This document discusses the etiology, pathophysiology, clinical presentation, and management of nausea, vomiting, dyspepsia, and diarrhea. It begins by describing nausea and vomiting as common symptoms of gastrointestinal disorders. It then discusses the etiology, pathophysiology involving the vomiting center and various neurotransmitter systems, and pharmacological management including antacids, H2 receptor antagonists, and serotonin antagonists. Next, it covers dyspepsia including definition, causes, pathophysiology, clinical presentation, and management with antacids, H2 receptor antagonists, and proton pump inhibitors. Finally, it addresses diarrhea by defining it, discussing pathophysiological mechanisms, and outlining non-pharmacological and pharmacological treatment

1. *
SUBMITED BY :
KHALIDA REHMANI
REG NO : 16AB1TOO19
UNDER THE GUIDELINES OF:
MR. RAMESH
Vignan pharmacy college ;vadlamudi; approved by AICTE; Pharmacy council of
India; new delhi;govt of AP ;affiliated to JNTUK ;kakinada.

2. *
•Nausea and vomiting are the most commonly seen
complaints in the patients suffering from gastro intestinal
disorders and chronic conditions like cancer.
•Nausea is a symptom , which is subjective and an
unpleasant sensation of urge to vomit.
•It is followed by variety of autonomic signs such as pallor ,
sweating , tachycardia , salivation and increased respiratory
rate .
•Vomiting or emesis is the reflux expulsion of the stomach
contents via the oesophagus and mouth and is usually
associated with nausea and retching.
•Retching is an involuntary but unsuccesfull effort to vomit

3. ETIOLOGY:
*Nausea and vomiting are experienced in various clinical
situations like gastrointestinal tract obstruction, mucosal
lesions such as ulcers , inflammation , liver diseases etc
*Cardio vascular diseases such as renal failure,
hyperparathyroidism , adrenal insufficiency ,pregnancy
and diabetic ketoacidosis
CLINICAL PRESENTATION:
The signs and symptoms of vomiting include,
•Dehydration
•Weight loss
•Mental confusion
•Reduced skin tuger
•Increased thirst, hypotension
Muscle weekness and cardiac disturbances and alkalosis

4. PATHOPHYSIOLOGY:
These are the three consecutive phases of emesis
Nausea
Vomiting
Retching
 Nausea is an urge to vomit and is associated with
gastric stasis and may be considered as a separate
singular symptom.
 Retching is a labored movement of abdominal and
thoracic muscles before vomiting .
 The final phase of emesis is vomiting , the forceful
expulsion of gastric contents caused by GI retro
peristalsis .
 Vomiting is mainly mediated via stimulation of
vomiting centre .

5. •The afferent fibres from the sensory receptors in the pharynx
, stomach , intestine , and other visceral organs directly
connect to vomiting centre through the values and sphlanchic
nerve stimulate the vomiting centre.
•Variety of stimulus such as sight , smell , medicines , toxins ,
metabolites , and motion sickness may stimulate the
chemoreceptor trigger zone[CTZ] to initiate the vomiting
reflex. When the vomiting centre is stimulated the efferent
impulses are sent to salivary , vasomotor and respiratory
centre .
•Five major , transmitter systems are involved in this process .
receptors are present in vomiting centre and chemo trigger
zone .
•When they receive stimulus they act via there respective
receptors to produce emesis .

6. •The main neuro transmitters involved in the process of
vomiting are:
•Dopaminergic
•Histaminic
•5-hydroxytryptamine
•Cholinergic
•Substance P
•The dopaminergic receptors are present in the CTZ and GI
tract.
•The dopamine agonists like apomorphine and levodopa
are thought to mediate via this pathway.
•Where as in motion sickness there is imbalance in the
cholinergic and adrenergic system in the region of the
medulla near the vomiting centre and CTZ or directly
stimulate CTZ.

7. •The chemotherapeutic agents produce nausea and vomiting
through serotonin stimulating the receptor located on afferent
vagal nerve terminals to initiate the vomiting reflex.
•Substance P – a neuropeptide that belongs to tachykinin
family is found in the higher concentration in the nucleus
tractus solitaries and the area postrema of CNS .
•The actions of substance P are mediated through NK1
receptor.
PHARMACOLOGICAL MANAGEMENT:
Medications in the management of nausea and vomiting are
classified as:
Ant acids and antisecretory agents
Eg: magnesium and aluminium hydroxide containing tablets
and suspensions.
Histamine 2-receptor antagonists:
Eg :cimetidine , famotidine ,nizatidine and ranitidine.

8. Proton pump inhibitors:
Eg : omeprazole , esomeprazole , lansoprazole , pantoprazole,
and rabeprazole.
Anticholinergics :
Eg : scopolamine : 0.5 mg every 72 hours.
Antihistamines :
Eg :diphenhydramine :10-150 mg every 4-6 hours needed.
Dopamine antagonists :
Eg : chlorpromazine :10-25mg Q4-6 hr ,promethazine :12.5 -
25mg Q 4-6hour needed , domperidone dose of 10mg 8th hourly.
Serotonin antagonists :
Eg :ondansetron :32mg 4 prior to chemotherapy as single
dose or 1.5mg per kg prior to chemotherapy, repeat every 4-
8 hr or 8mg orally prior to chemotherapy.

9. DYSPEPSIA:
•The term ‘dyspepsia’is derived from
greek word .The meaning of dyspepsia is
“improper digestion and is used to
describe upper abdominal discomfort ,
usually related to food or alcohol intake
or certain medications like antibiotics ,
non steroidal anti inflammatory drugs
[NSAID], digoxin , bisphosphonates ,
theophylline .
.

10. Aetiology :
•Peptic ulcer disease.
•Gastro esophageal reflux disease with or
without esophagitis
•Malignancy or functional or idiopathic
dyspepsia
•Smoking and stressfull lifestyle may
also contribute to the development of
dyspepsia.
•Chronic dyspepsia is defined as
recurrent symptoms that include
epigastric pain , abdominal bloating ,
belching , nausea , vomiting , and early
satiety .

11. Pathophysiology :
•Several pathophysiologic mechanisms are involved in the
development of functional dyspepsia , including visceral
hypersensitivity , both in the stomach and the duodenum , impaired
gastric accommodation , antral over distension , delayed gastric
emptying , and abnormal duodeno jejuna motility .
•Acute infrequent dyspepsia is commonly associated with irregular
intake of food , regular intake of alcohol , cigarette smoking and
stress.
•Chronic dyspepsia is related to peptic ulcer disease , esophageal
reflex disease H pylori infection and the malignancy .
Irritable bowel syndrome may also contribute to functional
dyspepsia

12. CLINICAL PRESENTATION:
SIGNS AND SYMPTOMS:
•Persistent vomiting
•Constant severe pain
•Concomitant weight loss
•Dysphasia
•Hematemesis or melena warrants endoscopy
•Abdominal and extra gastrointestinal complaints
•Anxiety or depression
•Early satiety
•Anorexia
•Jaundice
•GI bleeding

13. MANAGEMENT OF DYSPEPSIA:
Non pharmacological management:
•Lifestyle modifications
•Balanced diet
•Smoking cessation
•Reduced intake of alcohol
•Weight reduction through aerobics
•Reduced intake of caffeine and fatty foods
Pharmacological therapy:
Antacids
•Ant acids cause mucosal protection by neutralising the acid and
forming a coat on damaged tissue.
•Supensions are more effective than tablets .Antacids should be
taken regularly in a dose of 15 ml to relieve the symptoms.
Eg : mixture of aluminium and magnesium salts

14. H2 receptor antagonists:
•Ranitidine and famotidine block the action of histamine
on H2 receptors of the parietal cells thus reducing the
basal and stimulated gastric acid secretion.
•Due to good therapeutic efficacy Famotidine 20mg ;BID
or 40 mg;OD and ranitidine in 150mg ,BID or 300mg ; OD
are effective in providing relief in dyspepsia .
Anti secretory agents:
•Proton pump inhibitors [PPIs] binds irreversibly to the
Na+ K+ ATPase pump and inhibits the terminal step in the
acid production .
•They are more effective when taken 30-60min before the
first meal on an empty stomach .
Eg: omeprazole 20mg OD; Rabeprazole 20 mg
,Lansoprazole 30mg OD ; Pantaprazole 40 mg.

15. DIARRHEA
•Diarrhea is defined as an increase in fluidity and
frequency of stools
•Normally an healthy human individual defecate about
200 grams of stool per day. But during diarrhoea , more
than 200 gram stool containing 70-95% water will be
produced and the frequency increased upto 5-20 times a
day.
•In severe cases 1.4 L water will be lost.
•Dysentery is called low volume bloody diarrhoea.
•Diarrhea may be due to ingested contaminated food or
water with virus, bacteria or protozoan pathogens.

18. .
Pathophysiology :
Diarrhea occurs due to imbalances between absorption and
secretion of water and electrolytes. It may be associated with a
specific disease of intestine or secondary to the disease outside the
intestine.
The principal mechanisms of diarrhea :
•Change in the active ion transport by either decreased
sodium absorption or an increased chloride secretion.
•Change in intestinal motility.
•Increase in luminal osmolarity
•Increase in tissue hydrostatic pressure
•Malabsorption

19. MANAGEMENT:
Prevention of excessive water and electrolyte loss are the main
strategies in the management of diarrhea.
Non –pharmacological management:
•Eating balanced diet and avoiding solid foods and dairy products
atleast for 24 hours.
•In replenishing the lost electrolytes by oral rehydration salts.
•ORS formula can also be made at home by mixing a pinch a of salt
into 200ml of water and cooled water with one tea spoon full of
sugar.

20. Eg: loperamide –used in acute and chronic diarrhea;
initially 4mg then 2mg after each stool but should not
exceed 16mg per day.
Pharmacological management:
Anti motility drugs:These drugs delay the transit of
intraluminal content or increase the gut capacity prolonging
contact and absorption
Adsorbents :Adsorbents are used to provide symptomatic
relief.
Eg: kaolin –pectin given at a dosage range of 30 – 120 ml
after each stool.
Antisecretory agents: They are often used to treat travellers
diarrhea.
Eg :Bismuth sub salicylate

21. Bacterial replacement agents: Lactobacillus preparations are
intented to replace the colonic microflora therby retoring the
intestinal function and suppressing the growth of pathogenic
microorganisms.
Octreotide : It is the synthetic analogue of endogenous
somatostatin. It is given to the symptomatic treatment of
carcinoid tumours and vasoactive peptide secreting tumours. It
acts by blocking the release of serotonin and other active
peptides and thus controls diarrhea.
Antibacterial agents:
Flouroquinolones such as Norfloxacin 400mg ; or
ciprofloxacin 500mg ;oflaxacin 200mg.combinations of
flouruquinolones and anti amoebic agents are also used to
control infective bloody diarrheas.

22. CONSTIPATION :-
•Constipation is defined as an infrequent
bowel action of twice a week or less
then involves straining to pass hard
stools accompanied by a sensation of
pain or incomplete evacuation .
•Constipation appears to be more
common in upto 20% in elderly people
8% in middle aged and 3% of young
people .

24. Pathophysiology :-
*The upper GIT tract is responsible for
ingestion and digestion of the food ,where as
lower GIT is responsible for conserving body
water and electrolytes , drying the feces and
elimination .
*The remains of undigested food are swept
along the GI tract through peristalisis .These
peristaltic waves eventually move the faeces
from the colon to the rectum and induce urge
to defecate .

25. Normally there is net uptake of
fluid in the intestine and response
to osmotic gradiants involving the
absorption and secretion ions ,
absorption of sugars and amino
acids under the influence of ANS.
By the time stool reaches the
rectum it becomes more solid and
consistency because most of the
water has been absorbed

26. *Normally there is net uptake of fluid in the intestine and
response to osmotic gradiants involving the absorption
and secretion ions , absorption of sugars and amino acids
under the influence of ANS.
*In some situation absorption increases will generally lead
to constipation. Agents that alter intestinal motility either
directly or by acting on ANS , effect transit time of food .
* A slower transit time will lead to the formation of hot
stools and constipation
Managements :-
Non-pharmacalogical treatment :-
•Increased intake of water upto 2 litres
•Avoidence of excess intake of coffee or tea.
•Consuming foods that contain more fibres such as fruits,
vegetables and cerels..
•An increased level of exercise.

27. Pharmacological therapy :-
Emollient laxatives (docusates) :-
*These surfactant agents in various salts work by
facilitating the mixing of aqueous and fatty materials in
GIT.They may increase water and electrolyte secretion in
the small and large bowel.
*They result in softening of stools within 1-2 days .
Emollient laxatives are not effective in treating
constipation, but are used mainly to prevent constipation.
Lubricants :
*Mineral oil is the only lubricant laxative in the routine use
and acts by coating stool and allowing easier passage.
*It decreases colonic absorption of water,there by
increasing stool weight and stool transit time.

28. Lactotulose and sorbitol:
*Lactulose is a disaccharide that causes osmotic effect
retained in the colon.
*It is not generally recommended as first line therapy ,as it
is costly and not much effective than milk of magnesia.
Saline cathartics:
*Saline cathartics are composed of relatively poorly
absorbed ions such as magnesium , sulphate , phosphate ,
citrate,whose action is to retain fluid in GIT.
*Can be taken orally or rectally.
*Agents like milk of magnesia(8% suspension of
magnesium hydroxide.

29. Castor oil:
*Castor oil is metabolised in liver in to an active
compound ricinoleic acid.
*This acid stimulates secretory process, decreases glucose
absorption, promotes intestinal motilitywithin 1-3 hours
after administration.
Glycerine :
*Usually administered 3 gm and is most safest of all drugs
for children
*It occasionally causes rectal irritation.