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BUPA Basic Medical Sciences > Immunology/Inflammation/Vaccines > Flashcards

Immunology/Inflammation/Vaccines Flashcards

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USMLE® Step 1 flashcards
1
Q

What do COX-1 and COX-2 Inhibitors inhibit?

A

Cyclooxygenase (and therefore, thromboxane)

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2
Q

What cytokines are responsible for activating the anti-viral state in cells?

A

Type 1 IFNs

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3
Q

profound block in T cell development

A

Se vere combined Immunodeficiency (SCID)

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4
Q

What hypersensitivity is this?

Immune Thrombocytopenia - autoantibodies against protein antigens on platelet surface (NO INFLAMMATION)

A

Type II

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5
Q

The kinin cascade leads to the formation of what? Function?

A

Bradykinin - vasoactive

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6
Q

Lack of gamma chain (X-linked) or JAK3 (autosomal recessive) leading to lack of cytokine signaling (type of SCID)

A

Cytokine signaling deficiency

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7
Q

What hypersensitivity is this?

Graves Disease - autoantibody binds to TSH receptor —> activates receptor and causes inappropriate production of thyroid hormone

A

Type II

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8
Q

The clotting system leads to the formation of what? Function?

A

Thrombin and fibrin - clotting

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9
Q

What hypersensitivity is this?

Systemic Lupus Erythematosus (SLE) - cause by wide array of auto-antibodies leading to immune complex deposition

A

Type III

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10
Q

What hypersensitivity is this?

Myasthenia Gravis - autoantibody binds to Ach receptor; blocks Ach binding resulting in perceived muscle weakness; no inflammation

A

Type II

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11
Q

MHC II presents to which cell? What about MHC I?

A

MHC II: CD4+

MHC I: CD8+

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12
Q

What hypersensitivity is this?

anti-GBM; Goodpasture Syndrome - Autoantibodies against portion of collagen in glomerular and alveolar capillary membrane —> kidney inflammation and hemorrhage

A

Type II

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13
Q

Th1 CD4+ stimulates what?

A

Phagocytosis of microbes
IFN-gamma for macrophage activation
IgG production
Opsonization

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14
Q

Abnormal fibrils are produced when soluble precursors undergo conformational change and aggregate; Fibrils are deposited into extracellular tissues and disrupt normal function

A

Amyloidosis

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15
Q

accumulation of adenosine, resulting in premature death of lymphocyte precursors

A

ADA deficiency

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16
Q

What are the following antibodies responsible for: IgA, IgE, IgG, IgM?

A

IgA - mucosal immunity
IgG - everything; Th1 activated
IgE - allergies/mast cell degranulation; Th2 activated
IgM - classical pathway of compliment

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17
Q

What hypersensitivity is this?

Autoimmune Hemolytic Anemia - autoantibodies against protein antigen on RBC surfaces

A

Type II

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18
Q

block in granulopoesis (neutrophil production)

A

Severe congenital neutropenia

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19
Q

What are the secondary lymphoid organs?

A

Lymph nodes, spleen, mucosal and cutaneous lymphoid tissue

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20
Q

What are the co-stimulating receptors on T cells?

A

B7 - CD28

CD40L - CD40

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21
Q

A severe immunodeficiency due to lack of phagocyte oxidase

A

Chronic granulomatous disease (CGD)

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22
Q

An inherited deficiency in adhesion molecules required for cell migration; results in decreased innate immunity

A

Leukocyte adhesion deficiency

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23
Q

How can monoclonal bodies be used to target tumor cells?

A

Act as checkpoint inhibitors (CTLA-4 and PDL/PDL1) to maintain T cell function against tumor

24
Q

What hypersensitivity is this?

Rheumatoid Arthritis - chronic inflammatory disease of the joints/synovial cells (synovitis) via TNF and IFN

A

Type IV

25
Q

What are the main mediators of leukocyte recruitment?

A

Selectin
Integrin
PECAM-1
Chemokines

26
Q

BTK gene deficiency, decreased pre-B cell signaling

A

X-linked agammaglobunlinemia

27
Q

What cytokines are responsible for inflammation?

A

TNF, IL-1

28
Q

What does the hyperactute rejection of an organ rely on?

A

Already circulating alloantibodies

29
Q

Th2 CD4+ stimulates what?

A 
Eosinophil-mediated immunity against helminths
Release of IL-4, IL-5, and IL-13 for mast cell/eosinophil activation
IgE production (allergies)
30
Q

If free antigen gets into the blood, where does it trigger an immune response?

A

Spleen

31
Q

What are monoclonal antibodies?

A

genetically engineered antibodies that are very specific for one target; can remove one cell type or protein

32
Q

What cytokines are responsible for chemotaxis?

A

CXCL8

33
Q

lack of CD40L, leads to deficiency of IgG, IgA, IgE

A

Hyper-IgM

34
Q

What are the primary effector mechanisms of the immune system?

A

Phagocytosis
Membrane Attack Complex
Cytotoxicity
Neutralization

35
Q

What happens during direct acute organ rejection?

A
  1. Graft has an APC
  2. Donor MHC I/II antigens on APCs in the graft are recognized by CD8+ and CD4+ cells
  3. CD4+ cells proliferate/produce cytokines —> cause damage via delayed-type hypersensitivity
  4. CD8+ cells directly kill graft cells
36
Q

What happens during indirect acute organ rejection?

A
  1. recipient’s APCs presents graft antigens, which activates CD4+ T cells
  2. CD4+ damage graft via local delayed type hypersensitivity (cytokines + macrophages)
  3. B cells are stimulated by CD4+ to make antibodies
37
Q

What two checkpoints on T cells do tumors target? What are their normal functions?

A

CTLA-4 - inactivates T cell (negative signal)

PD-1 - inhibits TCR-mediated response and T cell survival

38
Q

Surface proteins used to define a specific cell type

A

Cluster of Differentiation

39
Q

What endogenous factors limit inflammation?

A

Short life-span of mediators
IL-10 and TGF-beta (anti-inflammatory)
Lipoxins
CTLA4 (inhibitory receptor on T cells)

40
Q

What is Type II Hypersensitivity?

A

Cell/antibody-mediated:

Antibodies bind to surfaces of cells and cause:

  • opsonization/phagocytosis
  • interference with protein function
  • Fc/complement activation
41
Q

What do steroid inhibit and how does it differ from COX-inhibitors?

A

Phospholipases from making arachidonic acid, thus lipoxin/leukotriene

Steroids inhibit both inflammation AND immune function where as COX-inhibitors only inhibit inflammation

42
Q

Th17 CD4+ stimulates what?

A

Inflammation
Recruitment of phagocytes for elimination of bacteria/fungi
Release of IL-17 for neutrophilic/monocytic inflammation

43
Q

What hypersensitivity is this?

Diabetes Mellitus - direct killing of pancreatic beta cells (insulin secreting cells)

A

Type IV

44
Q

What cytokines are responsible for activating liver synthesis of acute-phase proteins?

A

IN-6

45
Q

What is Type IV Hypersensitivity?

A

Delayed T-cell mediated:

  1. CD4+ T cells recognize antigen presented by APCs leading to generation of effector and memory TH1 cells
  2. Subsequent exposure to antigen results in TH1 activation and release of cytokines —> macrophages, neutrophils —> tissue injury

OR

No mediator; intracellular peptide is presented by MHC I to CD8+ —> subsequent direct killing by CTL

46
Q

characterized by aggregates of activated macrophages with scattered lymphocytes during certain pathological states; formation of granuloma walls off pathogen but does not always eradicate them

A

Granulmatous inflammation

47
Q

What pathways does the Hageman Factor trigger?

A

Clotting cascade
Kinin system
Complement
Fibrinolytic systems

48
Q

Improper thymus development; deceased production of T cells

A

DiGeorge Syndrome

49
Q

What is Type III Hypersensitivity?

A

Immune-complex-mediated: immune complexes form in the circulation between antigens and free body; deposit on vessel walls/joints/kidneys and lead to localized inflammation

50
Q

What are the primary lymphoid organs?

A

Bone marrow and thymus

51
Q

Competent T cells transplanted into recipient who is immunocompromised —> Activation of CD4+ and CD8+ T cells, with cytokine and cell-mediated tissue injury

A

Graft vs Host Disease (GVHD)

52
Q

The fibrinolytic system leads to the formation of what? Function?

A

Plasmin - limits clotting and activates compliment

53
Q

What are the 4 types of hypersensitivities?

A

A - allergic/anaphylactic/immediate (IgE) - I
C - cell-mediated/antibody-mediate (IgM, IgG) - II
I - immune-complex mediated (IgM, IgG) - III
D - delayed T-cell mediated (CD4+/CD8+) - IV

54
Q

What two receptors are involved in the Death Receptor pathway of apoptosis?

A

TNF

Fas

55
Q

deficiency of one Ig subtype (usually IgA)

A

Hypogammaglobulinemia/CVID

56
Q

What is the primary factor driving the diversity of the adaptive immune system?

A

Lymphocyte antigen receptor diversity

BUPA Basic Medical Sciences (3 decks)

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