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MOD 4 - Endocrine > MMI > Flashcards

MMI Flashcards

1
Q
A

Memorize!

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2
Q
A

Memorize

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3
Q

Nf-kB and glucocorticord interaction

A

Nf-kB activation:

  • (P) & removal of IkB inhibitor
  • txloc to nucleus
  • gene expression

Glucocorticoids:

  • induced expression of IkB –> seq NF-kB in cytoplasm
  • (-) gene Ts when activated GR (GC receptor) binds directly to NF-kB
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4
Q
A

Memorize

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5
Q

catecholamines drive a TH___ shift

A
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6
Q

How dod proinflammatory cytokines are a potently activate the HPA axis.

A

inflammation –> IL-1, TNF-alpha, IL-6 –> (+) CRH in hypoT –> (+) stress hormones

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7
Q

which pituiary hormones are immunostimulatory?

A

prolactin, GH

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8
Q

CD40-CD40L interaction

A

Th: bind cytokind receptors on B cells –> promote B cell proliferation and Ig production

B: proliferation, synthesis, secretion of Ab

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9
Q

autoimmune diseases are characterized by activity of ….

A

auto-reactive lymphocytes: formation of Ab or activation of effector T cells

  • organ specific: chronic T cell or Ab targetting of a particular organ
  • systemic: breakdown of immune tolerance to self –> immune complex dmg in several body sites
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10
Q

descrbie immuno-pathogenesis in hasimoto thyroiditis

A
  1. inflamm infiltrate of activated: CD8, CD4, B, plasma, macrophages
    * activated CD8 and CD4 –> IFNγ –> MHC II expression by thyrocytes –> CD4 T cell expansion and infiltration in the area
  2. delete and replacement of thyroid with above inflamm infiltrate
  • CD8: perforin/granzymes or FasL-Fas (CD95L-CD95) pathway
  • CD4: IFNγ –> recruitment of macrophages –> cytokine release –> dmg
  • anti-thyroid Ab –> bind thyrocytes –> C’ fixation –> ADCC
    • TPO
    • TBG
    • TSH receptor
  1. thyroid enlargement –> fibrosis
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11
Q

PTPN22

A

Potent inhibitor of the T cell receptor signaling pathway

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12
Q

CTLA-4

A

homologous structure to CD28 on T cells (binds B7 on APC)

fx: (-) T cell activation by counteracting signals DELIVERED by TCR complex and CD28 –> T cell signal termination

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13
Q

what could explain why some patients with Graves disease have episodes of hypothyroidism

A

presence of both stimulating and inhibiting Abs

  • TSI
  • TSII
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14
Q

what HLA is thought to protect pts from developing Graves

A

HLA DRB1*0701

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15
Q

what HLA-DR association with graves disease has been demonstated in caucasians?

A

HLA-DR3 and -DQA1 *0501

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16
Q

neonatal graves disease

A

transplacental transfer of thyroid-stimulating IgG from mom –> fetus

symptoms of hyperthyroidism

*** spontaneous recovery gradual!

  • 2-3 mo as materal IgG metabolized
17
Q

auto-Ag in T1D (4)

A

glutamic acid decarboxylase (GAD65)

  • highly predictive of subseq dev of T1D

insulin

IA-2 (tyrosine phosphatase)

zinc T8 transporter (ZnT8)

18
Q

what is the most important factor in determining disease susceptibility

A

MHC haplotype

19
Q

2 monogenic syndromes assoc with immune-mediated diabetes-

A

APS-1 (AIRE) and IPEX (FoxP3)

20
Q

Tregs

A

differentation & fx requires Foxp3 & production of IL-2

expression: CD4 & CD25 (alpha chain of IL-2 receptor)
fx: (-) activation of naive T cells & fx of effector T cells
* mainly through production of IL-10 & TGF-beta

21
Q

examples of autoimmune disorders associated with type 1A diabetes (5)

A
  1. celiac
  2. addison’s
  3. autoimmune thyroid disease
  4. pernicious anemia
  5. vitiligo
22
Q
A
23
Q

there is increased _____ in the adipose tissue of obese T2D mice

A

TNF-alpha

24
Q

elevated lvls of what immune cytokines are predictive of T2D (4)

A
  1. TNF-alpha
  2. IL-1
  3. IL-6
  4. CRP
25
Q

adipokines

A
26
Q

Hirata disease

A

Insulin Autoimmune Syndrome

  • presence of anti-insulin antibodies in a patient who has never been exposed to exogenous insulin
  • –> recurrent and spontaneous hypoglycemia
  • DRB1*0406
  • can follow thx with sulfhydryl-containing medication, such as methimazole
27
Q

autoimmune addison’s can have concimmitant autoimmunity with what other diseases?

A

autoimmune polyendocrine syndromes (APS-1 and APS-2)

28
Q

immuno-pathogenesis of autoimmune addison’s

A

B cells:

  • auto-Ab to 21-hydroxylase (in vitro but NOT in vivo)

T cells:

  • auto-Ab to IgG1 or IgG2
  • T cells reactive to fetal adrenal extracts
29
Q

pts with what diseases should be screened for 21-hydroxylase autoantibodies as a concommitant autoimmunity with Addison’s?

A
  1. T1D
  2. hypoparathyroidism
  3. APS
30
Q

idiopathic hypoparathyroidism may have autoAb to…

A
  1. parathyroid protein: NACHT leucine-rich repeat protein 5
  2. CaSR
31
Q

APS-1 major components

A
  1. Chronic mucocutaneous candidiasis (auto-Ab to Th17)
  2. Addison’s Disease (AAD)
  3. Autoimmmune Hypoparathyroidism:
  • manifests during childhood
  • mutation in AIRE
32
Q

APS-2 major components

A
  1. T1D
  2. Addison’s Disease (AAD)
  3. Autoimmmune thyroid disease
  • most common
  • genetically associated with certain HLA haplotypes & CTLA-4 gene polymorphisms
33
Q
A
34
Q

IPEX syndrome

A

Mutation in FoxP3 gene –> absent/dysfunctional Treg

presentation: during first few months of life:

  • dematitis
  • growth retardation
  • multiple endocrinopathies
  • recurrent infections
  • overwhelming autoimmunity
    • T1D (dev as early as 2 DAYS of age)

usually die within 2 years: sepsis, failure to thrive

35
Q

Overview of the steps in the maturation of lymphocytes

A
36
Q

regions of Ag receptor that dtermine Ag specificty are called

A

variable (V) regions

sequence variability within the V regions concentrated in CDRs (complementary determining regions)

37
Q
A
38
Q

Steps in the maturation and selection of MHC-restricted T lymphocytes.

A

recombination done by RAG-1/2

  • beta chain: D –> J: DJ –> V: VDJ (variable region that binds to Ag)
  • alpha chain: V –> J: VJ

mutation in RAG-1/2 –> SCID

MOD 4 - Endocrine (2 decks)

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