Disease Phatogenesis Therapeutics
ESOPHAGITIS 1.Gastric acid flow back to Antibiotic-Betamox
oesophagus (amoxicillin) - Adult
2.Acidity can corrosive lining 250 mg
oesophagus ,Child 20 mg/kg
3.Lining of oesophagus can be
irritated •Antifungal –
4.Infection/Inflammation of Fluconazole –
oesophagus • Antacids-
Magnesium
HIATUS HERNIA Trisilicate - 600-
1200mg
•Proton pump
1.Increasing of intraabdominal inhibitors-
pressure Omeprazole - IV :
2.Size of haitus not fixed 40 mg
3.Tear of phranoesophageal • H-2 receptor
ligament blockers-
4.Reduced LES pressure cimetidine - 400
5.Reduced oesophageal acid mg
clearence
Medication:
•Proton pump
inhibitors
(PPIs) –
Pantoprazole
GERD (Protonix) - IV : 40
mg
•Antacids –
magnesium
hidroxide – 10-20ml
• H-2 receptor
1.Smoking/alcohol/pregnency/ blockers-
overweight cimetidine – 400
2.Problematic at the lower mg • Prokinetic
Oesophagus sphincter Agents – Cisapride
3.Gastric acid can reflux to the 5-10 mg
esophagus
4.Inflammation at oesophagus Lifestyle changes
5.Symptoms develop
•Stress
management
•No smoking
•No alcohol
•Don’t sleep after
eat
•Antacids-
Magnesium
Trisilicate – 600-
1200mg
•Proton pump
inhibitors-
Omeprazole – IV :
40 mg
•Prokinetic Agents
– Cisapride 5-10 mg
GASTRITIS ACUTE •Antacids-
Magnesium
1.Due to any cause Trisilicate – 600-
2.Gastric mucosal barrier is 1200mg
penetrated
3.Hydrochloric acid comes into •Proton pump
contact with the mucosa inhibitors-
4.Injury to small vessels Omeprazole – IV :
5.Oedema, haemorrhage, and 40 mg
possible
Ulcer formation •Prokinetic Agents
– Cisapride 5-10 mg
CHRONIC GASTRITIS
1.The stomach lining first becomes
thickened and erythematous and
then becomes thin and atrophic.
2.Continued deterioration and
atrophy
3.Loss of function of the parietal
cells 4.Acid secretion decreases
5.Inability to absorb vitamin B12
6.Development of pernicious
anemia
PEPTIC ULCER 1.Smoking,emotional stress Antacids-
2.Reduction in blood flow Magnesium
3.Reduction of mucosal resistance Trisilicate – 600-
4.Peptic ulcer 1200mg
• Proton pump
1.Steroid therapy inhibitorsOmeprazo
2.Reduced mitotic activity le – IV : 40 mg
3.Reduce generation power of
epithelial cell
4.Reduction of mucosal resistance
5.Peptic ulcer
1.H.pylori infection & NSAIDs
2.Increased action of acid-pepsin
3.Peptic ulcer
IRRITABLE 1.bacterial/ viral infection
BOWEL
DISEASE Antispasmodic –
Hyoscine
2.Trigger immune respone butylbromide •
Antipyretic –
Paracetamol
3.Immune system respond the
invaders
4.digestive tract becomes inflamed
due to immune respond
CHOLERA 1.ingested contaminated •Antispasmodic.-
water/food Hyoscine
2.V. Cholerae resistand to gastric butylbromide
acid. • Antipyretic. –
3.Colonized at small instestine Paracetamol
4.Secrete enterotoxicin •Antibiotic.-
5.Enterotoxicin bind to intestine Doxycycline
cells 6.Chloride channel activated
7.Released large quantities of
electrolyte & bicarbonates
8.Fluid hypersecretion
9.Diarrhea
10.Dehydration
THYPHOID 1.Ingestion of contaminated food Antispasmodic.-
or water Hyoscine
2.Salmonella bacteria butylbromide
3.Invade small intestine and enter
the bloodstream Antipyretic.
4.Carried by white blood cells in Paracetamol
the liver, spleen, and bone marrow
5.Multiply and reenter the Antibiotic-
bloodstream Ciprofloxacin
DYSENTRY 1.Contaiminated food/water by Antispasmodic.-
infected faeces Hyoscine
butylbromide
2.Bacteria enter to the gutt
3.Growth in small intestine Antipyretic-
4.Spread to the colon, inflame the Paracetamol
epithelium mucosa cell Antibiotic –
5.Secrete / produce toxin metronidazole
6.Break through the colon wall &
necrosis ephitelium cell
7.Haemorrhage, more mucus
purulent at
the ephitelium surface
8.Ulcer colon happen.
APPENDIX 1.Obstruction of the appendiceal Pre:
lumen
(inside the appendix) 1.Assessment
2.Build up of mucous in the History taking
appendix physical
Appendix constantly secreting examinations,
mucous Regarding pain,
3.appendiceal lumen pressure nausea
4.blood flow to the appendix
5.oxygen delivery (hypoxia) Vomiting,
6.Ulceration (lesion) of the abdominal rebound
appendix mucosal lining tenderness,Anorexi
7.Promotes microbe invasion a.
(ex.Bacterial)
8.Inflammation and swelling of the 2.Monitor vital
appendix signs B.P.,
9.APPENDICITIS Temperature for
baseline data.
3.NPO and I.V.
Fluids be started. •
Naso-gastric
aspiration. •
Monitor for signs of
ruptured appendix
and peritonitis.
4.Position right-side
lying or low to semi
fowler position to
promote comfort. 5.
Uscultate Bowel
Sounds.
6.
Administer
antibiotics as
prescribed.
7. Preparation
for surgery
example: physically
& psychologically.
8.Alley anxiety &
fears. 9. Written
consent for surgery.
10.Prepare and
send the patient for
surgery without
delay. •
11.OT clothes and
pre medications to
be given 45
minutes before
operation Post :
1. Clear airway.
2. Proper
breathing and
adequate tissue
perfusion by IVF.
3. Naso-gastric
suction to be done
regularly to relieve
tension on sutures.
4. Provide
safety & effective
care environment
to the patient.
5. Care of all
drainage tubes.
6. Care of
surgical wounds.
Watch for
soapage/bleeding.
7. Daily A.S.
dressing and watch
for signs of
infections.
8. Nutritional
status maintained
by I.V. fluids
DIARRHEA 1.Osmotic diarrhoea occurs when Medication
excessive osmotically • Oral
Rehydration Salt
active particles are present in the
lumen, resulting in more (ORS)
• Ultracarbon -
Medicinal
charcoal/adsorbent
CONSTIPATION 1.The main cause of constipation Medication
are eating foods low in fiber ,not
drinking enough water and stress •Raven Enema
•Laxative :
2.The voluntarily sphincters Bisacodyl
constricts and and does not
evacuate bowel. Non medication
•Consume food
3.Rectal ampulla stretches and high in fiber
accommodates increasing amount •No alcohol
of stool •No smoking
•Exercise regularly
4.Water is mainly absorbed and
stool
becomes harder
5.With passage of time rectal
ampulla oversteches
6.Overstrecthing reduces the urge
to daefecate
7.Stool is pushed into the anal
canal also and starts collecting
there leading to soiling.
WORM 1.The most obvious forms of direct Medication
INFESTATION damage are those resulting from
the blockage of internal organs or •Albendazole
from the effects of pressure (Zentel)
exerted by growing parasites.
Large Ascaris or tapeworms can •Metronidazole
physically block the intestine, and (Flagyl)
this may occur after some forms of
chemotherapy; migrating Ascaris Non medication
may also block the bile duct.
•makan makanan
2.Intestinal worms cause a variety yang dibersihkan
of pathologic changes in the
mucosa, some reflecting physical •Makan makanan
and chemical damage to the yang dimasak
tissues, others resulting from sepenuhnya •
immunopathologic responses. Jangan merokok
Hookworms (Ancylostoma and
Necator) actively •Jangan minum
alkohol • Ubat
3.suck blood from mucosal makan mengikut
capillaries. waktu yang
Feeding by worms upon host ditetapkan
tissues is an
important cause of pathology,
particularly when it induces
hyperplastic and metaplastic
changes in epithelia. For example,
liver fluke infections lead to
hyperplasia of the bile duct
epithelium.
