Glucose regulation 1

tx with insulin

goal is to restore normal glucose patterns

• mimic basal and peak endogenous levels

• minimize risk of hypoglycemia

insulin administration

SC(90% of patients)

• SC needle injections→ common sites: abdomen, upper outer thighs, buttocks

• portable pen injectors

• insulin pumps- basal and bolus delivery

• IV for critically IV patients

• remember drug administration rights + patient teaching

• measured in units=U aka IU=international units

• dose double checked by 2 RNs

rapid acting insulin

onset: 10-15 minutes

• peak 1-2 hr, 

• duration 3-5 hrs 

• given immediately before eating and matches meals 

• ideal for: meal-time bolus, patient eats right away(food tray ready) 

• not given IV

• can be used for insulin pumps

• dose per carbohydrate content→ because we are matching glucose

• check blood glucose(BG) 1-2 hr post 

drugs: Humalog, Novo rapid, Apidra, Fiasp(more aggressive, faster acting) 

•  “hungry ninjas act fast’

rapid acting insulin in pumps

• slow infusion of rapid acting insulin only into hypodermis(SC) over 24 hrs 

• provides basal insulin requirement coverage

• check BG pre-meal and 1-2 hours post meal

• meal time boluses are per carbohydrate content 

long acting insulin

onset 90 minutes, plateaus up to 24 hrs(min 12)

ideal for:

• background administration, 1-2x daily(consistency is important)

• never given IV

• need something to cover basal insulin

• adjust dose according to bedtime BG level→ patient should have snack before bedtime to avoid nighttime hypoglycemia 

drugs: Tresiba(ultra long acting), levemir, lantus,

“truly long lasting insulin”

short acting insulin(regular)

onset: 30 minutes 

• peak 2-3 hr

• duration 6.5 hrs(dose dependent)

ideal for:

• 30-45 mins before meal, make sure patient eats

• some issues with hypoglycemia and balancing dose with intake may arise

• used IV for ketoacidosis, new diagnosis, and stabilizing patient in hospital 

drugs: novloin ge Toronto, humulin R, Entuzity→ 5x more concentrated 

intermediate acting insulin

onset: 1-3 hrs

• peak: 5-8 hrs

• duration: up to 18 hrs(dose dependent)

ideal for: 

• background replacement(basal)

• if patient is on steroids, it can match sugar levels, must monitor for hypoglycemia(evening snack is important) 

• never given IV

drugs: Humulin N, Novolin ge NPH

pre-mixed injectable pens

benefits:

• decreases injection frequency 

• basal and peak insulin pre-mixed in one syringe 

• multiple doses per pen

• patient use, not for RN administration in most settings

hypergylcemia

high blood glucose(high osmolality/solute in the blood) causes cellular dehydration and polyuria

• causes overall dehydration

• shift of potassium out of cells to ECF→ excreted causing hypokalemia

• low cellular function

• metabolic shift and ketone accumulation can progress to diabetic ketoacidosis(DKA)→ tells us how long the glucose has been high

• tx: regular insulin, IV fluids

• KCL→ to correct K+ levels

• neutralize metabolic acidosis using sodium bicarbonate→ stabilizes metabolic acidosis, returns blood pH to normal but does not treat the underlying cause

hyperglycemia S&S,

signs and symptoms:

• high blood glucose 

• high urine ketones

• glucose in urine

• high serum lactate→ lactic acid measured metabolic acidosis

• changes in LOC, N&V, 

• kussmaul respirations 

• acetone(fruity) breath 

hypoglycemia

rapid onset of S&S such as:

• loss of focus(anxiety, irritability)

• nervousness

• shakiness

hypoglycemia causes and response protocol 

causes:

• diet change

• increase in activity

• too much insulin

• sign→ blood glucose <4 mmol/L

• for conscious patients→ give glucose PO, 15 g e.g. glucose tablets, honey, apple juice 

• unconscious→ give glucagon IM or D50W, IV 

• 15-15 rule: test blood glucose, eat/drink 15 grams of fast acting carbs, wait 15 minutes, test again 

hypoglycemia 15-15 rule

protocol to response to conscious person with hypoglycemia

1. test blood glucose

2. eat/drink 15 grams of fast acting carbs e.g. honey, chocolate

3. wait 15 minutes, then test again until blood glucose is >70 mg/dL(or 3.9 mmol/L)

4. as

paracrine

communication through extracellular fluid into adjacent tissue

hormones

communicate via bloodstream

glucose

one of the primary energy sources

• the brain requires a constant supply of glucose, cannot store it for later

• extra glucose is stored as glycogen in the liver and muscles and triglycerides(adipose cells)

• a fall in blood glucose will stimulate the breakdown of glycogen via glycogenolysis triggered by glucagon

• formation of glucose from other sources= glucogenesis 

fatty acids

distributed via lymph to circulation

• CNS and RBCs cannot use fatty acids 

• extra fatty acids are stored as triglycerides→ 3 fatty acids and glycerol 

• fatty acids are not converted into glucose and cannot be used by the brian 

• fatty acid metabolism in liver produces ketone metabolites 

ketones

acids produced by the liver as an alternative fuel source when the body doesn't have enough glucose (sugar) to burn for energy

insulin

pancreatic hormone synthesized in beta cells(langerhans)

• causes cellular glucose uptake→ amino acids and triglycerides cells will take in glucose

• promotes storage formation→ triglyceride, glycogen, and protein synthesis

• prevents the breakdown of glycogen and fat(in order to first use glucose) and protein lysis(to preserve tissue)

• c 

glucagon

synthesized by alpha cells

• opposite of insulin

• stimulates the breakdown of glycogen(glycogenolysis)

• stimulates gluconeogenesis(amino acid conversion into glucose) 

• lipolysis→ triglyceride breakdown 

• triggered by low blood glucose(hypoglycemia) to mobilize stores and replenish blood glucose for cellular use

how does the body respond to high blood glucose?

• beta cells stimulate the release of insulin

• cells take up glucose from blood

• liver produces glycogen

• blood glucose drops

how does the body respond to low blood glucose?

alpha cells will trigger the release of glucagon

• liver breaks down glycogen

• blood glucose rises

beta cells

the synthesis of insulin is triggered by high serum glucose

glucose enters pancreatic beta cell via glucose transporter 

• it is metabolized via glucokinase into ATP

• this closes K+ channels on beta cells 

• leads to depolarization→ causes insulin secretion

• insulin from pancreas enters hepatic circulation(50% 1st pass metabolized) 

insulin in action: binds to cellular membrane receptor(tyrosine kinase)→ activates kinase enzyme wihtin cell→ stimulates glucose transporter channels to open to glucose 

diabetes mellitus

diagnosed if fasting glucose is >7 mmol/L(normal is <6)

• total destruction of beta cells→ Insulin dependent diabetes mellitus(IDDM) 

• diagnosed before age 30 

• type 1A: genetic predisposition and triggering event(infection, trauma)

→immune reaction to beta cell antigens=autoimmune

• type 1B: idiopathic, rare 

• tx: insulin

• no treatment can cause diabetic ketoacidosis→ death 

endogenous insulin levels

• basal/ background insulin levels= 5-15 IU/m→ cruise control, provides continuous low levels of insulin

• peak level= 60-90 IU/mL→ surge/booster of insulin at meals

• tx with exogenous insulin: focuses on mimicking basal and peak insulin levels

guide for intensive insulin treatment

• estimated daily insulin requirement= (0.55 U) x (Pt. wt kg)

• insulin estimates do not factor in BMR or activity/stress→ food is the starting point

• approx 40% of insulin estimate= basal insulin

• other 60% estimate= boluses

bolus/peak and basal/background insulin dosage

bolus/peak insulin dosage is based on: pre-meal BG levels and carbohydrate content

basal insulin dosage based on: bedtime blood glucose level

• am administration os preferred to avoid nighttime hypoglycemia

• similar amount each day, as long as the bedtime BG is normal

• given even if the patient is NPO

BBIT

Alberta’s protocol for blood glucose monitoring and insulin administration

• B=Basal(long acting insulin) given in the morning 

• B=Bolus(short/rapid acting insulin) given at meals

• I=Insulin correction(short/rapid acting) if necessary(based on BG post-meal)

• T=Titrate doses to achieve glucose levels 4-8 mmol/L(monitor glucose throughout the day)

 

blood glucose checks are recommended:

• before each meal

• 1-2 hours after each meal

• at bedtime

• 4 times a day minimum 

• 8 times a day for newly diagnosed patient( pre+ post meals, bedtime, nighttime) 

carbohydrate counting

average of 45-60 g/meal

• carb total- fiber= total count

• 15 g of carbohydrate= 1 unit rapid acting 

• regular meals and snacks are key to steady BG→ use bedtime snack to avoid nighttime hypoglycemia

• diet in DM matters for accurate bolus dosing

insulin bolus

• rapid or short acting insulin given at meals(right before eating)→ 3x day

• check BG before administering and 1-2 hrs post meal(at peak action) 

• carb cunt for this meal to match carbohydrate content 

• remember: 1 IU insulin decreases BG by 2-5 mmol/L (on average 2.5 mmol/L)

sliding scales

guideline of blood glucose level results and insulin dose based on it

• e.g. for BG 6.1-8 mmol/L give 2 units of insulin

• commonly used in hospitals and rural settings