One-liner#

Hypothyroidism management centers on levothyroxine replacement dosed at ~1.6 mcg/kg/day, titrated every 6-8 weeks to TSH goal (0.5-2.5 mIU/L for most adults), with special attention to starting low in elderly/cardiac patients and increasing requirements in pregnancy.

Quick nav#

• Definition and epidemiology
• Pathophysiology
• Clinical presentation
• Diagnostic workup
• Treatment
• Patient education
• Prognosis and monitoring
• Special populations
• When to refer
• Smartphrase snippets
• Related pages

Definition and epidemiology#

Diagnostic criteria#

Primary hypothyroidism classification:

Confirmation: Repeat TSH in 6-8 weeks if subclinical (TSH 4.5-10) to confirm persistence before treating. Overt hypothyroidism (elevated TSH + low free T4) can be treated after single measurement.

Hashimoto’s confirmation: TPO antibodies positive in >90% of autoimmune thyroiditis. Useful for predicting progression of subclinical hypothyroidism but not required if already planning to treat.

Epidemiology#

Prevalence is 4-5% of US adults (overt + subclinical combined); overt hypothyroidism affects ~0.5-2%. Female:male ratio is 5-8:1. Incidence increases with age—up to 10% of women >60 have subclinical hypothyroidism. Hashimoto’s thyroiditis is the most common cause in iodine-sufficient areas. Risk factors include female sex, age >60, family history of thyroid or autoimmune disease, other autoimmune conditions (type 1 DM, celiac, vitiligo, pernicious anemia), prior thyroid surgery or RAI, head/neck radiation, and medications (lithium, amiodarone, checkpoint inhibitors).

Pathophysiology#

Mechanism (clinical understanding)#

Hypothyroidism results from inadequate thyroid hormone production, most commonly due to autoimmune destruction of the thyroid gland (Hashimoto’s thyroiditis) or iatrogenic causes (surgery, radioactive iodine ablation).

Hashimoto’s thyroiditis (autoimmune): Anti-TPO and anti-thyroglobulin antibodies trigger lymphocytic infiltration and progressive destruction of thyroid follicular cells. Initially, the gland may enlarge (goiter) as it attempts to compensate; over time, it becomes fibrotic and atrophic. This explains why some patients present with goiter while others have a small, impalpable thyroid.

Post-ablative hypothyroidism: Following RAI therapy for Graves’ disease or thyroid cancer, or after thyroidectomy, the remaining thyroid tissue is insufficient for hormone production. These patients require lifelong replacement and typically need full replacement doses from the start.

Drug-induced hypothyroidism: Amiodarone (contains iodine; can cause hypo- or hyperthyroidism), lithium (inhibits thyroid hormone release), and checkpoint inhibitors (immune-mediated thyroiditis) are common culprits. Drug-induced hypothyroidism may be reversible if the offending agent is stopped.

Central hypothyroidism: Pituitary or hypothalamic disease causes inadequate TSH secretion. TSH may be low, normal, or slightly elevated (biologically inactive TSH). Free T4 is low. This is rare (<1% of hypothyroidism) but important to recognize because TSH cannot be used for monitoring, and concurrent adrenal insufficiency must be ruled out before starting levothyroxine.

Why symptoms occur: Thyroid hormone regulates metabolic rate in virtually every tissue. Deficiency causes slowed metabolism: decreased thermogenesis (cold intolerance), decreased GI motility (constipation), decreased cardiac output (bradycardia), and accumulation of glycosaminoglycans in tissues (myxedema, hoarseness, carpal tunnel).

How to explain to patients#

Your thyroid is a small gland in your neck that acts like your body’s thermostat—it controls how fast your body runs. When your thyroid is underactive, everything slows down.

Think of it like a car engine running too slow. Your body makes less heat (so you feel cold), your digestion slows down (causing constipation), your heart beats slower, and you feel tired because your cells are not getting enough energy.

In most cases, your immune system has mistakenly attacked your thyroid gland over time, damaging it so it cannot make enough hormone. The good news is we can replace the missing hormone with a pill you take once a day. Once we find the right dose, most people feel much better and can live completely normal lives.

Clinical presentation#

Characteristic symptoms#

Classic hypothyroid symptoms (the “slowing down”):

• Fatigue, low energy, feeling sluggish
• Weight gain (usually modest, 5-10 lbs—due to fluid retention and decreased metabolism)
• Cold intolerance (decreased thermogenesis)
• Constipation (decreased GI motility)
• Dry skin, brittle nails
• Hair loss, thinning hair (especially lateral eyebrows)
• Muscle aches, cramps, weakness
• Joint stiffness

Cognitive and mood symptoms:

• Depression, low mood
• Difficulty concentrating, “brain fog”
• Memory problems
• Slowed thinking and speech

Cardiovascular:

• Bradycardia (typically HR 50-60)
• Diastolic hypertension (increased peripheral resistance)
• Dyspnea on exertion
• Pericardial effusion (severe cases)

Reproductive:

• Menorrhagia or oligomenorrhea
• Infertility, recurrent miscarriage
• Decreased libido
• Erectile dysfunction

Other:

• Hoarseness (vocal cord edema)
• Hearing loss
• Carpal tunnel syndrome (myxedematous infiltration)
• Sleep apnea

Symptom onset: Usually gradual over months to years. Patients often attribute symptoms to aging, stress, or depression. Acute onset suggests subacute thyroiditis (hypothyroid phase) or postpartum thyroiditis.

Physical exam findings#

Vital signs:

• Bradycardia (HR 50-60; <50 in severe cases)
• Diastolic hypertension with narrowed pulse pressure
• Hypothermia (severe cases only)

General appearance:

• Dull, puffy facies
• Periorbital edema
• Slow movements and speech
• Hoarse voice

Skin, hair, nails:

• Dry, coarse, cool skin
• Non-pitting edema (myxedema)—hands, face, pretibial
• Coarse, brittle hair
• Lateral eyebrow thinning (Queen Anne sign)—present in ~30%
• Yellowish skin tint (carotenemia from impaired conversion)
• Brittle, ridged nails

Thyroid exam:

• Hashimoto’s: firm, rubbery, “pebbly” texture; may be enlarged (goiter) or atrophic
• Post-ablative: small or absent; surgical scar may be visible
• Note any nodules (require separate evaluation)

Neurologic:

• Delayed relaxation phase of deep tendon reflexes (“hung-up” reflexes)—classic finding
• Carpal tunnel signs (Tinel’s, Phalen’s)
• Proximal muscle weakness
• Cerebellar ataxia (severe cases)

Cardiovascular:

• Bradycardia
• Distant heart sounds (if pericardial effusion)
• Peripheral edema

Red flags#

Myxedema coma (medical emergency):

• Altered mental status + hypothermia + bradycardia + hypotension
• Precipitants: infection, cold exposure, sedatives, surgery, medication non-adherence
• Mortality 20-40% even with treatment
• Action: Call 911; do not attempt outpatient management

Severe symptomatic bradycardia:

• HR <40 with syncope, presyncope, or hypotension
• Action: ED evaluation

Concurrent adrenal insufficiency:

• Hypotension, hyponatremia, hypoglycemia
• Can be unmasked by starting levothyroxine (increases cortisol clearance)
• Action: Check cortisol before starting levothyroxine if suspected

Severe hyponatremia:

• Na <125 or symptomatic (confusion, seizures)
• Action: ED evaluation

Diagnostic workup#

Initial evaluation#

For suspected hypothyroidism:

TSH interpretation:

• TSH 4.5-10 mIU/L with normal free T4: subclinical hypothyroidism—repeat in 6-8 weeks to confirm before treating
• TSH >10 mIU/L with normal free T4: subclinical but high progression risk—treat
• TSH elevated with low free T4: overt hypothyroidism—treat
• TSH low/normal with low free T4: central hypothyroidism—refer to endocrinology

Additional initial labs:

Confirmatory testing#

When to check TPO antibodies:

• Subclinical hypothyroidism (helps decide whether to treat)
• Uncertain etiology
• Family history of autoimmune thyroid disease
• NOT needed if already planning to treat overt hypothyroidism

TPO antibody interpretation:

• Positive (>35 IU/mL): confirms autoimmune thyroiditis; higher progression risk
• Negative: does not rule out Hashimoto’s (10% are seronegative); consider other causes

When to suspect central hypothyroidism:

• Low or inappropriately normal TSH with low free T4
• Other pituitary hormone deficiencies (hypogonadism, adrenal insufficiency, growth hormone deficiency)
• History of pituitary surgery, radiation, tumor, or head trauma
• Headaches, visual field defects

If central hypothyroidism suspected:

• Check morning cortisol BEFORE starting levothyroxine (can precipitate adrenal crisis)
• Order pituitary hormone panel (LH, FSH, prolactin, IGF-1, morning cortisol, ACTH)
• MRI pituitary with contrast
• Refer to endocrinology

When to refer for specialist workup#

• Suspected central hypothyroidism (low/normal TSH with low free T4)
• Concurrent adrenal insufficiency suspected
• Thyroid nodule requiring evaluation
• Pregnancy (co-management with OB/endocrinology)
• Persistent symptoms despite normal TSH on adequate levothyroxine dose
• Difficulty achieving stable TSH (wide fluctuations)
• Patient requesting T3 or combination therapy

What NOT to order#

• Free T3: Not useful for diagnosis or monitoring of hypothyroidism; T4 is converted to T3 peripherally; T3 levels do not guide treatment
• Reverse T3: No clinical utility; often ordered inappropriately; does not guide treatment
• Thyroid ultrasound: Only if nodule palpated or goiter is asymmetric; not needed for routine hypothyroidism
• Thyroglobulin: Only for thyroid cancer monitoring; not useful for hypothyroidism
• Repeat TSH within 6 weeks of dose change: TSH takes 6-8 weeks to equilibrate; earlier testing is misleading
• TPO antibodies if already treating: Does not change management once treatment initiated

Biotin interference warning: Biotin supplements (common in hair/nail vitamins) can cause falsely low TSH and falsely low free T4 on some assays. Ask about supplements; hold biotin for 2-3 days before thyroid labs.

Treatment#

Goals of therapy#

TSH targets:

• Most adults: 0.5-2.5 mIU/L (lower half of normal range)
• Elderly (>70 years): 1-5 mIU/L acceptable (avoid overtreatment; higher TSH may be physiologically normal)
• Pregnancy: trimester-specific (1st: <2.5; 2nd: <3.0; 3rd: <3.5 mIU/L)
• Thyroid cancer survivors: per oncology (often suppressed to <0.5)

Symptom resolution:

• Most symptoms improve within 4-8 weeks of achieving euthyroid state
• Full resolution may take 3-6 months
• Some symptoms (hair loss, skin changes) may take longer

Secondary goals:

• Normalize lipids (LDL typically decreases 10-20% with treatment)
• Resolve anemia if present
• Restore normal menstrual cycles

Non-pharmacologic management#

Medication administration optimization:

• Take levothyroxine on empty stomach, 30-60 minutes before breakfast
• Alternative: bedtime dosing, 3+ hours after last meal (equally effective)
• Consistency is more important than timing—same time, same way daily
• Separate from interfering substances by 4 hours: calcium, iron, PPIs, antacids, sucralfate, bile acid sequestrants, coffee

Lifestyle factors:

• No specific diet required for hypothyroidism
• Avoid excessive iodine supplementation (can worsen autoimmune thyroiditis)
• Soy and high-fiber foods may slightly decrease levothyroxine absorption—take medication separately
• Maintain consistent dietary habits (major changes can affect absorption)

Weight management:

• Hypothyroidism causes modest weight gain (5-10 lbs), mostly fluid
• Achieving euthyroid state helps but is not a weight loss solution
• If significant weight gain, evaluate for other causes (diet, activity, other conditions)

Pharmacologic management#

Levothyroxine (T4) - First-line therapy:

Dosing by clinical scenario:

• Young healthy adult, new diagnosis: 50-100 mcg daily (or calculate 1.6 mcg/kg)
• Elderly (>65) or cardiac disease: 12.5-25 mcg daily, increase q4-6 weeks
• Post-thyroidectomy: full replacement from start (1.6 mcg/kg)
• Subclinical hypothyroidism: 25-50 mcg daily
• Pregnancy: increase pre-pregnancy dose by ~30% immediately upon confirmation

Dose adjustments:

• TSH above goal: increase by 12.5-25 mcg
• TSH below goal (overtreatment): decrease by 12.5-25 mcg
• Recheck TSH 6-8 weeks after any dose change

Brand vs generic:

• Generic levothyroxine is appropriate for most patients
• If switching brands or between brand and generic, recheck TSH in 6-8 weeks
• For patients with difficulty achieving stable TSH, consider consistent brand use
• Narrow therapeutic index—avoid frequent switching

What about T3 (liothyronine) or combination therapy?

PCP approach to T3 requests:

• First, optimize levothyroxine (adherence, administration, dose, stable TSH)
• If persistent symptoms despite normal TSH: evaluate for other causes (depression, sleep apnea, anemia, vitamin D deficiency, perimenopause)
• Randomized trials show no consistent benefit of T4/T3 combination over T4 alone
• If patient strongly prefers trial: refer to endocrinology
• Do NOT initiate liothyronine in primary care

Patient counseling points#

For levothyroxine initiation:

• “This medication replaces the thyroid hormone your body isn’t making enough of. You’ll likely need to take it for the rest of your life.”
• “Take it on an empty stomach, at least 30-60 minutes before eating. Many people take it first thing in the morning with water.”
• “Don’t take it at the same time as calcium, iron, or antacids—wait at least 4 hours.”
• “It takes 4-6 weeks to feel the full effect. Be patient—we’ll check your levels and adjust if needed.”
• “Don’t stop taking it even when you feel better. Your symptoms will come back.”

For dose adjustments:

• “Your thyroid level is [high/low], so we’re adjusting your dose. We’ll recheck in 6-8 weeks.”
• “Small dose changes can make a big difference. We adjust gradually to find your right dose.”

For persistent symptoms:

• “Your thyroid level is normal, which means the medication is working. Let’s look for other reasons you might still feel tired/[symptom].”
• “Many conditions can cause fatigue—depression, sleep problems, anemia, vitamin deficiencies. Let’s check for those.”

For overtreatment concerns:

• “Taking too much thyroid medication can cause heart racing, anxiety, tremor, and bone loss over time. That’s why we monitor your levels.”
• “If you feel jittery, have a racing heart, or can’t sleep, call us—your dose may be too high.”

Monitoring and follow-up#

Initial phase (first 6-12 months):

• TSH 6-8 weeks after starting or any dose change
• Continue adjusting until TSH at goal
• Typical time to stable dose: 3-6 months

Stable phase:

• TSH annually once stable
• Sooner if symptoms change, pregnancy, significant weight change, or new interacting medications

When to recheck TSH sooner:

• New symptoms of hypo- or hyperthyroidism
• Pregnancy (check immediately, then every 4 weeks in 1st trimester)
• Starting/stopping interacting medications (estrogen, PPIs, iron, calcium)
• Significant weight change (>10% body weight)
• Change in levothyroxine brand or formulation
• GI conditions affecting absorption (new celiac diagnosis, gastric bypass)

Lipid panel: Recheck 2-3 months after achieving euthyroid state; hyperlipidemia often improves.

Do NOT check:

• Free T3 for routine monitoring
• TSH more frequently than every 6 weeks (misleading results)

Patient education#

What is this condition?#

Your thyroid is a small gland in your neck shaped like a butterfly. It makes hormones that control how fast your body works—your metabolism. When your thyroid is underactive, it does not make enough hormone, and your body slows down.

This can make you feel tired, cold, and sluggish. You might gain a little weight, feel constipated, or notice your skin is dry. Your thinking might feel foggy, and you might feel down or depressed.

The most common cause is when your immune system slowly damages your thyroid over many years. This is called Hashimoto’s disease. It is not something you did wrong—it just happens, especially in women and as people get older.

What you can do#

Take your thyroid pill every day at the same time. Most people take it first thing in the morning on an empty stomach, then wait 30-60 minutes before eating. This helps your body absorb the medicine best.

Do not take your thyroid pill at the same time as calcium, iron vitamins, or antacids. These can block your body from absorbing the medicine. Wait at least 4 hours between them.

Keep all your appointments for blood tests. We need to check your thyroid level regularly to make sure your dose is right. It can take a few months to find the perfect dose for you.

Do not stop taking your medicine even when you feel better. Your thyroid cannot heal itself—you need the medicine to replace what it cannot make.

When to seek care#

Call your doctor if you have new or worsening symptoms like feeling very tired, gaining weight, feeling very cold, or feeling depressed. Your dose may need to be adjusted.

Call if you feel your heart racing, feel jittery or anxious, have trouble sleeping, or are losing weight without trying. These could mean your dose is too high.

Call if you become pregnant or are planning to become pregnant. Your dose will need to be increased right away.

Go to the emergency room if you become very confused, extremely cold, or very sleepy and hard to wake up. This is rare but serious.

Questions to ask your doctor#

• What is my TSH level, and what should it be?
• What dose of levothyroxine am I taking?
• When should I get my next blood test?
• Are any of my other medications affecting my thyroid medicine?
• Should I take brand-name or generic?
• What should I do if I miss a dose?
• Will I need to take this medicine forever?

Prognosis and monitoring#

Expected course#

With treatment:

• Excellent prognosis with proper levothyroxine replacement
• Most symptoms improve within 4-8 weeks of achieving euthyroid state
• Full symptom resolution may take 3-6 months
• Hair regrowth and skin changes may take longer (6-12 months)
• Normal life expectancy with appropriate treatment

Without treatment:

• Progressive symptoms: worsening fatigue, cognitive decline, depression
• Cardiovascular complications: diastolic hypertension, accelerated atherosclerosis, pericardial effusion
• Metabolic complications: hyperlipidemia, weight gain, hyponatremia
• Severe untreated hypothyroidism: myxedema coma (rare but life-threatening)

Disease progression:

• Hashimoto’s: progressive thyroid destruction; most patients eventually need full replacement doses
• Subclinical hypothyroidism: 4-5%/year progress to overt if TPO positive; 2-3%/year if TPO negative
• Post-ablative: permanent; requires lifelong replacement

Monitoring parameters#

Complications to watch for#

Overtreatment (iatrogenic hyperthyroidism):

• Symptoms: palpitations, anxiety, tremor, insomnia, weight loss, heat intolerance
• Risks: atrial fibrillation (especially elderly), osteoporosis (especially postmenopausal women)
• Prevention: maintain TSH in target range; avoid suppressed TSH unless indicated (thyroid cancer)

Undertreatment:

• Persistent hypothyroid symptoms
• Hyperlipidemia not improving
• Cardiovascular risk

Myxedema coma:

• Rare but life-threatening
• Precipitants: infection, cold exposure, sedatives, surgery, non-adherence
• Recognition: altered mental status, hypothermia, bradycardia, hypotension
• Action: emergency—call 911

Medication interactions:

• New medications may require dose adjustment
• Estrogen (increases TBG, may need higher dose)
• Androgens (decrease TBG, may need lower dose)
• Antiepileptics (increase T4 metabolism)

Special populations#

Elderly/geriatric#

Presentation differences:

• Symptoms often subtle or attributed to aging (“apathetic hypothyroidism”)
• May present primarily with cognitive decline, depression, or falls
• Classic symptoms (cold intolerance, weight gain) may be less prominent

TSH targets:

• Age >70: TSH 1-5 mIU/L is acceptable; avoid overtreatment
• Higher TSH may be physiologically normal in elderly (TSH increases with age)
• Overtreatment risks: atrial fibrillation, osteoporosis, falls

Dosing:

• Start LOW: 12.5-25 mcg daily
• Increase SLOWLY: 12.5-25 mcg every 4-6 weeks
• Full replacement dose often lower than younger adults (1.0-1.2 mcg/kg vs 1.6 mcg/kg)

Cardiac considerations:

• Can precipitate angina, arrhythmia, or heart failure exacerbation
• Monitor for chest pain, palpitations, dyspnea with dose increases
• May need to accept higher TSH if cardiac symptoms limit titration
• Coordinate with cardiology if significant CAD

Beers criteria considerations:

• Levothyroxine itself is not on Beers list
• Avoid overtreatment (TSH <0.5) due to AF and osteoporosis risk
• Desiccated thyroid (Armour) should be avoided—unpredictable T3 content

Polypharmacy:

• Review all medications for interactions
• Common interactions: calcium, iron, PPIs, bile acid sequestrants
• Simplify timing if possible (levothyroxine at bedtime may improve adherence)

Chronic kidney disease#

Dosing:

• No dose adjustment required for levothyroxine in CKD
• Levothyroxine is not renally cleared

Lab interpretation:

• TSH remains reliable in CKD
• Free T4 may be affected by altered protein binding—interpret with caution
• Uremia can cause “sick euthyroid” pattern (low T3, normal/low T4, normal TSH)

Monitoring:

• Standard TSH monitoring applies
• More frequent monitoring if on dialysis (protein binding changes)

Drug interactions:

• Phosphate binders (sevelamer, lanthanum) can decrease levothyroxine absorption—separate by 4 hours
• Iron supplements (common in CKD) interfere—separate by 4 hours

Comorbidity considerations:

• Hypothyroidism can worsen CKD-related anemia
• Hypothyroidism can worsen CKD-related hyperlipidemia
• Treating hypothyroidism may improve both

Other populations#

Pregnancy:

• Thyroid hormone requirements increase 25-50% in pregnancy
• Increase levothyroxine dose by ~30% as soon as pregnancy confirmed (or add 2 extra doses per week)
• TSH targets: 1st trimester <2.5; 2nd trimester <3.0; 3rd trimester <3.5 mIU/L
• Check TSH every 4 weeks in 1st trimester, then every 4-6 weeks
• Untreated hypothyroidism increases risk of miscarriage, preterm birth, preeclampsia, impaired fetal neurodevelopment
• Postpartum: reduce to pre-pregnancy dose; recheck TSH at 6 weeks
• Refer to endocrinology or MFM for co-management

Subclinical hypothyroidism in pregnancy:

• TSH >4.0 with positive TPO antibodies: treat
• TSH >10: treat regardless of TPO status
• TSH 2.5-4.0 with positive TPO: consider treatment

Postpartum thyroiditis:

• Occurs in 5-10% of pregnancies
• Typically: hyperthyroid phase (2-6 months postpartum) → hypothyroid phase (4-8 months) → recovery
• Hypothyroid phase may require temporary levothyroxine
• Most recover normal thyroid function within 12-18 months
• 20-30% develop permanent hypothyroidism

Cardiac disease:

• Start very low: 12.5-25 mcg daily
• Increase very slowly: 12.5-25 mcg every 4-6 weeks
• Monitor closely for angina, arrhythmia, heart failure exacerbation
• May need to accept higher TSH (2-5 mIU/L) if cardiac symptoms limit titration
• Coordinate with cardiology

Adrenal insufficiency (concurrent):

• Must treat adrenal insufficiency BEFORE starting levothyroxine
• Levothyroxine increases cortisol clearance—can precipitate adrenal crisis
• If suspected: check morning cortisol before initiating levothyroxine
• If confirmed: start hydrocortisone first, then levothyroxine

Malabsorption syndromes:

• Celiac disease, gastric bypass, IBD can impair levothyroxine absorption
• May need higher doses
• Consider liquid levothyroxine or soft gel capsules (better absorption)
• Screen for celiac if difficulty achieving stable TSH

Drug interactions (polypharmacy):

• Estrogen (OCPs, HRT): increases TBG, may need higher levothyroxine dose
• Androgens: decrease TBG, may need lower dose
• Antiepileptics (phenytoin, carbamazepine, phenobarbital): increase T4 metabolism
• Rifampin: increases T4 metabolism
• Sertraline: may increase levothyroxine requirements
• Tyrosine kinase inhibitors: may increase requirements

When to refer#

Specialist referral criteria#

Endocrinology referral:

• Suspected central hypothyroidism (low/normal TSH with low free T4)
• Concurrent adrenal insufficiency suspected or confirmed
• Difficulty achieving stable TSH despite adherence and proper administration
• Persistent symptoms despite normal TSH on adequate levothyroxine
• Patient requesting T3 or combination therapy trial
• Thyroid nodule requiring evaluation
• Pregnancy (co-management with OB)
• Thyroid cancer history (ongoing management)

Cardiology referral:

• Significant CAD and need for levothyroxine initiation
• Cardiac symptoms (angina, arrhythmia) limiting dose titration
• New atrial fibrillation in setting of thyroid disease

OB/MFM referral:

• Pregnancy with hypothyroidism (co-management)
• Difficulty conceiving with thyroid disease
• History of recurrent miscarriage

Psychiatry referral:

• Persistent depression despite euthyroid state
• Significant cognitive symptoms not improving with treatment

Urgency levels#

Smartphrase snippets#

Hypothyroidism, stable on levothyroxine: Hypothyroidism on levothyroxine [X] mcg daily, TSH [X] at goal. No hypo- or hyperthyroid symptoms. Continue current dose; recheck TSH in 12 months.

Hypothyroidism, dose adjustment needed: Hypothyroidism on levothyroxine [X] mcg, TSH [X] above goal. Increasing to [X] mcg daily; recheck TSH in 6-8 weeks.

Hypothyroidism, new diagnosis: New primary hypothyroidism, TSH [X], free T4 [X]. Starting levothyroxine [X] mcg daily. Counseled on proper administration and lifelong therapy; recheck TSH in 6-8 weeks.

Subclinical hypothyroidism, observation: Subclinical hypothyroidism with TSH [X], normal free T4, asymptomatic. Plan to observe with repeat TSH in 6 months; advised to report hypothyroid symptoms.

Related pages#

• Hypothyroid Symptoms (complaint) — symptom-based approach to hypothyroid presentation and initial workup
• Hyperthyroid Symptoms (complaint) — opposite presentation; important to distinguish
• Fatigue (complaint) — hypothyroidism as cause of fatigue
• Weight Gain (complaint) — hypothyroidism in differential
• Depression (complaint) — can mimic or coexist with hypothyroidism
• Hyperlipidemia (problem) — hypothyroidism causes secondary hyperlipidemia; screen and treat
• Type 2 Diabetes (problem) — common comorbidity; shared cardiovascular risk factors
• Atrial Fibrillation (problem) — risk with overtreatment; monitor TSH