Pharm 2-Exam 3 Study Guide Chapters 8, 26, 27, 28, 29, 38, 39, 49

Chap 8: Substance Use Disorder
 Know the risk factors and definition
o Risk Factors
 Cognitive development at the time drugs are introduced plays a major role
 Adolescents are in a period of brain development where they are especially
vulnerable to stress and risk-seeking behaviors
 Other risk factors
 Family-related risk factors-children who suffered neglect or abuse have
tried or use drugs
 Social risk factors-deviant peer relationships, peer pressure, popularity,
and bullying have all been correlated to drug use; gang affiliations is
associated with higher drug use and delinquent behavior
 Individual risk factors-individuals with ADHD are three times as likely to
use drugs such as nicotine, alcohol, and drugs other than cannabis;
depression is associated with alcohol use, particularly among young men
 Positive family relationships are a protective factor that has been related to a
decrease in drug use among adolescents
o Definition
 When the recurrent use of alcohol and/or drugs causes clinically and functionally
significant impairment, such as health problems, disability, and failure to meet
major responsibilities at work, school, or home
 Know the types of substance use disorders
 Alcohol use disorder-alcohol use inhibits the effects of GABA, thereby reducing
neurotransmission in the brain; short-term effects include nausea, vomiting,
headaches, slurred speech, impaired judgment, memory loss, hangovers, and
blackouts; long-term problems include stomach ailments, heart problems,
cancer, brain damage, serious memory loss, immune system compromise, and
liver cirrhosis
 Cannabis use disorder-most commonly used recreational drug; more common
among people in late teens to early 20s; feelings of alteration in their senses and
altered sense of time as well as changes in mood; impairs short-term memory,
learning, and ability to focus, and it can cause problems with balance and
coordination; increases heart rate and may cause hallucinations, anxiety, panic
attacks, and psychosis; long-term use associated with chronic cough, frequent
respiratory infections, and exposure to cancer-causing compounds because the
smoke has many of the same irritating and lung-damaging properties as tobacco;
ingestion of drug increases heart rate for hours, increasing risk for heart attack
and stroke
 Opioid use disorder-opioids are controlled substances legally prescribed to treat
moderate to severe pain; reduces pain and produces sense of euphoria and
tranquility; short term effects include drowsiness, mental confusion, nausea,
constipation, and dose-dependent respiratory depression; when taken with
alcohol may experience slowing of heart rate and breathing leading to coma or
death; when taken with serotonergic drugs, serotonin may occur (symptoms
include agitation, hallucinations, coma, tachycardia, hypertension, hyperthermia,
and rigidity; signs of opioid intoxication include depression mental status,

lowered respiratory rate, decreased tidal (inhalation-exhalation) volume,
constricted pupils, reduced bowel sounds
 Tobacco use disorder-nicotine stimulates release of dopamine, norepinephrine,
GABA, glutamate, and endorphins, resulting in stimulation and pleasure and
reduction in stress and anxiety, sensations fuel brain’s reward circuit; short-term
effects include increased blood pressure, breathing, and heart rate; long-term
does damage to nearly every organ often leading to cancers, respiratory
disorders, heart disease, stroke, immune dysfunction, and type 2 diabetes;
person attempting to quit experience irritability, anger, anxiousness, difficulty
thinking, cravings, and increased hunger
 Cough and cold products-dextromethorphan (DMX)-antitussive without
prescription; promethazine-codeine cough syrup, prescription required; DMX
side effects include nausea and vomiting, stomach pain, confusion, dizziness,
double or blurred vision, slurred speech, impaired coordination, tachycardia,
drowsiness, numbness, and disorientation; high doses can lead to hepatic failure
or damage, cardiovascular effects, and coma; promethazine-codeine cough syrup
can result in relaxation and euphoria
 Anabolic-Androgenic Steroids-synthetic agent used to treat conditions caused by
low levels of testosterone in the body, such as delayed puberty, hypogonadism,
and cachexia related to chronic disease states; by binding to androgen receptors,
these prescription drugs exert anabolic effects such as growth of muscle and bone
and red blood cell production and androgenic effect such as production of
primary and secondary sexual characteristics; short-term effects include
headache, acne, fluid retention in hands and feet, oily skin, yellowing of skin and
whites of eyes, aggression, extreme mood swings, anger, paranoid jealousy,
extreme irritability, delusions, impaired judgement, and infection at the injection
site; long-term effects include kidney damage or failure, liver damage, high blood
pressure, enlarged heart, or changes in cholesterol leading to increased risk of
stroke or heart attack; men may experience shrunken testicles, infertility,
baldness, development of breasts, and an increased risk for prostate cancer;
women may experience excess facial and body hair, male pattern baldness,
menstrual cycle changes, enlargement of clitoris, and deepened voice;
adolescents may experience stunted bone growth and height; withdrawal from
AAS use may lead to mood swings, fatigue, restlessness, loss of appetite, and
decreased sex drive; be alert when caring for person withdrawing from AAS
because withdrawal may cause depression lasting up to a year which can result
in suicide attempts
Drug-assisted treatment
o Naloxone-treat respiratory depression associated with opioid overdose; competitively
attaches to opioid receptors in CNS blocking activation by opioid drugs; careful
monitoring required to prevent opioid withdrawal; symptoms of withdrawal include
nausea and vomiting, abdominal cramps, hyperthermia, hypertension, and restlessness
o Naltrexone-approved by FDA to treat OUD; begins at 50mg daily after patient has been
opioid free 7-10 days; once treated with naltrexone, patients may have reduced tolerance
to opioids, if they relapse after a period of abstinence and resume opioid use at previous
doses, they may experience life-threatening consequences, including respiratory arrest
and circulatory collapse
o
o
Methadone-treat persons with OUD; boxed warning concerning risk of cardiac and
respiratory-related deaths due to QT prolongation and cardiac arrhythmias; changes way
person’s brain responds to pain; when taken daily, blocks sense of euphoria and
tranquility caused by opioid use and prevents opioid withdrawal and craving; concurrent
administration of rifampin, phenytoin, St. John wort, phenobarbital, and carbamazepine
can reduce serum methadone levels and precipitate withdrawal; administration with
zidovudine may lead to toxicity; methadone side effects include lightheadedness,
constipation, dizziness, sedation, nausea, and vomiting; excreted in breast milk
o Buprenorphine-long-acting, mixed narcotic agonist-antagonist; produce some euphoria
effect, there is a ceiling effect; increasing dose beyond moderate level does not increase
euphoria, so has low potential for misuse; initial dosing begins when person with OUD
has been opioid free for at least 12 hours and is beginning to experience withdrawal; side
effects include nausea, vomiting, and constipation; muscle aches and cramps, and
cravings, sedation, headache, depression, anxiety, and withdrawal symptoms; excreted
in breast milk
Chap 49: Pituitary, Thyroid, Parathyroid, and Adrenal Disorders
 Know the basic pathophysiology
o Growth Hormone (Somatropin)
 The anterior pituitary gland, called the adenohypophysis, secretes hormones that
target glands and tissues, including:
 Growth hormone (GH), which stimulates growth in tissue and bone
 Thyroid-stimulating hormone (TSH), which acts on the thyroid gland
 Adrenocorticotropic hormone (ACTH), which stimulates the adrenal gland
 Gonadotropins (follicle-stimulating hormone [FSH] and luteinizing hormone
[LH]), which affect the ovaries and testes
 Prolactin (PRL), which primarily affects the breast tissues
 The amount of each hormone secreted from the anterior pituitary gland is regulated
by a negative feedback system. If excess hormone is secreted from the target gland,
hormonal release from the anterior pituitary gland is suppressed. If there is a lack of
hormone secretion from the target gland, there will be an increase in that particular
anterior pituitary hormone
 Growth Hormone
 Two hypothalamic hormones regulate GH: (1) GH-releasing hormone (GH-RH;
somatropin) and (2) GH-inhibiting hormone (GH-IH; somatostatin).
 GH does not have a specific target gland. It affects body tissues and bone; GH
replacement stimulates linear growth when there are GH deficiencies.
 GH drugs cannot be given orally because they are inactivated by gastrointestinal (GI)
enzymes. Subcutaneous (subcut) or intramuscular (IM) administration of GH is
necessary.
 Because GH acts on newly forming bone, it must be administered before the
epiphyses are fused. Administration of GH over several years can increase height by
a foot. prolonged GH therapy can antagonize insulin secretion, eventually causing
diabetes mellitus. Athletes should be advised not to take GH to build muscle and
physique because of its effects on blood glucose along with other serious side
effects


o
o
Drug Therapy: Growth Hormone Deficiency
Somatropin is a GH used to treat growth failure in children because of GH
deficiency. Somatropin is a product that has an identical amino acid sequence as
human GH (hGH); it is contraindicated in pediatric patients who have growth
deficiency due to Prader-Willi syndrome, in those who are severely obese, or in
those who have severe respiratory impairment because fatalities associated with
GH can occur.
 Corticosteroids can inhibit the effects of somatropin; therefore they should not be
taken concurrently. Somatropin can enhance the effects of antidiabetics and can
cause hypoglycemia.
 SE/AE: Somatropin can cause paresthesia, arthralgia, myalgia, peripheral edema,
weakness, and cephalgia. Metabolic complications include glucose fluctuations,
hypothyroidism, and hematuria. Flulike symptoms and hyperpigmentation of the
skin can also occur. Adverse reactions include seizures, intracranial hypertension,
and secondary malignancy (e.g., leukemia).
Thyroid stimulating hormone (Thyrotropin)
 The adenohypophysis secretes thyroid-stimulating hormone (TSH) in response to
thyroid-releasing hormone (TRH) from the hypothalamus. TSH stimulates the
thyroid gland to release thyroxine (T4) and triiodothyronine (T3, or liothyronine).
Excess TSH secretion can cause hyperthyroidism, and a TSH deficit can cause
hypothyroidism. Hypothyroidism may be caused by a thyroid gland disorder
(primary cause) or a decrease in TSH secretion (secondary cause).
 Thyrotropin, a purified extract of TSH for thyroid cancer, is used as a diagnostic
agent to differentiate between primary and secondary hypothyroidism. Side effects
caused by thyrotropin include symptoms of hyperthyroidism. Other side effects
include urticaria, rash, pruritus, and flushing.
Adrenocorticotropic Hormone
 The hypothalamus releases corticotropin-releasing factor (CRF), which stimulates
the pituitary corticotrophs to secrete adrenocorticotropic hormone (ACTH), which
stimulates the release of glucocorticoids (cortisol), mineralocorticoids (aldosterone),
and androgen from the adrenal cortex and catecholamines (epinephrine and
norepinephrine) from the adrenal medulla. Usually, ACTH and cortisol secretions
follow a diurnal rhythm, in which the ACTH and cortisol secretion is higher in the
early morning and then decreases throughout the day. Stresses such as surgery,
sepsis, and trauma override the diurnal rhythm, causing an increase in secretions of
ACTH and cortisol. Hypocortisolism, or adrenal insufficiency, can occur and may be
due to inadequate secretion of ACTH or dysfunction of the adrenal glands.
 Cosyntropin
 Cosyntropin (synthetic ACTH) or corticotropin (exogenous ACTH) is administered
to establish the endocrine gland responsible for the inadequate serum cortisol.
 Cosyntropin, a synthetic ACTH, is only approved for diagnostic purposes and is
less potent and less allergenic than corticotropin. Cosyntropin stimulates the
production and release of cortisol, corticosterone, and androgens from the
adrenal cortex. It is administered via IM or intravenous (IV) routes.

o
Caution is advised when administering cosyntropin in patients receiving
diuretics; cosyntropin can increase electrolyte loss. Patients taking estrogens
can have an abnormal decreased response to the ACTH stimulation test. Side
effects and adverse effects include bradycardia, hypertension, sinus tachycardia,
and peripheral edema.
 Corticotropin
 The ACTH drug corticotropin is primarily used to diagnose adrenal gland
disorders, treat multiple sclerosis (MS), and treat infantile spasms; it is rarely
used for corticosteroid-responsive disorders. Corticotropin is available as
repository corticotropin injection (RCI), which is administered via IM or subcut
routes. RCI controls the synthesis of ACTH from cholesterol, which stimulates
adrenal glands in releasing its hormones. The effects of RCI are primarily due to
the glucocorticoid from the adrenal cortex. RCI decreases the symptoms of MS
during its exacerbation phase.
 The drug should be tapered over a 2-week period for infantile spasms to avoid
adrenal insufficiency.
 Corticotropin has numerous drug interactions. Diuretics and anti-Pseudomonas
penicillins, such as piperacillin, can decrease the serum potassium level
(hypokalemia). If the patient is taking a digitalis preparation and hypokalemia is
present, digitalis toxicity can result. Phenytoin, rifampin, and barbiturates
increase the metabolic rate, which can decrease the effect of the ACTH drug.
Persons with diabetes may need increased insulin and oral antidiabetic
(hypoglycemic) drugs because ACTH stimulates cortisol secretion, which
increases the blood glucose level.
 Side effects and adverse reactions are due to the activity of the adrenal glands
and their hormones.
Antidiuretic hormone (ADH) (Vasopressin)
o
ADH excess (Vaptans)
o
Hypothyroidism (Levothyroxine sodium)





Hyperthyroidism
 Methimazole
 Propylthiouracil
Parathyroid hormone (PTH)
o Hypoparathyroidism (Calcitriol)

o
Hyperparathyroidism (Calcitonin-Salmon)
o
Glucocorticoids (Prednisone)
o
Mineralocorticoids (Fludrocortisone)



Posterior Lobe
The posterior pituitary gland, known as the neurohypophysis, secretes antidiuretic hormone (ADH) and
oxytocin. ADH and oxytocin are produced by the hypothalamus and travel by way of the hypophysial
portal system into the posterior pituitary gland for storage and secretion.
ADH promotes water reabsorption from the renal tubules to maintain water balance in the body fluids.
When there is a deficiency of ADH, large amounts of water are excreted by the kidneys. This condition,
called diabetes insipidus (DI), can lead to severe fluid volume deficit and electrolyte imbalances.
The ADH preparations vasopressin and desmopressin acetate can be administered intranasally or by
injectionADH is contraindicated in patients with moderate to severe renal disease and in patients with
hyponatremia or a history of such. Side effects and adverse reactions include hyponatremia, cephalgia,
dyspepsia, diarrhea, nausea, and vomiting. Seizures may occur due to hyponatremia. Hypotension and
tachycardia can occur due to hypovolemia.
When secretion of ADH from the posterior pituitary gland is excessive, the most common cause is small
cell carcinoma of the lung. Medications, other malignancies, and stressors (e.g., pain, infection, anxiety,
trauma) may also be causative factors. These conditions lead to an excessive amount of water retention
expanding the intracellular and intravascular volume known as syndrome of inappropriate antidiuretic
hormone (SIADH). This increased fluid volume causes enhanced glomerular filtration and decreased
tubular sodium reabsorption. Natriuresis, excretion of urinary sodium, can occur and can cause
hyponatremia. SIADH can be treated by fluid restrictions, by hypertonic saline, or by drugs such as
demeclocycline, conivaptan, and tolvaptan.
Vaptans (e.g., conivaptan and tolvaptan) are vasopressin receptor antagonists and are indicated for the
treatment of euvolemic hyponatremia in SIADH. Their effects increase serum sodium and free water
clearance. Conivaptan is contraindicated in patients with corn allergy. Common complications with
conivaptan therapy are injection site reactions such as phlebitis, pain, edema, and pruritus; therefore
the drug must be administered only in large veins, and infusion sites should be rotated every 24 hours.
Other common side effects and adverse reactions include orthostatic hypotension, syncope,
hypertension, atrial fibrillation, and electrolyte imbalances.
Tolvaptan is given orally. It has black-box warnings for patients with alcoholism, hepatic disease, and
malnutrition; tolvaptan should be avoided in these patients. Common side effects and adverse reactions
are related to loss of fluids (e.g., thirst, dry mouth, constipation, hyperglycemia, dizziness, and
weakness). Fluid and serum electrolytes must be closely monitored.
Vaptans are contraindicated in patients with hypovolemia. Fluid restrictions should be avoided during
therapy to prevent sudden increase in serum sodium.
Thyroid Gland
The thyroid gland is an important regulator for many of the bodily functions. The three hormones
produced and secreted by the thyroid gland are triiodothyronine (T3); thyroxine (T4), which helps with
metabolism; and, to a lesser extent, calcitonin for regulating serum calcium. A majority of thyroid
hormone is synthesized as T4, which is then converted to T3 to act on target cells. Iodide, an inorganic
form of iodine, is needed for the synthesis of T3 and T4. These are carried in the blood by thyroxinebinding globulin (TBG) and albumin, which protect the hormones from being degraded. T3 is more
potent than T4, and only unbound (free) T3 and T4 have biologic actions and produce a hormonal
response.
Negative feedback mechanisms regulate hormone secretion from the thyroid gland. The hypothalamus
releases thyrotropin-releasing hormone (TRH), which stimulates the release of TSH from the pituitary
gland. TSH stimulates the synthesis and release of T3 and T4 from the thyroid gland. Excess free T3 and
T4 inhibit the hypothalamus-pituitary-thyroid (HPT) axis, which results in decreased TRH and TSH
secretion. Too low of an amount of T3 and T4 increases the function of the HPT axis.
For thyroid deficiency (hypothyroidism), synthetic thyroid hormones may be prescribed either alone or
in combination. When the thyroid gland secretes an overabundance of thyroid hormone
(hyperthyroidism), antithyroid drugs are usually indicated.
Hypothyroidism
Hypothyroidism, a decrease in thyroid hormone secretion, can have a primary cause (thyroid gland
disorder), a secondary cause (lack of TSH secretion [pituitary disorder]), or a tertiary cause (lack of TRH
[hypothalamus disorder]). Primary hypothyroidism occurs more frequently. Decreased T4 and elevated
TSH levels indicate primary hypothyroidism, the causes of which are acute or chronic inflammation of
the thyroid gland, radioiodine therapy, excess intake of antithyroid drugs, or surgical removal of the
thyroid gland. Myxedema is severe hypothyroidism in the adult; symptoms include lethargy; apathy;
memory impairment; emotional changes; slow speech; a deep, coarse voice; edema of the eyelids and
face; dry skin; cold intolerance; slow pulse; constipation; weight gain; and abnormal menses. In children,
hypothyroidism can have a congenital onset that can cause delayed physical and mental growth
(cretinism) or onset may be prepubertal (juvenile hypothyroidism). Drugs that contain T3 and T4, alone
or in combination, are used to treat hypothyroidism. Exogenous thyroid hormones are contraindicated
in patients with thyrotoxicosis, acute myocardial infarction (AMI), and adrenal insufficiency. Because
thyroid hormones are catabolized by the hepatic system, drugs with hepatic enzyme–inducing
properties (e.g., carbamazepine, hydantoins, rifabutin) should be used with caution. Elevated serum
calcium levels could also be related to hypothyroidism; exogenous calcitonin may also be prescribed.
Thyroid Drugs
Levothyroxine sodium is the drug of choice for replacement therapy for the treatment of primary
hypothyroidism. It increases the levels of T4 and metabolically is deiodinated to T3. Levothyroxine is also
used to treat simple goiter and chronic lymphocytic (Hashimoto) thyroiditis.
SE/AR: Nausea, vomiting, anorexia, diarrhea, cramps, tremors, nervousness, irritability, insomnia,
headache, weight loss, diaphoresis, and amenorrhea; usually due to undermedication or overmedication
Tachycardia, hypertension, palpitations, osteoporosis, and seizures; usually due to overmedication.
Other adverse reactions include urticaria, rash, and alopecia.
Life-threatening: Thyroid crisis, angina pectoris, cardiac dysrhythmias (atrial fibrillation), cardiovascular
collapse
Hyperthyroidism
Hyperthyroidism is an increase in circulating T3 and T4 levels, which usually results from an overactive
thyroid gland or excessive output of thyroid hormones from one or more thyroid nodules.
Hyperthyroidism may be mild, with few symptoms, or it may be severe, as in thyroid storm, in which
death may occur from vascular collapse. Graves disease, or thyrotoxicosis, is the most common type of
hyperthyroidism caused by hyperfunction of the thyroid gland. It is characterized by a rapid pulse
(tachycardia), palpitations, excessive perspiration (hyperhidrosis), heat intolerance, nervousness,
irritability, bulging eyes (exophthalmos), and weight loss.
Hyperthyroidism can be treated by surgical removal of a portion of the thyroid gland (subtotal
thyroidectomy), radioactive iodine therapy, or antithyroid drugs, which inhibit either synthesis or
release of thyroid hormone. Any of these treatments can cause hypothyroidism. By blocking beta
receptors, propranolol can control cardiac symptoms that result from hyperthyroidism, such as
palpitations and tachycardia.
Antithyroid Drugs
The purpose of antithyroid drugs is to reduce the excessive secretion of thyroid hormones by inhibiting
thyroid secretion. The use of surgery (subtotal thyroidectomy) and radioiodine therapy frequently leads
to permanent hypothyroidism; these patients will need to be on thyroid replacement therapy. Thiourea
derivatives (thioamides) are the drugs of choice used to decrease thyroid hormone production. This
drug group interferes with synthesis of thyroid hormone. Thiourea derivatives do not destroy thyroid
tissue; rather, they block thyroid action.
Propylthiouracil (PTU) and methimazole are effective thioamide antithyroid drugs. They are used to
control overactive thyroid due to Graves disease, toxic nodular goiter, or multinodular goiter; they are
also used before radioiodine treatment or thyroid surgery. Methimazole does not inhibit peripheral
conversion of T4 to T3 as does PTU; however, it is 10 times more potent, it has a longer half-life than
PTU, and the euthyroid state is achieved in 2 to 4 months. It is the preferred antithyroid because of the
less severe side effects. Methimazole is rapidly absorbed from the GI tract. Prolonged use of thioamides
may cause goiter because of increased TSH secretion and inhibited T4 and T3 synthesis. Minimal doses
of thioamides should be given when indicated to avoid goiter formation.
Strong iodide preparations such as potassium iodide have been used to suppress thyroid function for
patients who are undergoing subtotal thyroidectomy because of Graves disease. Table 49.3 lists the
antithyroid drugs used to treat hyperthyroidism along with their dosages, uses, and considerations.
Drug Interactions
Antithyroid drugs interact with many other drugs. When used with oral anticoagulants (e.g., warfarin),
they can cause an increase in the anticoagulation effect. In addition, thyroid drugs decrease the effect of
insulin and oral antidiabetics, digoxin and lithium increase the action of thyroid drugs, and phenytoin
increases serum T3 level.
Parathyroid Glands
The parathyroid glands secrete parathyroid hormone (PTH), or parathormone, which regulates serum
calcium levels in a number of ways:
• It enhances the release of calcium from the bones.
• It enhances calcium reabsorption in the renal tubules.
• It enhances calcium absorption in the intestines by increasing the production of activated vitamin D.
A decrease (negative feedback) in serum calcium stimulates the release of PTH. Calcitonin, one of three
thyroid hormones, decreases serum calcium levels by promoting osteoclast activity in bones and calcium
excretion by the kidneys and intestines.
For PTH deficiency, PTH analogues are used. Surgical removal (parathyroidectomy) is a common
treatment for hyperparathyroidism. Calcimimetic drugs, which mimic calcium in the blood, prevent the
parathyroid gland from releasing PTH.
Hypoparathyroidism
Damage to the parathyroid glands is a common cause of hypoparathyroidism. Hypomagnesemia (low
serum magnesium) can also cause PTH deficiency. Other causes of hypocalcemia (serum calcium deficit)
include vitamin D deficiency, renal impairment, or diuretic therapy; PTH replacement helps correct the
calcium deficit. The action of PTH is to promote calcium absorption from the GI tract, promote
reabsorption of calcium from the renal tubules, and activate vitamin D.
Calcitriol
Calcitriol is a vitamin D analogue that promotes calcium absorption from the GI tract and promotes
secretion of calcium from bone to the bloodstream.
SE/AR: Side effects are generally early signs of hypercalcemia: fatigue, weakness, somnolence,
cephalgia, nausea, vomiting, diarrhea, cramps, drowsiness, dizziness, vertigo, metallic taste, lethargy,
constipation, and xerostomia. Adverse effects are late signs of hypercalcemia: anorexia, photophobia,
dehydration, cardiac arrhythmias, decreased libido, hypertension, sensory disturbances, hypercalciuria,
hypercalcemia, and hyperphosphatemia.
Hyperparathyroidism
Hyperparathyroidism can be caused by malignancies of the parathyroid glands or ectopic PTH hormone
secretion from lung cancer, hyperthyroidism, or prolonged immobility, during which calcium is lost from
bone. Partial or full parathyroidectomy is the most common treatment for primary
hyperparathyroidism.
Calcitonin-salmon prevents bone loss and fractures, increases bone density, and alleviates pain due to
fractures and bone metastasis. Calcitonin is not as effective as other drugs for hyperparathyroidism.
Calcitonin is contraindicated in patients allergic to fish. Common side effects include allergic reactions,
GI symptoms (e.g., nausea and vomiting), cephalgia, and hypocalcemia. Adverse reactions due to severe
hypocalcemia (e.g., tetany and seizures) can also occur.
Adrenal Glands
The paired adrenal glands consist of the adrenal medulla and adrenal cortex. Hormones secreted from
the adrenal medulla are epinephrine and norepinephrine (catecholamines); Chapters 15 and 55 further
discuss these hormones. The adrenal cortex produces two types of steroid hormones, glucocorticoids
(cortisol) and mineralocorticoids (aldosterone), and, to a lesser extent, the adrenal androgens and
estrogens. Steroids are secreted by the adrenal cortex in response to signals from the hypothalamuspituitary-adrenal (HPA) axis; the levels are regulated by the negative feedback mechanism. A decrease in
serum steroid levels (hypocortisolism) increases CRF and ACTH secretions from the hypothalamus and
anterior pituitary gland, respectively; these stimulate the adrenal glands to secrete and release steroids.
An increased serum steroid level (hypercortisolism) inhibits the HPA axis, resulting in fewer steroids being
released. A decrease in steroid secretion is called adrenal hyposecretion (adrenal insufficiency, or Addison
disease), and an increase in steroid secretion is called adrenal hypersecretion (Cushing syndrome).
Because of the influences of steroids on electrolytes and on carbohydrate, protein, and fat metabolism,
hypocortisolism can result in serious illness or death.
Glucocorticoids
Glucocorticoids are the most potent natural cortisol produced by the body and are influenced by ACTH,
which is released from the anterior pituitary gland. Its functions include having an effect on the
inflammatory response, metabolism, growth, and biorhythms. Glucocorticoids also affect carbohydrate,
protein, and fat metabolism and muscle and blood cell activities. Indications for glucocorticoid therapy
include trauma, surgery, inflammation, emotional upsets, and anxiety.
Most of the glucocorticoid drugs, frequently called cortisone drugs, are synthetically produced. These
drugs have several routes of administration: oral, parenteral (IM or IV), topical (creams, ointments,
lotions), and aerosol (inhaler). Drugs administered via the (seldom used) IM route should be administered
deep into the muscle; subcutaneous administration is not recommended.
Glucocorticoids are used to treat many diseases and health problems, including inflammatory, allergic,
and debilitating conditions. Among the inflammatory conditions that may require glucocorticoids are
autoimmune disorders (e.g., MS, rheumatoid arthritis, myasthenia gravis), ulcerative colitis,
glomerulonephritis, shock, ocular and vascular inflammation, polyarteritis nodosa, and hepatitis. Allergic
conditions include asthma, drug reactions, contact dermatitis, and anaphylaxis. Debilitating conditions are
mainly caused by malignancies. Organ transplant recipients may require glucocorticoids to prevent organ
rejection.
Drugs used for adrenocortical insufficiency contain both glucocorticoids and mineralocorticoids, whereas
drugs with antiinflammatory or immunosuppressive properties contain mostly glucocorticoids with
minimal mineralocorticoid activity.
SE/AE: Side effects and adverse reactions of glucocorticoids that result from high doses or prolonged use
include increased blood glucose, abnormal fat deposits in the face and trunk (so-called moon face and
buffalo hump), decreased extremity size, muscle wasting, edema, sodium and water retention,
hypertension, euphoria or psychosis, thinned skin with purpura, increased intraocular pressure
(glaucoma), peptic ulcers, and growth retardation. Long-term use of glucocorticoid drugs can cause
adrenal atrophy (loss of adrenal gland function). When drug therapy is discontinued, the dose should be
tapered to allow the adrenal cortex to produce cortisol and other corticosteroids. Abrupt withdrawal of
the drug can result in severe adrenocortical insufficiency.
Drug Interactions
Glucocorticoids increase the potency of drugs taken concurrently, including aspirin and nonsteroidal
antiinflammatory drugs (NSAIDs), thus increasing the risk of GI bleeding and ulceration. Use of potassiumwasting diuretics (e.g., furosemide) with glucocorticoids increases potassium loss, resulting in
hypokalemia.
Barbiturates, phenytoin, and rifampin decrease the effect of prednisone because they increase
glucocorticoid metabolism. Larger doses of glucocorticoids may be required to achieve the desired effect.
Prolonged use of glucocorticoids can cause severe muscle weakness.
Herbal products such as cascara sagrada, yellow dock, and licorice can potentiate the effects of
corticosteroids, which can worsen potassium depletion.
Mineralocorticoids
Mineralocorticoids promote sodium retention and potassium and hydrogen excretion in the renal tubules.
The primary mineralocorticoid is aldosterone, which is controlled by the renin-angiotensin-aldosterone
system (RAAS). Mineralocorticoids maintain fluid balance by promoting the reabsorption of sodium from
the renal tubules. Sodium attracts water, resulting in water retention. When hypovolemia (a decrease in
circulating fluid) occurs, more aldosterone is secreted to increase sodium and water retention, thereby
restoring fluid balance. With sodium reabsorption, potassium is lost and hypokalemia (potassium deficit)
can occur. Some glucocorticoid drugs also contain mineralocorticoid properties; these include cortisone
and hydrocortisone. A severe decrease in the mineralocorticoid can lead to hypotension and vascular
collapse, as seen in Addison disease. Mineralocorticoid deficiency usually occurs with glucocorticoid
deficiency, frequently called corticosteroid deficiency.
Fludrocortisone is an oral mineralocorticoid that can be given with a glucocorticoid. Even though
fludrocortisone has significant glucocorticoid activity, it is not appreciable at usual therapeutic doses.
Fludrocortisone mimics the actions of endogenous aldosterone, facilitating sodium resorption and
promoting hydrogen ion and potassium excretion. In larger doses, it can inhibit endogenous hormone
secretions of adrenal cortex and pituitary gland, causing a negative nitrogen balance; therefore a highprotein diet is usually indicated. Because potassium excretion occurs with the use of mineralocorticoids,
serum potassium level should be monitored. Other adverse effects include fluid imbalance, fluid overload,
and hypertension. These usually indicate overdosage, at which point fludrocortisone should be
discontinued and then resumed at lower doses. Hypokalemia may cause metabolic alkalosis, which can
cause GI symptoms (nausea and vomiting), orthostatic hypotension, cardiac rhythm changes, weakness,
anorexia, and myalgia.
o
Chap 26: Penicillins, Other Beta-Lactams, and Cephalosporins
 Disease-producing organisms may be gram positive or gram-negative bacteria, viruses,
protozoans, or fungi; degree to which they are pathogenic depends on the microorganism
and its violence
 Bacteriostatic and Bactericidals
o Bacteriostatic drugs inhibit bacterial growth
o Bactericidal bacteria killing
 Resistance to antibiotics
o Bacteria can be sensitive or resistant to certain antibacterials; when bacteria are sensitive
to a drug the pathogen is inhibited or destroyed, if bacteria is resistant the pathogen
continues to grow despite administration of that antibacterial drug
o Bacteria resistance can result naturally (inherent resistance) or it may be acquired; natural
or inherent resistance occurs without previous exposure to antibacterial; drug; an
acquired resistance is caused by prior exposure to the antibacterial drug
o Another problem related to antibiotic resistance is that bacteria can transfer their
genetics instructions to another bacterial species and the other bacterial species then
becomes resistant to that antibiotic as well
o Antibiotic misuse increases antibiotic resistance


o Cross-resistance can also occur among antibacterial drugs that have a similar action
Penicillins-a natural antibacterial agent from mold genus Penicillium
 Penicillin G
 Penicillin beta-lactam ring structure interferes with bacterial cell wall synthesis
by inhibiting the bacterial enzyme necessary for cell division and cellular
synthesis; bacteria die of cell lysis
 Mainly bactericidal
 IM injection is painful so procaine is added to decrease the pain
 Amoxicillin
 Penicillins that are unaffected by food
 Contraindications: allergy to penicillins, hypersensitivity
 Geriatrics
 Most beta-lactam antibiotics are excreted via the kidneys. With older
adults, assessment of renal function is most important. Serum blood urea
nitrogen (BUN) and serum creatinine should be monitored. With a
decrease in renal function, the antibiotic dose should be decreased.
 Side Effects and Adverse Reactions
 AR: hypersensitivity and superinfection, the occurrence of a secondary
infection when the flora of the body are disturbed; Anorexia, nausea,
vomiting, and diarrhea are common GI disturbances, often referred to as
GI distress-may be alleviated by taking with food. Rash is an indicator of
a mild to moderate allergic reaction; severe allergic reaction leads to
anaphylactic shock. Clinical manifestations of severe allergic reaction:
laryngeal edema, severe bronchoconstriction with stridor, and
hypotension-close monitoring during the first and subsequent doses of
penicillin is essential.
 Drug Interactions
 The broad-spectrum penicillins, amoxicillin and ampicillin, may decrease
effectiveness of oral contraceptives. Potassium supplements can increase
serum potassium levels when taken with potassium penicillin G or V.
When penicillin is mixed with an aminoglycoside in IV solution, the
actions of both drugs are inactivated.
 Nafcillin (penicillinase-resistant penicillins/antistaphylococcal penicillins)
 Used to treat penicillinase-producing S. aureus.
 Not effective against gram-negative organisms and less effective than penicillin G
against gram positive organisms
 Treats endocarditis, meningitis, bacteremia, mastitis, and skin, respiratory, and
bone/joint infections
 May cause abdominal pain, arthralgia, stomatitis, nausea, vomiting, diarrhea,
tongue discoloration, rash, CDAD, superinfection, phlebitis, and injection site
reaction
Other Beta-Lactam antibacterials-bind to specific penicillin-binding proteins located inside the
bacterial cell wall and are bactericidal
 Meropenem
 Effective against broader spectrum of activity than other beta-lactam
antibacterials
 Less nephrotoxic than other antibacterials

o
SE/AE: headache, nausea, vomiting, diarrhea, anemia, eosinophilia, and
neutropenia; rash may occur
 AR: anaphylaxis, angioedema, seizures, C. Diffe associated diarrhea
 Cephalosporins-fungus against gram positive and gram-negative bacteria and resistant to
beta lactamase; act by inhibiting the bacterial enzyme necessary for cell wall synthesis; lysis
to the cell occurs, and bacterial cell dies; major antibiotic group used in hospital and in health
care offices
 Ceftriaxone-IM and IV; third gen: same effectiveness as 1st and 2nd gen and also
effective against gram negative bacteria but with increased resistance to destruction
by beta-lactamases;
 For treating otitis media, meningitis, gonorrhea, bacteremia, and skin,
respiratory, bone/joint, intraabdominal, and urinary tract infections; Ceftriaxone
is effective against Klebsiella, Haemophilus, Clostridium, Citrobacter,
Bacteroides, Acinetobacter, Neisseria, Proteus, Salmonella, Serratia, Shigella,
Staphylococcus, Staphylococcus, and Escherichia coli.
 Cefazolin-IM and IV; inhibit bacterial cell wall synthesis and produce a bactericidal
action; first gen: effective mostly against gram positive bacteria and some gramnegative bacteria
 All SE/AR: GI disturbances (NVD), alteration in blood clotting time (increased
bleeding) with administration of large doses, and nephrotoxicity (toxicity to kidney)
in individuals with a preexisting renal disorder
Chap 27: Macrolides, Oxazolidinones, Lincosamides, Glycopeptides, Ketolides, and Lipopeptides
 Macrolides-broad spectrum antibiotics; bind to 50S ribosomal subunit and inhibit protein
synthesis; al low doses they are bacteriostatic, at high doses they are bactericidal; not
administered IM because too painful, IV infused slowly to avoid unnecessary pain (phlebitis);
used to treat mild to moderate infections of respiratory tract, sinuses GI tract, and skin and
soft tissue in addition to treating diphtheria, impetigo contagiosa, and STIs
 Erythromycin-derived from fungus-like bacteria; gastric acid destroys it so salts are
added to decrease breakdown into small particles (dissolution) in the stomach which
allows drug to be absorbed in the intestine
 Used to treat mycoplasmal pneumonia and legionnaires disease; should be
diluted in normal saline
 Azithromycin
 Prescribed for upper and lower respiratory infections, STIs, and uncomplicated
skin infections; should be diluted in normal saline
o All SE/AR: GI disturbances such as nausea, vomiting, diarrhea, and abdominal cramping.
Severe diarrhea occurs when antibacterials kill normal flora, allowing an overgrowth of
Clostridium difficile. This superinfection is called Clostridium difficile–associated diarrhea
(CDAD), also known as pseudomembranous colitis. A release of bacterial toxins causes
injury, inflammation, and bleeding in the colon lining. This condition causes abdominal
cramping, 5 to 10 watery diarrheal stools per day, and bloody stools. Frequency of stools
may increase to 20 per day in severe cases. Conjunctivitis may develop as a side effect of
azithromycin, and the patient should avoid wearing contact lenses if this occurs. Allergic
reactions to erythromycin are rare. Hepatotoxicity (liver toxicity) can occur when
erythromycin and azithromycin are taken in high doses with other hepatotoxic drugs,
such as acetaminophen (high doses), phenothiazines, and sulfonamides. Liver damage is
usually reversible when the drug is discontinued. Erythromycin should not be taken with
clindamycin or lincomycin because they compete for receptor sites.
o
o
Macrolides can increase serum levels of theophylline (a bronchodilator), carbamazepine
(an anticonvulsant), and warfarin (an anticoagulant). If these drugs are given with
macrolides, their drug serum levels should be closely monitored. To avoid severe toxic
effects, erythromycin should not be used with other macrolides. Antacids may reduce
azithromycin peak levels when taken at the same time.
 Oxazolidinones
o Inhibit protein synthesis on 50S ribosomal subunit of bacteria; action prevents 70S
initiation complex which is necessary for bacterial reproduction
o Bacteriostatic or bactericidal and effective against gram positive bacteria
o SE/AR: headache, NVD, anemia, and thrombocytopenia
o AR: CDAD and serotonin syndrome
 Linezolid
 Lincosamides
o Inhibit bacterial protein synthesis and have both bacteriostatic and bactericidal actions
depending on dose
 Clindamycin-active against gram-positive organisms including S. aureus and
anaerobic organisms; not effective against gram-negative bacteria;
 SE/AR” Gi irritation, which may manifest as nausea, vomiting, stomatitis; rash may
occur; severe adverse reaction include colitis and anaphylactic shock
 Glycopeptides/ Vancomycin
o bactericidal antibiotic
o Vancomycin is used against drug-resistant S. aureus and in cardiac surgical prophylaxis for
individuals with penicillin allergies. Serum vancomycin levels should be monitored.
o Vancomycin has become ineffective for treating enterococci. Antibiotic-resistant
enterococci can cause staphylococcal endocarditis.
o Vancomycin is given orally for treatment of staphylococcal enterocolitis and antibioticassociated pseudomembranous colitis due to C. difficile. When vancomycin is given orally,
it is not absorbed systemically and is excreted in the feces. Vancomycin is also given
intravenously for septicemia; for severe infections due to MRSA; and for bone, skin, and
lower respiratory tract infections that do not respond or are resistant to other antibiotics.
Intermittent vancomycin doses should be diluted in 100 mL for 500 mg and 200 mL for 1
g of D5W, NS, or lactated Ringer’s (LR), and should be administered over 60 to 90 minutes.
o Vancomycin inhibits bacterial cell wall synthesis and is active against several grampositive microorganisms.
o SE/AR: nephrotoxicity and ototoxicity. Ototoxicity results in damage to the auditory or
vestibular branch of cranial nerve VIII. Such damage can result in permanent hearing loss
(auditory branch) or temporary or permanent loss of balance (vestibular branch);
headache, dizziness, fatigue, fever, nausea, vomiting, flatulence, abdominal pain,
diarrhea, back pain, peripheral edema, and injection site reaction. Too-rapid injection of
IV vancomycin can cause vancomycin infusion reaction, previously known as red man
syndrome or red neck syndrome-red blotching of the face, neck, arms, upper body, and
back, this is a toxic effect rather than an allergic reaction. Other effects: hypotension,
tachycardia, wheezing, dyspnea, paresthesia, erythema, pruritus, and urticaria, and may
lead to cardiac arrest.
o AE: eosinophilia, neutropenia, phlebitis, CDAD, hypokalemia, renal failure, and StevensJohnson syndrome.
Chap 28: Tetracyclines, Glycylcyclines, Aminoglycosides, and Fluoroquinolones
 Tetracyclines (Doxycycline)
o

broad-spectrum antibiotics effective against gram-positive and gram-negative bacteria;
act by inhibiting bacterial protein synthesis and have a bacteriostatic effect.
o not effective against S. aureus (except for the newer tetracyclines), nor are they effective
against Pseudomonas or Proteus species, but they can be used against Mycoplasma
pneumoniae; oral and topical tetracyclines have been used to treat severe acne vulgaris,
and low doses are usually prescribed to minimize the toxic effect of the drug.
o should not be taken with magnesium and aluminum antacid preparations, milk products
containing calcium, or iron-containing drugs because these substances bind with
tetracycline and prevent absorption of the drug.
o absorption of doxycycline and minocycline is improved with food ingestion.
o SE/AR: GI disturbances such as nausea, vomiting, and diarrhea; Photosensitivity (sunburn
reaction) may occur in persons taking tetracyclines; Pregnant patients should not take
tetracycline during the first trimester of pregnancy because of possible teratogenic
effects. Women in the last trimester of pregnancy and children younger than 8 years of
age should also not take tetracycline because it irreversibly discolors the permanent
teeth; Outdated tetracyclines should always be discarded because the drug breaks down
into a toxic by-product; Renal failure results with some tetracyclines, especially when
given in high doses with other nephrotoxic drugs. Because tetracycline can disrupt the
microbial flora of the body, superinfection (secondary infection resulting from drug
therapy) is another adverse reaction that might result. Blood dyscrasias may occur with
tetracyclines.
o Antacids and iron-containing drugs can prevent absorption of tetracycline from the GI
tract; doxycycline better absorbed from the GI tract when taken with milk products and
food.
o The desired action of oral contraceptives can be lessened
 Doxycycline
Aminoglycosides (Gentamicin Sulfate)
 act by inhibiting bacterial protein synthesis; used against gram-negative bacteria such as E.
coli and Proteus and Pseudomonas species. Some gram-positive cocci are resistant to
aminoglycosides, so penicillins or cephalosporins may be used.
 are for serious infections, cannot be absorbed from the GI tract, nor can they cross into the
cerebrospinal fluid; they cross the blood-brain barrier in children but not in adults. These
agents are primarily administered IM and IV; may be given orally to decrease bacteria and
other organisms in the bowel.
 The aminoglycosides currently used to treat P. aeruginosa infection include gentamicin,
tobramycin, and amikacin. P. aeruginosa is sensitive to gentamicin.
 Gentamicin inhibits bacterial protein synthesis and has a bactericidal effect. The onset of
action is rapid or immediate, and the peak action for gentamicin is 30 minutes to 1 hour for
IM and 30 minutes for IV administration.
 To ensure a desired blood level, aminoglycosides are usually administered IV; patient’s blood
levels are drawn periodically to determine the drug’s peak (highest concentration) and trough
(lowest concentration) blood levels. A therapeutic drug level maintained by monitoring the
trough level, and peak levels are useful to monitor for toxicity
 SE/AR: ototoxicity and nephrotoxicity. Renal function, drug dose, and age are all factors that
determine whether a patient will develop nephrotoxicity from aminoglycoside therapy; nurse
must assess changes in patients’ hearing, balance, and urinary output; Prolonged use could
result in a superinfection, and specific serum aminoglycoside levels should be closely
monitored to avoid adverse reactions.

o
Fluoroquinolones (Ciproflaxin)
o interfere with the enzyme DNA gyrase, which is needed to synthesize bacterial DNA;
bactericidal action on both gram-positive and gram-negative organisms useful in the
treatment of urinary tract, bone, and joint infections; bronchitis; pneumonia;
gastroenteritis; and gonorrhea.
o Ciprofloxacin is a synthetic antibacterial related to nalidixic acid; has a broad spectrum of
action on gram-positive and gram-negative organisms, including P. aeruginosa; is
approved for use for urinary tract and lower respiratory tract infections and for skin, soft
tissue, bone, and joint infections.
o Fluoroquinolones, especially levofloxacin, should be reserved for patients who have no
other alternative treatment options for uncomplicated urinary tract infection (UTI), acute
bacterial exacerbation of chronic bronchitis, or acute bacterial sinusitis due to disabling
and potentially irreversible serious adverse reactions. These adverse reactions include
tendon rupture, tendinitis, peripheral neuropathy, central nervous system (CNS) effects,
and exacerbation of myasthenia gravis. (Black Box Warning.)
o it should be taken before meals because food slows the absorption rate; antacids also
decrease the absorption rate. Ciprofloxacin increases the effect of theophylline and
caffeine.
Chap 29: Sulfonamides and Nitroimidazoles Antibiotics
 Sulfonamides
o are bacteriostatic because they inhibit bacterial synthesis of folic acid, which is essential
for bacterial growth. Humans do not synthesize folic acid; rather, they acquire it through
the diet; therefore sulfonamides selectively inhibit bacterial growth without affecting
normal cells. Folic acid (folate) is required by cells for biosynthesis of RNA, DNA, and
proteins.
o may be used as an alternative drug for patients who are allergic to penicillin. They are still
used to treat urinary tract and ear infections and may be used for newborn eye
prophylaxis. frequently a preferred treatment for urinary tract infections, which are often
caused by E. coli. They are also useful in the treatment of meningococcal meningitis and
against Chlamydia species and Toxoplasma gondii.
o are not effective against viruses and fungi.
o SE/AR: allergic response such as skin rash and itching. Anaphylaxis is uncommon. Blood
disorders such as hemolytic anemia, aplastic anemia, and low white blood cell (WBC)
and platelet counts could result from prolonged use and high dosages. GI disturbances
such as anorexia, nausea, and vomiting may also occur. The early sulfonamides were
insoluble in acid urine, and crystalluria (crystals in the urine) and hematuria (blood in
the urine) were common problems. Increasing fluid intake dilutes the drug, which helps
prevent crystalluria. Photosensitivity, an excessive reaction to direct sunlight or
ultraviolet (UV) light that leads to redness and burning of the skin, can also occur;
therefore the patient should avoid sunbathing and excess ultraviolet light. Crosssensitivity, a sensitivity or allergy to one sulfonamide that leads to sensitivity to another
sulfonamide, might occur with the different sulfonamides but does not occur with other
antibacterial drugs. Sulfonamides should be avoided during pregnancy to avoid
congenital malformations, neural tube defects, and kernicterus.
 Trimethoprim-sulfamethoxazole (TMP-SMZ)
o contains one part trimethoprim and five parts sulfamethoxazole to produce a synergistic
effect that increases the desired drug response.
o

Trimethoprim is an antibacterial agent that interferes with bacterial folic acid synthesis
just as sulfonamides do; it is classified as a urinary tract antiinfective that may be used
alone for uncomplicated urinary tract infections, and it is also effective against the gramnegative bacteria E. coli and also Proteus and Klebsiella species.
o combined with sulfamethoxazole, an intermediate-acting sulfonamide, to prevent
bacterial resistance to sulfonamide drugs and to obtain a better response against many
organisms. Giving both drugs causes bacterial resistance to develop much more slowly
than if only one of the drugs were to be used alone.
o TMP-SMZ is effective in treating urinary, intestinal, lower respiratory tract, and middle
ear (otitis media) infections; prostatitis; and gonorrhea. It is also used to prevent
Pneumocystis carinii in patients with acquired immunodeficiency syndrome (AIDS).
Increased fluid intake is strongly recommended to avoid complications such as
crystalluria.
o TMP-SMZ blocks steps in the bacterial synthesis of protein and nucleic acid, producing a
bactericidal effect.
o SE/AR: mild to moderate rashes, anorexia, nausea, vomiting, diarrhea, stomatitis,
crystalluria, and photosensitivity. Serious adverse reactions are rare; however,
agranulocytosis, aplastic anemia, and myocarditis have been reported as possible lifethreatening conditions.
Nitroimidazoles
o act by disrupting DNA and protein synthesis in susceptible bacteria and protozoa. The
nitroimidazoles are effective against H. pylori and bacterial species (such as Bacteroides,
Clostridium, Gardnerella, Prevotella, Peptococcus, Giardia), and protozoa (such as
Trichomonas vaginalis).
o used for prophylaxis for surgical infections and to treat Clostridium difficile–associated
diarrhea (CDAD), anaerobic infections, amebiasis, giardiasis, trichomoniasis, bacterial
vaginosis, and acne rosacea. Metronidazole and tinidazole are two of the most effective
drugs available to treat anaerobic bacterial infections.
o Nitroimidazoles are primarily administered orally, parenterally, and topically. When
metronidazole is given IV intermittently, it should be administered slowly over 30 to 60
minutes. Avoid contact with the eyes when using topical product.
 Metronidazole
 Nitroimidazoles disrupt DNA and protein synthesis becoming bactericidal,
amebicidal, and trichomonacidal.
 metronidazole can be given without regard to food.
 When metronidazole is used in the extended release form, it should be taken on
an empty stomach. The topical form is only minimally absorbed. The peak action
for both agents is 1 to 3 hours.
 SE/AR:Common side effects that may occur when taking nitroimidazoles include
headache, dizziness, insomnia, weakness, dry mouth, dysgeusia, anorexia,
nausea, vomiting, diarrhea, tongue/urine discoloration, and superinfection. More
serious adverse reactions that have occurred with metronidazole and tinidazole
are leukopenia, peripheral neuropathy, seizures, and Stevens-Johnson syndrome.
A disulfiram-like reaction may occur when metronidazole is taken with excessive
amounts of alcohol. Symptoms of disulfiram-like reaction include flushing,
throbbing headache, visual disturbance, confusion, dyspnea, nausea, vomiting,
tachycardia, syncope, and circulatory collapse.
o
Chap 38: Upper Respiratory Disorders
 Common Cold, Acute Rhinitis, Allergic Rhinitis
o The common cold is caused by the rhinovirus and affects primarily the nasopharyngeal
tract. Acute rhinitis, acute inflammation of the mucous membranes of the nose, usually
accompanies the common cold. Acute rhinitis is not the same as allergic rhinitis, often
called hay fever, which is caused by pollen or a foreign substance such as animal dander.
Nasal secretions increase in both acute and allergic rhinitis.
o A cold is most contagious 1 to 4 days before the onset of symptoms (the incubation
period) and during the first 3 days of the cold. Transmission occurs more frequently from
touching contaminated surfaces and then touching the nose or mouth than it does from
contact with viral droplets released by sneezing.
o Symptoms of the common cold include rhinorrhea (watery nasal discharge), nasal
congestion, cough, and increased mucosal secretions. If a bacterial infection secondary to
the cold occurs, infectious rhinitis may result, and nasal discharge becomes tenacious,
mucoid, and yellow or yellow green. The nasal secretions are discolored by white blood
cells and cellular debris that are by-products of the fight against the bacterial infection.
 Antihistamines
o Antihistamines, H1 blockers or H1 antagonists, compete with histamine for receptor sites
and prevent a histamine response.
o The two types of histamine receptors, H1 and H2, cause different responses.
o When the H1 receptor is stimulated, the extravascular smooth muscles—including those
lining the nasal cavity—are constricted. With stimulation of the H2 receptor, an increase
in gastric secretions occurs, which is a cause of peptic ulcer
o Antihistamines decrease nasopharyngeal secretions by blocking the H1 receptor.
o Although antihistamines are commonly used as cold remedies, these agents can also treat
seasonal allergies that cause allergic rhinitis. However, antihistamines are not useful in an
emergency situation such as anaphylaxis. Most antihistamines are rapidly absorbed in 15
minutes, but they are not potent enough to combat anaphylaxis.
o Diphenhydramine
 primary use is to treat rhinitis.
 Diphenhydramine blocks the effects of histamine by competing for and
occupying H1 receptor sites. It has anticholinergic effects and should be used
with caution by patients with closed-angle glaucoma. Drowsiness is a major side
effect of the drug; in fact, it is sometimes used in sleep aid products.
Diphenhydramine is also used as an antitussive to alleviate cough. Its onset of
action can occur in as few as 15 minutes when taken orally and IM. Intravenous
administration results in an immediate onset of action. The duration of action is
4 to 7 hours.
 Diphenhydramine can cause central nervous system (CNS) depression if taken
with alcohol, narcotics, hypnotics, or barbiturates.
 SE: drowsiness, dizziness, fatigue, and disturbed coordination. Skin rashes and
anticholinergic symptoms such as dry mouth, urine retention, blurred vision,
and wheezing may also occur.
 Nasal and Systemic Decongestants
o Phenylephrine hydrochloride
o Pseudoephedrine


Nasal congestion results from dilation of nasal blood vessels caused by infection,
inflammation, or allergy. With this dilation, a transudation of fluid into the tissue spaces
occurs that results in swelling of the nasal cavity.
 Nasal decongestants (sympathomimetic amines) stimulate the alpha-adrenergic receptors,
producing vascular constriction (vasoconstriction) of the capillaries within the nasal mucosa.
The result is shrinking of the nasal mucous membranes and a reduction in fluid secretion
(runny nose).
 Nasal decongestants are administered by nasal spray or drops or in tablet, capsule, or liquid
form. Frequent use of decongestants, especially nasal spray or drops, can result in tolerance
and rebound nasal congestion, rebound vasodilation instead of vasoconstriction. Rebound
nasal congestion is caused by irritation of the nasal mucosa.
 Systemic decongestants (alpha-adrenergic agonists) are available in tablet, capsule, and
liquid form, and are used primarily for allergic rhinitis, including hay fever and acute coryza
(profuse nasal discharge).
 (FDA) ordered its removal from OTC cold remedies and weight loss aids because reports
suggest that the drug might cause stroke, hypertension, renal failure, and cardiac
dysrhythmias.
 The advantage of systemic decongestants is that they relieve nasal congestion for a longer
period than nasal decongestants
 Nasal decongestants usually act promptly and cause fewer side effects than systemic
decongestants.
 National regulatory measures control pseudoephedrine drug sales with individual limits of
3.6 g/day and 9 g within 30 days
 SE/AR: is low with topical preparations such as nose drops.
 decongestants can make a patient nervous or restless. These side effects decrease or
disappear as the body adjusts to the drug.
 Use of nasal decongestants for as little as 3 days could result in rebound nasal congestion.
Instead of the nasal membranes constricting, vasodilation occurs, causing increased stuffy
nose and nasal congestion. The nurse should emphasize the importance of limiting the use
of nasal sprays and drops.
 As with any alpha-adrenergic drug such as decongestants, blood pressure and blood glucose
levels can increase. These drugs are contraindicated or used with extreme caution in
patients with hypertension, cardiac disease, hyperthyroidism, and diabetes mellitus.
Antitussives (Dextromethorphan)
o act on the cough control center in the medulla to suppress the cough reflex. The cough
is a naturally protective way to clear the airway of secretions or any collected material.
A sore throat may cause coughing that increases throat irritation. If the cough is
nonproductive and irritating, an antitussive may be taken. Hard candy may decrease the
constant, irritating cough. Dextromethorphan, a nonnarcotic antitussive, is widely used
in OTC cold remedies.
o The three types of antitussives are nonopioid, opioid, or combination preparations.
o Dextromethorphan, an antitussive, provides temporary cough relief, especially for
nonproductive cough due to sore throat, irritation, or the common cold. This drug acts
by decreasing the excitability of the cough center in the medulla.
o
o
Dextromethorphan has a duration of 3 to 6 hours. Usually preparations that contain
dextromethorphan can be used several times a day.
o SE: dizziness, drowsiness, confusion, fatigue, ataxia, nauseam\, vomiting, restlessness
 Expectorants (Guaifenesin)
o Expectorants loosen bronchial secretions so they can be eliminated by coughing. They
can be used with or without other pharmacologic agents. Expectorants are found in
many OTC cold remedies along with analgesics, antihistamines, decongestants, and
antitussives. The most common expectorant in such preparations is guaifenesin.
Hydration is the best natural expectorant. When taking an expectorant, patients should
increase fluid intake to at least 8 glasses per day to help loosen mucus.
o May cause drowsiness, dizziness, headache, NVD
Chap 39: Lower Respiratory Disorders
 Chronic Obstructive Pulmonary Disease
o Medications frequently prescribed for COPD include the following:
 Bronchodilators such as sympathomimetics (adrenergics), parasympatholytics
(anticholinergic drugs, ipratropium bromide), and methylxanthines (caffeine,
theophylline) are used to assist in opening narrowed airways.
 Glucocorticoids (steroids) are used to decrease inflammation.
 Leukotriene modifiers reduce inflammation in the lung tissue, and cromolyn acts
as an anti-inflammatory agent by suppressing the release of histamine and other
mediators from the mast cells.
 Expectorants are used to assist in loosening mucus from the airways.
 Antibiotics may be prescribed to prevent serious complications from bacterial
infections.
 Asthma
 is an inflammatory disorder of the airway walls associated with a varying amount
of airway obstruction. This disorder is triggered by stimuli such as stress,
allergens, and pollutants. When activated by stimuli, the bronchial airways
become inflamed and edematous, leading to constriction of air passages.
Inflammation aggravates airway hyperresponsiveness to stimuli, causing
bronchial cells to produce more mucus, which obstructs air passages. This
obstruction contributes to wheezing, coughing, dyspnea (breathlessness), chest
tightness, and bronchospasm, particularly at night or in the early morning.
o Sympathomimetics: Alpha- and Beta- Adrenergic Agonists (Epinephrine is an alpha1, beta
1, beta 2 adrenergic)
 Sympathomimetics increase cAMP, causing dilation of the bronchioles.
 Albuterol is a selective beta2 drug that is effective for treatment and
control of asthma by causing bronchodilation with a long duration of
action.
 Metaproterenol has some beta1 effect but is primarily used as a beta2
agent. It can be administered orally or by inhalation with a metered-dose
inhaler (MDI) or a nebulizer.
 SE/AR: of epinephrine include tremors, dizziness, hypertension, tachycardia,
palpitations, dysrhythmias, and angina. The patient needs to be closely
monitored when epinephrine is administered.
 The side effects associated with beta2-adrenergic drugs, such as albuterol,
include tremors, headaches, restlessness, increased pulse rate, and palpitations
o
o
(high doses). The beta2 agonists may increase blood glucose levels, so patients
with diabetes should be taught to closely monitor their serum glucose levels. Side
effects of beta2 agonists may diminish after 1 week or longer. The
bronchodilating effects may decrease with continued use. It is believed that
tolerance to these drugs can develop; if this occurs, the dose may need to be
increased. Failure to respond to a previously effective dose may indicate
worsening asthma that requires reevaluation before increasing the dose.
Anticholinergics
 Tiotropium
 is an anticholinergic drug used for maintenance treatment of
bronchospasms associated with COPD. This drug is administered by
inhalation only with the HandiHaler device (DPI).
 HandiHalers should be washed with warm water and dried.
 AE:dry mouth, constipation, vomiting, dyspepsia, abdominal pain,
depression, insomnia, headache, joint pain, and peripheral edema. Chest
pain has been reported after tiotropium administration.
Methylxanthine (Xanthine) Derivatives
 group of bronchodilators used to treat asthma
 Xanthines also stimulate the central nervous system (CNS) and respiration,
dilate coronary and pulmonary vessels, and cause diuresis. Because of their
effect on respiration and pulmonary vessels, xanthines are used in the
treatment of asthma.
 Aminophylline-Theophylline
 Aminophylline-theophylline relaxes the smooth muscles of the bronchi,
bronchioles, and pulmonary blood vessels by inhibiting the enzyme
phosphodiesterase, resulting in an increase in cAMP, which promotes
bronchodilation.
 Theophylline has a low therapeutic index and a narrow desired
therapeutic range (5 to 15 mcg/mL). The serum or plasma theophylline
concentration level should be monitored frequently to avoid severe
adverse effects. Toxicity is likely to occur when the serum level is greater
than 20 mcg/mL.
 potential danger of serious adverse effects—including dysrhythmias,
seizures, and cardiac arrest—and efficacy has not been found to be
greater than that of beta agonists or glucocorticoids.
 Because of its numerous adverse reactions, drug-drug interactions, and
narrow therapeutic drug range, theophylline is prescribed mostly for
maintenance therapy in patients with chronic stable asthma and other
COPDs when other drugs have failed to show improvement.
 Theophylline drugs are not prescribed for patients with seizure disorders
or cardiac, renal, or liver disease. Patients who receive theophylline
preparations need to be closely monitored for serious side effects and
drug interactions.
 SE/AR: anorexia, nausea, vomiting, diarrhea, gastric pain caused by
increased gastric acid secretion, hematemesis, dysrhythmias,
tachycardia, palpitations, and marked hypotension. Adverse CNS
reactions—headaches, irritability, restlessness, insomnia, dizziness, and
o
o
seizures—are often more severe in children than in adults. To decrease
the potential for side effects, patients should not take other xanthines
while taking theophylline.
 Theophylline toxicity is most likely to occur when serum concentrations
exceed 20 mcg/mL. Theophylline can cause hyperglycemia, decreased
clotting time, and, rarely, increased white blood cell count (leukocytosis).
Because of the diuretic effect of xanthines, including theophylline,
patients should avoid caffeinated products such as coffee, tea, cola, and
chocolate, and they should increase fluid intake.
 Rapid IV administration of aminophylline, a theophylline product, can
cause dizziness, flushing, hypotension, severe bradycardia, and
palpitations. To avoid severe adverse effects, IV theophylline
preparations must be administered slowly via an infusion pump.
Leukotriene Receptor Antagonists and Synthesis Inhibitors
 Montelukast
 Leukotriene (LT) is a chemical mediator that can cause inflammatory
changes in the lung.; promote an increase in eosinophil migration,
mucous production, and airway wall edema that results in
bronchoconstriction.
 LT receptor antagonists and LT synthesis inhibitors, called leukotriene
modifiers, are effective in reducing the inflammatory symptoms of
asthma triggered by allergic and environmental stimuli. These drug
groups are not recommended for treatment of acute asthmatic attacks;
rather, they are used for exercise-induced asthma.
 Leukotriene receptor antagonists and synthesis inhibitors should not be
used during an acute asthmatic attack. They are only for prophylactic
and maintenance drug therapy for chronic asthma.
 SE: headache, dizziness, drowsiness, cough, nasal congestion, fatigue,
infection, agitation, restlessness, insomnia, confusion, depression,
influenza, edema, palpitations, muscle cramps
Glucocorticoids (Steroids)
 members of the corticosteroid family, are used to treat respiratory disorders,
particularly asthma.
 have an antiinflammatory action and are indicated if asthma is unresponsive to
bronchodilator therapy or if the patient has an asthmatic attack while on
maximum doses of theophylline or an adrenergic drug.
 It is thought that glucocorticoids have a synergistic effect when given with a
beta2 agonist.
 can be given using the following methods:
 MDI inhaler: Beclomethasone
 Tablet: Dexamethasone, prednisone
 Intravenous: Dexamethasone
 Inhaled glucocorticoids are not helpful in treating a severe asthmatic attack
because it may take 1 to 4 weeks for an inhaled steroid to reach its full effect.






When severe asthma requires prolonged glucocorticoid therapy, weaning or
tapering of the dose may be necessary to prevent an exacerbation of asthma
symptoms and suppression of adrenal function.
Glucocorticoids can irritate the gastric mucosa and should be taken with food to
avoid ulceration.
does not replace fast-acting inhalers for sudden symptoms.
SE/AR:Side effects associated with orally inhaled glucocorticoids are generally
local (e.g., throat irritation, hoarseness, dry mouth, coughing) rather than
systemic. Oral, laryngeal, and pharyngeal fungal infections have occurred but
can be reversed with discontinuation and antifungal treatment. Candida
albicans oropharyngeal infections may be prevented by using a spacer with the
inhaler to reduce drug deposits in the oral cavity, rinsing the mouth and throat
with water after each dose, and washing the apparatus (cap and plastic nose or
mouthpiece) daily with warm water.
Oral and injectable glucocorticoids have many side effects when used long term,
but short-term use usually causes no significant side effects. Most adverse
reactions are seen within 2 weeks of glucocorticoid therapy and are usually
reversible. Side effects that may occur include headache, euphoria, confusion,
diaphoresis, insomnia, nausea, vomiting, weakness, and menstrual irregularities.
Adverse effects include depression, peptic ulcer, loss of bone density and
development of osteoporosis, and psychosis.
When oral and IV steroids are used for prolonged periods, electrolyte
imbalance, fluid retention (puffy eyelids, edema in the lower extremities, moon
face, weight gain), hypertension, thinning of the skin, purpura, abnormal
subcutaneous fat distribution, hyperglycemia, and impaired immune response
are likely to occur.