Stomach inflammation

Gastritis

Also known as Stomach inflammation, Gastric mucosal inflammation, Gastric irritation. Gastritis refers to the inflammation, irritation, or erosion of the gastric mucosa (the lining of the stomach). It can occur suddenly (acute gastritis) or gradually over time (chronic gastritis). The condition may be caused by various factors, including infections, medications, or autoimmune disorders.

Appendicitis

Appendicitis

Acute inflammation of the appendix. It is seen most commonly in older children and young adults, and it is uncommon in extremes of age.

Etiopathogenesis : Most often cause of appendicitis is low bulk or cellulose and high protein diet intake. Other cause of appendicitis are obstructive and non-obstructive -

A. Obstructive : 

1. Faecolith
2. Calculi
3. Foreign body
4. Tumour
5. Worms (especially Enterobius vermicularis)
6. Diffuse lymphoid hyperplasia, especially in children.

B. Non-obstructive :

1. Haematogenous spread of generalised infection
2. Vascular occlusion
3. Inappropriate diet lacking roughage

Appendicitis

You may also read - Dysentery

MORPHOLOGICAL FEATURES

Grossly : 

1. Acute appendicitis (early) - 

        i. The organ is swollen 

        ii. Serosa shows hyperaemia.
2. Acute suppurative appendicitis (well-developed) - 

        i. The serosa is coated with fibrinopurulent exudate.

        ii. Engorged vessels on the surface.
3. Acute gangrenous appendicitis (advanced) - 

        i. There is necrosis and ulceration of mucosa that extends through the wall, so appendix become soft and friable.

        ii. Surface is coated with greenish-black gangrenous necrosis.

Microscopically : Histological  criterion is neutrophilic infiltration of the muscularis.

1. In early stage - 

        i. Acute inflammatory changes. 

        ii. Congestion and oedema of the appendicial wall.
2. In later stages - 

        i. The mucosa is sloughed off. 

        ii. The wall become necrotic. 

        iii. Blood vessels may get thrombosed. 

        iv. Neutrophilic abscess in the wall.

3. In either case - 

        i. Impacted foreign body. 

        ii. Faecolith or concretion may be seen in the lumen.

Microscopic appearance

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CLINICAL FEATURES

1. Colicky pain, initially around umbilicus but later localised  to right iliac fossa.
2. Nausea and vomiting.
3. Mild grade fever.
4. Abdominal tenderness.
5. Increase pulse rate.
6. Neutrophilia with toxic granules in neutrophils.

Recurrent acute appendicitis is treated by surgery called appendectomy but after that chronic inflammation maybe observed.

COMPLICATIONS

1. Peritonitis - Perforated appendix ( gangrenous appendicitis) may cause localised or generalised peritonitis.
2. Appendix abscess - This is due to rupture of an appendix giving rise to localised abscess in the right iliac fossa. This abscess may spread to the liver, diaphragm (subphrenic abscess), urinary bladder and rectum, and in the females may involve uterus and fallopian tubes.
3. Adhesions - Late complications of acute appendicitis are fibrous adhesions to the  greater omentum, small intestine and other abdominal structures.
4. Portal pylephlebitis - Spread of infection into mesenteric vein may produce septic phlebitis and liver abscess. 
5. Mucocele - Distension of distal appendix by mucus following recovery from an attack of acute appendicitis called mucocele. An infected mucocele may result in formation of empyema of the appendix. It occur due to generally proximal obstruction but some time may be due to a benign or malignant neoplasm in the appendix.

Source : Textbook of pathology (Harsh Mohan) 7th edition

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Dysentery

Dysenteries

Definition : Diarrhoea with abdominal cramps, tenesmus and mucus in the stool called dysentery.

CLASSIFICATION 

1. Bacillary dysentery
2. Amoebic dysentery

1. BACILLARY DYSENTERY : It is the infection of Shigella species (S. dysenteriae, S. flexnery, S. boydii and S. sonnei).

Etiopathogenesis : Infection of the shigella species occurs by faeco-oral route with contaminated food and water. Infection is seen commonly in poor personal hygiene persons and overcrowding areas. The housefly play a major role in spread the infection.

MORPHOLOGICAL FEATURES

Grossly : 

• The lesions are mainly found in the colon sometime in the ilium.
• Superficial transverse ulcerations of mucosa of the bowel wall occurs in the region of lymphoid follicles and perforation maybe seen.
• The intervening mucosa is hyperaemic and oedematous.
• All of these recover completely after acute attack.

Microscopically : 

• Mucosa of the lymphoid follicles are necrosed.
• The surrounding mucosa shows congestion, oedema and infiltration by neutrophils and lymphocytes.
• The mucosa may be covered by greyish-yellow pseudomembrane consists of fibrinosuppurative exudate.

Trophozoites of entamoeba histolytica

COMPLICATIONS 

1. Haemorrhage.
2. Perforation.
3. Stenosis.
4. Poly-arthritis.
5. Iridocyclitis (inflammation of the iris).

2. AMOEBIC DYSENTERY : It is the infection of Entamoeba Histolytica.

Etiopathogenesis : It is most common in the tropical countries and primarily affects the large intestine. Infection occurs from ingestion of cysts in the form of parasite. The cyst wall is broken in the small intestine from where these free amoeba pass into the large intestine. Here, amoeba invade the epithelium of the mucosa to submucosa and produce ulcers.

Amoebic ulcers in large intestine

MORPHOLOGICAL FEATURES

Grossly : 

• In early stage - Intestinal lesions appears on the elevated mucosal surface.
• In advance cases - Seen, typical flask-shaped ulcers having narrow neck and broad base. They are more commonly found in caecum, rectum and flexures.

Microscopically : 

• Ulcerated area shows chronic inflammatory reaction consisting of lymphocytes, plasma cells, eosinophils and macrophages.
• Trophozoites of entamoeba are seen in the inflammatory exudate.
• Intestinal amoebae have ingested red cells and their cytoplasm.
• Oedema and vascular congestion also found in the surrounding area of ulcer. 

COMPLICATIONS

1. Amoebic hepatitis or amoebic liver abscess.
2. Perforation.
3. Haemorrhage.
4. Formation of amoeboma ( tumour like mass).

Source : Textbook of pathology ( Harsh Mohan) 7th edition

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Acute Peptic Ulcers

Peptic Ulcers

Definition : Peptic ulcers are the areas of degeneration and necrosis of gastrointestinal mucosa exposed to acid peptic secretions. They occur most commonly (98-99%)  in either the duodenum or the stomach in the ratio 4:1. It may be acute or chronic.

Acute Peptic Ulcers / Acute Stress Ulcers 

Definition : Acute peptic ulcers are multiple, small mucosal erosions, seen most commonly in the stomach but sometime involve duodenum also.

Etiology : Most common cause of ulcers are stress -

1. Psychological stress

2. Physiological stress - 

• Shock
• Severe trauma
• Septicemia or sepsis
• Extensive burns (Curling's ulcers in the posterior aspect of the first part of the duodenum)
• Intracranial lesions ( Cushing's ulcers developing from hyper-acidity due to excessive vegal stimulation) 
• Drug intake (aspirin, steroids, butazolidine, indomethacin)
• Local irritants (alcohol, smoking, coffee )

Pathogenesis :

1. Mucosal digestion from hyper-acidity (important factor).
2. Protective gastric mucus barrier may be damaged.

MORPHOLOGICAL FEATURES 

Grossly : Multiple ulcers (more than 3 ulcers in 75% cases) present in stomach but most common in the first part of duodenum. Ulcers are oval or circular in shape, usually less than 1 cm in diameter.

Histologically : Stress ulcers are -

1. Shallow and do not invade the muscular layer.
2. Margin and base show some inflammatory reaction depending upon the duration of ulcers.

COMPLICATIONS

1. Haemorrhage.
2. Perforation.

Source : Textbook of pathology (Harsh Mohan) 7th edition

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