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Pharm test 1
Undergraduate 4

Additional Nursing Flashcards




Amyotrophic Lateral Sclerosis
progressive weakness & wasting of muscles, destruction of motor neurons
Alzheimer’s disease
progressive loss of brain function (memory loss, confusion, & dementia)
Huntington’s Chorea
progressive dementia and involuntary spasmodic movement
Multiple Sclerosis
progressive weakness, visual disturbances, mood alteration, cognitive deficits
Parkinson’s Disease
Progressive loss of dopamine causes tremor, muscle rigidity, abnormal movement and posture

Parkinson’s Disease

  • Degenerative disorder of the CNS – progressive
  • Affects mostly people over 50
  • Lack of the neurotransmitter dopamine Affects more than 1.5 million Americans
  •  Pharmacology only partially relieves symptoms
Parkinson’s Disease Symptoms
  • Tremors –shakiness, pill rolling
  • Muscle rigidity – have difficulty bending over or moving extremities, face may be rigid
  •  Bradykinesia – difficulty swallowing, chewing, speaking, shuffling feet
  • Postural instability – may be slightly humped over, lose their balance easily, falls.


Parkinson’s Disease
—Degeneration and destruction of the dopamine producing neurons in the substantia nigra
—The substantia nigra neurons supply dopamine to the corpus striatum that controls unconscious muscle movement
—Neurotransmitters must be balanced in the corpus striatum (dopamine & acetylcholine)
—Drug therapy focuses on increasing dopamine and blocking the effects of acetylcholine


What do they do?
Either restore dopamine function or stimulate dopamine receptors balancing dopamine and acetylcholine
—Drugs of choice
—Levadopa (l-dopa, Laradopa) – prototype
—Carbidopalevadopa (Sinemet)
—Dopamine agonists
—Ropinirole (Requip)
—May be more effective in controlling dyskinesia



Levodopa (Larodopa)
  • Actions: Restores neurotransmitter dopamine
  • Administration alerts: Administer as ordered, do not stop taking abruptly (can cause an increase in acetocoline which causes parkinsonism)
  • Pharmacokinetics - Onset 30 min peak 1-3 hrs, half life 1 hr (can take weeks to see change)
  • Adverse effects - Purposeless movement, uncontrolled movement, loss of appetite, N&V, orthostatic hypotension(FALLS)
  • Drug interactions: Tricyclic antidepressants, MAOIs, antihypertensives, anticonvulsants, antacids, pyridoxine (B-6)  + ***Kava
  • Lab tests – liver enzymes  and BUN




Block the effects of actylcholine in the corpus striatum  Earliest drugs used to treat Parkinson’s disease.

 Benztropine mesylate (cogentin)  (.5-1 mg/day)  Sedation, nausea, constipation, dry mouth, blurred vision, drowsiness, dizziness, hypotension, tachycardia, nervousness

Nursing Considerations:  Careful monitoring of condition and adverse reactions to medication, Monitor B/P and heart rate, Muscle twitching and mood changes may indicate drug toxicity – report to HCP at once

Client Education

* Increase fiber and fluid intake

*Avoid foods high in pyridoxine (OTC, fortified foods)

*Report muscle spasms, spasmodic winking, and increase in bradykinesia

*Takes up to six months for therapeutic levels to be achieved

*Do not stop taking medicine abruptly

*Change positions slowly


Alzheimer’s Disease

  • Responsible for 70% of all dementia
  • Progressive memory loss, confusion, inability to think or communicate effectively
  • 4th leading cause of death in the US
  • Etiology unknown
  • Familial form; environmental, immunological, and nutritional factors, Structural damage in the brain- loss in number and function of neurons, Deficit in tasks that require the neurotransmitter acetycholine.


Impaired Memory Loss                                               Confusion and disorientation

Inability to recongnize family and friends                Aggressive Behavior

Depression                 Psychosis             Anxiety




Alzheimer's Disease

—<20 minutes, peak 3-4 hrs, half life 70 hours
—Enhances the effects of acetylcholine in the neurons that have not been damaged, effects may not be seen for six months, effects modest at best
—Give at bedtime

Acetylcholinesterase Inhibitors


Donepezil (Aricept)


  • Pharmacokinetics <20 minutes, peak 3-4 hrs, half life 70 hours
  • Actions/uses Enhances the effects of acetylcholine in the neurons that have not been damaged, effects may not be seen for six months, effects modest at best
  • Administration Give at bedtime NEED REGULAR SCHEDULE
  • Adverse effects V&D, dark urine, insomnia, syncope, depression, HA, irritability, muscle cramps, arthritis, bone fractures, fatigue, chest pain, >libido, hot flashes, incontinence, dehydration, blurred vision
  • Interactions- phenobarb, phenytoin, dexamethazone, and rifampin may speed metabolism (speed the metabolism of Aricept)
  • Nursing Considerations Careful monitoring of condition and adverse reactions to medication Monitor B/P and heart rate Monitor for changes in mental status, mood changes, dizziness, confusion, insomnia, anorexia, N&V
  • Client Education Take drug as prescribed Know and report major side effects Report changes in mental status or mood Takes up to six months for therapeutic levels to be achieved Frequent drinks of cool liquid or sugar free hard candy, or sugar free gum for dry mouth Increase fiber and fluid intake

Muscle Spasm


Associated with excessive use or local injury, antipsychotic drugs, epilepsy, hypocalcemia pain, and neurological disorders



  • Inflammation
  • Edema
  • Pain
  • Loss of mobility/coordination
  • Tonic (tightening of muscles) / Clonic spasms (relaxation)


Centrally Acting


Skeletal Muscle Relaxants



Probably inhibit upper motor neuron activity

 * CNS depression

 * Alter spinal reflexes

Commonly Used Drugs:

1: Baclofen (Lioresal)

2. Cyclobenzaprine (cycloflex, flexeril)

3. Tizanidine (Zanaflex)

4. Benzodiazepines (Valium, Klonopin, Ativan) (Seizure Control)





(cycloflex, flexeril)


Muscle Relaxant


Actions/Use: Depresses motor activity at the brain stem.

Increases circulating levels of norepinephrine.

Not effective for CP or diseases of the brain or spinal cord.


Administration: Not recommended for children

Maximum effects may take up to 2 weeks


Pharmacokinetics: Onset 1 hour Peak 3-8 hrs/duration 12-14 hrs Half life 1-3 days


Adverse effects: Drowsiness, blurred vision, dizziness, dry mouth, rash, tachycardia


Interactions: Alcohol, other CNS depressants, MAOIs


Muscle Spasticity


Usually secondary to cerebral cortex injury:

(CP, head and spinal cord injury or lesion, stroke.)

  • Symptoms: 1) Involuntary muscle contraction Painful movement or posture
  • Treatment: PT and antispasmodics




Centrally acting (CNS)


Baclofen (lioresal)

Diazapam (valium)


Direct acting (on muscle)


Dantrolene Sodium (Dantrium)

Botulinum toxin (botox)

Quinine sulfate


Dantrolene Sodium (Dantrium)



Action/Uses Interferes with the release of calcium ions from inside skeletal muscle cells Spinal cord injury, stroke, CP, MS,

Administration Use oral solution within days (no preservative) IV – high PH, very irritating Dantrolene Sodium (Dantrium) – prototype

Pharmacokinetics Onset 1-2 hours Peak 5 hours/ duration varies Half life 4-8 IV, 8-9 PO

Adverse effects Muscle weakness, dry mouth, drowsiness, dizziness, nausea, diarrhea, tachycardia, erratic B/P, urinary retention, photosensitivity

Interactions Not with OTC cough preparations or antihistamines Alcohol Other CNS depressants

Nursing Considerations Careful monitoring of client conditions  Monitor lab tests when indicated May need assistance in taking meds. (because of spasticity)

Client Education Avoid driving and other potentially hazardous activity Report changes in sensorium, chest pain, palpitations, dyspnea, fatigue, visual disturbances, urine retention Other medications, OTC, herbals DC alcohol ROM exercises Do not DC medicine abruptly – may cause seizures


Endocrine System

  • Consists of glands that secrete hormones
  • Maintains homeostasis using hormones as chemical messengers   *Secreted in response to changes in internal environment
  • Hormone release commonly controlled by negative feedback    *One hormone may control another
  • Negative Feedback: *Common for last hormone in a pathway to provide feedback * Turns off secretion from first hormone. * Prevents over responses by endocrine system.
  • Hypothalamus and Pituitary Glands: Control many other glands
  • Hypothalamus secretes releasing hormones (Directs anterior pituitary gland as to which hormones should be released)
  • Hypothalamus sends nerve signals (Posterior pituitary releases hormones)



Hormone Pharmacotherapy


Hormones used as

  • Replacement therapy
  • Antineoplastics
  • Natural therapeutic effects (Exaggerated response or suppression of body defenses)
  •  Hormone blockers used to inhibit actions of certain hormones



Pituitary and Hypothalamic Hormones


Only a few hormones have clinical application

  • Difficult and expensive to obtain
  • Usually more effective to give hormone that directly affects secretion

Commonly used for replacement are

*** Prolactin, oxytocin ** 


1) Corticotropin, growth hormone

2) Antidiuretic hormone (ADH)




Growth Hormone (GH)


Stimulates growth and metabolism

**Deficiency results in dwarfism

Recombinant DNA technology has produced pharmacotherapy Somatrem (Protropin) and Somatropin (Humatrope) "used most often"

**Recently approved to treat small stature associated with normal levels of growth hormone (GH)


Excess secretion results in acromegaly (adults)




Antidiuretic Hormone (ADH)


Conserves water in body

    **Diabetes insipidus is caused by deficiency of ADH (uncontrolled diaresis, Major fluid loss.. low ADH)


Most common form of ADH: desmopressin (DDAVP)

***Long duration of action (20 hours) *** Forms: nasal spray, oral, intravenous, subcutaneous


Other drugs: vasopressin (Pitressin) and lypressin (Diapid)

  • Short duration of action (2–8 hours)
  • Only given via intramuscular or subcutaneous routes



Anterior Pituitary Hormone

 vasopressin injection (Pitressin)


Mechanism of action: causes renal collecting tubules to increase their permeability to water. & Enhances water reabsorption


Primary use: treatment of diabetes insipidus


Adverse effects: hypertension! * Can precipitate angina episodes and myocardial infarction in clients with coronary artery disease.  * Excessive fluid retention can cause water intoxication.


Nursing Considerations: Assess for electrolyte imbalances, Assess for changes in specific gravity and fluid intake. Monitor serum sodium and potassium levels. Monitor urinary specific gravity, routine urinalysis. Monitor body weight and fluid intake/output. Assess vital signs, especially blood pressure and pulse


Thyroid Gland


Secretes thyroxine (T4) and triiodothyronine (T3)

     **Control basal metabolic rate and affect every cell in body

Parafollicular cells in thyroid secrete calcitonin

    **Responsible for calcium homeostasis

Follicular cells secrete thyroid hormone

  ***Thyroxine (T4) and triiodothyronine (T3)

  ***Iodine essential for synthesis of T4 and T3


   Negative-feedback loop controls secretion

 ***Low thyroxine levels signal hypothalamus to release thyroid-releasing hormone (TRH)

*** Signals pituitary to release thyroid-stimulating hormone (TSH)




Hypothyroidism in Adults (Myxedema)

  • Early symptoms are: general weakness, muscle cramps, and dry skin
  • More severe symptoms include: Slurred speech, bradycardia, weight gain, Decreased sense of taste and smell, Intolerance to cold environments
  • Elevated TSH (thyroid stimulating hormone) with diminished T3 and T4 levels



Pharmacotherapy for hypothyroidism


levothyroxine (Synthroid)


Mechanisms of action: same as those of thyroid hormone (how T3 T4 acts on the body naturally)


Primary use: drug of choice for replacement therapy in clients with low thyroid function


Adverse effects: hyperthyroidism, palpitations, dysrhythmias

***(Anxiety, insomnia, weight loss, heat intolerance Menstrual irregularities and osteoporosis in women <- these are signs of hyperthyroidism)

Nursing Considerations: ***(these are assesing for TOO MUCH stynthroid) Assess client’s weight and vital signs Assess tachycardia, irregular heart rate, hypertension Assess nervousness, weight loss, diarrhea, heat intolerance. Monitor clients with impaired renal function closely

***(these are assessing for TOO LITTLE synthroid)Monitor for excess fatigue, slow speech, hoarseness or slow pulse May indicate under dosage






Most common type: is Grave’s disease

Goal: is to lower activity of thyroid


Symptoms: Increased body metabolism Tachycardia, weight loss Elevated body temperature, anxiety.


1: Administer thioamides, which decrease activity of thyroid gland: Propylthiouracil(PTU) and methimazole (Tapazole).


2: Radioactive iodide that kills overactive thyroid cells.  SUCH AS: Sodium iodide-131, Lugol’s solution


Goal is to lower activity of thyroid gland






Antithyroid Pharmacotherapy 

 propylthiouracil (PTU)

(for hyperthyroidism)


Mechanism of action: to interfere with synthesis of T3 and T4 in thyroid gland. Also prevents conversion of T4 to T3 in target tissues


Adverse effects: symptoms of hypothyroidism....

***Rash and transient leucopenia are most common side effects

***Small percentage of clients experience agranulocytosis


Nursing Considerations:

Monitor vital signs

Monitor thyroid-function tests

Monitor for signs of infection, including CBC and WBC count

Monitor weight at least weekly

Monitor for drowsiness




Adrenal Cortex


Secretes glucocorticoids:

1) Mobilize body for long-term stress

2) Influence carbohydrate, lipid, and protein metabolism in most cells


Secretes mineralocorticoids:

1)Aldosterone promotes sodium reabsorption and potassium secretion


Secretes gonadocorticoids

1)Male sex hormones (androgens)




Selected Glucocorticoids

  • Adrenal glands secrete hormones affecting every body tissue
  • Specific pharmacotherapy depends on which portion of adrenal gland is responsible for the abnormal secretion
  • Chronic corticosteroid insufficiency requires replacement with glucocorticoids
  • Goal of replacement therapy is to reach appropriate level of hormones in blood
  • Glucocorticoids also prescribed to suppress inflammatory and immune responses



Control of Glucocorticoids


Hypothalamus releases corticotropin-releasing factor (CRF)

  • Causes adrenocorticotropic hormone (ACTH) to be secreted by pituitary

Adrenal cortex releases glucocorticoids


**When cortisol level rises, negative-feedback mechanism shuts off further release of glucocorticoids


Adrenocortical Insufficiency

(Addison’s Disease)


Primary adrenocortical insufficiency


It is rare; deficient of both glucocorticoids and mineralocorticoids



*Hypoglycemia, fatigue, hypotension

*Increased skin pigmentation

*GI disturbances: anorexia, vomiting, diarrhea

*Low plasma cortisol, accompanied by high plasma ACTH levels


Adrenal Drugs — Glucocorticoids



(Aeroseb-HC, Alphaderm)


Mechanism of action: acts as synthetic corticosteroid


Primary use: drug of choice for treating adrenocortical insufficiency


Adverse effects: sodium and fluid retention

CNS effects: insomnia, anxiety, headache, vertigo, confusion, depression

***Hypertension, tachycardia, peptic ulcer disease, Cushing’s syndrome (Can occur with long-term therapy)


Nursing Considerations: Assess: vital signs for temperature and blood-pressure elevations

Monitor: potassium, T3, T4, glucose levels

***Clients on long-term glucocorticoid therapy Monitor for osteoporosis and elevated serum cholesterol levels

***Assess for signs and symptoms of Cushing’s syndrome

Monitor: skin and mucous membranes for lacerations, abrasions, or break in integrity

Monitor: GI status for peptic ulcer development

Monitor: serum electrolytes

Monitor: changes in musculoskeletal system

Monitor: emotional stability




Cushing’s Syndrome


Caused by long-term administration of glucocorticoids


Signs and symptoms Moon face, buffalo hump, mood and personality disorders


Also:  Hyperglycemia, Na and fluid retention, bruises and petichia, thin skin, osteoporosis, fate deposits on back, thin extremities




Antiadrenal Drugs


Used to treat severe Cushing’s syndrome:

  • Occurs with prolonged glucocorticoid therapy 
    • Inhibits corticosteroid synthesis

Antiadrenal drugs NOT curative:

  • Use usually limited to three months of therapy
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