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what is gestational diabetes?
diabetes that develops during pregnancy in patients without a prior diabetes diagnosis
what are the clinical manifestation of diabetes?
the three P’s: polyuria, polyphagia, polydipsia
fatigue
blurred vision
slow-healing sores
tingling/numbness in the hand and feet
unexplained weight loss
ketoacidosis
what are the most generally known complications of diabetes?
heart and blood vessels: heart disease, stroke, peripheral artery disease (PAD)
eyes: retinopathy, cataracts, glaucoma
kidneys: diabetic kidney disease and nephropathy
nerves: diabetic neuropathy (e.g., tingling, numbness, or burning)
feet: nerve damage and por circulation make the feet vulnerable to sores
what level of blood sugar is considered hypoglycemia (generally vs. in real-world practice)?
generally - textbook - when BG is under 70 mg/dL
in real-world practice: when BG is under 75 mg/dL
what are the rule to treating patient with hypoglycemia?
the 15-15 rules: 15 grams of carbohydrates with a 15 minute check
what level of blood sugar is considered hyperglycemia (general vs. in real world-practice)
general - textbook: when BG is more than 110 mg/dL
in real-world practice: when BG is more than 150 mg/dL
why is glucagon to convert glycogen to glucose used to treat hypoglycemia if insulin is needed for glucose uptake?
glucagon raises blood glucose by stimulating the liver to break down glycogen and make new glucose
the brain, red blood cells, liver, and kidneys can take up glucose without insulin (via insulin-independent transporters), so the brain can use the released glucose immediately.
insulin is mainly needed for glucose storage in muscle and fat, not for emergency glucose use.
what is the peak, onset, and duration of insulin refer to?
peak: insulin at max strength
onset: when insulin begins working
duration: length of action
what is the MOA, indications, and adverse effects of insulin?
MOAL lowers BG level and provides cells with glucose for energy by helping cells absorb glucose
indications: hyperglycemia, glucose, homeostasis
adverse effects: weakness, HA, N, V, D, cough, weight gain, edema, injection site irritation and reactions
from where is insulin released?
released by the beta cells from the islets of Langerhans in the pancreas after eating
review the examples, onset, peak and duration of rapid-acting insulin…
examples: Lispro (Humanlog), Aspart (Novolog), Glulisine
onset: about 15 minutes
peak: about 1 hour
duration: about 3 hours
review the examples, onset, peak, and duration of short-acting insulin…
examples: Regular (Humulin R, Novolin R)
onset: about 30 minutes
peak: about 2 hours
duration: about 8 hours
review the examples, onset, peak, and duration for intermediate insulin…
examples: NPH (Humulin N, Novolin N)
onset: about 2 hour
peak: about 8 hour
duration: about 16 hours
review the examples: onset, peak, and duration for long-acting insulin…
examples: Glargine (Lantus), Detemir (Levemir), Degludec.
onset: about 2 hours
peak: none/minimal
duration: about 24 hours
can insulin be given via a fixed-dosed?
yes but that would require carb counting
a fixed-dosed mans the patient take the same amount of insulin at the same time everyday, usually before meals → this does not change based on what the person eats
carb counting is required as insulin and carbohydrates have to match, of which the patient have the eat roughly the same amount of carbohydrate at each meal every day!!! —> sliding scale offer more flexibility
what is sliding-scale insulin dosing?
Sliding-scale insulin is a method where short- or rapid-acting insulin is given based on the patient’s current blood glucose level before a meal.
The higher the blood sugar, the more insulin is given.
It is reactive — it treats high blood sugar after it happens instead of preventing it.
why is the sliding-scale insulin considered a weak or outdated strategy on its own?
this is because sliding-scale insulin only responds to high blood sugar after it occurs, which mean it does not prevent glucose spikes and can lead to large swings between hyperglycemia and hypoglycemia → it is best used with basal insulin and not by itself
what type of insulin is sliding-scale insulin based used with?
basal insulin
what is basal insulin and what is its purpose?
basal insulin is a long-acting insulin given once or twice daily to keep blood glucose stable all day and night (it controls fasting blood sugar and background glucose from the liver)
some examples includes glargine, detemir, degludec
what is bolus (mealtime) insulin used for?
bolus insulin is a rapid-acting insulin taken before meals to control the blood sugar spike caused by carbohydrate
what is the basal-bolus regimen?
a basal-bolus regimen mimics the body’s naturalinsulin pattern
basal insulin → steady background control
bolus insulin → cover meals
sometimes includes correction (sliding-scale doses)
when is IV insulin used?
IV insulin is used in critical care and emergency settings when rapid, precise control is needed
typically used for
diabetic ketoacidosis (DKA)
hyperosmolar hyperglycemic state (HHS)
ICU patients
periooperative management
why is iV insulin considered a SUPER HIGH ALERT medication?
because even a small dosing error can cause severe hypoglycemia, seizures, coma, and death of which it requires continuous glucose monitoring, IV pump, and strict protocols
insulinn, in general, is considered one of the most dangerous medication sif misused
which type of insulin can be given intravenously?
only regular insulin cna be given IV → rapid-acting, intermediate, and long-action insulin are never given IV
how do basal, bolus, sliding-scale, and IV insulin differ?
basal insulin → background control (long-acting)
bolus insulin → mealtime spikes (rapid-acting)
sliding-scale insulin → correction based on current glucose
IV insulin → emergency/critical care only (regular insulin)
can insulin be freeze or be heated?
freeze? NO
heated? NO - insulin can tolerate warmth up to about body temperature which is 98F/37C but it should never be intentionally heated
true or false: insulin is a high-alert medication
YES!
true or false: only use insulin syringes to administer insulin
true
what electrolytes must the nurse carefully monitor for patient taking insulin?
potassium - Nurses monitor potassium for insulin patients because insulin moves potassium from the bloodstream into cells, which can cause dangerously low blood potassium (hypokalemia), leading to severe symptoms like cardiac arrhythmias, muscle weakness, or even death.
what are the patient educations the nurse should provide for the patient starting on inuslin?
monitor for hypo/hyperglcyemia,
rotate insulin sites
needle safety
quickly state the difference between type 1 vs type 2 diabetes?
type 1 DM is when the pancreras does not make insulin because the body’s immune system attacks the islet cells in the pacreas that make insulin
type 2 DM is when the pancreas does not make enough insulin and the body is resistant to insulin
when is a patient most likely to develop hypoglycemia: at onset, peak, or end of action?
peak
what are non-insulin injectable diabetes medications?
non-insulin injectables are medications sued as an alternative or additon to insulin therapy
they work my mimicking or enhancing natural hormones released with insulin to control blood glucose
they are fairly new (with the oldest medication being about 20 year old)
mainly used for Type 2 Diabetes!!!
helpful for glucose control and weight loss
why use non-insulin injectables instead of just giving insulin?
non-insulin injectables are used instead of just giving insulin because they improve blood sugar control without directly forcing glucose into cells which mean they lower risk of hypoglycemia, weight loss instead of weight gain, and more provide more natural regulations after meals
how do non-insulin injectable diabetes medication lwoer blood sugar without forcing glucose into cells?
the medications lwoer blood sugar by controlling how much glucose enters the bloodstream instead of pushing glucose into cells by slowing down digestation (allowing glucose to enter the bloodstream more gradually), block glucagon release from the liver (which prevent the breaking down of glycogen into glucose), and increase insulin only when glucose is high
how does slow gastric emptying help control blood sugar?
slower gastric emptying means glucose enters the bloodstream more graudlly, preventing sharp post-meal blood sugar spikes
why does block glucagon lower blood sugar?
since glucagon tells the liver to release stored glucose, by blocking glucagon, the body reduces the liver’s glucose dumping into the bloodstream
why do GLP-1 receptor agonists have a lower risk of hypoglycemia?
they have lower risk of hypoglycemia because they only increase insulin release when blood glucose is high as when glucose is low, they do not stimulate insulin release
what is the MOA, indications, interactions, contraindication, and adverse effects of Amylin analogue?
MOA: mimics the hormone amylin, which is normally secreted with insulin after meals → slows gastric emptying, suppresses glucagon release from the liver, reduces post-meal blood glucose spikes, and increases satiety
indicationsL adjunct therpay for patient with diabetes using mealtime insulin | used in both Type 1 and Type 2 diabetes with insulin therapy
interactions: must be taking with insulin and dleays absorption of other oral medications and should be given before meal
contraindication: gastroparesesis (due to it slowing gastric emptying), history of severe hypoglycemia, and allergy to pramlintide
adverse effectsL nausea, loss of appetite, fatigue, headache, weight loss, hypoglycemia (especially with insulin)
what is the MOA, indications, interactions, contraindications, and adverse effects of GLP-1 receptor agonists (e.g, Ozempicm Trulicity, Byetta, Mounjaro)?
MOA: mimic the incretin hormone GLP-1 released form the GI tract after meals → increase insulin secretion (only use when glucose is high), decrease glucagon secretion, slow gastric emptying, and increase satiety and reduce appetite
indications: type 2 DM, weight management (only some are approved), and cardiovascular risk reduction in T2DM
interaction: delays absorption of oral medications, increased hypoglycemia risk when combined witrh insulin or sulfonylureas
contraindications: severe gastroparesis, history of pancreatitis
adverse effects: N, V, D, abdominal pain, decreased appetite, weight loss, risk of pancreatitis, possible thyroid C-cell tumors (boxed warning)
what type of medication is semaglutide (Ozempic)?
GLP-1 receptor agonists
what is the MOA, indications, interactions, contraindications, and adverse effects of semgaglutide (Ozempic)?
MOA: increase insulin secretion when glucose levels are elevated, decreases glucagon secretion, and delays gastric emptying
indications: adjunct to diet and exercise to improve glycemic control in patient over 10 years old, reduce risk of CV events in patients with T2Dm , and weight loss (only Wegovvy is approved asn an anti-obesity drug)
interactions: delays gastric emptying so can reduce rate of oral meds absorptions
contraindications: medullary thyroid carcinoma, multiple endocrine neoplasia, hypersensitivity
adverse effects: N, V, D, abdominal pain, decrease. appetite
what are oral antidiabetic drugs used for?
oral anti-diabetic drugs are used only for type 2 diabetes mellitus (T2DM(
they work by:
increasing insulin secretion
improving insulin sensitivity
decreasing glucose production
reducing glucose absorption
increasing glucose excretion
what is the MOA, indications, interactions, contraindications, and adverse effects of sulfonulureas?
MOA: stimulate pancreatic beta cells to release insulin by closing potassium channels
indications: type 2 DM (requires functioning beta cells)
drug/food interactions: alcohol → increased hypoglycemia risk, other antidiabetic which lead to additive hypoglycemia, beta blockers may mask hypoglycemia symptoms
contraindications: type 1 diabetes, diabetic ketoacidosis, several renal or level disease, sulfa allergy
adverse effects: hypoglycemia, weight gain, GI upset, rash
what is the MOA, indications, interactions, contraindications, and adverse effects of biguanides (metformin/glucophage)?
MOA: decrease hepatic glucose production, increases insulin sensitivity, decreases intestinal glucose absorption
indications: first-line therapy for T2DM
drug/food interactions: alcohol (increase lactic acidosis risk), contrast dye (hold metformin before/after imaging), and cimetidine (increased metformin levels)
contraindications: several renal impairment, metabolic acidosis, severe liver disease, alcohol abuse
adverse effects: N, D, metallic taste, vitamin B12 deficiency, and in rare cases: lactic acidosis
do we need to know how alpha-gluycosidase inhibitors, thiazolidinendiones, meglitinides, dipetidyl peptidsase 4 inhibitors, selective sodiyum glucose trnasportion 2 SGLT2, and fixed combination medication work?
what is the MOA, indications, interactions, contraindications, and advese effect of metformin (Glucophage, Glucophage XR)?
MOA: decreases intestinal absorption of glucose and improves insulin sensitivity and decrease hepatic glucose production
indicationsL control hyperglycemia in patients (including children) with T2DM
contraindications: renal and hepatic impairment, metabolic acidosis
interactions: fiber-rich foods, grapefruit juice, guar gum, psylliums, contrast dye, alcohol
adverse effects: dizziness, weakness, HA, hypoglycemia, palpitation, N, V, D, abdominal pain, vitamin B12 deficiency
patient taking metformin ten dot be deficient of what vitamin?
vitamin B12
what are the nursing consideration for metformin?
monitor for lactic acidosis - do not administer if the patient is to receive contrast within 4-48 hours and for 3-4 days after receiving dye
check BG often, especially receiving beta-blockers → BB can mask hypoglycemia symptoms
monitor patient A1c
what patient education should the nurse give for patient on metformin?
do not drink alcohol with metformin; can impair hepatic function
do not skip or double doses
may need to take vitamin B12
take with meals
why are oral antidiabetic drugs used for Type 2 diabetes but not Type 1 diabetes?
Type 1 diabetes is caused by autoimmune destruction of pancreatic beta cells, resulting in no insulin production. Most oral antidiabetic drugs require functioning beta cells or existing insulin to work.
Type 2 diabetes still has some insulin production and insulin resistance, so oral medications can improve insulin secretion and sensitivity.
Therefore, oral antidiabetic drugs are only effective in Type 2 diabetes.
what is glucagon and where is it produced?
hormone secreted by alpha cells in the islets of Langerhans in the pancreas
main function: increase blood glucose by stimulating glycogen breakdown (glycogenolysis) in the liver
how is glucagon administered and when does it peak?
Routes: Subcutaneous injection or nasal spray
Peak: ~15 minutes
Dosing: Based on age and weight
what drug interactions are associated with glucagon?
Can potentiate anticoagulant effects of warfarin if used repeatedly over several days
what is diazoxide and its mechanism of action? onset? duration?
Inhibits insulin release from the pancreas
Also acts as a vasodilator
onset: about 1 hour
duration: about 8 hours
Which insulin has the fastest onset?
A. Regular
B. NPH
C. Lispro
D. Glargine
C. Lispro
Which insulin has no peak?
A. Regular
B. NPH
C. Detemir
D. Lispro
C. Detemir
NPH insulin typically peaks at:
A. 1–2 hours
B. 4–12 hours
C. 12–24 hours
D. No peak
B. 4–12 hours (about 8 hours)
Which insulin should be given with meals?
A. Glargine
B. Detemir
C. Lispro
D. NPH
C. Lispro
Hypoglycemia is most likely during insulin’s:
A. Onset
B. Peak
C. Duration
D. Absorption
B. Peak
Semaglutide (Ozempic) works by:
A. Increasing insulin resistance
B. Slowing gastric emptying
C. Blocking glucose absorption
D. Stimulating glucagon
B. Slowing gastric emptying
Which adverse effect is common with GLP-1 agonists?
A. Hypoglycemia alone
B. Weight gain
C. GI upset
D. Bradycardia
C. GI upset
Sulfonylureas lower glucose by:
A. Increasing insulin secretion
B. Decreasing carb absorption
C. Blocking glucagon
D. Improving insulin sensitivity
A. Increasing insulin secretion
A major risk of sulfonylureas is:
A. Hyperglycemia
B. Hypoglycemia
C. Kidney stones
D. Lactic acidosis
B. Hypoglycemia - due to the increased insulin secretion
Metformin primarily:
A. Stimulates insulin release
B. Reduces hepatic glucose production
C. Causes hypoglycemia
D. Increases weight
B. Reduces hepatic glucose production by reducing glucagon secretion
Metformin should be held before:
A. Exercise
B. IV contrast studies
C. Meals
D. Bedtime
B. IV contrast studies
Lactic acidosis is a serious risk with:
A. Sulfonylureas
B. GLP-1 agonists
C. Metformin
D. Insulin
C. Metformin - it not only decrease hepatic glucose production but also produce lactates
Glucagon is used to treat:
A. Hyperglycemia
B. Hypoglycemia
C. DKA
D. Insulin resistance
B. Hypoglycemia
Diazoxide causes:
A. Insulin release
B. Insulin inhibition
C. Increased glucose uptake
D. Hypoglycemia
B. Insulin inhibition
After glucagon administration, the nurse should:
A. Keep patient NPO
B. Provide oral carbs once awake
C. Administer insulin
D. Monitor potassium only
B. Provide oral carbs once awake