Lecture 3 Flashcards

Altered Immune Response and Transplantation, Infection and Human Immunodeficiency Virus Infection, & Cancer

1
Q

Our body’s immunity is accomplished by

A

Defence
Homeostasis
Surveillance

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2
Q

Lymphocytes (B & T), Natural killer cells, Dendritic cells

A

Cells involved in our immune response

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3
Q

the immunity that is present from birth

A

Innate immunity

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4
Q

the immunity that is developed in an individual after exposure to a pathogen or through vaccination

A

acquired immunity

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5
Q

the ability of the host cells to recognize an antigen specifically as a unique molecular entity and distinguish it from another with exquisite precision

A

Antigenic specificity

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6
Q

Invasion of body by a virus

Enters a cell and starts to duplicate

The antigens on the surface are recognized by a macrophage - it eats the virus and now the virus antigen is displayed on it surface.

The antigen is recognized by the T helper cells and now they bind to the macrophage causing cytokines to be released.

T helper cells and T cytotoxic cells multiply. and B cells multiply and produce antibodies

T cytotoxic cells and natural killer cells destroy infected body cells

The virus is marked by binded antibodies for macrophage destruction

A

Immune response to a virus

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7
Q

small proteins that are crucial in controlling the growth and activity of other immune system cells and blood cells

A

Cytokines

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8
Q

produces antigen-specific antibodies and is primarily driven by B cells

A

Humoral immunity

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9
Q

does not depend on antibodies for its adaptive immune functions and is primarily driven by mature T cells, macrophages and the release of cytokines in response to an antigen

A

Cell-mediated immunity

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10
Q

↓ Autoantibodies
↓ Cell-mediated immunity
↓ Delayed hypersensitivity response
↓ Expression of IL-2 receptors
↓ IL-1 and IL-2 synthesis
↓ Primary and secondary antibody responses
↓ Proliferative response of T and B cells
Thymic involution

A

Effects of Aging on the Immune System

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11
Q

Anaphylactic reactions
Anaphylaxis
Atopic reactions

A

Hypersensitivity reaction - Type I

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12
Q

a severe, life-threatening allergic reaction. It can happen seconds or minutes after you’ve been exposed to something you’re allergic to

A

Anaphylaxis

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13
Q

the genetic tendency to develop allergic diseases such as allergic rhinitis, asthma and atopic dermatitis (eczema)

A

Atopic reactions

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14
Q

Neurological:
headache
dizziness
paresthesia
feeling of impending doom

A

Neurological manifestations of a systemic anaphylactic reaction

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15
Q

Skin:
pruitus
angioedema
erythema
urticaria

A

skin manifestations of a systemic anaphylactic reaction

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16
Q

Respiratory:
hoarseness
coughing
sensation of narrowed airway
wheezing
stridor
dyspnea, tachypnea
respiratory arrest

A

respiratory manifestations of a systemic anaphylactic reaction

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17
Q

Cardiovascular:
hypotension
dysrhythmias
tachycardia
cardiac arrest

A

cardiovascular manifestations of a systemic anaphylactic reaction

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18
Q

Gastro-intestinal:
cramping, abdominal bleeding
nausea, vomiting
diarrhea

A

gastro-intestinal manifestations of a systemic anaphylactic reaction

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19
Q

_______ result in: rhinitis, asthma dermatitis, urticaria and angioedema

A

atopic reactions

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20
Q

Cytotoxic and cytolytic reactions
Hemolytic transfusion reactions
Goodpasture’s syndrome

A

Type II

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21
Q

Immune-complex reactions

A

Type III

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22
Q

Delayed hypersensitivity reactions
Contact dermatitis
Microbial hypersensitivity reactions
Transplant rejection
Some drug reactions

A

Type IV

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23
Q

Antihistamines
Sympathomimetic/decongestant drugs
Corticosteroids
Antipruritic drugs
Mast cell–stabilizing drugs
Leukotriene receptor antagonists

A

Drug therapy for Allergic Disorders

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24
Q

Immunoglobulin E (IgE) mediated (classic immediate allergic reaction)
Contact dermatitis (delayed allergic reaction)

A

Two types of latex allergies

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25
Q

refers to the process of separating plasma from blood, typically by centrifugation or filtration

A

Plasmapheresis

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26
Q

refers to the process of separating the cellular and soluble components of blood using a machine

A

Apheresis

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27
Q
  • Genetic susceptibility
  • Initiation of autoreactivity
A

Theories of causation for Autoimmunity

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28
Q

Phagocytic defects
B cell deficiency
T cell deficiency
Combined B cell and T cell deficiency
Secondary immunodeficiency disorders

A

Primary immunodeficiency disorders

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29
Q

Hyperacute rejection
Acute rejection
Chronic rejection

A

Transplant rejection

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30
Q

occurs a few minutes after the transplant when the antigens are completely unmatched

A

Hyperacute rejection

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31
Q

happens when your body’s immune system treats the new organ like a foreign object and attacks it

A

Acute rejection

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32
Q

the leading cause of organ transplant failure. The organ slowly loses its function and symptoms start to appear. This type of rejection cannot be effectively treated with medicines.

A

Chronic rejection

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33
Q

(or tissue compatibility) is the property of having the same, or sufficiently similar, alleles of a set of genes called human leukocyte antigens (HLA), or major histocompatibility complex (MHC)

A

Histocompatibility

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34
Q

genes in major histocompatibility complexes (MHC) that help code for proteins that differentiate between self and non-self. They play a significant role in disease and immune defense

A

Human leukocyte antigens (HLA)

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35
Q

Activation of T helper lymphocyte

Sensitized T cytotoxic lymphocyte

Proliferation

T cytotoxic lymphocytes

Attack on transplanted organ

A

Transplant rejection

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36
Q

Calcineurin inhibitors
corticosteroids
Sirolimus (Rapamune)
Mycophenolate mofetil (CellCept)
Azathioprine (Imuran) and cyclophosphamide (Procytox) are also used but less frequently
Antithymocyte globulin, antilymphocyte globulin, and muromonab-CD3

A

Immuno-suppressive Therapy

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37
Q

Occurs when an immuno-incompetent (immunodeficient) client receives a transfusion or transplant with immuno-competent cells
The graft (donated tissue) rejects the host (recipient) tissue.
Response may begin 7–30 days after transplantation.
Once GVH disease is established, there is no adequate treatment.

A

Graft-versus-host Disease

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38
Q

man-made proteins that act like human antibodies in the immune system

A

Hybridoma technology: monoclonal antibodies

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39
Q

Invasion of the body by any microorganism that causes disease and the resulting signs and symptoms that develop in response to the invasion.
Localized or systemic
Caused by bacteria, viruses, fungi and protozoa

A

Infections

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40
Q

An infectious disease whose incidence has recently increased or threatens to increase in the immediate future
Can originate from unknown sources, contact with animals, changes in known diseases, natural disasters or biological warfare.
e.g COVID, SARS, WESTNILE,HIV, LYME, HEP C, Avian Flue, Ebola , Zika

A

emerging infections

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41
Q

unaffected by certain antibiotics – MRSA, VRE

A

Resistant organisms (superbugs)

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42
Q

Contribution of ______________ in the development of drug-resistant organisms:
- administering antibiotics for viral infections
- Prescribing unnecessary antibiotics
- Using inadequate drug regimes to treat infections.
- Using broad spectrum or combines ages for infections that should be treated with first-line medications.

A

health care workers

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43
Q

Formerly called nosocomial infections
Acquired from exposure to a microorganisms in a health care setting
Common organisms include – E-coli, streps, C-difficile, S. aureus, Enterobacter aerogenes.

A

Health Care Associated Infections (HAIs)

44
Q

Never rely on the presence of fever to indicate infection in __________ because many have lower core body temperatures and decreased immune responses

A

older adults

45
Q

Individuals in long-term care facilities are at risk
Impaired immune function, comorbid conditions contribute to higher infection rates.
Pneumonia, UTIs, skin infections, TB are common in older adults
Infections often have atypical features that can be misinterpreted

A

Infections in older adults

46
Q

RNA virus (retrovirus) discovered in 1983
Binds to specific CD4 and chemokine receptors to enter cell
Reverse transcriptase assists to make viral DNA.
Viral DNA enters cell nucleus and splices itself into genome permanently.
Integrase
Consequence of integration into genetic structure
All daughter cells are infected.
Viral DNA will direct cell to make

A

Pathophysiology of HIV

47
Q

Initial infection
Viremia (large viral levels in blood) for 2–3 weeks
Transmission is more likely when viral load is high.
Followed by prolonged period (years) of low viral load

A

Viral load in the blood - HIV

48
Q

Cells with CD4 receptor sites are infected.
CD4+ T cells (T helper cells)
Lymphocytes
Monocytes/macrophages
Astrocytes
Oligodendrocytes
Immune problems start when CD4+ T-cell counts drop to below 500 cells/μL.
Normal range is 800–1 200 cells/μL.
Allows for opportunistic diseases

A

Pathophysiology of HIV

49
Q

Flu-like symptoms
Fever, swollen lymph glands, sore throat, headache, malaise, nausea, muscle and joint pain, diarrhea, or a diffuse rash
Occurs about 1–3 weeks after infection
Lasts for 1–2 weeks

A

Acute infection - HIV

50
Q

Generally asymptomatic
Fatigue, headache, low-grade fever, and night sweats often occur.
Most are not aware of infected status.

A

Early chronic infection - HIV

51
Q

CD4+ T cells drop to 200–500 cells/mcL.
Viral load increases.
HIV advances to a more active state.

A

Intermediate chronic infection - HIV

52
Q

Thrush
Oral hairy leukoplakia
Persistent vaginal candida infections
Herpes
Bacterial infections
Kaposi’s sarcoma

A

Intermediate chronic symptoms of HIV

53
Q

Immune system severely compromised
Great risk for opportunistic disease
Possible malignancies, wasting, and dementia

A

Late chronic or AIDS

54
Q

Pneumocystis jirovecii pneumonia
Cryptococcal meningitis
Cytomegalovirus retinitis
Mycobacterium avium complex
Kaposi’s sarcoma
Influenza virus

A

Common opportunistic diseases

55
Q

For HIV may take _______ (window period) to detect antibodies

A

2 months

56
Q

CD4+ counts of ___________ cells/μL are generally considered normal.

A

800–1,200 cells/μL

57
Q

Main goals of HIV _________:
Decrease viral load
Maintain/raise CD4+ counts
Delay HIV-related symptoms and opportunistic infections
Prevent transmission

A

Drug therapy

58
Q

Inhibit the ability of HIV to make a DNA copy early in replication

A

Nucleoside, nonnucleoside, and nucleotide reverse transcriptase inhibitors

59
Q

Interfere with HIV CD4 receptor site binding and entry into cells

A

Fusion inhibitors

60
Q

Interfere with activity of enzyme protease

A

Protease inhibitors

61
Q

Three or more drugs from different groups are prescribed at full strength

A

Combination antiretroviral therapy

62
Q

treatment of people infected with human immunodeficiency virus (HIV) using anti-HIV drugs

A

Antiretroviral therapy (ART)

63
Q

Adherence to drug regimens is critical to prevent
Missing even a few doses can lead to medication resistance.

A

Antiretroviral therapy (ART)

64
Q

Group of more than 200 diseases
Characterized by uncontrolled and unregulated growth of cells
Occurs in people of all ages and ethnicities

A

Cancer

65
Q

Ask at-risk clients
Received blood transfusion or clotting factors before 1985?
Shared needles, syringes, or other injection equipment with another person?
Had a sexual experience with your penis, vagina, rectum, or mouth in contact with these areas of another person?
Had a sexually transmitted infection (STI)?

A

4 questions to ask someone at high risk of HIV

66
Q

Most human tissues contain _____, _____ stem cells

A

predetermined, undifferentiated stem cells

67
Q

give rise to mature cells of the type of tissue where they reside

A

Predetermined stem cells

68
Q

Loss of intracellular control of proliferation results from mutation of stem cells.
DNA is substituted or permanently rearranged.

A

Stem cell theory of cancer

69
Q

Orderly process progressing from a state of immaturity to a state of maturity
Stable and will not change
Exact mechanism of normal cellular differentiation not completely understood

A

Normal cellular differentiation

70
Q

Two types of genes that can be affected by mutation are:

A
  • Proto-oncogenes
  • Tumour suppressor genes
71
Q

Regulate normal cellular processes such as promoting growth

A

Proto-oncogenes

72
Q

Suppress growth

A

Tumour suppressor genes

73
Q

Genetic locks that keep cells functioning normally
Mutations that alter their expression can activate them to function as oncogenes

A

Proto-oncogenes

74
Q

Function to regulate cell growth
Suppress growth of tumours
Are rendered inactive by mutations
Result in loss of suppression of tumour growth

A

Tumour suppressor genes

75
Q

Well differentiated
Usually encapsulated
Expansive mode of growth
Characteristics similar to parent cell
Metastasis is absent.
Rarely recur

A

Benign

76
Q

Usually undifferentiated
Able to metastasize
Infiltrative and expansive growth
Frequent recurrence
Moderate to marked vascularity
Rarely encapsulated
Becomes less like parent cell

A

Malignant

77
Q

Mature cells of the:
brain
skin
glands

A

Ectoderm

78
Q

Mature cells of the:
muscles
bones
connective tissue

A

Mesoderm

79
Q

Mature cells of the:
trachea
lungs
epithelium

A

Endoderm

80
Q

In _____ phase:
Mutation of cell’s genetic structure
From inherited mutation
From exposure to a chemical, radiation, or viral agent
Mutated cell has the potential to develop into clone of neoplastic cells.

A

Initiation

81
Q

_________ may be
Chemical
Radiation
Viral

Effects in the stage of initiation are usually irreversible and additive.

A

Carcinogens

82
Q

Once initiated, mutation is __________.
Not all mutated cells form a tumour.
Mutated cells become tumours only when they establish the ability to self-replicate and grow.

A

Irreversible

83
Q

Long latency period makes identification of carcinogens difficult.
Certain drugs have been identified as carcinogens.

A

Chemical carcinogens

84
Q

Ionizing radiation can cause cancer in almost any human tissue.
Dose of radiation needed to cause cancer is unknown.
UV radiation is associated with melanoma and squamous and basal cell carcinoma.

A

Radiation

85
Q

Hepatitis B and C viruses, associated with hepatocellular carcinoma
Human papillomavirus, associated with squamous cell carcinomas such as cervical, anal, and head and neck cancers
Helicobacter pylori and gastric/duodenal ulcers, as well as of some gastric cancers
Genetic susceptibility

A

Viral carcinogens

86
Q

Second stage in development of cancer
Characterized by reversible proliferation of altered cells
Activities of _____ are reversible.
Obesity
Smoking, alcohol
Dietary fat

A

Promotion

87
Q

May range from 1 to 40 years
Length of _____ period associated with mitotic rate of tissue of origin and environmental factors
For disease to be clinically evident, tumour must reach a critical mass that can be detected.

A

Latent period

88
Q

Final stage
Characterized by
Increased growth rate of tumour
Invasiveness
Metastasis
Most frequent sites of metastasis are lungs, brain, bone, liver, and adrenal glands.

A

Progression

89
Q

Begins with rapid growth of primary tumour
Develops its own blood supply

A

Metastasis

90
Q

formation of blood vessels within tumour

A

Tumour angiogenesis

91
Q

Anatomical site
Histological analysis - grading and severity
Extent of disease - staging

A

Tumours classification

92
Q

Anatomical extent of disease is based on three parameters
Tumour size and invasiveness (T)
Spread to lymph nodes (N)
Metastasis (M)

A

TNM classification system

93
Q

C - Change in bowel or bladder habits
A - A sore that does not heal
U - Unusual bleeding or discharge from any body orifice
T - Thickening or a lump in the breast or elsewhere
I - Indigestion or difficulty in swallowing
O - Obvious change in a wart or mole
N - Nagging cough or hoarseness

A

Seven Warning Signs of Cancer

94
Q

The goal of cancer treatment is:

A

cure, control, or palliation

95
Q

Oldest form of cancer treatment

A

Surgical therapy

96
Q

cell cycle phase–nonspecific and cell cycle phase–specific drugs

A

The two major categories of chemotherapeutic drugs

97
Q

Repair of cellular damage,
Redistribution of cells in the cell cycle
Repopulation with normal cells
Reoxygenation of hypoxic tumor area.

A

The 4 Rs

98
Q

Occurs when you have too few neutrophils, a type of white blood cells, most common in patients receiving chemotherapy.

A

Neutropenia

99
Q

Involves the use of biological agents such as interferons, interleukins monoclonal antibodies and growth factors.

A

Biological & targeted therapy

100
Q

Obstructive
Metabolic
Infiltrative

A

Oncological emergencies

101
Q

Superior Vena Cava syndrome
Spinal Cord Compression
Third Space Syndrome
Intestinal Obstruction

A

Obstructive

102
Q

SIADH
Hypercalcemia
Tumor Lysis Syndrome
Septic Shock
Disseminated Intravascular Coagulation

A

Metabolic

103
Q

Cardiac Tamponade
Carotid Artery Rupture

A

Infiltrative

104
Q

Drug therapy includes nonsteroidal anti-inflammatory medications, opioids, and adjuvant pain medications.
Nonpharmacological interventions, including relaxation therapy and imagery, can be effectively used to manage pain

A

Cancer pain treatment

105
Q

disfigurement, dependency, unrelieved pain, financial depletion, abandonment, and death.

A

Common fears experienced by patients with cancer

106
Q

Most cancers occur in people older than 65 years.
Older adults are particularly vulnerable to the complications of both cancer and cancer therapy
Age alone is not a sufficient predictor of tolerance or response to treatment

A

Age related considerations (cancer)