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BIO 307 PATHOPHYSIOLOGY

BIO 307 PATHOPHYSIOLOGY. DR. GREENAMYER. BASIC TERMS. Vocabulary Hyper-- vs hypo-- --itis --osis --opathy Idopathic, Iatrogenic, Nosocomial Disease (Syndrome) vs Normalcy. Etiology: causes or reasons for a disease

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BIO 307 PATHOPHYSIOLOGY

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  1. BIO 307 PATHOPHYSIOLOGY DR. GREENAMYER

  2. BASIC TERMS • Vocabulary • Hyper-- vs hypo-- • --itis • --osis • --opathy • Idopathic, Iatrogenic, Nosocomial • Disease (Syndrome) vs Normalcy

  3. Etiology: causes or reasons for a disease • Virus/bacteria, occupation, age, sex, nutritional status, genetics • Can be used to classify disease • Inherited, congenital, toxic, infectious, traumatic, degenerative, neoplastic, metabolic

  4. Pathogenesis: development/evolution of disease • Manifestations of Disease • Signs: objectively identifiable changes (fever, BP, HR, PCV) • Symptoms: subjective feelings (nausea, pain)

  5. FACTORS THAT INFLUENCE DISEASE • Extrinsic factors—outside individual, may or may not be controlled • Diet, medication, exposure to harmful agents • Intrinsic factors—rarely under individual control • Age, sex, genetic inheritance • Congenital vs inherited • Most diseases are a combination (interaction) of factors

  6. Genetic disorders • Single gene disorders—may affect any tissue/organ system • Autosomal dominant—need only one bad copy of gene • Equally prevalent in males and females • No skipping of generations, delayed onset common • Typically less severe than recessive, structural protein defect • Huntingdon’s Disease, Adult polycystic kidney disease

  7. Autosomal recessive—need two bad copies of gene • Equally prevalent in males and females • May skip many generations, but often seen in siblings • Early age onset, more often enzymatic deficiency • Cystic fibrosis, sickle cell anemia

  8. Sex Linked disorders—carried on X (most often) or Y (rarely) chromosome • X linked recessive most common • More common in male; females are usually asymptomatic carriers unless unequal X inactivation or 2 copies of the mutated gene • All daughters of affected men are carriers • Hemophilia A, Duchenne’s muscular dystrophy

  9. Mitochondrial gene disorders—passed through maternal line • Extremely rare

  10. Chromosomal abnormalities • Aneuploidy—abnormal number of chromosomes • Down’s syndrome (trisomy 21) most common • Result of nondisjunction • Translocations—result in structural abnormalities • Genetic material exchanged between nonhomologus chromosomes • Robertsonian translocations most important clinically • Philadelphia chromosome in chronic myelogenous leukemia

  11. Fig. 4-18

  12. Causes of Cellular Injury • Hypoxic injury (ischemia is #1 cause) • Chemical injury (free radicals, heavy metals) • Physical injury (mechanical, thermal, radiation, electric shock) • Infectious injury (bacteria, viruses, fungi, parasites) • Immunological and inflammatory injury

  13. Terminology of Cellular Changes • Atrophy • Autophagy in malnutrition • Hypertrophy vs hyperplasia • Dysplasia (atypical hyperplasia) • Metaplasia • Senescence (aging) and death

  14. Common themes/results (T 2-2) • ATP depletion • Defects in membrane permeability • Increased intracellular calcium • Increased free radicals

  15. Manifestations of Cellular Injury • Accumulate water (cloudy swelling, oncosis, hydropic degeneration) • Accumulate lipids (steatosis), carbohydrates, or proteins • Atrophy—requires autophagy • accumulation of pigments (brown atrophy)

  16. Cloudy swelling (oncosis, hydropic degeneration)

  17. Cell death (necrosis) • Nuclear changes are most obvious • Pyknosis—shrunken, irregular, dark staining nucleus • Karyorrhexis—fragmentation of nucleus • Karyolysis—dissolution of nucleus

  18. Coagulative necrosis—most common type • Cells retain shape, tissue retains normal architecture • Indicates ischemia—dry gangrene • Liquifactive necrosis—most common in brain • Can result from hydrolases from bacteria • Wet gangrene • Caseous necrosis—cells degenerate but fragments remain--Mycobacterium infections

  19. Apoptosis • Active process of programmed cell death (scattered, single) • Deletes excess cells during development • Probably occurs in malignant cells or cells damaged by chemotherapy • NOT accompanied by inflammation • Should not stimulate an immune reaction

  20. Apoptosis

  21. Systemic Manifestations of Necrosis (Inflammation) • Fever (from pyrogens) • Increased heart rate • Increased WBCs • Elevated presence of tissue specific enzymes • CPK creatine phosphokinase • LDH lactic dehydrogenase • ALT alanine aminotransferase • Loss of some organ function • Pain

  22. LOCAL INFLAMMATION

  23. Purpose of Inflammation • Destroy and remove insult • Wall off and confine damage • Stimulate immune response • Promote healing

  24. Causes of inflammation • Infection • Trauma—physical, chemical, thermal, radiation • Immune hyper-sensitivity reactions

  25. INFLAMMATION---types • Acute • Redness, heat, pain, swelling (rubor, calor, dolor, tumor) • Altered function (functio laesa) has been added • Subacute • Chronic---Longer duration • Granuloma formation—massive numbers of macrophages

  26. Fig 6-3

  27. Clotting

  28. Cytokines in acute inflammation

  29. Local Inflammatory Response • Margination and diapedesis of WBC • Vascular Response—increased permeability • Arterial dilation—increased local BP • Endothelial cells of blood vessels (venules) separate • Exudation—significant amounts of protein lost into interstitial space • Water follows protein to maintain osmotic balance

  30. Results of water movement • Interstitial swelling pulls flaps of lymphatic capillaries apart • Increased flow of lymph • Protein, cells enter lymphatics • Lymphangitis/lymphadenitis (lymphadenopathy) may result

  31. Mediators of inflammation • Histamine—mast cells • Activated Factor XII--Clotting System • Arachidonic acid metabolites • COX and LOX pathways • Complement cascade • Miscellaneous cell factors

  32. Fatty acids

  33. Chronic inflammation

  34. Exudates • Serous—protein in interstitial fluid • Fibrinous—fibrinogen accumulates on serous surfaces • Mucinous—mucous membranes—cellular secretion • Neutrophillic—purulent—bacterial infection/necrotic cells • pus is suppurative exudate of neutrophils and dead bacteria

  35. Systemic Manifestations of Inflammation • Fever • Leukocytosis • Increased Erythrocyte Sedimentation Rate

  36. Wound Healing • Healing by first intention • Healing by second intention (granulation)

  37. Fig 6-21

  38. Indications of wound infection • Abscesses, furuncles (boils), carbuncles • Cellulitis—widespread purulent inflammation • Mixed exudate from wound • Fibrinopurulent • Mucopurulent • Serofibrinous

  39. Factors that Delay Wound Healing • Oxygen deficiencies/ Ischemia • Nutrition deficiencies • Fluid/ electrolyte imbalances • Age • Medications or other disease • Extent of tissue damage • Dehiscence/ evisceration may result from premature suture removal

  40. Complications of healing • Scaring • strictures, contractures • Adhesions • Keloids

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