Vitamins ch9 and 11 — Presentation Transcript

 1. Vitamins

 2. Two Categories of Vitamins Fat-soluble A, D, E, K Water-soluble The 8 B

vitamins, vitamin C

 3. Vitamin Storage in the Body Vitamin storage in the body Fat-soluble

vitamins are stored in adipose cells Water-soluble vitamins are not well stored, easily
excreted by the kidneys

 4. Vitamin Toxicity Megadose = 10 times the RDA Toxic levels of vitamins are
usually achieved only with supplements Although foods may be excellent sources of
vitamins, it is difficult to have toxic effects without supplementation Because fat-
soluble vitamins are stored and excess water-soluble vitamins are excreted by the
kidneys, toxicity from fat-soluble vitamins is more likely

 5. Preserving Vitamin Content Keep fresh produce cool, away from light Peel
and cut only right before serving Use soon after purchase Frozen and canned products
do provide substantial vitamin content still, particularly if use the fluid packed with it
For cooking, less water is best (steam, microwave, stir-fry)

 6. Fig. 8.15 Processing grains reduces natural vitamin and mineral content.
Some processed grain products are fortified, but much micronutrient content is not
restored.

 7. Vitamin A Vitamin A = retinol, retinal, retinoic acid Preformed vitamin A =

retinol Found in animal products (organ meat) Provitamin A Found in plant products
Beta-carotene, lycopene Only retinol can be toxic

 8. Vitamin A Functions: Eyes Prevents night blindness Protects mucus-

producing cells in the eyes Helps prevent xerophthalmia (“dry eye”)
Growth/reproduction Vitamin A attaches to DNA to stimulate the production of
proteins necessary for healthy growth Antioxidant: may protect against some cancers
Lycopene and prostate cancer

 9. Vitamin A Deficiency Common in countries with poor access to food

Toxicity Caused by excessive intake of retinol Acne cream, pregnancy

 10. Vitamin D: The Sunshine Vitamin Non-food source: sunlight exposure on

skin About 25% of the time it takes to get a sunburn, 2-3 times per week In Colorado,
not between October and March Body converts a cholesterol derivative into inactive
vitamin D when exposed to sun radiation Inactive vitamin D (also form found in
supplemented foods/beverages) is activated in the kidneys

 11. Fig. 8.5

 12. Vitamin D Function: encourages calcium absorption and deposition in

bones Deficiency: Rickets – malformation of skeletal tissue, soft bones from
inadequate calcium (“bowlegged”) Osteoporosis – bone loss disease

 13. Vitamin E Tocopherols Function: Most potent fat-soluble antioxidant,

protects PUFAs and LDL from free radical damage Deficiency: Hemolytic anemia –
preterm babies who do not have good vitamin E accumulation Food sources:
vegetable oils, nuts
 14. Fig. 8.8

 15. Vitamin K Non-food source: bacteria in the large intestine Function:

maintains healthy levels of blood clotting factors “ koagulation” Deficiency: Newborns
– sterile large intestine Long-term antibiotic use

 16. Fig. 8.11

 17. Vitamin C Ascorbic acid Functions: Maintains healthy collagen Major

structural protein in teeth, bones, tendons, blood vessels Antioxidant – prevents some
free radical damage May help protect against cardiovascular disease, cancers,
cataracts in the eye Immune system function

 18. Vitamin C So, does vitamin C cure colds? No, but…. Vitamin C can reduce
the duration of cold symptoms by about 1 day Body is saturated with 200 mg/day
Supplements often provide 1000 to 2000 mg Eat citrus!

 19. Vitamin C Deficiency: Scurvy – disease characterized by poor quality

collagen Fragile capillary walls, easy bruising, poor wound healing, bone pain and
fractures, diarrhea, pinpoint hemorrhages on arms and legs RDA for cigarette
smokers: 35mg extra Toxicity: UL = 2 grams (2000 mg), stomach inflammation,
diarrhea Cooking, water causes vitamin C loss Fig. 8.31

 20. Coenzymes All B vitamins are coenzymes Fig. 8.13

 21. Fig. 8.14

 22. Thiamin Functions: Coenzyme in energy metabolism Used in nutrition

therapy with alcoholism (alcohol interferes with thiamin absorption) Deficiency:
Beriberi Means “I can’t, I can’t” Peripheral nerve disease, pain and paralysis of
extremities, edema, muscle wasting Sources: Animal protein foods, whole grains,
enriched grain products, some vegetables and fruits Easily lost in cooking water

 23. Riboflavin Function: Coenzyme in energy and protein metabolism

Deficiency: Tissue inflammation and breakdown Swollen, reddened tongue Food
sources: milk, organ meats, whole or enriched grains, vegetables Easily destroyed by
light Milk in opaque containers Fig. 8.18

 24. Niacin Function: Coenzyme in system that converts protein into glucose
Deficiency Pellegra – dermatitis, sometimes fatal effects on nervous system
Tryptophan can be converted to niacin Milk has no niacin but is high in tryptophan
Milk can prevent deficiency www.medscape.com

 25. Vitamin B6 Pyridoxine Function: Coenzyme in protein metabolism in over

100 amino acid reactions Produces neurotransmitters, new amino acids, niacin from
tryptophan, hemoglobin Deficiency: Anemia Nervous system problems (irritability,
convulsions) Infant formulas – if sterilized, destroys B6

 26. Pantothenic acid Function: coenzyme in energy metabolism Biotin

Function: coenzyme in the synthesis of fatty acids, amino acids, DNA Some made by
intestinal bacteria

 27. Folate Folic acid Function: Coenzyme that transfers single carbons to
build larger molecules May help prevent heart disease

 28. Folate Deficiency: Macrocytic anemia Chemotherapy drugs inhibit folate

metabolism Neural tube defects – inability of nerve cells to divide and make new cells
Neural tube closes within 28 days of pregnancy Spina bifida Anencephaly
 29. Fig. 8.26

 30. Fig. 8.27

 31. Folate Food sources: green leafy vegetables, legumes, tomatoes, enriched
grains and flours RDA: 400 micrograms, average intake 220 micrograms for women

 32. Vitamin B12 Cobalamin Function: Coenzyme in amino acid metabolism

and hemoglobin production Assists in placing lipid coat on nerve cells Deficiency:
Pernicious anemia Neurological problems – tingling in arms and legs, paralysis, mental
decline

 33. Vitamin B12 Sources: Naturally only found in animal products Fortified
foods Supplements/injections B12 is poorly absorbed without intrinsic factor made by
stomach

 34. Vitamin B12 People at risk for B12 deficiency: Elderly Reduced intrinsic
factor production with age Vegans Eat no animal products, must use injections or
enriched foods Infants nursed by vegan mothers Symptoms: diminished brain growth,
spinal cord degeneration, anemia

Vitamins — Presentation Transcript

 1. VITAMINS BIOCHEM LEC WK 5

 2. VITAMINS VITAMINS- essential organic molecules needed in very small

amounts for cellular metabolism Primary Deficiency of a Vitamin- occurs when the
vitamin is not consumed in sufficient amounts to meet physiologic needs Secondary
Deficiency- develops when absorption is impaired or excess excretion occurs

 3. VITAMINS Categories Water Soluble Vitamins- Vitamin B Complex, Choline,

Vitamin C Fat Soluble Vitamins- Vitamins A, D, E, K Food Sources: Almost all foods, yet
NO one food group is a good source of all vitamins; fresh fruits and vegetables are
particularly rich sources

 4. WATER SOLUBLE VITAMINS THIAMINE (B1) functions: to serve as

coenzyme in energy metabolism; role in nerve functioning related to muscle actions
RDA: 1.2 mg for men/ 1.1 mg for women Deficiency: BERI-BERI—2 Types WET-
manifests with edema affecting cardiac function DRY- affects the CNS, producing
paralysis and extreme muscle wasting Toxicity: non-toxic; excess is excreted in urine

 5. WATER SOLUBLE VITAMINS RIBOFLAVIN (B2) function: coenzyme in the

release of energy from nutrients sensitive to light RDA: 1.3 mg for men/ 1.1 mg for
women Deficiency: ARIBOFLAVINOSIS—S/SX CHEILOSIS- lips become swollen and
cracks develop in corners of the mouth GLOSSITIS- inflammation of the tongue

 6. WATER SOLUBLE VITAMINS NIACIN (B3) functions: coenzyme for many

enzymes; critical for glycolysis and Kreb’s cycle occurs naturally in 2 forms:
NICOTINIC ACID and NIACINAMIDE RDA: 16 NE for men/ 14 NE for women Deficiency:
PELLAGRA—3D’s ( Diarrhea, Dermatitis, Dementia )

 7. WATER SOLUBLE VITAMINS PYRIDOXINE (B6) functions: coenzyme in the

metabolism of amino acids and CHON 3 forms ( pyridoxine, pyridoxal, pyridoxamine )
 all can be converted to the coenzyme pyridoxal phosphate for use in the body RDA: 1.3
mg for men and women Deficiency: S/SX: dermatitis, altered nerve function, weakness

 8. WATER SOLUBLE VITAMINS FOLATE function: coenzyme in reactions

involving the transfer of 1-Carbon units during metabolism 4 forms ( folate, folic acid,
folacin and pteroylglutamic acid ) for folate to be maintained for use in the body,
Vitamin B12 must be available folate has a role in proper formation of fetal neural
tubes (brain and spinal cord development) RDA: 400 mcg for men/women 600mcg for
pregnant women Deficiency: megaloblastic anemia—large RBC that cannot carry
oxygen

 9. WATER SOLUBLE VITAMINS COBALAMIN/CYANOCOBALAMIN (B12)

functions: coenzyme in nucleic acid metabolism; needed for maturation of RBC
absorption of Vitamin B12 relies on an intrinsic factor (IF) a substance produced by
stomach mucosa deficiency: Pernicious Anemia- inadequate RBC formation caused by
lack of IF in the stomach

 10. WATER SOLUBLE VITAMINS BIOTIN function: coenzyme in synthesis of fat,

glycogen and amino acids deficiency: S/SX: scaly red skin rash, hair loss, loss of
appetite, depression

 11. WATER SOLUBLE VITAMINS PANTOTHENIC ACID function: for metabolism

of CHO, FATS and CHON deficiency: do not occur in nature CHOLINE function: needed
for synthesis of acetylcholine, a neurotransmitter, and lecithin( phospholipid)
deficiency: rare

 12. WATER SOLUBLE VITAMINS ASCORBIC ACID ( VITAMIN C ) functions:

collagen synthesis and other CT; antioxidant; iron absorption; coenzyme RDA: 90 mg
for men/ 75 for women/ 125 mg for smokers Deficiency: SCURVY: S/SX—inflammation
of CT, gingivitis, muscle degeneration, bruising and hemorrhaging as the vascular
system weakens

 13. FAT SOLUBLE VITAMINS VITAMIN A functions: component of visual

pigments; needed for maintenance of epithelial tissues; antioxidant RDA: 900 mcg
RAE for men/ 700 mcg RAE for women Deficiency: XEROPHTHALMIA—night blindness
progressing to a hard, dry cornea (keratinization) resulting in complete blindness

 14. FAT SOLUBLE VITAMINS VITAMIN D function: aid in absorption and use of
calcium and phosphorus; promotes bone growth precursor: 7-dehydrocholesterol
(found in the skin) active form: 1,25- dihydrocholecalciferol deficiency: RICKETS- a
childhood disorder caused by Vitamin D or Calcium deficiency that leads to
insufficient mineralization of bone and tooth matrix

 15. FAT SOLUBLE VITAMINS VITAMIN E (TOCOPHEROLS) function: antioxidant

RDA: 15 mg TE for men/women Deficiency: rare VITAMIN K function: cofactor in the
synthesis of blood clotting factors deficiency: inhibits blood coagulation

Pharma4 — Presentation Transcript

 1. DRUGS ACTING ON THE GASTROINTESTINAL SYSTEM

 2. Four Major Activities of the GI System Secretion Absorption Digestion

Motility
 3.

 4. Secretion of digestive enzymes, acid, bicarbonate, and mucus facilitates

the digestion and absorption of nutrients.

 5. The GI system is controlled by the nerve plexus, which maintains a basic

electrical rhythm and responds to local stimuli to increase or decrease activity.

 6. A series of local reflexes within the Gi tract helps maintain homeostasis

within the system. Overstimuation of any of these reflexes can result in constipation
(underactivity) or diarrhea (overactivity).

 7. Swallowing is a centrally mediated reflex that us important in delivering

food to the GI tract for processing.

 8. Vomitting is controlled by the chemoreceptor trigger zone (CTZ) in the

medulla or by the emetic zone in immature or injured brains.

 9. The H2-receptor antagonists (H2RA, often shortened to H2 antagonist ) are

a class of drugs used to block the action of histamine on parietal cells in the
stomach , decreasing the production of acid by these cells. H2 antagonist are used in
the treatment of dyspepsia , although they have largely been surpassed in popularity
by the more effective proton pump inhibitors .

 10. examples Cimetidine Famotidine Nizatidine Ranitidine

 11. antacid An antacid is any substance, generally a base or basic salt ,

which counteracts stomach acidity . In other words, antacids are stomach acid
neutralizers .

 12. Action mechanism Antacids perform a neutralization reaction, i.e. they

buffer gastric acid , raising the pH to reduce acidity in the stomach. When gastric
hydrochloric acid reaches the nerves in the gastrointestinal mucosa , they signal pain
to the central nervous system. This happens when these nerves are exposed, as in
peptic ulcers . The gastric acid may also reach ulcers in the esophagus or the
duodenum . Other mechanisms may contribute, such as the effect of aluminum ions
inhibiting smooth muscle cell contraction and delaying gastric emptying.

 13. Indications Antacids are taken by mouth to relieve heartburn , the major
symptom of gastroesophageal reflux disease , or acid indigestion . Treatment with
antacids alone is symptomatic and only justified for minor symptoms. Peptic ulcers
may require H2-receptor antagonists or proton pump inhibitors . The utility of many
combinations of antacids is not clear, although the combination of magnesium and
aluminium salts may prevent alteration of bowel habits.

 14. Drug names Examples of antacids (brand names may vary in different
countries). Aluminium hydroxide (Amphojel, AlternaGEL) Magnesium hydroxide
(Phillips’ Milk of Magnesia ) Aluminum hydroxide with magnesium hydroxide (Maalox,
Mylanta, Diovol) gel (Basaljel) Calcium carbonate (Alcalak, TUMS, Quick-Eze, Rennie,
Titralac, Rolaids) Sodium bicarbonate (Bicarbonate of soda, Alka-Seltzer)
(Mg6Al2(CO3)(OH)16 ∙ 4(H2O); Talcid) Bismuth subsalicylate (Pepto-Bismol) Magaldrate
with Simethicone (Pepsil)

 15. Proton pump inhibitors Proton pump inhibitors (or "PPI"s) are a
group of drugs whose main action is a pronounced and long-lasting reduction of
gastric acid production. They are the most potent inhibitors of acid secretion available
today. The group followed and has largely superseded another group of
pharmaceuticals with similar effects, but different mode-of-action, called H2-receptor
 antagonists . These drugs are among the most widely-selling drugs in the world as a
result of their outstanding efficacy and safety. The vast majority of these drugs are
benzimidazole derivatives; however, promising new research indicates that
imidazopyridine derivatives may be a more effective means of treatment.

 16. Clinical use These drugs are utilized in the treatment of many conditions
such as: Dyspepsia Peptic ulcer disease (PUD) Gastroesophageal reflux disease
(GORD/GERD) Laryngopharyngeal Reflux Disease Barrett's esophagus prevention of
stress gastritis Gastrinomas and other conditions that cause hypersecretion of acid
Zollinger -Ellison syndrome

 17. Mechanism of action Proton pump inhibitors act by irreversibly blocking

the hydrogen / potassium adenosine triphosphatase enzyme system (the H+/K+
ATPase , or, more common, gastric proton pump ) of the gastric parietal cell . The
proton pump is the terminal stage in gastric acid secretion, being directly responsible
for secreting H+ ions into the gastric lumen, making it an ideal target for inhibiting
acid secretion. ("Irreversibility" refers to the effect on a single copy of the
enzyme; the effect on the overall human digestive system is reversible, as the
enzymes are naturally destroyed and replaced with new copies.) Targeting the
terminal-step in acid production, as well as the irreversible nature of the inhibition,
results in a class of drugs that are significantly more effective than H2 antagonists
and reduce gastric acid secretion by up to 99%. The lack of the acid in the stomach
will aid in the healing of duodenal ulcers, and reduces the pain from indigestion and
heartburn , which can be exacerbated by stomach acid. However, lack of stomach acid
is also called hypochlorhydria , the lack of sufficient hydrochloric acid , or HCl.
Hydrochloric acid is required for the digestion of proteins and for the absorption of
nutrients, particularly of vitamin B12 and of calcium. The proton pump inhibitors are
given in an inactive form. The inactive form is neutrally charged ( lipophilic ) and
readily crosses cell membranes into intracellular compartments (like the parietal cell
canaliculus) that have acidic environments. In an acid environment, the inactive drug
is protonated and rearranges into its active form. As described above, the active form
will covalently and irreversibly bind to the gastric proton pump, deactivating it.

 18. Examples of proton pump inhibitors Clinically used proton pump

inhibitors: Omeprazole (brand names: Losec, Prilosec, Zegerid, ocid, Lomac, Omepral,
Omez) Lansoprazole (brand names: Prevacid, Zoton, Inhibitol, Levant, Lupizole)
Dexlansoprazole (brand name: Kapidex) Esomeprazole (brand names: Nexium, Esotrex)
Pantoprazole (brand names: Protonix, Somac, Pantoloc, Pantozol, Zurcal, Pan)
Rabeprazole (brand names: Rabecid, Aciphex, Pariet, Rabeloc. Dorafem: combination
with domperidone ) All proton pump inhibitors except rabeprazole and dexlansoprazole
have intravenous formulations.

 19. prostaglandin A prostaglandin is any member of a group of lipid

compounds that are derived enzymatically from fatty acids and have important
functions in the animal body. Every prostaglandin contains 20 carbon atoms, including
a 5-carbon ring. They are mediators and have a variety of strong physiological effects.
Although they are technically hormones , they are rarely classified as such. The
prostaglandins together with the thromboxanes and prostacyclins form the prostanoid
class of fatty acid derivatives. The prostanoi is a subclass of eicosanoids .

 20. Function There are currently nine known prostaglandin receptors on

various cell types. Prostaglandins ligate a sub-family of cell surface seven-
transmembrane receptors, G-protein-coupled receptors . These receptors are termed
DP1-2, EP1-4, FP, Ip, and TP, corresponding to the receptor that ligates the
corresponding prostaglandin (e.g., DP1-2 receptors bind to PGD2 ). The diversity of
receptors means that prostaglandins act on an array of cells and have a wide variety
of effects: cause constriction or dilation in vascular smooth muscle cells cause
 aggregation or disaggregation of platelets sensitize spinal neurons to pain decrease
intraocular pressure regulate inflammatory mediation regulate calcium movement
control hormone regulation control cell growth Prostaglandins are potent but have a
short half-life before being inactivated and excreted. Therefore, they send only
paracrine (locally active) or autocrine (acting on the same cell from which it is
synthesized) signals.

 21. Laxatives Laxatives (or purgatives ) are foods, compounds, or drugs taken
to induce bowel movements or to loosen the stool , most often taken to treat
constipation . Certain stimulant, lubricant, and saline laxatives are used to evacuate
the colon for rectal and bowel examinations, and may be supplemented by enemas in
that circumstance. Sufficiently high doses of laxatives will cause diarrhea . Laxatives
work to hasten the elimination of undigested remains of food in the large intestine
and colon .

 22. Some vegetables and foods can be eaten to cure constipation and act as
laxatives, although the effectiveness may vary. These include: Almonds Aloe Vera
Apples / Apple Juice Bananas Basil Beets Carob Chicory Coconut Coffee Dandelion
Dates Dried apricots Endive Fenugreek Figs Flaxseed Grapes Kale Liquorice Mangos
Molasses Oranges Papayas Parsley Peaches / Apricots Pears Persimmons Pineapple
Plums Prunes /Prune Juice Rhubarb Soybeans Tamarind Tea Tomato Juice Vanilla
Walnuts Watercress Yams Olive oil

 23. Bulk-producing agents Site of Action: Small and large intestine Onset of
Action: 12 - 72 hours Examples: psyllium husk ( Metamucil ), methylcellulose ( Citrucel
), polycarbophil , dietary fiber , apples , broccoli Also known as bulking agents or
roughage, these include dietary fiber . Bulk-producing agents cause the stool to be
bulkier and to retain more water, as well as forming an emollient gel, making it easier
for peristaltic action to move it along. They should be taken with plenty of water. Bulk-
producing agents have the gentlest of effects among laxatives and can be taken just
for maintaining regular bowel movements.

 24. Stool softeners / Surfactants Site of Action: Small and large intestine
Onset of Action: 12 - 72 hours Examples: docusate (Colace, Diocto) These cause water
and fats to penetrate the stool, making it easier to move along. Many of these quickly
produce a tolerance effect and so become ineffective with prolonged use. Their
strength is between that of the bulk producers and the stimulants, and they can be
used for patients with occasional constipation or those with anorectal conditions for
whom passage of a firm stool is painful.

 25. Lubricants / Emollient Site of Action: Colon Onset of Action: 6 - 8 hours

These simply make the stool slippery, so that it slides through the intestine more
easily. An example is mineral oil , which also retards colonic absorption of water,
softening the stool. Mineral oil may decrease the absorption of fat-soluble vitamins
and some minerals.

 26. Hydrating agents (osmotics) These cause the intestines to hold more
water within, softening the stool. There are two principal types, saline and
hyperosmotic. Saline Site of Action: Small and large intestine Onset of Action: 0.5 - 6
hours Examples: Dibasic sodium phosphate , magnesium citrate , magnesium
hydroxide ( Milk of magnesia ), magnesium sulfate (which is Epsom salt ) , monobasic
sodium phosphate, . Saline laxatives attract and retain water in the intestinal lumen,
increasing intraluminal pressure and thus softening the stool. They will also cause the
release of cholecystokinin , which stimulates the digestion of fat and protein. Saline
laxatives may alter a patient's fluid and electrolyte balance. Sulfate salts are
considered the most potent.
 27. Hyperosmotic agents Site of Action: Colon Onset of Action: 0.5 - 3 hours
Examples: Glycerin suppositories , Sorbitol , Lactulose , and Polyethylene glycol
(PEG). Lactulose works by the osmotic effect, which retains water in the colon,
lowering the pH and increasing colonic peristalsis. Lactulose is also indicated in
Portal-systemic encephalopathy . Glycerin suppositories work mostly by hyperosmotic
action, but also the sodium stearate in the preparation causes local irritation to the
colon. Solutions of polyethylene glycol and electrolytes ( sodium chloride , sodium
bicarbonate , potassium chloride , and sometimes sodium sulfate ) are used for whole
bowel irrigation , a process designed to prepare the bowel for surgery or colonoscopy
and to treat certain types of poisoning . Brand names for these solutions include
GoLytely, GlycoLax, CoLyte, NuLytely, and others.

 28. Stimulant / Irritant These stimulate peristaltic action and can be

dangerous under certain circumstances. Long term use can lead to 'cathartic colon'.
[8] Stimulant laxatives act on the intestinal mucosa , or nerve plexus; they also alter
water and electrolyte secretion. They are the most severe among laxatives and should
be used only in extreme conditions. Castor oil may be preferred when more complete
evacuation is required.

 29. Castor oil Site of Action Small intestine Castor oil acts directly on
intestinal mucosa or nerve plexus and alters water and electrolyte secretion. It is
converted into ricinoleic acid (the active component) in the gut.

 30. Serotonin agonist Tegaserod is a motility stimulant that works through

activation of 5-HT4 receptors of the enteric nervous system in the gastrointestinal
tract . However caution must be taken due to potentially harmful cardiovascular side-
effects.

 31. GASTROINTESTINAL STIMULANTS Used for more generalized Gi

stimulation that results in an overall increase in GI activity and secretions. These
drugs stimulate parasympathetic activity or make the GI tissues more sensitive to
parasympathetic activity.

 32. Metoclopramide ( INN ) (pronounced /ˌ mɛtəˈkloʊprəmaɪd / or /ˌmɛtə

ˈklɒprəmaɪd) is an antiemetic and gastroprokinetic agent . Thus it is primarily used to
treat nausea and vomiting, and to facilitate gastric emptying in patients with
gastroparesis

 33. Clinical use Metoclopramide is commonly used to treat nausea and

vomiting (emesis) associated with conditions including: emetogenic drugs, uraemia ,
radiation sickness , malignancy , labor , and infection . It is also used by itself or in
combination with paracetamol (acetaminophen) ( paracetamol/metoclopramide
available in the UK as Paramax) or aspirin (MigraMax) for the relief of migraine . It is
considered ineffective in postoperative nausea and vomiting (PONV) at standard
doses, and ineffective for motion sickness . In nausea and vomiting associated with
cancer chemotherapy , it has been superseded by the more effective 5-HT3
antagonists (e.g. ondansetron ).

 34. anti-diarrheal drug An anti-diarrheal drug is any medication which

provides symptomatic relief for diarrhea .

 35. Types Electrolyte solutions are used to replace lost fluids and salts in
acute cases. Bulking agents like methylcellulose , guar gum or plant fibre ( bran ,
sterculia , , etc.) are used for diarrhea in functional bowel disease and to control
ileostomy output. Absorbents absorb toxic substances that cause infective diarrhea,
methylcellulose is an absorbent as well. Opioids ' classical use besides pain relief is
as an anti-diarrheal drug. Opioids have agonist actions on the intestinal opioid
receptors, which when activated cause constipation . Drugs such as morphine or
 codeine can be used to relieve diarrhea this way. A notable opioid for the purpose of
relief of diarrhea is Loperamide which only is an agonist of the μ opioid receptors in
the large intestine and does not have opioid affects in the central nervous system as
it doesn't cross the blood brain barrier in significant amounts. This enables
loperamide it to be used to the same benefit as other opioid drugs but without the
CNS side effects or potential for abuse.

 36. Emetics An emetic , such as syrup of ipecac , is a substance that induces

vomiting when administered orally or by injection. An emetic is used medically where
a substance has been ingested and must be expelled from the body immediately (for
this reason, many toxic and easily digestible products such as rat poison contain an
emetic). Inducing vomiting can remove the substance before it is absorbed into the
body. Ipecac abuse can cause detrimental health effects. Copper sulfate was also
used in the past as an emetic. It is now considered too toxic for this use.

 37. Antiemetics An antiemetic is a drug that is effective against vomiting and

nausea . Antiemetics are typically used to treat motion sickness and the side-effects
of some opioid analgesics and chemotherapy directed against cancer . Antiemetics
act by inhibiting the receptor sites associated with emesis. Hence, anticholinergics,
antihistamines, dopamine antagonists, serotonin antagonists, and cannabinoids are
used as anti-emetics.

 38. “Only as high as I reach can I grow, only as far as I seek can I go, only as
deep as I look can I see, only as much as I dream can I be.” Thank you for a wonderful
summer…Aim High Batch 2011…

Antacids and controlling agents — Presentation Transcript

 1. Antacids and Acid-Controlling Agents Antacids H 2 Antagonists Proton

Pump Inhibitors

 2. Acid-Related Pathophysiology The stomach secretes: Hydrochloric acid

(HCl) Bicarbonate Pepsinogen Intrinsic factor Mucus Prostaglandins

 3. Glands of the Stomach Cardiac Pyloric Gastric* *The gastric glands are
the largest in number

 4. Cells of the Gastric Gland Parietal Chief Mucoid

 5. Cells of the Gastric Gland Parietal Cells Produce and secrete HCl Primary
site of action for many acid-controller drugs

 6. Cells of the Gastric Gland Chief Cells Secrete pepsinogen, a proenzyme

Pepsinogen becomes PEPSIN when activated by exposure to acid Pepsin breaks down
proteins (proteolytic)

 7. Cells of the Gastric Gland Mucoid Cells Mucus-secreting cells (surface

epithelial cells) Provide a protective mucous coat Protects against self-digestion by
HCl

 8. Hydrochloric Acid Secreted by the parietal cells Maintains stomach at a pH

of 1 to 4 Secretion stimulated by: Large, fatty meals Excessive amounts of alcohol
Emotional stress
 9. Acid-Related Diseases Caused by imbalance of the three cells of the
gastric gland and their secretions Most common: Hyperacidity Most harmful: Peptic
ulcer disease (PUD) Lay terms for overproduction of HCl by the parietal cells:
indigestion, sour stomach, heartburn, acid stomach

 10. Antacids: Mechanism of Action Promote the gastric mucosal defense

mechanisms Secretion of: Mucus: Protective barrier against HCl Bicarbonate: Helps
buffer acidic properties of HCl Prostaglandins: Prevent activation of proton pump

 11. Antacids: Mechanism of Action Antacids DO NOT prevent the

overproduction of acid. Acids DO neutralize the acid once it’s in the stomach.

 12. Antacids: Drug Effects Reduction of pain associated with acid-related

disorders Raising gastric pH from 1.3 to 1.6 neutralizes 50% of the gastric acid.
Raising gastric pH 1 point (1.3 to 2.3) neutralizes 90% of the gastric acid.

 13. Antacids OTC formulations available as: Capsules and tablets Powders
Chewable tablets Suspensions Effervescent granules and tablets

 14. Antacids Aluminum salts Magnesium salts Calcium salts Sodium

bicarbonate Used alone or in combination

 15. Antacids Aluminum Salts Forms: carbonate, hydroxide, phosphate Have

constipating effects Often used with magnesium to counteract constipation Example:
aluminum carbonate (Basaljel)

 16. Antacids Magnesium Salts Forms: carbonate, hydroxide, oxide, trisilicate

Commonly cause a laxative effect Usually used with other agents to counteract this
effect Dangerous when used with renal failure—the failing kidney cannot excrete extra
magnesium, resulting in accumulation Examples: magnesium hydroxide (MOM);
combination products such as Maalox, Mylanta (aluminum and magnesium)

 17. Antacids Calcium Salts Forms: many, but carbonate is most common May
cause constipation Their use may result in kidney stones Long duration of acid action
may cause increased gastric acid secretion (hyperacidity rebound) Often advertised
as an extra source of dietary calcium Example: Tums (calcium carbonate)

 18. Antacids Sodium Bicarbonate Highly soluble Quick onset, but short
duration May cause metabolic alkalosis Sodium content may cause problems in
patients with CHF, hypertension, or renal insufficiency

 19. Antacids and Antiflatulents Antiflatulents: used to relieve the painful

symptoms associated with gas Several agents are used to bind or alter intestinal gas,
and are often added to antacid combination products.

 20. Antacids and Antiflatulents OTC Antiflatulents activated charcoal

simethicone Alters elasticity of mucus-coated bubbles, causing them to break. Used
often, but there are limited data to support effectiveness.

 21. Antacids: Side Effects Minimal, and depend on the compound used
Aluminum and calcium Constipation Magnesium Diarrhea Calcium carbonate
Produces gas and belching; often combined with simethicone

 22. Antacids: Drug Interactions Chelation Chemical binding, or inactivation, of

another drug Chemical inactivation Produces insoluble complexes Result: reduced
drug absorption
 23. Antacids: Drug Interactions Increased stomach pH Increased absorption
of basic drugs Decreased absorption of acidic drugs Increased urinary pH Increased
excretion of acidic drugs Decreased excretion of basic drugs

 24. Antacids: Nursing Implications Assess for allergies and preexisting

conditions that may restrict the use of antacids, such as: Fluid imbalances Renal
disease CHF Pregnancy GI obstruction Patients with CHF or hypertension should use
low-sodium antacids such as Riopan, Maalox, or Mylanta II.

 25. Antacids: Nursing Implications Use with caution with other medications
due to the many drug interactions. Most medications should be given 1 to 2 hours
after giving an antacid. Antacids may cause premature dissolving of enteric-coated
medications, resulting in stomach upset.

 26. Antacids: Nursing Implications Be sure that chewable tablets are chewed
thoroughly, and liquid forms are shaken well before giving. Administer with at least 8
ounces of water to enhance absorption (except for the “rapid dissolve” forms).
Caffeine, alcohol, harsh spices, and black pepper may aggravate the underlying GI
condition.

 27. Antacids: Nursing Implications Monitor for side effects: Nausea, vomiting,
abdominal pain, diarrhea With calcium-containing products: constipation, acid
rebound Monitor for therapeutic response: Notify heath care provider if symptoms are
not relieved.

 28. Histamine Type 2 (H 2 ) Antagonists

 29. H 2 Antagonists Reduce acid secretion All available OTC Most popular
drugs for treatment of acid-related disorders cimetidine (Tagamet) famotidine (Pepcid)
nizatidine (Axid) ranitidine (Zantac)

 30. H 2 Antagonists: Mechanism of Action Block histamine (H 2 ) at the

receptors of acid-producing parietal cells Production of hydrogen ions is reduced,
resulting in decreased production of HCl

 31. H 2 Antagonists: Drug Effect Suppressed acid secretion in the stomach

 32. H 2 Antagonists: Therapeutic Uses Shown to be effective for: Gastric

ulcer Gastroesophageal reflux disease (GERD) Upper GI Duodenal ulcer (with or
bleeding without H. pylori) May be effective for: Stress ulcers Peptic esophagitis
Prevention and management of allergic conditions, when used with H 1 blockers

 33. H 2 Antagonists: Side Effects Overall, less than 3% incidence of side

effects Cimetidine may induce impotence and gynecomastia

 34. H 2 Antagonists: Drug Interactions Cimetidine Binds with P-450

microsomal oxidase system in the liver, resulting in inhibited oxidation of many drugs
and increased drug levels All H 2 antagonists may inhibit the absorption of drugs that
require an acidic GI environment for absorption.

 35. H 2 Antagonists: Drug Interactions SMOKING has been shown to decrease

the effectiveness of H 2 blockers

 36. H 2 Antagonists: Nursing Implications Assess for allergies and impaired

renal or liver function. Use with caution in patients who are confused, disoriented, or
elderly. Take 1 hour before or after antacids. Ranitidine may be given intravenously;
follow administration guidelines.
 37. Proton Pump Inhibitors

 38. Proton Pump Inhibitors The parietal cells release positive hydrogen ions
(protons) during HCl production. This process is called the “proton pump.” H 2
blockers and antihistamines do not stop the action of this pump.

 39. Proton Pump Inhibitors: Mechanism of Action Irreversibly bind to H+/K+

ATPase enzyme. This bond prevents the movement of hydrogen ions from the parietal
cell into the stomach. Result: Achlorhydria—ALL gastric acid secretion is blocked. In
order to return to normal acid secretion, the parietal cell must synthesize new H+/K+
ATPase.

 40. Proton Pump Inhibitors: Drug Effect Total inhibition of gastric acid
secretion lansoprazole (Prevacid) omeprazole (Prilosec) rabeprazole (Aciphex)
pantoprazole (Protonix) esomeprazole (Nexium)

 41. Proton Pump Inhibitors: Therapeutic Uses GERD maintenance therapy

Erosive esophagitis Short-term treatment of active duodenal and benign gastric ulcers
Zollinger-Ellison syndrome Treatment of H. pylori-induced ulcers

 42. Proton Pump Inhibitors: Side Effects Safe for short-term therapy
Incidence low and uncommon

 43. Proton Pump Inhibitors: Nursing Implications Assess for allergies and
history of liver disease Pantoprazole is the only proton pump inhibitor available for
parenteral administration, and can be used for patients who are unable to take oral
medications May increase serum levels of diazepam, phenytoin, and cause increased
chance for bleeding with warfarin

 44. Proton Pump Inhibitors: Nursing Implications Instruct the patient taking
omeprazole: It should be taken before meals. The capsule should be swallowed whole,
not crushed, opened or chewed. It may be given with antacids. Emphasize that the
treatment will be short-term.

 45. Other Drugs sucralfate (Carafate) misoprostol (Cytotec)

 46. Sucralfate (Carafate) Cytoprotective agent Used for stress ulcers,

erosions, PUD Attracted to and binds to the base of ulcers and erosions, forming a
protective barrier over these areas Protects these areas from pepsin, which normally
breaks down proteins (making ulcers worse)

 47. Sucralfate (Carafate) Little absorption from the gut May cause
constipation, nausea, and dry mouth May impair absorption of other drugs, especially
tetracycline Binds with phosphate; may be used in chronic renal failure to reduce
phosphate levels Do not administer with other medications

 48. misoprostol (Cytotec) Synthetic prostaglandin analogue Prostaglandins

have cytoprotective activity: Protect gastric mucosa from injury by enhancing local
production of mucus or bicarbonate Promote local cell regeneration Help to maintain
mucosal blood flow

 49. misoprostol (Cytotec) Used for prevention of NSAID-induced gastric

ulcers Doses that are therapeutic enough to treat duodenal ulcers often produce
abdominal cramps, diarrhea
 Pharmacology Git Drugs — Presentation Transcript

 1. Pharmacology of the GIT system pinoynursing.webkotoh.com

 2. LECTURE Outline REVIEW the Anatomy of the GIT REVIEW the Physiology
of the GIT Review common GI drugs in the following categories: 1. Drugs affecting GI
secretions 2. Laxatives 3. Anti-diarrheals 4. Emetics and anti-emetics

 3. Fig. 16.1

 4. Fig. 16.10a

 5. Fig. 16.10b

 6. Fig. 16.11a

 7. Fig. 16.11b

 8. Fig. 16.12

 9. Drugs affecting GI secretions There are five types of drugs that affect
gastric acid secretions and are useful for the treatment of peptic ulcer. Histamine
(H2) receptor antagonist/blockers Antacids Proton pump inhibitors Mucosal
protectants Prostaglandin analogs

 10. Drugs affecting secretions: anti ulcer Misoprostol Prostaglandin analog

Sucralfate Mucosal protectants Omeprazole Proton pump inhibitors AlOH and MgOH
Antacids Cimetidine Histamine (H2) receptor antagonist/blockers Prototype Anti-ulcer
drugs

 11. General indication of the drugs affecting gastric acid secretion Peptic
ulcer Gastritis Patient on NPO to prevent stress ulcer

 12. General time of administration of the drugs affecting gastric acid

secretion Misoprostol WITH MEALS Prostaglandin analog Sucralfate BEFORE MEALS
Mucosal protectants Omeprazole BEFORE MEALS Proton pump inhibitors AlOH and
MgOH Usually after meals Antacids Cimetidine With FOOD or ONE hour after ANTACID
Histamine (H2) receptor antagonist/blockers Prototype Best time to give Anti-ulcer
drugs

 13. Pharmacodynamics Histamine (H2) receptor blockers These drugs BLOCK

the release of hydrochloric acid in the stomach in response to gastrin

 14. Drugs affecting GI secretions Antacids These drugs interact with the
gastric acids at the chemical level to neutralize them

 15. Drugs affecting GI secretions Proton pump inhibitors These drugs

suppress the secretion of hydrochloric acid into the lumen of the stomach

 16. Drugs affecting GI secretions Mucosal protectants These are agents that
coat any injured area in the stomach to prevent further injury from acid

 17. Drugs affecting GI secretions Prostaglandin analogs These are agents

that inhibit the secretion of gastrin and increase the secretion of mucus lining of the
stomach, providing a buffer.

 18. Histamine 2 receptor blockers

 19. The H2 Blockers- “tidines” Prototype: Cimetidine 1. Ranitidine 2.
Famotidine 3. Nizatidine

 20. The H2 Blockers- “tidines” Pharmacodynamics: Drug Action The H2

blockers are antagonists at the receptors in the parietal cells of the stomach. The
blockage results to inhibition of the hormone gastrin. There will be decreased
production of gastric acid from the parietal cells. Also, the chief cells will secrete less
pepsinogen.

 21. The H2 Blockers- “tidines” Therapeutic use of the H2 blockers Short-term

treatment of active duodenal ulcer or benign gastric ulcer Treatment of
hypersecretory conditions like the Zollinger-Ellison syndrome Prevention of stress-
induced ulcers and acute GI bleeding Treatment of erosive GERD (reflux disease)
Relief of Symptoms of heart burn and acid indigestion

 22. The H2 Blockers- “tidines” Precautions and Contraindications Any known

allergy is a clear contraindication to the use of the agents. Conditions such as
pregnancy, lactation, renal dysfunction and hepatic dysfunction should warrant
cautious use. Nizatidine can be used in hepatic dysfunction.

 23. The H2 Blockers- “tidines” Dynamics- Side effects/adverse effects GIT=

diarrhea or constipation CNS= Dizziness, headache, drowsiness, confusion and
hallucinations Cardio= arrhythmias, HYPOTENSION (related to H2 receptor blockage
in the heart) Cimetidine= Gynecomastia and impotence in males

 24. The H2 Blockers- “tidines” Drug-drug Interactions Cimetidine, Famotidine,

Ranitidine are metabolized in the liver- they can cause slowing of excretion of other
drugs leading to their increased concentration .

 25. The H2 Blockers- “tidines” Drug-drug Interactions These drugs can

interact with CIMETIDINE Anticoagulants Phenytoin, Alcohol Antidepressants.

 26. The H2 Blockers- “tidines” Nursing considerations: Administer the drug

WITH meals at BEDTIME to ensure therapeutic level One hour after Antacids Stress
the importance of the continued use for the length of time prescribed

 27. The H2 Blockers- “tidines” Nursing considerations Monitor the

cardiovascular status especially if the drugs are given IV Warn patient of the potential
problems of increased drug concentration if the H2 blockers are used with other drugs
or OTC drugs. Advise consultation first!

 28. The H2 Blockers- “tidines” Nursing considerations: Provide comfort

measures like analgesics for headache, assistance with ambulation and safety
measures because of confusion Warn the patients taking cimetidine that drowsiness
may pose a hazard if driving or operating delicate machines.

 29. The H2 Blockers- “tidines” Nursing considerations: Provide health

teaching as to the dose, frequency, comfort measures to initiate when side-effects are
intolerable Evaluate the effectiveness Relief of symptoms of ulcer, heart burn and
GERD

 30. Antacids

 31. The Antacids These are drugs or inorganic chemicals that have been used
for years to neutralize acid in the stomach
 32. The Antacids The following are the common antacids that can be bought
OTC: Aluminum salts (hydroxide) Calcium salts (carbonate) Magnesium salts (milk of
magnesia) Sodium bicarbonate Magaldrate (aluminum and magnesium combination)

 33. The Antacids Pharmacodynamics: drug action These agents act to

neutralize the acidic pH in the stomach. They do not affect the rate of gastric acid
secretion.

 34. The Antacids Pharmacodynamics: drug action The administration of

antacid may cause an acid rebound. Neutralizing the stomach content to an alkaline
level stimulates gastrin production to cause an increase in acid production and return
the stomach to its normal acidic state.

 35. The Antacids Therapeutic Indications Symptomatic relief of upset

stomach associated with hyperacidity Hyperacidic conditions like peptic ulcer,
gastritis, esophagitis and hiatal hernia Special use of AMPHOGEL (aluminum
hydroxide): to BIND phosphate

 36. The Antacids Precautions of Antacid Use Known allergy is a clear

contraindication Caution should be instituted if used in electrolyte imbalances, GI
obstruction and renal dysfunction. Sodium bicarbonate is rarely used because of
potential systemic absorption  metabolic alkalosis!!!

 37. The Antacids Pharmacokinetics These agents are taken orally and act
locally in the stomach

 38. The Antacids Pharmacodynamics: Effects of drugs GIT= rebound acidity;

alkalosis may occur. Calcium salts may lead to hypercalcemia Magnesium salts can
cause DIARRHEA Aluminum salts may cause CONSTIPATION and Hypophosphatemia
by binding with phosphates in the GIT. 2. Fluid retention due to the high sodium
content of the antacids.

 39. The Antacids Nursing Considerations: Administer the antacids apart from
any other medications by ONE hour before or TWO hours after- to ensure adequate
absorption of the other medications Tell the patient to CHEW the tablet thoroughly
before swallowing. Follow it with one glass of water Regularly monitor for
manifestations of acid-base imbalances as well as electrolyte imbalances

 40. The Antacids Nursing Considerations: Provide comfort measures to

alleviate constipation associated with aluminum and diarrhea associated with
magnesium salts. Monitor for the side-effects, effectiveness of the comfort measures,
patient’s response to the medication and the effectiveness of the health teachings

 41. The Antacids Nursing Considerations Evaluate for effectiveness:

Decreased symptoms of ulcer and pyrosis Decreased Phosphate level (Amphogel) in
patients with chronic renal failure

 42. proton-pump inhibitors

 43. The PPI These are the newer agents for ulcer treatment The “prazoles”
Prototype: Ome prazole Laniso prazole Esome prazole Panto prazole

 44. The PPI Pharmacodynamics: drug action They act at specific secretory
surface receptors to prevent the final step of acid production and thus decrease the
level of acid in the stomach. The “pump” in the parietal cell is the H-K ATPase enzyme
system on the secretory surface of the gastric parietal cells
 45. The PPI Clinical use of the PPIs Short-term treatment of active duodenal
ulcers, GERD, erosive esophagitis and benign gastric ulcer Long-term- maintenance
therapy for healing of erosive disorders.

 46. The PPI Precautions with the use of the PPIs Known allergy is a clear
contraindication Caution if patient is pregnant

 47. The PPI Pharmacodynamics: Adverse effects CNS- dizziness , headache,

asthenia (loss of strength), vertigo , insomnia, apathy GIT- diarrhea, abdominal pain,
nausea, vomiting, dry mouth and tongue atrophy Respi- cough, stuffy nose,
hoarseness and epistaxis.

 48. The PPI Nursing considerations: Administer the drug BEFORE meals.
Ensure that patient does not open, chew or crush the drug. Provide safety measures if
CNS dysfunction happens. Arrange for a medical follow-up if symptoms are NOT
resolved after 4-8 weeks of therapy.

 49. The PPI Nursing considerations: Provide health teaching as to drug name,
dosages and frequency, safety measures to handle common problems. Monitor patient
response to the drug, the effectiveness of the teaching plan and the measures to
employ

 50. The PPI Nursing considerations: Evaluate for effectiveness of the drug
Healing of peptic ulcer Decreased symptoms of ulcer

 51. Mucosal protectants

 52. The Mucosal Protectant Sucralfate (Caralfate/ Iselpin) This is given to

protect the eroded ulcer sites in the GIT from further damage by acid and digestive
enzymes

 53. Sucralfate Pharmacodynamics: Action of drug It forms an ulcer-adherent

complex at duodenal ulcer sites, protecting the sites against acid, pepsin and bile.
This action prevents further breakdown of proteins in the area and promotes healing.

 54. Sucralfate Clinical use of sucralfate Short and long term management of
duodenal ulcer. NSAIDs induced gastritis Prevention of stress ulcer Treatment of oral
and esophageal ulcers due to radiation, chemotherapy or sclerotherapy.

 55. Sucralfate Precautions on the use of Sucralfate This agent should NOT be
given to any person with known allergy to the drug, and to those patients with renal
failure/dialysis because of build-up of aluminum may occur if used with aluminum
containing products.

 56. The Mucosal Protectant Pharmacodynamics: Side-effects & adverse

reactions Primarily GIT= CONSTIPATION, occasionally diarrhea, nausea, indigestion,
gastric discomfort, and dry mouth may also occur CNS= dizziness, drowsiness, vertigo
Others= rash and back pain

 57. The Mucosal Protectant Drug-drug interactions If used with aluminum

salts= high risk of accumulation of aluminum and toxicity . If used with phenytoin,
fluoroquinolones and penicillamines- decreased levels of these drugs when taken with
sucralfate

 58. The Mucosal Protectant Nursing Considerations Administer drug ON AN

EMPTY stomach , 1 hour before meals , or 2 hour after meals and at BEDTIME Monitor
for side-effects like constipation and GI upset Encourage intake of high-fiber foods
 and increased fluid intake Administer antacids BETWEEN doses of sucralfate, NOT
WITHIN 30 minutes of sucralfate dose

 59. The Mucosal Protectant Nursing Considerations Provide comfort

measures if CNS effects occur Provide health teaching as to drug name, dosages and
frequency, safety measures to handle common problems. Monitor patient response to
the drug, the effectiveness of the teaching plan and the measures employed

 60. The Mucosal Protectant Nursing Considerations Evaluate effectiveness of

therapy Healing of ulcer No formation of ulcer

 61. Prostaglandin analogue

 62. Prostaglandin analogue Misoprostol This agent is a synthetic

prostaglandin E1 analog that is employed to protect the lining of the mucosa of the
stomach

 63. Prostaglandin analogue Misoprostol: Pharmacodynamics Being a

prostaglandin analog, it inhibits gastric acid secretion to some degree It INCREASES
mucus production in the stomach lining.

 64. Prostaglandin analogue Misoprostol: Clinical use NSAIDs-induced gastric

ulcers Duodenal ulcers unresponsive to H2 antagonists

 65. Prostaglandin analogue Precautions of Misoprostol Use This drug is

CONTRAINDICATED during pregnancy because it is an abortifacient. Women should be
advised to have a negative pregnancy test within 2 weeks of beginning therapy and
should begin the drug on the second or third day of the next menstrual cycle. They
should be instructed in the use of contraceptives during therapy.

 66. Prostaglandin analogue Pharmacodynamic effects: drug reactions GIT=

Nausea, diarrhea, abdominal pain, flatulence, vomiting, dyspepsia GU effects=
miscarriages, excessive uterine CRAMPING and bleeding , spotting, hyper-menorrhea
and menstrual disorders.

 67. Prostaglandin analogue Nursing Considerations Administer to patients at

risk for NSAIDs-induced ulcers during the full course of NSAIDs therapy Administer
four times daily with meals and at bedtime Obtain pregnancy test within 2 weeks of
beginning therapy. Begin the therapy on second or third day of menstrual period to
ensure that the woman is not pregnant

 68. Prostaglandin analogue Nursing Considerations Provide patient with both

written and oral information regarding the associated risks of pregnancy Provide
health teaching as to drug name, dosages and frequency, safety measures to handle
common problems. Monitor patient response to the drug, the effectiveness of the
teaching plan and the measures to employ

 69. laxatives

 70. Laxatives Generally used to INCREASE the passage of the colonic

contents The general classifications is as follows: 1. Chemical stimulants- irritants 2.
Mechanical stimulants- hyperosmotic agents and saline cathartics 3. Lubricants and
stool softeners

 71. Laxatives They promote bowel evacuation for various purposes They are
classified into their mode of action
 72. Laxatives Lubricating the intestinal material to promote passage through
the GIT Docusate Mineral oil Lubricants Increased fluid content of the fecal material
causing stimulation of the local reflex Lactulose Mechanical (bulk) stimulants Direct
stimulation of the GIT nerves Irritant laxatives Bisacodyl (Dulcolax) Chemical
stimulants Action Prototype Type

 73. Therapeutic Indications of the Laxatives SHORT term relief of

Constipation Prevention of straining in conditions like CHF, post-MI, post partum, post-
op Preparation for diagnostic examination Removal of poison or toxins Adjunct in anti-
helminthic therapy To remove AMMONIA by use of lactulose

 74. Contraindications in Laxative use ACUTE abdominal disorders

Appendicitis Diverticulitis Ulcerative colitis

 75. Chemical Stimulant Cathartics Prototype: Bisacodyl Irritant laxatives: 1.

Castor oil 2. Senna 3. Cascara 4. Phenolphthalein

 76. Chemical Stimulant Cathartics Pharmacodynamics These agents

DIRECTLY stimulate the nerve plexus in the intestinal wall The result is INCREASED
movement or motility of the colon

 77. Mechanical Stimulant Cathartics Prototype: LACTULOSE (Cephulac) Bulk-

forming laxatives 1. Magnesium ( citrate , hydroxide, sulfate)- saline cathatic 2.
Psyllium 3. Polycarbophil

 78. Mechanical Stimulant Cathartics Pharmacodynamics These agents are

rapid-acting laxatives that INCREASE the GI motility by Increasing the fluids in the
colonic material Stimulating the local stretch receptors Activating local defection
reflex

 79. Lubricants-Stool softener Prototype: Docusate 1. Glycerin 2. Mineral oil

 80. Lubricants-stool softeners Pharmacodynamics Docusate increases the

admixture of fat and water producing a softer stool Glycerin and Mineral oil form a
slippery coat on the colonic contents

 81. Pharmacokinetics: Common Side-effects of the Laxatives Diarrhea

Abdominal cramping Nausea Fluid and electrolyte imbalance Sympathetic reactions-
sweating, palpitations, flushing and fainting CATHARTIC dependence

 82. The Nursing Process and Laxative ASSESSMENT Nursing History- elicit
allergy to any laxatives, elicit history of conditions like diverticulitis and ulcerative
colitis Physical Examination- abdominal assessment Laboratory Test: fecalysis,
electrolyte levels

 83. The Nursing Process and Laxative NURSING DIAGNOSIS Alteration in

bowel pattern Alteration in comfort: pain Knowledge deficit

 84. The Nursing Process and Laxative IMPLEMENTATION Emphasize that it is

use on a SHORT term basis Provide comfort and safety measures like ready access to
the bathroom, side-rails Administer with a full glass of water

 85. The Nursing Process and Laxative IMPLEMENTATION 4. Encourage fluid

intake, high fiber diet and daily exercise 5. DO NOT administer if acute abdominal
condition like appendicitis is present 6. Advise to change position slowly and avoid
hazardous activities because of potential dizziness
 86. The Nursing Process and Laxative IMPLEMENTATION 7. Record intake and
output to assess fluid alteration 8. If possible, observe the character of stools 9.
Caution the patient that chronic use may promote dependence and use during
pregnancy may cause uterine cramping and Vitamin deficiency

 87. The Nursing Process and Laxative EVALUATION of drug effectiveness

Evaluate relief of GI symptoms, absence of staining and increased evacuation of GI
tract For Lactulose: decreased ammonia Nomal bowel fucntion is restored

 88. The Anti-diarrheals These are agents used to calm the irritation of the GIT
for the symptomatic relief of diarrhea General Classifications 1. Local anti-motility 2.
Local reflex inhibition 3. Central action on the CNS

 89. The Anti-diarrheals Stops GIT spasm by CNS action Opium derivatives
(paregoric) Central acting agent Directly inhibits the intestinal muscle activity to
SLOW peristalsis Loperamide Local anti-motility Locally coats the lining of the GIT to
soothe irritation Bismuth subsalicylate Local reflex inhibitor Action Prototype Type

 90. Clinical Indications of drug use Relief of symptoms of acute and chronic
diarrhea Reduction of fecal volume discharges from ileostomies Prevention and
treatment of traveler's diarrhea

 91. Contraindications of anti-diarrheal Use Poisoning Drug allergy GI

obstruction Acute abdominal conditions

 92. Pharmacokinetics: Side effects Constipation Nausea, vomiting Abdominal

distention and discomfort TOXIC MEGACOLON

 93. Nursing process and anti-diarrheals ASSESSMENT Nursing History – Elicit

history of drug allergy, conditions like poisoning, GI obstruction and acute abdominal
conditions Physical Examination- Abdominal examination Laboratory test- electrolyte
levels

 94. Nursing process and anti-diarrheals NURSING DIAGNOSIS Alteration in

bowel pattern Alteration in comfort: pain

 95. Nursing process and anti-diarrheals IMPLEMENTATION Monitor patient

response within 48 hours. Discontinue drug use if no effect Provide comfort measures
for pain Provide teaching regarding its short term use only

 96. Nursing process and anti-diarrheals EVALUATION Monitor effectiveness of

drug- RELIEF of diarrhea Monitor adverse effects, effectiveness of pain measures and
effectiveness of teaching plan

 97. Emetic and anti-emetics

 98. Emetics and Anti-emetics Emetic Agent Syrup of Ipecac Anti-emetics 1.

Phenothiazines 2. Non-phenothiazines 3. Anticholinergics/Antihistamines 4. Serotonin
receptor Blockers 5. Miscellaneous

 99. EMETIC Prototype: Ipecac Syrup

 100. EMETIC Pharmacodynamics Ipecac syrup irritates the GI mucosa

locally, resulting to stimulation of the vomiting center It acts within 20 minutes

 101. EMETIC Clinical Use of ipecac To induce vomiting as a treatment for

drug overdose and certain poisonings
 102. EMETIC Contraindications of Ipecac use Ingestion of CORROSIVE
chemicals Ingestion of petroleum products Unconscious and convulsing patient

 103. EMETIC Pharmacokinetics: side effects of Ipecac Nausea Diarrhea GI

upset Mild CNS depression CARDIOTOXICITY if large amounts are absorbed in the
body

 104. Nursing process and the EMETIC ASSESSMENT Nursing History- elicit
the exact nature of poisoning Physical Examination- CNS status and abdominal exam

 105. Nursing process and the EMETIC IMPLEMENTATION Administer to

conscious patient only Administer ipecac as soon as possible Administer with a large
amount of water Vomiting should occur within 20 minutes of the first dose . Repeat
the dose and expect vomiting to occur with 20 minutes

 106. Nursing process and the EMETIC IMPLEMENTATION 5. Provide comfort

measures like ready access to bathroom, assistance with ambulation 6. Offer support

 107. Nursing process and the EMETIC EVALUATION Evaluate patient response
within 20 minutes of drug ingestion Monitor for adverse effects Evaluate effectiveness
of comfort measures and teaching plan

 108. Anti-Emetics

 109. ANTI-EMETICS These are agents used to manage nausea and vomiting
They act either locally or centrally In general, they may inhibit the chemoreceptor
trigger zone in the medulla by blocking DOPAMINE receptor Others act by decreasing
the sensitivity of the vestibular apparatus

 110. ANTIEMETICS Dronabinol, hydroxyzine Miscellaneous “ setron”-

dolasetron Serotonin Receptor blockers Meclizine, buclizine Anticholinergics and
Antihistaminics Metoclopramide Non-phenothiazines Prochlorperazine, Promethazine
Phenothiazines Common examples Anti-emetic types

 111. ANTIEMETICS Act in the CNS , either in the medulla or in the cortex
Miscellaneous Centrally and locally inhibits the serotonin receptors Serotonin
receptor blockers Block the transmission of the impulses to the medulla
Anticholinergics Reduces the responsiveness of the nerve cell in the medulla; also
blocks the dopamine receptors Non-phenothiazine Centrally block the vomiting center
in the medulla Phenothiazines Pharmacodynamics Types

 112. ANTIEMETICS N/V associated with chemotherapy Miscellaneous N/V

associated with chemotherapy Serotonin-receptor Blockers N/V associated with
motion sickness Anticholinergics N/V associated with chemical stimulation Non-
phenothiazine N/V associated with anesthesia, intractable hiccups Phenothiazines
Clinical Use Types

 113. ANTIEMETICS Indications 1. Prevention and treatment of vomiting 2.

Motion sickness

 114. ANTIEMETICS Contraindications 1. Severe CNS depression 2. Severe

liver dysfunction

 115. ANTIEMETICS Pharmacokinetics: Oral absorption is good if vomiting is

not present IV drugs can be given if vomiting is active Most drugs are metabolized in
the liver excreted in the kidneys
 116. ANTIEMETICS Pharmacokinetics: Side-effects 1. PHOTHOSENSITIVITY 2.
Drowsiness, dizziness, weakness and tremors and DEHYDRATON 3. Phenothiazines =
autonomic anti-cholinergic effects like dry mouth, nasal congestion and urinary
retention Metoclopramide= EPS due to dopamine receptor blockage

 117. Nursing Process and the ANTIEMETICS ASSESSMENT Nursing History-

elicit allergy, impaired hepatic function and CNS depression Physical Examination-
CNS status and abdominal examination Laboratory test- Liver function studies

 118. Nursing Process and the ANTIEMETICS NURSING DIAGNOSIS Alteration

in comfort: pain High risk for injury Knowledge deficit

 119. Nursing Process and the ANTIEMETICS IMPLEMENTATION Assess

patient’s intake of other drugs that may cause dangerous drug interaction Emphasize
that this is given on a short term basis

 120. Nursing Process and the ANTIEMETICS IMPLEMENTATION 3. Provide

comfort and safety measures Advise to change position slowly Avoid hazardous
activities Provide mouth care and ice chips Monitor for dehydration and offer fluids if
it occurs

 121. Nursing Process and the ANTIEMETICS IMPLEMENTATION 4. Protect

from sun exposure Sunscreens Protective covering 5. Provide health teaching

 122. Nursing Process and the ANTIEMETICS EVALUATION 1. Monitor for the
drug effectiveness Relief of nausea and vomiting 2. Monitor for adverse effects 3.
Evaluate effectiveness of comfort measures and teaching plan