Infectious Diseases and Cancer Flashcards

1
Q

symbiosis

A

benefits only the human; no harm to the microorganism

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2
Q

mutualism

A

benefits the human and the microorganism

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3
Q

commensalism (satelliteism)

A

benefits the microorganism; no harm to the human

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4
Q

pathogenicity

A

ability of an agent to produce disease – success depends on communicability, infectivity, extent of tissue damage and virulence

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5
Q

opportunism

A

situation that occurs when benign microorganisms become pathogenic because of decreased human host resistance

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6
Q

communicability

A

ability to spread from one individual to others and cause disease

ex. measles, pertussis spread very easily

human immunodeficiency virus (HIV) is of lower communicability

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7
Q

immunogenicity

A

ability of pathogens to induce an immune response

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8
Q

infectivity

A

ability of the pathogen to invade and multiply in the host

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9
Q

mechanism of action

A

manner in which the microorganism damages tissue

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10
Q

pathogenicity

A

ability of an agent to produce disease – success depends on communicability, infectivity, extent of tissue damage and virulence

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11
Q

portal of entry

A

route by which a pathogenic microorganism infects the hose

direct contact, inhalation, ingestion, bites of animal / insect

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12
Q

toxigenicity

A

ability to produce soluble toxins or endotoxins, factors that greatly influence the pathogen’s degree of virulence

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13
Q

virulence

A

capacity of a pathogen to cause severe disease

ex. measles = low
rabies = high BATS!!! :)

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14
Q

Exotoxins

A

proteins released during bacterial growth

usually enzymes that have highly specific effects on host cells; they include:
cytotoxins, neurotoxins, pneumotoxins, enterotoxins, hemolysins

^immunogenic and elicit the production of antibodies known as antitoxins

vaccines are available for many of the exotoxins (tetanus, diphtheria, pertussis)

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15
Q

Endotoxins (lipopolysaccharides LPSs)

A

contained in the cell walls of gram - bacteria and are released during lysis, or destruction of bacteria

may be released also from the mbn of the bacteria during bacterial growth or during treatment with antibiotics → cannot prevent toxic effects of the endotoxin

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16
Q

Bacteremia

A

presence of bacteria in the blood

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17
Q

Septicemia

A

growth of bacteria in the blood and is caused by a failure of the body’s defense mechanisms

once in blood, endotoxins cause the release of vasoactive peptides and cytokines that affect blood vessels by producing vasodilation (reduces BP) = decreased O2 delivery → cardiovascular shock

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18
Q

six phases of the viral replication cycle

A
  1. Adsorption: attachment to cell
  2. Penetration
  3. Uncoating
  4. Replication
  5. Assembly
  6. Release
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19
Q

clinical manifestations of infection

A

Vary depending on pathogen and infected/affected organ system

May come from infecting microorganism and/or its products

Mostly come from host’s inflammatory immune response

Manifestations include:
fatigue 
malaise 
weakness
loss of concentration
general aching
loss of appetite 
FEVER- hallmark trait
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20
Q

Vaccines

A

intended to introduce a biological pathogen to the host’s immune system to cause a long-lasting protective immune response under conditions that will not result in disease

Primary response is often short lived
Thus the need for Boosters

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21
Q

Vaccine Types

A

Killed: use of inactive virus (does not normally lead to infection)

Attenuated: Live viruses that are weakened

Toxoids: purified toxins that have been chemically detoxified without the loss of immunogenicity

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22
Q

primary (congenital) immune deficiency

A

result of single gene defect, generally sporadic; not inherited; mutations occur before birth

GENERALLY RARE

5 groups of deficiencies:
B Lymphocyte 
T Lymphocyte 
Combined Immune
Complement
Phagocyte
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23
Q

secondary (acquired) immune deficiency

A

Not related to genetic defects

ARE complications of physiologic or pathologic conditions

Common, but many are not clinically relevant

May be very mild; can be very serious and life-threatening (AIDS)

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24
Q

HIV (human immunodeficiency virus)

A

Routes of transmission include:

  • blood or blood products
  • IV drug use
  • heterosexual and homosexual activity

-maternal-child transmission (before, during or after birth): contracted across the placenta, infected blood during delivery, through milk during breastfeeding

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25
Q

HIV Pathology

A

retrovirus: carry RNA

A viral enzyme reverse transcriptase converts RNA → ds DNA.

A second viral enzyme integrase, inserts the new DNA into the infected cell’s genetic material.

Protease processes the proteins needed from the capsid

The primary receptor on HIV is the envelope protein, gp120.

NOTE: The major immunologic finding in AIDS is the striking decrease in the number of CD4-positive (CD4+) T helper cells.

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26
Q

HIV Manifestations

A

Early stages of HIV initially presented as influenza-like symptoms. Symptoms are relatively mild and non-specific; disappearing after 1-6 weeks of onset

Window period: is the amount of time that passes between infection and appearance of antibody.

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27
Q

Diagnosis of HIV/AIDS : cell count

A

initially diagnosed by decrease in CD4+ T cells:

Normal range: 600/mm3-1200/mm3
HIV/AIDS: less than 200/mm3
Time frame from infection of HIV to development of AIDS is 10 years.

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28
Q

HIV Symptoms

A

Fever, Fatigue, Weight loss, Diarrhea
Swollen lymph nodes — often one of the first signs of HIV infection
Cough, Shortness of breath

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29
Q

Progression to AIDS

A

Fever, Fatigue, Weight loss, Diarrhea
Swollen lymph nodes — often one of the first signs of HIV infection
Cough, Shortness of breath

All of the above, PLUS:
Soaking night sweats
Shaking, Chills, Fever higher than 100F for several weeks
Headaches
Persistent, unexplained fatigue
Blurred and/or distorted vision
Persistent white spots or unusual lesions on your tongue or in your mouth
Skin rash or bumps
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30
Q

opportunistic infection

A

infection that would normally not bother someone with a “healthy” immune system, however, can be life-threatening to someone with HIV/AIDS. Some of their severities depend on certain levels of CD4+ cell count.

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31
Q

reverse transcriptase inhibitors

A

nucleoside and nonnucleoside inhibitors of reverse transcriptase; try to block recoding of RNA to DNA

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32
Q

protease inhibitors

A

without protease, HIV virions remain un-infectious

33
Q

entrance inhibitors

A

inhibits viral entrance into the CD4+ cell

34
Q

integrase inhibitors

A

blocking infected DNA from being integrated

and cell fusion inhibitors

35
Q

hypersensitivity reactions

A

Allergies, autoimmunity and alloimmunity (aka isoimmunity)

36
Q

Allergy

A

exaggerated response against noninfectious environmental substances. Such as mold, pollen, ragweed, dog dander, etc. Allergies refer to something that is not normally found in the body.

37
Q

Autoimmunity

A

disturbance in the immunologic tolerance of self-antigens. Autoimmune diseases occur when the immune system reacts against self-antigens to such a degree that autoantibodies or autoreactive T cells damage the individual’s tissues.

38
Q

Alloimmunity

A

body’s inappropriate reaction directed against beneficial foreign tissues, such as transfusions or transplants. An immunologic tolerance of self-antigens.

39
Q

Immediate Hypersensitivity

A

occur within minutes to few hours

40
Q

Delayed Hypersensitivity

A

several hours to days (maximal severity)

41
Q

Type I

A

IgE mediated reactions; most common allergic reactions

Histamine is the most potent mediator of IgE

  • bronchial constriction
  • vasodilation
  • increased vascular permeability [edema]
  • increased gastric acid secretion

NOTE: all mucosal lining in resp. tract is connected, so all tissues will be affected

42
Q

Type II

A

tissue specific reactions

1st mechanism: begins with antibody binding to tissue-specific antigens or antigens that are attached to specific tissues.
EX: ABO blood incompatibility or mismatched blood transfusion

2nd mechanism: antibody may cause cell destruction through phagocytosis by macrophages.

3rd mechanism: toxic products produced by neutrophils

4th mechanism: antibody-dependent cell-mediated cytotoxicity

5th mechanism: causes the cell to malfunction

43
Q

Type III

A

immune complex reactions; antigen-antibody immune complex

Type III reactions are not organ specific and symptoms are mostly unrelated to the antigenic target of the body

44
Q

Type IV

A

cell-mediated reactions

45
Q

ABO Blood group

A

ABO blood group - consist of two major carbohydrate antigens; A and B

Erythrocytes (red blood cells) express A, B, both, or none of the antigens (type O)

Blood type-A carries B antibodies. Blood type-B carries A antibodies. O-type carries A and B antibodies. AB does not carry blood-type antibodies.

Blood type O is universal donor

Blood type AB is universal recipient

46
Q

Rh blood groups

A

diverse group of 45 separate red blood cell antigens (only one of major importance, the D-antigen)

D-antigen: is expressed on red blood cells: Rh-positive; not expressed on red blood cells: Rh-negative

85% of people are Rh-positive, 15% Rh-negative

47
Q

Hyperacute rejection

A

Rare, but immediate rejection.

Grafted tissue turns white instead of pink when circulation is restored

Usually occurs because of preexisting antibodies (type II) to antigens on the grafted tissue

48
Q

Acute rejection

A

immune response that occurs within days to months after transplantation.

Occurs when recipient develops an immune response against unmatched HLA antigens. (infiltration of lymphocytes and macrophages characterization of type IV reaction)

49
Q

Chronic rejection

A

occurs after a period of months or years of normal function.

Characterized by slow, progressive organ failure.

May occur due to weak cell-mediated (type IV) reaction against minor histocompatibility antigens on grafted tissue.

50
Q

Cancer

A

a malignant (virulent or infectious) tumor

51
Q

Neoplasm

A

a new abnormal growth of tissue (usually cancer)

52
Q

Benign

A

tumors that are not cancerous. Cell retain function and stroma (structural framework) and do not invade beyond their capsule.

53
Q

Malignant

A

tumors with rapid growth rates, loss of differentiation, and absence of normal tissue organization.

54
Q

Metastasis

A

most deadly characteristic of malignant tumors. Growth spreads to nearby blood vessels, lymphatics, and surrounding structures.

55
Q

Carcinoma in Situ

A

cancerous growth found in epithelial tissues, but has not spread to the basement membrane or surrounding stroma.

56
Q

Tumor marker

A

substance produced by both benign and malignant cells that is either present in or on tumor cells or found in blood, spinal fluid or urine.

57
Q

Tumor markers benefits

A
  • screen and identify individuals at risk for cancer
  • diagnose the specific type of tumor in individuals with clinical manifestations relating to their tumor, as in adrenal tumors, or enlarged liver or prostate
  • follow the clinical course of a tumor.eg a falling PSA(Prostate Specific Antigen) level after radiation or surgical therapy for prostate cancer indicates successful treatment, and a later rise in the PSA may indicate a recurrence
58
Q

Cancer cell (transformed)

A

uncontrolled growth, are anchorage independent (continue to divide even when suspended in soft agar), they are immortal

59
Q

Proto-Oncogenes

A

are normal genes which, when altered by mutation, become an oncogene that can contribute to cancer

60
Q

Tumor suppressor genes

A

generally encode proteins that in one way or another inhibit cell proliferation. Loss of one or more of these “brakes” contributes to the development of many cancers.

61
Q

Point mutations

A

the alteration of one or a few nucleotide base pairs. (these are small scale changes in DNA)

62
Q

Chromosomal translocation

A

large changes in chromosome structure in which a piece of one chromosome is translocated to another chromosome

63
Q

Gene Amplification

A

A type of chromosome structural abnormality that can activate oncogenesis

64
Q

Oncogene (accelerate)

A

mutant genes that in their normal, non-mutant state direct synthesis of proteins that positively regulate (accelerate) proliferation

65
Q

Tumor-suppressor genes (brake)

A

in non-mutated state encode protons the negatively (“put the brakes on”, halt) proliferation

66
Q

Epigenetic silencing (turning off genes without mutation)

A

non-mutated gene silencing caused by reversible chemical modifications of histones and related chromatin components in DNA

67
Q

Loss of heterozygosity (LOH)

A

refers to the loss of one copy (allele) of a specific chromosome region in a tumor. ( i.e. in tumor suppressor genes)

68
Q

Apoptosis

A

self-destruct mechanism triggered by diverse stimuli including normal development and excessive growth.

69
Q

Telomeres

A

protective ends, or caps, on each chromosome and are placed and maintained by a specialized enzyme called telomerase.

70
Q

Caretaker genes

A

genes that are responsible for maintaining genomic integrity.

71
Q

Chemo

A

chemo agents take advantage of specific vulnerabilities in target cancer cells

72
Q

Chemo: Induction

A

seeks to cause shrinkage or disappearance of tumors

Ex. Hodgkin’s: chemo alone can be used to provide a cure for the disease

73
Q

Chemo: Adjuvant

A

given after surgical excision of the cancer to prevent any micro-mentastasism during removal

74
Q

Chemo: Neo-adjuvant

A

treat w/ chemo first so its hopefully easier to excise (smaller)

75
Q

Radiation

A

Well suited to treat localized diseases in areas that are hard to reach (brain and pelvis)

Kills cancer cells by minimizing damage to normal structures

76
Q

Radiation: Ionizing

A

damages cells by impairing enough energy to do damage to DNA

77
Q

Radiation: Brachytherapy

A

sublethal: cell potentially repair itself
- radiation sources in form of capsules or “seeds”
- can be temporarily placed into body cavities
- helpful in treatment in cervical, prostate, and head and neck

78
Q

Surgery

A

Biopsy: to initially diagnose
Removal: of tumors that will not spread (Stage 1 or 2)

Important role in prevention of cancer (removal of breasts if family history exists)

79
Q

Carcinogen

A

Cancer causing substances; substances that may increase the likelihood of developing cancer

Chemical, Radiation, Sexual, Dietary, Air Pollution, Obesity, Electromagnetic Radiation, Smoking