Organ - Specific Autoimmune Diseases Flashcards

1
Q

Normal Thyroid Function

A

thyrotropin-releasing hormone (TRH) is secreted from hypothalamus & acts on pituitary -> releases thyroid stimulating hormone (TSH) –> acts on thyroid to release thyroid hormones T3 & T4

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2
Q

Thyroid Hormone Function

A

metabolism, growth & maturation

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3
Q

Biosynthesis of Thyroid Hormones

A
  1. TSH binds to TSH receptor
  2. TSH causes iodine to be taken up into the thyroid
  3. iodine is oxidized to iodide by thyroid peroxidase (TPO)
  4. iodide is coupled to thyrooglobulin (TG)
  5. TG is converted to T3 or T4
  6. T4 is metabolized to T3
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4
Q

Throxine binding globulin (TBG)

A

serum protein that binds most circulating T3/T4

bound T3/T4 is inactive

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5
Q

Thyroid Feedback Mechanisms

A

low T3/T4 - piuitary gland produces TSH to stimulate more hormons
high T3/T4 - pituitary gland stops producing TSH

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6
Q

Thyroid autoantibodies

A

thyroid peroxidase antibody (TPOAb)
thyroglobulin antibody (TgAb)
thyroid stimulating hormone receptor antibody (TRAb)

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7
Q

Thyroglobulin (Tg)

A

protein produced exclusively by the thyroid gland

precursor to T3/T4

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8
Q

Anti-Tg antibodies

A

10-20% of ‘normal’ people have it
50-60% of patients w/ Hashimoto’s thyroiditis are +
>116 IU/ml is clinically relevant

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9
Q

Anti-TPO antibodies

A

50% + in thyroid inflammation
90% + in Hashimoto’s thyroiditis
75% + in Grave’s Disease
>75 IU/ml is clinically relevant

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10
Q

Anti TSH receptor antibodies

A

essentially all Grave’s patients are +

very difficult to test for so anti- TPO is normally ordered instead

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11
Q

Hashimoto’s thyroiditis

A

autoimmune process in which development of circulated cytotoxic Ab targets thyroid antigens
cellular damage & decreased production of thyroid hormones occur - hypothyroidism

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12
Q

Clinical Features of Hashimoto’s

A

30-60 yrs
5x more common in females
decreased T4 & increased TSH

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13
Q

Symptoms of Hashimoto’s

A

enlarged/lumpy thyroid
loss of energy, slowed metabolism, overweight, tiredness, constipation, cold sensitivity, slow pulse, dry skin, deep voice, dry hair, depression

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14
Q

Treatment for Hashimoto’s

A

synthetic T4 replacement (Synthroid)

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15
Q

Grave’s Disease

A

hyperthyroidism
mimics normal action of TSH by binding to & activating TSH receptors
increase T3/T4 & decrease in TSH

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16
Q

Clinical Features of Graves’

A
20-50 yrs
10x more common in females
enlarged thyroid
nervousness
fatigue
weightloss
bulging eyeballs (!)
17
Q

Lab testing for Graves’

A

increased T3/T4
low TSH
>75% have anti-TPO abs

18
Q

Treatment for Graves’

A

anti-thyroid drugs, surgery, radioactive iodine ablation

19
Q

Type 1 diabetes mellitus

A

hyperglycemia due to deficiency of insulin secretion -due to autoimmune pancreatic islet beta cell destruction

20
Q

Lab diagnosis for Diabetes type 1

A

increase in serum glucose
glucose present in urine
HbA1C >6%
elevated serum ketones

21
Q

Celiac Disease

A

inflamed small intestine -> malabsorption of food
chronic diarrhea
small stature / growth
genetic inappropriate immune response to gluten/gliadin

22
Q

Celiac Disease testing

A

perform an ELISA for the IgA-TTG

‘confirmatory’- colon biopsy; wide short villi & infiltration of lymphs are diagnostic

23
Q

Inflammatory Bowel Disease

A

marked chronic inflammation in the gut

abdominal pain, weight loss

24
Q

Ulcerative colitis

A

affects the colon, inflammation in mucosal area

positive p-ANCA seriology

25
Q

Crohn’s Disease

A

affects whole intestine
all layers inflammed w/ monocytes/macrophages
produce antibodies that react w/ baker’s yeast C. cerevisiae

26
Q

Anti-Neutrophil Cytoplasmic Antibody Testing (ANCA)

A

indirect IFA just like for ANAs but uses neutrophils instead of Hep-2 cells
c-ANCA - cytoplasmic; antibodies against proteinase -3
p- ANCA- peripheral; antibodies against myeloperoxidase

27
Q

Multiple Sclerosis

A

involves the CNS

autoantibodies against myelin basic protein

28
Q

Myasthenia Gravis

A

involves nerve cells in skeletal muscles

autoantibodies against acetylecholine receptors

29
Q

Goodpasture’s Syndrome

A

involves kidney glomeruli

autoantibodies against glomerular basement membrane