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Thermal Regulation:
Adrenal, Thyroid &
Pituitary Systems
Question
Where are the adrenal glands located?
A. Brain
B. Pancreas
C. Liver
D. Kidneys
Question
Where are the adrenal glands located?
A. Brain
B. Pancreas
C. Liver
D. Kidneys
Answer: D. They sit on top of the kidneys
Physiology: Adrenal Glands
The hormones of the endocrine system are
important chemical messengers in the
body.
Two adrenal glands are located one at the
top of each kidney. Each gland is
composed of two distinct parts—the
medulla and the cortex.
The adrenal glands are crucial to
metabolism (glucocorticoids) and fluid and
electrolyte balances (mineralcorticoids).
Cushing Syndrome
A disorder resulting
from increased
adrenocortical
secretion of cortisol,
resulting in chronic
elevation in
glucocorticoid and
adrenal androgen
(male) hormones.
Cushing syndrome also occurs in persons with
long-term use of cortisones (Prednisone,
Deltasone).
Melissa’s Story: Cushing’s
Disease
https://www.youtube.com/watch?v=IOXQ--XzwaA
Glucocorticoids
 The primary endogenous glucocorticoids produced by
the adrenal gland are cortisol and cortisone.
 All natural and synthetic glucocorticoids act by
binding to a specific cytoplasmic glucocorticoid
receptor.
 Abrupt discontinuation of a glucocorticoid following
prolonged administration may result in acute adrenal
insufficiency.
 Chronic, long-term use results in a chemically induced
Cushing syndrome.
Prototype drug: prednisone
(Deltasone)
Prednisone: Core Drug Knowledge
 Pharmacotherapeutics
Anti-inflammatory and immunosuppressive effects
 Pharmacokinetics
Absorbed from GI tract. Metabolized: liver.
Excreted: urine.
 Pharmacodynamics
Primarily glucocorticoid activity, although some
mineralocorticoid activity is present and more
apparent when the drug is administered in high
doses.
Prednisone: Core Drug Knowledge (cont.)
Contraindications and precautions
Hypersensitivity and systemic fungal
infections
Side effects & Adverse effects
Anxiety, mood swings, insomnia,
headache, GI complaints, menstrual
irregularities, hyperglycemia
Prednisone: Nursing Problems
Excess Fluid Volume related to sodium and
water retention.
Risk for Infection related to
immunosuppressive effects
Weight gain due to increased appetite
Altered Body Image related to physical
Cushingoid characteristics
Risk for injury with long-term use due to fragile
skins and organs (higher risk of peptic ulcers)
Drugs Affecting Pituitary,
Thyroid, Parathyroid, and
Hypothalamic Function
The Pituitary Gland
https://www.youtube.com/watch?v=qJj_-3dZ4ZQ
Hypothalamus
Physiology:
Pituitary gland function
Anterior lobe of the pituitary gland:
 Controls the function of glucocorticoid hormone levels
(ACTH)
 Body growth and metabolism (Growth Hormone)
 Function of the thyroid gland (Thyroid Stimulating
Hormone)
 Gonadal function (Folicular Stimulating Hormone and
Luteinizing Hormone) and
 Milk production and breast growth (prolactin).
Physiology:
Pituitary gland function
Posterior lobe of the pituitary gland:
 Stores and secretes two effector hormones
(hormones that produce an effect when stimulated):
Oxytocin, which stimulates labor
Vasopressin (also known as antidiuretic hormone
or ADH).
Physiology
Thyroid gland function
The thyroid gland controls cellular metabolism
and promotes normal growth and
development.
Thyroid Tests:
https://www.youtube.com/watch?v=yz15eiEuWQQ
Physiology
Parathyroid gland function
PTH affects three target organs: bone,
kidneys, and GI tract.
The major controlling factor for PTH secretion
is serum calcium.
Hyperparathyroidism
https://www.youtube.com/watch?v=sD9st1ZPFrQ
Recap: Pathophysiology of Pituitary Gland
 Anterior pituitary gland dysfunction:
 Includes growth hormone deficiency and excess.
 Posterior pituitary gland dysfunction:
 Major disorders are diabetes insipidus (DI) and syndrome
of inappropriate antidiuretic hormone (SIADH).
 Thyroid gland dysfunction:
 Hyper-functioning or hypo-functioning gland,
malfunctions that may be caused by either a congenital
defect or by a problem that occurs later in life.
 Parathyroid gland dysfunction:
 Parathyroid Hormone is a major regulator of serum
calcium and phosphate.
Human Growth Hormones
 GH deficiency, leading to short stature
 Initially treated with GH injections extracted from the
pituitary glands of cadavers.
 Presently, synthetic human GH (rhGH), produced
from recombinant DNA, is available.
Prototype drug: somatropin
Disorders of Human Growth
Hormone
Acromegaly
Dwarfism
Somatropin: Core Drug Knowledge
 Pharmacotherapeutics
Used as long-term replacement of inadequate
endogenous GH secretion
 Pharmacokinetics
Administered: SC and IM. Excreted: liver and
kidneys.
 Pharmacodynamics
It stimulates cell growth and cellular mitosis,
facilitates cellular uptake of amino acids for protein
synthesis, and promotes use of fatty acids for
energy.
Somatropin: Core Drug Knowledge (cont.)
 Contraindications and precautions
Growth promotion in children with closed epiphyses
 Adverse effects
Headache, hypertension, joint and back pain,
peripheral edema, muscle aches, and rhinitis
 Drug interactions
Anabolic steroids, androgens, estrogens, or thyroid
hormones may accelerate epiphyseal maturation.
Somatropin: Planning and Interventions
 Maximizing therapeutic effects
Hypothyroidism may develop during somatropin
therapy.
Patients who require chronic cycling peritoneal
dialysis should receive their doses of somatropin in
the morning, after the dialysis is completed.
 Minimizing adverse effects
GH therapy may induce insulin resistance.
Be alert for the development of a limp or complaints
of hip or knee pain, and tell parents to do the same.
Question
Patients taking somatropin should have which lab values
monitored on a routine basis due to adverse effects of
the drug therapy?
A. TSH
B. CBC
C. Glucose level
D. All of the above
Question
Patients taking somatropin should have which lab values
monitored on a routine basis due to adverse effects of
the drug therapy?
A. TSH
B. CBC
C. Glucose level
D. All of the above
Answer: Both A and C. Somatropin can cause
hypothyroidism and glucose intolerance; therefore, these
lab values should be monitored during therapy.
Posterior Pituitary Hormone Regulators
 The posterior pituitary stores two hormones that are
produced in the hypothalamus: vasopressin and
oxytocin.
 Desmopressin and vasopressin are synthetic analogues
of the naturally occurring posterior pituitary hormone.
 Desmopressin is commonly used to treat nocturnal
enuresis.
Prototype drug:
desmopressin (DDAVP)
Desmopressin: Core Drug Knowledge
 Pharmacotherapeutics
Manages central diabetes insipidus and nocturnal
enuresis and maintains homeostasis in hemophilia A
 Pharmacokinetics
Administered: intranasally, orally, or parenterally (IV
or SC route). Metabolism: liver. Excreted: kidneys.
 Pharmacodynamics
 It works at the level of the renal collecting duct by
binding to vasopressin (V2) receptors to
cause increasing water reabsorption from the
urine.
Desmopressin: Core Drug Knowledge
 Contraindications and precautions
 Hypersensitivity
 Side effects
 Transient headache, nasal congestion, nausea, rhinitis,
and facial flushing
 Adverse effects
 Risk for Fluid Volume Excess related to administration of desmopressin,
secondary to diabetes insipidus
 Watch for signs of water intoxication
 Low K+, Low Na+
 Confusion, ataxia (staggering gait)
 Drug interactions
 Carbamazepine, chlorpromazine, and nonsteroidal antiinflammatory drugs
Thyroid Drugs
 Thyroid hormones influence essentially every organ
system in the body.
 Thyroid disorders involve:
An alteration in the quantity of thyroid hormone
secretion
Enlargement of the thyroid gland (goiter)
Thyroid disorders are classified as either
hyperthyroidism or hypothyroidism.
Thyroid Goiter
Thyroid Drugs
 Hypothyroidism may be mistaken for the normal aging
process.
Fatigue, cold intolerance, sluggishness,
hypersomnia, weight gain
 Hypothyroidism may be mistaken for depression.
 The only treatment for hypothyroidism is lifelong
replacement of thyroid hormones adequate to meet
the individual’s metabolic needs.
 These drugs are considered safe for use in pregnancy.
Prototype drug:
levothyroxine (Levothroid, Synthroid)
Levothyroxine: Core Drug Knowledge
 Pharmacotherapeutics
Used as replacement therapy in hypothyroidism
 Pharmacokinetics
Administered: oral. Metabolism: liver. Excreted: bile.
Onset: 6 to 8 hours.
Protein bound
 Pharmacodynamics
Acts as replacement for natural thyroid hormone
Levothyroxine: Core Drug Knowledge
(cont.)
 Contraindications and precautions
 Hypersensitivity, thyrotoxicosis, and acute MI complicated by hypothyroidism
 Side and Adverse effects
 Hypertension, tachycardia, arrhythmias, anxiety, headache, nervousness, GI
irritation, sweating, and heat intolerance
 Drug interactions
 Many drugs
 Maximizing therapeutic effects
 Replacement therapy is a lifelong occurrence.
 During drug therapy, monitor cardiovascular response and serum thyroid
function.
 Ongoing assessment and evaluation
 In patients taking levothyroxine, monitor serum thyroid hormone levels
periodically.
Anti-thyroid Compounds
 Hyperthyroidism is treated with thyroid-hormone
antagonist drugs, surgery, or radioactive iodine.
 The purpose of treatment is to reduce the amount
of functional thyroid tissue.
Prototype drug:
Propylthiouracil (PTU)
Propylthiouracil: Core Drug Knowledge
 Pharmacotherapeutics
Palliative treatment of hyperthyroidism
 Pharmacokinetics
Administered: oral. Metabolism: liver. Excreted:
kidneys.
 Pharmacodynamics
Inhibits the synthesis of thyroid hormones
 Side effects
Hives, itching, rash, fever, arthralgia, joint swelling,
vertigo, drowsiness, nausea and vomiting, and
altered taste sensation
Adverse effects
Blood dyscrasias (e.g., agranulocytosis)
Propylthiouracil : Planning and Interventions
 Life span and gender
Pregnancy Category D drug (not safe to use)
 Drug interactions
Beta-blocking agents, theophylline, and warfarin
 Maximizing therapeutic effects
Ensure that the drug is being administered
appropriately.
 Minimizing adverse effects
During drug therapy, arrange for periodic blood
tests to monitor for hematologic and thyroid
functions.
Monitor the patient’s bone marrow function.
Radioactive Iodine
 Radioactive Iodine is absorbed by the thyroid and
destroys thyroid-hormone producing cells
Pharmacotherapeutics
 RI is used in the treatment of thyroid cancer and
severe hyperthyroidism
Adverse Effects
 Radiation sickness (vomiting blood, nosebleed,
nausea & vomiting)
 Bone marrow depression
 Drug-induced Hypothyroidism
Radioactive Iodine
 Radioactive Iodine is a Pregnancy Category X – DO
NOT USE
Minimizing Risk
 Limit contact with patients to 30 minutes/day
 Treat bodily wastes as contaminated (including cough
expectorants)
 Use gloves to handle the medication
 Pregnant nurses should not handle the product
 Encourage clients to void frequently to avoid
irradiating the gonads
 No breastfeeding
Anti-hypercalcemic, Calcium-Regulator
Drugs
 Anti-hypercalcemic
drugs do not directly
affect the parathyroid
gland (or PTH) but rather
inhibit bone reabsorption
of calcium.
 These agents are
frequently used in the
treatment of Paget’s
disease.
Antihypercalcemic, Calcium-Regulator
Drugs
 Paget’s Disease
Individuals with Paget’s disease experience bone
pain and deformity, fractures, spinal cord
compression, or cranial and spinal cord
entrapment.
Prototype drug:
calcitonin
Anti-hypo-calcemic Drugs
 Vitamin D works together with PTH and calcitonin to
regulate calcium homeostasis.
 Metabolites of Vitamin D metabolites control intestinal
absorption of dietary calcium, tubular reabsorption of
calcium by the kidney, and mobilization of calcium
from the skeleton, in conjunction with PTH.
 Vitamin D is also involved in magnesium metabolism.
Prototype drug:
calcitriol (Vitamin D3)
Case Study: Grave’s Disease
 Jane Winslow, age 43, has sought help at the urgent care
clinic, complaining of weakness, insomnia, awakening
during the night with “a rapid heart beat,” and “feeling
anxious.” Ms. Winslow denies chest pain or shortness of
breath associated with her rapid heartbeat. She also
complains of muscle tremors when doing small motor
activities and is “ready for summer to end” because she
cannot tolerate the heat. Past medical history includes
hypertension diagnosed 5 years ago. Family history
includes one sister with “thyroid problems.” She drinks
minimally and quit smoking 5-years ago.
 A system review reveals a thin woman with complaints of
increasing fatigue and weakness for the past 3 to 4
months, increased frequency of bowel movements—now
“watery”—hyperactive bowel sounds, 9-pound weight loss
over the past 6 weeks with a noticeable increase in
appetite—“I’ve lost weight without even trying”—and
slight hand tremor. Ms. Winslow complains “my eyes look
like they are bulging.”
Data from her nursing assessment are as follows:
•
She is diaphoretic.
• Vital signs: B/P 130/86, HR 132, RR, 16, Temp.
36.4°C
• Neck is supple with a nontender, palpable and
enlarged thyroid.
• Eyes are protruding, non-painful and equally
reactive to light and accommodation.
• Laboratory tests:
Free T3: 720 pg/dL
uU/mL
Free T4: 5.8 ng/dL
TSH: 0.2
A diagnosis of hyperthyroidism, specifically
Graves disease is made and prophylthiouracil
(PTU) 50 mg TID is prescribed.
Approximately 2 months later, Ms. Winslow returns to
the clinic for a follow-up visit. Her nursing
assessment indicates the following:
Vital signs: B/P 110/80, HR 88, RR 14, Temp. 35°C
Weight gain of 5 pounds.
During the interview, Ms. Winslow states, “My heart
is not beating as fast” and “I am not sweating as
much,” although she does have occasional periods
of vertigo and dizziness.
Labs: Free T3: 500 pg/dL Free T4: 2.9
ng/dL
TSH: 0.5 uU/mL
Questions
1. What is the mechanism of action of
prophylthiouracil (PTU)?
2. Describe the concept of thyroid crisis.
3. What are the potential minor side effects
and major adverse effects
ofprophylthiouracil (PTU)?