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BIOL 2200 > module 2: Immune System Disorders > Flashcards

module 2: Immune System Disorders Flashcards

1
Q

what is hypersensitivity?

A

an altered immunologic response to an antigen that results in disease or damage to the individual

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2
Q

what is an allergy?

A

hypersensitivity to environmental antigens

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3
Q

what is an allergen?

A

an antigen involved in an allergic response

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4
Q

what is an immediate hypersensitivity reaction?

A

type 1 reaction

  • occur against environmental antigens and are therefore allergic
  • IgE
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5
Q

what is anaphylaxis?

A

the most severe systemic allergic reaction
- generally a type 1 mechanism and potentially life threatening

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6
Q

what is delayed hypersensitivity reaction?

A

results typically peak 48-72 hours after exposure

  • type 4 cell mediated hypersensitivity
  • antibodies are not involved
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7
Q

what is an autoimmune response?

A

inflammation and attacking when not supposed to
- specifically attacking ourselves

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8
Q

what is an alloimmune response?

A

an immune response to alternative forms of an antigen not found in recipient’s body (allogen)

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9
Q

what is urticaria?

A

a localized pruritic skin disruption characterized by wheals and hives

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10
Q

what in an immunotolerance?

A

a state of immunological control whereby an individual does not make a detrimental immune response against their own cells and tissues

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11
Q

Describe the mechanism of a Type I hypersensitivity response and give examples

A

allergies for the most part

  • 2 major steps:
    1) first exposure: barely any reaction “sensitized”
  • stimulation of B- cells = production of IgE
  • IgE binds to mast cells

2) second exposure:

  • antigen/allergen comes in to bind to IgE on mast cells = degranulation
  • degranulation = histamine release
  • histamine release = inflammation, broncho spasms/constriction
  • longer term response:
    • mast cells generates leukotrienes, prostaglandins = further inflammtion and local/systemic effects (ex: mucous)
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12
Q

what are the two mechanisms of injury through type 2 hypersensitivity?

A
  1. causing damage through inflammation
  2. directly affecting cell metabolism
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13
Q

Describe the inflammation mechanism of a Type II hypersensitivity response and give examples

A
  • involves IgG & IgM
    1. produce a lot of inflammation (2 things can happen)
    a) complements & antibody-mediated cell destruction:
  • antibodies (IgG, IgM) bound to an antigen on the tissue cell surface =
    • phagocytosis OR activate complement = phagocytosis or cell lysis
  • ex: blood transfusion reaction

b) complement and antibody mediated inflammation:

  • antibodies bound to extracellular connective tissues = activate complement
  • complement components initiate inflammatory response
    • mast cells activated = release histamine
    • histamine = neutrophils & monocytes
  • cell injury
  • ex: tissue graft rejection
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14
Q

Describe the cell metabolism mechanism of a Type II hypersensitivity response and give examples

A
  • the antibody attaches to a receptor on cell surface = changes function of cell (2 things happen):
  1. replaces the chemical that normally fits into the receptor = inappropriate cell stimulation
  2. blocking/destroying the receptor
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15
Q

Describe the mechanism of a Type III hypersensitivity response and give examples.

A
  • IgG, IgM makes immune complex
  1. the antibody binds to free-floating antigen (aka bloodstream) = circulates through the bloodstream
  2. antigens in bloodstream deposits on cell surfaces/tissues = inflammation/tissue damage due to lysozymes
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16
Q

what is arthus reaction?

A

the localized immune complex reaction usually to an injected drug, producing a local inflammatory response that can be severe in some cases

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17
Q

what are the 2 mechanisms of type 4 hypersensitivity?

A
  1. delayed response
  2. direct cell-mediated cytotoxicity
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18
Q

Describe the mechanism of a delayed Type IV hypersensitivity response and give examples

A
  1. antigen ingested by an antigen-presenting cell (ex: macrophage)
  2. antigen transported to lymph node and bind to t-helper cells
  3. t-helper cells activate and go back to tissues = release inflammatory cytokines
  4. cytokines = macrophage recruitment

ex: TB skin test, contact dermatitis

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19
Q

Describe the mechanism of a direct cell-mediated cytotoxicity Type IV hypersensitivity response and give examples

A
  1. antigen ingested by antigen presenting cell
  2. antigen is transported to lymph node and presented to t-helper cells
  3. t-helper cells activate cytotoxic T cells
  4. cytotoxic T cells destroy body cells that display the antigen

ex: viral infections

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20
Q

what are 3 actions of histamine?

A
  1. increases vascular permeability
  2. causes vasodilation
  3. contracts bronchial smooth muscle tissue
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21
Q

Describe the general signs and symptoms of IgE (type I) mediated responses

A
  • most common “allergic reactions”
  • AKA : immediate hypersensitivity” (15-30 min after exposure)
  • most reactions occur against environmental antigens = allergic
  • IgE can play a part in autoimmune and alloimmune disorders
  • some allergic reactions are not type 1 reactions
  • strong genetic linkage shown
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22
Q

Outline the signs, symptoms, and treatment of allergic Rhinitis (hay fever)

A
  • signs & symptoms: sneezing, itching, watery nasal discharge
  • treatment: antihistamines, decongestants, nasal corticosteroids, allergen avoidance
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23
Q

Describe the mechanism, causes, signs, symptoms and treatment of anaphylaxis

A
  • mechanism:
    • substance injected/ingested = enters bloodstream
    • enters bloodstream = vasodilation through whole body
    • vasodilation through whole body = anaphylactic shock
    • anaphylactic shock = systemic BP drop
  • signs/symptoms:
    • itchy rash, flushed skin
    • laryngeal edema, wheezing/difficulty breathing
    • low blood pressure
    • tachycardia
  • treatment: epinephrine (epi-pen)
    • relaxes smooth muscle in bronchioles = bronchodilation
    • contracts smooth muscle in vessles = vasoconstriction
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24
Q

Describe the mechanism, causes, signs, symptoms and treatment of bronchial asthma

A
  • mechanism:
    • acute phase: 10-20 mins
    • IgE binds to mast cells = binds to bronchial smooth muscle
    • bronchial smooth muscle spasms/constricts
    • goblet cells produce mucus furtherign the difficulty to breath
    • late phase response: 4-8 hours
    • mucous pools in areas & cilia is not able to move mucous
    • infiltration of immune cells = vascular permeability & edema
    • thickening and narrowing of airways by edema mucus layer
  • causes:
    • extrinsic: type 1 response to environmental allergens (ex: pollen, animal dander)
    • intrinsic: respiratory infection, cold air, emotional stress
  • signs & symptoms:
    • wheezing, breathlessness, chest tightness, coughing (normally at night or early in morning)
  • treatment: inhaler
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25
Q

Define immunotolerance

A

a state of immunological control whereby an individual does not make a detriemental immune response against their own cells and tissues

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26
Q

Define autoimmune disease and give two possible mechanisms for its occurrence

A

an inappropriate immune response to tissues normally present in the body

2 mechanisms:

  1. release of sequestered antigens
  2. molecular mimicry
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27
Q

what is the release of sequestered antigens?

A

when some areas in the body does not have circulation of markers = lymphatic system does not recognize it when it gets damaged

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28
Q

what is molecular mimicry?

A

when pathogens have markers that look like your own cells, so our body starts attacking both markers since they are unsure/confused

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29
Q

Describe the mechanism, clinical manifestations and treatment of SLE (systemic lupus erythematosus

A
  • mechanism:
    • production of large variety of antibodies = body attacks itself in different ways
    • type 2 and 3 response
      • antibody complex are deposited into the tissues = inflammation (type 3)
  • clinical manifestations:
    • swollen, painful joints
    • butterfly rash on face
    • body rash
    • inflammation of various areas
  • treatment: no cure
    • NSAIDs to supress inflammation & pain
    • immunosuppressive drugs
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30
Q

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

A

transplant rejection

MCHI proteins (AKA human leukocyte antigens- HLA’s) are unique to each individual = antigenic (can’t tolerate other MCHI from different bodies)

  1. if you get tissue transplant, body may not recognize MHCI on new tissue = antibodies made to target MCHI on new tissue
  2. antibodies attack new tissue = inflammation
  3. inflammation = rejection

HLAs are more similar to a family member than some random person

  • try to match HLAs = reduce chance of inflammatory response to the transplant you’re receiving
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31
Q

what are 3 types of tissue rejection

A
  1. hyperacute
  2. acute
  3. chronic
32
Q

what is a hyperacute pattern of rejection?

A
  • occurs immediately
    • as soon as you hook up the bloos supply of that transplanted tissue
  • the donor antigen has already been in the recipient’s vody and the recipent already mounted an immune response to it = type 3 hypersensitivity
33
Q

what is an acute pattern of rejection?

A
  • occurs within days to months after transplant
  • type 4 reaction
34
Q

what is a chronic pattern of rejection?

A
  • occurs after months to years
  • slow progressive organ failure of transplanted tissue
  • weak type 4 hypersensitivity
35
Q

Describe immunodeficiency and differentiate between primary and secondary

A
  • immunodeficiency = the failure of the immune system to function normally, resulting in increased susceptibility to infections
  • primary (cogenital) = caused by genetic defect & rare
  • secondary (aquired) = caused by something else (ex: cancer, infection), much more common
36
Q

Outline the five main types of primary immunodeficiency (PID).

A
  1. B lymphocyte
  2. T lymphocyte
  3. combined
  4. complement
  5. phagocyte (neutrophils, macrophages)
37
Q

what are characteristics of a B lymphocyte primary immune deficiency?

A
  • no circulating antibodies/ not producing enough antibodies
  • only certain antibodies are beign produced
38
Q

what are characteristics of a T lymphocyte primary immune deficiency?

A
  • low cell-mediated immunity
  • low level of circulating antibodies due to lack of t-helper cells
39
Q

what are the characteristics of a combines primary immune deficiency?

A
  • most severe is SCIDs (ex: boy in bubble)
  • both B & T cells are not working/being produced
  • bare lymphocyte syndrome
40
Q

what is bare lymphocyte syndrome?

A

no MHC-1 or MCH-2 molecules = no way for cells to interact

death usually occurs before 5 years of age

41
Q

what are characteristics of a complement primary immune deficiency?

A
  • not producing the appropriate complement proteins
  • most severe is C3 deficiency
    • disrupts all the rest of the pathways of the complement system
42
Q

what are characteristics of phagocyte primary immune deficiency?

A
  • defects of phagocyte number, function, ro both
  • increased risk for infection by bacteria
43
Q

Outline the clinical warning criteria of immunodeficiency in infants

A
  • recurrent severe infections
  • 6-12 infections per year
  • numerous infrctions per year
44
Q

how would you treat a B cell deficiency?

A

replacing the missing component

  • regular infusions of gamma-globulins
45
Q

what treatment would you do for someone who is lymphycyte deficient?

A

replace stem cells through implantation with stem cell rich tissue (bone marrow)

46
Q

what treatment would you do for someone who has severe combined immunodeficiency?

A

transfusions of erythrocytes that contain adenosine deaminize

47
Q

Define secondary immune deficiencies and give at least one example

A

complications of other pathophysiological conditions (another infection affecting your immune response)

  • much more common than primary immune deficiencies
  • can be minor, short-term
  • can be severe (ex: AIDS)
48
Q

Describe the causative agent of AIDS and how HIV affects the immune system

A
  • causative agent = human immunodeficiency virus (HIV)
  • HIV targets helper- T cells = destoys them
  • destroyed helper T-cells = nohumoral and cell mediated immunity
49
Q

Describe how HIV is transmitted.

A

blood borne pathogen

  • IV drug use
  • sexual activity
  • maternal/child before or during birth
50
Q

Outline common diagnostic features of AIDS

A
  • flu-like symptoms
  • atypical infections
  • cancers
  • chronic disease syndromes
51
Q

what are some atypical infections and cancers associated with AIDs?

A
  • pneumocystis carinii pneumonia (PCP)
  • cytomegalovirus (CMV)
  • thrush
  • MAC (mycobacterium avium)
  • kaposi’s sarcoma
  • non-hodgkin’s lymphomas
  • cervical carcinoma
52
Q

what is pneumocystis carinii pneumonia (PCP)?

A

a fungal microbe found in lungs of healthy individuals

53
Q

what is cytomegalovirus (CMV)?

A
  • herpes genus
  • can cause retinitis encephalitis, or encephalitis and GI symptoms with AIDS
54
Q

what is thrush?

A
  • yeast infection
  • oropharyngeal or esophageal candidiasis
55
Q

what is MAC?

A

everyday soil and water pathogens producing fevers, diarrhea, malabsorption, and anorexia in immunocompromised individuals

56
Q

what is kaposi’s sarcoma?

A

viral induced skin cancer

57
Q

what is non-hodgkin’s lymphomas?

A

diverse group of lymphocyte cancers

58
Q

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

A
  1. cells of immune system not able to proliferate as rapidly
  2. total number of T cells is maintained, but they have decreased cytotoxicity
  3. antibody production is also decreased
59
Q

Anna L., a 69-year-old woman was fit and well until one August when she was stung on the back of her right hand by a wasp. She had previously been stung on several occasions, the last time 2 weeks earlier. Within 5 min, she felt faint, followed shortly by a pounding sensation in her head and tightness of her chest. She collapsed and lost consciousness and, according to her husband, became grey and made gasping sounds. After 2-3min, she regained awareness but lost consciousness immediately when her husband and a friend tried to help her to her feet. Fortunately, a doctor neighbour arrived in time to prevent her being propped up in a chair: he laid her flat, administered intramuscular epinephrine (adrenaline) and intravenous antihistamines and ordered an ambulance. She had recovered fully by the next day.

What kind of hypersensitivity is Anna experiencing? What lab test result clearly supports your diagnosis?

A

Type 1. The serum IgE is above normal range.

60
Q

Why hadn’t Anna experienced any symptoms when stung previously?

A

The first exposure only sensitizes – unlikely to have such a severe reaction the first time

61
Q

Describe the pathophysiology behind the process that occurred in Anna after she was stung this time (i.e., the mechanism of a Type I reaction after the first sensitization).

A
  1. Allergen enters the body.
  2. Allergen interacts with IgE that is already attached to mast cells.
  3. This causes the mast cell to degranulate
  4. Histamine is released
  5. There is an increase in vascular permeability, increase in vasodilation and bronchoconstriction
62
Q

Anna L., a 69-year-old woman was fit and well until one August when she was stung on the back of her right hand by a wasp. She had previously been stung on several occasions, the last time 2 weeks earlier. Within 5 min, she felt faint, followed shortly by a pounding sensation in her head and tightness of her chest. She collapsed and lost consciousness and, according to her husband, became grey and made gasping sounds. After 2-3min, she regained awareness but lost consciousness immediately when her husband and a friend tried to help her to her feet. Fortunately, a doctor neighbour arrived in time to prevent her being propped up in a chair: he laid her flat, administered intramuscular epinephrine (adrenaline) and intravenous antihistamines and ordered an ambulance. She had recovered fully by the next day.

What is the probable cause of the tightness in her chest and her problems in breathing, in particular?

A

The bronchoconstriction due to histamine

63
Q

It is apparent that Ana’s reaction has moved beyond an allergic response into a more serious type of response. What is this response called? Justify your answer by matching the characteristics of this response with Ana’s signs/symptoms.

A

Anaphylaxis

This affects more than one body system and she is having trouble breathing (respiratory system).

64
Q

Ana may also be developing an even more dangerous level of response – what would this be? (Hint: why did she lose consciousness every time she attempted an upright position?)

A

Anaphylactic shock – the circulatory system is also affected.

Systemic vasodilation decreases BP. In the upright position, there is not enough blood/oxygen going to the brain, so she loses consciousness.

65
Q

. Would you expect an elevated or a depressed heart rate in this patient (anna) at this time? Explain your choice.

A

Increased HR, to compensate for decreased BP

66
Q

. Explain how the administration of epinephrine was able to give her immediate relief.

A

Epinephrine causes increased vasoconstriction = increased BP = increased flow of blood to the brain.

Epinephrine causes an increase in airway diameter, which counteracts the bronchoconstriction

67
Q

Her total serum IgE was 147iu/ml (normal < 120iu/ml). Her antigen-specific IgE antibody level to wasp venom was 21U/ml (RAST class 4) but that to bee venom was 0.3U/ml (RAST class 0). (Note: “RAST” refers to results of blood tests that yield the amount of IgE specific to a particular allergen). The patient was a candidate for specific allergen injection immunotherapy (hyposensitization) for her wasp venom anaphylaxis. The slight but definite risk of desensitization was explained and balanced against the major risk of anaphylaxis should she be stung again. The first injection consisted of 0.1ml of 0.0001µg/ml of wasp venom vaccine given subcutaneously. Over the next 12 weeks, gradually increasing doses were given without adverse effects. Over this period, she tolerated injections of 100µg venom. She then continued on a maintenance regimen of 100µg of venom per month for 3 years

What was the purpose of the blood tests for specific antigens? (i.e., why is it advantageous to identify the specific antigen?)

A

So you know what to desensitize her with.

68
Q

Describe the process that occurred in Anna during her desensitization therapy, explaining the reason for the eventual reduction in her allergic reaction.

A

Inject a small amount of antigen multiple times over a series of months

This causes production of IgG

Over time, ther’s enough IgG that it can neutralize the anitigen before the entigen interacts with IgE on the mast cells.

69
Q

Give a name to a typical “local response” that might be observed at the point of injection in anna’s case. What term(s) would be used if there were many of these expressed over an area of the skin?

A

Wheal and flare. Urticaria / hives

70
Q

Jennifer Peterson (32 yrs) has been having a rough autumn. She has been feeling tired and “achy” in her joints for weeks, and now a reddish rash has appeared on her face. She attributed her state to looking after two preschoolers, with a third child experiencing a rocky start to the first grade of school. However, she has decided that an appointment with her GP is now necessary, as she has begun to notice a significant hair loss.

Based on the above signs and symptoms, from what autoimmune disease is Ms. Peterson most likely suffering?

A

Systemic lupus erythematosis

71
Q

Jennifer Peterson (32 yrs) has been having a rough autumn. She has been feeling tired and “achy” in her joints for weeks, and now a reddish rash has appeared on her face. She attributed her state to looking after two preschoolers, with a third child experiencing a rocky start to the first grade of school. However, she has decided that an appointment with her GP is now necessary, as she has begun to notice a significant hair loss.

Identify the two main types of hypersensitivity reactions that Ms. Peterson can be expected to exhibit. Explain the main difference between these two types of hypersensitivity.

A

Type 2 – the antibody combines with RBC, WBC, platelets and activates complement, causing inflammation that destroys the cell.

Type 3 – the antibody combines with free floating antigen (nucleic acids, coagulation proteins, complement proteins) that forms an immunocomplex that can be deposited anywhere in body tissue. The antibodies activate complement which causes inflammation in the tissue where it is deposited.

72
Q

. A common treatment for this disorder are NSAIDs. What is the rational for the use of this drug?

A

The disease is caused by inflammation and NSAIDs decrease the inflammatory response.

73
Q

. Should there be additional concern if Ms. Peterson begins to experience swelling in her legs? Explain the cause of this manifestation (Hint: think of a structure in an organ which could be a likely destination of immunocomplexes borne in the bloodstream (see slide 37). If this structure is affected, what important blood component would be decreased, due to it being lost in the urine? How would loss of this component cause tissue swelling? (Hint: google “what is responsible for the osmotic pressure of blood”).

A

Glomerulonephritis: proteins are lost in the urine. This decreases the protein content of the blood, which means fluid isn’t drawn back into the blood from the tissues, which results in edema.

The presence of edema in her legs suggests that she has glomerulonephritis.

74
Q

Further complications of lupus include anemia and an increased risk in bleeding. Explain how these complications could arise. (Hint: What blood components are involved in anemia and bleeding/clotting? How are these components possibly being reduced?)

A

Type 2 – loss of RBC will cause anemia, loss of platelets interferes with clotting Type 3 – loss of clotting proteins will interfere with clotting

75
Q

There is a possibility that lupus could cause an immunodeficiency. How could this happen? (There are actually two ways this could occur.) Choose whether this would be classified as a primary or secondary immunodeficiency, and explain your choice.

A

Type 2 – loss of lymphocytes

Type 3 – loss of complement proteins

Secondary, due to another disease.

BIOL 2200 (12 decks)

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