Thyroid disease Flashcards
Another name for Hyperthyroidism (HT)
thyrotoxicosis
Another name for Hypothyroidism (HoT)
myxedema
What causes the formation of a goiter/ what is a goiter
goiter’s are inflammed thryoid glands
Prolonged elevation of TSH cause them
What is a thyroid nodule?
an overgrowth of cells that can be benign or cancerous - overgrowth of cells can be called neoplasm
what is neoplasm
an overgrowth of cells that can be benign or cancerous
Describe the thyroid anatomy
hyoid bone
larynx
pyramidal lobe
right lobe and left lobe
what is thyroidal peroxidase
catalyzes iodine oxidizes so it can then interact with thyroglobulin and form T4 and T3
what are the two major cells in the thyroid and thier fucntions?
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
what are the full names of T3 and T4
T3 - Triiodothyronine
T4 - Thyroxine
Explain Thyroid hormone synthesis
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
Which thyroid hormone is more widely found?
T4 - 90%
T3 - 10%
Before stimulation by TSH, how are the thyroid hormones found?
T3 and T4 are attached to thyroglobulin
When the thyroid hormones are released what happens?
they bind to protein, are lipid-soluble, and diffuse from the follicle to the circulation
Discuss how thyroid hormone produce an effect when they are lipid soluble
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
What releases TSH
TRH - thyroid releasing hormone
What kind of disease is HT
autoimmune disease
What are some causes of HT
- ingestion of thyroid hormone preparations or excess iodine
- pituitary adenoma
- hypothalamic disease
- Inflammation: toxic thyroiditis of Hashimoto disease and sub-acute thyroidtis
what is Hasimoto’s thyroditis
thyroid follicular cell destruction with release of preformed T4 and T3
what is grave diseas
causes HT
- antibodies stimulate TSHR and we have excess T3 and T4 release
What are the classifications of HT and based on what criteria
primary: The thyroid gland is affected so T3 and T4
secondary: Hypophysis affects TSH
tertiary: Hypothalamus affected so TRH
ectopic: struma ovarii
When in life do we get graves disease?
2 or 3 decades of life
What HLA types make you more susceptible to graves disease?
HLA B-8, DR3 - caucasians
Bw46 and B5 - asaians
B17 - blacks
Graves disease more common in male or females?
females
Graves diseas is what kind of disease what’s it characterized by?
autoimmune disorder
- TSH-R (stim) antibody present in 90 % of cases
- serum levels correlate poorly with severity
Causes of graves disease?
- genetic
- molecular mimicry - TSH receptor
- Suppressor T lymphocyte defect
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
Histology of Graves disease
- colloid scant
- packed follicular with columnar epithelium
- scattered lymohocytes
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
Some more complicated clinical manifestations
- thyromegaly
- exophthalmos
- widening of the palpebral fissure resulting in exposed sclera
- vision changes (blindness), photophobia
Key features of primary HT
- undetectable levels of TSh however elevated serum T3 and T4
how to confirm the presence of graves diseases and rule out the presence of thyroid neoplasm
24-hour radioactive iodine uptake study
What is a thyroid storm?
dangerous levels of thyroid hormone acutely release
- life-threatening thyrotoxicosis
S and S of thyroid storm
- elevated temp, palpitations, arrhythmias, tachycardia
- extreme restlessness, agitation, and psychosis
- VND, and jaundice
Acquired HoT thru what means?
- primary lymphocytic thyrodidtis (Hasimotot or autoimmune thyroidtis)
- Irradtion of thyroid galnd
- surgical removal of thyroid gladn
- iodine defieincfy
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
Secondary causes of HoT
Defects in TSH production that result from:
- severe head trauama
- cranial neoplasms
- brain infections
- cranial irradiation
- neurosurgical procedures
Clinical manifesttaions in infants
- dull appearance, thick produlent tongue and lips, prolonged nenatal jaundice, poor mucle tone, bradycardia, mottled extremeites, hoarse cry, umbilical hernia
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
What does myxedema results from?
-prolonged/severe defienciy - edema due to accumulation of glycoaminoglycans in the interistal space
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
Diagnosis of HoT
- elevated TSH
- later in the disease low levels of T3 and T4
what results in low levels of TSh and T3 and T4
Hypothalamic-pituitary dysfunction