Lecture 3 Flashcards by Sydney Coopland

Our body’s immunity is accomplished by

Defence
Homeostasis
Surveillance

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

Cells involved in our immune response

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the immunity that is present from birth

Innate immunity

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

acquired immunity

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

Antigenic specificity

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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

Immune response to a virus

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

Cytokines

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

Humoral immunity

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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

Cell-mediated immunity

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↓ 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

Effects of Aging on the Immune System

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Anaphylactic reactions
Anaphylaxis
Atopic reactions

Hypersensitivity reaction - Type I

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

Anaphylaxis

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

Atopic reactions

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Neurological:
headache
dizziness
paresthesia
feeling of impending doom

Neurological manifestations of a systemic anaphylactic reaction

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Skin:
pruitus
angioedema
erythema
urticaria

skin manifestations of a systemic anaphylactic reaction

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

respiratory manifestations of a systemic anaphylactic reaction

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Cardiovascular:
hypotension
dysrhythmias
tachycardia
cardiac arrest

cardiovascular manifestations of a systemic anaphylactic reaction

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

gastro-intestinal manifestations of a systemic anaphylactic reaction

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

atopic reactions

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Cytotoxic and cytolytic reactions
Hemolytic transfusion reactions
Goodpasture’s syndrome

Type II

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Immune-complex reactions

Type III

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

Type IV

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

Drug therapy for Allergic Disorders

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

Two types of latex allergies

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

Plasmapheresis

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

Apheresis

- Genetic susceptibility - Initiation of autoreactivity

Theories of causation for Autoimmunity

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

Primary immunodeficiency disorders

Hyperacute rejection Acute rejection Chronic rejection

Transplant rejection

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

Hyperacute rejection

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

Acute rejection

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.

Chronic rejection

(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)

Histocompatibility

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

Human leukocyte antigens (HLA)

Activation of T helper lymphocyte ↓ Sensitized T cytotoxic lymphocyte ↓ Proliferation ↓ T cytotoxic lymphocytes ↓ Attack on transplanted organ

Transplant rejection

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

Immuno-suppressive Therapy

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.

Graft-versus-host Disease

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

Hybridoma technology: monoclonal antibodies

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

Infections

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

emerging infections

unaffected by certain antibiotics – MRSA, VRE

Resistant organisms (superbugs)

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.

health care workers

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.

Health Care Associated Infections (HAIs)

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

older adults

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

Infections in older adults

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

Pathophysiology of HIV

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

Viral load in the blood - HIV

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

Pathophysiology of HIV

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

Acute infection - HIV

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

Early chronic infection - HIV

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

Intermediate chronic infection - HIV

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

Intermediate chronic symptoms of HIV

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

Late chronic or AIDS

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

Common opportunistic diseases

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

2 months

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

800–1,200 cells/μL

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

Drug therapy

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

Nucleoside, nonnucleoside, and nucleotide reverse transcriptase inhibitors

Interfere with HIV CD4 receptor site binding and entry into cells

Fusion inhibitors

Interfere with activity of enzyme protease

Protease inhibitors

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

Combination antiretroviral therapy

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

Antiretroviral therapy (ART)

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

Antiretroviral therapy (ART)

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

Cancer

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)?

4 questions to ask someone at high risk of HIV

Most human tissues contain _____, _____ stem cells

predetermined, undifferentiated stem cells

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

Predetermined stem cells

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

Stem cell theory of cancer

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

Normal cellular differentiation

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

- Proto-oncogenes - Tumour suppressor genes

Regulate normal cellular processes such as promoting growth

Proto-oncogenes

Suppress growth

Tumour suppressor genes

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

Proto-oncogenes

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

Tumour suppressor genes

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

Benign

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

Malignant

Mature cells of the: brain skin glands

Ectoderm

Mature cells of the: muscles bones connective tissue

Mesoderm

Mature cells of the: trachea lungs epithelium

Endoderm

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.

Initiation

_________ may be Chemical Radiation Viral Effects in the stage of initiation are usually irreversible and additive.

Carcinogens

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.

Irreversible

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

Chemical carcinogens

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.

Radiation

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

Viral carcinogens

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

Promotion

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.

Latent period

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

Progression

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

Metastasis

formation of blood vessels within tumour

Tumour angiogenesis

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

Tumours classification

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

TNM classification system

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

Seven Warning Signs of Cancer

The goal of cancer treatment is:

cure, control, or palliation

Oldest form of cancer treatment

Surgical therapy

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

The two major categories of chemotherapeutic drugs

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

The 4 Rs

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

Neutropenia

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

Biological & targeted therapy

Obstructive Metabolic Infiltrative

Oncological emergencies

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

Obstructive

SIADH Hypercalcemia Tumor Lysis Syndrome Septic Shock Disseminated Intravascular Coagulation

Metabolic

Cardiac Tamponade Carotid Artery Rupture

Infiltrative

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

Cancer pain treatment

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

Common fears experienced by patients with cancer

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

Age related considerations (cancer)

Lecture 3 Flashcards

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