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STEP 1 (5) > Immunology-Immune Responses > Flashcards

Immunology-Immune Responses Flashcards

1
Q

What are acute-phase reactants?

A

Factors whose serum conc change significant;y in response to inflammation; produced by the liver in both acute and chronic inflammatory states

Notably induced by IL-6

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2
Q

What are the upregulated APRs (acute phase reactants)?

A

CRP

Ferritin (sequesters iron)

Fibrinogen

Hepcidin (prevents release of iron bound by ferritin= anemia of chronic disease)

Serum amyloid A (can lead to amyloidosis)

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3
Q

What are the downregulated APRs (acute phase reactants)?

A

Albumin (reduction converses AAs for positive reactants)

Transferrin

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4
Q

Describe the alternative complement pathway

A

C3 from the liver is broken down to C3b (and C3a), which binds with Bb (formed when factor D breaks down factor B) to form C3bBb (C3 convertase)

C3 convertase then leaves more C3 and some form C5 convertase (C3bBb3b) which cleaves C5 to C5a and C5b

C5b then binds to C6-9 to form the MAC

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5
Q

Describe the classic complement pathway

A

C1 becomes activated with Ab bind to C1q (IgM is the best since its a pentamer), which then cleaves C2 to Ca2/C2b and C4 to C4a/C4b. C4b and C2a combine to form C3 convertase of the classical pathway which cleaves C3 to combine with the other pathways

End-game: MAC complex

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6
Q

What is the effect of C1 esterase inhibitor deficiency?

A

hereditary angioedema (ACEIs are contraindicated)

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7
Q

What is the effect of C3 deficiency?

A

Increases risk of severe, recurrent pyogenic sinus and respiratory tract infections

susceptibility to type III hypersensitivity rxns

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8
Q

What is the role of IL-1?

A

Aka osteoclast-activating factor. Causes fever, acute inflammation.

Activates endothelium to express adhesion molecules

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9
Q

What is the role of IL-6?

A

Promotes fever and production of APRs

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10
Q

What is the role of IL-8?

A

chemotaxis of neutrophils

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11
Q

What is the role of IL-12?

A

Induces differentiatio of T cells into Th1 cells. Activates NK cells

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12
Q

What is the role of TNF-a?

A

Mediates septic shock.

Activates the endothelium

Causes vascular leak, cachexia in malignancy, and chemo-fog

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13
Q

What is the role of IL-3?

A

Secreted by ALL T cells to support growth and differentiation of bone marrow stem cells. Functions like GM-CSF

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14
Q

What is the role of IFN-y?

A

Secreted by NK cells in response to Il-12 from macrophages, stimulates macrophages to kill pathocytosed pathogens

Also activates NK cells to kill virus-infected cells. Increased MHC expression

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15
Q

What are the major Th2 cytokines?

A

IL-4 (promotes class switching to IgE and IgG)

IL-5 (promotes class switching to IgA; stimulates growth of eosinophils)

IL-10 (modulates inflammatory response; decrease of MHC class II and Th1 cytokines)

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16
Q

Describe the respiratory burst

A

This involves the activation of the phagocyte NAPDH oxidase complex (e.g. in neutrophils, monocytes, which utilize O2 as a substrate)

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17
Q

Describe the first two steps of the respiratory burst

A

In the phagolysosome:

  1. NAPDH oxidase converts O2 to O2*- using NADPH
  2. O2*- is converted to hydorgen peroxide via superoxide dismutase
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18
Q

Describe step 3 of the respiratory burst

A
  1. Hydorgen peroxide is convertd to HClO via MPO
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19
Q

Pts with CGD are at increased risk of what infections?

A

Those caused by catalse + organisms (e.g. S. aurues, Aspergillus) capable of neutralizing their own hydrogen peroxide

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20
Q

What does pyocyanin of P. aureginosa do?

A

fucntions to generate POS to kill competing microbes

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21
Q

What are interferons a and B?

A

Part of the innate host defense against BOTH RNA and DNA viruses. These are glycoproteins that act locally on uninfected cells, priming them for viral defense by helping to selectively degrade viral nucleis acid and protein

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22
Q

What are the major cell surface proteins of T cells?

A

TCR (binds antigen-MHC complex)

CD3

CD28 (binds to B7 on APCs)

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23
Q

What are the major cell surface proteins of regulatory T cells?

A

CD4, CD25

24
Q

What are the major cell surface proteins of B cells?

A

Ig

CD19/20

CD21 (receptor for EBV)

CD40

MHC II

B7

25
Q

What are the major cell surface proteins of macrophages?

A

CD14/40

MHC II

B7

26
Q

What are the major cell surface proteins of NK cells?

A

CD16 (binds to the Fc of IgG)

CD56

27
Q

What are the major cell surface proteins of hematopoietic stem cells?

A

CD34

28
Q

What is anergy?

A

State during which a cell cannot become actvated by exposure to its antigen. T and B cells become anergic when exposed to their antigen with costimulatory signal (another mechanism of self-tolerance)

29
Q

What are superantigens?

A

Seen in S. pyogenes and S. aureus- these cross-link the B region of the TCR to the MHC class II on APCs and can activate any CD4+ T cell leading to a massive release of cytokines

30
Q

What are some ex of bugs with antigenic variation?

A

Bacteria- Salmonnela (2 flagellar variants), Borrelia recurrentis (relapsing fever), No. gonorrhoeae (pilus protein)

Viruses- Influenza, HIV, HCV

Parasites- Trypanosoma

31
Q

Describe passive immunity

A

When you receive preformed Abs that yields RAPID immunity over the course of the Ab life (typically 3 weeks)

32
Q

When is passive (preformed Abs) immunity given?

A

After exposure to Tetanus toxin, Botulinum toxin, HBV, Varicella, or Rabies Virus

33
Q

Describe active immunity

A

Injecting foreign antigens and allowing for an endogenous immune response to form

34
Q

What are the advanatages and disadvanatages of liver attenuated vaccines?

A

This is when a microorganism loses its pathogenicity, but retins capacity for transient growth within an inoculated host and induces a CELLULAR and HUMORAL response.

Pros: induces strong, often lifelong immunity

Cons: may revert to active form

35
Q

What is the ONLY live attenuated vaccine iven to persons with HIV?

A

MMR

36
Q

What are some exs of live attenuated vaccines?

A

MMR

polio (Sabin)

infulenza (intranasal)

varicella

yellow fever

37
Q

Describe the basis of an inactivated or killed vaccine

A

The pathogen is inactivated by heat or chemicals, but maintains epitope structue on surface antigens to induce mainly a HUMORAL only response

Cons: weaker immune response

38
Q

What are some exs of killed/inactivated vaccines?

A

Rabies, Influenza (injection)

Polio (Salk)

Hep A

R.I.P Always

39
Q

What is a type I hypersensitivity rxn?

A

Anaphylatix and atopic in which free antigen cross-links IgE on presensitized mast cells and basophils, triggering IMMEDIATE release of vasoactive amines that act at POSTCAPILLARY VENULES

This rxn develops rapidly after antigen exposure due to preformed Ab formation and typically a delayed response follows due to production of arachidonic acid metabolites

Ex: allergic and atopic disorders such as rhinitis, hay fever, eczema, hives and asthma and anaphylaxis such as bee stings and food allergies

40
Q

What is a type II hypersensitivity rxn?

A

Cytotoxic (Ab-mediated)- IgM, IgG bind to fixed antigen on enemy cells and cause cellular destruction via 3 mechanisms:

Opsonization and phaocytosis

Complement

Ab mediated cellular destruction

41
Q

What is a type III hypersensitivity rxn?

A

Immune complex mediated in whch antigen-Ab complexes activate complement, which attract neutrophils to release lyosomal enzymes

42
Q

What is serum sickness?

A

An IMMUNE COMPLEX (type III) disease in which Abs to foreign proteins are produced (takes 5 days) and the immune complexes are deposited in membranes, where they fix complement (leads to tissue damage). (more common than arthus rxn)

43
Q

What are the most common causes of serum sickness?

A

Most commonly drugs acting as haptens

44
Q

How does serum sickness present?

A

Fever, urticaria, arthralgia, proteinuria, and LAD occuring 5-10 dys after antigen exposure

45
Q

What is an arthus rxn?

A

A local subacute Ab-mediate hypersensitivity rxn in which intradermal injection of antigen induces Abs, which form antigen-Ab complexes in the SKIN.

46
Q

How does an Arthus rxn present?

A

Edema, necrosis, and activation of complement

47
Q

Describe a type IV hypersensitivity rxn

A

Delayed (T-cell mediated)- sensitized T cells encounter antigens and then release cytokines

48
Q

What are some examples of type II hypersensitivity rxns?

A

Acute hemolytic transfusion rxns

Autoimmune hemolytic anemia

Bullous pemphigoid AND pemphigus vulgaris

Erythroblastosis fetalis

Goodpasture syndrome

Graves Disease

Guillian-Barre Disease

ITP

Myasthenia Gravis

Pernicious Anemia

Rheumatic Fever

49
Q

What are some examples of type III hypersensitivity rxns?

A

Arthus rxn

SLE

Polyarteritis nodosa

Poststrep glomerulonpheitis

Serum sickness

50
Q

What are some examples of type IV hypersensitivity rxns (response is delayed and DOES NOT involve antibodies)?

A

Contact dermatits (e.g. poison ivy, nickel allergy)

Graft-vs-host disease

MS

PPD test for M. TB

51
Q

What are the main blood transfusion rxns to look out for?

A

Allergic rxn (type I against plasma proteins in tranfused blood)

Anaphylactic rxn

Febrile nonhemolytic rxn

Acute hemolytic tranfusion rxn

52
Q

How might an Allergic rxn to blood transfusion present?

A

Urticaria, pruritis, wheezing, and fever

Tx with antihistamines

53
Q

How might an anaphlyactic rxn to blood tranfusion present?

A

Severe allergic rxn marked by dyspnea, bronchospasm, hypotension, and respiratory arrest/shock

Tx with epi

NOTE: IgA deficient persons must receive blood products without IgA

54
Q

How might a febrile nonhemolytic transfusion rxn present?

A

Type II rxn formed by host Abs against donor HLA antigens and WBCs presenting as fever, HA, chills, and flushing

55
Q

How might an acute hemolytic tranfusion rxn present?

A

Type II rxn in which intrasvascular hemolysis (ABO group incompatibility) or extravascular hemolysis (host Ab rxn against foreign antigen on donor RBCs) presenting with fever, hypotension, tachypnea, tachyacardia, flank pain, and hemoglobinuria/jaundice

56
Q
A

STEP 1 (5) (11 decks)

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