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Intro to Pathology

Intro to Pathology. The study of the origin and development of disease. Pathologists investigate etiology and pathogenesis By way of morphology ( morphe = form) Using techniques of histology ( histo = tissue) as well as biochemistry and molecular biology

dominic-kelley
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Intro to Pathology

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  1. Intro to Pathology

  2. The study of the origin and development of disease • Pathologists investigate etiology and pathogenesis • By way of morphology (morphe = form) • Using techniques of histology (histo = tissue) as well as biochemistry and molecular biology • With goal of easing clinical signs and symptoms • Where the clinician begins

  3. Language • Pathos = suffering, feeling • Logos = study • Genesis = origin, birth, development • Eti from aeiti = cause • Medical terms are compounded from prefixes, roots, and suffixes that are frequently Greek or Latin • Who speaks classic, dead languages? • Not your patients, but you will

  4. Comprehend and deduce • There are a lot of terms to “memorize” • There are patterns in the usage of the language • Learn the meaning of the parts of the language • Recognize the patterns, decode the terms, deduce the importance of their meaning • Back-translate to your patient, recalling when it was “all Greek to you”

  5. Elements of recognition Emergence Invariance Elements of comprehension Greek and Latin terminology Prefix, root, suffix Pattern recognition and language comprehension

  6. Case study: What does it mean, “Toll-like” receptor? • What language? • English, toll = fee for use, usually when crossing a bridge or travelling on a restricted-access road. • German, toll = crazy, weird, awesome, … • What usage? • Exclamation! Upon discovering a mutant drosophila that was all back and no front. • Toll is a maternal-dominant gene that controls segmentation and body plan patterning during embryonic development in flies • Toll is a receptor that provides protection from fungal infection in adult flies

  7. Does comprehending the name help understand the function? • Maybe not, but there is still a pattern • Toll-like receptors share primary (sequence), secondary (domain), tertiary (chain folding), and quaternary (protein-protein association) structure with the IL-1 receptor superfamily • Recognized patterns of amino acid sequence and folded shapes led to discovery of functional homologs from nematode to human—even fungal resistance in plants • Innate immunity as opposed to adaptive immunity is a concept with a foundation in discovery of TLRs • Pathogenic strains of E.coli secrete proteins that mimic the tertiary structure of TLRs, blocking signal transduction and enhancing survival of the bacteria. Toll!

  8. Emergence

  9. Emergence

  10. Emergence

  11. Invariance

  12. B A C D

  13. Start with cellular alterations • Rudolf Virchow, the father of modern pathology, pioneered the use of microscopes in modern (mid 1800s) medical education • “Omnis cellula e cellula” every living cell arises from a prexisting living cell • Disease caused by patterns of injuries (lesions) to cells, extracellular matrix, tissue, organ, person

  14. Hypertrophy hyper = above, more trophe = nourishment, food Hyperplasia plastein = (v.) to form, to shape; (n.) growth, development Dysplasia dys = bad or disordered Metaplasia meta = change or beyond Hypoplasia hypo = below, less Atrophy, Aplasia, Agenesis a = without nourishment, form, begining Altered demand (muscle activity) Altered stimulation (growth factors, hormones) Altered nutrition (including gas exchange) Adaptive responses

  15. Physiological hypertrophy—normal

  16. Microscopic physiological hypertrophy

  17. Physiological hypertrophy—normal?

  18. Exercise hypertrophy

  19. Hypertrophy resulting from pathological injury (hypertension) infarction scars

  20. Physiologic adaptation vs. pathology

  21. Scarred necrosis

  22. Mechanisms of muscle hypertrophy • Increased protein synthesis increased cell size  increased organ size • Nondividing cells produce more protein and membrane without division • Mechanosensors, PI3K /Akt signaling pathway important in exercise-induced growth • Growth factors, vasoactive agents, hormones mediate stress-induced response • Unrelieved stress eventually results in irreversible injury

  23. PI(3)K/Akt cascade promotes hypertrophy downstream of IGF-1

  24. Physiological, hormonal hyperplasia

  25. Thyroid hyperplasia—nodular goiter

  26. Thyroid hyperplasia—toxic goiter

  27. Prostate normal vs. hyperplasia

  28. Hyperplasias reversible with appropriate treatment Benign Prostate Hyperplasia BPH from accumulation of stable DHT-AR complexes Androgen-driven upregulation of Fibroblast Growth Factors and TGFb FGF stimulates proliferation of stroma Goiters Endemic—dietary iodine deficieny or goitrogen ingestion Production of T3 and T4 inhibited Feedback inhibition of TRH and TSH relieved Over-stimulation of thyroid by TSH Hyperplasia often nodular Euthyroid to hypothyroid metabolic status Grave’s disease Autoimmune stimulation of TSH receptor by an IgG Production of T3 and T4 stimulated Diffuse hyperplasia Hyperthyroid metabolic status Pathological hormomal hyperplasias

  29. Epithelial dysplasia This is cellular dysplasia in the uterine cervix. The normal cervical squamous epithelium has become transformed to a more disorderly growth pattern, or dysplastic epithelium. This is farther down the road toward neoplasia, but dysplasia is still a potentially reversible process.

  30. Skin dysplasia—actinic keratosis

  31. Intestinal epithelial dysplasia (congenital tufting enteropathy)

  32. Metaplasia respiratory epithelium Metaplasia of laryngeal respiratory epithelium has occurred here in a smoker. The chronic irritation has led to an exchanging of one type of epithelium (the normal respiratory epithelium at the right) for another (the more resilient squamous epithelium at the left). Metaplasia is not a normal physiologic process and may be the first step toward neoplasia

  33. Metaplasia of esophageal epithelium Glandular, or Barrett’s,metaplasia of the normal esophageal squamous mucosa has occurred here, with the appearance of gastric type columnar mucosa, secondary to gastric reflux.

  34. Gonadal hypoplasia Gonadal hypoplasia secondary to hypothalamic deficiency of Gonadotropin Releasing Hormone, which results in deficient release of LH and FSH from the pituitary. Called adiposogenital syndrome, Frölich's syndrome, or hypothalamic eunuchism

  35. Hypoplastic lung Microscopic examination of the lung reveals no alveolar development, only tubular bronchioles incapable of significant gas exchange, in this premature baby with pulmonary hypoplasia from oligohydramnios. This results in insufficient gas exchange from respiration following birth.

  36. Kidney atrophy

  37. Testicular atrophy

  38. Muscle fiber atrophy Some of these skeletal muscle fibers here show atrophy, compared to normal fibers. The number of cells is the same as before the atrophy occurred, but the size of some fibers is reduced. This is a response to injury by "downsizing" to conserve the cell. In this case, innervation to the small, atrophic fibers was lost. (This is a trichrome stain.)

  39. Spinal muscular atrophy

  40. Causes of cell injury • Ischemia and hypoxia • (ischein = hold back; haima = blood; hypo = below, less; oxi = presence of oxygen) • Physical agents (temperature, pressure, electricity, radiation) • Chemicals (drugs, poisons, venoms) • Microbes (viruses, bacteria, fungi, worms) • Immune reactions • Genetic defects • Nutrition (deficiency, imbalance) • Aging

  41. Mechanisms of cell injury • Energy depletion (ATP) • Mitochondrial permeability • Cytosolic calcium increase • Free radicals, reactive (activated) oxygen species (ROS) • Membrane damage and permeability changes • DNA and protein structural damage

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