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Pathophysiology: Introduction to Basic Pathology

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Title: Pathophysiology: Introduction to Basic Pathology


1
Pathophysiology Introduction to Basic Pathology
  • Lecture 1
  • Dr. Karen Ronquillo
  • Premed 2

2
Basic Pathophysiology
  • Basic Pathology
  • Basic Microbiology
  • Bacteriology
  • Virology
  • Mycology
  • Immunology
  • Basic Pharmacology

3
What is Pathology?
4
Pathology
  • Branch of Medicine
  • suffering
  • Studies the underlying causes of diseases
  • etiology
  • Mechanisms that result in the signs and symptoms
    of the patient
  • pathogenesis

5
Pathology
  • Bridge between basic science and clinical
    practice
  • Divisions
  • General Pathology
  • Systemic Pathology

6
The Cell
7
How do cells react to environmental stress?
  • Hypertrophy
  • Hyperplasia
  • Aplasia
  • Hypoplasia
  • Atrophy
  • Metaplasia

8
Hypertrophy
  • Increase in protein synthesis/ organelles
  • Increase in size of cells
  • Increase in organ/tissue size

9
Hypertrophy
10
Hyperplasia
  • Increase in NUMBER of cells
  • Increase in size of organ/tissue
  • Similar end result as hypertrophy
  • May occur with hypertrophy

11
Hyperplasia
12
Aplasia
  • Failure of cell production
  • Agenesis or absence of an organfetus
  • Loss of precursor cellsadults

13
Technetium scintigraphy
14
Aplasia
15
Hypoplasia
  • Decrease in cell production

16
Atrophy
  • Decrease in mass of preexisting cells
  • Smaller tissue/organ
  • Most common causes
  • disuse
  • poor nutrition
  • lack of oxygen
  • lack of endocrine stimulation
  • aging
  • injury of the nerves

17
Atrophy
18
Metaplasia
  • Replacement of one tissue by another tissue
  • Several forms
  • Squamous metaplasia
  • Cartilaginous metaplasia
  • osseous metaplasia
  • myeloid metaplasia

19
Metaplasia
Squamous to columnar change in cells
20
Barretts esophagus
21
What are the causes of injury/stress?
  • Hypoxic cell injury
  • Free radical injury
  • Chemical cell injury

22
Hypoxic cell injury
  • Complete lack of oxygen/ decreased oxygen
  • Anoxia or hypoxia
  • Causes
  • ischemia
  • anemia
  • carbon monoxide poisoning
  • decrease tissue perfusion
  • poorly-oxygenated blood

23
Hypoxic cell injury
24
Early stage Hypoxic cell injury
  • Decrease in production of ATP
  • Changes in cell membrane
  • Cellular swelling
  • endoplasmic reticulum
  • mitochondria
  • Ribosomes disaggregate
  • Failure of protein synthesis
  • Clumping of chromatin

25
Late stage
  • Cell membrane damage
  • myelin blebs
  • cell blebs

26
Cell Death
  • Irreversible damage to the cell membranes
  • Calcium influx
  • Mitochondria calcifies
  • Release of cellular enzymes
  • lab exams for AST, ALT, CKMB, LDH
  • Most vulnerable cells
  • neurons

27
Cardiac enzymes
28
CKMB kit
29
Free radicals superoxide and hydroxyl radicals
  • Seen in
  • normal metabolism
  • oxygen toxicity
  • ionizing radiation
  • UV light
  • drugs/chemicals
  • ischemia

30
What will neutralize free radicals?
31
Mechanisms to detoxify free radicals
  • Glutathione
  • Catalase
  • Superoxide dismutase
  • Vitamin A, C, E
  • Cysteine, selenium, ceruloplasmin
  • Spontaneous decay

32
Chemical Injury
  • Carbon tetrachloride and liver damage

33
Morphologic patterns of cell deathNECROSIS AND
APOPTOSIS
  • Necrosis
  • sum of all the reactions seen in an injured
    tissue, leads to cell death
  • autolysis cells enzymes
  • Heterolysis extrinsic factors

34
Types of necrosis
  • Coagulative necrosis
  • Liquefactive necrosis
  • Caseous necrosis
  • Gangrenous necrosis
  • Fibrinoid necrosis
  • Fat necrosis

35
Coagulative necrosis
  • Interruption of the blood supply
  • Poor collateral circulation
  • heart
  • kidney

36
Characteristic nuclear changes
37
Coagulative necrosis
38
Coagulative Necrosis
39
Liquefactive necrosis
  • Interruption of blood supply
  • Enzymes liquefy the tissue
  • Brain
  • Suppurative infections
  • Bacteria

40
Liquefactive necrosis
41
Caseous necrosis
  • Coagulative liquefactive
  • cheese - like
  • Part of granulomatous inflammation
  • Classic picture
  • Tuberculosis

42
Caseous necrosis
43
Gangrenous necrosis
  • Interuption of the blood supply to the lower
    extremities or bowels
  • 2 types
  • 1. Wet type complicated by liquefactive
    necrosis
  • 2. Dry type complicated by coagulative necrosis

44
Gangrenous necrosis types
45
Fibrinoid necrosis
  • Immune-mediated vascular damage
  • Protein like material in the blood vessel walls

46
Fat necrosis
  • Traumatic fat necrosis after injury
  • Breast

47
ENZYMATIC FAT NECROSIS PANCREAS
48
APOPTOSIS
  • falling away from
  • Another cell death pattern
  • Programmed cell death
  • Removal of cells
  • Prevents neoplastic transformation

49
Necrosis versus apoptosis
  • Gross irreversible cell injury
  • Passive form of cell death
  • Does not require genes, protein synthesis
  • Marked inflammatory reaction
  • Physiologic programmed cell removal
  • Active form of cell death
  • Requires genes, proteins, energy
  • No inflammatory reaction

50
Genes affecting apoptosis
  • Inhibits
  • bcl-2
  • Facilitates
  • bax
  • p53

51
Morphological features in apoptosis
  • Involves small clusters of cells only
  • No inflammatory cells
  • Cell membrane blebs
  • Cytoplasmic shrinkage
  • Chromatin condensation
  • Phagocytosis of apoptotic bodies

52
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53
Reversible Cellular changes
  • Fatty change
  • Hyaline change
  • Accumulation of exogenous pigments
  • Accumulation of endogenous pigments
  • Pathologic calcifications

54
Fatty change
  • Liver, heart, kidney
  • Accumulation of intracellular parenchymal
    triglycerides
  • -increased transport
  • -decrease mobilization
  • -decreased use
  • -overproduction

55
Fatty change LIVER
56
Hyaline change
  • Accumulation of hyaline
  • HYPERTENSION DIABETES MELLITUS
  • glassy appearance

57
Exogenous pigments
  • Lungs
  • carbon
  • silica
  • iron dust
  • Lead Plumbism
  • Silver - Argyria

58
Endogenous pigments
Bilirubin
Hemosiderin
59
  • Lipofuscin
  • wear and tear pigment
  • Elderly patients
  • Liver, heart
  • Brown atrophy

60
Pathologic calcifications
  • Previously damages tissues
  • dystrophic calcification
  • scarred heart valves

61
Pathologic calcifications
  • Hypercalcemia
  • metastatic calcification

62
Question
  • A young woman was admitted due to a bacterial
    infection. CT scan showed an abscess in her
    brain. What type of necrosis would you expect to
    see?
  • A.coagulative
  • B.Caseous
  • C.Liquefactive

63
Question
  • A 15 year old girl was brought into your clinic
    due to painful menses. She also said that her
    menstrual blood flow was heavy and had clumps of
    blood clots and tissues.Menstruation is
    classified as
  • A. Apoptosis
  • B. Coagulative Necrosis
  • C. Liquifactive Necrosis
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