week 2 Flashcards
1
Q
cells that produce antibodies
A
Plasma cells
2
Q
cytokines
A
Chemical messengers secreted by immune and other cells
3
Q
opsonization
A
The process of covering bacteria with antibodies to promote phagocytosis of the microorganisms
4
Q
Where are neutrophils produced and stored in the body?
A
Bone marrow
5
Q
Benefits of normal flora
A
In the intestines, they produce some B vitamins and vitamin K, which are absorbed into the body. During childhood, normal development of the immune system. - produce antibacterial factors and employ other mechanisms that prevent pathogenic organisms from becoming established. Antibiotic therapy that disrupts normal flora may allow overgrowth of pathogens such as fungi. If normal flora are displaced into areas of the body that are usually sterile, or if an individual becomes immunocompromised, they can cause glossary iconopportunistic infection.
6
Q
most common bacterial forms
A
spherical (cocci), rodlike (bacilli), and spiral (spirochetes)
7
Q
viruses consist of…
A
nucleic acids (DNA or RNA) surrounded by a proteinaceous glossary iconcapsid. Some viruses have an external membrane called an envelope. Viruses replicate by entering host cells and using their viral nucleic acids to direct the host cell to make new virus.
8
Q
fungi
A
are eukaryocytes (have a nucleus) that take the form of yeasts (single-celled spheres) or molds, or both (dimorphic). They are not motile and have thick polysaccharide cell walls.
9
Q
parasites
A
include protozoa, helminths, and arthropods. Protozoa are single-celled intracellular parasites that are larger than bacteria and have an organized nucleus. These organisms frequently infect the gastrointestinal tract, although infection of the liver, lungs, central nervous system, and other locations is possible. Protozoal infections usually occur in the presence of infected water (e.g., amebiosis) or by sexual transmission (e.g., Trichomonas vaginalis), ingestion (e.g., Toxoplasmosis gondii), inhalation (e.g., Pneumocystis jerovici), or insect vectors (e.g., malaria).
10
Q
pus
A
contains dead phagocytic cells, protein, and debris from damaged cells, is associated with bacterial infections.
11
Q
dermatophyte
A
a fungus that attacks the skin
12
Q
tinea pedis
A
“athlete’s foot”
13
Q
candidiasis
A
(infection with Candida albicans) in warm moist skin areas
14
Q
vulvovaginal candidiasis)
A
vaginal yeast infections
15
Q
the 4 major types of infectious organisms
A
bacteria, viruses, fungi and parasites
16
Q
What are the risks if pathogenic bacteria enter the blood?
A
septic shock, multiple organ dysfunction syndrome (MODS), and death.
17
Q
Viral replication depends on the ability of the virus to penetrate a permissive host. . Name the steps
A
1 - binding of the virus to the surface of the host cell
2 - penetration into the cytoplasm (can be by endocytosis)
3 - virus sheds its capsid (uncoating)
18
Q
thrus
A
presence of Candida albicans in the oral cavity
19
Q
cestodes
A
tapeworms
20
Q
4 classic manifestations of chronic inflammation
A
redness, heat, swelling, and pain
Latin names rubor (redness), calor (heat), tumor (swelling), and dolor (pain)
A fifth clinical sign is loss of function (functio laesa).
21
Q
inflamation
A
a protective response to injury that occurs in vascular tissue (tissue that has blood vessels). It assists in removing pathogens and other sources of injury from the body, cleaning up tissue debris caused by the injury, and beginning the processes of tissue repair. usually beneficial but can damage normal cells if prolonged or severe
22
Q
Mast cells
A
are the most important activators of inflammation. They are tissue cells that release vasoactive and chemotactic chemicals from their granules in response to tissue injury and other stimuli.
23
Q
Neutrophils
A
(polymorphonucleocytes, or PMNs) are the first phagocytes to arrive at the inflamed site; they ingest bacteria and debris and secrete oxidizing chemicals and cytokines.
24
Q
Macrophages
A
second major phagocytes to arrive at an inflamed site; they are strongly phagocytic, and also secrete cytokines and growth factors. Circulating monocytes become macrophages when they enter tissues.
25
Eosinophils
increase inflammation by releasing chemicals or by acting directly on parasites.
26
Basophils
function much like mast cells and release numerous vasoactive and chemotactic mediators.
27
Platelets
prevent bleeding from injured vessels by participating in clotting; they also can enhance the inflammatory response through the release of several inflammatory mediators.
28
Mast cell granules
contain many inflammatory mediators, including histamine, proteolytic enzymes, and chemotactic factors. Tissue injury and some other stimuli cause mast cells to degranulate, releasing these chemical mediators that trigger the inflammatory process.
29
hypermia
increased blood flow to an area; happens when there is a brief vasoconstriciton followed by prolonged vasolilation
30
Cause of vasodilation in inflamation
chemical mediators released by mast cells and other cells that become activated; increased blood flow brings white blood cells, fluids and proteins to area of injury = red and warm
31
What's the role of chemichal mediators in inflamation?
cause endothelial cells to retract in the blood vessel, oepening the spaces b/n them which allows fluid, WBCs and proteins to move out of the vessel and into the tissues. = swelling
32
What's thr role of WBCs in inflamation?
adhere to the vessel walls near area of injury by sticking to endothelial adgesion molecules. roll down the surface of the endothelial cells toward the openings in the vascular wall and squeeze through them (diapedesis)
33
Marginization
Phagocytes move to the edges (margins) of postcapillary venules near the site of tissue injury or other cause of inflammation.
34
Rolling and Firm Adhesion
Phagocytes begin to adhere to the glossary iconendothelium via interaction of leukocyte and endothelial glossary iconadhesion molecules, and then roll down the endothelial surface until they adhere firmly and stop rolling. Endothelial and these leukocyte adhesion molecules include selectins, integrins, intercellular adhesion molecules (ICAM), and vascular cell adhesion molecules (VCAM), which appear in the cell membranes due to the action of inflammatory mediators.
35
Diapedesis
Phagocytes squeeze between endothelial cells and cross the basement membrane into the tissues. Additional adhesion molecules help the phagocytes move between the endothelial cells.
36
Chemotaxix
After leukocytes have exited blood vessels through diapedesis, they move through the tissues toward the area of injury by this process
37
The functions of phagocytes in inflammation
removing foreign invaders and dead cells, helping to induce adaptive immunity, and promoting healing by clearing cellular debris and secreting cytokines, growth factors, and angiogenesis factors.
38
polymorphonucleocytes, PMNs)
neutrophils - one of the phagocytes of the inflammatory response
39
Role of macrophages in inflammatory response
arrive at the inflamed area later than the neutrophils but continue phagocytosis for longer periods of time, secrete more cytokines, and can help present antigens to adaptive immune cells.
40
Eosinophils
Release inflamatory mediators that intensify inflamation and release chemicals that can kill tissue, which is useful in the case of a parasite but in other cases can cause damage to the body
41
cause for redness in inflammation
arises from vasodilation caused by the chemical mediators of inflammation. Because the blood is red, bringing more blood to the inflamed area causes the skin to appear redder than usual.
42
cause for heat in inflammation
arises from the increase in warm blood due to vasodilation and from increased cellular metabolism in the inflamed area. The inflamed area is warmer than the surrounding tissue
43
cause of swelling (edema) in inflammation
occurs when the blood vessels in the area develop increased permeability. Normally, only a few small proteins enter the interstitial fluid. With the increased vascular permeability of inflammation, many proteins from the blood move into the interstitial area and draw fluid with them by osmotic forces. This increase of fluid in the interstitial space causes swelling. Accumulation of leukocytes in the tissues also may contribute to the swelling.
44
cause of pain in inflammations
that accompanies inflammation arises in part from activation of pain receptors by chemical mediators of inflammation, such as histamine and bradykinin. In addition, prostaglandins sensitize pain receptors so that they are more likely to respond to those chemical stimuli. Pressure on pain receptors due to swelling may be another contributor to the pain of inflammation.
45
Loss of function with inflammation
may arise from self-limited movement due to pain and swelling that causes physical restriction and movement limitation. Inflammation inside the body also may cause reduced function due to cellular dysfunction, edema, or other processes that interfere with organ function.
46
Exudates
are protein-containing fluids that leak out of blood vessels during inflammation. Different types of exudates have different components
47
Serous exudates
watery (like serum), containing only small amounts of protein; they are associated with mild inflammation
48
Fibrinus exudates
are thick and sticky because they contain fibrinogen, which is converted to fibrin.
49
Purulent exudates
(pus) are rich in protein, dead neutrophils and other leukocytes, and bits of dead tissue. They are common with bacterial infection.
50
Hemorrhaggic exudates
as their name implies, contain many red blood cells due to rupture of capillaries that occurs with severe inflammation and tissue damage
51
Systemic manifestations of inflammation
fever, lethargy, increased number of white blood cells in the blood (leukocytosis), muscle catabolism, and increased acute phase proteins in the blood.
52
Cytokine action on the brain produces...
lethargy, loss of appetite, and fever
53
Cytokine action on skeletal muscles
protein breakdown
54
Cytokine action on bone marrow
leukocytosis
55
Cytokine action on the liver
release of acute phase proteins
56
Dangers of fever
increases oxygen demand and may exacerbate cardiac, cerebrovascular, or pulmonary pathophysiologies. Susceptible children can develop febrile seizures.
57
Benefits of fever
It likely improves the effectiveness of phagocytic cells that help rid the body of microorganisms and clean up tissue debris, as well as increasing the responsiveness of lymphocytes to antigens
58
Endogenous pyrogens
pro-inflammatory cytokines such as IL-1, IL-6, and TNF-alpha. These cytokines cause endothelial cells in the hypothalamus to synthesize and secrete prostaglandin E2 (PGE2), which triggers mechanisms that cause thermoregulatory neurons to regulate body temperature to a higher set point.
59
Exogenous pyrogens
such as bacterial endotoxin, stimulate production of the pro-inflammatory cytokines and also stimulate hypothalamic endothelial cells directly to produce PGE2, with resulting elevation of the hypothalamic set point.
60
Leukocytosis
(an increase in the white blood cell count) commonly accompanies inflammation. With acute inflammation, leukocytosis usually is due to neutrophilia (increased neutrophils in the blood).
61
Reasons for chronic inflammation
a persistent foreign body or toxic agents, an unresolved infection, or an autoimmune disease process that causes continued tissue damage
62
Granulomatous inflammation
a type of chronic inflammation in which leukocytes accumulate around a focus such as Mycobacterium tuberculosis, the microorganism that causes tuberculosis, and form a granuloma
63
3 phases of tissue healing
inflammation, reconstructive, maturation
64
Inflammation phase of tissue healing
in which any toxins are diluted, cellular debris and any microorganisms are removed by phagocytosis, and cytokines and growth factors are secreted to stimulate the next phase.
65
reconstructive phase of inflammation
(also called proliferative), in which the collagen matrix and granulation tissue are produced, epithelium covers the surface (if a surface wound), and new blood vessels develop. Wound contraction occurs at the end of this phase or the beginning of the last phase.
66
Maturation phase of inflammation
(also called remodeling), in which the collagen in the area is reorganized over an extended period of time.
67
Debridement
Activation of the plasma fibrinolytic system and release of lysosomal enzymes from neutrophils begins dissolving the clot. Macrophages phagocytize residual debris and secrete cytokines, growth factors, and angiogenesis factors.
68
Fibroblast proliferation
Growth factors secreted by macrophages and other cells stimulate fibroblasts to enter the area, proliferate, and begin collagen synthesis.
69
Angiogenisis
Vascular endothelial growth factor (VEGF) and other angiogenic factors cause growth of new blood vessels from endothelial precursor cells and by budding from nearby blood vessels. New blood vessels and fibroblast proliferation form granulation tissue, as shown in the photograph.
70
Collagen deposition
Collagen produced by fibroblasts fills the wound. This process is limited in wounds that can heal by primary intention, but it is extensive in larger wounds that require healing by secondary intention and in some cases of internal tissue healing, such as after a myocardial infarction (heart attack).
71
Re-Epithelialization
: If the wound is in the skin or a mucous membrane, epithelial cells grow over and seal the wound surface. The epithelial cells differentiate gradually into the mature cells of the epidermal layers.
72
Wound contraction
causes inward movement of the wound edges, especially noticeable in wounds that heal by secondary intention. glossary iconMyofibroblasts in the granulation tissue connect to neighboring cells and anchor themselves in the wound bed, promoting contraction.
73
Factors that can impair tissue healing:
prolonged or excessive inflammation, lack of inflammation, poor oxygen supply to the area, poor nutrition, and infection
74
Fibrosis
excessive secretion of collagen, with extensive scar formation
75
Components of Fluid Homeostasis
•Fluid intake by oral and other routes
•Fluid absorption from the gastrointestinal tract or other portal of entry
•Fluid distribution between the vascular and interstitial compartments and the interstitial and intracellular compartments
•Fluid excretion through the normal routes of urinary tract, bowels, lungs, and skin
Fluid loss through abnormal routes such as emesis and bleeding (abnormal)
76
cytokines
polypeptide signaling molecules that affect the function of other cells by stimulating surface receptors; function in a complex intercellular communication network; made from macfrophages or T helper cells - generally function as chemotactic factors (chemokines), antiviral factors, mediators of inflammation, hemotpoietic factors, or activaton signals for specific types of WBCs.
77
Inflamation
occurs when cells are injured; protective mechanism that begins healing process; 3 purpses: to netralize and destroy invading and harmful agents, to limit the spread of harmful agents to other tissue, and to preapre any damaged tissue for repair.
78
5 cardinal signs of inflammation
redness (rubor), swelling (tumor), heat (calor), pain (dolor), and loss of function (functio laesa).
79
events of the inflammatory process
1) increased vascular permeability
2) recruitment and emigration of leukocytes
3) phagocytosis of antigens and debris
80
vasoactive chemicals released during inflammatory process
prosaglandins, histamine, and leukotrienes; all relaesed by mast cells.
81
role of platelets in early phase of tissue inflammation
move into site and adhere to exposed vascular gollagen; release fibronectin to form meshwork trap and stimulate intrinsic clotting cascade to reduce bleeding; release peptide growth factors to stimulate bibroblast cell proliferation act as chemotactic factor; leads to fibrin clot;
82
Lymphatic blockage in inflammation
fibrin is deposited in the lympgh system and walls off the area of inflammation from the surrounding tissue and delays the spread of toxins
83
margination or pavementing
as blood flows through areas of inflammation, neutrophils move to sides of blood vessels and roll along endothelium of vessel all
84
How do neutrophils stick to endothelials cells in inflammation?
Injured tissue triggers the expression of adhesion molecules on surface of endothelial cells; adhesion molecules bind to receptors on neutrophis; called selectin and chmokine receptors
85
emigration or diapedesis
process of leukocytes passing through the blood vessel walls and migrating to inflamed tissue
86
pus
a collection of dead neutrophils, bacteria and cellular debris; macrophages ramein in the system to remove spent neutrophils and prepare the site for healing;
87
What is signal that chronic inflammation is beginning?
a predominance of monocytes and machrphages in an inflamed area
88
Which one of these people is at highest risk for wet gangrene?
A. Mr. Smythe, who had a heart attack (myocardial infarction).
Think again. Myocardial necrosis causes coagulative necrosis.
B. Mr. Henley, who had a stroke that cut off the blood supply to an area in the parietal lobe of his brain.
Think again. Necrosis in the brain causes liquefactive necrosis.
C. Mr. Jeffers, who has diabetes and atherosclerosis of arteries that supply his toes.
Think again. Although wet gangrene is possible if a necrotic toe becomes infected, toes are exposed to the air and are likely to develop dry gangrene. Wet gangrene is highly likely to develop in a situation described in another answer choice.
D. Mr. Tallis, who has a clot in an artery that supplies his jejunum and other portions of his bowel.
D. Correct Mr. Tallis, who has a clot in an artery that supplies his jejunum and other portions of his bowel.
89
Caseous necrosis occurs in which disease?
Tuberculosis
90
Which of the following mediators of inflammation are produced by mast cells from arachidonic acid after they degranulate?
A. Platelet activating factor
Think again. Platelet activating factor is produced from membrane phospholipids but not via the arachidonic acid pathway.
B. Histamine and chemotactic cytokines
Think again. Histamine and chemotactic cytokines are released by mast cells during degranulation and are not products of arachidonic acid.
C. Leukotrienes and prostaglandins
C. Leukotrienes and prostaglandins
91
By what mechanisms does hyperglycemia from diabetes mellitus increase the risk of infection?
A. Bypasses protective mucus and impairs action of cilia in the respiratory tract
Think again. Hyperglycemia does not bypass mucus or impair action of cilia in the respiratory tract.
B. Impairs phagocytosis and provides an environment for pathogen growth
Hyperglycemia impairs phagocytosis and provides an environment for pathogen growth.
C. Increases microbial virulence and suppresses multiple components of the immune system
Think again. Hyperglycemia does not increase microbial virulence.
D. Causes death of T helper cells and suppresses cell-mediated immunity
B. Correct Impairs phagocytosis and provides an environment for pathogen growth
Correct! Hyperglycemia impairs phagocytosis and provides an environment for pathogen growth.
92
A. Clotting factors
Think again. Clotting factors do not contribute to lethargy and anorexia during inflammation.
B. Correct Cytokines
Correct! Circulating cytokines contribute to lethargy and anorexia during inflammation.
C. Opsonins
Think again. Opsonins do not contribute to lethargy and anorexia during inflammation.
D. Incorrect Angiogenic factors
What circulating factors contribute to lethargy and anorexia as a systemic response to inflammation?
93
Endotoxin is a toxic substance formed from which of the following?
A. Destructive enzymes in viral secretions
Think again. Viruses do not secrete enzymes.
B. Correct Fragments of cell membranes from lysed gram-negative bacteria
Correct! When gram-negative bacteria are lysed, lipopolysaccharide fragments from their cell membranes become inflammatory stimuli called endotoxins.
C. Incorrect Lysosomal enzymes released by fungi growing within the body
Think again. Fungi do not release lysosomal enzymes.
D. Poisons released by gram-positive bacteria
answer is there
