+ Did you take any medicine before vomiting blood?
+ Fresh blood or dark bruise?
+ Is there food in the blood?
+ Are there any warning signs before vomiting blood?
+ How much blood is vomited and how long does it take to vomit blood?
If the patient has bloody stools, ask:
+ When did the patient start having fresh blood in his stool?
+ Characteristics of blood in stool: fresh blood or blood clots?
+ Blood comes out before the stool, with the stool, or after the stool?
+ Is the blood mixed with mucus or pus?
+ Black blood or fresh blood?
+ Quantity much or little?
Before vomiting blood, having bloody stools, did you do any heavy work?
Any concerns?
Have a fever?
Do you have stomach pain when vomiting or defecating?
Do you have stomach or duodenal disease?
Medications used and previous illnesses
2.1.2. Observe the patient, pay attention;
Mental state
General condition
Properties of vomit and stool
Pain relief posture
2.1.3. Patient examination
Take vital signs: note pulse and blood pressure.
Abdominal examination: pay attention to the epigastric region.
Rectal examination if indicated.
Consider testing if available.
2.1.4. Assessment through collection of other data
Through records and test results
Use of drugs and how to use drugs
Through the patient's family
2.2. Nursing diagnosis
Some possible nursing diagnoses in gastrointestinal bleeding include:
1. Dizziness due to blood loss.
2. Bleeding due to gastric and duodenal ulcers.
3. Anxiety due to acute and severe illness.
4. Bleeding due to rectal polyp ulceration.
2.3. Care planning
- Let the patient fast and lie still for the first 24 hours.
- Reassure the patient.
- Carry out medical orders promptly and accurately.
- Monitor and detect severe blood loss.
- Instruct patient's family on how to monitor and care for them.
2.4. Implement the care plan
2.4.1. Basic care
- The patient must lie in bed, head not supported by a pillow. The room must be quiet.
- Encourage the patient to feel secure and avoid anxiety.
- Give the patient oxygen if the bleeding is severe and there is shock.
- Insert catheter and maintain vascular infusion with isotonic saline.
- Place a gastroduodenal tube to aspirate all blood clots in the stomach, and monitor bleeding through the tube.
- Defecate in bed to monitor stool characteristics.
- When the vomiting stops, give the patient a light meal: milk, porridge, soup...
2.4.2. Execute medical orders
Administer medications to patients as ordered promptly.
Take blood tests as ordered, take X-rays.
Assist in placing central venous pressure catheters when indicated.
2.4.3. Patient monitoring
- Take pulse, temperature, blood pressure, breathing rate every 30 minutes. If there is any abnormality, the doctor will handle it promptly.
- Monitor the patient's mental status.
- Measure urine output to detect symptoms of oliguria or anuria.
- Monitor vomiting and nature of vomitus.
- Monitor the patient's abdominal pain and stool characteristics (color, frequency, amount of blood and stool).
- Monitor medication use.
- Monitor general condition to detect early signs of blood loss (pale skin and mucous membranes, rapid pulse, low blood pressure, dizziness, etc.)
2.4.4. Health education
- Prevent and avoid illness by working, resting properly, and avoiding worry.
- Don't drink too much alcohol or coffee.
- Use anti-inflammatory drugs appropriately and correctly.
- Early detection of digestive tract diseases and thorough treatment.
- Early detection of signs of gastrointestinal bleeding and active treatment.
2.5. Evaluation of the care process
For patients with gastrointestinal bleeding, good care is considered when:
- Patients can rest quietly and receive treatment with peace of mind.
- Bleeding is reduced or absent.
- Vital signs are stable.
- Increased urine output.
- Patients are fed and given a reasonable diet.
- The cause of bleeding is resolved.
- Carry out doctor's orders promptly, completely and accurately.
- Upon discharge from the hospital, patients are instructed on how to detect gastrointestinal bleeding as early as possible and the possible causes of gastrointestinal bleeding.
SELF-ASSESSMENT
1. Describe the causes of upper gastrointestinal bleeding
2. Mark X on the correct answer.
2.1. Care for patients with upper gastrointestinal bleeding:
A. Let the patient lie with head elevated.
B. Take pulse, temperature, blood pressure every 2 hours.
C. Do not give the patient anything to eat or drink even after the bleeding has stopped.
D. Measure urine output to detect oliguria or anuria.
2.2. Common causes in patients with upper gastrointestinal bleeding
A. Colorectal polyps with bleeding inflammation.
B. Stomach cancer.
C. Colon and rectal cancer.
D. Gastric ulcer.
E. Ulcerative bleeding in the rectum and colon.
3. Choose the best answer
3.1. The earliest signs of change when following a patient with gastrointestinal bleeding:
a. Pulse b. Blood pressure c. Breathing rate d. Skin color e. Urine
3.2. When assessing a patient with hemorrhagic shock in case of gastrointestinal bleeding, which of the following symptoms is incorrect:
a. Pale, sweaty skin b. Cold hands and feet c. Rapid breathing
d. Fast, weak, difficult-to-detect pulse e. High blood pressure
CARE OF PATIENTS WITH GASTRIC AND DUODENAL ULCERS
TARGET
1. Describe the causes, pathogenesis and symptoms of gastric and duodenal ulcers.
2. Detect complications of gastric and duodenal ulcers.
3. Can use some drugs to treat gastric and duodenal ulcers.
4. Plan care for patients with gastric and duodenal ulcers.
1. SOME KEY POINTS ABOUT PATHOLOGY
1.1. General
Peptic ulcer is a fairly common disease in our country as well as in other countries in the world. Men are more likely to get the disease than women. The age of onset is from 20 to 40 years old, however, the disease can occur at any age.
The incidence of the disease has been increasing over time and varies by country or region. Duodenal ulcers are on the rise, and the current ratio of duodenal ulcers to gastric ulcers is 2:1, with the majority occurring in men. Approximately 10-15% of the world's population is affected by the disease.
stomach ulcer
duodenal thickening
In you and in
Australia is 5.29.9%,
in America
is 510%. Currently there are
About 10% of the world's population suffers from peptic ulcers.
1.2. Causes and pathogenesis
1.2.1. Causes
The imbalance between ulcerogenic and protective factors of the gastric mucosa is the most widely accepted hypothesis today. Ulcers occur due to increased concentration or activity of pepsin acid or due to decreased normal resistance of the gastric and duodenal mucosa. A damaged mucosa is often unable to secrete enough mucus to act as a protective barrier against hydrochloric acid. Recently, the role of Helicobacter Pylori, a gram-negative spiral bacterium, in the pathogenesis of gastric and duodenal ulcers has been increasingly demonstrated. Some of the following causes are common.
1.2.1.1. Genetics
Duodenal ulcers are believed to be hereditary, with high frequency in some families. Ulcers
Duodenal agenesis occurs more frequently in monozygotic than in dizygotic twins. Among
Known genetic factors are:
- Blood type O.
- Increased pepsinogen I secretion combined with increased HCL acid secretion.
- Hypergastrinemia due to gastrinoma in multiple endocrine neoplasia group I.
- Hypergastrinemia due to G-cell hypertrophy in the antrum.
- Other genetic diseases associated with ulcers: mastocytosis, tremor syndrome, trauma and ulcers.
1.2.1.2. Psychological factors
Ulcers also commonly occur in people with a lot of emotional trauma, or during periods of severe mental stress such as during war.
1.2.1.3. Movement disorders
It is the emptying of the stomach and reflux of the duodenum. In duodenal ulcers, the emptying of the stomach is too rapid, causing an increase in the amount of acid reaching the duodenum. Conversely, in gastric ulcers, the emptying of the stomach is too slow, causing acid stagnation in the stomach. In duodenal reflux, bile salts and lecithin cause inflammation of the antrum and then cause ulcers.
1.2.1.4. Environmental factors
Real factor.
The nature of the food, seasoning, time of meal or speed of eating do not seem to play a role in the etiology of ulcers. However, it cannot be ruled out that the geographical distribution of ulcers is due to dietary habits. Indeed, saliva contains many growth factors, the epidermis plays a role in nourishing the mucosa and reducing acid secretion. Milk does not have a protective effect on proteins, caffeine and calcium are acid-producing substances, and high doses of alcohol cause damage to the gastric mucosa.
Cigarette
Peptic ulcers are common in smokers, and smoking also causes new ulcers and slows healing or causes resistance to treatment. The mechanism of tobacco-induced ulcers is still not completely understood, possibly due to vagal stimulation, mucosal destruction due to gastric duodenal reflux or due to reduced bicarbonate secretion.
Medicine
+ Aspirin: causes ulcers and bleeding, more common in the stomach than the duodenum, due to local and systemic effects.
Locally: in the acidic environment of the stomach, aspirin does not dissociate and dissolve in fat, so it penetrates the mucus layer and corrodes the mucosa, causing ulcers.
Systemic: Aspirin inhibits prostaglandins, which hinders mucosal cell renewal and inhibits mucus production in the stomach and duodenum.
+ Nonsteroidal anti-inflammatory group: causes similar ulcers and bleeding but does not cause local corrosion.
like
aspirin
+ Corticoid: does not cause ulcers directly because it only
to prevent
synthetic
prostaglandin, so it only causes old ulcers to flare up again, or in people with existing ulcer-causing factors.
1.2.1.5. Helicobacter pylori (HP)
Discovered by Marshall and Warren in 1983, HP causes chronic gastritis, especially in the antrum (type B) and duodenitis due to gastric mucosal metaplasia into the small intestine, which then causes ulcers. 90% of gastric ulcers, and 95% of duodenal ulcers
Duodenum has HP presence in ulcer.
1.2.2. Pathogenesis
1.2.2.1. Pepsin
Secreted as a precursor pepsinogen, under the influence of hydrochloric acid, it turns into active pepsin when pH < 3.5, destroying mucus and collagen. There are 2 types of pepsinogen I and II, detected by immunoelectrophoresis. The amount of pepsinogen I is closely related to the amount of antral glandular cells and is increased in 2/3 of duodenal ulcer patients and 1/3 of gastric ulcer patients.
1.2.2.2. Back-dispersion of H+ ions
The ulcer process is initiated by increased secretion of HCl, due to excessive or overactive parietal cells, thus increasing basal or post-stimulated gastric juice, back-dispersion and entry of H+ ions damage the gastric wall and cause ulcers. Therefore, neutralizing H+ ions has greatly reduced the incidence of ulcers.
The risk of ulceration increases with increased acid secretion. However, acid alone does not explain all ulcers because in 1/3 of ulcers, gastric acid secretion is not increased.
1.2.2.3. Protective factors of the gastric mucosa
- Mucous barrier: to resist the attack of H+ ions, the main factor is the bicarbonate-rich mucus layer made of glycoprotein containing non-polar phospholipids, located on the surface of this gel layer with elastic mucus properties. When pepsin cleaves the peptide chain releasing glycoprotein subunits, they lose this elastic mucus property. H+ ions penetrate the mucus layer, but they are neutralized by bicarbonate. But when pH < 1.7, it exceeds its neutralizing capacity and H+ ions reach the gastric mucosa and cause ulcers.
- Gastric mucosa: secretes glycoprotein, lipid and bicarbonate, they have the ability to eliminate the entry of H+ ions into the cytoplasm in 2 ways: one is to neutralize by bicarbonate, two is to push H+ ions into the interstitium thanks to the H+K+ ATPase pump located at the base.
- Lamina Propria: has a regulatory function. Oxygen and bicarbonate are supplied directly to the submucosal layer by highly perforated capillaries, whose cells are very sensitive to metabolic acidosis. A sufficient amount of bicarbonate is supplied to the mucosal cells to prevent acidification in the stomach wall caused by H+ ions penetrating this mucosal barrier.
1.2.2.4. H. P. bacteria
Causes damage to the gastric and duodenal mucosa and produces ammonia that acidifies the local environment, creating ulcers. HP produces urease enzyme that damages the gastric mucosa. It also produces surface proteins that are chemotactic (+) with neutrophils and monocytes. It also secretes platelet-activating factor, pro-inflammatory substances, superoxide, interleukin 1, which are substances that cause inflammation and necrosis.
kind
HP also produces protease and phospholipase enzymes that destroy
matter
gastric mucosa
1.3. Clinical symptoms
The disease can present typically or atypically.
1.3.1. Typical form: The disease is characterized by ulcer syndrome.
Abdominal pain is the main symptom, manifestation;
+ Pain in the epigastric region, burning pain, cramping, twisting pain, or maybe just dull pain.
+ Pain is cyclical in nature during the day, season and year.
+ Pain in rhythm with meals: pain when hungry, pain is relieved after eating (duodenal ulcer) or pain right after eating (gastric ulcer). Pain lasts for 1, 2 or 3 weeks and then goes away on its own, often without any treatment.
The pain-free period lasts for weeks or months, sometimes even a year. Usually the following year, during the cold season, or when there is some favorable factor, a new pain cycle like the one above appears again.
Over time, the ulcer pain gradually loses its cyclical nature, the patient has many pain episodes during the year, then it becomes continuous pain.
In addition to pain, patients may also experience belching, heartburn or acid reflux.
Table 1. Comparison of some properties between duodenal ulcers and gastric ulcers
type
Duodenal ulcer | Stomach ulcer | |
Pain nature | Pain when hungry and at night Late pain after eating (4-5 hours) Eat to relieve pain | Early pain after eating (1 hour) Eating does not relieve pain, sometimes it makes it worse. |
Gastric juice test | Increased acidity | Decreased or normal acidity |
Gastrointestinal bleeding | Black stools are more common than vomiting blood. | Vomiting blood is more common than passing black stools. |
Cancerization | Not happening | There is a risk of cancer |
Evolution | Easy to relapse after recovery | If after 2 to 3 courses of active, proper medical treatment the ulcer does not heal, surgery should be performed. |
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