NSAIDs Pharmacology Lecture Notes Tissue Injury & Inflammatory Response Initial vasoconstriction occurs immediately after injury to minimize blood loss (temporary reaction) Chemical mediators released: histamines, kinins, and prostaglandins - crucial for inflammatory response Vasodilation follows - blood vessels widen, increasing blood flow to injured area Classic inflammatory symptoms: redness (erythema), swelling (edema), pain from nerve stimulation, fever/heat NSAIDs Classification & Examples Propionic derivatives: ibuprofen, naproxen Phenomates: mefenamic acid Available OTC: salicylates, propionic acid derivatives Prescription required: COX2 inhibitors, acetic acid derivatives, oxicams, phenomates Mechanism of Action COX enzymes: cyclooxygenase (COX1 & COX2) convert arachidonic acid to prostaglandins COX1: Always active, protects stomach lining, helps platelet aggregation COX2: Activated only during tissue injury, causes inflammation and pain NSAIDs inhibit COX enzymes, preventing prostaglandin production (prostaglandin inhibitors) Primary Effects Antipyretic: reduces fever Analgesic: pain relief Anticoagulant: prevents blood clots (especially aspirin) Specific Drug Categories Salicylates (aspirin): pain, inflammation, fever, anticoagulant effects Propionic acid derivatives: mild to moderate pain (1-6 on pain scale), inflammation, fever Acetic acid derivatives: more effective for inflammation but significant GI side effects COX2 inhibitors: second generation NSAIDs with better safety profile, target COX2 specifically Oxicams: long-term use for osteoarthritis/rheumatoid arthritis, longer half-life (once daily) Phenomates: especially effective for menstrual pain Major Side Effects Gastrointestinal Dyspepsia: heartburn, indigestion, abdominal pain, nausea Long-term risks: stomach lining damage, GI bleeding, perforation (holes in stomach/intestines) Bleeding signs to monitor: dark tarry stools, bleeding gums, petechiae, ecchymosis, purpura Higher risk patients: older adults, smokers, alcohol users, pre-existing ulcers Prevention: proton pump inhibitors or H2 receptor antagonists to reduce stomach acid Kidney Effects Impaired function: reduced urine output, fluid retention, weight gain, edema Monitor: BUN and creatinine levels for kidney function Mechanism: NSAIDs reduce blood flow to kidneys, worsening function and increasing kidney disease risk Cardiovascular Risk Non-aspirin NSAIDs increase heart attack and stroke risk Prescribe at smallest effective dose Special Considerations Menstrual Pain (Dysmenorrhea) Avoid aspirin for painful menstruation with heavy bleeding Use acetaminophen 2 days before and during first 2 days of menstrual period Aspirin-Specific Risks Salicylism/Aspirin toxicity: early symptoms from overdose, can progress to electrolyte imbalances, coma, respiratory depression Serum salicylate levels: >30 mg/dL mild toxicity, >50 mg/dL severe toxicity Treatment: activated charcoal, possible hemodialysis Reye's syndrome: rare but serious condition causing liver/brain swelling in children/adolescents recovering from viral infections (flu, chickenpox) Reye's syndrome symptoms: persistent vomiting, lethargy, confusion → irritability, aggression, disorientation, seizures, loss of consciousness Avoid aspirin in children/adolescents with viral infections Drug Interactions & Precautions Glucocorticoids: amplify stomach bleeding risk Alcohol: increases stomach bleeding - limit/avoid consumption Other NSAIDs: can negate heart protective effects of aspirin - space dosing apart Herbal supplements: garlic and ginseng enhance bleeding risk High-risk populations: older adults, smokers, certain health conditions (H7
NSAIDs Pharmacology Lecture NotesTissue Injury & Inflammatory Response
Initial vasoconstriction occurs immediately after injury to minimize blood loss (temporary reaction)
Chemical mediators released: histamines, kinins, and prostaglandins - crucial for inflammatory response
Vasodilation follows - blood vessels widen, increasing blood flow to injured area
Classic inflammatory symptoms: redness (erythema), swelling (edema), pain from nerve stimulation, fever/heat
NSAIDs Classification & Examples
Propionic derivatives: ibuprofen, naproxen
Phenomates: mefenamic acid
Available OTC: salicylates, propionic acid derivatives
Prescription required: COX2 inhibitors, acetic acid derivatives, oxicams, phenomates
Mechanism of Action
COX enzymes: cyclooxygenase (COX1 & COX2) convert arachidonic acid to prostaglandins
COX1: Always active, protects stomach lining, helps platelet aggregation
COX2: Activated only during tissue injury, causes inflammation and pain
NSAIDs inhibit COX enzymes, preventing prostaglandin production (prostaglandin inhibitors)
Primary Effects
Antipyretic: reduces fever
Analgesic: pain relief
Anticoagulant: prevents blood clots (especially aspirin)
Specific Drug Categories
Salicylates (aspirin): pain, inflammation, fever, anticoagulant effects
Propionic acid derivatives: mild to moderate pain (1-6 on pain scale), inflammation, fever
Acetic acid derivatives: more effective for inflammation but significant GI side effects
COX2 inhibitors: second generation NSAIDs with better safety profile, target COX2 specifically
Oxicams: long-term use for osteoarthritis/rheumatoid arthritis, longer half-life (once daily)
Phenomates: especially effective for menstrual pain
Major Side EffectsGastrointestinal
Dyspepsia: heartburn, indigestion, abdominal pain, nausea
Long-term risks: stomach lining damage, GI bleeding, perforation (holes in stomach/intestines)
Bleeding signs to monitor: dark tarry stools, bleeding gums, petechiae, ecchymosis, purpura
Higher risk patients: older adults, smokers, alcohol users, pre-existing ulcers
Prevention: proton pump inhibitors or H2 receptor antagonists to reduce stomach acid
Kidney Effects
Impaired function: reduced urine output, fluid retention, weight gain, edema
Monitor: BUN and creatinine levels for kidney function
Mechanism: NSAIDs reduce blood flow to kidneys, worsening function and increasing kidney disease risk
Cardiovascular Risk
Non-aspirin NSAIDs increase heart attack and stroke risk
Prescribe at smallest effective dose
Special ConsiderationsMenstrual Pain (Dysmenorrhea)
Avoid aspirin for painful menstruation with heavy bleeding
Use acetaminophen 2 days before and during first 2 days of menstrual period
Aspirin-Specific Risks
Salicylism/Aspirin toxicity: early symptoms from overdose, can progress to electrolyte imbalances, coma, respiratory depression
Serum salicylate levels: >30 mg/dL mild toxicity, >50 mg/dL severe toxicity
Treatment: activated charcoal, possible hemodialysis
Reye's syndrome: rare but serious condition causing liver/brain swelling in children/adolescents recovering from viral infections (flu, chickenpox)
Reye's syndrome symptoms: persistent vomiting, lethargy, confusion → irritability, aggression, disorientation, seizures, loss of consciousness
Avoid aspirin in children/adolescents with viral infections
Drug Interactions & Precautions
Glucocorticoids: amplify stomach bleeding risk
Alcohol: increases stomach bleeding - limit/avoid consumption
Other NSAIDs: can negate heart protective effects of aspirin - space dosing apart
Herbal supplements: garlic and ginseng enhance bleeding risk
High-risk populations: older adults, smokers, certain health conditions (H. pylori, hypovolemia, asthma, bleeding disorders)
Specific Drug ConsiderationsKetorolac
Never use with advanced kidney disease
Maximum 5 days of treatment
Best for moderate to severe post-operative pain
Routes: IV, IM for rapid onset, then PO
Celecoxib (COX2 Inhibitor)
Caution with heart disease - increases heart attack and stroke risk
Last resort for pain management
IV Ibuprofen
Infuse over 30 minutes to minimize vascular irritation and hypotension
Ensure adequate hydration to preserve renal function
Aspirin Surgery Considerations
Discontinue 1 week before elective surgery unless prescribed for cardiovascular protection
Acetaminophen
IV form: Ofirmev
Mechanism: works in brain and spinal cord, blocks prostaglandin production, inhibits COX2
Side effects: nausea, vomiting, headaches, insomnia
Prolonged use: can affect liver function
Dosage Limits
Most clients: no more than 4 grams per day
Undernourished patients: no more than 3 grams per day
Alcohol consumers (3+ drinks/day): no more than 2 grams per day
Toxicity & Treatment
Medical emergency requiring ER treatment
Antidote: acetylcysteine (Mucomist) via duodenal tube or IV to prevent vomiting/aspiration
Monitor liver function: ALT, AST, bilirubin, alkaline phosphatase
Key Clinical Points
Ibuprofen and diabetes: can mask hypoglycemia symptoms - use with caution
Aspirin for prevention: low-dose (81mg) for stroke/heart attack prevention in high-risk patients
Antibiotic Classification and MechanismsNarrow vs Broad Spectrum Antibiotics
Narrow spectrum: Target specific bacteria types when exact pathogen is known
Reduce bacterial resistance risk and preserve normal flora
Broad spectrum: Target wide variety (gram positive and negative)
Used when bacteria not yet identified or in critical conditions awaiting lab results
Bactericidal vs Bacteriostatic
Bactericidal: Directly kill bacteria ("the killers")
Bacteriostatic: Prevent bacterial growth without direct killing
Antibiotic Selection Process
Identify causative agent through body fluid analysis (blood, urine, sputum)
Perform sensitivity tests to determine effective antibiotics
Consider infection location, patient age, allergies, and immune status
Testing methods: Gram stain (quick assessment) vs Culture (detailed, several days)
Disk diffusion test: Bacteria sensitive if no growth near antibiotic disc
Key Laboratory Values
MIC: Minimum concentration to stop bacterial growth
MBC: Minimum concentration to kill 99.9% of bacteria
Nursing Responsibilities
Collect specimens for culture testing
Prevent contamination during sample collection
Ensure accurate test results
Combination Therapy and ProphylaxisDrug Interactions
Potentiating: One drug enhances the other's effect
Antagonistic: Combined drugs less effective than separate use
Additive: Combined effect equals sum of individual effects
Prophylaxis Use
Preventive medication use to prevent infections before they occur
Major Antibiotic ClassesPenicillins
Mechanism: Bactericidal - disrupts bacterial cell wall
Side effects: Anaphylaxis, renal impairment, electrolyte imbalances (hyperkalemia >5 mEq/L, hypernatremia >145 mEq/L)
Drug interactions: Cannot mix with aminoglycosides in same IV (inactivates both drugs)
Administration: Give penicillin 1 hour before or after aminoglycosides using separate IV lines
Probenecid interaction: Delays penicillin excretion, can cause kidney impairment
Cephalosporins (Five Generations)
1st generation: Effective against gram-positive bacteria
2nd & 3rd generation: Effective against gram-negative bacteria
4th generation: Effective against both gram-positive and gram-negative
5th generation: Effective against multi-drug resistant organisms
Advantages: Better tissue penetration, longer half-lives, less frequent dosing improves compliance
Side effects: Bleeding (interferes with vitamin K), thrombophlebitis at IV site
Monitoring: Check IV site for swelling, redness, warmth, pain; rotate IV every 72 hours
C. diff risk: Can cause pseudomembranous colitis - monitor for diarrhea
Vancomycin
Uses: C. diff, staph, MRSA infections
Administration: IV (most common), PO, or suppository
Red Man Syndrome: Histamine release from rapid infusion causing flushing, rash, hypotension, tachycardia
Prevention: Infuse over 60-90 minutes, pre-medicate with antihistamines
Ototoxicity: Monitor for tinnitus, hearing loss, vertigo, ear pressure
Tetracyclines
Mechanism: Bacteriostatic, prevents protein synthesis
Uses: Acne, periodontal disease, STI treatment
Contraindications: Children and pregnant women (tooth discoloration, enamel hypoplasia)
Side effects: Photosensitivity, hepatotoxicity, reduces hormonal contraceptive effectiveness
Macrolides
Mechanism: Bacteriostatic (bactericidal at higher doses)
Unique risk: Prolonged QT intervals leading to cardiac dysrhythmias and potential sudden death
Aminoglycosides
Mechanism: Bactericidal, effective for gram-negative bacteria
Side effects: Ototoxicity, nephrotoxicity, neuromuscular blockade (muscle weakness)
Monitoring: Peak and trough levels required
Trough: Lowest concentration, measured before next dose
Peak: Highest concentration, measured 30 minutes after dose completion
General Monitoring and SafetyAllergy Assessment
Always ask about medication allergies before first dose
Monitor for reactions: Immediate (2-30 min), accelerated (1-72 hours), delayed (days-weeks)
Treatment Effectiveness
Post-treatment culture to confirm absence of microorganisms
Clinical improvement (fever resolution, clear lung sounds)
Patient Education
Complete entire course even if feeling better to prevent resistance
For STI treatment: abstain from intercourse until negative culture results
Antibiotic Classification - Lecture NotesNarrow vs Broad Spectrum Antibiotics
Narrow spectrum: Target specific bacteria types when exact pathogen is known
Broad spectrum: Target wide variety (gram positive and negative) - used when bacteria not yet identified or in critical conditions
Bactericidal vs Bacteriostatic Mechanisms
Bactericidal: Directly kill bacteria ("the killers")
Bacteriostatic: Prevent bacterial growth without direct killing
Antibiotic Selection Process
Identify causative agent through body fluid analysis (blood, urine, sputum)
Testing methods: Gram stain (quick assessment) vs Culture (detailed, several days)
Disk diffusion test: Bacteria sensitive if no growth near antibiotic disc
MIC: Minimum concentration to stop bacterial growth
MBC: Minimum concentration to kill 99.9% of bacteria
Combination Therapy Effects
Potentiating: One drug enhances the other's effect
Antagonistic: Combined drugs less effective than separate use
Additive: Combined effect equals sum of individual effects
Major Antibiotic ClassesPenicillins
Side effects: Anaphylaxis, hyperkalemia >5 mEq/L, hypernatremia >145 mEq/L causing dysrhythmias
Critical drug interaction: Cannot mix with aminoglycosides in same IV (inactivates both drugs)
Administration: Give penicillin 1 hour before or after aminoglycosides using separate IV lines
Cephalosporins (Five Generations)
1st generation: Gram-positive bacteria
2nd & 3rd generation: Gram-negative bacteria
4th generation: Both gram-positive and gram-negative
5th generation: Multi-drug resistant organisms
Side effects: Bleeding (interferes with vitamin K), thrombophlebitis at IV site
C. diff risk: Monitor for diarrhea as early sign of pseudomembranous colitis
Vancomycin
Red Man Syndrome: Histamine release from rapid infusion causing flushing, rash, hypotension, tachycardia
Prevention: Infuse over 60-90 minutes, pre-medicate with antihistamines
Ototoxicity: Monitor for tinnitus, hearing loss, vertigo, ear pressure
Tetracyclines
Contraindications: Children and pregnant women (tooth discoloration, enamel hypoplasia)
Side effects: Photosensitivity, hepatotoxicity, reduces hormonal contraceptive effectiveness
Macrolides
Unique risk: Prolonged QT intervals leading to cardiac dysrhythmias and potential sudden death
Aminoglycosides
Side effects: Ototoxicity, nephrotoxicity, neuromuscular blockade (muscle weakness)
Monitoring: Peak and trough levels required
Trough: Lowest concentration, measured before next dose
Peak: Highest concentration, measured 30 minutes after dose completion
Critical Nursing Actions
Always ask about medication allergies before first dose
Monitor for reactions: Immediate (2-30 min), accelerated (1-72 hours), delayed (days-weeks)
Complete entire course even if feeling better to prevent resistance
IV site monitoring: Check for swelling, redness, warmth, pain; rotate every 72 hours
Pharmacokinetics Lecture NotesDefinition and Overview
Pharmacokinetics: Study of how drugs move within the body from administration to elimination
Encompasses the complete "journey of medication" through four main stages
Addresses key questions: How does medication reach target areas? What happens after administration?
Stage 1: Absorption
Process: How medication enters the bloodstream
Routes: Enteral (digestive system), parenteral (injection), sublingual, inhalation, topical, subcutaneous
Key factors: Speed of absorption, strength (amount absorbed), and administration method all impact drug potency
Stage 2: Distribution
Process: Transportation of medication to different body parts via bloodstream
Circulation factor: Blood flow issues (e.g., heart disease) impede medication transport
Cell membrane permeability: Medications pass through barriers to reach exclusive areas like the brain
Plasma protein binding: Medications attach to proteins (albumin) for distribution - limited availability creates competition among multiple drugs ("musical chairs" effect)
Stage 3: Metabolism
Process: Chemical alteration of drugs, primarily in the liver
Purpose: Makes medication more water-soluble, less active, or inactive to facilitate excretion
Other metabolic sites: Lungs, intestines, bloodstream (liver remains primary)
Factors Influencing Metabolism
Age: Infants have immature digestive systems vs. elderly patients
Enzyme levels: Can accelerate or slow metabolism
First pass effect: Some drugs inactivated by liver on first pass - doctors may change route (PO to sublingual/injection) to avoid this
Shared metabolic pathways: Multiple medications compete for same metabolic processes
Nutrition: Poor diet lacks necessary ingredients for proper drug metabolism
Stage 4: Excretion
Process: Removal of drugs and metabolites from the body
Primary organ: Kidneys (main site for dumping medication remnants)
Secondary sites: Liver and other organ systems also contribute to excretion
Pharmacology Lecture NotesDrug Half-Life
Dosing frequency depends on half-life: every 4-6 hours, 3x daily, or 1-2x daily based on drug's half-life
Pharmacodynamics Overview
Definition: Study of what a drug does in the body - how it produces both therapeutic and harmful side effects
Three Types of DrugsAgonist Drugs
Bind to receptor, activate it, produce full biological response
Analogy: Key that fully turns and opens the door
Example: Morphine - binds to opioid receptors in brain/spinal cord for full pain relief
Partial Agonist Drugs
Bind to receptor but produce weaker response than full agonist
Analogy: Key that partially opens the door
Example: Buprenorphine - provides milder pain relief effects
Antagonist Drugs
Bind to receptor but block activation by other substances
Analogy: Broken key that fits but doesn't turn
Example: Naloxone - antidote to opioid overdose, blocks opioid receptors and reverses morphine effects
Routes of AdministrationOral/Enteral Medications - Safety First
Do NOT give PO meds if patient:
Is vomiting
Has trouble swallowing
Is less alert
Has no gag reflex
Best position: High Fowler's (90 degrees) to help with swallowing
Food considerations: Medications that irritate stomach should be taken with food
Grapefruit juice warning: Can affect drug effectiveness - avoid with medications
Cannot crush: Enteric-coated or time-release tablets
Sublingual and Buccal Routes
Enter bloodstream directly, bypass liver and first-pass effect
Patient instructions: Keep tablet in place until dissolved, avoid eating/drinking for complete absorption
Nasal Administration
Use aseptic technique: Hand hygiene, clean gloves, alcohol cleaning
Review ATI for proper nasal drops and spray administration techniques
Rectal Suppositories
Position: Start supine, then turn to left side (Sims position) - takes advantage of natural colon curve
Post-insertion: Patient remains flat for 5 minutes to retain suppository and facilitate absorption
Vaginal Administration
Preparation: Perineal care to ensure clean area, may need lubrication
Insertion depths:
Suppositories: 3-4 inches deep in posterior vaginal wall
Creams/foams/jellies: 2-3 inches deep
Post-administration: Patient lies down for 5 minutes
Inhalers
Spacer benefits: Easier to use, more effective, increases lung delivery while decreasing throat deposition
Technique: Shake 5-6 times to mix medication, patient exhales completely, closes lips around spacer, then inhales
NG/G-Tubes
Preferred form: Liquid medications
If crushing needed: Only crush one medication at a time (not multiple together)
Special consideration: Sublingual drugs should still be given sublingually even with tubes present - maintains therapeutic effect
Administration: Check tube placement, use gravity flow (no plunger), flush after to clear remaining medication
Parenteral InjectionsBest Injection Sites
Ventrogluteal: Best for IM injections, especially >2cc volumes - away from major nerves/vessels
Vastus lateralis: Best for infants - largest thigh muscle
Deltoid: Adults, smaller muscle mass, limit to 1cc or 1ml
Injection Guidelines
Tuberculin syringe: For small volumes <0.5ml
Site rotation: Prevent tissue damage with repeated injections
Avoid injecting: Edematous, inflamed areas, or areas with moles/birthmarks
Injection Types and Angles
Intradermal: 10-15 degrees, for TB skin testing, do not massage site to avoid dispersing solution
Subcutaneous: For small, non-irritating, water-soluble drugs (insulin, heparin), use areas with good fat pads
Intramuscular: See angle chart
Needle Gauges
Higher number = smaller needle, lower number = bigger needle
16 gauge: Trauma patients
18 gauge: Surgery and blood administration
22-24 gauge: Children, elderly, stable post-op patients
Z-Track Method
Used for: Medications that stain skin or are irritating (e.g., iron preparations)
Purpose: Prevents leakage into subcutaneous tissue, avoiding skin discoloration and irritation
Side Effects vs Adverse EffectsSide Effects
Expected, unintended but not necessarily harmful
Occur at therapeutic doses, mild and tolerable
Examples: Drowsiness from Benadryl, dry mouth, mild nausea
Physician may continue drug despite side effects
Adverse Effects
Unintended AND harmful/undesirable effects
Can occur at normal doses or from improper use/overdose
Range: Mild to severe (life-threatening)
Can be: Predictable or unpredictable (allergic/idiosyncratic reactions)
Examples: Acetaminophen liver damage, penicillin allergic reactions
Drug Interactions
Medications interact with: Other drugs, food, herbal remedies, supplements
Example: Grapefruit juice can cause potential interactions
Contraindications vs Precautions
Contraindications: STOP sign - medication should NOT be used because it can be harmful
Precautions: YELLOW caution sign - medication should be used with extra care and monitoring, not a definite no but proceed with caution
Common Side Effect ProfilesCNS Effects
CNS Depressants (e.g., opioids): Decreased brain activity → drowsiness, sedation
CNS Stimulants (e.g., ADHD meds): Increased alertness/activity → seizure risk warning
Cardiovascular Effects
Anti-hypertensives: Commonly cause orthostatic hypotension
Anticholinergic Effects
Blocks acetylcholine → dry mouth, blurred vision, constipation, increased heart rate, urinary retention, reduced sweating, photophobia
Other Effects
GI: Nausea, vomiting, stomach irritation
Hematological: Bone marrow suppression/depression affecting blood and blood-forming organs
Drug Toxicity
Can be fatal when patients take excessive dosages or take medication too frequently
Acetaminophen example: causes liver damage in high amounts
Hepatotoxicity
Many medications processed in liver - impacts drug processing if liver damaged
Symptoms:
Fatigue, nausea, vomiting, loss of appetite
Right upper quadrant abdominal pain
Jaundice (yellowing of skin/eyes), dark urine, pale/clay-colored stool
Pruritus (itching), ascites (abdominal swelling)
Lab Tests:
ALT, AST, ALP, Bilirubin, Prothrombin time
Nephrotoxicity (Kidney Damage)Symptoms:
Fatigue, nausea, vomiting, loss of appetite
Oliguria (decreased urine output)
Fluid retention/swelling in legs, ankles, feet, face
Shortness of breath (fluid overload), hypertension
Lab Tests:
BUN, creatinine, electrolytes (potassium, sodium)
Hypersensitivity/Allergic Reactions
Immune response after exposure to substances like penicillin
Body creates antibodies; subsequent exposure triggers allergic reaction
Mild Symptoms:
Itching, rashes, watery eyes, sneezing
Inflammation of nose and sinuses
Severe: Anaphylaxis
Life-threatening reaction requiring immediate medical attention
Affects all body systems (vs angioedema affecting face/neck)
Initial signs: itching, redness, anxiety, weakness
Can lead to respiratory failure if untreated
Angioedema
Serious allergic reaction affecting deeper skin layers, blood vessels, subcutaneous tissue, mucous membranes
Primarily affects face, lips, neck
Medical emergency - throat swelling can block breathing
Stridor (high-pitched breathing sound) indicates airway compromise
Treatment:
Mild cases: antihistamines (diphenhydramine)
Moderate/severe cases: corticosteroids to reduce swelling
Drug Interactions
Combining drugs can increase/decrease therapeutic effects
Can increase/decrease side effects or lead to toxicity
Must warn patients about interactions with OTC drugs and herbal supplements
FDA Pregnancy Drug Categories
Category A: Safest - no risk shown in studies
Category B: Animal studies show no risk, limited human studies
Category C: Animal studies show adverse effects, no human studies
Category D: Evidence of human fetal risk, but benefits may outweigh risks
Category X: Proven risk in animals and humans - risk outweighs benefits
TB and Airborne Precautions
TB requires specific isolation room and special masks for nurses
Metronidazole (Antimicrobial/Anti-protozoal)
Kills anaerobic organisms (microorganisms that don't require oxygen)
Treats protozoal infections: giardiasis, trichomoniasis
Pre-surgical prophylaxis for vaginal, abdominal, colorectal surgeries
Combination therapy with tetracycline for H. pylori treatment
Side Effects & Complications
GI discomfort: nausea, vomiting, dry mouth, metallic taste
Take with food if metallic taste persists; contact provider if severe
Dark urine (normal side effect, don't be alarmed)
Neurotoxicity/CNS effects (concerning): numbness in hands/feet, ataxia, seizures
Stop medication immediately and contact provider if neurotoxicity occurs
Pseudomembranous colitis possible complication
Drug Interactions
Alcohol: causes severe aversion reaction (nausea, vomiting, flushing) - unique to metronidazole
Amplifies effects of warfarin, phenytoin, lithium (risk of toxicity)
Reduces effectiveness of hormonal birth control
Available oral or IV
STI Treatment Guidelines
Avoid sexual activity during treatment and after completion
Follow-up culture required to confirm infection clearance
Antifungal MedicationsAmphotericin B
Used for systemic fungal infections (whole body)
Ketoconazole
Used for superficial fungal infections (skin, nails, mucous membranes)
Mechanism of Action
Attaches to fungal cells and inhibits growth, killing the fungus
Effect depends on drug concentration
Nursing Actions for Amphotericin B
Monitor for infusion reactions - stay with patient for 15 minutes
Pre-treatment may include antihistamines or antipyretics
Monitor kidney function and electrolyte levels
Infuse slowly over 2-4 hours to reduce infusion reaction risk
Antiviral Drugs Lecture Notes
Overview
Short chapter on viral infections with reduced drug information
Focus on two main antiviral drugs: Acyclovir and Ganciclovir
Purpose: Stop virus from making copies of itself (like a stop sign in busy road)
Acyclovir
Therapeutic Uses
Cold sores on lips (herpes simplex)
Chicken pox (varicella zoster viral infection)
Ganciclovir
Therapeutic Uses
"Big gun" antiviral for patients with weakened immune systems
Targets cytomegalovirus in HIV/AIDS patients
Prevention of viral infections after organ transplant
Side Effects
Both Drugs
Phlebitis (inflammation)
Nephrotoxicity
Ganciclovir Specific
Weakens immune response further
Decreased white blood cell count (difficulty fighting infection)
Decreased platelet count (difficulty clotting blood)
Patient Education
Application Instructions
Use gloves when applying to skin
Ensure skin is clean and dry
Precautions
No intimate contact while active lesions present
No cure for herpes simplex - virus remains dormant
Drug Interactions
Acyclovir + Probenecid: Affects drug excretion from body
Ganciclovir + Cytotoxic drugs: Amplifies side effects
Effectiveness Indicators
Fewer or healed lesions
Key Facts About Herpes Simplex
Over 60% of adults have herpes simplex (often asymptomatic)
Type 1: Mouth sores, Type 2: Genital sores
Transmitted through kissing, sexual contact, sharing drinks/utensils
Important: Avoid stigma and judgment toward infected patients
Disease Overview
Metabolic disease group characterized by chronic hyperglycemia (high blood glucose)
Caused by defects in insulin secretion, insulin action, or both
Type 1 Diabetes Pathophysiology
Autoimmune response destroying insulin-producing beta cells in pancreas
Genetic predisposition - family history increases risk
Insulin deficiency prevents glucose from entering cells effectively
Body breaks down fats for energy → ketone production → diabetic ketoacidosis (dangerous condition)
Type 2 Diabetes Pathophysiology
Insulin resistance - cells become less responsive to insulin
Body requires higher insulin levels for same glucose uptake
Contributing factors: genetic predisposition (unavoidable), obesity, physical inactivity (preventable)
Beta cell dysfunction - pancreas produces less insulin over time
Increased hepatic glucose production - liver resistance leads to more glucose release
Long-term ComplicationsMicrovascular (Small Blood Vessel Damage)
Retinopathy (eye damage)
Nephropathy (kidney damage)
Neuropathy (nerve damage)
Macrovascular (Large Blood Vessel Damage)
Cardiovascular disease
Stroke/cerebrovascular accidents
Hypoglycemia SymptomsEarly Signs
Shakiness, sweating, dizziness, hunger, irritability, palpitations, anxiety
Moderate Symptoms
Confusion, difficulty concentrating, weakness, fatigue, blurred vision, headaches
Severe Symptoms
Loss of coordination, unconsciousness, seizures, coma
Insulin TherapyMechanism of Action
Hormone from pancreas that controls blood sugar levels
Attaches to receptors on muscle, fat, and liver cells
Activates cells to use glucose and convert to glycogen for storage
When Type 2 Patients Need Insulin
Blood sugar too high despite pills, diet, and exercise
Serious kidney/liver problems or neuropathy
Surgery, medical tests, or extreme stress (injury/infection)
Diabetic ketoacidosis or high potassium levels
Insulin Types - Onset, Peak, Duration Critical
Onset: Time to start lowering blood glucose after administration
Peak: Maximum strength period for glucose lowering
Duration: Total time insulin continues lowering glucose
Insulin Complications
Hypoglycemia from too much insulin or inadequate nutrition
Hypokalemia - insulin moves potassium into cells
Lipohypertrophy - abnormal fat masses from not rotating injection sites
Hypoglycemia TreatmentConscious Patients
15g carbohydrates: 4 oz orange juice, 2 oz grape juice, 8 oz milk, or glucose tablets
Unconscious Patients
IV/subcutaneous glucagon - cannot give oral glucose
Oral AntidiabeticsSulfonylureas (Glipizide, Glyburide, Glimepiride)
Help pancreas release more insulin by binding to beta cells
Metformin (Biguanide)
Tells liver to make less glucose
Helps body cells use insulin better
Decreases sugar absorption
Critical Metformin Warning
Excreted by kidneys - accumulates if kidney function compromised
HOLD before CT scans/angiograms - contrast dyes impair renal function
Can cause lactic acidosis - nausea, vomiting, confusion, shock, coma
Drug Interactions
Beta blockers hide hypoglycemia symptoms (tachycardia, shakiness)
Thiazide diuretics/glucocorticoids raise blood sugar, reduce insulin effectiveness
Sulfonylureas/meglitinides with insulin cause additive hypoglycemia
Pharmacology Lecture: Tuberculosis and Anti-TB MedicationsTuberculosis Overview
Causative agent: Mycobacterium tuberculosis bacterium
Primary target: Lungs (can also affect spine, kidneys, brain)
Transmission: Airborne through coughing, sneezing, speaking, singing
Isolation: Requires airborne precautions
TB Pathophysiology
Bacteria reaches alveoli where alveolar macrophages attempt destruction
Waxy cell wall resists destruction, allowing bacteria to survive and replicate inside macrophages
Infected macrophages release cytokines to attract other immune cells
Formation of granuloma structure to contain infection
Latent vs Active TB
Latent TB: Bacteria remains "sleeping" in healthy individuals - no symptoms, not contagious
Reactivation triggers: Immunocompromise (HIV, diabetes, malnutrition, immunosuppressive drugs)
Active TB symptoms: Persistent cough (>3 weeks), sputum production, hemoptysis, chest pain, fever, night sweats, weight loss, fatigue
TB Diagnosis
Tuberculin skin test to detect immune response
Chest X-ray for lung involvement imaging
Sputum culture to identify Mycobacterium tuberculosis
BCG vaccine scar indicates vaccination in high-prevalence countries (Asia, Philippines, Indonesia, India)
Isoniazid (Anti-TB Drug)
Mechanism: Stops mycolic acid synthesis in bacterial cell wall
Latent TB treatment: 9 months monotherapy, then combined with rifampin weekly for 3 months
Contraindications: Children under 2, HIV patients, pregnant patients
Isoniazid Complications
Hyperglycemia: Interferes with insulin secretion from pancreatic beta cells
Peripheral neuropathy: Inhibits enzyme needed for vitamin B6 activation - prevent with pyridoxine supplementation
Hepatotoxicity: Metabolized in liver creating toxic metabolites
Isoniazid Administration & Interactions
Best taken: Empty stomach (1 hour before/2 hours after meals)
With food: If stomach upset occurs
Drug interactions: Increases phenytoin levels causing toxicity; avoid tyramine-rich foods (cheese, cured meats, red wine)
Contraceptive interference: Recommend backup birth control method
Rifampin (Anti-TB Drug)
Mechanism: Stops bacterial protein synthesis ("wrench in machinery")
Unique characteristic: Red-orange pigmented compound causes discoloration of body fluids
Affected fluids: Urine, sweat, tears, saliva, sputum, breast milk - harmless but alarming to patients
Rifampin Drug Interactions
Warfarin: Reduces anticoagulant effect - monitor INR closely, frequent dose adjustments needed
HIV medications: Reduces efficacy of HIV drugs
Treatment Effectiveness Monitoring
Clinical improvement: Clear breath sounds, resolution of night sweats, return of appetite
Laboratory indicator: 3 consecutive negative sputum cultures (must be consecutive, not intermittent)
Treatment phases: Initial phase (2 months) kills bacteria, continuation phase (4-7 months) eliminates lingering bacteria