Pathophysiology Exam II Flashcards
1
Q
First Line of Defense
A
- innate, natural immunity
- physical barriers: skin, lining of tracts, sloughing off cells, coughing, sneezing – body shedding off unwanted things
- epithelial cell-derived chemical barriers: secrete saliva, tears, earwax, sweat, mucus, and antimicrobial peptides (naturally kill off bacteria)
- normal flora
2
Q
Second Line of Defense
A
- inflammatory response
- first response to injury
- vascular responses – vasodilation, increased vascular permeability and leakage, WBC adherence
- nonspecific response
- causes = infection, tissue death, physical or chemical injury, foreign bodies, immune response, ischemia
- manifestations = redness, heat, swelling, pain, loss of function
3
Q
Third Line of Defense
A
Adaptive, acquired immunity
4
Q
Goals of Inflammation
A
- limit and control inflammatory process – exclusive to location of injury
- prevent and limit infection and further damage
- initiate adaptive immune response
- initiate healing
5
Q
Complement System
A
- main goal: destroy bacteria, clear away pathogens, destroy cells, and continue immune response
- Produces biologically active fragments that recruit phagocytes, activate mast cells, and destroy pathogens
- activation of C3 and C5
1) opsonin – coat bacterial cells with sticky substances so they can phagocytize
2) chemotactic factors – bring in WBCs
3) anaphylatoxins – cause mast cells to open
4) MAC – membrane attack complex against bacterial infection
6
Q
Coagulation System
A
- clotting system, prevents infection
- forms a fibrinous meshwork at an injured or inflamed site: prevents spread of infection, localizes foreign bodies, forms a clot, provides framework for repair and healing
- Fibrin
7
Q
Kinin System
A
- function is to activate and assist inflammatory cells and recruit more
- Bradykinin
- causes dilation of blood vessels, pain and smooth muscle contraction; increases vascular permeability
8
Q
Cytokines
A
responsible for activating other cells and regulating inflammatory response
9
Q
Chemokines
A
induce chemotaxis (attraction of WBC) to promote phagocytosis and wound healing
10
Q
Interleukins
A
- work on leukocytes and give further instruction to them
- IL-1 is pro-inflammatory, IL-10 is anti-inflammatory
11
Q
Tumor Necrosis - Alpha
A
- secreted by macrophages
- induces fever by acting as endogenous pyrogen
- increases synthesis of inflammatory proteins
- causes muscle wasting and blood clots
12
Q
Interferon
A
- stop reproduction of viral infection
- protects against viral infection
- Produced and released by virally infected host cells
- Protect neighboring healthy cells
13
Q
Mast cells
A
- cellular bags of granules located in loos connective tissue close to blood vessels
- contain histamine, cytokines, and chemotaxis factors
- basophils just “tag along”
14
Q
Degranulation
A
- release of contents the mast cell granules
- Histamine = vasoactive amine that causes temporary, rapid constriction of the large blood vessels and the dilation of the post-capillary venules
- H1 = pro-inflammatory, present in smooth muscle cells of the bronchi
15
Q
Chemotactic Factor
A
- attract WBC
- Neutrophil chemotactic factors – attract neutrophils
- Eosinophil chemotactic factor – attract eosinophils
16
Q
Synthesis of Mediators
A
- leukotrienes – induce muscle contraction in airway, similar effects to histamines
- prostaglandins – induce pain
- platelet activating factors – similar effects to leukotrienes and blood clotting
17
Q
Acute inflammation
A
- local manifestations = result from vascular changes and corresponding leakage of circulating components into the tissue
- systemic manifestations = fever, leukocytosis, increased plasma protein synthesis
18
Q
Exudative Fluids
A
- serous exudate = watery exudate (early inflammation)
- fibrinous exudate = thick, clotted exudate
- purulent exudate = pus
- hemorrhagic exudate = exudate contains blood
19
Q
chronic inflammation
A
- lasts two weeks or longer
- often related to an unsuccessful acute inflammatory response
- characterized by pus formation, suppuration, and incomplete wound healing
- caused by: large invading organisms, ability to survive inside macrophage, toxins, chemical, particulate matter, physical irritants
20
Q
Wound Healing Terms
A
- regeneration = replace damaged tissue with healthy tissue
- resolution = returning injured tissue to the original structure and function
- repairs = replacement of destroyed tissue with scar tissue
21
Q
Phases of wound healing
A
- inflammatory phase = coagulation, infiltration of wound healing cells, growth of new blood vessels
- proliferative phase = granulation, epithelialization, requires fibroblast proliferation, collagen formation, wound contraction
- remodeling and maturation phase = continuation of cellular differentiation, scar tissue formation scar modeling
21
Q
Phases of wound healing
A
- inflammatory phase = coagulation, infiltration of wound healing cells, growth of new blood vessels
- proliferative phase = granulation, epithelialization, requires fibroblast proliferation, collagen formation, wound contraction
- remodeling and maturation phase = continuation of cellular differentiation, scar tissue formation scar modeling
22
Q
Dysfunctional Wound Healing
A
- occurs during any phase of wound healing
- dysfunctional collagen synthesis – keloid, hypertrophic
- wound disruption – dehiscence, impaired contraction, contracture
23
Q
Purpose of Adaptive Immunity
A
- destruction of infectious microorganisms that are resist to inflammation
- long-term
- specific
- long-lived
- has memory
24
Q
Adaptive Immunity
A
- elements = antigens and lymphocytes
- components = kills target directly, stimulate other leukocytes, stimulate B-cells
- both produce memory cells and interact
25
Q
Active Immunity
A
Exposure to antigen, immunization
26
Q
Passive immunity
A
antibodies or T-cells are administered via infusion, transferred of maternal antibodies to fetus
27
Q
Antigens
A
binds with antibodies or receptor on T&B cells, foreign invader
28
Q
IgG
A
- most abundant
- protection against infection
- transported across placenta
29
Q
IgA
A
- found in body secretions
- anchored by J chain and “secretory” piece
- secretory piece may function to protect against enzyme degradation
30
Q
IgM
A
- largest immunoglobulin
- pentamer stabilized by J chain
- first antibody produced during the primary response to an antigen
31
Q
IgE
A
- least concentrated
- mediator of common allergic responses
- provides protection from large parasites
32
Q
IgD
A
- low concentration in the blood
- function as one type of B cell antigen receptors
33
Q
Antibody Functions (direct)
A
- neutralization = activate or block binding formation
- agglutination = clumps particles together
- precipitation = inactive invading organism
34
Q
Antibody Functions (indirect)
A
- inflammation
- phagocytosis – cell eating
- complement = cascade in plasma proteins
35
Q
Clonal Diversity
A
Train T&B cells how to recognize foreign invaders
36
Q
B-Cell production
A
Production in bone marrow, travel to lymphoid tissue and immunocompetent cells, produce antibodies (IgG)
37
Q
T-Cell Development
A
Thymus is the center of T-cell development, when exposed to antigen, they divide and produce as many T-cells
38
Q
T-Helper Lymphocytes
A
- helps maturation of T&B cells
- Th1 = provide help in developing cell-mediated immunity
- Th2 = provide help in developing humoral immunity
- Differences based on cytokine production
39
Q
B-Cell Clonal Selection
A
- when an immunocompetent B cell encounters an antigen for the first time, B cells are stimulated to differentiate and proliferate
- Differentiated B cell becomes plasma cell
- Plasma cell is a factor for antibody production
40
Q
T-Cytotoxic Cells
A
- destroys cancer cells, kill virus infected cells
- destroys them by “punching” holes in infected cell membrane
- reject foreign cell
41
Q
Aging and Immune Function
A
- decreased T-cell activity
- Thymus size is about 15% of its maximum size
- Thymus hormone production drops, as does organ’s ability to mediate T-cell differentiation
- decreased antibody response to antigens
42
Q
Communicability
A
method of transmission, ability to spread
43
Q
Immunogenicity
A
ability of pathogens to induce an immune response
44
Q
Infectivity
A
ability of pathogen to invade and multiply in host
45
Q
Pathogenicity
A
ability of agent to produce disease
46
Q
Toxigenicity
A
ability to produce soluble toxins or endotoxins, factors that greatly influence the pathogen’s degree of virulence
47
Q
Virulence
A
capacity of pathogen to cause severe disease
48
Q
Microorganisms portal of entry
A
- direct contact
- inhalation
- ingestion
- bite of animal or insect
- route of entrance may also become site of shedding new infectious agents to others
49
Q
Pathogen Defense Mechanisms
A
- bacteria: produce surface coats that inhibit phagocytosis and toxins
- viruses: can mutate within cells where they are not available to immune and inflammatory mechanism
50
Q
Toxin Production
A
- endotoxins = when the bacteria is killed off
- exotoxins = enzymes released during growth, cause specific responses
51
Q
Bacteremia
A
presence of bacteria
52
Q
Septicemia
A
growth of toxins in the body
53
Q
Viral infection
A
- Characteristics dependent on host cell
- No metabolism
- Simple Organism
- Spreads cell to cell
- Self limiting infection
- Messes up cellular function
- Releases enzymes to damage host cell
- Transform host cell to cancer cell
- Infected cells clump together
54
Q
Fungal Infection
A
- Large microorganisms
- Eukaryotes
- Single celled or multi celled
- Adapt to host environment
- Suppress immune defenses
- Controlled by phagocytes, T-lymphcytes
- can invade hair, skin, and nails
- Ringworm
55
Q
Clinical manifestations of infectious disease
A
- depends on the pathogen – can be directly or indirectly caused
- fever – beneficial, resets hypothalamus
56
Q
Countermeasures to fight infection
A
- antimicrobials – bactericidal (kill microorganisms) and bacteriostatic (inhibit growth)
- antimicrobial resistance – genetic mutations, inactivation, MRSA, can destroy normal flora
- vaccines – long lasting protective immune response that will not result in disease in a health recipient
57
Q
Immune Deficiencies
A
- failure of immune mechanisms of self defense
- clinical manifestations = recurrent infection, T-cell deficiencies
- primary deficiencies are RARE – single gene defect
- secondary deficiencies are ACQUIRED – caused by age, stress, malnutrition, malignancies, physical trauma
58
Q
AIDS
A
- caused by viral disease HIV
- depletes the body’s T helper cells
- blood borne pathogen, spread primarily through sexual activity, increase at a faster rate in women than men
- retrovirus – genetic information in the form of RNA, converts RNA to double stranded
59
Q
HIV
A
- sequence of symptoms = negative blood test, positive blood test with no symptoms, window period, AIDS diagnosis
- AIDS diagnosis = atypical or opportunistic infections and cancer, presence of antibodies against HIV, western blot analysis test
- treatment = HAART, reverse transcriptase inhibitors, protease inhibitors, new drugs or vaccine development
