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Summer Patho > Infectious Diseases and Cancer > Flashcards

Infectious Diseases and Cancer Flashcards

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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
HIV Pathology
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.
26
HIV Manifestations
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.
27
Diagnosis of HIV/AIDS : cell count
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.
28
HIV Symptoms
Fever, Fatigue, Weight loss, Diarrhea Swollen lymph nodes — often one of the first signs of HIV infection Cough, Shortness of breath
29
Progression to AIDS
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 ```
30
opportunistic infection
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.
31
reverse transcriptase inhibitors
nucleoside and nonnucleoside inhibitors of reverse transcriptase; try to block recoding of RNA to DNA
32
protease inhibitors
without protease, HIV virions remain un-infectious
33
entrance inhibitors
inhibits viral entrance into the CD4+ cell
34
integrase inhibitors
blocking infected DNA from being integrated | and cell fusion inhibitors
35
hypersensitivity reactions
Allergies, autoimmunity and alloimmunity (aka isoimmunity)
36
Allergy
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
Autoimmunity
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
Alloimmunity
body’s inappropriate reaction directed against beneficial foreign tissues, such as transfusions or transplants. An immunologic tolerance of self-antigens.
39
Immediate Hypersensitivity
occur within minutes to few hours
40
Delayed Hypersensitivity
several hours to days (maximal severity)
41
Type I
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
Type II
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
Type III
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
Type IV
cell-mediated reactions
45
ABO Blood group
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
Rh blood groups
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
Hyperacute rejection
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
Acute rejection
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
Chronic rejection
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
Cancer
a malignant (virulent or infectious) tumor
51
Neoplasm
a new abnormal growth of tissue (usually cancer)
52
Benign
tumors that are not cancerous. Cell retain function and stroma (structural framework) and do not invade beyond their capsule.
53
Malignant
tumors with rapid growth rates, loss of differentiation, and absence of normal tissue organization.
54
Metastasis
most deadly characteristic of malignant tumors. Growth spreads to nearby blood vessels, lymphatics, and surrounding structures.
55
Carcinoma in Situ
cancerous growth found in epithelial tissues, but has not spread to the basement membrane or surrounding stroma.
56
Tumor marker
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
Tumor markers benefits
- 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
Cancer cell (transformed)
uncontrolled growth, are anchorage independent (continue to divide even when suspended in soft agar), they are immortal
59
Proto-Oncogenes
are normal genes which, when altered by mutation, become an oncogene that can contribute to cancer
60
Tumor suppressor genes
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
Point mutations
the alteration of one or a few nucleotide base pairs. (these are small scale changes in DNA)
62
Chromosomal translocation
large changes in chromosome structure in which a piece of one chromosome is translocated to another chromosome
63
Gene Amplification
A type of chromosome structural abnormality that can activate oncogenesis
64
Oncogene (accelerate)
mutant genes that in their normal, non-mutant state direct synthesis of proteins that positively regulate (accelerate) proliferation
65
Tumor-suppressor genes (brake)
in non-mutated state encode protons the negatively (“put the brakes on”, halt) proliferation
66
Epigenetic silencing (turning off genes without mutation)
non-mutated gene silencing caused by reversible chemical modifications of histones and related chromatin components in DNA
67
Loss of heterozygosity (LOH)
refers to the loss of one copy (allele) of a specific chromosome region in a tumor. ( i.e. in tumor suppressor genes)
68
Apoptosis
self-destruct mechanism triggered by diverse stimuli including normal development and excessive growth.
69
Telomeres
protective ends, or caps, on each chromosome and are placed and maintained by a specialized enzyme called telomerase.
70
Caretaker genes
genes that are responsible for maintaining genomic integrity.
71
Chemo
chemo agents take advantage of specific vulnerabilities in target cancer cells
72
Chemo: Induction
seeks to cause shrinkage or disappearance of tumors Ex. Hodgkin's: chemo alone can be used to provide a cure for the disease
73
Chemo: Adjuvant
given after surgical excision of the cancer to prevent any micro-mentastasism during removal
74
Chemo: Neo-adjuvant
treat w/ chemo first so its hopefully easier to excise (smaller)
75
Radiation
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
Radiation: Ionizing
damages cells by impairing enough energy to do damage to DNA
77
Radiation: Brachytherapy
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
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Surgery
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
Carcinogen
Cancer causing substances; substances that may increase the likelihood of developing cancer Chemical, Radiation, Sexual, Dietary, Air Pollution, Obesity, Electromagnetic Radiation, Smoking

Summer Patho (4 decks)

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