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(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)
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)
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)
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
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.
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.
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).
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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