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Phd Flashcards

0
Q

3 key features of tolerance

A

1) It is ANTIGEN SPECIFIC
2) Easier to introduce in the neonatal period or early life BUT it is nt restricted to this period
3) IT MUST be induced in new lymphocytes throughout life

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1
Q

Can an antigen be immunogenic and tolerogenic?

A

YES! Depending on the dose or method of delivery

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2
Q

What are the central tolerance mechs

A

Apoptosis, Development of T regs (T cells) and Receptor editing (B cells)

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3
Q

Peripheral tolerance mechanisms?

A

Apoptosis, anergy, suppression by T regs

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4
Q

Tell me about negative selection…

A

It acts on CD4 and CD8 cells that bind too tightly NB! Cells that bind weakly also die but this doesn’t result in tolerance. Only CD4 stimulated cells can become Tregs

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5
Q

What is the AIRE gene?

A

It is an autoimmune regulator that cuases some peripheral antigens (proteins that induce negative selection)to be expressed in the thymus

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6
Q

What are the mechanisms of T cell peripheral tolerance?

A

Anergy, Suppression by T regs and Activated induced cell death

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7
Q

What are the 2 ways by which T cells achieve anergy?

A

antigenic signaling w/o costimulation

Antigenic signaling w/ engagement of PD-1 or CTLA-4

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8
Q

What are the Treg markers?

A

CD25 (alpha chain of Il-2),Foxp3 and CD 4. Rem they need IL-2. they also ake emory cells.

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9
Q

IL-2 deficiency, will it affect all T cells?

A

Nope just Tregs. The other T cells respond to other growth factors but Tregs are solely IL-2 deficient

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10
Q

T regs mechanism of action?

A

Secrete cytokines that block macrophage and lymphocyte activation - IL-10 and TGf-beta

May also remove B7 from APC by transendocytosis

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11
Q

Tell me about AICD…

A

Normally: Antigen which is pro apoptotic and IL-2 which is anti apoptotic. With no costim : acid apoptosis by the mitochondrial pathway and by the FasL extrinsic pathway

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12
Q

What is receptor editing?

A

Strongly reactive B cells do this…
How ? Reactivate the rag gene and rearrange a new light chain gene. Old heavy + new light = new specificity

if receptor editing fails—negative selection saves the day.

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13
Q

A)Tolerance to proteins?

B)Tolearnace to proteins and non protein antigens?

A

A) T cells

B) B cells

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14
Q

What are the B cells peripheral tolerance mechs

A

Anergy and apoptosis

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15
Q

An autoimmune disease that is characterized by soluble self antigens and autoantibodies is a?

A

systemic disease- eg. Lupus

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16
Q

An autoimmune disease that is characterized by autoantibodies or autoreactive T cells againts tissue reactive antigen is a..

A

oragn specific disease- type 1 diabetes, hashimotos, thyroiditis, MS

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17
Q

A defect in the AIRE gene leads to

A

autoimmune polyendocrine syndrome

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18
Q

A defect in Fas/ Fas L leads to?

A

Autoimmune lympho proliferative syndrome

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19
Q

A defect in Foxp3 leads to

A

X linked polyendocrinopathy and enteropathy

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20
Q

How can diet affect autoimmunity?

A

Vit D deficiency–dec Th1 resp and inc Tregs
Celiac disease triggered by gluten..IgA antibodies to anti-transglutaminase 2
excess iodine—iodiated thryoglobulin, this is more immunogenic

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21
Q

What are the immune privileged sites in the body

A

brain, eyes, testes, placenta and fetus

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22
Q

How does the eye confer immune privilege?

A

Passive mechanism: sequester and segregation fr the immune system- trauma however can dsrupt this

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23
Q

What is the difference between extrinsic, intrinsic and chronic asthma?

A

Ext- classis mediated IgE hypersensitivity

Intrinsic- mast cells spontaneously degranulate due to pollutants, infections, exercise and drugs.

Chronic asthma- large numbers of eosinophils in bronchial mucosa and excessive mucous secretion. Bronchial smooth muscle also becomes hyperreactive.

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24
Q

What is the most severe form of hypersensitivity?

A

anaphylaxis- edema in many tissues and a fall in bp.

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25
Q

If your patient is on antihistamines, what alergy testing would you subject them to?

A

allergen specific IgE testing (RAST). The skin test may be false negative if the patient is on antihistamines.

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26
Q

Ways to treat hypersensitivity reactions?

A

Epinephrine for anaphylaxis, corticosteroids and phosphodiesteraseinhibitors for bronchial asthma
Cromolyn- inhibits mast cell degranulation
Anti IgE- neutralizes and eliminates IgE

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27
Q

Tell me about pemphigus vulgaris

A

Antibodies disrupt the cell-cell adhesions between keratinocytes. leads to superficial fluid filled vesicles and bullae.

The bullous pemphigoid- antibodies at the dermo-epidermal jxn deeper more tense more long lasting bullae

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28
Q

What is the classical test for autoantibodies in LE?

A

Antinuclear antibody test. Result is usually diffuse or homogenous staining

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29
Q

Serum sickeness today??

A

We use antitoxins to treat snake bites, rabies exosure

Monoclonal Ab therapy

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30
Q

An elevated SED rate indicates?

A

Systemic inflammation

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31
Q

Apart from elevated SED rate, what is anothe rmakrker of systemic inflammation?

A

CRP. It reacts with the C polysaccharide of pneumococcus. The CRP levels may rise more quickly than SED and return to normal more rapidly

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32
Q

Two methods of carrying out ANA screening?

A

Indirect immnuofluorescence on Hep cells
Multiplex bead assay

ANA tells you that something is going on but not which Ab is present. It can be followed up by a specific antibody test.

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33
Q

Diff between direct and indirect immunoflurescence?

A

Direct- looking in the patient tissue, while indirect is looking in the patient serum

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34
Q

Homogenous immunofluorescence stain is associated with what antibodies?

A

Anti histone and anti DNA

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35
Q

What about the speckled pattern of a ANA?

A

Most common but least specific.

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36
Q

Nucleolar ANA pattern?

A

Seen in scleroderma

37
Q

Centromere pattern of ANA?

A

Seen in CREST which is a variant of scleroderma

38
Q

Tell me the 3 ways by which antiphospolipid antibodies manifest..

A

1) IgG/ IgM Ab which eact with a beta 2 glycoprotein in phospholipids

2) Lupus anticoagulant- assoc with hypercoaguable state. Falsely elevated PPT.
3) false positive test for syphilis due to anticardiolipin antibodies

39
Q

This test is useful in diagnosis of vasculitis…

A

ANCA (Anti neutrophil cytoplasmic antibodies)

40
Q

A positive c_ANCA would mean which enzyme is present?

A

Proteinase-3

41
Q

A positive p-ANCA would indicate which enzyme is present?

A

myeloperoxidase

42
Q

What two test do you use to diagnose rheumatoid arthritis?

A

Rheumatoid factor- igM aginst Fc of IgG

Anti CCP- Advantageous because its specificity

43
Q

How would you detect antibodies against RBCs?

A

Direct Antiglobulin Test- it detects antibody and or complement bound to RBCs

Indirect Antiglobulin test- detects antibody to RBCs in serum

44
Q

Hyperglobinemia/ Abnla gobulins present?

A 
Serum elctrophoresis (see a spike)
then do immunofixation to see which one is present
45
Q

What chemical confers heat resistance to spores?

A

calcium dipicolinic acid

46
Q

What is a biofilm?

A

A polysaccharide capsule that forms a mechanical scaffold arund bacteria. It allows bacteria to bind to prosthetic devices.Planktovic cells form microcolonies. Biofilms represent a barrier to antimicrobial therapy

47
Q

Qurom sensing?

A

auto induction phenomenon. bacteria are able to sense their environment and mange their popn density.

LuxI- responsible for making the inducer
Lux R- binds the inducer and together they activate transcrption

48
Q

What is the bystander effect?

A

When an individual has more self reactive lymphocytes

49
Q

What is cryoglobulinemia?

A

Antibodies to antibodies..this is apparent at temps below 37 C- It is mixed when the antibodies have a monoclonal and polyclonal component

50
Q

What is the most important cause of mixed cryoglobulinemia?

A

Hep C..the immune complexes have the HCv virions..polyclonal anti-HCV IgG and monoclonal anti-IgG IgM

51
Q

Bystander autoimmune diseases?

A

Mixed cryoglobinulemia and HCV
Type I diabetes
Autoimmune myocarditis following a viral infection

52
Q

Which virus is most commonly associated with autoimmune mycarditis?

A

Enterovirus, Cockasackie b

53
Q

What are the 5 diseases to list on the differential for a person witha Strep A infection?

A 
Acute Rheumatic fever
Rheumatic heart disease
Post streptococcal glomerulonephritis
PANDAS
Syndenham chorea
54
Q

Pathogenesis of Acute Rheumatic fever?

A

Molecular mimicry between the M protein and the N acetyl glucosamine.

Joint involovement- Large joints are affected,symptoms are migratory. Swollen, red and painful joints

Cardiac involvement- hallmark of RHD is mitral valve damage

55
Q

How would you diagnose ARF?

A 
ASO, anti B DNASE,
Jones criteris (polyarthritis, carditis, nodules, erythema marginatum) Syndenham's chorea
Diff from reactive arthriris- It is non migratory, affects smalljoints and resistant to treatment w/ NSAIDs
56
Q

This disease is characterizedby an acute onsetof OCD and a tic in children

A

PANDAS

57
Q

This disease is usually seen after a skin infection (impetigo), affects the kidneys and is a post strep A disease..

A

Post streptococcal glomerulonephritis

58
Q

What is the cause of Cold agglutinin?

A

Mycoplasm pneumoniae, Epstein Barr virus

59
Q

Pathogenesis of autoimmune hemolytic anemia?

A

Make antibodiesto RBCs

IgM activate complement—> intravascular lysis
IgG activate phagocytosis —-> extravascular lysis

60
Q

Warm vs cold agglutinins?

A

Temp diff
Warm- IgG, epstein bar virus, cytomegalovirus, accounts for most cases, responds to steroids, usually anti Rh

Cold- IgM, Mycoplasm nuemoniae, Epstein Barr, clumping and cyanosis in extremities, chronic hemolysis

61
Q

Reactive arthritis?

A

Chlamydia bacteria

Chlamyidia pnuemoniae- respiratory prblems
Chlamydia trachomatis- urethritis- STD

Rem arthritis is assymetrical, uvetis, urethritis, keratoderma blenorrhagica

ASSOC with HLA-B27

62
Q

Lyme disease?

A

Arthritis in people infected withe bacterium burrella burgdorfelli
70% of people infected

63
Q

What are the fluid phase complement inhibitors?

A

C4BP, C1 inhibitor, Factor H and Clusterin

64
Q

What are the membrane bound complement inhibitors?

A

DAF, CD59 and membrane cofactor protein. DAF AND MCP AFFECT ACTIVATION OF C3B while CD59 prevents MAC formation which eventually leads to lysis

65
Q

C1 INH MOA?

A

Prevents C3 onvertase formation, Factor IC4BP splits C4b and C2a, and inactivates C3—> iC3b
Factor H- main one, prevents binding to make of factor B to makeC3bB, promotes dissociation of the C3 convertase and inactivates C3

66
Q

What causes hereditary angioedema?

A

C1 INH deficiency

67
Q

Paroxysmal Nocturnal hemoglobinurial?

A

GPI deficiency. This affects DAF and CD59..predisposes RBCs to lysis

68
Q

A disorder in which there a a factor H, I and CD 46 mutation, there is thromobosis and recurrent death..

A

Hemolytic Uremic Syndrome

69
Q

Anti C5 monoclonal antibody?

A

Eculizumab

70
Q

Complement C2 and C4 defects increase your chances of getting what autoimmune disease?

A

Lupus like disease

71
Q

NOD-2 defects increase your chances of getting what autoimmune disease?

A

Crohn’s disease, Blau syndrome

72
Q

FcyRllb defects increase your chances of getting what autoimmune disease?

A

Lupus like disease ( defective feedback B cell activation)

73
Q

PTPN22 defects increase your chances of getting what autoimmune disease?

A

Several diseases ( abnormal tyrosine phosphatase signaling)

74
Q

il-2 and il-2alpha/beta gene defects increase your chances of getting what autoimmune disease?

A

Ms, type 1 diabetes, others

75
Q

What does nod-1 do?

A

Present in monocytes, macrophages, dendritic cells and some epithelial cells; activates nf-kappaB in response to bacterial PAMPS

76
Q

What foods can cause auto immunities?

A

Vitamin D- decreases TH1and up regulates treg response. Vit d def can increase th1 response

Iodine- excess iodine can make iodinated thyroglobulin which is immunogenic

Celiac disease- caused in genetic susc pts, triggered by gluten, produce igA autoab to anti- transglutaminase 2

77
Q

Describe the life cycle of malaria

A

Mosquito bites human and injects sporozites into the skin. Some associate with DCs in the lymph nodes. These may present sporocytes to T cells. The sporozites then enter the liver and undergo acellular reproduction. From therethe merozoite enters the red blood cells

78
Q

Malaria has 5 tenets of acquired immunity

A

Effective in adults after lifelong exposure
Lose upon cessation of exposure
Species specific
Somewhat stage specific
Acquired at a rate that is dependent upon the degree of exposure

79
Q

This strain of malaria is the most severe, has anemia associated with it and cerebral complications.

A

P. falciparum

80
Q

This type of malaria has unique renal involvement..

A

Plasmodium malariae

81
Q

Morphology of nesseria?

A

Gram negative diplococci

82
Q

Morphology of streptococcus

A

Gram negative cocci

83
Q

Signs and symptoms of malaria

A

Fever, headache, myalia, cough, diarrhea, vomitting, abd pain

84
Q

How are you going to diagnose someone w/ malaria?

A

CBC- WBC and platelets should be decreased
Liver enzymes should be increased
Thick and thin smears (take a long time to read, they may miss low parisitemias and mixed infections)

85
Q

This drug is used forall blood staes ofmalaria. Its second line for severe malaria. It is a atiarrythmic.

A

Quinine

86
Q

This is the drug of choice for severe malaria- good for P.falciparum and chloroquine resistant P.vivax. It requires a partner drug

A

Artemesins

87
Q

This is the drug of choice forP. malariae. It is also usedin conjunction with primaquine for treatment of P. vivvax and P. ovale

A

Chloroquine

88
Q

This drug is effective against P vivax and ovale,late stage P.falciparum gametocytes

A

Primaquine

89
Q

Why can’t malaria be controlled?

A

Can’t develop a vaccine
Parasite is resistant to safe antimalarals
Vector control programs have gone downhill

Phd2 (1 decks)

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