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HB 2 > Cell Adaptations, Injury And Death (Dr. Nguyen) > Flashcards

Cell Adaptations, Injury And Death (Dr. Nguyen) Flashcards

1
Q

Define the term pathology.

A

Study of diseases (suffering)

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2
Q

What are the components of a pathological picture of a disease?

A

Etiology
Pathogenesis
Morphology
Clinical manifestations

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3
Q

What is etiology? What are some examples?

A

The cause/set of causes of a disease
Ex: genetics, environment, multifactorial

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4
Q

What is Pathogenesis?

A

Steps in development of disease (spread, infections)

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5
Q

What is morphology?

A

Ways in which cells, tissues, or organ changes

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6
Q

What are clinical manifestations?

A

Functional consequence

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7
Q

What did Virchow, the father of modern pathology, discover about pathology?

A

All diseases start with molecular or structural alterations in cells.

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8
Q

What are 4 types of cellular adaptions that can occur when under stress?

A

Hypertrophic
Hyperplasia
Atrophy
Metaplasia

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9
Q

What is hypertrophy?

A

An increase in the size of cells due to increase in protein in response to stress

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10
Q

Are new cells created in hypertrophy?

A

NO

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11
Q

What kind of cells does hypertrophy occur in?

A

Cells that can divide (epithelial, hematopoietic, connective tissue)
Cells that cannot divide (nerves, skeletal and cardiac)

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12
Q

What is the difference between physiological and pathological?

A

Physiological is normal
Pathological is abnormal, disease causing

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13
Q

What are the physiological causes of hypertrophy and their examples?

A

Growth factor or hormonal stimulation
Ex: growth of uterus during pregnancy

Increased functional demand
Ex: enlargement of muscle fibers from “pumping iron”

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14
Q

What are the pathological causes of hypertrophy and their examples?

A

Increased functional demand
Ex: cardiac enlargement from HTN or aortic valve disease

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15
Q

What is an examples of hypertrophic cells in the eye?

A

Congenital Hypertrophy RPE (CHRPE)- RPE cells enlarge, increasing proteins and pigment

Corneal endothelial cells- polymegethism, polymorphism

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16
Q

What is hyperplasia?

A

An increase the number of cells in an organ or tissue (controlled)

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17
Q

In what kind of cell does hyperplasia occur?

A

Cells that are capable of cell division

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18
Q

Can hyperplasia and hypertrophy occur simultaneously?

A

YES and often in response to the same stimuli

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19
Q

What are the physiological causes of hyperplasia and their examples?

A

Hormonal (female breast enlargement)

Compensatory (liver after hepatectomy, healing, regeneration after surgery) compensates for lost cells

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20
Q

What are the pathological causes of hyperplasia and their examples?

A

Excessive hormonal or growth factor stimulation (endometrial hyperplasia patient is not pregnant)

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21
Q

Is hyperplasia controlled? How can hyperplasia disappear?

A

YES

If signals that initiate it lessen; stimulus is removed response stops

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22
Q

What kind of hyperplasia can lead to cancer?

A

Pathological hyperplasia when it becomes uncontrolled

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23
Q

What is atrophy?

A

Skrinkage in the size of the cell and in the size of the organ as a result of loss of cell substance

Cell function is diminished but they are NOT dead

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24
Q

What are the causes associated with atrophy?

A

Decreased workload (atrophy of disuse)
Loss of innervation (denervation atrophy) Diminished blood supply
Inadequate nutrition
Loss of endocrine stimulation
Aging (senile atrophy)

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25
Q

How is protein synthesis and protein degradation affected in atrophy?

A

Decreased protein synthesis (reduced metabolic activity)

Increased protein degradation (ubiquitin proteasome pathway, autophagy)

26
Q

What is autophagy?

A

Consumption of body’s own tissue as metabolic process

27
Q

What is metaplasia? What is it a response to? How does it “help” the cell respond?

A

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

Usually in response to chronic irritation

Makes cells better able to withstand stress

28
Q

What are 2 examples of metaplasia?

A

Columnar epithelium to squamous (habitual cigarette smoking, trachea)

Squamous epithelium to columnar (chronic gastric reflux)

29
Q

What may result are a result of metaplasia?

A

May result in reduced functions or increased risk for malignant (uncontrolled) transformation

30
Q

How might metaplasia be reversed?

A

With removal (abatement) of stimulus

31
Q

Describe conjunctival squamous metaplasia?

A

Conjunctiva columnar epithelium with goblet cells becomes squamous

Affects tear film which affects cornea

32
Q

What is reversible cell injury?

A

Pathological changes reversible with removal of stimulus

33
Q

What is irreversible cell injury?

A

Pathological changes permanent & lead to cell death

34
Q

What are 7 causes of cell injury?

A

Oxygen deprivation
Physical agents
Chemical agents and drugs
Infectious agents
Immunologic reactions
Genetic defects
Nutritional imbalances
Aging

35
Q

Describe 3 mechanisms associated with hypoxia (oxygen deprivation)?

A

Ischemia (loss of blood supply)
Inadequate oxygenation of blood (pneumonia)
Loss of O2 carrying capacity of blood (anemia)

36
Q

What are some examples of physical agents causing cell injury?

A

Trauma, heat, cold, radiation, electric shock

37
Q

What are the 2 classifications of chemical agents and drugs causing cell injury?

A

Therapeutic and narcotic

38
Q

How can intracellular elements such as sodium or glucose cause cell injury?

A

Increases may disrupt osmotic gradient causing injury

39
Q

Describe an example of immunologic reactions causing cell injury.

A

Autoimmune diseases (body attacks normal cells)

40
Q

Describe the morphological changes that occur with reversible injury.

A

Cellular swelling
Fatty change (liver and heart muscle cells)
Intracellular changes

41
Q

Which necrosis that can only be seen microscopically?

A

Fibrinoid necrosis

42
Q

What kind of necrosis is associated with tuberculosis?

A

Caseous (queso) necrosis

43
Q

Describe gangrenous necrosis.

A

Coagulative necrosis of limb secondary to loss of blood supply

“wet”-liquefied by bacteria infection

44
Q

Describe fibrinoid

A

Immune complexes together with fibrin that has leaked out of vessels

45
Q

Describe fat as a pattern of tissue necrosis.

A

Areas of fat destruction
Enzymes (macrophage or pancreatic cell) degrade fat

Saponification
Calcification

46
Q

Describe caseous.

A

Soft, cheese like
Area of necrosis enclosed in inflammatory border (granuloma)

47
Q

Describe liquefaction.

A

Necrotic area soft and filled with fluid and cellular framework is destroyed

localized bacterial infections (abscesses) & in the brain

48
Q

Describe coagulation.

A

Most common type of necrosis
Denaturation of cytoplasmic proteins with preservation of framework of cells for several
days
Solid organs except brain

49
Q

What is the irreversible morphology of cell and tissue injury?

A

Necrosis

50
Q

What is necrosis associated with?

A

Loss of membrane integrity
Leakage of cellular content
Inflammation (influx of immune cells as membrane is disrupted)

51
Q

Describe how morphology occurs in necrosis.

A

Nuclear shrinkage, fragmentation and dissolution (pyknotic, karyorrhexis, karyolysis)
Breakdown of membranes
Leakage and enzymatic digestion of cellular contents
Myelin figures

52
Q

What is autolysis?

A

Occurs post cell death
Digestion of dead cell by its own lysosome

53
Q

What is heterolysis?

A

Occurs post cell death

Digestion by lysosomal enzymes of immigrant leukocytes

54
Q

What is dystrophic calcification?

A

Occurs post cell death

Necrotic cells attract calcium salts

55
Q

Describe cellular swelling associated with reversible injury.

A

Result of failure of energy dependent ion pumps in the plasma membrane (oxygen deficiency in pumps)

56
Q

Describe fatty change associated with reversible injury.

A

Occurs in hypoxic injury, and in various forms of toxic or metabolic
injury

Lipid vacuoles in the cytoplasm

57
Q

Describe the intracellular changes associated with reversible injury.

A

Plasma membrane alterations (blebbing, distortion of microvilli, and loosening of intercellular attachments)
Mitochondrial changes (swelling)
ER dilation (detachment of ribosomes)
Nuclear alterations (clumping of chromatin)
Myelin figures (phospholipid masses from damaged cellular membrane)

58
Q

What cellular components are most frequently damaged by injurious stimuli?

A

Mitochondria
Cell membrane
Protein synthesis and packaging machinery
DNA

59
Q

What is the definition of a free radical?

A

Atoms or groups of atoms with an odd (unpaired) number of electrons, typically highly reactive and short lived.

60
Q

What are some causes of free radicals?

A

During normal reduction -oxidation reaction of normal
metabolism
– Ionizing radiation
– Occurs during inflammation (oxidative burst)
– Metabolism of exogenous chemicals or drugs ex. CCl 4-→CCl3
– Transition metals

61
Q

What is ischemia reperfusion injury?

A

Restoration of blood flow to ischemic tissues
can promote recovery of cells if they are
reversibly injured, but can also paradoxically
exacerbate the injury and cause cell death.

HB 2 (17 decks)

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