Exam 1 Material Flashcards
1
Q
Pathology definition
A
“Study of suffering” or “study of disease”
2
Q
Etiology
A
Origin of disease, “why”
- genetics
- environmental exposures
- risk factors
3
Q
Pathogenesis
A
Steps in development, “how”
4
Q
Homeostasis
A
Tendency to maintain internal stability
5
Q
Disease definition
A
Structural or functional change in the body that is harmful to the organism
Deviation from optimal homeostasis
6
Q
Sign
A
Objective and observable indication that a disease is present
7
Q
Symptom
A
Subjective evidence of disease or physical disturbance
8
Q
Cells that are stressed will attempt to undergo..
A
Adaptation
9
Q
Two factors that influence a cell’s ability to adapt
A
- Cell type
2. Nature of the cellular stress
10
Q
Happens when a cell is no longer to adapt to a cellular stressor
A
Cellular injury
11
Q
Physiologic adaptations
A
Responses that would be expected to occur with normal physiological changes
12
Q
Pathologic adaptations
A
Responses to excessive cellular stress and indicate a loss of optimal structure and function
13
Q
Cellular adaptation definition
A
Reversible changes in cell populations
- Ex: number of cells, cell size, cell type
14
Q
Four main adaptations to stress
A
- Hypertrophy
- Hyperplasia
- Metaplasia
- Atrophy
15
Q
Hypertrophy
A
Increase in the size of a cell
16
Q
Hypertrophy is achieved by
A
Increase in synthesis of intracellular proteins and organelles
17
Q
Example of pathologic hypertrophy
A
“Ventricular hypertrophy”
18
Q
Pathology results from
A
Disruption in homeostasis
19
Q
Irreversible cellular injury results in
A
Death
20
Q
Two types of cell death
A
Necrosis (inflammatory) and apoptosis (controlled)
21
Q
Cardiac myocytes adapt to chronic hypertension via
A
Hypertrophy
22
Q
Which cellular adaptation is most likely to cause pre-cancerous cellular changes
A
Metaplasia
Some cases hyperplasia
23
Q
An HPV infection is most likely to cause which pathologic adaptation at the area of the infection?
A
Hyperplasia
24
Q
Stenosis definition
A
Narrowing
25
Steatosis definition
Fat accumulation
26
Hyperplasia
Increase in the number of cells
27
Hyperplasia can result from
Compensatory factors, gene activation or hormonal factors
28
Atrophy
Decrease in cell size, or reduced size and function
29
Decrease in cell size
Decrease protein synthesis or increase protein breakdown
30
Reduced size and function can be due to
1. Disuse
2. Denervation
3. Ischemia
4. Endocrine disruption
5. Aging
31
Metaplasia
Change of one cell type into another
32
Possible consequences of metaplasia
Decreased function, and malignant transformation
33
Three types of trauma
Physical
Thermal
Radiation
34
Injury occurs if stressors
1. Exceed ability to adapt
2. Direct damage
3. Intrinsic abnormalities
35
Type of stressor in a reversible injury
Transient or mild stressor
36
Examples of reversible injuries
Cellular swelling and fatty accumulation
37
Irreversible injuries due to what type of stressor
Prolonged or severe stressor
38
Examples of what prolonged or severe stressors cause
1. Irreparable mitochondrial damage
| 2. Damaged cellular membranes
39
Two types of cell death
1. Necrosis
| 2. Apoptosis
40
Inflammatory cell death
Necrosis
41
Type of cell death caused by trauma, toxins and ischemia
Necrosis
42
Type of cell death that is non-inflammatory
Apoptosis
43
Type of cell death due to decrease in growth factor or damage to DNA/proteins
Apoptosis
44
Pyknosis necrosis
Nucleus becomes a Solid, shrunken mass
45
Karyorrhexis necrosis
Nucleus becomes fragmented
46
Karyolysis necrosis
Nucleus fades and dissolutes
47
What happens to the Plasma membrane during necrosis?
Becomes disrupted
48
What happens to plasma membrane in apoptosis?
Stays intact, but structure is altered
49
Which type of cell death is considered pathologic?
Necrosis
50
Which type of cell death is often considered physiologic?
Apoptosis
51
5 patterns of necrosis
1. Coagulative
2. Liquefactive
3. Caseous
4. Fat
5. Fibrinoid
52
Coagulative necrosis
Severe ischemia, death of solid organ tissue
53
Infarction
Process of killing cells due to ischemia
54
Infarct
Area of dead tissue
55
Gangrene
Coagulative necrosis in an extremity
56
Major causes of gangrenous necrosis
Peripheral vascular disease
Frost bite
Trauma that obstructs blood supply
57
3 types of gangrene
Dry
Wet
Gas
58
Which pathology is most likely to cause gangrene in the U.S.?
Diabetes
59
Liquefactive necrosis
An infection occurs and dead cells are completely digested by WBC into a liquid/viscous mass
60
Liquefactive necrosis examples
1. CNS ischemia/hypoxia
| 2. Infections (bacterial and fungal)
61
Examples of stressors
Trauma, ischemia, hypoxia, poisons, infections, immune reactions, malnutrition, aging
62
Ischemia
Insufficient blood supply to a tissue
63
Hypoxia
When an organ is not receiving adequate oxygen within the arterial bloody supplying the organ
64
Cyanosis
Bluish discoloration of the skin which may develop following tissue ischemia or hypoxia
65
Cellular swelling develops because
Injured cells may not have enough ATP to power ATP-dependent pumps
66
Toxin definition
Poisonous substance secreted from a living organism
67
Poison definition
Substance that may kill, injure, or impair a living organism
68
Types of infectious microbes
Bacterial, viral, protozoan, or fungal
69
Ways an infection can arise
1. Microbes directly induce tissue damage
| 2. Microbes stimulate an excessive immune response that causes tissue damage
70
Nutritional imbalance
Deficiency or excess of dietary nutrients may inhibit homeostasis
71
Cellular senescence
Reduced capacity for cells to react to stress, and maintain homeostasis (result of age)
72
Fatty change (steatosis)
Accumulation of fat vacuoles within a cell’s cytoplasm
73
Apoptosis eliminates cells experiencing:
1. Severe DNA damage
2. Severe protein damage
3. A loss of cellular survival signals
4. Cells that have been infected by viruses
74
Dry gangrene
Uncomplicated gangrene
| Most common
75
Wet gangrene
If gangrenous tissue becomes infected w/ bacteria and the tissue liquefies
76
Gas gangrene
When bacteria (Clostridium perfringens) infects the tissue and gas byproducts become trapped within the tissues
77
Cytoplasmic changes during necrosis
Eosinophilia
| Myelin figures
78
Eosinophilia
Necrotic cells manifest with an increased pink/red appearance with H&E stain
79
Myelin figures
Necrotic cells contain membrane damage and myelin figures are “rolled-up” or “scroll-like”
80
Caseous necrosis
“Cheese-like” appearance— friable, yellow/white
81
Major cause of caseous necrosis
Tuberculosis
82
Granuloma definition
Walled-off collection of macrophages
83
Caseous necrosis via tuberculosis AKA
Caseous granuloma
84
Fat necrosis AKA
Enzymatic necrosis
85
Fat necrosis definition
Fat destruction, fat “saponification”
86
Causes of fat necrosis
Acute pancreatitis
Pancreatic trauma
Trauma to breast
87
Causes of acute pancreatitis
Gallstones
| Alcoholism
88
Enzyme defected in fat necrosis
Lipase enzyme
89
Fibrinoid necrosis
Due to an autoimmune reaction
90
Autoimmune reaction in fibrinoid necrosis induces the formation of
An immune complex + fibrin
91
Immune complex
Antibody + antigen
92
Apoptosis
Programmed/regulated cell death
93
Apoptotic bodies
Intact membranes, produce no inflammation
94
Apoptosis activates
caspases
95
Two apoptosis mechanisms
Mitochondrial pathway
| Death receptor pathway
96
Mitochondrial pathway caused by
Decreased growth factor
DNA damage
Misfolded proteins
97
Mitochondrial pathway activates
Caspase-9
98
Death receptor pathway signalled by
“Death receptors” binding with signaling molecules (extrinsic)
99
Death receptor pathway activates
Caspase-8
100
Autophagy
“Self-eating”; lysosomal digestion of a cell’s insides
101
What happens during autophagy
Organelles are sequestered/digested into autophagic vacuoles
102
Conditions when autophagy occurs
1. Survival during “lean times”
| 2. Rids misfolded proteins
103
Cellular injury frequently begins with
Reduced ATP
104
Vulnerable cellular structures for cellular injury
Mitochondria
Membranes
Protein synthesis
DNA
105
Ischemia/ Hypoxic Injury results in low oxygen, which results in
Low ATP
| Low ROS
106
Conditions when hypoxia will occur without ischemia
CO poisoning
Pneumonia
Choking
Premature baby (immature alveoli)
107
Persistent ischemia can result in
```
Ruptured membranes (necrosis)
Minimal apoptosis
```
108
Ischemia-Reperfusion Injury
Ischemia, followed by restoration of blood flow
109
Ischemia-Reperfusion injury results in cell injury by
Increase inflammatory cells (increase WBC)
| Increase ROS
110
Oxidative stress
Accumulation of ROS
111
Oxidative stress can result in
Cellular aging
Inflammation (neutrophils and macrophages)
Ischemia-reperfusion injury
112
ROS
Reactive oxygen species
Molecules with unpaired electrons in outer orbitals
113
Redox reactions
Partially reduced intermediate molecules
114
Inflammation/phagocytosis
Burts of ROS created by WBC when digesting phagocytized material
115
Nitric oxide
Natural free radical produced by macrophages or endothelial cells
116
Ionizing radiation
Hydrolyzed water into OH and H
117
Two types of chemical injury
```
Direct injury (rare)
Latent injury (MC)
```
118
Direct chemical injury
Toxins bind to cells
Inhibits use of ATP or damages membranes
119
Latent chemical injury
Require conversions into highly reactive or toxic metabolites
120
Cytochrome P-450 works in
Smooth ER of liver
121
Example of latent chemical injury
Acetaminophen (NAPQI created in liver via cytochrome P- 450)
122
Genetic Damage occurs via
Radiation or chemotherapy meds
Chemicals
Viral infections
123
Genetic damage can result in
ROS damage to DNA
Apoptosis
Future cancer risk
124
4 mechanisms of intracellular accumulations
Abnormal metabolism
Defective protein folding or transport
Defective or absent enzymes
Ingestion of indigestible materials
125
Abnormal metabolism example
Fatty liver disease (via alcoholism or diabetes)
126
Defective protein folding or transport example
Alpha 1- antitrypsin deficiency (results in emphysema in non-smokers)
127
Absent enzymes examples
Tay-Sachs Disease
| Gaucher Disease
128
Accumulation of indigestible materials examples
Pneumoconioses (carbon and silica)
129
Fatty change (steatosis)
Excessive lipid accumulation
130
Macroscopic fatty change
Hepatomegaly
131
Microscopic fatty change
Fat vacuoles
132
2 things that can lead to fatty changed
Alcoholic liver disease
| Nonalcoholic fatty liver disease
133
Alcoholic liver disease symptoms
Ascites
Caput Medusae
Mallory Bodies
134
Ascites
Edema in peritoneal cavity
135
Caput Medusae
Varicose veins of stomach
136
Mallory Bodies
Intracellular inclusion that accumulate in liver cells
| observed in alcoholic hepatitis and alcoholic liver disease
137
Causes of chronic liver disease that can result in hepatocellular carcinoma
Chronic HBV infection
HCV infection
Aflatoxin exposure
138
Inflammation of liver
Hepatitis
139
Scarring of liver
Cirrhosis
140
Percentage of heavy drinkers that will develop hepatic steatosis
90-100%
141
Percentage of heavy drinkers that will develop hepatitis
25%
142
Percentage of heavy drinkers that will develop cirrhosis
15%
143
About ___ years are required to cause cirrhosis
20
144
Steatosis and hepatitis are
Reversible
145
Liver cirrhosis is
Permanent
146
Ascites occurs because
Liver cirrhosis reduces ability to produce normal blood protein
Protein deficient blood causes fluid to leave circulation and accumulate in tissues
147
Caput Medusae occurs because
Liver cirrhosis prevents blood from flowing through liver, shunting venous blood from liver and to epigastric veins
148
Conditions that stimulate nonalcoholic fatty liver disease
Obesity
Type 2 DM
Dyslipidemia
Chronic hypertension
149
Africa and Asia patient are more likely to have __ between ages __ due to spreading from mother to baby
HBV
| 20 -40 years old
150
US patients are more likely to have
HCV
151
Males are about __ times more likely than females to develop hepatocellular carcinoma
3X
152
Aflatoxin is a carcinogen produced by
Aspergillus (mold)
153
Aflatoxin is present in
Peanuts
154
Up to __ of individuals with alcohol-induced liver cirrhosis will develop hepatocellular carcinoma
20%
155
Intracellular Pigment examples
Carbon
| Melanin
156
Lipofuscin
Wear and tear pigments
Found in elderly
157
Hemosiderin
Bleeding or hemosiderosis
158
Hemosiderosis
High iron levels = oxidative stress
Due to repetitive blood transfusions
159
Dystrophic Calcification
Calcification of damaged tissue
MC cause of pathological calcification
160
Fibrodysplasia Ossificans Progressiva
Dysfunctional soft tissue repair
Any trauma leads to heterotopic ossification
Ankylosis (fusion)
161
Fibrodysplasia ossificans progressiva is an ___ disorder and is ____
Autosomal dominant
| RARE (1 in 2 million births)
162
Metastatic calcification
Calcification of normal tissues (may deposit in any tissue)
| Abnormal Ca2+ homeostasis (hypercalcemia)
163
Causes of hypercalcemia
```
Bone cancer
Multiple myeloma
Paget disease
Leukemia
Hyperparathyroidism
Hypervitaminosis D
Renal failure
```
164
Cellular aging
Reduced functional capacity of cells
165
Theories of cellular aging
DNA damage
Replication Senescence
Defective protein homeostasis
166
Progeroid Syndromes
Extremely rapid aging
Cells can’t fix cellular damage
167
Bloom syndrome
Death in 20s
168
Werner syndrome
Death in 40s
