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
Neurotransmitter dysfunction r/t Ominous Octet
— It is the hormonal component to help control BS
— Can alter hormonal response in order to lower BS
Increased hepatic glucose production r/t ominous octet
— When you eat, liver will decrease amount of glucose it produces; if you don’t eat, you can still maintain BS, b/c liver stores glycogen and turn it to glucose to maintain BS
NOTE: sometimes diabetics will have an increase in HGP (will add more glucose to blood even if you don’t need it)
Islet alpha(a)-cells r/t hyperglycemia + the ominous octet
Purpose: to increase liver production of glucose
— Results in increased glucagon secretions
— Pancreas makes insulin which DECREASES the presence of sugar in the blood
Gas = pancreas makes insulin to decrease the presence of sugar in the blood (glucose levels), the way to decrease the levels by
Brake = but ALSO glucagon is made to INCREASE INCREASE BS
Islet beta(b)-cells r/t hyperglycemia + the ominous octet
Islet B-cells — Impaired insulin secretions results in hyperglycemia
Goals of treatment for the DM population
These are all the things we want a patient with DM to have:
— Normal range: 60-100 | with DM: (FSBS) 70-130
— 2 hr. Post-prandial (PP): BS <180
— w/in 2hrs your body should be responding to lower blood sugar
— A1C < 7%: how much glucose was circulating in the RBCs within the last 3 months to see how glucosylated they were
— Blood pressure (B/P) to be <130/80
— LDL < 100 (< 70 optimal); the “lousy” cholesterol
— HDL > 40 in men, > 50 in women; the “healthy” cholesterol
— Triglycerides (TG): <150
HbA1c Levels
Below 5% is nondiabetic
Between 5.7% to 6.4% is prediabetic
Above 6.5% is diabetic
The goal of therapy in a diabetic is to maintain fingerstick blood sugars _____.
FSBS b/w 70-130 mg/dL
Many DM patients die from which complications with prolonged/long-term DM
Cardiovascular
— These results create higher risks of strokes, PAD, heart attacks, and kidney disease (b/c impaired perfusion of disease; the body is working so hard to fight)
LADA (Latent Autoimmune Diabetes of Adults)
Getting diabetes as an adult
Type II/Non-insulin Dependent
Patients look: overweight, hungry, metabolic syndrome S/Sxs
Typical medications that can cause this secondary diabetes?
These medications can cause HYPERglycemia
Typically effect patients that are already borderline
— Glucocorticoids (e.g. cortisone, prednisone)
— Thiazide diuretics (e.g. hydrochlorothiazide (HCTZ))
— TZDs: does this cause iatrogenic diabetes? PLEASE DON’T CLICK IT
INSULIN
Used to use beef & pork insulin to use as regular insulin; use DNA technology to do that
Action: promote use of glucose by body cells, store glucose as glycogen in muscles
Use: reduce blood glucose
Interactions:
— Increased hypoglycemia with aspirin, oral anticoagulants, alcohol, oral hypoglycemics, BBs, TCAs, MAOIs, tetracyclines
— Decreased hypoglycemia with thiazides, glucocorticoids, oral contraceptives, thyroid drugs, smoking
Insulin pumps are either
rapid or short acting
Rapid-Acting Insulin
Color: clear
Taken insulin and made it quicker with the Analogs
Onset: 5 to 15 minutes
Peak: 30 minutes to 1 hour
Duration: 2 to 4 hours (can last up to)
MEDS:
— Insulin lispro (Humalog)
— Insulin aspart [rDNA origin] (NovoLog)
— Insulin glulisine (Apidra)
NOTE: lunch tray BETTER be at the bedside when giving rapid-acting unless HYPOglycemia is in your future
Short-Acting
Mixture: clear
Administration: only one given IV
mimics what the pancreas makes
MEDS:
—Regular (Humulin R, Novolin R)
—Regular insulin
Onset: 30 to 60 minutes
Peak: 2 to 3 hours
Duration (will be gone w/in): 3 to 4 hours
Intermediate-acting
Mixture: cloudy b/c protein (protamine) has been added
Insulin isophane NPH (Humulin N, Novolin N)
Onset of action (2 to 4 hours)
Peak (4 to 12 hours)
Duration (18 to 24 hours)
Long-acting insulin
Mixture: Clear
Covers basal range level by mimicking what it would do in the body
Administered at bedtime
MEDS:
— Insulin glargine (Lantus)
— Detemir (Levemir)
Onset of action (1 hour) then goes steady
Duration (24 hours), goes steady
Combination insulin
Composed of short- and intermediate-acting or rapid- and intermediate-acting
Humulin 70/30 (isophane NPH 70%, regular 30%)
Insulin isophane NPH 50/50 (Humulin NPH 50%, regular 50%)
Humalog 75/25 (lispro protamine 75%, lispro 25%) — give w/ food | will work quickly and then control BS throughout the day
NOTE: Helps with the goal of maintaining the A1C to stay below 7%
Gestational diabetes
— Gestational diabetes mellitus (GDM) during pregnancy
After pregnancy, the blood glucose level may decrease.
Some patients may develop diabetes.
Others may develop type 2 diabetes mellitus in later years.
During the second and third trimesters the levels of the hormones progesterone, cortisol, and human placental lactogen increase contributing to the occurrence of GDM.
What are the 3 P’s symptoms of diabetes mellitus?
- Polyuria – too much peeing
— elevated serum glucose and kidney’s attempt to try and get rid of it - Polydipsia – too much thirst (results from polyuria, XS glucose in brain)
— results from the polyuria; the h20 content that patient is losing causes them to feel thirsty
— elevated glucose makes brain feel as if the blood is too thick in attempt to increase hydration - Polyphasia – too much hunger
— elevated glucose, but the cells cannot utilized it d/t lack of insulin use (insulin is what gets glucose into the cell to be used for E); “cells still starving” which trigger hormonal responses to tell them ‘I’m hungry’
Why diabetic will have polydipsia?
Cells cannot utilize b/c of lack of insulin use (impaired)
–Cells are starving
HYPOglycemia
— Increased hunger (polyphagia)
— Cold, clammy skin
— Sweating
— Tremulousness d/t adrenergic response to central glucose deprivation
HYPERglycemia
increased urination r/t deficiency of insulin —> osmotic diuresis
Which insulin is used for basal, correctional, and bolus (prandial)?
Prandal = a meal
Who gets IV insulin?
Regular
Which insulins could be used in an insulin pump?
Rapid/Fast
Regular = only IV
— Aspart (the logs) —> NOT IV
What type of oral medication MOA has the highest risk of hypoglycemia?
If medication increases insulin reduction
All the stars + Insulins
Oral Agents
Ultimately decrease glucose, but MOA is different
*Biguanides
Sulfonylureas
(mainly 2nd generation)
*Glinides (meglitinides)
**Gliptins (DPP-4 inhibitors)
*Glitazones (thiazolidinediones/TZDs)
*Alpha-glucosidease inhibitors
*SGLT2 inhibitors (gliflozins)
The problem with Thiazolidinesdiones (TZDs)
Pioglitazone (Actos)
Antidiabetic
Rosiglitazone (Avandia)
Avandia users may be at greater risk for heart attack and possibly death.
Both drugs are contraindicated in symptomatic heart disease and Class III and IV CHF.
Meglitinides
for people that eat weird/irregular
Repaglinide (Prandin) and nateglinide (Starlix) — increase
“If i don’t take it and I don’t eat, I’m fine”
If I take it right before I eat at 8pm, it works fine.”
Repaglinide (Prandin) — Eat as soon as you take this medication
Drugs that DO/DO NOT increase insulin production
DO
— Sulfonyureas
— Meglitinides
could lead to hypoglycemia
DO NOT
— Metformin
— Alpha-Glucosidase Inhibitors
— Thiazolidinesdiones (TZDs)
Guidelines for Oral Antidiabetic Therapy for Type 2 Diabetes
Criteria for use of oral antidiabetic drugs:
Onset of diabetes mellitus at age 40 years or older
Diagnosis of diabetes for less than 5 years
Not underweight
Fasting blood glucose equal to or less than 200 mg/dL
Less than 40 units of insulin required per day
Normal renal and hepatic function
Renal + hepatic function = normal
Oral Antidiabetic Drugs
1st & 2nd Generation sulfonylureas
Used to treat type 2 diabetes
Stimulate pancreatic beta cells to secrete more insulin (tells pancreas to create more insulin)
First-generation sulfonylureas (doses were much higher)
Short-acting: tolbutamide (Orinase)
Intermediate-acting: tolazamide (Tolinase)
Long-acting: chlorpropamide (Diabinese)
Second-generation sulfonylureas (req. lower doses, tolerated better, problem if allergy to sulfa)
Glimepiride (Amaryl)
Glipizide (Glucotrol, Glucotrol XL) — it’s better to take med 30 minutes before a meal
Injectable Agents
*Incretin mimetics — not give to NIDDM if wanting to increasing insulin production
*Amylin mimetic — give to Type I, improve insulin use we’re giving them
Dawn phenomenon
H/A when waking b/c increased cortisol levels and then blood glucose is HIGH…therefore I need to increase medication
Somogyi phenomemon
Compensatory (released a bunch of sugar)…therefore decrease medicine so you don’t drop in the middle of the night so you don’t have a high spike
“Lower her basal” [little girl BS with cake]
Goals of treatment for the DM population
FSBS 70-130
2 hr. PP BS <180
A1C < 7%
B/P < 130/80
LDL < 100 (< 70 optimal)
HDL > 40 in men, > 50 in women
TG < 150
Short-Acting
Mixture: clear
Regular (Humulin R, Novolin R, regular insulin)
Onset of action (30 to 60 minutes)
Peak (2 to 3 hours)
Duration (3 to 4 hours)
Islet beta(b)-cells r/t hyperglycemia + the ominous octet
Exenatide (Byetta) + Liraglutide (Victoria)
MOA: Actions of exenatide and liraglutide are to enhance insulin secretion, increase beta-cell responsiveness, suppress glucagon secretion, slow gastric emptying, and reduce food intake.
Common side effects/adverse effects: Headache, dizziness, jitteriness, GI distress
RN Interventions:
It delays stomach emptying, which slows the absorption of carbohydrate and the resulting rise in blood glucose level after meals; it curbs appetite; and animal studies have shown that it may promote regeneration of the pancreatic beta cells and fight apoptosis (programmed cell death), improving the survival of existing beta cells.
Exenatide (Byetta) + Liraglutide
not a substitute for insulin and should not be
administered to Type 1 DM
Administration: Exenatide — injectable prefilled pens BID + significantly improves HbA1c levels + weight loss in many patients | Liraglutide — subQ 1x/day in arm, abdomen, or thigh
—
Exenatide (Byetta) + Liraglutide
not a substitute for insulin and should not be
administered to Type 1 DM
Administration: Exenatide — injectable prefilled pens BID + significantly improves HbA1c levels + weight loss in many patients | Liraglutide — subQ 1x/day in arm, abdomen, or thigh
