Pantoprazole Gastric acid Mechanism of Action Oral: Initial: 40 mg Administration: Flush IV line

(Pantoloc) suppression Proton pump inhibitor, suppresses gastric acid secretion by twice daily; before and after
inhibiting the parietal cell H+/K+ ATP pump administration with D5W,
Pharmacodynamics/Kinetics doses up to 240 mg NS, or LR
Onset of action: Acid secretion: Oral: 2.5 hours; IV: 15 to 30 daily have been
minutes administered
Maximum effect: IV: 2 hours
Absorption: Rapid, well absorbed IV: 80 mg every 12
Duration: Oral, IV: 24 hours hours;
Distribution: Adults: 11 to 23.6 L
Protein binding: 98%, primarily to albumin 160 to 240 mg daily
Metabolism: Extensively hepatic; CYP2C19 (demethylation), in divided doses has
CYP3A4; no evidence that metabolites have been used for a
pharmacologic activity limited period (up to
Bioavailability: ~77% 7 days
Half-life elimination:Adults: 1 hour; increased to 3.5 to 10
hours with CYP2C19 deficiency
Time to peak: Adults: Oral: 2.5 hours
Excretion: Urine (71% as metabolites); feces (18%);
pantoprazole clearance increased with weight and age
(Pettersen 2009)

Domperidone Upper Mechanism of Action Oral: 10 mg 3 times Administration: In GI motility

(Motilium) abdominal Domperidone has peripheral dopamine receptor blocking daily (maximum: 30 disorders, administer 15 to
pain properties and does not readily cross the blood-brain barrier. It mg/day). Use the 30 minutes prior to meals
increases esophageal peristalsis and increases lower lowest effective dose and at bedtime if needed.
esophageal sphincter pressure, increases gastric motility and for the shortest
peristalsis, and enhances gastroduodenal coordination, duration necessary. ADR: Central nervous
therefore, facilitating gastric emptying and decreasing small For gastroparesis, system: Headache (≤1%),
bowel transit time. the American College migraine (≤1%)
of Gastroenterology
Pharmacodynamics/Kinetics recommends
Protein binding: 93% initiating at 10 mg 3
Metabolism: Hepatic via CYP3A4, N-dealkylation and times daily (Camilleri
hydroxylation 2013).
Half-life elimination: 7 hours (increases to ~21 hours in severe
renal impairment)
Time to peak serum concentration: 30 minutes
Excretion: Feces (66%); urine (31%)

Fluconazole Treatment of Mechanism of Action

(Diflucan) oral fungal Interferes with fungal cytochrome P450 activity (lanosterol 14-
infections α-demethylase), decreasing ergosterol synthesis (principal
sterol in fungal cell membrane) and inhibiting cell membrane
formation

Pharmacodynamics/Kinetics
Absorption: Oral: Well absorbed; food does not affect extent of
absorption
Distribution: Vd: ~0.6 L/kg; widely throughout body with good
penetration into CSF, eye, peritoneal fluid, sputum, skin, and
urine
Relative diffusion blood into CSF: Adequate with or without
inflammation (exceeds usual MICs)
CSF:blood level ratio: Normal meninges: 50% to 90%;
Inflamed meninges: ~80%
Protein binding, plasma: 11% to 12%
Bioavailability: Oral: >90%
Half-life elimination: Normal renal function: ~30 hours (range:
20 to 50 hours); Elderly: 46.2 hours; Neonates (gestational
age 26 to 29 weeks): 73.6 to 46.6 hours (decreases with
increasing postnatal age); Pediatric patients 9 months to 15
years: 19.5 to 25 hours
Time to peak, serum: Oral: 1 to 2 hours
Excretion: Urine (80% as unchanged drug)

Potassium K = 3.0 Mechanism of Action Serum potassium Potassium must be diluted

chloride mmol/L Potassium is the major cation of intracellular fluid and is >2.5 to 3.5 mEq/L: prior to parenteral
syrup To increase essential for the conduction of nerve impulses in heart, brain, Maximum infusion administration. For IV
Potassium potassium and skeletal muscle; contraction of cardiac, skeletal and rate: 10 mEq/hour; infusion; do not administer
Chloride drip levels smooth muscles; maintenance of normal renal function, acid- maximum IV push.
base balance, carbohydrate metabolism, and gastric secretion concentration: 40
mEq/L; maximum 24- Adult: Some clinicians
Pharmacodynamics/Kinetics hour dose: 200 mEq recommend that the
Absorption: Well absorbed from upper GI tract maximum concentration for
Distribution: Enters cells via active transport from extracellular peripheral infusion is 10
fluid mEq/100 mL and maximum
Excretion: Primarily urine; skin and feces (small amounts); rate of administration for
most intestinal potassium reabsorbed peripheral infusion is 10
mEq/hour (Kraft 2005). ECG
monitoring is recommended
 for peripheral or central
infusions >10 mEq/hour in
adults (Kraft 2005). With
central line administration,
higher concentrations and
more rapid rates of infusion
may be used; concentrations
of 20 to 40 mEq/100 mL at a
maximum rate of 40
mEq/hour via central line
have been safely
administered (Hamill 1991;
Kruse 1990).

Lansoprazole For gastric Mechanism of Action Hypersecretory

(Prevacid acid Decreases acid secretion in gastric parietal cells through conditions:
FDT) suppression inhibition of (H+, K+)-ATPase enzyme system, blocking the Oral: Initial: 60 mg
final step in gastric acid production. once daily; adjust
dose based upon
Pharmacodynamics/Kinetics patient response and
Onset of action: Gastric acid suppression: Oral: 1 to 3 hours to reduce acid
Duration: Gastric acid suppression: Oral: >1 day secretion to <10
Absorption: Rapid mEq/hour (5
Distribution: Vd: Adults: 15.7 ± 1.9 L mEq/hour in patients
Protein binding: 97% with prior gastric
Metabolism: Hepatic via CYP2C19 and 3A4 to inactive surgery); doses of 90
metabolites, and in parietal cells to two active metabolites that mg twice daily have
are not present in systemic circulation been used;
Bioavailability: >80%; decreased 50% to 70% if given 30 administer doses
minutes after food >120 mg/day in
Half-life elimination: Adults: 1.5 ± 1 hour; Elderly: 1.9 to 2.9 divided doses
hours; Hepatic impairment: 4 to 7.2 hours
Time to peak, plasma: 1.7 hours
Excretion: Feces (67%); urine (33%; 14% to 25% as
metabolites and <1% as unchanged drug)
Clearance:
Adults: 11.1 ± 3.8 L/hour; Hepatic impairment: 3.2 to 7.2 hours

Vidagliptin + For high Mechanism of Action Vildagliptin 100

Meformin blood sugar Vildagliptin inhibits dipeptidyl peptidase IV (DPP-IV) enzymes mg/day plus current
(Galvusmet) resulting in prolonged active incretion levels. Incretin daily dose of
hormones [eg, glucagon-like peptide-1 (GLP-1) and glucose- metformin given in 2
dependent insulinotropic polypeptide (GIP)] regulate glucose equally divided
homeostasis by increasing insulin synthesis and release from doses..
pancreatic beta cells and decreasing glucagon secretion from
pancreatic alpha cells. Decreased glucagon secretion results
in decreased hepatic glucose production. Under normal
physiologic circumstances, incretin hormones are released by
the intestine throughout the day and levels are increased in
response to a meal; incretin hormones are rapidly inactivated
by DPP-IV enzymes.
Metformin decreases hepatic glucose production, decreasing
intestinal absorption of glucose, and improves insulin
sensitivity (increases peripheral glucose uptake and
utilization).
Vildagliptin:
Pharmacodynamics/Kinetics
Duration: >50% DPP-IV inhibition: ~14 hours (He 2007, He
2012)
Absorption: Rapid
Distribution: Vd: 71 L
Protein binding: 9.3%
Metabolism: 69% of the dose is metabolized (57%
hydrolyzed to a single inactive metabolite); not
metabolized by CYP450 enzymes
Bioavailability: 85%
Half-life elimination: ~3 hours
Time to peak: 1.7 hours (fasted); 2.5 hours (fed)
Excretion: Urine (85%, 23% as unchanged drug); feces
(15%)

Metformin:
Pharmacodynamics/Kinetics
Onset of action: Within days; maximum effects up to 2
weeks
Distribution: Vd: 654 ± 358 L; partitions into erythrocytes;
concentrates in liver, kidney, and GI tract
Protein binding: Negligible
Metabolism: Not metabolized by the liver
Bioavailability: Absolute: Fasting: 50% to 60%
Half-life elimination: Plasma: 4 to 9 hours; Blood ~17.6
hours
Time to peak, serum: Immediate release: 2 to 3 hours;
 Extended release: 7 hours (range: 4 to 8 hours)
Excretion: Urine (90% as unchanged drug; active
secretion)

Magnesium To neutralize Mechanism of Action Antacid (dosage in Administration: Oral

oxide (GNC) stomach acid Magnesium is important as a cofactor in many enzymatic terms of magnesium Administer at least 2 hours
reactions in the body involving protein synthesis and oxide salt): Oral: One apart from other
carbohydrate metabolism (at least 300 enzymatic reactions tablet (400 mg) twice medications.
require magnesium). Actions on lipoprotein lipase have been daily; maximum: 2 Dietary Considerations
found to be important in reducing serum cholesterol and on tablets (800 mg)/24 Should be taken with food
sodium/potassium ATPase in promoting polarization (eg, hours and at least 8 oz of water.
neuromuscular functioning). Whole grains, legumes, and
Pharmacodynamics/Kinetics dark-green leafy vegetables
Absorption: Oral: Up to 30% are dietary sources of
Excretion: Urine (IOM 1997); feces (as unabsorbed drug) magnesium.

Tramadol For pain Mechanism of Action IV, IM [International Injection [International

(Tramal) management Tramadol and its active metabolite (M1) binds to μ-opiate product]: Usual product]: May be
receptors in the CNS causing inhibition of ascending pain range: 50 to 100 mg administered by slow IV
pathways, altering the perception of and response to pain; every 4 to 6 hours injection over 2 to 3 minutes
also inhibits the reuptake of norepinephrine and serotonin, (maximum: 600 or further diluted and
which are neurotransmitters involved in the descending mg/day) administered as an IV
inhibitory pain pathway responsible for pain relief (Grond infusion.
2004)
Pharmacodynamics/Kinetics
Onset of action: Immediate release: Within 1 hour; Peak
effect: 2 to 3 hours
Distribution: Vd: IV: 2.6 L/kg (males); 2.9 L/kg (females)
Protein binding, plasma: ~20%
Metabolism: Extensively hepatic via demethylation (mediated
by CYP3A4 and CYP2D6), glucuronidation, and sulfation; has
pharmacologically active metabolite formed by CYP2D6 (M1;
O-desmethyl tramadol)
Excretion: Urine (~30% as unchanged drug; 60% as
metabolites)

Metoclopromi For gastric Mechanism of Action Diabetic Administration: IV

de (Vitamet) acid Blocks dopamine receptors and (when given in higher doses) gastroparesis. Injection solution may be
suppression also blocks serotonin receptors in chemoreceptor trigger zone IM, IV (for severe given direct IV push, short
of the CNS; enhances the response to acetylcholine of tissue symptoms): 10 mg infusion (15 minutes), or
in upper GI tract causing enhanced motility and accelerated over 1 to 2 minutes continuous infusion; lower
gastric emptying without stimulating gastric, biliary, or doses (≤10 mg) of
pancreatic secretions; increases lower esophageal sphincter metoclopramide can be
tone given IV push undiluted over
Pharmacodynamics/Kinetics 1 to 2 minutes; higher doses
Onset of action: IV: 1 to 3 minutes; IM: 10 to 15 minutes (>10 mg) to be diluted in 50
Duration: Therapeutic: 1 to 2 hours, regardless of route mL of compatible solution
Absorption: Oral: Rapid, well absorbed (preferably NS) and given
Distribution: Vd: Adults: ~3.5 L/kg IVPB over at least 15
Protein binding: ~30% minutes.
Half-life elimination: Adults: 5 to 6 hours (may be dose Note: Rapid IV
dependent) administration may be
Time to peak, serum: Adults: 1 to 2 hours associated with a transient
Excretion: Urine (~85%); feces (but intense) feeling of
anxiety and restlessness,
followed by drowsiness.

Cefazidin Prophylaxis Mechanism of Action: Inhibits bacterial cell wall synthesis by Usual dosage range: Administration: IVInject
(Stancef) prior to GI binding to one or more of the penicillin-binding proteins IM, IV: 1 to 1.5 g direct IV over 3 to 5 minutes
procedure (PBPs) which in turn inhibits the final transpeptidation step of every 8 hours, or may infuse as an
peptidoglycan synthesis in bacterial cell walls, thus inhibiting depending on intermittent infusion over 30
cell wall biosynthesis. Bacteria eventually lyse due to ongoing severity of infection; to 60 minutes.
activity of cell wall autolytic enzymes (autolysins and murein maximum: 12 g daily
hydrolases) while cell wall assembly is arrested. Store intact vials at room
temperature and protect
Pharmacodynamics/Kinetics from temperatures
Distribution: Widely into most body tissues and fluids including exceeding 40°C.
gallbladder, liver, kidneys, bone, sputum, bile, pleural, and Reconstituted solutions of
synovial; CSF penetration is poor cefazolin are light yellow to
Protein binding: 80% (Marshall 1999)
Half-life elimination: IM or IV: Neonates: 3 to 5 hours; Adults: yellow. Protection from light
1.8 hours (IV); ~2 hours (IM) (prolonged with renal is recommended for the
impairment) powder and for the
Time to peak, serum: IM: 0.5 to 2 hours; IV: Within 5 minutes reconstituted solutions.
Excretion: Urine (70% to 80% as unchanged drug) Reconstituted solutions are
stable for 24 hours at room
temperature and for 10 days
under refrigeration. Stability
 of parenteral admixture in
D5W, D5LR, D51/4NS,
D51/2NS, D5NS, D10W, LR,
or NS at room temperature
(25°C) is 48 hours. Stability
of parenteral admixture at
refrigeration temperature
(4°C) is 14 days.

Paracetamol For Mechanism of ActionAlthough not fully elucidated, the IV ≥50 kg: 650 mg Administration: IVInjection:
(Naprex) headache analgesic effects are believed to be due to activation of every 4 hours or For IV infusion only.
descending serotonergic inhibitory pathways in the CNS. 1,000 mg every 6 Administer undiluted over 15
Interactions with other nociceptive systems may be involved hours; maximum minutes.
as well (Smith 2009). Antipyresis is produced from inhibition of single dose: 1,000 For 1,000 mg doses (≥50
the hypothalamic heat-regulating center. mg/dose; maximum kg): Insert a vented IV set
Pharmacodynamics/Kinetics daily dose: 4 g/day through vial stopper or a
Note: With the exception of half-life, the pharmacokinetic non-vented IV set through
profile in pediatric patients (0-18 years) is similar to adult the administration spike port
patients. of the bag.
Onset of action: Storage/Stability
Oral: <1 hour Injection: Store intact vials
IV: Analgesia: 5 to 10 minutes; Antipyretic: Within 30 minutes and bags at 20°C to 25°C
Peak effect: IV: Analgesic: 1 hour (68°F to 77°F); do not
Duration: refrigerate or freeze. Use
IV, Oral: Analgesia: 4 to 6 hours within 6 hours of penetrating
IV: Antipyretic: ≥6 hours vial/bag or transferring to
Absorption: Primarily absorbed in small intestine (rate of another container. Discard
absorption dependent upon gastric emptying); minimal any unused portion.
absorption from stomach; varies by dosage form
Distribution: ~1 L/kg at therapeutic doses
Protein binding: 10% to 25% at therapeutic concentrations;
8% to 43% at toxic concentrations
Metabolism: At normal therapeutic dosages, primarily hepatic
metabolism to sulfate and glucuronide conjugates, while a
small amount is metabolized by CYP2E1 to a highly reactive
intermediate, N-acetyl-p-benzoquinone imine (NAPQI), which
is conjugated rapidly with glutathione and inactivated to
nontoxic cysteine and mercapturic acid conjugates. At toxic
doses (as little as 4 g daily) glutathione conjugation becomes
insufficient to meet the metabolic demand causing an increase
in NAPQI concentrations, which may cause hepatic cell
necrosis. Oral administration is subject to first pass
metabolism.
Half-life elimination: Prolonged following toxic doses
Neonates: 7 hours (range: 4 to 10 hours)
Infants: ~4 hours (range: 1 to 7 hours)
Children: 3 hours (range: 2 to 5 hours)
Adolescents: ~3 hours (range: 2 to 4 hours)
Adults: ~2 hours (range: 2 to 3 hours); may be slightly
prolonged in severe renal insufficiency (CrCl<30 mL/minute):
2 to 5.3 hours
Time to peak, serum: Oral: Immediate release: 10 to 60
minutes (may be delayed in acute overdoses); IV: 15 minutes
Excretion: Urine (<5% unchanged; 60% to 80% as
glucuronide metabolites; 20% to 30% as sulphate metabolites;
~8% cysteine and mercapturic acid metabolites)

PNSS For hydration Mechanism of Action Principal extracellular cation; functions Cl maintenance Administration: IV
in fluid and electrolyte balance, osmotic pressure control, and electrolyte >2% solutions:
water distribution requirement in Administration through a
Pharmacodynamics/Kinetics central line is recommended
parenteral nutrition:
Absorption: Oral: Rapid due to high osmolarity and
Distribution: Widely distributed IV: As needed to tonicity (Mortimer, 2006).
Excretion: Primarily urine; also sweat, tears, saliva maintain acid-base Consult individual
balance with institutional policies and
parenteral nutrition; procedures.
use equal amounts 3% solution: Osmolarity:
of chloride and 1027 mOsm/L; sodium
content: 513 mEq/L
acetate to maintain
Vesicant at higher
balance and adjust concentrations (>1%);
ratio based on ensure proper needle or
individual patient catheter placement prior to
needs and during infusion; avoid
extravasation.
Na maintenance
electrolyte
requirement in
parenteral nutrition:
IV: 1-2 mEq/kg/24
hours; customize
 amounts based on
individual patient
needs

D5W For hydration Mechanism of ActionDextrose, a monosaccharide, is a Administration:

source of calories and fluid for patients unable to obtain an IVInjectable is not for SubQ
adequate oral intake; may decrease body protein and nitrogen or IM administration;
losses; promotes glycogen deposition in the liver. When used concentrated dextrose
in the treatment of hyperkalemia (combined with insulin), solutions for peripheral
dextrose stimulates the transient uptake of potassium by cells, venous administration must
especially in muscle tissue, lowering serum potassium. be diluted (maximum
Pharmacodynamics/Kinetics concentration: 12.5%); in
Onset of action: Treatment of hypoglycemia: Oral: 10 minutes emergency situations only,
Maximum effect: Treatment of hyperkalemia: IV: 30 minutes 25% and 50% dextrose have
Absorption: Oral: Rapidly from the small intestine by an active been used peripherally; for
mechanism direct IV infusion, infuse at a
Metabolism: Metabolized to carbon dioxide and water maximum rate of 200 mg/kg
Time to peak, serum: Oral: 40 minutes over 1 minute; continuous
infusion rates vary with
tolerance and range from 4.5
to 15 mg/kg/minute;
hyperinsulinemic neonates
may require up to 15 to 25
mg/kg/minute infusion rates.
Refer to indication-specific
infusion rates in dosing for
detailed recommendations.
Vesicant (at concentrations
≥10%); ensure proper
needle or catheter
placement prior to and
during IV infusion. Avoid
extravasation.

Combiflex For poor oral Combiflex Lipid Peri Infusion works by providing energy and Adult & childn >10 Contraindications
1400 kcal intake and support to the body's cell wall; moisturizing and softening the yr 27-40 mL/kg/day Severe hyperlipidaemia.
dysphagia affected area; promoting protein synthesis and wound healing; Hyperglycemia not
replacing electrolytes in the body; increasing the blood sugar responding to insulin doses
level; >6 u/hr. Metabolic acidosis;
Pharmacokinetics: Distribution: Amino acids acute pulmonary edema,
(Combiflex Lipid Peri) administered orally are promptly decompensated cardiac
distributed and used via the same pathway as internal insufficiency.
Amino acids (Combiflex Lipid Peri). Absorption: When
Amino acids (Combiflex Lipid Peri) are administered
orally, each amino acid is absorbed via its transporter
in small intestine. Metabolism: Each amino acid is
pooled and can be used as substrates for synthesis of
protein and bioactive substances. On the other hand,
deaminated Amino acids (Combiflex Lipid Peri) enter
TCA cycle, gluconeogenesis or biosynthesis of fatty
acids as energy substrate. Nitrogen in Amino acids
(Combiflex Lipid Peri) decomposes into urea in urea
cycle. Excretion: The carbon skeleton in each amino
acid could be decomposed into carbon dioxide and
water. Carbon dioxide could be excreted into
expiration. Nitrogen could be excreted into urine as
urea or ammonia.

Hexetidine For surgical Mechanism of ActionHexetidine is a broad spectrum Oral antiseptic:

(Bactidol) prophylaxis antimicrobial with activity against gram positive and gram Oral: Rinse mouth or
negative bacteria, yeasts (Candida albicans), and fungi. gargle with at least
Pharmacodynamics/KineticsDuration of action: Retention 15 mL of undiluted
on buccal tissues: 8 to 10 hours after single oral rinse solution 2 to 3 times
daily, then spit; do
not swallow.

Benzydamine Oral care Mechanism of ActionNonsteroidal anti-inflammatory drug; Oral rinse: 15 mL Oral rinse: Patient should
HCl (Difflam- (prevention inhibits production of proinflammatory cytokines to reduce (undiluted solution) not swallow the liquid. If
C) of oral local pain and inflammation (Lalla, 2014). Also has local as a gargle or rinse 3 local irritation or burning
mouthwash candidiasis) anesthetic activity. or 4 times daily sensation occurs, dilute 1:1
Pharmacodynamics/Kinetics (depending on in lukewarm water.
Absorption: Oral rinse may result in some absorption through mucositis severity);
oral mucosa contact with inflamed
Time to peak: 2 hours mucosa should be
Excretion: Urine (primarily as unchanged drug) maintained for at
least 30 seconds,
followed by expulsion
from the mouth.
Begin the day before
radiation therapy,
continue during
 radiation therapy,
and after until
satisfactory
improvement occurs.

Povidone Oral care Mechanism of Action Povidone-iodine is known to be a

Iodine (prevention powerful broad spectrum germicidal agent effective against a
(Betadine) of oral wide range of bacteria, viruses, fungi, protozoa, and spores.
throat spray candidiasis) Pharmacodynamics/KineticsAbsorption: Absorbed
systemically as iodine; amount depends upon concentration,
route of administration, characteristics of skin

Insulin For high Mechanism of ActionInsulin acts via specific membrane- Diabetes mellitus, Insulin glulisine should be
Glulisine blood sugar bound receptors on target tissues to regulate metabolism of type 2: SubQ: administered within 15
(Apidra) carbohydrate, protein, and fats. Target organs for insulin Off-label: minutes before or within 20
include the liver, skeletal muscle, and adipose tissue. Initial: 4 units or 0.1 minutes after starting a
Within the liver, insulin stimulates hepatic glycogen synthesis. unit/kg or 10% of the meal. Cold injections should
Insulin promotes hepatic synthesis of fatty acids, which are be avoided. SubQ
basal insulin dose;
released into the circulation as lipoproteins. Skeletal muscle administration is usually
effects of insulin include increased protein synthesis and insulin glulisine (ie, a made into the thighs, arms,
increased glycogen synthesis. Within adipose tissue, insulin rapid acting insulin) buttocks, or abdomen; rotate
stimulates the processing of circulating lipoproteins to provide is administered injection sites within the
free fatty acids, facilitating triglyceride synthesis and storage before the largest same region to avoid
by adipocytes; also directly inhibits the hydrolysis of meal of the day and lipodystrophy. Insulin
triglycerides. In addition, insulin stimulates the cellular uptake is usually given in glulisine from a vial may be
of amino acids and increases cellular permeability to several mixed with insulin NPH only
addition to a regimen
ions, including potassium, magnesium, and phosphate. By (do not mix with other types
activating sodium-potassium ATPases, insulin promotes the that includes basal of insulin); insulin glulisine
intracellular movement of potassium. insulin (ie, a long- should be drawn into syringe
Normally secreted by the pancreas, insulin products are acting insulin such as first. Do not mix other insulin
manufactured for pharmacologic use through recombinant glargine, degludec, formulations with insulin
DNA technology using either E. coli or Saccharomyces or detemir) and glulisine contained in a
cerevisiae. Insulin glulisine differs from human insulin by metformin +/- other cartridge or prefilled pen.
containing a lysine and glutamic acid at positions B3 and B29,
noninsulin agents. If
respectively, in comparison to the asparagine and lysine found
at B3 and B29 in human insulin. Insulins are categorized HbA1c is still not
based on the onset, peak, and duration of effect (eg, rapid-, controlled despite
short-, intermediate-, and long-acting insulin). Insulin glulisine titrations to reach
is a rapid-acting insulin analog. glycemic targets, one
Pharmacodynamics/KineticsNote: Onset and duration of option is to advance
hypoglycemic effects depend upon the route of administration to ‘basal-bolus’ (ie,
(absorption and onset of action are more rapid after deeper IM
insulin glulisine
injections than after SubQ), site of injection (onset and
duration are progressively slower with SubQ injection into the administered before
abdomen, arm, buttock, or thigh respectively), volume and ≥2 meals per day) in
concentration of injection, and the preparation administered. addition to basal
Rate of absorption, onset, and duration of activity may be insulin and usually
affected by exercise, presence of lipodystrophy, local blood given in addition to
supply, and/or temperature. metformin +/- other
Onset of action: 0.2-0.5 hours
noninsulin agent
Peak effect: 1.6-2.8 hours
Duration: 3-4 hours (ADA 2017f)
Distribution: IV: 13 L Dosage adjustment:
Bioavailability: SubQ: ~70% To reach self-
Half-life elimination: monitoring glucose
IV: 13 minutes target: Adjust dose
SubQ: 42 minutes by 10% to 15% or 1
Time to peak, plasma: 60 minutes (range: 40-120 minutes) to 2 units; may adjust
Excretion: Urine at weekly or twice
weekly intervals
(ADA 2017f)
For hypoglycemia: If
no clear reason for
hypoglycemia,
decrease dose by 2
to 4 units or by 10%
to 20% (ADA 2017f)
General
considerations for
insulin use in type 2
diabetes:
Timing of initiation:
Dual therapy
(metformin + a
second
antihyperglycemic
agent) and then triple
therapy (metformin +
two
antihyperglycemic
agents) is
recommended in
patients who fail to
achieve glycemic
goals after ~3
months with lifestyle
intervention and
metformin
monotherapy or dual
therapy, respectively
(unless
contraindications to
metformin exist).
Preference is not
given for which
agent(s) should be
added to metformin
(drug choice should
be individualized
based on patient
characteristics). If
HbA1c target not
achieved after ~3
months of triple
therapy, consider
initiating basal insulin
(usually with
metformin +/- other
noninsulin agent) or
if patient already
receiving an
optimally titrated
basal insulin (ie, a
long-acting insulin
such as glargine,
degludec, or detemir)
as part of their
regimen, consider
combination
injectable therapy
(ADA 2017f).
Combination
injectable therapy: If
HbA1c target has not
been met with basal
insulin (ie, long-
acting insulin such as
glargine, degludec or
detemir) (usually
combined with
metformin +/- other
noninsulin agent),
despite titrating basal
insulin to provide
acceptable fasting
blood glucose
concentrations,
combination
injectable therapy
should be
considered. Options
include: adding a
rapid-acting insulin
(eg, lispro, aspart,
glulisine) prior to
largest meal or
adding a GLP-1
receptor agonist or
changing from basal
insulin to a twice
daily premixed
insulin. If HbA1c still
not adequately
controlled, consider
advancing from one
 rapid-acting insulin
prior to largest meal
to ‘basal-bolus’
regimen (ie, rapid-
acting insulin
administered before
≥2 meals) or
consider advancing
from a twice daily
premixed insulin to a
three times daily
premixed insulin
(ADA 2017f).
Patients with
elevated HbA1C at
therapy initiation: If
HbA1c is ≥9% at
initiation of therapy,
dual therapy
(metformin + a
second
antihyperglycemic
agent) should be
considered. If HbA1c
≥10%, blood glucose
is ≥300 mg/dL or if
patient is
symptomatic (eg,
polyuria, polydipsia),
insulin therapy (with
or without additional
agents) should be
considered (ADA
2017f).

Insulin For high Mechanism of Action Initial basal insulin Administration:

Glargine blood sugar dose: 0.2 units/kg Subcutaneous
(Toujeo) Insulin acts via specific membrane-bound receptors on target once daily; for Lantus
tissues to regulate metabolism of carbohydrate, protein, and or Basaglar, up to 10
fats. Target organs for insulin include the liver, skeletal Insulin glargine should be
units/day initially is
muscle, and adipose tissue.Within the liver, insulin stimulates administered once daily, at
recommended.
hepatic glycogen synthesis. Insulin promotes hepatic any time of day; however,
Adjust dosage
synthesis of fatty acids, which are released into the circulation administer at the same time
according to patient
as lipoproteins. Skeletal muscle effects of insulin include each day. Cold injections
response
increased protein synthesis and increased glycogen should be avoided. SubQ
synthesis. Within adipose tissue, insulin stimulates the administration is usually
processing of circulating lipoproteins to provide free fatty made into the thighs, arms,
acids, facilitating triglyceride synthesis and storage by General buttocks, or abdomen; rotate
adipocytes; also directly inhibits the hydrolysis of triglycerides. considerations for injection sites within the
In addition, insulin stimulates the cellular uptake of amino insulin use in type 2 same region to avoid
acids and increases cellular permeability to several ions, diabetes (off-label): lipodystrophy.
including potassium, magnesium, and phosphate. By
activating sodium-potassium ATPases, insulin promotes the Timing
intracellular movement of potassium.Normally secreted by the of initiation: Dual
pancreas, insulin products are manufactured for therapy (metformin +
pharmacologic use through recombinant DNA technology a second
using either E. coli or Saccharomyces cerevisiae. Insulin antihyperglycemic
glargine differs from human insulin by adding two arginines to agent) and then triple
the C-terminus of the B-chain in addition to containing glycine therapy (metformin +
at position A21 in comparison to the asparagine found in two
human insulin. Insulins are categorized based on the onset, antihyperglycemic
peak, and duration of effect (eg, rapid-, short-, intermediate-, agents) is
and long-acting insulin). Insulin glargine is a long-acting recommended in
insulin analog. patients who fail to
Pharmacodynamics/Kinetics achieve glycemic
goals after ~3
months with lifestyle
Note: Onset and duration of hypoglycemic effects depend intervention and
upon the route of administration (adsorption and onset of metformin
action are more rapid after deeper IM injections than after monotherapy or dual
SubQ), site of injection (onset and duration are progressively therapy, respectively
slower with SubQ injection into the abdomen, arm, buttock, or (unless
thigh respectively), volume and concentration of injection, and contraindications to
the preparation administered. Rate of absorption, onset, and metformin exist).
duration of activity may be affected by exercise, presence of Preference is not
lipodystrophy, local blood supply, and/or temperature. given for which
agent(s) should be
added to metformin
 (drug choice should
Onset of action: Lantus: 3 to 4 hours; Toujeo: 6 hours be individualized
based on patient
characteristics). If
HbA1c target not
Peak effect: Lantus, Basaglar: No pronounced peak achieved after ~3
months of triple
Duration: Lantus, Basaglar: Generally 24 hours or longer; therapy, consider
reported range (Lantus): 10.8 to >24 hours (up to ~30 initiating basal insulin
hours documented in some studies) (Heinemann 2000) (usually with
metformin +/- other
noninsulin agent) or
Absorption: Slow; upon injection into the subcutaneous tissue, if patient already
microprecipitates form which allow small amounts of receiving an
insulin glargine to release over time optimally
titrated basal insulin
Metabolism: Partially metabolized in the subcutaneous depot (ie, a long-acting
at the carboxyl terminus of the B chain to form two insulin such as
active metabolites, M1 (21A-Gly-insulin) and M2 (21A- glargine, degludec,
Gly-des-30B-Thr-insulin) or detemir) as part of
their regimen,
consider combination
Time to peak, plasma: Lantus: No pronounced peak; injectable therapy
(ADA 2017f).
Basaglar: ~12 hours
Combination
Excretion: Urine injectable therapy: If
HbA1c target has not
been met
with basal insulin (ie,
long-acting insulin
such as glargine,
degludec or detemir)
(usually combined
with metformin +/-
other noninsulin
agent), despite
titrating basal insulin
to provide acceptable
fasting blood glucose
concentrations,
combination
injectable therapy
should be
considered. Options
include: adding a
rapid-acting insulin
(eg, lispro, aspart,
glulisine) prior to
largest
meal or adding a
GLP-1 receptor
agonist or changing
from basal insulin to
a twice daily
premixed insulin. If
HbA1c still not
adequately
controlled, consider
advancing from one
rapid-acting insulin
prior to largest meal
to ‘basal-bolus’
regimen (ie, rapid-
acting insulin
administered before
≥2
meals) or consider
advancing from a
twice daily premixed
insulin to a 3 times
daily premixed
insulin (ADA 2017f).

Patients
with elevated
HbA1C at therapy
initiation: If HbA1c is
≥9% at initiation of
therapy, dual therapy
(metformin + a
second
 antihyperglycemic
agent) should be
considered. If
HbA1c ≥10%, blood
glucose is ≥300
mg/dL or if patient is
symptomatic (eg,
polyuria, polydipsia),
insulin therapy (with
or without additional
agents) should be
considered (ADA
2017f).

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