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AP III > DM Obesity Part 1 > Flashcards

DM Obesity Part 1 Flashcards

1
Q

Describe Type I DM

A

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

Not obese patient

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2
Q

What causes DM I?

A

ABSOLUTE deficiency of insulin

IA: autoimmune destruction of beta islet cells of langerhans

1B: unknown MOA, possibly genetic

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3
Q

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

A

Normally, 0.3-0.7 u/kg/day

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4
Q

What is DM II?

A

Gradual onset in adulthood
Obese patients

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5
Q

What causes DM II?

A

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

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6
Q

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

A

1u; 25-30 mg/dL

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7
Q

How do you calculate a regular insulin infusion rate?

A

Plasma glucose/ 150 = u/hr

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8
Q

How do you determine a maintenance glucose infusion rate?

A

1.5 ml/kg/hr

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9
Q

What are some of the cellular effects of insulin?

A

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

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10
Q

Where is insulin metabolized/

A

liver and kidneys

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11
Q

How are carbohydrates effected by insulin?

A

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

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12
Q

Why do DM pts become hyperglycemic?

A

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

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13
Q

How are proteins effected by insulin?

A

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

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14
Q

How are fats affected by insulin

A

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

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15
Q

In summary, what does insulin do?

A

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

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16
Q

What is glyconeolysis?

A

Breakdown of glycogen in liver into glucose

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17
Q

What is gluconeogenesis?

A

Formation of glucose from non-carbohydrate substrates

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18
Q

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

A

Glucagon
Somatostatin
Epinephrine
Cortisol

19
Q

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

A

Make them more insulin resistantW

20
Q

Where is glucagon produced?

A

Alpha cells of the islet of langerhanha

21
Q

What does glucagon do?

A

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

22
Q

What is glucagon stimulated by?

A

Hypoglycemia
Epinephrine
Cortisol

23
Q

What is glucagon suppressed by?

A

Glucose intake
Insulin secretion

24
Q

What is somatostatin and where is it produced?

A

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

Somatostatin is a hormone that suppresses HGH

25
Q

What does somatostatin do?

A

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

26
Q

When is somatostatin released?

A

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

27
Q

What is epinephrine and where is it secreted?

A

Adrenal medulla
Catecholamine

28
Q

What does epinephrine do to insulin?

A

Increases glyconeolysis to increase BG

29
Q

When is epi released in relation to insulin?

A

released when the patient is under a lot of stress (sick or postop)

This is why insulin resistance is so high in surgical patients

30
Q

What is cortisol and where is it released?

A

secreted from adrenal cortex

31
Q

What does cortisol do?

A

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

32
Q

What are some of the effects of hyperglycemia?

A

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

33
Q

What type of DM gets DKA?

A

DM I

34
Q

How does DKA happen?

A

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

35
Q

What are some s/sx of DKA?

A

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

36
Q

What is the treatment for DKA?

A

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

37
Q

What type of DM pts get IHHS?

A

DM 2, elderly ptsW

38
Q

How does IHHS occur?

A

Hyperglycemic diuresis –> dehydration and hyperosmolarity

Ketoacidosis IS NOT A PROBLEM because there is enough insulin to try and prevent it

39
Q

What are some s/sx of IHHS?

A

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

40
Q

How do you treat IHHS?

A

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)

41
Q

What is hypoglycemia?

A

Most feared consequence in the unconscious patient

BG <50 mg/dL
Sampling device and site can interfere with measurements

42
Q

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

A

Arterial&raquo_space; Venous&raquo_space; Capillary

43
Q

What are some s/sx of hypoglycemia?

A

Reflex catecholamine release
HTN
Tachycardia
Tearing
Diaphoresis
LOC +

44
Q

How do you treat hypoglycemia? (Formula)

A

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

AP III (25 decks)

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