PANEL MODUL BLOODY DEFECATION (BAB CAIR BERDARAH)

MEDICAL FACULTY

MUSLIM UNIVERSITY OF INDONESIA

2017

Tutor :

dr. Rachmat Faisal Syamsu, M.Kes

Innal Hamda 11020150019

Amirah Jihan Afry 11020150042

Rindang Cahyani Abas 11020150101

Gita Refina 11020150130

Ftiri Lestari 11020150142

Haerati Hairil 11020150144

Lilis Lestari 11020150152

Andi Mulia Sudirman 11020150154

A man aged 55 years, come to emergency unit with blood diarrhea

complaints. Patients also complain of heartburn. A history of using

medications for arthritic pain in the knee during the last 6 months.

A history of suffering from the DM and irregular treatment.

HEARTBURN

• Is retrosternal burning sensation in the area, which arise suddenly and spread up to the neck ; perhaps with reflux liquid into the mouth is often caused by gastroesophageal reflux

DM

• Is a chronic metabolic disease or disorders withmultiple etiologies characterized by high blood sugarlevels accompanied by impired metabolism ofcarbohydrates, lipids, and proteins as a result ofinsufficiency of insulin function

( Kamus Kedokteran Dorland. Edisi 28. Hal 501)

( Kamus Kedokteran Dorland. Edisi 28. Hal 309)

A man aged 55 years

Blood diarrhea complaints

Patients also complain of heartburn

A history of using

medications for arthritic pain in

the knee

Suffering from the DM and

irregular treatment

QUADRANT & REGIO

OESOPHAGUS

GASTER

DUODENUM

PANCREAS

Digestive system Motility Secretion Digestion Absorpsi

Mouth and saliva Chew Saliva

Amilase

Mukus

Lisozim

Digestion of

carbohydrates begins

The food was not;

some drugs such as

nitroglycerin

Pharynx and

esophagus

Swallow Flawless - -

Stomach Relaxation

receptive;

peristalsis

Gastric juice

• HCl

• Pepsin mucus

• Intrinsic factor

Carbohydrate

digestion continues in

the corpus of the

stomach; protein

digestion begins in

the gastric antrum

The food was not;

some fat soluble

ingredients, such as

alcohol and aspirin

Pancreatic exocrine There is no Pancreatic digestive enzymes

•Trypsin, chymotrypsin,

karboksipeptidase

•Amylase

•Lipase

NaHCO3 liquid secretion of

the pancreas

These pancreatic

enzymes complete the

digestion in the

duodenum lumen

-

• Heartburn is caused by a back-up of stomch acid into the esophagus. When

stomach acid comes into contact with the walls of the esophagus it often

causes a “burning” feeling.

• Certain foods and lifestyle choices can increase the back up of stomach

acid, making symptoms worse.

• The most common cause is due to the use of NSAIDs in the treatment of

artritisreumatoid and osteoartris. The use of NSAIDs (eg, aspirin,

piroxicam, ibuprofen, meloxicam, celecoxib, trisalicylate etc.), have a

direct effect on the gastric mucosa and causes the formation of ulcers. may

be caused because the destruction of one of the protective barrier in the

stomach.

NSAIDs can cause stomach ulcers through two ways:

a. Irritate the stomach epithelium directly

b. Through inhibiting the synthesis of prostaglandins.

However, the inhibition of prostaglandin synthesis is the dominant factor

that causes peptic ulcers by NSAIDs. Prostaglandins are compounds that

disentsis in the gastric mucosa that protects the body's physiological

functions such as renal function, homeostasis and gastric mucosa.

Based on the literature, the mechanisms involved still unknown but is

thought inhibited production of prostaglandins in the stomach so that the

protection of the gastric mucosa decreases and increases the risk of peptic

ulcers.

• The impact of the inhibition of COX- 1 is the reduction of prostaglandin synthesis so that the physiological

regeneration of the gastric mucosa becomes blocked.

• Long-term NSAID use cause local irritation of the gastric mucosa becomes longer and more intense. So the

gastric mucosa which originally was either be damaged or the gastric mucosa that is damaged can be

bleeding.

• Inhibition of COX-1 would result in a decrease in production tromboxan, followed by the extension of the

blood clotting time ease of bleeding.

• COX-2 inhibitor celecoxib, and other nimesulid experimentally not interfere with blood clotting. Along

with the growing process of vasoconstriction, increased blood clotting due to the more independent of

COX-1 pathway in synthesizing tromboxan will facilitate the occurrence of heart attack in users of

NSAIDs with inhibition of COX-2 which is highly selective.

• Inhibition of prostaglandin biosynthesis in the kidneys causing disruption of homeostasis. In patients with

hypovolemia, heart failure, hepatic cirrhosis, blood flow and filtration rate glomerolus Gijal will be

reduced, even acute renal failure can occur.

• Diabetes Mellitus patients with decreased insulin levels. Insulin plays a

role in stimulating the synthesis of bone matrix and cartilage formation. In

addition, insulin is also very important in normal bone mineralization, and

stimulate the production of IGF-1 by the liver.

• The role of insulin on matrix synthesis, especially in osteoblast

differentiation and function of IGF-1 increases the number of cells that can

synthesize the bone matrix.

• IGF-1 stimulating the synthesis of collagen matrix and bone, stimulate the

replication of cells derived osteoblasts and decreased bone collagen

degradation.

• So that a decrease in insulin levels lead to production of IGF I declined

which is a growth factor that plays a role in the process of cartilage repair.

Thus, there is an imbalance between the formation and bone breakdown

which affects the risk of osteoarthritis.

• Therefore, to reduce the pain experienced or lowers blood glucose levels,

patients taking medications such as allopurinol rheumatic NSAIDs,

medicines urikosirik, indomesatisin, or colchicine and corticosteroids and

ACTH hormone drugs.

• The drugs can inhibit the secretion of prostaglandins in the intestine and

stomach that can cause erosion, ulceration and even perforation of the

organ so that it can cause bleeding issued through the mechanism of

vomiting and defecation mechanism.

ETIOLOGY

PEPTIC ULCER DISEASE

• Damage to the mucosal or submucosal layer until the muscle layer of the GI tract due to the activity of pepsin and excessive stomach acid

GASTRITIS

• The state of inflammation or inflammatory process in the gastric mucosa and submucosa

ULCERATIVE COLITIS

• A chronic inflammatory disease of the intestine (Inflammatory bowel disease) causes inflammation and ulcers continuously on the innermost layer of the colon and rectum. Ulcerative colitis rarely affects the small intestine.

DEFINITION

GEJALA


• Helicobacter pylori

• The secretion of bicarbonate

• Feature genetic

• Stress

• NSAIDs

GASTRITIS

• Drugs - NSAIDs, such as aspirin, ibuprofen

• Potent alcoholic beverages

• Bacterial infections - H pylori (most frequent)

• Viral infections (eg, CMV)

• Fungal infections - Candidiasis, histoplasmosis, phycomycosis

• Parasitic infection (eg, anisakidosis)

• Acute stress (shock)

• Radiation

• Allergy and food poisoning

• Bile: The reflux of bile

• Ischemia

• Direct trauma

ULCERATIVE COLITIS

• Etiology is unknown, but the disease has a multifactorial and polygenic causes.

ETIOLOGY

GEJALA


• The most common symptom is burning pain

• The pain often occurs between meals and sometimes awakens people from sleep.

• May last minutes to hours

• Relieved by eating, taking antacids or acid blockers.

• include nausea, vomiting and loss of appetite and weight, and bleeding.

GASTRITIS

• Heartburn, anorexia, belching, nausea, vomiting, bleeding and hematemesis

ULCERATIVE COLITIS

• The predominant symptom is diarrhea, which can be associated with frank blood in the stool.

• Other symptoms : abdominal or rectal pain, fever and weight loss. Although

• Some patients may complain of constipation and rectal spasm.

CLINICAL MANIFESTATION

GEJALA


• In 70 percent of patients it occurs between the ages of 25 and 64 years

• Lifetime prevalence of PUD in the United States is ~12% in men and 10% in women.

• Moreover,an estimated 15,000 deaths per year occur as a consequence of complicated PUD.

GASTRITIS

• In developing countries the prevalence of Helicobacter pylori infection in adults is 90% whereas in children pravelensi Helicobacter Pylori infection is higher

ULCERATIVE COLITIS

• Most common between 15 and 40 years of age,

• with a second peak in incidence between 50 and 80 years.

• The disease affects men and women at similar rates.

• Studies indicate a decreased risk of ulcerative colitis for current smokers, however, former smokers are at increased risk of developing the disease.

EPIDEMIOLOGY

GEJALA


• Injury atthe mucosa as a result ofthe topical encounter with NSAIDs.NSAIDs are weak acids thatremain in a nonionized lipophilicform when found within the acidenvironment of the stomach.NSAIDs migrate across lipidmembranes of epithelial cells,leading to cell injury once trappedintracellularly in an ionized form.

• Topical NSAIDs can also alter thesurface mucous layer, permittingback diffusion of H+ and pepsin,leading to further epithelial celldamage.

GASTRITIS

• Helicobacter pylori attached to the gastric epithelium and destroy the protective mucous layer, leaving the epithelial area deforested

• Disrupt the gastric mucosal barrier

ULCERATIVE COLITIS

• There are three major hypotheses as tothese antigenic triggers. One hypothesisis that these triggers are microbialpathogens, as yet unidentified. Accordingto this theory, the immune response inUC is an appropriate but ineffectiveresponse to these pathogens. Thesecond hypothesis as to the antigenictrigger in UC is that there is somecommon dietary antigen ornonpathogenic microbial agent to whichthe patient mounts an abnormal immuneresponse. In UC, the immune cells ofthe lamina propria are exposed tonumerous luminal antigens. Theseluminal antigens are capable of triggeringimmune responses. As a result, specificimmune responses to the etiologicalagent may be overwhelmed by immuneresponses to thousands of luminalantigens that pass through the damagedepithelium.

PATOGENESIS

GEJALA


• Antacids

• Diet

• Anticholinergic

• Inhibiting H2 (cimetidine, ranitidine, famotidine)

• Anti-microbial therapy

• antibacterial

• Surgery: vagotomi, antrektomi, gastrectomy

GASTRITIS

• Antacids, such as aspirin, sodium bicarbonate, and citric acid (Alka-Seltzer); alumina and magnesia (Maalox); and calcium carbonate and magnesia (Rolaids). Antacids relieve mild heartburn or dyspepsia by neutralizing acid in the stomach.

• Histamine 2 (H2) blockers, such as famotidine and ranitidine. H2 blockers decrease acid production.

• Proton pump inhibitors (PPIs), such as omeprazole, lansoprazole, pantoprazole. PPIs decrease acid production more effectively than H2 blockers.

ULCERATIVE COLITIS

• Diet and supportive therapy

• The choice of drugs depending on the degree of disease. In mild to moderate cases can be administered 5-ASA (aminosalicylic acid) whereas in the case of complicated joints (arthritis) can be administered orally at a dose sulfasalazine gradually.

• Surgery. Surgical indications necessary if found no cases of drug response (cyclosporine) or cases with life-threatening complications, such as megacolon, perforation, ileus obstruction / paralytic ileus, and intestinal bleeding extensively.

MANAGEMENT

GEJALA


• Pola Healthy living and adequate rest, avoid excessive stress

• Quit smoking

• Modification of diet

GASTRITIS

• Set the feeding schedule

• Avoid greasy foods, sour and spicy

• Reduce alcohol

• Control stress

ULCERATIVE COLITIS

• Psychotherapy is sometimes necessary to prevent psychological stress. Avoid cigarettes and set the pattern for a healthier life

• A special diet is not required, it may be necessary to avoid cabbage and onions because many contain

PREVENTION

GEJALA


• If the underlying cause of peptic ulcer is resolved, it will provide a good prognosis.

• Most people recover with treatment of H. pylori infection, avoid taking NSAIDs and anti sekretorus in the stomach.

• Treatment with H.pylori infection will change the scientific history of the disease by lowering the incidence of this disease.

GASTRITIS

• If the underlying cause of gastritis is resolved, it will provide a good prognosis

• Many are cured with therapy Helicobacter and avoid NSAIDs

ULCERATIVE COLITIS

• Pretty much reported remisis spontaneous and in the long term. Prognosis influenced by the presence or absence of complications or the level of response to conservative treatment.

PROGNOSIS

GEJALA


• Penetration, perforation, bleeding and blockages

GASTRITIS

• Gastric Ulcers

• Bleeding in the stomach

• Gastric cancer

ULCERATIVE COLITIS

• Bleeding and toxic megacolon

COMPLICATION

PHYSICAL FEATURES OF DIAGNOSTIC

LABORATORY

Complete blood cell (CBC)

Liver and kidney function tests

Gallbladder and pancreatic

function tests

Stool for blood

RADIOLOGY

Abdominal XRay

Barium meal

CT-scan, MRI

USG

A HISTORY FROM IMAM MUSLIM IN HIS SHAHIH (NO. 2032) :

Told us yahya bin yahya, abu mu’awiya preach to us from Hisham ibn Urwah from Abdurrahman bin Sa’d of Ka’b bin Malik of a fatrher who said, “ The messenger

sallalahu ‘alaihi wa sallam was eaten by using three fingers, and licking the finger, before bringing it down”

ثنا يحيى بن يحيى، أخبرنا أبو مع بد اوية، عن هشام بن عروة، عن ع حد

حمن بن سعد، عن ابن كعب بن مالك، كان رسول »: عن أبيه، قال الر

يد قبل أ هللا صلى هللا عليه وسلم يأكل بثلث ، ويلع ن يمسحها أصاب »

THERE IS A HISTORY OF ABU HASAN BIN AL-MURQI IN SYAMAILNYA AS MENTIONED IN AL-

IHYA TAKHRIJ WORK OF AL-IRAQI (1/432)

عام استوفز على ركبته الي سرى وأقام اليمنىكان إذا قعد على الط

“That (the prophet shallalahu ‘alaihi wassalamu) when he sat down to eat

his knees left and uphold the right food”

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Education

PANEL MODUL BLOODY DEFECATION (BAB CAIR BERDARAH)