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Patho > Ch 8- Infection and Defects in Mechanisms of Defense > Flashcards

Ch 8- Infection and Defects in Mechanisms of Defense Flashcards

1
Q

what are the factors that influence infection?

A
  1. Communicability: ability to spread from one induvidual to others and cause disease
  2. Infectivity: pathogen ability to invade and multiply in host involving attachment, escape of phagocytes and dissemination (spread)
  3. Virulence: severity or harmfulness of a disease or poison
  4. Toxigenicity: ability to produce toxins (greatly influence pathogens virulence)
  5. Portal of entry: route by which a pathogen infects host
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2
Q

what is a bacterial disease?

A

bacteria. prokaryotes, aerobic or anerobic, gram + or gram -
gram negative is more difficult to defeat due to outer membrane and porin channels

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3
Q

what is staphylococcus aureus?

A
  • Life threatening
  • Major cause of nosocomial infections
  • Common on normal skin and nasal passages
  • Virulent abilities:
    1. Produce protein that blocks compliment attack
    2. avoid innate immunity by producing inhibitors that avoid recognition
    3. when engulfed by pahgocyte they resist lysosome by changning chemistry of their cell walls
    4. resist ation of many antibiotics
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4
Q

what is the toxin production of bacterial disease?

A
  1. Exotoxins: released from inside of pathogen, has enzymes that damage host cell plasma membranes or inactivate enzymes critical to protein synthesis
  2. Endotoxins: released from outer capsule and activate inflammatory response and produce fever
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5
Q

what is bacteremia or septicemia?

A

the presence or the growth. these both result in defense mechanisms failure

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6
Q

what do endotoxins do?

A

activate inflammatory response by activavting complement and clotting systems= increased capillary permeability= large volumes of plasma into surrounding tissue= resulting in hypotension

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7
Q

what is a viral disease?

A

most common affliction of humans, replication requires entry into host cell, it is a simple organism of RNA/DNA surrounded by capsid and perhaps envelope, self limiting and it transmitted by aerosol, infected blood, sexual contact, vector

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8
Q

what are the cytopathic (causing damage to living cells) effects of viruses?

A
  1. Inhibit host cell DNA or RNA synthesis
  2. cause release of lysosomes into host cell, killing cell
  3. fusion of host cells into multicellular giant cell
  4. alteration of host cells antigen properties= immune system attacks own cells
  5. transforming host cells into cancerours cells= uninhibited growth
  6. Utilization of host cell resources
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9
Q

what is influenza?

A

highly contagious viral infection of respiratory passages

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10
Q

what is antigenic variation?

A

ability to change viral antigen yearly
- Antigens utilized to activate adaptive immune response
- Ability to change antigen= dysfunction adaptive immune response (B cell/ T cells)

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11
Q

what virus is responsible for COVID-19?`

A

SARS-CoV-2 virus

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12
Q

what is a fungal infection?

A

large eukaryotes with thick, rigid cell walls, resist penicillin, exist as single celled yeasts, multicellular molds, or both, reproduction: simple division or budding

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13
Q

what is mycoses?

A

diseases caused by fungi

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14
Q

what is dermatophytes?

A

fungi that invade skin, hair, or nails. diseases they produce are called “tineas”

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15
Q

what is pathogenicity of a fungal infection?

A

adapt to host environment (wide temperature variations, low oxygen), suppress immune defenses, low white-blood-cell count promotes fungal infection

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16
Q

what is candida albicans?

A

most common cause of fungal infections, found in normal skin microbiome, GI tract and vagina of many individuals, most common fungal infections in cancer patients and transplantations, disseminated infection in immunocompromised, death rate= 30-40%

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17
Q

what is a parasitic infection?

A

unicellular protozoa to large worms, spread to human via vectors, tissue damage due to toxin damage or inflammatory/immune response, plasmodium occurs in RBC

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18
Q

what are antibiotics?

A

natural products of fungi, bacteria or other microorganisms that affect growth of specific mircoorganisms

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19
Q

what are antimicrobials?

A
  • Bactericidal (agent that kills other microorganisms)
  • Bacteriostatic (agent that inhibits growth of other microorgansims)
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20
Q

what are well known safeguards againsnt infections?

A

-hand hygiene
-proper sanitary disposal
- water treatment (prevention of water contamination)
- sanitary food transportation, preparation and serving
- control of insect vectors/draining standing waters/mosquito
- support research

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21
Q

what is the timeline for countermeasures?

A

1944- penicillin effective at treating infection in british hospital
1946- 14% of all staphylococcus aureus penicillin resistant
1950- 59% resistant
1990- 89%

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22
Q

what has caused antibiotic resistance?

A
  • Lack of compliance with therapeutic regimen: not using antibiotics for prescribed duration resulting in strongest microbes are left alive= repopulation with pathogens resistant to specific antibiotics
  • Overuse of antibiotics: destruction of normal microbiome= opens space for more infectious/resistant pathogens
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23
Q

what is the benefical process of vaccines?

A
  • Adaptive response usually requires two-weeks to activate
  • Vaccine (containing pathogen antigen) allows this two-week period to
    be performed against a non-viral pathogen
  • Result: when infection by viral pathogen occurs, Adaptive Immunity
    already prepared (no two-week delay)
  • Vaccine mixture: DTaP vaccine (diphtheria, tetanus, pertussis)
  • HERD immunity usually requires 85% of population immunized
24
Q

what is a vaccine?

A

biological preparations of weakened or dead pathogens

25
Q

what are toxoids?

A

chemically altered pathogen toxin injected into body = allows body to learn to defeat pathogens toxin

26
Q

what is passive immunotherapy?

A

preformed antibodies are given to individual
- human immunoglobulin (antibodies obtained from pathogen survivor)
- becoming focus after rise of antibiotic resistance

27
Q

what is primary immunodeficiency caused by?

A

a genetic defect

28
Q

what is secondary immunodeficiency caused by?

A

another illness ex cancer

29
Q

what are some primary facts?

A

Most result of a single gene defect
mutations are sporadic and not inherited and occurs before birth
1/200 70% undiagnosed
categorized into groups based upon what aspect of immune system is defective

30
Q

What is severe combined immunodeficiency?

A

An underdeveloped thymus= absence of T cells, few detectable lymphocytes

31
Q

what is DiGeorge syndrome?

A

Thymus and parathyroid gland dysfunction= inadequate T cell production and management of plasma

32
Q

What is hypogammaglobulinemia?

A

result of defect in B cell maturation or function, lower levels of circulating immunoglobulins (antibodies) in blood

33
Q

what are some facts about secondary?

A

acquired deficiencies, far more common than primary but not as clinically relevant/degree of immune deficiency usually relatively minor

34
Q

what is complete blood count?

A

total numbers of RBC, WBC, platelets

35
Q

what does differential mean?

A

individual numbers of lymphocytes, granulocytes and monocytes

36
Q

what does quantitative determination of immunoglobulins determine?

A

subpopulations of immunoglobulins

37
Q

what is total complement of assay mean?

A

total number of complements in blood

38
Q

what are some replacement therapies for immune deficiencies?

A
  1. stem cell transplantation
  2. mesenchymal stem cell injection
  3. gene therapy
39
Q

what is AIDS caused by?

A

Human immunodeficiency virus (HIV)

40
Q

how does AIDS work?

A

HIV depletes your helper T cells which are necessary for activation of both T and B cells causing a dysruption in your immune system increasing your susceptibility to disease = AIDS

41
Q

what is the epidemiology of AIDS?

A
  • heterosexual activity is most common transmission
  • women constitute more than 50% of people infected
  • children contact virus from mothers across placenta/breastfeeding milk
42
Q

what are some difficulties with vaccine development with HIV

A
  • HIV genetically and antigenically variable
  • indiviudals have high levels of antibodies but they dont work properly causing antibodies in a vaccine to not even work
43
Q

what does epidemiology mean?

A

branch of medicine that deals with incidence, distribution, and possible control of diseases

44
Q

what is the treatment of prevention of HIV?

A

Anti-retroviral therapy (ART): a combination of entrance inhibitors/reverse transcriptase inhibitors/integrase inhibitors/protease inhibitors. Doesnt cure but reduces death significantly

45
Q

what is hypersensitivity?

A

altered immunological response to an antigen that results in disease or damage to host

46
Q

what are some types of hypersensitivity?

A
  • Allergy: harmful effects of hypersensitivity to environmental antigens
  • Autoimmunity: disturbance in immunological tolerance of self-antigens (immune system doesn’t recognize bodies own antigens)
  • Alloimmunity: immune reaction to tissues of another individual
47
Q

What are the mechanisms of hypersensitivity?

A

Type I: IgE mediated (ex hay fever)
Type II: tissue-specific reactions (ex hemolysis in medication allergies)
Type III: immune complex-mediated (ex gluten)
Type IV: cell-mediated (ex poison ivy)
- These mechanisms are interrelated and often include more than one type.

48
Q

what is anaphylaxis?

A

most rapid and sever immediate reaction (within minutes)

49
Q

what are the symptoms of anaphylaxis?

A
  • pruritis: sever itching
  • erythema: red patches on skin
  • vomiting
  • diarrhea
  • breathing difficulties
50
Q

what is the difference between immediate and delayed hypersensitivity reaction?

A

immediate: occurs within minutes or hours
delayed: occurs after 7 hours and are at maximal several days later

51
Q

what is type I hypersensitivity?

A
  • mediated by antigen-specific IgE and products of mast cells
  • most common reaction
  • initial exposure to allergen= IgE binding to mast cell receptors= person now considered “sensitized”
  • subsequent exposure to allergen= mast cells release of cytokines= hypersensitive reactions
  • Tissues with high (mast cells) are most commonly affected: skin, GI tract, pulmonary tract
52
Q

what does atopic mean?

A

individuals predisposed to developing allergies
- One parent has allergies= 40% chance offspring will
- Both parents have allergies= high of 80%

53
Q

what is Type II hypersensitivity?

A
  • often called cytotoxic hypersensitivity: antibody-mediated destruction of healthy host cells
  • immune reactions against a specific cell or tissue
  • called tissue-specific antigens because they attach only on plasma membranes of certain cells ex platelets have antigens found on no other cell in body
54
Q

what are the 5 mechanisms of tissue specific hypersensitivity (A,B,C,D,E)?

A

A) Cell is destroyed by antibodies and complements
B) Cell destruction through phagocytosis by macrophage
C) Tissue damage caused by toxic products produced by Neutrophils
- Soluble antigens from infectious agent or hosts own cells bind to cell surface
- Neutrophils are attracted/release their granules into healthy cells= damage cells
D) Antibody-dependent cell-mediated cytotoxicity (ADDC)
- Binding of IgG antibodies to antigens. This attracts natural killer cells that releases toxic substances that destory cell
E) Target cell malfunction

55
Q

what is type III hypersensitivity?

A

Antigen-antibody immune complexes are formed in circulation and later deposited in vessel walls or extravascular tissues

56
Q

what is type IV hypersensitivity?

A

does not involve antibodies/mediated by T cells
ex graft rejection or allergic reactions from poison ivy or metals= T cell activation= macrophage activation= tissue damage

Patho (7 decks)

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