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Pathology Exam 1 > Cellular Pathology and Inflammation > Flashcards

Cellular Pathology and Inflammation Flashcards

1
Q

What are the 2 categories of etiology (causes of disease)?

A
  1. Genetic
  2. Acquired (infectious, nutritional, chemical, physical)
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2
Q

What represents those biochem rxns and cellular events that lead to disease?

A

Pathogenesis - mechanisms of its development

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3
Q

What are structural alterations induced in cells/organs of the body called?

A

Morphologic changes

-multiple etiologies/causes can give similar morphologic changes (flu) or very unique morphological alterations (herpes)

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4
Q

What are the functional consequences of the morphological changes called?

A

Clinical significance (signs/sx, course of disease, prognosis)

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5
Q

How is general pathology different than systemic pathology?

A

General - basic rxn of cells/tissues to abnormal stimuli that underlie all diseases (general inflamm 2’ to bacterial infx)

Systemic - specific responses of specialized organs/tissues to defined stimuli (ischemic heart diseases)

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6
Q

Under stress/injury, what 2 things can happen to the cell?

A
  1. Adaption
  2. Irreversible injury (injury is too severe) -> Death
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7
Q

7 causes of cell injury?

A
  1. Hypoxia and ischemia
  2. Physical agents
  3. Chemical agents and drugs
  4. Infectious agents
  5. Immunologic rxns
  6. Genetic derangements
  7. Nutritional imbalances
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8
Q

What is hypoxia?

A

Decreased availability of oxygen

  • severity of hypoxia -> spectrum of changes (atropy - cell death)
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9
Q

What are 3 causes of oxygen deprivation?

A
  1. Ischemia (insufficient blood supply; MCC)
  2. Cardiopulmonary fx
  3. Loss of oxygen carrying capacity of blood
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10
Q

What physical agents can cause cell injury?

A
  1. Mechanical trauma
  2. Deep cold
  3. Burns
  4. Sudden changes in atm pressure
  5. Ionizing radiation
  6. Electric shock
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11
Q

What are examples of chemical agents/drugs that cause cell injury?

A
  1. Elements (mercury)
  2. Salt
  3. Simple molecules (oxygen)
  4. Poisons
  5. Air pollutants
  6. Insecticides/herbicides
  7. Industrial/occupational chemicals
  8. Recreational drugs (alcohol and narcotic drugs)
  9. Therapeutic drugs
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12
Q

What are the 4 infectious agents that cause cell injury?

A
  1. Virus
  2. Bacteria
  3. Fungi
  4. Parasites
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13
Q

What are 3 immunologic rxns that cause cell injury?

A
  1. Anaphylaxis
  2. Deposition of immune complexes
  3. Rxns to self-antigens
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14
Q

What genetic derangements can lead to cell injury?

A
  1. Congenital malformations (i.e. Down’s syndrome)
  2. Gene insertions
  3. Gene deletions
  4. Gene translocations
  5. Frameshift mutations
  6. Point mutations
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15
Q

What nutritional imbalances can lead to cell injury?

A
  1. Protein - calorie deficiencies (i.e. Kwasiorkor and Marasmus)
  2. Vitamin - cofactor deficiencies and excesses
  3. Dietary excesses (i.e. fat)
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16
Q

What are the most common morphologically apparent adaptive changes?

A
  1. Atrophy
  2. Hypertrophy
  3. Hyperplasia
  4. Metaplasia
  5. Dysplasia
  6. Calcification
  7. Hyaline changes
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17
Q

What is atrophy? What are some causes?

A

Shrinkage in CELL SIZE by loss of cellular substances; caused by:

  • decreased workload (immobilization of limb in a cast)
  • pressure (physical injury)
  • diminished blood supply/nutrition (ischemia)
  • loss of endocrine stimulation (ablation of endocrine gland or denervation)
  • aging
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18
Q

What do atrophic cells usually contain?

A

Increased autophagic vacuoles w/ persistent residual bodies (such as lipofuscin)

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19
Q

What is hypertrophy? What are some causes?

A

Increase in CELL SIZE by gain of cellular substance; caused by:

  • Increased functional demand
  • Specific endocrine stimulations
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20
Q

Hypertrophy can affect not only the size of individual cells, but also the _____.

A

Phenotype

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21
Q

What is hyperplasia?

A

Increase in CELL NUMBER (tissue must contain cells that can divide; can occur concurrently w/ hypertrophy and in response to same stimuli)

  • typically caused by excessive endocrine stimulation
  • compensatory hyperplasia (liver tissue regrowth after part resected)
  • often a predisposing condition to neoplasia
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22
Q

What causes endometrial hyperplasia?

A

After normal MP -> burst of uterine epithelial proliferation -> excessive estrogen stimulation -> endometrial hyperplasia (common cause of abnormal menstrual bleeding)

-increases risk of developing endometrial cancer

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23
Q

What is metaplasia?

A

Reversible change in CELL TYPE

  • change in phenotype of differentiated cells
  • makes cells better able to withstand stress
  • normal protective mechanisms may be lost
  • persistence of signals that result in this often leads to neoplasia (metaplasia itself is NOT premalignant)
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24
Q

What is dysplasia?

A

Cells being replaced by ABNORMAL CELLS

  • cells do not differentiate properly, stay immature
  • precancerous cells which show genetic/cytologic features of malignancy but do not invade underlying tissue
  • can be reversible
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25
Q

Identify type of cell adaptation

A
  1. Atrophy
  2. Hypertrophy
  3. Hyperplasia
  4. Metaplasia
  5. Dysplasia
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26
Q

What is dystrophic calcification?

A

Abnormal deposition of calcium phosphate in dead or dying tissue

  • Calcium metabolism: normal
  • Serum calcium level: normal
  • Generally irreversible
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27
Q

What is metastatic calcification?

A

Calcium deposition in normal tissues as a consequence of hypercalcemia

  • Calcium metabolism: deranged
  • Serum calcium level: hypercalcemia
  • Reversible upon correction of metabolic disorder
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28
Q

Which type of calcification is an important component of pathogenesis of atherosclerosis disease and valvular heart disease?

A

Dystrophic calcification

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29
Q

Necrosis, infarcts, thrombi, haematomas, dead parasites, old scars, atheromas, Munckeberg’s sclerosis, certain tumors, cysts, and calcinosis cutis are all causes of what?

A

Dystrophic calcification

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30
Q

Hyperparathyroidism w/ subsequent bone resorption, bony destructive lesions (tumors, Paget’s), prolonged immobilization, vitamin D disorders (intoxication, Sarcoidosis, Williams Syndrome), milk-alkali syndrome, renal failure w/ secondary increased PTH, and hypercalcemia of infancy are all causes of what?

A

Metastatic calcification

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31
Q

What is the pathogenesis of dystrophic calcification?

A

Increased binding of phosphates w/ necrotic and degenerative tissue -> binds to calcium -> calcium phosphate precipitates

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32
Q

What is the pathogenesis of metastatic calcification?

A

Increased precipitates of calcium phosphate due to hypercalcemia at certain sites (in lungs, stomach, blood vessels, and cornea)

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33
Q

What is a hyaline change?

A

Histologic term for alteration intracellulary or extracellularly which stain glassy, pink with H&E

  • NOT specific marker for cell injury
34
Q

What happens in reversible cell injury?

A
  • Cell swelling 2/2 hypoxia (damage to Na-K pump)
  • Oxidative phosphorylation (hydropic change or ballooning)
35
Q

What happens in irreversible cell injury?

A

Injury to lysosomes w leakage of their enzymes into cytoplasm (cell death -> necrosis)

36
Q

What effect does ischemia have on mitochondrion?

A
  1. Decrease in oxidative phosphorylation -> decrease in ATP production
  2. Abnormal oxidative phosphorylation -> increase in release of ROS
37
Q

How does a decrease in ATP production in irreversible cell injury affect Na+ pump?

A

Na+ pump decreases -> Influx of Ca2+, H2O, and Na+ increases -> Efflux of K+ increases -> cellular swelling, loss of microvilli, blebs (from cell membrane dispersing), ER swelling

38
Q

How does a decrease in ATP production in irreversible cell injury affect glycolysis?

A
  • Glycogen production decreases
  • Lactic acid increases -> pH decreases -> clumping of nuclear chromatin
39
Q

What other effects does a decrease in ATP production in irreversible cell injury have?

A

Detachment of ribosomes -> protein synthesis decreases -> lipid deposition

40
Q

What is the central factor in the pathogenesis of irrreversible cell injury?

A

Cell membrane damage

41
Q

What are ultrastructural features of an injured cell?

A
  • Cell swelling
  • Cytoplasmic blebs
  • Distortion of microvilli
  • Mitochondrial swelling
  • Dilation of ER
42
Q

What is the importance of the Ca2+ influx during cell injury?

A
  • Activation of phospholipases (which cause membrane damage), proteases (break down both membrane and cytoskeletal proteins), ATPases (hastening ATP depletion), and endonucleases (which are responsible for DNA and chromatin fragmentation)
  • Increase in cytosolic Ca2+, oxidative stress, and lipid breakdown products -> formation of mitochondrial permeability transition
43
Q

What is the mitochondrial permeability transition pore?

A

High conductance channel in mitochondrial membrane -> opening of this channel -> loss of proton gradient and pH changes -> further compromises oxidative phosphorylation

  • cytochrome c also released from this pore -> triggers apoptosis of cell
44
Q

What pathway is vital to metabolism but leads to free radicals?

A

Oxidative phosphorylation

  • Molecular oxygen is sequentially reduced in mitochondria by addition of 4 electrons to make water
  • Imperfect rxn -> small amounts of highly reactive, short-lived toxic intermediates (superoxide -> hydrogen peroxide) -> in presence of metals H2O2 -> highly reactive hydroxyl radical
45
Q

What are free radicals?

A

Chemical species w/ a single unpaired free e- in outer orbital

46
Q

How do free radicals result in chemical damage?

A

Chemically unstable -> readily react w/ other molecules, resulting in:

  • lipid peroxidation in membranes
  • oxidative modification of proteins
  • lesions in DNA
  • membrane damage
  • initiate autocatalytic rxns (molecules that react w/ free rads are in turn converted to free rads)
47
Q

What are intracellular sources of free radicals?

A
  1. Normal redox rxns
  2. NO (produced in leukocytes and other cells)
  3. Ionizing radiation (UV, X-rays) can hydrolyze water into hydroxyl (OH) and hydrogen free rads
  4. Metabolism of exogenous chemicals (CCl4)
  5. Physiological antimicrobial rxn (produced in phagocytic leukocytes -> respiratory burst)
48
Q

How can free radicals be neutralized?

A
  1. Spontaneous decay
  2. Superoxide dismutase (SOD)
  3. Glutathione (GSH)
  4. Catalase
  5. Endogenous/exogenous antioxidants (Vitamins E, A, C, and beta-carotene)
49
Q

If not adequately neutralized, what are the 3 basic mechanisms free radicals can damage cells by?

A
  1. Lipid peroxidation of membranes: double bond in polyunsaturated membrane lipids are vulnerable to attack by oxygen free rads -> lipid-radical interaction yields peroxides -> autocatalytic chain rxn
  2. DNA fragmentation: free rads react w/ thymine in nuclear and mitochondrial DNA to produce single strand breaks
  3. Protein cross-linking: free rads promote SH-mediated protein cross-linking -> increased degradation/loss of activity
50
Q

Fill in the mechanisms of cell injury

A
  1. ER swelling, cellular swelling, loss of microvilli, blebs; clumping of nuclear chromatin; decrease in protein synthesis
  2. Damage to lipids, proteins, DNA
  3. Increase mitochondrial permeability
  4. Activation of multiple cellular enzymes
  5. Loss of cellular components
  6. Enzymatic digestion of cellular components
  7. Activation of pro-apoptotic proteins
51
Q

What is reperfusion damage?

A

If cells are reversibly injured due to ischemia, restoration of blood flow can paradoxically result in accelerated injury

  • significantly contributes to myocardial/cerebral infarctions
  • may be due to increased blood flow exposing compromised cells to high [Ca2+]
  • can result in increase free rad production
52
Q

What are 2 types of apoptosis?

A
  1. Physiologic (not always 2/2 injury)
  2. Pathologic
53
Q

What are morphologic characteristics of apoptosis?

A
  • General cell shrinkage
  • Chromatin condensation (MC)
  • Cytoplasmic bleb formation and apoptotic bodies (cytoplasm + condensed and packed organelles w/ or w/o fragments)
  • Phagocytosis of apoptotic cells
54
Q

What mechanisms does apoptosis use?

A
  • Activation of endonuclease -> protease cytoskeletal disruption and cell shrinkage, and transglutaminase
  • Changes in cell surface -> phagocytosis w/o inflammatory response
55
Q

What is the most common pattern of necrosis? What are its characteristics?

A

Coagulative

  • Cell outline remains after death (injury denatures not only structural protein but also enzymes -> blocks proteolysis of dead cells)
  • “City with no people”
  • Characteristic of infarcts (except in the brain)
56
Q

What is the specific type of coagulative necrosis usually from mycobacteria?

A

Caseous necrosis

57
Q

What type of necrosis has cellular destruction/pus formation?

A

Liquefaction

58
Q

What does fat necrosis result from?

A

Action of lipases on fat tissue

59
Q

What is the predominant pattern of necrosis for dry gangrene?

A

Coagulative gangrene

60
Q

What is the predominant pattern of necrosis for wet gangrene?

A

Liquefactive

61
Q

What is nuclear pyknosis?

A

Irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis

62
Q

What is karyorrhexis?

A

Destructive gradmentation of the nucleus of a dying cell whereby its chromatin is distributed irregularly throughout the cytoplasm

63
Q

What is karyolysis?

A

Dissolution of a cell nucleus

  • Typically happens in necrosis
64
Q

What is the stimuli for coagulation necrosis?

A

Hypoxia, toxins

65
Q

What is the stimuli for apoptosis?

A

Physiologic and pathologic factors

66
Q

What is the histologic appearance of coagulation necrosis?

A
  • Cellular swelling
  • Coagulation necrosis
  • Disruption of organelles
67
Q

What is the histologic appearance of apoptosis?

A
  • Single cells
  • Chromatin condensation
  • Apoptotic bodies
68
Q

How is DNA broken down in coagulation necrosis?

A

Random, diffuse

69
Q

How is DNA broken down in apoptosis?

A

Internucleosomal

70
Q

What are the mechansims of coagulation necrosis?

A
  • ATP depletion
  • Membrane injury
  • Free radical damage
71
Q

What are the mechanisms of apoptosis?

A
  • Gene activation
  • Endonucleases
  • Proteases
72
Q

What is the tissue rxn in coagulation necrosis?

A

Inflammation

73
Q

What is the tissue rxn in apoptosis?

A

No inflammation

Phagocytosis of apoptotic bodies

74
Q

The cell size in necrosis is ____

A

Enlarged (swelling)

75
Q

The cell size in apoptosis is ______

A

Reduced (shrinking)

76
Q

What happens to the nucleus in necrosis?

A

Pyknosis -> karyorrhexis -> karyolysis

77
Q

What happens to the nucleus in apoptosis?

A

Fragmentation into nucleosome-size fragments (karyorrhexis -> dissolution into apoptotic bodies)

78
Q

The plasma membrane in necrosis is _____

A

Disrupted

79
Q

The plasma membrane in apoptosis is _____

A

Intact (altered structure, especially orientation of lipids)

80
Q

What happens to the cellular contents in necrosis?

A

Enzymatic digestion; may leak out of cell

81
Q

What happens to the cellular contents in apoptosis?

A

Intact; may be released in apoptotic bodies

Pathology Exam 1 (5 decks)

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