Signs and symptoms of hypothyroidism and hyperthyroidism

Hypothyroidism:

Thick, coarse, dry Hyporeflexia, "hung up" patella reflex Slow thought process, Weight gain (5-

10 lbs./2.25-4.5 kg) Constipation, Menorrhagia, Cold intolerance: Cold all the time

Hyperthyroidism (aka graves disease):

Smooth, silky Hyperreflexia, Mind racing, Weight loss (10 lbs./4.5 kg) Diarrhea, loose, frequent 

stools, Oligomenorrhea, Heat intolerance: Hot all the time

pg. 418-419

What adjunctive therapy is good to prescribe to control symptoms of hyperthyroidism other than 

thyroid specific medications?

Know drug classes and examples of those drug classes.

β-Blockers and nonradioactive iodine may be used as adjunctive therapy. β-Blockers suppress 

tachycardia by blocking β-receptors on the heart. Nonradioactive iodine inhibits synthesis and 

release of thyroid hormones.

pg. 419

Monitoring needs and intervals for thyroid medications.

levothyroxine-Monitoring: Check TSH 6-8 weeks after initiating therapy and after any dosage 

change. Check TSH at least once a year after serum TSH is stabilized.

Methimazole-Monitoring: Check CBC with differential if signs or symptoms of infection. Check 

LFTs if signs or symptoms of liver dysfunction.

Propylthiouracil (PTU)- Treatment continues for 1-2 years

PTU has caused rare cases of liver injury. Onset is sudden and progression is rapid.

-Propylthiouracil (PTU) carries a risk for liver toxicity. Although rare, the FDA recommends 

against using PTU as a first-line treatment due to potential for hepatic toxicity.

Treatment continues for 1-2 years

PTU has caused rare cases of liver injury. Onset is sudden and progression is rapid. pg 421

-Effects of maternal hypothyroidism on offspring and appropriate patient teaching related to need 

for treatment.

Maternal hypothyroidism can result in permanent neuropsychological deficits in the child.

can decrease IQ and other aspects of neuropsychological function in the child.

teaching:

to help ensure healthy fetal development, maternal hypothyroidism must be diagnosed and 

treated very early.

some authorities currently recommend routine screening for hypothyroidism as soon as 

pregnancy is confirmed. If hypothyroidism is diagnosed, replacement therapy should begin 

immediately.

the signs and symptoms of pregnancy mimics those of hypothyroidism

When women taking thyroid supplements become pregnant, dosage requirements usually 

increase—often by as much as 50%. The need for increased dosage begins between weeks 4 and 

8 of gestation, levels off at approximately week 16, and then remains steady until parturition.

pg. 418

- Patient teaching for thyroid medications.

:levothyroxine:

should be taken on an empty stomach in the morning, at least 30 to 60 minutes before breakfast.

Inform patients about the symptoms of thyrotoxicosis and instruct them to notify the prescriber if 

these develop (Sweating, irritability, weight loss, tachycardia)Instruct patients to separate 

administration of levothyroxine and these drugs by 4 hours

Overdose may cause thyrotoxicosis. Symptoms include tachycardia, angina, tremor, nervousness, 

insomnia, sweating, and heat intolerance.

methamizole:

Agranulocytosis: Inform patients about early signs of agranulocytosis, including fever or sore 

throat. If follow-up blood tests reveal leukopenia, methimazole should be stopped.

Hypothyroidism: Methimazole may cause excessive reductions in thyroid hormone synthesis. If 

signs of hypothyroidism develop or if plasma levels of T3 and T4 become subnormal, dosage 

should be reduced.

Radioactive Iodine:

Inform patients about symptoms of iodism, including brassy taste, burning sensations in the 

mouth, and soreness of gums and teeth. Iodine can also cause corrosive injury to the GI tract. 

Instruct patients to notify the prescriber if severe abdominal distress develops.

PTU:

can cause rare cases of liver injury

What drug class can interfere with the assessment and monitoring of diabetes and why?

o You will need connect pathophysiology information of medications and diabetes together. 

Think about alpha and beta cells.

Hypoglycemic agents.

Drugs that lower blood glucose levels can intensify hypoglycemia induced by insulin. Among 

these drugs are sulfonylureas, glinides, and alcohol (used acutely or long term in excessive 

doses). When these drugs are combined with insulin, special care must be taken to ensure as best 

as possible that blood glucose does not fall too low.

Hyperglycemic agents.

Drugs that raise blood glucose (e.g., thiazide diuretics, glucocorticoids, sympathomimetics) can 

counteract the desired effects of insulin. When these agents are combined with insulin, insulin 

dosage may need to be increased.

β-Adrenergic blocking agents.

β-Blockers can delay awareness of and response to hypoglycemia by masking signs that are 

associated with stimulation of the sympathetic nervous system (e.g., tachycardia, palpitations) 

that hypoglycemia normally causes. Furthermore, because β-blockade impairs glycogenolysis 

and because glycogenolysis is one means by which the body can respond to and counteract a fall 

in blood glucose, β-blockers can make insulin-induced hypoglycemia even worse by preventing 

the body's natural counterregulatory response.

Coadministration of canagliflozin with Uridine 5'-diphospho-glucuronosyltransferase inducers—

such as rifampin, phenytoin, or phenobarbital—can decrease canagliflozin efficacy. Accordingly, 

if used with such an agent, the 300-mg canagliflozin dose should be considered. Because 

canagliflozin causes a diuretic effect, the risk for dehydration and hypotension may be increased 

when used in combination with thiazide and loop diuretics.

pg. 406