Diseases of Immune System Flashcards by Deleted Deleted

What chromosome encodes HLA molecular structure?

What are the 3 class I HLA alleles?

What are the 3 class II HLA alleles?

What chromosome encodes HLA molecular structure?

chromosome 6

What are the 3 class I HLA alleles?

A, B, C

What are the 3 class II HLA alleles?

DP, DQ, DR

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What is colostrum?

What Ig is secreted in it?

What is colostrum?

Mother’s 1st breast milk

What Ig is secreted in it?

IgA

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How do NK cells recognize damaged cells, as well as virally damaged cells?

A. Presence of MHC I

B. Presence of MHC II

C. Lack of MHC I

D. Lack of MHC II

Lack of MHC I

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How do we stimulate proliferation and differentiation of B cells?

A. CD8 T cell activation of naive B cells

B. CD4 T cell activation of naive B cells

C. APC exposure of B cells

D. None of the above

CD4 T cell activation of naive B cells

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What T cell lymphocyte is most involved in Type I hypersensitivity reactions?

A. CD4 Th1

B. CD4 Th2

C. CD4 Treg

D. CD4 Th17

CD4 Th2

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What 3 interleukins are involved in Type I hypersensitivity reaction?

What is the general role of each of these IL’s?

IL-4: class switching to IgE

IL-5: eosinophil signalling

IL-13: enhancing IgE production

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IgE primes mast cells by binding to what receptor on the mast cell?

FceRI

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All of the following are related to early phase reaction in Type I Hypersensitivity reactions and are born of membrane phospholipids EXCEPT which of the following that is the result of degranulation?

A. Histamine

B. Leukatrienes B4, C4, D4

C. Prostaglandin D2

D. PAF

Histamine

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In Type 1 hypersensitivity reaction what leukocyte is most involved in the late phase?

A. Basophil

B. Neutrophil

C. Eosinophil

D. None of the above

Eosinophil

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Which of the following syndromes/diseases of Type II Hypersensitivity develops as a result of inappropriate opsonization and phagocytosis?

A. Autoimmune hemolytic anemia and Autoimmune thrombocytopenia

B. Vasculitis caused by ANCA, Goodpasture syndrome, Acute Rheumatic fever

C. Myasthenia gravis, Grave’s Disease, Insulin-resistant diabetes

Autoimmune hemolytic anemia and Autoimmune thrombocytopenia

NOTE:

Type II with this mechanism usually results in lowered cell count, so if it has “penia” in it’s name it might be a good guess

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Which of the following syndromes/diseases of Type II Hypersensitivity develops as a result of Ab-mediated cell dysfunction, where the Ab binds and blocks receptors?

A. Autoimmune hemolytic anemia and Autoimmune thrombocytopenia

B. Vasculitis caused by ANCA, Goodpasture syndrome, Acute Rheumatic fever

C. Myasthenia gravis, Grave’s Disease, Insulin-resistant diabetes

Myasthenia gravis, Grave’s Disease, Insulin-resistant diabetes

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Which of the following syndromes/diseases of Type II Hypersensitivity develops as a result of complement and Fc-receptor mediated inflammation?

A. Autoimmune hemolytic anemia and Autoimmune thrombocytopenia

B. Vasculitis caused by ANCA, Goodpasture syndrome, Acute Rheumatic fever

C. Myasthenia gravis, Grave’s Disease, Insulin-resistant diabetes

Vasculitis caused by ANCA, Goodpasture syndrome, Acute Rheumatic fever

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What are 2 concepts illustrated by Rheumatic fever?

A. Type I hypersensitivity and Molecular mimicry

B. Type I hypersensitivity and Type II hypersensitivity

C. Type II and Type IV hypersensitivity

D. Molecular mimicry and Type II hypersensitivity

Molecular mimicry and Type II hypersensitivity

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How is a Type III hypersensitivity reaction like an Avenger’s movie?

A. The Abs are like Avengers in that they often dress up in a cape and fly around in the body

B. The Abs are like Avengers in the way that while they attack the Ags (the villains) they end up causing damage to the surrounding area

C. The Ags are actually the Avengers, attacking the Abs in the hopes of avenging their previously foiled attemps

D. Idk another MC option so its not this one I guess

B. The Abs are like Avengers in the way that while they attack the Ags (the villains) they end up causing damage to the surrounding area

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In the heart, post-streptococcal cross reactivity, Abs directly act on the myocardium which is a _________ hypersensitivity reaction. In the kidney, post-streptococcal cross-reactivity Abs are forming immune complexes that deposit in the glomeruli which is a ________ hypersensitivity reaction.

In the heart, post-streptococcal cross reactivity, Abs directly act on the myocardium which is a Type II hypersensitivity reaction. In the kidney, post-streptococcal cross-reactivity Abs are forming immune complexes that deposit in the glomeruli which is a Type III hypersensitivity reaction.

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What are the 2 inhibitory receptors expressed on T cells that help prevent it’s activation?

A. CTLA-4 and PD-1

B. B7 and PD-L1

C. CD28 and CCR5

D. B7 and CD4

CTLA-4 and PD-1

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What causes IPEX (immune polyendocrinopathy entropity X-linked) to develop, which results in ?

A. Presence of Class I HLA-B27

B. PResence of Class II HLA-DP27

C. mutation in FoxP3

D. mutation in AIRE gene

mutation in FoxP3

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Ankylosing spondylititis is a hereditary inflammatory condition of the joints, usually the spine, that leads to degeneration and fusion of vertebrae. Ankylosing spondylitis has a strong association with what HLA allele?

A. Class I HLA-B27

B. Class II HLA-DP27

C. Class I HLA-B24

D. Class I HLA-A27

Class I HLA-B24

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Crohns Disease is a condition characterized by an excessive immune response which erodes the intestinal epithelia. Polymorphisms in which of the following genes results in the defective killing and clearing of bacteria that leads to the accumulation of bacteria and contributes to the excessive immune response?

A. Class I HLA-B27

B. NOD-2 gene

C. FoxP3 gene

D. AIRE gene

NOD-2 gene

NOTE:

NOD is on innate immune cells and is used to “recognize” and kill bacteria

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Epitope spreading is a sort of secondary autoimmune response due to the “uncovering” of new antigens in the body. Explain how Oral Lichen PLanus exemplifies this.

An initial T cell response attacks the oral mucosa causing keratotic lesions that expose the basement membrane. The newly expose BM causes release of “unrecognized” Ags and triggers a secondary B cell response

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What is the primary immune mechanism involved in Systemic Lupus Erythematosis?

A. Neutrophil infiltration

B. Immune comlplex formation

C. Giant cell formation

D. B cells and CD4 T cells

Immune comlplex formation

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What stage of Lupus Nephritis is the most common stage at which people will present with symptoms?

A. Class I Minimal mesangial

B. Class III Focal Lupus nephritis

C. Class IV Diffuse Lupus Nephritis

D. Class VI Advanced sclerosing Lupus nephritis

Class IV Diffuse Lupus Nephritis

NOTE:

Diffuse Lupus nephritis is assoc. with proteinuria –> edema/ankle swelling, and hematuria

We start with Class I minimal mesangial, and end with Class VI Advanced sclerosing Lupus nephritis

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What staining should you see with Type III Hypersensitivity reactions?

A. Smooth, linear

B. Granular, grainy

C. Both A and B

D. None of the above

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What 3 variant or developments do we see in both DLE and Discoid Lupus?

A. Discoid rash only

B. Positive ANA only

C. Positive immunoflorescent only

D. Discoid rash, positive ANA, Positive immunofloruescent

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A patient was just prescribed Hydralazine to help control their BP, but recently they have developed arthralgias and fever. After testing revealed a positive ANA, you conclude Drug-Induced Lupus as the culprit. This patient is also likely positive for which of the following Abs? A. Anti-procainamide Ab B. Anti-hydralazine Ab C. Anti-histone Ab D. None of the above

Anti-histone Ab

Hydralazine confers high risk for Drug-Induced Lupus in people with what HLA? A. HLA-DR4 B. HLA-DR6

HLA-DR4

Procainamide confers high risk for Drug-Induced Lupus in people with what HLA? A. HLA-DR4 B. HLA-DR6

HLA-DR6

Sjogren syndrome is an AI disease that results in the destruction of the lacrimal glands and salivary glands leading to dry eye and dry mouth. Diagnosis of Sjogran syndrome relates to presence of which of the following? A. Anti-histone Ab B. Anti-Ro/SS-A and Anti-La/SS-B C. Class II HLA-DR4 D. Class II HLA-DR6

Anti-Ro/SS-A and Anti-La/SS-B

For the diseases: SLE, Sjogren syndrome, and systemic sclerosis, a sensitivity screening should determine that all of them are positive for what?

ANA (anti-nuclear Ab)

Mixed Connective Tissue Disease has features of SLE, Systemic Sclerosis, and polymyositis even sharing Raynaud phenomenon. A unique feature of Mixed Connective Tissue Disease is have a high titer of what? A. Anti-nucleic acid Abs B. Anti-ribonucleic acid Ab C. Anti-ribonucleoprotein (RNP) D. None of the above

Anti-ribonucleoprotein (RNP)

In autoimmune pancreatitis, riedel thyroiditis, mikulicz's syndrome, idiopathic retroperitoneal fibrosis, inflammatory pseudotumors, and inflammatory aortitis, all of them have what key event occuring? A. IgG4 plasma cells are triggering an immune response and causing irreversible fibrosis B. IgG1 plasma cells are triggering an immune response and causing irreversible fibrosis C. IgM plasma cells are triggering an immune response and causing irreversible fibrosis D. IgG1.3 plasma cells are triggering an immune response and causing irreversible fibrosis

A. IgG4 plasma cells are triggering an immune response and causing irreversible fibrosis

What are the staining patterns for the following AI diseases? SLE Systemic sclerosis Sjogen syndrome CREST syndrome

SLE: is homogenous Sjogren is speckled like systemic sclerosis

What mediates Hyperacute rekection that occurs within minutes to hours of transplantation? A. B cells and complement B. T cells C. preformed ABO Abs D. Preformed IgM

preformed ABO Abs

Acute and chronic Ab mediated rejection occurs within days or within years respectively. With these reactions we see tubulitis or fibrosis that's mediated by B cells and what? A. T cells B. Neutrophils C. Complement D. All of the above

Complement (can stain using C4d to confirm complement is afoot)

A C4d stain is able to help us determine between what 2 types of transplant rejection, which can help us in determining the correct treatment plan? A. Acute Ab mediated vs. Chronic Ab mediated B. Acute Ab mediated vs Hyperacute rejection C. Chronic Ab mediated vs. Hyperacute rejection D. Acute cell rejection (T-cell) vs, Acute Ab-mediated

D. Acute cell rejection (T-cell) vs, Acute Ab-mediated

The patient is depicted below. They've been brought in due to suffering from long standing and recurrent infections. You diagnose the patient with Chediak Higashi syndrome. What is the cause of this disorder? A. Failure of superoxide production in phagocytes B. Deficiency in C1 inhibitor C. Deficiency in MAC component complement proteins (C5, 6, 7, 8, 9) D. Failure of phagolysosome fusion

Failure of phagolysosome fusion The phagocytes never get the enzymes needed to break down these usually easy to kill pathogens

What is the fundamental issue that leads to development of Chronic Granulomatous diseases? A. Failure of superoxide production in phagocytes B. Deficiency in C1 inhibitor C. Deficiency in MAC component complement proteins (C5, 6, 7, 8, 9) D. Failure of phagolysosome fusion

Failure of superoxide production in phagocytes

Membrane attack complex deficiency is due to a defect in what complement components? Infection by what pathogen is most often seen with MAC complex deficiency?

Membrane attack complex deficiency is due to a defect in what complement components? **C5, C6, C7, C8, C9** Infection by what pathogen is most often seen with MAC complex deficiency? **Neisseria meningitis**

Hereditary angioedema is an Autosomal dominant disorder that may present in a multitude of ways including swelling of extremities, genitals, face, which are all due to which of the following? A. Failure of superoxide production in phagocytes B. Deficiency in C1 inhibitor C. Deficiency in MAC component complement proteins (C5, 6, 7, 8, 9) D. Failure of phagolysosome fusion

Deficiency in C1 inhibitor

SCID can be due to an X-linked mutation or Autosomal recessive mutation. Which of the followng is the most common cause of the autosomal recessive development of SCID? A. IL-receptor mutation B. Adenosine deaminase deficiency (ADA) which causes the accumulation of toxic purine metabolites C. AIRE mutation D. CD40/CD40L mutation

B. Adenosine deaminase deficiency (ADA) which causes the accumulation of toxic purine metabolites NOTE: IL-receptor mutation is usually due to the X-linked version

X-linked Agammaglobinemia is caused by a defect in the BTK gene (Bruton tyrosine kinase) on the X-chromosome. This mutation in the BTK gene causes what? A. Inability of pre-T cells to mature B. Inability to produce dimerized IgA C. Inability of pre-B cells to mature D. Inability to signal neutrophils

Inability of pre-B cells to mature For X-linked Agammaglobinemia we tend to see increase in disease later in childhood when maternal Abs wane

Hyper IgM syndrome causes an increase in infection by encapsulated bacteria due to lack of class switching o fB cells to produce more appropriate Abs. This impaired class switching seen in Hyper IgM syndrome is due to a mutation in which of the following? A. CTLA-4 and PD-1 B. AIRe gene C. CD40L/CD40 D. All of the above

CD40L/CD40 NOTE: Treat with IVIg and Stem Cell transplantation

Which of the following is the most common and significant primary immunideficiency, associated with higher recurrent sinus and pulmonary infections by Pyogenic bacteria, granulomas, or chronic diarrhea caused by Giardia lambliq? A. Common Variable Immunodeficiency (CVID) B. Hyper IgM syndrome C. SCID D. Hereditary angioedema

Common Variable Immunodeficiency (CVID)

If a patient has an anaphylactic reaction as a result of a blood transfusion, which of the following Abs might we believe is deficient due to the patient's allergic reaction to it? A. IgA B. IgG C. IgM D. IgE

IgA Can prevent by doing an Ab wash of the blood

A triad of Thrombocytopenia, eczema, and recurrent infection due to T cell loss and hypogammaglobinemia is characteristic of what syndrome with a WASP gene mutation? A. Common Variable Immunodeficiency (CVID) B. Hyper IgM syndrome C. Wisckott Aldrich syndrome D. DiGeorge

Wisckott Aldrich syndrome

Ataxia Telangiectasia is an autosomal recessive disorder due to ATM gene mutation and have an increase risk of respiratory infection, AI disease, and cancer due to resultant immune deficiencies in what 2 Igs? A. IgA and IgE B. IgA and IgG C. IgM and IgD D. IgM and IgG

IgA and IgG

Which of the following regions of the HIV viral genome initiates transcription and binds transcription factors like the host's NFkB? A. gag B. LTR C. env D. pol

LTR

Which of the following regions of the HIV viral genome encodes for the proteins inside the virus like p24? A. gag B. LTR C. env D. pol

gag *gag up what's inside of you*

Which of the following regions of the HIV viral genome encodes for the surface proteins gp120 and gp41? A. gag B. LTR C. env D. pol

env *envy can be very superficial*

Which of the following regions of the HIV viral genome encodes for the viral enzymes integrase, reverse transcriptase, and protease? A. gag B. LTR C. env D. pol

pol

In step 1 of HIV infection it looks for CD4 and binds receptors using what? A. gp41 B. gp120 C. integrase D. NFkB

gp120

In step 2 of HIV infiltration it "drills" into the cell membrane to allow for insertion of the viral genome. What protein allows this? A. gp41 B. gp120 C. integrase D. NFkB

gp41

In step 3 of HIV infiltration, reverse transcriptase turns its viral RNA into DNA and inserts it into the host cell DNA. What protein allows its insertion into the host DNA? A. gp41 B. gp120 C. integrase D. NFkB

integrase

In step 4 of HIV infiltration, HIV hijacks what transcription factor in order to trigger its LTR to promote its vrial transcription, instead of normally increasing T cell response? A. p53 B. ATM C. mTOR D. NFkB

NFkB

HIV's tropism allows for infection of not only T cells, but what other cells? (3)

Macrophages DC Microglia

What is the order of detectable substance in the detection of HIV from first to last? A. Viral RNA \> Ab to HIV \> p24 Ag B. p24 Ag \> Viral RNA \> Ab to HIV C. Viral RNA \> p24 Ag \> Ab to HIV D. None of the above

Viral RNA \> p24 Ag \> Ab to HIV

T/F: NAT testing is used to detect viral RNA, but still entails a 7-14 day window period from exposure to our ability to detect positive results

True

What is the clinical latency period? A. Period of silent massacre of CD4 cells B. Onslaught of clinical symptoms which resulted from CD4 cell destruction C. When HIV is minding it's own business and not causing any problems or destroying any cells. None. D. None of the above

Period of silent massacre of CD4 cells

Where does amyloid tend to manifest (4)?

Brain Liver Kidney Heart ***BLK Heart***

If we want to test for amyloid depositis, but don't want to affect major organs, what location can we biopsy? A. Palmar fat pad B. Plantar fat pad C. Abdominal fat pad D. Spine

Abdominal fat pad

Again x3