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Pathology > Cellular Pathology > Flashcards

Cellular Pathology Flashcards

1
Q

Plasma membrane

A

➢ phospholipid bilayer with embedded proteins / glycoproteins / glycolipids (eg
ion pumps, receptors, adhesion molecules, etc)
➢ semipermeable membrane with pumps for ionic / osmotic homeostasis

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2
Q

Nucleus

A

➢ chromatin (euchromatin vs heterochromatin)
➢ nucleolus (synthesis of ribosomal RNA/subunits)
➢ transcription of genes

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3
Q

Mitochondria

A

➢ inner & outer membrane, cristae
➢ intermembranous and inner matrix compartments
➢ oxidative phosphorylation (main source of ATP)

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4
Q

Endoplasmic reticulum (ER), Ribosomes, & Golgi Apparatus

A

➢ RER & Golgi - synthesis & packaging of proteins for export. Membranes,
lysosomes
➢ SER - lipid biosynthesis (eg membranes, steroids)
- Detoxification of harmful compounds (via P450’s)
- Sequestration of Ca 2+ ions

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5
Q

Chaperones & Proteasomes

A

➢ Chaperones assist proper folding of proteins and transport across organelle
membranes.
➢ Proteasomes degrade both excess proteins and incorrectly folded (misfolded)
proteins.

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6
Q

Lysosomes

A

➢ 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

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7
Q

Cytoskeleton

A

➢ Structure and movement of cells/organelles/ granules/ surface molecules/
phagocytosis

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8
Q

: actin in various forms – cell shape and movement

A

Microfilaments

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9
Q

: polymers of tubulin – organelle movement/flagella/cilia/ mitotic
spindle

A

Microtubules

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10
Q

Intermediate filaments:

A

cytokeratin, vimentin, desmin, GFAP, neurofilament
proteins

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11
Q

Peroxisomes

A

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

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12
Q

– metabolism of hydrogen peroxide and fatty
acids

A

Enzymes (eg catalase, oxidases)

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13
Q

CELLULAR INJURY CELL ADAPTATION AND CELL DEATH
The __________ are in constant fight for living from all kinds of aggressions
that could cause injury, and provided the operating environment is appropriate, could adapt to almost all situations. All these aggressions are called ______, and injury alters
the preceding normal steady state of the cell.

A

tissues and cells
stress

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14
Q

If the injury is acute, one of two possible
things can happen to the cell:

A
  1. It can either survive in a damaged state and adapt to the injury (reversible
    injury) or;
  2. It can die (irreversible injury or cell death). If the injury is of a chronic nature,
    the cell may be able to adapt to it, resulting in a variety of cellular changes
    known as adaptations. These include atrophy, hypertrophy, hyperplasia,
    intracellular accumulations, metaplasia and dysplasia, that will be described
    later
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15
Q

Homeostasis

A

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

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16
Q

Stress –

A

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

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17
Q

Cellular adaptation
▪

A

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.

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18
Q

cells may respond to these stimuli by either ___________ or __________
their content of specific organelles.

A

increasing or decreasing

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19
Q

adaptive processes:

A

atrophy, hypertrophy, hyperplasia and metaplasia
are forms of adaptation

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20
Q

Cell injury
▪ if the limits of adaptive response are exceeded, or in certain instances
when adaptation is not possible (eg with severe injurious stimulus), a
sequence of events called _______ occurs.

A

cell injury

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21
Q

Cell injury

A

A. Reversible cell injury
B. Irreversible cell injury / cell death

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22
Q

*removal of stress / injurious stimulus results in complete restoration
of structural and functional integrity.

A

a) Reversible cell injury

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23
Q

*if stimulus persists (or severe enough from the star) the cell will
suffer irreversible cell injury and death

A

b) Irreversible cell injury / cell death

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24
Q
  • is one of the most crucial events in pathology and can
    affect any type of cell.
A

cell death

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25
Q

Two principle morphologic patterns that are indicative of cell death:

A

Necrosis
Apoptosis

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26
Q

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

A

Necrosis

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27
Q

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

A

Apoptosis

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28
Q

CAUSES OF CELLULAR INJURY

A
  1. Hypoxia (Oxygen Deficiency)
  2. Physical agents
  3. Chemical, Drugs & toxins
  4. Infectious agents
  5. Immunologic Reactions
  6. Genetic Abnormalities
  7. Nutritional Imbalances
  8. Workload Imbalances
  9. Cell Aging
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29
Q

one of the most important and common causes of cell injury and cell
death.

A

Hypoxia (Oxygen Deficiency)

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30
Q

causes impairment of oxidative respiration, ie it interferes with
energy production.

A

hypoxia

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31
Q

Hypoxia (Oxygen Deficiency)
occurs with:

A

a) Deficient blood supply
b) Reduced oxygen-carrying capacity of the blood
c) Interference with respiratory chain / oxidative phosphorylation

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32
Q

= deficiency of blood supply from impeded
arterial flow or reduced venous drainage = hypoxia +
↓ delivery of nutrients and ↓ removal of metabolites.

A

ischemia

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33
Q

= localized area of ischemic necrosis.

A

infarction

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34
Q

Reduced oxygen-carrying capacity of the blood

A

due to anemia
due to Hb dysfunction

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35
Q

= reduction in numbers or volume of
erythrocytes or quantity of hemoglobin (Hb).

A

due to anemia

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36
Q

eg methaemoglobinemia - nitrate / nitrite poisoning,
carboxyhaemoglobinemia-carbon monoxide
poisoning

A

due to Hb dysfunction

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37
Q
  • nitrate / nitrite poisoning,
A

eg methaemoglobinemia

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38
Q

-carbon monoxide
poisoning

A

carboxyhaemoglobinemia

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39
Q
A

eg, cyanide poisoning inactivates cytochrome oxidase in
mitochondria → blocks oxidative phosphorylation.

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40
Q

________ may be increased by tissue hypoxia due to
associated local vascular injury.

A

physical injury

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41
Q

Physical agents

A

a) Direct mechanical trauma
b) Temperature extremes
c) Radiation
d) Electrocution
e) Sudden changes in atmospheric pressure

42
Q
  • lacerations or crush injuries.
A

Direct mechanical trauma

43
Q
  • heat (thermal burn), cold (frostbite).
A

Temperature extremes

44
Q
  • radioactive isotope emissions or electromagnetic
    radiation (eg UV light, x-rays).
A

Radiation

45
Q
  • pets chewing electric cords, faulty wiring in
    barns, lightning strike, etc.
A

Electrocution

46
Q

Sudden changes in atmospheric pressure - marine mammals
have mechanisms to mostly avoid the “______”

A

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

47
Q

Chemical, Drugs & toxins

A

a) Inorganic poisons
b) Organic poisons
c) Manufactured chemicals
d) Physiologic compounds
e) Plant toxins
f) Animal toxins
g)Bacterial toxins / Mycotoxins

48
Q

eg lead, copper, arsenic, selenium, mercury, etc.

A

Inorganic poisons -

49
Q
  • eg nitrate/nitrite, oxalate, hydrocyanic acid, etc.
A

Organic poisons

50
Q

eg drugs (overdose / idiosyncratic),
pesticides, herbicides, rodenticides, etc.

A

Manufactured chemicals -

51
Q

Physiologic compounds

A

eg salt, glucose, oxygen, etc

52
Q

Plant toxins -

A

eg ragwort, sweet clover, braken fern, etc.

53
Q

Animal toxins -

A

eg snake or spider venom, tick toxin, etc.

54
Q

Bacterial toxins / Mycotoxins -

A

eg botulinum toxin, aflatoxin, ergot, etc.

55
Q

Infectious agents

A

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

56
Q

Immunologic Reactions

A

a. Immune response - eg cells damaged as “innocent bystanders” in immune
/ inflammatory response.
b) Hypersensitivity (allergic) reactions - eg anaphylactic reaction to a foreign
protein or drug.
c) Autoimmune diseases - reactions to self-antigens

57
Q

Genetic Abnormalities

A

a) Cytogenetic disorders / chromosomal aberrations
b) Mendelian disorders (mutant genes)

58
Q
  • one cause of congenital
    anomalies.
A

Cytogenetic disorders / chromosomal aberrations

59
Q

• enzyme defects, eg lysosomal storage disease.
• structural / transport protein defects - eg collagen dysplasia, cystic
fibrosis, sickle cell anemia, etc.

A

b) Mendelian disorders (mutant genes)

60
Q
  • combined effects of environmental factors and 2
    or more mutated genes (eg neoplasia,
    hypertension, coronary artery disease, etc).
A

Multifactorial inheritance

61
Q

Nutritional Imbalances

A

a) Deficiencies - deficiencies of protein-calories (starvation), vitamins (A to E)
minerals (eg copper).
b) Overnutrition - eg excess lipids / calories → obesity, diabetes,
atherosclerosis, etc.

62
Q

Workload Imbalances

A

a) Overworked cells - cell injury occurs if stimulus prolonged and/or exceeds
ability to adapt.
b) Underworked cells - prolonged lack of stimulation (eg disuse, denervation,
lack of trophic hormones) can lead to atrophy and
eventually the loss of cells.

63
Q

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

64
Q

Mnemonic acronym for agents of disease = “double MINT”

A

Malformation (genetics, teratogens, etc)
Miscellaneous (metabolic, aging, hypoxia, etc)
Infectious (viruses, bacteria, fungi, etc)
Immune (immune mediated, hypersensitivity, autoimmune, etc)
Nutritional (protein-caloric intake, vitamins, minerals, etc)
Neoplastic (genetic, viral, chemical, radiation, etc)
Trauma (mechanical, temperature, radiation, etc)
Toxicity (inorangic, chemicals / drugs, plant toxins, etc.

65
Q

MECHANISMS OF CELL INJURY

A
  1. General consideration
  2. Biochemical Mechanisms
  3. Chemical (Toxic) Injury
66
Q

4 intracellular systems are particularly vulnerable to injury.

A

• cell membranes - especially ionic / osmotic homeostasis.
• mitochondria - oxidative phosphorylation / ATP production.
• protein synthesis, folding and packaging - structural and functional
proteins.
• genetic apparatus - DNA / RNA.

67
Q

sites are commonly damaged by a variety
of inciting causes.

A

Biochemical Mechanisms
▪ several molecular / biochemica

68
Q

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

69
Q

Generation of free radicals

A
  1. Cellular metabolism
  2. Enzymatic metabolism of exogenous chemicals
  3. Ionizing radiation
  4. Divalent metals
70
Q
  • small amounts produced from cell redox
    reactions, eg normal oxidative phosphorylation (leakage from
    mitochondria), other intracellular oxidases (eg peroxisomes), PMN’s
    in inflammation, excess O2, altered metabolism in cell stress (eg
    reperfusion injury)
A

Cellular metabolism

71
Q
  • some intermediary
    metabolites of chemical / drugs are highly reactive free radicals
A

Enzymatic metabolism of exogenous chemicals

72
Q
  • hydrolyzes water into hydroxyl (•OH) and
    hydrogen (H•
    ) free radicals.
A

Ionizing radiation

73
Q
  • the transition metals (copper and iron), accept or
    donate free electrons during certain intracellular reactions, ie
    catalyze free radical formation.
A

Divalent metals

74
Q

Important reactants

A
  1. superoxide anion (O2•) hydroxyl radical (•OH), hydrogen peroxide
    (H2O2) and peroxynitrite (ONOO•)
  2. H2O2 (not a free radical) is a frequent by-product of oxidative
    metabolism that can generate hydroxyl radicals from reactions with
    copper or ferrous ions (eg Fenton reaction = Fe2+ + H2O2 → •OH +
    OH- + Fe3+)
  3. most intracellular stored iron is in the ferric (Fe3+) state and must be
    reduced to the ferrous (Fe2+) state to act in the Fenton reaction (often
    reduced by O2 -.); iron & O2 -.
    required for maximal cell damage
75
Q

Main sites of damage

A
  1. Damage of Membranes (lipid peroxidation)
    • free radicals (esp •OH) are highly reactive & unstable (don’t
    last long or travel far) → “steal” single electrons from the
    hydrogen next to a double bond in unsaturated fatty acids in
    cell membranes → form lipid peroxides (which themselves
    are reactive & unstable) → autocatalytic chain reaction (selfpropagating) → can cause rapid widespread membrane /
    organelle damage.
  2. Damage of Proteins
    • free radicals cause fragmentation and cross-linkage between
    proteins → damaged structural proteins / loss of enzymatic
    activity → increased degradation by proteosomes.
  3. Damage to DNA
    • free radicals damage nuclear & mitochondrial DNA, producing
    strand breaks & DNA-protein adducts (short-term →
    apoptosis; long-term → low level damage implicated in cell
    aging & neoplasia).
76
Q

Protective mechanisms of the cell

A
  1. Storage and transport proteins:
    • iron & copper can catalyze formation of reactive oxygen
    forms; they are minimized by being bound to storage and
    transport proteins (eg ceruloplasmin, transferrin, lactoferrin,
    apoferritin/ferritin) and kept in an oxidized state.
  2. Antioxidants - either block the formation of free radicals or inactivate
    / scavenge them:
    • Vitamins A&E (lipid soluble, found in cell membranes),
    Vitamin C (aqueous-phase antioxidant) and glutathione
    (reduced form [GSH] reacts with H2O2 or •OH → oxidised
    glutathione [GSSG] + H2O).
  3. Enzymes which are involved in neutralizing free radicals:
    • Glutathione peroxidase - a selenium-containing enzyme
    which catalyzes GSH to GSSG.
    - this enzyme also catalyzes the reduction of lipid
    peroxides by glutathione, preventing propagation of lipid
    peroxidation reactions.
    • Superoxide dismutase (SOD) - catalyzes the conversion of
    O2-.
    to H2O2.
    • Catalase - catalyzes the breaks down H2O2 to O2 + H2O.
77
Q

Storage and transport proteins:

A

• iron & copper can catalyze formation of reactive oxygen
forms; they are minimized by being bound to storage and
transport proteins (eg ceruloplasmin, transferrin, lactoferrin,
apoferritin/ferritin) and kept in an oxidized state.

78
Q
  • either block the formation of free radicals or inactivate
    / scavenge them:
    • Vitamins A&E (lipid soluble, found in cell membranes),
    Vitamin C (aqueous-phase antioxidant) and glutathione
    (reduced form [GSH] reacts with H2O2 or •OH → oxidised
    glutathione [GSSG] + H2O).
A

Antioxidants

79
Q
  • a selenium-containing enzyme
    which catalyzes GSH to GSSG.
  • this enzyme also catalyzes the reduction of lipid
    peroxides by glutathione, preventing propagation of lipid
    peroxidation reactions.
A

Glutathione peroxidase

80
Q
  • catalyzes the conversion of
    O2-.
    to H2O2.
A

Superoxide dismutase (SOD)

81
Q
  • catalyzes the breaks down H2O2 to O2 + H2O
A

Catalase

82
Q

Chemical (Toxic) Injury
▪ chemicals and certain drugs/toxins produce damage in one of two ways.

A

a.) Direct interaction
b) Conversion to reactive toxic metabolites

83
Q

oxic metabolites usually produced by _________________
mixed function oxidase (MFO) in the SER of liver.

A

cytochrome P-450

84
Q

in humans & dogs most_________ is detoxified in liver to glucuronide
and sulfate conjugates which are then excreted in the urine; only small
amounts converted to highly reactive metabolite NAPQI by P450 MFO.

A

acetaminophen

85
Q

__________________ metabolized by P450 MFO enzyme system on the SER of the
hepatocyte (CCl4 + e → CCl3 • + Cl-).
______________ •
is highly reactive and causes lipid peroxidation (autocatyzing) →
see severe and rapid membrane destruction → ↓protein synthesis (30
min); ER swelling & ribosomal dissociation (2 hrs.).

A

Carbon Tetrachloride (CCl4) Toxicity
CCl4

CCl3

86
Q

CELLULAR ADAPTATIONS
▪ major adaptive responses:

A

atrophy, hypertrophy, hyperplasia

87
Q

Two main types of reversible cell injury are recognized →

A

cellular swelling and
fatty change.

88
Q

the critical transition point to irreversible injury is not known; however,
two features consistently characterize irreversibility (ie “point of no
return” or “lethal hit”):

A

▪ inability to reverse mitochondrial dysfunction.
▪ profound disturbances of membrane function.

89
Q
  • 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

90
Q
  • is the term used for the entire process of degeneration
    and death of cells
A

Necrobiosis

91
Q

Gross Indicators/Characteristics of Necrosis (Source:Dr. Camer)
- term used to describe the range of morphologic changes that occur
following cell death in living tissue.

A

• Loss of color or paleness of the tissue
• Loss of strength of the tissue as it softens
• A definite zone of demarcation between necrotic and
viable tissue
• The location or pattern of the lesion

92
Q

Types of Necrosis

A

1.Coagulation (coagulative) Necrosis
2. Liquefactive Necrosis
3. Caseous Necrosis
4. Gangrenous Necrosis
5. Fat Necrosis
6. Infarction (Ischemic Necrosis)
7. Zenker’s Necrosis (Zenker’s degeneration)

93
Q

OTHER TERMS USED IN ASSOCIATION WITH NECROSIS

A
  1. Erosion
  2. Ulcer
  3. Slough
94
Q

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

A

Erosion

95
Q

– 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

96
Q

– 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 piece of necrotic tissue separating from viable tissue.
-this term is applied to necrosis of surface epithelia

A

Slough

97
Q

Other terms used in reference to necrosis

A
  1. Malacia
  2. Sequestrum
98
Q

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

A

Malacia

99
Q

– an isolated necrotic mass
-process is called sequestration

A

Sequestrum

100
Q

Favorable outcome

A
  1. organization, replacement by connective tissue with formation of a scar or
    a capsule
  2. petrifaction
  3. ossification
  4. aseptic autolysis
101
Q

: saprogenic fusion of necrotic tissue followed by sepsis

A

Unfavorable outcome

Pathology (7 decks)

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