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MOD-Exam 3 > Diseases of Immune System > Flashcards

Diseases of Immune System Flashcards

1
Q

What chromosome encodes HLA molecular structure?

What are the 3 class I HLA alleles?

What are the 3 class II HLA alleles?

A

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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2
Q

What is colostrum?

What Ig is secreted in it?

A

What is colostrum?

Mother’s 1st breast milk

What Ig is secreted in it?

IgA

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3
Q

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

A

Lack of MHC I

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4
Q

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

A

CD4 T cell activation of naive B cells

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5
Q

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

A. CD4 Th1

B. CD4 Th2

C. CD4 Treg

D. CD4 Th17

A

CD4 Th2

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6
Q

What 3 interleukins are involved in Type I hypersensitivity reaction?

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

A

IL-4: class switching to IgE

IL-5: eosinophil signalling

IL-13: enhancing IgE production

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7
Q

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

A

FceRI

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8
Q

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

A

Histamine

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9
Q

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

A

Eosinophil

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10
Q

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

A

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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11
Q

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

A

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

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12
Q

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

A

Vasculitis caused by ANCA, Goodpasture syndrome, Acute Rheumatic fever

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13
Q

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

A

Molecular mimicry and Type II hypersensitivity

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14
Q

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

A

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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15
Q

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.

A

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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16
Q

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

A

CTLA-4 and PD-1

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17
Q

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

A

mutation in FoxP3

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18
Q

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

A

Class I HLA-B24

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19
Q

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

A

NOD-2 gene

NOTE:

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

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20
Q

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.

A

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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21
Q

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

A

Immune comlplex formation

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22
Q

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

A

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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23
Q

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

A
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24
Q

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

A

D. Discoid rash, positive ANA, Positive immunofloruescent

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25
Q

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

A

Anti-histone Ab

26
Q

Hydralazine confers high risk for Drug-Induced Lupus in people with what HLA?

A. HLA-DR4

B. HLA-DR6

A

HLA-DR4

27
Q

Procainamide confers high risk for Drug-Induced Lupus in people with what HLA?

A. HLA-DR4

B. HLA-DR6

A

HLA-DR6

28
Q

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

A

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

29
Q

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

A

ANA (anti-nuclear Ab)

30
Q

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

A

Anti-ribonucleoprotein (RNP)

31
Q

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

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

32
Q

What are the staining patterns for the following AI diseases?

SLE

Systemic sclerosis

Sjogen syndrome

CREST syndrome

A

SLE: is homogenous

Sjogren is speckled like systemic sclerosis

33
Q

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

A

preformed ABO Abs

34
Q

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

A

Complement

(can stain using C4d to confirm complement is afoot)

35
Q

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

A

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

36
Q

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

A

Failure of phagolysosome fusion

The phagocytes never get the enzymes needed to break down these usually easy to kill pathogens

37
Q

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

A

Failure of superoxide production in phagocytes

38
Q

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?

A

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

39
Q

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

A

Deficiency in C1 inhibitor

40
Q

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

A

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

41
Q

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

A

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

42
Q

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

A

CD40L/CD40

NOTE:

Treat with IVIg and Stem Cell transplantation

43
Q

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

A

Common Variable Immunodeficiency (CVID)

44
Q

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

A

IgA

Can prevent by doing an Ab wash of the blood

45
Q

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

A

Wisckott Aldrich syndrome

46
Q

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

A

IgA and IgG

47
Q

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

A

LTR

48
Q

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

A

gag

gag up what’s inside of you

49
Q

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

A

env

envy can be very superficial

50
Q

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

A

pol

51
Q

In step 1 of HIV infection it looks for CD4 and binds receptors using what?

A. gp41

B. gp120

C. integrase

D. NFkB

A

gp120

52
Q

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

A

gp41

53
Q

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

A

integrase

54
Q

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

A

NFkB

55
Q

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

A

Macrophages

DC

Microglia

56
Q

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

A

Viral RNA > p24 Ag > Ab to HIV

57
Q

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

A

True

58
Q

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

A

Period of silent massacre of CD4 cells

59
Q

Where does amyloid tend to manifest (4)?

A

Brain

Liver

Kidney

Heart

BLK Heart

60
Q

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

A

Abdominal fat pad

61
Q
A

Again x3

62
Q
A

Again x3

MOD-Exam 3 (6 decks)

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