STEPHANIE PEARL U.

MATILLANO,SN 1

Disturbances in Digestion 3. expulsion - relaxation of esophageal

sphincters, pyloric contraction, violent
a. Nausea and vomiting contraction of diaphragm and abdominal
b. Gastrointestinal bleeding muscles to expel gastric contents
c. Gastritis Red flags to suggest a serious cause of
d. Peptic Ulcer Disease vomiting:
Definition • Shock and volume depletion
• Nausea – unpleasant sensation often • Severe abdominal pain
localized to the abdomen that is typically • Abnormal vomit - hematemesis, coffee-
interpreted as an urge to vomit. ground appearance, bilious
• Vomiting – forceful oral expulsion of • Acute or focal neurological symptoms
gastric contents.

Retching: Rhythmic synchronized contractions

of the diaphragm, abdominal and intercostal
muscles against a closed glottis causing the
intra abdominal and decrease the intra thoracic
pressure causing the gastric contents to go up
through the esophagus.
Triggers for Vomiting
• Vomiting involves a vomiting centre seen
in medulla oblongata, the main part of Gastritis
brain with nucleus tractus solitarius (NTS) • Acute
and chemoreceptor trigger zone (CTZ). • Transient inflammation of the gastric
• When NTS and CTZ are activated, they mucosa; local irritants such as alcohol,
send impulses to the vomiting centre and aspirin, bacterial endotoxins
result in vomiting. • May be severe; usually self-limiting and
• NTS and CTZ can be activated by GI tract, heals within several days
blood vessels, through cortex by smell,
pain, sight, psychological stimuli, motion
sickness, ototoxic drugs etc…
• Vomiting centre in the brain receives
signals from vestibular apparatus, GI tract,
cerebral cortex, thalamus, and
chemoreceptor trigger zone (CTZ).
Neurotransmitters involved in vomiting are
dopaminergic receptors, histamine
receptors and 5 hydroxytryptamine
• The medicines used for nausea and
vomiting act against one of these receptors.
• There are six groups of antiemetics Chronic Gastritis
available: anticholinergics, antihistamines,
• chronic changes to the gastric mucosa
neuroleptics, D2 blockers, prokinetics and
caused by;
5 HT3 receptor antagonists.
• Helicobacter Pylori (H. Pylori)
Pharmacological targets (antiemetics) • Autoimmune disease
• Neurotransmitters involved in coordinating • Chemicals - alkaline reflux from
this response include: duodenum
• histamine
Helicobacter pylori (H. pylori) is a type of
• serotonin
bacteria that infects your stomach.
• acetylcholine and
• It can cause sores and inflammation in the
• dopamine
lining of your stomach or the upper part of
The process of vomiting involves three phases: your small intestine (the duodenum).
1. pre-ejection - prodromal nausea, • For some people, an infection can lead to
salivation, and retrograde peristalsis to stomach cancer.
force intestinal contents into the stomach Diagnosis
and lower oesophagus • Tests for H. pylori
2. retching - closure of epiglottis and • Passing a thin, flexible scope down the
elevation of soft palate throat, called an endoscopy.
• X-ray of your upper digestive system.
 STEPHANIE PEARL U. MATILLANO,SN 2

Treatment c. CT, BT, PT, APTT - monitor these times

• Antibiotics to kill H. pylori. (bcs. if these are increased/prolonged, the pt. is at
• Medicines that block acid production and risk for bleeding)
promote healing. d. Blood type - determine the blood type of the
• Medicines to reduce acid production. pt. (bcs. when the pt. is bleeding, we need to
• Medicines that neutralize stomach acid. manage it through surgery lead by the physician &
Gastrointestinal Bleeding administration of fresh whole blood)

• Massive GI bleeding can occur from Management

hematologic disorders that decrease platelet • Early identification of Hypovolemic &
levels or function such as dengue Hemorrhagic
hemorrhagic fever & thrombocytopenia. Shock (s/sx: decrease of BP, 1 pulse rate, weak &
• Lower Gi bleeding is most often caused by thready pulse, hypothermia)
hemorrhoids & colon polyps. • Hospitalization
• Vital Signs: BP & HR
• Fluids
• (isotonic solutions bcs. the pt. is losing
whole blood [administration of PNSS bolus
& PLR]

Peptic Ulcer Disease

• An ulceration in the mucosal wall of the
stomach, pylorus, duodenum, or esophagus
in portions accessible to gastric secretions
3 major causes: • Diameter of at least 0.5 cm
• Erosion may extend through the muscle
1. Peptic Ulcer Disease (PUD)
• Depth that reaches the muscularis mucosae
2. Gastritis
3. Esophageal varices
The ff. different areas:
Symptoms
• Stomach Mucosal wall (Gastric ulcer)
• Blood (vomit or stool)
• Pylorus (opening bet. stomach & duodenum)
• Black tarry stool
• Duodenum (Duodenal ulcer)
• Abdominal pain
• Esophagus (GERD/Esophageal Ulcer)
• Blood loss (Anemia)
• Fatigue
• Weakness Classifications (based on location)
• Pale skin • Gastric ulcer - occur commonly in the
• Shortness of Breath antrum, but also in the body/fundus
• Duodenal ulcer - occur in the upper portion
of the duodenum
• Esophageal ulcer - occur as a result of the
backward flow of HCl from the stomach
into the esophagus.

Classification (based on degree & duration of

mucosal involvement)
• ACUTE ULCER - short duration,
superficial erosion, and minimal
inflammation.
Diagnostic tests:
• resolves quickly when the cause is identified
a. Digital Rectal Exam (DRE) and removed
b. Endoscopy - if ruling out UGIB • CHRONIC ULCER - long duration,
c. Colonoscopy - if ruling out LGIB eroding through the muscular wall with the
formation of fibrous tissue.
Laboratory Tests • more common than acute erosions.
a. CBC - shows if the rbc level, hgb, & hot are • form usually in lesser curvature of stomach
decreased (indicatives if the pt. is losing blood) (Gastric ulcer)
b. Platelet - monitor its levels (bcs.
thrombocytopenia I the risk for bleeding) Etiology/Common causes
1. H. pylori infection (spiral shape)
 STEPHANIE PEARL U. MATILLANO,SN 3

• Most common cause mucous rich in bicarb, controls acid amounts

• Centive is the stomach acidic conditions via the parietal cells
because it secretes urcase which
• Spread from ingesting something
contaminated (fecal to oral / oral to oral).
• Predisposition to gastric carcinoma
2. Chronic NSAID use
• Increases gastric acid secretion
• Reduce the integrity of the mucosal barrier.
• They work to decrease the production of
prostaglandins (this causes us to feel pain,
inflammation, fever)
• The stomach uses prostaglandins to keep the Stomach Toxic System
stomach protected by promoting the • Hydrochloric acid via parietal cells
stomach cells to release mucus rich in • Pepsin via chief cells
bicarb, regulates acid amounts via parietal How are PEPTIC ulcers formed?
cells, and perfusion to the stomach.
3. Zollinger-Ellison Syndrome • Peptic ulcers can form when acid penetrates
• rare digestive disorder that results in too unprotected stomach mucosa.
much gastric acid • This causes histamine to be released which
• causes increased release of gastrin which signals to the parietal cells to release more
increases stomach acid production hydrochloric acid which erodes the stomach
4. Lifestyle factors/Genetics lining further.
• High alcohol intake
• Coffee Signs and Symptoms
• Psychologic distress • Mainly: Indigestion and Epigastric pain
• Smoking described as burning/dull/gnawing pain
• BUT certain foods and stress can only > Gastric ulcers (15% of PUD)
irritate ulcers/prolong healing but there is no • Food makes pain worst (pain 1-2 hours
evidence to suggest they cause them. minutes after eating)
• Report of pain dull and aching
Pathophysiology • Weight loss
• Role of the stomach: liquefies the food it • Severe: hematemesis is more common than
and release acids and enzyme such a pepsin melena.
to break down food. • Complications: hemorrhage, perforation,
• Mucosa: top layer of the mucosa that r and pyloric obstruction
mucous rich in bicarbonate that protect from • Duodenal ulcers (80% of PUD)
the stomach acid. • Pain happens when stomach empty...food
• It also contains gastric pits that contain th makes it BETTER (pain 3-4 hours after
cells, and g-cells. eating)
• Parietal cells: release hydrochloric acid • Wake in middle of night with pain
along factor • Weight normal
• Chief cells: release pepsinogen which mixes • Severe: tarry dark stool from Gi bleeding
acid and becomes PEPSIN (Melena is more common than hematemesis
• G-cells: release gastrin • Vitamin B12 deficiency
• Submucosa: made up of connective tissue, • Pernicious anemia results from a deficiency
nerves, vessels of intrinsic factor
• Muscularis externa (has 3 smooth muscle • Complications: bleeding, perforation, gastric
layers): function is to perform peristalsis outlet obstruction, and intractable disease
which pushes food down through the GI
tract Laboratory/Diagnostics
• Serosa: outer layer that has connective 1. Blood or stool test
tissue that connects to surrounding organs • Stools may be tested periodically until they
• Pylorus: opening from the stomach to the are negative for occult blood.
duodenum 2. Urea breath test
• Patient will ingest a urea tablet and if H.
Stomach Defense System: pylori is present, it will break down urea
• Bicarbonate (HCO3): coats the gastric into ammonia and carbon dioxide.
layer and protects the cells from acids • Breath samples will be analyzed for
• Prostaglandins: regulates perfusion to abnormally high carbon dioxide levels.
stomach, causes stomach cells to release • AKA Carbon 13 (13C) urea breath test
 STEPHANIE PEARL U. MATILLANO,SN 4

3. Scope of the stomach (EGD)

• Confirms the presence of an ulcer and
allows cytologic studies and biopsy to rule
out H. pylori or cancer.
4. Endoscopy.
• The preferred diagnostic procedure because
it allows direct visualization of
inflammatory changes, ulcers, and lesions.

Medications
• Antacids
• Proton Pump Inhibitors
• H2-receptor Antagonists
• Gastric mucosal protective agents
• Mucosal healing agent
• Sucralfate "Carafate"/Misoprostol "Cytotec"
- lines the stomach and adheres to the ulcer
site and protects it from acids and enzymes.
• Take on empty stomach 1 hour before eating
• Don't give at the same time as antacids or
H2 blockers (give 30-45 minutes apart).

With H. pylori infection

• Meds for H. Pylori infection that is causing
a peptic ulcer (NO ANTACIDS):
Antibiotics:
• Clarithromycin (Biaxin),
• Metronidazole (Flagyl),
• Tetracycline,
• Amoxicillin (Amoxil)
• Proton Pump Inhibitors
• H2-receptor Antagonists
• Bismuth Subsalicylates

What are Bismuth Subsalicylate ?

•Bismuth Subsalicylates "Pepto-Bismol"
•used for H. pylori infections by covering the
site of the ulcer and keeps the stomach acid
away.
• It is used with antibiotics. Dor or H2
blockers for treatment.
Brands
• Bismatrol
• Diotame
• Kaopectate