A

Lecture Notes: Inflammation, Infection, and Pharmacology Review

Major Concerns

  • Colonization: act of establishing presence
  • Agents of Disease: Inflammation and Infection

Characteristics of Organisms

  • Infection: presence and multiplication in host
  • Infectivity: ability to invade and multiply
  • Mutualism: organism and host derive benefits from each other

Terms

  • Opportunist pathogens: prey on host with weak immune system
  • Virulence: severe disease producing ability
  • Toxigenicity: ability to produce soluble toxins

Bacteria and Virus

  • Bacteria: killed by antibiotics; examples include E. coli, anthrax
  • Virus: antivirals; HIV, Hepatitis, rhinovirus

Panculture

  • Broad culture sampling from blood, sputum, urine, wound, stool, etc. covers infection sources
  • Growth in 24 hours prompts consideration of antibiotics; final at 48 hours helps determine meds

Environment

  • Germs like hot, humid, moist areas
  • Airborne: TB, anthrax (droplet spread for others e.g., COVID)
  • Contaminated food
  • Seasonal patterns: flu
  • Dense populations: colleges, campuses, schools
  • Contaminated water
  • Blood-borne: HIV

Diagnosis

  • Culture
  • Serology: study of plasma/serum
  • Monoclonal Antibodies: lab-made proteins that mimic antibodies and target specific diseases; effective with COVID

Systemic Manifestations

  • Anorexia
  • Arthralgia
  • Myalgia
  • Fever
  • Headache
  • Tachypnea
  • Tachycardia

Leukocytosis Manifestations

  • Systemic treatment vs localized treatment
  • Cytokine release can cause shock, organ failure, death
  • White blood cells should be 4{,}000-10{,}000 per mm³
  • Infection is present if white blood cells are elevated
  • Triggers: Stress, leukemia/lymphoma, burns and trauma, meds (heparin, steroids)
  • Smoking

Acute Phase

  • Begins within hours of inflammation
  • Localized inflammation may progress to lymphatic involvement; lymph nodes may enlarge and be painful
  • Acute phase proteins released from liver: Fibrinogen, CRP, and serum amyloid A (SAA)
  • Stimulated by cytokines
  • Body ramps up acute phase before illness is subjectively felt

Pyrexia

  • Fever
  • Antipyretics used to reduce fever
  • Prostaglandins: mediator chemicals released during trouble; promote fever, pain, inflammation
  • Prostaglandins produced via COX pathways; early signals include inflammation, pain, fever
  • Ibuprofen blocks prostaglandins (reduces fever/inflammation) but may affect other protective processes
  • Hypothalamus acts as the body's thermostat
  • Fever ↑ metabolism: higher heart rate, blood pressure, digestion changes; may necessitate more fluids and medication adjustments
  • Prodromal phase: nonspecific complaints

Cells of Inflammation

  • Histamines

Chronic Inflammation

  • (Conceptual level; ongoing inflammation can lead to tissue damage and remodeling)

Wound Healing

  • Phases: Inflammatory Phase, Proliferative Phase, Remodeling Phase
  • Chill, vasoconstriction to limit spread; flushing; defervescence (heat redirected to surface)
  • Acute Response: endothelial cells regulate vessel diameter; platelets accumulate
  • WBCs: neutrophils are primary responders; CBC with differential (diff) used to assess shift
  • Monocytes/macrophages produce prostaglandins, leukotrienes, platelet-activating factor, and cytokines
  • Vascular changes: initial vasoconstriction to contain; subsequent vasodilation to recruit more cells;↑ blood pressure locally; mediators drive inflammation
  • Prolonged irritation or foreign body presence sustains inflammatory mediators
  • Phases of healing: Inflammatory Phase → Proliferative Phase (cell production) → Remodeling Phase (scar formation)
  • Remodeling can result in abnormal scar formation (keloids)

Factors Affecting Healing

  • Nutrition
  • Age
  • Immunocompromised status
  • Blood flow
  • Infection presence

Chain of Transmission (Infection Control)

  1. Destroy the reservoir
  2. Block the portal exit
  3. Block the transmission
  4. Block portal entry
  5. Reduce victim susceptibility

H1 Antagonists

  • Therapeutic uses: mild allergy; severe allergy (adjunct); motion sickness; insomnia; common cold (anticholinergic effects reduce rhinorrhea)
  • Adverse Effects: sedation (less with newer generations); non-sedative CNS effects (dizziness, fatigue, coordination problems, confusion); GI effects (nausea, vomiting, loss of appetite, constipation)
  • Overuse risk: excessive diphenhydramine associated with increased dementia risk
  • Drug interactions

Anticholinergic Considerations and Second Generation Antihistamines

  • Anticholinergic effects: sympathetic nervous system actions; avoid with certain fruit juices; CNS depressant effects; caution in pregnancy/lactation
  • Acute toxicity: wide safety margin; generally accessible; CNS and anticholinergic reactions possible; children may exhibit CNS excitement; severe cases can cause coma or cardiac issues
  • Management: supportive care; activated charcoal; cathartics; seizures treated with IV benzodiazepines; hyperthermia managed with cooling
  • Second-generation antihistamines: less sedation; cross the blood-brain barrier poorly
    • Cetirizine (Zyrtec), Fexofenadine (Allegra), Loratadine (Claritin) among typical examples
    • Often taken orally; improved safety/efficacy profile
    • Some products advise avoiding certain foods or timings for absorption
    • Paradoxical reactions can occur in some patients

Glucocorticoid Drugs

  • Metabolic effects: elevated blood glucose due to cortisol; monitor for hyperglycemia
  • Potassium: risk of hypokalemia

Cyclooxygenase Inhibitors (and Corticosteroids)

  • Anti-inflammatory effects; include corticosteroids
  • Salt and water retention: edema risk
  • Musculoskeletal effects: reduced muscle mass; decreased bone matrix; thinning of skin
  • Interferes with tissue healing
  • Redistribution of fat: moon face, buffalo hump
  • Possible retinopathy/retinol effects

Nonendocrine Disorders

  • Cardiovascular effects: low dose may increase capillary permeability and alter vasoconstriction; potential blood pressure changes
  • Possible decreases in RBC and WBC counts

Stress Effects

  • During stress, adrenal glands secrete glucocorticoids and epinephrine to maintain BP
  • Prolonged stress can lead to adrenal gland atrophy and glucocorticoid insufficiency
  • In severe stress, risk of circulatory failure and death
  • Patients can become steroid-dependent and may struggle to raise BP after stress without steroids

Pharmacology (Anti-Inflammatory/Immunomodulatory Use)

  • Primary uses: anti-inflammatory, analgesic, antipyretic
  • Indications: rheumatoid arthritis, lupus, inflammatory bowel disease
  • Overuse can suppress immune response
  • Consider potential drug interactions

Uses

  • Anti-inflammatory, analgesic, antipyretic roles; broad therapeutic applications

Adverse Effects

  • Gastric ulceration
  • Bleeding
  • Renal impairment