1. Wound Management
a. Differentiate different types of wounds
i. Pressure injuries
1. Localized damage to skin or underlying issues
a. Usually over bony Prominence
b. Intense or prolonged pressure
i. Heel & sacrum are the most common
1. Aging, poor nutrition, low BP, hydration
status
2. Stage 1:
a. Non-blanchable (SKIN INTACT), erythema of skin
b. Changes in sensation, temp, firmness
3. Stage 2:
a. Partial thickness skin loss with exposed dermis
i. Would will be shallow and open
b. Wound bed is visible, pink/ red, moist
c. Important to note location and how it happened, don’t
mix up with incontinence/ abrasion
i. Get proper dressing on, may have to get wound
care onboard
4. Stage 3:
a. Full thickness skill loss
b. Wound depth varies by location
c. You should not see any muscle, bone, tendons
5. Stage 4:
a. Full thickness, skin/ tissue loss
b. May have exposed muscle, bone, tendons
i. Risk for osteomyelitis
6. Pressure injury on the mouth/lips **DO NOT STAGE**
7. Suspected Deep Tissue Injury*****
a. Purple or maroon localized area of discolored intact skin/
blood filled blister
b. If you think you might have DTI, report it, especially on
admission of new pts
8. Unstageable
a. Unable to see/tell due to necrotic tissue and eschar.
Requires debridement for staging
9. Medical device-related pressure injuries (MDRPIs)
a. Medical devices that can cause pressure injuries include
nasal cannulas, NG tubes, foley tubing…
10. Mucosal Membrane Pressure Injury
a. Found on mucous membranes from medical device
b. Don’t stage
11. Surgical incisionsa. Sometimes has drains such as JP, biliary drain, suprapubic
catheter, etc. often protected with split gauze
b. Other: tracheostomy, colostomy, chest tubes…
c. Sometimes incisions are closed with dermabond, steri
strips, sutures, staples, etc.
2. Understand wound healing processes
a. Healing Process:
i. Healing- final phase of the inflammatory resposne
ii. Two major components:
1. Regeneration- replacement of lost cells and tissues
2. Repair- most common, usually results in scar formation
iii. Types of Wound Healing:
1. Primary intentiona. Wound that is closed, wound edges approximated
i. Surgical incision, sutured/ stapled
b. Fine scar
2. Secondary intentiona. Wound that occur from trauma, stage 2 PI, infection, any
that have extensive tissue loss. Cannot approximate
wound edges
b. Granulation tissue fills in wound
c. Large scar
d. May need debridement
3. Tertiary intentiona. Delayed primary intention due to delayed suturing of the
wound
b. Contaminated wound left open or primary wound
becomes infected and is opened; after the infection is
controlled it is sutured
c. Large deeper scar
b. Complications of Healing:
i. Adhesions1. Bands of scar tissue
a. Develops around organs
ii. Contractions1. Excessive fibrous tissue formation
a. Can cause severe deformities, shortening of muscle and
scar tissue that can limit movement and ROM
iii. Dehiscence1. Separation of wound edges
a. Must keep an eye especially for abdominal surgeries
b. Can happen from force, hard cough
c. Splinting is important, educate patient
c. Eviscerationi. Intestines protrude through a dehiscence
1. Need help right away, RRT, cover with moist sterile covering
d. Excess granulation tissuei. Growing extra tissue
e. Fistulai. Abnormal passage between organs or organs and skin
f. Hemorrhagei. Internal or external blood loss
g. Keloid scarsi. Mass of scar tissue appears tumor like
h. Infectioni. Local signs: erythema, increased drainage, change in drainage, pain,
fever, increase in WBC
i. Factors that Delay Healing
i. Nutritional deficiencies
ii. Inadequate blood supply
iii. Corticosteroids
iv. Infection
v. Smoking
vi. Mechanical friction
vii. Advanced age
viii. Obesity
ix. Poor general health
x. Excessive moisture: diaphoresis, incontinence
xi. Immobility
xii. Altered mental status
xiii. Prolonged fever, infection
xiv. Edema
xv. Age - slowed collagen synthesis, impaired circulation
xvi. Chronic illnesses - DM, anemia
3. Learn various dressing and treatments for wounds
a. Antimicrobiali. CAUTION- can damage new epithelial tissue
ii. Used on- partial/ full thickness wounds (check orders)
iii. Should be followed by saline rinse
b. Hydrocolloid- Autolytic
i. Does not interfere with wound healing
ii. Supports debridement and prevents infection
iii. Creates moist healing environment
iv. “melts” as dressing absorbs
c.
d.
e.
f.
g.
h.
v. Does not allow O2 to enter wound
1. Not for infected wounds
Hydrogeli. Non-adherent
ii. Keeps wound moist- can rehydrate
iii. Not a good bacterial barrier
iv. Used for chronic wounds
v. Debridement (autolytic)
vi. Cooling effect
Aquacel- Ag
i. Silver kills wound bacteria
ii. Absorbs high amounts of fluid and bacteria
iii. Creates cohesive gel that conforms to wound
iv. Moist wound healing environment and control of bacteria
Alginatei. Derived from seaweed/kelp
ii. Forms a nonstick gel
iii. Twisted fiber ropes/ sponge-type material
iv. Non adherent
v. Requires secondary dressing
vi. Fibers absorb large amounts of exudate and form a gel
vii. Provides moist environment, but not soaking
Filmi. Non-absorbent
ii. Exudate will pool underneath
iii. Exudate may break the seal
iv. Used for superficial wounds, skin tears
v. Used as a retention over dressing
vi. Prevents friction damage
Foamsi. Mepilex
ii. Used for deep, heavily draining wounds
iii. Chronic wounds
iv. Used to prevent pressure ulcers
Treatments for wounds
i. Clean wounds1. Closure devices- adhesive strips (steri-strips)
2. Sutures- staples and tissue adhesives
3. Dressings- keep wound surface clean and slightly moist
a. Topical antimicrobials & antibactericidals can damage new
epithelium
ii. Contaminated wounds1. Must be cleaned for healing to occur
2. Debridement may be necessary
i.
a. Surgical, mechanical, autolytic, enzymatic
b. ESCHAR must be surgically removed
3. Absorptive or hydrocolloid dressing may be used
a. Absorb exudate
b. Clean the wound surface
iii. Cleaning Solutions1. Clean with noncytotoxic solutions
a. Normal saline
2. If irrigation is ordered, pressure is needed
a. 35 mL syringe and 19-gauge angiocatheter or tip
3. DO NOT ALLOW WOUND TO DRY
iv. Debridement:
1. If wound is dirty- must convert to clean before healing can begin
a. When Debridement is necessaryi. Autolytic
ii. Enzymatic
iii. Mechanical
iv. Surgical
v. Wound vac
1. Vacuum source creates continuous or intermittent negative
pressure
2. Uses suction to remove drainage and speed wound healing.
Removes fluid, exudate, and infectious materials
3. Exact patho- unknown
a. Thought to remove excess fluid, reduce bateria, and
encourage blood flow
vi. Hyperbaric oxygen therapy
1. Increases O2 content in serum, stimulating production of new
blood vessels. Kills anaerobic bacteria and increases killing power
of WBCs.
Evaluation
i. Pressure injury healing with restoration to skin integrity
ii. No further breakdown of intact skin
iii. Patient response to nursing therapies
iv. Did we meet the goals for this patient?
v. Closure devices
vi. Steri-strips
vii. Sutures
viii. Staples
ix. Tissue adhesives (fibrin sealants)
x. ** Dressings - keep wound surface clean and slightly moist
xi. ** Topical antimicrobials & antibactericidals - use with caution, can
damage new epithelium
4. Defines assessment for wounds
a. Wound classification
b. Black wound
c. Yellow wound
d. Red wound
e. Mixed-color wound
i. Assessment:
1. Always do a thorough skin assessment to catch PI’s upfront
a. Especially if a patient came in with a PI
2. Size, location, would base, drainage, margins, palpation
a. Tunneling- like a channel
b. Undermining- like a fan that sweeps under the skin
3. *Patients with dark skin:
a. Look for skin that is darker than surrounding skin
b. Use natural/ halogen light
c. Assess skin temp
d. Ask about pain and itchy sensation
4. Wound Culture
a. Whether it’s wound or blood cultures,
i. **THEY MUST BE COMPLETED BEFORE
ANTIBIOTICS ARE STARTED**
5. Planning:
a. What existing complication does the patient have?
i. Nutritional issues, uncontrolled diabetes,
decreased immunity, paralyzed
5. Wound cultures
a. Never collect samples from old drainage
b. Wound cultures must be obtained before starting antibiotics
6. Risk assessment/Nursing diagnosis
a. Risk for infection
b. Acute or chronic pain
c. Impaired mobility
d. Impaired peripheral tissue perfusion
e. Impaired tissue integrity
i. Nutrition
ii. High fluid intake
iii. Consider malabsorption problems
iv. High protein
v. High carbohydrate
vi. Increase vitamins
vii. Moderate fat intake
viii. If unable to eat, may need alternative nutritional route
7. Nursing Process/Documentation
a. Discuss the phases of the nursing process
i. Nursing process is circular
ii. Assess - gather information about the patient’s condition
iii. Diagnose - identify the patient’s problems
iv. Plan - set goals of care and desired outcomes and identify appropriate
nursing actions
v. Implement - perform the nursing actions identified in planning
vi. Evaluate - determine if goals and expected outcomes are achieved
b. Apply the nursing process in the development of a nursing care plan
c. Discuss the skills and attitudes of critical thinking
i. Knowledge
1. Underlying disease process
2. Normal growth and development
3. Normal physiology and psychology
4. Normal assessment findings
5. Health promotion
6. Assessment skills
7. Communication skills
ii. Standards
1. ANA Scope and Standards of Nursing Practice
2. Specialty standards of practice
3. Intellectual standards of measurement
iii. Experience
1. Previous patient care experience
2. Validation of assessment findings
3. Observation of assessment techniques
iv. Attitudes
1. Perseverance
2. Fairness
3. Integrity
4. Confidence
5. Creativity
d. Illustrate elements of critical thinking
e. Discuss the relationship between the nursing process and critical thinking
f. Analyze sociocultural factors utilizing the nursing process
g. Analyze growth and development factors utilizing the nursing process
h. Discuss cultural awareness
8. Introduction to Medication Administration
a. Differentiate between pharmacokinetic drug interactions and pharmacodynamic
drug interactions including ethnoicodynamics and food interactions
i. Pharmacology - study of medication
ii. Pharmacotherapy/pharmacotherapeutics - application of a drug for the
purpose of diagnosis, prevention or treatment of suffering
iii. Determinants that affect drug therapy:
iv. Clinical factors
1. Age, weight
2. Present health disorder
3. Other disease entities
4. Client drug compliance
v. Pharmacokinetics
1. Absorption
2. Distribution
3. Metabolism/biotransformation (t1/2)
4. Excretion
vi. Administration
1. Drug form
2. Route of administration
3. Multiple drug therapy
4. Drug interactions
vii. Pharmacodynamics
1. Onset, peak, and duration
2. Therapeutic range
3. Side effects and adverse effects
viii. Pharmacogenetics
b. Describe the pharmacodynamic interactions additive, synergistic, and
antagonistic
i. Pharmacodynamics - how a dug changes the body
ii. Medications can only mimic or block normal body functions. They cannot
confer new functions
iii. Plasma drug levels
1. Minimum effective concentration
a. Below MEC therapeutic effects of med will not occur
2. Toxic concentration
3. Therapeutic range
4. Drug half life (t5)
5. Loading and maintence doses
6. Peak & trough
iv. Medication dose responses
v. Serum half-life:
1. Time for serum medication concentration to be halved
vi. Onset:
1. Time it takes after a medication is administered for it to produce a
response
vii. Peak:
viii. Time at which a medication reaches its highest effective concentration
ix. Trough:
1. Minimum blood serum concentration before next scheduled dose
x. Duration:
1. Time during which the medication is present in concentration
great enough to produce a response
xi. Plateau:
1. Blood serum concentration is reached and maintained
xii. Medication actions
xiii. Therapeutic effect:
1. Expected or predicted physiological response that a medication
causes
xiv. Side effect:
1. Predictable and often unavoidable secondary effects produced at
a usual therapeutic dose
xv. Adverse effect:
1. Unintended, undesirable, and often unpredictable severe
responses to medication
xvi. Toxic effect:
1. Develop after prolonged intake of a medication or when a
medication accumulates in the blood because of impaired
metabolism of excretion
xvii. Idiosyncratic reaction:
1. Unpredictable. A patient overreacts or underreacts to a
medication or has a reaction different from normal
xviii. Allergic reaction:
1. Unpredictable. Repeated administration to the patient develops
an allergic response to it, its chemical preservatives, or a
metabolite
xix. Medication Interactions - occurs when one medication modifies the
action of another
1. Additive (1+1=2)
a. Adds another effect
b. Two drugs from a similar therapeutic class produce a
combined summative effect
2. Synergistic (1+1=3)
a. Adds the same effect as the other to create a stronger
effect
b. Medications acting together produce a greater effect than
each of them alone
i. Medication manufactured as a combination drug
1. Synercid - combined antibiotic - effective
against staph infections
3. Agonist
a. Medication that produces the same response as the
endogenous substance - (actual molecule in the body that
produces the desired effect; sometimes these substances
produce a greater effect than the endogenous substance)
4. Partial agonist
a. Medication that produces a weaker effect
5. Antagonistic
a. Blocks the effect of the other
b. Drug that prevents the agonist from producing the desired
effect
c. Describe the physiological mechanism of medication action including absorption,
distribution, metabolism, and excretion of medications
i. Route - how to enter the body
1. IVa. No barriers to absorption
b. Immediate and complete absorption
c. Disadvantages
i. Incontinent, costly, medication irretrievable
ii. Fluid overload
iii. Infection
iv. Emboli
2. IMa. Only barrier - capillary wall
b. Drug can easily pass through tissue
c. Absorption depends on
i. Solubility - water soluble will be absorbed more
rapidly
ii. Blood flow
d. Disadvantages
i. Discomfort
ii. Nerve damage
3. Subcutaneousa. Nearly identical to IM
4. Orala. Barriers: lining of GI tract and capillary wall
b. Absorption pattern: solubility, stability, gastric & intestinal
pH, gastric emptying, good in GI, other meds, special
medication coatings
c. Absorption takes place along the GI mucosa either in the
stomach or lower GI tract
d. Absorbed meds enter blood stream and go directly to the
liver
i. Hepatic first pass effect
1. Hepatic microsomal enzymes
2. Phenomenon where concentration of drug
is greatly reduced before it reaches
systemic circulation
3. After a drug is swallowed, it is absorbed by
the digestive system and enters the hepatic
portal system. It is carried through the
portal vein into the liver before it reaches
the rest of the body
a. The liver metabolizes many drugs,
sometimes to such an extent that
only a small amount of active drug
emerges from the liver to the rest of
the circulatory system. This first pass
through the liver thus greatly
reduces the bioavailability of the
drug
d.
e.
f.
g.
h.
i.
j.
ii. Alternative routes of administration like suppository, IV, IM, inhalation
aerosol, and sublingual avoid the first pass effect because they allow
drugs to be absorbed directly into the systemic circulation
Advantages
i. Easy & inexpensive enzymes
ii. Safer - potentially reversible
iii. Good choice for senior citizens
Disadvantages
i. Variable absorption rate
ii. Inactivation of certain medications
iii. Requires a conscious and cooperative client
iv. Age
1. Change in gastric pH can affect medication absorption
Pharmaceutical preparation
i. Tablets
ii. Enteric coating (do not crush)
iii. Sustained release preparations
Topical
i. Skin, eyes, ears, nose, mouth vagina
Inhalation
Rectal suppositories - cut in half lengthwise if needed
Absorption - from site into the blood
i. “Movement of medication from its site of administration into the
bloodstream”
ii. Rate of dissolution
1. Drugs that dissolve faster are absorbed faster
2. Repository
iii. Absorption dependent on the properties of the drug and on the
physiological and anatomical attributes of the surface
1. Surface area
a. The larger the surface area the faster the absorption
b. Anesthesia delivered via the lungs
2. Blood flow
a. Drugs absorbed most rapidly from sites with the most
blood flow
i. IV - directly into the bloodstream
ii. IM - muscles have a good blood supply
3. Anything that impedes or enhances blood supply can impact
absorption
a. Heating pad vs ice pack
4. Drug solubility
a. Lipid soluble drugs can readily cross the cell membranes
5. Ph partitioning
a. Acids tend to ionize in basic solutions
b. Bases tend to ionize in acidic media
c. Example: aspirin (acidic) is absorbed better in the stomach
acid than in the lower GI environment (basic).
d. Remaining non-ionized increased absorption
k. Distribution - from blood into cells, tissues, or organs/”movement of drugs
throughout the body”
i. Traveling via channels and pores
ii. Must have small ions
iii. Sodium and potassium are examples
iv. Transport systems - carriers that move drugs from one side of the cell
membrane to the other
v. Transportation depends on the structure of the drug molecule
vi. Affected by:
vii. Blood flow to the tissues, exiting the vascular tissue to site of action
viii. Drug solubility
1. Lipid soluble drugs are not limited by the barriers that
normally limit water soluble drugs
ix. Tissue storage
x. Some tissues have a greater ability to accumulate and store drugs
1. Bone marrow
2. Teeth
3. Eyes
4. Adipose tissue
xi. Determined
xii. Protein binding
1. Bonds reversible
2. Albumin - large molecule that remains in the bloodstream and
therefore amount of med available to the site of action may
be limited
3. Only a few molecules will bind at any one time
4. Multiple meds may compete at binding sites - resulting in
overdose
l. Special barriers
i. Blood brain barrier
1. Placental barrier
m. Action - how a medication acts
n. Metabolism - changed to prepare for excretion/the body chemically changes the
drug molecule, AKA “biotransformation”
i. Most often takes place in the liver
ii. Multiple enzymes
1. Hepatic microsomal enzymes - latest research is focusing on
identifying individual characteristics and specific function of these
enzymes
iii. Consequences of metabolism
1. Accelerated renal excretion
2. Drug inactivation
3. Increased therapeutic action
4. Activation of “prodrugs” (inactive substance changed to active
substance)
5. Increased toxicity
6. Decreased toxicity
o. Factors impacting drug metabolism
i. Age
ii. Induction of drug metabolizing enzymes
1. Stimulates liver to breakdown itself faster or this change my affect
other medications
iii. Hepatic first pass effect
iv. Nutritional status
v. Competition between drugs
vi. Competition between drugs and food
9. Excretion - how they exit the body
a. Options
i. Glomerular filtration - drugs removed from blood and discarded into the
urine
ii. Passive tubular reabsorption - frequently occurs with lipid soluble drugs
iii. Active tubular secretion - active pumping of drug into tubular urine
b. Modifiers of renal excretion
i. pH-dependent ionization
1. > excretion rate
ii. Competition (between drugs) for active tubular transport
c.
d.
e.
f.
g.
h.
i.
j.
k.
l.
m.
n.
o.
iii. Age
1. Very young immature kidneys - [???]
2. Senior citizens - decreased effectiveness of kidneys
a. Creatinine clearance
Non-renal routes of drug excretion
i. Breast milk
ii. Bile
iii. Lungs
iv. Sweat
v. Saliva
This knowledge is used when selecting timing, route, risks, and evaluating the
response.
Optimizes the benefits of the medication
Minimizes the harmful effects
Select the optimal schedule
Adjust the route
Educate our clients and their families
Enhances our understanding of physiology and pathophysiology
Discuss the student’s responsibilities including documentation during the
administration of medications (8 rights) including assessing for adverse reactions
and side effects.
i. 3 checks
1. Check before pulling meds
2. Check when pulling meds
3. Check outside patient’s room while prepping medication before
administering
ii. 8 rights
1. Right name
2. Right medication
3. Right dose
4. Right route
5. Right time
6. Right to education
7. Right to refuse
Utilizes the nursing process to develop an individualized nursing care plan for a
client requiring medication
Discuss factors that commonly cause medication errors
Describe the legal responsibilities associated with documentation for routine and
PRN medication administration within the scope of “Nurse Practice Acts”
Identify common medication errors and prevention strategies
10. Diabetes Assessment and Management
a. Describe pathophysiology of Diabetes
i. Both
1. Requires tight control of blood glucose levels in order to prevent
long-term complications
2. Also important to control blood pressure and blood lipids because
with uncontrolled blood glucose levels r/t DM, the blood is thicker
and will put greater strain on the heart and lower perfusion
3. Uncontrolled blood glucose r/t DM can cause kidney failure
ii. DM I1. Beta cells are attacked and destroyed by T-cells, resulting in
failure to create insulin.
iii. DM II1. Insulin resistance
b. Develop understanding of nursing assessment, planning and evaluation of
patients with diabetes
i. DM I1. Requires comprehensive plan
2. Integrated program of diet, self-monitoring of blood glucose,
exercise, and insulin replacement
3. Dietary measures
a. Total carbohydrates - not the type of carbohydrates - are
most important
b. Glycemic index
i. Foods w/ high glycemic index (eg. a muffin) will
make the person’s blood glucose spike very quickly
and drop very quickly (think sugar rush!)
ii. Foods w/ lower glycemic index (eg. fruit or some
other foods with natural sugars that will take more
time to metabolize) will not make the blood
glucose spike very high or very quickly but will
instead be more even and drop at a slower rate
over a longer period of time, which is better for the
pt.
iii. INSULIN NECESSARY
ii. DM II1. Requires comprehensive plan
2. Should be screened and treated for:
a. Hypertension, nephropathy, retinopathy, neuropathy,
dyslipidemias
3. Glycemic control with:
a. Diet and exercise
b. Drug therapy
4. Requires regular assessment (Q3months-ish) of patient’s labs
5. INSULIN MAY NOT BE NECESSARY
11. Learn medications management in relation to diabetes
a. Insulin I: Physiology
i. Biosynthesis
ii. Secretion
iii. Metabolic actions
iv. Metabolic consequences of insulin deficiency
b. Insulin II: Preparations and Administration
i. Sources of insulin
1. Recombinant DNA technology
2. Beef and pork pancreas
ii. 7 types of insulin
1. Short duration: rapid acting
a. Insulin lispro (Humalog)
b. Insulin aspart (NovoLog)
c. Insulin glulisine (Apidra)
2. Short duration: slower acting
a. Regular insulin (Humilin R, Novolin R)
3. Intermediate duration
a. Neutral protamine Hagedorn (NPH) insulin
b. Insulin detemir (Levemir)
4. Long duration
a. Insulin glargine
c. Concentration
i. 100 units/ml (U-100)
ii. 500 units/ml (U-500
d. Mixing insulins
i. NPH with short-acting insulins
ii. Short-acting insulin drawn first
e. Administration
i. Subcutaneous injection (*most common)
1. Syringe and needle
2. Pen injectors
3. Jet injectors
ii. Inhalation
1. Exubera - withdrawn 2007
a. Out on the market for a few years but found to be
ineffective
iii. Subcutaneous infusion
1. Portable insulin pumps
2. Implantable insulin pumps
3. Indication for pump: Dependent upon how much insulin one
needs and whether or not they have the skills or ability to inject
themselves
4. Cons: risk for infection due to invasiveness
iv. Intravenous infusion
f. Storage
i. Unopened vials should be stored under refrigeration until needed
ii. Should not be frozen
iii. Can be used until expiration date if kept in refrigerator
iv. After opening, can be kept up to 1 month without significant loss of
activity
v. Keep out of direct sunlight and extreme heat
vi. Mixtures of insulin in vials are stable for 1 month at room temp and 3
months in refrigeration
vii. Mixtures in prefilled syringes should be stored in refrigerator for up to 1
week and should be stored vertically - needle pointing up
g. Insulin III: Therapeutic Use
i. Indications
1. Principal - diabetes mellitus
2. Required by all DM I and some DM II patients
3. IV insulin for DKA (diabetic ketoacidosis)
a. Breakdown of ketones
b. Sugar stays in blood and does not go into the cells
c. Can lead to kidney failure bc the kidneys must now strain
itself to filter out these larger particles/molecules in the
blood
4. Hyperkalemia - can promote uptake of potassium
a. Can be used on patients that don’t have DM I/II if they
have hyperkalemia d/t kidney issues, being on diuretics, or
other reasons bc it can promote uptake of excess
potassium in blood
5. Aids in the diagnosis of GH deficiency
a. GH = growth hormones
ii. Insulin Therapy of Diabetes
iii. Tight glucose control: benefits/drawbacks
iv. Dosage
v. Dosing schedules
1. Conventional therapy
a. Dose scheduled Qmorning, Qafter food
b. Patients may have to check their glucose 3-4x in morning
before eating, then after every meal, then administer dose
based on sliding scale
2. Intensive conventional therapy
3. Continuous subQ infusion
vi. Achieving tight glucose control
vii. Complications of Insulin Treatment
viii. Hypoglycemia
ix. Lipodystrophies
x. Allergic reactions
xi. Hypokalemia
xii. Drug interactions
1. Hypoglycemic agents
2. Hyperglycemic agents
3. Beta adrenergic blocking agents
a. Can lower action of insulin
h. Oral hypoglycemics
i. Biguanides
ii. Metformin (Glucophage, Glucophage XR, Fortamet, Glumetza, Riomet)
1. Not just for DM, but also for weight reduction bc it decreases
appetite
2. Risk for hypoglycemia when starting this medication d/t
decreased appetite
3. Common suggestion for those starting this medication or for
those starting insulin: do not give yourself insulin if you do not
have food in front of you and make sure you eat that food
4. Particularly an issue in the hospital setting when administering a
short acting insulin and the patient doesn’t receive the food that
they wanted. In between the time it takes to switch out the meal
tray and the time from administration of short acting insulin, the
patient may dip.
iii. MOA
1. Inhibits glucose production in liver
2. Reduces glucose absorption slightly in gut
3. Sensitizes insulin receptors in target tissues
a. May be used as monotherapy or with a sulfonylurea, a
glitazone, or exenatide
b. More effective in combination
c. Well suited for patients who skip meals
d. Prevention of type 2 diabetes
e. Gestational diabetes
f. PCOS
g. Side effects
i. Decreased appetite, nausea, diarrhea
ii. Decreases absorption of B12 and folic acid
iii. Patients lose average of 7-8 lbs
h. Toxicity - lactic acidosis
i. Alcohol, cimetidine (Tagamet), and iodinated
radiocontrast media may intensify acidosis
i. Sulfonylureas
i. Tolbutamide (Orinase)
ii. First oral hypoglycemics
iii. MOA
1. Promotes insulin release
iv. Major side effect is hypoglycemia
v. First generation controversy
1. Cardiovascular toxicity
vi. Second generation agents
1. Much more potent than first generation drugs
2. Significant drug-drug interactions less common
vii. Interactions
1. Alcohol
2. NSAIDS
3. Sulfonamides
a. Used for treating infections
4. Cimetidine
a. H2 receptor blockers for GI problems (antacid effects)
5. Beta-adrenergic blocking agents
j. Thiazolidinediones (glitazones)
i. Rosiglitazone (Avandia)
1. Only minor side effects
a. Renal retention of fluid
i. Raises levels of plasma lipids
2. Drug interactions
a. Insulin also promotes fluid retention, hence the
combination poses increased risk for heart failure
b. Gemfibrozil (Lopid) can raise plasma levels of rosiglitazone
k. Pioglitazone (Actos)
i. Newest glitazone
ii. No hepatotoxicity
iii. Adverse effects - generally mild
1. URI, headache, sinusitis myalgia
2. Promotes water gain
iv. Drug interaction
1. Gemfibrozil (Lopid)
l. MOA
i. Reduces glucose levels by decreasing insulin resistance
ii. Not related chemically or functionally to sulfonylureas, biguanides, or
alpha-glucosidase inhibitors
m. Glinides (meglitinides)
i. Repaglinide (Prandin), Nateglinide (Starlix)
ii. Muraglitazar (Pargluva)
iii. MOA
1. Same as sulfonylureas - promotes insulin release
iv. Adverse effect: hypoglycemia
v. Interaction: gemfibrozil (Lopid)
n. Alpha-glucosidase inhibitors
i. Acarbose (Precose), Miglitol (Glyset)
o.
p.
q.
r.
s.
ii. MOA
1. Act in intestines to delay absorption of carbohydrates
iii. Does not depend on presence of insulin
iv. Monotherapy or combination
Gliptins
Combination products
i. Metformin/Glyburide
ii. Metformin/Glipizide
iii. Metformin/Rosiglitazone
iv. Metformin/Pioglitazone
v. Metformin/Repaglinide
vi. Metformin/Sitafliptin
vii. Pioglitazone/Glimepiride
viii. Rosiglitazone/Glimepiride
New Injectable Drugs for Diabetes
i. Pramlintide (Symlin)
1. Supplement to mealtime insulin (DM I or DM II)
2. Adverse effect: hypoglycemia
ii. Exenatide (Byetta)
1. Adjunctive therapy to improve glycemic control in patients with
DM II
2. Adverse effects: hypoglycemia, GI effects
iii. **GLUCAGON for INSULIN OVERDOSE**
Preferred treatment is IV glucose
i. Immediately raises blood glucose level
Glucagon can be used if IV glucose is not available
i. Delated elevation of blood glucose
ii. Will not work in starvation
1. Promotes glycogen breakdown and the malnourished have little
glycogen left
12. Understand blood glucose monitoring
a. Self-Monitoring of Blood Glucose (SMBG)
b. Glycosylated hemoglobin: HgbA1c
13. Demonstrate BG finger sticks and SQ injections