liver cirrhosis-hematemsis-peptic ulcer lecture

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الرحمن الله الرحمن بسم الله بسمالرحيمالرحيم

الثالثة الفرقة الثالثة اسنان الفرقة اسنان

Liver CirrhosisLiver CirrhosisHaematemesisHaematemesis

Peptic ulcer diseasePeptic ulcer disease

DysphagiaDysphagia

By Serag Esmat, MDBy Serag Esmat, MD

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Liver CirrhosisLiver CirrhosisDefinition

Liver CirrhosisLiver Cirrhosis is a is a Diffuse liver Diffuse liver disease characterized by disease characterized by degeneration, fibrosis, degeneration, fibrosis, regeneration nodules, and loss of regeneration nodules, and loss of architecturearchitecture

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Classification:Classification:

1.1.Post-hepatitis cirrhosis:Post-hepatitis cirrhosis:

Follows any chronic hepatitis, as:Follows any chronic hepatitis, as:• Hepatitis Virus C, B, or D on top of B.Hepatitis Virus C, B, or D on top of B.• Autoimmune hepatitis.Autoimmune hepatitis.• Drug induced hepatitisDrug induced hepatitis

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2.2. Alcoholic cirrhosis. Alcoholic cirrhosis.

3.3. Cardiac cirrhosis. Cardiac cirrhosis.

4.4. Biliary cirrhosis. Biliary cirrhosis.

5.5. Haemochromatosis. Haemochromatosis.

6.6. Wilson’s disease. Wilson’s disease.

Hepatic schistosomiasis is a mere fibrosis Hepatic schistosomiasis is a mere fibrosis of the liver and not cirrhosis, as there is no of the liver and not cirrhosis, as there is no degeneration, regeneration nodules or loss degeneration, regeneration nodules or loss of architecture.of architecture.

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7. Other possible causes:7. Other possible causes:

•Non alcoholic steatohepatitis (NASH)Non alcoholic steatohepatitis (NASH)•Toxins: methotrexate, isoniazid and Toxins: methotrexate, isoniazid and methyldopa.methyldopa.•Cryptogenic (Idiopathic) cirrhosis.Cryptogenic (Idiopathic) cirrhosis.

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Clinical PresentationsClinical Presentations

A.A. Latent Cirrhosis (Compensated)Latent Cirrhosis (Compensated)

Early in the disease there is no Early in the disease there is no impairment of liver functions and the impairment of liver functions and the patient is discovered accidentally patient is discovered accidentally when an enlarged liver and may be when an enlarged liver and may be an enlarged spleen are found during an enlarged spleen are found during examination of the patient for a non-examination of the patient for a non-related condition or during imaging.related condition or during imaging.

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B. Manifest Cirrhosis (Decompensated):B. Manifest Cirrhosis (Decompensated):Late in the disease there will be Late in the disease there will be complications of liver cirrhosis:complications of liver cirrhosis:1- Features of hepatocellular failure.1- Features of hepatocellular failure.2- Hepatic Encephalopathy2- Hepatic Encephalopathy3. Features of portal hypertension.3. Features of portal hypertension.4. Ascites4. Ascites

5. Hepatocellular carcinoma (HCC) may 5. Hepatocellular carcinoma (HCC) may occur.occur.

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Child- Pugh ClassificationChild- Pugh Classification

AABBCC

BilirubinBilirubin< 2< 22-32-3> 3> 3

AlbuminAlbumin> 3.5> 3.53 – 3.53 – 3.5< 3< 3

AscitesAscitesNoneNoneEasily Easily controlledcontrolled

Poorly Poorly controlledcontrolled

NeurologicalNeurological

DisorderDisorder

NoneNoneMinimalMinimalHepaticHepatic

PrecomaPrecoma

NutritionNutritionExcellentExcellentGoodGoodPoorPoor

WastingWasting

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INVESTIGATIONS:INVESTIGATIONS:

1- Ultrasonography :1- Ultrasonography :

Is helpful for the diagnoses cirrhosis, Is helpful for the diagnoses cirrhosis, portal hyper tension & HCC.portal hyper tension & HCC.

2. liver function tests: 2. liver function tests: PT,PC, albumin& PT,PC, albumin& bilirubin.bilirubin.

3. Investigations for portal hypertension:3. Investigations for portal hypertension:

Upper endoscopy for detection of Upper endoscopy for detection of oesophageal or gastric varices.oesophageal or gastric varices.

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4. Liver biopsy: 4. Liver biopsy:

diagnoses cirrhosis & its etiology.diagnoses cirrhosis & its etiology.

5. Specific investigations for the cause 5. Specific investigations for the cause of cirrhosis.of cirrhosis.

6. Alpha fetoprotein for early detection 6. Alpha fetoprotein for early detection of HCC.of HCC.

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IV- Skin ManifestationsIV- Skin Manifestations::

1. Palmar erythema:1. Palmar erythema:

This is erythema opposite the heads of This is erythema opposite the heads of metacarpal bones, thenar & hypothenar metacarpal bones, thenar & hypothenar eminences, with central palmar pallor.eminences, with central palmar pallor.

2. Spider naevi:2. Spider naevi:

Each spider naevus is a dilated arteriole Each spider naevus is a dilated arteriole with radiating capillaries. with radiating capillaries.

Spider naevi occur in the face, neck, U.L. & Spider naevi occur in the face, neck, U.L. & upper part of the chest.upper part of the chest.

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V- Ascites due to :V- Ascites due to :

1- Hypoalbuminaemia1- Hypoalbuminaemia

2- Portal hypertension2- Portal hypertension

3- Salt & Water retention3- Salt & Water retention

4- Development of spontaneous bacterial 4- Development of spontaneous bacterial peritonitis, malignant ascites or peritonitis, malignant ascites or tuberculous peritonitistuberculous peritonitis

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Other causes of ascites:Other causes of ascites:

1- Congestive heart failure1- Congestive heart failure

2- Nephrotic syndrome2- Nephrotic syndrome

3- Tuberculosis3- Tuberculosis

4- Malignancy4- Malignancy

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VI- Endocrinal ChangesVI- Endocrinal Changes::The cause of these changes is not yet The cause of these changes is not yet definite, but increased oestrogen, decreased definite, but increased oestrogen, decreased production of testosterone are the most production of testosterone are the most accepted possibilityaccepted possibilityA. Features in males:A. Features in males: Gynaecomastia, Female distribution of Gynaecomastia, Female distribution of suprapubic hair, Decreased libido, suprapubic hair, Decreased libido, impotence & testicular atrophy.impotence & testicular atrophy.B. Features in females:B. Features in females: Amenorrhea, sterility & Decreased libido.Amenorrhea, sterility & Decreased libido.

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VIII- Haematological Manifestations:VIII- Haematological Manifestations:

A. Bleeding tendencyA. Bleeding tendency: : Due toDue to

1. Hypoprothrombinaemia & 1. Hypoprothrombinaemia & hypofibrinogenaemia.hypofibrinogenaemia.

2. Diminished factors, V, VII, IX, X.2. Diminished factors, V, VII, IX, X.

3. Thrombocytopenia due to 3. Thrombocytopenia due to hypersplenism.hypersplenism.

4. Thrombocytasthenia 4. Thrombocytasthenia

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B. Anaemia:B. Anaemia: 1. Microcytic hypochromic anaemia:1. Microcytic hypochromic anaemia:Due to repeated haemorrhages, Due to repeated haemorrhages, causing iron deficiency.causing iron deficiency.2. Normocytic normochromic anaemia:2. Normocytic normochromic anaemia:Due to Acute haemorrhage, B.M. Due to Acute haemorrhage, B.M. depression or Hypersplenism.depression or Hypersplenism.3. Macrocytic hyperchromic anaemia:3. Macrocytic hyperchromic anaemia:Due to deficient storage of Vitamin Due to deficient storage of Vitamin B12.B12.

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VIII- Hapatic Encephalopathy:VIII- Hapatic Encephalopathy:

It is a neuropsychiatric syndrome that It is a neuropsychiatric syndrome that may complicate severe liver disease .may complicate severe liver disease .

Pathogenesis:Pathogenesis:

A. The bacteria in the color through A. The bacteria in the color through their action on proteins will liberate their action on proteins will liberate some toxic substances which will not some toxic substances which will not be detoxicated by the liver because of be detoxicated by the liver because of its failure and because of presence of its failure and because of presence of porto-systemic shunts. porto-systemic shunts.

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These toxic substances on reaching the These toxic substances on reaching the brain will cause encephalopathy. brain will cause encephalopathy.

The possible toxic substances are:The possible toxic substances are:

1. Ammonia:1. Ammonia:

It is the main toxic substance which It is the main toxic substance which interferences with Kreb’s cycle leading interferences with Kreb’s cycle leading to diminished energy production needed to diminished energy production needed for the brain cells.for the brain cells.

2.Gamma aminobutyric acid (GABA) & 2.Gamma aminobutyric acid (GABA) & Benzodiazepines:Benzodiazepines:

inhibits cortical functionsinhibits cortical functions

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3. Others : 3. Others : serotonin, false neuro serotonin, false neuro transmitterstransmitters

B. Alkalosis & hypokalemia, if present B. Alkalosis & hypokalemia, if present facilitate passage of toxins into the brain.facilitate passage of toxins into the brain.

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Precipitating Factors:Precipitating Factors:

1- Ingestion of excess proteins.1- Ingestion of excess proteins.

2- Infection e.g. spontaneous bacterial 2- Infection e.g. spontaneous bacterial peritonitis.peritonitis.

3- G.I.T. bleeding: This increases toxic 3- G.I.T. bleeding: This increases toxic production due to action of bacteria on production due to action of bacteria on haemoglobin & it decreases hepatic haemoglobin & it decreases hepatic blood flow.blood flow.

4- Transfusion of stored blood, rich in 4- Transfusion of stored blood, rich in ammonia.ammonia.

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5- Severe vomiting, diarrhoea, or 5- Severe vomiting, diarrhoea, or constipation.constipation.

6- Diuretics & morphia.6- Diuretics & morphia.

7- Aspiration of ascites: 7- Aspiration of ascites:

This leads to electrolyte disturbance.This leads to electrolyte disturbance.

8- Operation: impairs hepatic function.8- Operation: impairs hepatic function.

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Clinical Picture: Clinical Picture:

Passes through 2 stages:Passes through 2 stages:

1. Pre-Coma:1. Pre-Coma:-Hypersomnia & inverted sleep rhythm.Hypersomnia & inverted sleep rhythm.

-Micturition & defaecation in unsuitable Micturition & defaecation in unsuitable places.places.

- Childishness, phasic excitation & - Childishness, phasic excitation & depression.depression.

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- Apathy with slow response to - Apathy with slow response to questions.questions.

- Disturbed orientation for time, place & - Disturbed orientation for time, place & persons.persons.

- - Flapping Tremors:Flapping Tremors:

These are rapid flexion & extension These are rapid flexion & extension movements at the wrist & movements at the wrist & metacarpophalangeal joints in the metacarpophalangeal joints in the extended hands.extended hands.

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2- Coma:2- Coma:

Irritable coma with features of liver Irritable coma with features of liver failure.failure.

IX- Hepato-Renal Syndrome:IX- Hepato-Renal Syndrome:

It is acute renal failure with normal It is acute renal failure with normal renal histology occurring in patients renal histology occurring in patients with chronic liver diseasewith chronic liver disease

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TREATMENT OF LIVER FAILURE:TREATMENT OF LIVER FAILURE:

I. Treatment of the cause I. Treatment of the cause if possible.if possible.

II. Treatment of ascites II. Treatment of ascites

Provided that the features of liver failure Provided that the features of liver failure are minimal & there is no evidence of are minimal & there is no evidence of encephalopathy. Otherwise treatment of encephalopathy. Otherwise treatment of as will precipitate encephalopathy in these as will precipitate encephalopathy in these patients.patients.

III.Treatment of Encephalopathy:III.Treatment of Encephalopathy:

Avoid precipitating factors.Avoid precipitating factors.

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Diet:Diet:• Stop protein intake then gradually Stop protein intake then gradually increase the intake by 10gm protein increase the intake by 10gm protein every 3 days (if there is no every 3 days (if there is no encephalopathy) till you reach 40-encephalopathy) till you reach 40-60gm/day.60gm/day.• Avoid proteins of animal origin.Avoid proteins of animal origin.

• Excess carbohydrates will prevent Excess carbohydrates will prevent protein breakdown.protein breakdown.

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3. Colonic lavage:3. Colonic lavage:

Multiple enemas will wash the intestinal Multiple enemas will wash the intestinal contents and so prevent formation of contents and so prevent formation of toxic substances by the effect of toxic substances by the effect of bacteria on proteins. It is better to add bacteria on proteins. It is better to add lactulose to the enemaslactulose to the enemas

4. Lactulose :4. Lactulose :

It is a non absorbable synthetic It is a non absorbable synthetic disaccharide which is metabolized by disaccharide which is metabolized by intestinal bacteria leading to:intestinal bacteria leading to:

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i. Laxative effect, which will wash colonic i. Laxative effect, which will wash colonic contents.contents.ii. Production of acids, which will change ii. Production of acids, which will change pH of colon, so will change the bacterial pH of colon, so will change the bacterial flora to a non toxic producing one.flora to a non toxic producing one.5. Antimicrobials5. Antimicrobials-NeomycinNeomycin will prevent action of bacteria on will prevent action of bacteria on proteins. proteins. -MetronidazoleMetronidazole can be used instead of can be used instead of neomycinneomycin

6. L.Ornithine L-Aspartate (Hepamerz):6. L.Ornithine L-Aspartate (Hepamerz):

It decreases blood ammonia. It decreases blood ammonia.

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7- Artificial Biological Liver7- Artificial Biological Liver

8- Hepatic Transplantation:8- Hepatic Transplantation:

This is the only successful curative This is the only successful curative solution for liver failure till now. solution for liver failure till now. There is some success in the field There is some success in the field of hepatocytes transplantationof hepatocytes transplantation

الثالثة الفرقة الثالثة اسنان الفرقة اسنان

HaematemesisHaematemesis


DysphagiaDysphagia

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HaematemsisHaematemsis

Vomiting of blood & is associated with Vomiting of blood & is associated with Melena due to digestion of part of the Melena due to digestion of part of the bloodblood

Commonest causes:Commonest causes:Oesophageal varicesOesophageal varicesOesophageal erosions & ulcersOesophageal erosions & ulcersOesophageal cancerOesophageal cancer Acute gastritis & acute gastric ulcersAcute gastritis & acute gastric ulcers

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Chronic peptic ulcer gastric or Chronic peptic ulcer gastric or duodenalduodenal

Markedly inflamed hiatus herniaMarkedly inflamed hiatus hernia

Stomach cancerStomach cancer

Angiodysplasia of the stomachAngiodysplasia of the stomach

Haemorrhagic blood disordersHaemorrhagic blood disorders

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Reflux oesophagitisReflux oesophagitis

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Cancer OesophagusCancer Oesophagus

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Acute gastritis & acute gastric ulcersAcute gastritis & acute gastric ulcers

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Gastric ulcer with blood clot on topGastric ulcer with blood clot on top

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Bleeding duodenal ulcerBleeding duodenal ulcer

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Cancer stomachCancer stomach

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Angiodysplasia of the stomachAngiodysplasia of the stomach


EpidemiologyEpidemiology

Duodenal ulcers (Dus) are very common Duodenal ulcers (Dus) are very common and are two to three times more common and are two to three times more common than gastric ulcers (GUs) than gastric ulcers (GUs)

PathologyPathologyGastric ulcers are found in any part of Gastric ulcers are found in any part of the stomach, but are most commonly the stomach, but are most commonly seen on the lesser curve.seen on the lesser curve.

Most duodenal ulcers are found in the Most duodenal ulcers are found in the duodenal cap.duodenal cap. The surrounding mucosa appears The surrounding mucosa appears inflamed, haemorrhagic or friable. inflamed, haemorrhagic or friable.

EtiologyEtiology

1- H. 1- H. Pylori infection : Associated with Pylori infection : Associated with 90% of 90% of DUs and 70-90% of gastric ulcers DUs and 70-90% of gastric ulcers (GUs) (GUs)

2- Drugs : Mainly NSAIDs2- Drugs : Mainly NSAIDs

3- Hypersecretory syndromes : 3- Hypersecretory syndromes :

Zollinger-Ellison syndromeZollinger-Ellison syndrome

4- Radiation therapy and chemotherapy4- Radiation therapy and chemotherapy

5- Other factors :5- Other factors :

•SmokingSmoking•Family history of ulcersFamily history of ulcers•CorticosteroidsCorticosteroids•StressStress

HELICOBACTER PYLORI INFECTIONHELICOBACTER PYLORI INFECTIONH.pylori is a spiral shaped Gram negative H.pylori is a spiral shaped Gram negative urease producing bacteriumurease producing bacterium EpidemiologyEpidemiologyThe exact mode of transmission is The exact mode of transmission is unclear, but most theories suggests unclear, but most theories suggests person to person spread, either oral-oral person to person spread, either oral-oral or faeco-oralor faeco-oral..The prevalence of H. pylori is high in The prevalence of H. pylori is high in developing countries (80-90% of the developing countries (80-90% of the population)population)

HELICOBACTER PYLORI INFECTIONHELICOBACTER PYLORI INFECTIONIs the major cause of:Is the major cause of:

11 - -Duodenal ulcerDuodenal ulcer22 - -Gastric ulcerGastric ulcer

33 - -H.pylori gastritisH.pylori gastritis

Diagnosis of H. pylori infectionDiagnosis of H. pylori infection

Non-invasive methodsNon-invasive methods

11 - -Urea breath testUrea breath test

It is expensive, but very sensitive (97%) It is expensive, but very sensitive (97%) and specific (96%)and specific (96%) . .

The breath test is also used to The breath test is also used to demonstrate eradication of the organism demonstrate eradication of the organism following treatmentfollowing treatment..

22 - -Serological testsSerological tests

To detect IgG antibodies are reasonably To detect IgG antibodies are reasonably sensitive (90%) and specificsensitive (90%) and specific . .

They are used in the diagnosis and in They are used in the diagnosis and in studiesstudies..

IgG titres may take up to 1 year to fall by IgG titres may take up to 1 year to fall by 50% after eradication therapy and 50% after eradication therapy and therefore are not useful for confirming therefore are not useful for confirming eradication or the presence of a currenteradication or the presence of a currentinfectioninfection . .

33 - -Stool testStool test..

H. pylori H. pylori antigen in stools is widely antigen in stools is widely available. The overall sensitivity is 96% available. The overall sensitivity is 96% with a specificity of 97%with a specificity of 97%..

It is useful in the diagnosis of It is useful in the diagnosis of H. pylori H. pylori infection and for monitoring efficacy of infection and for monitoring efficacy of eradication therapyeradication therapy . .

Invasive methods (endoscopy)Invasive methods (endoscopy)

Rapid urease testRapid urease test

Gastric biopsies are added to a urea Gastric biopsies are added to a urea solution containing phenol red. If solution containing phenol red. If H. pylori H. pylori are present, the urease enzyme splits the are present, the urease enzyme splits the urea to release ammonia which raises urea to release ammonia which raises the pH of the solution and causes a rapid the pH of the solution and causes a rapid color changecolor change..

CultureCulture Biopsies obtained can be cultured on a Biopsies obtained can be cultured on a special medium and sensitivities to special medium and sensitivities to antibiotics can be detected.antibiotics can be detected.

HistologyHistology. . H. pylori H. pylori can be detected histologically oncan be detected histologically onroutine (Giemsa) stained sections of routine (Giemsa) stained sections of gastric mucosal endoscopic biopses.gastric mucosal endoscopic biopses.

Clinical features of peptic ulcersClinical features of peptic ulcers

The characteristic feature is epigastric The characteristic feature is epigastric painpain.. The relationship of the pain to food is The relationship of the pain to food is variable and on the whole not helpful in variable and on the whole not helpful in the diagnosis.the diagnosis.Nausea may accompany the pain. Nausea may accompany the pain. vomiting is infrequent but often relieves vomiting is infrequent but often relieves the pain.the pain.

Heartburn occurs owing to acid Heartburn occurs owing to acid regurgitation.regurgitation.

Anorexia and weight loss may occur, Anorexia and weight loss may occur, particularly with gastric ulcers.particularly with gastric ulcers.

Back pain suggests a penetrating Back pain suggests a penetrating posterior duodenal ulcer.posterior duodenal ulcer.

Patients can present for the first time Patients can present for the first time with either:with either:

Haematemesis or melaena or Haematemesis or melaena or perforation.perforation.

Clinical ExaminationClinical Examination

This is usually unhelpful; Epigastric This is usually unhelpful; Epigastric tenderness is quite common in non-ulcer tenderness is quite common in non-ulcer dyspepsia.dyspepsia.

InvestigationsInvestigationsUpper endoscopy is the main tool of Upper endoscopy is the main tool of diagnosis.diagnosis.Barium meal is much less sensitive Barium meal is much less sensitive diagnostic method and rarely used now diagnostic method and rarely used now for diagnosis of an ulcer.for diagnosis of an ulcer.

ComplicationsComplicationsHaemorrhageHaemorrhagePerforationPerforationPyloric stenosis or obstructionPyloric stenosis or obstructionTreatmentTreatmentThe most recommended medical The most recommended medical treatment regimen istreatment regimen is: :

Eradication therapy for H.pylori followed Eradication therapy for H.pylori followed by Proton-pump inhibitorsby Proton-pump inhibitors (PPIs) 4 (PPIs) 4 weeks for DU and 6 weeks for GUweeks for DU and 6 weeks for GU

Eradication therapyEradication therapyCurrent recommendations are that all Current recommendations are that all patients with duodenal and gastric ulcers patients with duodenal and gastric ulcers should have should have H. pylori H. pylori eradication therapy.eradication therapy.

Most eradication therapies are successful in Most eradication therapies are successful in approxi mately 90% of patients.approxi mately 90% of patients.

Currently favored regimens are triple Currently favored regimens are triple therapy with a PPI along with two therapy with a PPI along with two antibiotics for 7-10 daysantibiotics for 7-10 days..

For exampleFor example::

PPI as omeprazole 20 mg + PPI as omeprazole 20 mg + metronidazole 400 mg andmetronidazole 400 mg andclarithromycin 500 mg (all twice daily)clarithromycin 500 mg (all twice daily)

PPI as omeprazole 20 mg + PPI as omeprazole 20 mg + clarithromycin 500 mg and Amoxicillin clarithromycin 500 mg and Amoxicillin 1gm (all twice daily)1gm (all twice daily)

Treatment optionsTreatment options

11--Proton-pump inhibitors (PPIs)Proton-pump inhibitors (PPIs)::

OmeprazoleOmeprazoleLansoprazoleLansoprazoleRabeprazoleRabeprazolePantoprazolePantoprazoleEsomeprazoleEsomeprazole

22 - -H2 receptor antagonistsH2 receptor antagonists::

CimetidineCimetidineRanitidineRanitidineFamotidineFamotidineNizatidineNizatidine

33 - -Sucralfate 1gm 4 times /daySucralfate 1gm 4 times /day

44 - -Prostaglandin analogue :(Misoprostol)Prostaglandin analogue :(Misoprostol)

The prostaglandin E1 derivative The prostaglandin E1 derivative misoprostol is the only agent of this class misoprostol is the only agent of this class approved by the FDA for clinical use in approved by the FDA for clinical use in the prevention of NSAID-induced the prevention of NSAID-induced gastroduodenal mucosal injurygastroduodenal mucosal injury It enhances the mucosal defense and It enhances the mucosal defense and repair.repair.

5- Antacids:5- Antacids:

Simple antacids as Simple antacids as

magnesium trisilicate and aluminium magnesium trisilicate and aluminium hydroxide are readily available and are hydroxide are readily available and are often used initially by patients.often used initially by patients.

Antacids and SucralfateAntacids and Sucralfate are much less are much less commonly used now as a treatment commonly used now as a treatment option for peptic ulceroption for peptic ulcer

Surgical treatmentSurgical treatment

Surgery in peptic ulceration disease is used Surgery in peptic ulceration disease is used only for the complications:only for the complications:

•Recurrent uncontrolled haemorrhage.Recurrent uncontrolled haemorrhage.

•Perforation or obstruction.Perforation or obstruction.

DysphagiaDysphagiaDifficulty in swallowing which may be due Difficulty in swallowing which may be due to a local lesion or part of generalized to a local lesion or part of generalized disease.disease.Causes:Causes:•Diseases of the mouth and tongue.Diseases of the mouth and tongue.

•Oesophageal motility disorders as Oesophageal motility disorders as Achalasia and diffuse oesophageal Achalasia and diffuse oesophageal spasm.spasm.

• External pressure on the oesophagus External pressure on the oesophagus as: Enalrged mediastanal LN, Goitre as: Enalrged mediastanal LN, Goitre or Enalrged left atriumor Enalrged left atrium

• Foreign bodyForeign body• Strictures:Strictures:

Benign strictures: Corrosives, ulcersBenign strictures: Corrosives, ulcers

Malignant stricture: Cancer oesophagusMalignant stricture: Cancer oesophagus• Oesophageal webs and rings Oesophageal webs and rings

Diagnosis:Diagnosis:

•Upper endoscopy Upper endoscopy •Barium swallowBarium swallow•Oesophageal manometry (for motility Oesophageal manometry (for motility disorders)disorders)

Self assessmentSelf assessmentHelcobacter pylori is a common Helcobacter pylori is a common cause for:cause for:

a) Gastritis a) Gastritis

b) Duodenal ulcerb) Duodenal ulcer

c) Gastric ulcerc) Gastric ulcer

d) All of the aboved) All of the above

The chief symptom of peptic ulcer is :The chief symptom of peptic ulcer is :

a) Epigastric paina) Epigastric pain

b) Vomitingb) Vomiting

c) Heart burnc) Heart burn

d) All of the aboved) All of the above

The most recommended medical The most recommended medical treatment regimen for duodenal ulcer treatment regimen for duodenal ulcer

isis:: a)Eradication therapy for H.pylori a)Eradication therapy for H.pylori followed by antacids for 4 weeks followed by antacids for 4 weeks b)Proton-pump inhibitors (PPIs) for 4 b)Proton-pump inhibitors (PPIs) for 4 weeks weeks c) Eradication therapy for H.pylori c) Eradication therapy for H.pylori followed by Proton-pump inhibitors followed by Proton-pump inhibitors (PPIs) for 4 weeks.(PPIs) for 4 weeks.d) H2 blockers for 6 weeksd) H2 blockers for 6 weeks

Comment on the following sentences by Comment on the following sentences by (TRUE) or (FALSE):(TRUE) or (FALSE):

1- Gastric ulcers are two to three times 1- Gastric ulcers are two to three times more common than duodenal ulcers .more common than duodenal ulcers .

2- H. Pylori infection is associated with 90% 2- H. Pylori infection is associated with 90% of duodenal ulcers and 70-90% of gastric of duodenal ulcers and 70-90% of gastric ulcers.ulcers.

3- Barium meal is a very sensitive diagnostic 3- Barium meal is a very sensitive diagnostic method for diagnosis of peptic ulcers.method for diagnosis of peptic ulcers.

4- Upper endoscopy is the main tool of 4- Upper endoscopy is the main tool of diagnosis of duodenal ulcers.diagnosis of duodenal ulcers.

5- Eradication therapy for H.pylori is highly 5- Eradication therapy for H.pylori is highly recommended in the treatment of duodenal recommended in the treatment of duodenal ulcer.ulcer.

6- Oesophageal motility disorders as 6- Oesophageal motility disorders as Achalasia may cause dysphagia.Achalasia may cause dysphagia.

7- The chief symptom of peptic ulcer is 7- The chief symptom of peptic ulcer is recurrent vomiting.recurrent vomiting.

8- The chief symptom of peptic ulcer is 8- The chief symptom of peptic ulcer is epigastric painepigastric pain

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THANK YOUTHANK YOU

liver cirrhosis-hematemsis-peptic ulcer lecture

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