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Pathophysiology Exams > Pathophysiology Exam II > Flashcards

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
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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
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3
Q

Third Line of Defense

A

Adaptive, acquired immunity

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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
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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
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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
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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
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8
Q

Cytokines

A

responsible for activating other cells and regulating inflammatory response

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9
Q

Chemokines

A

induce chemotaxis (attraction of WBC) to promote phagocytosis and wound healing

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10
Q

Interleukins

A
  • work on leukocytes and give further instruction to them
  • IL-1 is pro-inflammatory, IL-10 is anti-inflammatory
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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
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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
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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”
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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
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15
Q

Chemotactic Factor

A
  • attract WBC
  • Neutrophil chemotactic factors – attract neutrophils
  • Eosinophil chemotactic factor – attract eosinophils
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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
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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
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18
Q

Exudative Fluids

A
  • serous exudate = watery exudate (early inflammation)
  • fibrinous exudate = thick, clotted exudate
  • purulent exudate = pus
  • hemorrhagic exudate = exudate contains blood
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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
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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
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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
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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
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22
Q

Dysfunctional Wound Healing

A
  • occurs during any phase of wound healing
  • dysfunctional collagen synthesis – keloid, hypertrophic
  • wound disruption – dehiscence, impaired contraction, contracture
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23
Q

Purpose of Adaptive Immunity

A
  • destruction of infectious microorganisms that are resist to inflammation
  • long-term
  • specific
  • long-lived
  • has memory
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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

Pathophysiology Exams (2 decks)

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