LI LBM 3 SGD 2

STEP 7

1. How the anatomy dan physiology from lower digestivus track?

Usus besar (colon)Motilitas : mengonsentrasikan dan menyimpan residu makanan yang tidak dicerna (serta, yaitu selulosa tanaman) dan bilirubin hingga keduanya dapat dieliminasi dalam tinja. Kontraksi haustra secara perlahan mengaduk isi colon maju-mundur untuk mencampur dan mempermudah penyerapan sebagian besar cairan dan elektrolit yang tersisa. Pergerakan massa beberapa kali sehari, biasanya setelah makan, mendorong feses dalam jarak jauh. Pergerakan feses ke rectum memicu refleks defekasiSekresi, digesti, dan absorbsi : skeresi mukus basa usus halus bersifat protektif. Tidak terjadi sekresi enzim pencernaan atau penyerapan nutrient dicolon. Penyerapan sebagian garam dan air yang tertinggal mengubah isi colon menjadi feses.

Colon sigmoid dan rectum Jika feses telah mencapai colon sigmoid maka menimbulkan gerakan peristaltik rectum sehingga feses berjalan menuju rectum dan jika feses sudah sampai ke rectum maka akan merangsang reseptor regang dan akan menginisiasi refleks defekasi

Source : Lauralle, sherwood. 2014. Fisiologi Manusia Dari Sel Ke Sistem. Edisi 8. Jakarta : EGC page 674

Source : Principles of Anatomy and Physiology 12th Edition - Tortora

2. What the mechanism of defecation and flatus?

Dengan kata lain adalah mekanisme "buang hajat". Semua diawali dengan adanya feces di colon sigmoideum, saat jumlah feces sudah melebihi kapasitas penyimpanan di colon sigmoideum, maka feces akan turun menuju ke rectum. Rectum biasanya kosong dan hanya terisi saat akan memulai defekasi. Dinding rectum mempunyai reseptor regangan yang dipersarafi oleh serabut viscero sensible parasymphatis segmen sacral 2-4. Rangsang yang diterima oleh reseptor regangan akan menjalar di serabut saraf, kemudian masuk ke cornu posterior medulla spinalis dan akan naik ke otak. Rangsang akan diproses di otak, apakah akan ditahan atau meneruskan proses defekasi.

Jika kita memutuskan untuk menahan defekasi, maka impuls akan turun menuju cornu anterior medulla spinalis segmen sacral 2-4 yaitu ke nervus pudendus yang mensarafi m. levator ani, lalu terus menuju ke cabangnya yaitu nervus rectalis inferior yang mensarafi musculus sphincter ani externus dan. Hal ini menyebabkan m. sphincter ani externus dan m. levator ani berkontraksi untuk menahan defekasi.

Jika kita memutuskan untuk meneruskan proses defekasi, maka impuls akan turun menuju ke berbagai saraf:

N. facialis (VII) untuk mengkontraksikan otot2 wajah. N. vagus (X) untuk menutup epiglottis. n. Phrenicus untuk memfiksasi diapraghma. nn. Thoracales segmen yang berhubungan untuk mengkontraksikan otot-otot

dinding abdomen. n. splanchnicus pelvicus, yang berisi pesan untuk mengurangi kontraksi m. sphincter

ani internus.

n. pudendus, yang berisi pesan untuk mengurangi kontraksi m. sphincter ani externus dan m. levator ani.

n. ischiadicus, untuk mengkontraksikan otot-otot hamstring.

Penutupan epiglottis dan kontraksi otot-otot dinding abdomen berfungsi untuk meningkatkan tekanan intra abdominal, sehingga mendukung pengeluaran feces. Selanjutnya feces dikeluarkan melalui canalis analis. Tunica mucosa bagian bawah canalis analis menonjol melalui anus mendahului massa feces. Pada akhir defekasi, tunica mucosa kembali ke canalis analis akibat tonus serabut-serabut longitudinal dinding canalis analis serta penarikan ke atas oleh m. puborectalis (bagian dari m. levator ani). Kemudian lumen canalis analis yang kosong ditutup oleh kontraksi tonik m. sphincter ani.

Diktat systema urogenital FK UNDIP & Anatomi klinik Snell.

Defecation When the mass in the rectum distention of rectum merangsang reseptor regang didinding rectum defecation refleks relaxation of m. sphincter ani internus more contraction of rectum and sigmoid if m. Sphincter ani eksternus has relaxation tooso the defecation is occure but because m. Sphincter ani externus is a scelet muscle so m. Sphincter ani axternus is volunter

a. gas yang masuk

i. gas yang ditelan lambung keluar ke sendawa atau GI

ii. gas yang terbentuk karna bakteri

bakteri di kolon bercampur dengan metana +hydrogen +o2 ledakan

iii. gas yang berdifusi ke traktus GI

1. normalnya

a. yang masuk 7-10 liter

b. yang keluar 0,6 liter

2. sisanya di absorpsi ke darah

iv. faktor

1. flatus lebih besar

a. makanan (kacang2an, kubis karbohidrat tidak terabsorpsi

2. Flatus berbau

a. Berasal dari sulfida

Mekanisme flatus

Gas dapat memasuki traktus gastrointestinal dari tiga sumber yang berbeda:

Udara yang ditelan

Gas yang terbentuk sebagai hasil kerja bakteri

Gas yang berdifusi dari darah ke dalam traktus gastorintestinal

Kebanyakan gas dalam lambung adalah nitrogen dan oksigen yang

berasal dari udara yang ditelan, dan pada orang normal biasanya dikeluarkan

melalui sendawa.

Hanya sebagian kecil gas yang biasanya ada dalam usus halus, dan

banyak dari udara ini berjalan dari lambung masuk ke dalam traktus

intestinal. Sebagai tambahan, karbon dioksida dalam jumlah cukup juga

sering timbul karena reaksi antara cairan lambung yang asam dan

bikarbonat dalam cairan pankreas kadang-kadang terlalu cepat untuk

membebaskan karbon dioksida yang diabsorbsi.

Dalam usus besar, bagian terbesar dari gas berasal dari kerja bakteri,

termasuk khususnya karbon dioksida, metana, dan hidrogen. Gas-gas

tersebut terjadi bersamaan dengan jumlah yang bervariasi dari oksigen dan

nitrogen dari udara yang dielan, kadang-kadang terbentuk campuran yang

benar-benar bisa meledak; penggunaan kauter elektrik selama

sigmoidoskopi bisa menyebabkan ledakan kolon, pada keadan yang jarang.

Makanan tertentu diketahui menyebabkan pengeluaran flatus yang lebih

besar dari usus besar dibandingkan makanan yang lain ( kacang-kacangan,

kubis, bawang, kembang kol, jagung, dan makanan tertentu mengiritasi

seperti cuka.

Beberapa dari makanan ini bertindak sebagai medium yang baik untuk

bakteri pembentuk gas, terutama karena tipe karbohidrat yang berfermentasi

tak terabsorbsi (sebagai contoh kacang-kacangan mengandung gula yang tak

dpat dicerna yang masuk ke dalam kolon dan merupakan makanan utama

bagi bakteri kolon), tetapi pada contoh lain, gas ledakan yang berlebihan

berasal dari iritasi usus besar, yang mencetuskan ekspulsi cepat dari gas,

sebelumgas diabsorbsi.

Fisiologi kedokteran, Guyton & Hall

Flatus Gas flatus berasal dari 2 sumber :1. Gas yang tertelan

Gas yang tertelan bisa dikeluarkan juga lewat sendawa (eruktasi) tetapi ada juga yang terbawa masuk sampai usus

2. Gas yang diprosuksi oleh fermentasi bakteri kolonMekanisme Secara selektif mengeluarkan gas ketika feces juga ada di rectum, yang bersangkutan secara sengaja mengontraksikan otot abdomen dan sfingter ani eksternus secara bersamaan. Ketika kontraksi abdomen meningkatkan yang menekan sfingter ani eksternut yang tertutup, terbentuk gradien tekanan yang memaksa udara keluar dengan kecepatan tisnggi melalui lubang anus yang terbentuk celah dan terlalu sempit untuk keluarnya feces. Lewatnya udara dengan kecepatan tinggi menyebabkan tepi lubang anus bergetar, menghasilkan nada rendah khas yang menyertai keluarnya gas

Source : Lauralle, sherwood. 2014. Fisiologi Manusia Dari Sel Ke Sistem. Edisi 8. Jakarta : EGC page 666 and 668

3. Why the patient compline the produce of urine is decrese?

Distention of the intestine is caused by the accumulation of gas and fluid proximal to and

within the obstructed segment. Between 70 and 80% of intestinal gas consists of swallowed

air, and because this is composed mainly of nitrogen, which is poorly absorbed from the

intestinal lumen, removal of air by continuous gastric suction is a useful adjunct in the

treatment of intestinal distention. The accumulation of fluid proximal to the obstructing

mechanism results not only from ingested fluid, swallowed saliva, gastric juice, and biliary

and pancreatic secretions but also from interference with normal sodium and water

transport. During the first 12–24 h of obstruction, a marked depression of flux from lumen

to blood of sodium and water occurs in the distended proximal intestine. After 24 h, sodium

and water move into the lumen, contributing further to the distention and fluid losses.

Intraluminal pressure rises from a normal of 2–4 cmH2O to 8–10 cmH2O. The loss of fluids

and electrolytes may be extreme, and unless replacement is prompt, hypovolemia,renal

insufficiency, and shock may result. Vomiting, accumulation of fluids within the lumen, and

the sequestration of fluid into the edematous intestinal wall and peritoneal cavity as a

result of impairment of venous return from the intestine all contribute to massive loss of

fluid and electrolytes.

Source : Harrison; Principles of Internal Medicine; 18th ed.; Part 14 Gastrointestinal System; Section

1 Disorder of Alimentary Tract; Chapter 299 Acute Intestinal Obstruction

4. Why the patient doesn’t passed stole and faltus?

Symptoms

Mechanical intestinal obstruction is characterized by cramping midabdominal pain, which tends to be more severe the higher the obstruction. The pain occurs in paroxysms, and the patient is relatively comfortable in the intervals between the pains. Audible borborygmi are often noted by the patient simultaneously with the paroxysms of pain. The pain may become less severe as distention progresses, probably because motility is impaired in the edematous intestine. When strangulation is present, the pain is usually more localized and may be steady and severe without a colicky component, a fact that often causes delay in diagnosis of obstruction. Vomiting is almost invariable, and it is earlier and more profuse the higher the obstruction. The vomitus initially contains bile and mucus and remains as such if the obstruction is high in the intestine. With low ileal obstruction, the vomitus becomes feculent, i.e., orange-brown in color with a foul odor, which results from the overgrowth of bacteria proximal to the obstruction. Hiccups (singultus) are common. Obstipation and failure to pass gas by rectum are invariably present when the obstruction is complete, although some stool and gas may be passed spontaneously or after an enema shortly after onset of the complete obstruction. Diarrhea is occasionally observed in partial obstruction. Blood in the stool is rare but does occur in cases of intussusception

Source : Harrison; Principles of Internal Medicine; 18th ed.; Part 14 Gastrointestinal System; Section 1

Disorder of Alimentary Tract; Chapter 299 Acute Intestinal Obstruction.

5. Why the patient vomit with greenish color?

Pathophysiology

Distention of the intestine is caused by the accumulation of gas and fluid proximal to and

within the obstructed segment. Between 70 and 80% of intestinal gas consists of swallowed air,

and because this is composed mainly of nitrogen, which is poorly absorbed from the intestinal

lumen, removal of air by continuous gastric suction is a useful adjunct in the treatment of intestinal

distention. The accumulation of fluid proximal to the obstructing mechanism results not only from

ingested fluid, swallowed saliva, gastric juice, and biliary and pancreatic secretions but also from

interference with normal sodium and water transport. During the first 12–24 h of obstruction, a

marked depression of flux from lumen to blood of sodium and water occurs in the distended

proximal intestine. After 24 h, sodium and water move into the lumen, contributing further to the

distention and fluid losses. Intraluminal pressure rises from a normal of 2–4 cmH2O to 8–10 cmH2O.

The loss of fluids and electrolytes may be extreme, and unless replacement is prompt,

hypovolemia,renal insufficiency, and shock may result. Vomiting, accumulation of fluids within the

lumen, and the sequestration of fluid into the edematous intestinal wall and peritoneal cavity as a

result of impairment of venous return from the intestine all contribute to massive loss of fluid and

electrolytes.

Billiary secretion Greenish color

Accumulation of fluid (ingested fluid, gastric juice, swallowed saliva, billiary and pancreatic secretion) on proximal of obstruction

Intraluminal pressure ↑↑↑

Vomiting

Hypovolemia

Source : Harrison; Principles of Internal Medicine; 18th ed.; Part 14 Gastrointestinal System;

Section 1 Disorder of Alimentary Tract; Chapter 299 Acute Intestinal Obstruction.

Source : Sibernagl/ Lang, Color Atlas of Patophysiology; Chapter6 Stomach, Intestine, Liver;

page 141-157

Source : Guyton and Hall; Textbook of Medical Physiology; 12thed; UNIT XII Gastrointestinal

Physiology; Chapter 66 Physiology of GI disorder; pg 803

6. Why the patient has hard, small, black colored stole like goat stole?Distention of the intestine is caused by the accumulation of gas and fluid proximal to and within the obstructed segment. Between 70 and 80% of intestinal gas consists of swallowed air, and because this is composed mainly of nitrogen, which is poorly absorbed from the intestinal lumen, removal of air by continuous gastric suction is a useful adjunct in the treatment of intestinal distention. The accumulation of fluid proximal to the obstructing mechanism results not only from ingested fluid, swallowed saliva, gastric juice, and biliary and pancreatic secretions but also from interference with normal sodium and water transport. During the first 12–24 h of obstruction, a marked depression of flux from lumen to blood of sodium and water occurs in the distended proximal intestine. After 24 h, sodium and water move into the lumen, contributing further to the distention and fluid losses. Intraluminal pressure rises from a normal of 2–4 cmH2O to 8–10 cmH2O. The loss of fluids and electrolytes may be extreme, and unless replacement is prompt, hypovolemia,renal insufficiency, and shock may result. Vomiting, accumulation of fluids within the lumen, and the sequestration of fluid into the edematous intestinal wall and peritoneal cavity as a result of impairment of venous return from the intestine all contribute to massive loss of fluid and electrolytes.

Source : Harrison; Principles of Internal Medicine; 18th ed.; Part 14 Gastrointestinal System; Section 1 Disorder of Alimentary Tract; Chapter 299 Acute Intestinal Obstruction.

7. Why the patient has bloating?Distention of the intestine is caused by the accumulation of gas and fluid proximal to and within the obstructed segment. Between 70 and 80% of intestinal gas consists of swallowed air, and because this is composed mainly of nitrogen, which is poorly absorbed from the intestinal lumen, removal of air by continuous gastric suction is a useful adjunct in the treatment of intestinal distention. The accumulation of fluid proximal to the obstructing mechanism results not only from ingested fluid, swallowed saliva, gastric juice, and biliary and pancreatic secretions but also from interference with normal sodium and water transport. During the first 12–24 h of obstruction, a marked depression of flux from lumen to blood of sodium and water occurs in the distended proximal intestine. After 24 h, sodium and water move into the lumen, contributing further to the distention and fluid losses. Intraluminal pressure rises from a normal of 2–4 cmH2O to 8–10 cmH2O. The loss of fluids and electrolytes may be extreme, and unless replacement is prompt, hypovolemia,renal insufficiency, and shock may result. Vomiting, accumulation of fluids within the lumen, and the sequestration of fluid into the edematous intestinal wall and peritoneal cavity as a result

of impairment of venous return from the intestine all contribute to massive loss of fluid and electrolytes.

Source : Harrison; Principles of Internal Medicine; 18th ed.; Part 14 Gastrointestinal System; Section 1 Disorder of Alimentary Tract; Chapter 299 Acute Intestinal Obstruction.

8. What the relation about his job?

Risk Factorso activities which increase intra-abdominal pressure:

obesity, chronic cough, pregnancy, constipation, straining on urination or

defecation, ascites,heavy lifting

o congenital abnormality (e.g. patent processus vaginalis)

o previous hernia repair

o Kulipasarmenggunakan otot2 abdomen terusmeneruskelemahanotot

– otot abdomen

Source : Toronto Notes; Comprehensive Medical Reference and Review for MCCQ I and USMLE II;

General Surgery; Hernia.

9. What are the etiology and risk factor about the cases?

Etiology

An indirect inguinal hernia is considered mainly to be a congenital lesion. It is denoted “indirect” because the bowel and peritoneum do not herniate directly through a weakness in the abdominal wall. Rather, the bowel and peritoneum move through a patent processus vaginalis (hence it being a congenital defect) and into the scrotum scroltalis hernia. This also lends to the analogy that “in”-direct hernias extend “in” through the internal ring. As such, they technically protrude lateral to the inferior epigastric vessels.

The hernia itself consists of a sac of peritoneum extending through the internal ring, antero-medial to the spermatic cord in males (or round ligament in females), through which omentum or bowel can traverse.

Risk Factors

Probably the largest single risk factor for developing an inguinal hernia is being male. Men are almost 10 times more likely to develop an inguinal hernia than females. Other factors (which mainly lead to an increased pressure in the lower abdomen) put the general population at risk. They include:

Family History: There is an increased risk of hernia with a close family historyCertain Medical Conditions: Cystic fibrosis, or conditions associated with a chronic cough increase the risk of developing a herniaSmoking: Like cystic fibrosis, a chronic cough increases riskChronic Constipation: Excessive straining over time can lead to herniaExcess Weight & Pregnancy: Increases risk by weakening and placing stress on lower abdominal musclesPast History: Having one hernia puts you at risk of having another

Source : http://fitsweb.uchc.edu/student/selectives/Luzietti/hernia_inguinal_indirect.htm10. How the pathogenesis about the cases?

The pinchcock action of the internal ring musculature during abdominal muscular straining prohibits protrusion of the intestine into a patent processus. Muscle paralysis or injury can disable the shutter effect. In addition, the transversus abdominis aponeurosis flattens during tensing, thus reinforcing the inguinal floor. A congenitally high position of the aponeurotic arch may preclude the buttressing effect. Neurapraxic or neurolytic sequelae of appendectomy or femoral vascular procedures may increase the incidence of hernia in these patients.

Clinical presentations suggest repetitive stress as a factor in hernia development. Increased intra-abdominal pressure is seen in a variety of disease states and seems to contribute to

hernia formation in these populations. Elevated intra-abdominal pressure is associated with chronic cough, ascites, increased peritoneal fluid from biliary atresia, peritoneal dialysis or ventriculoperitoneal shunts, intraperitoneal masses or organomegaly, and obstipation. (See the images below.)

Ventriculoperitoneal shunt, decreased activity, and acute scrotal swelling in 6-month-old boy.

Ventriculoperitoneal shunt, decreased activity, and acute scrotal swelling in 6-month-old boy. Abdominal radiograph shows incarcerated shunt within communicating hydrocele. Repair of hydrocele relieved increased intracranial pressure.

Other conditions associated with an increased incidence of inguinal hernias are exstrophy of bladder, neonatal intraventricular hemorrhage, myelomeningocele, and undescended testes. A high incidence (16-25%) of inguinal hernias occurs in premature infants; this incidence is inversely related to weight.

Inguinal hernias are commonly classified as either direct or indirect. A direct inguinal hernia usually occurs as a consequence of a defect or weakness in the transversalis fascia area of

the Hesselbach triangle. The triangle is defined inferiorly by the inguinal ligament, laterally by the inferior epigastric arteries, and medially by the conjoined tendon.[5]

An indirect inguinal hernia follows the tract through the inguinal canal. It results from a persistent processus vaginalis. The inguinal canal begins in the intra-abdominal cavity at the internal ring, approximately midway between the pubic symphysis and the anterior superior iliac spine, and courses down along the inguinal ligament to the external ring, located medial to the inferior epigastric arteries, subcutaneously and slightly above the pubic tubercle. The hernia contents then follow the tract of the testicle down into the scrotal sac.

Source : http://emedicine.medscape.com/article/189563-overview#a4

11. What are the diagnostic examination?

Abdominal x ray. An x ray is a picture recorded on film or on a computer using a small amount of radiation. The patient will lie on a table or stand during the x ray. The technician positions the x-ray machine over the abdominal area. The patient will hold his or her breath as the technician takes the picture so that the picture will not be blurry. The technician may ask the patient to change position for additional pictures.

Computerized tomography (CT) scan. CT scans use a combination of x rays and computer technology to create images. For a CT scan, the technician may give the patient a solution to drink and an injection of a special dye, called contrast medium. A health care provider injects the contrast medium into a vein, and the injection will make the patient feel warm all over for a minute or two. The contrast medium allows the health care provider to see the blood vessels and blood flow on the x rays. CT scans require the patient to lie on a table that slides into a tunnel-shaped device where the technician takes the x rays. A health care provider may give children a sedative to help them fall asleep for the test.

Abdominal ultrasound. Ultrasound uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure.

Source : http://www.niddk.nih.gov/health-information/health-topics/digestive-diseases/inguinal-hernia/Pages/facts.aspx

12. What the diagnosis and DD (with classification)? Hernia:1. Inguinalis Lateralis Pintu hernia terletak lateral dari Vasa epigastrica inferior = Inguinalis

Indirecta 2. Inguinalis Medialis Pintu hernia terletak medial dari Vasa epigastrica inferior = Inguinalis

Directa

Inguinal hernias are commonly classified as either direct or indirect. A direct inguinal hernia usually occurs as a consequence of a defect or weakness in the transversalis fascia area of the Hesselbach triangle. The triangle is defined inferiorly by the inguinal ligament, laterally by the inferior epigastric arteries, and medially by the conjoined tendon.[5]

An indirect inguinal hernia follows the tract through the inguinal canal. It results from a persistent processus vaginalis. The inguinal canal begins in the intra-abdominal cavity at the internal ring, approximately midway between the pubic symphysis and the anterior superior iliac spine, and courses down along the inguinal ligament to the external ring, located medial

to the inferior epigastric arteries, subcutaneously and slightly above the pubic tubercle. The hernia contents then follow the tract of the testicle down into the scrotal sac.

Source : http://emedicine.medscape.com/article/189563-overview#a4

13. What are the treatment?

Hernia surgery is also called herniorrhaphy. The two main types of surgery for hernias are

Open hernia repair. During an open hernia repair, a health care provider usually gives a patient local anesthesia in the abdomen with sedation; however, some patients may have

o sedation with a spinal block, in which a health care provider injects anesthetics around the nerves in the spine, making the body numb from the waist down

o general anesthesia

The surgeon makes an incision in the groin, moves the hernia back into the abdomen, and reinforces the abdominal wall with stitches. Usually the surgeon also reinforces the weak area with a synthetic mesh or “screen” to provide additional support.

Laparoscopic hernia repair. A surgeon performs laparoscopic hernia repair with the patient under general anesthesia. The surgeon makes several small, half-inch incisions in the lower abdomen and inserts a laparoscope—a thin tube with a tiny video camera attached. The camera sends a magnified image from inside the body to a video monitor, giving the surgeon a close-up view of the hernia and surrounding tissue. While watching the monitor, the surgeon repairs the hernia using synthetic mesh or “screen.”

Source : http://www.niddk.nih.gov/health-information/health-topics/digestive-diseases/inguinal-hernia/Pages/facts.aspx

14. What are the complications and prognosis from the cases?

Inguinal hernias can cause the following complications:

Incarceration. An incarcerated hernia happens when part of the fat or small intestine from inside the abdomen becomes stuck in the groin or scrotum and cannot go back into the abdomen. A health care provider is unable to massage the hernia back into the abdomen.

Strangulation. When an incarcerated hernia is not treated, the blood supply to the small intestine may become obstructed, causing “strangulation” of the small intestine. This lack of blood supply is an emergency situation and can cause the section of the intestine to die.

Source : http://www.niddk.nih.gov/health-information/health-topics/digestive-diseases/inguinal-hernia/Pages/facts.aspx