Peptic ulcers

- KALPNA
2ND YEAR
BSC (H) NURSING
Introduction
Ulcers are defined as a breach in the mucosa of the
alimentary tract, which extends through the
muscularis mucosa into the submucosa or deeper.

Peptic ulcers are chronic most often solitary, lesions

that occur in any portion of gastrointestinal tract
exposed to the aggressive action of acid-peptic
juices Typically occurs in stomach (Gastric ulcer)
and 1 few cm of duodenum (duodenal ulcer)

Peptic ulcers are produced by an imbalance between

the gastro- duodenal mucosal defense mechanisms
and damaging forces of gastric acid and pepsin,
combined with superimposed injury from
environmental or immunologic agents.
 Etiology
1. A peptic ulcer is a mucosal break, 3 mm or greater, that
can involve the stomach or duodenum.
2. The most important contributing factors are H pylori ,
NSAIDs, acid, and pepsin.

3. Additional aggressive factors include smoking ,ethanol,

bile acids, aspirin, steroids, and stress.

4. Important protective factors are mucus, bicarbonate,

mucosal blood flow, prostaglandins, hydrophobic layer,
and epithelial renewal

5. Frequent use of aspirin or other anti-inflammatory drugs

(risk associated with this behaviour increases in women
and people over the age of 60)Drinking too much
alcoholRadiation therapy
6. Stomach cancer
 The pathogenesis of duodenal ulcers (DU)
and gastric ulcers (GU) is multifactorial and
Pathophysiology most likely reflects a combination of
pathophysiologic abnormalities and
environmental and genetic factors. • Most
peptic ulcers occur in the presence of acid
and pepsin when HP, NSAIDs, or other
factors disrupt normal mucosal defense and
healing mechanisms.• Acid is an
independent factor that contributes to
disruption of mucosal integrity. Increased
acid secretion has been observed in
patients with DU and may result from HP
infection. Patients with GU usually have
normal or reduced rates of acid secretion.
 Pathophysiology
Due to etiological factor (NSAID’s, Alcohol fasting etc)

Excessive secretion of HCI and decrease mucous

secretion

Breakdown mucus membrane of stomach

Acids enters into gastric mucosa

Gastric ulcers
GASTRIC ULCERS
Stomach ulcers (gastric ulcers) are open
sores that develop on the lining of the
stomach. Ulcers can also occur in part of
the intestine just beyond the stomach.
These are called duodenal ulcers.

Stomach and duodenal ulcers are

sometimes called peptic ulcers. This
information applies to both.
Symptoms of gastric ulcers
the most common symptom of a stomach ulcer is a
burning or gnawing pain in the centre of the abdomen
(tummy). Not all stomach ulcers are painful.

Some people experience:

indigestion
heartburn
nausea (feeling sick)
Causes of stomach ulcers

Stomach ulcers occur when the layer protecting the

stomach lining from stomach acid breaks down. This allows
the stomach lining to become damaged.

This is usually caused by:

an infection with Helicobacter pylori (H. pylori) bacteria

taking non-steroidal anti-inflammatory drugs (NSAIDs),
such as ibuprofen or aspirin – particularly if they're taken for
a long time or at high doses
PATHOLOGY OF GASTRIC
ULCERS
Gastric ulcers are a break in the mucosa of the
stomach lining that penetrates through the
muscularis mucosa and extends more than 5
mm in diameter. When alterations occur to the
defense mechanisms of the stomach, it can
cause changes in the gastric mucosa which will
eventually result in erosion and then ulceration.
MANAGEMENT OF GASTRIC
ULCERS

Chemotherapy and radiation

therapy might be used first to
shrink the cancer.
GASTRIC H.PYLORI INFECTION

►By 3 Jeslin Cherian

nd
2 year
B.Sc.(Hons)
Nursing
Definition
► Helicobacter pylori infection occurs when
Helicobacter pylori (H. pylori) bacteria infect
your stomach. A common cause of stomach
ulcers (peptic ulcers), H. pylori infection may be
present in more than half the people in the
world.
Most people don’t realize they have H. pylori
infection because they never get sick from it. If
you develop signs and symptoms of a peptic ulcer,
your health care provider will probably test you
for H. pylori infection.
PATHOPHYSIOLOGY
► Overview of H. pylori infection and
pathogenesis
After entering the host stomach, H. pylori utilizes its urease
activity to neutralize the hostile acidic condition at the beginning of
infection.
► Flagella-mediated motility is then required for H. pylori to move
toward host gastric epithelium cells, followed by specific
interactions between bacterial adhesins with host cell receptors,
which thus leads to successful colonization and persistent
infection.
► Finally, H. pylori releases several effector proteins/toxins,
including cytotoxin-associated gene A (CagA), and vacuolating
cytotoxin A (VacA), causing host tissue damage
► In addition, the gastric epithelium layer, which forms the major
interface between H. pylori and the host, secretes chemokines to
initiate innate immunity and activate neutrophils, and further
lead to the formation of clinical diseases such as gastritis and
► After H. pylori enters the host stomach, four
steps are critical for bacteria to establish
successful colonization, persistent infection,
and disease pathogenesis:

► (1) Survival in the acidic stomach;

► (2) movement toward epithelium cells by
flagella-mediated motility;
► (3) attachment to host cells by adhesins/
receptors interaction;
► (4) causing tissue damage by toxin release.
 ETIOLOGY
► H. pylori infection occurs when
► H. pylori bacteria are usually passed from
person to person through direct contact
with saliva, vomit or stool.
► H. pylori may also be spread through
contaminated food or water.
► The exact way H. pylori bacteria causes
gastritis or a peptic ulcer in some people is
still unknown.
ORAL LEUKOPLAKIA

BY: KHUSHBOO RANI

B.Sc(H) NURSING

SECOND YEAR
 DEFINITION
❑ Oral leukoplakia is a white patch or plaque that develops in the oral
cavity. The condition is potentially malignant and is strongly
associated with tobacco use. This activity describes the evaluation
and treatment of oral leukoplakia and the role of the
interprofessional team in preventing, recognizing, and managing
patients with this condition
❑ Oral leukoplakia is a potentially malignant disorder affecting the
oral mucosa. It is defined as <essentially an oral mucosal white
lesion that cannot be considered as any other definable lesion.=
Oral leukoplakia is a white patch or plaque that develops in the
oral cavity and is strongly associated with smoking.
EPIDEMIOLOGY

• Prevalance:

Global: 1.5% – 4.3%

More prevalent in South Asia

• 80% of patient are > 40 years of age

• Affects more men than women

• Annual malignant transformation rate: 0.6% - 20%

ETIOLOGY
❖ Tobacco

❖ Alcohol

❖ U V Rays

❖ HPV-Type 16 and 18

❖ Trauma

❖ Sanguinaria

❖ Candida

❖ Nutritional factor
 PATHOPHYSIOLOG

Y
Tumor suppressor genes are genes involved in the

regulation of normal cell turnover and apoptosis

(programmed cell death).

One of the most studied tumor suppressor gene is p53,

which is found on the short arm of chromosome 17.

Mutation of p53 can disrupt its regulatory function and

lead to uncontrolled cell growth.

Mutation of p53 have been demonstrated in the cells from

areas of some leukoplakias, especially those with

dysplasia and in individuals who smoke and drink heavily.

 Squmaous cell carcinoma

By: khushboo singh

Bsc(H ) nursing
2 nd year
Definition

► Squamous cell carcinoma is a type of skin cancer that originates in

the squamous cells, which are thin, flat cells that make up the outer
layer of the skin. It can also occur in other tissues, such as the lining
of the respiratory and digestive tracts. Squamous cell carcinoma is
characterized by uncontrolled growth of these cells and can be
locally invasive.
Etiology

► 1 . Tobacco
► 2. Uv radiation
► 3.alcohol consumption
► 4.Hpv
► 5.chemical exposures
► 6. Immunosuppression
► 7.chronic skin inflammation
► 8.Genetic factor
 Pathology
► Morphology
Gross: Lession appear nodular,Ulcerated
Advanced: large ulceroproliferative

Microscope structure
Microscopically, squamous cell carcinoma is an invasive
carcinoma of the surface epidermis characterised by the
following features

1) There is irregular downward proliferation of epidermal cells into

the dermis.

Ii) Depending upon the grade of malignancy, the masses of

epidermal cells show atypical features such as variation in cell size
and shape

Absence of intercellular bridges, individual cell keratinisation and

occurrence of atypical mitotic figures.

Iii) Better-differentiated squamous carcinomas have whorled

arrangement of malignant squamous cells forming horn pearls.
The centres of these keratanised pearls may contain laminated,
keratin material.
Types
Pathophysiology
UV radiation causes mutations in ► Invasion of deep tissue layers
epithelial squamous cells

EPITHELIAL SQUAMOUS CELLS

ENTERS UNCONTROLLED PROLIFERATION
AND REDUCED APOPTOSIS HARD ON PALPATION

► Increased number of squamous

► Adherent keratotic
► cells lead to accumulation and
YELLOWISH APPEARANCE
► scale or keratin plug
► overproduction of keratin

KERATIN PLUG AND CELL PROLIFERATION

DISRUPTS VASCULAR SUPPLY UNDERLYING TISSUE NECROSIS

► If untreated, SCC cells will

ESCHAR (INTACT NECROTIC CRATER-LIKE CENTRE
► eventually metastasize to TISSUE) FORMATION
► other parts of the body
Diagnostic evaluation

1. Healh History

2. Physical Examination

3. Skin biopsy

- Confermative diagnosis

- obtain sample of skin tissue then carry cytological and histological

examination
Treatment

Treatment depend on the basis of –

- Tumor location

- cell type, depth

- cosmetic desire

- Metastasis
► 1. Surgical Excision : surgically removes malignant moles, lesions and
tumors from the skin along with a healthy margin around the tumor.
►
2. Electro surgery :surgeon scrapes away a lesion with a spoon-
shaped instrument (curette), then treats the area with an electrical
current to destroy any remaining cancer cells.
►
3.Cryo-Surgery

4. Radiation therapy:Expose the tumor surface to ionizing and

nonionizing radiation to kill cancerous cell
►
5. Chemotherapy : kill the cancer cell using cytotoxic drugs
ESOPHAGEAL
CANCER
JEHNIFER ALI KHAN
B.SC(H) NURSING [SECOND YEAR]
Topics DEFINITIONS

What we'll TYPES OF ESOPHAGEAL

CANCER

discuss Today ETIOLOGY

PATHOPHYSIOLOGY

MICROSCOPIC PATHOLOGY
 Esophagus
The esophagus is a hollow, muscular tube
that connects the throat to the stomach. It
lies behind the trachea (windpipe) and in
front of the spine.
Esophageal cancer
Cancer of the esophagus (also called
esophageal cancer) starts when cells in the
lining of the esophagus begin to grow out
of control. Cells in nearly any part of the
body can become cancer, and can spread
to other areas of the body
THERE ARE 2 MAIN TYPES OF
ESOPHAGEAL CANCER
 Squamous cell
Adenocarcinoma
carcinoma
This type of esophageal cancer starts in This type begins in the glandular
squamous cells that line the esophagus. tissue in the lower part of the esophagus
where the esophagus and the stomach come
together
 ETIOLOGY

SMOKING ALCOHOL CHEWING TOBACCO ACHALASIA OF THE OESOPHAG

 PATHOPHYSIO
• The esophagus is lined by nonkeratinized stratified squamous
epithelium. LOGY
• This lining is maintained as long as there are no risk factors
that can lead to a metaplastic change.
 PATHOPHYSIOLOGY
Chronic ingestion of hot liquids or food, GERD, nutritional deficiency, Barrett's esophagus,
poor oral hygiene, cigarette smoking etc.

Adenocarcinoma / squamous cell carcinoma

Cancer cell arise from the surface of esophagus causing Chronic esophageal irritation ,
tumor.

Dysphagia, sensation mass in throat, painful swallowing, substernal pain or fullness,

regurgitation of undigested food etc.

Obstruction of esophagus with possible perforation into mediastinum and erosion into
great vessels.
 Esophageal Squamous Carcinoma
01

PATHOPHYSIOLOGY

Esophageal Adenocarcinoma
02
 PATHOPHYSIOLOGY OF
ESOPHAGEAL SQUAMOUS CARCINOMA
• Risk factors: Smoking and alcohol.
• Synergistic effect: Alcohol + tobacco increase risk.
• Alcohol dissolves fat-soluble compounds.
• Tobacco carcinogens penetrate deeper with
alcohol.
• Alcohol damages DNA, lowers cell metabolism.
• Damaged DNA impairs detox, invites oxidative
damage.
• Oxidation squamous epithelium inflammation.
• Continuous irritation dysplasia, malignancy.
 PATHOPHYSIOLOGY OF
ESOPHAGEAL ADENOCARCINOMA
• Risk factors: GERD and obesity.
• Chronic reflux irritates esophageal lining.
• Chronic irritation esophagus metaplasia.
• From squamous to columnar epithelium.
• Result: Barrett's esophagus.
• Progression to adenocarcinoma linked to genetic
changes.
 Squamous cell carcinoma

Microscopic
pathology

Adenocarcinoma
 Squamous cell carcinoma
• Atypical squamous cells invade the basement membrane
⚬ Cytology of squamous cells:
￭ Eccentric nucleus
￭ High mitotic activity
￭ Eosinophilic cytoplasm
￭ Squamous whorls or keratin pearls
 Adenocarcinoma
• Atypical adenomatous cells show:
⚬ Invading cell clusters or glands
⚬ Cribriforming
⚬ Desmoplasia
⚬ Invasion into submucosa

Instruments Equipment Protection and security

AHILYA BAI COLLEGE OF NURSING

GASTRIC CANCER
BY- JILU MARIA JOSEPH
2ND YEAR
3RD SEM
 DEFINITION
Stomach cancer which is also called gastric cancer, is a
growth of cells that starts in the stomach.

The stomach is an organ on the left side of the upper

abdomen that digests food. The stomach helps to
break down and digest food.

Stomach cancer can happen in any part of the stomach.

Tumours can begin anywhere in the stomach but most
begin in the glandular tissue on the stomach's inner
surface. This type of cancer is an adenocarcinoma of
the stomach (gastric cancer).
ETIOLOGY
 PATHOPHYSIOLOGY
There is a strong correlation between Helicobacter pylori and gastric cancer incidence.The main cause of this
correlation is related to nitric oxides accumulation produced by inflammatory cells responding to H. pylori infection.
Nitric oxides may induce abnormalities in the DNA of epithelial cells.

This leads to persistent inflammation of the superficial portion of the gastric mucosa called superficial gastritis.

Atrophic gastritis (AG) is a chronic inflammation and thinning of your stomach lining accompanied by a change in
your stomach lining cells to mimic intestinal cells.

Intestinal metaplasia is a transformation of the cells in the lining of your upper digestive tract, often the stomach or
the esophagus (food pipe). It's called <intestinal= metaplasia because the cells change to become more like those
that line the intestines.

Dysplasia refers to the abnormal development of cells within tissues or organs.

Uncontrolled division of abnormal cells in a part of the body.

TOPICS :-
➢ TYPHOID ULCER

➢ INFLAMMATORY BOWEL DISEASE

1. CROHN’S DISEASE

-BY KAJAL
(2ND YEAR)
TYPHOID ULCERS
Typhoid fever is an acute systemic disease resulting from infection with salmonella paratyphi;
commonly a ects the ileum and the colon.

Pat gi c a g
Macroscopically

➔ Mainly seen in the terminal ileum(Peyer’s patch).

➔ Peyer’s patches show oval ulcers with a long axis along the length of the
bowel.
➔ Base of the ulcer is black due to sloughed mucosa with raised margins due to
inflammatory edema and cellular proliferation.
Microscopically

➔ Cellular proliferation consists of phagocytic histiocytes, lymphocytes and

plasma cells appear with hyperemia and edema.
➔ Peripheral blood smear reflects lymphocytosis with leukopenia and
neutropenia.

CLINICAL MANIFESTATIONS

Proliferation of large mononuclear cells in many different tissue leads to:

❖ Lymphadenopathy
❖ Splenomegaly
❖ Enlargement of lymphoid tissues in the intestine,bone marrow, liver and
lungs
❖ Lesion may extend deep into the intestinal wall and cause perforation of
the bowel, late in the disease usually in the distal ileum.
PATHOPHYSIOLOGY OF TYPHOID FEVER
Ingestion of typhoid bacilli through contaminated food and water

Bacteria invade the lymphoid follicles and peyer’s patches and proliferate their

Then, bacteria invade the bloodstream causing bacteremia Pass into circulation

Leads to appearance of red spots on the skin causing hyperpyrexia

Finally, bacteria localize themselves in intestinal in Intestinal perforation and

intestinal lymphoid tissue, mesenteric lymph nodes, liver, bleeding
gallbladder and spleen
INFLAMMATORY BOWEL DISEASE
INFLAMMATORY BOWEL DISEASE

CROHN’S DISEASE ULCERATIVE COLITIS

The term ‘inflammatory bowel disease (IBD),is commonly used to include two
idiopathic bowel diseases having many similarities but the conditions usually have
distinctive morphological appearance.

ETIOPATHOGENESIS

The exact etiology of IBD remains unknown. However, multiple factors are
implicated which can be considered under the following three groups:

1. Genetic Factors - more chances in monozygotic twins.

2. Immunologic Factors - defective immunologic regulation.
3. Exogenous Factors - environmental factors, smoking, oral contraceptives
CROHN’S DISEASE (REGIONAL ENTERITIS)

Crohn9s disease is an idiopathic chronic ulcerative IBD, characterized by transmural, granulomatous

in ammation, a ecting most commonly the segment of terminal ileum and /or colon, though any part of
the gastrointestinal tract may be involved.

The lumen of the a ected segment is markedly narrowed. The mucosa shows 8serpiginous ulcers9, while
intervening surviving mucosa is swollen giving 8cobblestone appearance9. There may be deep ssuring into
the bowel wall.
 Difference b/w ulcerative
colitis and crohn’s disease

Ulcer in colon in
crohn’s disease
 PATHOPHYSIOLOGY OF CROHN’S DISEASE

It is a subacute and chronic inüammation that extends through all layers of the bowel wall
from the intestinal mucosa.

The disease process begins with edema and thickening of the mucosa. Ulcers begin to
appear on the inüamed mucosa.

Lesions are not in continuous contact with one and are separately by normal tissue.

Fistulas,ûssures and abscesses form as the inüammation extends into the peritoneum.
Granulomas occur in one half of patients. In advanced cases, the intestinal mucosa has a
cobblestone appearance.

As the disease advances, the bowel wall thickens and becomes ûbrotic, and the intestinal
lumen narrows. Diseased bowel loops sometimes adhere to other loops surrounding them.
Topics
• Ulcerative Colitis
• Colorectal Cancer

By Kanchan
2nd year 3rd Sem
 Ulcerative Colitis

Definition
A chronic, inflammatory bowel disease that causes
inflammation in the digestive tract.
Ulcerative colitis is usually only in the innermost lining of
the large intestine (colon) and rectum. Forms range from
mild to severe. Having ulcerative colitis puts a patient at
increased risk of developing colon cancer.
• Symptoms
• Ulcerative colitis symptoms can vary, depending on
the severity of inflammation and where it occurs.
Signs and symptoms may include:
Diarrhea, often with blood or pus
Rectal bleeding 4 passing small amount of blood with
stool
Abdominal pain and cramping
Rectal pain
Urgency to defecate
Inability to defecate despite urgency
Weight loss
Fatigue
Fever
In children, failure to grow
 Causes
► The exact cause of ulcerative colitis remains unknown.
Previously, diet and stress were suspected. However,
researchers now know that these factors may
aggravate but don’t cause ulcerative colitis.
One possible cause is an immune system malfunction.
When your immune system tries to fight off an invading
virus or bacterium, an irregular immune response
causes the immune system to attack the cells in the
digestive tract, too.
Heredity also seems to play a role in that ulcerative
colitis is more common in people who have family
members with the disease. However, most people with
ulcerative colitis don’t have this family history.
 Risk factors
► Ulcerative colitis affects about the same number of
women and men. Risk factors may include.
Age. Ulcerative colitis usually begins before the age of 30,
but it can occur at any age. Some people may not develop
the disease until after age 60.
Race or ethnicity. Although white people have the highest
risk of the disease, it can occur in any race. If you’re of
Ashkenazi Jewish descent, your risk is even higher.
Family history. You’re at higher risk if you have a close
relative, such as a parent, sibling or child, with the
disease.
Pathophysiology
Etiological Factors

Superficial mucosa of colon

Diffuse inflammation, or shedding of the colonic epithelium

Bleeding occurs

Ulceration

(The mucosa becomes edematous and inflamed)

The disease process usually begins in the rectum and spread proximally to involve
the entire colon.
 Colorectal cancer
Definition
Colorectal cancer starts in the colon or
the rectum. These cancers can also be
called colon cancer or rectal cancer,
depending on where they start. Colon
cancer and rectal cancer are often
grouped together because they have many
features in common.

Cancer starts when cells in the body start

to grow out of control.
• Symptoms
A change in bowel habits that lasts more than a
few days, such as:
Diarrhea
Constipation
Feeling that the bowel does not empty completely
Your stool is narrower or has a different shape
than usual
Blood (either bright red or very dark) in the stool
Frequent gas pains, bloating, fullness, or cramps
Weight loss for no known reason
Fatigue
Etiology and Risk factors
► Advanced age
► Race
► Family history
► History of intestinal polyps
► History of IBD
► Inherited disorders
► Type 2 diabetes mellitus
► Previous radiation therapy
► Diet
► Smoking & alcohol
► Exposure to virus
► Obesity
► Physical inactivity
Pathophysiology of Colorectal Cancer
The patients in the early stages of the disease are
usually asymptomatic. If symptoms are present,
they usually depend on the site of the primary
tumor . Cancers of the proximal colon tend to grow
larger before symptoms appear than those in the
left colon and rectum.
Pathophysiology of Colorectal Cancer
Inflammatory bowel disease
Smoking
Abdominal radiation

Tubular
Uncontrolled cell adenomas
Cell line mutation division in the colon Colorecta
(Pre-
and rectum l cancer
cancerous
polyps)

Idiopathic Hereditary
syndrome
Obesity