MACOTO, AJ (BSN-II PHARMACOLOY FINALS NOTES)

DRUGS USED TO TREAT  GOBLET CELLS – produce

RESPIRATORY DISORDERS gelatinous mucus that forms a thin
layer over the interior surfaces of the
trachea and bronchi and bronchioles;
 Primary function of the lower
increased secretion produced by
respiratory tract (LRI) is the
exposure to irritants and bacteria
ventilatory cycle
COMMON RESPIRATORY DISEASES
 VENTILATION- the movement of
air in and out of the lungs; Respiratory Diseases are divided into 2 parts:
accomplished by contraction and 1. Obstructive airway diseases – those
relaxation of the diaphragmatic and that narrow passages ex.
intercostal muscles
Bronchospasms, edema,
 INHALATION – the process of inflammation, exces mucus secretion
transport of air containing oxygen for 2. Restrictive Airway diseases- those in
carbon dioxide (CO2) to the alveolar which lung expansion is limited from
sacs, exchange of carbon dioxide the loss of elasticity or physical
across the alveolar sacs, exchange of deformity
O2 for CO2 across the alveolar
 PARTIAL PRESSURE OF
membranes containing blood
ARTERIAL BLOOD GASES
capillaries, and exhalation of “stale
(ABGs) (PaO2 AND PaCO2) AND
air” including CO2.
Ph
 PERFUSION – blood flow to the  OXYGEN SATURATION- a readily
pulmonary arteries to the capillaries available non-invasive; the ratio,
surrounding the alveoli to the expressed in percentage, of the oxygen
pulmonary veins actually bound to hemoglobin
 DIFFUSION – the process by wc o2 compared with the maximum amount
passes across the alveolar membrane to of oxygen that could be bound to
the blood in the capillaries and co2 hemoglobin
passes from the blood to the alveolar  SPIROMETRY STUDIES- used to
sacs assess the capability of the patient’s
 GOBLET CELLS and SEROUS lungs, thorax, and respiratory muscles
GLANDS – origin of respiratory tract
fluids

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for moving volumes of air during TERMINOLOGY USED IN

inhalation and exhalation SPIROMETRY

 TIDAL VOLUME (TV) - volume of

HOW TO USE INCENTIVE
air inspired or expired during normal
SPIROMETER BASIC
breathing
 VITAL CAPACITY (VC) – volume
1. Sit-up tall holding the incentive
of air exhaled after maximal
spirometer upright and seal your
inspiration to full expiration
lips around the mouthpiece
 RESIDUAL VOLUME (RV) –
2. Breathe in slowly and deeply.
volume of air left in the lungs after
Hold breath as long as possible.
maximal exhalation
Then exhale slowly and allow
 FUNCTIONAL RESIDUAL
the piston to fall to the bottom of
CAPACITY (FRC) – volume of air
the column
left in the lungs after normal
3. As you inhale, notice the yellow
exhalation
indicator rise and reach the blue
 TOTAL LUNG CAPACITY (TLC)
outlined area. Position the
– VC + RV
yellow indicator at the side of
 FORCED EXPIRATORY
the spirometerto show your best
VOLUME (FEV) – vol. of air forced
effort. Use the indicator as the
out of the lungs by maximal exhalation
goal to work toward during each
 FORCED EXPIRATORY
slow deep breath
VOLUME IN 1 SEC (FEV1) – vol. of
4. Repeat the process 10 time in 1
air forced out in 1second to give the
hour.
rate of flow
5. After each set of 10 deep
 FORCED VITAL CAPACIY (FVC)
breaths, cough to be sure your
– maximal volume of air exhaled with
lungs are clear.
maximal forced effort after maximal
6. If you have an incision, support
exhalation
your incision when coughing by
placing a pillow firmly against  PEAK RESPIRATORY FLOW

it. RATE (PERF) – maximal rate of

airflow produced during forced
expiration

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 COUGH – one of the first symp. Of a o Alveolar sacs lose elasticity and
respiratory diseases; reflex initiated by collapse during exhalation,
the airway trapping air in lungs
 Productive Cough – if it helps remove o Dyspneic with minimal
accumulated secretions and phlegm for exertion, pursed lip breathing,
the tracheobronchial tree thin, barrel-chested and scanty
 NONPRODUCTIVE COUGH – sputum production with
results when irritant s repeatedly minimal cough.
stimulate the cough receptors but are DRUG THERAPY FOR LOWER
not removed by the coughing reflex RESPIRATORY DISEASES
 DRY, EXCESSIVE,
 EXPECTORANTS – liquefy mucus
NONPRODUCTIVE COUGH –
by stimulation the secretion of natural
discomforting; self-perpetuating
lubricant fluids from the serous glands
because rapid air expulsion further
 ANTITUSSIVES – act by
irritates the tracheobronchial mucosa
suppressing the cough center in the
 ASTHMA – inflammatory diseases of
brain; for patients with dry hacking
the bronchi and bronchioles;
nonproductive cough
intermittent periods of acute,
 MUCOLYTIC AGENTS – reduce
reversible airflow obstruction
the stickiness and viscosity of
(bronchoconstriction) caused by
pulmonary secretions by acting
bronchial inflammation
directly on the mucus plugs to cause
 CHRONIC BRONCHITIS – often
dissolution
called “BLUE BLOATERS”; chronic
 ANTI-INFLAMMATORY
irritation causes inflammation and
AGENTS – play an important role in
edema with excessive mucus
treating asthma by reducing
secretion; PRODUCTIVE COUGH
inflammation; most effective agent are
that is present for 3 mos. In each of 2
the corticosteroids.
successive years and has no
identifiable cause
NURSING Dx
 EMPHYSEMA – called “PINK
 Ineffective airway clearance
PUFFERS” diseases of the alveolar
 Activity intolerance
tissue destruction w/o fibrosis
 Impaired gas exchange
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 Anxiety - Rinse mouth and spit

following inhalation of
PATIENT EDUCATION
steroid medications
 Avoid irritants
 Activity and exercise
 Nutrition:
o Small frequent feeding for FOSTERING HEALTH MAINTENANCE
dyspneic patients
 Specialized filtration system in air
 Prevent infection
conditioners can reduce the exposure
o Annual flu vacc
to pollen and fungal sores
 Increased OFI
 DUST MITES – the most common
 Environmental elements
cause of allergies, found in carpeting
o Proper temp
and mattresses. Wash beddings in how
o Air humidification and
water and steam porous surfaces
ventilation
 All smoking should be ceased
 Breathing Techniques:
 Teach breathing and relaxation
o Postural drainage, abdominal
techniques
breathing, pursed lip breathing,
 Schedule daily activities
and coughing
 Psychosocial behavior – encourage DRUGS

open discussion of fears and Drug Class: EXPECTORANTS

expectaitons
 Guaifenesin – Robitussin
 Identify support people
ACTION:
 Medications- explain purpose and
 Enhances the output of respiratory
method of administration
tract fluid which decreases mucus
o Aerosol meds:
viscosity and promotes ciliary function
- Exhale completely before
USES:
initiating the first inhalation
 Symptomatic relief of conditions of
and the breath is held for 10
dry non-productive cough
sec during inhalation
 Combined with bronchodilators,
- Use bronchodialators first
decongestants, antihistamine, or
then steroids if prescribed at
antitussives
the same time
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 Most effective if patients are well properties; excellent agent to

hydrated suppress cough at night
 Not used for persistent cough that lasts
more then 1 week

COMMON ADVERSE EFFECTS:

Drug Class: Mucolytics
 GI Upset, N/V
 ACETYL.CYSTEINE –
MUCOMYST
Drug Class: ANTIUSSIVE ACTIONS:
 BUTAMIRATE CITRATE –  Dissolves chemical bonds within the
SINECOD mucus causing it to separate and
ACTIONS: liquefy

 Cough suppressants; suppress USES:

cough center of the brain  Dissolves abnormally viscous mucus
USES: that may occur in emphysema,
emphysema with bronchitis which
 Bothersome, dry, hacking,
allows for easier removal of secretions
nonproductive cough; will not stop
by coughing, percussion and postural
cough completely but decreases its
drainage.
frequency and suppress the severe
spasms COMMON ADVERSE EFFECTS:

 CODEINE – standard against  N/V

which other antitussives are
SERIOUS ADVERSE EFFECTS:
compared, not for CPD
 DEXTRO.METHORPHAN – as  Bronchospasm
effective as codeine; does not cause
respiratory depression or addiction
 DIPHEN.HYDRAMINE –
anticholinergic agent with both
antitussives and antihistaminic

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Drug Class: BETA-ADRENERGIC Drug Class: ANTICHOLINERGIC

BRONCHODILATING AGENTS BRONCHODILATING AGENTS

 SALBUTAMOL -VENTOLIN  IPRA.TROPIUM BROMIDE –

INHALER ATROVENT

ACTIONS: ACTIONS:

 Stimulate the beta-receptors in the  Administered via aerosol inhalation

smooth muscle of the tracheobronchial and produces bronchodilation by
tree to relax thus opening the airway competitive inhibition of cholinergic
receptors on bronchial smooth
USES:
muscles; has minimal effect on ciliary
 Mainstay in all asthma therapy
activity, mucus secretion, sputum
 Short-acting beta agonist volume and viscosity
(ALBUTEROL, TERBUTALINE) –
USES:
rapid onset, used to treat acute
bronchospasm and can be delivered  For long-term Tx of reversible
every 3-4 hrs bronchospasm associated with COPD
 Long-acting Beta Agonist (LABA)  Maximal effect seen in 1-2 hrs
(SALMETROL, FORMOTEROL) duration: 4-6 hours
-for patients with nocturnal asthma and  Prophylaxis and maintenance Tx of
those who wheeze with exercise; bronchospasm associated with COPD
onset: 15-20 min with duration: 12
CAE:
hours
 Mouth dryness, throat irritation
SERIOUS A/E
SAE:
 Tachycardia
 Anticholinergic- tachycardia,
 Tremors
urinary retention, exacerbation of
 N/V
pulmonary symptoms
 Nervousness, anxiety


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TIO.TROPIUM BROMDE – SPIRIVA 10.Open mouthpiece again and tip out

used capsule then discard
ACTIONS:
11.Wash hands and clean mouthpiece
 Administered by dry powder
inhalation (same w/ipratropium)
Drug Class: XANTHINE DERIVATIVE
USES:
BRONCHODILATING AGENTS
 Once-a day bronchodilator for (METHYL.XANTHINES)
long-term treatment of reversible
ACTIONS:
bronchospasm associated with
COPD including bronchitis and  Act directly on smooth muscle of
emphysema the tracheobronchial tree to dilate
the bronchi, thus increasing the
CAE:
airflow of the alveolar sacs
-same with ipra

HOW TO INHALE MEDICATION:

USES:
1. Open dust cover then the mouth piece
 Used in combination with
2. Place capsule in the center chamber
symathomimetic bronchodilators to
3. Close mouthpiece firmly
reverse airway constriction caused
4. Hold device upward and press piercing
by acute and chronic bronchial
button completely once then release
asthma, bronchitis and emphysema
5. Clear throat and mouth of sputum
6. Breath out completely CAE:
7. Raise device to mouth and close lips
N/v epigastric pain, abdominal cramps
tightly around mouth piece
SAE:
8. Keep head in upright position and
breath in slowly and deeply at rate Tachycardia, Tremors, Nervousness
sufficient to hear the capsule vibrate.
Breathe until the lungs are full then
hold breath
9. Resume normal breathing

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Drug Class: RESPIRATORY ANTI-  Alternate-day therapy (Single dose

INFLAMMATORY AGENTS every morning) is the nest
preferable program
Corticosteroids used for Obstructive Airway
Ds. CAE:

Inhalant Corticosteroid: Hoarseness, dry mouth

1. Budesonide phosphate – Pulmicort SAE:

Turbohaler
Fungal infections
2. FLUTICASONE- FLOVENT HFA

Inhalant Corticosteroid + beta-adrenergic

bronchodilator: Drug Class: ANTILEUKO.TRIENE
AGENTS
1. FLUTI.CASONE-SALMETROL –
ADVAIR DISKUS  Irritants (smoke, allergens)
 Triggers inflammatory cells
ACTIONS:
 Disruption of the phospholipid
 Direct effect on smooth muscle membrane in the epithelial lining of
relaxation; enhance the effect of the airway
beta-adrenergic bronchodilators  Chemical reaction from arachidonic
and inhibit inflammatory response acid release leukotrienes,
prostaglandin, thromboxanes, and
eicosanoids
USES:
 Leukotriene produce s/s of asthma
 Severe asthma and COPD who are  Bronchoconstriction, vascular
unresponsive to sympathomimetic permeability leading to edema and
agents or xanthine derivatives mucus hyperseretion
 1st course of therapy: short course
DC: ANTILEUKOTRIENE AGENTS
(5-7 days)of systemic
corticosteroids (PREDNISONE)  MONTELUKAST –
with intervals of several weeks or SINGULAIR
months ACTIONS:

 Selective competitive receptor

antagonist of the cysteinyl
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leukotriene receptor. This is the of inhaled corticosteroids for moderate

receptor that leukotriene D4 persistent astma
stimulates to trigger the asthma
CAE:
USES:
h/a nausea
 Can be used as prophylaxis and
chronic Tx in conjunction with
DC: MISCELLANEOUS ANTI-
other meds for asthma
INFLAMMATORY AGENTS
 Reduce early and late phase
bronchoconstriction, bronchial  CROMOLYN SODIUM – INTAL
hyperresponsiveness, daytime ACTIONS:
asthma s/s and night time
 A mast cell stabilizer that inhibits the
awakening
release of histamine and other
 Not a bronchodilator and should not
mediators of inflammation, making it
be used to treat episodes of asthma
an indirect anti-inflammatory agent.
CAE: Must be administered before the body
Nausea, dyspepsia is given a stimulus.

h/a

ZAFIRLEUKAST – ACCOLATE USES:

ACTIONS:  For patients with severe bronchial

asthma or allergic rhinitis
 Selective and competitive receptor
 Prophylactic management of exercise-
antagonist of cysteinyl leukotriene
induced bronchospasm and asthma
receptor. This is the receptor that
 No direct bronchodilatory,
Leukotriene D4 and E4 stimulate to
trigger asthma antihistaminic or anticholinergic
activity
USES:
CAE:
 Alternative to low dosed inhaled
 Oral irritation, dry mouth – nasal
corticosteroid for mild persistent
itching, nasal stuffiness
asthma and with low to medium doses

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SAE: bronchospasm, coughing 3. MUCUS CELLS: secretes mucus that

coats the stomach

DRUGS AFFECTING THE DIGESTIVE

SYSTEM  LIPASE – digest fats

DRUGS USED TO TREAT GERD AND  GASTRIC AMYLASE – digest carbs

PEPTIC ULCER DISEASE:  PROSTAGLANDINS – plays a major

role in protecting the stomach walls
Physiology of the stomach
from the acids and enzymes; produced
3 primary functions: by cell lining in the stomach and

1. Storing food until it can be used in the prevent injury by initiating gastric

lower GIT secretion, maintaining blood flow and

2. Mixing food with gastric secretions stimulating mucus and bicarbonate

until it is partially digested, semisolid production

mixture called as chyme COMMON STOMACH DISORDERS

3. Slowly emptying the stomach at a rate
1. GERD – aka heartburn, acid
that allows proper digestion and
indigestion or sour stomach
absorption of nutrients and medicine
 A reflux of gastric secretions
from the small intestine
primarily pepsin and HCl into
3 TYPES OF SECRETORY CELLS OF esophagus caused by weakened
THE STOMACH LINING: lowe esophageal sphincter,
1. CHIEF CELLS – secrete pepsinogen, delayed gastric emptying
and inactive enzyme  Burning sensation, bloating,
2. PARIETAL CELLS – stimulated by belching and regurgitation
acetylcholine from cholinergic nerve 2. PEPTIC ULCER DISEASE (PUD) –
fibers, gastrin, histamine, to secrete several stomach disorders that result
HCl w/c activate pepsinogen to pepsin from an imbalance between stomach
and provides 1-5 Ph, depending on the contents and the body’s normal
presence of food. Secretes intrinsic defencebarriers causing ulcerations in
factor that needed for the absorbtion of the GIT
Vit b12

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 GASTRIC AND DUODENAL Nursing Dx:

ULCERS – most common
 Acute pain
illness
 Chronic pain
 Burning, gnawing, or aching
 Imbalanced nutrtion: less than body
most noted when the stomach is
requirements
empty
 Proposed mechanisms:
oversecretion of HCl by PATIENT EDUCATION
excessive numbers of parietal
 Dietary changes – small frequent
cells, injury of the mucosal wall
meals, avoid seasoning that trigges
by H. Pylori
symptoms
RISK FACTORS OF PUD:  Avoid late night snacks – may cause
increased gastric acid
 Genetic predisposition
 Cease smoking
 No well-controlled studies support that
stress cause ulcers  Drink only small amounts of water
with the meal
 Cigarette smoking increases acid
secretion, alters blood flow in the
stomach and retards prostaglandin
DC: ANTACID
synthesis
 MAALOX, MYLANTA, TUMS –
 NSAIDS
USA
 Certain foods cause increased acid
 GAVISCON, KREMIL-S, SIMECO
secretions and alcohol irritate the
stomach lining – PH

ACTIONS:
GOALS OF TREATMENT:

1. GERD – to relieve symptoms,  Lower the acidity of gastric secretions

decrease the frequency and duration of by buffering they HCl 1-2 to as hgh as

reflux, heal tissue injury 3-4. Proteolytic action of pepsin is

MOST IMPORTANT TX - CHANGE reduced the gastric juices loses its

IN LIFESTYLE corrosive effects

USES:

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 MACOTO, AJ (BSN-II PHARMACOLOY FINALS NOTES)

 Long term self Tx with antacids may  For occasional indigestion . do not
masl symptoms of serious underlying contain enogh antacid to treat PUD
disease  Effective management of acute ulcer
 Most effective antacids available are diseases require large volumes of
combination of ALUMINUM antacids
HYDROXIDE, MAGNESIUM  Calcium carbonate and sodium
OXIDE, MAGNESIUM bicarbonate cause rebound
TRISILICATE, and CALCIUM hyperacidity
CARBONATE = ALL ACT by  Patients with renal failure should not
neutralizing gastric acid use amounts of antacids with
 Simethicone, alginic acid and bismuth magnesium
– other ingredients  Ca Carbonate in excess – constipation
 Simethicone – defoaming agent that  Mg in excess- diarrhea
breaks up gas bubbles in the stomach,
DC: HISTAMINE RECEPTOR
reducing the stomach distention and
ANTAGONIST
heart burn, effective in patients have
overeaten  CIME.TIDINE - TAGEMET

 ALGINIC ACID – produce highly  FAMO.TIDINE - PEPCID

viscous solution of sodium alginate on  RANI.TIDINE -ZANTAC

top of the gastric contents; only for ACTIONS:

patients with GERD OR HIATAL
 Act by blocking H2 receptor, resulting
HERNIA
in the decrease in the volume of acid
 Bismuth compounds – little acid -
secreted
neutralizing capacity
USES:
CAE: chalky taste
 Treat GERD, duodenal ulcers, and
SAE: diarrhea and constipation
pathologic hypersecretory conditions
such as Zollinger-Ellison syndrome
PRINCIPLES TO CONSIDER WHEN  CIMETIDINE – causes extensive liver
ANTACID THERAPY IS PLANNED: metabolism and has antiandrogenic
effect = gynecomastia
 INDIGESTION – not to be
administered >2 weeks
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 FAMOTIDINE – similar to CAE: Diarrhea h/a fatigue muscle pain

cimetidine; one dose a day, no SAE: Vascular Rash – OMEPRAZOLE
antiandrogenic effect, less drug
interactions
 RANITIDINE – 2x daily dosing, few DC: COATING AGENTS
drug interactions, no antiandrogenic
 SUCRAL.FATE – CARAFATE
effect
ACTIONS:
CAE:
 When swallowed, forms a complex
Diarrhea constipation dizziness h/a
that adheres to the crater to the ulcer,
SAE: protecting it from aggravators such as
acid, pepsin and bile salt. Does not
Confusion gynecomastia hepatotox
inhibit gastric secretions

USES:
DC: PROTON PUMP INHIBITORS
 Duodenal ulers, especially those that
 ESOME.PRAZOLE - NEXIUM
do not tolerate other forms of therapy
 LANSO.PRAZOLE -
CAE: constipation, dry mouth, dizziniess
PREVACID
 OME.PRAZOLE - PRILOSEC
 PANTO.PRAZOLE – DC: PROKINETIC AGENTS
PROTONIX
 METOCLOPRAMIDE - PLASIL,
ACTIONS: REGLAN
 Inhibit gastric secretions by inhibiting ACTIONS:
the gastric acid pump of the stomach’s
 INCREASING lower esophageal
parietal cells
sphincter pressure, thereby reducing
USES: the reflux, increasing stomach
 Treat severe esophagitis, GERD, contractions, relaxes pyloric valve,
gastric and duodenal ulcers and increases peristalsis in the GIT =
hypersecretory disorders. Used in increased gastric emptying and
combination with antibiotics intestinal transit
(Ampicillin) to eradicate h. pylori
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 Anti-emetic that blocks Dopamine in

the chemoreceptor trigger zone

USES:

 Relieve symptoms of gastric reflux COMMON CAUSES OF N/V:

esophagitis and diabetic gastroparesis,
 Postoperative nausea and vomiting –
aid in small bowel intubation,
dopamine antagonist, anticholinergic
stimulates gastric emptying and
agents and serotonin antagonist
intestinal transit of Barium after
 Motion sickness – antihistamines
radiologic exam of the upper GI series
 Nausea and vomiting in pregnancy-
CAE: Drowsiness fatigue lethargy nausea
phenothiazines and antihistamines
SAE: Extrapyramidal symptoms  Psychogenic vomiting –
metocloparamide
 Anticipatory nv – benzodiazepines
DRUGS USED TO TREAT NAUSEA
 CINV – ondansetron, dexamethasone
AND VOMITING
 Delayed emesis – combination of
 NAUSEA – the sensation of prochlor.perasine, lorazepam, and
abdominal discomfort that is diphen.hydramine
intermittently accompanied by the
desire to vomit
 VOMITING – is the forceful expulsion DC: DOPAMINE ANTAGONIST

of gastric contents up the esophagus PHENOTHIAZINE,

and out of the mouth BUTYROPHENONES,
 RETCHING – dry heaves, is the METOCLOPARAMIDE
involuntary labored, spasmodic
contractions of the abdominal and
respiratory muscles without the
expulsion of gastric contents

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ACTIONS: SCOPO.LAMINE TRANSDERMAL –

SCOPODERM
 Inhibit dopamine receptors that are
part of the pathway to the vomiting ACTIONS:
center. Causes EPS
 Motion sickness is thoughtot be caused
USES: by an excess of acetylcholine at the
CTZ and the vomiting center by
 PHENO.THIAZINE – anesthesia and
cholinergic nerves receiving impulses
surgery, radiation therapy
from the vestibular networks of the
 BUTYRO.PHENONES – surgery and
inner ear.
cancer chemo
 Anticholinergic agents are used to
 METO.CLOPRAMIDE – nv
counterbalance the excessive amounts
associated gastric cancer, peptic ulcer,
of acetylcholine present
radiation
USES:
DC: SEROTONIN ANTAGONIST
SCOPO.LAMINE- DOC short periods of
ONDAN.SETRON – ZOFRAN
motion sickness
ACTIONS:
ANTIHISTAMINE – longerperiods of
 Serotonin receptors of the 5-HT3 type motion sickness
are located centrally in the
MECLIZINE – Fewer adverse effects
chemoreceptor trigger zone of the
(sedation), shorter duration. Effective for
medulla and specialized cells of the
severe conditions
GIT and play a role in inducing NV
CAE: sedation blurred vision constipation
USES:
urinary retention dry mouth throat nose
 NV caused by radiation therapy
DC: BENZO.DIAZEPINES
CAE: h/a sedation, diarrhea, constipation
 APRASOL.AM - XANOR
 LORAZEP.AM- ANTIVAN
DC: ANTICHOLINERGIC AGENTS  MIDAZOL.AM - DORMICUM
 DIAZEP.AM – VALIUM
DIPHENYL.HYDRAMINE –
BENADRYL

MECLIZINE – BONAMINE

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ACTIONS:  CHRONIC CONST – ATLEAST 3

MONTHS
 Act as anti-emetics through
combination effects, including
sedation, reduction of anxiety, possible
depression of the vomiting center and
an amnesic effect

USES:

 Effective in reducing not only the

frequency nv but also anxiety often
associated with chemotherapy

DC: CANNABINOIDS
 DIARHHEA – increase in the
ACTIONS: frequency or fluid content of bowel
movements. Symptom rather than a
 Act through several mechanisms to
disease
inhibit pathways to vomiting center
 Causes: intestinal inf., spicy fatty
USES:
foods, enzyme deficiency, drug
 More effective than placebo and therapy
equally as effective as
DC: LAXATIVES
prochlor.perazine in patients receving
ACTIONS:
moderately emetogenic chemotherapy;
less effective than metoclopramide  Chemicals that act to promote
evacuation of the bowel
CSAE: dysphoric effects
CLASSIFICATIONS:

STIMULANT LAXATIVES:
DRUGS USED TO TREAT DIARRHEA
AND CONSTIPATION  BISACODYL – DULCOLAX
 Act directly on the intestine, causing
 CONSTIPATION – unsatisfactory
an irritation that promotes peristalsis
defecation and is characterized by
and evacuation. ORAL: act withing 6-
infrequent stools, difficult stool
10 hours, rectal 60-90 minutes
passage, straining, hard lumpy stool

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 MACOTO, AJ (BSN-II PHARMACOLOY FINALS NOTES)

OSMOTIC LAXATIVES  Must be administered with a full glass

of water. Causes water to be retained
 LACTULOSE – DUPHALAC,
within the stool, increases the bulk
LILAC
which stimulates peristalsis
 SORBITOL
 POLY.ETHYLENE GLYCOL – STOOL SOFTENERS
MIRALAX  DUCOSATE SODIUM
 Hypertonic compounds that draw
 DUCOSATE CALCIUM
water into the intestine from the
 Wetting agents; require 72 hours to aid
surrounding tissue
soft bowel movement; action depends
SALINE LAXATIVES on the patient’s state of hydration and
the GI Transit time
 MAGNESIUM HYDROXIDE -
PEDIA-LAX USES:
 MAGNESIUM SULPHATE –  Bulk-forming laxaives – DOC for
EPSOM SALT someone who is incapacitated and
 SODIUM PHOSPHATE needs laxatives regularly
 Hypertonic compounds that draw  Stimulant, osmotic, and saline –
water into the intestine from the acute constip.
surrounding tissue. The accumulated  Poly.ethylene glycol, lactulose –
water affects stool consistency and chronic constip.
distent the bowel, causing peristalsis
 Stool softeners – prophylactic
LUBRICAN LAXATIVES purposes
 Lubricant laxatives - helpful for
 MINERAL OIL
producing a SOFT STOOL without
 Lubricate the intestinal wall and soften
causing significant bowel spasm
the stool, allowing a smooth passage of
fecal contents. ONSET- 6-8 hrs may be CAE:abd. Spasms adb. Discomfort
up to 48 hours. Highly dependent on with flatulence
patients normal GI transit
SAE: abd tenderness pain bleeding
BULK-FORMING LAXATIVES vomiting

 PSYLLIUM – METAMUCIL
 METHYL.CELLULOSE

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 MACOTO, AJ (BSN-II PHARMACOLOY FINALS NOTES)

DC: ANTIDIARRHEAL AGENTS

ACTIONS:

Classifications:

1. Locally acting agents:

 LACTOBACILLUS
ACIDOPHILLUS -
LACTINEX
 BISMUTH
SUBSALICYLATE -
PEPTO-BISMOL
 ACTIVATED
CHARCOAL, PECTIN
 ABSORb excess water to
causeformed stool and to
absorb irritants or bact that
are causing diarrhea
2. Systemic agents
 DIPHENOXYLATE WITH
ATROPINE – LOMOTIL
 LOPERAMIDE – IMODIUM
 ACT through the autoimmune
nervous system to reduce
peristalsis and motility of the
GIT, allowing mucosal lining to
absorb nutrients, water, and
electrolytes

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