Diabeetus Flashcards

1
Q

Type 1 Diabetes

A
  • Develops during childhood or adolescence
  • Sx onset is abrupt
  • Primary defect is destruction of pancreatic beta cells from autoimmune processes - insulin levels decrease until they reach 0
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2
Q

Type 2 Diabetes

A
  • Develops later in life, becoming more common in children and adolescence
  • Sx result from combination of insulin resistance and impaired insulin secretion
  • Early disease, insulin levels tend to be normal or high, but insulin produced does not line up with plasma glucose level
  • Over time leads to diminished pancreatic beta cell function
  • Strong familial association
  • Tightly linked to weight gain and obesity
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3
Q

Causes of insulin resistance

A
  1. Reduced binding of insulin to it’s receptors
  2. Reduced receptor numbers
  3. Reduced receptor responsiveness
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4
Q

Short term complications of diabetes

A
  • Hyperglycemia
  • Hypoglycemia
  • Ketoacidosis - develops when hyperglycemia becomes severe and is allowed to persist; rare for T2, common for T1
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5
Q

Long term complications of diabetes

A
  • Macrovascular damage
  • Microvascular damage
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6
Q

Diabetes and Macrovascular Damage

A
  • CVD (leading cause of death in people with diabetes)
  • increased risk for: heart disease, hypertension, stroke d/t faster progression of atherosclerosis resulting from hyperglycemia and altered lipid metabolism
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7
Q

Diabetes and Microvascular Damage

A
  • retinopathy - major cause of blindness
  • nephropathy
  • sensory and motor neuropathy
  • autonomic neuropathy: gastroparesis
  • amputations secondary to infection
  • erectile dysfunction
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8
Q

Gestational Diabetes

A

defined as diabetes that appears in the pregnant patient during pregnancy and then subsides after delivery

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9
Q

Causes of Gestational Diabtes

A
  1. Placenta produces hormones that antagonize insulin’s actions
  2. Production of cortisol (promotes hyperglycemia) increases threefold during pregnancy
  3. Because glucose can pass freely from maternal to fetal circulation, hyperglycemia in mother will stimulate excess secretion of insulin in fetus. Resulting hyperinsulinsim can have adverse effects of fetus
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10
Q

Nursing considerations: Gestational Diabetes

A
  • monitor blood glucose 6-7 times per day
  • insulin preferred agent for management
  • if diabetes persists after delivery, it is no longer gestational and proper diagnosis should be sought out
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11
Q

Diagnostic Criteria for Diabetes

A

Fasting Blood Glucose > 126mg/dL

Casual Plasma Glucose > 200mg/dL plus sx of diabetes

Oral Glucose Tolerance Test: 2-hr plasma glucose > 200mg/dL

Hemoglobin A1C 6.5% or higher

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12
Q

Pre-diabetes

A

Fasting Blood Glucose between 100-125mg/dL

2-hr OGTT result of 140-199mg/dL

A1C of 5.7-6.4%

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13
Q

Overview of Treatment: T1D

A
  • Diet
  • Self-minotiring blood glucose
  • Physical activity
  • Insulin replacement
  • Management of hypertension: with ACE inhibitors and ARBs preferred; thiazide-like diuretics, or calcium channel blockers used if pt does not have albuminuria
  • Management of dyslipidemia: statins preferred
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14
Q

Overview of Treatment: T2D

A
  • Step 1. At diagnosis, initiate lifestyle changes plus metformin.
  • Step 2. Continue lifestyle changes plus metformin, and add a second drug
  • Step 3. Progress to three-drug combination (inclusive of metformin).
  • Step 4. If three-drug combination therapy that includes basal insulin fails to achieve treatment goals after approximately 3 months, it is recommended to proceed to a combination injectable regimen inclusive of insulin and possibly a GLP-1 receptor agonist.
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15
Q

Insulin: Biosynthesis

A

Synthesized in pancreas by beta cells within the islets of Langerhans

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16
Q

Insulin: Secretion

A
  • The principal stimulus for insulin release is a rise in blood glucose
  • Insulin release may also be triggered by amino acids, fatty acids, ketone bodies, and gut hormones
  • Activation of beta2-adrenergic receptors in the pancreas promotes secretion of insulin.
  • Activation of alpha-adrenergic receptors in the pancreas inhibits insulin release
17
Q

Insulin: Metabolic Actions

A
  • promotes the conservation of energy and buildup of energy stores such as glycogen
  • promotes cell growth and division
  • stimulates uptake of glucose, amino acids, nucleotides and potassium
  • promotes synthesis of organic molecules
18
Q

Insulin Deficiency: Metabolic Consequences

A
  • catabolic effects - favors breakdown of complex molecules
  • promotes hyperglycemia by three mechanisms:
    1. increased glycogenesis;
    2. increased gluconeogenesis;
    3. reduced glucose utilization
19
Q

Insulin: Appearance

A

With the exception of NPH insulins, all insulins are formulated as clear solutions

20
Q

Mixing Insulins

A
  • Of the longer-acting insulins in current use, only NPH insulin is appropriate for mixing with short-acting insulins
  • When a mixture is prepared, the short acting insulin should be drawn into the syringe first to avoid contaminating the stock vial of the short-acting insulin with NPH insulin.
  • As a rule, the mixtures are stable for 28 days
  • Premixed combinations are available
21
Q

Administration: SubQ Injection

A
  • Injection sites: upper arm, thigh (slowest absorption), and abdomen (fastest and more consistent).
  • To keep it consistent they should use the same general area
  • To reduce the risk of lipohypertrophy, within the chosen area they should use different spots about 1 inch apart and each spot should ideally only be used once a month
22
Q

Insulin Administration: SubQ infusion

A

Portable insulin pumps
- computerized devices that deliver basal infusion of insulin plus bolus doses before each meal
- delivers insulin from pump to a subcut catheter
- infusion set should be replaced about every three days at which catheter is moved to a new infusion site, at least 1 inch away from the old one

Implantable insulin pump
- surgically implanted in abdomen and deliver insulin intraperitoneally or intravenously

23
Q

Insulin Administration: IV infusion

A
  • Reserved for emergencies and for patients who are inpatient in the hospital
  • When used for intravenous infusion, regular human insulin is generally diluted by adding 100 units to 100 mL of 0.9% NaCl or other compatible intravenous fluid
  • An initial infusion rate of 0.1 unit/kg/hr is often recommended, but infusion rates and insulin doses must be individualized based on individual needs
24
Q

Insulin Administration: Inhalation

A
  • used for mealtime coverage and is inhaled at each meal
  • ability to fine-tine dose is limited to availability of 4-, 8- and 12-unit cartridges
  • good glycemic control, low incidence of hypoglycemia, no pulmonary effect
25
Q

Insulin: Storage

A
  • do not freeze unopened vials - should be refrigerated
  • vial in current use can be kept at room temp for up to one month
  • opened vial can be kept in fridge for 3 mo
  • avoid direct heat and sunlight
  • partially filled vials should be discarded after several weeks if left unused
  • injecting insulin at room term causes less pain than injecting cold insulin and reduces risk of lipodystrophy
  • mixtures in pre-filled syringes should be stored in a refrigerator - will be stable at least 1 week
  • pre-filled syringes should be stored vertically with needle pointing up to avoid clogging
  • before administering pre-filled syringe, agitate gently to re-suspend the insulin
26
Q

Insulin: Indications

A
  • T1 and most T2 diabetes
  • Ketoacidosis
  • Hyperkalemia
  • Gestational diabetes
  • Aid in dx of growth hormone deficiency
27
Q

Insulin: Dosage

A
  • T1D: initial doses typically range from 0.5-0.6 units/kg/day
  • T2D: initial doses typically range from 0.2-0.6 units/kg/day
28
Q

Insulin: Dosage Considerations

A
  • If carbohydrate intake is increased, insulin dosage must be increased too
  • when meal missed or is low in carb, dosage of insulin must be decreased
  • insulin needs are increased by infection, stress, obesity, growth spurts, and in pregnancy after the first trimester
  • insulin needs are decreased by exercise and the first trimester of pregnancy
29
Q

Insulin: Complications

A

Hypoglycemia
- Below 70 mg/dL
- When insulin levels exceed insulin needs
- can result from reduced intake of food, vomiting and diarrhea, excessive consumption of alcohol, unusually intense exercise, and childbirth
- may cause coma

Hypokaemia
- risk with excessive dosing
- insulin causes potassium uptake into cells

Lipohypertrophy
- Accumulation of subcutaneous fat when insulin is injected too frequently at the same site

Allergic Reactions
- develop rapidly
- characterized by widespread appearance of red and itchy welts
- breathing difficulty may occur
- desensitization procedure can be performed if person needs to continue insulin use

30
Q

Insulin: Drug Interactions

A

Hypoglycemic Agents
- drugs that lower blood glucose can intensify hypoglycemia induced by insulin
- include sulfonylureas, glinides, and alcohol

Hyperglycemic Agents
- drugs that raise blood glucose can counteract desired effect of insulin
- ex. glucocorticoids, sympathomimetics

Beta-Adrenergic Blocking Agents
- can delay awareness of and response to hypoglycemia by masking signs that are associated with stimulation of the sympathetic nervous system that hypoglycemia normally causes.
- nonselectives can make insulin induced hypoglycemia even worse by preventing the body’s natural counterregulatory response.

31
Q

Hyperosmolar Hyperglycemic State*

A
  • large amounts of glucose secreted in urine
  • dehydration and loss of blood volume
  • increases blood concentrations of electrlolytes (glucose, hematocrit)
  • blood thickens and becomes sluggish
  • metabolic changes begin 1-2 months before sx onset
  • if left untreated, can lead to coma, seizures, and death
  • correct with IV insulin, fluids and electrolytes
32
Q

Severe Hypoglycemia

A
  • preferred treatment is IV glucose
  • can use glucagon if IV glucose not available - delayed elevation in glucose
  • cannot correct hypoglycemia resulting from starvation