Pemicu 3

KGD
Oleh :

Erna Wati

405140024
 SHOCK

• Shock is abnormality of the circulatory system that results in

inadequate organ perfusion and tissue oxygenationis the clinical

syndrome that results from inadequate tissue perfusion

• Cause : the hypoperfusion-induced imbalance between the delivery

of and requirements for oxygen and substrate  cellular injury
 Types of shock

Hypovolemic Cardiogenic Obstructive Distributive

Lo 2
Describes OF GIT BLEEDING (UPPER AND LOWER)
 GIT BLEEDING
1. Upper abdomen
• Varices
• Esophageal/gastric varices
• Non varices
• Peptic ulcer
• Mallory weast tear
2. Lower abdomen

Longo DL, Fauci AS. Harrisons Gastroenterology and Hepatology. 17th ed. McGraw-Hill Education; 2010
• Endoscopic variceal ligation (EVL) 
Variceal band ligation
• Pharmacologic therapy : vasoconstricting
agen usually somatostatin or octreotide
• Balloon tamponade (Sengstaken-Blakemore
tube or Minnesota tube) can be used in
patients who cannot get endoscopic
therapy immediately
• TIPS should be reserved for individuals who
fail endoscopic or medical management or
who are poor surgical risks
 PEPTIC ULCER
(Duodenal ulcers & Gastric ulcers)
• Burning epigastric pain exacerbated by fasting and improved with
meals is a symptom complex associated with peptic ulcer disease
(PUD).
• Ulcer : disruption of the mucosal integrity of the stomach and/or
duodenum leading to a local defect or excavation due to active
inflammation

Source : Kasper, D.L, Hauser, S.L, Jameson, JL, et al. Harrison’s Principles of Interna Medicine. 19 th ed. McGraw-Hill Education; 2015.113
 Defined
• Ulcers : as breaks in the mucosal surface >5 mm in
size, with depth to the submucosa.
• Duodenal ulcers (DUs)
• Gastric ulcers (GUs)

share many common features in terms of pathogenesis,

diagnosis, and treatment, but several factors distinguish
them from one another.

Source : Kasper, D.L, Hauser, S.L, Jameson, JL, et al. Harrison’s Principles of Interna Medicine. 19 th ed. McGraw-Hill Education; 2015.116
 Epidemiology
• Duodenal ulcers (DUs)
• The reason for the reduction in the frequency of DUs is
likely related to the decreasing frequency of Helicobacter
pylori.

• Gastric ulcers (GUs)

• 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

Source : Kasper, D.L, Hauser, S.L, Jameson, JL, et al. Harrison’s Principles of Interna Medicine. 19 th ed. McGraw-Hill Education; 2015.116
 Pathology
Helicobacter pylori.
OAINS

• Duodenal ulcers (DUs)

• First portion of duodenum (>95%)
• 90% located within 3 cm of the pylorus.
• 1 cm in diameter but can occasionally reach 3–6 cm (giant ulcer).
• Ulcers are sharply demarcated, with depth at times reaching the
muscularis propria

• Gastric ulcers (GUs)

• Can represent a malignancy
• Benign GUs are most often found distal to the junction between the
antrum and the acid secretory mucosa

Source : Kasper, D.L, Hauser, S.L, Jameson, JL, et al. Harrison’s Principles of Interna Medicine. 19 th ed. McGraw-Hill Education; 2015.116
 Pathophysiology
• Duodenal ulcers (DUs)
• Hipotesis : accelerated gastric emptying of liquids,
Bicarbonate secretion is signifi- cantly decreased in the
duodenal bulb (cause H. pylori infection)

• Gastric ulcers (GUs)

• Occurs in the prepyloric area or those in the body
associated with a DU or a duodenal scar are similar in
pathogenesis to Dus
• Abnormalities in resting and stimulated pyloric sphincter
pressure with a concomitant increase in duodenal gastric
reflux

Source : Kasper, D.L, Hauser, S.L, Jameson, JL, et al. Harrison’s Principles of Interna Medicine. 19 th ed. McGraw-Hill Education;
2015.116-7
CLINICAL FEATURES
• History
• Abdominal pain
• Epigastric pain (burning or gnawing discomfort)
1. DU : 90 min-3 hour, after a meal  relieved by antacids/food, pain that awakes the
patient from sleep (between midnight and 3 A.M.)
2. ↑ also present 1/3 of patients with NUD
3. GU : discomfort may actually be precipitated by food. Nausea and weight loss occur
more commonly.
• Nausea, vomiting  ulcer complication
• Tarry stools or coffee-ground emesis bleeding

Source : Kasper, D.L, Hauser, S.L, Jameson, JL, et al. Harrison’s Principles of Interna Medicine. 19 th ed. McGraw-Hill Education; 2015.120
 • Physical Examination
• Epigastric tenderness
• Tachycardia and orthostasis : dehydration
• Severely tender, boardlike abdomen : perforation
• Succussion splash : retained fluid in the stomach
(suggesting gastric outlet obstruction)
• Diagnostic Evaluation
• Radiographic (barium study)
• Endoscopic procedure.

Source : Kasper, D.L, Hauser, S.L, Jameson, JL, et al. Harrison’s Principles of Interna Medicine. 19 th ed. McGraw-Hill Education; 2015.121
Source : Kasper, D.L, Hauser, S.L, Jameson, JL, et al. Harrison’s Principles of Interna Medicine. 19 th ed. McGraw-Hill Education; 2015.123
Lo 3
Describes OF ACUTE ABDOMEN
APENDISITIS
 Epidemiology
• Approximately 80,000 children experience appendicitis in
the United States annually
• A rate of 4/1,000 children younger than age 14 yr.
• Rare in developing countries, where diets are high in fiber.
• However, no causal relationship has been established between
lack of dietary fiber and appendicitis.
• The incidence of appendicitis increases with age, peaking
in adolescence and rarely occurring in children younger
than 1 yr old.
• A familial predilection to appendicitis has been reported.
• Cases occur more often in males.
• Cases occur more often in the autumn and spring.

Source : Kasper, D.L, Hauser, S.L, Jameson, JL, et al. Harrison’s Principles of Interna Medicine. 19 th ed. McGraw-Hill Education; 2015. 202-4
 Pathogenesis
• occur as a result of appendiceal luminal obstruction
• Obstruction is most commonly caused by a fecalith
• Enlarged lymphoid follicles associated with viral infections (e.g.,
measles)
• Inspissated barium
• worms (e.g., pinworms, Ascaris, and Taenia)
• tumors (e.g., carcinoid or carcinoma)
• appendiceal ulceration
• Infection with Yersinia organisms may cause the disease
• Luminal bacteria multiply and invade the appendiceal wall 
venous engorgement and subsequent arterial compromise 
gangrene and perforation occur 
• slow: terminal ileum, cecum, and omentum (localized abscess); rapid:
perforation with free access to the peritoneal cavity

Source : Kasper, D.L, Hauser, S.L, Jameson, JL, et al. Harrison’s Principles of Interna Medicine. 19 th ed. McGraw-Hill Education; 2015. 202-4
 Clinical manifestations
• abdominal discomfort and anorexia
• The pain is described as being located in the periumbilical
region initially and then migrating to the right lower
quadrant
• resulting from distention of the appendiceal lumen; pain is carried
on slow-conducting C fibers and is usually poorly localized in the
periumbilical or epigastric region
• In general, this visceral pain is mild, often cramping and
usually lasting 4–6 h
• As inflammation spreads to the parietal peritoneal surfaces
 pain becomes somatic, steady, and more severe and
aggravated by motion or cough
• Nausea and vomiting occur in 50–60% of cases

Source : Kasper, D.L, Hauser, S.L, Jameson, JL, et al. Harrison’s Principles of Interna Medicine. 19 th ed. McGraw-Hill Education; 2015. 202-4
 Physical findings
• tenderness to palpation will often occur at McBurney's point
• Abdominal tenderness may be completely absent if a
retrocecal or pelvic appendix is present  tenderness in the
flank or on rectal or pelvic examination
• Referred rebound tenderness is often present and is most likely to be
absent early in the illness
• Flexion of the right hip and guarded movement by the patient
are due to parietal peritoneal involvement
• The temperature is usually normal or slightly elevated [37.2°–
38°C (99°–100.5°F)], >38.3°C (101°F)  perforation
• Rigidity and tenderness  more marked as the disease
progresses to perforation and localized or diffuse peritonitis
• Perforation is rare before 24 h after onset of symptoms, but
the rate may be as high as 80% after 48 h

Source : Kasper, D.L, Hauser, S.L, Jameson, JL, et al. Harrison’s Principles of Interna Medicine. 19 th ed. McGraw-Hill Education; 2015. 202-4
 Laboratorium findings
• moderate leukocytosis of 10,000–18,000 cells/microL is
frequent
• Leukocytosis of >20,000 cells/microL  perforation
• Anemia and blood in the stool suggest a primary diagnosis
of carcinoma of the cecum, especially in elderly individuals
• urine may contain a few white or red blood cells without
bacteria if the appendix lies close to the right ureter or
bladder
• Urinalysis is most useful in excluding genitourinary
conditions that may mimic acute appendicitis

Source : Kasper, D.L, Hauser, S.L, Jameson, JL, et al. Harrison’s Principles of Interna Medicine. 19 th ed. McGraw-Hill Education; 2015. 202-4
 Radiographs
• opaque fecalith (5% of patients) is observed in the right
lower quadrant (especially in children)
• intestinal obstruction or ureteral calculus may be present
• Ultrasound  an enlarged and thick-walled appendix
• CT will include a thickened appendix with periappendiceal
stranding and often the presence of a fecalith

Source : Kasper, D.L, Hauser, S.L, Jameson, JL, et al. Harrison’s Principles of Interna Medicine. 19 th ed. McGraw-Hill Education; 2015. 202-4
Source : Kasper, D.L, Hauser, S.L, Jameson, JL, et al. Harrison’s Principles of Interna Medicine. 19 th ed. McGraw-Hill Education; 2015. 202-4
 Treatment
• early operation and appendectomy as soon as the patient
can be prepared
• A different approach is indicated if a palpable mass is found
3–5 days after the onset of symptoms  phlegmon /
abscess
• broad-spectrum antibiotics, drainage of abscesses >3 cm,
parenteral fluids, and bowel rest usually show resolution of
symptoms within 1 week
• Interval appendectomy can be performed safely 6–12 weeks later
• Antibiotics alone can effectively treat acute, nonperforated
appendicitis in 86% of male patients (higher recurrence
rate)

Source : Kasper, D.L, Hauser, S.L, Jameson, JL, et al. Harrison’s Principles of Interna Medicine. 19 th ed. McGraw-Hill Education; 2015. 202-4
PERITONITIS
 • Peritonitis : inflammation of the peritoneum; it may
be localized or diffuse in location, acute or chronic in
natural history, infectious or aseptic in pathogenesis.
• Acute peritonitis is most often infectious and is
usually related to a perforated viscus (and called
secondary peritonitis).
• When no intraabdominal source is identified,
infectious peritonitis is called primary or spontaneous.

Source : Kasper, D.L, Hauser, S.L, Jameson, JL, et al. Harrison’s Principles of Interna Medicine. 19 th ed. McGraw-Hill Education; 2015. 205-6
 • Acute peritonitis is associated with decreased
intestinal motor activity, resulting in distention of the
intestinal lumen with gas and fluid.
• The accumulation of fluid in the bowel together with
the lack of oral intake leads to rapid intravascular
volume depletion with effects on cardiac, renal, and
other systems.

Source : Kasper, D.L, Hauser, S.L, Jameson, JL, et al. Harrison’s Principles of Interna Medicine. 19 th ed. McGraw-Hill Education; 2015. 205-6
Primary (spontaneous) bacterial peritonitis

• Usually caused by single organism

• Etiology
• Occurs most commonly in conjunction with cirrhosis of the liver (frequently
the result of alcoholism)
• Metastatic malignant disease
• postnecrotic cirrhosis
• chronic active hepatitis & acute viral hepatitis
• congestive heart failure
• systemic lupus erythematosus
• lymphedema

Source : Kasper, D.L, Hauser, S.L, Jameson, JL, et al. Harrison’s Principles of Interna Medicine. 19 th ed. McGraw-Hill Education; 2015. 205-6
 • Clinical manifestation
• Fever (80%)
• Acites  predates infection
• Abdominal pain, an acute onset of symptoms, and peritoneal irritation
(physical examination)
• Nonlocalizing symptoms  malaise, fatigue, or encephalopathy

• Other examination
• >250 PMNs/L is diagnostic for PBP
• Blood culture
• enteric gram-negative bacilli (Escherichia coli)  most commonly encountered
• gram-positive organisms (streptococci, enterococci, or even pneumococci) 
sometimes found
• Aerobic bacteria
• Contrast-enhanced CT  intraabdominal source for infection
• Chest & abdominal radiography  to exclude free air

Source : Kasper, D.L, Hauser, S.L, Jameson, JL, et al. Harrison’s Principles of Interna Medicine. 19 th ed. McGraw-Hill Education; 2015. 205-6
 • Treatment
• Third-generation cephalosporins (cefotaxime 2 g q8h,
administered IV)  initial coverage in moderately ill patients
• Broad-spectrum antibiotics, such as penicillin/β-lactamase
inhibitor combinations (piperacillin/tazobactam 3.375 g q6h IV
for adults with normal renal function); ceftriaxone (2 g q24h IV)

• Prevention
• Up to 70% of patients experience a recurrence within 1 year
• Antibiotic prophylaxis reduces this rate to <20%
• Prophylaxis agents
• fluoroquinolones (ciprofloxacin, 750 mg weekly; norfloxacin, 400 mg/d)
• trimethoprim-sulfamethoxazole (one double-strength tablet daily)

Source : Kasper, D.L, Hauser, S.L, Jameson, JL, et al. Harrison’s Principles of Interna Medicine. 19 th ed. McGraw-Hill Education; 2015. 205-6
Secondary peritonitis
• Develops when bacteria contaminate the peritoneum as a result of
spillage from an intraabdominal viscus  chemical irritation and/or
bacterial contamination
• Found almost always constitute a mixed flora in which
• facultative gram-negative bacilli
• anaerobes predominate, especially when the contaminating source is colonic
• Early death in this  gram-negative bacillary sepsis and to potent
endotoxins circulating in the bloodstream
• E. coli, are common bloodstream isolates, but Bacteroides fragilis bacteremia
also occurs

Source : Kasper, D.L, Hauser, S.L, Jameson, JL, et al. Harrison’s Principles of Interna Medicine. 19 th ed. McGraw-Hill Education; 2015. 205-6
Source : Kasper, D.L, Hauser, S.L, Jameson, JL, et al. Harrison’s Principles of Interna Medicine. 19 th ed. McGraw-Hill Education; 2015. 205-6
 • Clinical manifestation
• local symptoms may occur in secondary peritonitis, ex:
• Epigastric pain from a ruptured gastric ulcer
• Appendicitis  vague, with periumbilical discomfort and nausea; number of
hours  pain localized right lower quadrant
• lie motionless
• knees drawn up to avoid stretching the nerve fibers of the peritoneal
cavity
• Coughing and sneezing  increase pressure within the peritoneal
cavity  sharp pain

• Physical examination
• voluntary and involuntary guarding of the anterior abdominal
musculature
• tenderness, especially rebound tenderness

Source : Kasper, D.L, Hauser, S.L, Jameson, JL, et al. Harrison’s Principles of Interna Medicine. 19 th ed. McGraw-Hill Education; 2015. 205-6
 Treatment
• antibiotics aimed particularly at aerobic gram-negative
bacilli and anaerobes
• penicillin/β-lactamase inhibitor combinations
(ticarcillin/clavulanate, 3.1 g q4–6h IV); cefoxitin (2 g q4–6h
IV)
• Patients in the intensive care unit  imipenem (500 mg
q6h IV), meropenem (1 g q8h IV), or combinations of drugs,
such as ampicillin plus metronidazole plus ciprofloxacin
• Surgical intervention + antibiotics (bacteremia)  decrease
incidence of abscess formation & wound infection; prevent
distant spread of infection

Source : Kasper, D.L, Hauser, S.L, Jameson, JL, et al. Harrison’s Principles of Interna Medicine. 19 th ed. McGraw-Hill Education; 2015. 205-6
PERFORASI INTESTINAL
 • Upper-bowel perforation can be described as either
free or contained.
• Free perforation : bowel contents spill freely into the
abdominal cavity, causing diffuse peritonitis (eg, duodenal
or gastric perforation).
• Contained perforation : when a full-thickness hole is
created by an ulcer, but free spillage is prevented because
contiguous organs wall off the area (as occurs, for example,
when a duodenal ulcer penetrates into the pancreas).

• Lower-bowel perforation (eg, in patients with acute

diverticulitis or acute appendicitis) results in free
intraperitoneal contamination

Source : http://emedicine.medscape.com/article/195537-perforation
 Etiology
• Penetrating injury to the lower chest or abdomen (eg.
knife injuries)
• Blunt abdominal trauma to the stomach
• Ingestion of aspirin, nonsteroidal anti-inflammatory
drugs (NSAIDs)
• Bacterial infections - Bacterial infections (eg, typhoid
fever) may be complicated by intestinal perforation

Source : http://emedicine.medscape.com/article/195537-perforation