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EndoRepro > Week 7 > Flashcards

Week 7 Flashcards

1
Q

What is the location of the thyroid in the body?

A
  • Two lobe located in lower neck, anterior and anterolateral to the trachea
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2
Q

Blood supply of the thyroid?

A
  • Blood supply
    • R + L superior thyroid arteries (from external carotid arteries)
    • R + L inferior thyroid arteries (from thyrocervical trunks)
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3
Q

Venous drainage of the thyroid

A
  • Venous drainage
    • R + L superior thyroid veins (into IJ veins)
    • R + L middle thyroid veins (into IJ veins)
    • R + L inferior thyroid veins (into brachiocephalic veins)
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4
Q

What is important to know about the recurrent laryngeal nerves? Also what is their function?

A
  • R+L Recurrent laryngeal nerves
    • Sensory below the vocal cords and motor function to all intrinsic muscles of the larynx
    • Risk of damage during thyroidectomy
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5
Q

How many parathryoid glands are there? Where are they located?

Blood supply of parathyroid?

A

Parathyroid Glands

  • 4 glands (2 on each side) located in posterior region of each thyroid lobe
  • Inferior thyroid arteries supply 100% of the inferior parathyroid glands and 85% of superior parathyroid glands
  • Superior thyroid arteries supply 15% of the superior parathyroid glands
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6
Q

What is the pathway of the hypothalamic-pituitary-thyroid axis?

How does negative feedback occur?

A

Regulation of Hypothalamic-Pituitary-Thyroid Axis

  • Pathway: Hypothalamus releases TRH → anterior pituitary release TSH → TSH stimulates gland growth → TSH stimulation + dietary iodine → T4 and T3 (less) release
    • Negative inhibition: TRH and TSH release inhibited by high levels of T3 and T4
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7
Q

How is the thyroid hormone synthesized? Provide a detailed pathway!

A
  • Pathway:
    • TSH binds to TSH receptor (basolateral) → activates Na-I symporter (basolateral) → iodine enters cells → iodine exits cell at apical side via Pendrin
    • Synthesis of thyroglobulin (Tg) in ER of cell → Tg secreted at apical side of cell → thyroid peroxidase (TPO) located on apical surface catalyzes reaction between iodine and Tg → Tg-T3/4 → Tg-T3/4 enters cells → exits basolateral side of cell as T3 or T4
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8
Q

Know this image.

A

yeah.

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9
Q

How much of thyroid hormone is bound? What is it bound by?

A
  • BOUND (99.95%) – to serum carrier proteins, which are made by the liver
    • Thyroxine-binding globulin (TBG) – principle binding protein
    • Thyroxine-binding prealbumin (transthyretin)
    • Albumin
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10
Q

How much of thyroid hormone is free? What functions and actions does free thryoid hormone have?

A
  • FREE (0.05%) – metabolically active form responsible for hormonal activity
    • Available to peripheral tissues for intracellular transport
    • Participates in negative feedback regulation
    • Undergoes degradation and excretion
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11
Q

How does the conversion of T4 to T3 occur? What enzyme is involved? What’s so special about T3?

A

Peripheral Conversion of T4

  • Serum T4 converted to T3 by intracellular 5’-deiodinase (D1) enzyme in many peripheral tissues
    • Accounts for 85% (most) of body’s T3
    • T3 is the biologically active and most potent form of thyroid hormone
  • T4 converted to inactive reverse T3 (rT3) by peripheral tissues
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12
Q

What is the general mechanism of thyroid hormone? How does it act on peripheral tissue?

Give some examples of what would occur when thyroid hormone acts (hypothalamus, pituitary, beta receptors)

A
  • MOA: binding to nuclear receptor at target tissues → interact with thyroid hormone response elements (TREs) sequences upstream of target gene promoters → regulation of gene expression
    • Ex: T3 decreases gene transcription of TRH (hypothal) and TSH (pituitary) = gives NEGATIVE FEEDBACK
    • T3 increases gene transcription of b-adrenergic receptors in heart, liver, muscle, adipocytes
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13
Q

What effects does thyroid hormone have on the following:

  • BMR?
  • O2/CO2
  • Carbs/lipids/proteins
  • Bones, intestines
A
  • Metabolic
    • Overall, increases Basal Metabolic Rate (BMR) and affects oxidative metabolism
    • Increase O2 consumption, CO2 production, thermogenesis
    • Affects Carbohydrate, lipid, and protein metabolism
      • Increases glycogenolysis, gluconeogenesis, lipolysis, proteolysis
    • Increase bone turnover, intestinal motility, erythropoiesis
    • Normal CNS function
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14
Q

What effects does thyroid hormone have on the following:

  • adrenergic?
  • Brain?
  • Bones?
  • Sexual characteristics?
A
  • Potentiates adrenergic stimuli/catecholamines
    • Positive chronotropic and inotropic effect – increases HR and CO; decreases SVR
  • Promotes normal Growth and Development
    • Brain development and maturation
    • Skeletal and muscle growth and maturation
    • Sexual maturation
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15
Q

What is the best way to test your thyroid initially?

A
  • Measurement of TSH level (highly sensitive; best initial test for primary thyroid dysfunction)
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16
Q

What are two other measurements of thyroid (other than TSH)?

A
  • Measurement of circulating thyroid hormone levels
    • FREE serum T4 (FT4) and free T3 (FT3) = most important
    • TOTAL serum T4 (TT4) and T3 (TT3)
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17
Q

What are some things that can increase your total serum T4? How does this occur?

A
  • Increase thyroid hormone binding proteins (increase total hormone levels):
    • Hyperestrogenic states (estrogen Tx, pregnancy)
    • Drugs (heroin, methadone, clofibrate, 5FU, major tranquilizers)
    • Acute hepatitis
    • Congenital TBG excess
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18
Q

What are some things that can decrease your total serum T4? How does this occur?

A
  • Decrease thyroid hormone binding proteins (decrease total hormone levels due excessive negative feedback):
    • Drugs (androgenic steroids, glucocorticoids, L-asparaginase)
    • Protein malnutrition or loss (nephrotic syndrome, protein losing enteropathy)
    • Cirrhosis
    • Major systemic illness
    • Congenital TBG deficiency
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19
Q

For the following conditions, know concentration of binding proteins, total plasma T4/T3, free plasma T4/T3, plasma TSH, and clinical thyroid state:

  • Hyperthyroidism
  • Hypothyroidism
  • Estrogens, methadone, heroin, etc
  • Glucorticoids, androgens, danazol
A
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20
Q

Describe thyrotoxicosis.

A
  • Description: hypermetabolic state and increased sympathetic tone due to excessive thyroid hormones
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21
Q

List symptoms/signs of thyrotoxicosis.

A
  • Clinical features: heat intolerance (due to high BMR), tachycardia/palpitations, arrhythmias (A-fib), weight loss (high BMR), nervous/tremor (increased sympathetic), warm/moist skin, excessive sweating, proximal weakness (proteolysis), frequent bowel movements, oligomenorrhea (prolactin induced), bone resorption, hypocholesterolemia (increased LDLr), hyperglycemia (gluconeogenesis)
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22
Q

What are labs of thyrotoxicosis?

A
  • Dx: decreased TSH, increased T4
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23
Q

What are some treatments of thyrotoxicosis?

A
  • Treatment: beta blockers, thionamides (methimazole, propylthiouracil), radioactive iodine (I-131 ablation), surgery (thyroidectomy)
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24
Q

What is the biggest complication of thyrotoxicosis? List pathophys, labs, and treatment for this.

A
  • Complication: thyroid storm
    • Pathophysiology: underlying hyperthyroidism + acute stress → elevated catecholamines → hormone excess → arrhythmias/hyperthermia/hypovolemic shock/coma
    • Labs: increased LFTs
    • Tx (4 Ps): propranolol, propylthiouracil, prednisolone, potassium iodide
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25
Q

List classifications of thyrotocicosis with different diseases listed.

A
  • High/normal iodine uptake
    • Production (primary hyperthyroidism)
      • Grave’s Disease
      • Multinodular goiter
      • Toxic adenoma
  • Suppressed iodine uptake
    • Destructive thyrotoxicosis
      • Subacute Granulomatous (De Quervain) Thyroiditis
      • Subacute Lymphocytic (Silent) Thyroiditis/Postpartum thyroiditis
    • Exogenous (factitious or iatrogenic)
      • Iodine-induced thyrotoxicosis
      • Exogenous ingestion of thyroid hormone
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26
Q

For Grave’s

  • Epidemiology
  • Pathophys
  • Dx
A

Classifications of Thyrotoxicosis

  • High/normal iodine uptake
    • Production (primary hyperthyroidism)
      • Grave’s Disease
        • Epidemiology: females, 20-40s, HLA DR3 or B8
        • Pathophysiology (type II hypersensitivity): TSH-receptor IgG autoantibody (TSI) → stimulates TSH receptor → increased synthesis of TH due to thyroid cell growth
        • Dx: iodine uptake scan (diffuse increased iodine uptake)
        • Histology: crowded epithelial follicular cells with scalloped colloids
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27
Q

For Grave’s

  • Histology
  • Unique features
A

Classifications of Thyrotoxicosis

  • High/normal iodine uptake
    • Production (primary hyperthyroidism)
      • Grave’s Disease
        • Histology: crowded epithelial follicular cells with scalloped colloids
        • Unique features: diffuse, symmetric goiter, myxedema (swelling of dermofibroblasts), Graves’ opathalomopathy (exophthalamos)
          • Exopthalamos: infiltration of retroorbital space by T-cells → increased cytokine release → increased fibroblast release of hydrophilic glycoaminoglycans → increased osmotic edema → bulging of eyes anteriorly
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28
Q

For multinodular goiter:

  • Description
  • Pathophys of two subtypes
  • Diagnosis
  • Micropathology
A
  • Multinodular goiter
    • Description: enlarged thyroid with multiple nodules due to iodine deficiency or TSH receptor mutations
      • Can be toxic or non-toxic
        • Toxic: leads to excessive T4 release → hyperthyroidism
    • Diagnosis:
      • Iodine uptake scan (focalized areas of increased uptake → multinodular goiter)
      • Micropathology: distended colloids
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29
Q

For toxic adenoma:

  • Descirbe it
  • Diagnosis
A
  • Toxic adenoma
    • Description: benign hyperplasia of thyroid glands
    • Dx: iodine uptake scan (singular hot nodule → focalized area of increased uptake)
      • If malignant: nodule is hypoechoic or “cold” on iodine uptake scan
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30
Q

For subacute granulomatous thyroiditis:

  • Whats another name for this?
  • Decription
  • Pathophys
  • Findings
  • Treatment
A
  • Destructive thyrotoxicosis
    • Subacute Granulomatous (De Quervain) Thyroiditis
      • Description: tender, PAINful (QuerVAIN), enlarged thyroid
      • Pathophysiology: viral infection → granuloma of thyroid
        • Early, transient hyperthyroidism → late hypothyroidism
      • Findings: increased ESR, jaw pain, negative antibodies, +/- fever
      • Treatment: NSAIDS, salicylates, beta blockers
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31
Q

For subacute lymphocytic thryoiditis:

  • What are some other names for it?
  • Description
  • Pathophys
  • Findings
  • Dx
A
  • Subacute Lymphocytic (Silent) Thyroiditis/Postpartum thyroiditis
    • Description: autoimmune, painless, enlarged thyroid
    • Pathophysiology: autoimmune attack on thyroid
      • Common post-partum when immune system is quickly picking back up (often recurs with subsequent pregnancies)
      • Early, transient hyperthyroidism → late hypothyroidism
    • Findings: antibodies positive (anti-TPO), no fever
    • Dx: low iodine uptake (distinguishes from Grave’s disease)
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32
Q

For iodine induced thyrotoxicosis:

  • Pathophys
  • Risk factors
A
  • Iodine-induced thyrotoxicosis
    • Pathophysiology: excessive exogenous iodine → negative feedback on thyroid → decreased iodine uptake (Jod-Basedow effect)
    • Risk factors: previous thyroid disease (Grave’s disease, MNG)
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33
Q

For exogenous ingestion of thyroid hormone:

  • Pathophys
A
  • Exogenous ingestion of thyroid hormone
    • Pathophysiology: over-ingestion of thyroid hormone → decreased serum thyroglobulin levels (high in other causes of hyperthyroidism)
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34
Q

Descirbe hypothyroidism

A

Hypothyroidism

  • Description: disorder in which the thyroid gland fails to secrete adequate amounts of thyroid hormone
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35
Q

What are the symptoms of hypothryoidism?

A

Hypothyroidism

  • Signs/symptoms:
    • Cold intolerance, weight gain (low BMR), decreased appetite, constipation, decreased reflexes (slowed sympathetic), muscle cramps (increased creatinine kinase), myxedema (accumulation of glycoaminoglycans → severe edema), anemia, hyponatremia, hypercholesterolemia (decreased LDLr), constipation, bradycardia, dyspnea, oligomenorrhea (prolactin-induced)
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36
Q

What is the outline of hypothryoidism with the diseases?

A
  • Primary: diseases or treatments that destroy thyroid tissue or interfere with thyroid hormone synthesis (increased TSH, decreased T4)
    • Chronic Lymphocytic Thyroiditis (Hashimoto’s thyroiditis)
    • Neonatal hypothyroidism (cretinism)
    • Riedel thyroiditis
    • Others: radiation injury, post-thyroidectomy, thyroid gland agenesis, idiopathic hypothyroidism, iodine deficiency, acute iodine excess in thyroid disease, meds
  • Central: results from pituitary (secondary) or hypothalamic (tertiary) disease
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37
Q

For chronic lymphocytic thyroiditis:

  • What is another name?
  • Epidemiology
  • Pathophys
  • Labs
  • PE
  • Complications
A
  • Chronic Lymphocytic Thyroiditis (Hashimoto’s thyroiditis)
    • Epidemiology: female, HLA DR5, most common cause of hypothyroidism (presents as hyperthyroidism early)
    • Pathophysiology: chronic antibodies against thyroglobulin or TPO → thyroid destruction
    • Labs: anti-TPO, firm goiter
    • PE: enlarged, non-tender thyroid
    • Complications: increased risk of B-cell lymphoma
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38
Q

For neonatal hypothyroidism:

  • Another name?
  • Etiologies (two groups)
  • Findings
  • Screening
  • Tx
A
  • Neonatal hypothyroidism (cretinism)
    • Etiologies:
      • Permanent hypothyroidism: thyroid dysgenesis, thyroid hormone defects, TSH/TRSH defects/deficiencies, TSH/TRH unresponsiveness
      • Transient hypothyroidism: extreme prematurity, maternal anti-thyroid meds, iodide deficiency (maternal/newborn), maternal TSHr antibodies, maternal hypothyroidism
    • Findings (6 P’s): Pot-bellied, Pale, Puffy-faced, Protruding umbilicus, Protuberant tongue, Poor brain development
      • Lack of epiphyseal growth and patent fontanelle
    • Screening: heel prick (day 2-5)
      • TT4 strategy: may miss compensated hypothyroidism due to normal TT4 levels, but high TSH
      • TSH strategy: TSH deficiency due to central hypothyroidism will be missed due to normal TSH levels
    • Tx: thyroxine immediately, monitor
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39
Q

For Riedel thyroiditis:

  • Pathophys?
  • Findings
  • Complications
A
  • Riedel thyroiditis
    • Pathophysiology: chronic inflammation → fibrosis of thyroid gland → hypothyroidism
    • Findings: VERY hard non-tender thyroid gland
    • Complications: fibrosis may spread to esophagus and trachea
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40
Q

What are some other causes of primary hypothyroidism?

A
  • Others: radiation injury, post-thyroidectomy, thyroid gland agenesis, idiopathic hypothyroidism, iodine deficiency, acute iodine excess in thyroid disease, meds
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41
Q

What are the labs associated with central hypothyroidism?

A
  • Central: results from pituitary (secondary) or hypothalamic (tertiary) disease
    • Low T4 with a low-normal TSH
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42
Q

For nonthyroidal illness syndrome

  • What are two other names?
  • Pathophys?
  • Treatment?
A

Nonthyroidal illness (NTI) syndrome/Euthyroid sick syndrome/Low T3 syndrome

  • Pathophysiology: severe illness → alterations in peripheral TH metabolism and transport → low T3
    • These changes are a “protective mechanism”
  • Treatment: NONE, do not assess thyroid function unless strong suspicion of disease
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43
Q

Describe PTH. What is it increased by?

A
  • Parathyroid hormone (PTH)
    • Description: protein secreted by the chief cells to regulate serum calcium levels
    • Increased by: decreased serum Ca (via Ca-sensing receptor), decreased active Vit D, increased phosphate, and decreased Magnesium/Aluminum/Strontium
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44
Q

What are 4 main actions of PTH? Understand the pathophys of each.

A
  • Actions
    • Increases bone osteoclast activity → releases Ca and PO4
      • Continuous PTH → RANKL release from osteoblasts → RANKL binds RANK on osteoclasts → stimulation of osteoclast activity → bone resorption → increased serum Ca
      • Intermittent PTH → bone formation
    • Activates Vit D via 1-alpha-hydroxylase → increases calcitriol → increased small bowel absorption of Ca and PO4
    • Increased renal calcium reabsorption at distal tubule
    • Decreased phosphate reabsorption at proximal tubule (balances increased PO4)
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45
Q

For primary hyperparathyroidism

  • Etiologies (3)
  • Labs
  • Complication
  • Treatment
A
  • Primary hyperparathyroidism
    • Etiologies: adenomas (majority), glandular hyperplasia, carcinomas
    • Labs: increased PTH, increased Ca, decreased phosphate, increased urinary cAMP, increased alkaline phosphate, decreased bone density
    • Complication: nephrogenic diabetes insipidus due to hypercalcemia (polyuria, polydipsia)
    • Treatment: parathyroidectomy, denosumab (RANKL inhibitor), bisphosphonates, cinacalcet (activates Ca-sensing receptors → decreases PTH secretion)
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46
Q

What are the clinical findings associated with primary hyperparathyroidism? Explain each one.

A
  • Clinical: bone pain, kidney stones, polyuria, abdominal pain, and depression (bones, stones, thrones, groans, and psychiatric overtones)
    • Bones: osteitis fibrosa cystica (brown fibrous tissue consisting of osteoclasts and deposited hemosiderin → lytic lesions and eating away of bones), osteomalacia, and osteoporosis
    • Stones: hypercalciuria → calcium oxalate and phosphate stones → nephrocalcinosis/renal insufficiency (due to damage)
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47
Q

For secondary hyperparathyroidism

  • Clinical
  • Labs
  • Tx
A
  • Secondary hyperparathyroidism
    • Clinical: renal osteodystrophy (osteitis fibrosa cystica, osteomalalcia), deformities, fractures
    • Labs: increased PTH, decreased Ca,
    • Tx: Ca, Vit D replacement, phosphate binders (indicated for CKD/ESRD)
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48
Q

Explain the etiologies associated with secondary hyperparathyroidism and why they cause the disease

A
  • Secondary hyperparathyroidism
    • Etiologies: Celiac’s, pancreatitis, antiseizure meds, vit D dependent rickets (1-alpha-hydrxylase mutation), vit D resistance
      • CKD/ESRD or nutritional deficiency/malabsorptive state: decreased 1-alpha-hydroxylation of Vit D → decreased calcium absorption from GI tract/decreased phosphate clearance from urine → hypocalcemia, hyperphosphatemia, hypomagnesemia, hypovitaminosis D
49
Q

For tertiary hyperparathyroidism:

  • Etiology
  • Labs
  • Clinical signs
  • Treatment
A
  • Tertiary hyperparathyroidism
    • Etiology: chronic ESRD → prolonged stimulation of parathyroid glands → glandular hyperplasia → increased PTH → hypercalcemia, decreased calcitriol, increased phosphate
    • Labs: VERY high levels of PTH (>800pg/mL), hypercalcemia, hyperphosphatemia
    • Clinical: osteitis fibrosa cystica, bone pain, fractures, extraskeletal calcification
    • Treatment: parathyroidectomy
50
Q

For hypoparathyroidism:

  • What are clinical signs?
  • Labs?
A
  • Hypoparathyroidism
    • Clinical: tetany (muscle spasms), prolonged QT interval/arrhythmia/HF, paresthesias/tingling (circumoral: around mouth)
      • Chvostek’s sign: tapping on facial nerve (Cheek) → contraction of facial muscles
      • Trousseau’s sign: occlusion of brachial artery (Tricep) with BP cuff → carpal spasms
    • Labs: hypocalcemia, hyperphosphatemia, low PTH
51
Q

What are etiologies of hypoparathyroidism? What is one syndrome?

For that syndrome, describe it, provide genetic etiology, and clinical signs.

A
  • Hypoparathyroidism
    • Etiologies: surgical removal/radiation of parathyroid gland, autoimmune destruction, infiltrative diseases/metastatic cancer, DiGeorge syndrome
      • DiGeorge syndrome:
        • Description: abnormal development of third and fourth branchial pouches
        • Etiology: deletion of chromosome 22q11
        • Clinical: hypocalcemia, thymic aplasia, cardiac defects, developmental delay, characteristic facial appearance (flat bridge of nose, low set ears, small jaw, cleft lip/palate)
52
Q

For psuedohyperparathyroidism:

  • Etiologies (name a disease)
    • gentic mutation
    • Clinical signs
      • Labs
  • Complications
  • Treatment
A
  • Pseudohypoparathyroidism
    • Etiologies: end-organ resistance to PTH (affecting kidneys, bones are spared)
      • Albright’s Hereditary Osteodystrophy (inherited maternal allele)
        • Autosomal dominant mutation in GNAS1 gene → failure to encode for PTH protein G receptor
        • Clinical: shortened 4th/5th digits, short stature
    • Labs: hypocalcemia, hyperphosphatemia, elevated PTH
    • Complications: end organ resistance in thyroid and gonads
    • Treatment: replace Ca, calcitriol, replaced respective hormones
53
Q

For pseudopsuedohyperparathyroidism:

  • Etiologies (name a disease)
    • gentic mutation
    • Clinical signs
  • labs
A
  • Pseudopseudohyperparathyroidism
    • Etiologies: NO end-organ resistance to PTH
      • Albright’s Hereditary Osteodystrophy (inherited paternal allele)
        • Clinical: shortened 4th/5th digits, short stature
    • Labs: normal lab findings (only physical exam findings)
54
Q

For MEN-1:

  • Genetics
  • Epidemiology
  • What do they present with?
  • Dx
  • Management
A

MEN-1

  • Genetics: associated with autosomal dominant mutation of menin (tumor suppressor on chromosome 11) – need two hits for inactivation
  • Epidemiology: rare, peak age (men: 4th decade/women: 3rd decade), high mortality
    • Mortality due to: malignant islet cell tumor, malignant carcinoid tumor
  • Clinical presentation (3 P’s): must have 2/3 for diagnosis
    • Parathyroid (90%): primary hyperparathyroidism
    • Pancreatic islet cell (70%): gastrinoma, insulinoma, non-functioning tumor, VIP-oma, glucagonoma, somatostatinoma
    • Pituitary (anterior) (20%): prolactinoma, pituitary tumors (GH, TSH, GnRH, ACTH)
  • Dx/screening: imaging, somatostatin-receptor scintigraphy, endoscopic US, labs annually (calcium, PTH, gastrin, pancreatic polypeptide, prolactin, IGF-1)
  • Management: treat underlying tumors
    • Will always remove parathyroid before treatment of gastrinoma → will decrease Ca++ and reduce size of gastrinoma
55
Q

For MEN-2A:

  • What is another name?
  • Genetics?
  • Epidemiology?
  • Clinical presentation?
A

MEN-2A (Sipple’s Syndrome)

  • Genetics: associated with autosomal dominant mutation in proto-oncogene RET (codes for receptor tyrosine kinase)
    • Gain of function → MEN syndromes; loss of function: Hirschprung’s disease
  • Epidemiology: peak incidence in 30s
  • Clinical presentation (2 P’s + MTC):
    • Medullary thyroid carcinoma (90%) – neoplasm of C-cells that produce calcitonin
    • Pheochromocytoma (50%)
    • Parathyroid hyperplasia (10%)
56
Q

For MEN-2B:

  • Genetics
  • Clinical presentation
A

MEN-2B

  • Genetics: associated with autosomal dominant mutation in proto-oncogene RET (codes for receptor tyrosine kinase)
  • Clinical presentation (1 P + others)
    • Medullary thyroid cancer (100%)
    • Pheochromocytoma (50%)
    • Mucosal ganglioneuromas (oral/intestinal)
    • Marfanoid habitus (75%)
57
Q

What action needs to be taken for someone with either medullary thyroid cancer or pheochromocytoma?

A
  • Any patient with pheochromocytoma or medullary thyroid cancer should be referred to geneticist to check for MEN
58
Q

What are the treatments/management for pheochromocytoma? For medullary thyroid carcinoma?

A
  • Treatments
    • Pheochromocytoma: surgical resection with possible partial adrenalectomy
    • Medullary thyroid carcinoma:
      • Evaluate for possible medullary thyroid carcinoma
      • Total thyroidectomy and resection of all involved structures (i.e. trachea)
59
Q

What are the prophylactic treatments indicated for MEN-2a and MEN-2b? By what ages do these need to be completed?

A
  • Prophylactic treatments
    • Prophylactic thyroidectomy indicated for MEN-2a (by 5-6 y/o) and MEN-2b (by 6 mo)
60
Q

Normal gross and microfeatures of thyroid

A
  • Gross: homogenous red surface with fibrous septae
  • Micro: Lobules (divided by fibrous septae) containing 20-40 follicles (functional unit of the thyroid)

Follicles are filled with colloid (blue arrow) and lined by cuboidal follicular cells (red arrow)

61
Q

Nodular hyperplasia

presentation and pathophys

A
  • Single to multinodular thyroid
  • Increased radioactive iodine uptake
  • Endemic – lack of iodine in diet, goitrogens
  • Sporadic
62
Q

Nodular hyperplasia

gross and micro features

A

Gross: Multiple variably sized heterogenous nodules

Micro: fibrotic changes (yellow), calcifications (blue), variable sized follicles (resembles normal)

63
Q

Lymphocytic Hyperplasia/ Hashitmoto’s Thyroiditis

presentation and pathophys

and micro features

A

Multinodular thyroid

Autoimmune (T-cell mediated)

Micro: Lymphocytic infiltration with germinal center formation, destruction of follicular cells, Hurthle cells (light pink blob – blue arrow)

64
Q

follicular ademonas

presentation, causes, genetics

A
65
Q

follicular ademonas

gross and micro features

A

Gross: completely encapsulated nodule

Micro: fibrous capsule (yellow), compression of normal parenchyma (blue), benign proliferation (uniform growth, but different from surrounding)

66
Q

Papillary thyroid carcinoma

presentation, causes, genetics

A
67
Q

Papillary thyroid carcinoma

micro?

A

Micro: Papillary architecture, empty-appearing nuclei (Orphan Annie – blue arrow), nuclear grooves (yellow arrows), psammoma bodies (calcifications – orange arrow)

68
Q

follicular carcinoma

presenation, causes, genetics

A
69
Q

Follicular carcinoma

gross and micro features

A

Gross:

  • Encapsulated nodule
  • Invasion through capsule (differentiates from follicular adenoma)
  • Poorly circumscribed tumor

Micro: proliferation of follicles with possible vascular invasion

70
Q

Medullary carcinoma

presentation, causes, genetics

A
71
Q

anaplastic carcinoma

presentation, causes, genetics

A
72
Q

Medullary carcinoma

gross and micro features

A

Gross: poorly-defined tan mass

Micro: Hyperplasia of c-cells and amyloid stroma (calcitonin deposits seen on Congo red stain – blue arrow)

73
Q

Anaplastic carcinoma

micro features

A

Micro: Large bizarre malignant cells with prominent mitotic activity and necrosis; no resemblance to any other structures

74
Q
A

normal thyroid

75
Q
A

normal thyroid

76
Q
A

nodular hyperplasia

77
Q
A

Lymphocytic Hyperplasia/ Hashitmoto’s Thyroiditis

78
Q
A

Lymphocytic Hyperplasia/ Hashitmoto’s Thyroiditis

79
Q
A

follicular adenoma

80
Q
A

follicular adenoma

81
Q
A

papillary carcinoma

82
Q
A

papillary carcinoma

83
Q
A

follicular carcinoma

84
Q
A

follicular carcinoma

85
Q
A

Medullary carcinoma

86
Q
A

Anaplastic carcinoma

87
Q

Hypoglycemia

clinical, labs, associated cancers, tx

A
  • Clinical: Sweating, anxiety, tremors, palpitations, hunger, weakness, seizures, confusion, coma
  • Labs
  • Non-islet cell tumor:
    • low glucose, low insulin, low c-peptide, elevated IGF-2:IGF-1 ratio

Islet cell tumor:

low glucose, elevated insulin and c-peptide; normal IGF-2:IGF-1 ratio
* Cancers:

Mesothelioma, sarcomas, lung cancer, hepatocellular carcinoma

  • Tx:

Tumor resection;

glucose infusion, corticosteroids, glucagon, diazoxide, octreotide, HGH

88
Q

Ectopic Cushing’s

clinical, labs, associated cancers, tx

A
  • Clinical:Muscle weakness; peripheral edema, hypertension weight gain
  • Labs:
    • Hypokalemia
    • Metabolic alkalosis
    • Elevated serum cortisol (>29 µg/dL)

Not suppressed by high dose dexamethasone
* Cancers:

Small cell lung; bronchial carcinoid; others: thymoma, medullary thyroid CA, GI, pancreatic, adrenal, ovarian

  • Tx:
    • Steroid synthesis inhibitors: ketoconazole, metyrapone, mitotane, aminoglutethimide, etomidate
      • Blocks ACTH release: octreotide
      • Binds glucorticoid receptor: mifepristone

Adrenalectomy

89
Q

Hypercalcemia

clinical, labs, associated cancers, tx

A
  • Clinical:Altered mental status, weakness, ataxia, lethargy, renal failure, nausea/vomiting, hypertension, bradycardia, coma
  • Labs:
      • Hypercalcemia (nl 8.5-10.2 mg/dL)
        • PTH: Low to normal (<20 pg/mL)

Elevated PTHrP

  • Cancers: Breast, myeloma, renal cell, squamous cell (PTHrP), ovarian, endometrial, Hodgkin’s lymphoma (Vit D secretion)
  • Tx: Saline; furosemide (after hydration); pamidronate/zoledronate (bisphosphonates); calcitonin, gallium nitrate (osteoclast inhibitor); hemodialysis; treat underlying malignancy
90
Q

SIADH

clinical, labs, associated cancers, tx

A
  • Clinical:

Abnormal gait, headache, nausea, fatigue, muscle cramps, confusion, seizures, coma, respiratory depression

  • No* orthostasis, No edema
  • Labs:
    • Decreased serum Na+(nl ~ 135-145 mEq/L)
    • Decreased BUN/uric acid

Decreased, but concentrated urine

  • Cancers: Small cell lung; squamous cell, lung; mesothelioma, GU, GI, brain, head/neck, prostate
  • Tx: Restrict fluids; encourage salt and protein intake; demeclocycline (interferes w/ renal response to ADH); Conivaptan/tolvaptan (vasopressor receptor antagonists); hypertonic saline
91
Q

Define “paraneoplasia”

A
  • Ectopic production of humoral factors (hormones, peptides, or cytokines) – by tumor cells, causing secondary disease, remote from the tumor itself
92
Q

Identify a cell type responsible for ectopic hormone peptide synthesis and secretion by some tumors

A
  • Both endocrine cells and non-endocrine tumor cells can secrete polypeptide hormones or inappropriately express a hormone’s receptor
    • Inappropriate repression or expression of certain genes → paraneoplasia
93
Q

APUD

A
  • APUD (amine precursor uptake and decarboxylation) cells: cells of neural crest or endodermal region that can produce, store, and secrete peptide hormones
    • Occur in clusters in normal and malignant tissues
94
Q

Growth Hormone Axis

A
  • GHRH → binds GPCR (GS) → release of GH at anterior pituitary → binds to Jak/Stat tyrosine kinase at peripheral tissues
95
Q

Thyroid Hormone Axis

also how does lithium, amiodarone, corticosteroid effects this

A
  • TRH from hypothalamus → Gq activation → TSH release at anterior pituitary → Gs activation → release of TH
    • Lithium decreases synthesis and release of thyroid hormone → hypothyroidism
    • Amiodarone is similar to TH → negative feedback → hypothyroidism
      • Can also cause hyperthyroidism (be careful in patients with existing arrhythmias)
    • Corticosteroid cortisol and glucocorticoids inhibits iodinase → decreased conversion from T4 to T3
96
Q

Liotrix

MOA, SE, Use, other fun facts

A

MOA: T4/T3

SE: Cardiac events

USE: Hypothyroidism

OTHER: EXPENSIVE

97
Q

Liothyronine (Ctyomel)

MOA, SE, Use, other fun facts

A

MOA: Synthetic T3 (fast onset, not protein bound)

SE: Cardiac events

USE: Hypothyroidism, myxedena

OTHER: higher cost

98
Q

Natural desiccated thyroid

MOA, SE, Use, other fun facts

A

MOA: Animal T4

SE: Allergic reactions

USE: Hypothyroidism

OTHER:

Drug interactions: warfarin (TH reduces clotting factors), beta blockers

Increased T4 clearance by: Rifampin, Phenytoin

99
Q

Synthroid, Levothroid, Levothryxine

MOA, SE, Use, other fun facts

A

MOA: Synthetic T4 (protein bound, can be converted to T3, slow onset)

SE: Cardiac events

USE: Hypothyroidism

OTHER:

Drug interactions: warfarin (TH reduces clotting factors), beta blockers

Increased T4 clearance by: Rifampin, Phenytoin

100
Q

Methimazole

MOA, SE, Use, other fun facts

A

MOA: Substrate for TPO, inhibits MIT/DIT coupling to thyroglobulin,

SE: Hypothyroidism, rashes, arthralgias, SLE-like syndrome, hypersensitivity reactions, birth defects

USE: Hyperthyroidism

OTHER:

101
Q

Propylthiouracil (PTU)

MOA, SE, Use, other fun facts

A

MOA: Substrate for TPO, inhibits MIT/DIT coupling to thyroglobulin, blocks peripheral conversion of T4/T3

SE: Hypothyroidism, rashes, arthralgias, SLE-like syndrome, hypersensitivity reactions, hepatotoxicity

USE: Thyroid storm, hyperthyroidism, when methimazole is not tolerated

OTHER: Indicated: pregnancy

102
Q

Iodides

MOA, SE, Use, other fun facts

A

MOA: Iodine analog → negative feedback of T3/T4 synthesis

SE: Hypothyroidism SE

USE: Short term hyperthyroidism (pre-operatively)

OTHER:

103
Q

Hydrocortisone

MOA, SE, Use, other fun facts

A

MOA: Activates cytosolic glucocorticoid receptors → release of cortisol

SE: Cushingoid effects

USE: Adrenal insufficiency, inflammation, asthma, eczema, etc

OTHER: Metabolism slowed by estrogens, liver disease, age, pregnancy, hypothyroidism

104
Q

Mifepristone

MOA, SE, Use, other fun facts

A

MOA: Progesterone and glucocorticoid receptor antagonist

SE: Vaginal bleeding, pregnancy termination, nausea

USE: Cushing’s syndrome

OTHER:

105
Q

Mitotane

MOA, SE, Use, other fun facts

A

MOA: Causes degeneration of zona fasiculata and reticularis cells → atrophy of adrenal gland

SE: Lethargy and extreme sedation, CNS effects

USE: Cushing’s syndrome

OTHER: Use: Inoperable cortical carcinoma

106
Q

Ketoconazole (antifungal)

MOA, SE, Use, other fun facts

A

MOA: Inhibits 11-hydroxylase activity

SE: Gynecomastia, low testosterone levels, elevates LFTs, CYP450 inhibitor

USE: Cushing’s syndrome

OTHER:

107
Q

Metyrapone

MOA, SE, Use, other fun facts

A

MOA: Inhibits 11-hydroxylase activity

SE: Hirsutism (increased androgens), acne, HTN, N/V, sedation

USE: Cushing’s syndrome

OTHER:

108
Q

Aminoglutethemide

MOA, SE, Use, other fun facts

A

MOA: Cholesterol desmolase inhibitor (rate-limiting step)

SE: Extreme sedation, nausea, severe skin rashes

USE: Cushing’s syndrome

OTHER:

109
Q

Spironolactone, Eplerenone

MOA, SE, Use, other fun facts

A

MOA: Aldo antagonist → blocks Na/H20 reabsorption

SE: Gynecomastia, menstrual issues (block androgen/ glucocorticoid receptors)

USE: HTN, hypokalemia

OTHER:

110
Q

Fludrocortisone

MOA, SE, Use, other fun facts

A

MOA: Aldo agonist → Na/H20 reabsorption

SE: Fluid retention, hypokalemia

USE: CAH: 11-beta hydroxylase deficiency, adrenal insufficiency

OTHER:

111
Q

Mecasemerin

MOA, SE, Use, other fun facts

A

MOA: Exogenous IGF-1 → acts at insulin-like receptor → growth

SE: Tonsillar hypertrophy, lipohypertrophy, hypoglycemia

USE: IGF-1 deficiency in children (not GH deficient, but resistant to effects of GH)

OTHER:

112
Q

GHRH injection: Sermorelin

MOA, SE, Use, other fun facts

A

MOA: Exogenous GHRH → GH

SE:

Kids: elevated HbA1c, eosinophilia, increased risk of secondary malignancies

Adults: fluid retention, myalgia

USE: Dwarfism (GH deficiency)

OTHER: Drug interactions: estrogens, androgens, thyroid hormones

113
Q

Growth hormone replacement: Somatotropin, Somatrem

MOA, SE, Use, other fun facts

A

MOA: Exogenous GH

SE:

Kids: elevated HbA1c, eosinophilia, increased risk of secondary malignancies

Adults: fluid retention, myalgia

USE: Dwarfism (GH deficiency)

OTHER: Drug interactions: estrogens, androgens, thyroid hormones

114
Q

Pegvisomant (subQ)

MOA, SE, Use, other fun facts

A

MOA: Growth hormone receptor antagonist

SE: Infection (subQ), elevated LFTs

USE: acromegaly

OTHER:

115
Q

Dopamine receptor antagonists: Metoclopramide

MOA, SE, Use, other fun facts

A

MOA: Inhibits dopamine → prolactin secretion occurs

SE:

USE: Hyperprolactinemia, acromegaly

OTHER:

116
Q

Dopamine receptor agonists: Bromocriptine

MOA, SE, Use, other fun facts

A

MOA: Inhibits prolactin secretion and decreases GH release (unsure MOA)

SE: Postural hypotension, N/V (CTZ), hallucinations

USE: Hyperprolactinemia, acromegaly

OTHER:

117
Q

Aquaretics: Conivaptan

MOA, SE, Use, other fun facts

A

MOA: ADH antagonist → water excretion

SE:

USE: Hyponatremia (too much ADH)

OTHER: Used in patients with CHF

118
Q

Desmopressin

MOA, SE, Use, other fun facts

A

MOA: ADH analog → fluid retention

SE: Rhinitis, hyponatremia

USE: Central diabetes insipidus (too little ADH)

OTHER: Contraindicated: HF, uncontrolled HTN

119
Q

Oxytocin

MOA, SE, Use, other fun facts

A

MOA: Peptide binds Gq → release of Ca → contractions

SE: Mom: Fluid retention (vasopressin is structurally similar to oxytocin)

USE: Uterine contractions

OTHER: Fetus: Uterine rupture, distress

EndoRepro (8 decks)

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