KURSK STATE

MEDICAL UNIVERSITY
Propaedeutics of Internal
Diseases Department
Professor T.A. Dronova
Lecture
GASTROENTEROLOGY
MAIN CLINICAL SYNDROMES

UPPER GASTROENTISTINAL BLEEDING

Upper GI bleeding - bleeding from lesion

of esophagus, stomach, duodenum

(above Treits ligament)
Upper GI bleeding features:
Hematemesis (vomiting of blood or
cofee ground vomiting)
Melena
Clinical features depend on rapidity & amount of

blood lost

GASTROENTISTINAL BLEEDING
Hematemesis - vomiting of blood (bright red or

coffee ground)
Melena - tarry black, sticky, foul smelling stool
(other stool darkness - iron & bismuth )
Special features:
a) approximately 60 ml of blood is required to
produce single black stool
b) the blood loss > 60 ml produces melena for
more than 7 days
c) to produce melena the blood must be in the
gut for 8 hours

UPPER GASTROENTISTINAL BLEEDING

Etiology
Common causes
Chronic duodenal ulcer
Chronic gastric ulcer
Gastric erosions (erosive gastritis)
Varices
Mallory-Weis tear
Esophagitis
Duodenal erosions
Stomach cancer
Miscellaneous

%
25
20
20
10
7
5
5
3
5

UPPER GASTROENTISTINAL BLEEDING

Subsequent cause evaluation

Peptic ulcer disease epigastric pain &

heartburn history
Gastric erosions NSAIDs or
corticosteroids using
Liver cirrhosis signs of chronic liver
diseases (jaundice, palmar erythema,
leukonychia, spider nevi,
hepatosplenomegaly & ascites)
Mallory-Weis syndrome - history of
forceful vomiting before hematemesis

UPPER GASTROENTISTINAL BLEEDING

Clinical features
Bleeding from upper GIT may present with

hematemesis (rapid bleeding presents as

hematemesis ) or melena (slow bleeding
presents as melena)
Hematemesis - vomiting of blood
Cofee ground vomiting (if blood remains in
stomach, it becomes partially digested &
appears brown in the vomit)
Melena - passage of black stools (after as little
as 50-100 ml of blood in upper GIT - black
colour due to altered blood by acid)

Severe bleeding
Symptoms:
weakness, faintness, nausea, sweating,
restlessness & disorientation
Signs:
postural hypotension > 10 mmHg - indication
of > 20% of blood volume lost
rapid pulse rate
decreased urinary output
patient may be in shock on arrival (systolic BP
< 90 mm Hg)

UPPER GASTROENTISTINAL BLEEDING

Initial assessment blood lost estimation

Clinical judgement of degree or rate of

bleeding
BP, pulse & postural changes (orthostatic drop
in blood pressure > 10mm Hg or pulse rise of
20 beats per minute or more indication of 1520% acute lost of blood volume)
Urine output monitoring (acute renal failure
due to hypovolemia)
Shock on arrival ( systolic BP < 90mmHg )
indication of massive 20-25% acute volume lost
(severe emergency)

UPPER GASTROENTISTINAL BLEEDING

Initial assessment blood lost estimation

Initial hemoglobin level & hematocrit - not

altered until 24-73 hours (reduced hematocrit

on admission to hospital suggests chronic
bleeding prior to acute episode)
Rised blood urea with normal serum creatinine
loss of at least 1 liter indication
Nasogastric tube passage - assessing
persistent rate of bleeding

UPPER GASTROENTISTINAL BLEEDING

Investigations
Endoscopy
Selective abdominal angiography
Urea, creatinine, electrolytes
Liver function tests, protrombin
Blood grouping & cross matching
Blood test
Radionuclide scan

UPPER GASTROENTISTINAL BLEEDING

Management
Intravenous access, oxygen, sedation
Blood volume replacement
Endoscopy
Pharmacological measures:
Proton pump inhibitor
Octreotide
Surgery

UPPER GASTROENTISTINAL BLEEDING

Emergency management
History & examination
Pulse & BP monitoring half-hourly
Blood examination for hemoglobin, urea, cretinine,

electrolytes, blood grouping & cross matching

IV line (in brisk bleeding central line)
Normal saline & blood trasfusion (indications: shock
BP < 100 mm Hg, pulse > 100, hemoglobin < 10 g/dl)
Oxygen for shocked patients
Urgent endoscopy
Re- endoscopy for continued bleeding
Surgery if bleeding persist

Lower gastrointestinal bleeding

Lower GI bleeding is defined as bleeding

arising below the ligament of Treitz:

small intestine & colon
majority of cases arise from colon &
particularly the anorectal region

Lower gastrointestinal bleeding

Etiology
Young patients (below 50 years):
Anorectal disease (hemorrhoids, anal fissure)
Infectious colitis (Shigella, E. coli)
Inflammatory bowel disease (ulcerative colitis)
Old patients (above 50 years):
Diverticulosis
Angiodysplasias
Neoplasms
Ischemic colitis

Lower gastrointestinal bleeding

Signs
Painless bleeding - internal hemorrhoids,

diverticulosis, angiodysplasia
Bleeding with pain - in anal fissure, ischemic
colitis & inflammatory bowel disease
Haematochezia - bright red blood from

rectum:
bleeding from anal & rectal lesions in
hemorrhoids, fissures, fistulas & carcinomas
amount of blood vary from few drops to
massive bleeding

Haematochezia
It is a passage of red (or maroon) blood from

the rectum, usually signifies bleeding from a

source distal to the ligament of Treitz (between
duodenum & small intestine)
it can also occur from massive upper
gastrointestinal bleeding (from esophagus,
stomach & duodenum)
Appearance of blood in stool depends not
only on bleeding site but also on hemorrhage
rate & rapidity of transit

Lower gastrointestinal bleeding

Patient evaluation
Diverticulosis: painless maroon or bright red

hematochezia in patient > 50 years of age, bleeding

stops spontaneously
Angiodysplasia: painless bleeding in patient > 70 years
Neoplasm: benign & malignant usually with chronic
occult bleeding
Inflammatory bowel disease (ulcerative colitis): diarrhea
with occult bleeding or recurrent hematochezia
associated with abdominal pain, tenesmus & urgency
Anorectal disease; hemorrhoids painless bleeding
mixed with stool or dripping into toilet bowl, painful
small bleeding in anal fissure
Ischemic colitis elderly patient with aterosclerosis
bloody diarrhea with mild abdominal cramps

COLONIC DISEASE
Rectal bleeding
Diagnostic stool appearance:
Blood coating exterior of formed stool - lesion in

anal canal or rectum

Blood admixed with feces - bleeding source higher
in colon
Brisk hemorrhage from colon or distal small
intestine - passage of fresh blood (hematochezia):
fresh blood & clots - lesion in left colon
dark, maroon-colored blood - bleeding from right
colon

Lower gastrointestinal bleeding

Diagnosis

1.

2.
3.
4.
5.

Sequence of diagnostic tools: 1) rectal examination,

anoscopy & sigmoidoscopy; 2) nasogastric tube; 3)
Technetium scan; 4) angoigraphy; 5) colonoscopy
Digital rectal examination, anoscopy & sigmoidoscopy
evidence of anorectal diseases, Iinflammatory bowel
disease or infections colitis
Exclude upper GI bleeding nasogastric tube
Technetium-99 scan to detect active bleeding course
Angoigraphy (choice method) rapid localization
Colonoscopy (if bleeding stops) identification of
angiodysplazia, tissue biopsy

Physical examination
in colonic diseases
Digital rectal examination (perianal,

sphinteric & ampullary lesions, prostatic &

uterine abnormalities, rectal masses &
metastatic tumor in perirectal tissues Blumers shelf
Fecal material on glove - immediate test with
guaiac-impregnated cards for occult blood

Lower gastrointestinal bleeding

Management
Bed rest, sedation & transfusion
Stop aspirin & other NSAIDs
Therapeutic colonoscopy: endoscopic

electrocoagulation of angiodysplasia
Intra-arterial vasopression or embolization
(90% effective in diverticulum or
angiodysplasia)
Surgery

Occult gastrointestinal bleeding

Loss of small amounts of blood into GIT

present in stool, but no hematochezia or

melena
Methods for detection:
Positive fecal occult blood test
Iron deficiency anemia in adult

Occult gastrointestinal bleeding

Etiology
All causes of upper & lower gastrointestinal

bleeding common causes:

Tumors: benign or malignant tumors of any
site in GIT especially colon canser
Peptic ulcer & esophagitis
NSAIDs
Angiodysplasia
Infections (hook worm most common cause)
Major causes: cecal carcinoma &
angiodysplasia (arteriovenous malformation
which can be visible on colonoscopy)

Occult gastrointestinal bleeding

Investigations
Webers guaiac test
detection of hemoglobin peroxidase:
3-5 g of feces mixed with strong acetic acid
(semiliquid paste) mixture stands for 30
min.
+ 1-2 ml of hydrogen piroxide
+ drop by drop (15-20 ml) of extemporarily
prepared alcoholic solution of guaiac resin
Blue or violet colour in blood presence

Occult gastrointestinal bleeding

Investigations
Gregersens benzidine test
Property of hemoglobin to catalyse oxidationreduction reactions:
Hydrogen piroxide + 1% benzidine
1% benzidine changes color in blood
presence (green or blue color)

Blood in stool
Blood mixed with stool: left sided colonic

tumor, inflammatory bowel disease, diverticular

disease, infective colitis & angiodysplasia
Fresh blood in small amounts: hemorrhoids,
Crohns disease of the anus, carcinoma of the
rectum
Severe bleeding (rare) : diverticular disease &
ischemic colitis

Difference between upper &

lower gastrointestinal bleeding
Features

Upper
gastrointestinal
bleeding

Lower
gastrointestinal
bleeding

Site

Above Treits
Below Treits
ligament (esophagus, ligament (small
stomach, duodenum) intestine & colon)

Presentation

Hematemesis
Cofee ground

vomiting
Melena

Hematochezia

Difference between upper &

lower gastrointestinal bleeding
Features

Upper
gastrointestinal
bleeding

Nasogastric Blood
aspiration

Bowel
sounds

Hyperactive

Lower
gastrointestinal
bleeding
Clear fluid

Normal

MALABSORPTION
Malabsorption - inadequate transport of one

or more of constituents of normal diet from

intestinal lumen across intestinal epithelium
into portal circulation
CLINICAL FEATURES:
Diarrhea
Abdominal pain
Distension
Weight loss
Nutritional deficiencies

Nutrient absorption
Sites

Duodenum: iron, calcium, magnesium,

folic acid, water soluble vitamins, amino

acids, monosaccharides
Jejunum: fatty acids, amino acids,
monosaccharides, water soluble vitamins
Ileum: monosaccharides, fatty acids,
amino acids, fat soluble vitamins (A, D, E,
K), vitamin B12 & conjugated bile salts

Nutrient absorption
Physiology - 3 phases
Luminal phase: hydrolysis &

solubilization of nutrients
Mucosal phase: further breakdown of
nutrients & transfer into cell
Transport phase: removal of nutrients
into vascular or lymphatic circulation

1. Intraluminal malabsorption
Disoders

Pancreatic insufficiency:
Chronic pancreatitis
Cystic fibrosis (autosomal disease)
Carcinoma of pancreas
Deficiency of bile acids:
Enterohepatic circulation interruption (resection or
terminal ileum disease)
Small intestine colonization with bacteria which
deconjugate bile acids (stagnant loop syndrome)
Uncoordinated gastric emptying:
Gastroenterostomy
Partial gastrectomy

2. Mucosal phase malabsorption

Disoders
Generalized mucosal abnormalities (histologically

abnormal mucosa):
Coeliac disease (gluten-sensitive enteropathy)
Tuberculosis
Tropical sprue
Lymphoma
Radiation enteritis
Whipples disease (macrophages infiltration)
Malabsorption of specific substances (histologically
normal mucosa):
Lactase deficiency

3. Transport phase malabsorption

Disoders
Vascular: vasculitis, atherosclerosis
Lymphatic: lymphangiectasia,

infiltrations

Malabsorption Syndrome
Symptoms
GIT system
Genitourinary system
Hematopoetic system
Musculoskeletal system
Nervous system
Skin

MALABSORPTION
Nutritional
deficiencies

Features

Fats

Steatorrhea, frothy
stools, watery diarrhea,
weight loss

Carbohydrates

Flatulent dyspepsia
(borborygmus),
abdominal distension,
flatus, watery diarrhea

MALABSORPTION
Nutritional
Features
deficiencies
Protein Weight loss, muscle wasting,
hypoalbuminuria, oedema,
leuconychia
Folic acid Macrocytic,
megaloblastic anemia,
glossitis, oral mucosa
ulceration in folic acid
deficiency

MALABSORPTION
Nutritional Features
deficiencies
Vitamin B12 Macrocytic, megaloblastic
anemia, glossitis, mental
& neurological
disturbances
Vitamin B
complex

Cheilosis, angular
stomatitis, dermatitis,
polyneuritis

MALABSORPTION
Nutritional
deficiencies

Features

Vitamin C

Bleeding tendency

Vitamin A

Follicular
hyperkeratosis,
xeropthalmia, night
blindness

MALABSORPTION
Nutritional
deficiencies

Features

Vitamin D &
Calcium

Osteomalacia
(rickets), proximal
myopathy,
paraestesia, tetany

Vitamin K

Purpura,
hemorrhages
(bruising & bleeding)

MALABSORPTION
Nutritional
deficiencies

Features

Iron

Hypochromic anemia,
cheilosis, spoon-shaped
nails (koilonychia),
apthous ulcers

Sodium

Muscular weakness,
cramps

MALABSORPTION
Nutritional
deficiencies

Features

Potassium

Flaccidity,
arrhythmias

Magnesium

Muscular weakness,
paraestesia, tetany

Water

Nocturnal diuresis

MALABSORPTION
Nutritional
deficiencies

Features

Zinc

Poor taste, dermatitis,

poor wound healing

Bile salts

Watery diarrhea

GASTRIC OUTLET OBSTRUCTION

(PYLORIC STENOSIS)
Etiology:
Peptic ulcer in the region of pylorus
(may lead to gastric outlet obstruction)
due to edema, spasm, fibrous stricture
Duodenal ulcer
Carcinoma of antrum

GASTRIC OUTLET OBSTRUCTION

(PYLORIC STENOSIS)
First - narrowing is compensated by hypertrophy

of the gastric muscles

Later - stomach becomes distended, food stays
inside for longer period & fermentation &
putrefaction occurs in the stomach
Absorption of water impaired
Upset of water-salt balance causing general
dehydration of the body & decrease of chloride
content in the blood & urine

GASTRIC OUTLET OBSTRUCTION

(PYLORIC STENOSIS)
Long history of peptic ulcer with prominent

nausea & vomiting

Without symptoms of peptic ulcer pyloric
carcinoma
Vomiting - striking relief
Vomitus: alkaline reaction (presence of

ammonia compounds) of food particle have

been eaten 24 hours or > previously

GASTRIC OUTLET OBSTRUCTION

(PYLORIC STENOSIS)

Clinical features

permanent pain (which intensifies at night)

eructation with rotten egg wind
vomiting with food that was ingested several

days ago
constipation is alternated with diarrhea
through irritation of the small intestine by
fermented food discharged into it from the
pylorus that is opened by intensified
peristalsis
alkalosis develops if large amount of HCl is
lost in vomiting

GASTRIC OUTLET OBSTRUCTION

(PYLORIC STENOSIS)

Clinical features

Wasting (cachexia) due to undernourishment

Dehydration
Examination of the epigastrium: peristalsis &

antiperistaltic contractions of the stomach visible gastric peristalsis (peristalsis wave

progressing from left hypochondrium &
epigastric region towards right lumbar region)
Late splashing sound (Hippocrates sign) > 7-8
hours after last meal or drink (in healthy person
splashing sound (succusion) < 1 hour after
meals because gastric emptying is rapid)

GASTRIC OUTLET OBSTRUCTION

(PYLORIC STENOSIS)

Investigation

Aspiration of stomach contents: volume

> 100 ml after fasting overnight or food

residue
Barium meal:
presence of barium in stomach > 6 hours
dilatation of stomach with or without
excessive peristalsis
Increase in fasting residue of stomach
Lesion at or near pylorus

GASTRIC OUTLET OBSTRUCTION

(PYLORIC STENOSIS)

Investigation
Endoscopy:

Lesion at pylorus
Increase in fasting residue of stomach

food
Serum electrolytes depletion

GASTRIC OUTLET OBSTRUCTION

(PYLORIC STENOSIS)
Management
Aspiration:
Nothing per os
2-4 hourly aspiration for 3-4 days (if aspiration

volume decreased fluid by mouth)

IV fluid rehydration
Vitamins
Surgery

INTESTINAL OBSTRUCTION
2 types of intestinal obstruction
Simple or dynamic: peristalsis working
against obstruction agent in the intestinal
lumen, in the wall or outside the wall (fecal
impaction, stricture or adhesion)
Strangulation or adynamic: peristalsis ceases
& no propulsive wave occurs - with intestinal
blood supply when the bowel is trapped or
twisted (paralytic ileus or mesenteric vascular
occlusion)

INTESTINAL OBSTRUCTION
Etiology
Luminal
obstruction

Fecal impaction
Gallstone ileus
Worms (ascaridiasis)

Intrinsic
lesions of
bowel wall

Tumors of large intestine

Strictures (tuberculosis, Crohns
disease)
Intussusception

Exstrinsic
compression

Adhesion
Hernias
Volvulus

Paralytic ileus Peritonitis

Postoperative
Vascular

INTESTINAL OBSTRUCTION
Clinical features
Pain:
Colicky pain in mechanical obstruction
Dull constant pain in paralytic ileus
Vomiting:
Copious in high small bowel
obstruction
Late or absent in lower small bowel or
colon obstruction

INTESTINAL OBSTRUCTION
Clinical features
Abdominal distention
Distention confined to some loops of bowel ridges across the abdomen forming Ladder
Pattern - visible intestinal peristalsis - distal
small bowel obstruction: step ladder form of
peristalsis waves (motile small intestine) in
umbilical region
Later diffuse distention indication of chronic
large bowel obstruction or paralytic ileum
Complete obstruction - feaces & flatus not
passed
First - increased bowel sounds, later - absent
peristaltic sounds

INTESTINAL OBSTRUCTION
Investigation
Finger examination of rectum:

ballooned & empty rectum (Obukhovs

hospital or Grekovs sign)

Plain X-ray abdomen (in erect & supine

position) - gaseous distention &

intestinal fluid levels (Kloibers cups horizontal fluid level & gas bubble)

INTESTINAL OBSTRUCTION
Management
Nothing per os
Decompression (gastrointestinal drainage
via nasogastric tube)
IV fluid & electrolytes
Antibiotics
Surgery

ACUTE ABDOMEN
ACUTE ABDOMEN a term used to

define a group of abdominal

conditions in which prompt surgical
treatment must be considered

ACUTE ABDOMEN
CAUSES
Bowel
Acute appendicitis
Perforated peptic ulcer or abdominal viscus
Diverticular disease
Intestinal obstruction & strangulation
Meckels diverticulum
Terminal ileitis (Yersinia infection)

ACUTE ABDOMEN
CAUSES
Vascular
Acute vascular insufficiency
Ruptured aortic aneurysm

Gynecological
Ruptured ectopic pregnancy
Ruptured ovarian cyst
Acute salpingitis

ACUTE ABDOMEN
CAUSES
Others
Cholecystitis
Acute pancreatitis
Acute mesenteric adenitis
Medical causes of abdominal pain

MIMIC ACUTE ABDOMEN

MEDICAL CONDITIONS
Common
Myocardial infarction
Pneumonia
Pleurisy
Acute pyelonephritis
Irritable bowel syndrome
Tonsillitis, otitis media in children
Uncommon
Diabetic ketoacidosis
Acute porphyria

ABDOMINAL PAIN
MECHANISMS
1. Visceral pain
a) Irritation or inflammation of peritonium

(peritonitis, pancreatitis)
b) Vascular insufficiency (strangulation of bowel
in hernia or volvulus, acute mesenteric vascular
obstruction)
c) Spasm of hollow viscus (intestinal colic, biliary
colic, ureteric colic)
d) Stretching of capsule of solid organs (liver,
spleen & kidney when they become enlarged)
e) Ulceration of tissue (peptic ulcer)

ABDOMINAL PAIN
MECHANISMS
2.

Referred pain

a) From the chest (myocardial infarction, pleurisy)

b) From the vertebral column (nerve root

compression, musculoskeletal disorders)

c) From the gonads (torsion of the testes)
3.

Miscellaneous

a) Metabolic disorders (uraemia, diabetes,

porphyria, hypercalcaemia, Addison's disease)

b) Psychogenic disturbances (irritable bowel
syndrome)

ACUTE ABDOMEN
Clinical picture
Paroxysm of severe abdominal pain
Peritoneal irritation signs (respiratory abdomen

excursions absent, Shchetkin-Blumberg sign +)

Signs of disordered peristalsis & tone of GIT (nausea,
vomiting, pronounced meteorism, constipation,
passage of flatus, visible peristalsis Wahls sign)
Circulatory collapse: pallor, syncope, cold sweat,
rapid & weak pulse, low BP, pinched face (facies
Hippocratica)
General rapidly progressing signs of inflammation:
fever, neutrophilic leucocytosis, accelerated ESR

Localization of abdominal pain

Organ

External localization
on abdominal wall

Stomach &
duodenum

Epigastrium, midline
or slightly to the right

Transverse & sigmoid Periumbilical or right

colon
iliac fossa

Localization of abdominal pain

Organ

External localization
on abdominal wall

Right colon

Right lower quadrant

Left colom

Left lower quadrant

Localization of abdominal pain

Organ

External localization
on abdominal wall

Rectosigmoid

Suprapubic

Bladder

Suprapubic

Localization of abdominal pain

Organ

External localization
on abdominal wall

Rectum

Lower back, midline

Gallbladder

Midepigastric,
radiating to right
upper quadrant & to
right scapular area

Localization of abdominal pain

Organ

External localization
on abdominal wall

Common bile duct

Midepigastric,
radiating to shoulder
or retrosternally to
neck

Pancreas

Midepigastric,
spreading laterally to
back if posterior
peritoneum is
involved

ACUTE ABDOMEN
Clinical picture
History
1. Pain
Onset: sudden in perforated duodenal ulcer &

acute intestinal ischaemia while gradual in

appendicitis
Nature: colicky in intestinal obstruction, biliary
colic & renal colic whereas continues pain in
peritonitis
Other fieatures: site, radiations, aggravating &
relieving factors
2. Vomiting
It can occur in any acute abdominal pain but
remains persistent in upper intestinal obstruction

ACUTE ABDOMEN
Clinical picture
Tongue furred in most acute abdominal

disease
Temperature fever more common in
acute inflammatory conditions

ACUTE ABDOMEN
Clinical picture
Examination
a) Signs of peritonitis
Site of tenderness
Guarding localized or generalized
Rebound tenderness
b) Signs of obstruction
Distension of abdomen due to gas
Increased gut sounds (borborygmi)
Absent gut sounds suggest peritonitis

ACUTE ABDOMEN
Investigations
Pelvic & rectal examination
Pelvic examination for gynecological disorders

(ruptured ectopic pregnancy)

Rectal examination to detect localized tenderness
d) Other observations:
Urinie analysis for:
a) Glucose & Ketones (for diabetic ketoacidosis)
b) WBC to exclude acute pyelonephritis
c) Phorphyrins - to detect porphyria (rare
condition)

ACUTE ABDOMEN
Investigations & treatment
Hospitalization
Hourly taking body temperature
Total blood counts
ECG
Radiographic abdomen examination (R-scopy &
R-graphy)
Surgery

ACUTE APPENDICITIS
SYMPTOMS
Pain begins as vague, central abdominal pain

(around umblicus or epigastrium) & shift's to the

right iliac fossa within a few hours
2. Anorexia (preceding the pain)
3. Nausea & vomiting (vomiting is not so
frequent)
4. Constipation or diarrhoea: mostly patients with
appendicitis develop constipation for a few days
before the attack of the pain - a few patients
have diarrhoea

ACUTE APPENDICITIS
SIGNS
1. Fever: low grade fever (100*F)
2. White & furred tongue
3. Tenderness in right iliac fossa
4. Localized guarding over the

inflamed appendix

ACUTE APPENDICITIS
Confirmatory signs
1) Rovsing's sign:- Pressure on the left iliac

fossa produces pain on the right iliac fossa

2) Psoas' sign: Pain on extension of right thigh
with the patient lying on the left side
3) Obturators sign:- Pain on internal rotation of
the flexed right thigh while the patient lying in
supine position
4) Rebound tenderness: Tenderness in the
right iliac fossa after releasing pressure
5) Rectal examination: may demonstrate,
tenderness in the pelvis

ACUTE APPENDICITIS
INVESTIGATIONS & TREATMENT
INVESTIGATIONS
Blood CP:- Shows leucocytosis (only

reaching upper limits - not so marked)

TREATMENT
Appendectomy

GASTRIC JUICE ANALYSIS

Nasogastric tube - into stomach
Gastric contents aspirated: 1st portion - from

fasting stomach (N = 50 ml)

4 Subsequent 15 min. samples of gastric juice
collected by continues aspiration (basal acid
output BAO)
Subcutaneously pentagastrin - 4 subsequent 15
min. samples (maximal acid output - MAO) samples titrated with NaOH to calculate BAO &
MAO secretory rate

GASTRIC JUICE ANALYSIS

Debit-hour of HCl - amount of free HCL secreted

during 1 hour
Formula: D ( HCl ) = A X B X 0.0365
D ( HCl ) - debit-hour of HCl
A - amount of gastric juice secreted in 1 hour
B - acidity of gastric juice in titrating units
0.0365 - molecular weight of HCl
Normal BAO level ranges from 50-150 mg HCL
& normal MAO level - from 200-400 mg HCl

GASTRIC JUICE EXAMINATION

Fasting stomach = 50 ml
Hourly basal secretion = 30 -150 ml (~50 ml)
Evacuating function by gastric juice volume

(after parenteral stimulants or 25 min. after test

meal) = 75 ml
Hourly secretion after stimulation:
~ 60 ml (intermittent aspiration)
~100 - 120 ml (continuous aspiration)

GASTRIC JUICE ANALYSIS

Pathological changes:
Level above normal BAO (50-150 mg) &

normal MAO (200-400 mg HCl)

hyperchlorhydria
Level below normal BAO (50-150 mg) & normal
MAO (200-400mg HCl) - hypochlorhydria
If both BAO & MAO = 0 - achlorhydria
Absence of pepsin in gastric juice - achylia
Achylia arises suspicion of stomach
carcinoma

INCREASED GASTRIC SECRETION

(HYPERSECRETION)
Hypersecretion - abnormal increase in gastric

juice amount
Gastric hyperacidity or hyperchlorhydria excessive gastric acidity
Hypersecretion: gastric juice > 160 ml extracted
in 1 hour during examination with thin tube
Hypersecretion manifested by constant
effusion of gastric juice containing free HCl:
amount of content in fasting stomach > 70 ml
(associated with complaints of heartburn,
vomiting & hunger pain)

DIMINISHED GASTRIC SECRETION

(HYPOSECRETION)
Hypochlorhydria - secretory function

impairment with reduced free HCl

secretion in stomach
Anacidity or achlorhydria - secretory
function impairment with totally absent
HCL
Gastric achylia - simultaneous absent of
pepsin & HCl from gastric juice

DIMINISHED GASTRIC SECRETION

(HYPOSECRETION)
HCl & pepsin may disappear as result of

functional disturbances (causes differentiated

by means of histamine test)
Organic stomach lesions - HCl not secreted

even after histamine injections

Functional disorder - free HCl in gastric

content

DIMINISHED GASTRIC SECRETION

(HYPOSECRETION)
Absence of free HCl - often in diseases

accompanied by toxicosis & derangement of

CNS function causing inhibition of stomach
secretion
Organic achylia in atrophic processes in
gastric glands due to inflammatory changes,
malnutrition, protein & vitamin deficiency in
food
Main signs: gastric & intestine dyspepsia

Gastric pH-metry
Normal pH in esophagus - neutral or slightly

alkaline (7,0-7,2)
Normal pH in stomach:
cardia = 1,3-2,0
antrum >2,5
0,9-1,3 hyperacidity
2,0-3,0 moderate hypoacidity
3,0-5,0 significant hypoacidity
> 6,0 veritable achlorhydria

Gastric pH-metry
After ingestion of 0.5 mg of NaHCO3,

stomach pH increases for about 20 min. &

then returns to initial level
Decreased esophagus pH - gastroesophageal reflux
Neutral gastric pH - achylia
Increase of gastric pH after administration
of NaHCO3 >30 min. - duodenogastric
reflux suspected

INADEQUATE DIGESTION
SYNDROME
Upset cavital digestion: stomach &

intestinal dyspepsia
Upset parietal digestion
Mixed form
DYSPEPSIA - term used as collective
description for variety of
alimentary symptoms

Dyspepsia
SYMPTOMS INCLUDED IN TERM DYSPEPSIA
Upper abdominal pain (may or not be related to
food)
Gastro-oesophageal regurgitation & heartburn
Anorexia, nausea & vomiting
Early repletion or satiety after meals
A sense of abdominal distension or bloating
(sense of abdominal distension)
Flatulence (burping, belching) & aerophagy

Dyspepsia
Etiology
Non-compensated secretory stomach

insufficiency
Exocrine pancreas dysfunction
Upset bile secretion
Disordered chyme passage through GIT:
stasis, stenosis, intestinal compression,
intense peristalsis accelerated passage
Intestinal infection & dysbacteriosis
Alimentary disorders (overeating, diet rich in
protein, fat, carbohydrate)

Dyspepsia
Most common causes
Stomach disorders (atrophic gastritis with

achylia or achlorhydria, stomach cancer)

Intestinal disorders (enteritis)
Disorders of regulation of digestive process
(so-called functional dyspepsia - in
depression)
Liver disorders (hepatitis, liver cirrhosis)
Disorders of pancreas (chronic pancreatitis)
Endogenous (uremia, diabetic ketoacidosis)
or exogenous (alcohol) intoxications

Dyspepsia
Pathogenesis
Incomplete breakdown of food particles
Active propagation of intestinal bacterial flora
Dysbacteriosis
Functional dyspepsia - psychological factors

Gastric Dyspepsia
Etiology
Dyspepsia - commonly associated with

organic diseases of upper GIT:

Peptic oesophagitis
Achlorhydria & achylia
Peptic ulcer
Gastric carcinoma
Pyloric stenosis
Gastritis

Gastric Dyspepsia
Clinical picture
Feeling of discomfort
Epigastrium pressure or distension after meals
Frequent eructation
Regurgitation (often with acid or fetid odor)
Unpleasant taste in mouth
Nausea
Poor appetite
Achylous diarrhoea
Meteorism
Gastric juice examination
achlorhydria or achylia (pepsin & HCL absence)

Functional Dyspepsia
(Nonulcer dyspepsia)
Complaints of persistent dyspepsia with

excluded organic causes - nonulcer

functional dyspepsia
Symptoms of disturbance in motorfunction

of GIT due to psychological factors

Patients - usually young (below 40 years ),

women / men = 2:1

FUNCTIONAL DYSPEPSIA
DISTINGUISHING FEATURES
Pain / discomfort - not episodic (tends to occur daily

for long periods at time)

Pain may persist throughout entire day from morning
to night, unaffected by food, antacids or bowel
movement
Pain diffuse (sweeping movements of hands over
abdomen, may be referred to more than one site)
Rare night pain, rare waking patient from sleep
When vomiting occurs - no relief from pain, patient
cannot eat for hours afterwards (by contrast, vomiting
almost always relieves pain in gastric dyspepsia of
peptic ulcer)

FUNCTIONAL DYSPEPSIA
Diagnosis
Anxious patient
History of previous psychotropic medication
In young women - rule out pregnancy
In old age - exclude intraabdominal malignancy
Liver palpation & LFTs

Investigations
No diagnostic investigation
In old age - endoscopy or barium meal to resolve
doubt of malignancy

INTESTINAL DYSPEPSIA
Reasons
Exocrine pancreas dysfunction
Small intestine chronic inflammatory

diseases

Clinical picture
Abdomen inflation
Rumbling (borborygmus) in abdomen
Intensive flatus passage
Diarrhea with putrefactive or acid smell
Constipation (rare)

INTESTINAL DYSPEPSIA
(Inadequate digestion)
Fermentative dyspepsia
Disturbance in carbohydrates digestion caused by

ingestion of fermented food & sustained by

overloading intestine with food abundant in
carbohydrates
Acid products formed in intestine - intensified
peristalsis
Fecal matter: putty-consistency & evacuated in
quantity
Stools - pale yellow color with acid odor, large
amount of gas bubbles & undigested starch - 3-7
times in 24 hours
Abdominal distention, splashing sound, rumbling
& tenderness by palpation

INTESTINAL DYSPEPSIA
(Inadequate digestion)
Putrefactive dyspepsia

Secondary to gastric achylia, pancreas hypofunction resulting disturbance of protein digestion

Decomposition process - in higher parts of intestine
(normally - in descending & sigmoid colon)
Inflammatory processes in intestine (protein exudate
undergoes putrefaction) - sustained & intensified by
ingestion of meat & fish
Stools: frequent, watery & copious
Fecal matter - dark colour with alkaline reaction &
extremely offensive odour with large amount of
remains of undigested food & muscle fibers with
retained striation
Patient undernourished & emaciated

INTESTINAL DYSPEPSIA
(Inadequate digestion)
Fatty dyspepsia
by rapid passage of food from small into
large intestine - inadequate secretion of
lipase & disturbance in bile supply of
intestine
Feces - pale yellow colour, with neutral or
slightly alkaline action & contain significant
amount of fatty acid crystals & soaps
Fecal fat loss > 6 mg per 24 hours - abnormal

INTESTINAL DYSPEPSIA
Investigations
Coprological findings (steatorrhea, amylorrhea)
Stool examination by physician - as soon as possible after

defecation for presence of visible blood on surface or

within the specimen, test for occult blood
Microscopic examination of fresh stool - diagnosis of
parasitic diseases (amebic colitis - motile trophozoits in
fresh, warm stool suspension)
Stool suspension stained with a drop of methylene blue for
polymorphonuclear leukocytes indication of presence of
acute inflammatory exudates (ulcerative colitis, amebic
colitis & bacillary dysentery)
Fixed & stained slides of stool for amoebas & other
parasites
Stool culture - for diagnosis of bacillary dysentery
Sudan III stain of stool - screening test for steatorrhea

DIARRHOEA
Stool weight increase > 300 g per day

accompanied by increased stool

frequency

Types:
Osmotic diarrhea
Secretory diarrhea
Inflammatory diarrhea
Abdominal motility diarrhea
Antibiotic-associated diarrhea

Osmotic diarrhea
Large quantities of non absorbed hypertonic
substances in gut lumen present
fluid enters bowel due to osmotic pressure:
Purgative intake
Generalized malabsorption
Specific malabsorption (disaccharidase
deficiency)
Osmotic diarrhea stops when patient stops
eating of malabsorptive substances

Secretory diarrhea
Active intestinal secretion of fluid &
electrolytes with decreased absorption:
Enterotoxin (cholera, E.coli)
Bile salts in colon following ileal
resection
Fatty acids in colon following ileal
resection
Food does not affect diarrhea - continues
during fasting

Inflammatory diarrhea
Damage to intestinal mucosal cells loss of fluid & blood:
Dysentery (Shigella)
Ulcerative colitis

Abdominal motility diarrhea

Not true diarrhea - volume &
weight of stool is not increased with
increased frequency of
defecation:
Irritable bowel syndrome
Diabetic neuropathy
Thyrotoxicosis

Antibiotic-associated diarrheaPseudomembranous colitis

After taking antibiotics (particularly
ampicillin, lincomycin & cephalosporin produce pseudomembranous colitis)
Sigmoidoscopy - multiple yellow plaques
& inflammation

Difference between small bowel

& large bowel diarrhea
Features

Small bowel
diarrhea

Large bowel
diarrhea

Stool
volume

Large

Small

Stool colour Light

Dark

Difference between small bowel

& large bowel diarrhea
Features

Small bowel
diarrhea

Large bowel
diarrhea

Stool smell

Very foul

Foul

Stool nature Soupy &

greasy

Mucinous &
jelly like

Difference between small bowel

& large bowel diarrhea
Features

Small bowel Large bowel

diarrhea
diarrhea

Stool type Watery

Mucoid

Blood in
stool

Common (usually
fresh blood, if
from caecum
maroon coloured

Rare (if
present
altered)

Difference between small bowel

& large bowel diarrhea
Features

Small bowel
diarrhea

Large bowel
diarrhea

WBCs in
stool

Rare

Common

Abdominal Periumbilical Lower abdomen

pain
region, mid (gripping &
location
abdomen
continuos)
(crampy &
intermittent)

Difference between small bowel

& large bowel diarrhea
Features

Small bowel Large bowel

diarrhea
diarrhea

Tenesmus

Absent

Present

Undigested
material

May be
seen

Invisible

Difference between small bowel

& large bowel diarrhea
Features

Small bowel Large bowel

diarrhea
diarrhea

Steatorrhea

May be
seen

Not seen

Frequency

Less

More

Abnormal stool - objective evidence

of colonic disease
Stool examination by physician - as soon as possible after

defecation for presence of visible blood on surface or within

the specimen, test for occult blood
Microscopic examination of fresh stool - diagnosis of
parasitic diseases (amebic colitis - motile trophozoits in
fresh, warm stool suspension)
Stool suspension stained with a drop of methylene blue for
polymorphonuclear leukocytes indication of presence of
acute inflammatory exudates (ulcerative colitis, amebic
colitis & bacillary dysentery)
Fixed & stained slides of stool for amoebas & other
parasites
Stool culture - for diagnosis of bacillary dysentery
Sudan III stain of stool - screening test for steatorrhea

Management
Restoration of blood volume

- restoration of blood volume can be best

achieved by transfusion of whole blood
- before blood arrangement, restored blood
volume with 0.9% normal saline and plasma
expender ( haemacel )
- the rate of blood transfusion must be
monitored carefully to avoid over transfusion
and consequent heart failure

Occult GI Bleeding
Is the lost of small amount of blood into tract

which is present in stool but cannot be seen

( no hematochezia or melena )
it is typically detected in 1 of the 2 settings :
a) positive feacal occult blood test
b) the presence of iron deficiency anemia in an
adult

Etiology
All causes of upper and lower GI bleeding may

also cause occult bleeding, following are the

common cases:
1. Tumors : benign or malignant
- tumor of any site of GIT, especially colon cancer
2. Peptic ulcer and esophagitis
3. NSAIDs
4. Infections : hookworm
Investigation : colonoscopy, barium enema, and
upper GI endoscopy
Management: according to the cause

Diagnosis
1. Rectal examination, anoscopy and
sigmoidoscopy are performed to look for
evidence of anorectal disease, inflammatory
bowel disease or infectious colitis
- if source is identified, no further investigations
are needed immediately unless bleeding persist
or is recurrent
2. Exclude an upper tract source : pass
nasogastric tube in patients with significant
bleeding to look for evidence of upper GI source