group 01 case 1a.ppt

““Gosh, Mrs. Doubtfire…you look pale”Gosh, Mrs. Doubtfire…you look pale”

Created by:Created by: Group 1Group 1

Tutor : dr. Krisnha LestadiTutor : dr. Krisnha Lestadi

Members• Leader : Liliana kencana (405070084)• Secretary : Melissa Santoso (405070077)• Member : Nathania KW (405070005)

Marwin Tjandra(405070006)

Dewi Gotama(405070008)

Toni Periyanto(405070018)

Marlene A. Sutanto(405070035)

Johan Winata(405070036)

Ledy Diana (405070091)

Muliyaman(405070103)

Linda Kartanegara(405070124)

Evaline Pasak(405070157)

• Fasilitator : dr. Krisnha LestadiKrisnha Lestadi

ProblemWhile you were watching “Harry Potter and The Goblet of Fire” in TV at the

emergency department you worked for as a doctor, suddenly came a woman, who looks pale, held by her husband. At the doorway, she’s vomiting blood with a coffee ground appearance.

Its known that the patient is Mrs. Doubtfire, a 55-years old woman. Tonight, at home, she had a sudden episode of hematemesis. She also feels dizzy. She describes abdominal discomfort in the epigastric area that started 3 days prior to presentation. But actually, she has felt that symptom comes and goes for about the past 6 months. Usually, it can be relieved either by eating food, or by taking the over the counter antacid. Yesterday, she had 2 bowel movements that were dark, sticky and foul-smelling. She woke up nauseated and has since twice vomited a small amount of bright red blood.

On physical exam, you find an alert patient. Her blood pressure is 90/60 mmHg, and her pulse is 110 beats/minute. Her abdomen is flat with hypoactive bowel sounds. She denies using aspirin or NSAIDs.

Learning Objective• To learn and know about :

– Anathomy of gastrointestinal system– Physiology of gastrointestinal system– Mechanism of vomit– Differential between UGIB and LGIB– Diseases of UGIB

Dyspepsia

Dyspepsia• Ascertaining the location of the pain (upper or

lower, localized or diffuse), its character (sharp, burning, cramping), and its relationship to meals will often provide clues into the most important diagnostic considerations.

Gastrointestinal Bleeding• Hematemesis is the vomiting of blood, which may be

obviously red or have an appearance similar to coffee grounds.

• Occasionally hemoptysis or vomiting of swallowed blood from epistaxis can be confused with hematemesis

• Melena is the passage of black, tarry stools. • Hematochezia is the passage of fresh blood per anus,

usually in or with stools.

Bleeding diagnosedBleeding diagnosed• X-rays or other imaging tests (abdominal CT scan,

abdominal MRI)• Endoscopy• Capsule endoscopy• Other procedures

– Angiography•is a technique that uses dye to highlight blood vessels

allows the dye to leak out of the blood vessel, which identifies the site of bleeding.

– Radionuclide scanning • is a non-invasive screening technique used for locating

sites of acute bleeding, especially in the lower GI tract.

Abdominal/bowel sound• Abdominal sounds (bowel sounds) are made by the

movement of the intestines as they push food through.

• Bowel sounds can echo throughout the abdomen much like the sounds heard from water-pipes.

• The majority of bowel sounds are harmless and simply indicate that the gastrointestinal tract is working.

• A doctor can evaluate abdominal sounds by listening to the abdomen with a stethoscope.

Abdominal/bowel sound• Reduced (hypoactive) bowel sounds include a reduction in the

loudness, tone, or regularity of the sounds. They indicate a slowing of intestinal activity.

• Hypoactive bowel sounds are normal during sleep, for a short time after the use of certain medications and after abdominal surgery.

• Decreased or absent bowel sounds often indicate constipation.

• Hyperactive bowel sounds reflect an increase in intestinal activity. This can sometimes occur with diarrhea and after eating.

Vomiting• Vomiting is abnormal emptying of stomach and upper part of

intestine via esophagus through mouth.• Causes:

1. Irritation in GIT2. Mechanical stimulation of pharynx3. Pregnancy4. Alcohol5. Stimulation of labyrinth of ear eg sea sickeness,

mountain sickeness6. Acute GI infection7. Metabolic disorders8.Increase Intracranial Pressure

Emesis mechanismEmesis mechanism

Emesis mechanismEmesis mechanism

Anatomy and Physiology

Physiology - Digestive System• The functions of the digestive system are:

– Ingestion - eating food– Digestion - breakdown of the food– Absorption - extraction of nutrients from the food– Defecation - removal of waste products

• The digestive system is a group of organs that breakdown the chemical components of food, with digestive juices, into micromolecul nutrients which can be absorbed to generate energy for the body

The bucal cavity (mouth) and salivary glands• Food enters the mouth and is chewed by the teeth,

turned over and mixed with saliva by the tongue.• Mouth: the salivary glands. Saliva produced by these

glands contains an enzyme that begins to digest the starch from food into smaller molecules. ptyalin enzyme

The Stomach• It is the widest part of the alimentary canal and acts as

a reservoir for the food where it may remain for between 2 and 6 hours.

• Here the food is churned over and mixed with various hormones, enzymes including pepsinogen which begins the digestion of protein, hydrochloric acid, and other chemicals

• The stomach has an average capacity of 1 liter, varies in shape, and is capable of considerable distension.

• At regular intervals a circular muscle at the lower end of the stomach, the pylorus opens allowing small amounts of food, now known as chyme to enter the small intestine.

Duodenum

Small Intestine• The small intestine measures about 7m in an average

adult and consists of the duodenum, jejunum, and ileum.

• Both the bile and pancreatic ducts open into the duodenum together.

• The small intestine, because of its structure, provides a vast lining through which further absorption takes place.

The Large Intestine• The large intestine averages about 1.5m long and

comprises the caecum, appendix, colon, and rectum. • Here most of the water and electrolytes is absorbed,

much of which was not ingested, but secreted by digestive glands further up the digestive tract.

• The colon is divided into the ascending, transverse and descending colons, before reaching the anal canal where the indigestible foods are expelled from the body.

Chase

Table 282-1. Overview of Approach to Patients with Common Gastrointestinal Disorders  

Site of Disorder Common Symptoms Possible PhysicalSigns

Potential Procedures orLaboratory Studies

Esophagus DysphagiaOdynophagiaHeartburn, chest painHematemesis/melena

EsophagoscopyBarium swallowManometryBernstein test

Stomach Nausea and vomitingEpigastric painHematemesis/melena

DistentionTendernessSuccussion splashMass

GastroscopyUpper GI x-ray seriesNasogastric aspirationGastric emptying

Small Intestine

Duodenum Epigastric PainNausea/vomitingHematemesis

TendernessAltered bowel soundsDistentionMass

DuodenoscopySmall bowel follow-through, enteroclysisKidney-ureter-bladder x-ray seriesD-Xylose absorption tests

Jejunum PainDiarrhea

Altered bowel soundsDistentionMass

CTStool cultures, stool examination for ova and parasitesSmall bowel biopsy

Gastrointestinal Bleeding

Esophagitis

Esophagitis Reflux esophagitis

– Often found in conjunction with sliding hiatal hernia.– Etiology:

• AGENTS (alcohol, chocolate, fatty foods, cigarette, drugs)

• Certain conditions (pregnancy, estrogen therapy, etc)• Gastric fluid (acid, pepsin) harmful for esophageal

mucosa– Phatogenesis

Agents that decrease the pressure of the lower esophageal sphincter frequent & long transient reflux inflamation necrosis mucose-submucose

Esophagitis Reflux esophagitis

– Clinical manifestations• Dysphagia• Heartburn• Hematemesis• Regurgitation of a sour brash• Melena

– Complication: Barrett esophagus

Barrett esophagus– Is a result of chronic gastroesophageal reflux– The distal squamous mucosa is replaced by metaplastic

columnar epithelium response of prolonged injury– Phatogenesis: still unclear

- Inflamation & ulceration ++ ingrowth of pluripotent stem cell differentiated into a columnar epithelium ---- more resistant to acid peptic injury.

– Clinical features:- Secondary complications of local ulcerations with

bleeding and stricture --- adenocarcinoma

Esophagitis

Varices Esophageal

Causes • Causes of portal hypertension usually are classified as

prehepatic, intrahepatic, and posthepatic.1. Prehepatic

– Splenic vein thrombosis– Portal vein thrombosis– Extrinsic compression of the portal vein

2. Posthepatic– Budd-Chiari syndrome– Thrombosis of the inferior vena cava– Constrictive pericarditis– Venoocclusive disease of the liver

3. Intrahepatic– Congenital hepatic fibrosis– Idiopathic portal hypertension– Sclerosing cholangitis– Schistosomiasis– Primary biliary cirrhosis– Alcoholic cirrhosis– Hepatitis B virus–related and hepatitis C virus–

related cirrhosis– Alpha-1 antitrypsin deficiency– Chronic active hepatitis

Causes

• Obstruction of the portal venous system at any level leads to increased portal pressure.

• An elevated portal venous pressure (>10 mm Hg) distends the veins proximal to the site of the block and increases capillary pressure in organs drained by the obstructed veins.

• The anastomoses connecting the portal and systemic circulation may enlarge to allow blood to bypass the obstruction and pass directly into the systemic circulation.

PATHOPHYSIOLOGY

• Studies have demonstrated the role of endothelin-1 (ET-1) and nitric oxide (NO) in the pathogenesis of portal hypertension and esophageal varices.

• ET-1 is a powerful vasoconstrictor synthesized by sinusoidal endothelial cells that has been implicated in the increased hepatic vascular resistance of cirrhosis and in the development of liver fibrosis.

• NO is a vasodilator substance that is synthesized by sinusoidal endothelial cells.

• In the cirrhotic liver, the production of NO is decreased, and endothelial nitric oxide synthase (eNOS) activity and nitrite production by sinusoidal endothelial cells are reduced.

PATHOPHYSIOLOGY

Gastritis

What is Gastritis?

• An inflammation, irritation or erosion of the stomach lining. Can be of acute or a chronic complaint.

• Acute gastritis often due to chemical injury (alcohol/drugs)

• Chronic gastritis: H. Pylori infection, chemical, autoimmune.

Etiology • Bile reflux Drugs

– NSAIDs, such as aspirin, ibuprofen, and naproxen – Cocaine – Iron – Colchicine, when at toxic levels, as in patients with failing

renal or hepatic function – Kayexalate – Chemotherapeutic agents, such as mitomycin C, 5-fluoro-2-

deoxyuridine, and floxuridine• Potent alcoholic beverages, such as whisky, vodka, and gin • Bacterial infections

– H pylori (most frequent) – H heilmanii (rare) – Streptococci (rare)

Etiology • Fungal infections

– Candidiasis – Histoplasmosis – Phycomycosis

• Parasitic infection (eg, anisakidosis) • Acute stress (shock) • Radiation • Allergy and food poisoning• Spicy food • Smoking• Viral infections (eg, CMV)

Acute Gastritis

• Acute gastritis can be broken down into 2 categories: – erosive (eg, superficial erosions, deep erosions,

hemorrhagic erosions) – nonerosive (generally caused by Helicobacter

pylori).

Erosive Gastritis• Acute erosive gastritis can result from the

exposure to a variety of agents or factors. This is referred to as reactive gastritis.

• These agents/factors include nonsteroidal anti-inflammatory medications (NSAIDs), alcohol, cocaine, stress, radiation, bile reflux, and ischemia.

• This results from oral or systemic administration of these agents either in therapeutic doses or in supratherapeutic doses.

Chronic Gastritis• Autoimmune• Bacterial (H. Pylori)• Chemical (NSAIDs)• Chronic noninfectious granulomatous gastritis• Lymphocytic gastritis• Eosinophilic gastritis• Ischemic gastritis• Radiation gastritis

PEPTIC ULCER DISEASE

Definition • Peptic ulcers are defects in the gastric or duodenal

mucosa that extend through the muscularis mucosa • Peptic ulcer disease (PUD) is one of the most common

diseases affecting the gastrointestinal (GI) tract. • It causes inflammatory injuries in the gastric or

duodenal mucosa, with extension beyond the submucosa into the muscularis mucosa.

Epidemiology • The incidence of DUs declined steadily from

1960 to 1980 and has remained stable since then.

• Gastric Ulcers GUs tend to occur later in life than duodenal lesions, with a peak incidence reported in the sixth decade.

• More than half of GUs occur in males

Etiology • H. pylori infection• NSAIDs• Cigarette smoking• Genetic predisposition • blood group O• Psychological stress

• The majority of GUs can be attributed to either H. pylori or NSAID-induced mucosal damage.

• The majority of DUs can be attributed to H. pylori

Predominant cause

Campylobacter pyloridis• It is S-shaped (~0.5 ´ 3 um in size) and contains

multiple sheathed flagella.• Its ability to colonize the gastric mucosa and

produce mucosal injury.• a gram-negative microaerophilic• This rate of colonization increases with age,

with about 50% of individuals age 50 being infected.

Figure 1: Helicobacter pylori invading epithelial cells.

Campylobacter pyloridis• Transmission of H. pylori occurs from person to

person, following an oral-oral or fecal-oral route.

•

PATHOPHYSIOLOGY H. pylori

PATHOPHYSIOLOGY NSAIDs

PATHOPHYSIOLOGY NSAIDs

CLINICAL FEATURES• Epigastric pain can be present in both DU and GU.• Pain pattern in DU occurs 90 min to 3 h after a meal and is

frequently relieved by antacids or food.• Pain that awakes the patient from sleep (between midnight

and 3 A.M.) is the most discriminating symptom, with two-thirds of DU patients describing this complaint.

• GU discomfort may actually be precipitated by food.• Nausea and weight loss occur more commonly in GU

patients.• Hematemesis

• Other symptoms are :– losing weight– not feeling like eating– having pain while eating– feeling sick to your stomach– vomiting

CLINICAL FEATURES

Related Complications• Gastrointestinal Bleeding• Perforation• Gastric Outlet Obstruction

Treatment

GASTRIC ADENOCARCINOMA

Epidemiology• Gastric cancer incidence has decreased worldwide but

remains high in Japan, China, Chile, and Ireland.• The risk of gastric cancer is greater among lower

socioeconomic classes.

Etiology

PATHOPHYSIOLOGY• Gastric carcinomas spread by direct extension through

the gastric wall to the perigastric tissues, occasionally adhering to adjacent organs such as the pancreas, colon, or liver.

• The disease also spreads via lymphatics or by seeding of peritoneal surfaces.

• The liver is the most common site for hematogenous spread of tumor.

Clinical Features• upper abdominal discomfort• Anorexia• slight nausea and vomiting• Weight loss• Dysphagia (caused by lesions of the cardia)• iron-deficiency anemia• occult blood in the stool

TREATMENT• Gastrectomy

subtotal gastrectomy is the treatment of choice for patients with distal carcinomas, total or near-total gastrectomies are required for more proximal tumors.

• chemotherapy combined with radiation therapy has been shown to reduce the recurrence rate and prolong survival

Conclusion• Mrs. Doubtfire probably having UGIB disease

based on the symptoms that she had• The diseases of UGIB are:

– Varices Esophagus– Gastritis – Peptic Ulcers (DU and GU)– Adenocarsinoma Gaster

Suggestion • Mrs. Doubtfire needs to have an endoscopy to

make sure what illness that she has • Take a meal in a small portion, but frequently• Give education to patients and other people

Summary 1. Contran, Kumar, Collins. Robbins Pathologic Basis of Disease. 6th edition.

Saunders company2. Rubin, Ravael. Rubin’s Phatology clinicopathologic foundation of

Medicine. 5th edition. Philadelphia3. Buku Ajar Ilmu Penyakit Dalam, edisi 3, jil. 1, Balai Penerbit FKUI: Jakarta,

2001.4. Litien,scott C. Mayo Clinic Family Heath Book. 5th edition. 2009. Jakarta :

Gramedia.5. http://digestive.niddk.nih.gov/ddiseases/pubs/cvs/index.htm6. http://www.nlm.nih.gov/medlineplus/ency/article/003118.htm7. http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1411788&blob

type=pdf