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MOD I Final > Chapter 6 Part 2 > Flashcards

Chapter 6 Part 2 Flashcards

1
Q

Autoimmune diseases effect mostly?

A

Woman

-IgG4 diseases effect men

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2
Q

Do autoantibodies mean there is an autoimmune disease

A

no, could be something else

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3
Q

3 things need to be met for autoimmune

A
  1. Immune reaction for self
  2. Not secondary to tissue damage (needs to be primary)
  3. Absence of other causes
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4
Q

Systemic diseases discussed in this chapter?

A
  1. Systemic Lupus erythematosus
  2. Rheumatoid arthritis
  3. Systemic Sclerosis (Sjogren syndrome)
  4. Polyarteritis nodosa
  5. Inflammatory myopathies
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5
Q

How does the immune system generate autoanitbodies?

A

Somatic recombination remember?? We need to eliminate these

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6
Q

There are 2 types of immune tolerance, what are they?

A
  1. Central (thymus and bone marrow)

2. Peripheral

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7
Q

How does central tolerance eliminate autoanitbodies (t-cells)?

A
  1. T cells for self are apoptosed in thymus.

2. Some CD4 cells allowed to live as regulatory T-cells

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8
Q

Central tolerance for B-cells?

A
  1. RECEPTOR EDITING is how B-cells are fixed.

2. Apoptosed if not

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9
Q

What is another word for peripheral tolerance?

A
  1. Anergy
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10
Q

How does peripheral tolerance work?

A
  1. Lymphocytes for self rendered functionally unresponsive
    - eliminate co-stimulater after APC presentation.
  2. Without TH, B-cells don’t function adequately
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11
Q

What allows fetus to be accepted?

A

Regulatory T-cells

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12
Q

Where are immune privileged sites?

A
  1. Testes, eyes, Brain

2. Sites where Ags are hidden from immune system

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13
Q

Changes contributing to autoimmunity (3)

A
  1. Defective tolerance
  2. Abnormal Ag display
  3. Inflammation or initial innate immune response
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14
Q

What disease is associated with the HLA-B27?

A

Ankylosins spondylitis (greater liklihood of happening)

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15
Q

HLA -DQA1?

A

Celiac disease

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16
Q

Role of Infections leading to autoimmune (the dark side): (3)

A
  1. Infection provides co-stimulation needed to cause self-antigen
  2. Molecularmimicry: microbe that looks like self Ag
  3. Viruses: (EBV or HIV) can drive B-cell activation that causes problems
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17
Q

Role of infections (the good side):

A
  1. Infections can help develop immunity.

2. Infections can decrease IL-2 and reg T-cell

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18
Q

What common disease decreases the likelihood of autoimmune problems?

A

Type 1 diabetes

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19
Q

Gen features of Autoimmune (AI)

A
  1. Chronic
  2. Relapse
  3. Damage=progressive
  4. Epitope spreading (1 bad Ag causes tissue damage and then stim other Abs
  5. Abnormal/excessive Th1 and 17
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20
Q

This disease effects skin, joints, kidney and serosal membranes. Pt has a malar rash, oral ulcers, renal problems and tests positive for syphilis.

A

Systemic Lupus Erythematosus (SLE)

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21
Q

Specific Abs for SLE?

A
  1. Double stranded DNA

2. Smith (SM) Ag

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22
Q

Antinuclear ABs are found in all AI and can be for? (4)

A
  1. DNA
  2. Histones
  3. Non-histone proteins on RNA
  4. Nuclear Ags
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23
Q

What can cause a false-+ syphilis test in SLE?

A

Antiphospholipid Abs

VDRL

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24
Q

What else can Antiphospholipid Abs do?

A

Cause hypercoagulable PTT test

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25
Q

What drugs are associated with SLE? (3)

A
  1. Hydralazine
  2. Procainamide
  3. D-penecillamine
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26
Q

What is linked to anti-DS DNA and Anti smith?

A

HLA-DQ

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27
Q

what in the Env may cause SLE?

A

UV-light

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28
Q

Morphologic effects of SLE are seen where? (5)

A
  1. Blood vessels
  2. Joints
  3. Kidneys
  4. Skin
  5. Pericardium/serosal surfaces
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29
Q

What are the morphologic changes of blood vessels?

A

Acute necrotizing vasculitis of small blood vessels

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30
Q

What are the morphologic changes of Joints?

A

Non-erosive synovitis, Just inflammed

!Rheumatoid arthritis is deformed joints!

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31
Q

What are the morphologic changes of Kidneys

A

Glomerular lesions related to the immune complex

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32
Q

What are the morphologic changes of Skin

A

Butterfly rash on face!

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33
Q

What are the morphologic changes of Pericardium/serosal surfaces

A

Inflammation

  • Acute = fibrisous exudate
  • Later = thickened
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34
Q

SLE can cause what cardiac problems?

A
  1. Tachycardia (due to myocarditis)
  2. Coronary artery disease
  3. Valvular abnormalaties
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35
Q

Other organs effected by SLE (3)

A
  1. CNS (due to vasculitis of small blood vessels)
  2. Splenomegaly
  3. Liver: pleural effusion/pleuritis
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36
Q

Clinical features of SLE

A
  1. Young woman
  2. Renal involvement (blood/protein in urine)
  3. Increased infections
  4. Disease can flare (corticosteroids help)
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37
Q

What is associated with Raised skin lesions that are deep and promote scarring?

A
  1. Chronic Discoid Lupus
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38
Q

What is associated with wide spread rash and no scars?

A

Subacute Cutaneous Lupus

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39
Q

Drug induced lupus

A
  1. Hydralazine
  2. Procainamide
  3. D-penecillamine
    - Spare CNS and Kidneys
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40
Q

Pt comes in complaining of dry eyes (keratoconjuctivitis sicca) and Dry mouth (xerostomia):

What is the disease and what causes these symptoms

A
  1. Sjogren Syndrome

2. Destruction of lacrimal and salivary glands

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41
Q

Will you find Sjogren syndrome on its own?

A

Generally not. Usually in conjunction with other diseases

42
Q

How do you diagnose Sjogren syndrome?

A
  1. Biopsy the lip and look for intense lymphocytic response
  2. Early onset = T and B mix
  3. Late = mostly B
43
Q

Sjogren syndrome mostly effects who?

A

Women ages 50-60

44
Q

This disease causes widespread damage to small blood vessels, progressive interstitial and perivascular Fibrosis in the skin and organs.

Pt with thick skin and Raynaud phenomenon.

What is the disease?

What causes death?

A
  1. Systemic Slerosis or Scleroderma

2. Fibrosis of kidney, heart or pulm

45
Q

Clinical features of Scleroderma? (6)

A
  1. Skin Thickening
  2. Raynaud phenomenon (vasoconstriction of extremities and discoleration in fingers)
  3. Dysphasia from esophageal fibrosis
  4. Resp diff
  5. Myocardial fibrosis
  6. Renal issues
46
Q

Pt with calcinosis, Raymond phenomenon, esophagea and scleradoma issues?

A

CREST syndrome.

-Limited form of scleroderma

47
Q

AI more likely in men?

A

IgG4 related

-Autoimune pancreatitis

48
Q

What is the major factor in Human organ transplants?

A

HLAs

49
Q

Rec of alloantigins in organ grafts, direct vs indirect?

A

direct: both CD8 and CD4

Indirect: CD4 only (IFN-gamma)

50
Q

Acute cellular rejections include

A
  1. Cytokines (CD4+ T-cells)

2. Increase vasc. perm and local mononuclear cells

51
Q

Chronic rejection includes?

A
  1. Lymphocytes react against alloantigens in vessel walls

2. Secrete cytokinse for local inflammation

52
Q

Hyperacute rejection includes

A
  1. Preformed antidonor Abs

2. Extremely rapid

53
Q

Acute ab-mediated rejections (2)

A
  1. Antidonor abs produced after transplant

2. graft vasculature is targeted

54
Q

Chronic AB-mediated

A
  1. Insidious

2. Also vascular components

55
Q

How to increase graft survival? (5)

A
  1. HLA matching
  2. Immunosuppressive Therapy
  3. T + B cell depleting Abs
  4. Pooled IgG
  5. Plasma Pherisis (pull out plasma from blood)
56
Q

HLA matching required for Kidney? (3)

A

HLA A, B and DR

-not done for liver, heart or lungs

57
Q

Immunosuppressive Therapies include? (2)

A
  1. Steroids = decreased inflammation

2. Mycophenolate mofetil = inhb lymphocytes

58
Q

This virus can reactivate, infect renal tubules and cause graft failure

A

Polyoma Virus

59
Q

Infections that increase AI risk? (3)

A
  1. EBV-induced lymphomas
  2. HPV
  3. Kaposi Sarcoma (HHV8)
60
Q

Where are hematopoitic cells taken from?

A

Peripheral blood (use colony stimulating factor to generate more stem cells)

61
Q

What is required for a bone marrow transplant?

A

Need to destroy immune system of recipient

62
Q

Graft vs host disease: Acute (2)

A
  1. Days to weeks.

2. Effects Immune system, skin, liver and intestines

63
Q

Graft vs host disease: Chronic

A
  1. Involution of thymus (some autoimmunity)

- gen same as acute but worse

64
Q

Graft vs host disease: is mediated through? (2)

A
  1. T-lymphocytes (if donor t-lymph killed than GVHD removed)

2. If you remove T-cells, Leukemia could come back and increase risk of graft failure

65
Q

B-cell related Immunodeficiency syndromes? (4)

A
  1. X-linked Agammaglobulinemia
  2. CVID
  3. Hyper-IgM syndrome (CD40L)
  4. IgA deficiency
66
Q

T-Cell Related Immunodeficieny syndromes (4)

A
  1. APA deficiency
  2. X-linked SCID (gamma chain)
  3. DiGeorge Syndrome
  4. MHC Class 2 deficiency
67
Q

What disease is a bubble boy?

What happens to da bboy?

A
  1. Severe combined Immunodeficiency (SCID)

2. Pro T-cell can’t become Immature T-cell thus effecting T-cell development

68
Q

Features of SCID?

A
  1. X-linked
  2. Infants w/early thrus
  3. Pt dies w/out bone marrow transplant
69
Q

Disease that is due to fail of B-cell precurssors and when do you see it?

A
  1. X-linked Agammaglobulinemia

2. At 6 months (when mothers Abs are gone)

70
Q

X-linked Agammaglobulinemia: do pt have Igs?

A

NOOOOO!

71
Q

X-linked Agammaglobulinemia: what is associated (3)

A
  1. giardia
  2. Blood stream viruses
  3. AI arthritis
72
Q

X-linked Agammaglobulinemia: Tx

A

Provide Immunoglobins

73
Q

Disease associated with a failure of 3rd and 4th pharyngeal pouches to close, t-cell deficiency and tetany.

A

DiGeorge syndrome

74
Q

DiGeorge syndrome features (4)

A
  1. Fail of 3rd and 4th pouch to close
  2. T-cell deficiency
  3. Hypoparathyroid = Hypocalcemia and tetany
  4. abnormal mouth and ears
75
Q

Can’t produce IgE, IgG or IgA

A

Hyper IgM syndrome

76
Q

Hyper IgM syndrome Features:

A
  1. CD40L mutation (Th to B messed up)
  2. X-linked
  3. Pyogenic infections
77
Q

What happens if IgM reacts w/blood cells?

A

hemolytic anemia

78
Q

Hypogamma globulinemia (blocking IgG) is a result of what disease?

A

Common Variable Immunodeficiency (CVID)

79
Q

CVID-do B-cells become plasma cells?

A

No, but they are normal

80
Q

Find this disease with blood transfusions

A

Isolated IgA

81
Q

IgA is usually

A

asymptomatic which is why you find it in transfusion pts.

82
Q

Immunodeficiencies Associated w/systemic diseases (2)

A
  1. Wiskoff-Aldrich syndrome

2. Ataxia Telangiectasia

83
Q

Wiskoff-Aldrich syndrome: facts (3)

A
  1. X-linked
  2. Thrombocytopenia
  3. Hematopoietic stem cell transplant = Tx
84
Q

Ataxia Telangiectasia: facts (3)

A
  1. Autosomal Recessive
  2. Abnormal gait and vascular malformations
  3. neurologic issues and increased tumors
85
Q

Acquired Immunodeficiency syndrome (AIDS): caused by?

A

HIV and transported by sexual, needles, mother to infant

86
Q

2 forms of HIV

A
  1. HIV 1 (Developed nations and Central america)

2. HIV 2 (3rd world)

87
Q

Virus core proteins of HIV

A
  1. Major Capsid Proteins-P24 (ELIZA test for this)
  2. copies of RNA
  3. Viral Enzymes
88
Q

HIV Matrix protein?

A

p17

89
Q

Proteins studding HIV envelope?

A

Gp120 and GP41

90
Q

HIV infection involves what cells?

A
  1. T cells
  2. Dendritic Cells
  3. Macrophages
91
Q

Chemokine receptors for HIV isolates (3)

A
  1. R5 => CCR5
  2. X4 => CXCR4
  3. R5X4 => dual tropic
92
Q

R5 => CCR5?

A
  1. Monocytes

2. Acute strain

93
Q

X4 => CXCR4

A
  1. T-cells

2. gradually accumulates

94
Q

HIV infects…

A
  1. Memory and active T-cells

2. Can’t infect Naive T-cells

95
Q

Why can’t HIV infect Naive T-cells?

A

ApoBEC36 gene/enzyme blocks it

-HIV’s VIF is learning to counteract this

96
Q

HIV thrives when…

A
  1. Host T-cell and macrophages activated

- Stim NF-kB and increase monocytes

97
Q

Polyclonal B-cells can

A

cause problems

98
Q

Macrophages from HIV1… (2)

A
  1. depend on VPR gene

2. Resevoirs of infection

99
Q

Dendritic Cells…

A
  1. Bring mucosal dendritic cells to lymph and CD4+
100
Q

Follicular cells…

A
  1. HIV resevoir

2. Trap virions and maintain CD4+ ability to infect

MOD I Final (4 decks)

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