3 P's 2- EXAM 3

Peristalsis

Wave-like muscle contractions that move GI contents from mouth to anus

Occurs in:

Lower 2/3 of the esophagus

Stomach

Small and large intestines

Stimulation of Peristalsis

Parasympathetic nervous system

Mechanoreceptors

Chemoreceptors

Parasympathetic nervous system

Vagus nerve and parasympathetic fibers
➜ Increases peristalsis

Mechanoreceptors

Activated by stretching or distension
➜ Increases peristalsis

Chemoreceptors

Respond to chyme composition (chemicals, nutrients)
➜ Increases peristalsis

What Slows Peristalsis

Opioid medications

Dehydration

Immobility

Electrolyte imbalances (especially low potassium)

Sympathetic nervous system activation (stress, pain, “fight or flight”)

Aging (slower GI motility)

Post-operative states (temporary ileus)

Clinical Examples of Altered Peristalsis

Constipation → reduced motility & slowed stool transit

Ileus → temporary absence of peristalsis

Diarrhea → increased motility reduces nutrient/fluid absorption

Obstruction → peristalsis increases early, then decreases if prolonged

Gastroesophageal Reflux Disease (GERD)

lower esophageal sphincter (LES) becomes weak or relaxes at the wrong time.

This causes

inflammation, irritation of the mucosal lining (esophagitis), and can lead to tissue damage if reflux continues.

Common factors contributing to LES dysfunction:

Obesity

Pregnancy

Hiatal hernia

Smoking

Foods that relax LES (chocolate, caffeine, alcohol, fatty/spicy foods)

Common Signs & Symptoms

Heartburn (burning sensation behind the sternum)

Regurgitation of sour or bitter fluid into throat or mouth

Dysphagia (difficulty swallowing)

Chest pain that may mimic cardiac pain

Chronic cough, hoarseness, or sore throat (especially worse at night or when lying flat)

Increased belching and bad breath (halitosis)

Complications (If GERD is not treated)

Esophagitis → inflammation that can cause ulcers

Strictures → scar tissue formation causing narrowing → worsens swallowing issues

Barrett’s esophagus

Lining of esophagus changes to a precancerous type of tissue

Increases risk for esophageal adenocarcinoma

Respiratory issues from aspiration:

Chronic cough

Asthma flare-ups

Pneumonia

Gastritis

Inflammation and redness of the gastric (stomach) lining.

Can be acute or chronic, and erosive or nonerosive

Often resolves once

underlying cause is treated

what can develop when gastritis is untreated

Peptic Ulcer Disease (PUD)

A defect in the lining of the stomach or duodenum

Acute Gastritis – Common Causes

Aspirin or NSAID use

Heavy alcohol consumption

Smoking

Certain infections

Stress-induced (↓ bicarbonate in mucosal lining)

Chronic Gastritis – Common Causes

Helicobacter pylori infection (most common)

Autoimmune disease

Crohn’s disease

Gastric surgery

Other infections (e.g., HIV)

Risks if Untreated

Gastric cancer

Peptic ulcers

Gastric bleeding

Perforation

Irritable Bowel Syndrome (IBS)

May occur due to:

Following infection

Triggered by stress

From food intolerances

Related to brain–gut interaction

Due to inflammatory processes

Clinical Manifestations of IBS

Diarrhea and/or constipation with abdominal pain (primary presentation)

Additional symptoms:

Cramping

Gas

Bloating

Fullness

Pain often worsens with

changes in bowel habits

pain improves

after a BM

Assessment Focus for IBS

GI signs and symptoms

Stress and psychosocial factors

History of food intolerances or triggers

— patient may have a history of mucus in the stool. Focused patient history information should include stool frequency, amount, and any precipitating factors

Diverticular Disease

Multiple contributing mechanisms believed:

Connective tissue abnormalities in the intestine → development of asymptomatic diverticulosis

Gut microbial changes and certain medications → may lead to acute diverticulitis and diverticular hemorrhage

Risk factors for diverticular disease:

Older age

Male sex

Smoking history

Higher BMI

Clinical Manifestations

Nonspecific GI symptoms:

Lower abdominal pain

Bloating

Diarrhea

More severe cases may include:

Fever

Bloody stools

Inflammatory Bowel Disease (IBD)

Chronic inflammation of the GI tract

Two primary types:

Crohn’s Disease (CD)

Ulcerative Colitis (UC)

Crohn’s Disease (CD)

inflammation can occur anywhere in the GI tract; affects multiple layers

Develops skip lesions — patchy inflammation with normal tissue between

Crohn’s Disease (CD) presents higher risk for

Strictures (narrowing from scarring)

Fistulas (abnormal connections between organs)

Associated systemic diseases: arthritis, kidney disease, gallstones

Ulcerative Colitis (UC)

inflammation only in innermost layer of large intestine/colon

Begins in colon

Continuous spreading of inflammation

Most common age of onset

15–30 years

ibd leads to

Chronic mucosal inflammation → edema, bleeding, ulcers, electrolyte loss

mnemonic for cd and uc

Think “C” for Crohn’s — “Cobblestone,” “Complications,” and “Can be anywhere.”

Think “U” for Ulcerative Colitis — “Ulcers in the Colon only.”

Clinical Manifestations

Weight loss

Abdominal pain & bloating

Diarrhea (often chronic)

Possible secondary symptoms:

Vomiting

Fever

Eye redness or pain

Joint pain

Skin rash

Stress does not cause IBD, but can

worsen symptoms

right upper quadrant (RUQ): houses

liver, gallbladder, right kidney (posterior abdomen), and a portion of the small intestine and large intestine

left upper quadrant (LUQ): houses

stomach, the spleen, pancreas, left kidney (posterior abdomen), another portion of the small intestine and large intestine, and a portion of the liver

right lower quadrant (RLQ): houses

appendix, part of the large intestine (cecum and ascending colon), the right ovary and fallopian tube in females, upper part of the right side of the bladder (the uterus is located below the lower quadrants in the abdominopelvic region)

left lower quadrant (LLQ): houses

lower part of the large intestine (descending colon), sigmoid colon, and the left ovary and fallopian tube in females, and the upper part of the left side of the bladder

Abdominal Assessment: Key Points

1. Inspection (Look First)

Patient supine, knees slightly bent, arms at sides (reduces muscle tension).

Look for contour: flat, rounded, scaphoid (sunken), or protuberant (bulging).

Check for symmetry and distention (gas, obesity, or fluid).

Note any masses or bulges → may indicate hernias.

Inspect skin: color, scars, striae (stretch marks).

Umbilicus should be midline and inward.

Watch for visible pulsations (may be normal in thin pts; otherwise abnormal).

Visible peristalsis may suggest intestinal obstruction

2. Auscultation (Listen Before Touching)

Use warm diaphragm of stethoscope.

Start in RLQ → move clockwise (RLQ → RUQ → LUQ → LLQ).

Listen 1 minute per quadrant; if no sounds, listen up to 5 minutes.

Normal = irregular gurgling sounds.

Hyperactive = loud/fast (e.g., gastroenteritis, obstruction).

Hypoactive = slow/faint (e.g., constipation, post-op, peritonitis).

Borborygmus = loud “stomach growling” → hyperactive.

Do NOT hear vascular bruits → if present, report (possible aneurysm or renal artery stenosis).

3. Palpation (Touch Last)

Have patient empty bladder first & bend knees to relax abdomen.

Light palpation only (about 1 cm/0.5 in deep).

Use flat fingers, not fingertips.

Move clockwise, starting in RLQ.

Palpate tender/painful areas last.

Feeling for: tenderness, guarding, rigidity, masses.

Deep palpation is performed only by advanced providers

Hernias are a common cause of

abdominal bulges

There are different types of hernias; they are named for

their location on the body

hernia types

epigastric hernia, involves the upper part of the stomach

femoral hernia, similar to the inguinal hernia but lower in the groin; most commonly found in females

incisional hernia, results from a surgical incision (healed or not fully healed)

inguinal hernia (direct or indirect), the most common type of hernia that occurs in the groin or scrotum

umbilical hernia, found at the belly button

stool chart

When taking a client’s health history, nurses should ask about:

Dietary practices: food preparation, food shopping and accessibility, healthy and unhealthy food choices, cultural or religious food preferences, meal timing, food allergies or intolerances

Nutritional supplements: vitamins, minerals, herbal or natural supplements, need for nutritional counseling

Oral health: dental history, tooth or gum disease, oral mucosal integrity

Appetite: recent changes

Preventive health: hydration habits, exercise habits, colonoscopy history

Bowel movements: changes in patterns

Weight: recent unintended weight gain or loss

Drug Therapy for Gastritis/ Peptic Ulcers- 6

•cimetidine (Tagamet) – Histamine (H2) Antagonist

•omeprazole (Prilosec) - Proton Pump Inhibitor

•sucralfate (Carafate) - Mucosal Protectant

•aluminum hydroxide (Amphojel) – Antacid

•misoprostol (Cytotec) - Prostaglandin E Analog

•Antibiotics- clarithromycin (Biaxin), amoxicillin (Amoxil), metronidazole (Flagyl), tetracycline

Histamine (H2) Antagonist – “dine”
cimetidine (Tagamet)
Action

•Blocks histamine receptors to stop gastric acid production

•Short-term tx of active duodenal and active benign gastric ulcers, erosive GERD, and hypersecretory conditions

Histamine (H2) Antagonist – “dine”
cimetidine (Tagamet)
ADR

diarrhea

headache

dizzy

confusion

agranulocytosis

gynecomastia

Histamine (H2) Antagonist – “dine”
cimetidine (Tagamet)
•Client instructions/Nursing considerations:

•Best if taken 30 minutes before breakfast

•Avoid antacids within 1 hour of administration

Histamine (H2) Antagonist – “dine”
cimetidine (Tagamet)
contraindi- •Drug Interactions

•Warfarin
Phenytoin
Theophylline
Metronidazole
Ketoconazole

Proton Pump Inhibitor (PPI) – “zole”
omeprazole (Prilosec)

Action

•Suppresses gastric acid secretion by inhibiting the H+, K+, ATPase enzyme system (proton pump)

Used for Peptic Ulcers, GERD, Erosive esophagitis, & H. pylori

Proton Pump Inhibitor (PPI) – “zole”
omeprazole (Prilosec)

ADR

diarrhea, abd pain, ha, n/v, zinc/magnes/b12 deficiency, pneumonia, osteoporosis

Proton Pump Inhibitor (PPI) – “zole”
omeprazole (Prilosec)

pt instruct

•Assess for worsening GI symptoms

•Given with or without food

•Avoid antacids within 1 hour of administration

•Monitor for respiratory infection and/or pneumonia with

Proton Pump Inhibitor (PPI) – “zole”
omeprazole (Prilosec)

contraind

•Rilpivirine

Proton Pump Inhibitor (PPI) – “zole”
omeprazole (Prilosec)

Assess for Worsening GI Symptoms

When assessing a client’s response to medications for hyperacidity and antiulcer treatment, monitor signs and symptoms of GI distress—weight, bowel habits, nausea, vomiting, abdominal pain, bloating, or belching. Follow provider instruction on dietary intake; some GI conditions require increased fiber and fluids, while others may require “bowel rest” that involves smaller meals with soft foods.

Proton Pump Inhibitor (PPI) – “zole”
omeprazole (Prilosec)

Drug Interactions

Amoxicillin
Clarithromycin
Diazepam
Proguanil
Moclobemide
Phenytoin
Warfarin

Mucosal Protectant
sucralfate (Carafate)
Action

•Coats ulcer via chemical reaction

Mucosal Protectant
sucralfate (Carafate)
ADR

constipation, generally well-tolerated

Mucosal Protectant
sucralfate (Carafate)
admin

Give on empty stomach 1 hour before meals

Avoid antacids 30 minutes before or after taking

Avoid all other other medications 2 hours before or after taking

Antacids
calcium carbonate

Action

•Antacids neutralize gastric acidity and elevate the pH of the stomach. Elevated pH also inactivates pepsin, a digestive enzyme.

Relieve heartburn, acid indigestion, and upset stomach.

Antacids
calcium carbonate

ADR

constipation, rebound hyperacidity, hypercalemia

Antacids
calcium carbonate

pt instruct

•Take with a full glass of water

•Do not administer calcium carbonate within 1-2 hours of other medicines

Antacids
calcium carbonate

contraindi

• preexisting kidney disease

Antibiotics types

•Clarithromycin (Biaxin)

•Amoxicillin (Amoxil)

•Metronidazole (Flagyl)

•Tetracycline

antibiotics used for

H. Pylori infections

Pathophysiology of Nausea & Vomiting

Nausea and vomiting are

protective reflexes controlled by the medulla oblongata in the brain.

three primary input pathways that trigger the vomiting response:

Vomiting Center (VC)

Chemoreceptor Trigger Zone (CTZ)

Vestibular Center

Vomiting Center (VC)

Located in the medulla

Directly stimulated by odor, taste, pain, and emotional stress

Coordinates the muscular response to produce vomiting

Chemoreceptor Trigger Zone (CTZ)

Located outside the blood–brain barrier

Sensitive to toxins, medications, metabolic imbalances

Activates the vomiting center when harmful substances are detected
→ This is why many anti-emetic drugs act on CTZ receptors

Vestibular Center

In the inner ear balance system

Stimulated by motion or vertigo

Uses acetylcholine and histamine pathways
→ Targeted by antihistamines for motion sickness

Motor Response

VC sends signals to: 3 places

Diaphragm – contracts forcefully

Abdominal muscles – compress stomach contents

Esophageal sphincters – relax to allow expulsion

Nausea vs. Vomiting

Nausea =

Vomiting =

Nausea = subjective sensation of needing to vomit

Vomiting = physical forceful expulsion of gastric contents

Key Takeaways

Nausea and vomiting are central-nervous-system mediated reflexes

Medications help by blocking neurotransmitters in one or more pathways (e.g., dopamine, serotonin, histamine)

Drug Therapy for Nausea- antiemetics

•ondansetron (Zofran) - Serotonin Antagonist

•Scopolamine- Antihistamine/Anticholinergic

•metoclopramide (Reglan) - Dopamine Antagonist/Prokinetic

Serotonin Antagonist – “tron”
ondansetron (Zofran)
Action

•Blocks serotonin receptors in the GI tract, the chemoreceptor trigger zone (CTZ), and the vomiting center (VC)

•Indication: Nausea

Serotonin Antagonist – “tron”
ondansetron (Zofran)
ADRs

dizzy, HA, constipation

Serotonin Antagonist – “tron”
ondansetron (Zofran)
pt instruct

admin PO or IV

30 min before chemo

1 hr pre op, and gain post op

1-2 hr prior radiation therapy

Serotonin Antagonist – “tron”
ondansetron (Zofran)
acts by

inhibiting the serotonin receptors and preventing activation of the vomiting reflex.

Serotonin Antagonist – “tron”
ondansetron (Zofran)
one of the most effective antiemetics used to treat

postoperative nausea and vomiting as well as nausea and vomiting associated with chemotherapy and radiation therapy.

Serotonin Antagonist – “tron”
ondansetron (Zofran)
what can occur if administered concurrently with other serotonin antagonists or selective serotonin reuptake inhibitors.

serotonin syndrome

rare but serious adverse effect of ondansetron is

QT prolongation that can cause an abnormal cardiac rhythm

Prokinetics
metoclopramide (Reglan)
Action

•Metoclopramide blocks dopamine and may also sensitize tissues to acetylcholine

• Promotes peristalsis

Prokinetics
metoclopramide (Reglan)
ADRs

drowsy, restless, •Movement disorders- Tardive Dyskinesia, SI/depression

Prokinetics
metoclopramide (Reglan)
pt instruct

•Report depression or abnormal muscle movements

• Can be administered orally, intramuscularly, and intravenously

Prokinetics
metoclopramide (Reglan)
contraindi

•Gastrointestinal hemorrhage, mechanical obstruction, or perforation

•Pheochromocytoma

•Seizures

Prokinetics
metoclopramide (Reglan)
Health Teaching & Health Promotion

Teach clients to immediately inform the health care provider if they experience new feelings of depression or abnormal muscle movements they cannot control

such as the following:

Lip smacking, chewing, or puckering of the mouth

Frowning or scowling

Sticking out the tongue

Blinking and moving the eyes

Shaking of the arms and legs

Antihistamine/Anticholinergic
scopolamine

Action

block ACh receptors in the vestibular center and within the brain to prevent nausea-inducing stimuli to the chemoreceptor trigger zone (CTZ) and the vomiting center (VC). They also dry GI secretions and reduce smooth muscle spasms

Antihistamine/Anticholinergic
scopolamine

indication

•Prevent motion sickness and treat nausea and vomiting

Antihistamine/Anticholinergic
scopolamine

ADRs

•sedation, anticholinergic effects

blind as bat- dilated pupils

dry as bone

red as beet- flushed skin

mad as a hatter

tcahycardic

Antihistamine/Anticholinergic
scopolamine

methods of admin

•oral, subcutaneous., or transdermal patch

Drug Therapy for Constipation

•psyllium (Metamucil) - Bulk-Forming Agent/Laxative (Fiber supplement)

•docusate sodium (Colace) - Surfactant Laxative/Stool Softener

•bisacodyl (Dulcolax) - Stimulant Laxative

•psyllium (Metamucil) - Bulk-Forming Agent/Laxative (Fiber supplement)

actions

Absorbs water from the intestines, stimulates peristalsis, adds bulk

•psyllium (Metamucil) - Bulk-Forming Agent/Laxative (Fiber supplement)

ADRs

esophageal obstruction

•psyllium (Metamucil) - Bulk-Forming Agent/Laxative (Fiber supplement)

pt instruct

Patient must take with at least 8 oz of liquid

Powder form is mixed with liquid & taken immediately

Monitor I&Os

Decreases absorption time of other PO meds

•docusate sodium (Colace) - Surfactant Laxative/Stool Softener

action

Changes surface tension of stool, increases absorption of water