Exam 1: Cell Injury, Death (highlights) Flashcards

1
Q

Define atrophy

A

Decrease in cell size

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2
Q

Define protooncogenes

A

Differentiation genes

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3
Q

Define hypertrophy

A

Increase in cell size

Enlargement in existing cells, increase in organelle number

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4
Q

Define etiology

A

Cause of disease

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5
Q

When does cell injury occur?

A

When limits of adaptation dare surpassed or when adaptive responses are not available

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6
Q

Symptoms are ___, signs are ____

A

Patient feels; doc observes

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7
Q

Define edema

A

Accumulation of fluid in body tissues and cavities

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8
Q

In reversible injury, limitations to survival include

A

the nature and duration of the injury and concurrent exposure to other cell stressors

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9
Q

Irreversible injury

A

When stimulus surpasses limits of survival

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10
Q

Will inflammation occur postmortem (autolysis)?

A

No

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11
Q

What is normal HR?

A

60-100 BPM

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12
Q

What is normal blood sugar?

A

80-100 mg/dL

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13
Q

Define necrosis

A

Cell disorganization

“Structural changes that result from cell death”

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14
Q

Define apoptosis

A

Programmed cell death

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15
Q

Atrophic cells have _____ but are not dead

A

Diminished function

E.g. muscle atrophy

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16
Q

Define idiopathic

A

Unknown cause

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17
Q

Define hypoxic

A

Tissue and organ atrophy associated with diminished blood or O2 supply

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18
Q

What is the most common reason for hypoxia?

A

Tissue or organ loose O2 supply

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19
Q

How does pressure influence pathological atrophy?

A

Compress adjacent structures

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20
Q

How does denervation contribute to pathological atrophy

A

Interruption of nerve supply

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21
Q

How does endocrine deficiency contribute to pathological atrophy

A

Pituitary insufficiency or another hormone inadequacy

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22
Q

Hypertrophy increases the size of structures that consists of

A

Non-dividing (permanent) cells

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23
Q

Example of hypertrophy with hypertension

A

Increase in size of heart

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24
Q

Example of idiopathic atrophy?

A

Alzheimer’s disease

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25
Q

What is an enlargement due to proliferation of cell (increase in number) usually concurrently with hypertrophy

A

Hyperplasia

E.g. prostate cancer

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26
Q

What promotes cancer development?

A

Hyperplasia

Note: if stimulus is removed, hyperplasia disappears

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27
Q

Define metaplasia

A

Substitution of one type of “mature” cell with another “mature” cell type that may be better suited to cope with altered environment.

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28
Q

Barrett’s Esophagus

A

Columnar cell metaplasia of lower esophagus (gastroesophageal reflux)

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29
Q

Marrow hyperplasia and extra-medullary hematopoiesis (severe anemia) are examples of

A

Metaplasia

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30
Q

Define dysplasia

A

Atypical metaplasia, bad growth

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31
Q

What kind of growth is pre-cancerous

A

Dysplasia

E.g. uterine cervical cancer causes cervical dysplasia from HPV virus

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32
Q

In what broad category of disorders would you see increased mitosis?

A

Dysplasia

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33
Q

Commons places of dysplasia

A

Uterine cervix, ducts of mammary gland, skin, oral, respiratory mucosa

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34
Q

Define ischemia

A

Hypoxic injury due to decreased blood flow

“Ischemic hypoxia”

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35
Q

If blood was being shunted away from a tissue to a different tissue (e.g. “steal syndromes”), this would cause what kind of injury in the original tissue?

A

Ischemia hypoxia

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36
Q

Define hypoxemia

A

Decreased blood oxygen levels

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37
Q

What happens in hypoxic injury?

A
  • Decreased synthesis and depletion of ATP (happens early on)
  • Oxidative phosphorylation is compromised
  • When ATP disrupted = work stops, increased membrane permeability and swelling due to increased Na2+ and water
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38
Q

What does a pathologically high amount of calcium activate?

A
  • Phospholipases
  • Proteases
  • ATPases
  • Endonucleases
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39
Q

Mitochondrial injury leads to

A

Irreversible damage and cell death

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40
Q

What is a “superficial” common sign early on in most forms of cell injury?

A

Loss of regulated membrane permeability

Which leads to ATP depletion, activation of phopholipases, direct membrane change

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41
Q

Function of antioxidants

A

To remove/degrade free radicals by spontaneous decay and/or enzyme action

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42
Q

A high number of enzymes is indicative of

A

Higher amount of damage, severe injury, death

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43
Q

Necrosis is a response from

A

exogenous stimuli

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44
Q

“Intrinsic” (autolysis)

A

Self-digestion by enzymes derived from lysosomes within injured cell

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45
Q

“Extrinsic” (heterolysis)

A

Enzymes derived from inflammatory leukocytes act on cell components

E.g. neutrophils, macrophages

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46
Q

Nuclear changes that look like shrinkage and increased basophilic staining

A

Pyknosis (condensation)

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47
Q

Nuclear changes that look like fragmentation and breakdown of nuclei

A

Karyorrhexis

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48
Q

Nuclear changes that look like dissolution of nucleus

A

Karyolysis

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49
Q

What type of necrosis is characterized by desaturation of cytoplasmic proteins

A

Coagulation

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50
Q

Clinical example of coagulation

A

Myocardial infarc

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51
Q

Tissue that ends up looking like “fried egg whites” is linked to what type of necrosis

A

Coagulation

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52
Q

Tissue that is lysed by enzymes is characteristically this type of necrosis

A

Liquefaction necrosis

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53
Q

A stroke is an example of what kind of necrosis?

A

Liquefaction necrosis

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54
Q

They of necrosis that has the characteristic of being pyogenic (pus forming)

A

Liquefaction necrosis

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55
Q

Pyogenic

A

pus forming

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56
Q

Type of necrosis that has the characteristic of being “cheesy” in nature

A

Casseous necrosis

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57
Q

What kind of necrosis is commonly caused by TB and leprosy infections?

A

Casseous necrosis

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58
Q

What kind of necrosis is associated with hydrolysis of lipid deposits present in adipose tissue?

A

Fat necrosis

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59
Q

Liver and acute pancreatitis is associated with what kind of necrosis?

A

Fat necrosis

60
Q

The type of necrosis that is characterized by forming fibrotic deposits (scars)

A

Gummatous necrosis

61
Q

The type of necrosis that is formed during tertiary stages of syphilis

A

Gummatous necrosis

62
Q

Coagulation necrosis modified by bacterial activity

A

Gangrene

63
Q

Mummification

A

Dry gangrene

64
Q

Moist necrosis combined with bacterial infection and more liquefaction

A

Wet (moist) gangrene

65
Q

Deep, blood-deprived wounds that get contaminated with spore forming anaerobic bacteria is characteristic of

A

Gas (infectious) gangrene

66
Q

Organisms that release phospholipases and other lyric enzymes that destroy cells and other tissue elements and produce “gas bubbles” at the sites of infection

A

Gas (infectious) gangrene

67
Q

Define apoptosis

A

Programmed cell death

68
Q

What happens with pathological increased blood, urea, creation levels?

A

Kidney problems

69
Q

Lipid “residual bodies” of certain cells

A

Lipofuscin

70
Q

Lipofuscin is common when?

A

During normal aging AND in response to chronic degenerative disease

71
Q

Induction

A

Expansion

72
Q

Intracellular accumulations also known as

A

Storage Disorders

73
Q

4 Causes of storage disorders

A
  1. Cell metabolism
  2. Abnormal endogenous substances
  3. Congenital enzyme abnormalities
  4. Abnormal exogenous substances
74
Q

Define fatty metamorphosis

A

Steatosis, fatty change

75
Q

Accumulation of lipids in parenchymal cells

A

Fatty metamorphosis

76
Q

What storage disorder is common in the liver resulting from alcohol abuse, diabetes and obesity

A

Fatty metamorphosis

77
Q

Gross changes in a fatty liver

A

Enlargement, softening, yellow color, blunted margins

78
Q

Accumulation of lipid products is

A

Pathogenic mechanism of fatty change in the liver

79
Q

Chronic hypoxia (anemia) leads to _____ in muscle

A

Tigered effect (Alternating yellow and red bands of tissue)

80
Q

Tigered effect

A

Alternating yellow (fat) and red (muscle) bands of tissue

81
Q

Tigered effect also known as

A

Thrush breast

82
Q

Tigered effect / thrush breast is associated with what organ?

A

Heart

83
Q

Clusters of lipid-containing macrophages in the dermis and tendons

A

Xanthoma

84
Q

Xanthoma associated with

A

Hyperlipidemia

85
Q

Increased lipids in the dermis and tendons…

A

Xanthoma

86
Q

“Foam cells” associated with

A

Lysosomal storage diseases

87
Q

Clinical sign: macular cherry red spot

A

Tay Sachs disease

88
Q

Clinical sign: cherry red spot in fovea

A

Niemann-Pick disease

89
Q

Accumulation of ganglioside

A

Tay Sachs disease

90
Q

Deficiency in sphingomyelinase

A

Niemann-Pick disease

91
Q

Deficiency in glucocerebrosidase which leads to accumulation of glucocerebrosides

A

Gaucher’s disease

92
Q

Synthesis of excessive quantities of immunoglobulins (Ig) by plasma cells give rise to large proteinaceous deposits known as

A

Russell bodies

93
Q

Russell bodies

A

large proteinaceous deposits

Note: caused by synthesis of excessive quantities of immunoglobulins (Ig)

94
Q

Mallory bodies

A

Alcoholic hyaline

95
Q

Lewy bodies

A

Parkinson’s

96
Q

Neurofibrillary tangles

A

Alzheimer’s and Huntington’s

97
Q

“mad cow disease” Or CDJ

A

Prion diseases

98
Q

Stress proteins include

A

Chaperonins and Upiquitin

99
Q

A stress protein that participates in activities of normal cells that include protein folding, disaggregation and intracellular transport

A

Chaperonins

100
Q

A stress protein that has a role in remolding denatured proteins

A

Ubiquitin

101
Q

Amyloidosis

A

Group of diseases in which amyloid is deposited in organs and tissues

102
Q

Where are amyloid materials derived from?

A

Peptide fragments of larger proteins

103
Q

Excess/abnormal amyloid proteins disease

A

Alzheimer’s disease

104
Q

Rheumatoid arthritis, Crohn’s disease and TB and leprosy are examples of

A

Amyloidosis

105
Q

T/F amyloidosis is curable

A

False.

Note: Conservative therapies such as dietary choices, supplements and antidote-inflammatory agents are employed.

106
Q

Glycogen storage diseases reflect

A

“Inborn errors” in glucose or glycogen metabolism

107
Q

Deficiency of G6P

A

Von Gierke’s disease (type I glycogen storage disorder)

108
Q

Defect in a1-glucosidase (a lysosomal enzyme) is the cause of

A

Pompe’s disease (type II glycogen storage disorder)

Note: Striated muscle including the heart is affected most, fatal by 1-2 yrs old.

109
Q

Protects against UV light

A

Melanin

110
Q

Congenital lack of melanin

A

Albinism

111
Q

Patchy areas of skin

A

Vitiligo

112
Q

Increased ACTH contributes to

A

Hyperpigmentation of the skin

113
Q

Ferric ion will block what?

A

Normal breakdown of melanin

This explains the darker pigmentation of skin in hemochromatosis

114
Q

Increased homogentisic acid in urine gives it a black color

A

Alkaptonuria

115
Q

Tissue discoloration secondary to accumulated homogentisic acid

A

Ochronosis

116
Q

Soluble deposits of iron-apoferritin complexes

A

Ferritin

117
Q

The relatively benign iron storage disorder as iron accumulate in macrophages

A

Hemosiderosis

118
Q

The iron storage is order associated with organ (perenchymal) damage

A

Hemochromatosis

119
Q

T/F. Small amounts of ferritin is normally in plasma

A

True. These levels are indicator fo adequacy of body stores

120
Q

“Bronze diabetes”

A

Hemochromatosis

121
Q

“perenchymal”

A

Organ

122
Q

Triad of hemochromatosis

A

Cirrhosis
Pancreatic fibrosis
Bronzed skin

123
Q

The triad (Cirrhosis, Pancreatic fibrosis, Bronzed skin) is indicative of

A

Hemochromatosis “bronze diabetes”

124
Q

Aging or wear-and-tear pigment

A

Lipofuscin

125
Q

brown-colored undigestible lipid derivatives

A

Lipofuscin

126
Q

“Plumbism”

A

Lead

127
Q

Most common exogenous pigment

A

Carbon

128
Q

Excess deposits that affect liver, basal ganglia and eyes

A

Copper

129
Q

What is Wilson’s disease?

A

Copper accumulation

130
Q

Fetus calcification is known as

A

dystrophic calcification or phleboliths

131
Q

Anything that increases calcium is

A

Hypercalcemia

E.g. increased secretion of parathyroid hormone

132
Q

Ectopic bone formation includes

A

Myositis ossificans

133
Q

Von Gierke’s disease (deposits in liver and kidney) and Pompe’s disease (accumulations in myocardium) are composed of

A

Glycogen

134
Q

Mallory bodies (inclusions in injured hepatocytes) and amyloidosis (deposits of complex insoluble materials that appear under a number of circumstances) are composed of

A

Proteins and protein complexes

135
Q

Tay Sachs disease is composed of

A

Ganglioside

136
Q

Neumann-Pick disease is composed of

A

Sphingomyelin

137
Q

Xanthoma is composed of

A

Cholesterol and other lipids

138
Q

Thrush breast is composed of

A

Intraparenchymal cell triglycerides

139
Q

Alkaptonuria is composed of

A

Homogentisic acid

140
Q

The “wear and tear” or brown atrophy seeing in aging and chronic injury is composed of

A

Lipofuscin

141
Q

Hemochromatosis “bronze diabetes” is composed of

A

Iron

142
Q

Plumbism is composed of

A

Lead

143
Q

Wilson’s disease is composed of

A

Copper

144
Q

How many doublings per adult cell according to Hayflick phenomenon?

A

50

145
Q

Limitations in doublin capacity are known as

A

Hayflick phenomenon