INTRODUCTION TO Pathophysiology

1. INTRODUCTION TOPathophysiology Mechanisms of Disease Diagnosis & Treatment Inflammation & Healing

2. Terms Used In Pathophysiology • Pathology = study of disease • Pathogenesis = the development of a disease • Diseases develops in stages • Infectious disease example: (A)incubation (b)disease (c)convalescence • Pathophysiology = the study of the functional changes associated with a specific disease • How the disease affects specific functions of the body • Subjective findings • The patient’s symptoms • Described by the patient----(the patient’s history) • Objective findings • Health provider’s findings---( the physical exam) • Occurrence of disease defined by 2 factors • Incidence = # new cases per unit of time • Prevalence = # new & old cases per unit of time

3. Disease terminology • Etiology = cause of the disease • Idiopathic = disease with unknown cause • Iatrogenic = disease caused by human intervention • Congenital diseases = diseases occurring at birth • Syndrome = common cause of different signs & symptoms • Remission = period when symptoms & signs of disease abates • Exacerbation = period when symptoms & signs increase • Endemic disease = disease native to local area • Epidemic = many people affected in a given area • Pandemic = many people affected in large areas • Incubation = latent period of the disease before develop signs & symptoms • Prognosis = probability for recovery • Morbidity = disease rates within a group • Mortality = death rates within a group • Epidemiology = how the disease occurs & spreads through an area

4. Predisposing Factors (riskfactors) • Age • Young are prone to accidents • Getting diseases such as diabetes, heart disease, and certain cancers increase with age • Very old are prone to drug interactions • Sex • More frequent in woman: MS, osteoporosis • More frequent in men: gout, Parkinson’s disease • Lifestyle • Examples of harmful lifestyle: • Perilous occupation • Smoking • Excess alcohol • Poor nutrition • Sedentary activity

5. Environment • Air pollution • Water pollution • Poor living conditions • Excessive noise • Chronic psychological stress • Heredity • Deals with genetic predisposition (inheritance) • Genetic predisposition + certain type of environment = mental retardation , lung cancer, etc. • Preventive health care • The best treatment of a disease is prevention !! • Deals with altering risk factors that can be changed

6. Homeostasis • Definition = internal constancyor astable internal environment • A “body in balance” is in homeostasis • Homeostatic regulation ---- works by using feedback loops • Feedback loops utilize 3 components • (1) receptor (2) control center (3) effector • 2 types of feedback loops • (1) negative feedback • Restores any change back to normal • Resembles “teeter-totter” • Stabilizing • Most common • (2) positive feedback • Exaggerates the change • Resembles “domino effect” • Stimulating • Least common

7. Homeostasis & disease • Disease is the failure to maintain homeostatic conditions • Disease mechanisms • Genetic = mutated or abnormal genes • Pathogens (microscopic organisms) • Loss of control mechanisms (e. G. Diabetes, immune problems) • Degenerative changes (normal aging) • Environmental hazards (trauma, chemicals) • Nutritional factors • Tumors (benign & malignant)

8. The Cell & Disease Changes in Growth • Changes in size of individual cell • Atrophy = decrease in cell size • Hypertrophy = increase in cell size • Changes in actual number of cells • Hyperplasia, Dysplasia, & Anaplasia = increase in rate of reproduction • Hyperplasia = increase in number of normal cells • Dysplasia = increase in number of atypical cells • Anaplasia = increase in number of frankly abnormal cells Change in Type of Cell • Change of one type of cell into another type (metamorphoses) • Metaplasia =change to different mature cell type

10. Cell damage is the main reason to lose homeostasis • Deficiency of oxygen (hypoxia) = most common reason • Mechanism of progression: ischemia -to- necrosis -to- gangrene • Cell death • Once it occurs, lysis occurs with release of lysosomal enzymes • This causes inflammation • After inflammation, the dead cells(tissue) is either: • Replaced by scar tissue • Regenerated to resemble original tissue

11. Diagnosis & Treatment • “SOAP” protocol: “S” = subjective “O” = objective “A” = assessment “P” = plan • Subjective Findings = the patient’s symptoms • Obtained by taking a medical history • includes: • Chief complaint (cc) • present illness (PI) • past history (PH) ------- med/ surg/ allergies/ lifestyles • family history (FH) • review of systems (ROS) • Objective Findings = the patient’s physical manifestations • Obtained by doing a physical exam • Begins with opening statement (WD/WN/WW) • Then vita signs ------ T, P, BP, RR, Pain • go from head to toes! • Includes techniques of: • inspection • auscultation • palpation • percussion

12. Assessment = arriving at a diagnosis • Differential diagnoses • Includes all possibilities • Lab • Basically a study of body fluids • Diagnostic tests • Imaging • X-ray, US, CAT, MRI, isotope scans • Endoscopies • Biopsies • Skin tests • Plan = all possible treatments with associated complications & prognoses • Includes a “Treatment Plan” • individualize • modalities available: • do nothing (primun non nocere) • Talk (counseling) • Medication • Surgery • Includes a Prognosis

13. The Inflammatory Response • Key purposes = DEFENSE • To hunt & kill invaders • To limit their spread • To prepare tissue for repair • Key events • Increase of vascular permeability • Recruitment (margination) & emigration (diapedesis) of WBC’s • Phagocytosis

14. The Inflammatory Response • Inflammatory response = normal body defense mechanism to tissue injury • Note: Inflammation is NOT infection • Cells of the inflammatory response when get tissue injury • Main groups; • Phagocytes --- “the eaters” • Macrophages --- become active as APC’s (antigen presenting cell) • Neutrophils --- “little eaters” • Monocytes --- become tissue macrophages • T- lymphocytes (helper-T) ---- produce cytokines which “ call all to action” • Platelets ---- release PAF (platelet activating factor) which in turn begins call to action and release of chemical mediators • Mast cells --- release chemical mediators that begin inflammation

15. Chemical Mediators • The initial “macrophage (APC cell) – antigen complex” causes chemical mediators to be released: • Histamine • From basophils & mast cells • Cause vasodilation & increased permeability of vessels via release of nitric oxide • Prostaglandins • Made in mast cell membrane from fatty acid (arachidonic) • Cause pain & vasodilation • Leukotrienes • “bad” prostaglandins since cause symptoms of inflammation (pain & swelling) • Cause chemotaxis • Very important for causing allergies, asthma, & anaphylaxis

16. Chemical Mediators • Complement • Coats bacterial surface; enhances phagocytosis & lyses bacteria • Inactive plasma proteins become activated by initial An-Ab complex • Interferon • Proteins that are released by helper T’s & kill viruses • Bradykinins • From inactivated plasma protein • Cause similar effects like histamine • Cause pain • Induce WBC’s into area (chemotaxis

17. Local effects of inflammation • 4 cardinal signs of inflammation • Redness (rubor) – from increased blood supply • Heat (calor) – from increased blood supply • Swelling (tumor) – from increased permeability & increased proteins in interstitial fluid • Pain (dolar) – from chemical mediators • Also get inflammatory exudate • Serous – from allergic reactions & burns • Purulent – from infections • May lead to abscess • Systemic effects of inflammation • General malaise • Fatigue • Headache • Fever • Caused by pyrogens (chemicals released from phagocytes) • Beneficial • Inhibits growth of pathogens • Enhances repair process via increased metabolic rate

18. Leukocytosis • Chemotaxis • Margination • Diapedesis

19. Potential complications of inflammation • Infection • Ulceration – from chronic inflammation • May lead to: • perforation of viscera • excess scar formation • Skeletal muscle spasm • Local tissue reactive changes • Joints from decreased ROM become stiff • Lungs cannot exchange gases • Diagnostic tests for inflammation • Leukocytosis • Differential WBC count • ESR • Cell enzymes – may or may not be tissue specific • C-reactive protein

20. Chronic Inflammation • The acute inflammatory reaction usually subsides within 48 –72 hours as long as the cause is removed (e.g. touching a hot stove) • If the cause persists, you get chronic inflammation • Clinically: • Increase in connective tissue reaction to the chronicity • Get more fibroblasts & more collagen • Thus get more scar tissue • Can get granulomas (collection of chronically inflamed tissue) • Treatment of inflammation • Aspirin • NSAID’s • Glucocorticoids • Heat & cold • Physiotherapy if chronic • Prevents contractures

21. Healing • 3 ways depending on the tissue involved & degree of injury • Resolution • Damaged cells recover in short time • Exp = mild sunburn • Regeneration • Damaged cells replaced by identical cells via mitosis • Only occurs in epithelia & connective tissue • If complex organ, some damaged tissue replaced by regeneration & some by scar • Scar formation • Keytissue = granulation tissue(highly vascular connective tissue) • Collagen produced by fibroblasts makes granulation tissue into scar tissue • Scar tissue is non-functional

22. Healing by primary or secondary intention • Depend weather edges of lesion can be brought together • Primary (first) intention gives small scar formation • Secondary intention gives large scar formation • Heals via granulation tissue

23. Complications from large scar formation (see next slide) • Loss of function • Contractures & obstructions • Can lead to stenosis • Adhesions • Ulceration • Factors promoting healing • Nutrition • Blood supply • Cleanness of area • Lack of complications • Factors delaying healing • Old age • Presence of foreign material • Poor blood supply • Poor nutrition • Complications (bleeding, hematoma, excessive mobility)

25. First degree burns Superficial partial-thickness Involves just epidermis Get redness but no blistering May peel in 1-3 days Get no scarring Second degree burns Deep partial-thickness Involves epidermis & dermis Get redness & blistering Can get scarring Can get some fluid loss Get significant pain Third degree burns Full-thickness Involves all 3 layers & may involve underlying tissue Get no pain Get serious fluid loss Rule of 9’s If burn 1st ,2nd , or 3rd & involves more than 20% ---- needs medical attention If burn 2nd or 3rd & involves greater 20% = serious If burn 2nd or 3rd & involves greater 40% = severe Complications Fluid imbalance Dehydration Anemia Infection Excess scar formation Burns