PATHOPHYSIOLOGY

OF DIGESTIVE
BY :
SYSTEM
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 Parkinsons 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
Dinding lambung terdiri dari :
a. Mukosa
b. Submukosa
c. Muskularis
d. Serosa

LAMBUNG
Pada lapisan mukosa terdapat beberapa
tipe sel :
1. Parietal cell = HCl
2. Enterochromafin cell = histamine
3. G cell = gastrin
4. D cell = somatostatin
5. Mucus cell = mucus, bicarbonate
6. Chief cell = pepsinogen

Pada parietal cell terdapat :

1. Reseptor gastrin
2. Reseptor histamin 2
HCl
3. Reseptor muskarinik
4. Reseptor prostaglandin

(+)

(-) HCl

Jalur Sekresi Gastric

Juice
(+)

PG

Sel
Mukus

(-)
(+)

GASTRIN

(-)
(-)
Somatostatin

(+)

(+)
HISTAMIN
(+)
ACh

Mukus
bikarbonat

Sel
parietal

HCl

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. Chronic use of NSAIDs

4. Cigarette smoking
5. Excess acid production from gastrinomas,
tumors of the acid producing cells of the
stomach that increases acid output (seen in
Zollinger-Ellison syndrome)
6. Excessive drinking of alcohol

The pathogenesis of peptic ulcer disease may

be considered as a combination scenario
involving an imbalance between defensive
factors (mucus-bicarbonate layer,
prostaglandins, cellular regeneration,
mucosal blood flow) and aggravating factors
(hydrochloric acid, pepsin, ethanol, bile
salts, drugs).

H. PYLORI
1. H. pylori induces an intense inflammatory
and immune response. There is increased
production of pro-inflammatory cytokines
such as IL-1, IL-6, TNF, IL-8. This cytokine is
produced by the mucosal epithelial cells, and
it recruits and activates neutrophils.

2. H.pylori secretes a urease that breaks down

urea to form toxic compounds such as
ammonium chloride and monochloramine.
Production of alkaline ammonia by bacteria
inhibit D cells. The organisms also elaborate
phospholipases that damage surface
epithelial cells. Bacterial proteases and
phospholipases break down the glycoproteinlipid complexes in the gastric mucus, thus
weakening the first line of mucosal defense.

3. H. pylori enhances gastric acid secretion and

impairs duodenal bicarbonate production,
thus reducing luminal pH in the duodenum.
NSAIDs
Chronic use of NSAIDs suppresses mucosal
prostaglandin synthesis. Prostaglandins are
important for mucosal integrity.
NSAIDs inhibit NO and H2S. NO and H2S
increase blood flow to mucosa, stimulate
mucus secretion, and inhibit neutrophil
adherence.

OTHERS
Cigarette smoking impairs mucosal blood
flow and healing.
Alcohol has not been proved to directly cause
peptic ulceration, but alcoholic cirrhosis is
associated with an increased incidence of
peptic ulcers.

A gnawing or burning pain in the middle or

upper stomach between meals or at night
Bloating
Heartburn
Nausea or vomiting
In severe cases, symptoms can include:
Dark or black stool (due to bleeding)
Vomiting blood(that can look like "coffeegrounds")
Weight loss
Severe pain in the mid to upper abdomen

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.

2.
3.

4.

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.
Bloating
Bowel habit : diarrhoea and constipation may
occur. There may be a feeling of incomplete
emptying after a bowel movement and may
be mucus present.
Nausea (sometimes), vomiting (less common)

Gallstone formation (cholelithiasis)

Gallstone disease (GD)/Cholelithiasis is chronic

recurrent hepotobiliary disease, the basis for
which is the impaired metabolism of cholesterol,
bilirubin and bile acids, which is characterized
by the formation of gallstones in the hepatic
bile duct, common bile duct, or gallbladder.
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.

The major components of all type of

Gallstones are :
1. Free unesterified cholesterol
2. Unconjugated bilirubin
3. Bilirubin calcium salts
4. Fatty acids
5. Calcium carbonates and phosphates
6. Mucin glycoproteins

Three main categories of

gallstones can be identified :
1.Cholesterol stones
2.Pigment stones
3.Mixed stones

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.
2.

3.

Kompres duduk panas

Analgesik (suppositoria), topical
steroid, local
anaesthetics,counter irritants.
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 Wilsons 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.