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VPATH 311 > Lecture 3: CELLULAR PATHOLOGY > Flashcards

Lecture 3: CELLULAR PATHOLOGY Flashcards

1
Q

It is a phospholipid bilayer with embedded proteins / glycoproteins / glycolipids (eg ion pumps, receptors, adhesion molecules, etc).

A

Plasma membrane

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2
Q

It is a semipermeable membrane with pumps for ionic/osmotic homeostasis.

A

Plasma membrane

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3
Q
  • Chromatin (euchromatin vs heterochromatin)
  • Nucleolus (synthesis of ribosomal RNA/subunits)
  • Transcription of genes
A

Nucleus

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4
Q
  • Inner & outer membrane, cristae
  • Intermembranous and inner matrix compartments
  • Oxidative phosphorylation (main source of ATP)
A

Mitochondria

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5
Q

Synthesis & packaging of proteins for export. Membranes, lysosomes.

A

Rough endoplasmic reticulum and Golgi apparatus

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6
Q
  • Lipid biosynthesis (eg membranes, steroids)
  • Detoxification of harmful compounds (via P450’s)
  • Sequestration of Ca 2+ ions
A

Smooth endoplasmic reticulum

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7
Q

These assist proper folding of proteins and transport across organelle membranes.

A

Chaperones

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8
Q

These degrade both excess proteins and incorrectly folded (misfolded) proteins.

A

Proteasomes

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9
Q
  • Enzymatic digestion (acid hydrolases) of materials in the cell
  • Primary vs secondary lysosomes; residual bodies
  • Autophagy vs heterophagy/endocytosis
  • Phagocytosis/phagosome; pinocytosis/pinocytic vesicle; receptor-mediated endocytosis
A

Lysosomes

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10
Q
  • Structure and movement of cells/organelles/ granules/ surface molecules/
    phagocytosis.
  • Microfilaments: actin in various forms – cell shape and movement.
  • Microtubules: polymers of tubulin – organelle movement/flagella/cilia/ mitotic spindle.
  • Intermediate filaments: cytokeratin, vimentin, desmin, GFAP, neurofilament proteins.
A

Cytoskeleton

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11
Q

Enzymes (eg catalase, oxidases) – metabolism of hydrogen peroxide and fatty acids.

A

Perixisomes

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12
Q

When cells are able to maintain normal structure and function (e.g. ion balance, pH, energy metabolism) in response to normal physiologic demands.

A

Homeostasis

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13
Q

It is any stimulus or succession of stimuli of such magnitude that tend to disrupt the homeostasis of the organism.

A

Stress

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14
Q
  • As cells encounter some stresses (eg excessive physiologic demand or some mild pathologic stimuli) they may make functional or structural adaptations to maintain viability/ homeostasis.
  • Cells may respond to these stimuli by either increasing or decreasing their content of specific organelles.
A

Cellular adaptation

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15
Q

These are adaptive processes. They forms of adaptation. (4)

A

Atrophy, Hypertrophy, Hyperplasia and Metaplasia.

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16
Q

If the limits of adaptive response are exceeded, or in certain instances when adaptation is not possible (e.g. with severe injurious stimulus), a sequence of events called ____________ occurs.

A

Cell injury

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17
Q

It is the removal of stress / injurious stimulus results in complete restoration of structural and functional integrity.

A

Reversible cell injury

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18
Q

If stimulus persists (or severe enough from the star) the cell will suffer through these.

A

Cell injury and cell death

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19
Q

Two principle morphologic patterns that are indicative of cell death: (2)

A

Necrosis and Apoptosis

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20
Q

It is a type of cell death characterized by sever membrane injury and enzymatic degradation; always a pathologic process.

A

Necrosis

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21
Q

It is regulated form of cell death; can be a physiologic or pathologic process.

A

Apoptosis

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22
Q

CAUSES OF CELLULAR INJURY: (9)

A

Hypoxia
Physical agents
Chemical, Drugs & Toxins
Infectious agents
Immunologic reactions
Genetic abnormalities
Nutritional imbalances
Workload imbalances
Cell aging

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23
Q

It is one of the most important and common causes of cell injury and cell death. It causes impairment of oxidative respiration, it interferes with energy production.

A

Hypoxia

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24
Q

Severity of a physical injury may be increased by tissue hypoxia due to associated local vascular injury.

a.) Direct mechanical trauma - lacerations or crush injuries.

b.) Temperature extremes - heat (thermal burn), cold (frostbite).

c.) Radiation - radioactive isotope emissions or electromagnetic radiation (e.g. UV light, x-rays).

d.) Electrocution - pets chewing electric cords, faulty wiring in barns, lightning strike, etc.

e.) Sudden changes in atmospheric pressure - marine mammals have mechanisms to mostly avoid the “bends”.

A

Physical agents

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25
Q

a.) Inorganic poisons - e.g. lead, copper, arsenic, selenium, mercury, etc.
b.) Organic poisons - e.g. nitrate/nitrite, oxalate, hydrocyanic acid, etc.

c.) Manufactured chemicals - e.g. drugs (overdose idiosyncratic), pesticides, herbicides, rodenticides, etc.

d.) Physiologic compounds - e.g. salt, glucose, oxygen, etc.

e.) Plant toxins - e.g. ragwort, sweet clover, braken fern, etc.

f.) Animal toxins - e.g. snake or spider venom, tick toxin, etc.

g.) Bacterial toxins / Mycotoxins - e.g. botulinum toxin, aflatoxin, ergot, etc.

A

Chemical, drugs & toxins

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26
Q

a. Viruses
b. Bacteria / rickettsiae / chlamydia
c. Fungi
d. Protozoa
e. Metazoan parasite

A

Infectious agents

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27
Q

a.) Immune response - e.g. cells damaged as “innocent bystanders” in immune/inflammatory response.

b.) Hypersensitivity (allergic) reactions - e.g. anaphylactic reaction to a foreign protein or drug.

c.) Autoimmune diseases - reactions to self-antigens

A

Immunologic reactions

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28
Q

a.) Cytogenetic disorders / chromosomal aberrations - one cause of congenital anomalies.

b.) Mendelian disorders (mutant genes)
* enzyme defects, e.g. lysosomal storage disease.
* structural / transport protein defects - e.g. collagen dysplasia, cystic fibrosis, sickle cell anemia, etc.

c.) Multifactorial inheritance - combined effects of environmental factors and 2 or more mutated genes (e.g. neoplasia, hypertension, coronary artery disease, etc.)

A

Genetic abnormalities

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29
Q

a.) Overworked cells - cell injury occurs if stimulus prolonged and/or exceeds ability to adapt.

b.) Underworked cells - prolonged lack of stimulation (e.g. disuse, denervation, lack of trophic hormones) can lead to atrophy and eventually the loss of cells.

A

Workload imbalances

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30
Q

It is the cumulative effects of a life time of cell damage (chemical, infectious, nutrition, etc.) leads to a diminished capacity of aged cells / tissues to maintain homeostasis and adapt to harmful stimuli.

A

Cell aging

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31
Q

Mnemonic acronym for agents of disease = “double MINT”

A

Malformation
Miscellaneous
Infectious
Immune
Nutritional
Neoplastic
Trauma
Toxicity

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32
Q

4 intracellular systems are particularly vulnerable to injury.

A
  • Cell membranes
  • Mitochondria
  • Protein synthesis, folding and packaging
  • Genetic apparatus
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33
Q

These are chemical species with a single unpaired electron in outer orbit (donate or steal electrons, extremely unstable); readily react with organic or inorganic chemicals, avidly attack/degrade membranes, proteins & nuclei acids.

A

Free radicals

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34
Q

It is an important mechanism of cell damage in many disease processes (chemical, radiation, O2 toxicity, inflammation, reperfusion, etc.)

A

Free radical-induced injury

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35
Q

It occurs when the free radical generation overwhelms antioxidant defense mechanisms.

A

Cell injury

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36
Q

Small amounts produced from cell redox reactions, e.g. normal oxidative phosphorylation (leakage from mitochondria), other intracellular oxidases (e.g. peroxisomes), PMN’s in inflammation, excess O2, altered metabolism in cell stress (e.g. reperfusion injury).

A

Cellular metabolism

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37
Q

Some intermediary metabolites of chemical/drugs are highly reactive free radicals.

A

Enzymatic metabolism of exogenous chemicals

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38
Q

Hydrolyzes water into hydroxyl (OH) and hydrogen (H) free radicals.

A

Ionizing radiation

39
Q

The transition metals (copper and iron), accept or donate free electrons during certain intracellular reactions, i.e. catalyze free radical formation.

A

Divalent metals

40
Q

It is a frequent by-product of oxidative
metabolism that can generate hydroxyl radicals from reactions with copper or ferrous ions (e.g. Fenton reaction = Fe2+ + H2O2 → *OH + OH- + Fe3+).

A

H2O2

41
Q

Main sites of damage. (3)

A

Damage of membranes, damage of proteins and damage to DNA.

42
Q

It is the decrease in the amount of a tissue or organ after normal growth has been attained. It is an adaptive response whereby a tissue or organ undergoes a reduction in mass (size), due to a decrease in the size and/or number of cells.

A

Atrophy

43
Q

Organs are increased in size due to an increase in cell size without cellular proliferation.

A

Hypertrophy

44
Q

It is an increase in organ size or tissue mass caused by an increase in the number of constituent cells.

A

Hypertrophy

45
Q

Two main types of reversible cell injury. (2)

A

Cellular swelling and fatty change

46
Q

It is the most common and most important response to cellular injuries of all types, including mechanical, anoxic, toxic, lipid peroxidation, viral, bacterial and immune mechanisms.

A

Cellular swelling

47
Q

It refers to the rapid death of a limited portion of an organism and is considered to be the final stage in irreversible degeneration.

A

Necrosis

48
Q

It is the term used for the entire process of degeneration and death of cells.

A

Necrobiosis

49
Q

It is the most common manifestation of cell death. It is characteristic of hypoxic / ischemic death of cells in all tissues (except brain).

A

Coagulation (coagulative) necrosis

50
Q

It occurs when enzymatic digestion of necrotic cells predominates over protein denaturation.

A

Liquefactive Necrosis

51
Q

It is typical lesion seen with specific bacterial diseases, e.g. tuberculosis, caseous lymphadenitis. It is common in birds since heterophils don’t have the potent hydrodrolytic enzymes to liquefy cells.

A

Caseous Necrosis

52
Q

Occurs when saprophytic bacteria grow in necrotic tissue.

A

Gangrenous Necrosis

53
Q

Two types of Gangrene. (2)

A

Dry gangrene and wet gangrene

54
Q

It occurs in necrotized portion of the skin with moisture loss due to evaporation and drainage and presence of saprophytic bacteria.

A

Dry gangrene

55
Q

When the coagulative necrosis of dry gangrene is modified by the liquefactive action of invading saprophytic/putrefactive bacteria.

A

Wet gangrene

56
Q

It is the production of gas bubbles in the necrotic tissue by invading bacteria (esp. Clostridia).

A

Gas gangrene

57
Q

It is a type of necrosis distinguished by its location within body fat stores, esp. abdominal or subcutaneous fat.

A

Fat Necrosis

58
Q

It is a form of coagulative necrosis resulting from a sudden deprivation of blood supply. Commonly occurring in areas or organs with end artery (i.e., kidney) blocked by thromboembolic lesions.

A

Infact

59
Q

It is a type of coagulative necrosis in striated muscles characterized by loss of striations following necrosis.

A

Zenker’s Necrosis (Zenker’s degeneration)

60
Q

It is a shallow area of necrosis confined to epidermis that heals without scarring.

A

Erosion

61
Q

It is an excavation of a surface produced by necrosis and sloughing of the necrotic debris and implies involvement of the tissue below the surface layer.

A

Ulcer

62
Q

It is a piece of necrotic tissue in the process of separation from viable tissue and implies a process of shedding when used with reference to a surface.

A

Slough

63
Q

It is an area of liquefactive necrosis of the nervous tissue. Literally means “softening”.

A

Malacia

64
Q

It is an isolated necrotic mass

A

Sequestrum

65
Q

It is the death of single cells as a result of activation of a genetically programmed “suicide” pathway.

A

Apoptosis

66
Q

It is occasionally seen in skeletal muscle and myocardium (sometimes called muscle steatosis).

A

Adipose (Fatty) Tissue Infiltration

67
Q

It is an excessive intracellular deposits of glycogen, i.e. seen with abnormalities of glucose or glycogen metabolism.

A

Glycogen Accumulation

68
Q

It is the name given to any substance, intracellular or extracellular, which has a homogeneous, glassy, eosinophilic appearance; the substance is often protein in nature (e.g. amyloid; Ag-Ab complexes causing thickened BM’s; protein droplets in renal tubular epithelium).

A

Hyaline

69
Q

It is a nonspecific term for hyaline material within an arterial wall.

A

Fibrinoid

70
Q

It is a pathologic proteinaceous substance (95% amyloid fibrils) which is resistant to proteolysis.

A

Amyloid

71
Q

These are insoluble aggregates that result from the self assembly of abnormally folded proteins (typically the abnormal folded protein has excess ꞵ sheet conformational change).

A

Amyloid fibrils

72
Q

It is a disorder of protein folding in which normally soluble proteins are deposited as abnormal, insoluble fibrils that disrupt tissue structure and function.

A

Amyloidosis

73
Q

It is derived from an acute phase protein called serum amyloid A (SAA) in chronic inflammation.

A

Protein AA

74
Q

It is derived from immunoglobulin light chains with plasma cell neoplasia.

A

Protein AL

75
Q

Seen in humans, Shar pei dogs, Abyssinian cats.

A

Familial amyloid

76
Q

It is derived from polypeptide hormones or prohormones in neoplastic or degenerative conditions, e.g. islet amyloidosis in cats & humans with type 2 diabetes mellitus.

A

Endocrine amyloid

77
Q

These are those that originate in the animal.

A

Endogenous pigments

78
Q

➢ also known as “wear-and-tear” or “aging” pigment.
➢ origin: breakdown products of lipids, usually derived from cell membranes (esp. lipid peroxidation).
➢ sites: aged cells, e.g. myocardial cells and neurons of old animals, or in chronically injured cells.
➢ grossly: when severe can give yellow-brown discoloration to tissue.
➢ microscopically: golden brown, finely granular, intracellular pigment.
➢ significance: does not injure cell, but is a sign of aging or excess free radical damage.

A

Lipofuscin

79
Q

These are disorders characterized by the excess storage of lipofuscin.
- e.g. “brown gut syndrome” of dogs with vitamin E/selenium deficiency → increased free radical damage.
- Grossly the intestine has a distinct yellow-brown discoloration (intestinal lipofuscinosis);
- Microscopically see increased amount of lipofuscin in smooth muscle cells

A

Lipofuscinosis

80
Q

Aariant of lipofuscin which is acid-fast positive and autofluorescent

A

Ceroid

81
Q

Insoluble, intracellular, brown-black pigment derived from tyrosine.

A

Melanin

82
Q

It is an essential trace element; the liver is the major organ involved in the regulation of copper levels, and homeostasis is maintained by the balance of dietary intake and copper excretion via the bile.

A

Copper

83
Q

It is common in sheep because of the reduced biliary excretion of copper in this species.

A

Copper toxicity

84
Q

It represents stored iron (ferric form = Fe3+), recovered from the hemoglobin of destroyed RBC’s.

A

Hemosiderin

85
Q

It is an end product of heme degradation (no iron); mostly from senescent RBC’s via macrophages.

A

Bilirubin

86
Q

It is a bright yellow-brown homogenous pigment occasionally seen at sites of previous hemorrhage.

A

Hematoidin

87
Q

It imparts black color to blood originating in stomach (e.g. gastric ulcers), i.e. blood + stomach HCl = melena.

A

Acid-Hematin

88
Q

It refers to the deposition of calcium salts in soft tissues. Usually occurs following tissue necrosis.

A

Calcification

89
Q

Types of Calcification

A

Dystrophic Calcification and Metastatic Calcification

90
Q

It is a calcification of injured cells (no hypercalcemia or other disturbances of calcium homeostasis).

A

Dystrophic Calcification

91
Q

Deposition of calcium salts in vital tissues and is always associated with hypercalcemia

A

Metastatic Calcification

92
Q

Term sometimes used for extensive metastatic calcification.

A

Calcinosis

93
Q

It is is a term that describes widespread of deposition of calcium in tissues of individual treated with a calcium sensitizer.

A

Calciphylaxis

94
Q
A

VPATH 311 (4 decks)

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