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NR565 WEEK #5 EXAM QUESTIONS WITH COMPLETE ASWERS
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NR565 WEEK #5 EXAM QUESTIONS WITH COMPLETE ASWERS
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NR565 WEEK #5 EXAM QUESTIONSWITH COMPLETE ASWERS
Signs and symptoms of hypothyroidism and hyperthyroidism - Answer-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. - Answer-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. - Answer-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. - Answer-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. - Answer-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. - Answer-: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. - Answer-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. - Answer-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.
Maturity-Onset Diabetes of the Young
MODY is characterized by impaired insulin secretion with minimal or no defects in
insulin action. It is inherited in an autosomal dominant pattern. Abnormalities at six
genetic loci on different chromosomes have been identified to date. The most common
form is associated with mutations on chromosome 12 in a hepatic transcription factor
referred to as hepatocyte nuclear factor (HNF)-1α. A second form is associated with
mutations in the glucokinase gene on chromosome 7p and results in a defective
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