DE LEON, KEO DOMINIQUE C.

APRIL 23,
2020

1. What is your primary working impression? Give your complete diagnosis. What are the salient
features of this patient that lead your diagnosis? Briefly explain your answer.

● Primary Working Impression: Primary Hyperthyroidism probably secondary to Graves’

Disease

● Salient Features: Patient has history of palpitations, easy fatigability, shortness of breath, heat
intolerance, irritability, excessive perspiration, progressive weight loss of 15% in 6 months
despite good appetite, difficulty falling asleep at night, recurrent attacks of nervousness, and
occasional bouts of throbbing bifrontal headache which common seen in patients with
hyperthyroidism.

● Physical findings of hyperthyroidism was also seen in the patient like diffusely enlarged anterior
neck mass that moves with deglutition, faint bruit at the anterior neck, exophthalmos, warm and
diaphoretic hands with onycholysis in the digits of the hands.

2. Concisely discuss the Wayne’s index for thyroid pathology and the Burch- Wartofsky scoring
system, in the context of this patient. What will be the Wayne’s and Burch-Wartofsky scores of the
patient? What is the clinical relevance of these scoring systems in an out-patient setting with
possible limited resources?

● Wayne’s index for thyroid pathology diagnostic index that scores the presence or absence of
various signs and symptoms of hyperthyroidism for the purpose of establishing a diagnosis of
thyrotoxicosis. Upon assessment of the patients signs and symptoms had a score of 39 which is
interpreted as toxic hyperthyroidism. A Wayne’s score of >19 implies toxic hyperthyroidism,
while a score less than 11 implies euthyroidism, a score between 11 and 19 is equivocal.

● Burch-Wartofsky-Score is a point scale used to identify the risk or probability of thyrotoxicosis

based solely on clinical and physical criteria. Patients having a score of score of ≥45 are
cosniderd to have thyroid storm, while a score 25–44 means that patient has an impending
thyroid storm and a score <25 implies that a thyroid storm unlikely to happen.

● These clinical scoring systems helps physician in an out-patient setting with limited resources in
terms of appropriately managing patients. They are able to refer patients to a bigger hospitals
especially in emergencies cases.

3. Considering the financial capacity of the patient and her family, what other cost- effective diagnostic
tests will you recommend for her in a community setting, such as Taytay, Rizal? Give the rationale
for requesting such ancillary test / procedure.
● Serum TSH because it is the best screening test for Hyperthyroidism and Serum Free T3 and T4
if thyrotoxicosis is highly suspected
● Complete Blood Count to rule out anemia and possible infection
 ● Serum electrolytes (Na, K) to rule out metabolic cause of palpitations, fatigue, weakness
● Baseline 12-lead ECG to rule out cardiac problem

4. Review the resting 12-lead electrocardiogram (ECG) of the patient. What is the main abnormality
noted, specifically in long lead 2 of the ECG tracing? Give your complete interpretation of the
tracing.

 Rate and rhythm: 150 bpm, tachycardic, irregularly irregular rhythm

 Axis: normal axis
 Hypertrophy: No hypertrophy
 Ischemia and infarction: no ischemia or infarction
 Miscellaneous: Atrial fibrillation, rapid ventricular response, no bundle branch block
5. If the consultation occurred at the Bro. Francisco Perez Clinic, what will be the final disposition the
patient? Will you manage the patient on an out-patient basis (i.e., on oral home medications) or
will you refer the patient to the nearest hospital for admission? Justify your answer.
● I will refer to a hospital for a possible admission because patient has manifestation of
thyrotoxicosis which is maybe life threatening. She will need close monitoring, additional
laboratory test and treatment with an antithyroid medication, or thyroidectomy.

6. Explain the clinical relevance of the different thyroid hormones, specifically thyroid stimulating
hormone (TSH), triiodothyronine (T3), thyroxine (T4), and the unbound forms of T3 and T4 (i.e.,
FT3 and FT4). Among these hormones, what ought to be monitored on a regular basis in patients
with thyroid abnormalities, and what is the frequency of monitoring?
TSH is the most useful physiologic marker of thyroid hormone action because TSH levels change
in response to alterations of T4 and T3. It has the highest sensitivity and specificity of any single
blood test used in the evaluation of suspected hyperthyroidism and should be used as an initial
screening test. Its diagnostic accuracy improves when free T4 is also asses at the time of
evaluation. Appropriate monitoring intervals are every 4–8 weeks until euthyroid levels are
achieved with the minimal dose of medication. Once the patient is euthyroid, biochemical testing
and clinical evaluation can be undertaken at intervals of 2–3 months.
● High values of T4 may indicate hyperthyroidism. T4 should be monitored after 4 weeks after
initiation of therapy for possible dose adjustment of medication.
● T3 is usually ordered if T4 tests and TSH tests suggest hyperthyroidism or if there are signs of
an overactive thyroid gland and T4 and TSH aren’t elevated
● High levels of free thyroid hormones (FT3 FT4) in the blood may be a sign of an overactive
thyroid, and low levels could be a sign of an underactive thyroid. For most purposes, the
unbound T4 level is sufficient to confirm thyrotoxicosis. Unbound T3 levels should be
measured in patients with a suppressed TSH but normal unbound T4 levels.
7. What maintenance medications will you prescribe to address all problems of the patient, given the
limited information that you have? Give the generic name/s, dose/s, and dosing regimen/s. What is
the mechanism/s of action of the prescribed medication/s?

● Based on the guidelines, methimazole is the 1 st line of treatment in antithyroid drug therapy,
except during the first trimester of pregnancy then propylthiouracil is preferred, in the treatment
of thyroid storm. Patient will be prescribed with Methimazole 10mg TID which Inhibits
synthesis of thyroid hormone by blocking oxidation of iodine in thyroid gland; blocks synthesis
of thyroxine (T4) and triiodothyronine (T3). For adrenergic symptoms of the patient she will be
prescribed with Metoprolol 50mg OD which Blocks response to beta-adrenergic stimulation;
cardioselective for beta1 receptors at low doses, with little or no effect on beta2 receptors.

8. The patient is also inquiring why there are changes in her finger nails. What do you call this
medical condition, and what is the pathophysiologic mechanism for this? What is the
recommended management for this condition?

● Patient has onycholysis which seen as spontaneous separation of the nail plate starting at the
distal free margin and progressing proximally. This separation is characteristically concave, and
the hyponychium commonly traps dirt, giving the nail a dark appearance.

● Since patient’s onycholysis is possibly caused by hyperthyroidism addressing this will also treat
the infection. She should also be given a topical antifungal imidazole or allylamine twice daily
to avoid superinfection of the nail. Patient will be advised to avoid trauma to the affected nails
and keep them dry. She should also stay away from irritants and always cut the nails short.

9. Give your clinical impression for the CBC result, with the background of possible thyrotoxicosis.
Briefly explain the main pathology and the possible cause of this abnormal condition.

 Clinical Impression: Agranulocytosis secondary to Propylthiouracil Intake

 Agranulocytosis may occur as an adverse effect of the use of PTU. When PTU is oxidized to
reactive metabolites by neutrophils, it indcues an immune response by activating
inflammasomes, which destroys neutrophils which results to low WBC count..

10. If and when the patient becomes biochemically euthyroid, what other treatment modalities (i.e.,
medical and surgical) will you recommend for this patient? Concisely discuss each treatment option,
highlighting their advantages and disadvantages.

TREATMENT ADVANTAGES DISADVANTAGES

MODALITIES
 Medical (Anti-thyroid  The avoidance of surgery,  May cause hepatotoxicity
drugs) and exposure to and agranulocytosis
radioactivity  High risk of recurrence
 Outpatient therapy  Frequent testing necessary

Surgery (Subtotal or Near  Definitive control of  Risks of damage to

Total Thyroidectomy) hyperthyroidism laryngeal nerve,
 No exposure to hypoparathyroidism,
radioactivity bleeding, infection,
 No potential side effects unsatisfactory cosmetic
of ATDs result
 Most effective in case of
pressure symptoms

Radioactive Iodine  Definitive control of  Risk of hypothyroidism

hyperthyroidism
 Side effect: Generally
mild, rare, transient
 May worsen
ophthalmopathy
 Hyperthyroidism can
persist for 2-3 months
before RAI takes effect
 Potential radiation hazard

11. What non-pharmacologic advice will you give to the patient who will undergo radioactive iodine
(RAI) therapy, with regard to exposure to radiation of other family members, especially pediatric
patients? What special preparations and precautionary measures must be addressed before and
while on RAI therapy? How is RAI administered, and how long will the duration of treatment
last?

● Patient must be placed on NPO after midnight on the day of procedure. She should also stop
taking her anti-thyroid medications at least 3 days before the RAI is administered. If the patient
stills present with signs of thyrotoxicosis she should be treated first with a beta-adrenergic
blockade (ie, atenolol or propanolol) or Methimazole prior to RAI therapy. Her diet should be
monitored food containg excess amounts of iodine should be avoided for ateast 7 days.

● Patient will be informed of the possible side effects of the therapy like nausea, vomiting,
swelling and tenderness of salivary glands, dry mouth, dry eyes, and taste changes, swelling and
neck tenderness so she can be prepared mentally.
 ● After the therapy, she should avoid sharing of clothes, linens and utensils for 2-3 days in order
not to exposed members of her family to radiation. She must distance herself from her kids and
sleep in another room if possible for 3-4 days. Her clothes and linen should be washed daily,
separately.

● RAI is administered orally as sodium iodide (131-I) in solution or capsule which is rapidly
incorporated into the thyroid and its beta emission results in extensive local tissue damage. TSH
levels should be monitored for 6-18 weeks to see the net effect is ablation. If the patient remains
thyrotoxic, biochemical montioring should be continued at 4-6wks interval. It can be done on an
outpatient basis provided that the patient will be compliant with the instructions.

12. What is the difference between primary hypothyroidism and secondary hypothyrodism? Briefly
explain.
● Primary hypothyroidism is due to disease in the thyroid that can causes injury to the thyroid. The
most common cause is autoimmune referred to as Hashimoto thyroiditis and is often associated
with a firm goiter or, later in the disease process, with a shrunken fibrotic thyroid with little or
no function. The 2nd most common cause is post-therapeutic hypothyroidism, especially after
radioactive iodine therapy or surgery for hyperthyroidism or goiter. Overt primary
hypothyroidism is indicated with an elevated serum TSH level and a low serum free T4 level.
On the contrary, secondary hypothyroidism occurs when the hypothalamus produces insufficient
thyrotropin-releasing hormone (TRH) or the pituitary produces insufficient TSH. Sometimes,
deficient TSH secretion due to deficient TRH secretion is termed tertiary hypothyroidism. In
patients with central hypothyroidism, the serum free T4 value is low-normal to low and serum
TSH may be frankly low, inappropriately normal (for the low T4), or slightly high (7 to 15
mU/L) due to secretion of biologically inactive TSH.

13. What medication will you recommend for this patient? Give the generic name, the dose, and dosing
regimen. Concisely discuss its pharmacokinetics and pharmacodynamics, including its potential
adverse effects.
● The patient should be prescribed levothyroxine with an initial dose of 1.6mcg/kg based on actual
body weight of the patient. Adjust dose by 12.5 to 25 mcg until TSH goal of lower half of
normal range is achieved (N: 0.4 – 4 mIU/L).

Levothyroxine

Mechanism of Action Levothyroxine is a synthetically prepared levo-isomer of the thyroid

hormone thyroxine that acts as a replacement in deficiency
syndromes such as hypothyroidism. It is chemically identical to the
 naturally secreted T4 that increases metabolic rate, decreases
thyroid-stimulating hormone (TSH) production from the anterior
lobe of the pituitary gland, and, in peripheral tissues, is converted to
T3.

Pharmacokinetics

Absorption Absorption of orally administered T4 from the gastrointestinal tract

ranges from 40% to 80%. The majority of the levothyroxine dose is
absorbed from the jejunum and upper ileum.

Distribution There is a higher affinity of both TBG and TBPA for T4 partially
explains the higher serum levels, slower metabolic clearance, and
longer half-life of T4 compared to T3.

Metabolism The liver is the major site of degradation for both T4 and T3, with
T4 deiodination also occurring at a number of additional sites,
including the kidney and other tissues.

Excretion Thyroid hormones are primarily eliminated by the kidneys. A

portion of the conjugated hormone reaches the colon unchanged and
is eliminated in the feces. Approximately 20% of T4 is eliminated in
the stool. Urinary excretion of T4 decreases with age.

Pharmacodynamics

Adverse Effects Headache, sleep problems (insomnia), nervousness, irritability,

fever, hot flashes, sweating, palpitations, changes in your menstrual
periods, or appetite or weight changes