• Converts arachidonic acid from cells into prostaglandins and their products

• The synthesis of prostaglandins causes inflammation and pain at the tissue injury site

• The greater the amount of tissue damage, the more prostaglandins are produced which means the greater the pain

COX-1: present in all tissues- produces prostaglandis, protects the stomach lining from gastric acid and regulates blood platelets, promotes renal blood flow, smooth muscle tone in blood vessels and in the broncial tree

COX-2: has only one action- triggers inflammation and pain at the injured site

reduces pain, fever and inflammation; do not cause gastric ulceration and have no effect on platelet function

• Inhibit prostaglandin synthesis
• Mimic the effects of corticosteroids but not chemically related

Inhibit COX-1 and COX-2

Side effects:

• GI irritation, sodium and water retention, HA, drowsiness, dizziness, fatigue, GFR impairment
• Genarally contraindicated in people w/CV dysfunction, hypertension, peptic ulcer disease

Nursing intervention: take w/food or milk to ↓ gastric upset

They are aspirin and aspirin like drugs

Have approximately the same efficacy, but may be variable in patients' responses & side effects

uses: reduce inflammation and pain (reduces swelling & stiffness)

Less antipyretic effects

Not recommended for fever or headaches, except for aspirin/ibuprofen

Redness

Swelling

Heat

Pain

Loss of Function

1st mediator: Released during inflammatory process

Stored in Mast cells located in tissue spaces under epithelial membranes: skin, bronchial tree, digestive tract, along blood vessels

Directly stimulates pain receptors

When released @ site of injury cause dilation of arterioles

Increase capillary permeability

Causes injured/affected area to be congested w/blood=swelling & pain

H₁ receptor: present in smooth muscle of vascular system, broncial tree, and digestive tract

stimulation causes itching, pain, edema, vasodilation, bronchoconstriction

H₂ receptor: present primarily in the stomach

stimulation causes secretion of large amounts of HCl

Three distinct actions:

anti-inflammatory (prostaglandin inhibitor)

antipyretic

antiplatelet- used w/CV disorders, DVT, TIA, prevention of MI

Therapeutic serum salicylate level: 10-30mg/dl

Toxic serum salicylate level: >30mg/dl

Well absorbed from GI tract; take w/milk and/or food

Short 1/2life; onset 30 minutes; peak 1-2 hours

Drug:

Do not take with other NSAIDs

Increases action of anticoagulants and hypoglycemic agents, increase gastric ulcer risk w/glucocorticoids, inhibits valproic acid metabolism (can cause toxicity), reduces the antihyperintensive effects of beta-blockers and ACE inhibitors

Lab:

increases PT, bleeding time, INR, uric acid

decrease potassium, cholesterol, T3 and T4 levels

Side effects:

tinnitus, vertigo

gastric distress/peptic ulcer, N/V/D

thrombocytopenia, leukopenia, agranulocytosis

hepatotoxicity, increased serum ammonia, encephalitis

decreases uric acid excretion

Toxicity:

convulsions, CV collapse, coma

It is a propionic acid derivative, and is relatively new

Act like ASA; have stronger effects and less GI irritation

Relieve pain, anti-inflammatory effect, reduce fever

Well absorbed; short onset of action, peak and duration

Highly protein-bound; therefore may displace other drugs

Use: non-selective COX inhibitor

Drug/drug:

↑ effects of warfarin, phenytoin, sulfonamides, calcium blockers

↓ effects if taken w/ASA

If taken w/insulin or oral hypoglycemics may lead to hypoglycemia

Side effects: gastric distress, GI bleeding (take w/food)

COX-2 inhibitor- a 2nd generation NSAID

Developed to eliminate the GI side effects associated w/ASA and other NSAIDs

Action: similar to NSAID; selectively inhibits COX-2 enzyme w/out inhibiting COX-1, so there is no impact on the stomach lining

Use:

-Decrease inflammation and pain; drug of choice for severe arthritic conditions when high doses of an anti-inflammatory drug are needed

-Antipyretic

Does not interfere w/low dose ASA

Contraindications: -individuals who have sulfonamide allergy

Caution: -avoid during 3rd trimester

-caution in renal/hepatic dysfunction

-hypertension, fluid retention, heart failure, infection

-may increase risk of lithium toxicity

-concurrent anticoagulant therapy

-steroids or ETOH use

Side effects:

-Mild: HA, dizzyness, N/D, sinusitis, peripheral edema; hypertension, heart failure

-Assess renal function & GI status

• inflammatory disease of joints, tendons

• uric acid crystals usually accumulate in base of big toe -may apear as bumps (tophi) in the subQ tissues

• defect in purine metabolism leads to uric acid accumulation and/or ineffective clearance of uric acid by the kidneys -purine containing foods: salmon, liver, sardines

An antigout drug

Properties: Inhibits migration of leukocytes to inflamed site

Effective in alleviating acute symptoms of gout attacks, but not effective in decreasing inflammation occurring in other inflammatory disorders

Does not inhibit uric acid synthesis; does not promote uric acid secretion

Side effects: N/V/D abd pain, gastric irritation, paralytic ileus, stomatitis, fever, malaise, pain, dehydration, oliguria

Nursing interventions: take w/food because of Gi distress; fluid intake

An antigout drug that inhibits uric acid (is not anti-inflammatory)

Action: decreases uric acid levels; inhibits the final steps of uric acid biosynthesis by inhibiting the enzyme xanthine oxidase

may be used w/pts who have renal obstructions caused by uric acid stones & for pts w/chronic tophaceous gout

frequently used prophylactically to prevent gout attacks

• Monitor CBC, liver enzymes, renal function

• Teach: avoid ETOH, caffeine, & thiazide diuretics that increase uric acid levlels

• Avoid foods rich in purines: organ meants, sardines, salmon, gravy, herring, meat soups, ETOH

• Increase fluid intake to increase uric acid excretion and prevent renal calculi

• Yearly eye exams for visual changes

is a uricosuric antigout drug

Action: increases rate of uric acid excretion; inhibits reabsorption of uric acid; do not use in acute attacks; affective in alleviating chronic gout; 1/2 life 8-10 hours; highly protein bound

Side effects: gastric irritation; severe blood dyscrasias, flushed skin, sore gums, headache

Nursing interventions: take w/food, not to be given w/other highly protein bound drugs; increase fluid intake to increase uric acid excretion; can be taken w/colchincine

Reflects the level of stimulus needed to create a painful sensation in an individual

• individual genetic makeup contributes to the variations

• the mu opioid receptor gene controls the number of mu receptors present; if a person has a large number of mu receptors than the pain threshold is high/pain sensitivity reduced

The amount of pain a person can endure w/out having it interfere w/normal functiong

• is a psychological aspect of pain; is very subjective

• varies greatly from person to person

• influenced by many factors such as age, gender, culture, ethnicity, previous experiences, anxiety level, specific circumstances

• Usually associated w/a specific tissue injury
• Generally short duration: occuring overa  defined time
• Can be mild, moderate, or severe

• Vague origin and onset
• Prolonged duration; >6 months
• May interfere w/daily activies and produce feelings of hopelessness or helplessness

Somatic: sharp, localized sensation

structural tissues: skeletal muscle, ligaments, joints

Visceral: generalized, dull, throbbing, aching pain

smooth muscles and organs

caused by physical dependence from chronic use

symptoms usually occur w/in 24-48 hours after last dose

intense, compelling desire to continue the drug: irritability, diaphoresis, restlessness, muscle twitching, increased pulse, and hypertension

Not usually lifethreatening

Patients w/head injuries:

opiods- decreased/depressed respiratory which increases CO₂ which causes cerebral blood vessel dilation which increases ICP

Patients w/respiratory disorders:

asthma: opiates decrease respiratory drive while simultaneously increasing airway resistance

Shock, hypotension: opiods may further decrease BP

Older/debilitated: use lower amounts of opiods 

• usually the 1st step in pain control
• treat mild-moderate pain: HA, dysmenorrhea, inflammation, minor abrasions, muscle aches & pain, arthritis
• non-addicting, inexpensive; many are OTC
• less potent than opioids
• salicylate analgesics
• NSAIDS
• nonsalicylate analgesic drugs

activate the same receptor sites as the endorphins; produce a natural feeling of pain relief w/out the use of drugs

prescribed for moderate to severe pain, and as a preopmed

low dose arcotic analgesics are generally safer than NSAIDs for longer-term use in the elderly

Schedule II: strictly regulated

inhibits prostaglandin synthesis and blocks pain impulse at pain receptor sites in peripheral NS

relieves pain, HA, discomfort, fever (use w/flu) muscular aches; can be used in children

antipyretic: acts on hypothalamus heat regulating center to dissipate heat through the process of vasodilation and sweating

weak antiinflammatory effects

325-650mg q4-6 hr; maximum dose 4g/day; do not use for more than 10 days w/out consulting PCP

if frequent acetaminophen user, limit to 2g/day to lesson hepatic/renal dysfunction

monitor liver enzymes and serum bilirubin levels

rapid onset of action 10-30 min; short 1/2life; duration of action ~5hrs; well absorbed from the GI tract

Benefits: minimal gastric distress, does not interfere w/platelet aggregation; no link w/reye's syndrome; many forms: tabs, capsules, caplet, chewable, gelcaps, liquid, infant drops, suppository;

ingredient in many OTC's ie: cold & flue relief, midol

Risks: side effects- rash, anorexia, N/V, low incidence gastric distress

toxic effects/overdose: varies ~10-12gm; hepatotoxicity (hepatic necrosis- death within 1-4 days) thrombocytopenia

Contraindications: renal dysfunction, anemia, ETOH

Potent opioid analgesic; the opioid analgesic prototype = all other opiods are measured in comparison to morphine

Effective against pain resulting from acute MI, cancer, & dyspnea from pulmonary edema; may be used as a preop med

Binds w/the mu & kappa opiate receptors in CNS

Can be given PO (but erratic due to 1st pass effect); can give rectally/epidurally; usually given IV w/severe pain; rapid onset

Readily depresses respirations

PF: 30% protein bound; short 1/2 life- 3-5hrs; 90% excreted;

MS Contin= controlled release PO, duration 8-12hrs

SE: respiratory depression, orthostatic hypotension, miosis, urinary retention, constipation, cough suppression

NI: monitor output, assess pain: location, intensity, characteristics, duration; assess bowel sounds for decreased peristalsis, pupiles for pinpoint (indicates overdose)

Caution: older adults and very young

Antidote: Narcan/Narloxone are opioid antagonists

Not as potent at morphine: 1/15 to 1/20 as potent

Use: relieves mild to moderate pain, supresses cough (antitussive)

can be used w/a nonopioid for pain

S/E: N/V, constipation, tachycardia, hypotension, respiratory depression, urinary retention, drowsiness, mental clouding

Prolonged Use: pupillary constriction, tolerance, and physical dependence

Use: semisynthetic opiod; similar to morphine

analygesic effect- ~6x more potent than morphine w/fewer hypnotic effects and less GI distress

faster onset, shorter duration of action than morphine

can be given during pregnancy; no antitussive, less constipation & urinary retention; not for chronic pain

S/E: hypotension, neurotoxicity (nervousness, tremors, agitation, irritability, seirzures)  w/older adults

Contraindications: long-term use, severe liver dysfunction, sever CAD, cardiace dysrhythmias, hx seizures: avoid ETOH & sedative-hypnotics (cause addive CNS depression); renal insufficiency

Use: antidote for opiate overdoses: reverses effects of opiates, including respiratory dpression, sedation, hypotension

respiratory distress, respiratory depression

Action: blocks the receptor and displaces any opioid that would normally be at the receptor, inhibiting the opioid action

Step 1: mild pain- nonopioids w/or w/out adjuvant med

Step 2: moderate pain- nonopioids and mild opioid w/or w/out an adjuvant

Step 3: severe pain- stronger opioid at higher dosage levels w/or w/out adjuvant med

Positive:

exaggeration of normal function or behavior (add on to normal behavior); agitation, incoherent speech, hallucinations, delusions, paranoia, and strange/irrational actions; are better managed by antipsychotics

Negative:

decrease or loss in function and motivation (subtract from normal behavior); poor self-care, poverty/loss of speech content, marked social withdrawal, poor job/acedemic performance, attitude of indifference or detachment towards life activities, tend to be more chronic and persistent; Not as well managed by antipsychotics

• Block D₂ dopamine receptors in the brain

- five subtypes of dopamine receptors (D₁-D₅)

- when D₂ receptor is blocked then extrapyramidal symptoms (EPS) resulting in pseudoparkinsonism

• Many antipsychotics also block the chemoreceptor trigger zone and vomiting center in the brain

Stooped posture

Masklike facial features

Rigidity

Tremors @ rest

Shuffling gait

Bradykinesia

Pill-rolling motion of the hand

• More pronounced w/high-potency typical antipsychotics (ie: Prolixin) and less pronounced w/low-strength antipsychotics such as Thorazine
• If EPS are reported early and the drug is withdrawn or dosage reduced the side effects can be reversible
• If anticholinergic also prescribed, may prevent some of EPS

• Can occur during early treatment w/typicals
• Occurs in 5% w/in a few days of taking typicals
• Muscle spasms of face, tongue, neck, and back
• Facial grimacing
• Abnormal or involuntary upward eye movements
• Prolonged muscle contractions w/twisting, repetitive movements
• Laryngeal spasms that can impair respirations
• Treatment: anticolinergics such as Cogentin

• Constant motion, pacing floor, difficulty standing still, restless
• Occurs in 20% of those who take typical antipsychotic drug
• May appear w/in days of initiating treatment
• Best treated w/benzos such as Ativan or beta-blockers such as Inderal

• A later serious adverse EPS reaction
• Occurs in pts who have taken a typical antipsychotic for more than one year (depends on dosage/duration)
• Protrusion and rolling of tongue, sucking and smacking of lips, chewing motion & involuntary movement of body & extremities
• May be more frequent & severe in older adults
• Stop the drug
• Treatment: benzos, calcium channel blockers or beta-blockers, high doses of Vitamin E, clozapine

-no one agent is effective for all clients

-anticholinergics have little effect

Rare, potentially fatal condition

Symptoms: muscle rigidity, sudden high fever, altered mental status, BP fluctuations, tachycardia, dysrhythmias, seizures, rhabdomyolysis (rapid breakdown of skeletal muscle releasing myoglobin into the bloodstream; may cause renal damage), acute renal failure, respiratory failure, coma

Treatment: immediate withdrawal of antipsychotics, hydration, hypthermic blankets, antipyretics, benzos, muscle relaxants

They are a typical antipsychotic that does not cause physical/psychological dependence

• Most effective for treating the positive signs of schizophrenia
• Block NE causing sedative & hypotensive effects early on
• Wide margin of safety between therapeutic and lethal dose
• Most can be given PO, IM, IV
• Most highly protein bound, metabolized by liver enzymes
• Slow excretion; may produce pinkish-red-brownish urine
• Full therapeutic effect may take 3-6 weeks, but observable effects may be w/in 7-10 days; noncompliance is common

Contraindications: CNS depressants, antihypertensives, coma, alcohol withdrawal, lactation; caution w/lung disorders

Nurisng interventsion: monitor liver and kidney function, eyes, mental status; monitor for EPS, drowsiness and sedation

-monitor for non-compliance

Adverse effects: EPS, anticholinergic effects, hypotension, parkinsonism, sedation, sexual dysfunction

1. Aliphatic: strong sedative and hypotensive effects; may cause moderate EPS

2. Piperazine: high potency; low sedative & strong antiemetic effects, little effect on BP; dry mouth, urinary retention, agranulocytosis; cause more EPS than other phenothiazines; ie: Prolixin

3. Piperidine: strong sedative effects, no antiemetic effect; cause few EPS, low to moderate effect on BP

A typical antipsychotic phenothiazine of the piperazine group

• Blocks D receptors in brain; also has anticholinergic properties
• Rapid onset & absorption, not affected by food, duration 6-8 hours, long half life
• Crosses the BBB, metabolized by liver, slowly excreted in urine

Side effects:

sedation, dizziness, HA, seizures

dry mouth, nasal congestion, blurred vision, urinary retention, photosensitivity

GI distress peripheral edema, tachycardia, EPS

its a typical antipsychotic

• Chemical structures are dissimilar to phenothiazines; but w/same therapeutic effects and equal efficacy
• May cause less sedation and fewer anticholinergic effects, but exhibit equal or greater EPS effects

1. Dibenzoxazepines: moderately potent, moderate sedative and hypotensive effects; strong EPS effects

2. Butyrophenomes: block only D; strong EPS

3. Thioxanthenes: block NE causing sedative & hypotensive effects; highly potent

4. Dihydroindolones: low sedative effects: high EPS

Use:

Management of acute and chronic psychotic disorders

Children w/severe behavioral problems such as unprovoked aggression and explosive hyperexcitability

Treat schizoprenia, tourette's syndrome, dementia

Side effects:

can begin 5-30 days after beginning therapy

drowsiness/sedation, EPS, HA, seizures

anticholinergic effects: dry mouth, blurred vision, tachycardia, urinary retention, constipation, photosensitivity, orthostatic hypotension, dysrhythmias

They are 2nd generation antipsychotics; also known as S/D antagonists

• Differ from typicals: broader spectrum of action than conventional
• Effective in treating both positive & negative symptoms of schizoprenia
• Not as likely to cause EPS or TD @ therapeutic doses
• Greater affinity for blocking S & D (D₄) receptors (rather than D₂)
• Weight gain is common; therefore compliance may be impacted

The first atypical antipsychotic

For schizophrenics not responding to or intolerant of tradition antipsychotics; treat both +/- symptoms

Action: blocks S and Dopaminergic D₄ receptors

Less likely to cause EPS or TD

Therapeutic effects: 2-4 weeks; peak of drug 2-4 hours

Side effects: agranuloctyosis (failure of bone marow to make WBC)

NI: monitor weekly WBC counts

Its an atypical antipsychotics that interferes w/the binding of D to D₂ and S receptors

low occurence of EPS and TD

Rapidly absorbed; 90% protein bound; mainly exrected in urine

SE: ECG changes, does NOT cause agranulocytosis

Interactions: increased effects of antihypertensives

decreased levels w/concurrent use of carbamazepine

Contraindications: hypersensitivity, dysrhythmias, blood dyscrasias, liver damage

Atypical antipsychotic

Does not cause EPS symptoms

Effective for treating pos/neg symptoms

Does not cause agranulocytosis

May cause HA, dizziness, agitation, insomnia, & somnolence

atypical antipsychotic

PO

less likely to cause EPS

may cause dizziness, HA, and sedation

used to treat primary anxiety and insomnia

SE: drowsiness, dizziness, weakness, confusion, blurred vision, GI distress, sleep disturbance, restlessness, hallucinations

Major group = benzodiazepines

Use: anxiolytic (antianxiety), anticonvulsant, sedative-hypnotic, preoperative drug

SE: drowsiness, dizziness, weakness, confusion, blurred vision, GI distress, sleep disturbance, restlessness, hallucination

Therapeutic onset: 1-2 weeks

May be related to insufficient amount of brain monomine (MAO) neurotransmitters (NE, S, and possibly D)

• Decreased S permits depression to occur (S is associated w/arousal and general activity levels of the CNS)
• Decreased level of NE cause depression (NE is associated w/control of arousal, attention, vigilance, mood, affect and anxiety)

Other factors: social/environmental; genetic predisposition; biologic conditions; postpartum blues/hormonal changes; SAD-reduced melatonin

Use: for major depression and agitated depression; elevates mood, increases interest in ADLs, decreases insomnia

block uptake of neurotransmitters NE and S in presynaptic nerve terminals of brain

blocks histamine receptors

SE: sedation, dizziness, nervousness, blurred vision, metallic taste, dry mouth/eyes, urinary retention, constipation, weight gain, GI distress, sexual dysfunction

Onset of therapeutic range: develop slowly over 1-4 weeks

Use: more commonly used than TCA's for depression; have ~ the same efficacy as TCA but have fewer side effects (safer) & may elicit a therapeutic effect more quickly. For major depression, anxiety disorders, PTSD, eating disorders, selective drug abuses, prevent migraines, minimizes aggression in borderline personality disorder, post-partum depression, chronic fatigue

Action: block/slow reuptake of S into the nerve terminal of the CNS which enhances the transmission @ the serotonergic synapse. Presynaptic receptors become less sensitive & postsynaptic receptors become more sensitive.

Does not block D/NE uptake; Does not block alpha₁ receptors or cholinergic receptors

Prozac is an SSRI

effective in ~50-60% of pts who do not respond to TCAs

onset of clinical effects: 1-4 weeks

PO: 20 mg each morning, increase by 20 mg at weekly intervals to 80mg/day

also comes in 90 mg sustained release capsule once/week

well-absorbed; peak concentration 4-8hr; 1/2 life 2-3 days

may have cumulative effect w/long-term use

strongly protein bound

metabolized and excreted by kidneys

Interactions: increased CNS effect w/ETOH & other CNS depressants

Many have grapefruit juice interactions

Se: HA, nervousness, restlessness, insomnia, tremors, GI distress- anorexia, N/V/D, dry mouth, blurred vision, sexual dysfunction

Seizures, suicidal ideation

Se often decrease over 2-4 weeks while waiting for therapeutic effect to emerge.

accumulation of serotonin with the use of SSRIs

may ocur when pt is taking another medication that affects the metabolism, synthesis/reuptake of S- mental status changes

Use: for mild, reactive, & atypical depress; chronic anxiety, hypersomnia, & fear

used only in ~1% pts taking antidepressents because of high risk of hypertensive crisis resulting from food interactions; so generally only used when depression can not be controlled by TCAs (have the same effectiveness as TCAs/SSRIs)

Action: MAO inactivates NE, D, E, & S; MAO enzymes are found primarily in the liver and brain

MAO-A inactivates D in brain; MAO-B inactivates NE and S

By inhibiting MAO, the levels of NE, D, E & S increase, which relieves symptoms of depression

Are nonselective, so inhibt MAO-A&B

Full therapeutic effect may take 4-8 weeks

Se: low margin of safety; CNS stimulation: agitation, restlessness, HA, insomnia, D, orthostatic hypotension, anticholinergic effects; Hypertensive crisis do to tyramine interactions from food and cause sympathomimetic like effects- rapid pulse, N/V/HA, sweating, tremors, hypertension, increased temperature

Foods to avoid: cheddar, swiss, blue cheese, sour cream, yogurt, bananas, avacados, raisins, papaya, canned figs, liver, yeast, coffee, chocoalte, beer, red wine, liver, pickled herring, anchovies, shrimp, sausage, soy sauce

Drug/drug: avoid barbiturates, TCAs, CNS depressants, antihistamines, vasoconstrictors, ginseng, ephedra, St. John's Wort

• thought to alter the activity of neurons containing D, NE, &S by influencing their release, synthesis, and uptake
• alteration of ion transport in muscles & nerve cells
• increased receptor sensitivity to S
• fast onset of action; well absorbed, 1/2 life 24 hrs; desired effect may take 5-6 days
• manic behaviro may return if drug is discontinued

• treat/stabilize manic episodes in bipolar psychosis
• has calming effect w/out impairing intellectual activity
• controls flight of ideas and hyperactivity
• narrow therapeutic range; monitor biweekly until reach therapeutic range, then monitor monthly
• metabolized by liver, most excreted unchanged in urine
• fast onset of action, but desirable effect may take 5-6 days

Increased lithium level w/thiazide diurectics, methyldopa, haloperidol, NSAIDs, antidepressants, theophylline, phenothiazines, tetracyclines

NSAIDs should not be givien w/Lithium on a continuous basis; avoid caffeine which can aggravate the manic phase

Monitor: vitals, sodium levels (tend to be depleted with Lithium); drug effectiveness, suicidal tendencies; urine output & for fluid loss/dehydration; renal function & thyroid function; Lithium levels ever 1-2 months; toxic >2 mEq/L

Encourage/push adequate fluid intake (1-2L daily)

Take w/food to decrease GI irritation

Instruct to wear medic-alert bracelet

Teach to take drug as prescribed & keep medical appointments

Do not drive/operate dangerous equip. until effect is known

Advise that drug effect may take 1-2 weeks

Encourage to avoid caffeine, crash diets, NSAIDs, diuretics

Do not get pregnant due to teratogenic effects

Natural: also called inherent- occurs w/out previous exposure to the drug

Acquired: caused by prior exposure to the antibacterial drug; ie: staph aureus has become resistant to pen G; pathogen acquires gene for bacteria resistance through mutation, as bacteria reproduce, some mutation occurs through cell division and eventually the mutant bacteria survive the effects of the drug; they may have grown a thicker wall

• can occur between antibacterial drugs that have similar actions (penicillin & cephalosporins)

• bacteria can transfer their genetic instruction to another bacterial species, and that species becomes resistant to that antibiotic as well

• bacteria can pass along high resistance to a more virulent and aggressive bacterium (such as S. aureus, or enterococci); many enterococcal strains are resistant to penicillin, ampicillin, gentamycin, streptomycin, and vancomycin

Infections acquired while pt is hospitalized

Many caused by drug-resistant bacteria

can prolong hospitalization (costly)

Can be very serious in critically ill

MRSA: methicillin-resistant staph aureus

VRE: vancomycin-resistent enterococci

-can cause death in weakened individuals

- staph bacteria tend to be resistant to every drug except vancomycin

• process of growing the pathogen and identify the most effective antibiotic
• determine the organism causing the infection by culture (blood, sputum, urine, CSF)
• ascertains the effect antibacterial drugs hae on specific microorgansims
• may take days to identify the bacteria
• is not always necessary; some infections are mild, or provider makes an accurate diagnosis based on client S&S

• Develop drugs that disable the antibiotic-resistance mechanism in the bacteria
• pts would take this disabler along w/the antibiotic which would make the antibiotic effective again
• bacterial vaccine

Broad Spectrum:

Effective against gram + & gram -

Used to treat infections when microorganism has not yet been identified by culture and sensitivity

Narrow Spectrum:

Primarily effective against one type of organism

Are selective (more active against those single organisms)

ie: penicillin or erythromycin for gram + bacteria

• 2° infection: occur when normal flora are killed by antibiotic; host flora normally prevent growth of pathogenic organisms but the chemical environment is altered and a new infection is "superimposed" on an original infection

• Occurs more commonly w/the use of broad specturm antibiotics

• Fungal infections are frequently superinfections
• Sites: mouth, skin, resp. tract, vagina, intestines, GU tract, bladder
• Usually occurs when treated more than 1 week

Occur in 5-10% of persons receiving penicillin

hypersensitivity, superinfection

N/V/D, rash

Decreased platelet aggregation w/high doses

Anaphylactic reaction/shock, laryngeal edema/bronchoconstriction, hypotension, glossitis, stomatitis, decreased RBC/WBC

Immediate reactions occur w/in first 30 minutes

Delayed reactions may take days or weeks to develop

Broad spectrums may decrease effectiveness of oral contraceptives; Potassium Pen G or Pen V can increase K+ levels

May have decreased absorption if taken w/juices or carbonated drinks

When mixed w/an aminoglycoside in IV solution, the action of both drugs in inactivated

Use decreased dose if decreased renal function (most beta-lactam antibiotics are excreted by kidneys)

Assess renal function (BUN) and serum creatinine, measure output

• Culture & sensitivity before initiating drugs; however 1st dose may be given pending the results of the C&S
• Allergy history before starting therapy; then monitor after starting 1st dose for development of allergy
• Monitor for bleeding
• Increase fluids, monitor urine output
• Take 1hr before or 2hr after meals
• Check for superinfection

1. Natural/Basic

2. Aminopenicillion (broad spectrum)

3. Penicillinase-resistant

4. Extended-spectrum

Pen G (Na/K): 1st drug; prototype; primarily bactericidal; drug of choice for almost all nonpenicillinase-producing nonmethicillin resistant gram + bacteria; poorly absorbed PO (only 1/3), can be givien IM or IV to maintain mroe therapeutic dose; Aqueous Pen G: short duration, painful IM; Pen G Procain: longer acting less painful

Pen V: less potent than Pen G; effective against mild/moderate infections & anthrax; better absorbed PO (2/3), can be taken after meals

Use: pharygitis, tonsillitis, otitis media, pneumonia, endocarditis, meningitis, soft tissue infections

Take w/full glass of water, NO FOOD

Bactericidal: interferes w/cell wall synthesis causing cell wall lysis

Use: for both gram + and -; E-coli, Salmonella, H influenza, Shigella dysenteriae, proteus mirabilis

NOT penicillinase resistant

Se: N/V/D, superinfections, anaphylaxis

Amoxicillin: most prescribed pen derivative for adults/children

Used for lower resp. tract infections, otitis media, sinusitis, skin infections, UTI; PO short 1/2 life, well absorbed from GI tract, 25% protein bound

also called anti-staphylococcal pen

Use: treat penicillinase-producing staph aureus

semisynthetic; bactericidal (cell lysis)

Not effective against gram -

less effective than Pen G against gram +

Cloxapen: PO only partially absorbed from GI tract; highly protein bound; short 1/2 life

Also called anti-pseudomonal pen

Broad spectrum; not penicillinase resistant; bactericidal

Use: for many gram -

pseudomonas aeruglycosides, proteus, klebsiella, pneumoniae, serratia, enterobacter

similar action as aminoglycosides but less toxic

treat bone, joint, skin, soft tissue, resp. tract, TUI

Pipracil: IM, IV

When combined w/ a broad-spectrum antibiotic it makes the antibiotic effective and extends its antimicrobial effect

penicillinase-sensitive pen such as amoxicillin, ampicillin, piperacillin, ticarcilline are combined with 3 beta-lactamase inhibitors: clavulanic acid, sulbactam, tazobactam

similar in structure to pen

beta-lactam structure

bactericidal: inhibits the bacterial enzyme for cell wall synthesis

Generally not first choice because queally effective and less expensive alternatives available

10% people allergic to pen are also allergic to cephalosporins

4 generations: based on gram - spectrum; not all are affected by beta-lactamases; each generation his stronger against gram - but weaker against gram +

destroyed by beta-lactamases

highest activity against gram +; mod effective against gram -

Cefazolin: use for serious resp., urinary, genital, skin/bone/joint infections, endocarditis; widely used prophylactically in surgical pts; decreased effects if given w/tetracyclines or erythromycin; IV: immediate onset of action, peak 5-15 min

not all affected by beta-lactamases

more active against gram -, less against gram+ than 1st gen

neisseria gonnorrhea, haemophilus influenzae, eisseria meningitidis

Ceclor: PO; resp., urinary, skin, ear infections

short 1/2 life; peak 30-60 min; excreted in urine; decreased effects if given w/tetracylines or erythromycin

considerably less active than 1st gen against gram +; have extended spectrum of activity against gram -

psuedomonas aeruginosa

more resistant to beta-lactamases; longer duration of action

Cefobid: IM/IV

expanded gram - coverage than 3rd gen

gram + and -: steptococci, staphylococci

resistant to most beta-lactamases

effective in treating sepsis & many strains of gram - bacilli

Maxipime: IM/IV

Se: Gi distress, N/V/D, abd pain, weakness, rash, pruritus

High Doses: increased bleeding time, seizures, nephrotoxicity, hypersensitivity, anaphylaxis

Drug/drug:

ETOH: may cause flushing, dizzy, HA/N/V, muscular cramps

DO NOT use w/other antibiotics-nephrotoxicity/ototoxicity

Diuretics: enhance nephrotoxicity & make some cephalosporins ototoxic

Uricosurics: decrease cephalosporin excretion

Probenecid: decrease excretion of cephalopsorings (toxicity)

take on empty stomach unless GI discomfort

assess for allergy: 10% of those allergic to pen are allergic to cepha

Culture and sensitivity before therapy

Assess renal/liver function (toxicity)

Administer IV over 30 min

Saftey: keep away from children