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Clinical Medicine 3 > Lecture 17 (Endocrine)-Exam 6 > Flashcards

Lecture 17 (Endocrine)-Exam 6 Flashcards

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2
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Vitamin D Background
* Found in what?
* If vit D is low, what is there a risk of?
* How does vitamin D enter circulation?

A
  • Vitamin D is also found in milk, fish oil and cereals
  • If vitamin D is low, bones become thin and there is a fracture risk
  • Vitamin D enters the circulation bound to vitamin D binding protein, and to a lesser extent, to albumin
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Vitamin D Background
* Vitamin D binding protein is synthesized where?
* The protein binds what?

A
  • Vitamin D binding protein is synthesized in the liver
  • The protein binds 25-OH-vitamin D (calcidiol) as well as 1,25-OH-vitamin D (calcitriol)
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4
Q

Vitamin D
* What happens in the liver?
* What happens in the kidney?

A

In the liver, vitamin D is changed into 25-OH vitamin D (calcidiol)
* T =2-3 weeks

In the kidneys, 1-α-hydroxylase changes 25-OH-vitamin D into 1,25-OH-vitamin D (calcitriol)
* T =6-8 hours

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5
Q

Vit D
* What induces 1-a-hydroxylase?
* What suppresses 1-α-hydroxylase?

A
  • PTH and low phosphate induce 1-α-hydroxylase
  • Calcium and 1,25-OH-vitamin D (calcitriol) suppress 1-α-hydroxylase
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6
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Vitamin D
* What lowers 1,25-OH-vitamin D (calcitriol)?
* What does Dilantin cause?

A
  • Ketoconazole lowers 1,25-OH-vitamin D (calcitriol)
  • Dilantin can cause resistance to 1,25-OH-vitamin D (calcitriol) and also increase the hepatic catabolism of vitamin D metabolites
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7
Q

Vitamin D
* Actions on what?

A

Actions on bone are multiple and probably the main action is to provide (by intestinal absorption of calcium and phosphate) an environment where bone mineralization can occur

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8
Q

Vitamin D
* Vitamin D moves what?
* What cells have parathyroid receptors and which ones don’t?
* Osteoblasts and their precursors signal what?

A
  • Vitamin D moves calcium into cells
  • Osteoblasts have parathyroid receptors, but osteoclasts do not!
  • Osteoblasts and their precursors signal osteoclast precursors to get bone to resorb
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10
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Vitamin D
* Vitamin D deficiency causes what?
* What is the lab value?

A
  • Vitamin D deficiency causes a myopathy with the loss of myofibrils, fatty infiltration and interstitial fibrosis
  • While 1,25-OH-vitamin D (calcitriol) is an active form of Vit D, 25-hydroxy-vitamin-D (calcidiol) level is the laboratory test to measure serum Vit D levels
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11
Q

Vitamin D Dependent Rickets Type 1
* What is the problem?
* What is low? What type of parathyroidism?
* There are normal or high what? What is low?

A
  • The problem is the 1-α-hydroxylase gene (kidney changes)
  • Low calcium, secondary hyperparathyroidism
  • There are normal or high vitamin D and 25-OH-vitamin D (calcidiol) but low 1,25-OH-vitamin D (calcitriol)
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12
Q

Vitamin D Dependent Rickets Type I
* What is the genetic pattern?
* What is the treatment?
* In infancy, there may be what?

A
  • Autosomal recessive
  • Treatment is physiologic replacement doses of 1-α-hydroxy metabolites of vitamin D (Alfacalcidol)
  • In infancy, there may be rickets and seizures
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13
Q

Vitamin D Dependent Rickets Type II
* What is the mechanism?
* The problem is what?
* In infancy, there may be what?

A
  • The mechanism is resistance to 1,25-OH-vitamin D (calcitriol)
  • The problem is mutation of the vitamin D receptor
  • In infancy, there may be rickets and seizures
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14
Q

Vitamin D Dependent Rickets Type II
* What is the genetic pattern?
* What is low? What type of parathyroidism?

A
  • Autosomal recessive
  • Low calcium and phosphorus, secondary hyperparathyroidism
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15
Q

Vitamin D Dependent Rickets Type II
* What is high?
* Sometimes, what is present?
* No ideal simple treatment but can try what?

A
  • 1,25-OH-vitamin D is high
  • Sometimes alopecia totalis
  • No ideal simple treatment but can try vitamin D or its metabolites in big doses and calcium infusion
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16
Q

Vitamin D Resistant Rickets
* Also called what?
* What is the mechanism?
* There is impaired synthesis of what?
* What is low?

A
  • Also called familial X-linked hypophosphatemic rickets
  • The mechanism is renal tubular phosphate wasting
  • There is impaired synthesis of 1,25-OH-vitamin D (calcitriol)
  • Low levels of serum phosphate, resistance to ultraviolet radiation or vitamin D intake.
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17
Q

Vitamin D Resistant Rickets
* Low what?
* What is normal or slightly low?
* What is the treatment?
* What is the heredity?

A
  • Low serum calcium; rickets
  • PTH is normal or slightly low
  • Treatment is calcitriol and phosphate but it is difficult to produce normal growth
  • Different forms of heredity
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18
Q

Hypoparathyroidism
* When does this occur?
* When PTN is low, what develops?

A
  • Hypoparathyroidism occurs when there is destruction of the parathyroid glands (autoimmune, surgical), abnormal parathyroid gland development, altered regulation of PTH production, or impaired PTH action.
  • When PTH secretion is insufficient, hypocalcemia develops.
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19
Q

Hypoparathyroidism
* Hypocalcemia due to hypoparathyroidism may be associated with what? What are the sxs?
* Rare or common?

A
  • Hypocalcemia due to hypoparathyroidism may be associated with a spectrum of clinical manifestations, ranging from few if any symptoms, if the hypocalcemia is mild, to life-threatening seizures, refractory heart failure, or laryngospasm if it is severe.
  • Hypoparathyroidism is rare, accounting for 10-40/100,000 cases
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20
Q

Hypoparathyroidism Etiology:
* What is the most common cause?
* What are other causes?

A
  • The most common cause is surgical destruction or injury to the parathyroid glands.
    * PTH is not produced
  • Other causes are autoimmune diseases or genetic disorders affecting parathyroid gland development or the biosynthesis or release of PTH.
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22
Q

Primary hypoparathyroidism is caused by what? What is the most commonly from?

A
  • Primary hypoparathyroidism is caused by a group of heterogeneous conditions in which hypocalcemia and hyperphosphatemia occur as a result of deficient parathyroid hormone (PTH) secretion.
  • This most commonly results from surgical excision of, or damage to, the parathyroid glands.
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23
Q

hypoparathyroidism clinical presentation
* The acute manifestations of hypoparathyroidism (eg, postsurgical hypoparathyroidism) are due to what?

A

due to acute hypocalcemia

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24
Q

hypoparathyroidism clinical presentation
* What is the hallmark issue? What are the sxs?

A
  • The hallmark of acute hypocalcemia is tetany.
  • The symptoms of tetany may be mild (perioral numbness, paresthesias of the hands and feet, muscle cramps) or severe (carpopedal spasm, laryngospasm, and focal or generalized seizures, which must be distinguished from the generalized tonic muscle contractions that occur in severe tetany).

HYPOCALEMIA

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25
Q

hypoparathyroidism clinical presentation
* What are the cardiac findings?(4)

A

Cardiac findings may include a prolonged QT interval, hypotension, heart failure, and arrhythmia.

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26
Q

hypoparathyroidism clinical presentation
* The classic physical findings in patients with neuromuscular irritability due to what?
* Other patients have less specific symptoms, such as what?

A
  • The classic physical findings in patients with neuromuscular irritability due to latent tetany are Trousseau’s and Chvostek’s signs.
  • Other patients have less specific symptoms, such as fatigue, hyperirritability, anxiety, and depression, and some patients, even with severe hypocalcemia, have no neuromuscular symptoms.
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29
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Diagnosis of hypocalcemia from hypoparathyrodism:
* What are the levels of labs?

A

Persistent hypocalcemia with a low or normal parathyroid hormone (PTH) level and hyperphosphatemia is, in the absence of hypomagnesemia, virtually diagnostic of hypoparathyroidism (PTH deficiency).
* Triad of hypocalcemia, decreased intact PTH and increased phosphate

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31
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DDX and Treatment of hypothyroidism
* What is the oral treatment of chronic hypocalcemia in hypoparathyroidism?

A
  • Calcium sypplementation + activated Vit D supplementation (eg calcitriol)
  • Acute symptomatic hypocalcemia: IV calcium gluconate plus oral calcitriol
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32
Q

Patient Education on hypoparathyroidism
* What are the complications?(6)

A
  • Changes in teeth
  • Development of cataracts
  • Brain calcifications
  • Stunted growth and mental delay in children
  • Pernicious anemia, Addison’s disease, and Parkinson’s disease
  • Overtreatment with Vit. D and Ca can lead to hypercalcemia and cause kidney injury
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33
Q

Pseudohypoparathyroidism Type Ia
* What is present?
* Giving PTH does not cause what?

A
  • Albright’s hereditary osteodystrophy (AHO) – type Ia
  • Giving PTH does not cause a phosphate diuresis or increase serum calcium
    * Relative PTH resistance and hypocalcemia
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34
Q

Pseudohypoparathyroidism Type Ia
* What is albright’s hereditary osteodystrophy?
* What are the sxs?
* What is the treatment?

A
  • Albright’s hereditary osteodystrophy is a form of osteodystrophy, and is classified as the phenotype of pseudohypoparathyroidism type 1A; this is a condition in which the body does not respond to parathyroid hormone.
  • Symptoms: Choroid plexus calcification, Full cheeks
  • Treatment: Phosphate binders, supplementary calcium
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35
Q

Pseudohypoparathyroidism Type Ia
* What is the dx methods?
* AHO is characterized by what?
* What is brachydactyly?

A
  • Diagnostic method: calcium, phosphorus, PTH, Urine test for phosphorus and cyclic AMP
  • AHO is characterized by a round face, short stature with a stocky habitus, brachydactyly, subcutaneous ossification, and dental anomalies
  • Brachydactyly is a medical term which literally means ‘short finger’
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36
Q

Pseudohypothyroidism Type Ia
* Type Ia has what?
* There may be resistance to what?(3)

A
  • Type Ia has the physical features and has low G8 alpha activity (in kidneys and some other tissues)
  • There may be resistance to other hormones also like TSH, glucagon, gonadotropins
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37
Q

Pseudohypoparathyroidism Type Ia
* What are some sxs?(5)

A
  • Short stature
  • Obesity
  • Round face
  • SQ ossifications
  • Brachydactyly
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38
Q

Pseudohypoparathyroidism Type Ib
* What is low and hig?
* Giving PTH does not cause what?
* No what? (2)
* AHO and g8 alpha?

A
  • Hypocalcemia, high PTH
  • Giving PTH does not cause an increase in urine cAMP
  • No physical features of AHO
  • No abnormality of G8 alpha in fibroblasts
  • The AHO physical features and PTH resistance but normal G8 alpha action
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39
Q

Pseudohypoparathyroidism Type Ib
* What type of resistance?
* What is there increase loss of? What does that cause?
* What reacts to PTH and does not react?
* Locus on what?

A
  • There is renal resistance to PTH
  • Increased renal loss of calcium and impaired 1-α-hydroxylase, so there is less intestinal absorption of calcium and osteomalacia
  • Sometimes bone reacts to PTH but kidneys do not
  • Locus on chromosome 20q 13.3
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40
Q

Pseudohypoparathyroidism Type Ic
* AHO? G8?

A

The AHO physical features and PTH resistance but normal G8 alpha action

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41
Q

*

Pseudohypoparathyroidism Type II
* Giving PTH causes an increase in what? What does it not cause?

A

Giving PTH causes an increase in urine cAMP (cyclic adenosine monophosphate) but it does not cause an increase in urine phosphorus.

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42
Q

Pseudohypoparathyroidism Type II
* Cyclic Adenosine Monophosphate (cAMP) functions as what?

A

Cyclic Adenosine Monophosphate (cAMP) functions as an intracellular “second messenger” regulating the activity of intracellular enzymes or proteins in response to a variety of hormones (eg, parathyroid hormone). Urinary cAMP is elevated

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43
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Pseudohypoparathyroidism Type II
* AHO?
* Genetic?
* No resistance to what? What changes do you see?

A
  • It does not have the special physical features of Albright’s hereditary osteodystrophy
  • Not familial
  • No resistance to PTH in bone cells and indeed you may see the bone changes of hyperparathyroidism
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44
Q

Pseudopseudohypoparathyroidism (PPHP)
* AHO? Ca and PTH levels?
* PTH?
* Curiously, when patients inherit what?

A
  • Same physical features of AHO but normal calcium and PTH
  • No resistance to PTH
  • Curiously, when patients inherit the mutant G8 alpha gene from their fathers, they get PPHP, but when they inherit this mutant gene from their mothers, they have pseudohypoparathyroidism TYPE Ia.
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45
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⭐️

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49
Q

Hyperparathyroidism
* Primary hyperparathyroidism common or rare?
* It is the most common cause of what?
* Primary hyperparathyroidism can occur when?

A
  • Primary hyperparathyroidism (PHPT) is a relatively common endocrine disorder, with prevalence estimates of one to seven cases per 1000 adults.
  • It is the most common cause of hypercalcemia, predominantly affecting elderly populations and W>M 3:1.
  • Primary hyperparathyroidism can occur at any age, but the great majority of cases occur in patients over the age of 50 to 65 years.
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50
Q

Hyperparathyroidism Pathophysiology
* Parathyroid hormone (PTH) is one of the two major hormones modulating what?

A

Parathyroid hormone (PTH) is one of the two major hormones modulating calcium and phosphate homeostasis, the other being calcitriol (1,25-dihydroxyvitamin D).

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51
Q

Hyperparathyroidism Pathophysiology
* The minute-to-minute regulation of serum ionized calcium is exclusively regulated by what?
* PTH secretion is, in turn, regulated by what?

A
  • The minute-to-minute regulation of serum ionized calcium is exclusively regulated through PTH, maintaining the concentration of this cation within a narrow range, through stimulation of renal tubular calcium reabsorption and bone resorption.
  • PTH secretion is, in turn, regulated by serum ionized calcium acting via an exquisitely sensitive calcium-sensing receptor (CaSR) on the surface of parathyroid cells.
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55
Q

What are the causes of hypercalcemia?

A
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56
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Hyperparathyroidism:
* What are the sxs?

A

hypercalcemia sings

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57
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Diagnosis-Primary Hyperparathyroidism (PHPT)
* What is the most common clinical presentation?
* If hypercalcemia is confirmed, what should happen?

A
  • The most common clinical presentation of PHPT is Asymptomatic hypercalcemia. Also, PHPT should be considered in a patient with nephrolithiasis.
  • If hypercalcemia is confirmed, intact parathyroid hormone (PTH) should be measured concomitantly with the serum calcium (should be elevated)
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58
Q

Diagnosis-Primary Hyperparathyroidism (PHPT)
* What levels would still make PHPT the most likely diagnosis

A

When the PTH is only minimally elevated orwithin the normal range (but inappropriately normal given the patient’s hypercalcemia), PHPT remains the most likely diagnosis, although familial hypocalciuric hypercalcemia (FHH), a rare disorder, is possible.
* Triad: Hypercalcemia, increased intact PTH, decreased phosphate

59
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⭐️

A
60
Q
  • What is the DDXs of hypercalcemia?
A
61
Q

How do you dx primary hyperparathyroidism?

A

Increased 24 hour urine calcium excretion

62
Q

Treatment
* What is the definitive therapy of primary hyperparathyroidism

A

Patients with symptomatic primary hyperparathyroidism (PHPT) (nephrolithiasis, symptomatic hypercalcemia) should have parathyroid surgery, which is the only definitive therapy.

63
Q

primary hyperparathyroidism
* Parathyroidectomy is what?
* What do you need to give post-surgery

A

Parathyroidectomy is an effective therapy that cures the disease, decreases the risk of kidney stones, improves bone mineral density (BMD), and may decrease fracture risk and modestly improve some quality-of-life measurements.
* Give Vit D and calcium supplementation to prevent hypocalemia

64
Q

Primary Hyperparathyroidism
* Mild asymptomatic PHPT =
* Avoid what?
* What is a temporary measure?

A
  • Mild asymptomatic PHPT = Keep active to minimize resorption, and drink adequate fluids (Calciuresis)
  • Avoid thiazides, lithium, large dosages of Vit A and D and any calcium containing supplements
  • Bisphosphonates (Alendronate) -temporary measure to decrease serum calcium levels.
65
Q

How does Bisphosphonates do?

A

Bisphosphonates are a group of drugs that work by slowing bone loss. They reduce the risk of hip and spine fractures. Bone renewal is a slow process, but in many people an increase in bone density can be measured over five years of treatment.
* Alendronate

66
Q

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Milk-alkali Syndrome
* What is the triad? Associated with what?

A

The milk-alkali syndrome consists of the triad of hypercalcemia, metabolic alkalosis, and acute kidney injury associated with the ingestion of large amounts of calcium and absorbable alkali.

67
Q

⭐️

A
68
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⭐️

A
69
Q

Hypothyroidism
* Primary hypothyroidism (local) is characterized by what? Subclinical hypothyroidism?

A
  • Primary hypothyroidism (local) is characterized by a high serum TSH concentration and low serum free thyroxine (T4) concentration
  • Subclinical hypothyroidism is defined biochemically as a normal free T4 concentration in the presence of an elevated TSH concentration.
70
Q

Hypothyroidism
* Secondary (central) hypothyroidism is characterized by what?

A

Secondary (central) hypothyroidism is characterized by a low serum T4 concentration and a serum TSH concentration that is not appropriately elevated.

71
Q

Hypothyroidism
* Is it common?

A
  • Present in 3-5% of US population
  • W>M 8:1, and more common in women with small body size at birth and during childhood
72
Q

What is the pathogenesis and clinical findings of hypothyroidism? (it is a lot lol)

A
73
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⭐️

A
74
Q

Hashimoto’s Thyroiditis
(aka Chronic Autoimmune Thyroiditis)
* Most common cause of what? What is it due to?

A

Most common cause of hypothyroidism in iodine-sufficient areas of the world.
* Due to autoimmune-mediated destruction of the thyroid gland involving apoptosis of thyroid epithelial cells. May be present with or without goiter.

75
Q

Hashimoto’s Thyroiditis
* Nearly all patients have high serum concentrations of what?

A

Nearly all patients have high serum concentrations of antibodies against one or more thyroid antigens; diffuse lymphocytic B and T cells infiltration of the thyroid; and follicular destruction.

76
Q

Hashimoto’s Thyroiditis
* The cause of Hashimoto’s thyroiditis is thought to be what?
* What indicates that the two disorders are closely related pathophysiologically, albeit not functionally.

A
  • The cause of Hashimoto’s thyroiditis is thought to be a combination of genetic susceptibility and environmental factors.
  • The familial association with Graves’ disease and the fact that Graves’ disease may sometimes evolve into Hashimoto’s thyroiditis (and vice versa) indicate that the two disorders are closely related pathophysiologically, albeit not functionally.
77
Q

Hashimoto’s: Chronic autoimmune thyroiditis
* Presence of what?
* Approximately 10 to 15 percent of children with this disorder have what?
* If autoimmune thyroiditis is suspected then what?

A
  • Has presence of antithyroid antibodies (TPO and/or Tg).
  • Approximately 10 to 15 percent of children with this disorder have negative anti-TPO and anti-Tg antibodies (“antibody-negative” autoimmune thyroiditis).
  • If autoimmune thyroiditis is suspected in a child with goiter despite negative antithyroid antibodies (with a family history of autoimmune thyroiditis or a finding of acquired hypothyroidism) ultrasonography may help establish this diagnosis.
78
Q

What are the sxs of hashimoto thyroiditis?

A
  • Decreased metabolic rate, fatigue, cold intolerance, dry thickened rough skin, constipation, weight gain despite decreased oral intake, menorrhagia, myxedema (eyelide and facial edema), weakness and lethargy
  • Goiter symptoms: hoarseness and dyspnea
  • Women may have galactorrhea
79
Q

What are the physical exam of hashimoto thyroiditis?

A
  • Thyroid might be normal, enlarged (goiter), or atrophic (later in the diease course)
  • Bradycardia, decreased DTR, loss of 1/3 of eyebrows
  • Myxedema- nonpitting edema
80
Q

Hashimoto’s Cont.
* What is the txt?

A
  • Normal thyroid: None just frequent labs
  • Overt hypothyroidism: Levothyroxine (Synthroid)
81
Q

What are the three Antithyroid antibody tests

A
  • Anti-Tg Ab
  • Anti-TPO Ab
  • Anti-TSHR Ab
82
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A
83
Q

Thyroglobulin
(Tg, formerly known as the colloid antigen)
* Tg is synthesized by what? stored as?
* Patients with Hashimoto’s thyroiditis or Graves’ disease may have what?

A
  • Tg is synthesized by follicular cells and secreted into the lumen of the thyroid follicle, where it is stored as colloid.
  • Patients with Hashimoto’s thyroiditis or Graves’ disease may have Tg antibodies, but Tg antibodies do not need to be measured to diagnose autoimmune thyroid disease.
84
Q

Thyroglobulin
(Tg, formerly known as the colloid antigen)
* thyroglobulin antibodies can interfere with what? Why is this important?

A

However, thyroglobulin antibodies can interfere with the measurement of serum thyroglobulin, and they are therefore always assessed when monitoring serum thyroglobulin levels in patients with differentiated thyroid cancer. (Thyroglobulin is used for the detection of residual, recurrent, or metastatic disease.)

85
Q

Thyroid peroxidase
(TPO, formerly known as the microsomal antigen)
* TPO does what? Nearly all patients with Hashimoto’s thyroiditis have what?
* Serum anti-TPO antibodies need not be measured in patients with what?

A
  • TPO catalyzes the iodination of tyrosine residues of Tg to form monoiodotyrosine and diiodotyrosine. Nearly all patients with Hashimoto’s thyroiditis have high serum concentrations of TPO antibodies.
  • Serum anti-TPO antibodies need not be measured in patients with overt primary hypothyroidism, because almost all have chronic autoimmune thyroiditis.
86
Q

Thyroid peroxidase
(TPO, formerly known as the microsomal antigen)
* a test for anti-TPO antibodies may be useful to predict what?

A

However, a test for anti-TPO antibodies may be useful to predict the likelihood of progression to permanent overt hypothyroidism in patients with subclinical hypothyroidism.

87
Q

The TSH receptor
Thyrotropin receptor antibodies (TRAbs)
* Thyrotropin receptor antibodies (TRAbs) are classified as what?
* What causes grave’s disease?
* Thyroid receptor-blocking antibodies can cause what?

A
  • Thyrotropin receptor antibodies (TRAbs) are classified as stimulating, blocking, or neutral.
  • Stimulating antibodies (thyroid-stimulating immunoglobulins, TSI) cause Graves’ disease.
  • Thyroid receptor-blocking antibodies can cause hypothyroidism.
88
Q

The TSH receptor-Thyrotropin receptor antibodies (TRAbs)
* Some patients will have a mixture of what? What will happen?

A

Some patients will have a mixture of both antibodies, and, depending on the relative titers of these antibodies, they may fluctuate between hyperthyroidism and hypothyroidism. Neutral antibodies bind the receptor but do not stimulate or block function.

89
Q

The TSH receptor-Thyrotropin receptor antibodies (TRAbs)
* What are two methods for measuring TRAb?

A
  • TSI assays measure only thyroid-stimulating antibodies
  • TSH receptor-binding inhibitor immunoglobulin (TBII or TBI) assays measure stimulating, blocking, and neutral antibodies.
90
Q

⭐️

The TSH receptor-Thyrotropin receptor antibodies (TRAbs)
* What has high sensitivity and specificity for dx of Grave’s disease

A

Third-generation TSI assays have a sensitivity of 97 percent and a specificity of 99 percent for the diagnosis of Graves’ disease

91
Q
A
92
Q

How does THS and free T4 vary in different diseases?

A

TSH
* Excellent screening test
* Released by pituitary, stimulates the thyroid to release T4/T3
* Elevated in Hypothyroidism, low in Hyperthyroidism

Free T4
* Released by thyroid, needs to be converted to active form (T3) (about 80% converted)
* Elevated in Hyperthyroidism, low in Hypothyroidism

93
Q

Free T3
* Only hormone that is what?
* High and low in what?
* What is another thyroid hormone?

A

Free T3
* The only thyroid hormone sensed by cells
* Elevated in Hyperthyroidism, low in Hypothyroidism

TRH (thyroid releasing hormone)

94
Q

May help identify central hypothyroidism. What happens with low t3/t4 and TSH?

A

May help identify central hypothyroidism. If TSH is low and T3/T4 are low, may give TRH stimulation
which will markedly raise TSH.

95
Q

Hypothyroidism Clues

A
96
Q
A
97
Q

⭐️

What is the txt of choice for hypothyrodisM

A

The treatment of choice for correction of hypothyroidism is synthetic thyroxine (T4,Levothyroxine).
* T4 is a prohormone with very little intrinsic activity.

98
Q

What happens with T4 in the tissues?

A

It is deiodinated in peripheral tissues to form T3, the active thyroid hormone. Approximately 70 to 80 percent of a dose of T4 is absorbed and, because the plasma half-life of T4 is long (seven days), once-daily treatment results in nearly constant serum T4 and triiodothyronine (T3) concentrations when a steady state is reached.

99
Q

⭐️

Hypothyroidism:
* For thyroid therapy, what sohuld be monitored?
* What is an option for those that do not want to wait?
* What else can be used?

A
  • TSH should be monitored every 4-6 weeks for treatment success
  • Crude thyroid is an option for those that do not want to wait - 2 weeks
  • Liothyronine (Synthetic T3) can also be used
100
Q

Patient Education-hypothyroidism
* What might need to happen to the dose?
* When does it need to change?

A
  • Changes in the T4 dose are based upon the person’s TSH and T4 level. The dose may need to be increased if thyroid disease worsens, during pregnancy, if gastrointestinal conditions impair T4 absorption, or if the person gains weight. A high-fiber diet, calcium- or aluminum-containing antacids, and iron tablets can interfere with the absorption of T4 and should be taken at a different time of day.
  • The dose may need to be decreased as the person gets older, after childbirth, or if the person loses weight.
101
Q

Patient Education-hypothyroidism
* What about advance age and heart disease?
* What are the metabolic syndrome complications?

A
  • Advanced age and heart disease — Thyroid hormone makes the heart work a bit harder. Therefore, a clinician may opt for more conservative T4 treatment in older adults and in people with coronary artery disease.
  • Metabolic Syndrome Complications – Hypercholesterolemia and hypertriglyceridemia are commonly see in hypothyroid patients
102
Q

Patient Education-hypothyroidism
* What happens with pregnancy?
* What happens with surgery?

A
  • Pregnancy — Women often need higher doses of T4 during pregnancy. Testing is usually recommended every four weeks, beginning after conception, until levels are stable, then once each trimester. After delivery, the woman’s dose of T4 will need to be adjusted again, usually returning to the pre-pregnancy dose.
  • Surgery — Hypothyroidism can increase the risk of certain surgery-related complications; bowel function may be slow to recover, and infection may be overlooked if there is no fever. If preoperative blood tests reveal low thyroid hormone levels, nonemergency surgery is usually postponed until treatment has returned T4 levels to normal.
103
Q

Hyperthyroidism Epidemiology
* Common in who?
* Graves’ disease is seen most often in who?

A
  • Hyperthyroidism is more common in women than men (5:1 ratio). The overall prevalence of hyperthyroidism, which is approximately 1.3 percent, increases to 4 to 5 percent in older women.
  • Hyperthyroidism is also more common in smokers.
  • Graves’ disease is seen most often in younger women, while toxic nodular goiter is more common in older women.
104
Q

What are the causes of primary and secondary hyperthyroidism?

A
105
Q

What are the clinical manifestations of hyperthyroisdism?

A
106
Q

⭐️

A
107
Q

Physical Examination for Hyperthyroidism
* Note what?
* Lock for what in hands/fingers?
* Examine what?

A
  • Shake hands and note excessive warmth and sweating.
  • Look for fine tremor of outstretched hands and acropachy of the fingers (hyperthyroidism).
  • Examine the radial pulse (usually rapid and high-volume unless on a β -blocker). An irregularly irregular pulse is likely to indicate atrial fibrillation.
108
Q

Physical Examination for Hyperthyroidism
* Examine the thyroid and describe what?
* Look for what?
* Inspect what?

A
  • Examine the thyroid and describe its size, surface and consistency. Listen for a thyroid bruit.
  • Look for evidence of thyroid eye disease.
  • Inspect the shins for pretibial myxedema
109
Q

Hyperthyroidism and Graves Disease
* What is graves disease?
* The terms Graves’ disease and hyperthyroidism are not synonymous, because why?

A
  • Graves’ disease is a syndrome that may consist of hyperthyroidism, goiter, thyroid eye disease (Graves’ orbitopathy), and occasionally a dermatopathy referred to as pretibial or localized myxedema (PTM).
  • The terms Graves’ disease and hyperthyroidism are not synonymous, because some patients may have orbitopathy but no hyperthyroidism, and there are many other causes of hyperthyroidism in addition to Graves’ disease.
110
Q

Hyperthyroidism and Graves Disease
* What is the most common feature of Graves’ disease caused by?

A

by autoantibodies to the thyrotropin receptor (TRAb) that activate the receptor, thereby stimulating thyroid hormone synthesis and secretion as well as thyroid growth (causing a diffuse goiter)

111
Q

Graves Disease
* What only occurs in graves disease?(4)

A

Exophthalmos, periorbital and conjunctival edema, limitation of eye movement, and infiltrative dermopathy (pretibial myxedema) occur only in patients with Graves’ disease

112
Q

Graves Disease
* What is Acropachy? What is it characterized by?
* Radiographic imaging of what?
* Toxic nodular goiter does not cause what?

A
  • Acropachy is a dermopathy associated with Graves’ disease. It is characterized by soft-tissue swelling of the hands and clubbing of the fingers.
  • Radiographic imaging of affected extremities typically demonstrates periostitis, most commonly the metacarpal bones.
  • Toxic nodular goiter does not cause the bulging eyes that can occur with Graves disease.
113
Q

Graves Disease Pathophysiology
* Graves disease results from what? Also known as what?

A

Graves disease results from production of thyroid-stimulating immunoglobulins (TSI) by stimulated B lymphocytes
* Also known as autoantibodies to the thyrotropin receptor (TRAb) or TBII, or TBI

114
Q

Graves Disease Pathophysiology
* thyroid-stimulating immunoglobulins (TSI) binds to what? What does that cause?
* What will develop?

A

TSI’s bind to TSH receptors, cause hyperproduction of thyroid hormone.
* As a result, hypervascularity develops leading to goiter formation
* A new-onset ophthalmopathy develops

115
Q

⭐️

Diagnosis of Hyperthyroidism (and Graves)
* Primary hyperthyroidism is consistent with what lab levels?

A

Primary hyperthyroidism is consistent with a low TSH, and a high free T4 and/or T3 blood test.

116
Q

⭐️

Diagnosis of Hyperthyroidism (and Graves)
* If TSH is elevated, and free T4 and T3 are what? What is necessary?

A

If TSH is elevated, and free T4 and T3 are high, an MRI of the pituitary gland is necessary to evaluate for central or TSH – induced hyperthyroidism.

117
Q

Diagnosis of Hyperthyroidism (and Graves)
* If TSH is low and T3 is high (but your free T4 is normal), the diagnosis is what? What can help differentiate between the two diagnoses?

A
  • If TSH is low and T3 is high (but your free T4 is normal), the diagnosis is either Graves disease or a thyroid nodule that is producing too much hormone.
  • A radioactive iodine uptake scan can differentiate between these two diagnoses. Alternatively, taking too much T3 (called exogenous T3 ingestion) is another possibility.
118
Q

⭐️

Iodine I-123 Nuclear Scintigraphy

A
119
Q

Differential diagnoses of hyperthyroidism?

A
120
Q

Treatment of Hyperthyroidism (and Graves)
* What are the two medications to treat hyperthyroidm?

A
  • Anti-thyroid medicines reduce the amount of hormone your thyroid gland makes (Thionamides->Propylthiouracil or methimazole). Can be use -/+ of radioiodine or surgery.
  • Beta-blocker medicines help reduce the symptoms of hyperthyroidism. Beta-blockers can make you more comfortable until the thyroid imbalance is under control.
    * Calcium channel blockers can be used if BB are contraindicated
121
Q

⭐️

Treatment of Hyperthyroidism (and Graves)
* What else besides anti-thyroid medicines and BB can be used? How do they work?
* Can cause problems in what?

A
  • Radioactive iodine (I-131) – Radioactive iodine comes in a pill or liquid you swallow. It destroys much of the thyroid gland causing Hypothyroidism
  • It can cause problems getting pregnant in the future or increase the risk of birth defects in future pregnancies.
122
Q

Treatment of Hyperthyroidism (and Graves)
* Radioactive iodine can make what worst?
* Throwback from Radiology! Iodinated contrast should be avoided when? Why?

A
  • Radioactive iodine can make eye bulging worse in people with Graves’ disease, especially if they smoke cigarettes. A steroid administration before radioactive iodine may help prevent bulging of the eyes.
  • Throwback from Radiology! Iodinated contrast should be avoided for two months before administration of iodine 131/123
    * Reduces uptake of I-131 and makes it ineffective
123
Q

Treatment of Hyperthyroidism (and Graves)
* What is the txt for those of fail medical therapy or those with malgnancy?

A

Surgery – Surgery for those that fail medical therapy or those with malignancy. But surgery is the best choice in some cases.

124
Q

Management of Hyperthyroidism in Pregnancy
* When do you patients have to wait for getting pregnant? Why?
* During pregnancy, what can the pregnancy develop? Can lead to what? Does not require what?

A

Patient must wait at least 6 months before trying to get pregnant after being treated with radioactive iodine.
* I-131 wipes out thyroid function, hypothyroidism in pregnancy can cause fetal complications. 6months timeframe allows work-up and stabilization of hormone level.

During pregnancy, mother can develop hCG-mediated hyperthyroidism (Not Graves disease)
* Can lead to pre-eclampsia, preterm labor or miscarriage
* Does not require treatment if mild and is self-limiting

125
Q

⭐️

Management of Hyperthyroidism in Pregnancy
* Severe symptoms of hCG-mediated hyperthyroidism and those with Graves disease will need what?
* What type of medications do you give when?

A

Severe symptoms of hCG-mediated hyperthyroidism and those with Graves disease will need thionamides (inhibit thyroid hormone synthesis)
* Propylthiouracil (PTU) in the first trimester (less fetal malformations)
* Methimazole in the second or third trimester (has longer half-life)
* Patients can continue PTU throughout pregnancy, or switch to methimazole at 16 weeks
* Methimazole may lead to an increased incidence of aplasia cutis, a fetal scalp defect. Avoid in first trimester.

126
Q

Thyroid storm
* What is it?

A

Thyroid Storm = “hyperthyroidism on steroids”, can develop in patients with longstanding untreated hyperthyroidism (Graves’ disease, toxic multinodular goiter, solitary toxic adenoma), but is often precipitated by an acute event such as thyroid or nonthyroidal surgery, trauma, infection, an acute iodine load, or parturition.

127
Q

Thyroid storm
* The classical symptoms of thyroid storm include what? (4)
* Physical examination may revel what?(6)

A
  • The classical symptoms of thyroid storm include tachycardia, hyperpyrexia, central nervous system dysfunction (agitation, delirium, psychosis, stupor, or coma), and gastrointestinal symptoms (nausea, vomiting, abdominal pain).
  • Physical examination may reveal goiter, ophthalmopathy (in the presence of Graves’ disease), lid lag, hand tremor, and warm and moist skin.
128
Q

Thyroid storm
* Thyroid function tests show what?

A

Thyroid function tests show hyperthyroidism (suppressed thyroid-stimulating hormone [TSH], elevated free thyroxine [T4] and triiodothyronine [T3]) generally comparable with that in patients with uncomplicated overt hyperthyroidism.

129
Q

Thyroid storm
* The diagnosis of thyroid storm is based upon what?

A

The diagnosis of thyroid storm is based upon the presence of severe and life-threatening symptoms (hyperpyrexia, cardiovascular dysfunction, altered mentation) in a patient with biochemical evidence of hyperthyroidism (elevation of free T4 and/or T3 and suppression of TSH)

130
Q

Diagnosis for Thyroid Storm
* what is the point scale for the dx of thyroid storm?

A
131
Q

Treatment of Thyroid Storm
* In addition to thionamides/BB/CCB/I-131, what else should be used? Do not treat fever with what and why?
* Where are they admitted to?

A
  • In addition to thionamides/BB/CCB/I-131, glucocorticoids and iodine solution (eg, saturated solution of potassium iodide [SSKI]) is used.
  • Don’t treat fever with ASA – can increase free T3/T4 concentration
  • ICU admission due to mortality rate of 10-30 percent.
132
Q

Treatment of Thyroid Storm

A
133
Q

Treatment of Thyroid Storm
* For patients with clinical features of thyroid storm, immediate treatment with what? (5)

A
  • Beta blocker (propranolol)
  • Thionamide (PTU is preferred)
  • Iodine solution (1 hour after a thionamide is given)
  • Glucocorticoids (hydrocortisone)
  • Bile acid sequestrants (cholestyramine) may also be of benefit in severe cases to decrease enterohepatic recycling of thyroid hormones.
134
Q

Treatment of Thyroid Storm
* What is for those that cannot get thionamides or those with obstructive goiter?
* What if iodine is contraindicated?

A
  • Surgery for those that cannot get thionamides or those with obstructive goiter
  • Potassium perchlorate if iodine is contraindicated (ex: amiodarone induced or due to allergy)
135
Q

Thyroiditis
* Inflammatory thyroid conditions that cause what?
* conditions in which there is no clinically evident what?
* Increased risk with who?

A
  • Inflammatory thyroid conditions that cause acute illness with severe thyroid pain (eg, subacute thyroiditis and infectious thyroiditis)
  • Or conditions in which there is no clinically evident inflammation and the illness is manifested primarily by thyroid dysfunction or goiter (eg, painless thyroiditis and fibrous [Riedel’s] thyroiditis)
  • Incidence increased with diabetes (25%)
136
Q

⭐️

Thyroiditis
* What are the causes?(5)

A
  • Suppurative or infectious
  • Subacute painful (de Quervain’s, granulomatous, or giant cell)
  • Drug-induced (usually Amiodarone)
  • Chronic lymphocytic (Hashimoto)
  • Fibrous thyroiditis (Riedel)
137
Q
A
138
Q

Thyroid strom-Suppurative:
* Caused by what?
* What are the sxs? (4)
* What lab levels?
* FNA with what?
* What is the treatment based on?

A
  • Caused by Staph. aureus
  • Tender Thyroid, fever, sore throat, overlying erythema
  • Leukocytosis and Elevated ESR
  • FNA with gram stain and culture
  • Treatment based on culture and surgical drainage

Rare and nonviral

139
Q

⭐️

Subacute (DeQuervain’s) Thyroiditis
* Typically follows what?
* What is on exam?
* What is high and low?

A
  • Typically follows URI disease
  • Painful enlarge thyroid on exam
  • ESR is elevated and antithyroid antibody titers are low
140
Q

⭐️

Subacute (DeQuervain’s) Thyroiditis
* What is both elevated? What may be normal or low?
* What is the txt? What can reduce sxs?

A
  • Both T3/T4 are elevated, TSH may be normal or low
  • Can last up to a year
  • Treatment is ASA with no steroids. BB and iodinated contrast products can reduce symptoms.
141
Q

What is De Quervain’s thyroiditis?

A

De Quervain’s thyroiditis, also known as subacute granulomatous thyroiditis or giant cell thyroiditis, is a health condition involving the thyroid gland that usually resolves spontaneously without treatment.Patients with this disease go through different phases over weeks to months. Initially, they will be hyperthyroid and then transition to a brief euthyroid phase, followed by a hypothyroid phase, before eventually returning to being euthyroid

142
Q

Drug-induced Thyroiditis
* What is most common?
* Can mimic both what? Why?
* After a couple of months, what will normalize?
* What is the txt?

A
  • Amiodarone induced (antiarrhythmic drug) which as 37% Iodine in it
  • Can mimic both hyper and hypothyroidism symptoms by increasing T4 by 20-40% during 1st month of taking the drug and reduces concentration of T3, therefore TSH will rise.
  • After 2-3 month, T4 and T3 and TSH levels normalize
    Stop the drug and find a replacement.
143
Q

Fibrous thyroiditis (Riedel’s)
* Caused by what?
* Common in who (gender)?
* What is on exam?

A
  • Very rare form caused by development of dense fibrous tissue in the thyroid gland. May have other extraglandular fibrosis such as sclerosing cholangitis.
  • 80% are female
  • Asymmetric, painless, hard (woody) thyroid on palpation
144
Q

Fibrous thyroiditis (Riedel’s)
* what is decreased?
* Dx is made via what?
* What is the treatment?(3)

A
  • RAIU is decreased in the involved areas of thyroid with possible thyroid antibodies in nearly half of patient
  • Diagnosis is made via biopsy.
  • Resection vs tamoxifen, methotrexate, or steroids treatment is warranted.
    * Tamoxifen (selective estrogen receptor modulator (SERM) used often for breast cancer patients).

Clinical Medicine 3 (27 decks)

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