Lecture 17 (Endocrine)-Exam 6 Flashcards

Question 1

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Question 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?

Answer

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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

Question 3

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Vitamin D Background
* Vitamin D binding protein is synthesized where?
* The protein binds what?

Answer

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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)

Question 4

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

Answer

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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

Question 5

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

Answer

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PTH and low phosphate induce 1-α-hydroxylase
Calcium and 1,25-OH-vitamin D (calcitriol) suppress 1-α-hydroxylase

Question 6

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Vitamin D
* What lowers 1,25-OH-vitamin D (calcitriol)?
* What does Dilantin cause?

Answer

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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

Question 7

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Vitamin D
* Actions on what?

Answer

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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

Question 8

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

Answer

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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

Question 9

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Question 10

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Vitamin D
* Vitamin D deficiency causes what?
* What is the lab value?

Answer

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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

Question 11

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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?

Answer

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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)

Question 12

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

Answer

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

Question 13

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

Answer

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

Question 14

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

Answer

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Autosomal recessive
Low calcium and phosphorus, secondary hyperparathyroidism

Question 15

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

Answer

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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

Question 16

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

Answer

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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.

Question 17

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

Answer

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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

Question 18

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

Answer

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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.

Question 19

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

Answer

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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

Question 20

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

Answer

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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.

Question 21

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Question 22

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

Answer

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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.

Question 23

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

Answer

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due to acute hypocalcemia

Question 24

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

Answer

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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

Question 25

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

Answer

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

Question 26

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

Answer

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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.

Question 27

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Question 28

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Question 29

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Diagnosis of hypocalcemia from hypoparathyrodism:
* What are the levels of labs?

Answer

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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

Question 30

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Question 31

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

Answer

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

Question 32

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

Answer

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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

Question 33

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

Answer

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

Question 34

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

Answer

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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

Question 35

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

Answer

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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’

Question 36

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

Answer

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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

Question 37

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

Answer

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Short stature
Obesity
Round face
SQ ossifications
Brachydactyly

Question 38

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

Answer

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

Question 39

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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?

Answer

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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

Question 40

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Pseudohypoparathyroidism Type Ic
* AHO? G8?

Answer

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

Question 41

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

Answer

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

Question 42

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

Answer

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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

Question 43

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

Answer

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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

Question 44

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

Answer

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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.

Question 45

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Question 46

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Question 47

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Question 48

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Question 49

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

Answer

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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.

Question 50

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

Answer

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

Question 51

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

Answer

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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.

Question 52

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Question 53

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Question 54

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Question 55

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What are the causes of hypercalcemia?

Question 56

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Hyperparathyroidism:
* What are the sxs?

Answer

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hypercalcemia sings

Question 57

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

Answer

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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)

Question 58

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

Answer

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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

Question 59

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Question 60

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What is the DDXs of hypercalcemia?

Question 61

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How do you dx primary hyperparathyroidism?

Answer

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Increased 24 hour urine calcium excretion

Question 62

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Treatment
* What is the definitive therapy of primary hyperparathyroidism

Answer

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

Question 63

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

Answer

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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

Question 64

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

Answer

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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.

Answer 49

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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

Answer 50

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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.

Answer 51

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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.

Answer 52

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

Answer 53

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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

Answer 54

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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.

Answer 55

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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.

Answer 56

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.

Answer 57

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.

Answer 58

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

Answer 59

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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

Answer 60

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Normal thyroid: None just frequent labs
Overt hypothyroidism: Levothyroxine (Synthroid)

Answer 61

A

Anti-Tg Ab
Anti-TPO Ab
Anti-TSHR Ab

Answer 62

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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.

Answer 63

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.)

Answer 64

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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.

Answer 65

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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.

Answer 66

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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.

Answer 67

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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.

Answer 68

A

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

Answer 69

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

Answer 70

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

Answer 71

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

TRH (thyroid releasing hormone)

Answer 72

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

Answer 73

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

Answer 74

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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.

Answer 75

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

Answer 76

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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.

Answer 77

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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

Answer 78

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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.

Answer 79

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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.

Answer 80

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.

Answer 81

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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

Answer 82

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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.

Answer 83

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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)

Answer 84

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

Answer 85

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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.

Answer 86

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

Answer 87

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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

Answer 88

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

Answer 89

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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.

Answer 90

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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.

Answer 91

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

Answer 92

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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.

Answer 93

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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

Answer 94

A

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

Answer 95

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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

Answer 96

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.

Answer 97

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.

Answer 98

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.

Answer 99

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.

Answer 100

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)

Answer 101

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.

Answer 102

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.

Answer 103

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)

Answer 104

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%)

Answer 105

A

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

Answer 106

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

Answer 107

A

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

Answer 108

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.

Answer 109

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

Answer 110

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.

Answer 111

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

Answer 112

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).