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Pathology Exam 1 > Lecture 1/2 - Cell Injury, Death, and Cell Adaptations > Flashcards

Lecture 1/2 - Cell Injury, Death, and Cell Adaptations Flashcards

1
Q

Fundamental concepts in cell injury

A
  • Clinical signs and symptoms are several steps removed morphologic changes that are preceded by the biochemical changes associated with cell injury
  • Cell injury is common to all pathologic processes
  • Cell injury results from a disruption of one or more of the cellular components that maintain cell viability
  • Cell injury may be reversible or result in cell adaptation ofdeath
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2
Q

Oxygen deprivation

A

hypoxia
ischemia
anemia

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3
Q

infectious agents

A

bacteria
viruses
fungi
parasites

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4
Q

physical changes

A 
trauma
electricity
pollutants
burns
UV light
radiation
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5
Q

chemical agents and drugs

A

tobacco
alcohol
posions
Rx/ OTC drugs

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6
Q

immunologic reactions

A

allergies and autoimmune disease

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7
Q

genetic derangement

A

chromosome abnormalities

gene mutations

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8
Q

nutritional imblanace

A

malnutrition
vitamin deficiecy
obesity

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9
Q

What are the causes of cell injury from the cell’s perspective?

A

cell injury results from a disruption of one of more of the cellular components that maintain cell viability
-Divergent factors can act at the same point on the cell to induce cell injury

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10
Q

The structures and processes that maintain cell viability include:

A

plasma membrane
mitochondria
macromolecular synthesis
nucleus

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11
Q

There are several basic biochemical themes in cell injury, what are they?

A 
ATP depletion
generation of ROS (oxidative stress)
loss of calcium homeostasis
altered plasma membrane permeability
mitochondrial damage
DNA and protein damage
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12
Q

Cell injury by impaired energy production - decreased oxygen (hypoxia) or no oxygen (anoxia) is due to:

A

impaired absorption of oxygen
decreased blood flow (ischemia)
disease of blood or blood vessels
inadequate oxygenation of the blood

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13
Q

decreased oxygen impairs oxidative phosphorylation in the…

A

mitochondria

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14
Q

reduced ATP reduces the ability of the plasma membrane to maintain homeostasis. This leads to …

A

a net gain of solute and an isosmotic gain in cytoplasmic water

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15
Q

an isosmotic gain in water leads to:

A
  • cell swelling with formation of cell surface blebs
  • swelling of mitochondria
  • dilation of the endoplasmic reticulum that leads to: detachment of ribosomes from RER and dissociation of polysomes an decrease in protein synthesis - can lead to increased lipid deposition
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16
Q

reduced oxidative phosphorylation leads to increased ________

A

glycolysis

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17
Q

increase glycolysis produces

A

lactic acid and inorganic phosphates that decrease intracellular pH leading to chromatin clumping

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18
Q

what is hypoglycemia

A

reduced substrate for ATP production can result in the same basic patterns
From wiki: is a medical emergency that involves an abnormally diminished content of glucose in the blood.[1] The term literally means “low blood sugar” It can produce a variety of symptoms and effects but the principal problems arise from an inadequate supply of glucose to the brain, resulting in impairment of function (neuroglycopenia)

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19
Q

ROS are free radicals that are generated by

A

normal endogenous oxidative reactions in the plasma membrane, mitochondria, cytoplasm and peroxisomes

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20
Q

Generations of ROS is associated with:

A 
Inflammation
oxygen toxicity
chemicals
irradiation
aging
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21
Q

Types of ROS (3 of them)

A
  1. Superoxide (O2-) - inactived spontaneously or by superoxide dismutase (SOD) to form H2O2
  2. Hydrogren peroxide (H2O2) - detoxified by glutathione peroxidase and catalase
  3. Hydroxyl radicals (OH) - generated by hydrolysis or water by ionizing radiation or by transitional metals such as Fe++ or Cu++
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22
Q

ROS damage cells by:

A
  • lipid peroxidation
  • protein (cytoplasmic and membrane bound) cross-linking
  • react with thymiddine and guanine to induce single strand DNA breaks
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23
Q

intracellular and extracellular antioxidant systems act to reduce the effects of ROS by blocking their initiation or by inactivating them. These include:

A
  • Intracellular - SOD, catalase and glutathione peroxidase
  • Extracellular - vitamins E, A, and C and serum proteins that bind free iron (transferrin, ferritin) and copper (ceruloplasmin)
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24
Q

Cytoplasmic Ca++ is maintained by protein sequestration in the…

A

cytoplasm, mitochondria, and endoplasmic reticulum

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25
Q

increase cytoplasmic Ca++ is a final common pathway of what?

A

cell injury

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26
Q

high levels of Ca++ will activate various degradative enzymes including:

A

phospholipases
proteases
endonucleases
ATPase

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27
Q

What are other causes of cell membrane injury? (5 of them)

A
  1. Complement - C5-C9 membrane attack complex
  2. Cytotoxic T cells - perforin
  3. Viral
  4. Bacterial endotoxins and exotoxins
  5. Chemicals
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28
Q

Biochemical alterations occur prior to

A

morphologic changes

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29
Q

degree of cell injury is partly determined by…

A
  • cell type and its physiological state

- the intensity, duration, and/or number of exposures to an etiological agent

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30
Q

cell injury may result in..

A
  • reversible cell injury
  • cellular adaptations associated with changes in cell number, size or differentiation
  • cellular adaptations associated with abnormal accumulations
  • cell death (necrosis or apoptosis)
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31
Q

reversible cell injury is acute in nature in occurs when the cell cannot maintain what?

A

normal homeostasis due to cell injury of short duration and minimal intensity

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32
Q

common etilogies of reversible(sub-lethal) cell injury include:

A

toxins
infectious agents
hypoxia
thermal injury

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33
Q

what are the two types of morphology with reversible cell injury?

A

hydropic change and fatty change

  • Plasma membrane injury leads to increase intracellular Na+ that leads to an isosmotic gain in water
  • organelles and cells swell, and the organ may appear pale and swollen
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34
Q

What are the concepts of cell death?

A
  1. There is NO SINGLE biochemical event that equates with cell death
  2. There are two morphologic forms of cell death - necrosis and apoptosis
  3. Cell death leads to the release of cellular constituents into the extracellular environment
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35
Q

Morphologic changes in necrosis include: (5 of them)

A
  1. Cell swelling
  2. Protein denaturation yielding a glassy homogenous pink staining cytoplasm
  3. Organelle breakdown may result in vacuolated cytoplasm
  4. Nuclei changes include: karyolysis, pyknosis, karyorrhexis, or total loss
  5. Inflammation - acute or granulomatous
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36
Q

The type of necrosis is dependent upon what?

A

patterns of enzymatic degradation and by bacterial byproducts when present

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37
Q

What is the most common from of necrosis?

A

coagulative
(cytoplasmic proteins are coagulated)
- The nucleus is lost, but the eosinophilic outline of the cell is retained for a short time prior to being removed by the inflammatory response

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38
Q

Which type of necrosis is described: tissue is totally digested by the release of lysosomal enzymes during the acute inflammatory response?

A

liquefactive necrosis (“pus”, purulence)

39
Q

Which type of necrosis is often associated with focal bacterial or fungal infections (eg. abscesses and wet gangrene), it is also seen in the CNS

A

liquefactive necrosis

40
Q

Which type of necrosis is associated with M. tuberculosis infection?

A

caseous necrosis

41
Q

Which type of necrosis displays gross features of the tissue having a white and “cheesy” appearance?
YUMMMMMMM this makes me want a cheeseburger

A

caseous necrosis

42
Q

Which type of necrosis is described: microscopically charactererized as amorphous pink granular material within a ring of granulomatous inflammation and loss of tissue architecture

A

caseous necrosis

43
Q

which type of necrosis is common in trauma to the breast or in cases of pancreatitis?

A

fat necrosis

44
Q

which type of necrosis has a gross appearance of chalky white-yellow

A

fat necrosis

45
Q

which type of necrosis give a “soap bubble” histologic appearance because of its dead adipocytes

A

fat necrosis

46
Q

What is another name for programmed cell death?

A

apoptosis

47
Q

What are the general concepts of apoptosis?

A
  • morphologically distinct, gene directed, form of individual cell death
  • it has a physiologic role
  • diseases may arise from an increase or from a decrease in the rate of apoptosis
48
Q

Morphologic features of apoptosis include: (4 of them)

A
  1. Cell shrinkage
  2. Chromatin condensation followed by fragmentation
  3. Apoptotic bodies formation
  4. Phagocytosis of the apoptotic bodies without a significant inflammatory response
49
Q

What are the SIGNALING mechanisms of apoptosis?

A 
intrinsic program
"death signals" (e.g. Fas- ligand binding to Fas receptor) 
removal of a trophic signal (hormones)
ROS, radiation and toxins
effect of cytotoxic T cells
50
Q

What are the CONTROL AND INTEGRATION mechanisms of apoptosis?
(two pathways)

A
  1. direct signaling (e.g. Fas ligand, TNF binding)

2. regulation of mitochondrial permeability

51
Q

In the control and integration mechanisms of apoptosis what is the role of the Bcl-2 gene?

A

Bcl-2 gene family serve as on and off switches that regulate the membrane permeability of the mitochondria (Bcl-2, Bax, Bak)

  • Bcl-2 and cl-x gene products INHIBIT apoptosis
  • Bax and bax gene products STIMULATE apoptosis
52
Q

What is released from the outer mitochondrial membrane and serves to disrupt the inhibitory function of Bcl-2, favoring apoptosis?

A

cytochrome-c

53
Q

mechanisms of apoptosis category execution - what are caspases?

A

apoptosis signaling pathways converge on an autocatalytic proteolytic cascade of caspases.
Their substrates include: cytoskeletal and nuclear matrix proteins, DNAse and transcription proteins

54
Q

In apoptosis the mitochondria release Ca that activates which two enzymes?

A
  1. transglutaminases cross link cytoplasmic proteins

2. Endonucleases cleave DNA at the linker regions b/w nucleosomes

55
Q

In apoptosis how are dead cells removed?

A
  • phagocytosis by neighboring cells and macrophages

- little or no inflammation

56
Q

How is apoptosis difference than necrosis in relation to STIMULI?

A

apoptosis: physiologic or pathologic
necrosis: hypoxia or toxins

57
Q

How is apoptosis difference than necrosis in relation to: MORPHOLOGY?

A

apoptosis: single cells, cell shrinkage, condensed chromatin, intact plasma membrane, apoptotic bodies
necrosis: multiple cells, cellular swelling, lysed plasma membrane, organelle disruption

58
Q

How is apoptosis difference than necrosis in relation to: MECHANISMS OF DNA DESTRUCTION?

A

Apoptosis: ATP DEpendent process, gene activation and endonuclease mediated DNA fragmentation

Necrosis: ATP INDEPENDENT process, random, diffuse, free radicals, membrane injury

59
Q

How is apoptosis difference than necrosis in relation to: TISSUE REACTION?

A

apoptosis: minimal inflammation, phagocytosis of apoptotic bodies
necrosis: inflammation

60
Q

Chronic cell injury leads to cell adaptations, the etiological factors are the same as those that cause reversible cell injury or cell death, but differ in….

A

duration and intensity

61
Q

cell adaptations include:

A
  • alterations in cell size (atrophy vs. hypertrophy)
  • alterations in cell number (hyperplasia)
  • alterations in cell differentiation (metaplasia)
  • intracellular accumulations
62
Q

What is the definition of atrophy

A

a decrease in cell size and function

*there is often concurrent decrease in organ size and/ or function

63
Q

What is the etiology of atrophy?

A
  • decreased workload
  • loss of innervation
  • decreased blood supply
  • inadequate nutrition
  • decreased trophic signals
  • aging
  • local pressure
64
Q

what is the morphologic appearance of atrophy?

A
  • atrophic cells are shrunken

- there is a reduction in structural components

65
Q

what is the definition of hypertrophy?

A

an increase in cell size

  • associated with an increase in functional capacity
  • tissue and/ or organ size may increase and may be accompanied by an increase in cell number (hyperplasia)
66
Q

in reference to hypertrophy, what is a NORMAL (physiologic) response to trophic signals (hormone stimulation)?

A

smooth muscle hypertrophy in the pregnant uterus

67
Q

in reference to hypertrophy, what is an ABNORMAL (pathologic) response to trophic signals (hormone stimulation)?

A
  • exogenous anabolic steroids induced muscle hypertrophy

- overproduction of TSH due to iodine deficiency induces thyroid follicle hypertrophy (goiter)

68
Q

increased functional demand (muscle hypertrophy) skeletal muscle cells hypertrophy in response to…

A

exercise

69
Q

When and why do myocardial cells hypertrophy?

A

due to increased workload of pumping against impaired aortic outflow or systemic hypertension

70
Q

What is the definition of hyperplasia?

A

an increase in the number of cells in a tissue or organ

  • may involve the proliferation of epithelial and/ or stromal cells
  • cell proliferation is stimulated by trophic factors (hormones and cytokines)
  • may increase the risk for subsequent neoplastic transformation
71
Q

what is the etiology of hyperplasia? (in relation to hormones)

A

hormones can stimulate hyperplasia:

  • endometrial glandular cells during the normal menstrual cycle
  • gynecomastia (hyperplasia of the breast in men) can be iatrogenic in its etiology (i.e. secondary to estrogen treatment for prostate cancer
  • erythrocyte hyperplasia can follow ectopic production or erythropoietin
72
Q

What is the etiology of hyperplasia? (in relation to growth factors)

A

growth factors can stimulate hyperplasia:

  • wound healing represents hyperplasia of CT cells as well as associated epithelial cells
  • lymph node hyperplasia is due to lymphocyte hyperplasia resulting during chromic inflammation and an immune response
  • epidermal cell hyperplasia leads to a callus due to repeated friction
  • chronic inflammation can induce hyperplasia of overlying epithelial cells
73
Q

definition of metaplasia

A

one adult cell type is replaced by another adult cell type in response to chronic stress

74
Q

intestinal metaplasia relates to replacement of

A

normal epithelium with goblet cells and other intestinal mucosal type cells

75
Q

what is Barrett’s esophagitis?

A

the normal stratified squamous epithelium of the esophagus being replaced due to prolonged exposure to reflux gastric contents

76
Q

squamous metaplasia is conversion of

A

normal columnar eptiehlium to stratified squamous epithelium

77
Q

what are some examples of squamous metaplasia

A
  • Resp. tract in response to chronic smoking
  • ductal epithelium of various glands in response to vitamin A deficiency
  • cervix in response to various agents
78
Q

categories of cell accumulations include:

A

-excess of normal cellular constituent such as water, lipids, proteins, and carbohydrates and pigments that may be exogenous or endogenous

79
Q

the mechanisms of intracellular accumulations include:

A
  • abnormal metabolism
  • lack of enzyme
  • abnormal protein folding or transport
  • ingestion of indigestible material
80
Q

what is a steatosis

A

it is a fatty liver

- an abnormal accumulation of triglycerides within paenchymal cells of the liver, heart, kidney, and skeletal muscle

81
Q

what is the etiology of lipid accumulation (steatosis)

A 
obesity
diabetes
alcohol
anorexia
toxins
protein malnutrition
82
Q

what is the gross appearance of a fatty liver?

A

enlarged yellow (3-6 kg) liver

83
Q

what is the microscopic appearance of a fatty liver?

A

hepatocytes contain clear cytoplasmic vacuoles that displace the nucleus

84
Q

where does cholesterol primarily accumulate?

A

macrophages (foam cells)
- skin - in subepithelial macrophages forming a xanthoma
vessels - in atheromas of atherosclerosis

85
Q

what is the histology of proteins

A

eosinophillic cytoplasmic droplets, vacuoles, or aggregates

86
Q

what are examples of proteins?

A
  • alpha 1 anti trypsin deficiency - impaired folding due to gene mutation
  • mallory bodies - impaired secretions due to improper folding or precipitation
  • neurofibrillary tangles in Alzheimer’s disease - accumulations of microtubule associated proteins and neurofilaments
87
Q

what is the morpholog of glycogen/ glucose?

A

clear cytoplasmic/ nuclear vacuoles, PAS (+)

88
Q

what is a glycogen storage disease?

A

abnormal glycogen metabolism due to enzyme deficiency

89
Q

what are some examples of exogenous pigments?

A
  • carbon is accumulated in makcrophages, (anthracosis vs. pneumoconiosis)
  • tattoos - pigment is accumulated locally
90
Q

what is lipofuscin?

A

“wear and tear” brown-yellow granular pigment

-lipoprotein complex due to ROS peroxidation of membranes

91
Q

definition of melanin?

A

black-brown pigment produced by melanocytes but accumulated in adjacent epidermal cells and in macrophages

92
Q

what is hemosiderin?

A
  • a yellow brown pigment represents aggregates of ferritin micelles
  • ## its accumulation arises from excess iron locally due to hemorrhage and can lead to hemosiderosis
93
Q

what is hemochromatosis

A

genetic disease associated with cell death due to uncompensated hemosiderin accumulation

94
Q

what is bilirubin?

A
  • brown yellow pigment
  • end produce of heme metabolism
  • accumulates in heptaocytes and bile ducts due to hemolysis, obstructed bile flow and or hepatocellular disease

Pathology Exam 1 (6 decks)

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