PATOFISIOLOGI SISTEM

DIGESTIVE
BY :
AGUSLINA KIRTISHANTI
ABNORMALITIES OF THE
ESOPHAGUS
1. DYSPHAGIA
 Difficulty swallowing that may be
caused by obstruction of the
esophagus or impaired motility of the
esophageal walls.
 Obstruction may be caused by tumors,
congenital narrowing or diverticula
 Neurologic disorders such as brain
injury, stroke or Parkinson’s disease
may affect voluntary swallowing or
peritalsis of the esophagus
2. Achalasia
 A condition caused by failure of the lower
esophageal sphincter (cardiac sphincter) to relax
and allow food to enter the stomach. It may be
related to defects in neural input to the
esophagus.
 Achalasia is a chronic condition that causes
distention of the lower esophagus that may lead
to chronic inflammation and eventual ulceration
of the esophagus.
 The condition presents with dysphagia, vomiting
and chest pain that is often exacerbated by
eating.
3. Esophageal diverticulum

 Diverticula are outpocketings of the

esophageal walls that occur most
frequently from congenital weakness of
the esophagus walls.
 Food can easily become trapped in these
divertucula, leading to inflammation and
infection of the esophagus with possible
ulceration.
4. Gastroesophageal reflux
disease (GERD)
 Gastroesophageal reflux is a condition caused
by the backflow of stomach contents into the
esophagus.
 It results from weakness or incompetence of the
lower esophageal sphincter that normally
blocks reflux of stomach contents into the
esophagus.
 It will cause irritation and inflammation of the
esophagus (esophagitis) that can lead to
ulceration of the esophagus
 A hiatal hernia may also cause
gastroesophageal reflux.
Manifestations GERD
 Heartburn that may be worsened by
alcohol consumption, caffeine, smoking,
exercise and obesity.
 Esophagitis
 Dysphagia, poor nutrition
 Possible increased risk of esophageal
cancer with chronic esophagitis.
Treatment GERD
 Consumption of frequent small meals
rather than large ones.
 Sleeping with head elevated.
 Comsumption of fluids with meals to
wash food out of the esophagus.
 Use of antacids or proton pump inhibitors
to reduce pH of stomach contents.
 Surgery if a hital hernia is present.
Hernia hiatus adalah : bentuk anatomi
abnormal lambung yang menekan diafragma
dan masuk ke dalam rongga dada.
Hernia hiatus dapat berkembang dan
memburuk pada keadaan hamil, obese, dan
penuaan (> 40 th).
Etiology of hiatal hernia :
1. Congenital abnormality
2. Trauma
3. Surgery
Sign and symptoms :
1. Heartburn
2. Sour or bitter taste in mouth
3. Belching
4. Coughng up of bloody mucus may occur when
the esophagus become irritated
5. Fullness in the upper abdomen after a meal
6. Dysphagia
7. A hourse voice
Ada 2 tipe hernia hiatus yaitu :
1. Sliding hiatal hernia
2. Rolling hiatal hernia (Paraesophageal
hernia)
 LAMBUNG
Lapisan mukosa lambung terdiri dari
beberapa kelenjar yaitu :
1. Kelenjar kardia
2. Kelenjar fundus/gastrik, terdiri dari 3 tipe
sel yaitu : sel zimogenik/chief cell, sel
parietal, sel leher.
3. Sel G menghasilkan hormon gastrin
Pengaturan Sekresi Lambung
Pengaturan sekresi lambung terbagi menjadi 3 fase yaitu
1. Fase sefalik
2. Fase gastrik
3. Fase intestinal
 Disorders of the stomach

GASTRITIS
Gastritis refers to inflammation of the gastric
mucosa
It may present as an acute or chronic disorder
 ACUTE GASTRITIS

Transient irritation and inflammation of the

stomach lining.
May be caused by factors such as alcohol
consumption, aspirin use and stress.
The inflammation associated with acute gastritis is a
self-limiting process that does not usually result in
long-term injury to the gastric mucosa.
Lanjutan gastritis akut ……

Tanda yang dpt terlihat pada mukosa lambung

adalah : mukosa memerah, edematosa, mukus
yang melekat, erosi kecil dan perdarahan sering
muncul.

Manifestasi klinis : anoreksia, mual & muntah, nyeri

epigastrium, perdarahan dan hematemesis.
 Chronic Gastritis

Chronic irritation and inflammation of the stomach

lining.
May be caused by bacterial infection, alcohol abuse
or long term aspirin and nonsteroidal anti
inflammatory drug (NSAID) use.
Can lead to atrophy and ulceration of the gastric
mucosa.
The term peptic ulcer refers to erosion of the
mucosa lining any portion of the G.I tract. If
the ulcer occurs in the stomach lining, it is
specifically referred to as a gastric ulcer.
The causes of peptic ulcers disease :
1. Infection with the bacteria Helicobacter
pylori (80-90% patients)
2. Stress : emotional, trauma, surgical
3. Injury or death of mucus-producing cells
4. Excess acid production in the stomach. The
hormone gastrin stimulates the production of
acid in the stomach.
5. Chronic use of aspirins and NSAIDs
 PATOGENESIS TUKAK PEPTIK
NSAID, H.pylori, rokok

Penghancuran epitel sawar

Asam kembali berdifusi ke mukosa

Penghancuran sel mukosa

Sekresi PG dan histamin Perangsangan Peningkatan asam/pepsin

kolinergik

Ulcer
 Episodes or remission and exacerbation
 Pain that for duodenal ulcers is often
relieved by eating or antacids
 G.I bleeding and possible hemorhage (20-25%
of patients)
 Perforation of ulcers with significant
mortalilty
 Obstruction of G.I tract
PEPTIC ULCER
 Avoidance of alcohol, smoking and NSAIDs
 Antibiotic therapy
 Antacids
 H2 antagonists
 Mucosal protectants
Disorder of the Intestines
Irritable bowel syndrome
 May be one of the most common G.I disorders
 Patients present with symptoms of G.I pain,
gas, bloating and altered bowel function
(diarrhea or constipation). Most symptoms are
localized to the lower intestine and colon.
Irritable bowel syndrome….
 No underlying pathophysiologic processes
have yet to be identified in these patients.
“Hiperreactivity” and excessive motility of
the bowels may be contributing factors.
 Emotional factors and diet may exacerbate
the symptoms.
 Treatment may include psychological
counseling, dietary changes such as
increased fiber consumption. Antidiarrhea,
anticholinergic and antispasmodic agents
might also be of value.
Symptoms IBS :

1. Abdominal pain : the pain can occur

anywhere in the abdomen. When pain occurs
in the upper abdomen, it can be confused
with peptic ulcer or gall bladder pain. The
pain can vary from person to person.
2. Bloating
3. Bowel habit : diarrhoea and constipation may
occur. There may be a feeling of incomplete
emptying after a bowel movement and may
be mucus present.
4. Nausea (sometimes), vomiting (less common)
Gallstone formation (cholelithiasis)
• Cholelithiasis is the most common disorder of
the G.I system.
• The gallstones that form in the gall bladder
are hardened precipitates of bile that
contain predominantly cholesterol.
• The size of gallstones can range from the
size of a grain of sand to several inches in
diameter.
 Factors such as aging, excess cholesterol,
obesity, sudden dietary changes or abnormal
fat metabolism may contribute to gallstone
formation.
 Gallstones may be detected by a number of
techniques including radiography,
ultrasonography and cholecystoscopy.
 Symptoms of gallstone formation will
generally not occur until the stones have
reached sufficient size to block the bile
ducts.
 Acute and severe abdominal pain.
 Nausea, vomiting, fever, chills.
 Jaundice from obstruction of bile outflow.
 Surgical removal of gall bladder
(cholecystectomy)
 Endoscopic removal of gallstones
 Lithotripsy : the use of sound waves to break
up the gallstones in the gall bladder.
 Low fat diet for prevention of additional
stone formation
• Cholecystitis is an acute or chronic
inflammation of the gall bladder.
• Caused of cholecystitis :

1. Presense of gallstones in the gall bladder

2. Infection
3. Reduced blood flow to the gall bladder
• Signs and symptoms are similar to those
observed with cholelithiasis.
• Treatment involves removal of gallstones and
antibiotics for treatment of infection if
present.
 Diverticular disease is a condition
characterized by the presence of diverticula,
which are multiple saclike protrusions of the
mucosa.
 Individuals who consume a low fiber, low
bulk diet also appear at greater risk for the
formation of diverticula
 Often asymptomatic
 Changes in bowel habits
 Excess flatulence
 A possible serious complication of
diverticular disease is infection or
inflammation of the diverticula
(diverticulitis) due to trapping of intestinal
contents and accumulation of intestinal
contents in the diverticula.
 Increased bulk and fiber in the diet
 Antibiotics if diverticulitis is present
 HEMOROID
Hemoroid atau wasir merupakan vena
varikosa pada anus.
Hemoroid timbul akibat kongesti vena yang
disebabkan gangguan aliran balik dari
vena hemoroidalis.
Ada 2 jenis hemoroid :
1. Hemoroid internal
2. Hemoroid eksternal
HEMOROID

Etiologi : konstipasi, diare, kongesti pelvis pada

kehamilan, pembesaran prostat, tumor rektum.
Hemoroid eksternal diklasifikasikan dalam bentuk
akut dan kronik.
Hemoroid eksternal akut merupakan hematoma
(hemoroid trombosis akut) dengan manifestasi
nyeri, gatal, sensasi terbakar dan bengkak.
Hemoroid eksterna kronis berupa satu atau lebih
lipatan kulit anus yang terdiri dari jaringan
penyambung dan sedikit pembuluh darah.
Lanjutan

Hemoroid internal diklasifikasikan dalam :

 Derajat I : tidak menonjol mll anus dan

tidak menimbulkan gejala.

 Derajat II : dapat mengalami prolapsus mll

anus stl defekasi, jenis ini dpt mengecil scr

spontan atau direduksi scr manual.
 Derajat III : mengalami prolapsus scr

permanen
Gejala hemoroid internal : perdarahan tanpa
nyeri karena tidak ada serabut pada
daerah itu.
 TERAPI HEMOROID

1. Kompres duduk panas

2. Analgesik (suppositoria), topical
steroid, local anaesthetics,counter
irritants.
3. Pembedahan (perdarahan menetap,
prolapsus, nyeri anus yang tidak
dapat diatasi).
HEMORRHOID
 JAUNDICE/IKTERUS
Penimbunan pigmen empedu dalam tubuh
menyebabkan warna kuning pada jaringan
yang dikenal sebagai ikterus.

Warna kuning dapat terlihat pada : sklera,

kulit atau kemih yang menjadi gelap bila
bilirubin serum mencapai 2-3 mg/100 ml.

Bilirubin serum normal : 0,2-0,9 mg/100 ml.

 IKTERUS
4 Mekanisme umum terjadinya ikterus yaitu :
1. Pembentukan bilirubin secara berlebihan
2. Gangguan pengambilan bilirubin tak
terkonjugasi oleh hati
3. Gangguan konjugasi bilirubin
4. Penurunan ekskresi bilirubin terkonjugasi
dalam empedu karena obstruksi
fungsional maupun mekanik.
 IKTERUS
Etiologi :
1. Viral infection
2. Alcoholism
3. Cancer : hepatocellular carcinoma
4. Gall stones : obstruction of the bile
duct.
 CIRRHOSIS
Cirrhosis is a chronic destruction of liver cells, it occurs when
normal liver cells are damaged and replaced by scar
tissue.
This decreases the amount of normal liver tissue and can
therefore limit blood flow through the liver and restrict liver
cell function.
What causes cirrhosis ?
1. Long term alcohol abuse (most common)
2. Chronic hepatitis
3. Obstruction of the bile duct
4. Certain inherited metabolic disorders (hemochromatosis
and Wilson’s disease)
5. Exposure to certain toxins
6. Adverse reaction to certain medications
7. Alpha 1-antitrypsin deficiency
 CIRRHOSIS
What are the symptoms of cirrhosis?
Early symptoms :
 Loss of appetite
 Nausea and vomiting
 Weight loss
 Weakness and fatigue
Later symptoms :
 Jaundice (yellow skin)
 Fluid accumulation/swelling in the abdomen and legs
 Bleeding
 Gallstone formation
 Intense itching
 Accumulation of toxins in the brain,resulting in :
unresponsiveness, forgetfulness, poor concentration,
changes in sleeping habits,and coma.
 CIRRHOSIS
How is cirrhosis treated? Scarring of the liver is
irreversible. Therefore, treatment focuses on
preventing further damage to the liver, may include :
 Abstinence from alcohol
 Dietary modifications
 Use of steroids or anti-viral drugs, to reduce liver
damage due to hepatitis.
 Medications to treat the symptoms of cirrhosis, i.e :
diuretics to reduce fluid retention and swelling.
 If necessary, surgery may be performed to control
any internal bleeding.
 In critical cases, liver transplant may be necessary.