Pharm 2 Exam #1 (Chpt. 47) Flashcards
TYPE 1 DIABETES MELLITUS
insulin-dependent DM
formerly known as juvenile-onset DM
due to: insufficient insulin secretion, impaired insulin use or bot
— absolute absence of insulin; beta cells in pancreas do not make insulin therefore cannot utilize glucose in the blood to get it into the cells (necessary to create E)
— Found in older adults r/t an autoimmune d/o triggered by health problem/condition: patient produces lack of insulin production within the pancreas
TYPE 2 DIABETES MELLITUS
Non-insulin-dependent DM
Formally known as adult onset
— You eat a meal, BG goes up, insulin production goes up, but cells get tired and cannot keep up, with time your insulin production begins to fall b/c not using properly
— Body gets tired of XS’ive need for insulin then becomes resistance to it
E.g.: body has had elevated glucose levels long enough that the body is now tired of trying to utilize XS insulin in order to lower serum glucose levels
Type 2 – insulin resistance: may make insulin, but do not utilize insulin correctly
–requires more insulin in order to promote same effect
What are the types of diabetes mellitus
– Type 1 (insulin-dependent)
– Type 2 (non-insulin-dependent, NIDDM)
– Secondary (Iatrogenic)
– Gestational (hormonal)
The more glucose you have the more _____ you need to get that _____ into the cell.
insulin, glucose
Describe the S/Sx of diabetes mellitus
Type 1: young, thinner,
Type 2 diabetics: overweight, hungrier, have metabolic syndrome, feeling tired and hungry
Medications that can cause hyperglycemia
— Glucocorticoids (cortisone, prednisone)
— Thiazide diuretics (hydrochlorothiazide)
— Epinephrine
Usually the blood glucose level returns to normal after the drug is discontinued
Insulin Resistance
— Body tissues do not respond to the action of insulin
— The more glucose you have, the more insulin you need to utilize resulting in tiring the body out, therefore begins to NOT respond to affect of the insulin which helps get into the cell —> less glucose getting into the cell, so being to store XS sugar as fat
— Why you’ll see Type 2 diabetics: overweight, hungrier, have metabolic syndrome, feeling tired and hungry
INSULIN TYPES
Rapid-acting — faster acting = analog
Short-acting — Regular (mimics what your pancreas makes, what we used to get from the cow/pig); only type given IV
Intermediate-acting (NPH)
Long-acting (Glargine (Lantus, Levemir, Detromir)
– Combinations
*If I want to make it faster acting than Regular = add Analog
*If I add a protein to it = becomes longer-acting = NPH = suspension (looks cloudy; protein added to make regular last longer)
*E.g. 70 (long term)/30
We make it long-acting
Basic insulin = REGULAR and how we adjust it determines if it’ll take a longer/quicker time to control glucose
Differentiate between the action of insulin, oral antidiabetic agents, and glucagon.
INSULINS
Currently manufactured by using deoxyribonucleic acid (DNA) technology
Humulin R
Novolin N
Human insulin analogs
Insulin lispro (Humalog)
Insulin aspart (Novolog)
Human insulin (Humulin and Novolin) was introduced in 1983 and duplicates insulin produced by the pancreas.
The insulin analogues are human insulins that have been modified to change the onset and duration of activity – they can be rapid acting (lispro and aspart) or long acting (glargine/Lantus, detmir/Levemir)
Intermediate acting insulins (NPH, Humulin N) contain protamine to prolong the action of the insulin – this protein additive makes them cloudy in appearance.
Insulin Side Effects + Hyper/Hypoglycemia
HYPOglycemia:
— H/A, dizziness, confusion, slurred speech
— Nervousness, anxiety, agitation
— Tremors, uncoordination, sweating, tachycardia, seizures
HYPERglycemia:
—
Kussmaul breathing/respirations: blow off acid b/c breaking down into fatty acids in attempt to create E for the cells
Hypoglycemia
Headache, dizziness, confusion, slurred speech
Hyperglycemia
Extreme thirst, dry mucous membranes
Poor skin turgor, polyuria, fruity breath
Fatigue, tachycardia, Kussmaul respirations
Insulin Side Effects
Lipodystrophy — please rotate sites
Somogyi effect = elevated BS effect b/c you took TOO much insulin before bed
— give insulin b4 bed (intermediate) to help control BS, if taking too much and BS drops, body will compensate to fix/increase BS, will see a dramatic bump in the morning r/t hypoglycemia that happened overnight, therefore…needs LESS insulin @ bedtime
Dawn phenomenon = Type 2 = FBS increased in the morning = cortisol levels increased, which increases
Elevated BS in the morning is telling you you need MORE insulin
What are some additional insulin side effects r/t the body?
Lipodystrophy
Somogyi effect
Dawn phenomenon
Insulin shock
Diabetic ketoacidosis
Weight gain
How to differentiate between Dawn phenomenon and Somogy effect?
— If not on any insulin dawn phenomenon
e.g check BS @ bedtime = 150, @ 3a = 150, @ 6am = 300 did not have drop just a chronic increase
— On insulins bedtime somogyi effect make sure to take blood sugars at/throughout the night
E.g. 150 @ bedtime, give insulin, 70 @ 3am, 300 @ 600; blood sugar dropped low and body responded by trying to bump it up
What is insulin shock?
Giving too much insulin than you already need b/c of being sick, throwing up
Too much insulin WILL result in hypoglycemia
Diabetic Ketoacidosis (DKA)
Diabetic keoacidosis – not enough insulin, hyperglycemia is present but the body cannot use it and instead is burning ketones (fatty acids) for energy which leads to acidosis, coma, and death if not treated
Apply the nursing process to the patient taking insulin and oral antidiabetic agents.
[review slide 17]
What is diabetes?
— Chronic disease of deficient glucose metabolism
— Insufficient insulin secretion from beta cells
— Impaired insulin use
What is the ominous octet?
– 8 core defects that can worsen or lead to affected blood sugar levels and ultimately DM
make your blood sugar go even higher
What are the 8 core defects of the ominous octet related to DM?
Defects all affect HYPERglycemia
1) Islet B-cell: impaired insulin secretion
2) Islet a[lpha] cells: increased glucagon secretions
3) Increased HGP
4) Neurotransmitter dysfunction
5) Deceased glucose uptake
6) Increased glucose reabsorption
7) Increased lipolysis
8) Decreased incretin effect
RN Interventions for Insulin Administration
— Monitor vital signs and glucose levels.
— Instruct patient to report hypoglycemia and hyperglycemia.
— Encourage compliance with diet, insulin, exercise.
— Advise patient to wear medical alert tag.
— Teach patient how to check blood glucose.
— Teach patient how to administer insulin.
Insulin storage
— Keep in refrigerator — will last 3 months
— Note in refrigerator — will only last 1 month
— Remove from refrigerator 30 minutes before injection
— Avoid storing insulin in direct sunlight or at high temperatures
— Can make pre-filled syringes on a 2-week notice
How do you draw up and administer insulins?
IF GIVING REGULAR INSULIN + NPH:
— Air in cloudy (NPH), air in clear, draw up clear, draw up cloudy, aspirate clear then aspirate cloudy ** START & END in cloudy or “STAY IN THE CLEAR” after injecting air to aspirate**
— Rub + rotate vial b/w hands to give consistent concentration when drawing up
NPH is a suspension, so gently rotate vial to mix to insure accurate dosing
Most/Greatest effective absorption = abdomen
Slowest absorption = the thighs (unless they do a lot of walking)
*NOTE: Avoid giving fat when giving snack to treat hypoglycemia, it can slow absorption. i.e. give skim milk instead of whole b/c of fat in whole milk slows down absorption
How is decreased incretin effect r/t hyperglycemia?
— Decreased Incretin Effect (from gut) hormone released by gut to tell pancreas (hey, someone just ate, bump up insulin production); also found in altered glucose metabolism, which is increased Decreased Incretin Effect (from gut) hormone released by gut to tell pancreas (hey, someone just ate, bump up insulin production)
— Found in altered glucose metabolism, which is increased
3 Ways to Treat Glucose presence in the blood + Insulin coverages
- BOLUS = rapid/short-acting
- CORRECTIONAL = rapid/short-acting
- BASAL = long-acting
Basal = pancreas is making low level of insulin throughout the night so my cells can utilize glucose/sugar in the blood for E (foh my brains, cells, and boday!)
— After you eat = bolus — pancreas figures out you ate and them bump up insulin production; you eat TID
— Correctional = say you bolus yourself (knows you’re gettin ready to eat), didn’t bolus you enough so it will correct it = rapid or short-acting |
Your body SHOULD figure it out that you’ve eaten and will fix it within 2 hours post-prandial and fix your levels (<180)
— Sliding scale insulin mimics correctional insulin (before people eat)
Increased Lipolysis r/t Ominous Octet
— Increased Lipolysis: change in lipid metabolism as a result of alteration in glucose so individual may break down more of lipids, fats in their body to get E into cell, so may affect change in lipid production throughout the body
— Individual may break down more of the lipids and fats in the body in efforts to get E into the cell
Increased glucose reabsorption
Increased Glucose Reabsorption if person’s kidneys not letting glucose into urine (normal kidney does not do that); glucose = E | elevated BS causes kidney to spill/release glucose b/c can’t hold on to all, but will try to reabsorb as much as possible (does not see glucose as a waste product), by adjusting amount of glucose that kidneys allowed to let through in body
Decreased glucose uptake r/t ominous octet
Decreased Glucose Uptake If you don’t use insulin properly or don’t make any insulin, cells cannot get insulin into them for E
