FINAL EXAM NOTES

*COAGULATION MODIFIERS*
Drugs that Affect Blood Coagulation: Anticoagulants, Antiplatelets, Thrombolytics
- Used in the prevention & management of thrombotic & thromboembolic disorders.
1. Anticoagulants prevent formation of new clots & extension of clots already present
a. DO NOT CALL THEM BLOOD THINNERS
2. Antiplatelet drugs: AKA platelet aggregation inhibitors prevent one or more steps in prothrombotic activity of platelets
a. The fxn is affected not the # of the platelets
b. Platelet aggregation is needed to stop bleeding. So if you are on any of these drugs & you cut yourself, bleeding is
going to last because the platelet plug will not develop
3. Thrombolytic drugs given to dissolve thrombi

Thrombosis: Involves formation (thrombogenesis) or presence of a blood clot (thrombus) in the vascular system. Can occur in veins
or arteries
- Arterial thrombosis: Associated with atherosclerotic plaque, hypertension, & turbulent blood flow.
o Thrombi cause disease by obstructing blood flow.
o Incomplete or temporary obstruction: local tissue ischemia.
o Complete or prolonged obstruction- infarction – local tissue death.

- Venous thrombosis: Associated with venous stasis. Activates the coagulation cascade.
o Less cohesive than arterial thrombosis
o Embolus can easily detach & travel to other parts of body.
o Cause disease in two ways:
 Causes local congestion, edema, & perhaps inflammation by impairing outflow of venous blood.
(thrombophlebitis, DVT)
 Embolus: obstructs blood supply to tissue when embolus becomes lodged.
Hemostasis: Physiologic process by which bleeding stops. It occurs in 2 stages. Processes are set in motion by blood vessel injury.

Blood contains: Platelets, cells that assist in blood clotting & clot formation, pro-coagulants & clotting factors, plasma proteins that
cause clotting – are inactive until an injury mobilizes them.

Keeping hemostasis under control:

- Need to protect against widespread coagulation.
- Body must inactivate clotting factors that stray from site of vessel injury.
- Antithrombin - protein that forms a complex with clotting factors & inhibits their activity.
Physiologic removal of clots:
- Essential in healing process.
- Plasminogen → plasmin – enzyme that digests fibrin meshwork of clot.

A. ANTICOAGULANTS
HEPARIN
- Rapid-acting anticoagulant.
o IV - acts immediately- generally given as IV infusion
o SubQ – acts within 20-30 minutes: 1 or 2x/d; used in pts who are not mobile so blood won’t clot
o NOT given IM*- any on an anticoagulant should never be given IM injections due to risk of bleeding ( will have a
terrible hematoma)
- Interferes with final steps of clotting cascade
o PREVENTS CLOTS FROM FORMING & GETTING BIGGER; DOES NOT DISSOLVE THEM
- Does not cross placenta, not found in breast milk: anticoagulant of choice for use during pregnancy & lactation
- Used in situations requiring rapid anticoagulation: PE, EVOLVING STROKE, MASSIVE DVT, MI
- Used for patients undergoing open heart surgery & renal dialysis.
- Used for treatment of disseminated intravascular coagulation (DIC).
- Adjunct therapy with thrombolytic to treat acute MI.
- Mechanism of Action:
o Along with anti-thrombin, rapidly promotes the inactivation of Factor X → prevents the conversion of prothrombin
to thrombin.

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 o Also has effect on fibrin → limits formation of a stable clot.
- Adverse effects: hemorrhage, heparin-induced thrombocytopenia, hypersensitivity rxns:
o HIT: life-threatening rxn  life-threatening bleeding – immune mediated rxn
 Heparin Induced Thrombocytopenia: ↓ platelet count
 If this happens, pt s should never get heparin again
- Drug Interactions: Any drug that suppresses platelet formation (aspirin, ibuprofen, indomethacin) weakens last defense
against hemorrhage
- Contraindication/Precautions:
o Pts with thrombocytopenia, bleeding disorders, active bleeding other than DIC.
o Those with a history of HIT
o During & immediately after any procedure where bleeding is likely and high risk- eye, brain, or spinal cord
surgeries & lumbar puncture & regional anesthesia.
o Used with caution in any pt with high likelihood of bleeding
- Laboratory Monitoring:
o aPTT (activated partial thromboplastin time) –the longer the T the greater the effect of anticoagulant
 normal value 40 seconds
 therapeutic levels increase aPTT by 1.5 to 2 times (60-80 seconds)
o Continuous IV infusion
 ptt may be drawn at any time
 1st lab draw often 4 hrs after therapy started & 4 hrs after dose changes
 Daily
o Intermittent administration → draw @ 1 hour before next dose is scheduled.
 Full dose heparin given, ptt needs to be obtained
 For LMWH ptt is not needed, but my need platelet count
- Dosage & Administration:
o Prescribed in units not milligrams
 L/U: GOOD START, UNITS/HR?
o Injection only – IV or SC
o Dosage varies with use and desired ptt

Nursing Actions:
- Prior to therapy – review aPTT, hematocrit, & platelet count.
- Check dosage on vial before administration.
- During therapy, monitor for signs of bleeding & review aPTT levels
o gum bleeding is usually common
o Blood in urine/stool, physician must be notified immediately (unusual & should not be happening)
o GUIAC test for occult blood
- If aPTT exceeds desired range, call prescriber for decrease in dosage.
- Use IV pump to administer.
- Patient education.

LOW-MOLECULAR- WEIGHT HEPARINS:

- As effective as heparin.
- Not used IV
- Advantages:
o Can be given on a fixed-dose schedule.
o Don’t require aPTT monitoring- plasma levels & effects are more predictable
- In US, three LMW heparins: these are indication specific
o Enoxaparin (Lovenox)
o Dalteparin (Fragmin)
o Tinzaparin (Innohep)
- Mechanism of Action: Same process as standard heparin except LMW preferentially inactivates factor Xa & fewer effects to
inactivate thrombin
o Can also cause HIT because they can affect platelets BUT have less risk
- Therapeutic Use:

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 o Prevention of DVT following surgery- right amount of LMWH may have the same effect as a low dose of heparin of
preventing DVT
o Treatment of established DVT
o Prevention of ischemic complications in patients with unstable angina or non-Q wave MI
o They are based on body wt (u/kg) & they’re used for a specific indication each

Protamine Sulfate: Reverses action of heparin; very unusual for this happen because once PTT is high, they will stop heparin infusion
and PTT will fall down fairly quickly
- Small protein with positive charges that binds with negative charges of heparin.
- Effects occur immediately & last about 2 hours.
- Dosage - 1mg of protamine will neutralize 100 units of heparin.
- Administered SC.
- Dosage based on body weight.
- Cost- higher in comparison to standard heparin
- Can be used at home & needs no aPTT monitoring
- Pharmacokinetics:
o LMW have longer half-lives
o plasma levels of LMW heparin are highly predictable
o Can be given on a fixed schedule with no coagulation monitoring.
- Adverse Effects: Bleeding, Immune-mediated thrombocytopenia (risk is ↓ though)

- IF AN ORDER SAYS ‘HOLD MED…’ & IT DOES NOT SAY WHEN TO RESTART, ASK PHYSICIAN!

WARFARIN
- Oral anticoagulant- only oral one available in the US.
- Has a delayed onset of action- inappropriate for emergency use
o That is why heparin and warfarin are given together when a is put on warfarin
- Mechanism of Action: Antagonist of vitamin K
o Inhibits synthesis of factors VII, IX, X, and prothrombin (II)
o Blocks biosynthesis of these clotting factors.
o Efficacy begins as the clotting factors are depleted and less new ones are produced
- Does not affect clotting factors already present
- Prevents new ones from being synthesized
o may be delayed 6 hours to 2.5 days.
o We overlap heparin for 3-5 days even if INR is therapeutic prior.
- When drug discontinued, effects still present for 2-5 days.
- Pharmacokinetics:
- Readily absorbed after oral administration.
- Hepatic metabolism & excretion in urine & feces.
o Metabolism is highly variable
 Clinical effects are highly variable
 Dose must be adjusted based upon INR
 No Standard dose
o Altered by various genetic factors
- Therapeutic uses
o Long-term prophylaxis of thrombosis
 Prevention of venous thrombosis and associated pulmonary embolism
 Prevention of thromboembolism (in patients with prosthetic heart valves)
 Prevention of thrombosis during atrial fibrillation
o DOES NOT break apart clots that are present
- Dosage: no standard dose; it’s based on ’s INR
o Based on achieving a therapeutic level as measured by changes is the prothrombin time (PT)
o International Normalized Ratio (INR) – standardized unit developed to measure therapeutic levels of warfarin.
 INR reflects the pt’s compared with the standardized value.
 /INR is a measure of anticoagulation
- INR: more consistent than for warfarin

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 o Therapeutic values are 2.0-3.0 in most conditions.
o When warfarin is started → assess daily until stable daily dose is reached.
o Thereafter → every 2-4 weeks for duration of drug therapy.
o If warfarin dose changed, INR measurements needed more often until stable daily dose is reached.
- Adverse effects:
o Hemorrhage
o Fetal hemorrhage and teratogenesis from use during pregnancy – Category X.
o Use during lactation – enters breast milk → woman should be advised against breast-feeding.
- Dosage & administration:
o Initial 10mg/day with maintenance or 2-10mg/day- old values
 Now 1-7.5 mg/day
o INR used to target dose.
- Drug Interactions
o More clinically significant drug interactions than any other drug.
o Interactions fall into 3 major categories:
 Drugs that increase anticoagulant effects.
 Drugs that promote bleeding.
 Drugs that decrease anticoagulant effects.
o Drugs can be combined but with caution.
 Risk for harm is greatest interacting drug is being added or deleted from regimen
 must be monitored & warfarin dose adjusted as needed.
o Platelet aggregation inhibitors: NSAIDS, ASA- risk of bleeding
 When used with ASA, med has to be titrated daily to see if warfarin dose needs to be lowered or not. THIS
IS ONLY OKAY IF ASA IS TAKEN DAILY NOT PRN
o P450 interactions: Drugs that inhibit or induce the CYP2C9, CYP1A2, and CYP3A4 isoenzymes have the greatest
potential to alter response to warfarin therapy.
 If these ↑ metabolism of warfarin- risk of clotting
 If these ↓ metabolism of warfarin- risk of bleeding
o Maintain a relatively consistent intake of vitamin K–rich foods- green leafy veggies
o stress consistency rather than abstinence
- Vitamin K: Used for warfarin overdose
o Reverses warfarin-induced inhibition of clotting factor synthesis.
o Can be given orally or IV.
o IV acts faster but can cause anaphylactic reactions
 must be diluted & given slowly
o Generally used when rapid reversal of INR is needed.
o If you have a consistent amount of salad everyday then it’s no problem, but if you eat some today then again in 2
wks: that’s a problem

Nursing Actions – Patient Education

- Signs of bleeding.
- Methods to prevent bleeding
- Correct way to take drug:
o Same time every day → maintains therapeutic levels.
o Don’t skip doses, don’t double up on doses.
- Must go for blood monitoring.
- Inform of potential for drug interactions.
- Use of “medical alert” bracelet
- If INR is high & is not bleeding then med can be held but if it’s extremely high, VIT K is needed to reverse warfarin actions
Warfarin is associated with necrosis- tell pt about it & tell them to report any issues

DIRECT THROMBIN INHIBITORS:

- Differ from heparin-like anticoagulants, these drugs work directly to inhibit the action of thrombin in clotting cascade.
o Used in place of warfarin, they are supposed to be safer BUT VERY DIFFICULT TO REVERSE
o aPTT is not measured
- Has some antiplatelet activity.

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 - Bivalirudin (Angiomax) - Given IV in combination with aspirin to prevent clot formation in patient with unstable angina who
is undergoing angioplasty.
- Other Drugs:
- Given IV under inpatient conditions
o Lepirudin (Refludan)
o Argatroban (Acova)
- Therapeutic Uses:
o Heparin-induced thrombocytopenia.
o Acute coronary syndrome
o Prophylaxis & treatment of venous thromboembolism.
o Management of atrial fibrillation.
- Dabigatran (Pradaxa)
o Oral direct thrombin inhibitor – FDA approved 2010
o 150 mg bid
o direct factor Xa inhibitor,
o Therapeutic use – reduce risk of stroke & systemic embolism in non-valvular atrial fibrillation
o No need for continual blood monitoring.
o Adverse Effects
 Increases risk for severe bleeding.
 Interacts with other drugs that affect bleeding times – heparin, NSAIDS, platelet inhibitors.
 Increased risk of bleeding – age > 75.
- Rivaroxaban (Xarelto): once-daily, oral
- Apixaban (Eliquis)- 5 mg bid
- Edoxaban (Savaysa)
o once-daily, oral, direct factor Xa inhibitor
o venous thromoboembolism (VTE)
o For prevention of stroke and systemic embolism in patients with non-valvular atrial fibrillation

B. ANTIPLATELET
Aspirin (ASA)
- Inhibition of cyclooxygenase – enzyme needed by platelets to synthesize thromboxane A2.
- Also causes vasodilation & suppresses platelet aggregation.
- Indications for Use:
o Prophylaxis of MI.
o Prevention of re-infarction.
o Prevention of stroke.
- Adverse Effects
o Increase risk of GI bleeding.
o Adverse effects uncommon with small doses used for antiplatelet effects.
o No antidote exists for effects of aspirin → causes irreversible platelet effects.
- Dosing
o Initial treatment of acute event – 325mg/day.
o Chronic therapy – 81 mg/day.

Adenosine Diphosphate (ADP) Receptor Antagonists

o Clopidogrel (Plavix)*
o Ticlopidine (Ticlid)- almost never used
- Mechanism of Action: Inhibits the binding of ADP to its platelet receptor and the subsequent ADP-mediated activation of
the GP IIb/IIIa complex → inhibits platelet aggregation.
o Platelets exposed to the drug are affected for the remainder of their life span.
- Therapeutic Uses: Reduces risk of thrombotic events – MI, ischemic stroke, and vascular death - in patients with
atherosclerosis.
- Adverse Effects:
o Similar to aspirin.
o Neutropenia (rare) – should be considered if patient develops s/s of infection.
o No antidote exists – produce irreversible platelet effects.

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 C. THROMBOLYTICS: Alteplase (tPA) & Retaplase
- Assist in breaking down formed blood clots- dissolve clots
- Used for patients who are diagnosed with:
o Evolving acute MI.
o Pulmonary embolus- one that is happening at the moment
o Acute ischemic stroke
o May also be used to unclog a central venous catheter.
- Can be given systemically or directly at site of blood clot.
- Adverse effects can be life-threatening- Bleeding is a major complication
- Drugs administered in emergency situation & should be given by clinician skilled with using these drugs.
- Five drugs available – streokinase, alteplase, reteplase, urokinase, & tenecteplase
o Thrombolytics with different indications
o Can be used for pts in dialysis
- Mechanism of Action: Promotes conversion of plasminogen to plasmin – an enzyme that digests the fibrin matrix of clots

Extra Notes:
- Excessive bruising = bleeding

*PAIN MEDS: PART II*

MIGRAINE DRUGS:
- Migraine headaches are accompanied by pain nausea and increased sensitivity to lights and sound
- Strong genetic influence→ Occurs in families
- In adults more common in females
- Caused by neural hyper-excitability that results vasodilatation of the vessels in the brain
- Migraine triggers: foods high in Monosodium gluconate (MSG), chocolate, aged cheese, wine, ↑ incidence during menses
o affected person should avoid triggers
- Two categories:
o Treatment of acute pain: (Acetylsalicylic acid, ASA, NSAIDS)
- Prevention/Prophylactic (Propranolol, calcium channel blocker, anticonvulsants)
o Menstrual migraines
 Oral contraceptives & SSRIs

Treatment for Migraine

- Triptans (Serotonin receptor 5-HT1B and 5-HT1D agonists):
 Almotriptan (Axert)
 Eletriptan ( Replax)
 Sumatriptan (Imitrex); acts within 10 min
 Rizatriptan (Maxalt)
o Bind to serotonin receptors in the intracranial blood vessels results in vasoconstriction
o Reduces vascular inflammation
o Aborts migraine headaches
o Most act within 1-2 hours

SUMATRIPTAN
- Route:
o SC: relief within 2 hours in about 80% of patients
o Nasal spray: relief in about 60% of patients after 2 hours
o Oral: relief in about 50-60% of patients after 2 hours
o Most useful is Nasal & SC
o almotriptan, eletriptan, rizatriptan and zolmitriptan- Similar in efficacy to sumatriptan
- Naratriptan & frovatriptan: longer half-lives & have slower onset of action & lower initial response rate than other triptans
Triptans
- Contraindicated in patients with history of angina pectoris, MI or uncontrolled hypertension
- Use cautiously with medications that increase serotonin levels such as antidepressants, meperidine, dextromethorphan

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 - Serotonin syndrome- hallucinations, restlessness, tachycardia- triptans cannot be taken together w/ a SSRI due to this
- ADR’s:
o Pressure in the chest may occur with all triptans: most commonly with injectable sumatriptan.
o Tingling
o Flushing
o Dizziness
o Drowsiness
- Interactions:
o Generally not used within 24 hours of another triptan
o > risk of serotonin syndrome with SSRIs
o Triptan specific

Ergot- Ergotamine Tartrate

- Ergot preparations relieve headache by activating 5-HT1d receptors on intracranial blood vessels →Vasoconstriction
- Usual route of administration is sublingual. May also be given nasally
- Most effective when given at first symptoms

Contraindications to Ergotamine
o Pregnancy
o Severe hypertension
o Peripheral vascular disease
o Coronary Artery Disease
o Severe infections
o Vasospasms- can even see gangrene!

Cafergot
- Ergotamine Tartrate and caffeine
- Caffeine increases the absorption and vasoconstrictive effects of Ergotamine Tartrate

NSAIDs: Nursing Implications

o Before beginning therapy, assess for conditions that may be contraindications to therapy, especially:
o GI lesions or peptic ulcer disease
o Bleeding disorders
o Assess for conditions that require cautious use
o Perform lab studies as indicated (cardiac, renal, and liver function studies, CBC, platelet count)
o Perform a medication history to assess for potential drug interactions (Several serious drug interactions exist)
o Monitor for therapeutic effects, which vary according to the condition being treated
o Decrease in swelling, pain, stiffness, and tenderness of a joint or muscle area

BONE DISORDER DRUGS

Osteoporosis: Medical condition characterized by low bone mass and increased bone fragility.
- About 10 million Americans have osteoporosis: @ 80% of them older women.
- Another 34 million have reduced bone mass → risk factor for osteoporosis.

Osteoporosis – Primary Prevention

- Educate pts to implement lifelong measures that help maximize bone strength.
- Sufficient intake of calcium: need supplementation if dietary intake not enough.
- Vitamin D – needed for calcium absorption: 10-15 minutes sunshine daily & Supplement as needed.
- Weight-bearing exercise.
- Avoid excessive alcohol consumption.
- Avoid smoking.

Vitamin D Supplementation
Age Recommendations
- 6 months – 24 years old 400 IU daily

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 - 25-50 years old 200 IU daily
- 51-70 years old 400 IU daily
- >70 years old 600 IU daily
- 800 IU daily – individuals at risk for vitamin D deficiency due to lack of sunlight exposure.
- Vitamin D → Fat-soluble vitamin – use with caution! – risk for toxicity.

Bisphosphonates
- Inhibit osteoclast-mediated bone resorption
 Prevents calcium from being reabsorbed into circulation
 Enhances bone mineral density.
- Drugs of choice for osteoporosis
 Clinical evidence indicates reversal of lost bone mass & reduction of fracture risk.
- Therapeutic uses:
- In women to treat & prevent postmenopausal osteoporosis.
- In men with osteoporosis.
- For patients with osteoporosis produced by the use of glucocorticoid-induced osteoporosis.
- For clients who have Paget’s disease of the bone and hypercalcemia of malignancy.
- Drugs:
o Alendronate (Fosamax)
o Ibandronate sodium (Boniva)
o Risedronate (Actonel)

Side/Adverse Effects Nursing Interventions/Patient Education

Esophagitis To facilitate passage through the esophagus, administer with full
glass of water & instruct patient to sit up or stand for 30 minutes
after taking medication

Risk for hyperparathyroidism at higher dose – used for Paget’s Monitor patient’s parathyroid hormone (PTH) levels.
disease
Risk of jaw necrosis Make sure pt has required dental work done prior to therapy
Risk for femur Monitor for length of total therapy- 5 yrs

- Contraindications/Precautions
o Cautious use in lactating women.
o Pts with prior esophageal disorders (i.e., gastroesophageal reflux disease) should not use bisphosphonates.
- Medication/Food Interactions: Calcium supplements, antacids, orange juice, & caffeine – bisphosphonate absorption
decreased when taken concurrently
- Nursing Interventions/Patient Education: Advise to take medication on an emy stomach with at least 8 ounces of water

Additional Patient Education

Instructions about medication administration should include:
- Take med first thing in morning after getting out of bed.
o if a cannot move they do not get these meds
o Need to be able to sit up (at least sit up) because of risk of esophageal erosion
- Take med on an empty stomach with full glass of water.
- Sit or stand for 30 minutes after taking med.
- Do not take any other meds within 30 minutes of taking bisphosphonate.
- Understand correct dosage schedule – once daily, weekly, or monthly
- Monitor patient’s bone density – bone density scan should be performed every 12-18 months.
- Monitor serum calcium. Normal range between 9.0- 11 mg/dL.
- For maximum benefit of medication, patients should, consume adequate amounts of calcium & Vitamin D.
- Encourage weight-bearing exercise daily.
- Teach pt to notify provider with sxs such as difficulty swallowing, painful swallowing, and/or new or worsening heartburn.

GOUT DRUGS:
- Recurrent inflammatory disorder characterized by:
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 o Hyperuricemia – blood uric acid levels ↑ 7 mg/dl in men; ↑ 6 mg/dl in women
o Episodes of severe joint pain – typically in large toe.
- Chronic hyperuricemia:
o Tophi form in affected joint.
o Renal damage from deposition of urate crystals in kidney.
- Treatment of gout:
o Short-term to relieve sxs of acute gout attack.
o Long-term to lower blood levels of uric acid.

Drugs for Acute Gouty Arthritis

NSAIDS – 1st choice drug.
Corticosteroids: For acute episodes

Colchicine
- Anti-inflammatory agent specific for gout treatment.
- Can be used by those that cannot tolerate a NSAID
- Used to treat an acute attack & to help to prevent attacks in chronic gout.
- Side effects – GI disturbances – N/V, diarrhea, abdominal pain.
o If GI sx occur, drug should be discontinued
- Anti-inflammatory agent specific for gout treatment: can be used by those that cannot tolerate a NSAID
- Used to treat an acute attack & to help to prevent attacks in chronic gout.
- Initially 1.2-mg dose (2 tabs) followed by 0.6 mg one hour later is as effective as higher doses, with less toxicity
o Then 0.6 mg once to twice a day for several months
o BACK IN THE DAY: one tablet would be given every hr until developed diarrhea
- Deadly in an OD

Drugs for Hyperuricemia

- Allopurinol (Zyloprim) – drug of choice for chronic tophaceous gout.
o Inhibits uric acid formation
o Prevents tophus formation- long term promotion of reversion
o Promotes regression of tophi that have already formed
o Long-term use
o Generally well-tolerated.
o GI side effects (occasionally)
o Hypersensitivity syndrome (rare but potentially fatal)- dermatologic rxns
 When allopurinol is used with Hydrochlorothiazide the risk for this ↑
 DRESS rxn: drug rash, with eosinophilia & systemic sxs (renal, liver, & other organ dysfxn)
o Drug interactions:
 Can inhibit hepatic drug-metabolizing enzymes → delays inactivation of other drugs.
 Warfarin – dosage may need to be reduced.
Probenecid
- Acts on renal tubules to inhibit reabsorion of uric acid- uric acid will be peed out
- ↑ excretion of uric acid lowers plasma urate levels:
o Prevents formation of new tophi.
o Facilitates regression of tophi already formed.
- Generally well-tolerated.
o GI effects (occasional)
o Hypersensitivity can occur.
- Drug interactions
o Aspirin & other salicylates
o PCN

Additional Patient Education

- Instruct on preventive measures:
o Avoid alcohol consumption.
o Avoid foods high in purine – red meat, scallops, cream sauces, etc

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 o Ensure adequate intake of water.
o Maintain appropriate body wt.
*BASIC PRINCIPLES OF ANTIMICROBIAL THERAPY*:
ANTIMICROBIAL/ANTIBIOTIC DRUGS:
- Drugs used to kill or suppress microorganisms
- Selective toxicity- Ability to kill or suppress the target organism microorganism without harming the host
- Antibiotics DO NOT treat viral or fungal infections.
o Pts do not become resistant to the drugs, the organisms do
o There is no such thing as a ‘strong’ antibiotic

Community-associated infections
- An infection that is acquired by a person who has not been hospitalized or had a medical procedure (such as dialysis,
surgery, catheterization) within the past year

Healthcare-associated infections: Contracted in a hospital or institutional setting

- Were not present or incubating in the patient on admission to the facility
- More difficult to treat because causative microorganisms are often drug resistant and the most virulent
- One of top ten leading causes of death in the U.S.
- MRSA most common
- Previously known as nosocomial

Healthcare-Associated Infections: Prevention:

- Hand washing
- Antiseptics: Generally only inhibits the growth of microorganisms but does not necessarily kill them. Applied exclusively to
living tissue
- Disinfectant: Kills organisms & Used only on nonliving objects

Antibiotics: Medications used to treat bacterial infections

- Empiric: start antibiotic treatment before it’s definitive that the has a certain issue, it’s given due to sxs present
o Treat w/o knowing type of infection before specific culture info has been reported
o Ex. Female with cystitis at a college; Antibx A is given because health professionals know that other antibxs do not
work on s around that area
- Definitive: C/S report came back, shows which bacteria caused the problem
o Antibx treatment tailored to treat organism identified w/ cultures
o If results come back & the bacteria matches the drug, then the treatment stays the same, if not then med is
switched
- Prophylaxis against infections: to PREVENT an infection
o Surgical prophylaxis: prevent infection during surgery; given before the incision is made , once they are in the OR
o Dental work: people with arrhythmias, faulty valves, will get antibx to prevent bacteria affecting heart
- Ideally, before beginning antibiotic therapy, the suspected areas of infection should be cultured to identify the causative
organism and potential antibiotic susceptibilities
o Obtain clean catch urine sample
o C/S of sputum

How Do Antibiotics Work? Disruption of the cell wall, Inhibition of bacterial enzymes, Disruption of bacterial protein synthesis

Antibiotic actions:
- Bactericidal- Kills microorganism; penicillins
- Bacteriostatic- Slows growth- macrolides
- Allows the host to kill the bacteria

Selection of Antibiotics
First rule- Match the Bug with the Drug!
How? Agar plates, MIC (Minimum Inhibitory Concentration)

Therapeutic response: ↓ in specific signs & sxs of infection are noted (fever, elevated WBC, redness, inflammation, drainage, pain)

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Subtherapeutic response: Signs & sxs of infection do not improve
Almost all antibiotics are associated with
- Superinfection- Reduction or complete elimination of normal bacterial flora & ↑ risk of infections
o Pseudomembranous colitis (diarrhea, abdominal pain due to Clostridium difficile)
o Vaginal yeast infection (unbalance vaginal bacterial flora due to AB Rx)
- Allergies: Some have cross reactions with each other
- N/V, diarrhea (C.diff and none C. diff related- 2 different disease states)

Assess: Age, allergy history (allergy-crossing varies among antibxs), liver function, pregnancy status, host defenses, site of infection,
genetic characteristics

Genetic host factors

- G6PD deficiency →hemolysis
- Slow acetylation →slow metabolism →drug accumulation →Toxicity

ANTIBIOTIC CLASSES:
- Sulfonamides
- β-Lactams: Penicillins, Cephalosporins, Carbapenems, Monobactams
- Macrolides
- Tetracyclines
- Aminoglycosides
- Quinolones
- Others: Miscellaneous antibiotics

Antibiotic Therapy: Mechanism of Action

- Interference with cell wall synthesis
- Interference with protein synthesis
- Interference with DNA replication
- Acting as a metabolite to disrupt critical metabolic reactions inside the bacterial cell

A. BETA-LACTAM ANTIBIOTICS: Penicillins, Cephalosporins, Carbapenems, Monobactams

a. PENICILLINS:
i. Bactericidal: inhibit cell wall synthesis
ii. Kill a wide variety of bacteria
iii. A LOT OF Bacteria produce enzymes capable of destroying penicillins
iv. These enzymes are known as betalactamases- this is why the organism may be resistant to this antibx
v. Is a result, the medication is not effective
vi. Natural Penicillins: penicillin G, penicillin V potassium
1. No longer commonly used because of resistance
vii. Penicillinase-resistant penicillins: cloxacillin, dicloxacillin, nafcillin, oxacillin
1. Skin infections that are not methicillin resistant (I.E, that are methicillin sensitive)
a. Penicillinase= betalactamase
b. Cellulitis for example
c. If pt is resistant to methicillin, these drugs won’t work against it
- Along with other beta-lactams are not see being used often due to: needs to be taken 4x/d, on an empty stomach, resistance
has developed
- It is important for pts to finish all the prescribed antibx because there are a few strands that stay behind and become
resistant to the meds

b. AMINOPENICILLINS: AMOXICILLIN (2-3x/d), AMPICILLIN (4x/d)- work more on gram neg bacteria
i. Otitis, sinusitis & Cystitis in special situations
ii. If allergic to penicillin, may be allergic to these drugs
iii. Although sometimes the physicians will give it anyways because some pts would think they were allergic to the
meds but they actually had Mononucleosis (viral infection)

11
 1. When given an aminopenicillin with viral infection, a rash is caused due interaction of antimicrobial
with the virus
c. Extended-spectrum penicillins: piperacillin, ticarcillin, carbenicillin
i. Usually used with other drugs; rarely used alone
ii. If allergic to ampicillin or amoxicillin alert physician

- Chemicals have been developed to inhibit the enzymes that break down penicillins/aminopenicillin. These chemicals bind
with beta-lactamase and prevent the enzyme from breaking down the penicillin, thus making the drug more effective
o Clavulanic acid
o Tazobactam
o Sulbactam
- Once these (↑) are added to Penicillin, the following beta-lactamase inhibitor combination drugs are formed:
o Ampicillin + sulbactam = Unasyn
o Amoxicillin + clavulanic acid = Augmentin
o Ticarcillin + clavulanic acid = Timentin
o Piperacillin + tazobactam = Zosyn

Penicillins: Mechanism of Action

- Penicillins enter the bacteria via the cell wall
- Inside the cell they bind to penicillin-binding protein
- Once bound, normal cell wall synthesis is disrupted
- Result: bacteria cells die from cell lysis
- Penicillins do not kill other cells in the body

Penicillins: Indications: Prevention and treatment of infections caused by susceptible bacteria, such as:
- Gram-positive bacteria: Streptococcus spp., Enterococcus spp., Staphylococcus spp.

Penicillins: Adverse Effects

- Allergic reactions occur in 0.7% to 4% of cases
- Urticaria (rash), pruritus, angioedema
- Those allergic to penicillins have an increased risk of allergy to other beta-lactam antibiotics
- Cross-reactivity between penicillins and cephalosporins is between up to ~10-20%
o Varies, depends upon severity of allergy, depends on specific agents involved.
- COMMON: Nausea, vomiting, diarrhea, abdominal pain
- Interactions: MANY interactions!
o Oral contraceptives: tell female s to use back-up protection
o Warfarin

d. CEPHALOSPORINS:
i. There are 4 generations of cephalosporins, with a 5th generation on the fast track to be marketed
ii. Structurally and pharmacologically related to penicillins
1. If is allergic to penicillin, they will most likely be allergic to these meds
iii. Bactericidal action
iv. Broad spectrum
v. Divided into groups according to their antimicrobial activity
- First Generation
o Good gram-positive coverage
o Poor gram-negative coverage
o Parenteral and PO forms
 Examples: CEFAZOLIN, CEPHALEXIN (Keflex), CEFADROXIL, CEPHRADINE
o Used for surgical prophylaxis, and for susceible staphylococcal infections (skin infections)
 Cefazolin (Ancef and Kefzol): IV or IM
 BID- q12h; 3x/d- q8h
 Cephalexin (Keflex): PO
- Second Generation: cross-allerginicity to penicillin risk is less; narrower spectrum is narrower
o Good gram-positive coverage

12
 o Better gram-negative coverage than 1st generation
o Examples: generic names
 Cefaclor
 Cefprozil
 Cefoxitin
 CEFUROXIME
 Loracarbe
 Cefotetan
 Cefoxitin (Mefoxin): IV and IM
 Used prophylactically for abdominal or colorectal surgeries
 Also kills anaerobes
 Cefuroxime
 Zinacef is parenteral form; Ceftin is PO
 Surgical prophylaxis
 Does not kill anaerobes
- Third Generation: cross-allerginicity to penicillin risk is less; narrower spectrum is narrower
o Most potent group against gram-negative bacteria
o Less active against gram-positive bacteria
o Examples
 Ceftibuten;
 Cefotaxime
 Cefdinir
 Ceftizoxime
 CEFTRIAXONE*(Rocephine)- most used
 IV and IM, long half-life, once-a-day dosing
 Elimination is primarily hepatic
 Easily passes meninges and diffused into CSF to treat CNS infections
 Ceftazidime (ceaz)
 IV and IM forms
 Excellent gram-negative coverage
 Used for difficult-to-treat organisms such as Pseudomonas spp.
 Eliminated by renal instead of biliary route
 Excellent spectrum of coverage
 Resistance is limiting usefulness
- Fourth Generation
o Broader spectrum of antibacterial activity than third generation, especially against gram-positive bacteria
o Uncomplicated and complicated UTI- cefepime (Maxipime)
- Fifth Generation
o Cefaroline (Teflaro) and Ceftobiprole (not available in the US)
o Broader spectrum of antibacterial activity
o Effective against a wide variety of organisms: MRSA, Pseudomonas spp.

Adverse Effects
- Similar to penicillins
- Mild diarrhea, abdominal cramps, rash, pruritus, redness, edema
- Potential cross-sensitivity with penicillins if allergies exist

Nursing Implications:
- Assess for penicillin allergy; may have cross allergy
- Give orally administered forms with food to decrease GI upset, even though this will delay absorption
- Some of these drugs may cause a disulfiram (Antabuse)-like reaction when taken with alcohol

B. MACROLIDES:
a. erythromycin (E-mycin, E.E.S, others)- least used
b. azithromycin (Zithromax)
c. clarithromycin (Biaxin)
13
 d. dirithromycin- rarely used if at all

Mechanism of Action
- Prevent protein synthesis within bacterial cells (gram positive & negative)
- Considered bacteriostatic- not kills, slows growth so bacteria will eventually die
o No cross-allerginicity with penicillins or cephalosporins
o Anyone w/ severe allergies to anything has a risk of being allergic to anything
o A pt could also be allergic to them independently
o However, if you are allergic to a macrolide, you can be allergic to the other macrolides
- In high enough concentrations, may also be bactericidal

Indications
- Strep infections: Streptococcus pyogenes (group A beta-hemolytic streptococci)
- Mild to moderate URI and LRI: Haemophilus influenzae
- Spirochetal infections: Syphilis and Lyme disease
- Gonorrhea, Chlamydia, Mycoplasma
- Azithromycin and clarithromycin: Recently approved for mycobacterium avium intracellular complex infection
(opportunistic infection associated with HIV/AIDS)
- Clarithromycin: Recently approved for use in combination with omeprazole for treatment of active ulcer disease associated
with Helicobacter pylori infection

Adverse Effects
- GI effects, primarily with erythromycin, FOLLOWED BY CHLARITHROMYCIN, Nausea, vomiting, diarrhea, hepatotoxicity,
flatulence, jaundice, anorexia
- Azithromycin and clarithromycin: fewer GI adverse effects, longer duration of action, better efficacy, better tissue
penetration
- Interact with Digoxin; levels of dig may ↑
- Oral contraceptives: use back up protection
- Can cause liver damage
- Erythromycin burns when given IV (potassium burns as well)
- QT prolongation: if a is already on a QT prolongation drug, macrolides can add to those prolongation effects- azi & erythro
have this effect
o Citalopram (Celexa) & *Escitalopram
o Atypical Antipsychotics
Nursing Implications
- These drugs are highly protein-bound and will cause severe interactions with other protein-bound drugs
- The absorption of oral erythromycin is enhanced when taken on an empty stomach, but because of the high incidence of GI
upset, many drugs are taken after a meal or snack

C. TETRACYCLINES: no cross-allerginicity to either penicillin or macrolides; they are a different type of drug
- Demeclocycline (Declomycin)
- Oxytetracycline
- Tetracycline*
- Doxycycline (Doryx, Vibramycin)*
- Minocycline*
- Tigecycline (Tygacil)
- Natural and semisynthetic
- Obtained from cultures of Streomyces
- Bacteriostatic—inhibit bacterial growth
- Inhibit protein synthesis
- Stop many essential functions of the bacteria
- A Tetracycline med treats leginarie’s disease

CAUTIONS:
- Bind (chelate) to Ca2+ and Mg2+ and Al3+ ions to form insoluble complexes
o Thus, dairy products, antacids, and iron salts reduce oral absorption of tetracyclines

14
 - Should not be used in children under age 8 or in pregnant/lactating women because tooth discoloration will occur if the
drug binds to the calcium in the teeth
o RISK VS BENEFIT: given to pregnant women & kids during the anthrax scare for prophylaxis
- Do not go in the sun!

Indications
- Wide spectrum
o Gram-negative and gram-positive organisms, protozoa, Mycoplasma, Rickettsia, Chlamydia, syphilis, Lyme
disease, acne, others
- Demeclocycline is also used to treat the syndrome of inappropriate antidiuretic hormone secretion (SIADH) by
inhibiting the action of ADH
o One dose of demeclocycline upon tick removal has been shown to ↓ chances of getting Lyme’s

Adverse Effects
- Strong affinity for calcium
- Discoloration of permanent teeth and tooth enamel in fetuses and children, or nursing infants if taken by the mother
- May retard fetal skeletal development if taken during pregnancy
- Photosensitivity
- Alteration in intestinal flora may result in: Superinfection (overgrowth of non-susceptible organisms such as Candida),
Diarrhea, Pseudomembranous colitis
- May also cause:
- Vaginal candidiasis
- Gastric upset
- Enterocolitis
- Maculopapular rash
- Other effects

Tetracyclines
- Avoid milk products, iron preparations, antacids because of the chelation and drug-binding that occurs
- Take all medications with 6 to 8 ounces of fluid, preferably water
- Because of photosensitivity, avoid sunlight and tanning beds

D. SULFONAMIDES: NO cross-rxn w/ penicillins, macrolides, tetracyclines, HOWEVER watch out with other sulfa drugs
- Sulfadiazine, Sulfamethoxazole, Sulfisoxazole
- Often combined with another antibiotic
- Sulfamethoxazole combined with trimethoprim (a nonsulfonamide antibiotic), known as Bactrim, Sera, or Cotrimoxazole
(SMX-TMP)
- This combination is used commonly

Mechanism of Action
- Bacteriostatic action
- Prevent synthesis of folic acid required for synthesis of purines and nucleic acid
- Do not affect human cells or certain bacteria—they can use performed folic acid
- Only affect organisms that synthesize their own folic acid

Indications
- Effective against both gram-positive and gram-negative bacteria
- Treatment of UTIs caused by susceible strains of: Enterobacter spp., Escherichia coli, Klebsiella spp., Proteus mirabilis,
Proteus vulgaris, Staphylococcus aureus
- Pneumocystis jirovecii pneumonia
- Co-trimoxazole
- Upper respiratory tract infections
- Other uses (opportunistic infections in patients with HIV)

Adverse Effects
- Blood- Hemolytic and aplastic anemia, agranulocytosis, thrombocytopenia

15
 - Integumentary- Photosensitivity, exfoliative dermatitis, Stevens-Johnson syndrome, epidermal necrolysis
- GI: Nausea, vomiting, diarrhea, pancreatitis
- Other: Convulsions, crystalluria, toxic nephrosis, headache, peripheral neuritis, urticaria

Nursing Implications:
- Take with 2000 to 3000 mL of fluid/24 hr
- Assess RBCs prior to beginning therapy
- Take oral doses with food
- Penicillins
- Take oral doses with water (not juices) as acidic fluids may nullify drug’s antibacterial action
- Monitor patients taking penicillin for an allergic reaction for at least 30 minutes after administration

GENERAL ANTIBIOTIC NURSING IMPLICATIONS:

- Before beginning therapy, assess drug allergies; renal, liver, and cardiac function; and other lab studies
- Be sure to obtain thorough patient health history, including immune status
- Assess for conditions that may be contraindications to antibiotic use or that may indicate cautious use
- Assess for potential drug interactions
- It is ESSENTIAL to obtain cultures from appropriate sites BEFORE beginning antibiotic therapy
- Instruct patients to take antibiotics exactly as prescribed and for the length of time prescribed; they should not stop taking
the medication early when they feel better
- Assess for S/S of superinfection: fever, perineal itching, cough, lethargy, or any unusual discharge
- For safety reasons, check the name of the medication carefully because there are many drugs that sound alike or have
similar spellings
- Each class of antibiotics has specific adverse effects and drug interactions that must be carefully assessed and monitored
- The most common adverse effects of antibiotics are nausea, vomiting, and diarrhea
- All oral antibiotics are absorbed better if taken with at least 6 to 8 ounces of water
- Monitor for therapeutic effects: Improvement of S/S of infection, Return to normal vital signs, Negative culture and
sensitivity tests, Disappearance of fever, lethargy, drainage, and redness, adverse reactions

Nursing Considerations In Antibiotic Therapy

- Age- Elderly and Young are more susceptible to toxicity
- Pregnancy and lactation
- Allergies- Penicillin has the most frequency of drug rxns
- Genetics – Some antibiotics cause Hemolysis (G6PD) or the individual may not metabolize them well

E. Aminoglycosides: no cross-allerginicity with the previous drugs

- Kill mostly gram-negative bacteria; some gram-positive also
- Poor oral absorption; no PO forms- IV only ran over 30 mins or an hr; get peak level 30 mins after 30-min infusion stops;
trough level 30 mins before the next dose
- Very potent antibiotics with serious toxicities
- Bactericidal; prevent protein synthesis
- Examples:
o Gentamicin (Garamycin)
o Neomycin (Neo-fradin)
o Tobramycin (Nebcin)
o Amikacin (Amikin)
o Kanamycin
o Streomycin

Indications
- Used to kill gram-negative bacteria such as Pseudomonas spp., E. coli, Proteus spp., Klebsiella spp., Serratia spp.
- Often used in combination with other antibiotics for synergistic effects
- Used for certain gram-positive infections that are resistant to other antibiotics
- Aminoglycosides are poorly absorbed through the GI tract, and given parenterally
- Exceion: neomycin

16
 o Given orally to decontaminate the GI tract before surgical procedures
o Also used as an enema for this purpose

Toxicities
- Ototoxicity: Temporary or permanent hearing loss, balance problems
- Nephrotoxicity: Varying degrees of reduced renal function.
- Monitor trough levels every 5 to 7 days while on therapy or as ordered
- Monitor serum creatinine levels at least every 3 days as an index of renal function

Adverse Effects
- Cause serious toxicities
o Nephrotoxicity (renal damage)
o Ototoxicity (auditory impairment and vestibular impairment [eighth cranial nerve])
o Must monitor drug levels to prevent toxicities
o Ototoxicity and nephrotoxicity are the most significant
- Headache, Paresthesia, Fever, Superinfections, Vertigo, Skin rash, Dizziness

F. QUINOLONES: no cross-allerginicity with other drugs mentioned before

- Also called “fluoroquinolones”
- Excellent oral absorption
- Absorption reduced by antacids
- Effective against gram-negative organisms and some gram positive organisms
- Examples:
o ciprofloxacin (Cipro)
o norfloxacin (Noroxin)
o levofloxacin (Levaquin): IV & PO AMOUNTS ARE EQUAL DUE TO GREAT ABSORION
o moxifloxacin (Avelox)
- Bactericidal
- Alter DNA of bacteria, causing death
- Do not affect human DNA
- Not used in pregnant women/breastfeeding, it affected bone & cartilages in tested animal fetuses.
o RISK vs Benefit: this med was also used during the anthrax scare
Notes: this class increases risk of Achilles tendon tear

Indications
- Gram-negative bacteria such as pseudomonas
- Respiratory infections
- Bone and joint infections
- GI infections
- Skin infections
- Sexually transmitted diseases
- Anthrax

Adverse Effects
CNS: Headache, dizziness, fatigue, depression, restlessness, insomnia
GI: Nausea, vomiting, diarrhea, constipation, thrush, increased liver function studies, others
Cardiac: Prolonged QT interval
Integumentary: Rash, pruritus, urticaria, flushing, photosensitivity (with lomefloxacin)
Other: Fever, chills, blurred vision, tinnitus, also affects oral contraceptives
Black box warning: ↑ risk of tendonitis and tendon rupture (watch out with runners)

G. OTHER ANTIBIOTICS: don’t belong to a specific class, miscellaneous antibxs

- Clindamycin (Cleocin)*: used for chronic bone infections, GU infections, intra-abdominals infections, other serious infections,
may cause C diff (p. colitis), topically for acne
- Linezolid (Zyvox)*:
o New class: oxazolidinones

17
 o Used for staph infections
o Used to treat vancomycin-resistant Enterococcus faecium (VREF, VRE), hospital-acquired skin and skin structure
infections, including those with MRSA
o May cause hypotension, serotonin syndrome, & rxns if taken with tyramine-containing foods
 Do not give to pts who take SSRI’s or MAOI’s
- Metronidazole (Flagyl)*- anaerobic organisms, prophylaxis infections, intraabdominal & gynecologic infections, protozoal
infections, trichomonas, metallic taste, darkening of the urine, CNS sxs like ataxia, numbness, seizures
o DRUG OF CHOICE FOR C DIFF
o Oral or IV
o DO NOT TAKE WITH ALCOHOL- for several days after taking this antibx
 Disulfiram Rxn – GI pain, facial flushing, SOB, ↑HR, etc
- Nitrofurantoin (Macrodantin)
- Quinupristin and Dalfopristin (Synercid)
- Daomycin (Cubicin)
- Vancomycin (Vancocin)*:
o Destroys cell wall
o very poorly absorbed, not used orally except for C. Diff; anything else it is used IV
o Gram positive infections: Staph
 Treatment of choice for MRSA
o Ototoxicity & nephrotoxicity
o Peaks & troughs need to be obtained
o Ran over at least one hr or 2 hrs because it is associated with RED MAN NECK SYNDROME when given too quickly
 Flushing of face, neck, chest- anaphalactoid rxn, NOT allergic; not immune mediated; an allergic-LIKE rxn
 Give antihistamine to reduce effects
 monitor IV site closely
- Colistimethate (Coly-mycin)

EXTRA NOTES:
- TEN: toxic epidermal necrolysis- skin peels off in sheets; can be a rxn to antibiotics
- Stevens-Johnsons sxs: rare, serious disorder of your skin and mucous membranes; can be a rxn to antibiotics.
o Facial swelling, tongue swelling, hives, skin pain, red/purple skin rash, blisters on skin & mucous membranes, skin
shedding
__________________________________________________________________________

*DIGESTIVE SYSTEM DRUGS:*

The stomach secretes:
- Hydrochloric acid (HCl)- helps digest foods that we eat
- Bicarbonate- buffers acid, prevents too low of a pH
- Pepsinogen- break down food
- Intrinsic factor- absorption of B12
- Mucus- protect the lining of the stomach, GI tract from the acid
- Prostaglandins (Ex: PGE2)- beneficial in GI tract because they ↑ mucosal flood flow – if this is blocked GI upset is caused
(REMEMBER NSAIDS)

Why doesn’t the stomach digest itself?

- Defensive factors:
o Mucous secreted by the mucosa of the GI tract form a protective barrier against the digestive enzymes and acids.
o Bicarbonate is secreted by the epithelial cells. This mixes with the mucous and neutralizes acid.
o Prostaglandins stimulate blood flow, secretion of mucous and bicarbonate. Also suppress secretion of gastric acid.

Glands of the Stomach: Cardiac, Pyloric, Gastric

Cells of Gastric Glands: Parietal, Chief, Mucous, Endocrine, Enterochromaffin

Hydrochloric Acid
- Secreted by parietal cells when stimulated by food
- Maintains stomach at pH of 1-4

18
 - Secretion also stimulated by: Large fatty meals, Excessive amounts of alcohol, Emotional stress

Chief cells: Secrete pepsinogen, a proenzyme

- Pepsinogen becomes pepsin when activated by exposure to acid & Pepsin breaks down proteins (proteolytic)

Mucous cells: Mucus-secreting cells (surface epithelial cells)

- Provide a protective mucus coat & Protect against self-digestion by HCl

ACID-RELATED DISEASES
- Caused by imbalance of the three cells of the gastric gland and their secretions
- Most common: hyperacidity
- Lay terms for overproduction of HCl by the parietal cells: Indigestion, sour stomach, heartburn, acid stomach
- Peptic ulcer disease (PUD)
- Gastroesophageal reflux disease (GERD)
- Helicobacter pylori (H. pylori)
o Bacterium found in GI tract of 90% of patients with duodenal ulcers and 70% of those with gastric ulcers
o Can be detected by serum antibody tests
o Antibiotics are used to eradicate H. pylori

Factors That Promote Ulcer Disease

- Infection –specifically Helicobacter Pylori
- NSAIDS- inhibit the synthesis of prostaglandins
- anti -prostaglandin effect inhibits: blood flow, gastric mucous production , bicarbonate production
- Smoking-affects gastric secretion and production of bicarbonate
- Excessive consumption of fatty meals, alcohol, caffeine, chocolate as well as emotional stress
- Increased production of HCl

PEPIC ULCER DRUG THERAPY:

- Goals : improve symptoms, promote the healing process
- Classes of Drugs used: Antibiotics, Anti-secretory agents, Mucosal protectant, Anti-secretory agent that promotes mucosal
defenses, Antacids

Antibacterial Drugs in Ulcer Diseases:

- Usually used in combinations of two or three antibiotics
- Common antibiotic regimens used are amoxicillin, clarithromycin, tetracycline and metronidazole
- The most effect way to treat PUD is to use 2 or 3 antibiotics with an anti-secretory agent or a protein pump inhibitor

TYPES OF ACID-CONTROLLING DRUGS: Antacids, H2 antagonists, Proton pump inhibitors

ANTACIDS
Mechanism of Action
- Neutralize stomach acid that has already been produced
- Promote gastric mucosal defense mechanisms
- Secretion of:
o Mucus: protective barrier against HCl
o Bicarbonate: helps buffer acidic properties of HCl
o Prostaglandins: prevent activation of proton pump
o Antacids DO NOT prevent the overproduction of acid
o Antacids DO neutralize the acid once it is in the stomach

Drug Effects
- Reduction of pain associated with acid-related disorders
- Raising gastric pH from 1.3 to 1.6 neutralizes 50% of the gastric acid
- Raising gastric pH 1 point (1.3 to 2.3) neutralizes 90% of the gastric acid
- Reducing acidity reduces pain

19
Over-the-counter formulations available as: Capsules and tablets, Powders, Chewable tablets, Suspensions, Effervescent granules
and tablets

Used alone or in combo: Aluminum salts, Magnesium salts, Calcium salts, Sodium bicarbonate
- Aluminum Salts
o Have constipating effects
o Often used with magnesium to counteract constipation
o Often recommended for patients with renal disease (more easily excreted)
o Examples:
 Aluminum carbonate: Basaljel
 Hydroxide salt: AlternaGEL
 Combination products (aluminum and magnesium): Gaviscon, Maalox, Mylanta, Di-Gel
- Magnesium Salts
o Commonly cause diarrhea; usually used with other drugs to counteract this effect
o Dangerous when used with renal failure—kidney cannot excrete extra magnesium, resulting in accumulation
o Examples
 Hydroxide salt: magnesium hydroxide (Milk of Magnesia)
 Carbonate salt: Gaviscon (also a combination product)
 Combination products such as Maalox, Mylanta (aluminum and magnesium)
- Calcium Salts
o May cause constipation, kidney stones
o Also not recommended for patients with renal disease—may accumulate to toxic levels- hypercalcemia
o Short duration of acid action—may cause increased gastric acid secretion (hyperacidity rebound)
o Often advertised as an extra source of dietary calcium
o Example: Tums (calcium carbonate)

- Sodium Bicarbonate
o Highly soluble
o Buffers the acidic properties of HCl
o Quick onset, but short duration- needs to be taken a few times, better used for acute issues
o May cause metabolic alkalosis
o Sodium content may cause problems in patients with HF, HTN, or renal insufficiency
-
- Antiflatulents: used to relieve the painful sxs associated with gas
o Several drugs are used to bind or alter intestinal gas and are often added to antacid combination products
o Over-the-counter antiflatulents
o Activated charcoal
o Simethicone
 Alters elasticity of mucus-coated bubbles, causing them to break
 Used often, but there are limited data to support effectiveness

Adverse Effects
- Minimal, and depend on the compound used
- Aluminum and calcium: Constipation
- Magnesium: Diarrhea
- Calcium carbonate: Produces gas and belching; often combined with simethicone to prevent these

Drug Interactions
- Absorption of other drugs to antacids: Reduces the ability of the other drug to be absorbed into the body
- Chelation: Chemical binding, or inactivation, of another drug- DO NOT USE WITH TETRACYCLINES
o Produces insoluble complexes
o Result: reduced drug absorion
- Increased stomach Ph: Increased absorption of basic drugs, Decreased absorption of acidic drugs
- Increased urinary pH: Increased excretion of acidic drugs, Decreased excretion of basic drugs

Nursing Implications

20
 - Assess for allergies and preexisting conditions that may restrict the use of antacids, such as:
o Fluid imbalances, Renal disease, GI obstruction, Heart failure (HF), Pregnancy
- Patients with HF or hypertension should not use antacids with high sodium content
- Use with caution with other medications because of the many drug interactions
- Most medications should be given 1 to 2 hours after giving an antacid
- Antacids may cause premature dissolving of enteric-coated medications, resulting in stomach upset
- Be sure that chewable tablets are chewed thoroughly, and liquid forms are shaken well before giving
- Administer with at least 8 ounces of water to enhance absorption (except for “rapid-dissolve” forms)
- Long-term self-medication with antacids may mask sxs of serious underlying diseases, such as cancer or bleeding ulcers
- If sxs remain ongoing, patient should seek medical evaluation
- Monitor for adverse effects: Nausea, vomiting, abdominal pain, diarrhea
o With calcium-containing products: constipation, acid rebound
- Monitor for therapeutic response
- Notify health care provider if sxs are not relieved

HISTAMINE TYPE 2 (H2) ANTAGONISTS

- Reduce acid secretion
- All available over the counter in lower dosage forms
- Most popular drugs for treatment of acid-related disorders
o Cimetidine (Tagamet)- P450*- risk of drug interactions, CNS effects
 Do not use on the elderly- causes mental issues, confusion
o Cizatidine (Axid)
o Famotidine (Pepcid)
o Ranitidine (Zantac)

Mechanism of action: Block histamine at the (H2) receptors of acid-producing parietal cells. Production of hydrogen ions is reduced,
resulting in decreased production of HCl gut pH is increased

Drug Effect and Indications

- Drug effect: Suppressed acid secretion in the stomach
- Indications: GERD, PUD, Erosive esophagitis, Adjunct therapy to control upper GI bleeding, Pathologic gastric
hypersecretory conditions

Adverse Effects
- Overall, very few adverse effects
- Cimetidine may induce impotence and gynecomastia
- May cause headaches, lethargy, confusion, diarrhea, urticaria, sweating, flushing, other effects

Drug Interactions
- Cimetidine (Tagamet): Binds with P-450 microsomal oxidase system in the liver, resulting in inhibited oxidation of many
drugs and increased drug levels
o All H2 antagonists may inhibit the absorption of drugs that require an acidic GI environment for absorption
- Smoking has been shown to decrease the effectiveness of H2 blockers

Nursing Implications
- Assess for allergies and impaired renal or liver function
- Use with caution in patients who are confused, disoriented, or elderly
- Take 1 hour before or after antacids
- For intravenous doses, follow administration guidelines

PROTON PUMP INHIBITORS – more potent gp of drugs that inhibit HCl

- The parietal cells release positive hydrogen ions (protons) during HCl production- proton pump
- H2 blockers and antihistamines do not stop the action of this pump

Mechanism of Action
- Irreversibly bind to H+/K+ ATPase enzyme

21
 - This bond prevents the movement of hydrogen ions from the parietal cell into the stomach
- Results in achlorhydria—ALL gastric acid secretion is temporarily blocked
- To return to normal acid secretion, the parietal cell must synthesize new H+/K+ATPase

Drug Effect
- Total inhibition of gastric acid secretion
o lansoprazole (Prevacid)
o Omeprazole (Prilosec)*
o Rabeprazole (AcipHex)
o Pantoprazole (Protonix) (IV form available)
o Esomeprazole (Nexium)

Indications
- GERD maintenance therapy
- Erosive esophagitis
- Short-term treatment of active duodenal and benign gastric ulcers
- Zollinger-Ellison syndrome: ondition in which a gastrin-secreting tumor or hyperplasia of the islet cells in the pancreas
causes overproduction of gastric acid, resulting in recurrent peptic ulcers.
- Treatment of H. pylori–induced ulcers: Given with an antibiotic

Adverse Effects
- Safe for short-term therapy
- Some approved for long-term therapy
- Adverse effects uncommon

Nursing Implications
- Assess for allergies and history of liver disease
- Not all are available for parenteral administration
- May increase serum levels of diazepam and phenytoin; may increase chance for bleeding with warfarin
- The granules of pantoprazole capsules may be given via NG tubes, but NG tube must be at least 16 g or tube will get
clogged
- Capsule contents may be opened and mixed with apple juice, but do not chew or crush delayed-release granules
- Proton pump inhibitors often work best when taken 30 to 60 minutes before meals

OTHER DRUGS: SUCRALFATE (CARAFATE), MISOPROSTOL (CYTOTEC), SIMETHICONE (MYLICON)

- Sucralfate (Carafate)
o Cytoprotective drug
o Used for stress ulcers, peptic ulcer disease
o Attracted to and binds to the base of ulcers and erosions, forming a protective barrier over these areas
o Protects these areas from pepsin, which normally breaks down proteins (making ulcers worse)
o Little absorption from the gut
o May cause constipation, nausea, and dry mouth
o May impair absorption of other drugs—give other drugs at least 2 hours before sucralfate
o Do not administer with other medications
o Binds with phosphate; may be used in chronic renal failure to reduce phosphate levels
- Misoprostol (Cytotec)
o Synthetic prostaglandin analog
o Prostaglandins have cytoprotective activity
 Protect gastric mucosa from injury by enhancing local production of mucus or bicarbonate
 Promote local cell regeneration
 Help to maintain mucosal blood flow
o Used for prevention of NSAID-induced gastric ulcers
o Doses that are therapeutic enough to treat duodenal ulcers often produce abdominal cramps, diarrhea
o Some women have used this to induce an abortion
- Simethicone
o Antiflatulent drug

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  Used to reduce the discomforts of gastric or intestinal gas (flatulence)
 Alters elasticity of mucus-coated gas bubbles, breaking them into smaller ones
 Result is decreased gas pain and increased expulsion via mouth or rectum

*ANTIDIARRHEAL DRUGS & LAXATIVES*

DIARRHEA:
- Abnormal passage of stools with increased frequency, fluidity, and weight, or with increased stool water excretion
Acute diarrhea: Sudden onset in a previously healthy person. Lasts from 3 days to 2 weeks. Self-limiting. Resolves without sequelae
- Causes: bacterial, viral, drug induced, nutritional factors
Chronic diarrhea: Lasts for more than 3 weeks. Associated with recurring passage of diarrheal stools, fever, loss of appetite, nausea,
vomiting, weight loss, and chronic weakness
- Causes: tumors, DM, Addison’s Disease, Hyperthyroidism, IBS, AIDS

Mechanism of Action: Adsorbents, anticholinergic

- Adsorbents
o Coat the walls of the GI tract
o Bind to the causative bacteria or toxin, which is then eliminated through the stool
o Examples: bismuth subsalicylate (Pepto-Bismol), activated charcoal, aluminum hydroxide, others
 Bismuth subsalicylate: form of aspirin so if allergic to ASA do not take this
 Increased bleeding time, Constipation, dark stools, Confusion, twitching
 Hearing loss, tinnitus, metallic taste, blue gums
- Antimotility drugs: anticholinergics
o Decrease intestinal muscle tone and peristalsis of GI tract
o Result: slows the movement of fecal matter through the GI tract
o Examples: belladonna alkaloids (atropine, hyoscyamine)- anticholinergic effects
- Anticholinergics: Urinary retention, hesitancy, impotence, headache, dizziness, confusion, anxiety, drowsiness, confusion,
dry skin, flushing, blurred vision, hypotension, bradycardia
- Antimotility drugs: opiates
o Decrease bowel motility and relieve rectal spasms
o Decrease transit time through the bowel, allowing more time for water and electrolytes to be absorbed
o Reduce pain by relief of rectal spasms
o Examples: PAREGORIC, OPIUM TINCTURE, CODEINE, LOPERAMIDE (OTC product), DIPHENOXYLATE
o Adverse Effects: Drowsiness, sedation, dizziness, lethargy, Nausea, vomiting, anorexia, constipation, Respiratory
depression (if taken in high amounts), Hypotension, Urinary retention, Flushing
- Intestinal flora modifiers:
o Probiotics or bacterial replacement drugs
o Bacterial cultures of Lactobacillus organisms work by:
 Supplying missing bacteria to the GI tract
 Suppressing the growth of diarrhea-causing bacteria
o Example: L. acidophilus (Lactinex)

Interactions
- Adsorbents decrease the absorption of many drugs, including digoxin, clindamycin, quinidine, hypoglycemic drugs, others
- Adsorbents cause increased bleeding time and bruising when given with anticoagulants
- Antacids can decrease effects of anticholinergic antidiarrheal drugs

Nursing Implications
- Obtain thorough hx of bowel patterns, general state of health, & recent history of illness or dietary changes; assess for
allergies
- Do NOT give bismuth subsalicylate to children or teenagers w/ chickenpox or influenza because of risk of Reye’s syndrome
- Use adsorbents carefully in elderly s or those with ↓ bleeding time, clotting disorders, recent bowel surgery, confusion
- Do not administer anticholinergics to s with a hx of narrow-angle glaucoma, GI obstruction, myasthenia gravis, paralytic
ileus, and toxic megacolon
- Teach s to take medications exactly as prescribed and to be aware of their fluid intake and dietary changes
- Assess fluid volume status, I&O, and mucous membranes before, during, and after initiation of treatment

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 - Teach patients to notify their physician immediately if symoms persist
- Monitor for therapeutic effect

CONSTIPATION: Abnormally infrequent & difficult passage of feces through the lower GI tract. Symom, not a disease. Disorder of
movement through the colon and/or rectum. Can be caused by a variety of diseases or drugs

LAXATIVES: Bulk forming, Emollient, Hyperosmotic, Saline, Stimulant, Peripherally acting opioid antagonists

A. BULK FORMING LAXATIVES:

- High fiber
- Absorb water to increase bulk
- Distend bowel to initiate reflex bowel activity
- Examples: PSYLLIUM (METAMUCIL) & METHYLCELLULOSE (CITRUCEL)
- INDICATIONS: acute & chronic constipation, IBS, diverticulosis
- ADVERSE EFFECTS: impaction. Fluid overload, electrolyte imbalances*, esophageal blockage

B. EMOLIENT LAXATIVES:
- Stool softeners and lubricants
- Promote more water and fat in the stools
- Lubricate the fecal material and intestinal walls
- Examples:
o Stool softeners: DOCUSATE SALTS (Colace, Surfak)
o Lubricants: Mineral oil
 Do not use orally due to risk of aspiration
- INDICATIONS: acute & chronic constipation, fecal impaction facilitation of bowel movements in anorectal conditions
- ADVERSE EFFECTS: skin rashes, ↓ absorption of vitamins, electrolyte imbalances*, lipid pneumonia

C. HYPEROSMOTIC LAXATIVES: high osmotic load

- Increase fecal water content
- Results in bowel distention, increased peristalsis, and evacuation
- Examples: POLYETHYLENE GLYCOL (PEG; not absorbed, same ingredients as in golytely or miralax), SORBITOL, GLYCERIN,
LACTULOSE
o Lactulose is also used to reduce elevated serum ammonia levels
o PEG is safest- molecule is not absorbed so it doesn’t cause an electrolyte abnormality
o Others can cause electrolyte and fluid abnormalities
o Glycerin used in suppositories
o Sorbitol- sucking candies have sorbitol- sugar free anything has sorbitol
- INDICATIONS: chronic constipation, dx & surgical preps
- ADVERSE EFFECTS: abdominal bloating, electrolyte imbalances*, rectal irritation

D. SALINE: Increase osmotic pressure within the intestinal tract, causing more water to enter the intestines
o Results in bowel distention, increased peristalsis, and evacuation
o Examples:
 MAGNESIUM HYDROXIDE (Milk of Magnesia)
 MAGNESIUM CITRATE (CITROMA)
- INDICATIONS: constipation, dx & surgical preps
- ADVERSE EFFECTS: Mg toxicity (w/ renal insufficiency), cramping, electrolyte imbalances*, diarrhea, ↑ thirst

E. STIMULANT LAXATIVES:
- Increases peristalsis via intestinal nerve stimulation
- Examples: SENNA (SENEKOT), BISACODYL (DULCOLAX)
- Give bisacodyl with water because of interactions with milk, antacids, and juices
- INDICATIONS: acute constipation, dx & surgical preps
- ADVERSE EFFECTS: nutrient malabsorion, skin rashes, gastric irritation, electrolyte imbalances*, discolored urine, rectal
irritation, GI cramping

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F. PERIPHERALLY ACTING OPIOD ANTAGONISTS
- Treatment of constipation related to opioid use and bowel resection therapy
- Block entrance of opioid into bowel
- Strict regulations for use
- Allow bowel to function normally with continued opioid use:
o METHYLNALTREXONE (RELISTOR) & ALVIMOPAN (ENTEREG)
-

NURSING IMPLICATIONS FOR LAXATIVES:

- Obtain a thorough history of presenting symoms, elimination patterns, and allergies
- Assess fluid and electrolytes before initiating therapy
- Inform patients not to take a laxative or cathartic if they are experiencing nausea, vomiting, and/or abdominal pain
- A healthy, high-fiber diet and increased fluid intake should be encouraged as an alternative to laxative use
- Long-term use of laxatives often results in decreased bowel tone and may lead to dependency
- All laxative tablets should be swallowed whole, not crushed or chewed, especially if enteric coated
- Patients should take all laxative tablets with 6 to 8 ounces of water
- Patients should take bulk-forming laxatives as directed by the manufacturer with at least 240 mL (8 ounces) of water
- Inform patients to contact their physician if they experience severe abdominal pain, muscle weakness, cramps, and/or
dizziness, which may indicate possible fluid or electrolyte loss
- Monitor for therapeutic effect

*ANTIEMETIC DRUGS*
- Nausea: Unpleasant feeling that often precedes vomiting
- Emesis (vomiting): Forcible emying of gastric, and occasionally, intestinal contents
Antiemetic drugs: Used to relieve nausea and vomiting

Vomiting Center and Chemoreceor Trigger Zone: Both located in the brain. Once stimulated, cause the vomiting reflex

Antiemetics and Antinausea Drugs: Most work by blocking one of the vomiting pathways, thus blocking the stimulus that induces
vomiting

INDICATIONS:
- Specific indications vary per class of antiemetics
- General use for each type: prevention and reduction of nausea and vomiting

A. ANTICHOLINERGIC DRUGS ( Ach blockers)

- Bind to and block acetylcholine (ACh) receptors in the inner ear labyrinth
- Block transmission of nauseating stimuli to CTZ
- Also block transmission of nauseating stimuli from the reticular formation to the VC
- SCOPOLAMINE: Also used for motion sickness (transdermal patch)-applied behind the ear
- Effects: dry mouth, dry eyes, urinary retention, etc

B. ANTIHISTAMINE DRUGS (H1 receptor blockers)

- Inhibit ACh by binding to H1 receptors
- Prevent cholinergic stimulation in vestibular and reticular areas, thus preventing nausea and vomiting
- Also used for motion sickness, nonproductive cough, allergy symptoms, sedation
- DIMENHYDRINATE (DRAMAMINE), DIPHENHYDRAMINE (BENADRYL), MECLIZINE (ANTIVERT)

C. ANTIDOPAMINERGIC
- Block dopamine receptors on the CTZ
- Also used for psychotic disorders, intractable hiccups
- PROCHLORPERAZINE (COMPAZINE)- very sedating
- PROMETHAZINE (PHENERGAN)
- DROPERIDOL (INAPSINE)- use is controversial because of associated cardiac dysrhythmia
- All may cause sedation
- Rare dystonic reactions-block dopamine receptors

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D. PROKINETIC DRUGS:
- Block dopamine in the CTZ
- Cause CTZ to be desensitized to impulses it receives from the GI tract
- Also stimulate peristalsis in GI tract, enhancing emptying of stomach contents
o Treats Diabetic Gastroparesis
- Also used for GERD, delayed gastric emptying
- METOCOPRAMIDE (REGLAN)
o Long-term use may cause irreversible tardive dyskinesia

E. SEROTONIN BLOCKERS:
- Block serotonin receptors in the GI tract, CTZ, and VC
- Used for nausea and vomiting in patients receiving chemotherapy and for postoperative nausea and vomiting
o Given in advanced
- DOLASETRON (ANZEMET)
- GRANISETRON (KYTRIL)
- ONDANSETRON (ZOFRAN)
- PALONOSETRON (ALOXI)

F. TETRAHYDROCANNABINOIDS
- Major psychoactive substance in marijuana
- Inhibitory effects on reticular formation, thalamus, cerebral cortex
- Alter mood and body’s perception of its surroundings
- Example: DRONABINOL (MARINOL)
- Used for N/V associated with chemotherapy, and anorexia associated with wt loss in AIDS patients

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