Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathophysiology > 8. Infection and Defects in Mechanisms of Defense > Flashcards

8. Infection and Defects in Mechanisms of Defense Flashcards

1
Q

ability to spread from one individual to others and cause disease

A

communicability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

ability of a pathogen to invade and multiply in the host

A

infectivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

capacity of a pathogen to cause severe disease

A

virulence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ability of an agent to produce disease

A

pathogenicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does pathogenicity of an agent depend on?

A

their communicability, infectivity, extent of tissue damage, and virulence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

route to infect a host

A

portal of entry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

ability to produce soluble toxins or endotoxins (greater influence pathogen’s degree of virulence)

A

toxigenicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

opportunistic bacteria that is commonly found on skin and nasal passages but is also a major cause of HAI and abx resistance

A

staphylococcus aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

thick capsule that helps microbes adhere to plastic/prosthetics

A

biofilm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

T/F: S. aureus uses biofilms to colonize but doesn’t produce toxins

A

False: produces and secretes exotoxins as well as uses biofilms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

proteins created and secreted by the bacteria to have a virulence effect -> can damage plasma membranes or inactivate enzymes needed for protein synthesis

A

exotoxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Explain how endotoxins can activate inflammatory response and produce fever

A

When bacterial cell dies -> membrane is disrupted -> releases LPS (lipid A portion) -> lipid A exposed to the immune system -> causes fever, shock, and DIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what type of bacteria produce endotoxins?

A

gram-negative bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Explain what causes endotoxic shock

A

bacteria growing in blood (septicemia) -> release endotoxins -> activate complement and clotting systems -> increased capillary permeability -> large volumes of plasma escape to surrounding tissues -> hypotension -> shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

4 ways of transmitted viruses

A
  • aerosol - infected blood - sexual contact - vector (ex. mosquitos)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

changing of viral surface antigens to evade the immune system (seen in influenza)

A

antigenic variation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

antigenic drift vs shift

A
  • antigenic drift: minor change in surface antigens due to mutations -> leads to weakened protection against virus - antigenic shift: major change where genome is segmented and undergoes recombination (usually zoonotic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What 2 proteins classify influenza and what do they do?

A
  • H protein (hemagglutinin): attachment and fusion (entry into cell) - N protein (neuraminidase): facilitates release of viral proteins from host cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

large microorganisms w/ thick, rigid cell walls without peptidoglycan

A

fungus/mycoses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Because fungus cell wall is missing peptidoglycans, what medications are they resistant to?

A

penicillins and cephalosporins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q
  • most common cause of fungal infections - opportunistic fungus that is normally found in the skin, GI tract, and vagina but can cause localized infection if overgrown -> disseminates if immunocompromised
A

Candida albicans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

eukaryotic, unicellular microorganisms include malaria, amoeba, and flagellates

A

protozoa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

how do protozoa spread?

A

via vectors or ingestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Bactericidal vs Bacteriostatic

A
  • bactericidal: kill bacteria; # of cells in the colony will decline after administration of abx - bacteriostatic: arrest growth -> stops cells from doubling and allows host immune system to take care of them
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What causes antibiotic resistance?

A
  • genetic mutations - lack of compliance (selective resurgence) - overuse (destruction of normal microbiome)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

live viruses that are weakened

A

attenuated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Who should not receive live attenuated vaccines?

A

individuals w/ deficient or suppressed immune systems -> may cause life-threatening infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

purified exotoxins that have been chemically detoxified without the loss of immunogenicity (used in vaccines)

A

toxoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

countermeasure against pathogens where preformed antibodies are given to individuals

A

passive immunotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Lab/serum tests used to evaluate immunodeficiencies

A
  • CBC w/ diff - quantitative determination of immunoglobulins - assay for total complement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Name 6 types of treatments for immunodeficiencies

A
  • gamma-globulin therapy (IVIg) - stem cell transplantation - transfusion of erythrocytes - BM transplants - mesenchymal stem cell injection - gene therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What type of immunity are vaccines?

A

active artificial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What do bacteria produce to destroy penicillin and become resistant to it?

A

B-lactamase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

List the 6 stages of viral infection of a host cell

A
  • attachment - penetration - uncoating - replication - assembly - release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What do all viruses contain?

A

genome and capsid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

MOA of most antibiotics (4)

A
  • inhibition of function/production of cell wall/membrane - prevent protein synthesis - blockage of DNA replication - interference w/ folic acid metabolism
37
Q

primary vs secondary immune deficiencies

A
  • primary: congenital - secondary: acquired
38
Q

3 most common primary immune deficiencies

A
  • common variable immune deficiency - selective IgA deficiency - IgG subclass deficiency
39
Q

deficiencies that result from defects that affect development of both B and T cells

A

combined deficiencies

40
Q

group of AD and X-linked disorders where T cell function is always impaired and function will vary with B cells

A

severe combined immunodeficiencies (SCID)

41
Q

immune deficiency characterized by inability of lymphocytes and macrophages to produce HLA I or HLA II

A

bare lymphocyte syndrome

42
Q

x-linked disorder where IgM production is greatly depressed

A

Wiskott-Aldrich Syndrome

43
Q

clinical triad of wiskott-aldrich syndrome

A

eczema, thombocytopenia, and immune deficiency

44
Q

congenital mutation that causes thymic hypoplasia or aplasia, hypoparathyroidism, congenital heart defects, and characteristic facial features

A

DiGeorge syndrome

45
Q

What do each of the following mutations in DiGeorge syndrome lead to? - thymic hypoplasia/aplasia - hypoparathyroidism

A
  • thymic hypoplasia/aplasia: decreased number of T cells and T cell function - hypoparathyroidism: low blood calcium levels -> develop tetany
46
Q

What facial features are seen in DiGeorge syndrome?

A

low ears and wide eyes

47
Q

What complications are seen from selective IgA deficiency

A

recurrent sinus infections, respiratory infections, and stronger environmental allergies

48
Q

caused by a mutation in the pathway for B cell development but pt will have normally developed T cells

A

Bruton’s syndrome (X-linked agammaglobulinemia)

49
Q

What types of infections will be seen in Bruton’s syndrome?

A

recurrent upper and lower respiratory infections w/ encapsulated bacteria

50
Q

mutation in NADPH oxidase -> phagocytes take up Ags but can’t destroy them -> chronically infected

A

chronic granulomatous disease (CGD)

51
Q

What happens in patients with C3 deficiency?

A

loss of C3 (central to complement pathway) -> inability to activate C5 -> recurrent life-threatening infections soon after birth

52
Q

What cells are destroyed by HIV? What is the purpose of these cells?

A

CD4 Th cells -> necessary for development of plasma cells and CD8 cytotoxic T cells

53
Q

How is HIV spread?

A

blood-borne and sexual contact (more common)

54
Q

viruses that carry genetic material in the form of RNA rather than DNA

A

retroviruses

55
Q

What do retroviruses use to implant their ds DNA into host cells?

A
  • reverse transcriptase: RNA -> DNA - HIV integrase: inserts DNA into host genes
56
Q

essential enzyme in processing proteins needed from the viral internal structure (capsid)

A

protease

57
Q

Describe the general steps of HIV life cycle (6)

A
  • virion binds to CD4 and chemokine receptor - fusion of membrane w/ host cell membrane -> genome enters cytoplasm - reverse transcriptase -> integration of virus genes into host genome - transcription of HIV genome into RNA - synthesis of proteins and assembly of virion core - budding and release of mature vision
58
Q

List 4 types of medication MOAs that treat/prevent AIDS

A
  • HIV fusion inhibitors (prevents entrance into host cell) - reverse transcriptase inhibitors - HIV protease inhibitors - HIV integrase inhibitors
59
Q

current regimen for treatment of HIV (combination of drugs)

A

antiretroviral therapy (ART)

60
Q

Name 2 lab tests use to determine the progression of HIV

A
  • HIV RNA levels: determines viral load - CD4 T cell count
61
Q

Normal CD4 T cell count and value that begins to cause opportunistic infections

A
  • Normal: 800-1000 - Opportunistic infections: < 200
62
Q

Describe typical HIV progression without treatment

A
  • exposure: viral load is high (first 6-12 weeks) - clinical latency: viral load is low (no sxs) but it could still be transmitted (12 weeks - 7 years); CD4 count drops slowly over time - Constitutional sxs as viral load begins increasing - Opportunistic diseases occur as CD4 < 200
63
Q

Clinical symptoms of AIDS

A
  • cachexia (severe weight loss) - Kaposi sarcoma - PCP pneumonia - other atypical or opportunistic infections or cancers
64
Q

How can HIV be transmitted to infants?

A

during pregnancy, at delivery, or through breastfeeding

65
Q

Which system is typically involved in pediatric AIDS?

A

neurologic involvement -> HIV encephalopathy

66
Q

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

A

hypersensitivity

67
Q

deleterious effects of hypersensitivity to environmental (exogenous) antigens

A

allergy

68
Q

disturbance in the immunologic tolerance of self-antigens

A

autoimmunity

69
Q

immune reaction to tissues of another individual

A

alloimmunity

70
Q

Hypersensitivity I, II, III are mediated by what? How does this differ from hypersensitivity IV?

A
  • mediated by Abs - Type IV is cell mediated
71
Q

type I hypersensitivity is mediated by what?

A

IgE mediated against environmental antigens (allergens)

72
Q

sensitizing exposure and re-exposure in type I hypersensitivity

A
  • sensitizing exposure: allergen binds to APC -> B cell + Th2 cell -> plasma cell -> creates IgE -> binds to IgE Fc receptor on mast cell - re-exposure: allergen enters -> binds to IgE on mast cells -> mast cell degranulation -> histamine release -> edema/smooth muscle contraction/mucous secretion
73
Q

Symptoms of type I hypersensitivity

A
  • itching/urticaria - angioedema - hypotension - bronchospasm (anaphylaxis) - dysrhythmia
74
Q

type II hypersensitivity is mediated by what?

A

specific cell or tissue (tissue-specific antigens)

75
Q

5 mechanisms of type II hypersensitivity

A
  • cell is destroyed by abs and compliment - cell destruction through phagocytosis - soluble antigen may enter circulation and deposit on tissues -> destroyed by complement and neutrophils - Ab dependent cell mediated cytotoxicity (ADCC) - target cell malfunction
76
Q

Ex. of type II hypersensitivity

A
  • Graves disease (hyperthyroidism) - myasthenia gravis - Hemolytic disease of newborn (HDNB)
77
Q

type III hypersensitivity is mediated by what?

A

immune complex mediated (not organ specific) -> antigen-antibody complex circulate and later deposited in vessel walls or extravascular tissues

78
Q

Ex. of type III hypersensitivity

A
  • serum sickness (includes Raynaud phenomena) - arthus reaction - SLE
79
Q

type IV hypersensitivity is mediated by what?

A

cell-mediated; either cytotoxic T lymphocytes or lymphokine-producing Th1 and Th17 cells -> direct killing of target cells

80
Q

Ex. of type IV hypersensitivity

A
  • graft rejection - TB skin test - contact dermatitis (poison ivy, metals, and latex)
81
Q

T/F: individuals w/ allergies are typically genetically predisposed to them

A

True

82
Q

may reduce severity of allergic reaction but could also cause anaphylaxis

A

desensitization

83
Q

breakdown of tolerance to where the body recognizes self-antigens as foreign

A

autoimmunity

84
Q

autoimmune disease characterized by production of a large variety of antibodies (autoantibodies)

A

systemic lupus erythematosus (SLE)

85
Q

Explain how SLE is a type III hypersensitivity

A

causes deposition of circulating immune complexes containing antibody against host DNA

86
Q

List some of the clinical manifestations of SLE

A
  • arthritis/arthralgia - vasculitis/rash - renal disease - hematologic changes - CV disease
87
Q

How is SLE diagnosed?

A

presence of 4 or more: - facial rash - discoid rash (raised patches w/ scaling) - photosensitivity - oral/nasal lesions - arthritis of at least 2 peripheral joints - pleurisy/pericarditis - renal, neuro, or hematologic disorders - presence of ANA (antinuclear antibodies) in blood

88
Q

Where are Rh antigens expressed?

A

only on RBCs

89
Q

3 types of transplant rejection

A
  • hyperacute: due to preexisting ab to the antigens of the graft - acute: cell-mediated immune response (type IV) against unmatched HLA antigens - chronic: takes months-years; weak cell-mediated reaction against minor HLA antigens

Pathophysiology (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions