Pharm 2 Exam #3 (Chpt. 42, 13, 12, 14) Flashcards
Compare the pharmacologic treatment of vomiting, diarrhea, and constipation
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Chapter 42, objective #1
Vomiting: vestibular system and chemoreceptor trigger zone are very close to one another causing N/V sensory input; S/Sx: salivate, dry heaving
Diarrhea:
Constipation:
RN Implications for taking drugs for the GI tract
Obtain diet, travel, illness and medication history
Monitor vitals
Monitor hydration (vomiting and diarrhea can lead to severe dehydration and shock)
Monitor bowel sounds – hypoactivity or hyperactivity
Provide oral hygiene
Provide pericare
Monitor for side effects of medications
Encourage nonpharmagological therapies as first line treatment
Drugs to treat GI problems
— Antiemetics
— Emetics
— Antidiarrheals
— Laxatives
Location of chemoreceptor trigger zone (CTZ) + vomiting center
CTZ: lies near the medulla
Vomiting center: inside the medulla
What are things to trigger the CTZ?
— Drugs
— Toxins
— Vestibular center is in the middle ear
Which stimulates the vomiting center?
What are the direct triggers of the vomiting center?
Think sensory impulses
— Odors
— Smells,
— Taste
— Gastric mucosal irritation
Neurotransmitter actions of CTZ and vomiting center
— Dopamine stimulates the CTZ
— Acetylcholine stimulates the vomiting center
Non-pharmacological measures for vomiting
1st step to treatment of GI problems
Weak tea
Flat soda
Gelatin
Pedialyte (for use in children)
Gatorade
Crackers
Dry Toast
Peppermint/ginger
Mild nausea may be relieved by applying acupressure on the inside of your wrist
BRAT diet when Tx of GI d/o’s: bananas, rice, applesauce, toast
Nonprescription Antiemetics
2nd step to Tx of GI problems
Antihistamines:
Dimenhydrinate (Dramamine) —
— provides anticholinergic effects = drowsiness, dry mouth, constipation so increase fluid and fiber intake, take 30-60minutes before activity
Bismuth subsalicylate (Pepto-Bismol)
may have allergic rxn b/c has trace amounts of sulfa/aspirin
NOTE: RISK OF REYE’S SYNDROME FOR CHILDREN WITH VIRAL SYNDROMES WHEN TAKING PEPTO-BISMOL!!
Prescriptive Antiemetics: Antihistamines
3rd option to tx to imitigate nausea/GI problems
_Action: act primarily on the vomiting center | decrease stimulation of CTZ + vestibular pathways
NOTE: Antihistamines have CNS depressive effects so sedation and respiratory depression is a concern, especially if combined with OTHER CNS depressants = problem if drug is used to counteract the emetogenic properties of opiates!
Prescriptive Antiemetics Examples: Antihistamines + Anticholinergics
3rd option to Tx GI problems
Hydroxyzine (Vistaril)
Promethazine (Phenergan)
Scopolamine (Transderm-Scop)
Side effects for Antiemetics: Antihistamines + Anticholinergics
Side effects: drowsiness, dry mouth, blurred vision caused by pupillary dilation, tachycardia (with anticholinergic use), and constipation
— These drugs should not be used by patients with glaucoma
Differences b/w: emesis, emetogenic, antiemetic
Emesis = vomiting
Emetogenic = something that causes nausea/vomiting; e.g. chemotherapy drugs
Antiemetics = medicines that imitigate nausea
How long should OTC antihistamines for motion sickness be taken before travel?
30 minutes before travel
NOTE: antihistamines inhibit vestibular stimulation in the middle ear
Antiemetics Drugs
— Dopamine antagonists
Phenothiazine antiemetics: Chlorpromazine (Thorazine) | Prochlorperazine edisylate (Compazine) | Promethazine (Phenergan) |
— Droperidol (Inapsine): Butyrophenone (NOT for patients w/ QT prolongation) |
Diphenidol (Vontrol), trimethovbenzamide (Tigan)
Miscellaneous Antiemetics
Action:
— suppress impulses to CTZ and reduce sensation of nausea
Side Effects:
— drowsiness + anticholinergic Sx b/c meds reduce availability of dopamine, which will relieve of N/V, but may cause EPS effects (Parkinson’s)
— Trimethobenzamide can cause HoTN, diarrhea, and EPS
Causes of Diarrhea
Spoiled foods or excessively spicy foods
Bacteria (Escherichia coli, Salmonella), virus (parvovirus, rotavirus), toxins
Drug reactions
Fecal impaction, laxative abuse
Malabsorption disorders, bowel tumor, inflammatory bowel disease
Stress, anxiety
Non-pharmacological measures for treating diarrhea
— Clear liquids
— Oral solutions (Gatorade, Pedialyte, Rehydralyte [both if use in children])
— IV electrolyte solutions
— Grab a small cup (~30mL/cc) and pour liquid (H2O, flat soda, Pedialyte, etc) and have person sip on it every few minutes; if capable of drinking 2 “cups” per hour = 1/2 cup drunken within the 1 hour
Purpose, caution, and types of Antidiarrheals
Purpose: decrease hypermotility in the gut
Caution: should nOT be used for more than 2 days or if fever present
Types:
— Opiates and opiate-related agents
— Somatostatin analogue
— Adsorbents
— MIschellaneous
Diarrhea = constipation = opstimation (chronic constipation) = colon rupture/perforation (trying to get rid of stool) = sepsis = death
Metoclopramide (Reglan)
Mischellaneous Antiemetics
Action: suppress impulses to CTZ and increases GI transit time
Side effects: high doses can cause sedation and diarrhea; occurrence of EPS is more prevalent in children than adults (tardive dyskinesia) |
Contraindicated w/: GI obstruction, hemorrhage, or perforation
Ipecac (OTC)
Emetic
Action: stimulates CTZ and acts directly on gastric mucosa
Use: induces vomiting after toxic substance
Caution:
— avoid vomiting if substance is caustic or petroleum
— if vomiting contraindicated, activated charcoal or gastric la age can be used
Substances that induce emetics + use of Ipecac
Caustic substances: ammonia, chlorine bleach, lye, toilet cleaners, battery acid
Petroleum substances: gasoline, kerosene, paint thinners, lighter fluid
Activated charcoal is used when emesis is contraindicated.
RN Interventions:
— Ipecac is considered appropriate in isolated cases for the patient who is alert and if administered within 1 hour of poisoning
— Be sure to use ipecac syrup and not ipecac fluid extract
— Give with glass of water…not milk or sodas Vomiting usually begins within 15 to 30 minutes of ingestion
Diarrhea can lead to
— Malabsortion disorders (UC, Crohn’s, Celiac Disease)
— Bowel tumor
— Inflammatoy bowel disease
Antidiarrheals: Opiates, Opiate-related agents
Diphenoxylate with atropine (Lomotil) — contraindicated with IBD b/c can cause severe complications of toxic mega colon
Difenoxin (Motofen)
Loperamide (Imodium)
Opiates decrease GI motility.
Opiates may cause respiratory depression.
Especially children and older adults
May cause physical dependence
Atropine contraindicated in glaucoma.
What is the key differences between Imodium vs. Lomotil
Imodium is structurally related to Lomotil but causes less CNS depression and can be purchased as an OTC drug.
NOTE: Prolonged use of these meds may cause physical dependence.
What Antidiarrheals do you NOT use to treat Traveler’s Diarrhea? Why?
**Ioperamide (Imodium) **
— Is used cautiously as it slows peristalsis and may also slow the exit of infectious organism from the GI tract (causing infectious diarrhea).
— Allow patient to poop it out as opposed to slowing and maintaining bacteria in the gut if using this drug
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NOTE: Traveler’s diarrhea can be reduced by drinking bottled water, washing fruit, and eating cooked vegetables. Meats should be cooked until well done.
Pharmacological options for nausea
Prescriptive antiemetics
Antihistamines
Anticholinergics
Dopamine antagonists
Benzodiazepines
Serotonin antagonists
Glucocorticoids
Cannabinoids (for patients with cancer)
Miscellaneous
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NOTE: these drugs act as antagonists to dopamine, histamine, serotonin, and acetylcholine, which are all associated with N/V
— Cannabinoids: dronabinol (Marinol)
— Miscellaneous: Diphenidol (Vontrol), Trimeth (reduce availability in Dopamine that can trigger EPS), Metoclopramide (Reglan),
Antihistamines + Anticholinergics to combat N/V
Hydroxyzine (Vistaril)
Promethazine (Phenergan)
Scopolamine (Transderm-Scop)
Side effects: drowsiness, dry mouth, blurred vision caused by pupillary dilation, tachycardia (with anticholinergic use), and constipation
These drugs should not be used by patients with glaucoma.
Why can you not give patients Antihistamines and Opiates together?
** — Antihistamines + Opiates = additive effects r/t respiratory depression**
— Antihistamines and anticholinergic agents reduce opioid-induced vestibular sensitivity.
— Antihistamines have CNS depressant effects and adding an opiate will have sedating effect adding to respiratory depression
Dopamine antagonists that combat N/V
Phenothiazine antiemetics
Chlorpromazine (Thorazine) — used as an antipsychotic
Prochlorperazine edisylate (Compazine)
Promethazine (Phenergan)
droperidol (Inapsine)
Butyrophenone — (Haldol found in this category for antipsychotic patients)
Contraindicated in patients with QT prolongation
Side effects: moderate sedation, hypotension, EPS, CNS effects, and mild anticholinergic symptoms
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Benzodiazepines
Lorazepam effectively provides emesis control, sedation, anxiety reduction, and amnesia when used in combination with a glucocorticoid and serotonin 5-HT3 receptor antagonist (can cause ischemic colitis).
Promethazine (Phenergan)
Category: Phenothiazines
MOA: blocks H1-receptor sites and inhibits CTZ
Onset: 15-60 minutes (oral); 20 minutes (IM); 3-5 minutes (IV)
Duration: 4-6 hours (oral, IM, IV)
*— Treats/prevents motion sickness, N/V and sedation induction
— A CNS depressant and an additive if taken with EtOH, narcotics/opiates, sedative-hypnotics, and general anesthetics
— Anticholinergic effects increase when combined with antihistamines (e.g. atropine)
Side effects: have antihistamine + anticholinergic properties, watch for EPS and CNS effects (restlessness, weakness, systolic rxns, agitation)
Contraindications: Narrow angle glaucoma, intestinal obstruction, blood dyspraxia’s, liver dysfunction, COPD
Serotonin antagonists for Antiemetics
Ondansetron (Zofran), granisetron (Kytril), dolasetron (Anzemet), palonosetron (Aloxi)
— work on 5H-T receptors
— Best used for patients CINV, PONV, radiation therapy NV, viral gastritis NV & NVP (pregnancy)
Serotonin antagonists benefits r/t nausea, vomiting + side effects
Benefits: reduces N/V r/t chemotherapy, post-op, radiation, viral gastritis, & pregnancy
Common side effects: headache, diarrhea, dizziness, and fatigue
These drugs DO NOT block dopamine so will not cause EPS effects
These drugs can also prolong the QT measurement —> TORSADES de Pointes
— Antidote: Magnesium IV
Glucocorticoids (corticosteroids) for N/V
Dexamethasone (Decadron)
Methylprednisolone (Solu-Medrol)
Administered IV
Effective in suppressing emesis associated with cancer chemotherapy
NOTE: Because these are administered IV and for only a short while, side effects normally associated with glucocorticoids are minimized
IBD vs. IBS
IBD = inflammatory bowel disease
— electrolytes, biologic? Med, malabsorption
e.g. ulcerative colitis, celiac, crohn’s
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IBS = irritable bowel syndrome
— no inflammation
— usually diet/stress-related
— C(constipation predominant; don’t poop for 2 weeks) | D(diarrhea predominant)
Diphenoxylate with Atropine
Class: Antidiarrheals CSS V
Dose: initially, 2 tabs (2.5mg diphenoxylate, 0.025mg atropine each tablet); MAX = 8 tablets
MOA: inhibits gastric motility by exerting effect on smooth muscle cells of GI tract
Therapeutic effects: Tx diarrhea by slowing intestinal motility
Contraindications: severe diarrhea d/t pseudomembranous colitis; Increased CNS depression when drinking EtOH, antihistamines, opioids, sedative-hypnotics; MAOIs = may enhance HTNive crisis
Labs to check: increased serum liver enzymes, amylase
S/Eff: drowsiness, dizziness, confusion, euphoria, H/A, restlessness, abd pain, N/V, flushing, urine retention
A/Eff: angioedema, pancreatitis, tachycardia, lieu’s, toxic mega colon
Differentiate the actions and side effects of antiemetics, emetics, antidiarrheals, and laxatives
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Chapter 42, objective #2
Apply the nursing process for the patient taking antiemetics, antidiarrheals, and laxatives
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Chapter 42, objective #3
What is PUD and it’s causes?
Peptic Ulcer Disease (PUD)
— Group of upper GI disorders characterized by varying degrees of erosion of the gut wall
— Develops when aggressive factors outweigh defensive factors
Difference b/w aggressive factors vs. defensive factors related to PUD
Aggressive factors: H pylori, NSAIDs, acid, pepsin, hyperstimulative
—purpose: disorders stimulates the gut causing issues
Defensive factors: mucus, bicarb, submucosal blood blow, prostaglandins
— purpose: to keep/maintain gut health
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NOTE: NSAIDs inhibits prostaglandins =setting person up to development of erosions in the gut wall
H. pylori + how to treat
most common cause of PUDs
— Gram negative bacillus that can colonize the stomach and duodenum
— 60-75% of patients with peptic ulcer disease (PUD) have it
— Tx: control acid production, but will not cure, but trying to create conditions conducive to stomach; e.g. Take an anti acid (will neutralize acid in stomach and allow healing to occur) but will not FIX the hyper acidity problem that originally caused the problem — use antibiotics in conjunction to get RID of H.pylori and CURE problem
Examples of peptic ulcers
Esophageal ulcer
Results from reflux of acidic gastric secretions into esophagus due to an incompetent cardiac sphincter
Gastric ulcer
Results from a breakdown of gastric mucosal barrier
Duodenal ulcer
Results from hypersecretion of acid
Stress ulcer
Results from trauma, burns, major surgery
Stomach diagram
— Cardiac sphincter = top of stomach = lower esophageal sphincter (LES)
— Pyloric sphincter = @ end of stomach
— duodenum = beginning of small intestine
— stomach = starts digestion and makes hydrochloric acid
— lower stomach used to low pH
— small intestine = not used to low pH ( if lots of acid in tummy and moves to duodenal —> duodenal ulcers
Once you impair the mucosal barrier
Pepsin = used to start digestion of protein (stomach muscle is made of protein)
Heartburn = fluid refluxing through cardiac sphincter/LES and damaging the esophageal mucosa (not made for acidic pH)
Stomach can develop erosion = more difficult to heal in presence of more acid and pepsin
Differentiate contraindications to the use of antiemetics, emetics, antidiarrheals, and laxatives
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Chapter 42, objective #4
Differentiate between peptic ulcer, gastric ulcer, duodenal ulcer, and gastroesophageal reflux disease (GERD)
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Chapter 43, objective #2
Explain the predisposing factors for peptic ulcers
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Chapter 43, objective #1
What is GERD? Cause? Triggers?
GERD Gastroesophageal Reflux Disease aka reflux esophagitis
— inflammation of the esophageal mucosa caused by reflux of gastric content into the esophagus
Cause: incompetent lower esophageal sphincter — cannot maintain it’s competency (can’t stay shut very well), will allow reflux, creating sensation of heartburn of reflux esophagitis
Triggers: EtOH, smoking, stress, spicy foods
What is LPR? What are its triggers? Why is this dangerous?
*When reflux moves all the way to oropharynx and throat causing laryngapharyngeal reflux (LPR) — dangerous b/c opportunity to aspirate gastric content to the lungs —> aspiration pneumonia —> DEATH
Triggers: EtOH, spicy foods, smoking
NONPHARMACOLOGIC Measures for GERD
— Avoid tobacco
— Avoid alcohol
— Avoid hot, spicy, greasy foods
— Take any NSAIDS (2nd leading cause of PUD and aggregate the GI tract); including aspirin and oroal glucocorticoids, w/ food or in decreased dosage
— Sit upright
— Do not eat before bedtime
— Wear loose fitting clothing (e.g. tight belts, pants can increase risk of reflux)
Antiulcer Drugs
1) Tranquilizers
2) Anticholinergic drugs
3) Antacids
4) H2 blockers
5) Proton pump inhibitors
6) Pepsin inhibitor
7) Prostaglandin E1 analog
Tranquilizers MOA + Drugs + Side Effects
MOA: reduce acetylcholine (ACh) production = reduce vagal stimulation, decrease anxiety
Calms vagus nerve | When vagus nerve is activated and releases ACh, it can increase histamine receptors —> increased HCl acid ==> less ACh, less histamine, HCl acid produced
Drugs
Chlordiazepoxide (Librium)
Clidinium bromide (Quarzan)
Anticholinergic drugs for Antiulcers
MOA: Inhibit ACh and inhibit histamines that will promote HCl acid production
decrease ACh (breaking pathology chain leading to ulcer development/erosion)
Drugs
—
Antiulcer Drugs: Antacid
MOA: compounds that neutralize HCl acid + reduce pepsin activity, which is not healthy for erosion|
acid back diffusion: have an erosion in the mucosa of gastric stomach and with that erosion comes ability for acid to diffuse back into the ulcer and make it worse so need to get env’t conducive to healing to get mucosa back in tact*
Not going to be effective when you made the HCl, but now can neutralize the acid you have produced; not systemically absorbed, but can change the pH WITHIN the tract; do not give w/ other meds b/c binds with contents in GI tract and if take w/ medicines = will impair absorption/efficacy; take 1-2 hours AFTER meal (acid production at its highest)
Drugs
Sodium bicarbonate (Alka-Seltzer) — NOT FOR: HTN, Cardiovascular diseases, fluid overload, heart failure
Calcium carbonate (Tums) = taking as supplement and not for Hburn
Magnesium (Mg) hydroxide/aluminum hydroxide (Maalox) = cause diarrhea; NOT FOR renal patients (their Mg runs high)
— Aluminum (Al) hydroxide (Amphojel) = cause constipation; NOT FOR hx of chronic constipation
Aluminum (Al) hydroxide (Amphojel)
antacid
MOA: neutralizes gastric activity
Onset: 15-30 minutes | Peak = 0.5hr | Duration = 1-3hrs
Therapeutic effects: hyperacidity, gastric/duodenal ulcer, reflux esophagitis; reduce hyperphosphoatemia
Side effects:
— N/V
— Anorexia
— Abdominal cramping/constipation
— Weakness
— Impaired cognition
RN Intervention:
NOT for patients with diarrhea, hepatic/renal disease, HYPOphosphatemia, HYPERcalcemia, HYPOmagnesemia, dehydration, GI bleeding/obstruction, older adults, osteoporosis, children, pregnancy
Antiulcer Drugs: Histamines (H2) Blockers
MOA:
(found in stomach mainly) = reduce production of HCl acid; reducing stress (from ACh) that can lead to HCl production
Drugs:
— Cimetidine (Tagamet) — 1stG
— Ranitidine (Zantac) — 2ndG
— Famotidine (Pepcid) — 2ndG — can cause anemia
— Nizatidine (Axid) — 2ndG
Antiulcer Drug: Ranitidine (Zantac)
Oldest
MOA:
— reduce gastric acid production by blocking H2 receptors of parietal cells in stomach
— promote healing of ulcer by eliminating cause
Therapeutic effect: The patient’s abdominal pain is expected to decrease after 1 to 2 weeks of drug therapy, but healing may take 1 to 2 months.
Side effects:
— H/A
— Dizziness
— Diarrhea
— Constipation
— Reversible impotence
— Gynecomastia: histamine tube blockers resemble hormones in chemical structure hence possible side effect for men
removed from the market b/c of some inactive ingredients found harmful
Antiulcer drugs: Proton Pump Inhibitors (PPI)
MOA: reduce gastric acid by inhibiting hydrogen/potassium ATPase
Newest, expensive, most effective = suppress gastric acid secretions; even if you have simulation of ACh + histamine production, a PPI can prevent hyper secretions of HCl that leads to ulcer development
Side Effects:
H/A, insomnia, dizziness, dry mouth, flatulence, abdominal pain, malabsorption of minerals and vitamins, increase risk of ventilator-assisted pneumonia (VAP) b/c of LER (have a higher pH, some bacteria may grow and reflux into throat and aspirate a little bit), increase risk of C.diff (abnormal bacteria growing), chronic use can lead to osteoporosis/fractures
— Swallow whole; do not crush/chew capsules/tablets b/c unstable in stomach acid
Drugs:
Omeprazole (Prilosec)
Lansoprazole (Prevacid)
Rabeprazole (Aciphex)
Pantoprazole (Protonix)
Esomeprazole (Nexium)
Dexlansoprazole (Dexilant)
Esomeprazole (Nexium)
MOA: reduce gastric acid by inhibiting hydrogen/potassium ATPase
Therapeutic effects: healing erosive GERD. dyspepsia, Helicobacter pylori infection, pyrosis, and Zollinger-Ellison syndrome, and for NSAID-induced ulcer prophylaxis
Side Effects: H/A, insomnia, dizziness, dry mouth, flatulence, abdominal pain, malabsorption of minerals/vitamins (B12, Ca, Mg, Fe, lead) increase risk of ventilator-assisted pneumonia (VAP) b/c of LER (have a higher pH, some bacteria may grow and reflux into throat and aspirate a little bit), increase risk of C.diff (abnormal bacteria growing), chronic use can lead to osteoporosis/fractures
Histamine 2 Blocker Drug + Lab Interactions
— Cimetidine interacts with oral anticoagulants, theophylline, caffeine, phenytoin (Dilantin), diazepam (Valium), propranolol (Inderal), phenobarbital, and calcium channel blockers.
— Cimetidine can cause an increase in blood urea nitrogen (BUN), serum creatinine, and serum alkaline phosphatase.
Neither cimetidine nor ranitidine should be taken with antacids.
— If want to take Zantac + Tums = separate within at least an hour
— Teach patient to eat foods rich in vitamin B12 to avoid deficiency as a result of cimetidine and ranitidine therapy.
DO NOT TAKE TOGETHER WITH Tagmet, Zantac, Cimetidine, Rinitadine
Best given 2-3hrs AFTER eating and BEFORE bedtime b/c acid production is the highest and you will receive biggest neutralization of acid at that time
Pepsin inhibitor: Sucralfate (Carafate)
Pepsin inhibitors
MOA: mucosal protective drugs; combines w/ protein to form a thick paste covering ulcer, protects from acid and pepsin
Side effect: constipation
RN Interventions:
— Do not take with antacids
— Take as a slurry: immediately coat ulcer bed, does not have to break down tablet
— Given 30 minutes before meals & @ bedtime
coats ulcer bed (nothing in pathology chain) and doesn’t let pepsin aggregate it further, creating an env’t conducive to healing; ulcer is like a raw sore and pepsin can further deepen the sore
Antiulcer Drugs: Prostaglandin E1 Analogs
defensive factors in the gut
MOA:
— inhibits gastric acid secretion and increases cytoprotective mucus in GI tract; counteracts effects of NSAIDs on prostaglandins (from diminishing/ help maintain)
— Defensive factors = help protect stomach from HCl acid (no pathological impact in altering hypersecretions, but can help stomach deal with increase in HCl acid)
Patients who complain of gastric distress from NSAIDs such as aspirin or indomethacin prescribed for long-term therapy can benefit from misoprostol. Who would you expect this would be??
RN Interventions:
— Cytotec is contraindicated in pregnancy as it can cause uterine contractions
Compare the actions of seven groups of antiulcer drugs used in the treatment of peptic ulcer: tranquilizers, anticholinergics, antacids, histamine2 blockers, proton pump inhibitors, pepsin inhibitor, and prostaglandin analogue antiulcer
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Chapter 43, objective #3
Plan patient teaching for the following drug groups: anticholinergics, antacids, and histamine2 blockers
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Chapter 43, objective #4
Anticholinergics: not taken with acute/narrow angle glaucoma d/t drying up Sx’s
____________________
Antacids: best taken 1-3hrs after meals; may experience acid rebound; watch out for HYPERcalcemia, Burnetts syndrome (milk-alki syndrome) r/t XS use of Tums; NBicarb = HYPERNa + H2O retention, metabolic alkalosis, caused by XS bicarbonate, and acid rebound
______________
Histamine 2 blockers: abdominal pain will decrease after 1-2 weeks of drug therapy, but healing may take 1-2 months
Differentiate between the side effects of anticholinergics and systemic and nonsystemic antacids
________
Chapter 43, objective #5
Apply the nursing process, including patient teaching, to antiulcer drugs
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Chapter 43, objective #6
slide
Describe osmolality and tonicity
______
Chapter 12, objective #1
Discuss normal range for serum osmolality
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Chapter 12, objective #2
Describe the classifications of intravenous fluids
______
Chapter 12, objective #3
Discuss the functions of major electrolytes: potassium, sodium, calcium, magnesium, chloride, and phosphorus
________
Chapter 12, objective #4
Differentiate between major intracellular and extracellular electrolytes
_________
Chapter 12, objective #5
Key To Remember (KTR): if the serum range is larger, it will be OUTSIDE the cell (ECF), if smaller serum range, it will be INSIDE cell (ICF)
Discuss the importance of blood and blood products
_______
Chapter 12, objective #6
Apply the nursing process to fluid volume deficit and fluid volume excess
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Chapter 12, objective #7
Describe major signs and symptoms of deficiency and excess of potassium, sodium, calcium, magnesium, chloride, and phosphorus
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Chapter 12, objective #8
Explain the methods used to correct potassium, calcium, and magnesium excess
________
Chapter 12, objective #9
Apply the nursing process to the care of the patient experiencing potassium, sodium, calcium, and magnesium imbalances
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Chapter 12, objective #10
Discuss the four justifications for the use of vitamin supplements
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Chapter 13, objective #1
Differentiate between water- and fat-soluble vitamins
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Chapter 13, objective #2
FAT-soluble = not stored in body = Vitamins ADEK = megadoses may cause toxic effects
— A = teratogenic effect, hypervitaminosis, nightblindness, leukopenia, aplastic anemia | 3000mcg/day
— D = HYPERcalcemia, anorexia, N/V | if deficient = rickets —> osteomalacia (soften bone)
— E = fatigue, weakness, GI upset, H/A, breast tenderness, fat malabsorption syndromes, breakdown of RBCs
— K = hyperbilirubinemia (kernicterus in newborns), MUST have EKG ready! | if deficient —> spontaneous hemorrhaging
WATER-soluble = stored in body and XS vitamins are excreted through urine (not really toxic) = C, B1-12
___________________
Mnemonic: ”A DEK of cards are FAT”
Mnemonic: “I C you B in the bathroom a lot”
Relate food sources and deficiency conditions associated with each vitamin
________
Chapter 13, objective #3
Explain the need for iron and foods that are high in iron content
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Chapter 13, objective #4
Explain the uses for iron, copper, zinc, chromium, and selenium
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Chapter 13, objective #5
Describe the nursing interventions, including patient teaching, related to vitamin and mineral uses
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Chapter 13, objective #6
Explain the differences between enteral nutrition and parenteral nutrition
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Chapter 14, objective #1
— Nasogastric tube – can be used to give nutrition or empty stomach contents (gastric decompression)
— Nasoduodenal or nasojejunal tube – goes through pyloric sphincter; weighted Dobhoff tube; smaller bore and more flexible than NG; decreases aspiration risk; clogs easily!
— Gastrostomy and PEG (percutaneous endoscopic gastrostomy) – both gastric feeding tubes; flexible, larger bore than Dobhoff; difference is surgeon puts in gastrostomy tube; GI specialist can take patient to endoscopy and insert PEG tube; so PEGs are cheaper and require less anesthesia then gastrostomy tubes
— Jejunostomy tube – bypasses stomach and still can be used for feedings or intestinal decompression.
Describe the routes for enteral feedings
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Chapter 14, objective #2
— Blenderized = formulas made with natural foods in liquid form to pass through tubes. i.e. thinned baby food
— Polymeric (milk-based or lactose-free) = can be milk based or lactose free; provide complete nutritional requirements if given in sufficient amounts; multiple formulas….Nephro (for renal), Pulmocare (for COPD), Glucerna (for diabetics), NutriHep (for liver failure), etc.
— Elemental or monomeric = supplemental formulas that provide specific nutrients for specific GI dysfunction or malabsorption syndromes (i.e. pancreatic enzymes, low fat/high protein mixes, etc)
Discuss examples of enteral solutions and explain the differences
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Chapter 14, objective #3
— Blenderized = thinned baby food (be able to pass through tubes)
— Polymeric = can be milk-based or lactose-free; complete nutritional requirements; multiple formula options
— Elemental/monomeric = specific nutrients for specific GI dysfunction/malabsorption syndromes like pancreatic enzymes, low fat/high protein mixes
Explain the advantages and differences of the methods used to deliver enteral nutrition
_________
Chapter 14, objective #4
— Bolus = 250-400mL of solution rapidly administered q4-6/day
— Nocturnal = only @ night
— Infusion
- Intermittent drip = q3-6h over 30-60 minutes by gravity drip or infusion pump
- Continuous drip = @ slower rate over 24hr period
- Cyclic infusions
Major side effect of enteral feedings = diarrhea
NOTE: dehydration can occur if an insufficient amount of H2O is given with/or b/w feedings | Watch for aspiration pneumonia = biggest complication of enteral nutrition
DO NOT FEED PATIENT WHILE LYING DOWN OR UNCONSCIOUS
Describe the complications that may occur with use of enteral nutrition and parenteral nutrition
________
Chapter 14, objective #5
BMI is 1st step of nutrition assessment
Aseptic technique
Label enteral equipment
Elevate HOB at least 30 degrees
Rriht patient, formula, tube
Trace all lines and tubing back to patient
Why are enteral feedings preferred over parenteral feedings?
— Less risk of infection
— Maintains GI integrity
— Less costly
— Body uses it more efficiently
Common mistakes with Enteral medications + Results From Mistakes
Common mistakes:
— Drug incompatible with administration through a tube
— Failure to prepare drug properly
— Use of faulty techniques
_______________
Results in:
— Occluded feeding tube
— Reduced drug effect
— Drug toxicity
— Harm, death
Discuss the nursing interventions for patients receiving enteral nutrition and parenteral nutrition
________
Chapter 14, objective #6
Nursing Implications:
BMI is first step of nutrition assessment.
Diarrhea can be managed by decreasing the rate of the infusion or diluting the concentration.
Be sure patient is receiving “free” water.
Keep HOB elevated.
Turn off feeding pump when turning, changing sheets.
Provide meticulous oral care.
Monitor patient’s weight and vital signs.
Check gastric residual before feeding and q4-6 hours if continuous feedings…over 100 ml notify MD.
Flush tube, after meds and feedings to prevent clogging.
GI and respiratory assessments are key.
Change feeding bag daily.
Ask pharmacy to change meds to liquid formulations if possible, but always add water to reduce osmolality – this helps prevent GI upset and tube clogging.
Watch labs – renal panel (hydration status), albumin (nutritional status), white blood count (infection)
Indications + Nutrients for TPN
TPN + Total Parenteral Nutrition
Indications:
Bowel obstruction
Inflammatory bowel disease
Severe pancreatitis
Need bowel rest
Severe trauma
Severly malnourished
Nutrients:
Hyperosmolar glucose
Amino acids
Vitamins
Water & Electrolytes
Minerals
Trace elements
Lipids
TPN Complications
— Air embolism
— Pneumothorax, hemothorax
— Hyper/Hypoglycemia
— Infection
— Hypervolemia (fluid overload); hyperosmolar concentrated formula — weak hearts beware! Increasing preload + if cannot tolerate it —> HEART FAILURE
What is the prevention for an air embolism when giving TPN?
Valsalva maneuver = bearing down to temporarily increase pressure in venous system so less likely to get air in system when pulling catheter out
If unable to = hold breath
If unable to do that = pull tube out when they inhale
COVER WITH OCCLUSIVE DRESSING + APPLY WITH TEGADERM+ LEAVE WITH 24HRS TO ENSURE PUNCTURE IS HEALED
PICC line + Lines
PICC = Peripheral = inserted all the way to the R atrium from the brachial area (down the arm)
Subclavian = catheter inserted below clavicular into subclavian vein
Internal Jugular (IJ) vein = central line where line goes down to a R atrium
External Jugular (EJ) vein =
Place the gauze and pause + 5 minutes + patient needs to bear down — b/c DO NOT want air into ducted into the vascular system
Describe osmolality vs. tonicity
Discuss the different ranges b/w normal, hyperosmolar, hypo-osmolar, and iso-osmolar serum osmolality
Normal osmolality: 180-200mOsm/kg
Hyperosmolality:
Hypo-osmolality:
Iso-osmolality:
At risk for HYPOkalemia related to fluid loss
— Vomiting
— Diarrhea
— NG hook to suction
Intravenous fluids: CRYSTALLOIDS
Isotonic: D5W (isotonic then hypotonic inside body) | 0.9%NS | Lactated Ringers
Hypotonic: 0.45%NaCl
Hypertonic: D51/2NS | D5NS | D10H2O
Dextrose5 in water (D5W)
Isotonic (unless continuous or rapid)
Lactated Ringer’s
Isotonic solution
Normal saline solution (0.9% NSS)
Isotonic solution
D5 LR
Hypertonic solution
D5W and 0.45% NSS
Hypotonic solution
D10W
Hypertonic solution
Constipation Types + Interventions
— Laxatives: soft stool
— Cathartics: soft to watery stool w/ cramping
— Purgatives: for watery stool w/ cramping
Types:
— Osmotic (saline) = pull water to gut = tx of constipation; for Go-Lytely = for procedure to clean out the gut
— Stimulant (irritants) = irritates gut to relieve the constipation to stimulate defecation
— Bulk forming = safer, not irritating to gut, not habit-forming (can be used daily) to keep stool soft; can use them for diarrhea b/c act as an absorbent, when constipated, will draw water to gut to relieve
Emollient (stool softeners) = do not promote peristalsis, decreases surface tension of stool to help make stool softer
Diarrhea = acts as an absorbent
Go-Lytely = bowel prep, osmolality, finish entire bottle w/in ~3hours
Where to find your vitamins in your foods
Why would you hold the dose for patient taking Lactulose (Chronulac)? Why wouldn’t you?
— Prolific diarrhea…If cannot get off the toilet ALL day
— Never? If elevated serum ammonia levels in patient’s with Liver Diseases (e.g. fibrosis, cirrhosis) b/c high levels are toxic to the brain and can cause encephalopathy
S/Sx we see: confusion, agitation, disorientation
What are the problems with using Bisacodyl (Dulcolax), Senna (Senokot)?
Can leads to dependency where you are unable to poop without using these
FOLIC ACID therapeutic + administration + adverse effects
Therapeutic use — megaloblastic (macrocyclic) anemia, folate deficiency (EtOH), prevent neural tube defects in in developing fetus
Administration — orally (preferred), subQ, IM, IV; Check Vitamin B12 levels to confirm absence of B12 deficiency, baseline serum folate, Hgb, RBC, and reticulocyte count and monitor periodically thereafter; HCTZ should start to improve w/in 2 weeks
Adverse Rxns —
Difference b/w Docusate (Colase) + Bisacodyl (Dulcolax)
Docusate (Colase) = stool-softener
Bisacodyl (Dulcolax) = stimulant (contact) laxative
Metoclopramide (Reglan)
Miscellaneous Antiemetics
Action: suppress impulses to CTZ + increases GI transit time; have prokinetic effect (increases peristalsis) on the gut
— Used in the tx of post-op emesis, cancer chemotherapy, and radiation therapy
Metoclopramide (Reglan) Side effects
EPS; tardive dyskinesia = chewing, licking
Other prokinetics for N/V
Erythromycin (low dosages, not antibiotic dosing levels)
Renzapride (2008, a Phase III trial in USA has been completed)
Cisapride (still available under compassionate-release programs) – a serotonin active agent; Cisapride was voluntarily pulled from the market by Janssen Pharmaceutica in July 2000 (in the United States) due to the risk of rare but serious cardiac events, which in some cases led to deaths. A significant proportion of these reported cases had other known risk factors. In less than one percent of the cases, the events occurred in the absence of risk factors.
Prescriptive Antiemetics: Anticholinergics
Prescriptive Antiemetics: Anticholinergics
What are the direct triggers of the vomiting center?
Think sensory impulses
— Odors
— Smells,
— Taste
— Gastric mucosal irritation
F
What is LPR? What are its triggers? Why is this dangerous?
*When reflux moves all the way to oropharynx and throat causing laryngapharyngeal reflux (LPR) — dangerous b/c opportunity aspirate gastric content to the lungs —> aspiration pneumonia —> DEATH
What is LPR? What are its triggers? Why is this dangerous?
*When reflux moves all the way to oropharynx and throat causing laryngapharyngeal reflux (LPR) — dangerous b/c opportunity aspirate gastric content to the lungs —> aspiration pneumonia —> DEATH
Antiulcer Drugs: Prostaglandin E1 Analogs
When caring for a patient with a serum potassium of 2.8 mEq/L, what is the priority nursing intervention when giving IV replacement therapy?
A. Apply ice packs to site of IV administration
B. Maintain infusion rate no greater than 20mEq/hr
C. Administer potassium as a bolus over 10minutes
D. Teach the patient S/Sx of HYPOkalemia
Apply ice packs to site of IV administration.
Too rapid an infusion of potassium may cause cardiac arrest. Therefore, IV potassium infusion rates should not exceed 20 mEq/hr.
CORRECT
Maintain infusion rate at no greater than 20 mEq/hr.
Too rapid an infusion of potassium may cause cardiac arrest. Therefore, IV potassium infusion rates should not exceed 20 mEq/hr.
INCORRECT
Administer potassium as a bolus over 10 minutes.
Too rapid an infusion of potassium may cause cardiac arrest. Therefore, IV potassium infusion rates should not exceed 20 mEq/hr.
Teach the patient signs and symptoms of hypokalemia.
Too rapid an infusion of potassium may cause cardiac arrest. Therefore, IV potassium infusion rates should not exceed 20 mEq/hr.
During the IV administration of a hypertonic saline solution to treat a patient with severe hyponatremia, the nurse monitors for which signs and symptoms of hypernatremia?
Flushes skin and increased thirst
Mental confusion + Seizures, V/D, and Lethargy and HoTN are ALL HYPONatremia S/Sxs
A patient receiving an IV infusion of one unit of packed red blood cells suddenly develops shortness of breath, chills, and is feeling hot. What is the nurse’s priority action?
Stop the blood transfusion
The nurse is caring for a patient with renal insufficiency and thrombocytopenia. Along with platelet transfusions, the nurse would expect to administer which blood product to increase deficient clotting factors in this patient?
FFP
Albumin
Plasma protein factors
Whole blood
FFP
Fresh-frozen plasma is indicated to increase clotting factors in patients with a known deficiency. Albumin and plasma protein factors do not contain clotting factors. Although whole blood does contain the same ingredients as fresh-frozen plasma, the amount of volume that must be administered to give the patient the necessary clotting factors may be contraindicated in a patient with renal insufficiency.
While assessing the patient, the nurse notes edema of the hands and feet at +3 from third spacing. The patient is having signs and symptoms of intravascular dehydration, and the total protein laboratory result is 4.6 g/dL. The nurse anticipates the health care provider will prescribe which IV solution for this patient?
—5% albumin
—NS
—Whole blood
— Lactated ringers
5% albumin
If the total protein level falls below 5.3 g/dL, fluid shifts out of blood vessels into the tissues. When this happens, colloid replacement therapy is required to reverse this process by increasing the colloid oncotic pressure. The three most commonly used are 5% albumin, dextran 40, and hetastarch. They all have a very rapid onset of action as well as a long duration of action.
While the nurse is providing care to a patient, the health care provider prescribes an IV potassium chloride infusion. For which condition would this prescription be given?
Renal failure
Potassium replacement therapy is indicated in the treatment or prevention of potassium depletion in patients with severe renal disease, acute dehydration, untreated Addison’s disease, severe hemolytic disease, conditions involving extensive tissue breakdown (e.g., multiple trauma, severe burns), and hyperkalemia from any cause.
