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Thyroid disease Flashcards

1
Q

Another name for Hyperthyroidism (HT)

A

thyrotoxicosis

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2
Q

Another name for Hypothyroidism (HoT)

A

myxedema

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3
Q

What causes the formation of a goiter/ what is a goiter

A

goiter’s are inflammed thryoid glands

Prolonged elevation of TSH cause them

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4
Q

What is a thyroid nodule?

A

an overgrowth of cells that can be benign or cancerous - overgrowth of cells can be called neoplasm

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5
Q

what is neoplasm

A

an overgrowth of cells that can be benign or cancerous

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6
Q

Describe the thyroid anatomy

A

hyoid bone
larynx
pyramidal lobe
right lobe and left lobe

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7
Q

what is thyroidal peroxidase

A

catalyzes iodine oxidizes so it can then interact with thyroglobulin and form T4 and T3

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8
Q

what are the two major cells in the thyroid and thier fucntions?

A

Follicular cells
- trap dietary iodine and transport it to colloid along with enzyme thyroidal peroxidase
-produce and secret thyroid hormone T3 and T4

Parafollicular cells
- secrete calcitonin

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9
Q

what are the full names of T3 and T4

A

T3 - Triiodothyronine
T4 - Thyroxine

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10
Q

Explain Thyroid hormone synthesis

A

The TSHR receptor on the outside of colloids is stimulated via TSH (whihc is produced from the pituitary gland)

Upon stimulation, it stimulates thyroglobulin, thyroid peroxide and iodine channels

idoien cahnnels allow idoine to enter collloid

iodine and thyroglobulin work together to form T3 and T4

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11
Q

Which thyroid hormone is more widely found?

A

T4 - 90%
T3 - 10%

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12
Q

Before stimulation by TSH, how are the thyroid hormones found?

A

T3 and T4 are attached to thyroglobulin

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13
Q

When the thyroid hormones are released what happens?

A

they bind to protein, are lipid-soluble, and diffuse from the follicle to the circulation

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14
Q

Discuss how thyroid hormone produce an effect when they are lipid soluble

A

since they are lipid soluble they travel bound to a protein

Only a small percanetge dissolve in plasm as free hormone and are ble to cross directly to their traget cell

T3 bind to its receptor and exerts its action, mediated thorugh alternation in gene transcript

T4 is acted on by cellualr enzymes that cleave one iodine unit converting it to active T3 form

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15
Q

What releases TSH

A

TRH - thyroid releasing hormone

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16
Q

What kind of disease is HT

A

autoimmune disease

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17
Q

What are some causes of HT

A
  • ingestion of thyroid hormone preparations or excess iodine
  • pituitary adenoma
  • hypothalamic disease
  • Inflammation: toxic thyroiditis of Hashimoto disease and sub-acute thyroidtis
18
Q

what is Hasimoto’s thyroditis

A

thyroid follicular cell destruction with release of preformed T4 and T3

19
Q

what is grave diseas

A

causes HT

  • antibodies stimulate TSHR and we have excess T3 and T4 release
20
Q

What are the classifications of HT and based on what criteria

A

primary: The thyroid gland is affected so T3 and T4

secondary: Hypophysis affects TSH

tertiary: Hypothalamus affected so TRH

ectopic: struma ovarii

21
Q

When in life do we get graves disease?

A

2 or 3 decades of life

22
Q

What HLA types make you more susceptible to graves disease?

A

HLA B-8, DR3 - caucasians
Bw46 and B5 - asaians
B17 - blacks

23
Q

Graves disease more common in male or females?

24
Q

Graves diseas is what kind of disease what’s it characterized by?

A

autoimmune disorder
- TSH-R (stim) antibody present in 90 % of cases

  • serum levels correlate poorly with severity
25
Causes of graves disease?
1. genetic 2. molecular mimicry - TSH receptor 3. Suppressor T lymphocyte defect
26
Pathogenis of graves disease
defect in T helper cell allows for B cell generation in response to thryoid antigens producing antibodies, Inflammation of orbit due to sensitization of T celler cells
27
Histology of Graves disease
- colloid scant - packed follicular with columnar epithelium - scattered lymohocytes
28
Clinical manifestations of HT
Behavioral changes: insomnia, restlessness, tremor, irritability, palpitations, heat intolerance, diaphoresis, inability to concentrate, Increase appetite and dietary intake paradoxical weight loss Scant menses
29
Some more complicated clinical manifestations
- thyromegaly - exophthalmos - widening of the palpebral fissure resulting in exposed sclera - vision changes (blindness), photophobia
30
Key features of primary HT
- undetectable levels of TSh however elevated serum T3 and T4
31
how to confirm the presence of graves diseases and rule out the presence of thyroid neoplasm
24-hour radioactive iodine uptake study
32
What is a thyroid storm?
dangerous levels of thyroid hormone acutely release - life-threatening thyrotoxicosis
33
S and S of thyroid storm
- elevated temp, palpitations, arrhythmias, tachycardia - extreme restlessness, agitation, and psychosis - VND, and jaundice
34
Acquired HoT thru what means?
1. primary lymphocytic thyrodidtis (Hasimotot or autoimmune thyroidtis) 2. Irradtion of thyroid galnd 3. surgical removal of thyroid gladn 4. iodine defieincfy
35
Idoine in HoT
- is essential for T3 and T4 synthesis - defeincy leads to lack of T3 and T4 but not thyrogloblulin levels - therefore ther is insuffient hormone to inhibit TSH secretion - increased TSH cause cells to secret large amounts of thyroglobulin, which leads to a goiter
36
Secondary causes of HoT
Defects in TSH production that result from: - severe head trauama - cranial neoplasms - brain infections - cranial irradiation - neurosurgical procedures
37
Clinical manifesttaions in infants
- dull appearance, thick produlent tongue and lips, prolonged nenatal jaundice, poor mucle tone, bradycardia, mottled extremeites, hoarse cry, umbilical hernia
38
Clinical manifestations in children/adults
- decreas basal metbolic rate, weakness, lethargy, cold intolerance, decreased apapetite, bradycardia, narrowed pulse pressure, mild/moderate weight gain, elevated cholesterol and triglycerides, enlarged thyroid, dry skin, constipation, depression, difficulties with memory and concentration, menstrual irregulairty
39
What does myxedema results from?
-prolonged/severe defienciy - edema due to accumulation of glycoaminoglycans in the interistal space
40
what can myxedema patient present with? and what can it progress to?
- altered mental status, altered temperature regulation, history of precipitating event (trauma/sepsis/infections) - can progress to myxedema coma and life-threatening condition
41
Diagnosis of HoT
- elevated TSH - later in the disease low levels of T3 and T4
42
what results in low levels of TSh and T3 and T4
Hypothalamic-pituitary dysfunction

Patho (8 decks)

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