Ch7: Thyroid Flashcards

1
Q

what is T4

A

thyroxine

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2
Q

what is T3

A

triiodothyronine

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3
Q

what is the function of T3 and T4

A

these hormones act as cellular energy release catalysts and influence the function and health of every cell in the body

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4
Q

most common thyroid disorder encountered in primary care

A

hypothyroidism

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5
Q

MOMS SO TIRED mnemonic for hypothyroidism presentation

A
Memory loss
Obesity 
Menorrhagia
Slowness
Skin/hair dry
Onset gradual
Tiredness
Intolerance to cold
Raised BP
Energy levels fall
Depression/delayed relaxation phase of all reflexes (especially patellar, Achilles)
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6
Q

what is the natural history of weight gain with hypothyroidism?

A

modest weight gain of <10lbs that is mostly fluid, will pee off this fluid when adequately treated

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7
Q

DTRs with hypothryoidism

A

delayed relaxation of DTRs - slow arc out and an even slower arc back

“hung up patellar reflex”

most noticeable in patellar and achilles DTRs

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8
Q

most common cause of hypothyroidism in the USA

A

chronic autoimmune hypothyroidism

aka Hashimotos thyroiditis

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9
Q

classic patient characteristics of someone with Hashimotos thyroiditis

A

> 50yo

female

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10
Q

causes of hypothyroidism

A
  • autoimmune (Hashimotos)
  • post-radioactive iodine treatment (e.g., after Graves dx)
  • select medications (Lithium, amiodarone, interferon)
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11
Q

medications that can cause HYPOTHYROIDISM

A
  • lithium (up to 1/3)
  • amiodarone
  • interferon
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12
Q

SWEATING mnemonic for hyperthyroidism

A
Sweating
Weight loss
Emotional lability
Appetite increased but losing weight
Tremor/tachycardia
Intolerance of heat/irregular menstruation/irritability
Nervousness
Goiter, GI problems (diarrhea)
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13
Q

what is a goiter

A

descriptor for thyroid enlargement

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14
Q

most common cause of hyperthyroidism

A

Grave’s disease (autoimmune)

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15
Q

cluster of autoimmune conditions to keep on your radar if someone has autoimmune thyroid disease (5)

A
  • rheumatoid arthritis
  • lupus SLE
  • vitiligo
  • celiac dz
  • T1DM
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16
Q

exophthalmos, suspect….

A

Grave’s hyperthyroidism

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17
Q

What is a toxic adenoma

A

benign (non-malignant) metabolically-active thyroid nodule that causes typical hyperthyroid symptoms but with palpable unilateral thyroid mass and NO exophthalmos

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18
Q

what is thyroiditis

A

inflammation of the thyroid

usually transient

can be caused by a viral infection, autoimmune condition, postpartum, drug-induced, etc.

typically has a milder symptom presentation with thyroid tenderness but without exophthalmos

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19
Q

medications that can cause hyperthyroidism (2)

A
  • amiodarone

- interferon

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20
Q

hyper or hypothyroid: dry skin

A

hypothyroid

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21
Q

hyper or hypothyroid: fine tremor

A

hyperthyroid

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22
Q

hyper or hypothyroid: hypoactive DTRs (delayed relaxation)

A

hypothyroid

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23
Q

hyper or hypothyroid: mood changes

A

both

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24
Q

hyper or hypothyroid: menorrhagia

A

hypothyroid

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25
Q

hyper or hypothyroid: exophthalmos

A

hyperthyroid

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26
Q

normal range for TSH

A

0.4-4.0 mIU/L

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27
Q

what is the single most reliable test to diagnose all common forms of hypo and hyperthyroidism

A

TSH

thyroid-stimulating hormone

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28
Q

TSH is released by the…..

A

anterior pituitary

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29
Q

when TSH results are normal, can you rule out thyroid disease?

A

yes, very good sensitivity and specificity

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30
Q

normal range for free T4

A

10-27 pmol/L

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31
Q

normal range for thyroid peroxidase antibody (anti-TPO ab)

A

<35 IU/mL

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32
Q

second most helpful test for diagnosing hypo or hyperthyroidism

A

FREET4

not total

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33
Q

% of all T4 that is free

A

0.025%

majority of T4 is protein-bound

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34
Q

anti-TPO antibodies are used to detect….

A

Hashimoto’s thyroiditis

35
Q

dx: TSH 84, free T4 3

A

high TSH
low free T4

untreated hypothyroidism

36
Q

levothyroxine replacement doses for hypothyroidism

A

based on ideal body weight if obese, actual body weight if BMI WNL or underweight

  • 1.6 mcg/kg/day in most adults
  • 1.0 mcg/kg/day in elderly
37
Q

check TSH after ____ weeks after starting levothyroxine for hypothyroidism

A

q6-8 weeks until euthyroid, then in 4-6 months, then yearly if stable

she says 8 WEEKS and any earlier can lead to errors in clinical decision-making

38
Q

weight based dosing for levothyroxine: most adults

A

1.6 mcg/kg/day

ranges 50-200mcg for adults, typically

39
Q

weight based dosing for levothyroxine: elderly

A

1.0 mcg/kg/day

40
Q

T4/T3 combination medication?

A

Armour Thyroid

use is not recommended by the AACE due to variable pharmcokinetics

41
Q

instructions for patient administration of levothyroxine

A

levothyroxine should be taken with plain water on an empty stomach, same time every day

should not be taken within 2 hours of cation such as calcium, iron, aluminum, magnesium , or others due to chelation effect with reduced drug absorption

42
Q

dx: TSH 0.15, free T4 79

A

low TSH, high free T4

hyperthyroidism

43
Q

treatments for hyperthyroidism

A
  • non-cardioselective beta blockers (propanolol, nadolol) for counteracting tachycardia and tremor
  • thyroid-ablative therapies (e.g., methimazole, PTU, RAI)
44
Q

thyroid ablative therapy options in hyperthyroidism

A
  • methimazole PO (Tapazole)
  • PTU (Propylthiouracil)
  • radioactive iodine

use the PO methimazole or PTU first to reduce thyroxine production to become euthyroid. Once euthyroid from antithyroid medications, use radioactive iodine with the goal of thyroid ablation with resulting hypothyroidism

usually treated in conjunction with endocrinology consult

45
Q

do you want cardioselective or non-cardioselective beta blockers for hyperthyroidism?

A

non-cardioselective beta blockers

most commonly, propanolol

46
Q

priority risk of methimazole and PTU

A

acute hepatic failure even in the absence of liver disease risk factors (e.g., alcohol use)

can happen to anyone

47
Q

dx: TSH 8.9, total T4 15, TPO-ab 76

A

subclinical hypothyroidism

48
Q

treatment for subclinical hypothyroidism?

A

recommend treatment if TSH >5 and presence of a goiter or TPO-antibodies, symptomatic, infertility/pregnant/trying to conceive

49
Q

what range should you treat TSH to ideally with levothyroxine

A

0.5-2 uIU/mL

50
Q

If you start levothyroxine, they come back in 6-8 weeks later and the TSH is still elevated (>4) – Dose titration?

A

increase levothyroxine dose by 12.5mcg to 25mcg

51
Q

If you start levothyroxine, they come back in 6-8 weeks later and the TSH is now low (<0.5) – Dose titration?

A

decrease levothyroxine dose by 12.5 - 25mcg

52
Q

follow-up interval for checking TSH after levothyroxine adjustments

A

q6-8 weeks until euthyroid, then 6 months, then annually

53
Q

risk that any given thyroid nodule is malignant?

A

5%

54
Q

role of a NP primary care provider in pt with a thyroid nodule

A

initiate evaluation, refer to specialist

55
Q

what is a thyroid nodule

A

a palpable thyroid mass, not a term specific to a diagnosis. is clinically evident, typically >1cm in diameter

presentation of benign and malignant tends to be the same

5% risk of being malignant

56
Q

findings most consistent with a MALIGNANT thyroid nodule?

A
  • h/o head or neck irradiation
  • size >4cm
  • firmness, nontender on palpation
  • relatively fixed position (nonmobile)
  • persistent non-tender cervical lymphadenopathy
  • dysphonia
  • hemoptysis
57
Q

pt presents with clinically evident thyroid nodule >1cm, next step?

A

labs: TSH
imaging: thyroid US

58
Q

pt presents with clinically evident thyroid nodule >1cm. you order TSH and a thyroid US. lab results return low TSH. what is your next step?

A

refer for nuclear medicine thyroid scan to determine the nodule function and structure

will determine “hot” (releasing T4) aka toxic or non-toxic (not releasing excess T4) nodules

59
Q

pt presents with clinically evident thyroid nodule >1cm. you order TSH and a thyroid US. lab results return low TSH. nuclear medicine thyroid scan reveals a “hot” nodule, diagnosed with toxic nodular goiter. what is the next step?

A

radioiodine ablation or surgery to remove it

60
Q

pt presents with clinically evident thyroid nodule >1cm. you order TSH and a thyroid US. lab results return low TSH. nuclear medicine thyroid scan reveals a non-toxic goiter, nodule is not releasing excess T4. what is the next step?

A

FNA biopsy
(fine needle aspiration)

this is very unusual for it to be not “hot”, non-toxic

61
Q

pt presents with clinically evident thyroid nodule >1cm. you order TSH and a thyroid US. Lab results return a normal TSH. what is the next step?

A

refer for FNA biopsy (fine needle aspiration)

62
Q

one of the most common causes of asymptomatic hypercalcemia in an otherwise well adult?

A

primary hyperparathyroidism

63
Q

hypothalamic-pituitary-thyroid axis

A

hypothalamus releases TRH (thyroid hormone releasing hormone) –> stimulates anterior pituitary to release TSH (thyroid stimulating hormone) –> stimulates the thyroid to produce T3 and T4

64
Q

TSH production requires which nutritional components (3)

A
  • protein
  • magnesium
  • zinc
65
Q

T4 production requires which nutritional components (3)

A
  • iodine
  • vitamin C
  • vitamin B2
66
Q

T3 production requires which nutritional and body system requirements

A
  • selenium
  • healthy liver function
  • healthy adrenal gland function
67
Q

hyper vs. hypothyroid: which can you treat as NP in primary care vs. which do you refer out?

A

NP can treat hypothyroid (levothyroxine replacement)

refer out hyperthyroid for consultation

68
Q

what is deQuervein’s thyroiditis?

A

aka subacute granulomatous thyroiditis

transient thyroid inflammation (hyperthyroidism, transient) usually s/t a viral infection

69
Q

possible physical exam findings indicative of hyperthyroidism

A
  • thyroid bruit
  • exophthalmos
  • hyperactive DTRs
  • tachycardia
  • proximal muscle weakness
  • lid lag
  • atrial fibrillation
70
Q

world-wide most common cause of hypothyroidism

A

iodine-deficiency (uncommon in US)

71
Q

% of hypothyroidism that is caused by Hashimoto’s autoimmune thyroiditis?

A

90-95%

72
Q

(3) most common causes of hypothyroidism

A
  • autoimmune Hashimoto’s
  • ablative therapy for hyperthyroidism treatment
  • iodine deficiency
73
Q

role of PTH (parathyroid hormone) in the body

A

increases serum calcium

opposite of calcitonin

74
Q

what is primary hyperparathyroidism

A

elevated level of parathyroid hormone (PTH)

excess PTH = hypercalcemia

caused by overactivity of one or more of the four parathyroid glands, via enlargement (hyperplasia), adenoma (benign tumor), or malignant tumor

75
Q

clinical presentation of primary or secondary hyperparathyroidism

A

variable
“moans, groans, stones, and bones with psychic overtones”

common s/s include:

  • loss of energy
  • poor concentration or memory
  • depression
  • OSTEOPOROSIS/OSTEOPENIA
  • insomnia
  • GERD
  • decreased libido
  • hair loss
  • bone and joint aches

other s/s:

  • kidney stones
  • hypertension
  • arrhythmias, atrial fibrillation
  • liver dysfunction
  • abnormal blood protein levels
76
Q

diagnostic evaluation of primary hyperparathyroidism

A

elevated serum calcium found on labs without other obvious cause

confirmed by elevated PTH level

additional test could include a 24-hour urine calcium to determine disease severity – specialty consult advised

77
Q

priority sequelae of primary hyperparathyroidism

A

osteoporosis

78
Q

what is secondary hyperparathyroidism

A

elevated PTH as a result of another condition that lowers serum calcium levels, thus causing the parathyroid glands to overproduce PTH

causes include:

  • severe calcium deficiency
  • severe vitamin D deficiency
  • chronic kidney disease
79
Q

most common causes of secondary hyperparathyroidism (3)

A
  • calcium deficiency
  • vitamin D deficiency
  • chronic kidney disease
80
Q

diagnostic evaluation of secondary hyperparathyroidism

A

low-normal serum calcium
elevated PTH on labs
presence of severe renal dysfunction (often on dialysis or have significant kidney problems over several years)

81
Q

treatment options for hyperparathyroidism

A
  • surgery to remove the problematic gland is curative 95% of the time for primary hyperparathyroidism, only considered as last resort in secondary
  • cinacalcet (Sensipar) is a calcimimetic used to treat hyperparathyroidism in CKD or parathyroid cancer, causes less parathyroid hormone to be released
  • bisphosphonates and/or hormone replacement therapy for post-menopausal women should be considered to prevent bone loss
  • phosphate binders and/or vitamin D analogs can be used in secondary hyperparathyroidism if vitamin D deficiency or calcium deficiency is the cause
  • ensure adequate intake of vitamin D and calcium
  • stop use of lithium or thiazide diuretics which may exacerbate
82
Q

avoid use of (2) medications in someone with hyperparathyroidism as these can elevate levels of both PTH and calcium, exacerbating the condition

A
  • thiazide diuretics

- lithium

83
Q

if a patient is taking either of these (2) medications when hyperparathyroidism is found on labs, they should stop medications and have calcium levels reassessed after a medication-free interval to confirm the diagnosis

A

lithium or thiazide diuretics (e.g., HCTZ)