PHARMA MT
LESSON 5
I. AUTONOMIC NERVOUS SYSTEM DRUGS
- regulates the body's involuntary functions including heart rate, respi rate and digestion, and sexual arousal
*Sympathetic: "fight and flight"; increased BP, HR, blood sugar
*Parasympathetic: "rest and digest"; decrease BP, HR, peristalsis and digestion restart
A. CHOLINERGIC DRUGS
- promote action of the neurotransmitter acetylcholine
- also called "parasympathomimetic drugs" because they imitate parasympathetic nervous system
- 2 major classes:
a. Cholinergic agonists: mimic the action of the neurotransmitter acetylcholine
b. Anticholinesterase: inhibits the destruction of acetylcholine at the cholinergic receptor sites
B. CHOLINERGIC AGONISTS
- mimic the action of acetylcholine by directly stimulating cholinergic receptors
- include: acetylcholine, bethanecol, carbachol, pilocarpine
- poorly penetrate the CNS and its effects are primarily peripheral with a widespread action
- when combined with the receptors on the cell membranes of the target organs, they stimulate the muscle and produce: salivation, bradycardia, vasodilation, bronchoconstriction, increased activity of GI tract, increased tone and contraction of the muscles of the bladder, constriction of the pupils of the eye
- rapidly destroyed in the body; rarely administered by IM or IV
C. ANTICHOLINESTERASE DRUGS
- block acetylcholinesterase at the cholinergic receptor sites; breaks down acetylcholine
- 2 categories:
a. Reversible Anticholinesterase: short duration of action
b. Irreversible Anticholinesterase: long lasting effect, used primarily as toxic insecticides
- Reversible anticholinesterase block the break down of acetylcholine for minutes to hours; Irreversible anticholinesterase lasts for days or weeks
- most are readily absorbed from GIUT, SQ, and mucous membranes
- most are metabolized in the body by enzymes in the plasma and excreted in urine
*Nursing Responsibilities:
- take as prescribed, compliance is essential
- report side effects such as: dizziness, decreased HR, signs and symptoms of respiratory distress
- arise from a lying position slowly
- effective oral hygiene
D. CHOLINERGIC BLOCKING DRUGS
- interrupt parasympathetic nerve impulses in CNS
- prevent acetylcholine from stimulating cholinergic receptors
- block only muscarinic receptor sites
- can have paradoxical effects on the body depending on the dosage and condition being treated
- produce a stimulating or depressing effect depending on the target organ
*Nursing Responsibilities:
- advice client of common side effects: dry mouth, decreased urination, constipation as a result of long-term use of anticholinergics
- increase OFI to prevent constipation
- hard candies, ice chips or chewing gum
- urinate before taking
II. ADRENERGIC AND ADRENERGIC BLOCKING DRUGS
A. ADRENERGIC DRUGS
- also know as "sympathomimetic drugs"
- can affect alpha-beta adrenergic receptors, beta-adrenergic receptors and dopamine receptors
- most produce their effects by stimulating the alpha and beta receptors; these drugs mimic the action of norepinephrine or epinephrine
- dopamine drugs act primarily on receptors in the sympathetic nervous system stimulated by the dopamine
Classification based on chemical structure:
a. Catecholamines
- stimulate the nervous system, constrict peripheral blood vessels, increase the heart rate and dilate the bronchi
- can’t be taken orally; SQ absorption is slowed because the drug causes the surrounding blood vessels to constrict; IM is more rapid because there is less constriction
- widely distributed, metabolized predominantly in the liver but can also be inactivated in the GIT, lungs, kidneys, plasma and other tissues
- excreted primarily in the urine
b. Non-Catecholamines
- local or systemic constriction of blood vessels
- nasal and eye decongestion and dilation of the bronchioles
- smooth muscle relaxation (ritodrine hydrochloride and terbutaline)
- metabolism and inactivation occur primarily in the liver but can also occur in the lungs, GIT and other tissues
- excreted primarily in the urine
- absorption depends on the route of administration:
inhaled drugs (albuterol) are absorbed from the bronchi in the lungs
oral drugs are well absorbed from the GIT and distributed widely in the body fluids and tissues
some (ephedrine) cross BBB and can be found in high concentrations in the brain and CSF
Classifications based on how they act:
- Direct acting: drugs act directly on organ or tissue innervated by SNS; stimulate alpha activity (methoxamine and phenylephrine)
- stimulate Beta 2 activity (albuterol, isoetharine, metaproterenol, ritodrine and terbutaline)
- Indirect acting: drug triggers the release of a neurotransmitter, usually norepinephrine; phenylpropanolamine
- Dual-acting: drug has both direct and indirect actions; ephedrine, mephentermine and metaraminol
B. ADRENERGIC BLOCKING DRUGS
- also called "sympatholytic drugs"
- used to disrupt the sympathetic nervous system’s function
- Inhibition of catecholamine receptors
- Inhibition of the production, storage, and/or release of catecholamines (especially norepinephrine)
- block neurotransmitter from binding to the receptors
- classifications include alpha-adrenergic blockers or beta-adrenergic blockers
a. Alpha-Adrenergic Blockers
- interrupt the actions of the catecholamines epinephrine and norepinephrine at alpha receptors resulting in
- relaxation of the smooth muscle in the blood vessels
- increased vasodilation
- decreased blood pressure
- work by interfering or blocking the synthesis, storage, release and reuptake of norepinephrine by neurons or by antagonizing epinephrine, norepinephrine or adrenergic drugs at alpha receptor sites
- occupy alpha receptor sites on the smooth muscle of the blood vessels preventing catecholamines form occupying and stimulating the receptor sites
- indicated for: hypertension; peripheral vascular disorders such as Raynaud’s disease, acrocyanosis and frostbite; pheochromocytoma
b. Beta-Adrenergic Blockers
- most widely used adrenergic blockers
- prevent stimulation of the sympathetic nervous system by inhibiting the action of catecholamines at the beta-adrenergic receptor sites
- commonly referred as beta-blockers
LESSON 6
I. MUSCLE RELAXANTS
- relieve msk pain or spasm and severe msk spasticity
- 2 MAIN CLASSES:
a. CENTRALLY ACTING
- acts on the central nervous system
- used to treat acute spasms caused by anxiety, inflammation, pain and trauma
- onset: oral (30 min - 1 hr.)
- duration: varies from 4-6 hrs.
- cyclobenzaprine has the LONGEST DURATION of 12-25 hrs.
- depress the cns
- a patient with acute muscle spasms may receive one of the following drugs:
BACLOFEN – used for the treatment of muscle spasticity; multiple sclerosis, muscle rigidity and spinal cord injuries (oral intrathecal – injection thru the spinal cord via pump)
CARIOPRODOL – indicated to relief of discomfort ass with msk pain, safe with older patient, renal or hepatic dysfunction
CHLORPHENESIN – same carioprodol long duration in action
CHLORZOXAZONE – relief with painful acute msk condition
CYCLOBENZAPRINE – relief of discomfort ass with msk – few adverse effect – oral form
METAXALONE – caution for patient with hepatic impairment – with an established pediatric dose for children older than 12 yrs old
METHOCARBAMOL – used to alleviate s&s of tetanus
ORPHENADRINE – parenteral drug relief acute and painful msk condition
TIZANIDINE – acute and intermittent management of increase muscle tone ass with spasticity 0 ass with liver toxicity and hypotension
b. PERIPHERALY ACTING
- most common is dantrolene sodium (direct acting skeletal muscle relaxant)
- major effect is on the muscles (cerebral palsy , multiple sclerosis muscular dystrophy, polio, tetanus, quadrelegia, als)
- high therapeutic doses are toxic to the liver
- peak: 5 hrs after ingestion
- half life: 4-8 hrs (9hrs. for healthy adults; longer for patients w liver dysfunction)
II. SEDATIVES, ANXIOLYTICS, HYPNOTIC AGENTS
- Sedation: loss of awareness and reaction to environmental stimuli (restless, nervous, irritable, or overreacting)
- Anxiety: "fear of the unknown"; feeling of tension, nervousness, apprehension or fear that usually involves unpleasant reaction to a stimuli – ass with sympathetic stress
- Hypnosis: extreme sedation result in further central nervous system depression and sleep
Sedatives and Hypnotics
- sedatives reduce activity or excitement
- when given in large doses, sedatives are considered hypnotics
- 3 main classes of synthetic drugs used as sedatives and hypnotics are:
A. BENZODIAZEPINES
- minor tranquilizer; anxiolytic; "-am"
- low dose: decrease anxiety by acting on the limbic system and other areas of the brain that help regulate emotional activity; calm and sedate
- high dose: induce sleep
B. BARBITURATES
- highly addicting and causes drug dependence
- reduce overall CNS alertness
- low dose: depress sensory and motor cortex of the brain causing drowsiness
- high dose: cause respiratory depression and death because of their ability to depress all levels of the CNS
C. NONBENZODIAZEPINES-NONBARBITURATES
- act as hypnotics for short-treatment of simple insomnia
- Lose their effectiveness by the end of the 2nd week except zolpidem (35 days)
ANTIANXIETY DRUGS
- "anxiolytics"
- used primarily to treat anxiety disorders
- 3 main types:
A. Benzodiazepines
B. Barbiturates
C. Buspirone
- the first anxiolytic in a class of drugs known as azaspirodecanedione derivatives
- less sedation
- no increase in CNS depressant effects when taken with alcohol or sedative-hypnotics
- low abuse potential
- affects midbrain
- does not interact with alcohol or other CNS depressants
- slow onset makes it ineffective when quick relief from anxiety is needed
III. ANTIDEPRESSANTS
- Affect: refers to the persons feeling in response to their environment
- Mood: state of emotion
- Depression: most common affective disorder – feeling of sadness is much more serve and longer
- treat affective disorders
- include:
A. Monoamine Oxidase Inhibitors (MAOIs)
- work by inhibiting monoamine oxidase making more norepinephrine and serotonin available to the receptors and thereby relieving the symptoms of depression
- MAOI + antidiabetics = may enhance hypoglycemic effects
- MAOI + meperidine = excitation, hypertension or hypotension, extremely elevated body temperature and coma
- severe reaction may occur if taken with tyramine rich food such as red wines, aged cheese and fava beans, and sympathomimetic drugs
- 2 classifications:
HYDRAZINE - include phenelzine sulfate
NONHYDRAZINE - comprised of a single drug, tranylcypromine sulfate
Mao – break down norepi and 5ht(serotonin) to be recycled and restored in the neurons; used rarely because they require specific dietary regimen to prevent toxicity
NArdil (phenelzine) – reserved for use in patients who do not respond to other antidepressant or who can not take other antidepressant for some reason
Parnate (tranylcypromine) – used for adult patients with reactive depression, associated with potentially fatal food-drug interaction
B. Tricyclic Antidepressants (TCAs)
- used to treat major depression, effective and less expensive than SSRIs and other drugs
- block the uptake of the neurotransmitter norepinephrine and serotonin
- absorbed completely when taken orally but undergo first-pass effect
- fat solubility makes these drugs widely distributed, excreted slowly and long half-lives
- effective in treating depression of insidious onset accompanied by weight loss, anorexia or insomnia
- physical symptoms may respond after 1 to 2 weeks of therapy; psychological after 2 to 4 weeks
C. Selective Serotonin Reuptake Inhibitors (SSRIs)
- formerly known as 2nd generation antidepressants
- developed to treat depression with fewer side effects
- chemically different from TCAs and MAOIs
- used to treat the same major depressive episodes as TCAs and have the same degree of effectiveness; some are used to treat OCD
- use of drugs with MAOIs can cause serious potentially fatal reactions
IV. ANTIPARKINSONIAN AGENTS
- Parkinson's disease – a progressive, chronic neurological disorder and may develop in people of any age
- cause is unknown. No cure for Parkinson's disease, therapy is aimed to manage signs and symptoms and provide optimal functioning for as long as possible.
- 2 goals:
a. promote the secretion of dopamine (dopaminergic drugs) which helps in muscle tone
b. inhibit the cholinergic effects (anticholinergic drugs)
ANTICHOLINERGIC
- drugs that opposes the effects of acetylcholine at the receptor sites
- Synthetic: they have been developed to have a greater affinity for cholinergic sites in the CNS than those in the PNS
- Antihistamine (benadryl): often used in combination with other agents indicated for treatment of any type of Parkinsonism including drug induced disease esp in elderly patients who cannot tolerate other drugs and for patients in early stage of the disease
- 2 chemical categories according to their chemical structure:
a. synthetic tertiary amines: benztropine, biperiden hydrochloride, biperiden lactate, procyclidine, and trihexyphenidyl
b. antihistamines with anticholinergic properties such as diphenhydramine and orphenadrine
- well absorbed from the GIT and cross the BBB(blood brain barrier) to their action site in the brain
- levodopa: metabolic precursor to dopamine; still inactive until it crosses the BBB and is converted to dopamine by enzymes in the brain
- antipsychotic drugs decrease the effectiveness of anticholinergics
- OTC cough and cold preparations increase the anticholinergic effects
- carbidopa enhances levodopa's effect
DOPAMINERGIC
- drugs that increase the effects of dopamine at the receptor sites, have been proven to be more effective than anticholinergic in treatment of Parkinson's disease
- Dopamine itself does not cross the blood brain barrier; others that act as dopamine or increase dopamine concentrations indirectly must be used to increase dopamine levels in the brain
- Remains effective as long as enough intact neurons respond to increase dopamine level; at some point patients no longer respond to these drugs
- absorbed from the GIT into the bloodstream and are
delivered to their action site in the brain
- absorption is slowed and reduced when ingested with food
- act in the brain to improve motor function in or two ways – increasing dopamine concentration and/or enhancing the neurotransmission of dopamine
adverse reactions:
- levodopa: causes nausea and vomiting
- amantadine: orthostatic hypotension, constipation
- bromocriptine: persistent orthostatic hypotension, ventricular tachycardia, bradycardia, worsening angina
- pergolide: confusion, dyskinesia, hallucinations,
nausea
- pramipexole: orthostatic hypotension, dizziness, confusion, insomnia
V. ANTIEPILEPTIC AGENTS
Seizure classification:
A. PARTIAL
- seizure originates in one part/area of the brain; do not spread throughout the entire organ
1. SIMPLE - one area only; no loss of consciousness; may involve a single muscle movement or sensory alterations
2. COMPLEX - altered awareness; loss of consciousness; hallucinations; no physical S&S
B. GENERALIZED
- begins in one area and spreads throughout both hemispheres of the brain
1. ABSENCE - "tulala"; 3-5 seconds period of loss of consciousness
2. MYOCLONIC - sudden, brief jerks of muscles; lasts several minutes
3. TONIC CLONIC - (grandmal seizure); stiffening(tonic) followed by jerking movements (clonic); recovery period characterized by confusion and exhaustion
4. TONIC - muscle stiffening, no jerking; very brief and happens without warning
5. ATONIC - sudden loss of muscle tone, causing falls
ANTICONVULSANT DRUGS
- also known as antiepileptic drugs
- long term management of chronic epilepsy (recurrent seizures)
- short term management of acute isolated seizures not caused by epilepsy, such as after trauma or brain injury
- have 5 major classes:
A. HYDANTOINS
- 1st anticonvulsant to treat seizures
- include phenytoin (10-20 mcg/ml), phenytoin sodium, fosphenytoin, mephenytoin
- phenytoin is absorbed slowly after oral and IM; mephenytoin is absorbed rapidly after oral
- phenytoin is distributed rapidly in all tissues; fosphenytoin is widely distributed
- stabilize nerve cells to keep them from overexcited; works in the motor cortex of the brain where it stops seizure activity
- phenytoin is most commonly prescribed because of its effectiveness and low toxicity
- manage: complex partial seizure(psychomotor or temporal lobe seizures); tonic clonic seizures
- adverse effects: may cause severe liver toxicity, bone marrow suppression
B. BARBITURATES
- long-acting barbiturate phenobarbital was one of the most widely used anticonvulsants, now less frequent due to adverse effects
- therapeutic serum range for phenobarbital is 15-40 mcg/ml
- phenobarbital is absorbed slowly but well from GIT
- 20-45% bound to serum proteins; 75% is metabolized by the liver; 25% is excreted in the urine unchanged
- inhibit impulse conduction in the ascending RAS, the cerebral cortex, alter cerebellar function, depress motor nerve output
- manage: partial, tonic-clonic, and febrile seizures
- adverse effects: CNS depression; can produce sedation, hypnosis, and deep coma; may be associated with physical dependence and withdrawal syndrome
C. IMINOSTILBENES
- most common is carbamazepine
- therapeutic serum range is 5-12 mcg/ml
- absorbed slowly and erratically from GIT; distributed rapidly to all tissues; 75-90% protein bound; metabolized in the liver and excreted in the urine
- inhibit spread of seizure activity or neuromuscular transmission in general
- manage: partial and generalized tonic-clonic seizures; mixed seizure types
D. BENZODIAZEPINES
drugs that provide anticonvulsant effects include:
- diazepam (parenteral form)
- clonazepam (rec for long term treatment of epilepsy; 20-80 mg/ml)
- clorazepate (adjunct therapy in treating partial seizures)
- can be given orally or parenterally; absorbed rapidly and almost completely from GIT; distributed at different rates; 85-90% protein-bound
- act as anticonvulsants, anxiolytics, sedative-hypnotics, muscle relaxants
stabilize nerve membranes throughout CNS to decrease excitability and hyperexcitability to stimulation
- manage: absence, atonic and myoclonic seizures
E. VALPROIC ACID
- unrelated structurally to other anticonvulsants
- used cautiously when giving this drug to very young children and clients with liver disorders because hepatoxicity is one of possible adverse reaction
- 2 major drugs: valproate (40-100 mch/ml) and divalproex
- valproate is converted rapidly to valproic acid in the stomach; divalproex is a precursor of valproic acid and separates into valproic acid in the GIT
- absorbed well, strongly protein bound; metabolized in liver and excreted in urine
- unknown MOA but thought to increase level of GABA
- manage: long term treatment of absence, myoclonic, and tonic-clonic seizures
VI. ANTIPSYCHOTIC AGENTS
- control psychotic symptoms such as delusion, hallucinations and thought disorders that can occur with schizophrenia, mania and other psychoses
*Various names:
- antipsychotics: eliminate the S&S of psychoses
- major tranquilizer: calm an agitated patient
- neuroleptic: can cause adverse neurobiological effect that causes abnormal body movements
*3 Distinct class of phenothiazines accd to adverse reactions that they can cause:
1. ALIPHATICS: primarily cause sedation and anticholinergic effects, moderately potent; strong sedative effect, decrease BP, and may cause moderate EPS(pseudo parkinsonism)
2. PIPERAZINES: primarily cause involuntary movements; low sedative effects, little effect on BP, and strong antiemetic effect
3. PIPERIDINES: primarily cause sedation; strong sedative effect, cause few EPS, low to moderate effect on BP, and have no antiemetic effect
*Major Groups:
A. TYPICAL ANTIPSYCHOTICS: phenothiazines and nonphenothiazines
- absorbed erratically; very lipid-soluble and highly protein-bound
- distributed in many tissues and highly concentrated in brain
- metabolized in the liver and excreted in urine
- block postsynaptic dopaminergic receptors in the brain
*Phenothiazines: schizophrenia; calm anxious/agitated patients; improve patient's thought process; alleviate delusions and hallucinations
*Non-phenothiazines: psychotic disorders; thiothixene: controls acute agitation; haloperidol and pimozide: Tourette's syndrome
B. ATYPICAL ANTIPSYCHOTICS: clozapine, olanzapine, and risperidone
- lesser side effects; most common is weight gain
- 2 advantages over typical antipsychotics: effective in treating negative symptoms; not likely to cause EPS
- include clozapine, olanzapine, risperidone
- absorbed after oral administration; metabolized by liver and is highly protein bound; eliminated in urine with a small portion in feces
- block the dopamine receptors but not as effectively as the typical antipsychotics
- given to schizophrenic patients who are unresponsive to typical antipsychotics
- counteract the effects of levodopa and other dopamine agonists
LESSON 7
I. DIURETICS
- promote excretion of water and electrolytes by kidneys
- 2 main purposes: a. lower BP; b. decrease edema in heart failure and renal or liver disorder
- major diuretics: thiazide & thiazide-like; loop; potassium-sparing; osmotic; carbonic-anhydrase inhibitors
1. THIAZIDE & THIAZIDE-LIKE
- sulfonamide derivatives
- used to treat edema and to prevent development or recurrence of renal calculi
a. THIAZIDE
- absorbed rapidly but incompletely from GIT after oral administration
- cross placenta and secreted in breastmilk
- differ in how well they are metabolized, but all are excreted primarily in urine
b. THIAZIDE-LIKE
- absorbed from GIT
- metabolized in liver; excreted primarily in urine
- work by preventing Na from being reabsorbed in kidney
- increase excretion of chloride, potassium and bicarbonate
- cause loss of Na, K and Mg; promote Ca reabsorption
- alter fluid volume, BP and serum electrolyte levels
2. LOOP DIURETICS
- high ceiling diuretics (highly potent drugs)
- act on the thick ascending loop of Henle to inhibit chloride transport of Na into the circulation
- bumetanide, ethacrynate sodium, ethacrynic acid, torsemide, furosemide
- absorbed well and distributed rapidly; highly protein bound
- undergo partial or complete metabolism in the liver except for furosemide, which is excreted primarily unchanged
- excreted by kidneys
- for: edema associated with heart failure and liver disease of nephrotic syndrome; hypertension: usually a K-sparing diuretic or a K supplement to prevent hypokalemia
- adverse reactions: reduced blood volume, orthostatic hypotension, hyponatremia, hypokalemia, hypocalcemia, hypomagnesemia, hypochloremia
3. POTASSIUM-SPARING DIURETICS
- referred to as aldosterone inhibiting diuretic
- have weaker diuretic and antihypertensive effects than other diuretics but have the advantage of conserving K
- include amiloride, spironolactone and triamterene
- available orally and absorbed in GIT
- metabolized in liver except for amiloride; excreted primarily i urine and bile
- urinary excretion of sodium and water increases as does the excretion of chloride and calcium ions
- excretion of potassium and hydrogen ion decreases
- for: edema; diuretic-induced hypokalemia in patients with heart failure; cirrhosis; nephrotic syndrome; hypertension
- adverse reactions: can lead to hyperkalemia especially when taken together with K supplement or a high K diet
4. OSMOTIC DIURETICS
- pull water into renal tubule without Na loss; example is mannitol
- used in acute situations when it is necessary to decrease IOP before eye surgery or during acute attacks of glaucoma
- freely filtered at the renal glomerulus, poorly reabsorbed by the renal tubule and resistant to metabolism
- mannitol is only available for IV use
- adverse reactions: sudden drop in fluid levels; nausea, vomiting, hypotension, light headedness, confusion, and headache can be accompanied by cardiac decomposition and even shock
5. CARBONIC ANHYDRASE INHIBITORS
- mild diuretics
- include acetazolamide and methazolamide
- rapidly absorbed and widely distributed; excreted in urine
- can be taken orally or IV
- peak: 2-4 hrs; 15 mins if given orally
- duration: 6-12 hrs
- have been associated with fetal abnormalities, and should not be used during pregnancy
- block effects of carbonic anhydrase thereby slowing down movement of hydrogen ions; as a result, more sodium and bicarbonate are lost in urine
- adverse reactions: disturbance in acid-base and electrolyte balances such as acidosis and hypokalemia; others include paresthesia, confusion, and drowsiness
II. DRUGS FOR FLUID AND ELECTROLYTE IMBALANCE
A. POTASSIUM
- major cation in ICF
- adequate amounts must be ingested daily
- normal amount: 3.5-5.5mEq/L
- dietary requirement: 40-60 mEq
- absorbed readily from GIT; after absorption into the ECF, almost all K passes into the ICF
- normal serum levels of K are maintained by kidneys, which excrete most of the excessive K intake; the rest is excreted in feces and sweat
- moves quickly into the ICF to restore depleted K levels and re-establish balance
- used to decrease toxic effects of digoxin
- adverse reactions: oral K sometimes causes nausea, vomiting, abdominal pain and diarrhea; IV infusion of K preparations can cause pain at the injection site and phlebitis; if given rapidly, IV admin may cause cardiac arrest
B. CALCIUM
- almost all Ca in the body is stored in the bone, where it can be mobilized if necessary
- chronic insufficient Ca intake can result in bone demineralization
- promotes normal nerve and muscle activity and increases contraction of the heart's muscle
- normal amount: 4.5-5.5 mEq/L or 8.5-10.5 mg/dl
- daily requirement: 1,300 mg (14-18 yo); 1,000 mg (19-50 yo); 1,200 mg(above 50 yo)
- absorbed readily from duodenum and proximal jejunum
- distributed primarily in the bone; pH of 5 to 7
- Ca salts are eliminated primarily in the feces, the rest is excreted in urine
- integral to normal functioning of the heart, kidneys and lungs and it affects blood coagulation rate as well as cell membrane and capillary permeability
- helpful in treating magnesium intoxication
- adverse reactions: hypercalcemia (early signs include drowsiness, lethargy, muscle weakness, headache, constipation, metallic taste in mouth); ECG: elevated serum Ca levels may lead to a shortened QT internal and heart block
C. MAGNESIUM
- most abundant cation in ICF after K
- normal value: 1.5-2.5 mEq/L
- daily requirement: 19-30 yo, 400mg (men) and 310mg (women); 31 and older, 420mg (men) and 320mg (women)
- distributed widely throughout the body; IV magnesium sulfate acts immediately, whereas after IM administration, it acts within 30 minutes
- not metabolized and is excreted unhanged in urine, some are excreted in breastmilk
- replenishes and prevents Mg deficiencies; also prevents seizures by blocking neuromuscular transmission
- adverse reactions: hypotension, circulatory collapse, flushing, depressed reflexes, respiratory paralysis
D. SODIUM
- major cation in ECF
- contributes to nerve conduction and neuromuscular function
- normal value: 135-145 mEq/L
- daily dietary requirement: 2g
- quickly absorbed and widely distributed throughout the body
- not significantly metabolized, primarily eliminated in urine
- adverse reactions: pulmonary edema, hypernatremia, K loss
LESSON 8
I. ANTIULCERANT DRUGS
A. ANTACIDS
- group of inorganic chemicals that neutralize stomach acid; available OTC
- used alone or with combination with other drugs to treat peptic ulcers, relieve pain; relieve symptoms of acid indigestion, heartburn, dyspepsia or GERD
- neutralize gastric acid; reduces the total amount in the GIT allowing peptic ulcers time to heal
- distributed throughout the GIT and are eliminated primarily in the feces
- interfere with the absorption of oral drugs if given at the same time
B. H2 RECEPTOR ANTAGONISTS
- H2 blockers
- commonly prescribed include cimetidine, nizatidine, ranitidine and famotidine
- cimetidine, nizatidine, and ranitidine are absorbed rapidly and completely from GIT; famotidine is not absorbed completely
- food and antacids may reduce absorption
- distributed widely through the body, metabolized by the liver and excreted in the urine
- block histamine from stimulating the acid secreting parietal cells of the stomach
- help treat active duodenal ulcer or benign gastric ulcer; relieve symptoms of heartburn, acid indigestion, and sour stomach
- adverse reactions: headache, dizziness, malaise, muscle pain, nausea, diarrhea, rashes, itching, impotence
C. PROTON PUMP INHIBITORS
- "prazole"
- given orally in enteric-coated formulas to bypass the stomach because they're highly acid labile
- dissolved in small intestine and absorption is rapid
- highly protein bound and are extensively metabolized by liver to inactive compounds and then eliminated in urine
- block the final step of gastric acid production
- adverse reactions: dizziness, headache, abdominal pain, diarrhea, nausea, cough, stuffy nose, epistaxis
D. OTHER PEPTIC ULCER DRUGS
1. SUCRALFATE
- GI protectant; works locally in the stomach
- rapidly absorbed after oral administration, metabolized in liver, excreted in feces
- should not be given to those with renal failure or undergoing dialysis; caution to clients who are pregnant or lactating
2. MISOPROSTOL
- synthetic prostaglandin
- inhibits gastric acid secretion and increases bicarbonate and mucus production in the stomach
- given orally; rapidly absorbed from the GIT; metabolized in liver; excreted in urine
- contraindicated during pregnancy because it is an abortifacient
II. LAXATIVES
A. CHEMICAL STIMULANTS
- directly stimulate the nerve plexus in the intestinal wall, causing increased movement and the stimulation of local reflexes
- include Bisacodyl (Dulcolax), cascara, castor oil, and Senna (Senokot)
- most are minimally absorbed and exert their therapeutic effect directly in the GIT
- castor oil has an onset of action of 2-6 hrs; others are 6-8 hrs
- castor oil is used when a thorough evacuation of the intestine is desired; Bisacodyl acts in a similar manner but milder in effect; cascara is milder than castor oil and often used when effects are needed overnight; Senna is available orally in tablet and syrup form and as a rectal suppository
- adverse effects: diarrhea, abdominal cramping, nausea, sweating, palpitations
B. BULK STIMULANTS
- "mechanical stimulants"
- rapid acting, aggressive laxatives that cause the fecal matter to increase in bulk
- taken orally
- directly effective within GIT and not generally absorbed systematically
- rapidly acting, causing effects as they pass through the GIT
- administration of laxatives and other meds should be separated by at least 30 minutes
- adverse effects: diarrhea, abdominal cramping, nausea, sweating, palpitations
C. LUBRICANTS
- make defecation easier without stimulating GIT movement
- include docusate (Colace), glycerin (Sani-Supp), and mineral oil
- docusate has a detergent action on surface of the intestinal bolus; glycerin is used in suppository form to gently evacuate the rectum; mineral oil is the oldest of these laxatives, it's not absorbed and forms a slippery coat on the contents of the intestinal tract
- docusate and mineral oil are given orally
- frequent use of mineral oil can interfere with the absorption of vitamins A,D, E, K
III. GASTROINTESTINAL STIMULANTS
- stimulate parasympathetic activity or make the GI tissues more sensitive to parasympathetic activity
- include dexpanthenol and metoclopramide
- increase the motility of the GI system
- indicated when more rapid movement of GI contents is desirable
- dexpanthenol is given by IM and reaches its peak levels within 4 hrs
- metoclopramide is given orally or by IM or IV infusion and has a peak effect by all routes in 60-90 minutes
- metabolized in liver; excreted in feces and urine
IV. ANTIDHIARRHEALS
- block stimulation of GIT for symptomatic relief from diarrhea
- include bismuth subsalicylate, crofelemer, loperamide, opium derivatives
- bismuth subsalicylate is absorbed from GIT after oral administration, metabolized in liver, and excreted in urine
- loperamide is slowly absorbed after oral administration, metabolized in liver, and excreted in urine
- opium derivatives is a category C-III controlled substance, is readily absorbed after oral administration, metabolized in liver, and excreted in urine
- crofelemer is minimally absorbed, and its half-life, metabolism, and excretion are unknown