Endocrine pt 1 Thursday Flashcards

(49 cards)

1
Q

Are thyroid nodules benign? Explain

A

90% of nodules are benign
Often these are follicular adenoma or cysts. Only 10% are suspicious

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2
Q

List the benign types of thyroid nodules

A

Follicular adenoma (colloid) most common type of thyroid nodule, accounting for 50-60%
Other: adenomas, cysts, localized thyroiditis

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3
Q

Describe the clinical Sx of thyroid nodules

A

Most of the time, they are asymptomatic
May have compressive symptoms:
Difficulty swallowing or breathing
Neck, jaw, or ear pain
Hoarseness
Rarely, patients may develop a functional nodule which causes hyperthyroid symptoms

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4
Q

Describe benign vs malignant thyroid nodules on PE

A

Benign: smooth, firm, irregular, sharply outlined, discrete, painless
Malignant: rapid growth, fixed, no movement with swallowing

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5
Q

What type of testing do you need for thyroid nodules? Explain

A

Thyroid function testing:
1) You will order TSH, T3/T4 and ultrasound
-If TSH is in the subclinical hyperthyroid range or overtly hyperthyroid, then radioactive iodine uptake scan should be ordered in addition to ultrasound
>“Hot” nodules have a lower risk for malignancy but need to be treated
-Ultrasound will guide the need for FNA with biopsy

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6
Q

“_____” thyroid nodules have a lower risk for malignancy but need to be treated

A

Hot

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7
Q

Ultrasound interpretation of thyroid nodules:
1) Describe what would have high suspicion

A

Solid hypoechoic nodule, or a cyst with hypoechoic segment PLUS one of the following
1) Irregular margins, microcalcifications, taller than wide shape, evidence of extrathyroidal extension
2) Recommended FNA with bx if > than 1.0 cm

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8
Q

Ultrasound interpretation of thyroid nodules:
Describe what would have intermediate suspicion

A

Hypoechoic solid nodule with smooth margins WITHOUT the following:
1) Microcalcifications, extrathyroidal extension, taller than wide shape
2) Recommended FNA with bx if > 1.0 cm

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9
Q

Ultrasound interpretation of thyroid nodules:
Describe what would have low suspicion

A

Isoechoic or hyperechoic solid nodule, or partially cystic nodule with eccentric solid areas WITHOUT
1) Microcalcifications, extrathyroidal extension, taller than wide shape
2) Recommend FNA with bx if > 1.5 cm

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10
Q

Ultrasound interpretation of thyroid nodules:
Describe what would have very low suspicion

A

1) Spongiform or partially cystic nodules WITHOUT any of the features described above
2) Recommend FNA with bx if > 2.0 cm

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11
Q

Ultrasound interpretation of thyroid nodules:
Describe what you could say is benign

A

1) Purely cystic nodules with no solid component
2) No FNA with bx recommended

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12
Q

List the 4 main types of thyroid cancer

A

1) Papillary
2) Follicular
3) Medullary
4) Anaplastic

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13
Q

Papillary thyroid CA:
1) Describe the pathogenesis
2) Describe the pt profile

A

1) Most common and least aggressive cancer of the thyroid (80%)
2) More often female
Painless thyroid nodule
Had radiation exposure to the head and neck
Possible family history

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14
Q

Papillary thyroid CA:
1) How do you Dx?
2) How do you Tx?

A

1) Fine needle aspiration
2) Thyroidectomy (near or total)
-Followed by post op levothyroxine
-+/- Post surgery radioactive iodine
-Monitor thyroid levels

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15
Q

Follicular Thyroid Carcinoma:
1) Describe the pathogenesis
2) Describe the demographic

A

1) Second most common type of thyroid cancer (10%)
Associated with iodine deficiency
2) 40-60 years old

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16
Q

Follicular Thyroid Carcinoma:
1) How do you Dx?
2) How do you Tx?

A

1) Fine needle aspiration with post surgical histologic testing
This will be done after thyroidectomy
2) Thyroidectomy (full or partial) > post op levothyroxine
+/- radioiodine
Monitoring of thyroid levels

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17
Q

Medullary Thyroid Carcinoma: Describe the pathogenesis and prevalence

A

1) Cancer of calcitonin-synthesizing parafollicular cells
2) 5% of thyroid carcinoma
-90% of these are sporadic
-10% are associated with MEN IIa or IIb; RET mutation
2) May have ectopic production of ACTH, with a pheochromocytoma present in 50-70% cases, Hyperparathyroidism in 50%

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18
Q

Medullary Thyroid Carcinoma:
1) How do you Dx?
2) How do you Tx?

A

1) FNA
-Increased calcitonin on lab
-On pathology- proliferation of parafollicular cells ( C cells) that produce excess calcitonin
-Check urinary metanephrine levels; Pheochromocytoma also associated with MEN II
2) Total thyroidectomy
Levothyroxine supplementation and monitoring

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19
Q

Anaplastic Thyroid Carcinoma
1) Describe the pathogenesis
2) Describe the pt profile

A

1) Most aggressive + rarest thyroid cancer
Poorest prognosis
2) Rapid growth
Compressive symptoms; dyspnea
May invade the trachea
Dysphagia
Rock hard thyroid mass

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20
Q

Anaplastic Thyroid Carcinoma:
1) How do you Dx?
2) How do you Tx?

A

1) Fine needle biopsy
2) Resection doesn’t work
Radiation or chemo
Palliative tracheostomy

21
Q

Describe PTH (parathyroid hormone)
1) What does it do?
2) What secretes it>?
3) What inhibits it? What stimulates the receptor on the gland?

A

1) Increases calcium when it’s low
-Causes the kidneys to excrete PO4
2) Secreted by parathyroid glands on back of thyroid whose default is “ON”
3) High calcium inhibits PTH release
Ca++ stimulates Ca receptor on gland

22
Q

What does PTH normally do to bone?

A

Bone resorption = taking Ca and Phosphate from bone
Does this through osteoclast activity

23
Q

What does the GI tract normally have to do with PTH?

A

Absorbs Ca and Phosphate
Does this through 1,25 Vit D (active form) secreted by kidney

24
Q

1) What does PTH normally do to the kidneys?
2) How does this affect urine?

A

1) Signals the release 1, 25 Vit D; tells kidney to resorb Ca and ELIMINATE Phosphate
-The kidney will waste more phosphate than is resorbed through bone or absorbed through GI tract
-Serum Ca++ is HIGH and Phosphate is LOW
2) Increase in urine phosphate
-Increase in URINE Calcium; yes, because there is so much Ca around, some still gets excreted

25
Describe how the end product of vit D processing is created
D2 is the Vit D you eat UV light creates D3 - Vit D precursor in your skin Liver takes both forms and makes 25 Vit D which is still an intermediate form Kidney turns 25 Vit D into 1, 25 Vit D in the proximal convoluted tubule
26
List some Sx of Hyperparathyroid
1) Bones: Osteoclast activity increased = watch for osteopenia and bone pain 2) Stones: Urine Calcium UP, urine phosphate UP > calcium phosphate and calcium oxalate kidney stones 3) Abdominal groans: Increased CA = constipation and pain 4) Psychic moans: Ca > encephalopathy -Note: most of the time, a Ca high enough to cause encephalopathy is actually caused by malignancy (not parathyroid hormone)
27
List 2 causes of hyperparathyroid
MEN 1 syndrome Chromosome XI inversion
28
What are 2 causes of hypoparathyroid? explain
The surgeon tried to resect some of the thyroid and cut out parathyroid glands or cut their vascular supply. . . LOW calcium Hyperactive nerves Calcium is not available to block sodium channels on neuron, increasing total activity
29
List 3 Sx of hypoparathyroid
Perioral tingling Digital paresthesia Trousseau and Chvostek's sign
30
List a bunch of Sx of hypercalcemia
-Muscle weakness -Fatigue -Volume depletion -Nausea and vomiting -Coma and death -Depression and confusion -Memory problems -Polydipsia/polyuria -Decreased appetite -Abd pain -Constipation -Acute pancreatitis -HTN -EKG- short QT -Left Ventricular Hypertrophy Kidney stones Asymptomatic
31
Hypercalcemia: Describe the pathogenesis
1) Lab error! 2) Primary hyperparathyroidism most common -Parathyroid adenoma, MEN 3) Lithium therapy 4) Malignancy -PTH related protein
32
Hypercalcemia: What will the pt be like? Explain
Usually, asymptomatic unless they have cancer and are delirious from extremely high calcium
33
For every deviation of 1 on albumin, change Ca in opposite direction 0.8; give examples
1) Alb 4 -0-> CA lab is 10 and actually is 10 2) Alb 5 > Ca lab is 10.8 and actually is 10 3) Albumin 3 > Ca lab is 9.2 and actually IS 10! These equations show that the Ca is 10 You would confirm this with ionized calcium 4.65-5.25
34
What if the ionized calcium is high? (even with correction)
Go looking for the cause
35
Hypercalcemia: How do you Dx?
1) Repeat the lab! -Get ionized calcium! 2) Once confirmed elevation  get PTH and see if it’s high 3) You can get PTH related protein (which is what cancer emits) if the PTH is normal 4) You can check 1,25 Vit D and 24-hour urinary calcium -Calcium is high or high normal in hyperparathyroidism, and can be the same or VERY high in malignancy 5) Check an EKG
36
How do you Tx hypercalcemia?
1) Mild hypercalcemia, which is < 12, does not often require treatment 2) Moderate to severe, >12: -IV fluids -IV fluids -IV fluids -IV loop diuretics – furosemide -In malignancy: calcitonin +/- bisphosphonates & Denosumab -In granulomatous disease: Steroids
37
Primary Hyperparathyroidism: How is it diagnosed?
1) Kidneys “win” once stimulated by PTH 2) Therefore, calcium is HIGH and PO4 is low 3) On lab: High Calcium High PTH Low PO4
38
Primary Hyperparathyroidism: How is it treated?
1) Surgery 2) Post op Sestamibi scans monitor subsequent parathyroid function
39
What can happen with Untreated Hyperparathyroidism?
1) Osteoporosis 2) Kidney stones ( from excess calcium in blood- hard deposits can form in kidneys) 3) Cardiovascular disease assoc with hypercalcemia -Hypertension, arrhythmia
40
Untreated Hyperparathyroidism: What are some findings on Xrays?
1) “Salt and pepper” skull 2) Distal clavicle resorption
41
Hyperparathyroidism during Pregnancy: 1) How may it manifest? 2) Do fetuses have complications? Explain
1) May manifest as hyperemesis, pancreatitis, muscle weakness -Hypercalcemic crisis 2) 80% of fetuses experience complications -Fetal demise, preterm delivery, low birth weight -Neonatal tetany -Permanent hypoparathyroidism
42
Secondary Hyperparathyroidism: Describe the main pathogenesis
Kidney disease: 1) Kidneys not making enough vit D 2) Nothing tells the gut to absorb Ca 3) Ca doesn’t inhibit PTH 4) Parathyroid glands proliferate and make lots of PTH
43
Secondary Hyperparathyroidism: 1) Describe the pt presentation (main symptom) 2) Describe how to Dx 3) How do you Tx?
1) Bones get weak > osteomalacia 2) Phosphate would classically be low, but may be normal because kidneys aren’t filtering well -The above process is occurring to normalize low calcium to begin with, so calcium may be normal -Look for high creatine, high BUN, potentially low GFR 3) Treat the kidney disease
44
Secondary Hyperparathyroidism: 1) Describe the Vit D deficiency pathogenesis
Low vit D = Calcium is not being resorbed  calcum begins to lower PTH goes high Calcium trands back toward normal PO4 should be low because the kidneys have not trouble dumping it
45
Secondary Hyperparathyroidism bc of Vit D def: 1) Dx? 2) Tx?
1) Check 25 vit D Not 1,25 – that one is too variable and changes based on PTH 2) Give them Ca and Vit D
46
slide 91
PTH is absent- either by parathyroid injury (after thyroid surgery) or hereditary (DiGeorge syndrome) PTH is ineffective (intestinal malabsorption, pseudohypoparathyroidism) PTH is overwhelmed (acute renal failure, or rhabdomyolysis, or septic shock) Primary hypoparathyroidism- lifelong risk of symptomatic tetany without access to calcium- a patient may die
47
slide 92
Lab Ca is 6-7 or lower
48
Describe the pt in hypoparathyoidism
paresthesia of lips, tongue, fingers, feet Carpopedal spasm- Trousseau’s sign Spasm of facial muscles Fatigue Anxiety Hoarseness Wheezing Could have slowly developing mild diffuse encephalopathy. Suspect in any patient with unexplained dementia or psychosis
49
Hypoparathyroidism: Describe the Tx
Acute attack of tetany- IV calcium gluconate Administer calcium 1 to 2 grams/day Calcitriol (0.25- 1 ug/day)- ( Vitamin D as soon as calcium rx started) Adjust according to serum calcium levels and urinary excretion. Restoration of magnesium stores may be required to reverse hypocalcemia if severe hypomagnesemia is present.