Quiz 1 Flashcards

1
Q

Peptic Ulcer Disease

Overview

A

Group of upper GI disorders Characterized by varying degrees of erosion of the gut wall
-Most commonly found in lesser curvature of stomach and duodenum

Complications

  • Hemorrhage
  • Perforation
  • Obstruction

Causes
-Imbalance between mucosal defensive and aggressive factors

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2
Q

Aggressive Factors

A
H.pylori
NSAIDs
Acid
Pepsin
Smoking
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3
Q

Defensive Factors

A

Mucus
bicarbonate
blood flow
Prostaglandins

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4
Q

Pathophysiology of

A

¥ Dyspepsia (upper gastric discomfort, abdominal distention, burping)
¥ GERD (reflux is present, acid coming up, burning, indigestion, cough, exacerbation of asthma)
¥ Hiatal Hernia (Stomach herniates up through the esophageal hiatus)
¥ Ulcers
Ð layers involved
Ð Gastric ulcer v. Duodenal ulcer
Ð Stress ulcer (physiological stress, surgery, trauma, burns, etc.)
¥ Zollinger-Ellison Syndrome

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5
Q

Treatment for PUD

A
  • alleviate sxs
  • promote healing
  • prevent complications
  • prevent reoccurrence
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6
Q

Classes of antiulcer Drugs

A
  • Antibiotics
  • Antisecretory agents
  • Mucosal protectants
  • Antisecretory agents that enhance mucosal defenses
  • Antacids

Actions:
-eradicate H. Pylori
reduce gastric acid
enhance mucosal defenses

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7
Q

If h. pylori is present then what??

A
Combination therapy:
-Two (or three) antibiotics
 AND One of the following:
-Proton pump inhibitor (PPI) 
-H2RA
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8
Q

Antibiotics often used

A

Clarithromycin
Ð Distortion of taste, nausea, diarrhea

Amoxicillin
Ð Best in neutral pH

Bismuth
Ð Turns tongue and stool black

Metronidazole
High resistance (WORKS LIKE ANTIBUSE- NO ALCOHOL)

Tetracycline
Stains teeth and can effect bones of children < 8 or pregnant women

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9
Q

Production of gastric acid is stimulated by 3 endogenous compounds- what are they??

A

Acetylcholine (Ach)
-Acts at muscarinic receptors

Histamine
-Acting at H2 receptors

Gastrin
-Acting at gastrin receptors

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10
Q

MOA H2 Blockers ( H2RAs)

A

When histamine is released, strong gastric acid is released and caused h2 receptors on the parietal cell to increase hydrochloric acid production

H2 blockers- BLOCK this action, thereby decreasing volume of gastric juices and decreasing H+ concentration.

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11
Q

H2 Blockers continue…

A

h2blockers end in -tidine

  • cimetidine
  • ranitidine
  • famotidine

“take me tidine with you”

D- don’t take with antacids
I- inform HCP of bleeding
N- no alcohol, smoking or NSAIDs
E- Elevate HOB

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12
Q

Cimetidine ( Tagamet)

A

( 1st one invented, used less now, more side effects, available OTC)

Pharmacokinetics:

  • PO
  • Food decreases rate of absorption, but not the extent
  • Possible prolonged benefit (take the same way everytime)
  • Crosses BBB ( keep an eye out for CNS sxs)
  • Hepatic metabolism; eliminated in urine

Therapeutic Uses:

  • Gastric and duodenal ulcers
  • GERD
  • Zollinger-Ellison Syndrome –
  • Acid-related symptoms (OTC use)

Adverse Effects:

  • Gynecomastia (antiandronergic effects)
  • CNS effects
  • Pneumonia

DRUG INTERACTIONS
-acts as hepatic inhibitor (CYP450) thus increasing the toxicity of other meds

Specifically:
warfarin
phenytoin
theophylline

Patient Teaching:
-antacids cause decreased absorption of cimetidine

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13
Q

Zollinger-Ellison Syndrome

A
  • Hyper-secretion of gastric acid
  • Development of peptic ulcers caused by a secretion of gastrin from a gastrin-producing tumor

-Cimetidine at high doses can heal HOWEVER- significant adverse effects can occur at high doses

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14
Q

Ranitidine (Zantac) H2RA

A

More potent than cimetidine (Tagamet)

Can be given PO, IM, IV
Food has no impact
-Fewer adverse effects
-No antiandrogenic effects
-Does not cross the blood-brain barrier as easily- less cns effects
-Weak inhibitor of hepatic drug-metabolizing enzymes
thus Fewer drug interactions

Therapeutic Uses

  • Gastric and duodenal ulcers
  • Prophylaxis of recurrent duodenal ulcers
  • Zollinger-Ellison Syndrome
  • GERD
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15
Q

Famotidine (Pepcid)

A
  • No antiandrogenic effects
  • Does not inhibit hepatic drug-metabolizing enzymes

Therapeutic Uses

  • Gastric and duodenal ulcers
  • GERD
  • Zollinger-Ellison Syndrome
  • Heartburn, acid indigestion, sour stomach
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16
Q

Proton Pump Inhibitors

A

End in -PRAZOLE

Inhibits H+, K+-ATPase (proton pump), the enzyme that generates gastric acid

prodrugs

decrease acid, increase PH

P = Protonix
U =“Ue” my head hurts, I am constipated
M = Maximum 16 weeks
P = Prilosec

prototype: Omeprazole

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17
Q

omeprazole (Prilosec)

A

Therapeutic Uses

  • Gastric and duodenal ulcers
  • GERD
  • Erosive esophagitis
  • Zollinger-Ellison Syndrome

Formulations:

  • extended release capsules, suspensions, powders
  • Reconstitute for IV therapy

Pharmacodynamics:

  • Causes irreversible inhibition of H, K, -ATPase (proton pump), enzymes that generate gastric acid
  • Blocks the pathway of gastric production

Nursing Considerations/Patient Education

  • Take before meals: 30min -1hr
  • Do not crush or chew

Adverse effects with short-term therapy
-N/V, Headache, diarrhea

Adverse effects with long-term therapy

  • Pneumonia (because PPIs weaken the ability of WBCs to do their job)
  • Fractures (decreased absorption of calcium d/t decreased acid)
  • Rebound acid hypersecretion (SLOWLY TAPER always, but specifically with rebound acid)
  • Hypomagnesemia
  • C.difficile (because of the change in gastric PH) – if diarrhea occurs test for C-dif (Teaching point!!!)

Drug interactions :

  • Alter gastric pH
  • Inhibit CYP2C19
  • Some HIV drugs
  • Some antifungals
  • Clopidogrel (Plavix)- antiplatelet – can cause MORE bleeding
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18
Q

What do Prostaglandins do in the stomach?

A

Prostaglandins are found in high concentration in the gastric mucosa and gastric juice. Exogenous prostaglandins inhibit acid secretion, stimulate mucus and bicarbonate secretion, alter mucosal blood flow, and provide dramatic protection against a wide variety of agents which cause acute mucosal damage.

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19
Q

Mucosal Protectants:

A

Sucralfate (Carafate)

Misoprostol (Cytotec)

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20
Q

Sucralfate (Carafate)

A

Complex: Aluminum salt & sulfated sucrose

  • Forms a non-absorbent paste that protects the ulcerated lesion (protective barrier)
  • No acid neutralizing capacity & does not decrease acid secretion

Side effects: Constipation and decrease absorption of other meds

Used to treat and prevent duodenal ulcers

Drug Interactions:
-Antacids interfere with drug effect
Decreases absorption of phenytoin, digoxin, theophylline, warfarin, fluoroquinolones

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21
Q

Misoprostol (Cytotec)

A

Synthetic prostaglandin

Pharmacotherapeutics:

  • Prevention of NSAID induced gastric ulcers in high risk patients
  • Does NOT prevent duodenal ulcers in patients on NSAIDs
  • PREGNANCY RISK!!!

Adverse effects

  • Diarrhea
  • Abdominal pain
  • Spotting & dysmenorrhea in females
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22
Q

Antacids

A

Pharmacodynamics

  • Increase gastric pH
  • Neutralize stomach acid
  • Inactivate pepsin if pH greater than 5

Commonly used salt compounds:

  • Magnesium
  • Calcium
  • Sodium
  • Aluminum

Pharmacotherapeutics
-Symptom management of PUD, GERD dyspepsia

Potency- check book
ANC- Acid neutralizing Capacity

Dosage

  • Usual schedule is 7 times/day
  • 1 and 3 hours after each meal and at bedtime
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23
Q

4 major groups of antacids

constipation/diarrhea; salt load

A
  1. Magnesium Hydroxide
  2. Aluminum Hydroxide
  3. Calcium Carbonate
  4. Sodium Bicarbonate
  5. Magnesium hydroxide (Milk of Magnesia)
    - Use with caution in patients with renal impairment
    - Causes diarrhea (stimulates the bowels)
    - Avoid use in undiagnosed abdominal pain
  6. Aluminum hydroxide (Amphogel, Alternagel)
    - Aluminum binds with PO4, so used in patients with renal failure.
    - Causes constipation
    - Has high amount of sodium, avoid in HTN, HF

Sometimes milk of mag and alternagel combined to even out bowel issues

  1. Calcium carbonate (TUMS)
    - Associated with acid rebound

Adverse effects

  • Constipation
  • Eructation & flatulence due to CO2 production
  1. Sodium Bicarbonate (not usually used for PUD or GI problems, Systemically absorbed- can make pt. alkolotic)
    - Not an agent of choice for PUD
    - Use for increasing ph (treating/decreasing acidosis in blood/urine)
    - Avoid in patient with hx of HTN
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24
Q

A –>C
M–>D

THIS IS IMPORTANT FOR TEST

A

Antacids with aluminum alone can cause constipation (A-C)

Magnesium alone can cause diarrhea (M-D)

Combination agent of Maalox to balance this.
-Suspensions have the highest acid neutralizing capacity

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25
Q

Pt Teaching and Antacids

A
  • NOT a substitute of RX drugs or continuing primary care
  • Tablets should be chewed thoroughly followed by glass of water or milk
  • Liquid preparation should be shaken before pouring
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26
Q

What is constipation?

A

Change in consistency /effort, alteration from normal pattern

can be cause by:

  • Pregnancy
  • iron supplements
  • lack of mobility
  • diet,
  • medications
  • anal, perineal, rectal surgery, etc.
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27
Q

Indications for laxative use

A

see pg.973

28
Q

Laxtaives

A

Classified by either therapeutic effect or mechanism of action

Contraindicate if undiagnosed abdominal pain/possible obstruction

29
Q

Laxatives by group and MOA

A

Class 1- Produce watery stool in 2-6 hours
Osmotic Laxatives

Class 2-Produce semifluid stool in 6-12 hours

  • Stimulant Laxatives
  • Osmotic Laxatives

Class 3- Produce soft stool in 1-3 days

  • Bulk Forming Laxatives
  • Surfactant Laxatives

4th class is miscellaneous

30
Q

Class 3 bulk forming laxatives

A

TAKE WITH at least 8 OZ of water

Pharmacodynamic action:
keep water in the stool, softening fecal mass, increasing bulk; distends colon & helps evacuation!

-Helps to produce soft, formed stools after 1-3 days

Adverse effects:

  • Esophageal obstruction
  • Intestinal obstruction or impaction
  • methylcellulose (Citrucel)
  • Also used in treatment of diarrhea, absorbs free fecal water
  • psyllium (Metamucil)

Unlabeled use: cholesterol lowering agent

**Shouldn’t be used for people with chronic constipation-cancer pts on opiods, etc. can CAUSE obstruction*******

31
Q

Surfactant Laxatives - group 3

A

Docusate -docusate sodium (Colace) or docusate calcium

Pharmacodynamic action: facilitates addition of fat & water to soften stool over a few days

  • Prophylactic agent**
  • Give with a full glass of water!

Pharmacodynamic action 2 effects
-stimulate intestinal motility
-increases water & electrolytes within intestinal lumen (decrease their absorption).
+ Results in 6-12 hours with oral preparations

What does this mean?

  • Widely used and abused
  • Direct effect on the intestinal mucosa & stimulates peristalsis (Works in the colon)

Bisacodyl (Dulcolax)

  • Oral works in 6-12 hours
  • Suppositories work in 15-60 min

Anthraquinones: Senna (Senokot)- herbal source

Patient teaching point: change in urine color

  • Oral Works in 6-12 hours
  • Give at bedtime, high abuse potential
32
Q

Stimulant Laxatives (Group I)

A
Castor Oil (also considered as Group I)
-Works in small intestine 
Can work quicker, but usually within 2-6 hours
33
Q

Osmotic laxatives

A

Onset of action depends on dosages

Pharmacodynamics:

  • poorly absorbed salts whose osmotic action draws water into the intestinal lumen…
    • Results in 6-12 hours (2-6 hours if given in large doses)

Adverse effect: substantial loss of water
-Use cautiously in renal dysfunction

Magnesium hydroxide: Milk of Magnesia (MOM)

  • Use in caution with patients with renal failure, HF
  • Increases effect of sulfonylureas, quinidine, and others

Sodium phosphate

  • Causes fluid retention
  • Caution use in patient with renal failure, HTN, & HF

Polyethylene Glycol (Miralax)

  • For chronic constipation
  • Mix with 4-8 ounces of liquid
34
Q

Lactulose ( osmotic diuretic)

A

pulls ammonia into stool – can help with hepatic diseases that cause ammonia build up- such as hepatic-encephalopathy

  • Semi-synthetic disaccharide of lactose
  • Metabolized by colonic bacteria into acids & CO2, draws water into stool (think osmotic pull)

-Acids draw ammonia into stool for treatment of hepatic encephalopathy secondary to liver disease
Pathophysiology, Lab values

35
Q

Miscellaneous Laxatives

A

Mineral Oil –orally or by enemea ( but long term oral can fuck up absorption)

Pharmacodynamic action: emollient or lubricant
-Excessive oral administration decreases absorption of fat soluble vitamins

Glycerin suppositories

  • Gentle laxative, safe in infants, children
  • Re-establish bowel patterns after laxative abuse

Newer Miscellaneous Laxatives
Lubiprostone (Amitiza) – (oral, gel-like capsule)
-Newer class (chloride channel activators)

Therapeutic uses: chronic idiopathic constipation, IBS with constipation in females, & opioid induced constipation (non-cancer)

Adverse effects: N/V, abdominal pain & distention, gas, headache, diarrhea, and chest tightness (rare)

Plecanatide (Trulance) (oral tablet)
-Indicated for chronic idiopathic constipation
-MOA : pulls fluid into the intestines
BLACK BOX WARNING FOR KIDS UNDER 6 , 6-18 limit use
-CAN CAUSE SEVERE DEHYDRATION

36
Q

Bowel Cleansing Laxatives

A

For colonoscopy

Polyethylene Glycol- Electrolyte Solutions (ex: GoLYTELY)

  • Isosmotic with body fluids. Water is not lost & electrolyte balance is preserved
  • Used primarily prior to diagnostic procedures for bowel cleansing
37
Q

Opioid Induced Constipation (OIC)

A

Methylnaltrexone (Relistor) – subq or oral

Subcutaneous & now oral route daily

-For use when laxatives have not been effective

Pharmacodynamics: Peripheral acting opioid antagonist; works on the mu-opioid receptors to block constipating effect of opioids

Adverse effects: abdominal pain, nausea, diarrhea, flatulence, flushing, tremors, etc.

-Decreased dosing needed in renal/hepatic dysfunction

38
Q

BIGGEST LAXATIVE TAKE AWAY

A

Make sure your patient does not have a bowel obstruction or other GI problem before administration
-x-ray

Do not use laxatives in the presence of undiagnosed abdominal pain!
WHY??? – because pt could have an obstruction and you can kill the patient if you give a laxative by perforating their BOWEL

39
Q

Abuse of laxatives

A

Most frequently abused over the counter drug

Misconception: daily bowel movement needed for good health

Patient’s misdiagnose a normal bowel pattern for constipation and self-medicate

Educate Patients:
-Normal bowel function

Alternatives: diet high in fiber, fluids, exercise, regular bowel habits

Do not use in presence of undiagnosed abdominal pain!!!!!!!

40
Q

Other GI MEDs

A
¥	Antiemetic Agents
¥	Drugs for Motion Sickness
¥	Antidiarrheal agents
¥	Drugs for Irritable Bowel Syndrome
¥	Drugs for Inflammatory Bowel Disease
¥	Prokinetic Agents
¥	Pancreatic Enzymes
¥	Drugs for Gallstones
¥	Anorectal Preparations
¥	Drugs for Treating Obesity
41
Q

Antiemetics

A

Why are they given:

Common Causes:

  • GI disorders
  • Infections
  • Drug Therapy
  • Pain
  • Emotions
  • Radiation
  • Motion sickness
  • Post-op
  • Pregnancy……
42
Q

Normal Patho of Vomiting

A

Vomiting Center located in the medulla

Direct stimulation

  • Signals from sensory organs (pain, odors)
  • Signals from the cerebral cortex (psychic stimulation, fear, stress, anxiety)
  • Signals from the vestibular apparatus (vagus nerve stimulus, motion sickness)

Indirect stimulation

  • Activation of the chemoreceptor trigger zone (CTZ) (located near the vomiting center)
  • Stimulated by signals from stomach and small intestine
  • Direct action of emetogenic compounds
43
Q

Receptors involved in Vomiting response

A
  • Serotonin
  • Dopamine
  • Acetylcholine
  • Histamine
  • Also Neurokinin
44
Q

Serotonin receptor (5-HT3) Antagonists

A
  • Most effective agents for N/V related to chemo/radiation/anesthesia
  • PO, IV (more effective)

Prototype: Ondansetron (Zofran)
Medicate 30 to 60 minutes prior to chemotherapy
-More effective when used with dexamethasone

Side effects: diarrhea, HA, dizziness

-Monitor for prolonged QT on EKG – special precautions in pts who have prolonged QT intervals already

OTHER Serotonin receptor antagonists

Granisetron (Kytril) : IV, PO, Transdermal
Similar to Ondanestron

Palonosetron (Aloxi) IV only

  • Longer acting (longer half life)
  • Effective for Acute & Delayed N/V

Dolasetron (Anzemet) – older drug- NOT first line

Can cause Dysrhythmias!!!*Do not give in the presence of hypomagnesemia or hypokalemia

45
Q

Substance P/Neurokinin1 Antagonists

A

MOA blocks Neurokinin 1 receptors

Therapeutic use prevention of CINV (chemo induced N/V) When combined with other antiemetics – delayed or acute N/V

A 5HT3 antagonist and a glucocorticoid (steroid)
Prototype  Aprepitant (Emend)

Think suffix – pitant

Adverse effects fatigue, hiccups, dizziness & diarrhea

Drug Interactions inhibits several liver metabolizing enzymes (Ex: decrease levels of warfarin & oral contraceptives; increase glucocorticoid levels: may see more steroid effects in pts who also receive other steroids)

46
Q

Antiemetics Dopamine Antagonists

A

Phenothiazines:

Prochlorperazine (Compazine) – Prototype
Promethazine (Phenergan)- derivative

-Giving this IV can cause serious side effects-tissue destruction
-IM is better but PO is best
Due to blockade of dopamine receptors, may cause extrapyramidal side effects (acute dystonia, akathisia) “Act like Dopey”

don’t use promethazine in children <2 years old

**caution use in children > 2 ** - due to respiratory depression

Lorazepam (Ativan), a benzodiazepine, is used in combination regimens for CINV as an adjunct therapy.

Also, helps control EPS secondary to phenothiazines

47
Q

Antiemetics: Cannabinoid

A

Dronabinol (Marinol) – synthetic form for THC

Pharmacotherapeutics:

  • N/V associated with cancer chemotherapy (CINV) *higher doses than when used as appetite stimulant
  • Appetite stimulant in patients with AIDS

Unknown Mechanism of Action (MOA)
-Thought to activate cannabinoid receptors

Adverse effects: dissociation, dysphoria

  • hypotension, prolonged QT : Use caution in clients with cardiac disease
  • Slow onset of action
  • Do not take with alcohol, CNS depressants

Abuse potential – DEA Schedule III

Nabilone: structurally different from Marinol but acts similarly for CINV effects

- risk for abuse is similar
- used less
- doesn’t stimulate appetite
48
Q

Prokinetic Agents:

A

-Increase tone and motility of GI tract, but as an effect of that can decrease N/V

Prototype agent: Metoclopramide (Reglan)

Therapeutic Uses
-Nausea & Vomiting related to gastroparesis (slow GI movement), GERD, post-operatively, chemotherapy can also help in NG pts who have a lot of residual

Mechanism of Action

  • Sensitizes tissues to the effect of acetylcholine
  • Increases peristalsis & gastric emptying – does not increase gastric juices
  • Dopamine receptor antagonist with antiemetic effects on the CTZ
  • Doesn’t require vagal stimulation to work- good for conditions where vagas nerve is poorly functioning.

N/V, diagnostic studies of small intestine: IV

Gerd- PO

Off-label use for N/V in pregnancy

Adverse effects

  • CNS depression
  • EPS - EDUCATE ON THESE SXS
  • Tardive Dyskinesia, Acute Dystonia, Parkinsonism, Akathisia
  • Diarrhea Why? Moves it tooooo fast

Nursing Administration
Traditionally, give prior to symptoms of N/V
-30 minutes prior to a meal and at bed time ( 4x per day)
-Do not use in bowel obstruction can lead to perforation

49
Q

Anti-spasmodics

A

Bentyl

Cholinergic nerve fibers are throughout the gastrointestinal tract and when stimulated cause increased motility and secretion of acids and enzymes. This stops that

Antispasmodic agents are anticholinergic agents

So what do we expect these drugs to do?? – relax smooth muscle, and decreased secretion of acids and enzymes

Which side effects would you expect?

  • decreased urination
  • blurred vision
  • dry mouth
  • constipation
50
Q

Cholinergic effects

A
PNS effects when stimulated:
SLUG BAM (cholinergic effects)
Salivation, secretions, sweat
Lacrimation
Urination
GI upset (diarrhea)
Bradycardia, BM, Bronchoconstriction, 
Abdominal cramps, Anorexia
Miosis (constriction of pupils)
51
Q

AntiCholinergic effects

A

If cholinergic agents make you “wet”, then anticholinergic agents make you ”dry”

Can’t pee urinary retention
Can’t see blurred vision
Can’t spit dry mouth
Can’t poop constipation

  • Avoid in the elderly if possible, watch closely
  • Avoid in pts with preexisting urinary retention
  • Avoid in MI or CHF pts.
52
Q

Drugs for Motion Sickness

A

Anticholinergic/Muscarinic antagonist

Scopolamine
-Most effective for motion sickness ( start prior to sickness begins)

Adverse effects: dry mouth, blurred vision, & drowsiness
Given: Po, Subcutaneous, or Transdermal

Anticholinergic/Antihistamines- not first line for motion sickness due to sedation

Dimenhydrinate (Dramamine) &
Meclizine (Antivert)- primarily used for vertigo

  • Dry mouth, blurred vision, drowsiness, and sedation
  • educated pts on the sedation; avoid things that require alertness and coordination until they know how the drugs will affect them.
53
Q

Diarrhea

A

Diarrhea (stools of excess volume and excess fluid)
-Symptom of GI disease

Causes: Infection, maldigestion, medications, inflammation, and functional disorders

SXS of a problem- figure out the problem

Complications:
-Dehydration and electrolyte imbalances

What else??: Malnutrition, vascular compromise/collapse: LOW BP - arrhythmias

Treatment

  • Diagnose & treat the cause
  • Replace lost fluids
  • Relive cramping
  • Decrease amount of stool

if it’s infectious diarrhea-we don’t want to stop it- because we want the toxic agent to get out

what do antidiarrheals do to gi Motility- SLOW IT DOWN

54
Q

Prototype for antidiarrheal

A

Prototype agent: Diphenoxylate HCl with atropine sulfate

  • Controlled substance
  • Atropine added to discourage misuse
55
Q

Diphenoxylate HCl (Lomotil)

A

Diphenoxylate HCl with atropine sulfate
Acts on Mu recptors in the gut -Slows motility

Contraindications:

  • diarrhea of infectious nature
  • obstructed jaundice
  • children under age 2

Adverse effects: related to opioids & anticholinergics (mostly in high doses)

Drug interaction: MAO inhibitors

Opioids: Controlled substance (Schedule V)
-Atropine added to discourage misuse

56
Q

Loperamide (Imodium)

A

Used in treatment of acute or chronic diarrhea (gastroenteritis)

-Also can be used to reduce effluent from an ileostomy
¥	Does not cross blood brain barrier 
¥	Little to no abuse potential 
¥	Does not contain atropine
Ð	Less adverse effects 

UPDATE ON IMODIUM:
Recommendation approved dosages in 24 hrs – (9-13 hr half life)
At 16 mg or higher (half-life as high as 41 hrs)

57
Q

Difenoxin with atropine (Motofen)

A

¥ Higher abuse potential (Schedule IV)

¥ -new drug

58
Q

Other Anti-diarrheals

A

Bismuth Subsalicylate (Pepto Bismol)

Anti-inflammatory and anti?????

  • PRN
  • Age related concern (ASA and Children)

Adverse effects :
Tongue and stool can turn black, risk for RISE syndrome in children like in aspirin

Kaolin and Pectin (Kaopectate)

  • Absorbent property (doesn’t decrease volume, just formation)
  • Sometimes, bulk-forming laxatives and antibiotics

All anti-diarrheals must be used with caution in patients with IBD

WHY?? It can cause colon dilation (mega colon)- lead to all kinds of problems including obstruction or death.

59
Q

IBD vs IBS

A

Inflammatory Bowel Disease (IBD) autoimmune

examples:

  • Ulcerative Colitis
  • Crohn’s Disease

Irritable Bowel Syndrome (IBS)

  • Unknown cause
  • Hyper-sensitive/hyper-responsive bowel
  • Pain that’s relieved with defecation
  • Drug therapy is not great with IBS
60
Q

Irritable Bowel Syndrome- D

A

Alosetron (Lotronex) (PO)

-For use in women only with severe disease (last resort)

What are the expected therapeutic effects??

  • Decreased abdominal pain
  • Decrease transition time through colon
  • More formed stool

MOA: blocks 5-HT3 receptors in lower GI tract

  • Fatal GI effects
  • Constipation obstruction perforation
  • Ischemic colitis- pain
  • Need to follow strict criteria and consent to a risk management program
  • Stop drug immediately if constipation or abdominal pain occur

When should this drug not be taken??

Lubiprostone (Amitiza) – Chloride channel activator-IBS in women greater than 18

Linaclotide (Linzess)- associated with dehydration

Other possible medications: tricyclic antidepressants, antispasmodics, anti-diarrheals, bulk forming meds, and antibiotics

61
Q

Inflammatory Bowel Disease Drug Therapies- autoimmune

A

NO curative medications

Pharmacological Treatments:

  • 5-Aminosalicylates - inflammation
  • Glucocorticoids- inflammation
  • Immunomodulators
  • Immunosuppressants

Antibiotics

  • Metronidazole (Flagyl)
  • Ciprofloxacin (Cipro)
62
Q

5-Aminosalicylates - metabolized by intestinal bacteria

A

Sulfasalazine (Azulfadine) only given PO
-Anti-inflammatory effect

Contraindication: be aware of sulfa allergies

Nursing administration: give with food & monitor CBC (can cause anemia)

Mesalamine (Asacol, Cantasa, Pentasa, Rowasa) –PO, PR, Enema
-Better tolerated than sulfasalazine

Others: Olsalazine (Dipentum) & Balsalazide (Colazal, Giazo)

63
Q

Inflammatory Bowel Disease Drug Therapies

Glucocorticoids

A

-first line for flares

Intravenous
-Hydrocortisone, Methylprednisolone, or Dexamethasone

Oral
-Prednisone, Methylprednisolone, or Dexamethasone

New :
Budesonide- newer and can be given as extended release- helpful for Crohn’s
weight gain, infection risk, altered glucose metabolism- increased insulin needs, taper when stopping

Administration and Patient Teaching
Nursing Assessments?
-Mood swings
-Nutrient metabolism
-Watch for infection – fever
64
Q

Immunosuppresants

A

Azathioprine (Imuran) & Mercaptopurine (Purixan)

Watch for infection
-For refractory disease, onset of action may take up to 6 months

Adverse effects: pancreatitis & bone marrow suppression

Monitor lab values which ones??
- WBCs

Cyclosporine – renal function, drug levels

Methotrexate - renal function

Azathioprine and Allopurinol (gout med)- can be bad

65
Q

Immunomodulators – BIG GUNS

A

Infliximab (Remicade) (IV)

  • Monoclonal antibody (TNF inhibitor)
  • For mod to severe IBD
  • IV infusion
  • Risk for hypersensitivity/infusion reaction
  • RISK FOR INFECTION- TB

Ustekinumab (Stelara) (IV, SubQ)
-Monoclonal antibody that blocks specific interleukins

66
Q

Pancreatic Enzymes

A

Used for exocrine pancreatic insufficiency (EPI)

  • People who can’t digest food normally because their pancreas does not make enough enzymes
  • Normally Enzymes are secreted into the duodenum, digest fats, carbohydrates & proteins.
  • Deficiency of pancreatic enzymes compromise digestion especially of fats.
  • If pancreatic enzyme secretion is reduced, replacement therapy is needed
  • All drugs except Viokase tablets are delayed release capsule so they dissolve in the duodenum

Deficiencies in pancreatic enzymes occur in:
¥ Cystic Fibrosis
¥ Duct Obstruction
¥ Pancreatectomy
¥ Chronic Pancreatitis (swelling of the pancreas that lasts a long time). CP may cause irreversible damage to the pancreas, including the cells that make digestive enzymes
-Fatty stools are characteristic, foul smelling - steatorrhoea

Pancrelipase (Creon)
-Helps break down food into fats, proteins, and carbohydrates that your body can use
-Enteric coated, contains 
-lipase, 
-protease, 
&amp; amylase
67
Q

Pancrelipase-

A

GIVE WITH FOOOOOOOOOOD
¥ May be from bovine or porcine source
¥ Adverse effects: abdominal discomfort, flatulence, headache, & cough.
¥ Do not crush or chew capsule; can cause irritation in the oral mucosa.
¥ How do we know if a patient is experiencing a therapeutic effect?
¥ Decrease in steatorrhoea

Gallstone- stores bile, bile is composed primarily of cholesterol, and is used primarily to reduce fats and metabolize cholesterol

  • If gallstones can be dissolved by drugs- they will be cholesterol containing stones – 20mm in size or smaller