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Internal Medicine EOR > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is acromegaly?

A

acromegaly and gigantism are usually caused by a pituitary adenoma that secretes excessive amounts of Growth Hormones; rarely, they are caused by non-pituitary tumors that secrete GHRH

  • gigantism occurs if growth hormone (GH) hypersecretion begins in childhood, before the closure of the epiphyses
  • acromegaly involves growth hormone GH hypersecretion beginning in adulthood; a variety of bony and soft tissue abnormalities develop
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2
Q

What is the presentation of acromegaly?

A
  • large hands, feet, nose, lips, ears, jaw, tongue

- presents as gigantism (excessive height) if occurs before epiphyseal closure

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3
Q

How is acromegaly dx?

A
  • GH test 2 hour after glucose load
  • increased IGF-1
  • MRI/CT shows a pituitary tumor
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4
Q

What is the tx for acromegaly?

A

pituitary tumor removal

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5
Q

What is Addison’s disease?

A

typically autoimmune, may be due to tuberculosis in endemic areas

  • destruction of the adrenal cortex resulting in loss of cortisol production (decrease cortisol)
  • nonspecific symptoms: hyperpigmentation, hypotension, fatigue, myalgias, GI complaints, weight loss
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6
Q

What are the lab findings for Addison’s disease?

A

decreased sodium, decreased 8 AM cortisol, increased ACTH (primary), increased potassium (primary), low DHEA

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7
Q

How is Addison’s disease dx?

A

high dose cosyntropin (synthetic ACTH) stimulation test

  • blood or urine cortisol is measured after an IM injection of cosyntropin (synthetic ACTH)
  • the normal response is a rise in blood and urine cortisol levels after synthetic ACTH is given
  • primary adrenal insufficiency results in little or no increase in cortisol levels (< 20 mcg/dL) after ACTH is given
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8
Q

What is the tx of Addison’s disease?

A

hydrocortisone/prednisone PO daily

  • Crisis: hypotension, altered mental status
  • treatment: emergent IV saline, glucose, steroids
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9
Q

What is Cushing’s syndrome?

A

a collection of signs and symtpoms due to prolonged exposure to excess cortison

  • symptoms from increased cortisol secretion
  • it doesn’t specify cause or soure of excess
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10
Q

What is Cushing disease?

A

ACTH secreting pituitary microadenoma usually very small on anterior pituitary, F 3x >M
-secondary - increased cortisol due to ACTH excess, typically caused by pituitary adenoma -ACTH causes adrenals to secrete cortisol

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11
Q

What are the features of Cushing disease?

A
  • hypercortisolism (increased cortisol) = obesity (buffalo hump, moon facies, supreclavicular pads), HTN, thirst, polyuria, hypokalemia
  • proximal muscle weakness, pigmented striae; backache, headache, oligomenorrhea/amenorrhea/ED; emotional lability/psychosis
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12
Q

How is Cushing disease dx?

A

confirming high cortisol with a 24 hr urine free cortisol, late-night serum cortisol, and/or low-dose dexamethasone suppression test

  • 24-hr urinary free cortisol is the most reliable index of cortisol secretion
  • once confirmed, the source of the high cortisol needs to be determined with an ACTH level
  • a high ACTH level indicates an ACTH dependent cause, a low ACTH level indicated an ACTH independent cause (plasma or serum ACTH < 20 pg/mL suggest adrenal tumor
  • if it is an ACTH dependent cause, an MRI of the brain should be done to look for a pituitary adenoma (Cushing disease)
  • if it is an ACTH independent cause, a CT of adrenals should be done to look for an adrenal mass such as an adenoma
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13
Q

What is low dose dexamethason suppresion test?

A
  • give a steroid (dexamethasone) = failure of steroid to decrease cotisol levels is diagnostic = proceed next to high dose dexamethason suppression test = no suppression = Cushing’s syndrome
  • supression < 5 ugs/dL excludes Cushing with some certainty
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14
Q

What is the tx for Cushing disease?

A

trnasphenodial selective resection of pituitary tumor cures 75-90%

  • irradiation provides remission in 50-60%
  • 95% 5-year survival
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15
Q

What is diabetes insipidus?

A

caused by a deficiency of or restance to vasopressin (ADH), which decreases the kidney’s ability to reabsorb water, resulting in massive polyuria

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16
Q

What is central diabetes insipidus?

A

deficiency of ADH from posterior pituitary/hypothalamus
-no ADH production most common type: idiopathic, autoimmune destruction of posterior pituitary from head trauma, brain tumor, infection, or sarcoidosis

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17
Q

What is nephrogenic diabetes insipidus?

A

Lack of reaction to ADH
-partial or complete insensitivity to ADH: caused by drugs (lithium, amphoterrible), hypercalcemia and hypokalemia affect the kidney’s ability to concentrate urine, acute tubular necrosis

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18
Q

How is diabetes insipidus dx?

A

serum osmolality (concentration) is high (unable to stop the secretion of water into the kidneys so blood becomes more concentrates) and urine osmolality is low because it is so dilute

  • water deprivation test - simplest/most reliable method - continued production of dilute urine despite water deprivation
  • desmopression stimulation test:
  • central: reduction in urine output indicating a response to ADH
  • nephrogenic: continued production of dilute urine (no response to ADH) because kidenyes can’t respond
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19
Q

How is diabetes insipidus tx?

A
  • central = desmopression/DDAVP

- nephrogenic = sodium and protein restriction, HCTX, indomethacin

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20
Q

What is the etiology of diabetes mellitus type 1?

A

autoimmune - HLA-DR3/4/O antiboies

-Islet cell antibodies

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21
Q

What is the presentation os Type 1 DM?

A
  • children
  • polyuria, polydipsia, polyphagia, fatigue and weight loss
  • often first recognized as diabetic ketoacidosis:
  • symptoms: fruity breath, nausea, vomintg, dehydration
  • treatment: IV regular insuling
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22
Q

What is the the treatment of type I DM?

A

insulin

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23
Q

What is the dawn phenomenon?

A

normal glucose until 2-8 am when it rises

  • results from decreased insulin sensitivity and a nightly surge of counter-regulatory hormones during nighttime fasting
  • treat with bedtime injection of NPH to blunt morning hyperglycemia, avoiding carbohydrate snak late at night
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24
Q

What is the somogyi effect?

A

nocturnal hypoglycemia followed by rebound hyperglycemia due to a surge in growth hormones
-treat with decreased nighttime NPH dose or give bedtime snack

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25
Q

What is insulin waning?

A

a progressive rise in glucose from bedtime to morning

-treat with a change of insulting dose to bedtime

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26
Q

What is DKA?

A

fruity breath, weight loss, rapid respirations, hypotension

  • diabetic ketoacidosis (DKA) should always be handled in a hospitalized setting, usually an intensive care unit, and often with an endocrinologist’s consultation, if appropriate
  • TREAT WITH FLUIDS! patinets with DKA are always dehydrated and need large-volume IV fluid resucitation, usually isotonic fluids such as normal saline
  • if corrected serum sodium level is high, this can be reduced to half-normal saline
  • insuling should always be administered by an IV pump to guard against accidental overdose
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27
Q

How is the diagnosis of DM made?

A
  • randoma blood glucose level of > 200 mg/dL + diabetic symptoms
  • 2 separate fasting (8 hours) glucose levels of >126 mg/dL
  • 2-hour plasma glucose of > 200 on an oral glucose tolerance test (3-hour GTT is the gold standard in GDM)
  • hemoglobin A1c of >6.5%
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28
Q

What are the insulin and c-peptide levels with Type I DM?

A

low or inappropriately normal fasting C-peptide and insulin levels with concomitant hyperglycemia
-high fasting insulin and C-peptide level suggest T2DM

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29
Q

What are insulin, GAD65, and IA-2 antibodies?

A

if one or more the antibodies are present, and especially if two or more are positive, the patient should be presumed to have type 1 diabetes and should be treated with insulin replacement therapy

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30
Q

How you monitor/evaluate glycemic control?

A
  • hemoglobin A1c
  • represents mean glucose level from previous 8-12 weeks (approx lifespan of an RBC)
  • useful to gauge the ‘big-picture’ overall efficacy of glucose control in patients (either type 1 or type 2) to assess the need for changes in medication/insulin levels
  • treatment goal of A1c <7.0%
  • “finger-stick” blood glucose monitoring
  • useful for insulin-dependent (either type 1 or type 2) diabetics to monitor their glucose control and adjust insulin doses according to variations in diet or activity
  • treatment goals: <130 mg/dL fasting and <180 mg/dL peak postprandial
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31
Q

What is diabetes mellitus type 2?

A

diagnosis: random glucose > 200 x two or fasting glucsoe >126 x two

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32
Q

What are the characteristics of Metformin?

A

decreases hepatic glucose production and peripheral glucose utilization, decreases intestinal glucose absorption (these are reasons it leads to weight loss)

  • side effects: lactic acidosis, GI side effects, initiation is contrindicated with eGFR <30 mL/min and not recommended with eGFR 30 to 45 mL/min, discontinue 24 hours before contrast and resume 48 hours after with monitoring for creatinine, stop if creatinine is >1.5
  • benefits: weight loss, inexpensive
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33
Q

What are the characteristics of sulfonylureas?

A

stimulates pancreatic beta-cell insulin release (insulin secretagogue)

  • Glyburide (diabeta), glipizide (glucotrol), glimepride (amaryl)
  • side effects: hypoglycemia
  • benefits: cheap, rapidly effective
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34
Q

What are the characteristics of thiazolidinediones?

A

increases insuling sensitivity in peripheral receptor site adipose and muscle has no effect on pancreatic beta cells

  • pioglitazone (Actos), rosiglitazone (avandiaz0
  • contraindictions: CHF, liver disease, fluid retention, weight gain, bladder cancer (pioglitazone), a potential increase in MI (rosiglitazone)
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35
Q

What are the characteristics of alpha-glucosidase inhibitors?

A

delays intestinal glucose absorption

  • acarbose (precose), miglitol (glyset)
  • GI side effects, three times a day dosing
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36
Q

What are the characteristics of meglitinides?

A

stimulates pancreatic beta-cell insulin release

  • repaglinide (prandin) and nateglinide (starlix)
  • side effects: may cause hypoglycemia
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37
Q

What are the characteristics of GLP-1 Agonists?

A

lowers blood sugar by mimicking incretin - causes insulin secretion and decreased glucagon and delays gastric emptying

  • Exenatide (bydureon, Byetta), dulaglutide (trulicity), semaglutide (Ozempic), liraglutide (Victoza, saxenda)
  • side effects: requires injection, frequent GI side effects, caution is gastroparesis
  • benefits: weight loss, reduced CV mortality (semaglutide, Liraglutide) in patient with CVD
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38
Q

What are the characteristics of DPP-4 Inhibitors?

A

dipetpidylpetase inhibition - inhibits degradatino of GLP-1 so more circulation GLP-1

  • sitagliptin (januvla), saxagliptin (onglyza)
  • side effects: expensive, possible increased risk of heart failure with saxagliptin
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39
Q

What are the characteristics of SGLT2 inhibitor?

A

SGLT2 inhibition lowers renal glucose threshold which results in increased urinary glucose excretion

  • canagliflozin (invokana or sulisent)
  • side effects: vulvovaginal candidiasis, urinary tract infections, bone fractures, lower limb amputations, acute kidney injury, DKA, long-term safety not established
  • benefits: weight loss, reduction in systolic blood pressure, reduced cardiovascular mortality in pateitns with established CVD
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40
Q

When do you add insulin?

A

add if HbA1C > 9

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41
Q

What is the follow up with DM2?

A

annual - ophthalmologist visit, urine microalbumin

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42
Q

What are the complications of DM?

A

neuropathy (most common), retinopathy (a leading cause of blindness), nephropathy

43
Q

What is normal fasting glucose?

A

between 70 and 100

44
Q

What is the diagnostic criteria for prediabetes?

A
  • A1C 5.7 -6.4
  • fasting glucose 100-125
  • 2-hour oral glucose tolerance test 140-100
45
Q

What are the glucose goals and basic management?

A
  • A1C <7.0% check every 3 months if not controlled and 2x per year if controlled
  • preprandial glucose 80-110 (60-90 if pregnant)
  • postprandial blood glucose goal (1.5 - 2 hours after a meal) is <140
  • annual dialted eye exams, ACEI if microalbuminuria, annual foot examination
  • blood pressure should be maintained at <130/80
  • new statin guidelines: recommend statins in persons with diabetes mellitus who are 40 to 75 years of age with LDL-C levels of 70 to 189 mg per dL but without clinical ASCVD
46
Q

What is hypercalcemia?

A
  • serum total calcium > 10.5 mg/dL

- ionized fraction of calcium > 5.6 mg/dL

47
Q

What is the presentation of hypercalcemia?

A

“stones, bones, abdominal groans, psychiatric moans”, EKG: shortened QT interna

  • blood: increased PTH, increased calcium, decreased phosphorus
  • associated with malignancy and hyperparathyroidism
48
Q

What is the treatment for hypercalcemia?

A

IV normal saline and furosemide

49
Q

What is the definitiion of hypernatremia?

A

serum sodium of >145 mmol/L

50
Q

What is the etiology of hypernatremia?

A

diarrhea, burns, diuretics, hyperglycemia, diabetes insipidus, a deficit of thirst

51
Q

What are the signs and symptoms of hypernatremia?

A

poor skin turgor, dry mucous membranes, flat neck veins, hypotension, increased BUN/CR ratio >20:1
-decrease circulating volume = decrease of flow to kidneys means more bound urea in the blood which means increased BUN

52
Q

What is the tx of hypernatremia?

A

intravenous (IV) 5% detrose in water (D5W)

-rapid overcorrectio ncaused cerebral edema and pontine herniation

53
Q

What is hyperparathyroidism?

A

a condition in which one or more of the parathyroid glands become overactive and secrete too much parathyroid hormone (PTH)
-this causes the levels of calcium in the blood to rise

54
Q

What are the characteristics of hyperparathyroidism?

A
  1. increased PTH = bone breakdown = releases Ca
  2. kidney holds on Ca and increased Vitamin D3
  3. the intestine absorbs more Ca = increased Ca in blood levels
55
Q

What are the causes of hyperparathyroidism?

A

primary and secondary

  • primary: increased PTH usually caused by a PTH secreting parathyroid ADENOMA
  • secondary: increased PTH by a physiologic response to hypocalcemia or vitamin D deficiency
  • chronic kidney disease is the most common cause of secondary hyperparathyroidism
56
Q

What is the presentation of hyperparathryoidism?

A

weakness, fatigue, constipation = stones, bones, abdominal groans, psych moans, and fatigue overtones

  • bone loss from increased PTH and Ca absorption from bones = pain in bones
  • renal loss of Ca and phosphorus = kidney stone
  • increase GI absoprtion of Ca and abdominal cramps = graons
  • irritability, psychosis, depression = moans
57
Q

What are the labs for hyperparathyroidism?

A
  • blood = increased Ca, increased PTH, and decreased phosphorus
  • urine = hyperphosphaturia, hypercalciuria (all CA and phosphorus go out through kidneys to urine)
58
Q

What is the tx of hyperparathryoidism?

A
  • primary = surgical correction to remove the overactive parathyroid gland = if all 4, remove 3.5 glands
  • secondary = replace cause (vitamin D/Ca supplementation)
  • If Ca very high: IV fluids, lasix, calcitonin; treat osteoporosis with bisphosphonates
59
Q

What is hyperthyroidism?

A

the production of too much thyroxine hormone
-it can increase metabolism and accelerate the body’s metabolism, causing unintentional weight loss and a rapid or irregular heartbeat

60
Q

What is the etiology of hyperthyroidism?

A

Grave’s disease (autoimmune), toxic adenoma, thyroiditis, pregnancy, amiodarone

61
Q

What is the presentation of hyperthyroidism?

A

heat intolerance, palpitations sweating, weight loss, tremor, anxiety, tachycardia

  • graves - diffuse goiter with a bruit, exophthalmos, pretibial myxedema
  • thyroid storm - fever, tachycardia, delirium
62
Q

How is hyperthyroidism dx?

A
  • TSH (best test): decreased in primary disease (decreased TSH and increased free T4), elevated in secondary disease (increased TSH and increased free T4)
  • T4: elevated although may be normal
  • thyroid radioactive iodine uptake:
  • graves: diffusely high uptake
  • toxic multinodular: discrete areas of high uptake
63
Q

What are the antibodies of hyperthyroidism?

A

graves: anti-thyrotropin antibodies

64
Q

What is the tx for hyperthyroidism?

A
  • beta-blockes (symptomatic), methimazole/propylthiouracil, radioactive iodine, thyroidecotmy
  • thyroid storm - prompt beta-blockers, hydrocortisone, methimazole/propylthiouracil, iodine
  • thyroidecotmy - most likely complication is injury to the recurrent laryngeal nerve (hoarseness)
65
Q

What do you do about antithyroid drugs during pregnancy and nursing?

A
  • propylthiouracil used to be the drug of choice during pregnancy because it causes less severe birth defects than methimazole
  • experts now recommend that propylthiouracil be given during the first trimester only
  • this is because there have been rare cases of liver damage in people taking propylithiouracil
  • after the first trimester, women should switch to methimazole for the rest of the pregnancy
  • for women who are nursing, methimazole is probably a better choice than propylthiouracil (to avoid liver side effects)
66
Q

What is thyroiditis?

A

a general term that refers to “inflammation of the thyroid gland”

  • includes a group of individual disorders causing thyroidal inflammation but presenting in different ways
  • painful va painless may be hypo or hyperthyroid
67
Q

What is hashimoto’s thyroiditis?

A

diffusely enlarged, painless, nodular goiter

68
Q

What is subacute thyroiditis?

A
  • young women, after a viral infection
  • painful enlarged thyroid with dysphagia, mild fever
  • aspirin
69
Q

What is postpartum thyroiditis?

A
  • 1-2 months of hyperthyroidism after delivery

- completely resolves, give propranolol for cardiac symptoms

70
Q

What is suppurative thyroiditis?

A
  • fever, pain, redness, fluctuant mass, increased WBC

- antibiotic/surgical drainage

71
Q

What is hypocalcemia?

A
  • serum total calcium <8.4 mg/dL

- ionized fraction of calcium <4.4 mg/dL

72
Q

What is the presentation of hypocalcemia?

A

QT prolongation, trousseau’s sign, chvostek’s sign

  • labs: decreased Ca, decreased PTH, increased phosphate
  • EKG = prolonged QT
73
Q

What is the tx of hypocalcemia?

A

IV calcium gluconate or calcium chloride

74
Q

What is hyponatremia?

A

serum sodium of <135 mmol/L
-peripheral and presacral edema, pulmonary edema, JVD, hypertension, decreased hematocrit, decreased serum protein, decreased BUN/CR

75
Q

What is the presentation of hyponatremia?

A

msucle cramps and seziures

  • hypervolemic hyponatreia - CHF, nephrotic syndrome, renal failure, cirrhosis
  • euvolemic hyponatremis - SIADH, steroids, hypothyroid
  • hypovolemic hyponatremia - sodium loss (renal, non-renal)
76
Q

What is the tx of hyponatremia?

A
  • asymptomatic: free water restriction
  • moderate hyponatremia: IV normal saline and loop diruetics may be added
  • severe hyponatremia: hypertonic (3%) saline

-serum Na should be corrected slowly - by <10 mEq/L over 24 h to avoid osmotic demyelination syndrome

77
Q

What is hypoparathyroidism?

A

an uncommon condition in which your body secretes abnormally low levels of parathyroid hormone (PTH)
-thic causes calcium levels in the blood to decrease

78
Q

What is the etiology of hypoparathyroidism?

A

thyroidectomy

79
Q

What is the presentation of hypoparathyroidism?

A

tingling, tetany, cataracts

80
Q

What is the physical exam of hypoparathyroidism?

A
  • chvostek’s sign - tap facial nerve illicity cheek twitch

- trousseau’s sign - BP cuff inflation illicit carpal spasm

81
Q

What are the labs for hypoparathyroidism?

A

hypocalcemia decreased CA, low decreased PTH, hyperphosphatemia, low urinary calcium

82
Q

What is the tx for hypoparathyroidism?

A

Vitamin D and calcium

-tetany - secure airway, IV calcium gluconate

83
Q

What is the etiology of hypothyroidism?

A

Hashimoto’s (chronic lymphocytic/autoimmune), previous thyroidecotmy/iodien ablation, congential

84
Q

What is the presentation of hypothyroidism?

A
  • cold intolerance, fatigue, constipation, depression, weight gain, bradycarida
  • congenital: round face, large tongue, hernia, delayed milestones, poor feeding
85
Q

What are the labs for hypothyroidism?

A

TSH - elevated in primary diease, low T4 (increased TSH and decreased free T4)
-Hashimoto’s antithyroid peroxidase, antithyroglobulin antiboides

86
Q

What is the tx for hypothyroidism?

A

levothyroixine, follow up with serial TSH monitoring

87
Q

What is Paget disease?

A

bone remodeling disorder that results in the formation of an unorganized mosaic of woven and lamellar bone that is less compact and weaker than the normal bone

88
Q

What are the characteristics of Paget disease?

A
  • the exact cause is unknown but can be triggered by infections (e.g measles) and linked to genetic mutations
  • Paget’s disease of bone most commonly occurs in the pelvis, skull, spine, and legs
  • risk factors include increasing age and a family history of the condition
  • over time, affected bones may become fragile and misshapen
  • this condition can be sympotmless for a long period of time
  • when symptoms do occur, they may include bone deformiteis, broken bones, and pain in the affected area
  • may lead to osteosarcoma - Paget’s Sarcoma
89
Q

How is Paget disesse dx?

A

the x-ray shows lytic lesions and thickened bone cortices, a bone biopsy to exclude malignanices
-labs: increased alkaline phosphatase and bone-specific alkaline phosphatase; increased osteoclast activity and osteoblastic activity

90
Q

What is the tx of Paget disease?

A 
includes bisphosphonates (which reduce bone resorption and may improve pain and quality of life), and occasionally, calcitonin 
-surgery can help correct bone deformities, decompress an impinged nerve, and reduce fractures
91
Q

What is a pheochromocytoma?

A

catecholamine secreting adrenal tumor - secretes norepinephrine and epinephrine autonomously and intermittently

  • 5 P’s: pressure, pain (HA), perspiration, palpitations, pallor
  • associated with neurofibromatosis type 1, MEN 2A/B
92
Q

How is a pheochromocytoma dx?

A
  • 24-hour catecholamines including metabolities (metanephrine and vanillylmandelic acid)
  • MRI or CT of the abdomen to visualize the tumor
93
Q

What is the tx for a pheochromocytoma?

A
  • resect tumor - complete adrenalecotmy
  • medical treatment preoperative: Alpha-blocker (phenoxybenzamine) preop, phentolamine (acute HTN crisis), sodium nitroprusside (acute HTN crisis), nicardipine (acute HTN crisis)
  • pre-op nonselective alpha blockade: phenoxybenzamine or phentolamine 7-14 days followed by beta-blocker to control HTN (NO solo beta-blockers = prevent unopposed alpha constriction = life-threatening HTN)
94
Q

What is a pituitary adenoma ?

A

noncancerous tumors in the pituitary gland that don’t spread beyond the skull

  • most common tumors are microadenomas that are functional (hypersecretion of pituitary hormones), nonfunctional or compressive
  • microadenomas are less than 1 cm in diameter, whereas adenomas that are 1 cm or more are commonly referred to as macroadenomas
  • microadenoma < 10 mm
  • macroadenoma > 10 mm
95
Q

What are the s/s of pituitary adenoma?

A

diminished temporal vision or bitemporal hemianopsia = MC visual

96
Q

What are lactotroph adenomas?

A

(prolactinomas = MC) are pituitary masses = hypersecretion of prolactin

  • s/s: amenorrhea, galactorrhea, and headaches
  • location of the mass at the sella turcica = tumor applies pressure on the optic chiasm of the optic nerve resulting in loss of vision in the temporal visual fields
97
Q

What is a growth hormone tumor?

A

gigantism, acromegly

98
Q

What is a corticotroph adenoma?

A

secrete ACTH = present with Cushings syndrome

99
Q

What is a thyrotroph adenoma?

A

secrete TSH = presents with hyperthyroidism

100
Q

How is a pituitary adenoma dx?

A

MRI is the study of choice to look for sellar lesions/tumors
-endocrine studies: prolactin, GH, ACTH, TSH, FSH, LH

101
Q

What is the tx of pituitary adenoma?

A

dopamine agonists cabergoline and bromocrptine; if dopamine agonsts are unsuccessful, transsphenoidal resection of the pituitary tumor should be considered
-in women, estrogen therapy can also be used due to the associated hypogonadism

102
Q

What is thyroid cancer?

A

thyroid cancer occurs in the cells of the thyroid

  • MC risk is radiation exposure; MC F 40-60 y/o
  • hoarse voice, solitary cold nodule on thyroid uptake scan
  • most often papillary carcinoma (80%) = papillary = popular
103
Q

How is thyroid cancer dx?

A

ultrasound - all lesions >1 cm should be biopsied; smaller lesions can be followed/reevaluated if they grow

  • high-risk malignancy on U/S: microcalcifications, hypoechogenicity, a solid cold nodule, irregular nodule margins, chaotic intranodular vasculature, and a nodule that is more tall than wide
  • to eval malignancy: thyroid uptake scan - cancerous does not up take iodine (cold); non-cancerous will take up iodine (hot)
  • if cold = fine needle aspiration
104
Q

What is the tx of tyroid cancer?

A

depends on staging (99% 5-year survival with local confined, <1 cm papillary carcinoma)

  • always involves complete/parital thyroidectomy with chemo and radiation for anaplatic thyroid CA
  • recommended TSH level for pt: 1-2.0

Internal Medicine EOR (10 decks)

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