JL

Pathophysiology and Pharmacology: Pain, Inflammation & Infection

Introduction to Pain and the Nervous System

  • Pain as a Warning Mechanism: Pain serves as a crucial signaling system to alert the body to potential harm or injury.
  • Pain Assessment: Registered Nurses (RNs) are responsible for thorough pain assessment.

Nervous System (NS) Overview

  • Information Processing: The NS integrates, processes, and coordinates sensory input and motor commands.
  • Central Nervous System (CNS): Comprises the brain and spinal cord.
  • Peripheral Nervous System (PNS): Consists of nervous tissue located outside the CNS and the Enteric Nervous System (ENS).
    • Afferent Division (Sensory Information): Relays sensory input to the CNS.
      • Special sensory receptors: Monitor smell, taste, vision, balance, and hearing.
      • Visceral sensory receptors: Monitor internal organs.
      • Somatic sensory receptors: Monitor skeletal muscles, joints, and the skin surface.
    • Efferent Division (Motor Commands): Transmits motor commands from the CNS to effectors.
      • Somatic Nervous System (SNS): Controls skeletal muscle.
      • Autonomic Nervous System (ANS): Controls smooth muscle, cardiac muscle, glands, and adipose tissue.
        • Parasympathetic Division
        • Sympathetic Division

Afferent Pathway of Pain (Sensory Information Flow)

  • Pathway: Sensory information travels from the PNS to the CNS, termed 'afferent'.
  • Origin: Starts at sensory receptor(s) in a specific body part.
  • Termination: Ends in the Somatosensory Cortex (parietal lobe) of the CNS.
  • Action Potential: The sensory impulse must be strong enough to reach a threshold to initiate an action potential. If not strong enough, no action potential is generated, and thus no message is transmitted.
  • Nociceptor Pathway: Nociceptor (pain receptor) \rightarrow \text{1st order neuron (A or C fibers in PNS)} \rightarrow \text{CNS} \rightarrow \text{thalamus} \rightarrow \text{related sensory homunculus area} .

Neuron Fibers and Neurotransmitters Involved in Pain

  • Type A Nerve Fiber:
    • Speed: Fast transmission.
    • Myelination: Myelinated.
    • Pain Sensation: Associated with 'sharp pain'.
    • Reflexes: Often triggers reflexes.
  • Type C Nerve Fiber:
    • Speed: Slow transmission.
    • Myelination: Unmyelinated.
    • Pain Sensation: Associated with 'aching' or 'burning' pain.
  • Substance P: An excitatory Central Nervous System (CNS) neurotransmitter that plays a role in pain transmission.
  • Terminology:
    • Cutaneous pain: Superficially triggered pain, originating from the skin.
    • Visceral pain: Organ-related pain, originating from internal organs.
  • Interneurons: Communicate information within synapses, facilitating processing, modifying, and relaying of signals.

Pain & Flexor Reflexes (Withdrawal Reflex)

  • Mechanism: A sharp pain stimulus triggers a reflex withdrawal without requiring cerebral control.
  • Pathway: Activation of a sensory neuron (afferent) \rightarrow \text{interneuron (at level of stimulus in CNS)} \rightarrow \text{automatic activation of a motor neuron (efferent)} \rightarrow \text{response by the effector} .

Pain Treatment: Analgesia

  • Analgesia: Refers to the treatment of pain.

Centrally Acting Agents

  1. Non-opioid Centrally Acting Agent: Acetaminophen (Tylenol)

    • Administration: Per os (PO), every 4 hours (q4h); pediatric dosage is weight-based (per kg).
    • Therapeutic Actions: Primarily an antipyretic (fever reducer) and analgesic (pain reliever).
    • Antipyretic Mechanism: Stimulates the hypothalamus, leading to peripheral vasodilation and subsequent cooling of the body.
    • Efficacy: Highly efficacious for pain and fever.
    • Anti-inflammatory Properties: Not anti-inflammatory.

  2. Centrally Acting Analgesics: Opioids (aka 'Narcotics')

    • Examples: Morphine, Fentanyl, Hydromorphone (Dilaudid), Meperidine (Demerol), Methadone (Metadol), Hydrocodone, Oxycodone (OxyNeo), Oxycontin, Tramadol (Ultram), Codeine.
    • Receptor Agonism: Act as agonists for mu ( \mu ), kappa ( \kappa ), and delta ( \delta ) opioid receptors, with drug-specific affinities.
    • Mechanism of Action: Opioid binding inhibits the release of Substance P, reducing pain signal transmission.
    • Mu ( \mu ) Receptor: Binding to mu receptors has high analgesic efficacy.
    • Other Receptor Stimulations: Receptor binding also stimulates the release of histamine and dopamine.
    • Mimicry: Opioids mimic 'Endogenous opioid peptides' (endorphins, enkephalins, dynorphins).
      • These are endogenous inhibitory neurotransmitters (neuromodulators).
      • Released from: Hypothalamus, limbic system, and reticular formation.
      • Action: Act on the descending (efferent) pathway to inhibit Substance P, thereby modulating pain.
    • Clinical Use: Used for moderate-to-severe pain, often in synergy with NSAIDs and Acetaminophen.
    • Efficacy Levels:
      • High Efficacy: Fentanyl, hydromorphone (Dilaudid), meperidine (Demerol), Morphine, methadone (Metadol).
      • Moderate Efficacy: hydrocodone, oxycodone (OxyNeo), oxycontin, tramadol (Ultram).
    • Combination Drugs:
      • Percocet: oxycodone + acetaminophen
      • Percodan: oxycodone + ASA
      • Vicodin: hydrocodone + acetaminophen
      • Tramacet: Tramadol + acetaminophen
      • Tylenol #1 - #4: Varying dosages of acetaminophen + codeine ( + caffeine)
    • Side Effects (Adverse Effects):
      • Common: CNS depression (sedation, decreased respiratory rate (RR), decreased heart rate (HR), decreased blood pressure (BP), decreased level of consciousness (LOC), pupillary constriction), psychomimetic effects (euphoria, depression, nightmares), nausea and vomiting (N&V), constipation, pruritus (itching), urinary retention.
    • Cautions (Nursing Actions):
      • Hold Opioids: If respiratory rate (RR) falls below 12/min. This indicates low oxygenation/ventilation, which can lead to high carbon dioxide (CO_{2}) levels, causing CNS vasodilation and a risk of increased intracranial pressure (ICP).
      • Opioid Allergy: Always check for an opioid allergy, as it is common.
      • Severe Asthma Patients: Use with caution as opioids can stimulate histamine release, potentially worsening bronchoconstriction.
      • Pregnancy: Use with caution and assess risks/benefits.

Peripheral Level Agents

  1. Non-steroidal Anti-inflammatory Drugs (NSAIDS)

    • Examples: Ibuprofen and ibuprofen-like drugs, Aspirin (ASA).
    • Mechanism of Action: Inhibit prostaglandin formation from arachidonic acid, primarily by inhibiting the cyclooxygenase (COX) enzyme.
    • Clinical Use: High efficacy for pain associated with tissue injury and inflammation.
    • Combination Drugs: Can be found in combination drugs (e.g., Robax contains Ibuprofen with a muscle relaxant).
    • Allergy: Contraindicated in patients with NSAID allergy.
    • Non-selective COX Inhibitors (Inhibit COX-1 and COX-2):
      • Acetylsalicylic acid (Aspirin, ASA, Enteric coated ASA (ECASA)).
      • Ibuprofen (Advil, Motrin).
      • Ibuprofen-like drugs: Diclofenac (Voltaren), Naproxen (Aleve, Naprosyn), Ketorolac (Toradol), Indomethacin (approximately 20 \times the potency of ASA, prescription (Rx) only).
    • Selective COX-2 Inhibitors (Inhibit COX-2 only):
      • Celecoxib (Celebrex®).
      • Clinical Use: Not considered first-line treatment; Rx only.

  2. Steroidal Drugs (Glucocorticoids)

Inflammation Pathway (Simplified Diagram Explanation)
  • Tissue Damage: Leads to cellular injury.
  • Mediator Release: Macrophages and mast cells at the injury site release chemical signals (e.g., histamine, bradykinin, complement, leukotrienes).
  • Vascular Changes: These signals cause nearby capillaries to widen (vasodilation, leading to redness and heat) and become more permeable (allowing fluid, antimicrobial proteins, and clotting elements to move from blood to the site, causing edema).
  • Clotting: Clotting begins to wall off the injured area.
  • Cellular Infiltration: Chemokines attract more phagocytic cells (e.g., neutrophils, macrophages) from the blood to the injury site (leading to pus formation and thrombosis).
  • Phagocytosis: Neutrophils and macrophages phagocytose pathogens and cell debris.
  • Nerve Stimulation: Chemical mediators also stimulate nerve endings, causing pain.
  • Tissue Healing: The tissue then begins to heal.
Cyclooxygenase (COX) Pathway Explained
  • Arachidonic Acid: A precursor molecule in the inflammatory pathway.
  • COX Enzyme: Converts arachidonic acid into prostaglandins (PGs).
  • COX-1: Produces PGs vital for various physiological functions, including stomach protection and platelet aggregation.
    • Non-selective COX inhibitors (e.g., Aspirin, Ibuprofen) block both COX-1 and COX-2, leading to side effects like gastrointestinal issues and altered platelet function.
  • COX-2: Produces PGs primarily associated with pain and inflammation.
    • Selective COX-2 inhibitors (e.g., Celecoxib) specifically target COX-2, aiming to reduce pain and inflammation with fewer COX-1 related side effects.
  • Pain Mediators: Histamine and pyrogens (substances that cause fever by signaling the brain to increase body temperature) are also involved in the pain and inflammatory response.
  • Opiates: Alter the perception of and emotional responses to pain.

Pain Rating and Treatment Options (Critical Thinking)

  • Pain < 4/10 (Mild Pain):
    • Treatment: Non-opioid medications.
    • Route: Per os (PO).
    • Agents: NSAIDs, Tylenol, often used in synergy (combination for enhanced effect).
  • Pain 4-6/10 (Moderate Pain):
    • Treatment: Opioids, combination medications.
    • Route: Per os (PO).
    • Agents: Used in synergy.
  • Pain > 6/10 (Severe Pain):
    • Treatment: Higher potency opioids.
    • Route: Parenteral (e.g., intravenous (IV), subcutaneous (SC)).
    • Consideration: Patient-Controlled Analgesia (PCA).
    • Agents: Used in synergy.

Steroidal Drugs: Glucocorticoids

  • Nature: Endogenous hormones, often referred to as 'survival/stress hormones'.
  • Secretion Site: Adrenal cortex.
  • Physiological Effects:
    • Stimulates gluconeogenesis (formation of glucose from non-carbohydrate sources).
    • Stimulates protein degradation.
    • Facilitates lipolysis (breakdown of fats).
  • Drug Examples: Prednisone, Prednisolone, Methylprednisolone, Dexamethasone, Hydrocortisone, Cortisone.
  • Clinical Uses:
    • Inhibit prostaglandin synthesis (acting on COX-2).
    • Suppress phagocytes and lymphocytes (white blood cells, WBCs).
    • Suppress histamine release.
    • Specific Efficacy: Used for local, chronic inflammation, systemic diseases, chronic diseases, and anaphylaxis.
    • Specific Applications:
      • Systemic Inflammation: Used as an adjunct in autoimmune conditions like Inflammatory Bowel Disease (IBD) or Lupus (e.g., Dexamethasone PO, low dose, daily).
      • Anaphylaxis: For patient stabilization during severe allergic reactions.
      • Local - Joints: Cortisone injections.
      • Local - Intranasal: For allergic rhinitis (e.g., budesonide (Rhinocort), fluticasone (Flonase), mometasone (Nasonex)).
      • Asthma - Inhalation: (e.g., Budesonide (Pulmicort), Beclomethasone (Qvar), Fluticasone (Flovent)).

Asthma Treatment Connection

  • Normal Sympathetic Stimulation: \beta_2 adrenergic receptor stimulation leads to bronchodilation, increased lung perfusion, and improved ventilation.
  • Asthma Treatment Goals: Focus on \beta_2 adrenergic stimulation (bronchodilation) and anti-inflammatory modalities.
  • Asthma Treatment Strategy: Prevention + Rescue
    • Prevention Focus ('Controllers'): Anti-inflammatory medications.
      • Glucocorticoids.
      • Leukotriene modifiers.
      • Mast cell stabilizers.
      • Control of irritants.
    • Rescue Focus (ER Treatment - 'Relievers/Rescue'): Bronchodilators.
      • \beta_2 adrenergic agonists (Short-Acting Beta Agonists, SABA; e.g., Salbutamol (Ventolin, albuterol)).
      • Anticholinergics (inhibit PNS; e.g., Ipratropium (Atrovent)).
      • Epinephrine (Racemic Epinephrine) – short onset, short half-life ($t_{1/2}$); administered via endotracheal tube (ET) or intramuscular (IM)/intravenous (IV) in advanced rescue.

Allergy-Related Inflammation and Histamine

  • Pathophysiology: Cellular injury \rightarrow \text{mast cell activation} \rightarrow \text{release of chemical mediators (histamine, bradykinin, complement, leukotrienes)} \rightarrow \text{vasodilation (redness, heat) and vascular permeability (edema)} \rightarrow \text{cellular infiltration (pus), thrombosis (clots), and stimulation of nerve endings (pain)} .
  • Histamine:
    • Primary Mediator: Key mediator in sensory-stimulated inflammation, such as allergic reactions.
    • Storage and Release: Stored within mast cells and released upon contact with an allergen.
    • Receptor Binding: Binds to \text{H1-receptors} (a G-protein coupled receptor type), located in smooth muscles of the vascular system, digestive tract, bronchial tree, and CNS.
    • Undesirable Effects of \text{H1} Receptor Activation:
      • Capillary vasodilation and increased permeability.
      • Itching (pruritus).
      • Urticaria (hives).
      • Pain.
      • Increased heart rate (HR).
      • Bronchoconstriction.

Histamine 1 Receptor Antagonists (Antihistamines)

  • Mechanism: Antagonize \text{H1} receptors.
  • Generations: Classified into 1st and 2nd generations, differing primarily in sedation profiles.
  • First Generation Antihistamines:
    • Mechanism: Block histamine receptors.
    • CNS Effects: Cross the Blood-Brain Barrier (BBB), leading to CNS effects like sedation.
    • Medications: diphenhydramine (Benadryl, Allerdryl), chlorpheniramine (ingredient in some cough/cold medications like Benylin).
  • Second Generation Antihistamines:
    • Mechanism: Selectively block \text{H1} histamine receptors.
    • CNS Effects: Decreased CNS distribution, resulting in 'non-drowsy' effects.
    • Medications: fexofenadine (Allegra), loratadine (Claritin), cetirizine (Reactin - fast melt tabs; onset 10-20 min, duration 24 hrs), desloratadine (Aerius).

Combination Medications (Example Ingredients)

  • Combination cold and allergy medications often contain various active ingredients to target multiple symptoms.
    • Robitussin: Codeine (antitussive), guaifenesin (expectorant).
    • Triaminic: Hydrocodone (antitussive), pseudoephedrine (decongestant), chlorpheniramine (antihistamine), guaifenesin (expectorant).
    • Actifed Sudafed: pseudoephedrine (decongestant), chlorpheniramine (antihistamine).
    • Benadryl (allergy/cold): pseudoephedrine (decongestant), diphenhydramine (antihistamine), acetaminophen (analgesic).
    • Benylin: Dextromethorphan (antitussive), chlorpheniramine (antihistamine), menthol, guaifenesin (expectorant).

Body Defenses Against Infection

  • Physical Barriers:
    • Skin: Keratin layers provide a robust outer defense.
    • Mucous Membranes: Found in areas like the nose and GI tract, trapping pathogens.
  • Cellular Defenses (Phagocytosis):
    • Neutrophils, monocytes/macrophages, Natural Killer (NK) cells, eosinophils, cytotoxic T cells engulf and destroy pathogens.
  • Specific Immune Response (Adaptive Immunity):
    • Memory B and T cells provide long-term immunity.
    • B cells secrete antibodies.
  • Interferons: Immunogenic proteins secreted by WBCs (lymphocytes, macrophages) that stimulate immune responses.
  • Pro-inflammatory Chemical Mediators: Initiate and sustain inflammation, a key part of the immune response.
  • Fever: An increase in body temperature activated by pyrogens, which can inhibit pathogen growth and enhance immune cell activity.

Cells of the Immune Response: White Blood Cells (WBCs)

  • Neutrophils:
    • Constitute up to 70 \% of WBCs.
    • First responders to sites of tissue damage.
    • Lifespan: Up to 1 week in blood and tissues.
    • Immature neutrophils are known as 'band cells'.
  • Lymphocytes:
    • Involved in both innate and adaptive (memory) immunity.
    • Three main types: NK cells, B cells, and T cells.
  • Monocytes:
    • Circulate in the blood.
    • Mature into macrophages in tissues, which are specific to their locations (e.g., hepatic Kupffer cells in the liver).
  • Eosinophils:
    • Primary responders in allergic reactions.
    • Release enzymes and chemical mediators.
    • Destroy allergens and parasites.
  • Basophils:
    • Involved in allergic responses.
    • Release pro-inflammatory and anticoagulating substances (e.g., histamine, heparin).

What Causes an Infection?

  • Pathogenicity: An organism's inherent ability to evade or overcome the body's defenses.
  • Pathogens: The causative agents of infection, including bacteria, viruses, fungi, and parasites.
  • Port of Entry: Pathogens must gain entry into the body past endogenous defenses.
  • Mechanisms of Infection:
    • Strength in numbers: A high microbial load can overwhelm defenses.
    • Toxin production: Pathogens release toxins that directly damage host cells or interfere with host functions.
  • Prevention:
    • 80 \% of infections are spread by hands.
    • Handwashing: The most effective preventive measure.
    • Technique: Use water and soap, rubbing for 15-20 seconds.
    • Example: Prevention of Streptococcus septicemia through proper hygiene.

Microorganisms: General Information

  • Microflora: Microorganisms naturally present on or in the human body.
    • Commensalism: A relationship where the host is not negatively affected, but the bacteria benefit from the environment (e.g., skin flora).
    • Mutualism: A relationship where both the host and bacteria benefit (e.g., intestinal flora which aids in Vitamin K formation).
  • Infectious Disease ('Pathogens'): Occurs when the host is negatively affected by microorganisms, representing a 'parasitic relationship'.
    • Causative agents: Bacteria, viruses, parasites, fungi.
  • Opportunistic Pathogens: Any microorganism capable of causing disease if an opportunity arises.
    • Example: Intestinal flora causing infection in an immunocompromised host.
    • High-Risk Patients: Opportunistic infections are common in individuals with chronic illness, the elderly, newborns, those undergoing drug treatment (e.g., immunosuppressants), and those experiencing malnutrition.

Site of Infection

  • Suffix '-itis': Indicates an infected or inflamed body part (e.g., appendicitis, laryngitis).
  • Suffix '-emia': Indicates the presence of a pathogen in the blood (e.g., bacteremia - bacteria in blood, fungemia - fungi in blood).
  • Important Note: A single pathogen may infect a variety of body areas or organs, and conversely, a specific body area or organ may be infected by various pathogens. Therefore, an accurate diagnosis is complex and imperative for effective treatment.

Course of Infection

  1. Incubation Period:
    • Pathogen is present and replicating.
    • No symptoms are typically observed.
    • The infected individual can still infect others.
  2. Prodromal Stage:
    • Initial, non-specific symptoms emerge (e.g., malaise, mild fever, headache, myalgia).
    • Symptoms are generic, making it difficult to differentiate from other illnesses.
  3. Acute Stage:
    • Maximum presence of the pathogen in the body.
    • Maximum host immune response.
    • Maximum impact of the infection, with more specific symptoms arising.
  4. Convalescent Period:
    • The pathogen's numbers begin to decrease.
    • Progressive host repair of damages caused by the infection.
  5. Resolution:
    • No signs of disease remain; the infection has cleared.

Antibacterial (Abx) Treatment Process

Step 1: Where is the Illness?

  • Assessment: Based on health history (Hx) and focused health assessment findings (signs and symptoms, S&S).

Step 2: Identify What is Causing the Illness?

  • Diagnosis: Differentiating between bacterial and viral causes.
  • Tools: Complete Blood Count (CBC) and differential, S&S, Hx, and culture from the suspected source.
  • Culture Tests: Involve collecting samples to grow and identify the causative microorganism.
  • Culture Results: Clinical Classification of Bacteria:
    • Characteristics: Single-cell organisms, generally larger than viruses.
    • Gram Staining: A laboratory method to classify bacteria based on their cell wall composition.
      • Staining involves applying crystal violet, then iodine, followed by alcohol treatment to remove iodine.
    • Gram Negative Bacteria: Do not retain the crystal violet stain after decolorization due to a thinner peptidoglycan layer and outer membrane (e.g., E. coli, Klebsiella, Pseudomonas, Salmonella, Haemophilus influenzae (Hib), Cholera, Syphilis, Gonorrhea, Neisseria meningitidis).
    • Gram Positive Bacteria: Retain the crystal violet stain due to a thick peptidoglycan layer (e.g., Staphylococci, Streptococci (Pneumococci), Enterococci, Listeria, Clostridioides difficile (C-diff)).

Step 3: Antibacterial (Abx) Treatment

  • Antibiotic Empiric Treatment:
    • Basis: Initiated based on the suspected bacterial pathogen, guided by clinical presentation and evidence.
    • Spectrum: Broad-spectrum antibiotics may be used if multiple regions are affected or more than one pathogen is suspected.
    • Timing: Should be started as soon as possible (ASAP) if bacterial infection is suspected.
    • Pharmacokinetics: The drug must reach its target site (ADME: Absorption, Distribution, Metabolism, Excretion).
    • Patient Compliance: Crucial for treatment success.
    • Viral Infections: No antibiotics should be administered if the illness is viral.
  • Antibiotic Focal Treatment:
    • Basis: Treatment initiated or adjusted once Culture & Sensitivity (C&S) results are known.
    • Switching Therapy: Empiric treatment may be switched to focal treatment.
    • Spectrum: Typically involves a narrow-spectrum antibiotic, which is a better choice for the specific identified pathogen.
    • Viral Infections: No antibiotic used if the cause is definitively viral.

Antimicrobial (Anti-infective, Antibiotic) Major Categories & Drug Classes

  • Always evaluate treatment efficacy to ensure the antibiotic is working.
  • Important Reminder: Various pathogens can cause the same illness, and illnesses can be caused by various pathogens.

Antimicrobial Mechanisms of Action: 4 Classes

  1. Cell Wall Synthesis Inhibitors:
    • Drug Category: Beta-lactam antibiotics (characterized by a beta-lactam ring structure).
    • Drug Classes:
      • Penicillins:
        • Nomenclature: End in the suffix '-illin'.
        • Efficacy: Effective against both Gram-positive ( + ) and Gram-negative ( - ) bacteria.
        • Spectrum: Can be narrow- or broad-spectrum.
        • Allergy: Approximately 10 \% of patients with a penicillin allergy may also have a cross-allergy to cephalosporins.
        • Treatment Examples:
          • Pharyngitis (Bacterial cause: Streptococcus Pyogenes (Gram + )): 1^{st} choice is Penicillin V (PO).
          • Otitis Media (Bacterial causes: S. pneumoniae; Hib; Moraxella): 1^{st} choice is Amoxicillin (PO); may be combined with beta-lactamase inhibitors.
      • Beta-lactamase Inhibitors:
        • Mechanism: Inhibit the resistance enzyme beta-lactamase, which bacteria produce to break down beta-lactam antibiotics.
        • Drugs: Clavulanic Acid, Tazobactam.
        • Combination Drugs (Broad Spectrum Penicillins): Often combined with penicillins to overcome resistance.
          • Amoxicillin + Clavulanic Acid (co-amoxiclav (Augmentin)).
          • Ticarcillin + Clavulanic Acid (co-ticarclav (Timentin)).
          • Piperacillin + Tazobactam (Pip-Taz (Tazosin, Zosyn)).
      • Cephalosporins:
        • Nomenclature: Start with the prefix 'cef-'.
        • Class Size: The largest antibiotic class, with 5 generations.
        • Clinical Use: 1^{st} choice for skin infections (e.g., Cefazolin (Ancef) IV, Cephalexin (Keflex) PO, Cefuroxime).
        • BBB Penetration: Higher generations (3^{rd} - 5^{th}) cross the Blood-Brain Barrier (BBB).
          • Examples: Ceftriaxone, Ceftazidime, Ceftaroline.
          • Efficacy: Effective for bacterial meningitis and resistant bacterial infections, such as MRSA.
      • Carbapenems:
        • Nomenclature: End with the suffix '-penem'.
        • Potency: Potent antibiotics, generally not 1^{st} line therapy; administered IV.
        • Medications: Imipenem, Meropenem.
        • Efficacy: Broad-spectrum, used for serious and mixed infections (e.g., Meningitis, Aspiration pneumonia).
      • Bacitracin:
        • Brand Name: Polysporin.
        • Efficacy: Effective against Gram-positive bacteria and has a broad spectrum.
        • Formulations: Topical, ophthalmic, and ear preparations.
        • Treatment: Used for conjunctivitis, topical skin/soft tissue infections, and as a prophylactic agent.
  2. Protein Synthesis Inhibitors: (e.g., Macrolides, Tetracyclines, Aminoglycosides).
  3. Nucleic Acid Inhibitors (DNA, RNA): (e.g., Fluoroquinolones, Rifampin).
  4. Antimetabolites: (e.g., Sulfonamides, Trimethoprim).

Resistance and Adverse Effects of Antibiotics

  • Resistance:
    • Common Resistant Pathogens:
      • Staphylococcus Aureus (specifically Methicillin-Resistant Staphylococcus Aureus, MRSA).
      • Enterococci (specifically Vancomycin-Resistant Enterococci, VRE).
      • Other multi-drug resistant organisms (e.g., Tuberculosis, TB) will be noted in C&S results.
  • Adverse Effects to Note:
    • Common, Non-Threatening: Gastrointestinal (GI) issues such as diarrhea, abdominal pain, and nausea.
    • Compatibility Check: Always check for drug interactions that could decrease antibiotic efficacy.
    • Allergy Check: Crucial to check for allergies to penicillins, cephalosporins, and sulfa drugs.
      • If a patient reports a symptom, always inquire further about it.
    • Resources: Lexicomp app provides drug monographs including side effects.
    • Opportunistic Infections: Long-term treatment with antibiotics can disrupt normal flora and lead to opportunistic infections, such as Clostridioides difficile (C-diff).

Viruses & Treatment

  • Characteristics:
    • Non-living entities.
    • Consist of genetic material (DNA or RNA) enclosed in a protein or lipid coat.
    • Parasitic Nature: Require a host cell to survive and replicate; they contain only replication material and need the host's cellular machinery.
    • Mutation: Mutation is frequent, making treatment difficult to derive.
  • Common Viruses:
    • Common Cold: Rhinoviruses, coronaviruses, parainfluenza viruses.
    • Herpes Family: Herpes simplex virus I & II, Varicella (causes chickenpox and shingles).
    • Hepatitis A-E: Hepatitis A (food-borne), Hepatitis B (body fluids), Hepatitis C (blood), Hepatitis D (blood), Hepatitis E (mostly water-borne).
    • HIV: Human Immunodeficiency Virus, the cause of AIDS (Acquired Immunodeficiency Syndrome).
  • Treatment (Tx):
    • Difficulty: Treatment is challenging because viruses target and replicate inside human cells.
    • Strategy: Unless antivirals can reach the virus prior to entering host cells, treatment is mostly suppressive.
    • Antiviral Drugs: Aim to decrease the severity of the disease but do not typically eliminate the virus from the body.
    • Immunizations: The most effective strategy, focusing on prevention of viral infections.