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Pathophysiology > Basic Pathologic Process Part II > Flashcards

Basic Pathologic Process Part II Flashcards

1
Q

What is the difference between reversible and irreversible cellular injury?

A

Reversible injury is when damaged cells can return to normal if stimulus is removed.
Irreversible injury is when damaged cells cannot return to normal.

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2
Q

Common causes of cellular injury.

A
  1. Hypoxia, ischemia
  2. Toxins
  3. Infectious disease
  4. Immunologic agents
  5. Genetic abnormalities
  6. Nutritional imbalance
  7. Physical agents
  8. Aging
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3
Q

What are the two main morphologic correlates of reversible cellular injury?

A
  1. Cellular swelling - increased permeability of plasma membrane
  2. Fatty change - appearance of triglyceride-containing lipid vacuoles.
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4
Q

What are the 3 characteristics of irreversible cellular injury?

A
  1. Inability to restore mitochondrial function.
  2. Loss of structure/functions of plasma membrane.
  3. Loss of DNA/chromatin integrity.
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5
Q

Necrosis v. Apoptosis

A
  1. Necrosis - accidental cell death due to severe damage
  2. Apoptosis - programmed cell death when cell is deprived of growth factors (no host response)
  3. Necroptosis - necrosis morphology and apoptosis mechanically
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6
Q

What are the morphological changes of necrosis?

A
  • discontinuities in plasma and organelles
  • increase in eosinophils
  • breakdown of DNA/chromatin (pyknosis, karyorrhexis, karyolysis)
  • calcification due to degradation into fatty acids binding calcium salts
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7
Q

What are the gross appearance of each type of necrosis?

A
  1. Coagulative
  2. Liquefactive
  3. Gangrenous
  4. Caseous
  5. Fat
  6. Fibrinoid
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8
Q

What are the mechanisms of serum lab test to detect cellular necrosis?

A
  • intracellular proteins in general circulation; detection of tissue-specific necrosis
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9
Q

What is similar and different between physiologic and pathologic apoptosis?

A

Physiologic - during development, some cells die and are replaced, no inflammation response
Pathologic - elminiates damaged cells beyond repair

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10
Q

What are the general principles that determine the cellular response and consequences of an injurious stimulus?

A

Principle - type of injury, duration, severity

Consequences depends on the above.

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11
Q

What are the principle biochemical mechanisms of cellular injury?

A
  1. Hypoxia, ischemia - failure of many energy-dependent pathways (necrosis)
  2. Multiple injurious stimuli - oxidative stress (necrosis)
  3. Mutations, cell stress, infection (apoptosis)
  4. Radiation - (necrosis/apoptosis)
  5. Infection, immunologic disorder (necrosis/apoptosis)
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12
Q

What are the four main cellular adaptations to stress?

Distinguish between physiologic and pathologic adaptation.

A
  1. Hypertrophy
  2. Hyperplasia
  3. Atrophy
  4. Metaplasia

Physiologic - response to hormone/endogenous chemical mediators/stress

Pathologic - cell modulates structure/functions to allow cell escape at expense of normal function

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13
Q

What are the main categories of intracellular accumulations?

A
  1. Fatty change - triglyceride accumulation (fatty liver)
  2. Cholesterol, cholesteryl esters - lipid-filled phagocytic cells (atherosclerosis)
  3. Proteins - too much proteins presented or too much production in cell (immunoglobins/protein defects)
  4. Glycogen - glycogen deposits (diabetes)
  5. Pigments - endogenous v. exogenous (lack of enzymes v indigested materials)
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14
Q

What are the differences between dystrophic and metastatic calcification?

A

Dystrophic - normal Ca2+ metabolism, Ca+ deposits into injured cells causing atherosclerotic lesions (aortic stenosis).

Metastatic - Ca2+ deposits into healthy tissues due to hypercalcemia due to tumors/disease

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15
Q

Describe a typical inflammation reaction.

A
  1. Recognition - host cells recognizes stimulus
  2. Recruitment - of leukocytes and plasma cells
  3. Vasodilation - increases vascular permeability
  4. Activation - of leukocytes and plasma cells
  5. Regulation - reaction is controlled
  6. Healing - damage tissue is repaired
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16
Q

Distinguish between acute and chronic inflammation.

A

Acute - initial, rapid response, short duration; accumulation of fluid and plasma proteins (edema) and the emigration of neutrophils

Chronic - reaction progresses to protracted type of inflammation, longer duration, more tissue destruction, the presence of lymphocytes and macrophages, the proliferation of blood vessels and fibrosis.

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17
Q

Describe the reaction of blood vessels in acute inflammation.

A 
Vasodilation (increase diameter arterioles --> capillary) slows down blood flow for leukocyte adhesion
Increased permeability (retraction of endothelial cells) allows exudate to enters ECF
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18
Q

Describe leukocyte recruitment (from margination to chemotaxis)

A
  1. Margination - leukocytes rolls along the periphery of endothelial vessel walls around site of inflammation. (selectins)
  2. Integrins activated by chemokines at the site of inflammation
  3. Stable adhesion of leukocytes
  4. Migration through endothelium - leukocytes squeeze through intercellular junctions into extravascular tissues
  5. Chemotaxis - movement of leukocytes by chemical gradient (chemoattractants) toward the stimulus of inflammation
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19
Q

Describe the roles of the dominant molecules during leukocyte recruitment.

A

Selectins: receptors on endothelium that mediate weak interactions between leukocytes and endothelium

Integrins: receptors on leukocytes that allow firm interactions between leukocytes and endothelium

Chemokines: activates integrins from low-affinity to high-affinity

Chemoattactants - chemical gradient attacting leukocytes toward the stimulus of inflammation

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20
Q

Describe steps of phagocytosis.

A
  1. Recognition and attachment of the particle to be ingested by the leukocyte
  2. Engulfment, with subsequent formation of a phagocytic vacuole (phagosomes)
  3. Killing or degradation of the ingested material
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21
Q

List the mediators of inflammation (source and action).

A
  1. Histamine
    Source: Mast cells, basophils and platelets.
    Action: Vasodilation, increased vascular permeability, endothelial activation.
  2. Prostaglandins
    Source: Mast cells, Leukocytes
    Action: Vasodilation, pain and fever.
  3. Leukotrienes
    Source: Mast cells, leukocytes
    Action: Increased vascular permeability, chemotaxis, leukocyte adhesion and activation.
  4. Cytokines (TNF, IL-1, IL-6)
    Source: Macrophages, endothelial cells, and mast cells
    Action: Local: endothelial activation (expression adhesion molecules).
    Systemic: fever, metabolic abnormalities, hypotension (shock).
  5. Chemokines-
    Source: Leukocytes, activated macrophages
    Action: Chemotaxis, leukocyte activation.
  6. Platelet-activating factor-
    Source: Leukocytes, mast cells
    Action: Vasodilation, increased vascular permeability, leukocyte adhesion,
    Chemotaxis, degranulation, oxidative burst.
  7. Complement-
    Source: Plasma (produced in liver)
    Action: Leukocyte chemotaxis and activation, direct target killing, (membrane attack complex), vasodilation (mast cell stimulation)
  8. Kinins
    Source: Plasma (produced in liver)
    Action: increased vascular permeability, smooth muscle contraction, Vasodilation and pain.
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22
Q

What are the 3 main functions of the complement system?

A
  1. Inflammation
  2. Opsonization/Phagocytosis
  3. Cell Lysis
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23
Q

What is the critical step in activating the complement system?

A

Splitting of inactive C3 into activated C3a and C3b.

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24
Q

What are the pathways that leads to activation of the complement system?

A
  1. Classical pathway
  2. Alternative pathway
  3. Lectin pathway
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25
Q

What are the four (4) main morphologic patterns of acute inflammation?

A
  1. Serous
  2. Fibrinous
  3. Purulent, abscess
  4. Ulcers
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26
Q

What is the cause, result and example of serous inflammation?

A

Exudation of cell-poor fluid, effusion, skin blisters

27
Q

What is the cause, result and example of fibrinous inflammation?

A

Large vascular leaks or procoagulant stimulus, fibrin forms in extracellular space, scar

28
Q

What is the cause, result and example of purulent inflammation?

A

By pus-producing bacteria, pus-containing abscess, appendicitis

29
Q

What is the cause, result and example of ulcers?

A

Shedding of inflamed necrotic tissue near surface of tissue, margins and based becomes scarred, diabetic ulcers

30
Q

Describe the 3 usual outcomes of acute inflammation.

A
  1. Complete resolution - Elimination of offending agent, restoration of site to normal
  2. Healing by connective tissue replacement (scarring or fibrosis) - tissue incapable of regeneration, abundant fibrin exudation that cannot be cleared
  3. Progression to chronic inflammation response - persistence of injurious agent or interference with normal process of healing
31
Q

What is chronic inflammation and some common settings in which it may arise?

A

Response of prolonged duration
(weeks/months) in which inflammation, tissue
injury, and attempts at repair coexist, in varying combinations.

Settings: persistent infections, prolonged exposure to toxic agents, autoimmunity, some cancers

32
Q

What are the morphologic changes of chronic inflammation?

A

Cellular infiltrate (WBC’s), fibrosis (severe or progressive

33
Q

What are the characteristic features of granulomatous inflammation?

A

Chronic inflammation with collection of activate macrophages sometimes with associated central necrosis.

Immune v. Foreign body

34
Q

What are the differences between the two main types of granulomas?

A

Immune - persistent T-cell mediated response when inciting agent cannot be eliminated

Foreign body - response to immobile foreign body, forms around talc, sutures, other fibers

35
Q

Compare and contrast the two main types of reactions that lead to tissue repair.

A

Regeneration - proliferation of cells that survive injury; in only some tissues

Connective deposition - scar formation, when regeneration is not possible, framework is damaged, fibrosis.

36
Q

Describe common systemic effects of inflammation.

A
  1. Fever (eleveation by 1-4 degree C)
  2. Acute-phase proteins (C-reactive protein, serum amyloid, fibrinogen, hepcidin)
    Leukocytosis (elevated, 15-20K)
    Increased HR, BP, decreased sweating.
37
Q

Define etiology.

A

Underlying causes responsible for disease initiation and progression.

38
Q

Define pathogenesis.

A

Cellular and molecular changes that produce structural/functional abnormalities specific to a disease

39
Q

Define homeostasis.

A

maintenance and regulation of stable, constant internal environment

40
Q

Define adaptation.

A

New steady state while still preserving viability and function.

41
Q

Define necrosis.

A

form of cell death where cellular membranes deteriorate causing cellular enzymes to leak out and digest cell

42
Q

Define apoptosis.

A

Regulated, programmed cell death via enzymatic degradation of cells DNA, nuclear and cytoplasmic proteins

43
Q

Define hemotoxylin.

A

Blue dye –> basophilia

44
Q

Define eosin.

A

Red dye –> eosinophilia

45
Q

Define pyknosis.

A

Nuclear shrinkage and increased basophilia; DNA = dark, shrunken mass

46
Q

Define karyorrhexis.

A

Shrunken nuclear mass undergoes fragmentation.

47
Q

Define: Karyolysis

A

Basophilia fades because DNAase digests DNA

48
Q

Define autophagy.

A

“Self eating” as survival mechanism when nutrient deprived, lysosomal digestion of cell’s own component

49
Q

Define hypoxia

A

Oxygen deficiency in tissues

50
Q

Define ischemia

A

Reduced blood supply; lead to deficiency in nutrients and build up of toxic metabolites

51
Q

Define hypertrophy

A

An increase in the SIZE of cells resulting in increased size of the organ

52
Q

Define hyperplasia

A

An increase in the NUMBER of cells in an organ that stems from increased proliferation

53
Q

Define atrophy

A

Shrinkage in the size of cells by the loss of cell substance

54
Q

Define metaplasia

A

A change in which one adult cell type is replaced by another cell type

55
Q

Define exudate

A

Escape of fluid, proteins and blood cells from vascular system into interstitial tissue or cavities due to inflammation

56
Q

Define transduate

A

Extravascular fluid with low protein content, little or no cellular material pushed out of capillaries due to high blood pressure

57
Q

Define edema

A

Accumulation of extravascular fluid; known as swelling at site of injury

58
Q

Define lymphangitis

A

Red streaking, swelling near a skin wound as a telltale sign of infection

59
Q

Define lymphadenitis

A

Inflammation of the lymph node.

60
Q

Define effusion.

A

Accumulation of fluid into a space or cavity created by injury

61
Q

Define purulent (suppurative)

A

Pus, inflammatory exudate consisting of neutrophils, liquefied debris of necrotic cells

62
Q

Define abscess

A

Localized collection of pus

63
Q

Define ulcer

A

Local defect of surface of an organ or tissue that is produced by shedding of inflamed necrotic tissue.

Pathophysiology (9 decks)

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