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Immunity > Pathology I > Flashcards

Pathology I Flashcards

1
Q

The tendency of the body to seek and maintain a condition of balance or equilibrium within its internal environment, even when faced with external changes

A

Homeostasis

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2
Q

Refers to the mechanisms of development and progression of disease, which account for the cellular and molecular changes that give rise to the specific functional and structural abnormalities that characterize any particular disease

A

Pathogenesis

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3
Q

Refers to why a disease arrises

A

Etiology

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4
Q

Describes how a disease develops

A

Pathogenesis

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5
Q

Metabolism, differentiation and specialization, neighboring cells, availability of substrates are all?

A

Constraints on a cell

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6
Q

Reversible functional and structural responses to changes in physiologic and some pathologic stimuli to maintain homeostasis

A

Adaptations

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7
Q

If the limits of adaptive response are exceeded, we see

A

Reversible injury, irreversible injury, and cell death

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8
Q

New cells from proliferating mature cells & stem cells

A

Hyperplasia

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9
Q

Non-dividing permanent cells (muscle, nerve) get bigger

A

Hypertrophy

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10
Q

What is an example of

  1. ) Physiologic hypertrophy?
  2. ) Pathologic hypertrophy?
A
  1. ) Skeletal muscle

2. ) Cardiac muscle

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11
Q

Endometrial & prostatic hyperplasia is an example of

A

Pathologic hyperplasia

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12
Q

An increase in the size of cells => increase in size of

A

Organ

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13
Q

Occurs in tissue whose cells have a limited capacity to divide

A

Hypertrophy

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14
Q

Turn on signal transduction pathways => induction of genes => protein synthesis

A

Mechanical and trophic triggers of hypertrophy

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15
Q

The normal adult prostate gland shows compound tubulo-acinar glands lined by pseudostratified columnar and/or cuboidal epithelium and separated by a supporting

A

Stroma

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16
Q

The supporting stroma consisting of bundles of smooth muscle cells separated by bands of

A

Fibrous tissue

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17
Q

An extremely common condition seen in men over the age of 50 years

A

Benign Prostatic Hyperplasia

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18
Q

The histologic hallmark of BPH is the

A

Expansile Nodule

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19
Q

The cause of BHP is most likely related to excess stimulation of the prostate gland by

A

Testosterone or DHT

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20
Q

A proliferation of cells in organs whose cells can replicate

A

Hyperplasia

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21
Q

Hyperplasia is controlled: remove stimulus and proliferation

A

Ceases

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22
Q

Decrease in stress or trophic factors => decrease in organ size

A

Atrophy

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23
Q

Atrophy can be caused by an increased degredation due to

A

Ubiquitin-proteosome degradation

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24
Q

A reversible change whereby one adult cell type is replaced by another one

A

Metaplasia

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25
Q

A cell type vulnerable to a particular stress is replaced by one that is less vulnerable in

A

Metaplasia

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26
Q

The drawbacks of metaplasia is the loss of

A

Specialized function, and growth deregulation

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27
Q

Change in metaplasia results from altering the maturation program of

A

Stem cells

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28
Q

In a smoker’s bronchi, ciliated columnar cells => tougher squamous cells. This is an example of

-But protective mucus secretion and ciliary clearance is lost

A

Metaplasia

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29
Q

As the stress continues to affect the metaplastic epithelium, we may see

A

Malignant transformation

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30
Q

Characterized by generalized swelling of the cell and its organelles; blebbing of the plasma membrane; detachment of ribosomes from the endoplasmic reticulum; and clumping of nuclear chromatin

A

Reversible injury

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31
Q

Characterized by increasing swelling of the cell; swelling and disruption of lysosomes; presence of large amorphous densities in swollen mitochondria; disruption of cellular membranes; and profound nuclear changes

A

Irreversible injury

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32
Q

Nuclear condensation (pyknosis), followed by fragmentation (karyorrhexis) and dissolution of the nucleus (karyolysis) is an example of

A

Irreversible injury

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33
Q

Laminated structures (myelin figures) derived from damaged membranes of organelles and the plasma membrane first appear during the

A

Reversible stage

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34
Q

Can cause direct membrane damage

A

Ischemia

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35
Q

What are the earliest, i.e. reversible changes seen in cell injury?

A

Decreased ATP and cell swelling

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36
Q

What are two signs of irreversible cell injury?

A

Extensive membrane injury and severe mitochondrial damage

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37
Q

On a microscopic scale, reversible injury shows

A

Swelling and fatty change

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38
Q

Lysosome rupture and mitochondrial amorphous densities are signs or

A

Irreversible damage

39
Q

One of the events that occurs in hypoxic or ischemic injury is

A

Cellular swelling

40
Q

The decrease of oxygen tension in the cell results in impairment of mitochondrial

A

Oxidative phosphorylation

41
Q

Since ATP is used to maintain the cellular ion pumps, the lack of ATP leads to an influx of

A

Sodium and water

42
Q

There is also an efflux of calcium. However, we still see a net increase in

A

Osmotic load

43
Q

In addition inorganic phosphates, lactate, and purine nucleosides accumulate in the cell and contribute to the

A

Osmotic load

44
Q

The microvilli (mv) are lost and have been incorporated in apical cytoplasm; blebs have formed and are extruded in the lumen (L). Mitochondria are slightly dilated in a proximal tubule with

A

Reversible injury

45
Q

Markedly swollen mitochondria containing amorphous densities, disrupted cell membranes, and dense pyknotic nucleus are seen in a proximal tubule with

A

Irreversible damage

46
Q

Oxygen deprivation such as hypoxia and ischemia are major agents of

A

Cell injury

47
Q

Anaphylaxis and autoimmune disease are both agents of

A

Cell injury

48
Q

With cellular injury, ATP levels drop to

A

5-10% of normal

49
Q

What are the three major causes of the ATP depletion seen in cellular injury?

A

Decreased O2 nutrients, mitochondrial damage, and toxins (ex: cyanide)

50
Q

ATP depletion, mitochondrial damage, loss of Ca2+ homeostasis, oxidative stress, defects in plasma membrane, and protein/DNA damage are mechanisms of

A

Cellular injury

51
Q

The loss of Ca2+ homeostasis can be seen by initial release of Ca2+ from intracellular stores. Followed later by influx across the

A

Plasma membrane

52
Q

Some diseases such as Alzheimer’s, Huntington’s, Parkinson’s, and +/- type II diabetes are the result of

A

Protein/DNA damage

53
Q

Unregulated cell death from damage to cell membranes, loss of ion homeostasis, and denaturation of cellular proteins

A

Necrosis

54
Q

A passive response to injury, i.e. there is no energy required

A

Necrosis

55
Q

Necrosis is always

A

Pathologic

56
Q

There is no individual cell phagocytosis with

A

Necrosis

57
Q

What are the 5 types of Necrosis?

A
  1. ) Coagulative
  2. ) Liquefactive
  3. ) Gangrenous
  4. ) Caseous
  5. ) Fat
58
Q

Underlying tissue architecture is preserved

–Characteristic of infarcts (ischemic necrosis)

A

Coagulative necrosis

59
Q

Focal bacterial/fungal infections

–Characteristic of CNS infarcts
–Liquid, viscous mass

A

Liquefactive Necrosis

60
Q

Clinically, an ischemic limb with coagulative necrosis.

–Called “wet” if bacterial superinfection => liquefaction

A

Gangrenous necrosis

61
Q

Tissue architecture & cell outlines obliterated

–Surrounded by distinctive inflammation: granuloma

A

Caseous necrosis

62
Q

Caseous necrosis is mainly due to

A

Tuberculosis

63
Q

Shows vague outlines of necrotic fat cells

A

Fat necrosis

64
Q

Typically from release of activated pancreatic lipases in acute pancreatitis

A

Fat necrosis

65
Q

Since the etiology of coagulative necrosis is often ischemia, the infarct occurs in a vascular distribution that is wedge-shaped with a base at the

A

Organ capsule

66
Q

Outline of the myocardial cells are preserved, but the fibers have a “smudgy” appearance with increased eosinophilia and decreased numbers of nuclei

A

Coagulative necrosis due to MI

67
Q

In coagulative necrosis the necrotic process is due mainly to

A

Protein denaturation

68
Q

When hypoxic injury leads to cell death, it often results in coagulative necrosis except in the

A

Brain (where we see liquefactive necrosis)

69
Q

Usually the result of a bacterial or fungal infection, because these processes evoke a massive influx of inflammatory cells, which release various degradative enzymes

A

Liquefactive necrosis

70
Q

For unclear reasons, a hypoxic insult to the brain (as opposed to most other organs) results in

A

Liquefactive necrosis

71
Q

As this infarct in the brain becomes organized and resolved, the liquefactive necrosis leads to resolution with

A

Cystic spaces

72
Q

Often the result of mycobacterial or fungal infection

A

Caseous necrosis

73
Q

Characterized by acellular pink areas of necrosis

A

Caseous necrois

74
Q

Necrosis of the acinar cells of the pancreas releases lipase and proteases that in turn lead to injury and death of

A

Adipose cells

75
Q

If fat necrosis is extensive, sufficient calcium may be deposited to result in hypocalcemia and in some cases even

A

Tetany

76
Q

Programmed cell death

-a rational way of getting rid of cells

A

Apoptosis

77
Q

In apoptosis, activation of caspase cascade => catabolism of

A

Proteins and DNA

78
Q

Results in: chromatin condensation, cytoplasmic blebs/apoptotic bodies, phagocytosis

A

Activation of caspase cascade

79
Q

What are the two pathways for apoptosis?

A

Intrinsic and extrinsic

80
Q

In the intrinsic pathway, cell injury leads to

  1. ) Activation of?
  2. ) Inhibiton of?
A
  1. ) Bax and Bak

2. ) Bcl-2

81
Q

This causes mitochondrial membrane channels to release

A

Cytochrome c

82
Q

Cytochrome c release into the cytoplasm leads to activation of

A

Caspase cascade

83
Q

Cell surface death receptors (Type I TNF receptor, Fas) bind their ligands => activate caspase cascade in

A

Extrinsis Apoptosis

84
Q

Most apoptosis is actually

A

Physiologic

85
Q

However, DNA damage, misfolded protein response, and certain infections are three types of

A

Pathologic apoptosis

86
Q

Proteolytic enzymes that are important in the chain of intracellular events that lead to apoptosis

A

Caspases

87
Q

The extrinsic pathway functions through the

A

Death receptor

88
Q

The death receptor binds

A

Fas and TNF

89
Q

Members of the TNF receptor family

A

Death receptors

90
Q

The death domains bind to the

A

Adapter proteins

91
Q

Too little apoptosis leads to increased cell survival which can cause

A

Cancer and autoimmune diseases

92
Q

Mutated cells survive without apoptosing in

A

Cancer

93
Q

Increased apoptosis leads to excessive cell death. This can result in

A

Neurodegenerative diseases, ischemic injury, and death of virus infected cells

94
Q

Failure to eliminate self-reactive lymphocytes

–failure to eliminate dead cells, a source of self-antigens

A

Autoimmune diseases

Immunity (33 decks)

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