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Pathology > Adaptation, Injury, and Death + Cell Injury (SS 01) > Flashcards

Adaptation, Injury, and Death + Cell Injury (SS 01) Flashcards

1
Q

define necrosis

A

death of cells, tissues, or organs in a living person

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2
Q

define apoptosis

A

programmed cell death of single cells

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3
Q

define ischemia

A

reversible injury due to inadequate blood supply

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4
Q

define infarction

A

irreversible necrosis due to ischemia that is not relieved in time

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5
Q

is the same treatment used for all types of necrosis?

A

no, type of necrosis determines treatment

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6
Q

what type of treatment is used in the case of liquefactive necrosis?

A

drainage

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7
Q

what type of treatment is used in the case of caseous necrosis?

A

anti-fungal and TB

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8
Q

what type of treatment is used in the case of gangrenous necrosis?

A

amputation

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9
Q

pathologic apoptosis is important in ___

A

certain cancers (lack of it), chemo, radiation, transplant rejection, hypoxia, certain viral infections

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10
Q

define etiology

A

cause

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11
Q

define morphology

A

visible manifestation

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12
Q

define gross

A

visible without a microscope

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13
Q

what is the gradation of response to stress and noxious stimuli?

A

adaptation –> injury –> death

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14
Q

define adaptation

A

physiologic and morphologic changes, modulating function, bringing it to a new altered steady state of homeostasis

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15
Q

when it comes to adaptive ability, most vital organs have a large ___

A

reserve capacity

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16
Q

what is the relationship bw disease and reserve capacity?

A

disease commonly uses up an organ’s reserve capacity silently until it’s too late

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17
Q

define injury

A

reversible pathophysiologic and morphologic response to stress or noxious stimuli exceeding the capacity of cell, tissue, organ or person to adapt, though not enough to be lethal

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18
Q

what are the injurious reactive oxygen species (ROS)?

A

superoxide, hydrogen peroxide, hydroxyl radical, and peroxynitrite

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19
Q

what is reperfusion?

A

restoration of blood supply to ischemic cells

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20
Q

what can reperfusion lead to?

A

can be injurious bc brings oxygen that can be converted to ROS and calcium that can increase mitochondrial permeability and activate enzymes inappropriately in cells already damaged

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21
Q

injured and dead cells leak their contents into the bloodstream which are useful how?

A

blood tests can detect these contents to diagnose tissue injury or necrosis

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22
Q

what is amylase?

A

enzyme that digests carbs

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23
Q

what is amylase secreted by?

A

pancreas (into duodenum) and salivary glands (into saliva)

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24
Q

what is lipase?

A

enzyme that digests fats

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25
Q

what is lipase secreted by?

A

pancreas (into duodenum)

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26
Q

in a case of pancreatitis where is lipase released?

A

retroperitoneal peri-pancreatic fat (leading to fat necrosis)

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27
Q

what is creatine phosphokinase (CPK or CK)?

A

enzyme concentrated in muscle and brain composed of M and B dimers

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28
Q

what is CK secreted by?

A

myocytes –> MB fraction is secreted into blood with myocardial injury

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29
Q

what is ALT?

A

alanine aminotransferase, transaminase that catalyzes interconversion of glutamate and alanine

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30
Q

what is ALT secreted by?

A

liver normally releases it, but more is secreted by liver injury than AST

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31
Q

what is AST?

A

aspartate aminotransferase, transaminase that catalyzes interconversion of glutamate and aspartate

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32
Q

what is AST secreted by?

A

muscle, liver, and other organ injury

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33
Q

what is ALP?

A

alkaline phosphatase, phosphatases that transfer phosphate from donor to receptor molecules at alkaline pH

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34
Q

what is ALP secreted by?

A

liver and bone injury, esp. with biliary obstruction and space-occupying disease

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35
Q

what is GGT?

A

gamma-glutamyl-transferase, outer cell membrane enzyme that transports amino acids into cells

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36
Q

what is GGT secreted by?

A

liver injury (esp. toxic)

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37
Q

what is LDH?

A

lactate dehydrogenase, enzyme that catalyzes conversion of lactate to pyruvate by removing 2H

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38
Q

what is LDH secreted by?

A

injury to RBCs, liver, muscle, other organs

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39
Q

what is coagulative necrosis?

A

morphological manifestation of irreversible injury to cell, tissue, organ due to ischemia (except in brain)

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40
Q

is ischemia reversible or irreversible?

A

reversible

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41
Q

is infarction reversible or irreversible?

A

irreversible

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42
Q

what is pyknosis?

A

condensation, shrinkage , and hyperbasophilia (increased blue) of a dead cell nucleus

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43
Q

what is karyorrhexis?

A

clumping and fragmentation of nuclear DNA in a pyknotic dead nucleus

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44
Q

what is karyolysis?

A

fading away of a dead cell nucleus

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45
Q

what are the features of coagulative necrosis?

A

1) preservation of ghost outline
2) cytoplasm has increased pink eosinophilia
3) nucleus exhibits pyknosis, karryorhexis, karyolysis
4) acute inflammatory response

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46
Q

what is liquefactive necrosis?

A

necrosis with conversion of solid tissue to liquid due to severe acute infection, toxicity, or (brain only) ischemia

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47
Q

what is an abscess?

A

localized area of liquefactive necrosis

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48
Q

what is a microabscess?

A

localized area of liquefactive necrosis visible only microscopically

49
Q

what is caseous necrosis?

A

distinctive form of coagulative necrosis grossly resembling cheese

50
Q

what are the features of caseous necrosis?

A

amorphous, granular, eosinophilic, no ghost cells

51
Q

what is gangrene necrosis?

A

distinctive form of coagulative necrosis with blackening and shrinkage , typically of distal extremities, but sometimes of internal organs such as gallbladder

52
Q

what is fat necrosis?

A

adipose tissue digested by pancreatic lipase, creating white saponification (most common form) –> can result from trauma

53
Q

what does saponification of fat entail?

A

chalky white deposits of calcium + fatty acid soap from digestion by pancreatic lipase

54
Q

what 2 pathways can initiate apoptosis?

A

mitochondrial (internal/intrinsic) and death receptor (external/extrinsic)

55
Q

can protein misfolding lead to pathologic apoptosis?

A

yes

56
Q

what are the features of apoptosis?

A

1) cell shrinkage
2) cytoplasmic hypereosinophilia
3) chromatin condensation and karyorrhexis
4) phagocytosis by macrophages

57
Q

do apoptosis and necrosis occur within 1) single cells/small clusters or 2) large groups of cells?

A 
apoptosis = single cells/small clusters
necrosis = large groups of cells
58
Q

do apoptosis and necrosis occur with 1) cell membrane intact or 2) cell membrane disrupted?

A 
apoptosis = intact
necrosis = disrupted
59
Q

do apoptosis and necrosis produce an inflammatory response?

A 
apoptosis = no
necrosis = yes
60
Q

physiologic apoptosis is important in ___

A

embryogenesis, involution, ending inflammation, eliminating self-reactive lymphocytes, eliminating virally infected and tumor cells, etc.

61
Q

define lesion

A

discrete visible manifestation of disease

62
Q

define physiology

A

normal function

63
Q

define pathophysiology

A

abnormal function, rendered abnormal by disease

64
Q

define pathogenesis

A

sequence of events in response of person, organ, or cell to etiologic agent of disease (from initial stimulus to ultimate manifestation of disease)

65
Q

what is Occam’s razor as it applies to medicine?

A

a single diagnosis that explains all of a patient’s symptoms, signs and other manifestations of disease is most likely the correct diagnosis

66
Q

the electrolyte potassium is most important to what?

A

muscle

67
Q

the electrolyte sodium is most important to what?

A

brain (and nerves)

68
Q

the electrolyte bicarbonate is most important to what?

A

acid-base balance

69
Q

which part of the small intestine is most difficult to diagnose injury to?

A

jejunum

70
Q

liver injury is more likely than any other organ to elevate ___ out of proportion to ___

A

ALT; AST

71
Q

what four factors have influence on whether reversible ischemia becomes irreversible infarction?

A

1) vulnerability of the disease
2) rate of development
3) alternative blood supply
4) blood oxygenation

72
Q

infarctions tend to be ___, ___, and ___-shaped

A

peripheral, subcapsular, and wedge-shaped

73
Q

white anemia infarcts are typical of ___

A

solid organs with end-arterial circulation (e.g., heart, spleen, kidneys)

74
Q

red hemorrhagic infarcts have what different mechanisms?

A

venous occlusion, dual or anastomosing blood supply or reperfusion

75
Q

the brain tends to develop what type of necrosis?

A

liquefactive

76
Q

do all cell types react to stress and injury the same way?

A

no

77
Q

define atrophy

A

decrease in size and function of cell or organ due to disuse, aging (senile atrophy), denervation, decreased blood supply, etc.

78
Q

define hypertrophy

A

increase in size of a cell caused by augmented functional demand or specific hormonal stimulation; can be physiologic or pathologic

79
Q

define hyperplasia

A

increase in number of cells in an organ or tissue; can be physiologic or pathologic

80
Q

define polyploidy

A

the state of a cell nucleus containing 3+ haploid chromosomal sets

81
Q

define metaplasia

A

conversion of one differentiated cell type to another differentiated cell type; can be epithelial or mesenchymal

82
Q

define dysplasia

A

alteration of size, shape, and organization of cellular components of a tissue

83
Q

what is the difference bw hypertrophy and hyperplasia?

A 
hypertrophy = larger cells
hyperplasia = more cells (but same size)
84
Q

is polyploidy always indicative of unrestricted cell growth?

A

no

85
Q

metaplasia is based on what concept?

A

entire genetic code is contained within every cell

86
Q

metaplasia typically begins where (within epithelium)?

A

at base of epithelial surface along basement membrane, first in reserve cells then the rest of the cells

87
Q

what is dysplasia characterized by?

A

1) abnormalities in size and shape of cells
2) enlargement, irregularity, and hyperchromasia of nuclei
3) disorderly arrangement of cells within epithelium
4) generally preneoplastic condition

88
Q

name the common intracellular, endogenous brown pigments

A

iron compds, lipofuscin, melanin

89
Q

what are the entities responsible physiologically for iron stores?

A

ferritin and hemosiderin

90
Q

what is the principal storage form of iron?

A

ferritin, a “hollow” protein loaded with iron

91
Q

is ferritin visible by routine microscopy?

A

no

92
Q

is hemosiderin visible by routine microscopy?

A

yes

93
Q

hemosiderin is composed of what?

A

intracellular granules in iron storing cells - autophagosomes loaded with semidigested ferritin molecules

94
Q

iron stores may be increased due to ___

A

hemochromatosis (hereditary, too much iron absorbed or retained) or hemosiderosis (iron overload bc of other systemic or local causes)

95
Q

what is the function lipofuscin?

A

“wear and tear” pigment, polymer of oxidized lipids, present in long-lived cells; no real use proven

96
Q

what is melanin?

A

naturally occurring pigment normally present in basal layer of skin, retina, and some other ectodermal derived tissues

97
Q

what is the function of melanin?

A

absorbs harmful UV light and may be useful as free radical ‘sink’, in neoplasms may indicate malignant melanoma

98
Q

name the most commonly encountered black pigment in pathology

A

carbon

99
Q

what is the main route of ingestion of carbon?

A

pulmonary

100
Q

can carbon be seen microscopally? grossly?

A

yes and yes

101
Q

what is anthracosis?

A

permanent condition of black pigment in the lungs, pulmonary lymph nodes, and distant tissues

102
Q

is anthracosis harmful?

A

no, as long as surrounding tissues don’t react to inert carbon

103
Q

what causes tissue calcification?

A

calcium salts deposit in abnormal, diseased or dead tissues of many types

104
Q

what are the types of pathologic calcification?

A

dystrophic type and metastatic type

105
Q

which type of calcification is more common?

A

dystrophic

106
Q

what are the features of dystrophic type calcification?

A
  • more common
  • generally localized process, usu. related to some tissue injury
  • plasma calcium levels are normal
107
Q

what are the features of metastatic type calcification?

A
  • less common
  • generalized process where there may be calcification of many tissues
  • generally related to more systemic derangement of calcium levels (elevated)
108
Q

what abnormal accumulations can build up in cells?

A

water, electrolytes, lipids, carbs, proteins

109
Q

how do water and electrolytes accumulate in cells?

A

leaking into cells due to vacuole formation or to hydropic swelling, resulting in diffuse waterlogging of entire cell

110
Q

what is hydropic swelling?

A

early and often reversible indicator of cell damage

111
Q

what are the 2 significant lipids that can accumulate in cells?

A

cholesterol and triglycerides

112
Q

what is xanthelasma?

A

soft, yellow-orange like plaques on eyelids or medial canthus (associated with LDL)

113
Q

how are triglycerides seen in accumulation?

A

seen grossly as greasy, yellow deposits on diseased organs whose cells are engorged with triglyceride droplets and vacuoles (steatosis) –> most common in liver

114
Q

kwashiorkor is caused by what type of diet?

A

low protein, high carb

115
Q

kwashiorkor results from the lack of what?

A

protein synthesis, which blocks synthesis and export of LPPs from liver, with retention of lipid components

116
Q

abnormal deposition or storage of cholesterol can lead to what?

A

severe disease or may be histologic curiosity only (e.g., foam cells in wall of gallbladder)

117
Q

what is an example of a carbohydrate accumulant that is seen pathologically?

A

glycogen, may increase intracellularly in conditions like diabetes or hypoxia but accumulation tends to diffuse

118
Q

most carbohydrate accumulations can’t be seen as discrete bodies, except for ___ found in the aging CNS.

A

corpora amylaceae (extracellular, not harmful)

119
Q

what proteins tend to accumulate and when do they do so?

A

cytoskeletal proteins may accumulate or condense in a variety of disease states

Pathology (2 decks)

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