Midterms topic 1 Flashcards
(118 cards)
1
Q
Body’s overall reaction to injury or invasion by an infectious agent.
A
Inflammation
2
Q
Each individual reactant plays a role in following processes:
A
- initiating
- amplifying
- or sustaining the reaction
3
Q
Primary objective of Inflammation
A
To localize and eradicate the irritant and repair the surrounding tissues.
4
Q
Purpose of localizing the area of inflammation
A
To prevent it from becoming systematic
5
Q
Prolonged inflammatory response cause severe consequences on the body due to:
A
release of cytokines, chemokines, and the action of your macrophages.
6
Q
body’s immune system causing harm or damage to its own
A
Auto immune disease
7
Q
Major events of ACUTE inflammation
A
- Increased blood supply to the infected area
- Increased capillary permeability
- Migration of white blood cells
- Migration of macrophages to the injured area
8
Q
Released from injured mast cells that causes vasodilation, which increases blood supply/flow
A
Chemical mediators like Histamine
9
Q
Due to increase blood supply and vasodilation
A
Rubor (redness)
10
Q
Due to the release of histamine and other chemical mediators brought upon by the dilation of blood vessels
A
Calor (Heat)
11
Q
Chemical mediators such as histamine, which are released from injured mast cells, cause dilation of the blood vessels and bring additional blood flow to the affected area, resulting in Rubor and Calor.
A
Increased blood supply to the infected area
12
Q
The increased permeability of the vessels allows fluids in the plasma to leak to the tissues caused by contraction of the endothelial cells lining the vessels, thus some plasma would go to the tissue which result to Tumor and Dolor.
A
Increased capillary permeability
13
Q
Major type of cell present in acute inflammation
A
Neutrophils
14
Q
neutrophils migrate from the capillaries to the surrounding tissue
A
Diapedesis
15
Q
Soluble mediators that act as chemoattractant to initiate and control the response
A
Chemokines
Cytokines
Acute-phase reactants
16
Q
Neutrophils are mobilized within ______(1)________ after the injury and their emigration may last ________(2)__________.
A
- 30-60 minutes
- 24-48 hours
17
Q
Neutrophils move inside the blood vessels in the process known as _______________.
A
Rolling
18
Q
The ______(1)________ on the neutrophil will bind with the ________(2)_________ on the endothelial cells allowing it to roll on the blood vessel wall.
A
- L-selectin
- Sialyl-Lewis X
19
Q
Carbohydrate structures that bind to the L-selectin
A
Sialyl - lewis x
20
Q
Neutrophils adhere to the blood vessel wall prior to being squeeze out through binding themselves to ____________________.
A
Integrin
(L-selectin - rolling; Integrin - adhesion)
21
Q
An event if inflammation that involves the migration of macrophages dendritic cells from surrounding tissue and from blood monocytes
A
Migration of macrophages to the injured area
22
Q
Peak of the migration of macrophages/dendritic cells
A
16-48 hours
23
Q
Stimulate phagocytosis of microorganisms
A
Acute phase reactants
24
Q
There are instances that inflammation is triggered without breached in innate immune system through _______________.
A
Hypoxia
25
What is hypoxia?
o Decrease in oxygen
o Usually happens in
organ grafts which triggers inflammation and rejection of the
transplanted organ.
o Has multiple effects on the innate and adaptive
immune systems
26
Prolonged inflammation
Chronic; failure to eliminate the irritant, which caused continuous damage.
27
Decrease in oxygen and nutrients. It also increases the risk of inflammation and graft failure or rejection.
Ischemia
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What is SIRS
Systematic Inflammatory Response Syndrome
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Criteria for SIRS:
1. Alteration of body temperature (>38°C or <36°C)
2. Increased heart rate
3. Increased respiratory rate
4. Total leukocyte count of >12.0 × 109/L (or >10% immature forms)
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SIRS + Infection
Sepsis
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Sepsis + Organ dysfunction
Severe Sepsis
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Decrease blood pressure + shock
Septic Shock
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Sepsis begins when…
when the innate immune system responds aggressively to the presence of bacteria.
34
__________________ of bacteria cause the antigen presenting cell (APC) to produce proinflammatory cytokines (also a biochemical marker associated with sepsis)
Toll - like receptors
35
Pro-inflammatory Cytokines:
Tissue Necrosis Factor - alpha
IL 6
IL 1
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produce systemic inflammation by activating circulating polymorphonuclear leukocytes (PMNs)
Pro-inflammatory cytokines (TNF-alpha, IL 6, IL 1)
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TNF alpha, IL 6 and IL 1, trigger the release of substances that follows thrombin formation. What are these substances?
Platelet activating factor
Plasminogen activator inhibitor
Leukotruenes
Arachidonic acid
38
involve the adaptive immune system by presenting bacterial antigen to T-cell
39
Co-stimulation of CD28
APC
40
APC uses what MHC protein?
MHC II
41
Gaining notoriety as a very effective biomarker of infection and systemic inflammation that increases in response to pro-inflammatory stimulus, especially of bacterial origin
Procalcitonin
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Levels of procalcitonin in:
Viral -
Bacterial -
Viral - Normal
bacterial - increase
43
What happens to the levels of calcium and calcitonin if procalcitonin is increased in bacterial infection?
Remains normal;does not change
44
Main purpose of inflammatory response
attract cells to the site of infection and remove foreign cells or pathogens.
45
Process whereby specialized cells engulf and destroy foreign particles, such as microorganisms or damaged cells.
Phagocytosis
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Phagocytic cells
Segemented Neutrophils (PMNs)
Monocytes
Macrophages
Dendritic cells
47
Enumerate the steps of Phagocytosis:
1. Chemotaxis
2. Adherence
3. Engulfment
4. Phagosome maturation and phagolysosome formation
5. Destruction and digestion
6. Exocytosis
48
a change in the direction of movement of a motile cell in response to a concentration gradient of a specific chemical, chemotaxin.
Chemotaxis/chemotactic response
49
cells are attracted to the site of inflammation by chemical substances
Chemotaxis
50
Enumerate the acute phase reactants (chemical substances that attract cells)
1. Soluble bacterial factors
2. Complement components
3. C-reactive protein
51
Why is there a change in the direction of movement in chemotaxis?
Because usually when exiting the blood vessel they form zigzag pattern, and once they receive a signal from chemoattractant, they then zoom in to that, and that becomes their concentration gradient
52
Function as chemoattractants
Antigens
53
Identify which step of Phagocytosis: when antigenic material is present in the body, phagocytes are attracted to its source by moving up its concentration gradient. Phagocytes detect antigens using various cell surface receptors.
Adherence
54
Enumerate the substances or attachment devices that enhance phagocytosis
1. Opsonins
2. Complement receptor
3. FC receptors
55
It binds the Fc portion of antibody molecules,
FC receptor
56
It binds the Fc portion of antibody molecules
FC receptor
57
Serum proteins that attach to a foreign cell or pathogen and help prepare it for phagocytosis
- It enhances the binding process of receptors on neutrophils, macrophages, and dendritic
Opsonins
58
Sequence of cells arriving at the site of infection
Neutrophils → Monocytes → Macrophages and Dendritic cells
59
Once contact with surface receptors occurs, ___________ secrete chemoattractants such as cytokines and chemokines; these recruit additional cells to the site of infection.
Phagocytic cells
60
Five steps appear to be necessary for effective leukocyte recruitment to the site of injury
1. Capture
2. Rolling
3. Slow rolling
4. Firm adhesion
5. Transmigration
61
the cell membrane invaginates and pseudopodia (outflowing of cytoplasm) surround the pathogen.
Engulfment
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The pseudopodia fuse to completely enclose the pathogen, forming a structure known as a_______________.
Phagosome
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Fusion between granules and phagosome
Phagolysosome
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The granules contain the following and are released into the phagolysosome and digestion occurs.
1. Lysozyme
2. Myeloperoxidase
3. and other proteolytic enzymes
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ingestion of particles, with the required energy primarily provided by anaerobic glycolysis.
Digestion
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Degradatory enzyme:
1. Primary -
2. Secondary -
3. Tertiary -
1. Primary (azurophilic) - lysozyme and myeloperoxidase
2. Secondary (Specific) - lactoferrin
3. Tertiary - caspases
67
releases antibacterial substances (e.g., lactoferrin, lysozyme, defensin) from the granules; released enzymes promote bactericidal activity by increasing membrane permeability.
Degranulation
68
How does the released enzymes promote bactericidal activity?
Increasing membrane permeability
69
one of several substances that can damage host tissues, is also released
Elastase
70
2 ways of eliminating pathogens
1. Oxygen - dependent pathway
2. Oxygen - independent pathway
71
An increase in oxygen consumption that occurs within the cell as the pseudopodia enclose the particle within a vacuole.
Oxidative/Respiratory burst
72
Drawback of O2-dependent pathways
The NADPH oxidase generates reactive oxygen species (ROS) by generating the superoxide radical (O2−); the associated cyanide-insensitive increase in oxygen consumption is the respiratory burst.
73
Reduces NADP to NADPH
HMP (Hexose Monosphate)
74
What happens when the NADPH Oxidase Complex (NOC) is assembled in the membrane of the phagolysosome?
NADPH reduces O2 to Superoxide
75
Catalyzes the conversion of superoxide to hydrogen peroxide
Superoxide Dimutase (SOD)
76
Important bactericidal agent and more stable than any of the free radicals
Hydrogen peroxide
77
Powerful oxidizing agent
Hypochlorite
78
Catalyzes the formation of hypochlorite
MPO (Myeloperoxidase)
79
Depolarizes the membrane when fusion with the
phagosome occurs, allowing hydrogen and potassium ions to enter the vacuole
NADPH oxidase
80
What happens when Hydrogen and Potassium ions enter the vacoule?
alters the pH, which in turn activates proteases that contribute to microbial elimination.
81
What are Defensins?
Defensins are small cationic ions that are released from the lysosomal granules. They have the ability to cleave segments of bacterial cell walls without the benefit of oxygen.
82
kill a wide spectrum of organisms, including
both gram-positive and gram-negative bacteria, many fungi, and some viruses
Defensins
83
Contents of phagolysosome are expelled to the outside by exocytosis.
Excretion
84
IDENTIFY:
- lymphocytes that are part of the innate immune response.
- the first line of defense against cells that are virally infected, cells infected with other intracellular pathogens, and tumor cells.
Natural Killer Cells
85
How is NK cells stimulated?
Exposure to Interleukin 12, Interferon alpha, and Interferon Beta
86
Activated NK Cells produce cytokines such as:
Interferon gamma
Tumor Necrosis Factor Alpha
Colony Stimulating Factors
87
What are the two main classes of binding receptors on NK cells?
1. Inhibitory receptors – which deliver inhibitory signals
2. Activating receptors – which deliver signals to activate the cytotoxic mechanisms.
88
If NK cells react with class I MHC proteins, then
_____________________________________.
inhibition of natural killing occurs.
89
NK cells are triggered by a lack of?
Lack of “missing self”
90
What are Perforins and Granzymes?
These are substances that are released by NK cells after being triggered:
Perforins
- are proteins that form channels (pores) in the target cell membrane.
Granzymes
- are packets of enzymes that may enter through the channels and mediate cell lysis.
91
A second method of destroying target cells is also available to NK cells. They recognize and lyse antibody-coated cells.
ADCC (Antibody-dependent cell cytotoxicity)
92
Produced primarily by hepatocytes that may act by binding to microorganisms and promoting adherence, help to limit destruction caused by the release of proteolytic enzymes from
WBCs as the process of phagocytosis takes place.
Hepatocytes
93
Some of the most important acute phase reactants are
C-reactive protein
Serum amyloid A Complement components Alpha1-antitrypsin
Haptoglobin
Fibrinogen
Ceruloplasmin.
94
Cytokines involved in the release of acute phase reactants
IL-1
IL 6
TNF - alpha
95
A trace constituent of serum that acts like an antibody and can be thought of as a primitive, nonspecific form of an antibody molecule
C-reactive protein
96
What are the antibody-like capabilities of CRP?
1. Opsonization (the coating of foreign particles)
2. Agglutination
3. Precipitation
4. Activation of complement by the classical pathway.
5. Promote phagocytosis by binding to specific receptors found on:
- Monocytes
- Macrophages
- Neutrophils.
97
Binding of CRP
Calcium dependent and nonspecific
98
Main substrate of CRP that is common in microbial membranes
Phosphocholine
99
The most widely used indicator of acute inflammation
CRP
100
Normal range of CRP
0.47 to 1.34 mg/L
101
CRP is easily destroyed by
Heating serum to 56 degrees celsius for 30 minutes
102
A lipoprotein that is synthesized in the liver and has high affinity for HDL cholesterol, as well as transported by HDL to the site of infection
Serum Amyloid A
103
Act as a chemical messenger, like a cytokine, and it activates monocytes
and macrophages to then produce products that increase inflammation.
Serum Amyloid A
104
Increases more in bacterial infection than viral
SAA
105
Reference range of SAA
5-8 ug/mL
106
Serum proteins that have the function of opsonization, chemotaxis, and lysis of cells
Complement
107
52-kD protein and a general plasma inhibitor of proteases released from leukocytes
Alpha1-antitrypsin
108
Defeciency of alpha1 antitrypsin can cause
Premature Emphysema
109
An anti 2globulin that acts as an antioxidant by binding to free hemoglobin to prevent oxidative damages
Haptoglobin
110
Reference range of haptoglobin
40 to 290 mg/dL
111
An acute-phase protein involved in the coagulation pathway that makes blood more viscous and serves to promote aggregation of redblood cells (RBCs) and platelets.
Fibrinogen
112
Increased levels of Fibrinogen is at risk of
Coronary Artery Disease
113
Reference range of Fibrinogen
200-400 mg/dL
114
It is the principal copper-transporting protein in human plasma.
Ceruplasmin
115
Function of Ceruplasmin
Converts toxic ferrous ion to non toxic ferric form
116
Autosomal recessive genetic disorder characterized by a massive
increase of copper in the tissues.
Wilson’s disease (due to the depletion of ceruplasmin)
117
Treatment of wilson’s disease
Liver transplant
chelation therapy (long term)
118
Reference range of ceruplasmin
20-40 mg/dL
