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UWorld - Immunology > Immunology > Flashcards

Immunology Flashcards

1
Q

Type 1 Hypersensitivity

  1. What are the humoral components?
  2. What are the cellular components?
A
  1. IgE
  2. Basophils and Mast Cells
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2
Q

Type 2 Hypersensitivity

  1. What are the humoral components?
  2. What are the cellular components?
A
  1. IgG, IgM, complement activation
  2. NK cells, eosinophils, macrophages, neutrophils
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3
Q

Type 3 Hypersensitivity

  1. What are the humoral components?
  2. What are the cellular components?
A
  1. Ag-Ab Complex Deposition, complement activation
  2. Neutrophils
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4
Q

Type 4 Hypersensitivity

  1. What are the humoral components?
  2. What are the cellular components?
A
  1. NONE
  2. T-cells & Macrophages
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5
Q

What are examples of Type 1 Hypersensitivity?

A

Anaphylaxis

Allergies

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6
Q

What are examples of Type 2 Hypersensitivity Reactions?

A

Autoimmune Hemolytic Anemia

Goodpasture Syndrome

(glomerulonephritic + hemoptysis)

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7
Q

What are examples of Type 3 Hypersentivity Reactions?

A

Serum Sickness (joint pain + pruritic rash)

Poststreptococcal Glomerulonephritis

Polyarteritis Nodosa

(vasculitis with fibrinoid necrosis)

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8
Q

What are examples of Type 4 Hypersensitivity reactions?

A

Contact Dermatitis (poison ivy, nickel allergy)

Graft vs. Host Disease

(maculopapular rash, jaundice, diarreha, hepasplenomegaly)

Tuburculin Skin Test (PPD)

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9
Q

How does serum sickness present?

A
  • Pruritic skin rash
  • arthralgia (joint pain)
  • Decreased C3 & C4
  • fever
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10
Q

What activates macrophages?

What cell secretes it?

A

Interferon-gamma and LPS

secreted by Th1 cells

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11
Q

What do macrophages secrete to recruit other macrophages and monocytes?

A

TNF-alpha

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12
Q

What cell is responsible for killing cells with decreased or absent MHC class I?

A

Natural Killer Cells

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13
Q

What are the common causes of SCID?

A
  1. Defective IL-2R gamma chain
  2. Adenosine Deaminase Deficiency
  3. MHC Class II Deficiency
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14
Q

How does SCID present?

A

-chronic diarrhea

-failure to thrive

-thrush

-recurrent infections

(due to Decreased T-Cells and B-cells)

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15
Q

Which 4 key mediators attract and activate neutrophils?

A

1. LTB4

2. C5a

3. IL-8

4. bacterial products

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16
Q

Chronic Granulomatous Disease

  1. Pathogenesis
  2. What are u at increased risk for?
  3. What test is used to detect it?
A

1. NADPH Oxidase deficiency

(decreased oxidative burst in neutrophils)

  1. Infection via Catalase Positive organisms
  2. Nitroblue Test: failure to turn blue

DHR Flow Cymmetry: decreased fluorescenst green

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17
Q

Toxic Shock Syndrome Toxin

(superantigens)

What cells are activated?

A

T lymphocytes

(very large amount get activated by the superantigen)

Macrophages

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18
Q

Which cell belongs to the surface marker:

  1. CD4
  2. CD8
  3. CD14
  4. CD20
A

1. CD4 = T-helper cell

2. CD8 = T-killer cell

3. CD14 = Macrophage

4. CD20 = B-cells

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19
Q

Anaphylaxis

  1. What are the 2 main cells involved?
  2. Degranulation of these cells releases what?
A
  1. Mast Cells and Basophils
  2. Histamine and Trypsin

(Note: Trypsin is often used as a marker for mast cell activation)

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20
Q

What triggers the release of histamine (and trypsin) from mast cells or basophils?

A

Binding of IgE to the mast cell via the IgE receptor (FCΣR1) results in cross-linking of multiple bound IgE molecules resulting in aggregation of FCΣR1 receptors which causes degranulation

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21
Q

What substance is most likely to be released following a bee-sting in an allergic child?

A

Histamine

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22
Q

What region of the Antibody is A+B?

What attaches there?

A

The hypervariable region of the FAB

(antigen binding fragment)

It is where the antigen binds

(only 1 antigenic specificy expressed per B cell)

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23
Q

What region of the Antibody is E?

What attaches there?

A

The Fc (phagocytic) Region

The Fc receptors bind macrophages, neutrophils and B-cells

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24
Q

What region of the Antibody is D?

What attaches there?

A

The Compliment Binding region

It is where the compliment (C1) binds

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25
Q

What region of the Antibody is C?

What attaches there?

A

The Disulfide bonds that hold the 2 heavy chains together

Nothing attaches there

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26
Q

What are the 2 main cells activated in Tuberculosis?

A

Macrophages and CD4+ T-cells

(since Tb replicates within the phagosome, it will be displayed on MHC class II)

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27
Q

alpha and Beta (Type 1) Interferons

  1. Which cells secrete them ?
  2. What is their function?
A
  1. They are secreted by cells is response to viral infections

2.

They downregulate protein synthesis in infected cells

increase MHC class I expression in all cells

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28
Q

gamma (Type 2) Interferon

  1. Which cells secrete them ?
  2. What is their function?
A
  1. They are secreted by T-cells and NK cells

2.

Promotes Th1 differentiation

Increases expression of MHC Class II on APCs

Activates and improves macrophage killing ability

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29
Q

Calcineurin

  1. What does it do?
  2. How does it do it?
  3. Which drugs inhibit it?
A
  1. It promotes growth and differentiation of T-cells
  2. It phoshorylates NFAT which then binds IL-2 and promotes growth+differentiation of T-cells
  3. Cyclosporine and Tacrolimus

(immunosuppresants)

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30
Q

Bcl-2

  1. What is it?
  2. What it is associated with?
A

1. Apoptosis inhibitor

  1. Follicular lymphomas t(14;18) translocation
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31
Q

p53

  1. What is it?
  2. How does it work?
A
  1. Tumor supressor
  2. It causes cell cycle arrest and apoptosis
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32
Q

Neurofibromin

  1. What is it?
  2. How does it work?
A
  1. Tumor supressor
  2. It supresses Ras

(a cell proliferation activator)

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33
Q

What enzyme is activated in both pathways of apoptosis?

A

Caspases

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34
Q

Metalloproteinases

  1. What is it?
  2. What is their function?
A
  1. Zinc containing enzyme that degrades ECM components

(degrades collagen, fibronectin, laminin)

  1. Wound Healing
35
Q

What is the main function of IL-1?

A

Fever

Acute Inflammation

“Hot T-Bone stEAK”

36
Q

What is the main function of IL-2?

A

Stimulates growth of all T-cells

Stimulates growth of NK cells

“Hot T-Bone stEAK”

37
Q

What is the main function of IL-3?

A

Stimulates growth of and differentiation of bone marrow stem cells

“Hot T-Bone stEAK”

38
Q

What is the main function of IL-4?

A

Promotes IgE class switching

Promotes Th2 differentiation

Promotes B-cell growth

“Hot T-Bone stEAK”

39
Q

What is the main function of IL-5?

A

Promotes IgA class switching

Stimulates growth/proliferation of Eosinophils

Promotes B Cell Growth

“Hot T-Bone stEAK”

40
Q

What is the main function of IL-6?

A

Stimulates akute-phase protein production

Causes Fever

41
Q

What is the main function of IL-8?

A

Chemotaxis for neutrophils

42
Q

What is the main function of IL-10?

A

Attenuates the inflammatory response

“TGF-_B_ and IL-10 Both atTENuate the immune response”

43
Q

What is the main function of IL-12?

A

Induces differentiation of T cells in Th1 cells

Activates NK cells

44
Q

What is a major result of impaired interferon signalling?

A

Increased likelihood of mycobacterial infection

45
Q

What are the most common ways that Toxic Shock Syndrome occurs?

How does it present?

A

Prolonged tampon use

Prolonged nasal packing

Presents as fever, hypotension, end-organ failure, diffuse eythematous rash

46
Q

What is the difference between a superantigen and a normal antigen?

A

Superantigens bind to the invariant region of MHC-II without being processed

(this results in massive T-cell activation and cytokine release)

NOTE: antigents are normally processed in the lysosome before being presented

47
Q

What is the difference between the structure of MHC-I and MHC-2?

A

MHC-I:

- Heavy chain (alpha 1,2,3)

- Beta-2 Microglobullin

MHC-II

Alpha chain (alpha 1,2)

- Beta chain (beta 1,2)

48
Q

Which cells express:

1. MHC Class I

2. MHC Class II

A
  1. All nucleated cells
  2. APCs only (dendritic cells, B-cells, macrophages)
49
Q

X-Linked (Bruton) Agammaglobulinemia

  1. What causes it?
  2. What does it result in?
  3. What does it increase risk for?
A
  1. BTK mutation (x-linked recessive)
  2. No B-cells

3.

  • pyogenic bacteria infections
  • Giardia infections
  • enteroviruses
50
Q

Which surface markers (CD??) will be absent in a patient with X-linked (Bruton) Agammaglobulinemia?

A

CD19

CD20

CD21

(B-cell surface markers)

51
Q

Poliovirus

What is the diffrence between the Live Attenuated Oral (Sabin) Vaccine and the Inactivated IntraMuscular (salk) vaccine?

Where is this difference seen the most?

A

The live attenuated oral (sabin) vaccine produces a much stronger mucosal IgA response since it actually goes through the digestive system

The difference in IgA response is seen mainly at the intestinal and oropharyngeal mucosa since the oral live vaccine directly stimulates these areas.

52
Q

Wiskott-Aldrich Syndrome

What mutation causes it?

What does it result in?

How does it classically present?

A
  1. WASp gene mutation
  2. B+T-cell disorder: defective Ag presentation

3. Thrombocytopenia, Eczema, Recurrent pyogenic infections

“WATER”:

Wiscott Aldrich: Thrombocytopenia Eczema, Recurrent pyogenic infections

53
Q

Which antibody subtype can cross the placenta?

(Ig?)

A

IgG

54
Q

Which antibody is seen in the following blood type:

  1. Type A
  2. Type B
  3. Type AB
  4. Type O
A
  1. Anti-B (IgM)
  2. Anti-A (IgM)
  3. None

4. Anti-A + Anti-B (IgG)

(NOTE: IgG can cross placenta)

55
Q

ABO Hemolytic Disease of the Newborn

How come fetal hemolysis can occur in mothers of Type O blood but not the others?

A

Mothers of type O contain IgG antibodies to type A and type B blood, so if their child is born type A or B the antibodies can cross the placenta.

Other blood types result in IgM antibodies which cannot cross the palcenta (Only IgG can cross placenta)

56
Q

Why is the H. Influenzae Tybe B vaccine given conjugated to a carrier protein?

A

Since the conjugated elicits a B-cell and T-cell

It will also allow for immunogenicty in infancy.

(A nonconjugated polysaccharide vaccine will only elicit a B-cell response)

57
Q

Which cells and cell products are primarily responsible in formation of granulomas?

A

Macrophages secrete IL-12, which stimulates Th1 differentiation

Th1 cells secrete IL-2 which increases Th1 proliferation and IFN-Y which activates macrophages

58
Q

Which cytokines result in reduced inflammation?

A

TGF-B and IL-10

“TGF-_B_ and IL-_10_ Both atTENuate inflammation”

59
Q

Hyperacute Transplant Rejection

  1. Time of onset
  2. Etiology
A
  1. minutes to hours
  2. Recipient has preformed antibodies to the graft (organ)
60
Q

Acute Transplant Rejection

  1. Time of onset
  2. Etiology
A
  1. <6 months
  2. Exposure to donor antigens induces humoral/cellular response
61
Q

Chronic Transplant Rejection

  1. Time of onset
  2. Etiology
A
  1. >6 months
  2. Chronic low-grade immune response
62
Q

How does Hyperacute Transplant rejection present?

Can it be reversed?

A

Thrombosis of graft vessels which causes ischemia/necrosis

No it cannot be reversed, graft must be removed

63
Q

How does Chronic Transplant rejection present?

A

Vasuclar wall thickeninig, intersitial fibrosis and parenchyma atrophy

Heart: accelerated atherosclerosis

Kidney: fibrosis

Liver: vanishing bile duct syndrome

Lungs: Brochiolitis obliterans

64
Q

How does Acute Transplant rejection present?

Can it be reversed?

A

Vasucilitis of graft vessels with a dense intersitial lymphocitic infiltrate

Yes, can be reversed with immunosupressants

65
Q

The Candida Antigen Skin Test

  1. What is it testing?
  2. What type of hypersensitivity is it?
A
  1. It asses the activity of T-cell mediated immunity via the recruitment of CD4, CD8 T-cells and macrophages

2. Type IV sensitivity (T-cell)

66
Q

Eosinophils

  1. Against what type of organism to they play a role in defence?
  2. What is their role?
A
  1. Against parasites
  2. They get stimulated by antibodies bound to the parasitic organism and destroy the parasite via antibody-dependant-cell-mediated cytotoxicity
67
Q

Chediak-Higashi Syndrome

  1. What is it?
  2. How does it classically present?
A
  1. A disorder of neutrophil phagasome-lysosome fusion

(autosomal recessive)

2.

  • immunodeficiency (defective neutrophils)
  • albinism
  • neurological defects
68
Q

What type of vaccine is the tetanus vaccine?

How does it work?

A

Inactivated toxoid vaccine

It triggers the production of antitoxin antibodies

(active immunity)

69
Q

What tests can be used to detect Chronic Granulomatous Disease?

A

1. Nitroblue Tetrazolium (NBT) Testing

Properly functioning neutrophils will produce reactive oxygen species that will turn the NBT from yellow to blue

2. Dihydrorhodamine (DHR) Flow Cymmetry

Asseses the production of superoxide radicals by measuring the conversion of DHR to Rhodamine (a fluorescent green compound)

70
Q

Rh Hemolytic Disease of the Newborn

  1. What is the mother and child bloodtype?
  2. Does it occur after the first pregancy?
  3. How does it occur?
A
  1. Rh- mother & Rh+ fetus
  2. No it does not occur in the 1st pregnancy, only subsequent pregnancies
  3. Mother is exposed to fetal blood during delivery where she forms anti-D (Rh) IgG. In subsequent pregnancies the Abs can cross the placenta and cause hemolysis of RBCs
71
Q

How does Rh hemolytic disease of the newborn present?

A

Jaundice shortly after birth

Kernicterus (bilirubin deposits in basl ganglia - often fatal)

Hydrops Fetalis / Generalized Edema

+ Direct Coombs Test (RBCs coated with antibodies)

72
Q

PD-1 Receptor

(Programmed Cell Death Protein-1)

  1. When its bound by its ligand what occurs?
  2. What cells upregulate this ligand?
A
  1. It downregulates the immune response by inhibiting cytotoxic T-cells
  2. Cancer cells

(therefore antibodies against PD-1 and its ligand can be used for cancer therapy)

73
Q

Poststeptococcal Glomerulonephritis

  1. How does it present
  2. What type of hypersensitivity reaction is it?
  3. What causes it?
A
  1. it is a nephritic syndrome (hematuria, edema, HTN) caused by immune complex deposition along the glomerular basement membrane
  2. Type III hypersentivity (antibody-antigen complex)
  3. It occurs 2-4 weeks after a streptococcal infection (impetigo, cellulitis, pharyngitis)
74
Q

Which part of the Lymph Node are the arrows pointing at?

What cellular process is undergone there?

A

Germinal Centers

Isotype Switching

75
Q

In a patient with Small Intestine Bacterial Overgrowth which vitamins would we expect to see elevated? Decreased?

A

Elevated: Vitamin K , Folate

Decreased: A, D, E, B12

76
Q

What are the 2 most important opsonins for phagocytosis?

A

IgG & C3b

77
Q

In SLE what autoantibodies are present?

A
  1. Antinuclear Antibodies (non-specific)
  2. Anti-double-stranded DNA antibodies (specific)
  3. Anti-smith Antibodies (Specific)
78
Q

C1 Esterase Inhibitor Deficiency

  1. What does it cause?
  2. Labs
  3. What medication is contraindicated in these patients?
A

1. Hereditary Angioedema

(swelling of the skin, most common in face, lips, tongue)

2. Overactive C1, decreased C4, increased bradykinin

3. ACE Inhibitors

(since they can cause angioedema due to inc. bradykinin)

79
Q

The inflammatory response to Septic Shock is mediated by what cytokines?

A

TNF-alpha

IL-1

IL-6

80
Q

A patient presents with jaundice, hepatosplenomegaly, rash and diarrhea 1 months after getting a liver transplant.

  1. Most likely diagnosis
  2. Pathogenesis
A
  1. Graft vs Host Disease

2.

T-cells from the transplanted organ reject host cells

(results in severe organ dysfunction)

81
Q

Hepatitis B Vaccine

  1. What type is it?
  2. What is it made of?
  3. How does it prevent infection?
A
  1. Subunit Vaccine
  2. HBsAg

(which then generates antibodies)

  1. Antibodies bind to viral envelope inhibiting viral entry
82
Q

A patients who has been diagnosed with celiac disease and 3 previous episodes of pneumonia develops anaphylaxis in response to a blood transfusion, what is the most likely diagnosis?

A

Selective IgA Deficency

Clinical Features

  • Asymptomatic (usually)
  • Airway + GI infections
  • Autoimmune Diseases
  • Anaphylaxis during blood transfusion
83
Q

A patient has painful and deformed hands and fingers which improve as the day goes on.

  1. What is the most likely diagnosis?
  2. This patients serum is most likely to contain antibodies against what?
A
  1. Rheumatoid Arthritis
  2. IgM antibodies against Fc portion of human IgG

UWorld - Immunology (1 decks)

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