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Chapter 8. Thyroid Dysfunction
187
of the thyroid. In the USA, RAI is general favored for initial
treatment (58.6%) followed by 40.5% of endocrinologists
opting for antithyroid drugs, and only a small minority (1%)
recommending surgical therapy [18], though there has been
an increase in the use of antithyroid drugs as first-line therapy [19]. Beta blockade is important to minimize clinical
symptoms such as palpitations and tremulousness, while
other treatments to lower thyroid hormone levels are undertaken. Propranolol, atenolol, and metoprolol are commonly
prescribed. Of note, the treatment for toxic nodular goiter or
toxic adenoma generally follows that for Graves’ disease.
Antithyroid drugs include methimazole and propylthiouracil (PTU). The use of these medications for 12–18months
results in remission in 40–50% of patients [20]. Both of these
medications decrease hormone synthesis by interfering with
thyroid peroxidase (TPO). Methimazole is the preferred primary treatment for most patients, as PTU has been associated
with hepatotoxicity. PTU is utilized in the first trimester of
pregnancy and in patients intolerant of methimazole. The
starting dose of methimazole is 10–30mg a day, generally in
a single dose, and thyroid function tests are performed within
2–6 weeks. The duration of therapy is approximately
12–18months, followed by a taper if the patient is felt to be
in remission. Adverse effects of the antithyroid drugs include
pruritic rash and arthralgias (5%). Agranulocytosis occurs in
1 in 500 patients [21] and typically presents with fever and
pharyngitis. Patients taking antithyroid drugs should be
warned about this potential side effect. Checking routine
white blood cell counts is controversial, though roughly 50%
of prescribers routinely check CBCs on patients on thyroid
medications [18].
Radioactive Iodine (RAI)
The goal of RAI is to render the patient hypothyroid. RAI is
incorporated into thyroid hormone, which causes damage to
follicular cells and eventual destruction of the thyroid gland.
Most patients develop hypothyroidism 2–3 months after a
188
N. A. LaVine
single dose of RAI is administered. Serial thyroid hormone
measurements should be done at 2–6 week intervals and
levothyroxine therapy initiated with free T4 levels drop
below normal range.
Surgery
Indications for surgery include large goiters with compressive symptoms, suspicious thyroid nodules, and hyperparathyroidism [22].
Treatment: Subclinical Hyperthyroidism
The need for treatment in subclinical hyperthyroidism is controversial but may be advised in patients with persistently
suppressed TSH (<0.10), the elderly, or those with cardiac
disease, particularly since the risk of atrial fibrillation is
higher in these groups.
Clinical Pearls
• Graves’ disease is the most common cause of hyperthy-
roidism, accounting for 75% of cases, and is mediated by
antibodies to the thyroid-stimulating hormone (TSH)
receptor.
• Older patients tend to have fewer symptoms of
hyperthyroidism.
• Consider treatment of subclinical hyperthyroidism in
patients over the age of 65 with persistently suppressed
TSH and cardiac history.
Don’t Miss This!
• Agranulocytosis occurs in roughly 1/500 patients treated
with antithyroid medications, and patients should be
alerted to the signs and symptoms of this side effect (fever,
sore throat, oral ulcers).
• In older patients, TSH should be measured in the setting of
new-onset atrial fibrillation.
Chapter 8. Thyroid Dysfunction
189
Thyroid Nodules
Brief Introduction
The identification of thyroid nodules can occur by several
means. The patient may note a change in the neck, or a clinician may identify a nodule on physical exam. Additionally,
thyroid nodules may be noted incidentally when patients
undergo imaging (ultrasound, CT scanning, etc.) for other
reasons. Palpable thyroid nodules are found in 4–7% of the
population [23], whereas ultrasound may detect nodules in
19–68% of a random population sample [24]. Workup of thyroid nodules is important to exclude thyroid malignancy,
which can occur in 7–15% of thyroid nodules [25].
Key H&P
Thyroid nodules are often asymptomatic. Important history
to note in a patient with a thyroid nodule includes history of
radiation treatment to the head or neck, family history of
thyroid cancers, neck discomfort, rapid growth of the nodule,
dysphagia, and hoarseness. Exam should focus on the thyroid,
with special attention to the adjacent lymph nodes of the
neck.
Decision-Making/Differential Diagnosis
The presence of a nodule on exam should be further evaluated with ultrasonography of the neck and a serum TSH [23,
25]. If the TSH is below normal (suggesting hyperthyroidism),
the nodule should be assessed for hyperfunctioning with a
radioiodine scan. Hyperfunctioning nodules are rarely malignant, and further workup would include a free thyroxine level
and treatment for hyperthyroidism as appropriate. If the
nodule is nonfunctional, the characteristics of the nodule will
190
N. A. LaVine
Thryoid
Nodule on
Ultrasound
Hyperfunctioning
Nodule
Check Free T4 and
T3; treat for
Hyperthryoidism as
appropriate
TSH
Suppressed
Radionuclide
Scanning
Non/Hypofunctioning
Nodule
Size <1 cm
Low Risk features:
No Family Hx
Age >60
Well defined
margins
Cystic lesions
Consider
Observation
TSH Normal
or Elevated
Evaluate
Sonographic
Characteristics
Size
>1.5cm
FNA
Size >1cm
and/or
suspicious
features:
Solid hypoechoic
Irregular margins
Calcifictions
Extrathyroidal
extension
FNA
F . Diagnostic algorithm for thyroid nodules
dictate further workup, including possible fine-needle aspiration (FNA). If the TSH is normal or elevated, the characteristics of the nodule will influence further workup (Fig.8.3).
Treatment
If FNA is performed, further testing and diagnosis will be
dependent on the results and may include observation or
surgical thyroidectomy [25].
Clinical Pearls
• Thyroid nodules are common in the general population,
though most are benign.
• Thyroid ultrasound and TSH measurement are the main
factors in guiding diagnosis of thyroid nodules.
Chapter 8. Thyroid Dysfunction
191
Don’t Miss This!
• Ultrasound characteristics of suspicious thyroid nodules
include: solid hypoechoic nodules with irregular margins,
microcalcifications, abnormal cervical lymph nodes, and
extra-thyroidal extension.
References
1. Tunbridge WM, Evered DC, Hall R, et al. The spectrum of
thyroid disease in a community: the Whickham survey. Clin
Endocrinol. 1977;7:481–93.
2. Vanderpump MP, Tunbridge WM, French JM, et al. The incidence of thyroid disorders in the community: a twenty-year
follow-up of the Whickham survey. Clin Endocrinol. 1995;43:55.
3. Johansen ME, Marcinek JP, Doo Young Yun J.Thyroid hormone
use in the United States, 1997–2016. J Am Board Fam Med.
2020;33(2):284–8.
4. Biondi B, Wartofsky L.Treatment with thyroid hormone. Endocr
Rev. 2014;35(3):433–512.
5. Canaris GJ, Manowitz NR, Mayor G, Ridgway EC. The
Colorado Thyroid Disease Prevalence Study. Arch Intern Med.
2000;160(4):526–34.
6. Canaris GJ, Steiner JF, Ridgway EC. Do traditional symptoms of hypothyroidism correlate with biochemical disease? J Gen Intern Med. 1997;12(9):544–50. https://doi.
org/10.1046/j.1525- 1497.1997.07109.x.
7. Roberts CG, Ladenson PW. Hypothyroidism. Lancet.
2004;363:793–803.
8. Ylli D, Soldin SJ, Stolze B, et al. Biotin interference in assays
for thyroid hormones. Thyrotropin and thyroglobulin. Thyroid.
2021;31(8):1160–70.
9. Biondi B, Klein I.Hypothyroidism as a risk factor for cardiovascular disease. Endocrine. 2004;24:1–13.
10. Roos A, Linn-Rasker SP, van Domburg RT, Tijssen JP, Berghout
A.The starting dose of levothyroxine in primary hypothyroidism
treatment: a prospective, randomized, double-blind trial. Arch
Intern Med. 2005;165:1714–20.
11. Biondi B, Cooper DS. Thyroid hormone therapy for hypothyroidism. Endocrine. 2019;66(1):18–26.
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12. Huber G, Staub JJ, Meier C, Mitrache C, Guglielmetti M, Huber
P, Braverman LE.Prospective study of the spontaneous course
of subclinical hypothyroidism: prognostic value of thyrotropin,
thyroid reserve, and thyroid antibodies. J Clin Endocrinol Metab.
2002;87(7):3221–6.
13. Peeters RP. Subclinical hypothyroidism. N Engl J Med.
2017;376(26):2556–65.
14. Stott DJ, Rodondi N, Kearney PM, et al. Thyroid hormone
therapy for older adults with subclinical hypothyroidism. N Engl
J Med. 2017;376:2534–44.
15. Hollowell JG, Staehling NW, Flanders WD, Hannon WH, Gunter
EW, Spencer CA, Braverman LE. Serum TSH, T(4), and thyroid antibodies in the United States population (1988 to 1994):
National Health and Nutrition Examination Survey (NHANES
III). J Clin Endocrinol Metab. 2002;87(2):489–99.
16. Biondi B, Cooper DS. Subclinical hyperthyroidism. N Engl J
Med. 2018;378(25):2411–9.
1 7. Nyström HF, Jansson S, Berg G. Incidence rate and clinical
features of hyperthyroidism in a long-term iodine sufficient
area of Sweden (Gothenburg) 2003–2005. Clin Endocrinol.
2013;78:768–76.
18. Burch HB, Burman KD, Cooper DSA.A 2011 survey of clinical
practice patterns in the management of Graves’ disease. J Clin
Endocrinol Metab. 2012;97(12):4549–58.
19. Brito JP, Payne S, Singh Ospina N, Rodriguez-Gutierrez R,
Maraka S, Sangaralingham LR, Iñiguez-Ariza NM, Montori
VM, Stan MN. Patterns of use, efficacy, and safety of treatment options for patients with Graves’ disease: a Nationwide
population- based study. Thyroid. 2020;30(3):357–64.
20. Sundaresh V, Brito JP, Wang Z, et al. Comparative effectiveness of therapies for Graves’ hyperthyroidism: a systematic
review and network meta-analysis. J Clin Endocrinol Metab.
2013;98(9):3671–7.
21. Nakamura H, Miyauchi A, Miyawaki N, Imagawa J.Analysis of
754 cases of antithyroid drug-induced agranulocytosis over 30
years in Japan. J Clin Endocrinol Metab. 2013;98(12):4776–83.
22. Bahn Chair RS, Burch HB, Cooper DS, etal., American Thyroid
Association; American Association of Clinical Endocrinologists.
Hyperthyroidism and other causes of thyrotoxicosis: management guidelines of the American Thyroid Association and
American Association of Clinical Endocrinologists. Thyroid.
2011;21(6):593–646.
Chapter 8. Thyroid Dysfunction
23. Burman K, Wartofsky L. Thyroid nodules. N Engl J Med.
2015;373:2347–56.
24. Tan GH, Gharib H. Thyroid incidentalomas: management
approaches to nonpalpable nodules discovered incidentally on
thyroid imaging. Ann Intern Med. 1997;126:226–31.
25. Haugen BR, Alexander EK, Bible KC, et al. 2015 American
Thyroid Association management guidelines for adult patients
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193
Chapter 9
Lipids
AnjaliManavalan
Introduction
Hyperlipidemia encompasses a group of conditions characterized by an increase in serum total or low-density lipoprotein (LDL) cholesterol or triglycerides (TGL). When this
occurs due to genetic defects in lipid metabolism, it is called
primary hyperlipidemia [1]. However, it may also occur secondary to other diseases—such as diabetes mellitus, HIV,
nephrotic syndrome, hypothyroidism, obesity, and other
endocrine disorders, or due to lifestyle factors such as smoking, alcohol use, and inactivity. Hyperlipidemia is a wellstudied and important risk factor for atherosclerotic
cardiovascular disease (ASCVD) [2], which is the leading
cause of death not only in the United States but also
worldwide [3]. Screening and treating hyperlipidemia for primary and secondary prevention of cardiovascular disease are
extremely important in primary care practice.
A. Manavalan (*)
Department of Endocrinology, Jacobi Medical Center,
Bronx, NY, USA
e-mail: manavala@nychhc.org
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2022
E. Sydney et al. (eds.), Handbook of Outpatient Medicine,
https://doi.org/10.1007/978-3-031-15353-2_9
195
196
A. Manavalan
Key History andPhysical
History
Lipid disorders are usually asymptomatic. The history is
focused on the patient’s other medical conditions, family history, lifestyle, and risks of cardiovascular disease, all of which
can help inform treatment decisions.
Medical History
A review of the patient’s medical history is critical to identify
possible medical conditions or risk factors that could lead to
hyperlipidemia and to estimate the risk for ASCVD.Personal
histories of hypertension, diabetes, obesity, cardiovascular
disease (CVD), or peripheral vascular disease (PVD) are risk
factors that warrant further screening for lipid disorders,
according to the USPSTF guidelines (see Decision-Making
session for further details).
Family History
A complete family history of chronic metabolic diseases
including diabetes, lipid disorders, and cardiovascular disease
should be obtained. Early-onset cardiovascular disease in
first-degree family members is an important risk factor for
ASCVD and should also be ascertained.
Social History
A complete history of the patient’s dietary habits, physical
activities, and alcohol and tobacco use should be evaluated.
They are parameters to evaluate a patient’s risk of lipid disorders, metabolic syndrome, and cardiovascular events. In
Chapter 9. Lipids
addition, these factors are also significant points of possible
intervention after establishing the clinical diagnosis of hyperlipidemia (see Treatment Strategies session for details).
197
Physical Exam
In most patients there is no specific physical exam for lipid
disorder. Xanthomas are circumscribed plaque or nodule-like
lesions in the skin, tendons, or fasciae and could be seen occasionally in patients with primary or secondary hyperlipidemia. They are derived from macrophages containing a high
amount of LDL particles [4]. Xanthelasma are soft, yellow
plaques that are usually symmetric and occur on the medial
aspect of the eyelids. These are also associated with disorders
of LDL metabolism. On the other hand, physical exam might
reveal signs of atherosclerotic vascular diseases, such as
carotid bruits, cardiac murmurs due to aortic valve atherosclerosis, renal artery bruits due to atherosclerotic stenosis,
and signs of peripheral vascular disease (e.g., diminished
pulses; cold, dry, and shiny skin; ulceration or gangrene; etc.).
In addition, the presence of obesity or acanthosis nigricans
should prompt further evaluation for dyslipidemia.
Decision-Making/Differential Diagnosis
Screening Population
The US Preventive Services Task Force (USPSTF) strongly
recommends screening for lipid disorders in men ≥35years of
age and women ≥45years of age (Grade A recommendation).
The screening is also recommended in men of age 20–35 and
women of age 20–45, with increased risks for cardiovascular
disease (Grade B recommendation). The risk factors for
CVD include hypertension, diabetes, obesity (BMI ≥ 30),
tobacco use, family history of early-onset CVD (onset before