it explains about the hyperacidity ie acute gastritis

2. Introduction
• Hyper acidity is also called Acid Dyspepsia, which is
one of the most common problem. Hyperacidity is a
medical condition in which the stomach secretes a
lot of acids. It can be caused due to various
medications, stressed lifestyle and spicy foods.
• Hyperacidity has various symptoms, which can
include sudden stomach pain, vomiting, loss of
appetite, flatulence and heartburn. Sometimes, the
problem aggravates and lead to other complications
such as chronic indigestion and gastric ulcers.

3. Symptoms
• Acidity Symptoms
• Following are some of the symptoms of acidity –
• Respiratory problems
• Coughing
• Vomiting
• Long heartburn
• Stomach and chest pain
• Flatulence
• Bloating

4. • Stomach ulcers
• Pain in ears
• Gastroesophageal reflux
• Pain in muscular contraction
• Inadequate weight and turning down food in infants
are the symptoms of acidity.

5. Etiology
• Acute gastritis has a number of causes, including
certain drugs; alcohol; bacterial, viral, and fungal
infections; acute stress (shock); radiation; allergy and
food poisoning; bile; ischemia; and direct trauma.
• Note the following:
• Drugs - NSAIDs, such as aspirin, ibuprofen, and
naproxen; cocaine; iron; colchicine, when at toxic
levels, as in patients with failing renal or hepatic
function; kayexalate; chemotherapeutic agents, such
as mitomycin C, 5-fluoro-2-deoxyuridine, and
floxuridine

6. • Potent alcoholic beverages, such as whisky, vodka,
and gin
• Bacterial infections - H pylori (most frequent), H
heilmanii (rare), streptococci (rare), staphylococci
(rare), Proteus species (rare), Clostridium species
(rare), E coli (rare), tuberculosis (rare), secondary
syphilis (rare)
• Viral infections (eg, CMV)
• Fungal infections - Candidiasis, histoplasmosis,
phycomycosis

7. • Parasitic infection (eg, anisakidosis)
• Acute stress (shock)
• Radiation
• Allergy and food poisoning
• Bile: The reflux of bile (an alkaline medium is
important for the activation of digestive enzymes in
the small intestine) from the small intestine to the
stomach can induce gastritis.
• Ischemia: This term is used to refer to damage
induced by decreased blood supply to the stomach.
This rare etiology is due to the rich blood supply to
the stomach.
• Direct trauma

8. Epidemiology
• Data from a national administrative database (2009-
2011) revealed standardized estimated prevalence
rates of 6.3 per 100,000 population for eosinophilic
gastritis and 3.3 per 100,000 population for
eosinophilic colitis; women were affected more
often.
• Gastritis affects all age groups. The incidence of H
pylori infection increases with age.

9. I. REFLUX OESOPHAGITIS
• The disorder may be defined as damage to the
esophageal mucosa due to reflux of gastric contents.
• Etiology: Increased reflux of gastric contents into the
esophagus from reduced pressure in the lower
oesophageal sphincter and an increased number of
transient relaxation of the sphincter are the main
factors in the development of reflux esophagitis.

10. • Clinical Features / Symptoms:
• Heartburn: This is a sensation of burning or burning
pain located high in the epigastria or behind the
lower end of the sternum often radiating upwards
behind the sternum. It occurs after meals and is
characteristically brought on by lifting or straining
due to an increase in the abdominal pressure.
Heartburn may also occur on lying down in bed at
night, preventing sleep or awakening the patient
several hours after the onset of sleep.It is sometimes
precipitated immediately by acid food or drink –
tomatoes, orange, cola, and alcohol.
• Painful Dysphagia: The usual cause is the bolus of
food passing through an inflamed segment of
esophagus.

11. • Regurgitation of gastric contents into the mouth
may occur during bending, after large meal or at
night. The patient becomes aware of the
regurgitation because of a bitter taste in the mouth.
• Sore throat, Globus sensation (‘lump in throat’),
and hoarseness are other consequences.
• Management:
• Weight reduction
• Stopping cigarette smoking
• Meals should be of small volume
• Alcohol, fatty food, and caffeine should be avoided

12. • No snacks must be taken after evening meal to
prevent nocturnal regurgitation
• Heavy stooping or bending at the waist should be
avoided especially after meals
• Head in the bed should be elevated by 15 cm.

13. Peptic ulcer
• The term ‘peptic ulcer’ refers to an ulcer in the lower
esophagus, stomach, or duodenum.
• Etiology: Following factors play a role
• Heredity
• Helicobacter pylori
• NSAID’s
• Smoking
• Chronic stress
• Alcohol
• Corticosteroids
• Duodenogastric reflux of bile.

14. • Pathology: An ulcer forms when there is an
imbalance between aggressive forces, i.e., the
digestive power of acid and pepsin, and defensive
factors i.e., the ability of the gastric and duodenal
mucosa to resist this digestive power. However, in
the majority of patients acid secretion is within
normal limits or is moderately raised. In these
individuals, damage to the gastric mucosal barrier is
necessary to facilitate the damaging effect of acid
and pepsin. The initial damage results from
Helicobacter pylori, NSAID’s, and smoking.

15. • Clinical Features / Symptoms:
– Epigastric pain: Pain is referred to the epigastrium
and is often so sharply localized that the patient
can indicate its site with two or three fingers-the
‘pointing sign’.
– Hunger pain: Pain occurs intermittently during the
day, often when the stomach is empty, so that the
patient identifies it as ‘hunger pain’ and obtains
relief by eating.
– Night pain: Pain wakes the patient from sleep and
may be relieved by food, a drink of milk, or
antacids; this symptom when present is virtually
pathognomonic for ulcer.

16. – Water brash: This is a sudden filling of mouth with
saliva which is produced as a reflex response to a
variety of symptoms from the upper GIT, e.g.,
peptic ulcer pain
– Heartburn
– Loss of appetite
– Vomiting

17. Gastric acid
• Gastric acid, gastric juice or stomach acid, is a digestive fluid
formed in the stomach and is composed of hydrochloric
acid(HCl), potassium chloride(KCl) and sodium chloride(NaCl).
The acid plays a key role in digestion of proteins, by
activating digestive enzymes, and making ingested proteins
unravel so that digestive enzymes break down the long chains
of amino acids. Gastric acid is produced by cells in the lining of
the stomach, which are coupled in feedback systems to
increase acid production when needed. Other cells in the
stomach produce bicarbonate, a base, to buffer the fluid,
ensuring that it does not become too acidic. These cells also
produce mucus, which forms a viscous physical barrier to
prevent gastric acid from damaging the stomach.
The pancreasfurther produces large amounts of bicarbonate
and secretes bicarbonate through the pancreatic ductto
the duodenum to completely neutralize any gastric acid that
passes further down into the digestive tract.

18. • The main constituent of gastric acid is hydrochloric acid which
is produced by parietal cells(also called oxyntic cells) in
the gastric gland in the stomach. Its secretion is a complex
and relatively energetically expensive process. Parietal cells
contain an extensive secretory network (called canaliculi)
from which the hydrochloric acid is secreted into the lumen of
the stomach. The pH of gastric acid is 1.5 to 3.5in the human
stomach lumen, the acidity being maintained by the proton
pump H+/K+ ATPase. The parietal cell releases bicarbonate into
the bloodstream in the process, which causes a temporary
rise of pH in the blood, known as an alkaline tide.
• The highly acidic environment in the stomach lumen
causes proteins from food to lose their characteristic folded
structure (or denature). This exposes the protein's peptide
bonds.

19. • The gastric chief cells of the stomach secrete
enzymes for protein breakdown
(inactive pepsinogen, and in
infancy rennin). Hydrochloric acid activates
pepsinogen into the enzyme pepsin, which then
helps digestion by breaking the bonds linking amino
acids, a process known as proteolysis. In addition,
many microorganisms have their growth inhibited by
such an acidic environment, which is helpful to
prevent infection.

20. Secretion
• A typical adult human stomach will secrete about 1.5 liters of
gastric acid daily. Gastric acid secretion happens in several
steps. Chloride and hydrogen ions are secreted separately
from the cytoplasm of parietal cells and mixed in the
canaliculi. Gastric acid is then secreted into the lumen of
the gastric gland and gradually reaches the main stomach
lumen. The exact manner in which the secreted acid reaches
the stomach lumen is controversial, as acid must first cross
the relatively pH neutral gastric mucus layer.
• Chloride and sodium ions are secreted actively from
the cytoplasm of the parietal cell into the lumen of the
canaliculus. This creates a negative potential of -40 mV to -70
mV across the parietal cell membrane that causes potassium
ions and a small number of sodium ions to diffuse from the
cytoplasm into the parietal cell canaliculi.

21. • The enzyme carbonic anhydrase catalyses the reaction
between carbon dioxide and water to form carbonic acid .
This acid immediately dissociates into hydrogen and
bicarbonate ions. The hydrogen ions leave the cell
through H+/K+ ATPase antiporter pumps.
• At the same time, sodium ions are actively reabsorbed. This
means that the majority of secreted K+ and Na+ ions return to
the cytoplasm. In the canaliculus, secreted hydrogen and
chloride ions mix and are secreted into the lumen of the
oxyntic gland.

22. • The highest concentration that gastric acid reaches in the stomach is 160 mM in
the canaliculi. This is about 3 million times that of arterial blood, but almost
exactly isotonic with other bodily fluids. The lowest pH of the secreted acid is 0.8,
but the acid is diluted in the stomach lumen to a pH between 1 and 3.
• There is a small continuous basal secretion of gastric acid between meals of
usually less than 10 mEq/hour.
• There are three phases in the secretion of gastric acid which increase the secretion
rate in order to digest a meal:
• The cephalic phase: Thirty percent of the total gastric acid secretions to be
produced is stimulated by anticipation of eating and the smell or taste of food.
This signalling occurs from higher centres in the brain through the vagus
nerve(Cranial Nerve X). It activates parietal cells to release acid and ECL cells to
release histamine. The vagus nerve (CN X) also releases gastrin releasing
peptide onto G cells. Finally, it also inhibits somatostatin release from D cells.
• The gastric phase: About sixty percent of the total acid for a meal is secreted in
this phase. Acid secretion is stimulated by distension of the stomach and by amino
acids present in the food.
• The intestinal phase: The remaining 10% of acid is secreted when chyme enters
the small intestine, and is stimulated by small intestine distension and by amino
acids. The duodenal cells release entero-oxyntin which acts on parietal cells
without affecting gastrin.

23. • Gastric acid production is regulated by both the autonomic nervous
system and several hormones. The parasympathetic nervous system, via
the vagus nerve, and the hormone gastrin stimulate the parietal cell to
produce gastric acid, both directly acting on parietal cells and indirectly,
through the stimulation of the secretion of the
hormone histamine from enterochromaffine-like
cells (ECL). Vasoactiveintestinal peptide, cholecystokinin, and secretin all
inhibit production.

24. • The production of gastric acid in the stomach is tightly
regulated by positive regulators and negative
feedback mechanisms. Four types of cells are involved in this
process: parietal cells, G cells, D cells and enterochromaffine-
like cells. Besides this, the endings of the vagus nerve (CN X)
and the intramural nervous plexus in the digestive tract
influence the secretion significantly.
• Nerve endings in the stomach secrete two
stimulatory neurotransmitters: acetylcholine and gastrin-
releasing peptide. Their action is both direct on parietal cells
and mediated through the secretion of gastrin from G cells
and histamine from enterochromaffine-like cells. Gastrin acts
on parietal cells directly and indirectly too, by stimulating the
release of histamine.
• The release of histamine is the most important positive
regulation mechanism of the secretion of gastric acid in the
stomach. Its release is stimulated by gastrin and acetylcholine
and inhibited by somatostatin.

25. Neutralization
• In the duodenum, gastric acid is neutralized
by sodium bicarbonate.
• This also blocks gastric enzymes that have their
optima in the acid range of pH. The secretion of
sodium bicarbonate from the pancreas is stimulated
by secretin. This polypeptide hormone gets activated
and secreted from so-called S cells in the mucosa of
the duodenum and jejunum when the pH in the
duodenum falls below 4.5 to 5.0. The neutralization
is described by the equation:
• HCl + NaHCO3 → NaCl + H2CO3

26. • The carbonic acid rapidly equilibrates
with carbondioxide and water through catalysis
by carbonic anhydrase enzymes bound to the gut
epithelial lining, leading to a net release of
carbon dioxide gas within the lumen associated
with neutralisation. In the absorptive upper
intestine, such as the duodenum, both the
dissolved carbon dioxide and carbonic acid will
tend to equilibrate with the blood, leading to
most of the gas produced on neutralisation being
exhaled through the lungs.

27. Role in disease
• In hypochlorhydria and achlorhydria, there is low or
no gastric acid in the stomach, potentially leading to
problems as the disinfectant properties of the gastric
lumen are decreased. In such conditions, there is
greater risk of infections of the digestive tract (such
as infection with Vibrio or Helicobacter bacteria).
• In Zollinger–Ellison syndrome and hypercalcemia,
there are increased gastrin levels, leading to excess
gastric acid production, which can cause gastric
ulcers.

28. • In diseases featuring excess vomiting, patients
develop hypochloremic metabolic
alkalosis (decreased blood acidity
by H+ and chlorine depletion).

29. pharmocology
• The proton pump enzyme is the target of proton pump inhibitors, used to
increase gastric pH (and hence decrease stomach acidity) in diseases that
feature excess acid. H2antagonists indirectly decrease gastric acid
production. Antacids neutralize existing acid.

30. Let us take a look at some of the home remedies for acidity
• Calcium gives immediate relief from acidity. Drinking cold milk in small
quantities after meals can help bring down acidity. Ice creams are also known
to help in acidity.
• A pinch of baking soda added to a glass of water can give immediate relief
from gas and acidity.
• Acidic and sour condiments like sauces, hot sauce, vinegar, pickles etc should
be avoided.
• Fried and oily food can give a bad time and should be kept away.
• Keep away from eating raw vegetables like onion, radish, cucumber, tomatoes
and peppers.
• Sipping on mint juice after meals can be very useful.
• Suck on a small clove to get relief from acidity. It helps in subsiding any acid
reflux tendencies.
• Bananas are full of potassium and can help reduce acidity symptoms if taken
daily.
• Coconut Water sipped throughout the day can give relief from incessant heart
burn.

31. • Ginger is very useful in treating digestion problems. A spoonful of ginger
juice 2-3 times a day can relieve acidity.
• Stay away from alcohol, caffeine and tobacco.
• Eat small meals at regular intervals and chew food slowly. Skipping meals
worsens the acidity problem.
• Not having sufficient sleep can also aggravate the acidity problem.
• Exercising is very helpful. Don’t go to bed right after a meal. A small stroll
or walk post meal is very beneficial.
• Overweight or obese people may have the problem more because of the
excess pressure on the digestive tract.So try losing weight to see an
improvement in your GERD symptoms.
• Lastly, drink lots of water, about 8-10 glasses a day. However, don’t drink
water during or immediately after a meal. It dilutes gastric juices and can
inhibit proper digestion.
• The home remedies for acidity are without any side effects and can bring
immense relief if consistently pursued.