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Exam 1 Material Flashcards

1
Q

Pathology definition

A

“Study of suffering” or “study of disease”

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2
Q

Etiology

A

Origin of disease, “why”

  • genetics
  • environmental exposures
  • risk factors
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3
Q

Pathogenesis

A

Steps in development, “how”

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4
Q

Homeostasis

A

Tendency to maintain internal stability

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5
Q

Disease definition

A

Structural or functional change in the body that is harmful to the organism

Deviation from optimal homeostasis

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6
Q

Sign

A

Objective and observable indication that a disease is present

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7
Q

Symptom

A

Subjective evidence of disease or physical disturbance

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8
Q

Cells that are stressed will attempt to undergo..

A

Adaptation

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9
Q

Two factors that influence a cell’s ability to adapt

A
  1. Cell type

2. Nature of the cellular stress

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10
Q

Happens when a cell is no longer to adapt to a cellular stressor

A

Cellular injury

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11
Q

Physiologic adaptations

A

Responses that would be expected to occur with normal physiological changes

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12
Q

Pathologic adaptations

A

Responses to excessive cellular stress and indicate a loss of optimal structure and function

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13
Q

Cellular adaptation definition

A

Reversible changes in cell populations

- Ex: number of cells, cell size, cell type

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14
Q

Four main adaptations to stress

A
  1. Hypertrophy
  2. Hyperplasia
  3. Metaplasia
  4. Atrophy
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15
Q

Hypertrophy

A

Increase in the size of a cell

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16
Q

Hypertrophy is achieved by

A

Increase in synthesis of intracellular proteins and organelles

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17
Q

Example of pathologic hypertrophy

A

“Ventricular hypertrophy”

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18
Q

Pathology results from

A

Disruption in homeostasis

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19
Q

Irreversible cellular injury results in

A

Death

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20
Q

Two types of cell death

A

Necrosis (inflammatory) and apoptosis (controlled)

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21
Q

Cardiac myocytes adapt to chronic hypertension via

A

Hypertrophy

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22
Q

Which cellular adaptation is most likely to cause pre-cancerous cellular changes

A

Metaplasia

Some cases hyperplasia

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23
Q

An HPV infection is most likely to cause which pathologic adaptation at the area of the infection?

A

Hyperplasia

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24
Q

Stenosis definition

A

Narrowing

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25
Q

Steatosis definition

A

Fat accumulation

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26
Q

Hyperplasia

A

Increase in the number of cells

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27
Q

Hyperplasia can result from

A

Compensatory factors, gene activation or hormonal factors

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28
Q

Atrophy

A

Decrease in cell size, or reduced size and function

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29
Q

Decrease in cell size

A

Decrease protein synthesis or increase protein breakdown

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30
Q

Reduced size and function can be due to

A
  1. Disuse
  2. Denervation
  3. Ischemia
  4. Endocrine disruption
  5. Aging
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31
Q

Metaplasia

A

Change of one cell type into another

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32
Q

Possible consequences of metaplasia

A

Decreased function, and malignant transformation

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33
Q

Three types of trauma

A

Physical
Thermal
Radiation

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34
Q

Injury occurs if stressors

A
  1. Exceed ability to adapt
  2. Direct damage
  3. Intrinsic abnormalities
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35
Q

Type of stressor in a reversible injury

A

Transient or mild stressor

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36
Q

Examples of reversible injuries

A

Cellular swelling and fatty accumulation

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37
Q

Irreversible injuries due to what type of stressor

A

Prolonged or severe stressor

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38
Q

Examples of what prolonged or severe stressors cause

A
  1. Irreparable mitochondrial damage

2. Damaged cellular membranes

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39
Q

Two types of cell death

A
  1. Necrosis

2. Apoptosis

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40
Q

Inflammatory cell death

A

Necrosis

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41
Q

Type of cell death caused by trauma, toxins and ischemia

A

Necrosis

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42
Q

Type of cell death that is non-inflammatory

A

Apoptosis

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43
Q

Type of cell death due to decrease in growth factor or damage to DNA/proteins

A

Apoptosis

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44
Q

Pyknosis necrosis

A

Nucleus becomes a Solid, shrunken mass

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45
Q

Karyorrhexis necrosis

A

Nucleus becomes fragmented

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46
Q

Karyolysis necrosis

A

Nucleus fades and dissolutes

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47
Q

What happens to the Plasma membrane during necrosis?

A

Becomes disrupted

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48
Q

What happens to plasma membrane in apoptosis?

A

Stays intact, but structure is altered

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49
Q

Which type of cell death is considered pathologic?

A

Necrosis

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50
Q

Which type of cell death is often considered physiologic?

A

Apoptosis

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51
Q

5 patterns of necrosis

A
  1. Coagulative
  2. Liquefactive
  3. Caseous
  4. Fat
  5. Fibrinoid
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52
Q

Coagulative necrosis

A

Severe ischemia, death of solid organ tissue

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53
Q

Infarction

A

Process of killing cells due to ischemia

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54
Q

Infarct

A

Area of dead tissue

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55
Q

Gangrene

A

Coagulative necrosis in an extremity

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56
Q

Major causes of gangrenous necrosis

A

Peripheral vascular disease
Frost bite
Trauma that obstructs blood supply

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57
Q

3 types of gangrene

A

Dry
Wet
Gas

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58
Q

Which pathology is most likely to cause gangrene in the U.S.?

A

Diabetes

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59
Q

Liquefactive necrosis

A

An infection occurs and dead cells are completely digested by WBC into a liquid/viscous mass

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60
Q

Liquefactive necrosis examples

A
  1. CNS ischemia/hypoxia

2. Infections (bacterial and fungal)

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61
Q

Examples of stressors

A

Trauma, ischemia, hypoxia, poisons, infections, immune reactions, malnutrition, aging

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62
Q

Ischemia

A

Insufficient blood supply to a tissue

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63
Q

Hypoxia

A

When an organ is not receiving adequate oxygen within the arterial bloody supplying the organ

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64
Q

Cyanosis

A

Bluish discoloration of the skin which may develop following tissue ischemia or hypoxia

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65
Q

Cellular swelling develops because

A

Injured cells may not have enough ATP to power ATP-dependent pumps

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66
Q

Toxin definition

A

Poisonous substance secreted from a living organism

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67
Q

Poison definition

A

Substance that may kill, injure, or impair a living organism

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68
Q

Types of infectious microbes

A

Bacterial, viral, protozoan, or fungal

69
Q

Ways an infection can arise

A
  1. Microbes directly induce tissue damage

2. Microbes stimulate an excessive immune response that causes tissue damage

70
Q

Nutritional imbalance

A

Deficiency or excess of dietary nutrients may inhibit homeostasis

71
Q

Cellular senescence

A

Reduced capacity for cells to react to stress, and maintain homeostasis (result of age)

72
Q

Fatty change (steatosis)

A

Accumulation of fat vacuoles within a cell’s cytoplasm

73
Q

Apoptosis eliminates cells experiencing:

A
  1. Severe DNA damage
  2. Severe protein damage
  3. A loss of cellular survival signals
  4. Cells that have been infected by viruses
74
Q

Dry gangrene

A

Uncomplicated gangrene

Most common

75
Q

Wet gangrene

A

If gangrenous tissue becomes infected w/ bacteria and the tissue liquefies

76
Q

Gas gangrene

A

When bacteria (Clostridium perfringens) infects the tissue and gas byproducts become trapped within the tissues

77
Q

Cytoplasmic changes during necrosis

A

Eosinophilia

Myelin figures

78
Q

Eosinophilia

A

Necrotic cells manifest with an increased pink/red appearance with H&E stain

79
Q

Myelin figures

A

Necrotic cells contain membrane damage and myelin figures are “rolled-up” or “scroll-like”

80
Q

Caseous necrosis

A

“Cheese-like” appearance— friable, yellow/white

81
Q

Major cause of caseous necrosis

A

Tuberculosis

82
Q

Granuloma definition

A

Walled-off collection of macrophages

83
Q

Caseous necrosis via tuberculosis AKA

A

Caseous granuloma

84
Q

Fat necrosis AKA

A

Enzymatic necrosis

85
Q

Fat necrosis definition

A

Fat destruction, fat “saponification”

86
Q

Causes of fat necrosis

A

Acute pancreatitis
Pancreatic trauma
Trauma to breast

87
Q

Causes of acute pancreatitis

A

Gallstones

Alcoholism

88
Q

Enzyme defected in fat necrosis

A

Lipase enzyme

89
Q

Fibrinoid necrosis

A

Due to an autoimmune reaction

90
Q

Autoimmune reaction in fibrinoid necrosis induces the formation of

A

An immune complex + fibrin

91
Q

Immune complex

A

Antibody + antigen

92
Q

Apoptosis

A

Programmed/regulated cell death

93
Q

Apoptotic bodies

A

Intact membranes, produce no inflammation

94
Q

Apoptosis activates

95
Q

Two apoptosis mechanisms

A

Mitochondrial pathway

Death receptor pathway

96
Q

Mitochondrial pathway caused by

A

Decreased growth factor
DNA damage
Misfolded proteins

97
Q

Mitochondrial pathway activates

98
Q

Death receptor pathway signalled by

A

“Death receptors” binding with signaling molecules (extrinsic)

99
Q

Death receptor pathway activates

100
Q

Autophagy

A

“Self-eating”; lysosomal digestion of a cell’s insides

101
Q

What happens during autophagy

A

Organelles are sequestered/digested into autophagic vacuoles

102
Q

Conditions when autophagy occurs

A
  1. Survival during “lean times”

2. Rids misfolded proteins

103
Q

Cellular injury frequently begins with

A

Reduced ATP

104
Q

Vulnerable cellular structures for cellular injury

A

Mitochondria
Membranes
Protein synthesis
DNA

105
Q

Ischemia/ Hypoxic Injury results in low oxygen, which results in

A

Low ATP

Low ROS

106
Q

Conditions when hypoxia will occur without ischemia

A

CO poisoning
Pneumonia
Choking
Premature baby (immature alveoli)

107
Q

Persistent ischemia can result in

A 
Ruptured membranes (necrosis)
Minimal apoptosis
108
Q

Ischemia-Reperfusion Injury

A

Ischemia, followed by restoration of blood flow

109
Q

Ischemia-Reperfusion injury results in cell injury by

A

Increase inflammatory cells (increase WBC)

Increase ROS

110
Q

Oxidative stress

A

Accumulation of ROS

111
Q

Oxidative stress can result in

A

Cellular aging
Inflammation (neutrophils and macrophages)
Ischemia-reperfusion injury

112
Q

ROS

A

Reactive oxygen species

Molecules with unpaired electrons in outer orbitals

113
Q

Redox reactions

A

Partially reduced intermediate molecules

114
Q

Inflammation/phagocytosis

A

Burts of ROS created by WBC when digesting phagocytized material

115
Q

Nitric oxide

A

Natural free radical produced by macrophages or endothelial cells

116
Q

Ionizing radiation

A

Hydrolyzed water into OH and H

117
Q

Two types of chemical injury

A 
Direct injury (rare)
Latent injury (MC)
118
Q

Direct chemical injury

A

Toxins bind to cells

Inhibits use of ATP or damages membranes

119
Q

Latent chemical injury

A

Require conversions into highly reactive or toxic metabolites

120
Q

Cytochrome P-450 works in

A

Smooth ER of liver

121
Q

Example of latent chemical injury

A

Acetaminophen (NAPQI created in liver via cytochrome P- 450)

122
Q

Genetic Damage occurs via

A

Radiation or chemotherapy meds
Chemicals
Viral infections

123
Q

Genetic damage can result in

A

ROS damage to DNA
Apoptosis
Future cancer risk

124
Q

4 mechanisms of intracellular accumulations

A

Abnormal metabolism
Defective protein folding or transport
Defective or absent enzymes
Ingestion of indigestible materials

125
Q

Abnormal metabolism example

A

Fatty liver disease (via alcoholism or diabetes)

126
Q

Defective protein folding or transport example

A

Alpha 1- antitrypsin deficiency (results in emphysema in non-smokers)

127
Q

Absent enzymes examples

A

Tay-Sachs Disease

Gaucher Disease

128
Q

Accumulation of indigestible materials examples

A

Pneumoconioses (carbon and silica)

129
Q

Fatty change (steatosis)

A

Excessive lipid accumulation

130
Q

Macroscopic fatty change

A

Hepatomegaly

131
Q

Microscopic fatty change

A

Fat vacuoles

132
Q

2 things that can lead to fatty changed

A

Alcoholic liver disease

Nonalcoholic fatty liver disease

133
Q

Alcoholic liver disease symptoms

A

Ascites
Caput Medusae
Mallory Bodies

134
Q

Ascites

A

Edema in peritoneal cavity

135
Q

Caput Medusae

A

Varicose veins of stomach

136
Q

Mallory Bodies

A

Intracellular inclusion that accumulate in liver cells

observed in alcoholic hepatitis and alcoholic liver disease

137
Q

Causes of chronic liver disease that can result in hepatocellular carcinoma

A

Chronic HBV infection
HCV infection
Aflatoxin exposure

138
Q

Inflammation of liver

139
Q

Scarring of liver

140
Q

Percentage of heavy drinkers that will develop hepatic steatosis

141
Q

Percentage of heavy drinkers that will develop hepatitis

142
Q

Percentage of heavy drinkers that will develop cirrhosis

143
Q

About ___ years are required to cause cirrhosis

144
Q

Steatosis and hepatitis are

A

Reversible

145
Q

Liver cirrhosis is

146
Q

Ascites occurs because

A

Liver cirrhosis reduces ability to produce normal blood protein

Protein deficient blood causes fluid to leave circulation and accumulate in tissues

147
Q

Caput Medusae occurs because

A

Liver cirrhosis prevents blood from flowing through liver, shunting venous blood from liver and to epigastric veins

148
Q

Conditions that stimulate nonalcoholic fatty liver disease

A

Obesity
Type 2 DM
Dyslipidemia
Chronic hypertension

149
Q

Africa and Asia patient are more likely to have __ between ages __ due to spreading from mother to baby

A

HBV

20 -40 years old

150
Q

US patients are more likely to have

151
Q

Males are about __ times more likely than females to develop hepatocellular carcinoma

152
Q

Aflatoxin is a carcinogen produced by

A

Aspergillus (mold)

153
Q

Aflatoxin is present in

154
Q

Up to __ of individuals with alcohol-induced liver cirrhosis will develop hepatocellular carcinoma

155
Q

Intracellular Pigment examples

A

Carbon

Melanin

156
Q

Lipofuscin

A

Wear and tear pigments

Found in elderly

157
Q

Hemosiderin

A

Bleeding or hemosiderosis

158
Q

Hemosiderosis

A

High iron levels = oxidative stress

Due to repetitive blood transfusions

159
Q

Dystrophic Calcification

A

Calcification of damaged tissue

MC cause of pathological calcification

160
Q

Fibrodysplasia Ossificans Progressiva

A

Dysfunctional soft tissue repair

Any trauma leads to heterotopic ossification
Ankylosis (fusion)

161
Q

Fibrodysplasia ossificans progressiva is an ___ disorder and is ____

A

Autosomal dominant

RARE (1 in 2 million births)

162
Q

Metastatic calcification

A

Calcification of normal tissues (may deposit in any tissue)

Abnormal Ca2+ homeostasis (hypercalcemia)

163
Q

Causes of hypercalcemia

A 
Bone cancer
Multiple myeloma
Paget disease
Leukemia
Hyperparathyroidism 
Hypervitaminosis D
Renal failure
164
Q

Cellular aging

A

Reduced functional capacity of cells

165
Q

Theories of cellular aging

A

DNA damage
Replication Senescence
Defective protein homeostasis

166
Q

Progeroid Syndromes

A

Extremely rapid aging

Cells can’t fix cellular damage

167
Q

Bloom syndrome

A

Death in 20s

168
Q

Werner syndrome

A

Death in 40s

Gen Path (10 decks)

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