mod 2 Flashcards

1
Q

Explain Type 1 Hypersensitivity

A

-igE is mediated
first exposure could have little to no response - it will prime the response causing sensitization - stimulate b cells into plasma cells then IgE is produced that binds to mast cells.
subsequent exposure - allergen binds to the IgE on the mast cells which causes degranulation (histamine release) - inflammation, vasodilation and increase in permeability of membranes begin + bronchoconstriction.

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2
Q

Explain Type 2 Hypersensitivity

A

Involves IgG and IgM antibodies and binds to extracellular tissues directly. Produces a lot of inflammation and affecting cell metabolism which leads to negative outcomes.
- binding causes phagocytosis or complement of cells (destruction) and affects cell metabolism which binds to a receptor that inappropriately activate the cell + block and destroy the receptor.

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3
Q

Explain Type 3 Hypersensitivity

A

Involves IgG and IgM antibodies
It does not bind to something, but to something in the blood (floating antigens) - nucleic acids, proteins and peptides.
- deposits in tissues and causes inflammation and tissue damage.
neutrophil recruitment which activate ROS and compounds to kill pathogens which could be direct (bind to cell surface) + within connective tissue.

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4
Q

Explain Type 4 Hypersensitivity

A

Does not involve antibodies

  1. delayed response - antigen is ingested by antigen presenting cells - TH cells - inflammation (cytokines) macrophage recruitment = tissue damage.
  2. Direct cell mediated cytotoxicity - same as delayed but cytotoxic activation but destroys all cells with the antigen (inflammation + damage occurs) w/ not macrophage recruitment + autoimmune disease and condition.
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5
Q

Define Hypersensitivity

A

An altered immunological response to an antigen that results in a disease or damage to an individual

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6
Q
  1. You eat a delicious peanut butter cookie. Suddenly you experience a tingling sensation and swelling around your mouth. You start to have some airway constriction. This hypersensitivity is called (a/an):
    a) Allergic reaction
    b) IgE-mediated reaction
    c) Immediate hypersensitivity
    d) Type I hypersensitivity
    e) All of the above
A

e)

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7
Q
  1. Describe, with a diagram, the mechanism of a Type I response. Include the sensitizing exposure and the re-exposure (with the immediate and longer-term response).
A

sensitizing exposure
1. allergen stimulates iGE production which attracts mast cells
Re-exposure to allergen binds to the igE on mast cells and activates them.

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8
Q
  1. What are 3 actions of histamine?
A

vasodilation, increase membrane permeability and smooth muscle contraction (broncoconstriction)

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9
Q

Where are the antigens located that react with the antibodies in a Type II response vs a Type III response?

A

Tissues (connective tissue) or blood cells - destroy by inflammation or damage.
Antigens bind to the antibodies (tissues) - non specific - inflammation or tissue damage.

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10
Q
  1. Describe the following mechanisms (and be familiar with the examples) of a Type II response: a) cell destruction b) inflammation c) altered cell metabolism
A

a) complement + antibody mediated cell destruction.
- IgG + IgM binds to an antigen on the tissue’s cell surface (opsonization) OR. complement is activated and PHAGocytosis occurs. (ex. blood transfusions)

b) antibodies bind to the extracellular connective tissue - matrix, basement membranes - then it activates the complement to initiate the inflammatory response by - mast cell activation or act as chemokines to attract neutrophils + monocytes.

c) antibodies attach to the receptors, 2 ways.
- blocks or destroys the receptors
- alters the chemicals that usually attach there.

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11
Q

Where are the antigens initially located that react with the antibodies in a Type III response? Describe the general mechanism of a Type III response and give an example.

A

Any tissues - non specific (could be connective)

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12
Q

Describe the difference between a systemic immune complex disorder occurring, versus a localized immune complex reaction occurring?

A

Systemic - affecting the whole body.

Localized - affecting a certain area.

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13
Q

Which of the above two mechanisms causes “serum sickness” and what can it be caused by?

A

Type 3 hypersensitivity - systemic immune complex disorders.

  • Ab - Ag complexes are deposited in. a wide range of body tissues.
  • ex. venom, antibiotics, foods and drugs.
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14
Q

Which of the above two mechanisms causes the “Arthus reaction” and what can it be caused by?

A

Type 3 - localized immune response.

- usually to be injected drug, producing a local inflammatory response which can be severe.

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15
Q

What is not involved, and what is involved, in a Type IV response?

A

Antigens are not involved and it involves helper T cells (Th1) and cytotoxic cells and inflammatory cells (macrophages)

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16
Q

Describe Delayed hypersensitivity

A

Antigen is ingested by an antigen presenting cell eg. macrophage and transported to the lymph nodes and presented to TH1 cells - then activated to profilterate and migrate to the tissues to release cytokines then chemotaxis of monocytes occur - macrophages release lysosomal enzymes + ROS and comes tissue destruction.

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17
Q

Describe cell mediated cyotoxicity

A

Antigen is ingested and transported to the lymph node + presented to Th1 cells then activated to activate cytotoxic t cells and travels to destroy the cells containing the antigen. (autoimmune disease - diabetes mellitus + viral infections hepititis)

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18
Q

Name 3 areas of the body where the effects of mast cell degranulation can be significant.
Describe the effects in each area and relate these to the signs and symptoms that occur in each area.

A

Gastrointestinal tract - increase peristalsis snd fluid secretion - GI tract expulsion (vomit, diarrhea)

Airways - increase mucus secretion and decrease in diameter - blockage/congestion of airways (wheezing, coughing, phlegm) - swelling and mucus secretion in nasal passage.

Blood vessels - increase in blood flow and permeability - increase tissue fluid - increase lymph flow to lymph nodes, increase in cells + protein in tissues, increase tissue effector response (bp)

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19
Q

Allergic Rhinitis: signs + symptoms, treatment and diagnostic test

A

Signs + symptoms: sneezing, itching and watery eyes
Treatment: antihistamines, decongestants, nasal cortisteroids, allergen avoidance, desensitization therapy.
Diagnostic test: scratch test

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20
Q

Describe the mechanism behind desensitization therapy.

A

Small doses of the antigen over a long period of time. Developing igG so that it neutralizes the allergens, so it does not bind to IgE that causes an allergic reaction.

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21
Q

Identify the mechanism behind anaphylaxis and the significance about the types of substances that cause it.

A

mechanisms: substances that is injected into the blood stream or ingested - affects various tissues.
causes: insect bites/strings, food and antibiotics.

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22
Q

What part of this mechanism can cause anaphylactic shock?

A

inflammatory mediators that cause massive vasodilation and increase in capillary permeability.

23
Q

Anaphylaxis: signs and symptoms and treatment.

A

itchy rash, flushed skin (red rash), laryngeal edema, wheezing, difficulty breathing, *low bp and tachycardia.

epineprhine

24
Q

What is the difference between an extrinsic and an intrinsic trigger for bronchial asthma?

A

extrinsic - type 1 - environmental allergens (pollen, animal dander)
intrinsic - not type 1 - respiratory infection, cold air and emotional stress.

25
Q

Describe the signs and symptoms of bronchial asthma.

A

recurrent episode of wheezing, tight chest, coughing and breathlessness.

26
Q

Define immunotolerance. What occurs if immunotolerance breaks down?

A

when one does not create a detrimental imnune response to its own cells and tissues (immunological control)

autoimmune disorder

27
Q

Define immunotolerance. What occurs if immunotolerance breaks down?

A

when one does not create a detrimental imnune response to its own cells and tissues (immunological control)

autoimmune disorder

28
Q

By which two hypersensitivity reactions are autoimmune reactions usually caused?

A

Type 2 + Type 3

29
Q

Describe two possible mechanisms for an autoimmune disease.

A

Sequested antigen release - areas not drained by lymph nodes that is full of antigens, with no self antigen release the immune system cab ignore this (fetal development)
Molecular mimicry - where infection w/organism having aG close in structures to a self antigen - not confirmed except for rhueamatic fever/acute glomerulonephritis w/strep.

30
Q
  1. Describe systemic lupus erythematosus (SLE) to include the following:
    a. two self-antigens that are molecular (what type of hypersensitivity would this be?)
    b. three self-antigens that are cellular (what type of hypersensitivity would this be?

c. the most characteristic self-antigens
d. be familiar with signs and symptoms (easier to remember if you relate the mechanism of the hypersensitivity to the S&S)
e. treatment

A

a. type 2 - lymphocytes and platelets.
b. type 3 - nucleic acids, erythrocytes, and coagulative proteins.
c. nucleic acids, erythrocytes, coagulation proteins, lymphocytes and platelets.
d. swelling, painful joints, butterfly rash on face, body rash ^ w/sun exposure and various inflammation.
e. no cure, but NSAID’s can suppress inflammation and pain. Immunosuppressive drugs can be used in more serious instances (internal organ environment)

31
Q

Define “alloimmune response”.

A

Every cell has various compounds on the surface of cells which is unique per person.
If someone gives blood with CHO chain on the RBC that is the wrong type, they do not have that RBC therefore their body will attack and see it as an antigen.
Thus, create an immune response and destroy it (Type 3)

32
Q

Identify and explain the type of hypersensitivity reaction on which the alloimmune response involved with the ABO blood grouping is based.

A

Type 3 - IgG and igM is binds to the blood cells which is then damaged by inflammation and destructs its function.

33
Q

Describe the influence of HLA’s/MHCI’s on tissue transplantation.

A

HCL - produced in chromosome 6 - in relatives it is similar.
Needs tissue typing or else the immune response will react and attack.

34
Q

3 types of tissue rejection

A

hyper acute: immediate, preexisting recipient Ab to a donor Ag (from previous transplant or transfusion_ - type 3 - Arthus type

acute: within days to months post transplant - biopsy has many lymphocytes and macrophages - type 4 reaction.
chronic: months to years: slow progressive failure of organ transplant (blood vessel damage and fibrosis - weak type 4.

35
Q

Describe graft vs. host disease and in which type of transplant it most often occurs

A

Transplanted tissue contains the donor’s TH + TC cells that sees the recipients tissues as foreign material then attack it - most common in bone marrow.

Transplant and the recipient is usually immunocompromised, hard to fight back.

36
Q

Describe immunodeficiency and differentiate between primary and secondary.

A

The failure of the immune system to function normally/properly.

Primary - rare (congential) genetic defect presented at birth

Secondary - common - (acquired) by cancer, aging and infection

37
Q

What is the main clinical manifestation of immunodeficiency?

A

recurrent severe infections ex. pneunonia, bronchitis, sinusitis, menginiitis, septicemia.

38
Q

What would the type of recurring infection tell you about the type of insufficiency (e.g., viral vs bacterial?)

A

viral - colds, sore throat - middle ear infection.

bacterial per year - 8+ ear infections, 2 sinitis, 2+ pneumonia or persistent abscessed/fungal infection within a year.

39
Q

Identify the usual cause of a primary immune deficiency (PID), and describe the 5 main classes of PID.

A

Usually a single gene defect that affects # or function of immune cells.

B lymphocytes - no antibodies circulating - one class sometimes are affected (IgG + IgE)

T lymphocytes - cell mediated immunity = low and Th cells are important for B cells - low antibodies - defect in defence of pathogen or group of pathogen.
Combined (b+t) - most severe (SCID) no Ab, few lymphocytes, thymus reduction.

Complement - severe (c3) - involved in complement protein production pathway (increase infection risk with encapsulated bacteria).
Phagocyte (neutrophils + macrophages) - defects of # and function of macrophages or both + increase bacterial infection rate.

40
Q

Describe the treatments for B cell deficiency, lymphocyte deficiency, and SCID.

A

Replacing the components.

B cell - gamma globulins are regularly infused (antibody rich plasma)

Lymphocyte - stem cell replacement through implantation w/stem cell rich tissue (bone marrow)

Severe combined - erythrocyte transfusion of adenosine deaminize.

41
Q

Define secondary immune deficiencies and give one example

A

Acquired deficiency - complications of other pathophysiological conditions.
Eg. Aids. Diabetes mellitus

42
Q

What does “AIDS” stand for? Identify the causative agent of AIDS. How is it transmitted?

A

acquired auto immunodeficiency syndrome
profound immunosuppression, related to opportunistic infections, malignancies, weight loss (progressive wasting) and CNS degeneration
transmitted through blood, semen, vag fluid, breast milk, IV, sex - not contact or insects.

43
Q

How does the virus actually cause AIDS?

A

HIV destroys helper T cells that is required for cytotoxic t cells and plasma development that is needed for immunity.

44
Q

What are the early stage symptoms of HIV infection?

A

flu like symptoms then dissapears.

45
Q

How is AIDS diagnosed? (Be familiar with common opportunistic infections and malignancies, especially one example of an opportunistic infection, and one example of a malignancy.)

A

Antibodies, antigens and viral RNA. Atypical infections, cancers and chronic disease syndromes - such as thrush. orophangael or esophagael and kaposi sarcoma - skin induced cancer that is viral

46
Q

How is an HIV infection treated? Why is treatment difficult and why is a vaccine unlikely?

A

Target mechanisms for viral transmission and replication - cannot cure HIV bc it hosts in DNA which antimicrobial agents cannot work well on.

47
Q

What are 3 reasons for the poor antigenic response of the elderly?

A
  • immune system cells cannot profilterate fast
  • increase cell numbers the same but decrease cytotoxicity.
  • decrease antibody production.
48
Q

Define Allergen

A

Antigen involved in an allergic response

49
Q

Define Allergy

A

Hypersensitivity to an environmental antigen

50
Q

Define Pruritus

A

Symptoms of itching mf

51
Q

Define Urticaria

A

localized pruritic skin disruption characterized by wheals and hives (reddened bumps + swelling)

52
Q

Define Autoimmune response

A

Inappropriate response to tissues normally present in the body.

53
Q

Define Alloimmune response #2

A

in a single species - an immune response to alternate forms of an antigen not found in the recipient’s body (allogen) = eg. ABO Antigen, Rh antigens and tissue transplant.