Barium-Based Gastroduodenal X-ray: Good Method for Diagnosing Lesser Curvature and Duodenal Ulcers, Less Sensitive for Superficial Ulcers or Inflammation, Now Gradually

- Pain occurs regularly after eating (1-3 hours after eating in gastric ulcers) or slowly from

3-5 hours after eating in duodenal ulcers.

- The pain recurs regularly every day at a certain time after meals, lasting 2-3 weeks if not treated; if treated, the pain only decreases or disappears when taking medication and only disappears completely after 1 week to 10 days. This point helps us distinguish it from "pseudo-ulcer" pain (less than 3 days), a variation of liver colic.

- The pain recurs periodically after 1 or more years, usually in the cold season.

- Pain is reduced when eating, drinking milk or taking antacids, increased with sour foods,

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- Pain characteristics: like twisting, rarely hot, burning like in inflammation

Barium-Based Gastroduodenal X-ray: Good Method for Diagnosing Lesser Curvature and Duodenal Ulcers, Less Sensitive for Superficial Ulcers or Inflammation, Now Gradually

stomach.

- Accompanied by belching or heartburn. Vomiting when there are complications. Constipation.

- Patients may lose weight due to decreased appetite due to pain, but some people gain weight due to eating.

or drink a lot of milk to relieve the pain.

2.1.2. Atypical form :

- Burning pain, after eating and cyclical.

- Twisting pain, after eating but irregular cycle during the year.

- Twisting pain, not much related to meals but cyclical.

- Painless form is only detected when there are complications of perforation or hemorrhage.

20-25% of cases.

- Only 30% of duodenal ulcer patients have typical pain.

2.1.3. Physical signs: in gastric ulcer are very poor, however, a comprehensive examination is necessary to find lesions of other diseases that can cause pain in the epigastric region (atypical). Usually the patient has mild anemia, insomnia, or anxiety. Sometimes the patient can pinpoint a pain point in the epigastric region.

2.2. Paraclinical

2.2.1. Contrast-enhanced gastroduodenal X-ray: a good method for diagnosing lesser curvature and duodenal ulcers, less sensitive to superficial ulcers or inflammation, now gradually being partially replaced by endoscopy.

2.2.2. Gastroduodenoscopy: is the best means to diagnose and monitor gastric and duodenal ulcers. Through endoscopy, we can biopsy or stain the mucosa for a more accurate diagnosis. Biopsy is a means to diagnose degenerative ulcers (cancer) and Helicobacter pylori infection by staining with Giemsa, Starr or doing a rapid urease test (Clo test), detecting urea released by Helicobacter pylori on biopsy tissue samples.

2.2.3. Other means: to detect Helicobacter pylori infection: diagnostic serum, gastric biopsy culture,...

3. Complications

3.1. Gastrointestinal bleeding

3.2. Perforation of the stomach and duodenum

3.3. Pyloric stenosis

3.4. Cancerization

4. Treatment principles:

4.1. Lifestyle changes: avoid factors that favor ulcers.

4.2. Use of medication

- Antacids.

- Acid-reducing drugs: H2 receptor antagonists, proton pump inhibitors.

- Medicine to protect the stomach lining and increase the resistance of the stomach lining.

- HP killer.

HEPATITIS


TARGET

1. List the causes of hepatitis.

2. Describe the clinical and paraclinical presentation of acute and chronic hepatitis.

1. Definition

Hepatitis is a condition of liver parenchyma damage, characterized by the presence of

inflammatory cells

Hepatitis lasting less than 6 months is called acute hepatitis, lasting more than 6 months is called chronic hepatitis.

2. Causes

2.1. Caused by viruses: A, B, C, D, E.

2.2. Caused by bacteria: leptospira infection, typhoid, riskettsia infection,...

2.3. Due to alcohol

2.4. Fatty liver disease

2.5. Due to drugs: high doses of acetaminophen, anti-tuberculosis drugs, birth control pills, etc.

2.6. Due to toxins

2.7. Autoimmune hepatitis

2.8. Wilson's disease

2.9. Hereditary hemochromatosis

2.10. Due to α1-antitrypsin deficiency

2.11. Due to ischemia

3. Clinical

Most patients have no obvious symptoms and are discovered incidentally during testing. About 25% of patients have typical clinical manifestations suggestive of hepatitis such as right hypochondriac pain and jaundice.

3.1. Acute hepatitis

The disease can be divided into 4 stages:

3.1.1. Incubation period

Lasts on average from several weeks to several months depending on the pathogen. Most patients have no specific symptoms.

3.1.2. Onset period

- Mild fever without chills.

- Fatigue, poor appetite, muscle pain, joint pain.

- Sometimes there is pain in the liver area, dark yellow urine.

3.1.3. Full development period

- Dark urine appears first, then jaundice and mucous membranes appear. At this time, the fever gradually decreases and then disappears completely.

- Symptoms of physical weakness (fatigue, poor appetite, nausea or vomiting, etc.).

- May itch.

- May cause bowel disorders: diarrhea or constipation.

- The liver may be enlarged and painful on examination.

- Can progress to fulminant hepatitis with symptoms of acute liver failure causing blood clotting disorders (skin and mucous membrane bleeding, gastrointestinal bleeding, etc.), impaired consciousness, gradually entering hepatic coma within 8 weeks from the onset of the disease, and possibly death. In acute liver failure, leg edema and ascites are usually very mild while blood clotting disorders and impaired consciousness are prominent.

3.1.4. Recovery period

Symptoms gradually decrease and disappear, and the patient recovers completely after 1-2 months. Some patients may have prolonged jaundice, but not more than 6 months.

3.2. Chronic hepatitis

In the early stages, there are usually no clinical symptoms of fistula. The patient may only feel slightly tired, have poor appetite, mild jaundice, etc., or have no symptoms at all. After many years, the first symptom that concerns the patient is often a manifestation of complications such as decompensated cirrhosis (leg edema, ascites, oliguria, abnormal skin and mucosal bleeding, etc.) or liver cancer (enlarged, hard, painful liver, rapid deterioration of general condition).

4. Paraclinical

4.1. Tests to diagnose hepatitis

- Quantification of liver transaminase enzymes: AST (SGOT) and ALT (SGPT).

- Lactate dehydrogenase (LDH).

- Bilirubin.

- Alkaline phosphatase (ALP).

- γ glutamyl transpeptidase (GGT).

- Protein electrophoresis.

- Blood clotting function.

- Diagnostic imaging: ultrasound, CT scan, MRI,…

- Liver biopsy.

4.2. Diagnostic tests for the cause:

Depending on different causes, for example:

- Hepatitis B: HBsAg, Anti-HBs, Anti-HBc (IgM: acute inflammation), HBeAg,

Anti-HBe, HBV DNA.

- Hepatitis C: Anti-HCV, HCV RNA.

5. Treatment principles

Depending on the specific cause of hepatitis, we have separate treatment directions.

CIRRHOSIS


TARGET

1. List the causes of cirrhosis.

2. Describe clinical and paraclinical symptoms of cirrhosis.

3. List the prognostic factors for cirrhosis according to Child-Pugh.

4. List common complications.

5. State the treatment principles.

1. Definition:

- Cirrhosis is the result of chronic and progressive liver disease, resulting in the widespread destruction of liver parenchyma cells, replaced by scar tissue and regenerative nodules that disrupt the normal structure of blood vessels and liver lobules.

- Histologically cirrhosis is defined as:

Liver parenchymal cell necrosis.

Portal fibrosis extends into the lobule.

The tumors regenerate but are non-functional.

2. Cause:

2.1. Alcohol:

Alcohol causes liver damage to varying degrees:

- Fatty liver.

- Alcoholic hepatitis.

- Cirrhosis.

2.2. Hepatitis B, C

2.3. Medicine

2.4. Iron overload

- Congenital: due to iron metabolism disorders.

- Secondary: due to diseases requiring long-term blood transfusion.

2.5. Copper overload: Wilson's disease

2.6. Biliary obstruction:

- Congenital (no extrahepatic biliary obstruction).

- Secondary (with extrahepatic biliary obstruction).

2.7 . Budd-chiari syndrome: hepatic vein obstruction.

2.8. Heart failure : chronic right heart failure cardiac cirrhosis.

2.9. Malnutrition

2.10 . Infections, parasites: liver flukes, congenital syphilis.

2.11. Spontaneous: no cause is known.

Cirrhosis can be caused by one cause or by many causes.

same impact

3. Symptoms

3.1 . Compensated cirrhosis

- This is the early stage of cirrhosis, clinical symptoms are not obvious, rarely detected, only discovered by chance because of its complications: gastrointestinal bleeding due to ruptured esophageal varices, or other diseases detected through abdominal surgery or through routine health check-ups.

- The liver is usually large, painless, firm, with sharp edges, smooth or bumpy surface,...

- Definitive diagnosis at this stage is based on liver biopsy showing cirrhosis.

3.2 . Decompensated cirrhosis

This is the late stage of cirrhosis, clinical manifestations are quite obvious with many

symptoms. There are two syndromes:

3.2.1. Portal hypertension syndrome : about 60% of cases of cirrhosis have

portal hypertension (> 20 cmH 2 O).

Clinical symptoms of portal hypertension syndrome include:

+ Dilation of portal-systemic veins:

. Subcutaneous abdominal collateral circulation.

. Esophageal varices.

. Rectal varicose veins.

+ Ascites.

+ Enlarged spleen.

3.2.2. Hepatocellular failure syndrome

The liver has a great capacity for compensation. Therefore, when cirrhosis is in the late stage and decompensated, the symptoms become obvious. The main symptoms are as follows:

- Digestive disorders: loss of appetite, indigestion, diarrhea, unusual constipation.

- Jaundice - mucous membranes

- Skin and mucous membrane bleeding.

- Dropsy.

- Swollen feet.

- Pulse, red palms.

- Endocrine disorders: Men: impotence, breast enlargement.

Female: menstrual disorders, inability to conceive.

- Neuropsychiatric disorders: memory loss, more severe disorientation of space and time, more severe coma.

3.2.3. Liver examination: decompensated cirrhosis usually has a shrunken liver, there are also cases of enlarged liver with the following characteristics: no pain, sharp edges, firm density, surface is often not smooth or can have a smooth surface depending on the cause.

3.3. Paraclinical

3.3.1. Liver function tests : disturbances

* Protein electrophoresis: decreased albumin, increased globulin (gamma globulin), A/G ratio <1.

* Prothrombin ratio: decreased, in cirrhosis often decreased < 60%. Quick time: prolonged.

Estered cholesterol

* Rate ---------------------------: decrease

Total cholesterol

* BSP discharge test (+)

* Tests for liver cell necrosis: transaminase enzymes (SGOT, SGPT) may be normal or increased.

Increased transaminase indicates progressive cirrhosis. Conversely, normal transaminase indicates stable cirrhosis.

3.3.2 . . Peritoneal fluid testing

Peritoneal fluid in cirrhosis is classified as: transudates

Based on the serum-peritoneal fluid albumin gradient (SAAG)

In cirrhosis: SAAG 1.1g/dl

3.3.3. Endoscopy: to look for signs of portal hypertension.

3.3 . 4. Ultrasound

Ultrasound contributes to diagnosis through imaging of changes in liver tissue structure, peritoneal fluid, splenomegaly, and dilated portal veins.

3.3.5. Liver biopsy

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