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MedSurg 1 > Type 2 Diabetes Mellitus > Flashcards

Type 2 Diabetes Mellitus Flashcards

1
Q

4 Types of Diabetes Mellitus

A

1) Type 1 - Insulin dependent diabetes mellitus (IDDM) aka Juvenile Diabetes
2) Type 2 - Non-Insulin dependent diabetes mellitus (NIDDM) aka Adult Onset Diabetes
3) Gestational Diabetes
4) Other: prediabetes, secondary diabetes (due to autoimmune disease or viral disease)

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2
Q

Stable BG

A

74-106 mg/dl

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3
Q

Type 1 Diabetes

A

Peak onset between 11-13yo

Most often occurs in people under 40yo

Causes: genetic predisposition, exposure to virus (usually hand, foot, mouth disease)

Progressive destruction of pancreatic cells that produce insulin by body’s own T cells

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4
Q

Prediabetes

A

Known as IGT (impaired glucose tolerance) or IFG (impaired fasting glucose).

IFG: Fasting glucose levels (8-12 hour fast) between 100-125 mg/dl

IGT: 2 hour plasma glucose higher than normal (between 140-199 mg/dl)

At increased risk of developing type 2 diabetes.

Usually develop diabetes within 10 years if no preventative measures are taken.

Often presents with no symptoms.

Long term damage is already occurring to heart and blood vessels.

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5
Q

Type 2 Diabetes

A

Gradual onset, may go years with undetected hyperglycemia.

Most prevalent type of diabetes.

80-90% of pt’s are overweight

Usually occurs in those over 35yo, prevalence increase with age.

Genetic component.

Greater in some ethnic populations.

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6
Q

Type 2 Diabetes: Etiology and Pathophysiology

A

Pancreas continues to produce some endogenous insulin.

Insulin produced is either insufficient or poorly utilized by tissues.

Obesity = most powerful risk factor.

Genetic mutations = lead to insulin resistance and increased risk for obesity.

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7
Q

Type 2 Diabetes: 4 Types of Metabolic Abnormalities

A

1) Insulin resistance: body tissues do not respond to insulin (insulin receptors either unresponsive or insufficient in number), resulting in hyperglycemia.
2) Pancreas has decreased ability to produce insulin: beta cells are fatigued from compensating or beta cell mass is lost).
3) Inappropriate glucose production from liver: liver’s response of regulating release of glucose is haphazard
4) Alteration in production of hormones and adipokines: play a role in glucose and fat metabolism (contribute to pathophysiology of type 2 diabetes). Two main adipokines = adiponectin and leptin.

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8
Q

Metabolic Syndrome

A

Grouping of health conditions associated with an increased risk for heart disease and type 2 diabetes.

Conditions include:

  • hypertension
  • central obesity
  • high triglyceride levels
  • low HDL cholesterol levels
  • above-normal blood glucose levels

MUST HAVE AT LEAST 3 METABOLIC RISK FACTORS TO BE DIAGNOSED WITH METABOLIC SYNDROME

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9
Q

Secondary Diabetes

A

Results from another medical condition such as:

  • cushing’s syndrome
  • hyperthyroidism
  • pancreatitis
  • parenteral nutrition (TPN)
  • cystic fibrosis
  • hematochromatosis

Tx of medical condition or removal of medication that causes abnormal BG usually resolves secondary diabetes.

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10
Q

Type 1 DM: S/Sx

A
  • 3 P’s: Polyuria (frequent urination), Polydipsia (excessive thirst), Polyphagia (excessive hunger).
  • weight loss
  • weakness
  • fatigue
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11
Q

Type 2 DM: S/Sx

A
  • nonspecific symptoms (could potentially have classic symptoms of type 1)
  • fatigue
  • recurrent infections
  • recurrent vaginal yeast or monilia infections
  • prolonged wound healing
  • visual changes (due to damage to small blood vessels in the eyes)
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12
Q

DM Glucose Ranges

A

Fasting glucose: >126 mg/dl

Random or casual glucose: greater than or equal to 200 mg/dl plus symptoms

Two-hour OGTT (oral glucose tolerance test) level: greater than or equal to 200 mg/dl using a glucose load of 75g

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13
Q

Hemoglobin A1C Test

A

Ideal: per ADA = less than or equal to 7.0%, per American college of endocrinology = less than 6.5%

Not diagnostic but monitors success of tx.

Shows the amount of glucose attached to hemoglobin molecules over RBC lifespan (90-120 days).

Normal A1C reduces risk of retinopathy, nephropathy, and neuropathy.

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14
Q

Interventions for DM

A

Health promotion:

  • identify those at risk
  • routine screening for overweight adults over 45yo (FPG is preferred method in clinical settings)

Diet:

  • after dx of diabetes, start with education on diet
  • cornerstone of care for person with diabetes
  • most challenging for many people
  • recommended that diabetes nurse educator and registered dietitian with diabetes experience be members of team.
  • overall goal: assist people in making changes in nutrition and exercise habits that lead to improved metabolic control.
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15
Q

Diet Interventions for Type 1 vs Type 2 DM

A

Type 1: meal plan based on individual’s usual food intake and is balanced with insulin and exercise patterns. Insulin regimen managed day to day.

Type 2: emphasis on achieving glucose, lipid and blood pressure goals. Calorie reduction.

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16
Q

Healthy Plate Percentages

A

Carbs and monounsaturated fats = 45-65% of total energy intake

Fats = 25-30% max with <7% from saturated fats.

Protein = <10%

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17
Q

Alcohol

A
  • high in calories
  • no nutritional value
  • promotes hypertriglyceridemia
  • detrimental effects on liver
  • can cause severe hypoglycemia
  • mixed drinks can cause hyperglycemia
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18
Q

Exercise

A

Essential part of diabetes management

  • increases insulin receptor sites
  • lowers blood glucose levels
  • contributes to weight loss

Best done after meals with small carb snack taken ever 30 min during exercise to prevent hypoglycemia.

Exercise plans should have medical clearance, be individualized, and start slowly.

Monitor BG levels before, during, and after exercise

19
Q

Exogenous Insulin

A

Insulin from outside source.

Required for type 1 diabetes, may be Rx for pt’s with type 2 diabetes who cannot control BG by other means.

Regimen that closely mimics endogenous insulin production is basal-bolus

  • long acting (basal) = once a day
  • rapid/short acting (bolus) = before meals
  • both admin subcutaneous or IV (no such thing as oral insulin b/c insulin is a hormone and gastric juices in stomach deactivate insulin).
20
Q

Insulin Pump

A

Continuous subcutaneous infusion

Battery operated device

Connected via plastic tubing to a catheter inserted into subcutaneous tissue in abdominal wall

Potential for tight glucose control

21
Q

PO Meds

A

Not insulin!

Work to improve mechanisms by which insulin and glucose are produced and used by the body.

Work on 3 defects of type 2 diabetes:

  1. Work on insulin resistance
  2. Decrease insulin production when insulin is being overproduced
  3. Increase hepatic glucose production
22
Q

Sulfonylureas and Meglitinides

A

PO Meds for Type 2 DM

Sulfonylureas are more long acting. Ex: glipizide (glucotrol) and glimepiride (amaryl)
-decrease chance of prolonged hypoglycemia

Meglitinides are more short acting. Ex: repaglinide (prandin) and nateglinide (starlix).
-should be taken 30 min before each meal and not taken if meal is skipped.

Both do the same thing:
-increase insulin production from pancreas

23
Q

DPP-4 Inhibitors

A

PO Med for Type 2 DM

slows incretin metabolism, increases insulin production/release and decreases glucagon levels

taken once daily

24
Q

SGLT2 Inhibators

A

PO Med for Type 2 DM

inhibits glucose reabsorption in urine causing increase urinary glucose excretion

taken before first meal of day typically

25
Q

Biguanides

A

PO Med for Type 2 DM

first line, used when pt is first diagnosed

  • reduce glucose production by liver
  • enhance insulin sensitivity at tissues
  • improve glucose transport into cells
  • do not promote weight gain

Ex) Metformin

*effects kidneys and can cause acute kidney injury if it’s used with other meds (specifically contrast). keep in mind when you send pt for imaging, they will need to stop taking metformin before they go in.

26
Q

Alpha-Glucosidase Inhibitors

A

PO Med for Type 2 DM

“starch blockers”

  • slow down absorption of carbs in small intestine
  • rarely used
27
Q

Thiazolidinediones

A

PO Med for Type 2 DM

  • most effective in those with insulin resistance
  • improves insulin sensitivity, transport, and utilization at target tissues

*rarely used

28
Q

Amylin Analog

A

Subcutaneous Injection for Type 1 or Type 2 DM

  • hormone secreted by beta cells of pancreas
  • cosecreted with insulin
  • slows gastric emptying, reducing postprandial glucagon secretion, and increasing satiety

Make you feel fuller faster so you aren’t as hungry and therefore not taking in as much hyperglycemic calories as you normally would.

*not used as often as PO meds and insulin

29
Q

GLP-1 Agonist

A

Similar to Amylin Analog

  • suppresses glucagon secretion
  • reduces food intake
  • slows gastric emptying

DO NOT TAKE WITH INSULIN B/C YOU WILL HAVE HYPOGLYCEMIA FAST

*not used as often as PO meds and insulin

30
Q

When do you need to check BG?

A
  • before meals (ac)
  • before bed (hs)
  • ac, 2 hour post-prandial (pp) and hs
31
Q

HHNS: Cause and S/Sx

A

Hyperosmolar Hyperglycemic Non-Ketotic Syndrome

HOT AND DRY - SUGAR IS HIGH

  • specific to Type 2 DM
  • life threatening syndrome
  • caused by recent illness/infection (most common cause is fever)
  • Inadequate fluid intake (dry)
  • increasing mental depression
  • polyuria
  • BG >600mg/dl
  • minimal ketone bodies
  • increase in serum osmolality
  • less common than DKA (specific to type 1 DM)
  • often occurs in pt over 60yo
  • pt has enough circulating insulin so ketoacidosis does not occur.
  • few symptoms in early stages
  • neurologic manifestations occur due to increased serum osmolality

Tx similar to DKA but with greater fluid replacement

32
Q

Ketoacidosis

A

Ketones dumping into urine and circulation.

  • ketones are acid byproducts of fat
  • with enough circulating insulin, there’s enough to keep this from occurring
  • not enough insulin means byproducts of fat circulate and are let go through urine
  • causes change in pH balance which causes high serum osmolality
33
Q

HHNS: Tx

A
  • admin: IV fluids, insulin therapy, electrolytes
  • assess: renal status, cardiopulmonary status, LOC
  • closely monitor

NS (0.9% NaCl) + IV Insulin, when BG becomes <250 add dextrose to solution to prevent hypoglycemia.

Note: watch electrolytes as insulin pushes K out of cells and into periphery which then gets excreted so you’ll probably want to be giving IV K

34
Q

Hypoglycemia: Cause and S/Sx

A

COLD AND CLAMMY - NEED SOME CANDY

Cause: too much insulin in proportion to glucose in the blood. BG <70mg/dl

S/Sx: confusion, irritability, diaphoresis, tremors, hunger, weakness, visual disturbance (can mimic alcohol intoxication)

35
Q

Hypoglycemia: Tx

A

if alert enough to swallow:

  • 15-20g simple carb (4-6oz juice, or regular soft drink)
  • avoid foods with fat (decrease absorption of sugar)
  • do not overtreat, recheck BG in 15 min
  • repeat until BG is >70mg/dl
  • check BG again 45 min after tx

If no improvement after 2 or 3 doses of simple carb OR pt not alert enough to swallow, then:

  • admin 1 mg of glucagon IM or subQ
  • have pt ingest complex carb after recovery to prevent rebound hypoglycemia
  • in acute care setting: 20-50ml of 50% dextrose IV push
36
Q

Chronic Complications of DM: Macrovascular

A

-atherosclerosis (tight glucose control may delay this)

Risk factors:

  • obesity
  • smoking
  • hypertension
  • high-fat intake
  • sedentary lifestyle

pt’s with DM should be screened for dyslipidemia at dx

37
Q

Chronic Complications of DM: Microvascular

A

results from thickening of vessel membranes in capillaries and arterioles (in response to hyperglycemia)

  • specific to DM unlike macrovascular
  • areas most notably affected = eyes, kidneys, skin

usually appears within 10-20 years of DM

38
Q

Diabetic Retinopathy

A

Microvascular

  • damage to retina due to chronic hyperglycemia
  • most common cause of new blindness in 20-74yo

Nonproliferative: occurs slowly, most common type of diabetic retinopathy. Partial occlusion occur in small vessels (capillaries) causing microaneurysms in the retina. Very weak and allow leaking of capillary fluid causing retina edema. Increase of cataracts in early stage and increase in glaucoma because flow of fluid is being cut off and slowing down of vascular fluid.

Proliferative: most severe diabetic retinopathy, capillaries are occluded so new vessels form since they can’t get through old vessels, but they are very fragile and hemorrhage easily.

39
Q

Diabetic Nephropathy

A

associated to damage to small blood vessels that supply the glomeruli of the kidney

  • leading cause of end-stage renal disease

Critical factors for prevention/delay = tight control of glucose and BP management

Yearly screening

40
Q

Diabetic Neuropathy

A

Autonomic:

  • can affect nearly all body systems
  • complications: gastroparesis, CV abnormalities, sexual function, neurogenic bladder (don’t feel when you have to urinate, can either have retention or leaking)

Sensory:
distal symmetric (most common form)
-affects hands and/or feet bilaterally
-loss of sensation, abnormal sensations, pain, and paresthesias
-usually worse at night
-foot injury and ulcerations can occur without the pt having pain
-can cause atrophy of small muscles of hands/feet

41
Q

DM: Foot Complications

A

most common cause of hospitalization in DM

results from combo of micro and macrovascular diseases

Risk factors: sensory neuropathy and PAD

Other contributors: smoking, clotting abnormalities, impaired immune function, autonomic neuropathy

42
Q

DM: Integumentary Complications

A

Acanthosis nigricans: dark, coarse, thickened skin

43
Q

DM: Infection

A

More susceptible to infections due to:

  • defects in mobilization of inflammatory cells
  • impaired phagocytosis by neutrophils and monocytes
  • loss of sensation may delay detection

Tx must be prompt and vigorous

44
Q

DM: Gerontologic Considerations

A
  • prevalence increases with age
  • hypoglycemia unawareness is more common
  • presence of delayed psychomotor function could interfere with tx of hypoglycemia
  • must consider pt’s own desire for tx and coexisting medical problems
  • recognize limitations in physical activity, manual dexterity and visual acuity
  • educate based on individual’s needs, using slower pace

MedSurg 1 (18 decks)

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