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Pathophysiology (L3) > Immunity > Flashcards

Immunity Flashcards

1
Q

Difference between cellular and humoral

A

Cellular: Involves targeted killing of infected or abnormal cells
Humoral: Involves production of soluble immunoglobulins that confer protection from specific pathogens that are freely circulating

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2
Q

What is the difference between negative and positive selection?

A

Negative selection we are looking for attributes we don’t want and getting rid of it
Positive selection we are looking for attributes we WANT and keeping them

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3
Q

There are 4 different types of hypersensitivity reactions. What are they and give a brief description of each

A

Type I: Sensitization to antigen resulting in prod of IgE which primes mast cells, basophils and eosinophils
Type II: Antibodies bind cells and fix complement resulting in cell lysis
Type III: Deposition of antigen-antibody complexes in joints, tissues and vessel walls
Type IV: Host cells destroyed by cytotoxic T-Cells

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4
Q

What is the pathophysiology for type 1 hypersensitivity reaction?

A

Naive T and B cells come in contact with an allergen, generates a humoral responses with a prod of IgE antibodies

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5
Q

What are clinical manifestations for type 1 hypersensitivity reaction?

A

Erythema, edema, wheezing, rhinitis, coughing, diarrhea, vomiting, hives, pruritus, conjunctivitis

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6
Q

What are treatment options for type 1 hypersensitivity reaction?

A 
Epinephrine: Dilates airways, decrease mucus prod, contract vasc smooth muscle, dec vas perm, and improve myocardial contractility
Avoidance
Antihistamines
Corticosteroids
Desensitization
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7
Q

Compare T cell and B Cell: which pathogens are targeted

A

T: Intracellular pathogens and cancers
B: Extracellular pathogens

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8
Q

What is negative selection and where does it occur?

A

Clonal detection
If T-cell bind to self-antigens they are told to undergo apoptosis
Only T-cells which don’t bind are chosen

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9
Q

What is positive selection and where does it occur?

A

Testing whether a T cell binds to MHC. If it binds then it is chosen however it does not bind with MHC it is apoptosized

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10
Q

Describe the pathophysiology of lupus

A

A type III hypersensitivity reaction which causes inflammation of multiple body systems caused by an autoimmune reaction

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11
Q

Describe the treatment options of lupus

A

No cure
Control with use of:
NSAIDS: Control inflamm
Corticosteroids: Reduce severity and duration of disease symptoms
Immunosuppressants: Reduces antibody prod
Biologics: (Belimumab) Inhibs cell survival factor BLyS needed for b-cell survival
Low dose IL-2 therapy: Cytokine that promotes survival of regulatory T-helper cells

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12
Q

Describe the treatment options of lupus

A

No cure
Control with use of:
NSAIDS: Control inflamm and pain
Corticosteroids: Reduce severity and duration of disease symptoms (acute active disease)
Immunosuppressants: Treat severe symptoms involving internal organs
Biologics: (Belimumab) Inhibs BLyS needed for b-cell survival
IL-2 therapy: Promotes survival of regulatory T-helper cells

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13
Q

What is the clinical path from infection to death for HIV? Three phases

A
  1. Primary Infection: Dramatic increase in viral load and drop in CD4+ cell then bounce back to normal after adaptive intervention
  2. Latency: Gradual decline of CD4 with T-cells dying quicker than production
  3. AIDS: Acquired immunodeficiency syndrome with a dangerously low CD4 count
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14
Q

What is the pathophysiology of HIV?

A

Infection with HIV which targets CD4+ cells resulting in deficiency in adaptive responses

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15
Q

What are opportunistic infections? What are their importance and significance

A

Infections that occur frequently and easily with people with weak immune systems
Death occurs due to OIs

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16
Q

How is the process of negative selection different for a B cell?

A

If a B cell recognizes MHC it undergoes apoptosis

17
Q

Where does central tolerance occur for a B cell?

A

Bone marrow

18
Q

If a T cell recognizes self antigens it undergoes apoptosis, how is this different for a B cell?

A

B cells that recognize self antigens undergo somatic recombination to change their BCR

19
Q

What are measures that the body uses to prevent autoimmunity? 4

A

Negative selection (Clonal deletion)
Need for costimulatory molecules
Anergy
Regulatory T cells

20
Q

What is molecular mimicry?

A

When antibodies created for a specific infection cross-react to a self-antigen expressed in our body

21
Q

Autoimmunity may occur if self-antigens that were not present during T-cell and B-cell development become assessible. What are three situations where this occurs?

A
  1. Mutations in host genes results in expression of new proteins on cells surfaces (Ex. Cancer)
  2. Self-antigens are altered by attachment of small molecules (Ex. Drugs or toxins)
  3. Tissue trauma causes release of self-antigens that were previously sequestered from the immune system
22
Q

What are the three types of T-cells and what are their roles?

A

CD8: Cytotoxic, induces apoptosis in target cells
CD4: Helper T-cells, aid in providing signals which drive t and b cells differentiation and clonal expansion
Regulatory T-cells: Suppresses adaptive immune responses

23
Q

CD4 (Helper T-cells) are broken into three subtypes: Th1, Th2, and Th17. What do these do?

A

Th1: Secrete IL2 to activate cytotoxic T-cells
Th2: Secrete IL-4 provides co-stim signals for b cells
Th17: Secrete IL-17 which activates neutrophils

24
Q

What is the role of B-cells?

A

To differentiate into antibody secreting plasma cells and produce antibodies

25
Q

How do antibodies inactivate toxins?

A

Neutralization: Inactivate it
Agglutination: Bind multiple toxins to create precipitation
Precipitation: Tags antigens (opsonization) so macrophages can engulf easier

26
Q

Main difference between T and B cells

A

T: Resp for cell-mediated immunity
B: Mediate humoral response

27
Q

What are the main differences between MHC I and MHC II in terms of which cells are affected, which antigens are presented and which response it induces?

A

MHC I: All nucleated cells affected, presents endogenous antigens, induces a cellular response
MHC II: Antigen-presenting cells only, presents exogenous antigens and induces a humoral response

28
Q

What are the main differences between MHC I and MHC II in terms of which cells are affected, which antigens are presented and which response it induces?

A

MHC I: All nucleated cells affected, presents endogenous antigens, induces a cellular response
MHC II: Antigen-presenting cells only, presents exogenous antigens and induces a humoral response
AKA MHC 1 = destruction, MHC II = Protection

29
Q

What is the effect of histamine on: Blood vessels, resp system, GI system, integument and eyes

A

BV: Vasodilation and inc vas perm
Resp: Constriction of airways and inc mucus prod
GI: Inc mucus secretion and peristalsis
Integument: Inc vas perm and stim of free nerve endings
Eyes: Inc mucus secretion and stim of free nerve endings

30
Q

What is anaphylactic shock?

A

System wide vasodilation and increased vascular permeability due to a massive release of histamine

31
Q

How do antibodies inactivate toxins? Think PLAN

A

Neutralization: Inactivate it
Agglutination: Bind multiple toxins to create precipitation
Precipitation: Tags antigens (opsonization) so macrophages can engulf easier
L: Lysis (MAC)

32
Q

What is HAART?

A

Highly Active Anti-Retro Viral Therapy

Aggressive therapy with antiretroviral form to improve CD4+ cells

33
Q

What is the mechanism of action for nucleoside/nucleotide analogs?

A

Inhibit elongation of viral DNA by preventing addition of nucleosides

34
Q

What is the mechanism of action for reverse transcriptase inhibitors

A

Bind RT active site to prevent transcription of viral RNA into DNA

35
Q

What is the mechanism of action for protease inhibitors?

A

Prevent cleavage of viral polypeptides necessary for viral assembly

36
Q

What is the mechanism of action for entry inhibitors?

A

Block HIV fusion with CD4 and blocks CCR5 receptors

37
Q

What is the mechanism of action for integrase inhibitors?

A

Prevent viral DNA integration into host genome

Pathophysiology (L3) (8 decks)

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