Course: Infectious

Module: Pallor and Ecchymosis

Facilitator: Dr. J. Sarapuddin
Date: June 8-10, 2020

I. ANATOMY
A. BILIARY SYSTEM
- The biliary system consists of the organs and ducts (bile
ducts, gallbladder, and associated structures) that are
involved in the production and transportation of bile.

- Bile is the greenish-yellow fluid (consisting of waste products,

cholesterol, and bile salts) that is secreted by the liver cells to
perform 2 primary functions: to carry away waste and to
break down fats during digestion

- Biliary anatomy parallels the portal venous supply of the

liver. The right hepatic duct drains the entire right lobe of the
liver. It is formed by the union of the anterior right hepatic
duct, which drains the anterior segments V and VIII, and the
posterior right hepatic duct, which drains the posterior
segments VI and VII. The anterior right hepatic duct lies
vertically, whereas the posterior hepatic duct is more - However, not all bile runs directly into the duodenum. About
horizontal. The left hepatic duct is formed by the union of 50% of the bile produced by the liver is first stored in the
ducts draining segments II and III and one or more ducts from gallbladder. This is a pear-shaped organ located directly
segment IV. Segment I normally drains to both the left and below the liver.
the right hepatic ducts. The bile ducts, together with
branches of the hepatic artery and portal vein, form the - Then, when food is eaten, the gallbladder contracts and
portal triad. releases stored bile into the duodenum to help break down
the fats.

C. BILE DUCTS OF THE LIVER

- Bile is secreted by the liver cells at a constant rate of about

40 mL per hour.

- When digestion is not taking place, the bile is stored and

concentrated in the gallbladder; later, it is delivered to the
duodenum.

- The bile ducts of the liver consist of the right and left hepatic
ducts, the common hepatic duct, the bile duct, the
gallbladder, and the cystic duct.

C.1. HEPATIC DUCTS

B. TRANSPORT SEQUENCE OF BILE
- When the liver cells secrete bile, it is collected by a system
of ducts that flow from the liver through the right and left
hepatic ducts.
- These ducts ultimately drain into the common hepatic duct.
- The common hepatic duct then joins with the cystic duct
from the gallbladder to form the common bile duct. This runs
from the liver to the duodenum (the first section of the small
intestine).
- The right and left hepatic ducts emerge from the right and
left lobes of the liver in the porta hepatis. After a short
course, the hepatic ducts unite to form the common hepatic
duct.
- The common hepatic duct is about 1.5 in. (4 cm) long and
descends within the free margin of the lesser omentum. It is
joined on the right side by the cystic duct from the
gallbladder to form the bile duct
C.2. COMMON BILE DUCT
- It is about 3 in. (8 cm) long. In the first part of its course, it lies
in the right free margin of the lesser omentum in front of the
opening into the lesser sac. Here, it lies in front of the right
margin of the portal vein and on the right of the hepatic

Manus Dei Patriae 2019-2024|MD MPH Page 1 of 13

 artery. In the second part of its course, it is situated behind middle with the bile duct on the major duodenal papilla.
the first part of the duodenum to the right of the
gastroduodenal artery. In the third part of its course, it lies in
a groove on the posterior surface of the head of the
pancreas. Here, the bile duct comes into contact with the
main pancreatic duct.

- The bile duct ends below by piercing the medial wall of the
second part of the duodenum about halfway down its length.

- It is usually joined by the main pancreatic duct, and together

they open into a small ampulla in the duodenal wall, called
the hepatopancreatic ampulla (ampulla of Vater).

- The ampulla opens into the lumen of the duodenum by

means of a small papilla, the major duodenal papilla. The
terminal parts of both ducts and the ampulla are surrounded
by circular muscle, known as the sphincter of the
hepatopancreatic ampulla (sphincter of Oddi).
C.3. CYSTIC DUCT
- It is about 1.5 in. (3.8 cm) long and connects the neck of the
gallbladder to the common hepatic duct to form the bile duct.
- It usually is somewhat S-shaped and descends for a variable
distance in the right free margin of the lesser omentum.
- The mucous membrane of the cystic duct is raised to form a
spiral fold that is continuous with a similar fold in the neck of
the gallbladder. The fold is commonly known as the “spiral
valve.” The function of the spiral valve is to keep the lumen
constantly open.
- Sometimes, the main duct drains separately into the
duodenum. The accessory duct of the pancreas, when
present, drains the upper part of the head and then opens
into the duodenum a short distance above the main duct
on the minor duodenal papilla. The accessory duct
frequently communicates with the main duct.
- Blood supply: The splenic and the superior and inferior
pancreaticoduodenal arteries.
- Nerve supply: Sympathetic and parasympathetic (vagal)
nerve fibers.
C.5. APPENDIX
- It is a narrow, muscular tube containing a large amount of
lymphoid tissue. It varies in length from 3 to 5 in. (8 to 13
cm). The base is attached to the posteromedial surface of
the cecum about 1 in. (2.5 cm) below the ileocecal
junction. The remainder of the appendix is free.

- It has a complete peritoneal covering, which is attached to

the mesentery of the small intestine by a short mesentery
of its own, the mesoappendix.

C.4. PANCREATIC DUCT
- The main duct of the pancreas begins in the tail and runs
the length of the gland, receiving numerous tributaries on
the way.
- It opens into the second part of the duodenum at about its
- The mesoappendix contains the appendicular vessels and
nerves.
- The appendix lies in the right iliac fossa, and in relation to
the anterior abdominal wall its base is situated one third of
the way up the line joining the right anterior superior iliac

Page 2 of 13
 spine to the umbilicus (McBurney’s point).
- Inside the abdomen, the base of the appendix is easily
found by identifying the teniae coli of the cecum and
tracing them to the base of the appendix, where they
converge to form a continuous longitudinal muscle coat.
II. PHYSIOLOGY
A. MECHANISM OF ABDOMINAL COLIC
- The correct interpretation of acute abdominal pain is
challenging. Few other clinical situations demand greater
judgment, because the most catastrophic of events may be
forecast by the subtlest of symptoms and signs. A
meticulously executed, detailed history and physical
examination are of the greatest importance.
A.1. INFLAMMATION OF THE PARIETAL PERITONEUM
- The pain of parietal peritoneal inflammation is steady and
aching in character and is located directly over the
inflamed area.
- Its exact reference being possible because it is transmitted
by somatic nerves supplying the parietal peritoneum.
- The intensity of the pain is dependent on the type and
amount of material to which the peritoneal surfaces are
exposed in a given time period.
- The pain of peritoneal inflammation is invariably
accentuated by pressure or changes in tension of the
peritoneum, whether produced by palpation or by
movement, as in coughing or sneezing.
- Another characteristic feature of peritoneal irritation is
tonic reflex spasm of the abdominal musculature, localized
to the involved body segment. The intensity of the tonic
muscle spasm accompanying peritoneal inflammation is
dependent on the location of the inflammatory process, the
rate at which it develops, and the integrity of the nervous
system.
- Spasm over a perforated retrocecal appendix or
perforated ulcer into the lesser peritoneal sac may be
minimal or absent because of the protective effect of
overlying viscera.
A.2. OBSTRUCTION OF HOLLOW VISCERA
- The pain of obstruction of hollow abdominal viscera is
classically described as intermittent, or colicky.
- The colicky pain of obstruction of the small intestine is
usually periumbilical or supraumbilical and is poorly
localized. As the intestine becomes progressively dilated
with loss of muscular tone, the colicky nature of the pain
may diminish. With superimposed strangulating
obstruction, pain may spread to the lower lumbar region if
there is traction on the root of the mesentery.
- The colicky pain of colonic obstruction is of lesser intensity
than that of the small intestine and is often located in the
- infraumbilical area. Lumbar radiation of pain is common in
colonic obstruction.
- Sudden distention of the biliary tree produces a steady
rather than colicky type of pain; hence, the term biliary
colic is misleading.
- Acute distention of the gallbladder usually causes pain in
the right upper quadrant with radiation to the right
posterior region of the thorax or to the tip of the right
scapula, but is not uncommonly midline.
- Distention of the common bile duct is often associated
with pain in the epigastrium radiating to the upper part of
the lumbar region.
- The pain of distention of the pancreatic ducts is similar to
that described for distention of the common bile duct but,
in addition, is very frequently accentuated by recumbency
and relieved by the upright position.
- Obstruction of the urinary bladder results in dull
suprapubic pain, usually low in intensity.
A.3. VASCULAR DISTURBANCES
- The pain of embolism or thrombosis of the superior
mesenteric artery or that of impending rupture of an
abdominal aortic aneurysm certainly may be severe and
diffuse.
- Abdominal pain with radiation to the sacral region, flank,
or genitalia should always signal the possible presence of a
rupturing abdominal aortic aneurysm. This pain may persist
over a period of several days before rupture and collapse
occur.
A.4. ABDOMINAL WALL
- Pain arising from the abdominal wall is usually constant
and aching.
- Movement, prolonged standing, and pressure accentuate
the discomfort and muscle spasm.
- Simultaneous involvement of muscles in other parts of the
body usually serves to differentiate myositis of the
abdominal wall from an intraabdominal process that might
cause pain in the same region.
B. NUTRIENT ABSORPTION – GIT
- The major foods on which the body lives (with the
exception of small quantities of substances such as vitamins
and minerals) can be classified as carbohydrates, fats, and
proteins.
B.1. ANATOMICAL BASIS OF ABSORPTION
- The total quantity of fluid that must be absorbed each day
by the intestines is equal to the ingested fluid (about 1.5
liters) plus that secreted in the various gastrointestinal
Page 3 of 13
 secretions (about 7 liters), which comes to a total of 8 to 9
liters.
- The stomach is a poor absorptive area of the
gastrointestinal tract because it lacks the typical villus type
of absorptive membrane, and also because the junctions
between the epithelial cells are tight junctions.
- Folds of Kerckring, Villi, and Microvilli Increase the Mucosal
Absorptive Area by Nearly 1000-Fold. Folds of Kerckring
increase the surface area of the absorptive mucosa about
threefold. These folds extend circularly most of the way
around the intestine and are especially well developed in
the duodenum and jejunum, where they often protrude up
to 8 millimeters into the lumen.
- Each intestinal epithelial cell on each villus is characterized
by a brush border, consisting of as many as 1000 microvilli
that are 1 micrometer in length and 0.1 micrometer in
diameter and protrude into the intestinal chyme.
- This brush border increases the surface area exposed to
the intestinal materials at least another 20-fold.
B.2. ABSORPTION IN THE SMALL INTESTINE
- Absorption from the small intestine each day consists of
several hundred grams of carbohydrates, 100 grams of fat,
50 to 100 grams of amino acids, 50 to 10 grams of ions, and
7 to 8 liters of water.
- The large intestine can absorb still more water and ions,
although it can absorb very few nutrients.
B.3. ISOSMOTIC ABSORPTION OF WATER
- Water is transported through the intestinal membrane
entirely by diffusion.
- When the chyme is dilute enough, water is absorbed
through the intestinal mucosa into the blood of the villi
almost entirely by osmosis.
B.4. ABSORPTION OF IONS
- Sodium Is Actively Transported Through the Intestinal
Membrane. Sodium absorption is powered by active
transport of sodium from inside the epithelial cells through
the basal and lateral walls of these cells into paracellular
spaces.
- Active transport of sodium through the basolateral
membranes of the cell reduces the sodium concentration
inside the cell to a low value (≈50 mEq/L).
- At the same time, they also provide secondary active
absorption of glucose and amino acids, powered by the
active sodium-potassium (Na+-K+) ATPase pump on the
basolateral membrane.
B.5. NUTRIENT ABSORPTION
- Carbohydrates Are Mainly Absorbed as Monosaccharides.
By far the most abundant of the absorbed
monosaccharides is glucose, which usually accounts for
more than 80 percent of the carbohydrate calories
absorbed.
- Glucose Is Transported by a Sodium Co-Transport
Mechanism. In the absence of sodium transport through
the intestinal membrane, virtually no glucose can be
absorbed because glucose absorption occurs in a co-
transport mode with active transport of sodium.
- It is the initial active transport of sodium through the
basolateral membranes of the intestinal epithelial cells that
provides the eventual force for moving glucose through the
membranes as well.
- Galactose is transported by almost exactly the same
mechanism as glucose. Fructose transport does not occur
by the sodium co-transport mechanism. Instead, fructose is
transported by facilitated diffusion all the way through the
intestinal epithelium and is not coupled with sodium
transport.
- Most proteins, after digestion, are absorbed through the
luminal membranes of the intestinal epithelial cells in the
form of dipeptides, tripeptides, and a few free amino
acids. The energy for most of this transport is supplied by a
sodium co-transport mechanism in the same way that
sodium co-transport of glucose occurs.
- When fats are digested to form monoglycerides and free
fatty acids both of these digestive end products first
become dissolved in the central lipid portions of bile
micelles.
- In this form, the monoglycerides and free fatty acids are
carried to the surfaces of the microvilli of the intestinal
cell brush border and then penetrate into the recesses
among the moving, agitating microvilli.
- Both the monoglycerides and fatty acids diffuse
immediately out of the micelles and into the interior of the
Page 4 of 13
 epithelial cells, which is possible because the lipids are also
soluble in the epithelial cell membrane.
- Thus, the micelles perform a “ferrying” function that is
highly important for fat absorption.
- They are mainly used to form new triglycerides that are
subsequently released in the form of chylomicrons through
the base of the epithelial cell.
III. PARASITOLOGY/PATHOLOGY
A. ASCARIS LUMBRICOIDES (aka: giant intestinal round
worm, lumbricus teres, eenworm)
- Infective stage: embryonated egg
- Habitat: Lumen of small intestine/Jejunum (human body);
eggs (soil)
- MOT: Ingestion/ Inhalation
- Diagnostic stage: unfertilized egg, fertilized egg and adult, Symptoms due to Migrating Larva:
X-ray for obstruction 1.
- Procedures: Direct fecal smear, kato thick and kato katz
Note: If negative stool exam:
• No infection
• Early infection
• All MALE WORM infection 2. Larva in General Circulation
Life Cycle: filtered (Brain, spinal cord, heart, kidney)
- Stage 1: Eggs in Feces – fertilized and unfertilized eggs are Symptoms due to the Adult worm:
passed out through defecation (not yet infective) - Incubation peroid
- Stage 2: Development in soil - rhabidiform larva is
developed (10 – 40 days/18 days to several weeks/ 2 – 3
weeks) depending on the atmospheric temperature and
humidity.
Note:
a. Excessive heat and dryness soon kill them.
b. They remain viable in moist soil for long periods.
- Stage 3: Infection by ingestion of larva – ingested
embryonated egg through food drinks and raw vegetables.
Pathway: Mouth -> Stomach -> Duodenum (digestive
juices breakdown/weaken their shell releasing the LARVA)
- Stage 4: Migration to Lungs – liberated larva burrow
through the mucus membranes of small intestine -> blood
and lymphatics -> Liver (3-4 days) -> heart (right) ->lungs (
grow bigger) -> Capillaries -> alveoli
Note:
a. They moult twice in the lungs
- Stage 5: Re-Entry into the stomach and small intestine
Alveoli -> bronchi -> trachea (they travel by crawling, and
aided by the ciliated ephithelium of the respiratory system)
-> Larynx -> Pharynx (coughing then swallowing) -> Esophagus
-> Stomach -> Small Intestine
- Stage 6: Sexual Maturity and Egg liberation
Note:
a. Grow into adult worm – 6 to 10 weeks
b. Female gravid - 2 months after
Molting: 1 outside (soil), 2 in the lungs, 1 in the small intestine
Immunology:
a. Partial immunity may be acquired
- Antigens are liberated during the moulting period of
larvae and produce protective antibodies which lower the
worm burden and play a part in the immune response.
b. Severe allergic reaction (Urticaria and fall of BP) if larva
reaches the small intestine the secnd time around.
c. Eosinophilic count is increased at time of invasion
Larva in the lungs
• Ascaris Pneumonia (Loeffler’s Syndrome)
• Fever, cough, dyspnea
• Blood-tinged sputum may contain Ascaris larva
• Urticaria and eosinophila
• May have unusual symptoms as to where the larva is
• It takes 60 to 75 days
- Pathogenesis – mostly GI
1. Spoliative action
• robbing the host of its nutrition protein and vitamin
content
• Protein-energy malnutrition
• Vitamin A deficiency – night blindness
• Anti-enzymes (antitryptic and antipipetic) causes
malnutrition
2. Toxic Action
• The body fluid of the Ascaris is highly toxic and when
absorbed may give rise to typhoid-like fever
• Responsible for allergic manefestations: urticaria,
edema of the face, conjuctivitis, irritation of upper
respi tract
3. Mechanical Effects
• GI obstruction
4. Ectopic Ascariasis
• Worms migrate and may go out through the mouth or
nose
• May also block the rima glottidis or may enter
bronchus causing suffocation
• Wandering Ascaris may also enter the lumen of the
appendix causing appendicitis
Page 5 of 13
 B. ANCYLOSTOMA DUODENALE. NECATOR AMERICANUS
(HOOKWORKM)
Characteristics:
- Soil-transmitted helminthes
- Blood-sucking nematodes that attach to the mucosa of the
small intestines.
- Most commonly found in tropical and subtropical countries
- Females can release more than 10,000 eggs per day into
the feces, where a larva hatches from the egg within a day
or two.
- Larvae can survive in moist soil for several weeks, waiting
for an unsuspecting barefooted host to walk by.
- Females are larger than males.
- N. americanus adults are small, cylindrical, fusiform,
grayish-white nematodes.
- The head is curved opposite to the curvature of the body,
which is like a hook at the anterior end.
- The buccal capsule has a ventral pair of semilunar cutting
plates.
- The posterior end of the male has a broad, membranous
caudal bursa with rib-like rays, which are used for
copulation.
- The head of the A. duodenale adult continues in the same
direction as the curvature of the body.
- The buccal capsule has two pairs of curved ventral teeth.
Life Cycle:
PATHOLOGY & PATHOGENESIS
▪ The pathology of hookworm infection involves:
(a) the skin at the site of entry of the filariform larvae,
(b) the lung during larval migration, and
(c) the small intestine, the habitat of the adult worms.
▪ Feet and ankles are common sites of infection due to
exposure from walking barefoot.
CLINICAL MANIFESTATION
▪ Penetration of the filariform larvae through the skin
produces maculopapular lesions and localized erythema.
▪ Itching is often severe, and it is known as “ground itch” or
“dew itch,”
▪ Itching, edema, erythema, and later papulovesicular
eruptions can last for 2 weeks.
▪ If the larvae migrating through the lungs are abundant,
bronchitis or pneumonitis may result.
▪ In the course of migration, these larvae produce minute
hemorrhages with eosinophilic and leukocytic infiltration,
but these manifestations seem to be rare in the tropics.
▪ In the stage of maturation of the worm in the intestine,
there is abdominal pain, steatorrhea, or sometimes
diarrhea with blood and mucus, as well as eosinophilia.
▪ Other symptoms are exertional dyspnea, weakness,
dizziness, and lassitude, while signs include rapid pulse,
edema, and albuminuria.
▪ Unlike in ascariasis, the complications in hookworm
infection are quite mild, and remedial measures are
readily applied. In general, the prognosis of hookworm
infection is good.
C. TRICHURIS TRICHIURA (WHIPWORM)
- Common name: Whipworm
- Mode of transmission: Ingestion of embryonated egg
- Incubation Period : 12 weeks
- Morphology: Eggs – barrel/ football/ Japanese lantern
with bipolar plugs
- Adult- Holomyarian ( cells are small, numerous, and closely
packed in narrow zone); has thick and fleshy posterior and
threadlike anterior
- Reservoir: HUMANS
- NO MIGRATION OUTSIDE GIT
Pathogenesis:
PETECHIAL HEMORRHAGE, APPENDICITIS, DYSENTERY
SYNDROME, BLOODY MUCOID DIARRHEA, RECTAL
PROLAPSE, TRICHOCEPHALIASIS
Life Cycle:
The unembryonated eggs are passed with the stool . In the soil, the
eggs develop into a 2-cell stage, an advanced cleavage stage , and
then they embryonate ; eggs become infective in 15 to 30 days. After
ingestion (soil-contaminated hands or food), the eggs hatch in the
small intestine, and release larvae that mature and establish
themselves as adults in the colon . The adult worms (approximately 4
Page 6 of 13
cm in length) live in the cecum and ascending colon. The adult worms
are fixed in that location, with the anterior portions threaded into the
mucosa. The females begin to oviposit 60 to 70 days after infection.
Female worms in the cecum shed between 3,000 and 20,000 eggs per
day. The life span of the adults is about 1 year.
D. ENTEROBIUS VERMICULARIS (PINWORM)
Life cycle:
Parasite biology:
- Found in cecum and adjacent portions of small and large
intestines, migrate to the anus and deposit eggs on the
perianal skin, usually evening (nocturnal migration)
-
Female pinworms:
• 10 mm in length
• Slender, pointed posterior end
• Deposit up to 15,000 eggs per night
Male pinworms:
• 3 mm in length
• Curved posterior end
• Usually die after copulation
CLINICAL FEATURES
■ Most pinworm infections are asymptomatic.
■ Perianal pruritus is the cardinal symptom.
■ The itching may lead to excoriation and bacterial
superinfection.
■ Restless sleep secondary to nocturnal perianal or perineal
pruritus.
■ Eosinophilia is not observed in most cases.
■ Aberrant migration to ectopic sites occasionally may lead to
appendicitis, pelvic inflammatory disease, peritonitis,
hepatitis, and ulcerative lesions in the large or small bowel.
DIAGNOSIS
■ Since pinworm eggs are not released in feces, the diagnosis
cannot be made by conventional fecal ova and parasite
tests.
■ SCOTCH TAPE TEST
E. STRONGYLOIDES STERCORALIS (THREADWORM)
• Also known as the Thread worm
• 2mm long intestinal worm causing a disease called
strongyloidiasis
• Common in tropical and subtropical areas but also occurs
in temperate zones
• Penetrates skin usually in people who walks barefooted
Life cycle
• Once the filariform larvae penetrates the skin it goes into
the blood stream and will eventually end up in the lungs.
There it grows and gets coughed up and swallowed into
the small intestine where it will mature and will lay eggs
• Eggs does not get passed in the stool.
• The filariform larvae can do 3 things:
a) Autoinfection
b) Direct cycle
c) Indirect cycle
Autoinfection
• The filariform larvae burrows into the small intestine then
goes into the bloodstream and goes to the lungs to
repeat the cycle without leaving the host
Direct cycle
• The filariform larvae goes out of the body when the
infected host defacates. It will survive in the soil then
penetrate the skin of the next potential host that passby,
travel to the lungs and repeat the cycle.
Indirect cycle
• The filariform larvae gets passed in the stool then instead
Page 7 of 13
 of infecting a passerby, it will reproduce in the soil. The
eggs will hatch and the filariform will infect the
unfortunate passerby repeating the cycle.

IV. RADIOLOGY
A. DOT SIGN IN ABDOMINAL X-RAY

Central Dot Sign

- Display an appearance of small portal venous branches
surrounded by SEVERELY DILATED INTRAHEPATIC BILE
DUCTS.
- This is best seen using cross-sectional imaging in axial
imaging plane (CT/MRI).

- On PE, dry rales and wheezes may be observed.

Radiologic features:
- display patchy infiltrates (few mm to cm in size)
- Infiltrate may be transient and clear after several weeks

V. PHARMACOLOGY
Etiology:
A. CLINICAL PHARMACOLOGY OF THE ANTIHELMINTHIC
- Caused by Ascaris lumbricoides
DRUGS
- In heavy infections, a large bolus of entangled worms can
cause mechanical small-bowel/biliary obstruction
- Antihelminthic drugs have diverse chemical structures,
- Single worms can occlude biliary tree causing complications
mechanisms of action, and properties.
such as cholecystitis

Management: - Most were discovered by empiric screening methods. Many

- Partial obstruction is managed by: act against specific parasites, and few are devoid of
a. Nasogastric suction significant toxicity to host cells.
b. Instillation of piperazine by NGT
- Complete obstruction is managed by: - In addition to the direct toxicity of the drugs, reactions to
a. immediate surgical intervention dead and dying parasites may cause serious toxicity in
patients.
B. ACUTE TRANSIENT PNEUMONIA (Loeffler Syndrome)
- The drugs are divided into 3 groups on the basis of the type
of helminth primarily affected (nematodes, trematodes,
- Caused by A. lumbricoides, S. stercoralis, and hookworm
and cestodes).
which migrates to the lungs in their life cycle.
- In the lungs, they break into the alveolar spaces, ascend the
bronchial tree, are swallowed and thereby reach the small
intestine.
- When helminths invade lung tissue, it may elicit immune-
mediated hypersensitivity response
- Gram negative bacteria and other gut organisms may be
carried by the migrating larvae.

Page 8 of 13
 B. ALBENDAZOLE
BASIC PHARMACOLOGY:
- It is a benzimidazole carbamate.
- There is an Increased absorption of the drug if taken with a
fatty meal, then rapidly undergoes first-pass metabolism in
the liver to the active metabolite albendazole sulfoxide.
- Reaches peak plasma concentrations about 3 hours after a
400 mg oral dose
- Half-life is about 8 to 12 hours.
- Albendazole metabolites are excreted in the urine.
MECHANISM OF ACTION:
- Inhibits the microtubule synthesis.
- Larvicidal Effects in Ascariasis, and Hookworm infections.
- Ovicidal Effects in Ascariasis and trichuriasis.
CLINICAL USES:
- For Adults and Children older than 2 years old with
ascariasis and pinwom infections, the treatment for
ascariasis is a single dose of 400 mg orally (repeated 2-3
days for heavy infections and in 2 weeks for pinworm
infections).
- For hookworm infections and trichuris, albendazole at 400
mg orally once daily for 3 days is now recommended. For
children between ages of 12 and 24 months, WHO
recommeded a reduced dose of 200mg.
ADVERSE REACTIONS, CONTRAINDICATIONS, & CAUTIONS:
- When used for 1-3 days, it is nearly free of significant
adverse effects.
- GI Upset can occur.
- Blood counts and liver function tests should be monitored
for long term therapy.
C. IVERMECTIN
BASIC PHARMACOLOGY:
- It is a semisynthehic macrocyclic lactone derived from the
soil actinomyocete.
- Available only for oral administration in humans.
- Peak plasma concentration is 4 hours after a 12 mg dose.
- Half-life of 16 hours.
- Excretion of the drug and its metabolites via feces.
MECHANISM OF ACTION:
- Paralyzes nematodes by intensifying y –aminobutyric acid
(GABA) – mediated transmission of signals in peripheral
nerves
- ADVERSE REACTIONS, CONTRAINDICATIONS, & CAUTIONS:
CLINICAL USES:
- Stronglyodiasis – Treatment consists of 200mcg/kg once
daily for 2 days.
- For immunosuprred patients, once monthly may be helpful.
ADVERSE REACTIONS, CONTRAINDICATIONS, & CAUTIONS:
- Infrequent adverse effects include fatigue, dizziness,
nausea, vomiting, abdominal pain, and rashes.
D. MEBENDAZOLE
BASIC PHARMACOLOGY:
- It is a synthetic benzimidazole..
- Less than 10% of orally administered mebendazole is
absorbed.
- Half-life of 2-6 hours.
- Excreted in the urine.
- Increased absorption with fatty meal.
MECHANISM OF ACTION:
- Inhibits the microtubule synthesis.
- Efficacy of the drug varies with gastrointestinal transit time,
with intensity of infection, and perhaps with the strain of
parasite.
- The drug kills hookworm, ascaris, and trichuris eggs.
CLINICAL USES:
- Mebendazole is indicated for use in ascariasis, trichuriasis,
hookworm and pinworm infections.
- For pinworm, the dose is 100mg once, repeated at 2 weeks.
- For ascariasis, trichuriasis, and hookworm infections, a
dosage of 100 mg twice daily for 3 days is used for adults
and children older than 2 years.
ADVERSE REACTIONS, CONTRAINDICATIONS, & CAUTIONS:
- Short term use is nearly free of significant adverse effects.
- GI Upset can occur.
- Contraindicated in pregnancy.
E. PIPERAZINE
BASIC PHARMACOLOGY:
- It is an alternative for the treatment of ascariaisis with cure
rates over 90% when taken for 2 days.
- Pleak plasma levels are reached in 2-4 hours.
- Drug excreted in the urine in 2 to 6 hours, and excreted
complete within 24 hours.
MECHANISM OF ACTION:
- Causes paralysis of ascaris by blocking acetylcholine at the
myoneural junction, live worms are expelled by peristalsis.
CLINICAL USES:
- For ascariasis, the dosage of piperazine is 75 mg/kg
(maximum dose, 3.5 g), orally once a daily for 2 days.
- For heavy infections, treatment should be continued for 3-4
days or repeated after 1 week.
- Occasional mild adverse effects include nausea, vomiting,
diarrhea, abdominal pain, dizziness, and headache.
Page 9 of 13
 F. PYRANTEL PAMOATE

BASIC PHARMACOLOGY:
- It is a broad-spectrum antihelminthic highly effective for
the treatment of pinworm, ascaris infections.
- Pleak plasma levels are reached in 1-2 hours.
- It is a tetrahydropyrimidine derivative,

MECHANISM OF ACTION:
- It is effective against mature and immature forms of
suscpetible helminths within the intestinal tract but not
against migratory stages in the tissues or against ova.
- It is a neuromuscularblocking agent that causes release of VI. CLINICAL PATHOLOGY
acetylcholine and inhibition of cholinesterase; this results in A. MINIMUM ENTERO-PARASITOGRAM
paralysis of worms, followed by expulsion. - Entero – referring to intestine
- Parasito – referring to parasite
CLINICAL USES: - gram – recording
- The standard dose is 11 mg (base)/kg (maximum, 1 g), given - Therefore, Minimun Entero-Parasitogram, just like
orally once with or without food. For pinworm, the dose is “Hemogram or CBC” is intestinal parasite count or
repeated in 2 weeks. recording

ADVERSE REACTIONS, CONTRAINDICATIONS, & CAUTIONS: B. OVUM COUNT TECHNIQUE

- Adverse effects are infrequent, mild, and transient. Four ways:
1. McMaster Technique
2. Stoll Quantitative Technique
G. THIABENDAZOLE 3. Beaver Technique
4. Kato-Katz/Kato-Miura
BASIC PHARMACOLOGY:
- It is an alternative to ivermectin or albendazole for the B.1. McMaster Technique
treatment of strongyloidiasis. - Identification and quantification of the number of
- It is a benzimidazole compound. parasitic elements per gram of feces Eggs/gram;
- It is rapidly absorbed after ingestion. Oocyst/gram; Cysts/gram; Larvae/gram
- Peak Plasma within 1 to 2 hours, the half life is 1.2 hours. - Parasitic elements multiplied by 100 if one chamber,
- It is excreted in the urine in 48 hours. multiply by 50 if two chambers
- It can be absorbed through the skin. - Example:
30 eggs were seen in one chamber
MECHANISM OF ACTION: Therefore,
- Inhibition of microtubule synthesis. 30 100 = 3,000 eggs/gram
- It has ovicidal effects against some parasites. 60 eggs were seen in two chambers
Therefore,
CLINICAL USES: 60 X 50 = 3,000 eggs/gram
- The standard dosage, 25 mg/kg (maximum 1.5 g) twice
daily, should be given after meals. Tablets should be B.2. Stoll Quantitative Technique
chewed. - Used for estimating the amount of worms and to determine
- For strongyloides infection, treatment is for 2 days. severity of infection
- Estimate effectiveness of antihelminthic treatment
ADVERSE REACTIONS, CONTRAINDICATIONS, & CAUTIONS: - For soil transmitted helminthes the number of eggs is
- Thiabendazole is much more toxic than other counted; number of eggs per gram feces is calculated by
benzimidazolees and more toxic than ivermectin. multiplying the count with 100
- Irreversible liver failure and Steven-Johnson Syndrome have
been reported. If feces is not formed, multiple by the correction factors
- Contraindicated for pregnant women. • Mushy Stool (pulpy or soft) – X2
- Common adverse reactions include dizziness, anorexia, • Mushy Formed – X1.5
nausea, and vomiting. • Mushy Diarrhoeic – X3
Example
30 eggs were counted
Therefore,
30 X 100 = 3,000 eggs/gram feces
If,
• Mushy Stool (pulpy or soft) – 3,000 X 2 = 6,000 eggs/gram feces
• Mushy Formed – 3,000 X 1.5 = 4,500 eggs/gram feces

Page 10 of 13
• Mushy Diarrhoeic – 3,000 X 3 = 9,000 eggs/gram feces granules in blue cytoplasm.

B.3. Beaver Technique

- Smear is made by using 2 mg of feces mixed in a drop of
saline in a slide and examined under microscope (LPO)
- Number of eggs in 2 mg of feces is counted and then
MULTIPLIED BY FACTOR 500 to calculate the number of
eggs per gram feces
- Example:
30 eggs were counted
Therefore,
30 X 500 = 15,000 eggs/ gram feces

B.4. Kato-Katz/Kato-Miura
- For monitoring large-scale treatment program - Eosinophils play important roles in immune regulation.
implemented for the control of soil transmtted helminth They transmigrate into the thymus of the newborn and are
infection believed to be involved in the deletion of double-positive
- Number of eggs counted multiplied by: thymocytes.
20 for 50 mg template (9 mm on a 1 mm thick temp)
50 for 20 mg template (6.5 mm on a 0.5 mm thick temp) - Eosinophils regulate mast cell function through the release
24 for 41.7 mg template (9 mm on a 1.5 mm thick temp) of major basic protein (MBP) that causes mast cell
- Example: degranulation as well as cytokine production, and they also
30 eggs were counted in the 50 mg template produce nerve growth factor that promotes mast cell
30 X 20 = 600 eggs/ gram feces survival and activation.
30 eggs were counted in the 20 mg template
30 X 50 = 1,500 eggs/gram feces - Eosinophil production is increased in infection by parasitic
30 eggs were counted in the 41.7 mg template helminths, and in vitro studies have shown that the
30 X 24 = 720 eggs/ gram feces eosinophil is capable of destroying tissue-invading
helminths through the secretion of major basic protein and
WHO classification of intensity of infections wIth soil-transmitted eosinophil cationic protein as well as the production of
helminthes and Schistosoma Spp reactive oxygen species.There is also a suggestion that
Organism Light Intensity Moderate Heavy eosinophils play a role in preventing reinfection.
Intensity intensity
Ascaris 1-4,999 epg 5,000-49,999 ≥50,000 epg B. PATHOPHYSIOLOGY OF ALLERGIC VASCULITIS SYNDROME
lumbricoides epg
Trichuris 1-999 epg 1,000-9,999 ≥10,000 epg - Cutaneous necrotizing vasculitis (CNV) presents as
trichiura epg “palpable purpura,” and has also been called allergic
Hookworm 1-1,999 epg 2,000-3,999 ≥4,000 epg cutaneous vasculitis, leukocytoclastic vasculitis and
epg hypersensitivity angiitis.
Schistosoma 1-99 epg 100-399 epg ≥400 epg
japonicum - The internal organs most commonly affected in
Schistosoma hypersensitivity vasculitis are the joints, gastrointestinal
mansoni tract, and kidneys. Hypersensitivity vasculitis may be acute
and self-limited, recurrent, or chronic.

- Hypersensitivity vasculitis is thought to be mediated by

VII. IMMUNOLOGY
immune complex deposition.
A. EOSINOPHILIA IN PERIPHERAL BLOOD SMEAR
- In this form of vasculitis, circulating antigens in the body
- Eosinophils make up 1% to 3% of nucleated cells in the
(produced by factors such as medications, infections, and
bone marrow.
neoplasms) induce antibody formation. These antibodies
bind to the circulating antigen and create immune
- Eosinophil development is similar to that described earlier
complexes, which then deposit within vessels, activating
for neutrophils, and evidence indicates that eosinophils
complement and inducing inflammatory mediators.
arise from the common myeloid progenitor (CMP).
Inflammatory mediators, adhesion molecules, and local
factors may affect the endothelial cells and play a role in
- Eosinophil lineage is established through the interaction
the manifestations of this disease.
between the cytokines IL-3, IL-5, and GM-CSF and three
transcription factors (GATA-1, PU.1, and c/EBP).
- Autoantibodies, such as antineutrophil cytoplasmic
antibody (ANCA), may be associated with disease
- Eosinophil myelocytes are characterized by the presence of
manifestations.
large (resolvable at the light microscope level), pale,
reddish orange secondary granules, along with azure

Page 11 of 13
 SAMPLE EXAM SAMPLE EXAM
1. A 31-year old female from Southern Mindanao is brought in 6. The drug of choice for mixed round worm infection:
for chronic diarrhea of two months duration. Stool A. Pyrantel pamoate C. Niclosamide
examination reveals larvae with prominent genital B. Mebendazole D. Praziquantel
primodium. What is your probable diagnosis?
A. Capillariasis 7. Which of the following anthelmintics possesses a potent
B. Hookworm infection inhibitory effect on the feeding behavior of worms by
C. Strongyloidiasis acting on glutamate-gated channels expressed in the
D. Ascariasis pharyngeal muscles of these worms?
A. Ivermectin C. Diethylcarbamazine
2. A 10-year-old girl, with perianal pruritus, was brought by B. Thiabendazole D. Pyrantel pamoate
her mother to her pediatrician. What is your most probable
diagnosis? 8. A 15-year old boy from Davao del Norte is noted to have
A. Ascariasis pallor and malnutrition. Stool examination reveals an ovum
B. Trichuriasis with thin colorless cell wall. What is your diagnosis?
C. Enterobiasis A. Ascariasis
D. Hookworm infection B. Trichuriasis
C. Enterobiasis
3. Adult roundworm, measuring 27 cm. in length, was seen in D. Hookworm infection
the colon of a 10-year old boy who died of pneumonia.
Manifestations such as lung infiltration, asthmatic attacks, 9. All these parasites have a lung phase during their
and edema of the lips were documented before the patient developmental cycle EXCEPT:
died. What is the most probable parasitic infection can you A. Ascaris lumbricoides C. Strongyloides stercoralis
identify in this case? B. Enterobius vermicularis D. Necator americanus
A. Trichuriasis.
B. Ascariasis 10. Embryonated ovum is the infective stage of this parasite:
C. Capillariasis A. Trichinella spiralis C. Capillaria philippinensis
D. Hookworm infection B. Enterobius vermicularis D. Strongyloides stercoralis

4. Which of the following statements is correct about the

cystic duct?
A. It forms the medial boundary of the triangle of Calot.
B.The proximal portion contains the spiral valves of Heister.
C.It lies at the thickened distal portion of the lesser
omentum.
D. It is about 8-10 cm in length.

5. The most important pancreatic enzyme needed for protein

digestion is:
A. aminopeptidase C. chymotrypsin
B. carboxypeptidase D. trypsin

Page 12 of 13
Page 13 of 13