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207 Cards in this Set
- Front
- Back
what type of gland is the thyroid gland?
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ENDOCRINE
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What are the glands inside the thyroid gland?
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Parathyroid glands
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What is the histological composition of a thyroid gland?
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Follicles
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what are the follicle cells lined by?
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Cuboidal cells
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what is the function of the cuboidal cell
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thyroxine (T4)
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Where does the thryoxine get stored?
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in the follicle in the COLLOID
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what is the mechanism with which the colloid exits the gland and enters the blood stream?
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Pinocytosis- binds to membrane proton and goes to organ
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Once the membrane bound colloid has reached the organ what does it do?
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It converts the T4 to its T3 active form
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What is the function of T3
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activates:
in children: brain tissue and muscle tissue in adults: primarily muscle tissue |
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Why is the thyroid important in children
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it is important to produce effective neurological functioning in the child
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What is thyrotoxicosis?
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when the patient has high levels of free T3/T4 in the serum and causing organ involment
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What are the effects of Thyrotoxicosis?
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GIT- steatorhea, malabsorption diarrhea
Cardiac: palpitation, tachycardia, atrial fibrillation Constitutional: heat intolerance, weight loss despite increased appetite, sweating Thyroid Myopathy (muscle breakdown-proximal muscle weakness) Tremor(76%) Staring gaze and lid lag |
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How can thyrotoxicosis produce sudden death
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Atrial fibrillations
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What can Thyrotoxicosis cause with hyperthyroidism?
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1.) Graves disease (Ab +ve)
2.) Toxic MNG 3.) Toxic adenoma ALL lead to increase in I141 uptake |
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What is produced by basophilic cells of the anterior pituitary?
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TSH
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what is produced by parafollicular or C cells?
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Calcitonin
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What is the etiology of Primary hyperthyroidism?
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Autoimmune
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What is another name of Primary hyperthyrodism?
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Grave's disease
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30yr old Female, exopthalamus( accumulation of fat retro orbital),
pretibial myxedema( dermal accumulation of myxoid tissue) and diffuse symmetric hyperplasia of thyroid gland. |
Grave's disease/ Primary hyperthyroidism
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What are the different autoimmune etiologies of Grave's disease
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-Thyroid stimulating immunoglobulin(TSI)
- Thyroid growth stimulating immunoglobulin (TGI) - TSH- receptor binding inhibitory immunoglobulin |
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What is the mechanism of TSH receptor binding inhibitory immunoglobulin.
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blocks binding of TSH to TSH-R but stimulates thyroid gland
- fibroblastogenic- stimulates fibroblast change to adipocytes- myxedema and periorbital edema(exophthalamus) |
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What are the associations of Primary hyperthyroidism?
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SLE, pernicious anemia
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What is the morphology of Grave's disease?
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-follicles lined by columnar cells
- papillary projections - "scalloped" appearance in follicles: devoid of colloid |
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What are the lab findings of Grave's disease?
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-Low TSH, high free T3 or T4
-Auto antibodies + -Diffuse increase I131 uptake - increase in resin T3 uptake |
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What are the complications of Primary hyperthyroidism?
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Thyroid storm: sudden onset of sweating, palpitation, hyperthermia (greater than105F), atrial fibrillation increase cardiac arrest
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What is the I131 Uptake in Grave's disease?
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There is diffuse increased uptake
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What is the I131 uptake in Primary hypothyroidism?
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diffuse reduced uptake
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what is the I131 uptake in exogenous thyroid hormone?
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reduce uptake
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What is the I131 in a toxic Adenoma?
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Localized increase uptake
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What is the pathogenesis behind secondary hyperthyroidism?
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Pituitary adenoma of the basophilic cells - increase in TSH
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What are the lab findings of Secondary hyperthyroidism?
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normal or high TSH- highly elevated T3/T4
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What are the lab findings of primary hypothyroidism
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increase in TSH, decrease in T3/T4
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What are the lab findings of secondary hypothyroidism?
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decrease in TSH, decrease in T3/T4
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What are the etiologies of primary hypothyroidism?
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-Cretinism
- iodine defny (Sub himalayan- Goiter) -Hashimotos Thyroiditis: goiter idiopathic (MC in USA: no change in shape/size of gland |
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What causes secondary hypothyroidism?
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hypothalamic failure or pituitary necrosis- sheehan's syndrome..
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What are the clinical fts of hypothyroidism?
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-fatigue and lethargy
- sensitivity to cold -alopecia - increased cholestral and TG- weight gain (chance of coronary ath) -reduced cardiac output-Myxedema |
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What is myxedema?
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accumulation of mucopolysaccharide in subcutaneous tissue
- may progress to myxedema coma- end stage of severe long standing hypothyroidism -mental obtundation, bradycardia, hypotension, hypothermia.. |
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Child has a low level of T4 and goiter. His IQ is very low, and has a pot belly, with an umbilical hernia, and a protruded tongue. He is very short (dwarf)
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Cretinism
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What is another name for inflammation of the thyroid gland. follicles?
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Hashimoto's thyroiditis
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What is the pathogenesis behind Hashimoto's thyroiditis?
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Autoimmune: T cell stimulated B cells to produce AB locally:
- antithyroglobulin: Ab to colloid -Antimicrosoma: Ab to thyroid peroxidase in cuboidal epithelium -Anti- TSH receptor inhibitory antibody: Ab to TSH receptor |
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What is Hashimoto's associated with?
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Rheumatic Arthritis and SLE
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What is the morph of Hashimoto's?
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symmetrical enlargedment of gland
-Hurthle cells: degenerated follicular cells -Diffuse infiltrate of lymphoid follicles in thyroid (CD8 and CD4) |
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Female 45-65y/o, presents with painless diffuse enlargement of gland.
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Hashimoto's thyroiditis
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What is the genetic association with Hashimoto's
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HLA DR3 and HLA DR5
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what is the d/d of myxedema in an adult suffering of hypothyroidism?
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Secondary- Hypopituitarism( decrease in T4 AND T3 AND TSH)
Primary thyroid disease- Autoimmune vs non autoimmune thyroiditis ( decrease in t4, t3 and increase in TSH) |
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What is there an increased risk of developing in a Hashimoto's patient?
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Non Hoddgkin's lymphoma
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What is the most common cause of hypothyroidism in adults
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Hashimoto's thyroidititis
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What happens when there is an increase in T3/T4 in hashimoto's?
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Hashitoxicosis (due to release of thyroxin form damaged follicles), it is followed by persistent hypothyroidism
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when do you get temporary loss of colloid cells?
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Hashitoxicosis
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What is the etiology of Subacute granulomatous thyroiditis?
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Post viral infection
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What is another name for De Quervin's disease?
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Subacute Granulomatous thyroiditis
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Female 30-50yr, has a tender, firm, enlarged gland. She has been feeling hot, sweating, has palpitations, tremors and diarrhea with an increased wbc count and ESR
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Subacute granulomatous thryoidiits
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What is the morphology of DeQuervin's disease
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prescence of large foreign body giant cells and granuloma with inflammatory destruction of thyroid follicles.
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What it the pathogenesis of Reidal thyroidititis?
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dense fibrosis in thyroid and around trachea and esophagus.
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Pt. presents with stridor, dyspnea, and dysphagia
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Riedel thryoiditis
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What is riedel thyroiditis associated wtih?
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retroperitoneal and severe mediastinal fibrosis (Idiopathic pulmonary Fibrosis/ scleroderma- ANA's)
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Pt. has hx of pneumonia/ septicimea, malnutrition, starvation. what might they suffer from later?
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Euthyroid Sick Syndrome
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Pt presents with hypothyroid like ft. with low T3 and normal T4 and TSH
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Euthyroid Sick Syndrome
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What is the pathogenesis of Euthyroid Sick Syndrome?
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Destruction of T3 by INF- alpha and IL-2
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Why is there myxedema in both Hyperthyrodism and hyperthyrodism?
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This is because they both have an activate TSH-R Ab which activates a fibroblast in soft tissue, causing the production of lymphocytes and the myxedema
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What receptors are found in soft tissues of fibroblast as well?
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TSH-R Ab.
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What happens when you activate the fibroblast TSH-R in tissue cells?
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It causes production of soft tissue matrix- known as proteoglycan
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Is TSH-R localised to follicular cells in the thyroid?
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No it can be found in soft tissue
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Hypothyroidism myxedema
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is generalised all over the body
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what happens in proptosis?
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same as myxedema- seen in Hypo and hyper. same mechanism.
Fat/Adipose tissue accumulates behind the eye causing the protrusion |
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Is the accumulation of fat + lymphocytes behind the eyes reversible or irreversible in proptosis?
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irreversible
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Is the accumulation of proteoglycan and matrix formation reversible or irreversible?
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reversible if treated properly.
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What happens in a thyroglossal duct cyst?
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accumulation of atrophic thryoid tissue around the thryoid.
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where does the thyroglossal duct cysts arise from?
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Foramena cecum, midline of neck below the hyoid bone, and moves with deglutination
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What is a branchial cyst
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is infront of the SCM(lateral portion)
Huge amts of lymphoctes/plasma cells accumulate here and hence it can be confused for a lymph node. |
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What is the d/d of a branchial cyst?
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Reactive Lymph node
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Fluctuant, non tender, smooth mass
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Branchial Cyst
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Definition of Goiter
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Enlargement of thyroid gland due to any cause
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what is the most common cause of goiter?
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prolonger iodine defny (seen in areas surrounded by large land masses, away from the sea, oceans)
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What are the types of Goiter?
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-Colloid goiter: single nodule, euthryoid- huge amts of thyroxine
-Multiple Nodular Goiter(MNG) usually non toxic and euthyroid |
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What is the purpose of goiter formation?
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To physiologically balance out the thyroxine level
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If you see a goiter what do you not expect to see
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Hypothyroidism
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What are the complications of Multiple Nodular Goiter?
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- Plummer Syndrome- nodules of MNG become toxic- produce T4 and develop hyperthyroidism
- Follicular Carcinoma |
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What is the morphology of goiter?
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Gross: enlarged thyroid gland with multiple colloid nodule (not deficient of thyroxine)
Micro: Follicles of varying size, calcification, and fibrosis |
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What is I131 scan finding in MNG?
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usually non-toxic and euthyroid (pt. can live with it for years)
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What is the primary problem of MNG?
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cosmetic effect
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What does I131 tell you?
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The functioning of the gland
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What happens as a result of the patient developing Plummer Syndrome
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Increased chance of thyroid storm and death by hyperpyrexia
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What is the cause of death in a thyroid storm?
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Hyperpyrexia
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What is the cause of the hyper functioning of the Goiter in Plummer Syndrome
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It is genetic, the same gene that is responsible for causing Glioblastoma Mulitforme of the brain
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What is the age group of plummer syndrome patients?
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Elderly
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What type of calcifications is seen in multiple nodular goiter?
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Dystrophic
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What is "hot" thyroid?
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produces more T3/T4( hyper functioning)- thryotoxicosis, taking up MORE I131
usually non neoplastic lesion |
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What is "cold" thyroid?
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Produces less T3/T4 (non functional)- takes up LESS I131
usually neoplastic(adenoma/carcinoma) |
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What is the name of a benign thyroid tumor?
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Adenoma
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What is the most common type of thyroid adenoma
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Follicular adenoma ( involves follicular cells)
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What are the ft s of a thyroid adenoma?
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usually single,
capsulated firm "cold"- non functional: neoplastic. |
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what happens when a thyroid adenoma is active?
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It becomes "HOT" but it is still single, capsulated and firm.
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What is another name for a "HOT" thyroid adenoma?
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toxic adenoma
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What is the etiology of papillary carcinoma?
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radiation therapy early in life due to having a cancer and getting chemotherapy.
more common in females |
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Pt has a painless mass in anterior neck, it has metastasized to the enlarged cervical LN
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Papillary Carcinoma
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What is the gene specifically related to papillary carcinoma?
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rearrangements of Tyrosine Kinase receptors of RET gene
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What is the morphology of papillary carcinoma?
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- psammoma body
- intranuclear pseuodoinclusion - Orphan Annie nucleus (hypochromic nuclues) |
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What are the I131 findings of papillary carcinoma?
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It is "COLD"
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What is the age group where you would find papillary carcinoma
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2nd decade and 5th decade
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What is d/d of papillary carcinoma?
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-Thyroglossal cyst
-Branchial(cleft) cyst - thyroid adenoma |
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Why is FNAC(fine needle aspiration cytology) used to see in papillary carcinoma
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pseudo inclusion
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which cancers are produced by follicular cells?
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Papillary carcinoma
Follicular carcinoma Anaplastic carcinoma |
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What is the percentage of cases where you end up with papillary carcinoma?s
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75-85%
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What cancers are produced by C cells of parafollicular cells
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Medullary carcinoma
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Which is tumor in the thyroid is neuroendocrine in nature?
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Medullary carcinoma
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What is the etiology of follicular carcinoma?
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iodine defny i.e. Multiple nodular goiter
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What kind of spread is involved in papillary carcinoma?
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lymphatics- to regional LN(cervical group)
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what are the C/F of follicular carcinoma
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- greater in females than males
- btw age 40-60 |
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what are the I131 findings of follicular carcinoma?
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Mostly "cold", but sometimes "hot"
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What is the means of spread of follicular carcinoma?
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Hematogenous spread to bone and lung
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what is prognosis of papillary carcinoma?
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Good, despite early metastasis
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what can be seen on the microscopy of a follicular carcinoma?
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capsular and vascular invasion
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What disesase comes before follicular carcinoma?
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MNG
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What is the mutation involved in follicular carcinoma?
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KRAS, HRAS, AND NRAS- therefore it is an adenocarcinoma of the thyroid gland
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why is the scan finding important clinically in follicular carcinoma?
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you can measure the anticancer drug uptake with I131 to kill cancer more effectively
- helps to measure metastasis- acts as an area of single uptake |
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What is prognosis of follicular carcinoma?
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bad
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What must you do to help diagnose follicular carcinoma?
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A full body scan with I131
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what type of carcinoma is a follicular carcinoma?
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adenocarcinoma
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Explain the mechanism by which capsular invasion takes place
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-tumor cells express laminin receptors
- tumor cells anchors into the laminin in the receptors - it produces collagenase 4 and Cathepsin D -t hese enzymes break through protein |
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What is produced by medullary thyroid carcinoma?
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Calcitonin
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Thyroid storm vs myxedema coma what is the difference?
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high temperature, diarrhea, taccychardia,atrial fibrillations
in thyroid storm but in myxedema coma: there is loss of brain functioning, cold intolerance, weight gain, lethargy, fatigue, constipation, headaches |
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What are the associations responsible for Medullary carcinoma?
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MEN 2A: medullary carcinoma and pheochromocytoma + hyperparathyroidism
MEN IIB: medullary carcinoma+ pheochromocytoma + neuroma of GIT/schwannoma |
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What are the other neuroendocrine tumors?
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- carcinoid
-Small cell carcinoma -Pheochromocytoma -Neuroblastoma -Medullary thyroid carcinoma |
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Does the calcitonin produced by medullary thyroid carcinoma cause changes in the body?
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No, because it is localised to the tumor, and does not cause an increase in the serum levels of calcitonin
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What is the mode of inheritance in Medullary Thyroid Carcinoma?
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old age= sporadic
young patient= autosomal dominant familial |
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What is the gene mutation involved in Medullary carcinoma?
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RET gene mutation
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What are the associations of MEN IIA
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Medullary carcinoma+ pheochromocytoma+ hyperparathyroidism
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What are the associations of MEN IIB
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meduallary carcinoma+ pheochromocytoma+ neuroma of GIT /schwanoma
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What is the morphology of medullary thyroid carcinoma?
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spindle cells and amyloid stroma (calcitonin acts like this)
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what are the fts of MEN IIA?
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Episodic fluctuating HTN, hypercalcemia
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what are the findings of schwanoma?
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Antony A area, Antony B area and Vercay bodies
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what is an important marker to differentiate between MEN IIA and MEN IIB?
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Calcium, as it is elevated in A and normal in B
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what is the full form of MEN
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multiple endocrine neoplasia
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How do you manage thyroid carcinoma?
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-total or partial resection
-Thyroxine replacement 1.)basal ganglia calcification- muscle rigidity 2.) overdose - check parathyroid status after sx- hypocalcemia produces tetany |
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what structure in Medullary Carcinoma acts like amyloid
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calcitonin
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What is intact PTH
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broken down product of PTH release from parathyroid gland (used PTH by tissues)
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How does a surgeon recognize a parathyroid and thyroid?
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parathyroid- typically looks golden yellow
thyroid- looks pink |
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What is PTH-related protein?
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it is due to paraneoplastic syndrome- sq c carcinoma of lung, RCC
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How does PTH act on the tubules of the kidney/
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increase in phosphate excretion
absorption of calcium |
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How does PTH act on the bone?
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Resorption of calcium- takes calcium out of the bone
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How does PTH affect the GIT
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It is in conjunction with Vit d- REUPTAKES calcium in the GIT
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what does parathyroid look like histologically?
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typically has a capsule
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what are the two cells that make the parathyroid
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chief cells
clear cells |
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what is the additional tissue you can see in the parathyroid gland?
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adipose tissue, a lot of it around the chief cells and clear cells
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which is the only organ in the body which has a normal amount of adipose tissue?
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parathyroid gland
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what is hyperparathyroidism?
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increased levels of PTH
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What is the most common cause of Primary hyperparathyroidism?
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Adenoma of parathyroid
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if a patient is suffering from primary hyperparathyroidism what are the affects on the renal system?
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Calcium Oxalate stone formation
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What effects does Primary Hyperparathyroidism have on the GIT system?
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-Peptic ulcer- due to hypercalcemia
-pancreatitis |
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What effect does Primary hyperparathyroidism have on calcium
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it increases it
|
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What causes hyper secretion of the PTH in primary hyperparathyrodism?
|
the adenoma of they parathryoid- increase in bone resorption- increase in GIT absorption, increase in kidney absorption of Calcium
|
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What effects does Primary Hyperparathyroidism have on the GIT system?
|
-Peptic ulcer- due to hypercalcemia
-pancreatitis |
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Which MEN is associated with primary hyperparathyrodism?
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MEN 2 A
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What effect does Primary hyperparathyroidism have on calcium
|
it increases it
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What type of medullary carcinoma do you get in MEN 2A
|
RET protooncogene- familial
|
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What causes hyper secretion of the PTH in primary hyperparathyrodism?
|
the adenoma of the parathryoid- increase in bone resorption- increase in GIT absorption, increase in kidney absorption of Calcium
|
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Which MEN is associated with primary hyperparathyrodism?
|
MEN 2 A
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What type of medullary carcinoma do you get in MEN 2A
|
RET protooncogene- familial
|
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What effects does Primary Hyperparathyroidism have on the GIT system?
|
-Peptic ulcer- due to hypercalcemia
-pancreatitis |
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What effect does Primary hyperparathyroidism have on calcium
|
it increases it
|
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What causes hyper secretion of the PTH in primary hyperparathyrodism?
|
the adenoma of the parathryoid- increase in bone resorption- increase in GIT absorption, increase in kidney absorption of Calcium
|
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Which MEN is associated with primary hyperparathyrodism?
|
MEN 2 A
|
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What type of medullary carcinoma do you get in MEN 2A
|
RET protooncogene- familial
|
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what is the typical morphological finding that is unique to papillary carcinoma?
|
hypochromatic nucleus
|
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what is the marker for Medullary carcinoma?
|
Calcitonin
|
|
How does I131 differentiate:
a. Grave's disease b.) Plummer Syndrome c.) Toxic adenoma |
a.) diffuse excess uptake
b.) multiple focal areas of "HOT" uptake c.) one single area of "hot" uptake |
|
what are the lab findings of Primary Hyperparathyroidism?
|
increase in PTH, increase in Ca2+ and decrease in Phosphate
|
|
What is the most common cause of Secondary Hyperparathyroidism
|
CRF:
chronic pyelonephritis chronic GN Adult polycystic kidney disease |
|
what is the typical morphological finding that is unique to papillary carcinoma?
|
hypochromatic nucleus
|
|
what is the marker for Medullary carcinoma?
|
Calcitonin
|
|
How does I131 differentiate:
a. Grave's disease b.) Plummer Syndrome c.) Toxic adenoma |
a.) diffuse excess uptake
b.) multiple focal areas of "HOT" uptake c.) one single area of "hot" uptake |
|
what are the lab findings of Primary Hyperthyroidism?
|
increase in PTH, increase in Ca2+ and decrease in Phosphate
|
|
what is the typical morphological finding that is unique to papillary carcinoma?
|
hypochromatic nucleus
|
|
What is the most common cause of Secondary Hyperparathyroidism
|
CRF:
chronic pyelonephritis chronic GN Adult polycystic kidney disease |
|
what is the marker for Medullary carcinoma?
|
Calcitonin
|
|
How does I131 differentiate:
a. Grave's disease b.) Plummer Syndrome c.) Toxic adenoma |
a.) diffuse excess uptake
b.) multiple focal areas of "HOT" uptake c.) one single area of "hot" uptake |
|
what are the lab findings of Primary Hyperthyroidism?
|
increase in PTH, increase in Ca2+ and decrease in Phosphate
|
|
What is the most common cause of Secondary Hyperparathyroidism
|
CRF:
chronic pyelonephritis chronic GN Adult polycystic kidney disease |
|
what are the other causes of Secondary hyperparathyroidism
|
Malabsorption, as well as Vit D defny
Lack of Vit D= activated parathyroid gland, as there is decreased levels of serum calcium due to lack of absorption |
|
What is the mechanism behind which CRF causes 2dary Hyperparathyroidism?
|
It causes uremia:
causes: astrexis, there is hyperkalemia, in GIT- there is acute hemorrhagic gastritis, as well as colonic gastritis, In bone- suppresion of it leading to anemia, cardiac- fibrinous pericarditis |
|
What is the morphology of secondary hyperparathyroidism?
|
produce parathyroid hyperplasia involves multiple glands
|
|
what causes primary hyperparathyroidism?
|
parathyroid adenoma
parathyroid hyperplasia parathyroid carcinoma |
|
What is a parathyroid adenoma?
|
Involves single gland, is capsulated and composed of mainly chief cells that release PTH
|
|
What happens in primary parathyroid hyperplasia?
|
it involves multiple glands
occurs as part of MEN 2B and microscopically you see water clear cell hyperplasia |
|
What happens to the phosphate levels in chronic renal failure?
|
it is secretion is impaired therefore it is increased..
|
|
What is the lab values when a pt suffers of Acute Polycystic kidney disease?
|
decrease in Hb and RBC, Increase in in K+
it has CRF fts and uremia ft s |
|
What happens as a result of impaired phosphate secretion?
|
-increase in serum phosphate, decrease in serum calcium
- low Ca++ produces PTH production (constant activation leads to parathyroid hyperplasia) -Leads to osteopenia (fractures) and increase in serum Ca+ -Eventually as CRF continues you get decrease in Ca++ |
|
How does loss of renal substance cause secondary hyperparathyroidism?
|
Reduced availability of ALFA-1- HYDROYXLASE imp for Vitamin D synthesis. results in
- reduced Ca++ absorption from GIT -Increase in PTH to increase se. Ca++ - increase in PTH cannot act of failing kidney to excrete Phosphate therefore increase in phosphate |
|
How does malabsorption cause secondary hyperparathyroidism?
|
Vitamin D defny
Impaired Ca2+ and P uptake in GIT= increase in PTH High PTH cannot compernsate of loss of Ca2+ but causes excretiong of phosphate from functioning kidney |
|
What are the lab values of 2dary hyperparathyroidism in malabsorption?
|
increase in PTH, se. Decrease in Ca++ and Phosphate, but urine increase in phospate
|
|
What are the skeletal complications of 2dary hyperparathryoidism?
|
Osteitis fibrosa cystica: diffuse bone loss resulting in osteoclastic resorption and fibrous replacement of bone
|
|
What are the characteristics of osteitits fibrosa cystica?
|
-sub periosteal thinning and bone cysts
|
|
what are the xray findings of osteitis fibrosa cystica?
|
Multiple lytic lesions/fractures and small hemorrhages- brown tumors
effects small bones(phalanges), skull, cetre |
|
What is the composition of brown tumors?
|
depostion of hemosiderin and formation of osteoclastic giant cells
|
|
What are the other findings that are associated with Primary/Tertiary hyperparathyroidism
|
Moan, Bone, Groans and stones:
- Nephrocalcinosis: metastatic calcifciations - Peptic ulcer:- G cells stimulates secretion -Acute pancreatits: trypsinogen stimulation -Gall stone: calcium+ bilirubin - Psychic moans: depression, seizures hypotonia |
|
What are the lab findings of Secondary hyperparathyroidism?
|
increase in serum calcium (action of PTH on bones)
-Radioimmunoassay of PTH (brown tumor) -Hypophosphatemia - increased urine phosphate and calcium (Action of PTH on kidney) |
|
What is the etiology of hypoparathyroidism?
|
-Thyroidectomy
-Di George syndrome |
|
What is the gene association of Di George syndrome?
|
CATCH 22 (22q11 deletion)
failure or 3rd and 4th pharyngeal pouch |
|
What are the clinical fts of Di George's syndrome?
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Cardiac Defects, abnormal face, thymic hypoplasia, cleft palate, hypocalcemia
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What are the clinical fts. of hypoparathyroidism
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-tetany: tingling sensation with muscle spasm
-prolonged QT interval -Cataract, dental abnormality -Positive for Trousseau's and Chvotsek's sign |
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What are the lab values in hypoparathyroidism?
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decrease in Ca++, decrease in PTH, increase in P
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What is another name for pseudo- hypoparathyroidism?
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Albright's Hereditary Osteodystrophy (lack of response to PTH)
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What is the pathogenesis of Pseudo- hypoparathyroidism?
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PTH-resistant hypocalcemia(bone, kidney, GIT)
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What is Albright's hereditary osteodystrophy associated with?
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Resistance to TSH and FSH/LH
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What are the c/f of pseudo-hypoparathryoidism?
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-short stature, rounded face, shortened 4th metacarpal, obesity, dental hypoplasia
-primary hypothyroidism -primary hypogonadism |
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what is the D/D of Albright's osteodystrophy?
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-Hypothyroidism
-Cushings's syndrome -Cretinism |