NR565 week 5 Study Guide
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
- HgbA1C goals- what are they generally? Review goal guidelines for different age groups within the ADA DM
Guidelines linked in the Endocrine Case Studies and on your Student Lesson Plan.
Neonatal Diabetes
Diabetes diagnosed in the first 6 months of life has been shown not to be typical autoimmune type 1 diabetes. This so-
called neonatal diabetes can either be transient or permanent. The most common genetic defect causing transient disease
is a defect on ZAC/HYAMI imprinting, whereas permanent neonatal diabetes is most commonly a defect in the gene
encoding the Kir6.2 subunit of the β-cell KATP channel. Diagnosing the latter has implications, since such children can be
well managed with sulfonylureas.
