Primary Care of the Maturing and Aged Family Practicum NR601

INFJayne Nurse 💜

NR601 PHASE 2 MASTER VOLUME
Ultra-Detailed Textbook-Level Board Review
Weeks 5–8
WEEK 5 — ENDOCRINE DISORDERS

Hypothyroidism — Advanced Pathophysiology & Management

Hypothyroidism results from deficient thyroid hormone production and is most
commonly caused by autoimmune destruction (Hashimoto thyroiditis) in iodine-sufficient
regions. Pathophysiologically, thyroid hormone deficiency reduces basal metabolic rate,
decreases cardiac output, slows gastrointestinal motility, and impairs neurologic
processing. Clinical manifestations include fatigue, weight gain, constipation,
menorrhagia, bradycardia, depression, coarse skin, alopecia, and delayed deep tendon
reflex relaxation. Severe untreated disease may progress to myxedema coma,
characterized by hypothermia, hypoventilation, hypotension, and altered mental status.

Diagnostic evaluation begins with serum TSH. Elevated TSH with low free T4 confirms
primary hypothyroidism. Elevated TSH with normal free T4 indicates subclinical disease.
Low free T4 with inappropriately normal or low TSH suggests central hypothyroidism
requiring pituitary imaging prior to hormone replacement.

Levothyroxine is a first-line therapy. Full replacement dosing approximately 1.6
mcg/kg/day for healthy adults. Elderly patients or those with coronary artery disease
should begin at 12.5–25 mcg daily and titrate every 6–8 weeks. TSH should be reassessed
after dose changes. Patients must take levothyroxine on an empty stomach and separate
from calcium, iron, and certain medications.

Most common causes (big picture)

 Autoimmune thyroiditis (Hashimoto’s) is the classic/most common cause in
iodine-sufficient settings. Your textbook notes that once hypothyroidism is
confirmed, the cause is often established by checking TPO and Tg antibodies,
which are present in >95% of patients with autoimmune hypothyroidism.
 Other common causes to keep on your radar (testable): thyroid ablation/surgery,
thyroiditis, medications (amiodarone, lithium), iodine deficiency/excess, and
central (pituitary/hypothalamic) disease.

,What labs/tests to order + how to interpret

Step 1: TSH (best screen for primary hypothyroidism).

 A normal TSH essentially excludes primary hypothyroidism (but not
secondary/central).

Step 2: Free T4 if TSH is abnormal.

 If TSH is elevated, order FT4 to confirm clinical (overt) hypothyroidism.
 T4 alone is not a great screening test because it can miss subclinical
hypothyroidism.
 T3 levels are not helpful (often normal), so T3 measurement is generally not
indicated.

Step 3: Autoimmune confirmation (etiology): Check TPOAb/TgAb: present in >95%
with autoimmune hypothyroidism. Treatment (age-based “test-taking”
approach)

 Levothyroxine (LT4) is standard.
 Younger/healthy adults: closer to “full replacement” dosing is typically
appropriate.
 Older adults and/or CAD risk: “start low and go slow” to avoid precipitating
angina/arrhythmias; titrate based on TSH re-checks (often every ~6–8 weeks after
changes in real-world practice).

42F, fatigue/weight gain/cold intolerance/constipation, delayed reflex relaxation;
TSH high, FT4 low → Primary hypothyroidism most consistent with autoimmune
destruction (Hashimoto’s). This fits the “overt hypothyroid pattern” (↑TSH + ↓FT4)
and autoimmune is the most likely underlying cause (supported by the high prevalence of
thyroid antibodies in autoimmune hypothyroidism).

Why the others are wrong (quick):

 Iodine excess can cause hypothyroidism, but the vignette is more classic for
Hashimoto’s (esp. when antibodies are involved in other questions).
 Pituitary adenoma (TSH-secreting) would usually give high/normal TSH with
high T4/T3 (hyperthyroid picture).
 Thyroid hormone resistance typically has high T4/T3 with non-suppressed
TSH, not low FT4.

Practice question (diagnosis)

, TSH 8.9 (elevated), “T4 0.7” (low), TPO antibodies positive, diffuse nontender goiter
→ Hashimoto’s thyroiditis. Antibody-based confirmation is exactly what your text
emphasizes.

Why the others are wrong:

 Subclinical hypothyroidism = elevated TSH with normal FT4 (not low FT4).
 Graves’ usually has low TSH and high FT4/T3.
 Central hypothyroidism typically has low/normal TSH with low FT4 (TSH
wouldn’t be elevated like this).



Hyperthyroidism & Thyrotoxicosis
Hyperthyroidism is characterized by excessive thyroid hormone production. Graves
disease is mediated by TSH receptor antibodies causing diffuse gland stimulation.
Clinical features include weight loss, tremor, heat intolerance, atrial fibrillation, anxiety,
diarrhea, and goiter. Ophthalmopathy may occur in Graves' disease. Suppressed TSH
with elevated free T4/T3 confirms diagnosis.

Management includes beta-blockers for symptomatic relief and methimazole for hormone
suppression. PTU is preferred during first trimester pregnancy. Patients must be
counseled regarding agranulocytosis symptoms such as fever or sore throat. Definitive
therapy includes radioactive iodine ablation or thyroidectomy when indicated.

Start with TSH, then free T4 (and often total/free T3 if needed):

 Overt hyperthyroidism: low/suppressed TSH + high FT4 and/or T3
 Subclinical hyperthyroidism: low TSH + normal FT4/T3

Then determine etiology (high-yield):

 TSI/TRAb (supports Graves)
 Radioactive iodine uptake (RAIU) / scan (when appropriate)
o High uptake → Graves/toxic nodular disease
o Low uptake → thyroiditis, exogenous thyroid hormone, iodine load

Treatment (high yield)

 Symptom control: beta blockers (propranolol or atenolol) help adrenergic
symptoms, especially early before antithyroid meds take effect.