatty acids from adipose tissue
What are some of the effects of hyperglycemia?
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
What type of DM gets DKA?
DM I
How does DKA happen?
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
What are some s/sx of DKA?
BG >250
Glycosuria
Acidosis (pH <7.3)
Dehydration
Tachypnea
Abdominal Pain, N/V
mental status chages
serum K+ might be slightly elevated
What is the treatment for DKA?
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
What type of DM pts get IHHS?
DM 2, elderly ptsW
How does IHHS occur?
Hyperglycemic diuresis –> dehydration and hyperosmolarity
Ketoacidosis IS NOT A PROBLEM because there is enough insulin to try and prevent it
What are some s/sx of IHHS?
BG >600
Hyperosmolarity >360 mOsmo
Hyponatremia
Formation of intravascular thrombiWh
How do you treat IHHS?
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)
What is hypoglycemia?
Most feared consequence in the unconscious patient
BG <50 mg/dL
Sampling device and site can interfere with measurements
What is the preferred method of sampling if the patient is thought to be hypoglycemic?
Arterial»_space; Venous»_space; Capillary
What are some s/sx of hypoglycemia?
Reflex catecholamine release
HTN
Tachycardia
Tearing
Diaphoresis
LOC +
How do you treat hypoglycemia? (Formula)
In a 70 kg pt, 1mL of D50 will increase a patient’s BG level by 2 mg/dL
