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PAS 753 (Molecular Pathophysiology) > Immunopathology > Flashcards

Immunopathology Flashcards

1
Q

how does a normal immune response cause disease

A

damage from inflammation in response to pathogen can exceed the damage done by the pathogen

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2
Q

three infections that trigger a damaging immune response

A
  1. tuberculosis
  2. leprosy
  3. sarcoidosis
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3
Q

hypersensitivity

A

altered immune response to an antigen which results in disease or damage

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4
Q

allergy (atopy)

A

hypersensitvity to environmental allergies

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5
Q

autoimmunity

A

hyper sensitivity to self-antigens

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6
Q

alloimmunity

A

reaction to antigens from someone else

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7
Q

four types of hypersensitivity

A

Type 1: IgE mediated (anaphylaxis)

Type 2: cytotoxic reaction to self allergens (lmyastheia gravis)

Type 3: immune complex reactions (lupus)

Type 4: cell mediated (chronic transplant reaction)

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8
Q

what is the difference between atopic individuals and non atopic

A

atopic individuals developed more Th1 lymphocytes vs Th2

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9
Q

how does IgE cause atopy

A

IgE binds to mast cells, which degranulate and release high amounts of histamine

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10
Q

where are three locations of concentrated mast cells

A
  1. skin
  2. airway mucosa
  3. GI
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11
Q

what is the physical interaction between allergens and IgE on mast cell receptors

A

IgE binds to mast cells, allergens form cross links between IgE to produce a stronger response

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12
Q

what is the difference between Th1 and Th2

A

helper lymphocyte 1 produces more IgG

Th2 produces more IgE

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13
Q

why do some people produce more Th2 lymphcytes

A

the mechanism isn;t know but may be related to the hygiene hypothesis

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14
Q

what is the potential link between infection and allergies

A

exposure to bacterial infection increases the production of Th1, if there is no infection exposure then Th2 dominates

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15
Q

what is the cut off age that a person must be exposed to certain antigens to produce more Th1 cells vs Th2 cells

A

exposure before age 2 will result in more Th1 cells, after more Th2 cells

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16
Q

T/F everyone has the potential for autoimmune disease

A

True, everyone has some defective cells

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17
Q

genetic risk factors for autoimmune disorders

A

family and species genetics

18
Q

civilization hypothesis

A

the formation of cities with close proximity of people and animals increased the number of epidemics and pandemics

this created an evolutionary pressure to develop a strong resistance to infection but decreased our ability to regulate immune response to self antigens and neoplasm

19
Q

autoimmune pathophysiology

A

T cell antigen receptors will bind with antigens they have a lower affinity for (like self antigens) if they are activated molecular mimicry

20
Q

molecular mimicry

A

when an autoimmune disease is triggered by an infection due to T cell cross reactivity

21
Q

two examples of molecular mimicry

A
  1. strep pyogenes and rheumatic fever
  2. coxsackie and type I diabetes
22
Q

antigen spreadng

what specific disease can this cause

A

when damage from an intial autoimmune response allows T and B cells to cross react with other self antigens

can cause lupus

23
Q

what are four ways to treat autoimmune disease

A
  1. decrease number of lymphocytes
  2. reduce production of antibodies
  3. interfere with T cell activation
  4. reduce cytokines (interleukin and tumor necrosis factor)
24
Q

two categories of immunodeficiency symdromes

A
  1. congenital
  2. acquired
25
Q

three examples of congenital immunodeficiency

A
  1. isolated T cell deficiency
  2. isolated B cell deficiency
  3. SCIDS
26
Q

what lymphocyte does HIV attack to cause AIDs

A

CD4 helper T cells

27
Q

what are four causes of acquired immunodeficiency

A
  1. AIDS
  2. immunosuppressive therapy
  3. inadequate nutrition
  4. tuberculosis
28
Q

what are the symptoms of acute HIV infection

A

flu like symptoms that occur 2-4 weeks after exposure and last 1-4 weeks

29
Q

latent HIV infection

A

gradually decreasing CD4 counts and increasing viral load

30
Q

what are three factors that influence the length of the latent phase of AIDS

A
  1. nutrition
  2. other diseases
  3. antiviral treatment
31
Q

what is the goal of current HIV treatment

A

prolonging the latent phase

32
Q

what is the primary indicator of the AIDS phase of an HIV infection

A

opportunisitc infection or unusualy cancer

33
Q

if an HIV positive patient is diagnosed with leukemia and receives a blood marrow transplant which decreases the amount of HIV in his blood, what happened

A

the bone marrow donation was homozygous for a chemokine receptor mutation which removed the receptor needed for HIV to bind with CD4 cells

34
Q

why is there a difference between HIV mortality in developed countries vs Africa

A

because developed nations have better nutrition, less exposure to disease, and better access to healthcare

35
Q

what is an example of an excessive immune response

A

cytokine storm

36
Q

what causes cytokine storm

A

introduction of super antigens that cause a feedback loop leading to excessive activation of cytokines and their effectors

37
Q

what are two historical instances of cytokine storm

A
  1. 1918 flu pandemic
  2. 2006 trail of CD28 agonist monoclonal antibodies
38
Q

why was the flu of 1918 unique?

how did most people die?

A

it was most fatal in young healthy people due to cytokine storm

either from intial cytokine storm or secondary pneumonia

39
Q

how is cytokine storm relevant to modern cancer therapy

what is the risk of this therapy?

A

patient T cells can be modified in vitro and given back to the patient to target cancer cells

it can cause a cytokine storm

40
Q

what are two sources of “super antigens”?

what are two pathologies associated with cytokine release

A

bacterial toxins or viral proteins

toxic shock and septic shock

PAS 753 (Molecular Pathophysiology) (17 decks)

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