Immunity Pt. 3 Flashcards

1
Q

What are the effects of aging on immune system?

A
  • Increased susceptibility to infections and malignancies
  • Increased production of autoantibodies
  • Decreased response to vaccines
  • Decreased immune system function
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2
Q

What are the effects of aging on T and B cells?

A

T cells become less responsive
- Thymus atrophies as we age, decrease production of thymic hormones – which are needed for functioning of T lymphocytes

B cells become less responsive, cannot produce enough antibody, response to antigen

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3
Q

What is the cause of assortment of infections in AIDS patient?

A

The HIV virus bonds to the Helper T Lymphocyte (CD4) and destroys them.

Over time, this reduces the body’s immunity and opens up the body to more infections with no ability to fight them off.

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4
Q

What are the modes of transmission of HIV virus? How the virus can be killed at hospital and home settings?

A

blood, semen, vaginal, secretions, and breast milk

The virus can be killed by standard disinfecting, most effective Bleach, but also heat (135 degree) and cloth washing, hydrogen peroxide, rubbing alcohol, or germicidal cleanser such as betadine or hibiclens.

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5
Q

What are the ways by which transmission of HIV infection can be blocked?

A
  • Abstinence and/or condoms
  • Don’t share needles, use only sterile hypodermic needles
  • Avoid pregnancy and especially breast feeding
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6
Q

What are the type and structure of HIV virus? Why is it called retrovirus?

A

HIV is a Retrovirus - Genetic information is carried by RNA not DNA.

RNA genome transcribes/copies back into the DNA in the host cell (RNA to DNA is backwards)

Structure: inner core of RNA covered by a protein coat (capsid), envelope composed of a lipid bilayer penetrated by glycoproteins

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7
Q

What are the 3 enzymes HIV has?

A
  • Reverse Transcriptase – enzyme that reads the RNA strand and makes a DNA copy
  • Integrase - integration of viral DNA into the host genome, inserts the HIV DNA copy into host cell DNA
  • Protease – Viral enzyme that cuts proteins into pieces to assemble the protein coat of newly produced HIV particles (Cleaving / activating)
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8
Q

Generally how a virus makes its copies?

A

Outside a living host cell the virus is unable to replicate – in the cell it uses the host cells enzymes and ribosomes to make thousands of copies of the virus

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9
Q

What are the stages in the life cycle of HIV?

A
  1. Attachment of HIV Virus to CD4 Receptors / bonding
  2. Internalization and uncoating of the virus with viral RNA and reverse transcriptase
  3. Reverse transcription, which produces a mirror image of the viral RNA and double stranded DNA molecule
  4. Integration of viral DNA into host DNA using the integrase enzyme
  5. Transcription of the inserted viral DNA to produce viral messenger RNA
  6. Translation of viral messenger RNA to create viral polyprotein
  7. Cleavage of viral polyprotein into individual viral proteins that make up the new virus (using protease)
  8. Assembly and release of the new virus from the host cell
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10
Q

Why HIV can only attach CD4 T cells?

A

Gp120 glycoprotein on the HIV virus is specifically able to bond to the receptors on the Helper T Cell (CD4)

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11
Q

How an HIV infected patient present early after contacting the infection?

What are the responses of immune system to HIV infection in a few weeks?

A

Soon after being infected, most people experience a brief flulike illness - common signs are fever, fatigue, rash, headache, joint pain, sore throat, and swollen lymph nodes (about 50% experience night sweats)

3-4 weeks after infection, plasma cells begin secreting antibodes, they are detectible in a blood test, but not able to destroy the HIV virus

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12
Q

How the progression of HIV infection to AIDS happen?

A

HIV progresses to AIDS after a period of 2-10 years when it has destroyed enough Helper T cells that they begin to experience immunodeficiency symptoms - the immune system collapse and they become susceptible to “opportunistic infections” because the immune system is no longer able to hold these diseases in check

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13
Q

What measures can help HIV positive patients in addition to drugs?

A

Treatment can improve life expectancy by slowing down the virus/reducing viral load via
- Reverse Transcriptase Inhibitors
- Integrase Inhibitors
- Protease inhibitors
Recommended treatment is Highly Active Antiretroviral Terapy (HAART) - combination from at least two drug classes.

In addition to drugs, a healthy lifestyle, good food, sleep, no drugs/alcohol can help someone who is HIV positive have a better outcome

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14
Q

What is the cause of hypersensitivity reactions in general? Define an allergen.

A

Overly reactive to a substance that is tolerated by most other peopls

Antigens that induce an allergic reaction are called allergens

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15
Q

Name common allergens.

A

Common allergens:

  • Food - milk, peanuts, shellfish, eggs
  • Antibiotics - penicillian, tetracycline
  • Vaccines - pertussis, typhoid
  • Venoms - honeybee, wasp, snake
  • Cosmetics
  • Chemicals in plants - poison ivy, pollens, dust, molds, iodine containing dyes
  • Even Microbes
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16
Q

What are the 4 types of hypersensitive reactions?

Which is most common?

A

Type I: Anaphalactic
Type II: Cytotoxic
Type III: Immune-Complex
Type IV: Cell-Mediated

The first three are antibody mediated, only Type IV is cell-mediated

Type I Anaphalactic are most common

17
Q

What is the mechanism of type 1 hypersensitivity?

What are the cells and chemicals involved in it?

Give examples of type 1 hypersensitivity disorders.

A

IgE antibodies, Mast Cells, Basophils

In response to the first exposure, B lymphocytes are activated and plasma cells produce antibodies to a antigen/allergen, when they are re-exposed to the allergen there are antibodies present and mast cells and basophils release histomine, prostaglandins, leukotrienes, and kinins.
They cause vasodilation - resulting in inflammatory responses, difficulty breathing

Diseases caused by Type I Reactions
Asthma, Eczema/Atopic Dermatitis, Allergic Rhinitis/Hay Fever, Anaphylactic Shock – widespread vasodilation, BP low

18
Q

What is the mechanism of type II hypersensitivity?

What are the cells and chemicals involved in it?

Give examples of type 1 hypersensitivity disorders.

A

Cytotoxic reactions are caused by antibodies (IgG or IgM) directed against a person’s blood cells or tissue cells

Mediated by IgG or IgM which forms antigen-antibody complexes on cell membrane or basement membrane -> complexes activates complement lysis of the cells

Diseases

  • Hemolytic anemia – against RBC
  • Goodpasture’s syndrome – lung, kidney cell – antibodies directed at the basement membrane – bleeding
  • Graves’ disease – causes hyperthyroidism, produces too much T3, T4 hormone
  • Myasthenia gravis – joint – muscle fatigue, ACH receptors is decreased, cannot produce enough to contract
19
Q

What is the mechanism of type III hypersensitivity?

What are the cells and chemicals involved in it?

Give examples of type 1 hypersensitivity disorders.

A

Immune-Complex reactions involve antigens (not part of a host tissue cell) antibodies (IgA or IgM) and complement

Formed in the circulation, precipitated in some organs

Mediated by circulating immune complexes (precipitate) between antigens and appropriate antibodies -> activate complement -> Attraction of PMNs -> Acute inflammation

Diseases

  • Systemic Lupus erythematosus
  • Rheumatoid arthritis
  • Poststreptococcal glomerulonephritis – strep throat - kidney and other organs
  • Postarterisis Nodosa
20
Q

What is the mechanism of type IV hypersensitivity? What are the cells and chemicals involved in it? Give examples of type 1 hypersensitivity disorders.

A

Cell-mediated, delayed type hypersensitivity reaction - No antibody (T Lymphocytes)

Exposure to an allergen and occur when allergens are taken up by antigen=presenting cells to lymph nodes and present the allergen to T cells. Intracellular bacteria, such as the one that causes tuberculosis, trigger this type of cell mediated immune response
Macrophages transform into epithelioid cells -> formation of giant cells by fusion of Epitheloid cells -> formation of granuloma

Diseases

  • Caseous necrosis (‘cheese like’ on the center of this giant granuloma)
  • Tuberculosis – latent phase, contained by the granuloma, active when the body immunity is lower
  • Sarcoidosis
  • Contact Dermatitis
21
Q

What are the causes of autoimmune diseases?

A

The immune system fails to display self-tolerance and attacks the person’s own tissues

22
Q

How self-tolerance can be broken in a susceptible person? What is the results of this?

A

The influence of unknown environmental triggers and certain genes that maek some people more susecptible, self-tolerance breaks down, leading to activation of self-reactive clones of T cells and B cells .

These cells then generate cell-mediated or antibody-mediated immune responses against self-antigens

23
Q

What are the possible mechanisms of different autoimmune diseases? Give examples of each.

A
  • Production of autoantibodies - antibodies that bind to and stimulate or block self antigens
  • Autoantibodies that mimic thyroid stimulating hormone are present in Graves disesase and stimulate secretion of thyroid hormones - producing hypothyroidism
  • Autoantibodies bind and block ACH receptors cause muscle weakness in Mysathenia Gravis
  • Activation of Cytotoxic T Cells that desctroy certain body cells
  • Type 1 diabetes melltus - t cells attack the insulin-producing pancreatic beta cells
  • MS - T cells attack myelin sheats around axons of nerons

Innapropriate activation of Helper T Cells or excessive produciton of Gamma-interferon occur

24
Q

What are the possible mechanisms of SLE pathogenesis? What are the organs usually affected?

A

Lupus - Cause is not known - a genetic predisposition to the disease and environmental factors (infections, antibiotics, ultraviolet light, stress, and hormones) may trigger it

  • Abnormalities in apoptosis, a type of programmed cell death in which aging or damaged cells are neatly disposed of as a part of normal growth or functioning
  • During an immune reaction to a foreign stimulus, such as bacteria, virus, or allergen, immune cells that would normally be deactivated due to their affinity for self-tissues can be abnormally activated in SLE

Organs impacted: Skin (butterfly rash, ulcers, hair loss, Raynauds phenomenon - blue hands), Joint pain, arthritis, brain-CNS symptoms, Kidney - Lupus nephritis, Lymphnode & Spleen, Red blood cells - anemia

25
Q
A