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DISEASES Muscle Spasms Involuntary contractions of a muscle or groups of muscles. The muscles become tightened and develop a fixed pattern of resistance, resulting in diminished levels of function. Severe muscle spasms seen in patients who have other disorders such as stroke, injury, neurodegenerative diseases, cerebral palsy. A single prolonged contraction is a tonic spasm. Multiple, rapidly repeated contractions are clonic spasms. Other causes of muscle spasms include overmedication with antipsychotic drugs, epilepsy, hypocalcemia, pain and neuro disorders. Spasticity: muscles in a continuous state of contraction; usually contracted muscles become still with increased muscle tone; other signs and symptoms include pain, muscle spasms, involuntary crossing of the legs, and fixed joints. Etiologies for spasticity: cerebral palsy, head injury, spinal cord injury, stroke. Dystonia: chronic neuro disorder; involuntary muscle contraction that forces body parts into abnormal/painful positions and postures. Medications alone are not adequate in reducing the complications of spasticity. Physical therapy is

Nursing Pharmacology Study Guide

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Page 1: Nursing Pharmacology Study Guide

DISEASES

Muscle Spasms

Involuntary contractions of a muscle or groups of muscles. The muscles

become tightened and develop a fixed pattern of resistance, resulting in

diminished levels of function. Severe muscle spasms seen in patients who

have other disorders such as stroke, injury, neurodegenerative diseases,

cerebral palsy.

A single prolonged contraction is a tonic spasm. Multiple, rapidly repeated

contractions are clonic spasms.

Other causes of muscle spasms include overmedication with antipsychotic

drugs, epilepsy, hypocalcemia, pain and neuro disorders.

Spasticity: muscles in a continuous state of contraction; usually contracted

muscles become still with increased muscle tone; other signs and symptoms

include pain, muscle spasms, involuntary crossing of the legs, and fixed joints.

Etiologies for spasticity: cerebral palsy, head injury, spinal cord injury, stroke.

Dystonia: chronic neuro disorder; involuntary muscle contraction that forces

body parts into abnormal/painful positions and postures.

Medications alone are not adequate in reducing the complications of

spasticity. Physical therapy is needed, including strengthening and stretching

exercises.

Alzheimer’s

AD is responsible for 70% of all dementia. Dementia is a degenerative

disorder with signs of progressive memory loss, confusion, and an inability to

think or communicate effectively.

Consciousness and perception usually unaffected.

Associated with cerebral atrophy/structural changes of the brain. Patients

generally live 5-10 years following a DX of AD, which is the 4th leading cause

of death.

Etiology of AD remains mostly unknown. Early onset form of the disease is

associated with chromosomal defects. Amyloid plaques/neurofibrillary

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tangles are found in nearly all patients with AD, upon autopsy. Loss in both

the number and function of neurons.

AD patients experience a loss in the ability to perform tasks that require

acetylcholine as the neurotransmitter. Acetylcholine is a major

neurotransmitter in the area of the brain responsible for learning/memory,

neuronal function is affected. Symptoms of AD are as follows: impaired

memory/judgement; confusion/disorientation; inability to recognize

friends/family; aggressive behavior; depression; psychoses, paranoia,

delusions; anxiety.

Parkinson’s

Degenerative disorder of the CNS caused by death of neurons that produce

the brain neurotransmitter dopamine. The second most common

degenerative disease of the nervous system. Pharmacotherapy often

successful at reducing some of the symptoms of this disease.

Progressive disease, and full symptoms take many years to show. Symptoms

include: tremors, when the hands and head are shaky at rest, patients rub the

thumb and forefinger together as if a pill were between them; muscle rigidity,

stiffness may resemble symptoms of arthritis, difficulty bending over or

moving limbs, become more obvious in later years; bradykinesia, marked by

difficulty chewing, swallowing, speaking, patients with Parkinson’s have

problems initiating movement and controlling fine muscle movement,

walking becomes difficult, patients shuffle their feet without taking normal

strides; postural instability, patients may be humped over and easily lose

balance; affective flattening, patients often have “masked face” with little

facial expression or blinking of eyes.

Symptoms develop due to the destruction of dopamine-producing neurons in

the area of the brain that controls unconscious muscle movement.

Balance, posture, muscle tone and involuntary movement depend on a

balance of dopamine (inhibitory) and acetylcholine (stimulatory) in the brain.

If dopamine is absent, then acetylcholine has a more dramatic effect.

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Drug therapy for parkinsonism focuses on restoring dopamine function and

blocking the effect of acetylcholine.

Extrapyramidal Side Effects (EPS) develop for the same reasons as

Parkinson’s disease. Antipsychotic drugs act through a blockade of dopamine

receptors. Treatment with certain antipsychotic drugs can induce

parkinsonism-like symptoms, or EPS, by interfering with the same neural

pathway and functions affected by the lack of dopamine. EPS may occur

suddenly and become a medical emergency. With acute EPS, patient’s mescles

may spasm or become locked up. Fever and confusion are other signs. Give IV

Benadryl.

Schizophrenia

A type of psychoses characterized by abnormal thoughts and thought

processes, disordered communication, withdrawal from other people, and a

high risk for suicide.

It is the most common psychotic disorder, and affects 1-2% of the population.

Symptoms appear in early adulthood, and they may appear quickly or take

several years. Other symptoms include: hallucinations, delusions, paranoia;

strange behavior, communicating in rambling statements of made-up words;

alternating between extreme hyperactivity and stupor;

indifference/detachment toward life activities; strange/irrational actions;

deterioration of personal hygiene, job/school performance; withdrawal from

social interactions, interpersonal relationships.

Nurses should look for both positive and negative symptoms. Positive

symptoms ar those that add on to normal behavior (hallucinations, delusions,

disorganized thought and speech patterns); while negative symptoms are

those that subtract from normal behavior (lack of interest and motivation,

lack of response, no pleasure in daily activities).

Cause not known for sure, but there may be a genetic link. May be caused by

imbalances in neurotransmitters in areas of the brain. Overactive

dopaminergic pathways in the area of the brain that controls neuro activity.

Symptoms of schizophrenia seem to be associated with the dopamine type 2

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(D2) receptors. All antipsychotic drugs act by entering the dopaminergic

synapses and competing with dopamine. By blocking a majority of the D2

receptors, antipsychotic drugs reduce the symptoms of schizophrenia.

Schizoaffective Disorder: patient feels schizo symptoms and mood disorders.

Acute Achizoaffective pt will have hallucinations followed by extreme

depression.

Insomnia

The inability to fall asleep or stay asleep. This is bad because the body repairs

itself during sleep. Deals with electrical charging and discharging of the brain.

The brain needs time to process and file new information collected

throughout the day. Sleeping and waking are synchronized to bodily functions

like temperature, blood pressure, hormone levels, respiration.

Increased levels of the neurotransmitter serotonin help initiate the various

processes of sleep.

Insomnia is sometimes associated with anxiety. Short-term/behavioral

insomnia: when a hectic lifestyle inhibits sleep because the mind is too active.

Caffeine and some foods may interrupt sleep. Tobacco products might make

someone edgy and restless. Alcohol causes people to fall asleep, but can cause

vivid dreams and frequent awakening. Ingesting a large meal high in protein

and fat can interfere with sleep due to the increased metabolic rate needed to

digest the food. Long-term insomnia is often caused by depression, manic

disorders, chronic pain.

Long-term use of sleep meds is likely to worsen insomnia and may cause

physical or psychologic dependence. Rebound insomnia: when a sedative

drug is discontinued abruptly after it has been taken for a long time,

symptoms become much worse.

When PRN meds are required for sleep, the nurse needs to conduct an

individualized assessment of the individual, as well as follow-up evaluation

and documentation of the medication’s effect on the patient.

Insomnia linked to type 2 diabetes.

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Depression

Characterized by a sad or despondent mood. Symptoms include lack of

energy, sleep disturbances, abnormal eating patters, feelings of despair,

hopelessness, guilt. Most common mental health disorder among elderly

adults.

Major Depression: affects up to 10% of adults in the U.S.; to diagnose the

disorder, the patient should have a depressed affect and at least 5 of the

following symptoms lasting for a minimum of 2 weeks: difficulty sleeping or

sleeping too much; extremely tired, without energy; abnormal eating

patterns; vague physical symptoms like GI pain, muscle pain, headaches;

inability to concentrate/make decisions; feelings of despair/guilt/misery,

lack of self-worth; obsessed with death; avoiding interpersonal relations; lack

of interest in appearance; delusions or hallucinations.

Psychotic Depression: intense mood shifts and unusual behavior. Loss of

contact with reality, hallucinations, delusions, disorganized speech patterns.

Seizures

Clinically detectable sign of epilepsy. A disturbance of electrical activity in the

brain that may affect consciousness, motor activity, and sensation. Cause by

abnormal or uncontrolled neuronal discharges. Uncontrolled charges may

remain in one focus or propagate to other areas of the brain.

Electroencephalogram (EEG) is useful in diagnosing seizure disorders.

Seizure and convulsion are not synonymous. Convulsions refer to

involuntary, violent spasms of the large skeletal muscles of the face, neck,

arms, and legs. Not all seizures involve convulsions. All convulsions are

seizures, but not all seizures are convulsions.

Antiseizure Drugs: treat some/all symptoms related to seizures, including

signs of epilepsy.

A seizure is a symptom of an underlying disease, not the disease itself.

Triggers include exposure to strobe/flickering lights, or fluid and electrolyte

imbalances. Seizures can be acute or chronic, and can be caused by too-high

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doses of come meds for mood disorders, or with drug abuse from cocaine or

while withdrawing from alcohol.

Known causes of seizures include: infectious diseases like meningitis and

encephalitis that cause inflammation in the brain; trauma, like a physical blow

to the skull, which may increase intracranial pressure, or chemical trauma

such as the presence of toxic substances or poison; metabolic disorders, such

as changes in fluid and electrolytes (hypoglycemia, hyponatremia, water

intoxification); vascular diseases, such as changes in oxygenation caused by

respiratory hypoxia and carbon monoxide poisoning, changes in perfusion

caused by hypotension, cerebral vascular accidents, shock, cardiac

dysrhythmias. Pediatric disorders, such as a rapid increase in body

temperature. Neoplastic disorders, such as tumors, especially rapidly gorwing

ones that may increase intracranial pressure and damage brain tissue by

disrupting blood flow.

Several antiseizure durgs decrease the effectiveness of birth control.

If the patient is pregnant, some antiseizure drugs can cause folate deficiency.

Simple Partial Seizure: Olfactory, auditory and visual hallucinations; intense

emotions; twitching of arms, legs and face.

Complex Partial: aura preceding the seizure; brief period of confusion or

sleepiness afterward with no memory of the seizure; fumbling with or

attempting to remove clothing; no response to verbal commands.

General, absence seizure, or petit mal: Lasting a few seconds; seen most often

in children when the child stares into space and doesn’t respond but has

fluttering eyelids or jerking movements; misdiagnosed as ADD or

daydreaming.

General, atonic seizures, or drop attacks: Falling or stumbling for no reason;

lasting a few seconds.

General, tonic-clonic seizure, or grand mal: Aura preceding the seizure;

intense muscle contraction (tonic phase) followed by alternating contraction

and relaxation of muscles (clonic phase); crying at beginning as air leaves the

lungs, loss of bowel/bladder control; shallow breathing with periods of

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apnea, usually lasting 1-2 minutes; disorientation and deep sleep after

seizure.

Myoclonic Seizure: large jerking movements of a major muscle group, such as

an arm; falling from a sitting position or dropping what is held.

Status epilepticus: a medical emergency; continuous seizure activity, which

can lead to coma and death.

Asthma

One of the most common chronic conditions in the U.S. Characterized by acute

bronchospasm, it can cause intense breathlessness, coughing and gasping for

air. An acute inflammatory response stimulates histamine secretion, which

increases mucus and edema in the airways. Some patients experience asthma

when exposed to certain triggers, and others experience the disorder when

exercising. Status asthmaticus is a severe, prolonged disorder that may lead

to respiratory failure.

The goals of drug therapy are to terminate acute bronchospasms in progress

and to reduce the frequency of asthma attacks.

Beta2-adrenergic agonists (beta agonists, sympathomimetics) are effective

bronchodilators to manage asthma and other pulmonary diseases. They are

the drug of choice for acute bronchoconstriction. Beta-adrenergic agonists

activate the sympathetic nervous system, relaxing bronchial smooth muscles,

and resulting in bronchodilation.

Beta1 receptors are located primarily in the heart. Beta2 receptors are

located in smooth muscle of the lung, uterus, and other organs. These have no

anti-inflammatory properties, which is why other classes of drugs are used to

control chronic asthma.

Short-acting beta agonists have a rapid onset of action, usually several

minutes, and are most frequently prescribed as rescue agents for aborting or

terminating an acute asthma attack. Their effects only last 2-6 hours,

however.

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Intermediate duration beta agonists like albuterol and levelbuterol have

effects that last approximately 8 hours and long-acting agents last up to 12

hours. The intermediate and long-acting agents are used in combination with

inhaled corticosteroids for the prophylaxis of moderate to severe, persistent

asthma.

Taking a long-acting beta agonist can result in death if a person takes it for an

acute attack.

Osteoporosis

The skeletal system is the primary repository for calcium. It is the primary

mineral responsible for maintaining bone health throughout the lifespan. It is

also critical to proper functioning of the nervous, muscular, and CV systems.

Calcium balance in the body is regulated by parathyroid hormone (PTH),

calcitonin, and vitamin D. In response to low levels of calcium in the

bloodstream, PTH is released which stimulates the release of calcium from

bones and increased calcium reabsorption from the kidneys. Higher levels of

calcium in the bloodstream trigger calcitonin release by the thyroid which

leads to calcium being added to bone, and decreased absorption of calcium in

the small intestine. Vitamin D and calcium disorders are often associated.

Vitamin D is increased by exposure to sunlight, and it is eventually etabolized

to calcitriol which increases calcium absorption from the GI tract. Dietary

calcium is absorbed more efficiently in the presence of active vitamin D and

parathyroid hormone.

Osteoporosis is the most common metabolic bone disorder. It is usually

asymptomatic until bones begin to break. The following are risk factors for

osteoporosis: menopause, high alcohol/caffeine consumption; anorexia;

tobacco use; physical inactivity; low vitamin D and calcium; corticosteroid

use, anticonvuldants use and immunosuppressants tha lower the serum

calcium levels. Greatest risk factor is menopause because estrogen secretion

declines, and bones become weak. Bone demineralization is accelerated,

resulting in loss of bone density. Drug therapies include calcium and vitamin

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D, estrogen replacement therapy, estrogen receptor modulators, statins, etc.

The most common drug class for treating osteoporosis is the biphosphonates,

which inhibit the breakdown of bone. They suppress osteoclast activity which

increases bone density and reduces the incidence of fractures. Bone mass

density increases rapidly during the first year of therapy and then plateaus.

Patient must take med with adequate calcium and vitamin D in the diet.

Dysrhythmias

Abnormalities of electrical conduction that may result in alterations in heart

rate or cardiac rhythm. Some produce no symptoms and others are life

threatenening and require immediate treatment. Symptoms include dizziness,

weakness, decreased exercise tolerance, shortness of breath, fainting. They

may experience palpitations or that their heart has skipped a beat.

Atrial fibrillation, a complete disorganization of rhythm, is the most common

dysrhythmia. Those that originate in the ventricles are generally more

serious. The following conditions are associated with dysrhythmias: HTN,

cardiac valve disease/mitral stenosis, coronary artery disease, digoxin use,

low potassium levels in the blood, MI, stroke, DM, CHF.

Atrial/Ventricular Tachycardia: HB more than 100 in adults.

Atrial/Ventricular Flutter: rapid, regular heartbeats, may range between 200-

300 per minute, usually not fatal if atrial but ventricular requires immediate

treatment.

Atrial/Ventricular Fibrillation: rapid, uncoordinated beats; complete

disorganization of rhythm, lack of adequate cardiac contraction; requires

immediate attention.

Heart Block: area of nonconduction in the myocardium.

Premature atrial/premature ventricular contractions: An extra beat

originating from a source other than the SA node; normally not serious unless

it’s frequent.

Sinus bradycardia: slow HB, less than 60 BPM, may require a pacemaker.

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Glaucoma

An eye disease caused by damage to the optic nerve, resulting in a gradual

loss of vision, possibly advancing to blindness. Usually the disorder is

accompanied by increased intraocular pressure. Glaucoma occurs when the

IOP is so high that it causes damage to the optic nerve. Glaucoma as a primary

condition without an identifiable cause is most frequently found in persons

older than 60. This disease can be associated with genetic factors, it can be

congenital and in young children. It can also be secondary to eye trauma,

infection, diabetes, inflammation, hemorrhage, tumors, and cataracts. The

long-term use of topical corticosteroids can cause glaucoma, in addition to

some anti-hypertensives, antihistamines, and antidepessants. Other risk

factors for glaucoma include HTN, migraines, high degrees of near-or-far-

sightedness, and normal aging. It is the leading cause of preventable

blindness.

Closed-angle glaucoma: not as common. Can be caused by stress, impact

injury, or meds. Displacement of the iris due to pressure inside the eye.

Causes dull to severe eye pain, headaches, bloodshot eyes, and a bulging iris.

Open-angle glaucoma: most common type. Cause is not known, and many

people don’t have symptoms. Usually bilateral. Develops over years.

Patient is treated when their IOP is high or they present with signs of optic

nerve damage or visual field changes. When beginning meds for this, a target

IOP is identified and the IOP is reevaluated after 2-4 months. Some

antiglaucoma meds take up to 8 weeks to reach peak effect. It is common to

add a 2nd drug if just one is not working. The meds work by either increasing

the outflow of aqueous humor or decreasing the formation of aqueous humor.

Many glaucoma meds work by affecting the autonomic nervous system.

Peptic Ulcer Disease

Parietal cells secrete intrinsic factor, which is essential for the absorption of

vitamin b12. Parietal cells also secrete hydrochloric acid every day, which

helps to break down food, activates pepsinogen and kills microbes.

Chief cells secrete pepsinogen, which chemically breaks down proteins.

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The combined secretion of the chief and parietal cells – gastric juice – is the

most acidic fluid in the body, having a PH of 1.5-3.5. To pretect against this

acid, cells on the surface of the stomach secrete a thick mucous and

bicarbonate ion to neutralize the acid.

An ulcer is an erosion of the mucosa layer of the GI tract, usually associated

with inflammation. The duodenum is a common ulcer site although they can

happen anywhere in the alimentary canal. Peptic Ulcer refers to a lesion in

either the stomach (gastric) or the small intestine (duodenal). Peptic Ulcer

Disease is associated with a family history of the disease; blood group O;

smoking tobacco; beverages with caffeine; corticosteroids, NSAIDs, aspirin;

psychological stress; infection with H. Pylori. The primary cause of PUD is

infection by H. Pylori. In noninfected patients, the most common cause of PUD

is NSAID usage.

The classic symptom of a duodenal ulcer is burning and upper abdominal

pain that occurs 1-3 hours after a meal. The pain is worse when the stomach

is empty and often disappears with the ingestion of food. Most heal

spontaneously. Gastric Ulcers are less common and have different symptoms.

Although relived by food, the pain may continue even after a meal. Anorexia,

weight loss, and vomiting are more common. Follow-up for gastric ulcers

should continue for several years, as they can become cancerous. Gastric

ulcers are more common in women older than 60. Ulceration in the distal

small intestine is known as Crohn’s Disease, and erosions in the large

intestine are called ulcerative colitis.

GERD

A common condition in which the acidic contents of the stomach move

upward into the esophagus. It causes intense burning (heartburn) and is

sometimes accompanied by belching. In some cases, untreated GERD can lead

to esophagal complications. Can occur in adults and infants. The cause of

GERD is usually a weakening of the lower esophageal sphincter – it may no

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longer close tightly, thereby allowing contents of the stomach to move up

when the stomach contracts. GERD is associated with obesity, and losing

weight may eliminate the issues. Other lifestyle changes that can improve

GERD symptoms include elevating the head of the bed, avoiding fatty or acidic

foods, eating smaller meals at least 3 hours before sleep, and eliminating use

of tobacco/alcohol.

Many drugs used for PUD can be used for GERD, with the primary goal being

to reduce gastric secretions.

Constipation

Constipation is a decrease in the frequency of bowel movements. Stools may

become dry, hard, and difficult to evacuate without straining. When waste

material remains in the colon for too long, too much water is reabsorbed,

leading to small, hard stools. Constipation can cause abdominal distention,

discomfort and flatulence. It is a symptom of an underlying disorder. May be

related to a lack of exercise, insufficient food/fiber intake; or drugs that

reduce intestinal motility. Opioids, anticholinergics, antihistamines, certain

antacids and iron supplements can cause constipation. Foods that can cause

constipation inclue alcohol, white flour products, dairy, and chocolate.

Hypothyroidism, diabetes and IBS can also cause constipation.

Hypertension

Most common CV disease. Consistent elevation of systemic arterial blood

pressure. Greater than 140/99. Blood pressure changes through the lifespan,

rising with age.

Factors responsible for creating the pressure are cardiac output, blood

volume and peripheral resistance. The volume of blood pumped per minute is

cardiac output, and the higher the cardiac output, the higher the BP. Friction

in the arteries that can reduce the velocity of blood is called peripheral

resistance, and more resistance will create a higher BP. The normal blood

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volume is 5L, and more blood in the system will exert additional pressure on

the walls of the arteries and raise BP. IV fluids increase blood volume and

raise BP, like when hypotension is being treated due to shock; diuretics can

cause fluid loss through urination, declining blood volume and lowering BP.

Hypotension can cause dizziness and lack of adequate urine formation,

wheras HTN can cause blood vessels to rupture, or restrict blood flow to

critical organs. The vasomotor center in the medulla oblongata regulates

blood pressure. Nerves travel from the vasomotor center to the arteries,

where smooth muscle is either directed to constrict, raising BP, or relax,

lowering BP. Baroreceptors that also control BP are deteriorated with

diabetes. Emotions have an effect on BP; anger and stress can cause BP to

rise, where as depression and lethargy cause it to fall. Strong emotions can

cause chronic HTN. Antidiuretic hormone ADH is a potent vasoconstrictor

that can increase BP by raising blood volume.

HTN having no identifiable cause is primary/idiopathic/essential, and is 90%

of all cases. Secondary HTN is a result of certain diseases like Cushing’s

disease, hyperthyroidism, and chronic renal disease. Drugs that cause HTN

include corticosteroids, oral contraceptives, and erythropoietin. The

therapeutic goal for secondary HTN is to treat or remove the underlying

condition, which will often cure the HTN.

Chronic HTN may produce no symptoms. Four target organs affected are the

heart, the brain, the kidneys and the retina. The heart must work harder to

pump blood to the organs and tissues, and excessive cardiac workload can

cause the heart to fail and the lungs to fill with fluid, which is known as heart

failure. High BP also adversely affects the vascular system, and damage to the

blood vessels supplying blood and oxygen to the brain can result in transient

ischemic attacks and stroke. It can also lead to a loss of renal function. Vessels

in the retina can rupture or become occluded, leading to blindness. It is

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important to treat this in the pre-HTN stage, bc if it is allowed to progress it

may be irreversible.

CHF

One of the most common/fatal of the CV diseases. It is the inability of the

ventricles to pump enough blood to meet the body’s metabolic demands. The

amount of blood received by the right side should be exactly that sent out by

the left side of the heart. If the heart is unable to completely empty the left

ventricle, HF may occur. Can be caused by any disorder that affects the heart’s

ability to receive or eject blood. Can be caused or accelerated by coronary

artery disease; mitral stenosis; MI; HTN; DM. There is no cure for HF, so the

goals are to treat, prevent, or remove the underlying causes when possible.

Controlling lipid levels and keeping BP WNL reduces the incidences of CAD

and MI. Maintaining glucose WNL reduces the CV consequences of diabetes.

HF is a preventable disease for many patients. Pharmacotherapy is targeted

at prevention and slowing the progression of HF.

Drugs that increase heart contractility are called positive inotropic agents,

and examples of these are epinephrine, norepinephrine, thyroid hormone,

and dopamine. Drugs that decrease contractility are called negative inotropic

agents, and examples include quinidine, and beta-adrenergic antagonists such

as propranolol.

In HF, the myocardium becomes weakened and the heart cannot eject all the

blood it receives. It can occur on the left, right, or both sides. If it occurs on the

left side, excess blood accumulates in the left ventricle. The wall of the left

ventricle thickens and enlarges (hypertrophy). Blood “backs up” in the lungs,

resulting in the classic symptoms of cough and shortness of breath. Left

failure is sometimes called congestive heart failure. The right side can also

weaken, although left is more common. In right HF, blood backs up into the

veins, resulting in peripheral edema and engorgement of organs such as the

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liver. Lung congestion causes cough and orthopnea; pulmonary edema causes

the pt to feel as if they are suffocating and extreme anxiety may result, and

the condition often worsens at night.

The nurse must stress the importance of sodium restriction and drug

adherence to maintain a properly functioning heart.

HF is treated with:

ACE inhibitors;

angiotensin II receptor blockers;

diuretics;

beta-adrenergic blockers;

direct vasodilators;

cardiac glycosides;

phosphodiesterase inhibitors.

Angina

Angina is acute chest pain caused by insufficient oxygen to a portion of the

myocardium. The classic presentation is steady, intense pain in the anterior

chest, sometimes accompanied by a crushing or constricting sensation. The

pain may radiate to the left shoulder and down the left arm and extend to the

posterior thoracic spine or move up to the jaw.

Angina pain is usually precipitated by physical exertion or emotional

excitement, events associated with increased myocardial oxygen demand.

Narrowed coronary arteries containing atherosclerotic plaques prevent the

proper flow of oxygen and nutrients to the stressed cardiac muscle. Angina

episodes are usually short in duration and subside in 5-10 minutes with rest.

Psoriasis

Chronic, noninfectious, inflammatory skin disorder; affects 1-2% of the

population; is generally established by age 20 but may occur later. Plaques

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are seen on the skin due to an extremely fast skin turnover rate, with skin

cells reaching the surface in 4-7 days instead of the usual 14 days. Underlying

skin becomes inflamed and irritated. Has both genetic and autoimmune

components. About 50% have a genetic base. Factors such as stress, smoking,

alcohol, climate changes and infections can cause flare ups.

Certain drugs like ACE inhibitors, beta-adrenergic blockers, tetracyclines and

NDAIDs can act as triggers.

Topical corticosteroids are the first treatment for psoriasis. Topical

immunomodulars can also be used. Calcipotrient can induce hypocalcemia

and is not used typically on an extended basis.

Hypogonadsism

Androgens include testosterone and related hormones that support male

reproductive function. Other androgens include androstenedione and DHEA.

Therapeutically, androgens are used to treat hypogonadism and certain

cancers.

Lack of sufficient testosterone secretion by the tested can result in

hypogonadism, which may be congenital or acquired later in life. Primary

Hypogonadism is when it is caused by a testicular disorder. Disease states

that may cause primary testicular failure include mumps, testicular trauma or

inflammation, and certain autoimmune disorders. Secondary Hypogonadism

is when the pituitary is not secreting sufficient amounts of FSH and LH. Lack

of these secretions may be caused by Cushing’s syndrome, thyroid disorders,

estrogen secreting tumors, and therapy with GnRH agonists like Lupron.

Symptoms of male hypogonadism include sparse facial and pubic hair,

increased subcutaneous fat; and small testicles.

In adult men, lack of testosterone can lead to erectile dysfunction and

disinterest in sex. In young men, a lack of testosterone can delay puberty.

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It is treated with replacement therapy using testosterone or other androgens

and libido is improved within days or weeks. Male sex characteristics

reappear, which is called virilization. Depression resolves and muscle

strength improves.

BPH

BPH affects 50% of men older than 60 and 90% of men older than 90. Only a

few drugs are available for BPH. An enlarged prostate gland decreases the

outflow of urine by obstructing the urethra. Urination is difficult.

S&S: urinary frequency with drops of urine; increased urgency to pee;

leakage; excessive night-time urination/nocturia; decreased force of urine

stream; sensation that bladder did not fully empty. The obstruction can lead

to urinary infections and renal failure.

Surgery can be done to restore patency of urethra. Static Factors of BPH are

related to the prostate doubling/tripling its size with aging and causing block

of urine. Dynamic Factors are due to an excessive number of alpha1-

adgrenergic receptors in the urinary bladder and prostate; when activated,

the alpha1 receptors compress the urethra and obstruct urine flow.

Alpha-adrenergic meds like pseudoephedrine and phenlephrine can worsen

symptoms. Anticholinergic drugs like antihistamines, TCAs, may also worsen

urinary retention. Testosterone/anabolic steroids can enlarge the prostate.

Goal of therapy is focused on minimizing urinary obstruction and preventing

complications. Drugs can only treat symptoms. They can’t reverse or cure

BPH. Not all BPH is progressive and many pts never experience advanced

symptoms.

Pt should avoid caffeine and alcohol. Restrict fluids close to bedtime.

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Alpha1-adrenergic blockers are the first choice for treating moderate

symptoms. These relax smooth muscle in the prostate and bladder and

urethra and ease urination.

Cardura and Hytrin are good for men with BPH and HTN. Flomax is just good

for BPH, and it is an alpha1 blocker. Symptoms should improve within 2

weeks; primary AEs are dizziness, fatigue, and headache. Reflex tachy is

common with alpha blockers due to stimulation of baroreceptors. Pts unable

to take alpha1 blockers can take Proscar, a 5-alpha-reductase inhibitor, which

blocks an enzyme in the testoterone metabolic pathway and eliminates the

hormonal signal for prostate growth. Proscar can take months to work and

cause sexual side effects.

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CONCEPTInhalation

Respiratory system is a rapid/efficient mechanism for delivering drugs.

Almost instantaneous action for inhaled substances. Aerosol therapy is used

often. Delivers pulmonary drugs to their immediate site of action and reduces

systemic effects.

Anesthesia

Pain

Selective/nonselective

Fight or flight

Rest and digest

Phagocytosis

Inflammatory response

Anaphylaxis

A potentially fatal condition when the body defenses produce a

hyperresponse to a foreign substance known as an antigen or allergen. During

anaphylaxis the body releases massive amounts of histamine and other

mediators of the inflammatory response. Itching, hives and a tightness in the

throat/chest may occur. The larynx swells causing a nonproductive cough and

a hoarse voice. The pt experiences a rapid fall in BP and can’t breathe due to

bronchoconstriction. The hypotension causes reflex tachycardia. Anaphylaxis

can lead to shock, which is often fatal.

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To treat, epinephrine is given SQ or IM because it causes vasoconstriction and

can relieve bronchoconstriction. Dose can be repeated up to 3 times at 10-15

minute intervals.

Crystalloids/colloids can be used for volume depletion.

Antihistamines can be administered IV or IM to prevent further release of

histamine.

Albuterol can be used to relieve acute SOB. High-flow oxygen also usually

administered.

Glutocorticoids given to dampen the inflammatory response that may occur

several hours after the initial event.

The most common drugs causing anaphylaxis include:

antibiotics (penicillins, cephalosporins, sulfonamides);

NSAIDs (aspirin, ibuprofen, naproxen);

ACE inhibitors;

opioid analgesics;

iodine-based contrast media.

Pts can be pretreated with antihistamines or glucocorticoids to

suppress inflammatory response.

Betalactam ring

The portion of penicillin that is responsible for its antibacterial activity is the

betalactam ring.

Some bacteria secrete an enzyme called beta-lactamase or penicillinase which

splits the beta-lactam ring. This structural change allows the bacteria to

become resistant to the effects of most penicillings.

Cephalosporings, carbapenems and monobactams also contain the beta-

lactam ring. Several drugs are available that inhibit the bacterial beta-

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lactamase enzyme and when combined with penicillin protect the penicillin

from destruction. These include Augmentin and Timentin. (Inhibitor names

are clavulanate, sulbactam, tazobactam.)

Pharmacokinetics

The study of drug movement throughout the body. How the body deals with

meds. The plasma membranes determine movement of drugs throughout the

body.

The four components of pharmacokinetics are absorption, metabolism,

distribution, and excretion.

Pharmacodynamics

Concerned with how drugs produce CHANGE in patients, and the differences

in pt responses to meds. Therapeutic indexes = represent the margin of safety

of a drug. The higher the therapeutic index, the safer the drug. Graded dose-

response relationship = how the therapeutic response to a drug changes as

the med dose is increased. Potency = dose required to produce a response.

Efficacy = magnitude of maximal response to drug. Drug-receptor theory =

explains the MOA of many meds.

Agonists, partial agonists and antagonists are substances that compete with

drugs for receptor binding and can cause drug-drug and food-drug

interactions.

Pharmacology of the future will likely be tailored to match the genes of each

pt.

Oral contraceptives

Female reproductive function is controlled by the secretion of GnRH from the

hypothalamus and FSH and LH from the pituitary.

Estrogens are secreted by ovarian follicles and responsible for the maturation

of the sex organs and 2ndary sex characteristics of the female.

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Progestins prepare the endometrium for implantation.

Low doses of estrogens ad progestins prevent conception by blocking

ovulation.

Emergency contraception prevents implantation of fertilized eggs. Uterine

contractions can be stimulated to expel an implanted embryo.

Estrogen-Progestin combos used for hormone replacement therapy during

and after menopause; may have serious effects.

Progestins can be used for uerine bleeding. Also used as antineoplastics.

Oxytocins stimulate uterine contractions and induce labor. Tocolytics slow

labor.

With heavy bleeding, high estrogen doses may be used for 3 weeks and then

progesterone is added. D&C may be necessary if that does not work. Estrogen

proliferates the endometrium and progesterone limits and stabilizes

endometrial growth.

Anabolic steroids

Testosterone-like compounds with hormonal activity. Taken inappropriately

by athletes who hope to build muscle mass and strength, thereby obtaining a

competitive edge.

If taken in large doses for long periods of time, these can cause adverse effects

that last for months after stopping the drug. Cholesterol levels will rise and

sperm counts will be lowered in men. Females will start to look like men. Oral

androgens are hepatotoxic and permanent liver damage may result.

Behavioral changes include aggression and psychologic dependence. Most

androgens are schedule 3.

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High doses of androgens are occasionally used as a palliative measure to treat

certain types of breast cancer in combo with other antineoplastics.

Virilization will occur in most patients. Androgens shouldn’t be prescribed for

older men unless the possibility of prostate cancer has been ruled out, as

prostate carcinomas are dependent on testosterone. Patients with prostate

carcinoma are sometimes given a GnRH agonist like Lupron to reduce

circulating testosterone levels.

Crystalloid vs. Colloid

For treating shock with IV fluid therapy.

Hypovolemic shock, triggered by:

Hemorrhage

Burns

Dehydration

Vomiting/diarrhea

Diuretic therapy

Immediate maint. of blood volume through IV infusion of fluid and

electrolytes or blood products is essential. Admin of whole blood to expand

volume has been largely replaced by fluid infusion therapy.

Colloids & Crystalloids used when up to a third of an adult’s BV has been lost.

Colloids are proteins or other large molecules.

They stay suspended in the blood a long time bc too large to cross

membranes.

Draw water from the cells and into the blood vesssels, increase plasma

osmotic pressure.

Colloids: Albumin; Plasma; Globulins.

Can treat shock, burns, acute liver failure, neonatal diseases.

Crystalloids are IV solutions; contain electrolytes that resemble the

concentrations in plasma.

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Crystalloids can readily leave the blood and enter cells.

Replace fluids that have been lost and promote urine output.

Normal saline; lactated Ringer’s; Plasmalyte; hypertonic saline.

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DRUG

Certain drugs, such as glucocorticoids, levodopa and oral contraceptives can

cause the same symptoms as depression, and the health care provider should

rule out this possibility.

Dilantin

The oldest and most commonly prescribed antiseizure med is phenytoin

(Dilantin). It is a broad-spectrum hydantoin drug, useful in treating all types

of epilepsy except absence seizures.

Doesn’t have the abuse potential or CNS depression associated with

barbiturates. Dosages are individualized. There is a very narrow range

between a therapeutic dose and a toxic dose, so patients must be carefully

monitored.

Dilantin’s therapeutic class is as an antiseizure and antidysrhythmic drug. The

Pharm class is hydantoin, sodium-influx suppressing drug. Phenytoin acts by

desensitizing sodium channels in the CNS responsible for neuronal response.

This prevents the spread of disruptive electrical charges that produce

seizures. (Doesn’t work for absence seizures.) It has antidysrhythmic activity

similar to lidocaine, and an unlabeled use is for digitalis-induced

dysrhythmias.

When giving IV, mix with only saline. Flush IV lines before hanging as a

piggyback because traces of dextrose solution can cause emboli. Use an IV line

with a filter. Injectable version causes local tissue damage, so do not give IM.

Don’t inject into hand veins or they will turn purple.

The drug may cause dysrhythmias, hypotension, and hyperglycemia. It may

cause CNS reactions (nystagmus, ataxia, confusion); peripheral neuropathy

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may occur with long-term use; it can cause agranulocytosis and aplastic

anemia. Skin rashes and S-J syndrome may occur. Can cause lupus, gingival

hypertrophy, other connective tissue reactions.

Don’t use if the pt has sinus bradycardia or a rash.

Don’t use with these drugs:

oral anticoagulants;

glucocorticoids;

H2 antagonists;

antituberculin drugs;

folic acid;

calcium;

vitamin D.

If used with a tricyclic, it can cause seizures.

Carbamazepine (Tegretol) is a phenytoin-like medication used for tonic-

clonic and partial seizures.

Levodopa

Antiparkinsonism agents are given to restore the balance of dopamine and

acetylcholine in the brain. Meds used include dopaminergic drugs and

anticholinergics. Dopaminergics either restore dopamine function or

stimulate the brain’s dopamine receptors, and they are used for the initial

treatment of Parkinson’s.

The goal of med therapy for PD is to increase the pt’s ability to perform daily

ADLs. Meds should restore the balance of dopamine and acetylcholine;

dopaminergic drugs are used to increase dopamine.

Levodopa is the drug of choice for parkinsonism; and it can cross the blood-

brain barrier which dopamine cannot. It’s sometimes combined with

carbidopa.

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Adverse Effects: dizziness; light-headedness; difficulty concentrating;

confusion; anxiety; headache; sleep dysfunction; fatigue; n&v; constipation;

ortho hypo; dystonia; dyskinesia. Really bad AEs include: MI, shock,

neuroleptic malignant syndrome; agranulocytosis; depression/suicidal

thoughts; EPS; liver failure; liver cell injury.

Pt can take with food, but not high-protein bc it will impair absorption and

reduce effectiveness. Possible dizziness when standing up quickly. Change

positions slowly, dangle legs before getting out of bed, use elastic stockings.

B6 and multivitamins OK to take.

Watch for neuroleptic malignant syndrome, which also happens in pts

receiving antipsychotic meds. S&S are muscle rigidity, fever, delirium.

Elevated CPK.

Morphine

Opioid analgesic. Binds with both mu and kappa receptor sites to produce

analgesia. Causes euphoria, constriction of the pupils, stimulation of cardiac

muscle. Used for acute and chronic pain. Used as a pre-anesthetic medication

to relieve SOB associated with HF and pulmonary edema. Used for acute chest

pain connected with MI.

Causes peripheral vasodilation, which results in ortho hypo. May cause

dysphoria (restlessness, depression, anxiety); hallucinations, nausea,

constipation, dizziness, itching. OD can result in resp depression and death.

Tolerance develops to the sedative, nausea-producing and euphoric effects of

the drug. Cross-tolerance develops for heroin, methadone.

Drug may intensify or mask pain of gallbladder disease due to biliary tract

spasms. Avoid in pts with severe asthma, GI obstruction, hepatic or renal

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failure. Don’t use with other CNS depressants; or antidepressants like MAOIs

and tricyclics which increase the risk of resp depression.

Codeine

Opioid agonist with moderate effectiveness. Adverse effects include sedation,

nausea, constipation, dizziness. Serious side effects include liver damage,

respiratory depression, circulatory collapse, coma. Codeine is most often

prescribed as a cough suppressant. For coughing, codeine is considered an

“antitussive.”

Antitussives are drugs used to dampen the cough reflex when treating

allergies and colds; a dry, hacking cough can be irritating to the membranes of

the throat and can deprive a patient of much-needed rest.

Opioids are the most effective antitussives, and they act by raising the cough

threshold in the CNS. Codeine and hydrocodone are the most frequently used

opioid antitussives. Doses needed to suppress the cough are low, so there is

not as much of a risk for dependence.

Care must be taken when using these meds in patients with asthma, because

bronchoconstriction may occur. They can be combined with nonopioid

antitussives like antihistamines and decongestants. Codeine suppresses the

cough reflex by direct action on the cough center in the medulla.

Codeine can also be used for mild to moderate pain other than from coughing.

To administer, give with milk or meals to avoid GI upset. Don’t use with other

CNS depressants, anesthetics, MAOIs, tricyclics. Don’t use with alcohol. Take

caution when using with pts who have head injuries or increased intracranial

pressure, hepatic/renal disease, seizures, COPD. Breast-feeding mothers

shouldn’t use it. Reassess pain level 15-30 minutes after admin. Give drug

before intense pain sets in.

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Don’t use when cough is beneficial, such as after thoracic surgery. Assess for

constipation. May delay gastric emptying; GI distress can be eased with milk

or meals.

Narcan

Naloxone. For the treatment of acute opioid overdose and misuse. Pharm

Class: Opioid receptor antagonist. Drug is a pure opioid antagonist, blocking

both mu and kappa receptors. Used for complete or partial reversal of opioid

effects in emergency situations/opioid ODs.

Given IV, can reverse CNS and respiratory depression within minutes. Will

immediately cause withdrawal symptoms in pts physically dependent on

opioids. Also used to treat post-op opioid depression. Can also reverse

hypotension caused by septic shock. Administer when RR is less than 10 per

minute. Narcan is not toxic but the withdrawals it might cause can lead to

increased BP, pain, hyperventilation, n&v and drowsiness. Only for resp

depression caused by opioids. OD of this is treated with oxygen, IV fluids,

vasopressors.

Robinol

Glycopyrolate. Used in combo with other meds to treat ulcers.

It is anticholinergic. Decreases stomach acid production. Usually taken 2-3

times per day.

Take on an empty stomach, at lease 2-3 hours from meal time. Can cause

paralytic ileus. Don’t use with megacolon or ulcerative colitis or myasthenia

gravis. Overdose symptoms may include weak or shallow breathing, feeling cold,

jerky muscle movements, or seizure (convulsions). Glycopyrrolate can decrease

sweating and you may be more prone to heat stroke. Don’t use with Haldol,

levodopa or digoxin.

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Atropine

Anticholinergic.

Antispasmodic.

Antidysrhythmic.

Inhibits acetylcholine. Acts on heart, exocrine glands, smooth muscles, eye.

Incr. HR; decreases secretions; dilates pupils; lowers GI motility.

Hot as a hare (temp rises); mad as a hatter (delirium); red as a beet )flished

face); dry as a bone (decreased secretions and thirst).

Blocks vagal response during surgery.

Serious AEs = bradycardia, anaphylaxis.

Don’t use with antacids; other anticholinergics; levodopa; potassium tabs; not

for pts with glaucoma; GI obstruction patients shouldn’t use; nor pts with CV

disease; or myasthenia gravis.

Causes urinary retention. Pt may be sensitive to sunlight.

Albuterol

Beta-Agonist/Sympathomimetric.

2 inhalations every 4-6 hours as needed. Max is 12 inhalations per day.

Proventil, Ventolin, VoSpire.

May cause headache, dizziness, tremor, nervousness, throat irritation, drug

intolerance. Inhaled beta agonists produce minimal systemic toxicity because

only small amounts of the drug are absorped. When given orally, a longer

duration of action is achieved, but systemic adverse effects are more

frequently experienced. Systemic effects may include activation of beta1

receptors in the heart, which could cause an angina attack or a dysrhythmias

in patients with cardiac impairment.

Tolerance may develop to bronchodilation effect with long-term use.

Increased use of the drug is an indication that the patient’s condition is

deteriorating. Can also be used to prevent exercise-induced bronchospasm by

taking 15 mins before exercise.

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Method of Action: Relaxes bronchial, uterine and vascular smooth muscle by

stimulating beta2 receptors.

Don’t use with CNS stimulants; may decrease digoxin levels; if used with

MAOIs and tricyclics, it may increase adverse CV effects; propranolol and

other beta blockers may cancel the albuterol out and vice versa.

Drug may decrease the patient’s potassium level.

Tell patient to shake the inhaler, clear nasal passages and throat, breathe out,

expelling as much air from the lungs as possible, place mouthpiece well into

mouth, seal lips around mouthpiece, and inhale deeply as you release a dose

from the inhaler. Hold breath for several seconds, remove mouthpiece and

exhale slowly. Tell patient to wait at least 2 minutes before repeating

procedure.

If patient is also on a corticosteroid inhaler, tell them to use the

bronchodilator first and wait about 5 minutes before using the corticosteroid.

This lets the bronchodilator open the air passages for maximal effectiveness

of the corticosteroid. Wash inhaler after removing canister, wash at least once

a week with soapy water.

Atrovent

Can be used for asthma, COPD and nasal congestion.

It is a bronchodilator and anticholinergenic.

Delivered by inhalation and intranasal routes. Relieves/prevents

bronchospasms seen with asthma and COPD. Combined with albuterol to

treat COPDs. Off-label for asthma.

Alternative to short-acting beta agonists, for pts with severe acute probs.

Can be comined with beta agonists.

Provides relief within minutes, although peak effect may take 1-2 hours.

Effect can continue for 6 hours.

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InWhen used for runny nose, it inhibits nasal secretions but doesn’t have

decongestant action.

Treatment limited to 3 weeks.

Not for pts allergic to lecithin, soybean, peanuts.

Don’t use with other anticholinergics.

Dextromethorphan

Estrogen and Estrogen Antagonist (tamoxifen)

Oral antiestrogen preferred drug for treating metastatic breast cancer.

Effective against breast tumor cells that require estrogen for growth, which

are known as estrogen receptor positive cells.

Blocks estrogen receptors on breast cells but tamoxifen activates estrogen

receptors in other parts of the body, resulting in typical estrogen like effects

such as reduced LDL levels and increased mineral density of bone.

One antineoplastic approved for prevention of breast cancer. For high risk pts

at risk of developing the disease.

Adjust therapy in women following mastectomy to decrease potential for

cancer in opposite breast.

Give with food/fluids to decrease GI irritation. Do not crush or chew drug.

Avoid antacids fr 1-2 hours following PO dose. Pregs category D.

Side effects include n and v, little serious toxicity. Association of tamoxifen

therapy with incr. risk of endometrial cancer and thromboembolic disease

such as strokes and pulm embolisms.

Hot flashes, fluid retention, vag discharges are common.

Tumor flare initially, increase in tumor size but is expected. Hypertension and

edema occur in 10% of people taking this.

Don’t use with anticoagulants. History of thromboembolitic disease a no-no;

no pregs or lactation; precaution in pts with blood disorders, visual

disturbances, cataracts, hypercalcemia, hypercholesterolemia. Don’t use

estrogens.

Labs: calcium levels may increase.

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Serious neurotox dysrhythmias may occur with OD.

Cialis

Erectile dysfunction. Promotes smooth muscle relaxation, promotes blood

flow to the corpus cavernosum.

Don’t use w nitrates, alpha blockers, rifampin, erythromycin, grapefruit,

alcohol.

Not for pts with unstable angina. Or for pts with retinal disorders.

Don’t use if pt has bleeding disorder.

Sickle cell anemia, ultiple myeloma, leukemia will predispose them to

priapism.

Sex can increase cardiac risk.

Pt should seek immediate med help if chest pain occurs after taking drug. Or if

erection lasts more than 4 hours. Take 60 mins before sex. Drug has no effect

without sexual stim. Notify doc of hearing or vision changes.

Timolol

For angina and MI.

For glaucoma.

For HTN.

For migraines.

Non-selective beta-adrenergic blocker. Lowers IOP in open angle glaucoma,

reduces the formation of aqueous humor. Can take 2-4 weeks to work. As oral

med, it can treat mild HTN, stable angina, prophylaxis of MI and migraines.

Can mask signs of hypoglycemia.

Common to have burning/stinging on instillation. Vision may temporarily

blur. HypoTN and dysrhythmias are possible but uncommon. Not for pts with

asthma, COPD, bradycardia, AV block, heart failure.

Using w epinephrine can cause HTN followed by severe bradycardia.

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Tetracycline

Inhibs gram pos and neg. Inhibs bacterial protein synthesis. Slows microbial

groth. Bacteriostatic, some can enter CSF.

Don’t take w milk or iron.

Broad spectrum.

Can cause yellow teeth in young kids. Fetal bone disruption. Risk of

superinfection. High dose = hep toxic. Old pills = kidney toxic.

Prazosin

Used for BPH and HTN.

Antiypertensice and Adrenergic-Blocking Agent.

Selective alpha1 antagonist & compets with norepinephrine on smooth

muscles of arterioles and veins.

Rapid decrease in peripheral resistance, reduces BP. Little effect on cardiac

output or HR.

Tolerance to HTN lowering effect can occur.

Often used with beta blockers/diuretics.

Taken 2-3 times per day dur to short half life.

Like other alpha blockers, can cause ortho hypo dur to alpha 1 inhibition.

Rarely can cause unconsciousness 30 mins after 1st dose. First dose should be

low at at bedtime. Reflex tachy may occur from fall in BP.

May cause nasal congestion or inhibit ejaculation.

Heparin

Nitroglycerin

For treatment/prevention of angina.

Can cause fatal hypotension when used with Viagra.

A potent vasodilator in vascular smooth muscle. Relaxes arteries and veins,

which reduces the amount of blood returning to the heart and chambers

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contain a lower volume. Myocardial oxygen demand is lowered. Chest pain is

fixed and angina happens less often w use.

Tolerance is a problem. Stop drug overnight.

Can cause hypoTN, anaphylaxis, syncope.

Lasix

Can be used for pulmonary edema.

It is a loop diuretic.

Hypotension is a poss. Side effect but pt doesn’t have to stay in bed. Diureses

is expected to start within an hour and peak over 2.

If IV, the onset is 5 minutes and peak is half an hour.

Pt needs easy access to a toilet.

Inhibits reabsorption of sodium and chloride in the loop of Henle and distal

renal tubules.

Nurse should monitor BP, I&O, monitor K, weigh pt daily, don’t give right

before bedtime; encourage K foods.

Digoxin

Cardiac glycoside used for treating congestive HF and atrial fib, flutter or

tachy. Has direct effect on the heart so pt must take accurate pulse measures

before admin.

Withhold if HR less than 60. Take resting HR.

MOA = decreases HR and increases force of contraction. Can cause

bradycardia, anorexia, n&v, dysrhythmias, diaphoresis.

Nurse should know baseline VS

Check for toxicity = visual disturbances, GI upset, confusion.

Take apical for 1 minute. Withhold and notify doc if HR lower than 60. Obtain

12-lead ECG.

Inhibits sodium-potassium activated adenosine triphosphates, producing

movement of calcium from extracellular to intracellular and strengthening

myocardial contraction.

Also acts on CNS.

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Use caution when combining w anticholinergics, beta/calcium channel

blockers.

Can cause hypercalcemia and hypomagnesemia.

Therapeutic level = .125-.5 mg or .8-2 nanograms.

Insulin Regular (Humulin R/Novolin R)

Short Action. Onset is 30-60 mins. Peak is 1-5 hours. Give SQ 30-60 min

before a meal. Can mix with NPH, sterile water, normal saline. Promotes

cellular uptake of glucose, amino acids, and potassium. Promotes protein

synthesis, glycogen formation/storage, fatty acid storage as triglycerides;

conserves energy stores by promoting utilization of glucose for energy needs.

Inhibits gluconeogenesis.

Since it is short-acting, it is often used in combo with intermediate or long-

acting insulin. Do not mix with Lantus. Can be used as emergency treatment

for diabetic ketoacidosis, for gestational diabetes, and in combo with oral

antidiabetic agents for Type 2 pts.

The only type of insulin that can be used IV.

Pts with hypokalemia should be monitored carefully bc insulin may worsen

this condition.

Insulin Glargine (Lantus)

Long acting. Onset 1.1 hour. No peak. Give SQ, 1 time a day, same time each

day. Don’t mix with any other insulin or dilute with solutions. For Type 1 and

Type 2 diabetes. Reduces glucose by stimulating peripheral glucose uptake,

esp. by muscle and fat; inhibits hepatic glucose production. Common serious

side effect is hypoglycemia. Serious drug interaction – don’t use with MAOIs.

Don’t use with oral antidiabetics.

Due to prolonged duration, it isn’t the insulin to be used for diabetic

ketoacidosis. Treat mild hypoglycemia with oral glucose tabs. If solution is

cloudy, discard vial. Use only if clear/colorless. Avoid alcohol bc it lowers the

glucose levels. Avoid vigorous exercise after injection.

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Ibuprofen

Therapeutic class is as an analgesic/anti-inflammatory and antipyretic.

Pharm class is as an NSAID. Can treat mild to moderate pain, fever, and

inflammation. Effectiveness is equal to aspirin and other NSAIDs. Inhibits

synthesis of prostaglandins, which are lipids found in all tissues and promote

inflammation.

Give drug on an empty stomach as tolerated. OK to give with food if GI upset

occurs. Pts with asthma or allergies might have hypersensitivity reaction to

ibuprofen. Side effects mild. GI ulcers with occult blood may occur if pts take

high doses for long periods of time. Pts with PUD shouldn’t take this. Chronic

use can lead to renal impairment. Don’t use for peri-op pain for coronary

bypass due to risk for stroke or MI. Don’t use with pts who have renal/hepatic

impairment. Not for pts with nasal polyps, angioedema, or bronchospasm.

Use cautiously in pts with HF, HTN or history of stroke/MI.

Avoid while taking anticoagulants bc it can affect platelet function. Aspirin

can decrease ibuprofen’s anti-inflamm effect. Ibuprofen can cause lithium

toxicity. GI events can occur if taken w other NSAIDs, alcohol or

corticosteroids.

May incr. bleeding time, AST and ALT levels, and may decrease HB and HCT.

Aspirin/Salicylic Acid

Aspirin. The large doses of aspirin needed for severe inflammation may result

in adverse effects on the digestive system. It increases gastric secretion and

irritates the stomach lining. Can cause GI pain, heartburn, bleeding/ulcers.

Enteric coating minimizes GI effects. Salicylism is a syndrome that includes

tinnitus, which is ringing in the ears; dizziness; headaches; excessive

sweating.

Aspirin interferes with clotting by keeping a platelet-aggregating substance

from forming. Can cause thrombocytopenia and leucopenia; hepatitis;

angiodema; Reye Syndrome. Don’t use with Heparin bc it may increase

bleeding. Don’t use with pts who have bleeding disorders. Reye Syndrome can

develop in children recovering from chicken pox. Can cause hyperthermia;

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dehydration; tinnitus; vertigo; headache; confusion & drowsiness;

diaphoresis; hyperventilation; vom & runs. Buffered aspirin contains sodium.

Take with food/antacid/milk/water to avoid GI probs.

Aspirin’s significant anticoagulant activity give it the ability to reduce the risk

of mortality following an MI, and to reduce the incidence of strokes. It has also

been found to reduce the risk of colorectal cancer. Discontinue aspirin 1 week

before elective surgery. Excreted in urine and affects urine testing for glucose.

Acetaminophen

Prednisone

Anti-inflammatory agent. Glucocorticoid.

When used for inflammation, therapy is limited to 4-10 days. For long-term

therapy, alternate-day dosing is used. Occasionally used to terminate acute

bronchospasm in pt with asthma and as an antineoplastic agents for prs with

certain cancers. When using for more than 10 days, dose must be gradually

withdrawn.

Short-term use has few side effects. Long-term use can result in Cushing’s and

gastric ulcers. Don’t take if have an active viral, bacterial, fungal or protozoan

infection. When used to treat inflammation, the doses are many times higher

than the amount naturally in the body. Most effective meds for severe

inflammatory disorders. Inhibit biosynthesis of prostaglandins, suppress

histamine, inhibits functions of lymphocytes and phagocytes.

Acetylcholine

Potassium Chloride

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CATEGORY

Central muscle relaxant

These drugs generate their effects by inhibiting motor neurons within the

brain and/or spinal cord. This means the origin is within the central nervous

system. It is believed they generate their effects within the brain and/or

spinal cord by inhibiting upper motor neuron activity, causing CNS

depressant effects, or altering simple spinal reflexes.

All the centrally acting agents have the potential to cause sedation.

Adverse effects can include drowsiness; dizziness; dry mouth; sedation;

ataxia; lightheadedness; urinary hesitancy or retention; hypotension;

bradycardia.

Serious adverse effects can include edema of the tongue; anaphylactic

reaction; respiratory depression; coma; laryngospasm; cardiovascular

collapse.

Prototype for centrally active skeletal muscle relaxants: Clobenzaprine

(Cycoflex, Flexeril). Causes relaxation in causes of acute muscle spasticity, but

not effective for cerebral palsy or diseases of the brain/spinal cord. Meant to

provide therapy for only 2-3 weeks. Maximum effects may take 1-2 weeks.

Use with caution in patients with MI, dysrhythmias, CV disease. Don’t take

with alcohol or MAO inhibitors (hyperpyretic crisis/convulsions may occur).

Antiepileptic/Antiseizure

For the treatment ofall seizure-related symptoms, including signs of epilepsy.

Once a med is selected, the patient is placed on a low initial dose, and it is

gradually increased until seizure control is achieved or until drug side effects

prevent additional dose increases. If seizures continue, a second drug is

added and the first is slowly reduced. Seizures are likely to occur if

antiseizure drugs are abruptly withdrawn, so they are usually withdrawn

over a period of 6-12 weeks. An FDA report analyzing newer nontraditional

drugs showed that 11 popular meds might double the risk of suicidal

behavior among patients. Most patients only need one drug, though two is OK.

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The goal of antiseizure therapy is to suppress the neuronal activity just

enough to prevent abnormal or repetitive firing. The drugs either stimulate

an influx of chloride ions, an effect associated with the neurotransmitter

GABA; or they delay an influx of sodium; or they delay an influx of calcium.

The drugs should control the movement of electrolytes across neuronal

membranes or if they are affecting neurotransmitter balance. An influx of

sodium or calcum into the neuron enhances neuronal activity, while an influx

of chloride or an efflux of potassium suppresses neuronal activity.

Some drugs change the activity of GABA (primary inhibitory

neurotransmitter of the brain). These drugs mimic the effect of GABA by

stimulating an influx of chloride ions that interact with GABA receptors.

Chloride ions move into the cell and suppress the firing of neurons.

Barbiturates, benzodiazepines, etc. reduce seizure activity by intensifying

GABA action.

Several drugs dampen CNS activity by delaying an influx of sodium ions

across neuronal membranes. Hydantoins act by this mechanism. Sodium ion

movement is the major factor that determines if a neuron will undergo an

action potential. If these channels are temporarily inactivated, neuron activity

will be suppressed. Hydantoin and phenytoin drugs block/desensitize the

sodium channels, and neuronal activity completely stops.

Drugs that suppress calcium influx: bind to neuronal membrances and

stimulate the entry of calcium and without calcium influx, neuronal

transmission would not be possible. Succinimides delay entry of calcium into

neurons by blocking calcium channels, increasing the electrical threshold of

the neuron and reducing the liklihood that an action potential will be created.

Succinimides keep neurons from firing too quickly.

Acetylcholinesterase inhibitors (Cholinergics, Parasympathomimetrics)

Stimulation of the parasympathetic nervous system: These drugs are called

cholinergic agents or parasympathomimetrics. They produce the

characteristic symptoms of the rest-and-digest response.

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Inhibition of the sympathetic nervous system: These drugs are called

adrenergic-blocking agents, or adrenergic antagonists, or sympatholytics.

They produce actions opposite of sympathomimetics. Produce mane of the

same rest-and-digest symptoms as the parasympathomimetrics and have a

wide therapeutic application in the treatment of HTN.

The classic parasympathomimetic is acetylcholine, the neurotransmitter at

cholinergic synapses in the ANS. However, it has almost not therapeutic use

because it is rapidly destroyed after administration and produces many side

effects. Acetylcholine in the synaptic cleft is rapidly destroyed by

acetylcholinesterase AchE and choline is reused, and taken up by the

presynaptic neuron to make more Ach. Direct-acting parasympathomimetics

are relatively resistant to AchE and have a longer duration than Ach. Direct-

acting parasympathomimetics can also be described as muscarinic agonists

because they are moderately selective to muscarinic receptors. Indirect-

acting parasympathomimetics such as neostigmine inhibit the action of AchE,

which allows endogenous Ach to avoid rapid destruction and remain on

cholinergic receptors for a longer time, prolonging its action. The indirect

meds are also called cholinesterase inhibitors and are nonselective, and affect

all Ach sites, including ganglia, muscarinic receptors, skeletal muscle, and Ach

sites in the CNS.

These are used sparingly due to many side effects. Used in ophthalmology to

reduce intraocular pressure in glaucoma patients and for stimulatory effects

on the smooth muscle of the bowel or urinary tract. Used for myasthenia

gravis, a disease characterized by the destruction of nicotinic receptors in

skeletal muscles. Paras stimulate skeletal muscle contraction and reverse

severe muscle weakness. Aricept and Cognex are used to treat AD because

they increase the amount of acetylcholine binding to receptors located in the

CNS.

Opioids

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Analgesics are meds used to relieve pain. The two categories of analgesics are

opioids and nonopioids. Opioids are narcotic substances, meaning they

produce numbness or stupor-like symptoms. Opioids exert their actions by

interacting with at least 6 types of receptors. Drugs that stimulate a particular

opioid receptor are called opioid agonists. Those that block an opioid

receptor are called opioid antagonists. Opioid blockers like Narcan inhibit

both mu and kappa receptors, the most important ones when dealing with

opioids. Morphine is a prototype opioid agonist used to treat severe pain. It is

considered the standard by which the effectiveness of other opioids are

compared. Other than analgesia, opioid are effective at suppressing the cough

reflec and slowing the motility of the GI tract for cases of severe diarrhea.

Opioids also cause sedation , and some people experience euphoria and

relaxation which is why the drugs are sometimes abused. Adverse effects

include respiratory depresson, sedation, nausea and vomiting.

Barbiturates

Powerful CNS depressants prescribed for their sedative, hypnotic, and

antiseizure effects. Until benzodiazepines, barbiturates were the drug of

choice for treating anxiety and insomnia. They are now rarely prescribed for

anxiety and insomnia because of significant adverse effects and the

availability of more effective meds. The risk of dependence is high, and

several are schedule 2 drugs. The withdrawal syndrome is severe and can be

fatal. OD results in respiratory depression, hypotension and shock.

They act by binding to GABA receptors and intensifying the effect of GABA

throughout the brain. Low doses reduce anxiety and cause drowsiness;

moderate doses inhibit seizure activity; higher doses can induce anesthesia.

With repeated use, tolerance develops to the sedative effects of barbiturates

but not the respiratory depressant effects. Include Nembutal, Seconal, Amytal,

Alurate, Luminal for treating insomnia/anxiety.

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Phenobarbital is able to suppress abnormal neuronal discharges without

causing sedation; it is inexpensive, long-acting, and produces a low incidence

of side effects. It is the drug of choice when treating neonatal seizures.

Overall, barbiturates are effective against all major seizure types except

absence seizures. Amobarbital is an intermediate-acting barbiturate given IM

or IV to terminate status epilepticus. Amobarbital is not given orally as an

antiseizure med.

SSRI

Drugs that slow the reuptake of serotonin into presynaptic nerve terminals

are the SSRIs, which have become the drugs of choice in the treatment of

depression because of a better side-effect profile. Serotonin is important to

several body functions, including cycling between NREM and REM sleep, pain

perception, and emotional states. Lack of serotonin can lead to depression.

Serotonin is metabolized to a less active substance by the enzyme monoamine

oxidase (MAO). While tricyclics inhibit the reuptake of both norepinephrine

and serotonin, the SSRIs selectively target serotonin. SSRIs have the same

efficacy at relieving depression as MAOIs and tricyclics, but the advantage of

SSRIs is their greater safety. Sympathomimetic effects like increased heart

rate and HTN; and anticholinergic effects like dry mouth, blurred vision,

urinary retention and constipation are less common with this drug class.

Sedation is also less common and cardiotoxicity is not observed. One common

side effect is sexual dysfunction, and up to 70% of men and women

experience this. Other common side effects include nausea, headache, weight

gain, anxiety, and insomnia. Serotonin syndrome may occur, and this is when

serotonin accumulates in the body. Symptoms begin as early as 2 hours after

taking the first dose, or several weeks after starting the med. Symptoms of SS

include mental status changes like confusion, anxiety, and restlessness;

hypertension; tremors; sweating; hyperpyrexia, and ataxia. Discontinue SSRIs

and provide supportive care if this happens. Mechanical ventilation and

muscle relaxants might be used in extreme cases. Can cause death if left

untreated. Zoloft is an SSRI. Lexapro is an SSRI, along with Celexa, Prozac,

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Luvox and Paxil. SSRIs can cause nausea, dry mouth, insomnia, headache,

nervousness, anxiety, GI disturbances, dizziness, anorexia, fatigue, sexual

dysfunction, SS, stephens-johnson.

MAOI

Anticholinergic blocking

Beta adrenergic agonist and antagonist

Alpha adrenergic agonist

Symmpathomimetics

Antitussive

Dampen the cough reflex. Treats coughs due to allergies or the common cold.

For dry, hacking, nonproductive cough, which can be irritating to the throat

and deprive a patient of sleep. Opioids are the most effective antitussives.

They raise the cough threshold in the CNS. Rarely, opioid cough remedies can

cause respiratory depression. Use caution with asthma patients as

bronchoconstriction may occur. The most frequently used nonopioid

antitussive is dextromethorphan, which is OTC. Chemically similar to opioids,

and also acts on the CNS. In large doses, it can cause slurred speech, dizziness,

drowsiness, euphoria, lack of motor coordination.

Mucolytic

Acetylcysteine (Mucomyst) is one of the few drugs available to directly loosen

thick bronchial secretions. It is a mucolytic, which is a class that breaks down

the chemical structure of mucous molecules. Mucus becomes thinner and can

be removed more easily by coughing. It is delivered via the inhalation route

and not available OTC. Used with pts who have cystic fibrosis, chronic

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bronchitis, or any disease that causes this bronchial secretions. It can trigger

bronchospasm and has an odor resembling rotten eggs. Another mucolytic,

called dornase alfa breaks down DNA molecules in the mucous, thinning it.

Acetadote is also administered oral/IV to patients who OD’d on

acetaminophen.

Antihistamine

H1-Receptor Antagonists. Block the actions of histamine at the H1 receptor.

OTC for allergy symptoms, motion sickness, insomnia. Histamine is released

from mast cells & basophils and causes itching, increased mucus secretions,

congestion. May cause bronchoconstriction, edema, hypotension, anaphylaxis.

(H1 receptors = allergic symptoms/H2 receptors = gastric mucosa/peptic

ulcers). Antihistamines selectively block the actions of histamine at the H1

receptor and alleviate symptoms. Most effective when taken to prevent

allergic symptoms. Cause typical anticholinergic effects. Anticholinergic effect

= drying of mucous membranes.

Don’t take alcohol with these because sedating effects may be addictive. Some

pts can exhibit CNS stimulation though, causing insomnia/nervousness.

Anticholinergic effects = dry mouth, dry mucous membranes, urinary

hesitancy. Diphenhydramine and clemastine produce the greatest incidence

of anticholinergic effects. Astelin causes less drowsiness bc it is applied

locally to the mucous membranes.

Bronchodilators

Beta2 adrenergic agonists (beta agonists) are effective bronchodilators and

are the drug of choice for ACUTE bronchoconstriction. They activate the

sympathetic nervous system, which relaxes smooth muscle resulting in

bronchodilation. Effective at widening the airway but provide no

inflammation relief. Not good for chronic asthma. Short-acting beta agonists

abort acute attacks and are rescue agents. Intermediate beta agonists include

albuterol. Don’t use LABAs to abort an asthma attack, it won’t work (like

Severent). Minimal systemic toxicity if inhaled. Adverse effects more common

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if taken PO because they can act on beta1 receptors in the heart and cause

angina or dysrhythmias in pt with heart disease.

Glucocorticoid

Inhaled glucocorticoids (corticosteroids) are used for long-term prevention of

asthmatic attacks. Oral corticosteroids may be used for the short-term mgmt

of acute severa asthma. Most potent anti-inflammatory substance known.

Dampen the activity of inflammatory cells and increase production of anti-

inflammatory mediators. They are not bronchodilators, but sensitize the

smooth muscle to be more responsive to beta-agonists. Reduce bronchial

hyper-response that causes some asthma attacks. Inhaled corticosteroids can

cause hoarseness, dry mouth, cough, sore throat, candidiases, hypercorticism,

hypersensitive reactions. (Other anti-inflamm drugs for asthma: Mast cell

stabilizers can cause nausea, sneezing, nasal stinging. Anapylaxis,

bronchospasm; leukotriene modifiers can cause headache, dizziness,

diarrhea, liver toxicity, increased AST.) Prototype inhaled corticosteroid is

beclomethasone (Beconase, Qvar).

Preferred therapy for PREVENTING asthma attachs; when inhaled daily, they

suppress inflammation without major side effects. May take 4-8 weeks to see

improvements. Must be taken daily; won’t work for acute episodes. For

severe asthma, prednisone may be prescribed to take orally. Inhaled corticoid

steroids produce few side effects, but when taken PO they cause many. Some

side effects from the oral form include adrenal gland atrophy, peptic ulcers,

osteoporosis, hyperglycemia.

Glucocorticoids R/T the endocrine system

The adrenal cortex secretes three classes of steroid hormones:

glucocorticoids, mineralocorticoids, gonadocorticoids. The term

CORTICOSTEROID imples that the drug has both glucocorticoid and

mineralocorticoid. The drugs are used as replacement therapy for patients

with adrenocortical insufficiency and to dampen inflammatory and immune

responses. They are short, intermediate, and long-acting.

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SySymptoms of adrenocortical insufficiency: hypoglycemia; fatigue;

hypotension; increased skin pigmentation; anorexia; vomiting; diarrhea.

Addison’s Disease is primary adrenocortical insufficiency, is quite rare, and is

a deficiency of glucocorticoids and mineralocorticoids. Addison’s is caused by

autoimmune destruction of the adrenal glands. Secondary adrenocortical

insufficiency occurs when corticosteroids are suddenly withdrawn as a med.

When glucocorticoids are taken for a long time, the adrenal cortex shrinks

and causes adrenal atrophy. Symptoms of acute adrenocortical insufficiency

include nausea, vomiting, lethargy, confusion, coma. Treatmeant is IV therapy

with hydrocortisone. To avoid, discontinue glucocorticoids gradually.

Insulin

Released by the pancreas to decrease blood glucose levels. After meals, the

pancreas recognizes rising serum glucose and releases insulin. Without

insulin, glucose stays in the blood and can’t enter cells. Cells can be

surrounded by glucose but can’t use it without insulin. Insulin is said to have

a hypoglycemic effect because it causes glucose to leave the blood and enter

the cells, therefore there is less glucose in the blood.

Insulin’s actions are as follows: promotes entry of glucose into cells; provides

storage of glucose, as glycogen; inhibits breakdown of fat and glycogen;

increases protein synthesis and inhibits gluconeogenesis (the production of

“new” glucose from noncarb molecultes).

Type 1 DM = severely deficient in insulin production and insulin therapy is

required in normal physiologic amounts.

Type 2 DM = insulin needed for those who can’t manage their glucose levels

with diet, exercise and oral antidiabetic meds.

The right amount of insulin must be available to cells when glucose is

available in the blood; admin when glucose is NOT available can lead to

serious hypoglycemia and coma. This happens when a person admins insulin

correctly but then skips a meal – the insulin is available to cells but glucose is

not. Serious effects can also occur it the person exercises heavily – the insulin

was admin on schedule and food was eaten, but the muscles quickly used all

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the glucose in the blood and the patient becomes hypoglycemic. Pts with

diabetes should consume food/sports drinks prior to activity.

If pts skip or forget their insulin dose, glucose from a meal can build up in

high levels and cause hyperglycemia and possible coma.

Time of peak action of insulin is when risk for hypoglycemia is greatest.

Must be given by injection or insulin pump.

Primary adverse effect is too much insulin, resulting in hypoglycemia. If a pt is

hypoglycemic, they will have pale, cool, moist skin with blood glucose less

than 50 mg/DL and sudden onset of symptoms.

Anticoagulant

Antibiotics

Diuretics (thiazide, loop, potassium sparing)

Chemotherapeutic

Aminoglycosides

ACE Inhibitors

Penicillins

Bactericidal disrupts and weakens the cell wall, leading to cell lysis and death.

Types include narrow spectrum that are penicillinase sensitive – penicillin G,

penicillin V. Penicillinase-resistant include nafcillin, oxacillin, dicloxacilin

Broad-spectrum include ampicillin, amoxicillin, Augmentin. Extended-spectrum

penicillins include ticarcillin, piperacillin

Side effects:

Allergic reactions: rash, itching, hives, anaphylaxis. Nursing considerations:

Contraindicated in pts with hypersensitivity to penicillin, cephalosporins, or

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carbapenems; not for neonates either. Not for neonates. Monitor pt for 30 mins after

admin.

Cephalosporins

Each generation has increasing bactericidal activity to break down gram-

negative bacteria and anaerobes, as well as reach the cerebrospinal fluid.

Cephalosporins interfere with bacterial cell wall synthesis and are considered

broad-spectrum. The cell weakens, swells, bursts, and dies as a result of

increased osmotic pressure inside the cell.

Side effects:

Rash, priritus, fever, nausea, vomiting, diarrhea

Uncommon side effects: anorexia, flatulence, some of these may cause

bleeding tendencies. Taking cefotetan and drinking alcohol may cause a

serious reaction.

Adverse effects:

Hypersensitivity reactions such as rash, pruritus, fever.

Possible suprainfection.

Nursing considerations:

Contraindicated in patients allergic to penicillins.

Monitor rate of infusion; check labeling for rate of IV infusion. Monitor renal

and hepatic studies throughout therapy.

If GI upset occurs, patient can take med with food.

Evaluate IM and IV sites for reaction, such as abcess and thrombophlebitis.

Minimize complication of thrombophlebitis by rotating injection sites and

slowly injecting a dilute solution.

Monitor for bleeding. IM injections are frequently painful, so warn the patient.

Patient teaching:

Advise patient to hydrate; notify health care provider if patient is

experiencing diarrhea

Teach patient to refrigerate oral suspensions

Instruct patient to report signs of allergy such as skin rash, itching, hives.

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Antiviral

Viruses are non-living.

Infect bacteria, plants, animals.

None of the cellular organelles necessary for self-survival. Quite primitive

even compared to simplest cell. Surrounded by protective coat. Capable of

remarkable feats. Infect host by locating and entering a target cell and using

machinery of the host to replicate. Intracellular parasites.

Antivirals the least effective of all anti-infective drugs.

Pharm therapy challenging bc of rapid mutation rate of viruses. Quickly

render drugs ineffective. Intracellular nature of virus makes it difficult to

eliminate pathogen without injuring normal cells. Narrow spectrum of

activity. Usually limited to one type of virus.

Laxatives

PPIs

Prilosec, Nexium. Act by blocking the enzyme responsible for secreting

hydrochloric acid in the stomach. Drugs of choice for short-term therapy of

PUD and GERD. PPIs reduce acid secretion to a greater extent than the H2

receptor antagonists and have a longer duration of action. PPIs heal more

than 90% of duodenal ulcers within 4 weeks and about 90% of gastric ulcers

in 6-8 weeks. Several days of therapy may be needed before the pt feels relief

from ulcer pain. The typical length of therapy is 4 weeks. Some are used

concurrently with antibiotics to eradicate H. pylori. Serious adverse effects

from drugs in this class are uncommon and all PPIs have similar efficacy and

adverse effects. Headache, abdominal pain, diarrhea, nausea, and vomiting

are the most frequently reported symptoms.

H2 Blockers

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Widely used in the treatment of hyperacidity disorders of the GI tract.

Tagamet, Pepcid, Zantac (prototype). Histamine has two receptors, H1 and

H2. H1 produces the symptoms of inflammation and H2 increase acid

secretion in the stomach. The H2-receptor antagonists suppress the volue and

acidity of parietal cell secretions. These drugs are used for GERD and PUD. All

H2-receptor antagonists have similar safety profiles and adverse effects are

minor: patients taking high doses or with renal/hepatic disease may

experience confusion, restlessness, hallucinations, depression. Tagamet is

used less frequently than the others because of numerous drug-drug

reactions, as it inhibits hepatic drug-metabolising enxymes. Don’t take

antacids with these drugs bc the absorption of the H2-receptor antagonist

will be diminished.

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VOCABULARY

Identify the key components included in a Complete Blood Count to

include normal value ranges

RBC (erythrocyte) (4.5-5.5)

Hemoglobin (12-16 g/dL): Protein molecule of blood that carries oxygen

Hematocrit: Percentage of RBC by volume 38-54%

WBC (4,000-10,0000)

Platelets (thrombocyte) (140,000-500,000)

Red Blood Cell Count

(4.5-5.5)

Closely related to the HGB and HCT levels and represents a different way of

evaluating the number of RBCs. Used in pts with ongoing bleeding or to evaluate

anemic pts. Test counts the number of circulating RBCs in a small amount of venous

blood. Low values can be caused by many things, like hemmorhage, hemolysis,

dietary deficiency, genetics, drugs, marrow failure, chronic illness.

Hematocrit

Critical values: Lower than 15% or higher than 60%

An indirect measurement of RBC number and volume. Used as a rapid measurement

of RBC count. Integral part of evaluation of anemic patients. Normal values vary

with age. Pregnancy can decrease values. HCT falsely elevated in dehydration.

Decreased in overhydration.

Hemoglobin

Critical values: Less than 5 g/DL or more than 20 g/DL

Measures the total amount of hemoglobin in the blood. Used as a rapid direct

measurement of RBC count. Used to evaluate anemic patients. Living at high

altitudes causes increased HGB.

Hemoglobin serves as a vehicle for oxygen and carbon dioxide transport. The

oxygen carrying capacity of the blood is determined by the HGB concentration.

Other Key Components

WBC-differential: Determines the percent of different types of WBC’s

Neutrophils (54-75%) of WBCs

Lymphocytes (25-40%) of WBC

Reticulocyte Count: Response to erythropoiesis

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NA-values

Potassium-values

Creatinine… what does it measure?

Autonomic

Tinnitus

Mast Cell

Histamine

Prostaglandin

Leukotriene