DISEASES OF AND

ACQUIRED
THROUGH GASTROINTESTINAL TRACT

 To be able to gain understanding about the

different diseases acquired through
gastrointestinal tract.
To be able to gain understanding about the
different causes of the different diseases
acquired through gastrointestinal tract.
To be able to know the different nursing
interventions done with the different
diseases.

DISEASES CAUSED
BY BACTERIA

a. TYPHOID FEVER

Typhoid Fever

Typhoid Fever is a lifethreatening illness caused by the

bacterium Salmonella Typhi.
enteric fever, bilious fever or
Yellow Jack.

Incubation period
The incubation period is 10
to 20 days and depends
on, among other things, how
large a dose of bacteria
has been taken in.

Pathology
After ingestion, the bacteria temporarily enter
the blood stream and travel to the small
intestine.
White blood cells carry the disease to the liver,
spleen and bone marrow where it reproduces
and reenters the blood stream.
The bacteria then invades the gallbladder,
biliary system, and the lymphatic tissue of the
bowel.

Affected Organs
Abdominal Cavity including:
Liver
Gallbladder
Stomach
Small intestine
Large intestine

Mode of Transmission

Feco- oral route

 Typhoid can be passed through

animals, only through humans.
Flies however, are known to help
transmit the disease because when
they land on human excrement, it
remains on their appendages and
can be transmitted when they land
on something else.

Signs and Symptoms

Symptoms include:
Fevers up to 103 or 104
Weakness
Headaches
Poor appetite
Generalized aches and pains
Diarrhea
Occasionally a rash of flat, rose-colored spots
Abdominal Tenderness

Constipation, then diarrhea

Bloody Stools
Nosebleed
Chills
Delirium
Confusion
Agitation
Fluctuating moods
Hallucinations

Stages of Typhoid Fever

Classically, the untreated typhoid fever is broken down into
four different stages, each lasting about a week.
Stage One:

A slowly rising temperature

Relative bradycardia (unusually slow heart rate),
malaise (discomfort or uneasiness), headache and
cough.
In of cases, epistaxis (acute hemorrhage from
the nostril, nasal cavity, or nasopharynx) can
occur.

Stage Two:

Continuing high fever

Extremely distended abdomen
Considerable weight loss
Bradycardia continues
Dicrotic pulse wave
Delirium is frequent, frequently calm and
sometimes agitated.

 Stage Three:
A number of complications can occur:
Intestinal hemorrhage due to bleeding
Intestinal perforation
Encephalitis (inflammation of the brain)
Fever is still very high
Dehydration occurs and increases delirium
Lies motionless with eyes half-opened
Stage Four:
Defervescence (very high fever) commences that continues
into the fourth week.

Complications
Death occurred from the development of other
complications such as:
Overwhelming infections
Pneumonia
Intestinal bleeding
Intestinal perforation
Kidney Failure
Peritonitis

 Inflammation of the pancreas

Infections of the spine
Inflammation of the membranes surrounding
the spinal cord and brain (meningitis)
Inflammation of the heart muscle
Psychiatric problems

Diagnosis
Diagnosis is made by blood, bone marrow, or stool.
The Widal test is commonly used to diagnose
Typhoid.
A blood culture that shows the bacteria
A stool culture
A platelet count (low platelet count)

Carriers of Typhoid Fever

A carrier is usually a healthy person
who survived the disease but in
whom the bacteria are able to
survive without causing further
symptoms.
Carriers continue to spread the
disease through their excrement
without realizing it.
It is believed that Mary Mallon
never actually had the disease
however, her mother had typhoid
while pregnant with her.

Typhoid Mary

She infected 47 people and killed 3

She constantly changed her employment but
the members of the household always got sick.
She was forced into containment for two years
and then released under the conditions that
she could no longer be a cook.
She assumed a false name and began cooking
again and of course, infecting numerous people.
She was forced into life-time containment
where she died 26 years later of pneumonia.

Treatment
Typhoid is treated with an antibiotic that
kills the Salmonella bacteria.
With antibiotics, improvement can be seen
in 1-2 days and recovery in 7-10 days.
Intravenous fluids and electrolytes may
also be given to patients.

Treatment

In most cases typhoid fever is

not fatal.
Antibiotics such as ampicillin,
chloramphenicol,
trimethethoprimsulfamethoxazole, and
ciprofloxican.
These antibiotics have been used
in most developed countries .

Prevention

Choose foods processed for safety

Prepare food carefully
Foods prepared by others (avoid if possible)
Keep food contact surfaces clean (3 wash cycle)
Eat cooked food as soon as possible
Maintain clean hands
Steam or boil shellfish at least 10 minutes
All milk and dairy products should be pasteurized
Control fly populations

CHOLERA

 Cholerais an acute bacterial entric

diseases of the GIT characterized by
profuse diarrhea, vomiting, massive
loss of fluid and electrolytes that
could result to hypovolemic shock,
acidosis and death.
Sometimes known asAsiaticor

epidemic cholera

Etiologic Agent:
Vibrio Cholerae/Vibrio coma
An enterotoxin, choleragen, is elaborated by
the organism as they grow in theintestinal
tract.

Source of Infection:

Vomitus and feces of

infected persons and feces
of convalescent or healthy
carriers. Contacts may be
temporary carriers.

Incubation Period:

Theincubation periodranges
from a few hours to five
days; usually one to three
days.

Period of Communicability:
The organisms are communicable
during stool positive stage, usually
a few days after recovery,
however occasionally the carrier
may have the organism for several
months.

Mode of Transmission:
fecal transmission passes via oral
route from contaminated water,
milk, and other foods.
through ingestion of food or water
contaminated with stool or vomitus
of patient.
Flies, soiled hands and utensils also
serve to transmit the infection.

Pathogenesis and Pathology:

Fluid loss is attributed to the enterotoxin
elaborated by the organism as they lie in
opposition with the lining cells of the
intestines.
The toxin stimulates adenylate cyclase, which
results in the conversion of the adenosine
truphosphate (ATP) to cyclic adesine
monophosphate (CAMP).
The mucosal cell is stimulated to increase
secretion of chloride, associated with water
and bicarbonate loss.

 The toxin acts upon the intact epithelium

on the vasculator of the bowel, thus,
resulting in outpouring of intestinal fluids.
Fluid loss of 5 to 10 percent of the body
weight resulting in dehydration and
metabolic acidosis.
If treatment is delayed or
inadequate,acute renal failureand
hypokalemia become secondary problems.

Clinical Manifestations
There is an acute, profuse, watery
diarrhea with no tenesmus or intestinal
cramping.
Initially, the stool is brown and contains
fecal materials, but soon becomes pale
gray, rice-water in appearance with an
inoffensive, slightly fishy odor.
Vomiting often occurs after diarrhea
has been established.

 Diarrhea causes fluid loss

amounting to 1 to 30 liters per
day owing to subsequent
dehydration and electrolyte
loss.
Tissue turgor is poor and eyes
are sunken into the orbit.

 skin is cold, the fingers and toes are

wrinkled, assuming the characteristic
washer-momans hand.
Radial pulse become imperceptible and
the blood pressure unobtainable.
Cyanosis
The voice becomes hoarse and then, is
lost, so that the patient speaks in
whisper (aphonia).
Breathing is rapid and deep.

 Despite marked diminishedperipheral

circulation, consciousness is present.
oliguria and may even develop anuria.
Temperature could be normal at the onset of
the disease but becomes subnormal in later
When the patient is in deep shock, the passage
of diarrhea stops.
Death may occur as short as four hours after
onset, but usually occurs on the first or second
day if not properly treated.

Diagnostic Exams:

Rectal Swab
Darkfield or phase
microcopy
Stool Exam

Modalities of Treatment:
Intravenous treatment - achieved by rapid
intravenous infusion of alkalinesaline solution
containing sodium, potassium, chloride and
bicarbonate ions in proportions comparable to
that in water-stool.
Oral therapy rehydration can be completed by
oral route (Oresol, Hydrites) unless
contraindicated or, if the patient is not
vomiting.

 Maintenance ofthe volumeoffluids and

electrolytesto ensure rehydration. This is done
by careful intake and output measurement.
Antibiotics
Tetracycline
Furazolidone
Chlorampenicol
Cotrimoxazole

NursingManagement:

Medicalsepticprotective care must be provided.

Enteric isolation must be observed.
Vital signsmust be recorded accurately.
Intake and output must be accurately measured.
A thorough and careful personal hygiene must be
provided.
Excreta must be properly disposed
Concurrent disinfection must be applied.
Food must be properly prepared.
Environmental sanitation must be observed.

Prevention:
Food and water supply must be protected
from fecal contamination.
Water should be boiled or chlorinated.
Milk should be pasteurized.
Sanitary disposal of human excreta is a must.
Sanitary supervision is important.

Bacillary
Dysentery
Shigellosis

The term dysentery is used in

connection with various intestinal
disturbances. The modifying word
bacillary is employed to denote that
form of dysentery caused by specific
bacilli of the dysentery group.

Bacillary Dysentery is an acute

bacterial infection of the intestine.
It is a contagious infection,
occurs in epidemics and occurs more
frequently in the summer and fall.

E t I o l o g I c A g e n t
The causative agent is a bacteria of the Shigella
(Kiyoshi Shiga ) group, a short, non-motile, gram
negative organism
There are four serologic groups:
1. Shigella dysenteriae (Group A)
considered as the most infectious
their habitat is almost exclusively the GIT of
man
they rarely invade the blood stream, and are
cultured from the stools

like other gram negative bacilli, they

develop resistance against
antibiotics
2. Shigella flexneri (Group B)
predominant in developing countries
common in the Philippines
3. Shigella boydii (Group C)

4. Shigella sonnei- the most common but

also the mildest form. Many milder
cases are probably never diagnosed
and so never reported, so the true
incidence may be substantially higher.

I n c u b a t I o n

P e r I o d

Seven hours to seven

days with an average of
three to five days.

Period of
The disease is communicable during
the acute phase and until the
Communicability

microorganism is absent from the

bowel discharges, usually within a
few weeks even without specified
therapy. A few individuals became
carriers for a year or two.

Mode of
Transmission
ingestion of contaminated food or
drinking contaminated water or milk.

by flies or through other objects

contaminated by feces of the patient.

 Fecal-oral transmission is possible.

Hand-to

mouth

transfer

of

contaminated

material
Swimming in infected waters.
Eating contaminated food with human sewage
(either directly or via contaminated water)
especially with cold uncooked foods such as
salads.

P a t h o l o g y

the organism invades the intestinal

mucosa and causes inflammation. The
organism invades the cell lining the
large bowel and multiplies there,
killing the cell; this is the cause of
the symptoms produced. However, it
occasionally invades the bowel beyond
the surface lining .

Dirty, fibrinous sloughing areas or

ulcers are formed
Within the few days, the stool may
contain pus, mucus and blood.

Clinical
Fever especially in children
Manifestations

Tenesmus, nausea, vomiting, and headache

Colicky or cramping abdominal pain (days to

weeks) associated with anorexia and body
weakness.
Diarrhea with bloody-mucoid stool that is
watery at first
Rapid dehydration and loss of weight

ComplIcatIo
Rectal prolapse particularly in
undernourished children.
ns
Non-suppurative arthritis with one
or several joints involved
(accompanied with fever and a
serous effusion into the joint,
which has sometimes been found to
contain Shigas bacillus).
Anemia

Parotitis (due to secondary

infection from mouth organism)
Bacteraemia occurs primarily in
malnourished children
Hemolysis (destruction of RBC)
Ulceration in the intestine can
lead to severe blood loss

Diagnostic
Procedures
Fecalysis or microscopic

examination of the stool.

Rectal swab
Peripheral blood examination.

Blood tests
>Full blood count looking for anemia,
infection or inflammation
>Electrolytes to assess loss e.g. low
potassium, magnesium and calcium
>Iron studies looking for iron deficiency
due to blood loss or malabsorption

INTERVENTION
Rehydration goal
Emphasize principles of safe food preparation, with
special attention to meat preparation and cooking
>adequate provision for storage and reheating to
meat temperature thresholds is important.

> Excreta must be properly disposed.

>Concurrent and terminal disinfection
should be employed.
*Diarrheal diseases should be reported to
local health departments
*The need for rehydration and refeeding
should be taught to parents.

 Good hygiene in the health care delivery

and home settings must be a focus.
>the principles of hand washing and glove
use that are emphasized with Standard
Precautions
Diet: Liquid or soft diet until diarrhea
stops, then return to normal diet

ModalItIes of

T rAntibiotics
e a tsuch
m aseAmpicillin,
n t Tetracycline or

Cotrimoxazole is useful in severe cases or when

the spread of infection to other people is likely
and when the patient is very young
IV therapy with normal saline (with electrolyte)
to prevent dehydration.
Anti diarrheal drugs are contraindicated because
they delay fecal excretion that can lead to
prolong fever.

Methods of Prevention
Sanitary disposal of human feces.
and supervision
Control
Sanitary
of processing, preparation and
serving of food particularly those eaten raw.
Adequate provision and protection for safe water
supplies.
Fly control and screening to protect foods against
fly contamination.
Construction of safe privy.
Emphasizing good personal hygiene.
Provision of adequate hand washing facilities.

Control of infected individual contacts

and environment.
Reporting to Local Health Officer.
Rigid personal precautions by attendants.
Isolation of patient during acute illness.

DISEASES
CAUSED BY
VIRUSES

POLIOMYELITIS
Acute Anterior Poliomyelitis; HeineMedin Disease: Infantile Paralysis.

 - is an acute infectious disease caused by any of

the three types of Poliomyelitis virus which
affects chiefly the anterior horn cells of the
Spinal cord and the medulla, cerebellum and
midbrain.
- Characterized by two febrile episodes, a minor
andmajorillnessseparatedby a remission of one
or two days followed by varying degrees of
muscle weakness or occasionally a progressive
Paralysis that ends fatally.

ETIOLOGY

- the causative virus is poliovirus (Legio Debilitants)

- there are 3 distinct serelogic types of poliovirus
(with no cross Immunity)
1) Type I is the most paralytogenic or the most
frequent cause of Paralytic poliomyelitis, both
epidemic and endemic.
2) Type II the next most frequent.
3) Type III the least frequently associated with
paralytic disease.

1)

2)

3)
4)

Types of Poliomyelitis

Spinal
`Cervical
Thoracic
Lumbar
Bulbar
Cranial nerves
Circular System
Respiratory System
Bulbo-spinal
Polioencephalitis

PERIOD OF COMMUNICABILITY:
Most contagious a few days
before and after the onset of
symptom when the virus is found
in the oropharynx for about a
week, and in large quantities in
the small bowel, and continues to
be in feces up to about 3 months.

Modes of Transmission:

- transmitted through saliva, vomitus and feces

1) Direct contact from one person to another person
through healthy carriers via the intestinal/oral pathways.
- it has been shown that poliovirus excretors are much more
commonly found among household or family contacts than
among noncontact.
2) Indirect contact fecal-oral through food, water,
utensils and objects contaminated by human exreta.
- occasionally, the virus may be implanted through the
oropharynx and in very rare instances by parenteral.

INCUBATION PERIOD:
Usually

7-14 days, with a range of

5-35 days, for paralytic and nonparalytic forms; 3-5 days for the
minor illness.

PATHOGENESIS:

polio
virus
reaches
theintestinal
tractthroughthe mouth, enters the intestinal
mucosa and lodges and multiplies in undetermined
sites, possibly reticuloendothelial system. This is
known as the IntestinalPhase.
- The organism may then reach the blood
(viremicphase) and then proceed to CSN
(neuralphase)
- In each of these stages the body defences
respond and resist the invading organisms.

 - The disease may stop in any of this sites,

depending on the promptness and effectiveness of
the hosts antibody response at that
particularphase.
- Thus if the virus is inhibited or is stopped from
increasing at the intestinalphase, adequate
immunity develops locally in the intestine as well as
systematically, with hardly any clinical
manifestations. This is what happens in the
asymptomatic, silent or subclinical manifestations.
This is also theprincipleof oral vaccination.

 If the virus proceeds unabated, it enters

blood
stream
resulting
in
systemic
manifestations which, depending on the
severity of infection may present dregs of
fever,headache, vomiting, and irritability.
- The milder manifestations constitute the
Abortive type of the disease and the more
severe manifestations; the Meningitic or
preparalytic Type.

 - Unchecked, the organism proceed via nerve

pathways to the CNS and again depending on the
site they invade, manifestations may
correspondingly be Spinal, Bulbospinal or
Encephalitic.

CLINICAL MANIFESTATIONS:
4 Clinical forms are described:
1) Inapparent/Subclinical/Asymptomatic/Silent
Type
- person who are expose to poliomyelitis ward
like the nurses and other members of the
health team. But not all polio victim has small
leg or both.

2) Abortive Type/Minor Illness of Poliomyelitis:

- starts with a mild to moderateupper respiratory
infectionor with symptoms of mild influenza like
slight fever, malaise,headache, sore throat, inflamed
pharynx and vomiting. This is follows by a remission
of 1-2 days at which time the child may be active and
playful.
- This case may be unnoticed.

3) Preparalytic or Meningitic Type/Major Illness of

Poliomyelitis:
- then the second febrile stage is observe, this time with
higher temperature,headache, vomiting, restlessness,
anorexia, lethargy and pain in theneck and back, arms,
legs, and abdomen.
- It cause also muscle spasms and tenderness in the
extension or extensora ofneck and back.
- Is usually lasts about a week with meningeal irritation
persisting for about 2 weeks.

4) Paralytic Type
- early manifestations are pain and some degree of stiffness
followed by twitching and diminished deep tendon reflexes.
- There may be hyperesthesia and irritability.
- Loss of tendon reflexes, positive Kernigs Sign and
Brudzinskis Sign
- In one or two days later, weakening of muscle plus paralysis.
- Positive Hoynes Signs- his head will fall back when he is in
supine and his shoulders are elevated. He wont be able to
raise his legs at full 90 degrees.

DIAGNOSIS:

Isolation of the Virus

Blood- end offirst week; WBC may be normal or
slightly increased
Throat- end offirst weekuntil second week
Fecal/Stool-first weekuntil third week
With CNS, CSFexamination
a. CHON- normal and moderately elevated as disease
progress
b. Sugar/Glucose content is normal

TREATMENT:
1. Abortive Type/Minor Illness
Bed rest
Analgesic-to easeheadache,back painsand muscle
spasm
2. Preparalytic or Meningitic Type/Major Illness
Moist hot packs for 15-30 min every 2-4 hrs over the
affected muscles
Anxiety and fear should be allayed
The limb should be in a position of comfort

3.Paralytic Type ( hospitalization required)

Suitable body alignment; feet at the right angle, knees
slightly flexed, hips and spine straight, with the use of board,
sand bags, and occasionally light splint shells
Active and passive movements as soon as pain disappears
Avoid fecal impaction
Maintain good body alignment by using boards, sand bags, etc.
Make bed with cotton or woollen blanket both under and over
the pt.
Change position frequently
Daily bath if necessary and change wet clothes

4. To avoid spread of microorganism

Secretions should be properly disposed
Avoid contact with person having known cases
Nasal and oral hygiene

PREVENTION:
1. Administration of polio vaccine
a. Salk Vaccine- solution of killed viruses that
given intramuscularly
b. Sabin Vaccine- which is preparation
attenuated living viruses that is administered
orally.
2. Effective Immunization-programs may be
achieved carried out community wide to
include all infants over 2 months old, children
and young adults with the preschool age
group as priority target.

COMPLICATION
1.Respiratory paralysis- which includes the
diaphragm and the inter costal muscle
2. Pneumonia
3. Myocarditis
4. Atelectasis
5. Pulmonary edema

6. Acute gastric dilatation, melena

7.Hypertension
8. Renal calculi
9. Late complication- skeletal and soft tissue
deformity

DIAGNOSIS
a) Blood- by the end of the 1stweek,WBC
countmay be normal or slightly increased.
b) Throat- by the end of the 1stweek until the
2ndweek
c) Fecal/stool- by the end of the 1stweek until
the 3rdor throughout the disease and even up
o 3 months.
d) CSF- is not a path gnomonic but may be help
when considered with other manifestations
and the course of the disease.

2) SEROLOGIC DIAGNOSIS
- is of value when there is at least a 4 rise of
antibody titer from the acute to the acute to
the convalescent stage, as determined by
neutralization orcomplement fixation tests.

3) WITH CNS INVOLVEMENT,

CSFEXAMINATION:
a) Pleocytosis with early predominance of
polymorph nuclear cells followed by a shift to
mononuclear cells.
b) Proteins- normal in the early stage of the
disease and may be moderate elevated as
disease progresses
c) Glucose/sugar content is normal.

PROGNOSIS
recoveryfromthenonparalyticformofpoliomyelitisisusuallycomplete.
Inparalyticpoliomyelitis,thedegreeofdisabilitythatresultsdepends
ontheextentofinvolvementandthemanagement.
Recoveryofmusclefunctionusuallyoccursspontaneouslywithina
fewweeks.
Muscleswhichareparalyzedin1monthaftertheonsetofillness
recovercompletelyonlyinlessthan2%ofthecases.
Overallmortalityfortheparalyticformisabout4%
Prognosisispoorerinorderchildrenandadults.
Bulbarpoliomyelitisisalwaysseriousparticularlywhenthemedulla
andrespiratorymusclesareinvolved.

PREVENTION
1.AdministrationofpoliovaccineSalk
Vaccine-solutionofkilledvirusesthatgiven
intramuscularly.
SabinVaccine-whichisapreparation
attenuatedlivingvirusesthatisadministered
orally:

NURSINGINTERVENTIONS
1.Isolationofthepatient(-entericprecautions)
2.Torelievepanandpromotecomfort
-Applymoisthotpackstotheaffectedmuscleand
torelievemuscleshortening.
-maintaingoodbodyalignmentbyusingboard,
sandbags,etc.
-Makebedwithcottonorwoolenblanketboth
underandoverthepatient
-Changepositionfrequently
-Dailybathifnecessaryandchangewetclothes.

3.Toavoidspreadofmicroorganisms
isolation;secretionsshouldbeproperly
disposed
avoidcontactwithpersonhavingknowncases
Nasalandoralhygienesuchasmouthandteeth
mustbeclean,noseshouldbecleansedfor
easilypassageofair;moistenthemucus
membranewithsomeprescribedlubricant.

4.Whenacaseofpoliomyelitisorendemicoccurs
inacommunity,panicandtensionshouldbe
minimized
5.Childrensactivitiesshouldbereducedtoavoid
physicalexertionandfatigueandchillingshould
notbeoverlooked.
6.Sanitationofthepremisesandproperfood
handlingtoavoidcontaminationbyfliesshould
beoverlooked.

7.Unvaccinatedchildrenandsusceptiblemaybe
immunized.
8.Anyonewhopresentsaminorfebrileillness
shouldbeputtobed.
Goldenperiodofpoliois6MONTHS,thisis
wherethegreatestreturnofmotorfunctionis
evident
Butrecoverywillcontinueupto2years
Mortalityis1to4%butmayincreaseto10%if
bulbarinfrom

Sharrads index
1.Extentofneurologicrecoveryandfunctional
dependson:
no.ofmotorneuronsthatsurvivedunimpaired
no.ofmotorneuronsthatrecoverandresumenormal
function,spontaneousimprovementin34mos.
no.ofmotorneuronsthatdevelop
terminalaxonsprouting,responsibleforslowrecovery
evenupto1yearormore

2.Rateofrecoveryfastestinchildren
3.90%ofmusclethatarestillcompletelyparalyzed
after6moswouldremainpermanentlyparalyzed.

Surgical management
a.Muscleandtendontransplantation
OperationofTendons
tenotomy-divisionoftendon
myotomy-divisionofmuscle
fasciotomy-operationondeepfasciathemost
usefulprocedureinthesurgicaltreatmentof
poliomyelitisareoperationsthatrestorestability
tofailedjoints.

b.Arthrodesis-fusionofbonesacrossajointspace
bysurgicalmeans,whicheliminatesmovement,
usuallyperformedtoeliminatepainoverajoint.
c.Osteotomy-cuttingofboneinto2partsfollowed
byrealignmentofendstoallowhealing
d.Operationtoequalizedtheleglengthdiscrepancy
Afterpoliomyelitis,growthaffectedlegisslowed
downasmuch6to7cmbydisuse,atrophyand
diminishedbloodflowtothelimb.Thedegreeof
shorteningdependsoftheseverityoftheparalysis
andtheageatwhichparalysisbegins.

Orthotic devices:
1.Hookscorset
Preventdeformity
2.Longlegbrace
Toprovideneededsupport
3.OppenensSplints
Preventweakeningofmuscles
4.Mobilearmsupport
Toincreasehandfunction

HEPATITIS

Isaviralinfectionoftheliverassociatedwitha
broadspectrumofclinicalmanifestationsfrom
asymptomaticinfectionthrough
icterichepatitistohepaticnecrosis.

Five forms of
viral hepatits

Type A Hepatitis
(HAV)
IscausedbyanRNAvirusoftheenterovirus
family.
Itspreadsprimarilybyfecal-oralroute,usually
throughtheingestionofinfectedfoodorliquids.
Itmayalsospreadfromperson-to-person
contactand,rarely,bybloodtransfusion.
TypeAhepatitisoccursworldwide,especiallyin
areaswithovercrowdingandpoorsanitation.

 Incubationperiod,3to5weeks.
Prodromalsymptoms:fatigue,anorexia,
malaise,headache,low-gradefever,nausea,
vomiting.Highlycontagiousatthistime,usually
2weeksbeforeonsetofjaundice.
Ictericphase:jaundice,tea-coloredurine,
clay0coloredstools,rightupperquadrant
painandtenderness.
Symptomsoftenmilderinchildren.

Type B Hepatitis (HBW)

Iscausedbyadouble-shelledviruscontainingDNA.
Itspreadsprimarilythroughblood(percutaneous
andpermucosalroute).
Itcanalsospreadbywayofsaliva,breastfeeding,
orsexualactivity(blood,semen,saliva,orvaginal
secretions.
Malehomosexualsareathighriskforinfection.
Afteracuteinfection,10%ofpatientsprogressonto
carrierstatusordevelopchronichepatitis.
HBVisthemaincauseofcirrhosisand
hepatocellularcarcinoma.

 Incubationperiod,2to3months.
Prodronalsymptoms(insidiousonset):fatigue,
anorexia,transientfever,abdominaldiscomfort,
nausea,vomiting,headache.
Mayalsohavemyalgias,photophobia,arthritis,
angioedema,urticaria,maculopapularrash,
vasculitis.
Ictericphaseoccurs1weekto2monthsafter
onsetofsymptoms.

Type C Hepatitis (HCV)

Formerlycallednon-A,non-Bhepatitis,usually
spreadsthroughbloodorbloodproduct
transfusion,usuallyfromasymptomaticblood
donors.
Itmayalsobetransmittedthroughunsterile
piercingortattooingtoolsordyes.
ItcommonlyaffectsI.V.drugusersandrenal
dialysispatientsandpersonnel.
HCVisthemostcommonformof
postransfusionhepatitis.

 Incubationperiod,6weekstoseveralmonths.
SimilartoHBVbutlesssevere.

Type D Hepatitis (HDV)

AlsoknownasDeltahepatitis.
IscausedbyadefectiveRNAvirusthatrequires
thepresenceofhepatitisB-specifically,hepatitis
Bsurfaceantigen(HBsAg)toreplicate.
HDVoccursalongwithHBVormaysuperinfect
achronicHBVcarrier,andcannotoutlasta
hepatitisBinfection.
ItoccursprimarilyinI.V.drugabusersorthose
whohavehadmultiplebloodtransfusions,but
thehighestincidenceisintheMediterranean,
MiddleEast,andSouthAmerica.

 Unclearincubationperiod.
SimilartoHBVbutmoresevere.

Type E Hepatitis (HEV)

Iscausedbyanonenveloped,single-strand
RNAvirus.
Ittransmittedbythefecal-oralroutebutishard
todetectbecauseitisinconsistentlyshedinthe
feces.
ItsoccurenceisprimarilyinIndia,Africa,Asia,or
CentralAmerica.

Fulminant Hepatitis
Isararebutseverecomplicationofhepatitis,
whichmayrequirelivertransplantation.

Applicable to all type:

Obtainapatienthistory.AskaboutI.V.druguse,
bloodtransfusions,contactwithinfected
persons(includingsexualactivity),travelto
endemicareas,andingestionofpossible
contaminatedfoodorwatertohelpdetermine
causeofhepatitis.

Diagnostic Evaluation:
Allformsofhepatitis;elevatedserum
transferaselevels(aspartateaminotransferase,
lanineaminotransferase);mayhaveabnormal
clottingtests.
HAV:radioimmunoassaydetects
immunoglobulinM(IgM)antibodiestohepatitis
Avirusintheacutephase.
HBV:radioimmunoassaysdetecthepatitisB
surfaceantigen(HBsAg),antibodytohepatitisB
coreantigen(anti-HBc),anti-HBsAginvarious
stagesofhepatitisBinfection.

 HCV:hepatitisCantibodymaynotbedetected
for3to6monthsafteronsetofillness(usedfor
screening);polymerasechainreactiontesting
evaluatesviralactivity.
HDV:anti-deltaantibodiesinthepresenceof
HBsAg,ordetectionofIgMinacutediseaseand
IgGinchronicdisease.
HepatitisEantigen(withHCVruledout).
Ifindicated,preparethepatientforliverbiopsyto
detectchronicactivedisease,trackprogression,
andevaluateresponsetotherapy.

Pharmacologic Interventions:
VitaminKinjectedsubcutaneously(S.C.)if
prothrombintimeisprolonged.
I.V.fluidandelectrolytereplacementsas
indicated.
Antiemeticfornausea.
Long-terminterferontherapyincombinationwith
oralribavirinmayproduceremissioninHCV
patients.Peginterferonalfa-2bisalong-acting
preparationgivenS.C.,onceperweek,and
ribavirinistakentwicedaily.
AntiviraltreatmentisbeinginvestigatedforHBV.

Nursing Interventions:
Monitorhydrationthroughintakeandoutput.
Monitorprothrombintimeandforsignsof
bleeding.
Encouragethepatienttoeatmealsinasitting
positiontoreducepressureontheliver.
Encouragepleasingmealsinanenvironment
withminimalnoxiousstimuli(odors,noise,and
interruptions).
Teachself-administrationofantiemeticsas
prescribed.

 Encouragerestduringsymptomaticphase,
accordingtoleveloffatigue.
Encouragediversionalactivitieswhenrecovery
andconvalescenceareprolonged.
Encouragegradualresumptionofactivitiesand
mildexerciseduringconvalescentperiod.
Stressimportanceofproperpublicandhome
sanitationandproperpreparationand
dispensationoffoods.
Encouragespecificprotectionforclosecontacts.

 Explainprecautionsabouttransmissionand
preventionoftransmissiontootherstothe
patientandfamily.
Warnthepatienttoavoidtraumathatmay
causebruising.
Stresstheneedtofollowprecautionswithblood
andsecretionsuntilthepatientisdeemedfree
ofHBsAg.
Emphasizethatmosthepatitisisself-limiting,
butfollowupisneededforliverfunctiontests.

DISEASE
CAUSED BY
PARASITES

AMOEBIC
DYSENTERY
(AMOEBIASIS)

 Anacutediseasecausedbyingesting
substancescontaminatedwiththe
amoebaEntamoeba histolyticaand
characterizedbyseverediarrhea,
nausea,andinflammationofthe
intestines.

Prevalent in unsanitary areas

Common in warm climate
Acquired by swallowing
Cyst survives a few days
outside the body
Cyst passes to the large intestine
and hatches into trophozoites.
It passes into the mesenteric veins
to the portal vein , to the liver,
thereby forming amoebic liver abscess.

Trophozoites / Vegetative
Form
-Trophozoites are
facultative parasites that
may be found in
the
parasitized tissues and
liquid colonic contents.

Cyst
-Cyst is passed out with formed or
semi formed stools
and are resistant
to
environmental conditions.
-This is considered as the infective
stage in the life cycle of E. Histolytica.

Whenthecystisswallowed,itpasses
throughthestomachunharmedandshows
noactivitieswhileinanacidicenvironment.
Whenitreachesthealkalinemediumof
theintestine,themetacystbegintomove
withinthecystwall,whichrapidlyweakens
andtears.

Thequadrinucleateamoebaemergesanddivides
intoamebulasthataresweptdownintothececum.
This is the first opportunity of the organism to
colonize, and its success depends on one or more
metacystic trophozoites making contact with the
mucosa.
Mature cyst in the large intestines leaves the
host in great numbers
(the host remains asymptomatic).

Thecystremainviableandinfectiveinmoistandcool
environmentforatleast12days,andinwaterfor30
days.
The cyst are resistant to levels of chlorine
normally used for water purification.
They are rapidly killed by purification,
desiccation and temperatures below 5 and above
40 degree celcius.

The incubation period in severe

infection is three days.
in sub-acute and chronic form it lasts
for several months.
In average cases the incubation
period varies from three to four
weeks.

The microorganism is
communicable for the entire
duration of the illness.

The disease can be passed from one

person to another through fecal-oral
transmission.
The disease can be transmitted through
direct contact, through sexual contact by
orogenital, oroanal, and proctogenital
sexual activity.

Through indirect contact, the disease

can infect humans by ingestion of food
especially uncooked leafy vegetables or
foods contaminated with fecal
materials containing E. histolica cysts.
Food or drinks maybe contaminated by cyst through
pollution of water supplies, exposure to flies.

1. Acute amoebic dysentery

Slightattackofdiarrheaalteredwith
periodsofconstipationandoften
accompaniedbytenesmus
Diarrhea,wateryandfoul-smellingstool
oftencontainingbloodstreakedmucus .

 Colicandgaseousdistensioninlower
abdomen.
Nausea,flatulence,abdominal
distensionandtendernessintheright
iliacregionoverthecolon.

2. Chronic amoebic dysentery

Attackofdysenterythatlastfor
severaldays,usuallysucceededby
constipation.
Tenesmusaccompaniedbydesireto
defecate.
Anorexia,tenesmusandweakness
Livermaybeenlarge

1. Stoolexam(cyst,whiteand
yellowpuswithplentyof
amoeba).
2.Bloodexam
3.Proctoscopy/Sigmoidoscopy

 Metronidazole(flagyl)800mgTIDx5
days
Tetracycline250mgevery6hours
Ampicilin,quinolones,sulfadiazine
StreptomycinSO4,clorampenicol
Lostfluidandelectrolytesshouldbe
replaced.

1.Observeisolationandentericprecaution.
2.Providehealtheducationandinstructthe
patientto:
a.Boilwaterfordrinkingorused purifiedwater.
b.Avoidwashingoffoodfromopendrumorpail
c.Coverleftoverfoods
d.Washhandsafterdefecationor beforeeating.
e.Avoidgroundvegetables (lettuce,carrotsand
etc.)

3.Propercollectionofstoolspecimen.
a. Nevergiveparaffinoranyoilforatleast48
hourspriortocollectionofthespecimen.
b. Instructthepatienttoavoidmixing urine
andstools.
c. Ifwholestoolcannotbesenttolaboratory,
selectasmuchportionaspossiblecontaining
bloodandmucous.
d. Sendspecimenimmediatelytothelaboratory;
stoolthatisnotfreshisnearlyuselessfor
examination.
e. Labelspecimenproperly.

4.Skincare-Cleanliness,freedomfrom

wrinklesonthesheetwillbe helpfulwithallthe
usualprecautionarymeasuresagainstpressure
sores.
5.Mouthcare
6.Provideoptimumcomfort-Patientshouldbe
keptwarm.Dysentericpatientshouldneverbe
allowedtofeelcold,evenforamoment.

7.Diet
a. Duringtheacutestage,fluidsshould beforced.
b. Inthebeginningofanattack,cerealandstrained
meatbrothswithoutfatsshouldbegiven.
c. Chickenandfishmaybeaddedwhen
convalescenceisestablished.
d. Blanddiet

Health education
Sanitary disposal of feces
Protect chlorinate, and purify drinking water
Observe scrupulous cleanliness in food
preparation and food handling
Detection and treatment of carriers
Fly control (it can serve as a vector)

ASCARIASIS
(roundworm
infestation)

 Is an infection caused by
ascariasis lumbricoides (intestinal
roundworm). It is characterized
by an early pulmonary invasion
from larval migartion and a later
more prolonged intestinal phase.

Causative agent

Ascariasis lumbricoides
The adult ascariasis worms
are elongated, cylindrical,
tapering bluntly at the end
and somewhat more pointed
at the anal end

Mode of Transmission
FECAL-ORAL route, i.e., by ingestion
of infective eggs with food or drink.
Foods that are eaten raw such as
salads and vegetables readily convey
the infection and so is polluted water.
Other means of spread are by fingers
contaminated with soil or by ingestion
of contaminated soil as usually
happens

Clinical manifestations
In the lungs
Persistent cough
Shortness of breath
Wheezing
In the intestine
Vague abdominal pain
Nausea and vomiting
Diarrhea or bloody stools

 Heavy intestinal infestation

severe abdominal pain
Fatigue
Vomiting
Weight loss
A worm in vomit or stool

Complications

Energy protein
undernutrition, anemia
Intestinal obstruction
perforationsecondary
peritonitis

Diagnosis
History of passing out adult
worms
Patient occasionally vomits a worm
Stool specimen
X-ray
Blood exams

Treatment
Anti-parasite medications are the
first line of treatment against
ascariasis. The most common are:
Albendazole (Albenza)
Ivermectin (Stromectol)
Mebendazole

Nursing interventions and

prevention
The best defense against ascariasis is good

hygiene and common sense. Follow these tips to

avoid infection:

Practice good hygiene.Ascariasis is spread by

ingesting parasite eggs from contaminated soil.
Before handling food, always wash your hands with
soap and water, and wash fresh fruits and
vegetables thoroughly.

 Use care when traveling.Ascariasis is the

most common roundworm infection in the
world, with higher infection rates in
developing and warm-climate countries.
When traveling, use only bottled water and
avoid raw vegetables unless you can peel
and wash them yourself. As a rule, eat only
foods that are hot and cooked

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