Module 7A & 7B - Pathology Flashcards
1
Q
Pathology
A
• Pathos= suffering
• -ology= study
• Study of disease- the causes of disease and the associated changes at the levels of
cells, tissues, and organs
2
Q
Etiology
A
• Etio= cause
• -ology= study
• Study of the origin of disease, including causes and modifying factors
Refers to why a disease occurs, and pathogenesis describes how a disease
develops
3
Q
Pathogenesis
A
• Pathos= suffering
• -genesis= beginning, development, or production of something
• Reviewing the steps in the development of a disease
• Biochemical and molecular mechanisms
4
Q
Morphology
A
• Gross and microscopic appearance of cells and tissues
• Associated structural changes
5
Q
Clinical Manifestations
A
• End results of genetic, biochemical, structural changes in cells and tissues that lead to physiological changes/impairment
• Lead to signs and symptoms of disease
• Functional alterations in cells and organs, and the resulting clinical consequences
6
Q
What is the concept of homeostasis in relation to cells?
A
Homeostasis refers to the ability of cells to maintain a stable internal environment within a normal range of function and structure.
7
Q
What are adaptations in cells?
A
Adaptations are reversible functional and structural responses of cells to changes in physiological states, allowing cells to survive and function under stress.
8
Q
What happens if the limits of adaptive responses are exceeded?
A
If the limits of adaptive responses are exceeded or if cells face further stress, it can lead to cell injury, loss of nutrients, and mutations that compromise cellular function, ultimately resulting in irreversible injury and cell death.
9
Q
What are two Categories of Adaptations?
A
- Physiologic Adaptations
• Stimulation from hormones, chemical mediators - Pathologic Adaptations
• Responses to stress
• Cells adapt and change their structure and function
• “Escape” injury
10
Q
The reason or causation of why a disease occurs is referred to:
• A) Clinical manifestations
• B) Pathology
• C) Pathogenesis
• D) Etiology
A
D) Etiology
11
Q
Cellular adaptations can be reversible if the stimulus is removed?
• A) True
• B) False
A
A) True
12
Q
What happens when stressors persist in cellular adaptations?
A
When stressors persist, cells may progress beyond adaptive changes, leading to irreversible injury and potentially cell death.
13
Q
What is hypertrophy?
A
Hypertrophy is the increase in the size of cells, resulting in an overall enlargement of the tissue or organ.
14
Q
What is hyperplasia?
A
Hyperplasia is the increase in the number of cells within a tissue or organ, leading to tissue enlargement.
15
Q
What is atrophy?
A
Atrophy is the shrinking of cells due to the loss of cell substance, leading to a decrease in tissue or organ size. It may involve loss of cell function but not cell death.
16
Q
What is metaplasia?
A
Metaplasia is the change in phenotype where one adult cell type is replaced by another adult cell type, usually as an adaptive response to stress. It is reversible.
17
Q
What is dysplasia?
A
Dysplasia is the abnormal development or growth of cells within a tissue, often characterized by irregular cell size, shape, and organization, and can be a precursor to cancer.
Dysplasia is the presence of abnormal cells within a tissue or organ, where cells lose their normal morphological characteristics and undergo dedifferentiation.
18
Q
What is physiological hypertrophy?
A
Physiological hypertrophy occurs in response to normal, healthy stimulation, such as changes in the uterus during pregnancy or skeletal muscle growth from exercise.
19
Q
What is pathological hypertrophy?
A
Pathological hypertrophy occurs in response to abnormal stress or injury, such as the enlargement of the myocardium due to high blood pressure (HBP) or stenosis.
20
Q
What happens if the stress causing pathological hypertrophy is not removed?
A
If the stress is not removed, pathological hypertrophy can lead to impaired function and potentially irreversible damage, as seen in conditions like heart failure.
21
Q
Can hyperplasia occur with hypertrophy?
A
Yes, hyperplasia can occur simultaneously with hypertrophy, as both are cellular adaptations to stress or stimulation.
22
Q
What is physiological hyperplasia?
A
Physiological hyperplasia includes hormonal hyperplasia (such as tissue growth during pregnancy) and compensatory hyperplasia (such as tissue regeneration after part of an organ is lost).
23
Q
What is pathological hyperplasia?
A
Pathological hyperplasia is usually caused by excessive hormonal or growth factor stimulation. It is important to differentiate it from cancer, as hyperplasia can stop once the stimulus is removed.
24
Q
What are common causes of atrophy?
A
Common causes include decreased workload, loss of innervation, ischemia, malnutrition, loss of endocrine stimulation, and aging.
25
What is the mechanism of atrophy?
Atrophy results from a combination of decreased protein synthesis and increased protein degradation within cells.
26
Why does metaplasia occur?
Metaplasia occurs when a cell type sensitive to a specific stressor is replaced by another type that can better withstand and adapt to the stressor.
27
What is an example of metaplasia?
An example is the change from columnar epithelium to squamous epithelium in response to chronic irritation (like in the lungs of smokers).
28
Is dysplasia reversible?
Yes, dysplasia is reversible, but it may become cancerous if the stress or damage continues and the abnormal cells proliferate.
29
How does dysplasia relate to cancer?
Dysplasia itself is not cancer, but it is considered a precancerous condition. It can be mild, moderate, or severe, with severe cases having a higher risk of developing into cancer if left untreated.
30
What happens if dysplasia continues?
If the stress or stimulus causing dysplasia is not removed, it may progress to more severe forms, possibly leading to cancer.
31
What is anaplasia?
Anaplasia is an advanced form of dysplasia where there is a total loss of structural and functional differentiation of normal cells. Cells in this state do not resemble their original counterparts and exhibit uncontrolled division.
32
How does anaplasia relate to cancer?
Anaplasia is commonly used to describe cancer cells, which divide rapidly and show little or no resemblance to normal, differentiated cells. It indicates a loss of differentiation and is often associated with more aggressive tumors.
33
What happens to cells in anaplasia?
Cells in anaplasia lose their original structure and function, and they often proliferate uncontrollably, contributing to tumor growth and cancer progression.
34
The term that refers to when a cell changes its phenotype and
even function is called:
• A) Atrophy
• B) Hyperplasia
• C) Metaplasia
• D) Dysplasia
C) Metaplasia
35
Dysplasia can be a reversible process and sometimes is referred to
as pre-cancerous.
• A) True
• B) False
A) True
36
What is the difference between reversible and irreversible cell injury?
• Reversible Cell Injury: The structure and function of the cell can return to normal if the damaging stimulus is removed, but only to a certain extent.
• Irreversible Cell Injury: If the damaging stimulus persists or is severe, the cell damage becomes irreversible, leading to cell death.
37
What happens if the damaging stimulus is not removed?
If the damaging stimulus is not removed, the injury progresses from reversible to irreversible, eventually leading to cell death.
38
What are the key principles of most forms of cell injury?
1. The response of a cell to injury depends on the nature, duration, and severity of the stimulus.
2. The consequences of injury depend on the type, state, and adaptability of the cell.
3. A single injurious stimulus can activate multiple interconnected mechanisms that damage the cell.
39
What are the common variables that lead to cell injury?
• Oxygen Deprivation
• Physical Agents
• Oxidative Stress
• Chemical Agents and Drugs
• Infectious Agents
• Immunologic Reactions
• Genetic/DNA Abnormalities
• Nutritional Imbalances
• Aging
40
What is ischemia, and why is it significant in cellular injury?
• Ischemia is the reduction of blood flow to tissues, resulting in inadequate perfusion and oxygen delivery.
• Ischemia is one of the most common causes of cell injury in a clinical setting.
41
Can hypoxia occur without ischemia?
Yes, hypoxia (reduction of oxygen levels below metabolic needs) can occur without ischemia if oxygen levels are insufficient, even if blood flow is not reduced.
42
What is ischemia-reperfusion injury?
• Ischemia-Reperfusion Injury occurs when blood flow is restored to ischemic tissues.
• While it can promote recovery of reversibly injured cells, it can paradoxically worsen the injury and lead to cell death.
43
How do chemical agents and drugs cause cellular injury?
Chemical agents and drugs can cause cell injury through:
1. Direct toxicity (e.g., cyanide).
2. Conversion to toxic metabolites (e.g., acetaminophen, which is converted to a toxic product in the liver, causing injury).
44
What are some physical agents that can cause cellular injury?
• Trauma: Both micro (small scale, repeated injury) and macro (large, acute injury).
• Extreme temperatures: Can damage proteins and cell membranes.
• Radiation: Causes DNA damage, leading to mutations and cell death.
45
How do infectious agents contribute to cellular injury?
Infectious agents (e.g., bacteria, viruses, parasites, fungi) can lead to:
1. Cellular infection: Direct invasion and damage to cells.
2. Toxin production: Toxins released by pathogens can cause cellular damage.
46
What are immunological reactions that can cause cellular injury?
• Autoimmune disorders: The immune system attacks the body’s own cells.
• Hypersensitivity reactions: Overreaction of the immune system to harmless substances, leading to tissue damage.
47
How do genetic abnormalities cause cellular injury?
• Genetic abnormalities, either congenital or acquired, result in faulty protein production or function.
• These can involve entire chromosomes or single genes, leading to dysfunctional cellular processes.
48
What role do nutritional imbalances play in cellular injury?
• Increased caloric intake: Leading to obesity, which causes cellular stress.
• Decreased caloric intake: Nutrient deficiencies can impair cellular function and repair.
49
How does aging contribute to cellular injury?
• Cellular senescence: As cells age, they lose their ability to adapt to stresses.
• Senescence: Deterioration over time, making cells less capable of repair and function.
50
What is oxidative stress, and how does it contribute to cellular injury?
• Free radicals are molecules with a single unpaired electron in their outer orbit, causing damage to cells.
• Normally, the body produces free radicals, but scavengers (antioxidants) degrade and remove them.
• Oxidative stress occurs when there’s excess free radicals or inadequate removal, leading to cell damage.
• Implicated in cancer, aging, Alzheimer’s disease, and general cell injury.
51
How do antioxidants help in the removal of free radicals?
• Antioxidants block the production of free radicals or inactivate them.
• They act as scavengers, neutralizing harmful free radicals and preventing cell damage.
• Certain enzymes in the body also help neutralize free radicals as part of a natural defense system.
52
How does mitochondria damage lead to cellular injury?
• Mitochondrial damage affects energy production (ATP), impairing essential cell functions.
• It can lead to calcium imbalance, the release of reactive oxygen species (ROS), and activation of cell death pathways (e.g., apoptosis).
53
How does membrane damage cause cellular injury?
• Membrane damage disrupts the integrity of cell membranes and organelle membranes (like mitochondria and lysosomes).
• This can lead to leakage of enzymes and increased permeability, disrupting cellular homeostasis and leading to cell death.
54
How does nucleus/DNA damage result in cellular injury?
• DNA damage leads to mutations, cell cycle arrest, or failure to repair DNA.
• This damage can result in impaired cellular function or trigger apoptosis. Inability to repair DNA can lead to cancer or irreversible cellular dysfunction.
55
How does ATP depletion contribute to cellular injury?
• ATP depletion causes impaired energy production, which affects cellular processes like protein synthesis, ion transport, and cell repair.
• Without ATP, cells cannot maintain their structure or function properly, leading to cell injury and death.
56
What happens during incomplete phosphorylation in mitochondria?
• Incomplete phosphorylation in mitochondria leads to impaired oxidative phosphorylation, reducing ATP production.
• This can result in the formation of reactive oxygen species (ROS), causing further mitochondrial and cellular damage.
57
How does leakage of mitochondrial proteins contribute to cell injury?
• Leakage of mitochondrial proteins (like cytochrome c) triggers apoptosis (programmed cell death).
• This releases pro-apoptotic signals that activate caspases and lead to cell death pathways.
58
What is the impact of early loss of selective membrane permeability on the plasma membrane?
• The loss of selective permeability disrupts the cell membrane’s barrier function, allowing harmful substances to enter the cell and enzymes to leak out.
• This causes membrane damage and can lead to cellular swelling, necrosis, and cell death.
59
How do reactive oxygen species (ROS) contribute to membrane injury?
• ROS cause oxidative damage to lipids, proteins, and DNA in the cell membrane.
• This leads to increased membrane permeability, decreased integrity, and membrane breakdown.
60
What role do decreased phospholipid synthesis and increased phospholipid degradation play in plasma membrane damage?
• Decreased phospholipid synthesis impairs the membrane’s structural integrity, while increased degradation breaks down essential lipids in the membrane.
• This results in membrane instability, contributing to cell injury and death.
61
What are cytoskeletal abnormalities and how do they affect the plasma membrane?
• Cytoskeletal abnormalities disrupt the structural framework of the cell.
• This affects membrane stability, leading to membrane rupture, which is a key feature of necrosis.
62
What is the difference between hypoxia and ischemia is?
• A) Hypoxia is reduced blood flow and ischemia is reduced oxygen levels
• B) Ischemia is reduced blood flow and hypoxia is reduced oxygen levels
• C) Hypoxia is increased oxygen levels and ischemia is reduction in blood flow
• D) Hypoxia is when a cell is injured due to ischemia which is a reduction in
blood flow
B) Ischemia is reduced blood flow and hypoxia is reduced oxygen levels
63
What is the difference between reversible and irreversible cell injury?
• Reversible Cell Injury: The damage can be repaired, and normal function can be restored once the damaging stimulus is removed (to an extent).
• Irreversible Cell Injury: If the damaging stimulus persists, it leads to permanent damage and cell death.
64
What are the two types of cell death?
• Necrosis: Uncontrolled cell death due to severe injury, often accompanied by inflammation.
• Apoptosis: Programmed cell death, a controlled process to eliminate damaged or unnecessary cells.
65
What happens during reversible cell injury?
• The cell structure and function become abnormal but can return to normal if the damaging stimulus is removed.
• The cell may undergo swelling or fatty changes, but these are reversible if the cause is addressed.
66
What are the two major morphological changes in reversible cell injury?
1. Cellular Swelling: Due to increased permeability of the plasma membrane, causing an influx of water into the cell.
2. Fatty Change: Accumulation of triglycerides in lipid vacuoles in the cytoplasm, mainly seen in the liver.
67
What happens during cellular swelling in reversible injury?
• Cellular swelling occurs when the plasma membrane becomes more permeable, leading to an influx of water and ions into the cell.
68
What is fatty change in reversible cell injury?
• Fatty change occurs when triglyceride molecules accumulate in lipid vacuoles in the cytoplasm.
69
What are the additional morphological changes in reversible cellular injury?
• Plasma Membrane Alterations:
• Blebbing, blunting, or distortion of microvilli
• Loosening of intercellular attachments
• Mitochondrial Changes:
• Swelling
• Dilation of Endoplasmic Reticulum (ER):
• Loss of ribosomes
• Nuclear Alterations:
• Clumping of chromatin
70
What are the additional morphological changes in reversible cellular injury?
• Plasma Membrane Alterations:
• Blebbing, blunting, or distortion of microvilli
• Loosening of intercellular attachments
• Mitochondrial Changes:
• Swelling
• Dilation of Endoplasmic Reticulum (ER):
• Loss of ribosomes
• Nuclear Alterations:
• Clumping of chromatin
71
What are the additional morphological changes in reversible cellular injury?
• Plasma Membrane Alterations:
• Blebbing, blunting, or distortion of microvilli
• Loosening of intercellular attachments
• Mitochondrial Changes:
• Swelling
• Dilation of Endoplasmic Reticulum (ER):
• Loss of ribosomes
• Nuclear Alterations:
• Clumping of chromatin
72
What are the additional morphological changes in reversible cellular injury?
• Plasma Membrane Alterations:
• Blebbing, blunting, or distortion of microvilli
• Loosening of intercellular attachments
• Mitochondrial Changes:
• Swelling
• Dilation of Endoplasmic Reticulum (ER):
• Loss of ribosomes
• Nuclear Alterations:
• Clumping of chromatin
73
What happens in irreversible cellular injury?
• When a cell is exposed to persistent or excessive damaging stimuli, it passes a “point of no return,” leading to cellular death.
• There is no specific line for the transition from reversible to irreversible injury; it’s a gradual process that leads to permanent damage.
74
What are the two types of cellular death?
• Necrosis: Irreversible, uncontrolled cell death, often resulting from significant damage and inflammation.
• Apoptosis: Controlled, programmed cell death that occurs in response to damage or as part of normal cellular processes.
75
What are the characteristics of irreversible cellular injury?
1. Inability to restore mitochondrial function:
• Even after the original injury is resolved, the mitochondria fail to regain normal function.
2. Loss of structure and function of the plasma membrane and intracellular membranes:
• Membranes lose their integrity, leading to leakage of cellular contents.
3. Loss of DNA and chromatin structural integrity:
• DNA and chromatin undergo fragmentation, leading to cell death.
76
What are the two distinct features seen in cells with reversible cell injury?
Generalized swelling and fatty changex
77
All of the following are characterizations of irreversible cell injury,
except?
• A. Loss of DNA integrity
• B. Loss of function and structure of plasma membrane
• C. Increased lysosome function
• D. Inability to restore mitochondrial function
C. Increased lysosome function
78
What needs to occur to move from reversible to irreversible cell injury?
Exposure to persistent or excessive damaging stimuli
79
What happens if the damaging stimulus is not removed in cellular injury?
• The cell damage becomes irreversible and leads to cell death.
• There are two categories of cell death:
1. Necrosis
2. Apoptosis
80
What are the key differences between Necrosis and Apoptosis?
1. Inflammation:
• Necrosis causes inflammation as cellular contents leak out.
• Apoptosis does not cause inflammation.
2. Cellular Leakage:
• Necrosis leads to leakage of cellular content into surrounding tissues, causing damage.
• Apoptosis involves the formation of apoptotic bodies, which are then cleared without spilling their contents.
81
What is the difference between Necrosis and Apoptosis?
• Necrosis is accidental cell death that results from severe injury, leading to inflammation and cell damage.
• Apoptosis is programmed cell death, a controlled process that does not cause inflammation and is important for normal development and health.
82
What are the key characteristics of Necrosis?
• Accidental cell death caused by severe injury.
• Leads to local inflammation due to leakage of cellular contents.
• Characteristics:
• Denaturation of cellular proteins
• Leakage of contents through damaged membranes
• Local inflammation
• Enzymatic digestion of the injured cell
83
What leads to Necrosis?
• Reversible to irreversible injury: Once a cell reaches a “point of no return,” it cannot recover.
• Key factors causing necrosis:
• Mitochondrial dysfunction
• Membrane damage
• Loss of DNA/chromatin integrity
• Causes: Ischemia, toxins, chemical/physical injury
• All leads to membrane damage.
84
What are DAMPs and how do they contribute to necrosis?
• DAMPs (Damaged Associated Molecular Patterns) are cellular contents leaked through the damaged plasma membrane into the extracellular fluid.
• Components include ATP, uric acid, proteins, and other cellular organelles.
• DAMPs are recognized by macrophages in the extracellular fluid, initiating an inflammatory response.
85
What is the role of DAMPs in necrosis and inflammation?
• DAMPs (Damaged Associated Molecular Patterns) are released when cells undergo necrosis.
• They trigger an inflammatory response by activating the immune system, which leads to inflammation.
• DAMPs enter blood circulation and can be detected via blood work.
• Example: Cardiac Troponin is a DAMP that appears in the blood as soon as 2 hours after myocardial cell necrosis, indicating heart damage.
86
All of the statements are true, except?
• A. DAMPS are released when mitochondria break down with necrosis
• B. Cellular components are released when necrosis occurs
• C. Apoptosis doesn’t cause inflammation, but necrosis does
• D. Necrosis and apoptosis are a result of irreversible cell injury
A. DAMPS are released when mitochondria break down with necrosis
87
When a cell is undergoing necrosis it will shrink in size.
• A. True
• B. False
B. False
88
Describe the pathogenesis of necrosis and how it leads to inflammation.
Necrosis leads to membrane damage and the release of DAMPs. These DAMPs activate the immune system, causing inflammation that can become systemic and contribute to further tissue injury and healing.
89
What is the primary difference between necrosis and apoptosis in terms of inflammation?
• Necrosis causes inflammation due to the leakage of cellular contents into the extracellular space.
• Apoptosis does not cause inflammation because the cell’s contents are contained in apoptotic bodies and are phagocytized without triggering an immune response.
90
How does cellular leakage differ between necrosis and apoptosis?
• In necrosis, cellular contents leak into the extracellular space, leading to inflammation.
• In apoptosis, the cell breaks down into apoptotic bodies that are phagocytized without leaking harmful substances.
91
What causes inflammation in necrosis?
Inflammation in necrosis is caused by the leakage of cellular contents (such as DAMPs) into the extracellular space, which triggers an immune response.
92
What are DAMPs, and how are they related to necrosis?
DAMPs (Damage-Associated Molecular Patterns) are cellular contents (like ATP, proteins) that are released when cells die via necrosis. They trigger an inflammatory response when recognized by immune cells.
93
Does apoptosis lead to inflammation? Why or why not?
No, apoptosis does not cause inflammation because the cell undergoes controlled fragmentation into apoptotic bodies, which are cleared by macrophages without causing immune activation.
94
What is the key difference in the way necrosis and apoptosis affect surrounding tissue?
• Necrosis damages surrounding tissue through inflammation and leakage of cellular contents.
• Apoptosis leaves surrounding tissue intact as the cell is dismantled in a controlled, non-inflammatory way.
95
How do the mechanisms of necrosis and apoptosis differ in terms of cellular breakdown?
• In necrosis, cells rupture due to injury or stress, releasing their contents.
• In apoptosis, cells undergo programmed cell death where they shrink and break into apoptotic bodies without rupturing.
96
What is the key difference between necrosis and apoptosis?
• Necrosis is trauma-induced cell death leading to inflammation.
• Apoptosis is a regulated, programmed cell death without inflammation, where cells break into apoptotic bodies that are phagocytized.
97
What are apoptotic bodies?
Apoptotic bodies are plasma membrane-bound fragments of a cell that result from apoptosis. They are then phagocytized by immune cells without triggering an immune response.
98
How does apoptosis avoid inflammation?
Apoptosis avoids inflammation because the cell breaks into apoptotic bodies that are cleared by phagocytes without releasing harmful contents into the extracellular space.
99
In which physiologic situations does apoptosis occur?
Apoptosis occurs in processes like embryogenesis, hormonal withdrawal, cell turnover, and elimination of harmful lymphocytes or cells that have reached the end of their life cycle.
100
What are some pathological conditions that lead to apoptosis?
Apoptosis can occur in response to DNA damage, infections, misfolded proteins, or cellular stress, such as from excessive exposure to toxins (e.g., too much Mt. Dew).
101
What role do caspases play in apoptosis?
Caspases are proteases that, when activated, degrade the cell’s DNA, proteins, and structures. Their activation is essential for a cell to undergo apoptosis.
102
What are the two main pathways to activate caspases in apoptosis?
• Intrinsic (Mitochondrial) Pathway: Triggered by DNA damage, oxidative stress, or growth factor withdrawal, leading to mitochondrial membrane permeabilization and release of pro-apoptotic molecules like cytochrome c.
• Extrinsic (Death Receptor) Pathway: Initiated by engagement of plasma membrane death receptors (e.g., TNFR1) that activate caspases.
103
What is the role of cytochrome c in apoptosis?
Cytochrome c is a mitochondrial protein that, when released into the cytoplasm, triggers the apoptotic cascade by activating caspases.
104
How does the extrinsic death receptor pathway activate apoptosis?
The extrinsic pathway is activated when death ligands bind to plasma membrane receptors like Fas, which then activate caspases and initiate apoptosis.
105
What is autophagy?
Autophagy is a process in which a cell “eats” its own contents by delivering cytoplasmic materials to lysosomes for degradation.
106
What are some physiological responses that involve autophagy?
Physiological responses to autophagy include exercise and aging, where it helps maintain cellular health and function.
107
In what pathological situations is autophagy involved?
Pathological responses include stress situations, where autophagy helps manage cellular damage and stress.
108
How does autophagy serve as an adaptive response?
During nutrient deprivation, autophagy is an adaptive response that helps the cell survive by recycling cellular components for energy.
109
What is the process of forming autophagosomes?
Autophagy involves a complex sequence of protein activations that ultimately result in the formation of autophagosomes, which are cytoplasmic vacuoles containing cellular material to be degraded.
110
What happens when autophagosomes bind to lysosomes?
Autophagosomes bind to lysosomes, and their contents are degraded by the lysosomal enzymes.
111
What statement is TRUE?
• A) Cytochrome C found within the mitochondria will lead to apoptosis
• B) The mitochondrial pathway of apoptosis has FADD activate the caspases
• C) A cell undergoing apoptosis will undergo swelling
• D) With the lack of survival signals, stimulation of synthesis of BAX/BAK occurs
D) With the lack of survival signals, stimulation of synthesis of BAX/BAK occurs
112
Describe how apoptosis occurs.
Apoptosis is a programmed and tightly regulated process, initiated through either intrinsic or extrinsic pathways, involving the activation of caspases that lead to the degradation of cellular components and the formation of apoptotic bodies. This process is crucial for removing unwanted, damaged, or harmful cells without causing inflammation. Describe how apoptosis occurs.
113
What are the main morphological changes in cellular necrosis?
• Cellular swelling: Cells become enlarged due to ion pump failure and water influx.
• Cytoplasmic changes: Breakdown of organelle membranes.
• Nuclear changes:
• Pyknosis: Nucleus shrinks and chromatin condenses.
• Karyorrhexis: Nucleus fragments and chromatin disintegrates.
• Karyolysis: Nucleus swells and chromatin fades.
114
What is coagulative necrosis?
• Coagulative necrosis is the most common type, caused by ischemia or hypoxia.
• The affected tissue becomes firm and pale, with the basic tissue architecture preserved, but the cells within the tissue are dead.
• Infarct refers to the localized area of coagulative necrosis due to inadequate blood supply.
115
What causes cellular necrosis?
Cellular necrosis is caused by severe injury, leading to irreversible damage to cells. This can result from ischemia, toxins, infections, or physical damage, causing membrane damage and leakage of cellular contents.
116
What is the significance of recognizing necrotic morphology?
Recognizing necrotic morphology helps in identifying the underlying cause of necrosis (e.g., ischemia, infection). It can also differentiate between types of necrosis and guide treatment strategies.
117
How does an infarct form in tissue?
An infarct is a localized area of necrotic tissue caused by inadequate blood supply, typically due to coagulative necrosis following ischemia.
118
What is liquefactive necrosis?
• Liquefactive necrosis occurs when dead cells are completely digested by enzymes, leading to the tissue becoming soft and viscous.
• This type of necrosis typically happens in the brain or abscesses.
119
What is gangrenous necrosis and how is it classified?
• Gangrenous necrosis refers to the loss of blood supply leading to coagulative necrosis in multiple tissue layers.
• It is classified into two types:
• Dry Gangrene: Occurs due to slow reduction in blood supply, often from conditions like diabetes or atherosclerosis, causing tissues to become hard, black, and purplish, with no bacterial infection.
• Wet Gangrene: Results from a sudden loss of blood supply, often due to trauma (e.g., frostbite, blood clots), with bacterial infection present, leading to pus formation.
120
What is caseous necrosis and where is it commonly seen?
• Caseous necrosis involves necrotic tissue enclosed within a distinct inflammatory border, forming a granuloma.
• It is typically associated with chronic inflammation and infections like tuberculosis.
121
What is a granuloma?
• A granuloma is a mass or nodule of chronically inflamed tissue with granulations, often associated with an infectious process.
• It forms as a response to chronic infection, like tuberculosis.
122
What is fat necrosis and how does it occur?
• Fat necrosis is the destruction of fat cells, often due to the release of activated pancreatic lipases.
• It typically occurs in tissues such as the pancreas and surrounding areas.
123
What is fibrinoid necrosis?
• Fibrinoid necrosis is characterized by vascular (endothelial) damage, often seen in immune reactions involving blood vessels.
• Antigen-antibody complexes are deposited into the walls of blood vessels, resulting in a fibrinoid appearance.
124
What are the main features of cellular apoptosis morphology?
• Cell Shrinkage: The cell becomes denser and shrinks.
• Chromatin Condensation: The chromatin of DNA condenses, which is the most characteristic feature.
• Formation of Cytoplasmic Blebs/Apoptotic Bodies: The cell breaks into smaller droplets, called apoptotic bodies.
• Phagocytosis of Apoptotic Cells: The apoptotic bodies are phagocytized by neighboring cells.
125
What are intracellular accumulations, and what causes them?
• Intracellular accumulations refer to the abnormal buildup of substances within the cell, which can either be harmless or lead to injury.
• The four main mechanisms leading to abnormal accumulations are:
1. Inadequate removal
2. Defects in folding, packaging, transporting, or secretion
3. Failure to degrade a metabolite
4. Accumulation of abnormal exogenous substances
126
What is steatosis, and what causes it?
• Steatosis (or fatty change) is the abnormal accumulation of triglycerides in cells or organs, particularly the liver.
• It can result from metabolic disturbances such as excessive alcohol consumption, obesity, or diabetes.
127
How does cholesterol accumulation occur in the body?
• Cholesterol accumulation, specifically LDL (low-density lipoprotein), can lead to conditions like atherosclerosis.
• It results from an imbalance in cholesterol metabolism, leading to the deposition of cholesterol in the arteries.
128
What is the cause of protein accumulation in cells?
• Protein accumulation can happen for a variety of reasons, often due to the aggregation of abnormal proteins, such as denatured or misfolded proteins.
• This can be associated with diseases like Alzheimer’s or Parkinson’s, where protein buildup occurs in the brain.
129
What causes excessive glycogen accumulation in cells?
• Excessive glycogen accumulation results from abnormalities in glucose or glycogen metabolism.
• This may be seen in conditions like glycogen storage diseases.
130
What is lipofuscin, and where is it commonly found?
• Lipofuscin is an insoluble, brownish-yellow granular intracellular material.
• It accumulates in various tissues with aging or atrophy and is commonly referred to as “wear-and-tear pigment.”
131
What is hemosiderin, and how does it accumulate?
• Hemosiderin is a hemoglobin-derived granular pigment that is golden yellow to brown.
• It accumulates in tissues when there is a local or systemic excess of iron, often seen in conditions like hemochromatosis or repeated blood transfusions.
132
This type necrosis morphology is associated with a granuloma
• A. Caseous
• B. Liquefactive
• C. Coagulative
• D. Fibrinoid
A. Caseous
133
This type of nuclear changes involves the nucleus fragments and chromatin
disintegrates into granules?
• A. Pyknosis
• B. Karyolysis
• C. Karyorrhexis
• D. Paryolysis
C. Karyorrhexis
134
Which option is the most common type of tissue necrosis morphology?
• A. Caseous
• B. Liquefactive
• C. Coagulative
• D. Fibrinoid
C. Coagulative
135
This term is given for insoluble brownish-yellow granular intracellular material that accumulates in a variety of tissues with aging or atrophy?
• A) Senescence
• B) Lipofuscin
• C) Hemosiderin
• D) Dystrophic calcification
B) Lipofuscin
136
Steatosis is when there is an accumulation of cholesterol in a cell or organ.
• A) True
• B) False
B) False
137
6. This type of cellular accumulation is due to excessive amounts of iron?
• A) Melanin
• B) Lipofuscin
• C) Hemosiderin
• D) Dystrophic calcification
C) Hemosiderin
138
What is inflammation?
• A protective response involving host cells, blood vessels, and mediators aimed at eliminating the cause of cell injury and initiating repair.
139
What is the primary goal of inflammation?
• To eliminate the initial cause of cell injury, remove necrotic cells and tissues, and begin the repair process.
140
What happens after the damaging stimulus is removed in inflammation?
• The process of tissue repair is initiated.
141
Which type of tissues exhibit an inflammatory response?
• Vascularized tissues.
142
How does inflammation help in host defense?
• It delivers leukocytes and defense molecules from circulation to the site of infection or damage to eliminate offending agents.
143
Is inflammation part of innate or adaptive immunity?
• It is part of innate immunity.
144
What is the difference between innate and adaptive immunity?
• Innate immunity is the body’s first line of defense, providing a rapid, non-specific response, while adaptive immunity is specific, slower to activate, and involves memory cells.
145
What does the suffix “-itis” indicate?
• It indicates inflammation of a specific tissue or organ.
146
What are key components of the inflammatory response?
• Phagocytic leukocytes, blood vessels, antibodies, complement proteins, and chemokines.
147
Where are inflammatory cells found in the body?
• Some circulate in the blood, while others reside in tissues.
148
How can inflammation be harmful?
• The inflammatory response and repair process can cause significant tissue damage and contribute to disease.
149
Why is inflammation essential for survival?
• Without it, the body would be unable to fight infections, remove damaged tissue, or initiate repair, leading to severe complications or death.
150
How can inflammation itself lead to disease?
• If uncontrolled, the damage it causes can become the dominant feature of a disease.
151
What are the three main functions of inflammation?
• Limit the spread of pathogens/damaged tissue, remove cellular debris and foreign substances, and initiate tissue repair.
152
What are two major causes of inflammation?
• Trauma and infection
153
What are the main types of infections that can cause inflammation?
• Bacterial, viral, fungal, parasitic, and microbial toxins.
154
What determines the outcome of an infection-related inflammatory response?
• The type of pathogen and the host’s immune response.
155
How does tissue necrosis lead to inflammation?
• Cellular necrosis releases signals that trigger an inflammatory response.
156
What causes cell death?
• Trauma, ischemia, toxins, and infections.
157
Does apoptosis cause inflammation? Why or why not?
• No, apoptosis is a controlled form of cell death that does not trigger inflammation, unlike necrosis.
158
How do foreign bodies trigger inflammation?
• They can physically damage tissues or introduce pathogens, leading to an immune response.
159
What is an example of an endogenous substance that can trigger inflammation?
• Uric acid crystals (in gout) or cholesterol deposits (in atherosclerosis).
160
What type of immune reaction can cause inflammation?
• Hypersensitivity reactions, where the immune system overreacts to a stimulus.
161
What are the five cardinal signs of inflammation?
• Redness (rubor), warmth/heat (calor), swelling (tumor), pain (dolor), and loss of function (functio laesa).
162
What are the five steps (5 R’s) of the inflammatory response?
• Recognition, Recruitment, Removal, Regulation, and Resolution.
163
What happens during the Recognition phase of inflammation?
• The immune system detects a noxious agent or harmful stimulus.
164
What occurs during the Recruitment phase of inflammation?
• Leukocytes and plasma proteins are mobilized to the site of injury or infection.
165
What is the goal of the Removal phase?
• To eliminate the harmful stimulus and clear cellular debris.
166
Why is the Regulation phase important in inflammation?
• It ensures the inflammatory response stops once the threat is eliminated to prevent excessive tissue damage
167
What happens in the Resolution phase?
• The body heals, repairs, or replaces damaged tissue.
168
How does acute inflammation differ from chronic inflammation?
• Acute inflammation is rapid and self-limiting, whereas chronic inflammation is prolonged and may not completely eliminate the harmful stimulus.
169
What are the two main components of acute inflammation?
• A vascular reaction and a cellular response.
170
Why does chronic inflammation cause more tissue damage?
171
What is an example of a disease associated with chronic inflammation?
• Osteoarthritis.
172
Where can inflammation happen?
Any where in the body
173
What is the first step in the inflammatory vascular response?
• Dilation of small blood vessels, leading to increased blood flow.
174
What is the purpose of increasing blood vessel permeability during inflammation?
• It allows plasma proteins and leukocytes to leave circulation and enter tissues to fight infection and begin repair.
175
What two vascular changes contribute to edema?
• Dilation of small blood vessels and increased vessel permeability.
176
What is the role of leukocytes in inflammation?
• They migrate from capillaries, remove the damaging stimulus, and initiate tissue repair.
177
Which type of leukocyte arrives first at the site of acute inflammation?
• Neutrophils.
178
Which leukocyte follows neutrophils in the inflammatory response?
• Macrophages.
179
Which type of immune cells predominantly infiltrate tissues during chronic inflammation?
• Macrophages (sustain the inflammatory process), along with lymphocytes and plasma cells.
180
What causes tissue destruction in chronic inflammation?
• Ongoing inflammatory processes and immune cell activity.
181
How does chronic inflammation lead to tissue damage?
• The persistent presence of inflammatory cells and mediators damages the affected tissue.
182
What are examples of diseases associated with chronic inflammation?
• Osteoarthritis and hepatitis
183
What are the two key processes involved in tissue repair during chronic inflammation?
• Angiogenesis (formation of new blood vessels) and fibrosis (scarring).
184
. All of the following options are signs of inflammation, except…?
• A. Swelling
• B. Heat
• C. Pain
• D. Fever
• E. Redness
• F. All of the options are signs of inflammation
D. Fever
185
2. The ability to initiate tissue repair is part of the inflammatory process.
• A. True
• B. False
A. True
186
Fibrosis is commonly seen with acute inflammation.
• A. True
• B. False
B. False
187
Edema associated with acute inflammation is primarily due to:
• A. Broken blood vessels
• B. Vasodilation
• C. Leukocyte activation
• D. Increased vascular permeability
• E. Two of the answers are correct
E. Two of the answers are correct
188
All of the options are true regarding inflammation, except?
• A. Acute inflammation can happen within minutes
• B. Chronic inflammation primarily has neutrophil infiltration
• C. Chronic inflammation does not have as prominent local and systemic signs
• D. Hypersensitivity disorders can lead to chronic inflammation
• E. Acute inflammation has increased vascular permeability
B. Chronic inflammation primarily has neutrophil infiltration
189
What are chemical mediators of inflammation?
• Substances that initiate and regulate inflammatory reactions.
190
What are the four common characteristics of chemical mediators?
• They are produced only in response to stimuli, can stimulate other mediators, may be produced at the site of inflammation or derived from plasma precursors, and are short-lived.
191
What are two examples of stimuli that trigger the production of active mediators?
• Microbial products and substances released from necrotic cells.
192
How do mediators amplify or regulate inflammation?
• By stimulating the release of additional mediators.
193
Where can chemical mediators be produced?
• At the site of inflammation by specific cells or from inactive precursors in circulation.
194
Which cells are the major producers of chemical mediators at inflammation sites?
• Macrophages, dendritic cells, and mast cells.
195
What are plasma-derived mediators?
• Inactive precursors present in circulation that must be activated at the site of inflammation.
196
What is an example of a plasma-derived mediator?
• Complement proteins.
197
Why are chemical mediators short-lived?
• They quickly decay or are inactivated by enzymes to prevent excessive inflammation.
198
What are the five major categories of chemical mediators?
• Vasoactive amines, cytokines and chemokines, kinins, arachidonic acid metabolites, and complement system proteins.
199
Why are vasoactive amines named “vasoactive”?
• Because they affect blood vessels
200
When are vasoactive amines released during inflammation?
• They are among the first mediators released.
201
What are the two main vasoactive amines?
• Serotonin and histamine.
202
Where is serotonin found, and what is its role in inflammation?
• It is found in platelets and plays a role in inflammation and coagulation by causing vasoconstriction.
203
Where is histamine stored, and what are its effects?
• It is stored in mast cell granules and causes vasodilation and increased vascular permeability.
204
Which mediator is considered the principal initial mediator of inflammation?
• Histamine.
205
What are kinins?
• Vasoactive peptides derived from plasma proteins.
206
What is the most influential kinin?
• Bradykinin.
207
What are the effects of bradykinin?
• It increases vascular permeability and causes vasodilation, similar to histamine.
208
What are cytokines?
• Proteins secreted by many cells that mediate and regulate immune and inflammatory responses.
209
What are chemokines, and what is their function?
• They are smaller proteins that act as chemoattractants, guiding leukocytes to sites of infection or tissue damage outside of blood vessels.
210
What are arachidonic acid metabolites?
• Lipid mediators that regulate vascular and cellular inflammatory reactions.
211
What are the two main types of inflammatory mediators derived from arachidonic acid?
• Prostaglandins and leukotrienes.
212
Where is arachidonic acid found?
• In phospholipids of cell membranes.
213
How is arachidonic acid released from membranes?
• It is released when phospholipids are hydrolyzed by enzymes like phospholipase
214
What happens to arachidonic acid after it is released from the membrane?
• It is rapidly converted into bioactive chemical mediators called eicosanoids.
215
What are the three main types of eicosanoids?
• Prostaglandins, thromboxanes, and leukotrienes.
216
What roles do eicosanoids play in the body?
• They regulate inflammation and have other physiological functions.
217
Which enzyme converts membrane phospholipids into arachidonic acid?
• Phospholipase.
218
What are the two enzymes that metabolize arachidonic acid into prostaglandins and thromboxane A2?
• COX-1 and COX-2 (Cyclooxygenase).
219
Which enzyme metabolizes arachidonic acid into leukotrienes?
• Lipoxygenase.
220
What are the effects of leukotrienes?
• They mediate vascular and smooth muscle reactions.
221
What is the role of cyclooxygenase inhibitors in inflammation?
• They block COX-1 and COX-2 enzymes, which are involved in the production of prostaglandins.
222
What are some examples of cyclooxygenase inhibitors (NSAIDs)?
• Aspirin, Ibuprofen, and Naproxen.
223
Is acetaminophen (Tylenol) an NSAID?
• No, acetaminophen is not considered an NSAID.
224
What is the function of phospholipase inhibitors in inflammation?
• They block the formation of arachidonic acid, preventing the inflammatory pathway from proceeding.
225
Which class of drugs acts as phospholipase inhibitors?
• Corticosteroids.
226
What is the complement system?
• A collection of soluble proteins and their membrane receptors that play a key role in host defense against microbes and in pathological inflammatory reactions.
227
How many complement proteins are there?
• More than 20 complement proteins.
228
How are complement proteins activated?
• Complement proteins are present in inactive forms in plasma and are activated to become proteolytic enzymes that degrade other complement proteins.
229
What happens after complement proteins are activated?
• They trigger immunological and inflammatory responses.
230
What is the critical step in the activation of the complement system?
• The proteolysis of C3.
231
What are the three pathways that lead to the cleavage of C3?
• Classical pathway, alternative pathway, and lectin pathway.
232
How is the classical pathway initiated?
• By C1 binding to an antibody (IgM or IgG) that has combined with an antigen.
233
What triggers the alternative pathway?
• The absence of antibodies, where bacterial surface proteins or endotoxins activate C1.
234
How does the lectin pathway work?
• Plasma mannose-binding lectin binds to carbohydrates on bacteria and directly activates C1.
235
What are the three main outcomes of the complement system?
• Inflammation (C3a and C5a), opsonization (C3b), and cell lysis (C5b).
236
Which complement proteins are involved in inflammation?
• C3a and C5a.
237
How do C3a and C5a contribute to inflammation?
• They stimulate histamine release from mast cells, increasing vascular permeability and vasodilation, and recruit and activate leukocytes.
238
What is opsonization?
• It is the process by which a substance (like an antibody or C3b) binds to foreign microorganisms or cells, making them more susceptible to phagocytosis.
239
What role does C3b play in opsonization?
• C3b binds to the membrane of pathogens, acting as an opsonin to enhance phagocytosis.
240
What complement protein is involved in cell lysis?
• C5b.
241
What does C5b do in the complement system?
• C5b activates other complement proteins to form the Membrane Attack Complex (MAC).
242
What is the function of the Membrane Attack Complex (MAC)?
• MAC punctures holes in the cell membrane, leading to cell lysis
243
All of the options are true regarding histamine, except….?
• A. It causes vasodilation
• B. Released from mast cells
• C. Cyclooxygenase enzyme activity creates histamine
• D. It leads to vascular permeability
C. Cyclooxygenase enzyme activity creates histamine
244
NSAIDs block the production of arachidonic acid.
• A. True
• B. False
B. False
245
Both C3b and C5b are necessary for the MAC process to occur?
• A. True
• B. False
B. False
246
All of the options are true of opsonization, except?
• A. It is part of the complement system
• B. It is dependent upon the complement protein C3b
• C. Leads to a puncture in the cell membrane
• D. Causes phagocytosis of cell
C. Leads to a puncture in the cell membrane
247
All of the following options are outcomes of complement proteins, except?
• A. Opsonization
• B. Vasodilation
• C. Increased vascular permeability
• D. Phagocytosis
• E. All of the above are outcomes
E. All of the above are outcomes
248
What is the role of C3 convertase in the complement system?
• C3 convertase cleaves C3 into two fragments: C3a and C3b.
249
What are the functions of C3a and C3b?
• C3a: Leads to the recruitment and activation of leukocytes, increases vascular permeability, and causes vasodilation.
• C3b: Becomes attached to the cell or molecule where the complement is activated, forms and activates C5 convertase, and promotes opsonization.
250
What does C5 convertase do?
• C5 convertase cleaves C5 into C5a and C5b.
251
What are the functions of C5a and C5b?
• C5a: Leads to the recruitment and activation of leukocytes, increases vascular permeability, and causes vasodilation.
• C5b: Leads to the formation of the Membrane Attack Complex (MAC), which results in cell lysis.
252
What is the first step in the inflammatory response?
• The recognition of microbes and necrotic cells by cellular receptors and circulating proteins.
253
What are the primary stimuli that trigger recognition during inflammation?
• Cellular receptors for microbes, receptors for cell damage/necrosis, and plasma proteins recognizing microbes and cell damage.
254
What are PAMPs?
• Pathogen-Associated Molecular Patterns, which are molecular structures or portions of pathogens recognized by Pattern Recognition Receptors (PRRs).
255
What are DAMPs?
• Damage-Associated Molecular Patterns, which are derived from damaged cells and released extracellularly after tissue injury.
256
What are PRRs?
• Pattern Recognition Receptors are receptors found in various immune and inflammatory cells that detect PAMPs and DAMPs.
257
What is the role of Toll-Like Receptors (TLRs)?
• TLRs are a class of PRRs that are found on immune, inflammatory, and tissue cells. They activate transcription factors to stimulate the production of cytokines.
258
What are NOD-Like Receptors (Inflammasomes)?
• NOD-Like Receptors are intracellular soluble proteins that also function as PRRs, playing a role in detecting cellular stress and initiating inflammation.
259
All of the options are stimuli for recognition within inflammation,
except _____.
• A. Plasma proteins recognition of microbes and cell damage
• B. Increase leukocytes
• C. Cell receptors for necrosis
• D. Cell receptors for microbes
B. Increase leukocytes
260
Pattern recognition receptors (PRR) recognize PAMPs and DAMPs to initiate the inflammatory process.
• A. True
• B. False
A. True
261
What happens after PAMPs and DAMPs are recognized during inflammation?
• Leukocytes are recruited to the area where PAMPs and DAMPs were detected.
262
What two major changes are involved in the recruitment process during acute inflammation?
• Vascular changes and cellular changes (leukocytes).
263
What are the key components of vascular changes during acute inflammation?
• Vasodilation, increased vascular permeability, and adhesion of leukocytes.
264
What causes vasodilation during inflammation?
• Chemical mediators, such as histamine, relax smooth muscle, increasing vessel diameter.
265
What effects does vasodilation have on the body?
• It increases blood flow, leading to increased heat and redness (erythema) in the affected area.
266
What is the role of histamine in acute inflammation?
• Histamine is a chemical mediator that causes vasodilation and is responsible for the early manifestations of inflammation, such as increased heat and redness.
267
What happens after vasodilation in acute inflammation?
• Increased vascular permeability follows, causing endothelial gaps to increase and allowing proteins, leukocytes, and other components to leak into surrounding tissues.
268
What is the effect of increased vascular permeability on the body?
• It leads to swelling (edema) as fluids and other components leak out of the blood vessels.
269
Which cardinal signs of inflammation are associated with vasodilation and increased vascular permeability?
• Redness (rubor), heat (calor), and swelling (tumor).
270
What is stasis of blood flow, and what causes it?
• Stasis refers to slower blood flow, which is caused by increased vessel diameter and the loss of fluid during inflammation.
271
What is vascular congestion, and what effects does it have?
• Vascular congestion refers to the prolonged redness in the involved tissue due to RBC congestion. It also aids in the recruitment and migration of leukocytes
272
What is the main difference between non-inflammatory and inflammatory edema/swelling?
• Non-inflammatory edema has low protein and cellular content, while inflammatory edema has high protein and cellular content.
273
What is the fluid in non-inflammatory edema called?
• Transudate.
274
What is the fluid in inflammatory edema called?
• Exudate.
275
What is edema?
• Edema is the excess fluid in the interstitial tissue or serous cavities.
276
What is exudation in the context of inflammation?
• Exudation is the escape of fluid, proteins, and blood cells from the vascular system into the interstitial tissue or body cavities.
277
What characterizes exudate fluid?
• Exudate has a high protein concentration and contains cellular debris, indicating an inflammatory process.
278
What characterizes transudate fluid?
• Transudate has low protein content with little or no cellular material, caused by osmotic or hydrostatic imbalance rather than increased vascular permeability.
279
What is pus, and what does it contain?
• Pus is a purulent exudate rich in leukocytes, debris of dead cells, and microbes.
280
What happens as a result of vascular changes during acute inflammation?
• Vasodilation and loss of fluid from blood vessels, leading to stasis (blood congestion) and slower blood flow.
281
What is stasis in the context of inflammation?
• Stasis refers to slower blood flow, increased RBC concentration, and higher blood viscosity due to fluid loss from blood vessels.
282
What role do endothelial cells play during stasis in inflammation?
• Endothelial cells express Cellular Adhesion Molecules (CAM), which are essential for the recruitment of leukocytes to the site of inflammation.
283
What happens to leukocytes during the recruitment phase of inflammation?
• Leukocytes adhere to the endothelial wall and then squeeze through the blood vessel into the surrounding tissue, a process called diapedesis.
284
What is TRUE regarding vascular changes within inflammation?
• A. Serotonin release stimulates vascular changes
• B. Diapedesis is an outcome of vascular changes
• C. Monocytes are the primary leukocyte associated with recruitment
• D. Vascular changes cause redness, heat, and swelling symptoms
C. Monocytes are the primary leukocyte associated with recruitment
285
Describe how edema can occur due to inflammation.
Histamine leading to vasodilation and increased vascular permeability
286
An exudate has a high protein content.
• A. True
• B. False
A. True
287
What is the main function of leukocytes during acute inflammation?
• Leukocytes, including neutrophils and macrophages, phagocytize bacteria, microbes, necrotic tissue, and foreign substances.
288
What is stasis and how does it relate to leukocyte recruitment?
• Stasis refers to slower blood flow, increased RBC concentration, and higher blood viscosity, which triggers endothelial cells to express adhesion molecules (CAM) for leukocyte recruitment.
289
What is the process called when leukocytes exit the blood vessels and move to the surrounding tissue?
• This process is called diapedesis (also known as extravasation).
290
What is the role of Cellular Adhesion Molecules (CAM) during inflammation?
• CAMs on endothelial cells allow leukocytes to adhere to the blood vessel walls, facilitating their movement into tissues.
291
How do chemokines assist in leukocyte recruitment?
• Chemokines create a gradient that guides leukocytes to the site of inflammation, mediating their migration and extravasation.
292
What is the first phase of leukocyte recruitment in acute inflammation?
• Margination: Leukocytes move toward the endothelial surface due to changes in blood flow during stasis.
293
What happens during the second phase of leukocyte recruitment?
• Rolling and adhesion to the endothelium: Leukocytes “roll” along the endothelial surface and then adhere to it through interactions with adhesion molecules (CAM).
294
What is the process that occurs during the third phase of leukocyte recruitment?
• Transmigration (Diapedesis): Leukocytes squeeze between endothelial cells and exit the blood vessel into the surrounding tissue.
295
What occurs during the fourth phase of leukocyte recruitment?
• Migration into the interstitial tissues: Leukocytes move through the tissue toward the site of injury or infection, following a chemotactic gradient created by chemokines.
296
What are the two main leukocytes within acute inflammation?
• A. Macrophages and Monocytes
• B. Neutrophils and Macrophages
• C. Eosinophils and Neutrophils
• D. Neutrophils and Monocytes
B. Neutrophils and Macrophages
297
What is the process of the leukocytes squeezing between two endothelial
cells?
• A. Chemotaxis
• B. Diapedesis
• C. Cellular adhesions
• D. Stasis
B. Diapedesis
298
Chemotaxis is the process of leukocytes migrating to the source of injury.
• A. True
• B. False
A. True
299
What is the first step in inflammatory responses?
Recognition of microbes and necrotic cells by cellular receptors and circulating proteins.
300
What are PAMPs and DAMPs?
• PAMPs (Pathogen-Associated Molecular Patterns): Molecular patterns found on pathogens that are recognized by the immune system.
• DAMPs (Damage-Associated Molecular Patterns): Molecules released from damaged or necrotic cells that are recognized by the immune system.
301
What is the role of Toll-like receptors (TLRs) in inflammation?
TLRs are pattern recognition receptors (PRRs) found on immune, inflammatory, and tissue cells that activate transcription factors to stimulate the production of cytokines.
302
What are the main vascular changes during acute inflammation?
• Vasodilation: Increased blood flow, leading to heat and redness.
• Increased vascular permeability: Fluid and proteins leak into the surrounding tissue, leading to swelling.
303
What is the difference between exudate and transudate?
• Exudate: Fluid with high protein and cellular content, associated with inflammation.
• Transudate: Fluid with low protein content, usually resulting from osmotic or hydrostatic imbalance, not inflammation.
304
What are the cardinal signs of inflammation and what causes them?
• Redness (erythema) and Heat: Caused by vasodilation and increased blood flow.
• Swelling: Caused by increased vascular permeability and fluid leakage into tissues.
• Pain: Often due to the release of chemical mediators like prostaglandins.
• Loss of function: May occur due to pain or tissue damage.
305
What is the role of neutrophils and macrophages in acute inflammation?
• Neutrophils: First responders to infection or injury, primarily involved in phagocytosis and killing pathogens.
• Macrophages: Later responders that also help in phagocytosis and play a role in tissue repair and regulating inflammation.
306
What are the four phases of leukocyte recruitment during acute inflammation?
1. Margination: Leukocytes move toward the vessel wall.
2. Rolling: Leukocytes slow down and begin to roll along the endothelium.
3. Adhesion: Leukocytes adhere to endothelial cells.
4. Transmigration: Leukocytes squeeze through endothelial gaps to enter the tissue.
307
What is phagocytosis, and what are the steps involved?
Phagocytosis is the process by which leukocytes ingest and digest particles such as pathogens and dead cells.
Steps:
1. Recognition and attachment of the particle.
2. Engulfment: Formation of a phagocytic vacuole around the particle.
3. Killing or degradation of the ingested material.
308
Which option defines the role of opsonins in acute inflammation?
• A. Provides digestive enzymes to break down foreign and dead materials and substances
• B. Allows for the chemotactic process to occur
• C. Provides an increased ability for a substance to be phagocytized
• D. Creates the pathway for apoptosis to occur in foreign substances
C. Provides an increased ability for a substance to be phagocytized
309
Opsonization can occur from the complement system and/or antibodies?
• A. True
• B. False
A. True
310
Commonly, chemical mediators are still secreted after the offending agent is removed?
• A. True
• B. False
B. False
311
What cardinal signs of inflammation are directly due to increased
blood flow and vascular permeability? (Select all that apply)
• A. Heat
• B. Pain
• C. Edema
• D. Redness
• E. Loss of function
A. Heat
C. Edema
D. Redness
312
Acute inflammation can lead to chronic inflammation when the
offending stimuli cannot be removed.
• A. True
• B. False
A. True
313
A similarity between acute and chronic inflammation is both tend to have
fibrosis occur in the resolution process?
• A. True
• B. False
B. False
314
All of the following options are mechanisms for the development chronic
inflammation, except?
• A. Autoimmune diseases
• B. Prolonged exposure to toxins
• C. Prolonged infection
• D. Hypersensitivity reactions
• E. All of the options are a common cause or initiation to chronic inflammation
E. All of the options are a common cause or initiation to chronic inflammation
315
Within chronic inflammation, activated neutrophils will lead to activation of
lymphocytes which in turn, activates more neutrophils.
• A. True
• B. False
B. False
316
All of the options are necessary for the process of scar formation, except?
• A. Fibroblasts
• B. Collagen fiber reorganization
• C. Neutrophil infiltration
• D. Angiogenesis
C. Neutrophil infiltration
317
Collagen fibers are initially laid down in a disorganized fashion and then are
re-organized to align along tension lines and eventually crossed linked.
• A. True
• B. False
A. True
318
Fibrosis can occur in the skin and within internal organs.
• A. True
• B. False
A. True
319
What is opsonization in the context of phagocytosis?
Opsonization is the process by which complement proteins or antibodies bind to antigens, making them more susceptible to phagocytosis by neutrophils and macrophages.
320
What role do opsonins play in phagocytosis?
Opsonins (such as antibodies or complement proteins) bind to pathogens or particles, marking them for phagocytosis by neutrophils and macrophages by making them recognizable to phagocytic cells.
321
What happens during the engulfment phase of phagocytosis?
Leukocytes express receptors for opsonins. When opsonized particles bind to these receptors, it triggers the engulfment of the particles and activates the leukocytes to enhance the degradation of the ingested material.
322
What occurs during the killing or degradation phase of phagocytosis?
Once the foreign particle is engulfed, it is enclosed in a phagocytic vacuole, which fuses with lysosomes to form a phagolysosome, where the ingested material is destroyed.
323
What are the five steps of the inflammatory process (the 5 R’s)?
1. Recognition of the noxious agent/stimulus.
2. Recruitment of leukocytes and plasma proteins.
3. Removal of the stimulus (microbes, dead cells).
4. Regulation to stop the inflammation once the stimulus is removed.
5. Resolution, where tissue healing, repair, or replacement occurs.
324
How is the regulation of inflammation mediated?
Inflammation regulation is mediated by chemical mediators produced during the process. Inflammation declines after the offending agent is removed, and anti-inflammatory mediators are produced to stop the process.
325
What is the fate of neutrophils after they perform their role in inflammation?
Neutrophils have a short lifespan in tissues, typically dying by apoptosis within hours to a day after leaving the blood, once their job is done.
326
What are the three potential outcomes of acute inflammation?
1. Resolution
2. Scar tissue formation
3. Chronic inflammation
327
What are the two types of tissue repair?
1. Regeneration – The tissue regains normal function.
2. Scar formation – Deposition of connective tissue, leading to a loss of function.
328
What happens during complete resolution of inflammation?
• The offending stimulus is eliminated.
• The damaged tissue is replaced with the same type of cells.
• Macrophages remove cellular debris and microbes.
• This occurs when the injury is limited and tissue damage is minimal.
329
What leads to scar tissue (fibrosis) formation?
• Scar tissue forms when there is substantial tissue damage or when the tissue is unable to regenerate.
• It involves the replacement of damaged tissue with connective tissue.
330
What is chronic inflammation, and when does it occur?
Chronic inflammation occurs when the acute inflammatory response cannot be resolved. This can happen due to:
• The persistence of the injurious agent.
• Interference with the normal healing process.
331
What defines chronic inflammation?
Chronic inflammation is inflammation that lasts for a prolonged duration (weeks to years), involving continuing inflammation, tissue injury, and healing, often with fibrosis.
332
How does chronic inflammation differ from acute inflammation in terms of cellular components?
• Acute inflammation: Primarily involves neutrophils.
• Chronic inflammation: Involves mononuclear cells, including macrophages, lymphocytes, and plasma cells.
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What are the characteristics of chronic inflammation?
• Infiltration with mononuclear cells (macrophages, lymphocytes, plasma cells).
• Tissue destruction, initiated by chemical mediators.
• Repair processes involving angiogenesis (new blood vessel formation) and fibrosis (scarring).
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What are the main causes of chronic inflammation?
1. Persistent infections (e.g., Mycobacterium tuberculosis, Hepatitis C virus).
2. Immune-mediated inflammatory diseases (e.g., hypersensitivity diseases, autoimmune diseases).
3. Prolonged exposure to toxic agents (e.g., inhaled particulate silica).
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What cells are primarily involved in chronic inflammation?
• Monocytes/Macrophages
• Lymphocytes
• Chemical mediators
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What is the role of macrophages in chronic inflammation?
• Macrophages differentiate from monocytes when they exit the blood and enter tissues.
• They help eliminate injurious agents, initiate repair, and are responsible for much of the tissue injury in chronic inflammation.
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What are the different names for macrophages depending on their location?
• CNS: Microglial cells
• Lungs: Alveolar macrophages
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What are the outcomes of activated macrophages in chronic inflammation?
A. Eliminate injurious agents
B. Initiate the process of repair
C. Responsible for much of the tissue injury in chronic inflammation
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What role do lymphocytes play in chronic inflammation?
• Lymphocytes are involved in both adaptive immunity and innate immunity, and they regulate the inflammatory process.
• They are key in strong chronic inflammatory responses, particularly in autoimmune and hypersensitivity diseases.
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What are the types of lymphocytes involved in chronic inflammation, and their roles?
• B Lymphocytes: Differentiate into plasma cells which produce antibodies.
• T Lymphocytes: Include T helper cells and cytotoxic T cells.
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What are the two types of tissue repair?
Regeneration: Regaining the normal function of injured tissue.
Scar formation: Deposition of connective tissue, leading to a loss of function of tissue, also known as scarring/fibrosis.
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What are the steps involved in scar formation (fibrosis)?
1. Formation of granulation tissue
2. Collagen synthesis and secretion
3. Remodeling of scar tissue
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What happens during the formation of granulation tissue in tissue repair?
• New connective tissue and blood vessels fill in the “gap” of a wound.
• Provides a replacement scaffolding for the damaged area.
• Angiogenesis (the formation of new blood vessels) occurs, and blood flow is crucial for healing.
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Why is blood flow important in the formation of granulation tissue?
• Blood flow is needed to deliver nutrients, oxygen, and growth factors to the damaged area.
• Any impairment of blood flow or blood vessel formation can slow the healing process.
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What role do fibroblasts play in collagen synthesis during tissue repair?
• Fibroblasts are key in synthesizing collagen, elastic fibers, reticular fibers, and other extracellular matrix (ECM) components.
• They migrate to the damaged area, proliferate, and secrete ECM components, forming a matrix that bridges the gap in the tissue.
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How is collagen deposited during tissue repair?
• Collagen fibers are initially deposited in a disorganized manner during the early stages of scar formation.
• This results in a weaker tissue than the original and can contribute to the characteristic raised appearance of scars.
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What happens during the remodeling of scar tissue?
• Connective tissue in the scar continues to be modified and remodeled.
• This process can take several months to years after the initial injury.
• It involves a balance between synthesis and degradation of ECM proteins.
• Collagen fibers are reorganized and aligned along tension lines, improving strength and flexibility.
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What enzymes are involved in the degradation of ECM proteins during scar tissue remodeling?
• Matrix metalloproteinases (MMPs) are the enzymes responsible for the degradation of collagen fibers and other ECM components.
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How are collagen fibers reorganized during the remodeling phase of scar tissue?
• Collagen fibers become organized and aligned along tension lines and are cross-linked to improve the strength and flexibility of the scar tissue.
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What role do myofibroblasts play in wound healing during the remodeling phase?
• Myofibroblasts assist with wound contraction, helping to close the wound during healing.
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What is the outcome of scar tissue maturation?
• As the scar matures, it becomes less red, raised, and firm.
• Blood vessels that initially formed to supply healing tissue regress, making the scar less vascular.
• This maturation results in a stronger, less prominent scar.
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What are contracture and hypertrophy in the context of scar tissue?
• Contracture: The scar tissue may contract further, reducing range of motion.
• Hypertrophy: In severe injuries or burns, the scar tissue may become excessively thick, leading to a hypertrophic scar or keloid.
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What factors influence the rate and outcome of tissue repair?
• Extrinsic factors: Infection, nutrition, glucocorticoids, mechanical variables, foreign bodies, location of injury.
• Intrinsic factors: Aberrations of cell growth, poor perfusions.
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What is a keloid?
• A keloid is an overgrowth of scar tissue due to excessive accumulation of collagen fibers, often resulting in a raised, thickened scar.
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What is fibrosis?
• Fibrosis is the process where normal parenchymal cells are replaced by connective tissue, leading to the formation of a scar.
• It involves excessive deposition of collagen and ECM components.
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How are the terms “scar” and “fibrosis” related?
• The terms “scar” and “fibrosis” are often used interchangeably.
• However, fibrosis typically refers to excessive collagen deposition in chronic diseases.
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How does fibrosis contribute to organ dysfunction?
• Chronic fibrosis in organs like the lungs (pulmonary fibrosis) or liver can lead to organ dysfunction and, if left unresolved, organ failure.
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What causes fibrosis in tissues?
• Fibrosis is induced by persistent injurious stimuli, such as infections, immunologic reactions, and other types of tissue injury.
