SlideShare a Scribd company logo
1 of 59
Download to read offline
Diseases of Mouth
- Since mouth is the entry point of various pathogens and microorganisms,
be it with food or as such, there are chances of a number of diseases to
occur in the mouth.
• Thrush (Oral Candidiasis)
- Thrush acute fungal infection is caused by the yeast Candida albicans,
which occurs when the commensal microbe grows in white patches on the
tongue and oral mucosa.
- Caused by – Candida albicans (Yeast)
- Symptoms – Itching and rash at the infected site.
- Risks - In adults it causes opportunistic infection mainly in those whose
immunity is lowered by, e.g., steroids, antibiotics or cytotoxic drugs. In
children it occurs most commonly in bottle-fed babies.
- Diagnosis – Physical examination of the lesions in mouth; Blood test –
Candida specific antibody test is used to detected candidiasis – IgM, IgA &
IgG.
- Treatment – Antifungals (Clotrimazole, Fluconazole, etc.), Antiseptics,
etc.
• Gingivitis
- This is inflammation of the gums.
- May be Acute or Chronic.
- It occurs in response to accumulation of bacterial plaque around the teeth.
- It gradually destroys the tissues supporting the teeth.
- Symptoms – Swollen gums, bleeding gums.
- Risks – Poor oral hygiene, Smoking or chewing tobacco, Older age, etc.
• Dental Caries
- Dental caries cause destruction of the calcified tissues of the teeth.
- If untreated - microorganisms may invade the pulp, causing inflammation and infection.
- Bacteria - produce acids that demineralize the enamel.
- Dextran, a sticky polysaccharide produced from sucrose, causes the bacteria to stick to the
teeth.
- Masses of bacterial cells, dextran, and other debris adhering to teeth constitute dental plaque.
- Root canal treatment helps to treat the decay of pulp caused due to the infection.
Diseases of Pharynx
• Tonsilitis
- This is the inflammation of palatine tonsils, palatine arches and walls of the pharynx
caused byViruses and Streptococcus pyogenes.
- There may be production of abscess at the site of infection.
- The infection, if untreated may spread to the neck and cause cellulitis.
- Repeated infection may lead to chronic inflammation, fibrosis and permanent
enlargement.
- Surgical removal of the tonsils (Tonsillectomy) can help to reduce the pain and
inflammation.
- NSAIDs, analgesics and antibiotics can be used.
• Diphtheria
- Causative agent - Corynebacterium diphtheriae
- This is a bacterial infection of the pharynx – extends to the nasopharynx
and trachea, caused by a bacteria in which thick fibrous membrane
forms over the area and may obstruct the airway.
- The microbe produces powerful exotoxins that may severely damage
cardiac and skeletal muscle, the liver, kidneys and adrenal glands.
- It may be treated by using antitoxin to diphtheria toxin.
- Vaccination with diphtheria toxoid is the best way to prevent its
occurrence.
Diseases of Salivary Glands
• Mumps
- Caused by - Mumps virus
- This is an acute inflammatory condition of the salivary glands, especially the parotids.
- The virus is spread by inhalation of infected droplets.
- Viruses multiply elsewhere in the body before spreading to the salivary glands.
- Complications may affect:
a. the brain, causing meningitis or meningoencephalitis
b. the testes, causing orchitis (testicular inflammation)
c. Pancreatitis, Heart problems, miscarriage, etc.
Risks – Unvaccinated individuals are at a high risk, children between 2-12 years, etc.
Symptoms – Pain while swallowing, Fever, Loss of appetite, etc.
• Tumor of Salivary Glands
1. Salivary adenoma
- This benign tumor occurs mainly in the parotid gland and is the
most common tumor of the salivary glands.
- A second tumor may develop in the same gland several years -
malignant type.
2. Carcinoma
- Malignant tumors most commonly affect the parotid glands.
- Some forms have a tendency to infiltrate nerves in the
surrounding tissues, causing severe pain.
• Symptoms – Swelling near the jaw or in neck or mouth,
difficulty swallowing, numbness in part of the face, etc.
• Causes – Genetic mutations (predominantly), smoking,
tobacco chewing, etc.
Diseases of Esophagus
• Gastro-esophageal reflux disease (GERD)
- This disease is characterised by the reflux of gastric juice and acids from
the stomach into the esophagus.
- It may be due to a fault in the lower esophageal sphincter to close and
prevent the gastric contents from entering into the esophagus.
- It results in inflammation of the lower esophagus.
- It the reflux persists, fibrous tissues form at the site of inflammation.
- Reflux of gastric contents is associated with:
• increase in the intra-abdominal pressure, e.g. in pregnancy, constipation
and obesity.
• low levels of secretion of the hormone gastrin, leading to reduced sphincter
action at the lower end of the oesophagus.
• the presence of hiatus hernia.
Symptoms – Heartburn, nausea, regurgitation, discomfort in upper
abdomen, etc.
Cause – Failure of the lower Oesophageal sphincter to constrict properly.
• Barrett’s oesophagus
- This disease is actually a consequence of Reflux Oesophagitis.
- In this stratified squamous epithelium of the lower oesophagus is replaced
by columnar epithelium (columnar metaplasia).
- If not treated on time, may progress to Carcinoma of Oesophagus
followed by Adenocarcinoma.
- Symptoms – Difficulty in swallowing food, Chest pain, heartburn and
regurgitation.
- Causes – Not know, but is thought to be a consequence of Reflux disease.
- Risk – Family history, Gender (Men are more likely to develop it), Smoking,
GERD, Obesity, etc.
• Achalasia
- Achalasia of the oesophagus is a neuromuscular dysfunction
due to which the cardiac sphincter fails to relax during
swallowing and results in progressive dysphagia and dilatation
of the oesophagus.
- It occurs when the intramural neurons in the wall of the
oesophagus are damaged.
- Symptoms – Heartburn, regurgitation of food, belching, chest
pain, vomiting, etc.
- Causes – Loss of nerve cells from oesophagus.
- Risk – Allgrove syndrome, Herpes infection, Measles,
Autoimmune diseases, etc.
• Oesophageal Diverticula
- These are the protrusions or pouches of oesophageal wall at the
point of weakness.
1. Congenital diverticula occur either at the upper end of the
oesophagus or at the bifurcation of trachea.
2. Acquired diverticula may be of 2 types:
a) Pulsion (Zenker’s) type—It is seen in the region of hypopharynx and
occurs due to oesophageal obstruction such as due to chronic
oesophagitis, carcinoma etc. The mucosa and submucosa herniate
through the weakened area or through defect in the muscularis propria.
• b) Traction type—It occurs in the lower third of oesophagus from
contraction of fibrous tissue such as from pleural adhesions, scar tissue
of healed tuberculous lesions in the hilum, silicosis etc.
• Complications of diverticula include obstruction, infection, perforation,
hemorrhage and carcinoma.
Oesophageal
Diverticula
Congenital
Acquired
• Carcinoma of Oesophagus
- Although exact etiology of carcinoma of the oesophagus is not known, a number of conditions
and factors have been implicated as under:
1. Diet and personal habits:
- i) Heavy smoking
- ii)Alcohol consumption
2. Oesophageal disorders:
- i) Oesophagitis (especially Barrett’s oesophagus in adenocarcinoma)
- ii)Achalasia
- iii) Hiatus hernia
- iv) Diverticula
3. Other factors:
- i) Family history—association with tylosis (keratosis palmariset plantaris).
- ii) Genetic factors—predisposition with coeliac disease, epidermolysis bullosa, tylosis.
- iii) HPV infection—is a recent addition in etiologic factors.
- Abnormality of p53 tumor suppressor gene is found to be associated with the onset of the
disease.
• Carcinoma of the oesophagus is mainly of 2 types—
A. Squamous cell carcinoma
- 90% of primary oesophageal cancers are of this type.
- Majority of the squamous cell carcinoma occur in the middle third, followed by lower third,
and the upper third of oesophagus in that order of frequency.
- 3 types of patterns are recognized (Fig. 18.4,B):
i) Polypoid fungating type—is the most common form. It appears as a cauliflower-like
friable mass protruding into the lumen.
ii) Ulcerating type—is the next common form. It looks grossly like a necrotic ulcer with
everted edges
iii) Diffuse infiltrating type—appears as an annular, stenosing narrowing of the lumen due
to infiltration into the wall of oesophagus.
Oesophageal
Carcinoma
Squamous cell
carcinoma
Adenocarcinoma
B. Adenocarcinoma
- 10% of primary oesophageal cancers are of this type.
- The common locations are lower and middle third of the oesophagus.
- Oesophageal adenocarcinoma appears as nodular, elevated mass in the lower
oesophagus.
- Three patterns recognized:
1. Intestinal type—is the adenocarcinoma with a pattern similar to that seen in
adenocarcinoma of intestine or stomach.
2. Adenosquamous type—is the pattern in which there is an irregular admixture of
adenocarcinoma and squamous cell carcinoma.
3. Adenoid cystic type—is an uncommon variety and shows a cribriform appearance in an
epithelial tumour.
Diseases of Stomach
❖Congenital and Acquired Condition:-
• Pyloric Stenosis
- In this disease, there is narrowing of the pyloric opening
especially in male children as a congenital defect
(infantile pyloric stenosis).
- It is rarely observed in adults – may be due to acquired
inflammatory fibrosis or by invasion of tumors
- Causes:
1. For infantile pyloric stenosis – Genetic and
environmental factors responsible.
2. For adult pyloric stenosis – related to antral gastritis,
and tumors in the region (gastric carcinoma,
lymphoma, pancreatic carcinoma, etc.)
- In both the types, there is hypertrophy as well as hyperplasia of the circular layer of
muscularis in the pyloric sphincter accompanied by mild degree of fibrosis.
- Symptoms – Vomiting after feeding/eating, Stomach contractions, Dehydration, Changes
in bowel movement, etc.
- Risks – Gender (More seen in males), Premature birth, Family history, Smoking during
pregnancy, etc.
- Complications – Jaundice (rare), Stomach irritation, etc.
❖Inflammatory Conditions:-
• Gastritis
- It is a condition in which the lining of the stomach becomes inflamed which may be cause
upper abdominal discomfort like indigestion or dyspepsia.
- In worst cases, it may progress to peptic ulcer or gastric cancer.
• Types:
A. Acute Gastritis
- Acute gastritis is a transient acute inflammatory involvement of the stomach, mainly
mucosa, and is usually a response to irritant drugs (NSAIDs like Aspirin, etc.) or alcohol.
- Causes-
1. Diet and personal habits: - Highly spiced food, Excessive alcohol consumption,
Malnutrition, Smoking.
2. Infections: - Bacterial infections e.g. Helicobacter pylori, diphtheria, salmonellosis,
pneumonia, staphylococcal food poisoning, etc.
3. Drugs:- Intake of drugs like NSAIDs, aspirin, cortisone, phenylbutazone, indomethacin,
preparations of iron, chemo therapeutic agents.
Gastritis
Acute Chronic
4. Severe stress:- Emotional factors (like shock, anger), Extensive burns,Trauma, Surgery.
• Mechanism of Injury:
B. Chronic Gastritis
- Chronic gastritis is a milder but longer-lasting condition.
- It is usually associated with Helicobacter pylori but is sometimes due to autoimmune
disease or chemical injury.
1. Reduced blood flow
2. Increased acid secretion and its accumulation
3. Decreased production of bicarbonate buffer.
1. Helicobacter-associated gastritis.
Helicobacter pylori is a bacterium that can survive in the gastric mucosa
and is
commonly associated with gastric conditions, especially chronic gastritis
and peptic ulcer disease.
2. Autoimmune gastritis
- It is called autoimmune gastritis due to the presence of circulating
antibodies and is sometimes associated with other autoimmune diseases
such as Hashimoto’s thyroiditis and Addison’s disease.
- Antibodies against parietal cells and intrinsic factor are produced, as a
result there is depletion of parietal cells and impaired secretion of intrinsic
factor.
- May lead to significant gastric atrophy where intestinal metaplasia may
occur.
• Consequences include:
- pernicious anemia due to lack of intrinsic factor
- increased risk of cancer of the stomach
- Symptoms- Nausea, Vomiting, Burning ache or pain in upper
abdomen, etc.
- Risks – Bacterial infection, Frequent use of pain relievers, Stress,
Excessive alcohol use, Autoimmune disease, etc.
- Complications – If left untreated, may lead to stomach ulcers
and bleeding.
- Prevention – Frequent washing of hands with soap and water,
consuming completely cooked food.
• Peptic Ulcer Disease (PUD)
- Peptic ulcers are the areas of degeneration and necrosis of
gastrointestinal mucosa exposed to acid-peptic secretions.
- These are basically open sores that develop on the inner
lining of the stomach and duodenum.
- They can occur in any part of the GIT which are exposed to
HCl and Pepsin, but majority occur in Stomach and
Duodenum.
A. Acute Peptic Ulcer
- These are a result of severe stress.
- These are multiple, small mucosal erosions, seen most
commonly in the stomach but occasionally involving the
duodenum.
- Causes -
B. Chronic Peptic Ulcer
- If not specified – chronic peptic ulcers would mean gastric and
duodenal ulcers – the two major forms of peptic ulcer disease of the
upper GI tract.
- More common in duodenum than in stomach.
- H. pylori infection is found associated in 90% of duodenal and 70% of
stomach ulcer cases.
Causes
Physiological
stress
Severe
trauma
Extensive
burns
Septicaemia
Local irritants
(e.g. alcohol)
Psychological
stress
- Three distinct causes of PUD are recognized:
- the bacterium Helicobacter pylori
- (2) nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin
- (3) hypersecretion of HCl
- Causes - Helicobacter pylori gastritis, NSAIDs-induced mucosal injury, Psychological
factors, Genetic factors, etc.
• Symptoms – Burning stomach pain, Bloating, Intolerance to fatty food, Heartburn, etc.
• Risks – Smoking,Alcohol consumption, Consuming spicy food, Stress, etc.
• Complications - 1. Haemorrhage
2. Perforation
3. Anaemia
4. Gastric outflow obstruction
5. Gastric cancer
• Tumors
A. Polyps
1. Hyperplastic (Inflammatory) Polyps
- regenerative, nonneoplastic lesions which are the most common type
(90%).
- Often located in the pyloric antrum.
2. Hamartomatous Polyps
- not true neoplasms but are malformations.
B. BenignTumor
1. Adenomas
- true benign epithelial neoplasms and are much rare in the stomach
than in the large intestine.
2. StromalTumors
- Firm, circumscribed nodules, that appear as submucosal nodules.
B. BenignTumor
Gastric Carcinoma
- Carcinoma of the stomach is responsible more than 90% of all gastric
malignancies.
• Causes - H. pylori infection, Genetic factors, Pre-malignant changes in
the gastric mucosa, etc.
• Symptoms - Digestion, Heartburn, Stomach pain, Difficulty
swallowing,Vomiting, etc.
• Risks – GERD, Obesity, Smoking, Stomach polyps, Familial history, H.
pylori infection, etc.
• Prevention – Stop smoking, consume lots of fruits and vegetables,
reduce the amount of salty food, etc.
• Classification:-
1. Early gastric carcinoma (EGC)
Types:
Type I : Polypoid type
Type IIa : Superficial elevated
Type IIb : Superficial flat
Type IIc : Superficial depressed
Type III : Ulcerated type
2. Advanced gastric carcinoma
Types:
i) Ulcerative carcinoma
ii) Fungating (Polypoid) carcinoma
iii) Scirrhous carcinoma
iv) Colloid (Mucoid) carcinoma
v) Ulcer-cancer
Diseases of Small Intestine
❖Congenital Abnormality:
• Meckel’s Diverticulum
- Meckel’s diverticulum is an outpouching containing all the layers of
the intestinal wall in their normal orientation.
- It is more common in males.
- Causes – It occurs as a result of incomplete absorption of the vitelline
duct by the foetus during the 7th week of pregnancy.
- Symptoms – GI bleeding, Abdominal pain, Obstruction of the
bowels, diverticulitis (swelling of the intestinal wall), etc.
• Other congenital conditions:
1. Intestinal atresia (congenital absence of intestinal lumen)
2. Intestinal stenosis (congenital narrowing of the intestinal lumen)
3. Intestinal malrotation (failure of normal rotation of midgut)
• Hernia
- Protrusion of an organ or part of an organ through a weak point or aperture in the
surrounding structures.
- External hernia - protrusion of the bowel through a defect or weakness in the peritoneum.
- Internal hernia - herniation that does not present on the external surface
- Most common type – Inguinal hernias; followed by femoral and umbilical hernias.
Factors involved in
formation of Hernia
Increased intra-
abdominal pressure
Local weakness
- Inguinal hernias may be of 2 types:
➢ Direct when hernia passes medial to the inferior epigastric artery and it
appears through the external abdominal ring.
➢ Indirect when it follows the inguinal canal lateral to the inferior epigastric
artery.
- Strangulated hernia - blood flow in the hernial sac is obstructed; results in
infarction or gangrene of the affected loop of intestine.
• Sites of Hernias:-
1. Inguinal hernia – Inguinal canal; occurs more commonly in males.
2. Femoral hernia - femoral canal through which the femoral artery passes.
3. Umbilical hernia – umbilicus, where the umbilical blood vessels from the
placenta enter the fetus before birth.
4. Incisional hernia - repeated stretching of fibrous (scar) tissue formed
after previous abdominal surgery.
5. Hiatus hernia - protrusion of a part of the fundus of the stomach through
the esophageal opening in the diaphragm. (Types – Rolling & Sliding)
(Figures: A. Common sites of herniation. B. Strangulated hernia formation.)
- Causes – Congenital, Aging, Damage from injury, Pregnancy,
Previous surgery, Obesity, etc.
- Symptoms – Bulge or Lump in the affected area (which
disappears on lying down), Pain, Heartburn, Difficulty in
swallowing,Chest pain (in case of Hiatus hernia), etc.
- Risks – Family history, Pregnancy, Smoking, Premature birth,
Cystic fibrosis, etc.
Figure: Hiatus hernia
• Inflammatory Bowel Disease (IBD)
- This is a term used to describe disorders that involve
chronic inflammation of the digestive tract.
- It basically includes 2 conditions:
1. Crohn’s disease
2. Ulcerative colitis
A. Crohn’s disease
- It is characterized by inflammation of the lining of the
digestive tract, often involving deeper layers of the
digestive tract.
- There is chronic patchy inflammation with oedema –
causing partial obstruction of the lumen – skip lesions.
- Complications - Fistula formation, Malabsorption,
Development of malignancy, Bowel obstruction, etc.
B. Ulcerative colitis
- Involves inflammation and ulcers along the lining of the colon and
rectum.
- Ulcerative colitis begins in the rectum, and extends upwards into the
sigmoid colon, descending colon, transverse colon, and sometimes
may involve the entire colon.
• Complications - Fulminant colitis (Toxic megacolon), Perforated colon,
Perianal fistula, Colon cancer, Severe dehydration, etc.
• Symptoms for both:
- Diarrhoea, Blood in stools, Reduced appetite,Weight loss, etc.
• Risks for both:
- Smoking, Familial history, Excessive use of NSAIDs, etc.
• Causes – Mostly Idiopathic; may be due to immune system
malfunction, hereditary, etc.
• Enteric Fever (Typhoid & Paratyphoid)
- Causative agents – Salmonella typhi (Typhoid) and S. paratyphi A or B
(Paratyphoid).
Typhoid:
- The incubation period is about 10–14 days during which time bacteria invade
the lymphoid tissue of the small intestine, especially the aggregated lymph
follicles (Peyer’s patches).
- The bacilli invade the bloodstream causing bacteremia, and the
characteristic clinical features of the disease like continuous rise in
temperature and rose spots on the skin are observed.
- Eventually, the bacilli are localized in the intestinal lymphoid tissue, in the
mesenteric lymph nodes, in the liver, in the gallbladder, and in the spleen.
Paratyphoid:
- Paratyphoid fever follows a similar course but is usually milder and of shorter
duration although the onset can be more sudden; complications are less
frequent.
- Causes – Ingestion of food or water contaminated with Salmonella
typhi and S. paratyphi A or B.
- Mode of spread - Through typhoid carriers, Fecal-oral transmission
route.
- Symptoms – High fever, Stomach pain, Constipation or Diarrhoea,
Rashes, etc.
- Risks – Close contact with an infected person, Drinking contaminated
water,Travelling to affected areas, etc.
- Complications- Myocarditis, Endocarditis, Pneumonia, Pancreatitis,
etc.
- Prevention – Washing hands properly, Avoid drinking untreated
water, Avoid raw fruits and vegetables, Consumption of hot food,
Getting vaccinated, etc.
• Dysentery
- The term refers to a condition in which diarrhoea is accompanied with abdominal cramps
and passage of mucus in the stools.
- Types:
1. Bacillary dysentery
2. Amoebic dysentery
A. Bacillary dysentery
- Causative agent - Shigella species
- Vector - common housefly
- Infection caused by Shigella species: S. dysenteriae, S. flexneri, S. boydii and S. sonnei.
- Superficial transverse ulcerations of mucosa of the bowel wall occur in the region of
lymphoid follicles.
- The mucosa overlying the lymphoid follicles become necrosed and the surrounding
mucosa shows congestion and oedema.
Shigella dysenteriae
- Complications - The complications of bacillary dysentery are haemorrhage, perforation,
stenosis.
B. Amoebic dysentery
- Causative agent - Entamoeba histolytica
- Vector - common housefly, rodents, cockroaches
- The disease primarily affects the large intestine.
- Infection occurs from ingestion of cyst form of the parasite.
- The cyst wall is dissolved in the small intestine from where the liberated amoebae pass
into the large intestine.
- Here, they invade the epithelium of the mucosa, reach the submucosa and produce the
characteristic flask-shaped ulcers.
- Complications - amoebic liver abscess, amoebic hepatitis, perforation, haemorrhage.
Entamoeba histolytica
- Symptoms – Loose water stools, Blood in stools, Fever, Mucus in
stools, Bloating, etc.
- Risks – Contaminated food, Poor hand washing, Swimming in
contaminated water - lakes, etc.
- Complications – Excessive thirst, Dry mouth, Dark coloured
urine, etc.
- Prevention – Wash hands frequently and properly, Use hand
sanitizer, etc.
Diseases of Large Intestine
• Appendicitis
- It refers to acute inflammation of the appendix (a narrow, worm-like pouch at
some distance away from the junction of ileum – caecum i.e. ileocecal
junction).
- A diet with low bulk or cellulose and high protein intake more often causes
appendicitis.
- It causes intense pain in the lower right abdomen.
- It is common is people between 10-30 years of age.
- Causes – Blockage in the lining of appendix, Obstructive (Faecolith, Calculi,
Tumor, etc.), Low bulk or cellulose and high protein intake diet, Bacterial
infections, etc.
- Symptoms – Sudden pain in the right side of the lower abdomen, Nausea
and Vomiting, Loss of appetite, Constipation or Diarrhoea, Bloating,
Flatulence, etc.
- Complications – Ruptured appendix, Appendix abscess, Mucocele, etc.
• Hemorrhoids (Piles)
- These are varicosities of the hemorrhoidal veins in the anus and lower rectum.
- Internal piles - dilatation of superior hemorrhoidal plexus covered over by mucous
membrane; inside the rectum.
- External piles - involve inferior hemorrhoidal plexus; under the skin around the anus.
- Causes - Portal hypertension, Chronic constipation and straining at stool,Cardiac failure,
Venous stasis of pregnancy, Hereditary predisposition,Tumors of the rectum, Eating low
fiber diet, etc.
- Symptoms:
➢External hemorrhoids – Itching or irritation in anal region, Bleeding, Swelling around
anus, Pain, etc.
➢Internal hemorrhoids – Painless bleeding during bowel moment, Pain, Irritation, etc.
➢Thrombosed hemorrhoids – Severe pain, Swelling, Inflammation, Hard lump in anus,
etc.
- Risks – Aging, Pregnancy, etc.
- Complications – Anemia, Strangulated hemorrhoid,
Blood clot, etc.
- Prevention – Eat high fiber foods, Drink plenty of
fluids, Exercise, Avoid long periods of sitting, etc.
Diseases of Liver
• Jaundice
- It refers to the yellow pigmentation of the skin or sclerae of the eye by bilirubin.
- Bilirubin is derived from degradation of hemoglobin from the worn out RBCs.
- Jaundice is the result of elevated levels of bilirubin in the blood termed
hyperbilirubinaemia (serum bilirubin exceeds 2 mg/dl).
- Types:
1. Pre-hepatic jaundice
- Occurs as a result of increased hemolysis of red blood cells that results in production of
excess bilirubin.
- Because the excess bilirubin is unconjugated (unconjugated bilirubin is fat soluble) it
cannot be excreted in the urine, which therefore remains normal in colour.
- Neonatal haemolytic jaundice - high rate of hemolysis coupled with a shortage of
conjugating enzymes in the hepatocytes of the still immature liver in the neonates.
2. Intra-hepatic jaundice
- This is the result of damage to the liver itself by: Viral hepatitis, Toxic
substances, such as drugs, Amoebiasis, Cirrhosis, etc.
- Excess bilirubin accumulates in the liver.
- Because it is mainly in the conjugated form, it is water-soluble and excreted in
the urine making urine dark in colour.
3. Post-hepatic jaundice
- Causes of obstruction to the flow of bile in the biliary tract include: Gallstones in
the common bile duct, Tumor of the head of the pancreas, Fibrosis of the bile
ducts, following cholangitis or injury by the passage of gallstones.
- In this situation excess bilirubin is also conjugated and is therefore excreted in
the urine.
- The effects of raised serum bilirubin include: Pruritus (itching), Pale feces due to
absence of stercobilin, Dark urine due to the presence of increased amounts of
bilirubin.
- Causes – High rate of synthesis of bilirubin, gall stones, Liver
damage,Alcoholism, etc.
- Symptoms – Fever, Chills, Abdominal pain. Dark coloured urine,
Yellowing of skin, etc.
- Complications – Bloating, Stomach pain, Diarrhoea, Vomiting,
etc.
- Prevention – Avoid alcohol consumption, Maintain healthy
weight, Manage cholesterol levels, etc.
- Risks- Liver infections like hepatitis, cirrhosis, etc.
• Gilbert’s Syndrome
- It is a familial, genetically-determined, autosomal disease of the liver.
- It is characterised by mild, benign, unconjugated hyperbilirubinaemia which is not due
to haemolysis.
- It may be due to reduced conjugation of bilirubin or impaired hepatic uptake of
bilirubin.
- Causes – Genetically inherited disease due to an abnormal gene.
- Symptoms – Occasional yellowing tinge of the skin and whites of the eyes due to
slightly elevated levels of bilirubin as seen in Jaundice,
- Risks – Gender (Males are at a high risk), Both the parents carry the abnormal gene
for the disorder.
- Complications – Low levels of the enzyme (UDP-glucuronosyl transferase) causing
Gilbert’s syndrome may increase the side effects of other drugs (like Irinotecan, etc.)
that are metabolized by the same enzyme.
• Hepatic failure
- May develop from severe acute liver injury with massive necrosis of liver cells (acute
hepatic failure), or from advanced chronic liver disease (chronic hepatic failure).
- It occurs when liver function is markedly impaired.
- Liver failure has serious effects on other parts of the body.
- Manifestations:
1. Jaundice
2. Hepatic encephalopathy (Hepatic coma)
3. Hyperkinetic circulation
4. Hepatorenal syndrome
5. Hepatopulmonary syndrome
6. Oedema and ascites
7. Jaundice
8. Endocrine changes
- Causes – Certain medicines (like Paracetamol), Viral hepatitis, Toxins, Certain
autoimmune disease, etc.
- Symptoms – Loss of appetite, Jaundice, weight loss, bruising or bleeding,
Itching, Edema, Ascites, etc.
- Complications – Cerebral edema, Bleeding disorders, infections, Kidney
failure, etc.
- Prevention – Get vaccinated for HBV, HAV, avoid alcohol consumption, etc.
• Viral Hepatitis
- It refers to the infection and inflammation of the liver by hepatotropic
viruses.
- Currently there are 5 main varieties of these viruses causing distinct
types of viral hepatitis:
➢ Hepatitis A virus (HAV) - causing a faecally-spread self-limiting disease.
➢ Hepatitis B virus (HBV) - causing a parenterally transmitted disease
that may become chronic.
➢ Hepatitis C virus (HCV) - involved chiefly in transfusion-related
hepatitis.
➢ Hepatitis delta virus (HDV) - associated as superinfection with hepatitis
B infection.
➢ Hepatitis E virus (HEV) - causing water-borne infection.
- Only HBV is a DNA virus, all other human hepatitis viruses are RNA
viruses.
Hepatitis A
- It affects mainly children, causing a mild illness although it is often
asymptomatic.
- Infection is spread by the fecal– oral route, e.g. via contaminated hands,
food, water and fomites.
- Hepatitis A is usually a benign, self-limiting disease and has an incubation
period of 15-45 days.
- Most frequently affected age group is 5-14 years; adults are often infected by
spread from children.
- Serologic and viral markers: IgM anti-HAV antibody, IgG anti-HAV antibody.
- Causes – Infection from Hepatitis A virus.
- Symptoms – Vomiting, Low-grade fever, Clay-coloured bowel movement,
Dark urine,Yellowing of eyes, Intense itching, etc.
- Risks – HIV positive, Clotting factor disorders, Physical contact with infected
person, etc.
- Complications – Loss of liver function, etc.
- Prevention – Hepatitis AVaccine. Fig: Structure of hepatitis A virus
Hepatitis B (serum hepatitis)
- It is transmitted parenterally, such as in recipients of blood and blood products, patients
treated by renal dialysis and hospital workers exposed to blood.
- The virus has a longer incubation period - 30-180 days.
- The infection causes more severe form of illness that includes: acute hepatitis B, chronic
hepatitis, progression to cirrhosis.
- It leads to the development of hepatocellular carcinoma.
- Serologic and viral markers:
HBsAg
Anti-HBs
HBeAg
Anti-Hbe
HBcAg
Anti-HBc
HBV-DNA
- Causes – Infection from Hepatitis B virus.
- Symptoms – Abdominal pain, Dark urine, Fever, Loss of appetite,Weakness, Jaundice, etc.
- Risks – Unprotected sex with infected person, Sharing of needles, Infant born to an
infected mother, etc.
- Complications –Cirrhosis, Liver cancer, Liver failure, etc.
- Prevention – Hepatitis B vaccine.
Fig: Structure of hepatitis B virus
Hepatitis C
- This disease is acquired by blood transfusions, blood products,
hemodialysis, parenteral drug abuse and accidental cuts and needle-pricks
in health workers.
- Acute HCV hepatitis is milder than HBV hepatitis but HCV has a higher rate
of progression to chronic hepatitis than HBV.
- The infection is asymptomatic and infection is usually diagnosed later in life
when cirrhosis or chronic liver failure becomes evident.
- Currently, HCV is considered more important cause of chronic liver disease
worldwide than HBV.
- Serologic and viral markers: Anti-HCV antibodies, HCV-RNA.
- Causes – Infection from Hepatitis C virus.
- Symptoms – Dark urine, Fluid buildup in abdomen, Swelling of legs,
Bruising and bleeding easily, Jaundice, Poor appetite, etc.
- Risks – HIV, Piercing or tattoo, Infant born to an infected mother, etc.
- Complications – Cirrhosis, Liver cancre, Liver failure, etc.
- Prevention – Practice safe sex, Hepatitis C vaccine. Fig: Structure of hepatitis C virus
Hepatitis D
- HDV is a defective virus for which HBV is the helper; hepatitis D develops
when there is concomitant hepatitis B infection.
- Co-infection – HDV infection and hepatitis B occur simultaneously.
- Superinfection – HDV infects a chronic HBsAg carrier.
- Serologic and viral markers: HDV identification in the blood and in the
liver cell, HDAg, Anti-HD antibody.
- Causes – Infection from Hepatitis D virus
- Symptoms – Abdominal pain, Loss of appetite, Vomiting, Dark urine,
Fatigue, etc.
- Risks – Unprotected sex, Infant born to an infected mother, HVB infected
individuals, etc.
- Complications – Cirrhosis, Liver cancer, Liver diseases, etc.
- Prevention – Get vaccinated, Practice safe sex, Cautious about Piercing or
tattoo, etc.
Fig: Structure of hepatitis D virus
Diseases of the BiliaryTract
• Gallstones (Cholelithiasis)
- Gallstones consist of deposits of the constituents of bile, most
commonly cholesterol.
- Many small stones or one or more large stones may form but they
do not necessarily produce symptoms.
- Types of Gall stones:
a. Pure gallstones – Pure cholesterol gallstones, Pure pigment
gallstones, Pure calcium carbonate gallstones.
b. Mixed gallstones – contain more than 50% cholesterol
monohydrate plus an admixture of calcium salts, bile pigments
and fatty acids.
c. Combined gallstones – has a pure gallstone nucleus and outer
shell of mixed gallstone; or a mixed gallstone nucleus with pure
gallstone shell.
- Causes – Too much cholesterol in bile, Too much bilirubin in bile,
obstruction of bile duct, etc.
- Symptoms – Sudden and rapidly intensifying pain in upper right
portion of the abdomen, Pain in right shoulder, Back pain between
shoulder blades, etc.
- Risks – Gender (Females are more prone), Age above 40, Low fiber
diet, Familial history, Diabetes, Liver disease, etc.
- Complications – Cholecystitis, Blockage of common bile duct,
Blockage of pancreatic duct, Gallbladder cancer, etc.
- Prevention – Don’t skip meals, Consume high fiber food, etc.
Fig: Effects of gallstones in different locations
• Cholecystitis
- This is usually accompanied with Gallstones.
A. Acute cholecystitis
- In this there is acute inflammation of the gall bladder that occurs when a gallstone
becomes stuck in the cystic duct.
- It does not cause jaundice because bile from the liver can still pass directly into the
duodenum.
- It may be complicated by bacterial infection and distension of the gall bladder, which
carries the risk of perforation and peritonitis.
B. Chronic cholecystitis
- Chronic cholecystitis is the commonest type of clinical gallbladder disease.
- The onset is usually insidious, sometimes following repeated acute attacks.
- Gall stones are present and there may be accompanying biliary colic.
- This condition is associated with cancer of the gall bladder.
- Causes – Gallstones,Tumor, Bile duct blockage, Infection, etc.
- Symptoms – Severe pain in upper right abdomen, Tenderness
in abdomen,Vomiting, Fever, etc.
- Risks – Gallstones
- Complications – Infection within gallbladder, Necrosis or
gallbladder, etc.
- Prevention – Healthy diet, Maintain a healthy wait, etc.
Diseases of Pancreas
• Pancreatitis
- Pancreatitis is inflammation of the pancreas.
- Proteolytic enzymes produced by the pancreas are secreted in inactive forms,
which are not activated until they reach the intestine – this protects the
pancreas from digestion by its own enzymes.
- If these precursor enzymes are activated while still in the pancreas, pancreatitis
results.
A. Acute pancreatitis
- The onset is sudden and lasts for a few days.
- The severity of the disease is dependent on the amount of pancreatic tissue
involved.
- The condition occurs in adults between the age of 40 and 70 years and is
commoner in females than in males.
- There is elevation of serum amylase level within the first 24 hours and elevated
serum lipase (specific for pancreatic disease) level after 3 to 4 days.
B. Chronic pancreatitis
- The condition is either due to repeated attacks of acute pancreatitis
or may arise gradually without evidence of pancreatic disease.
- It is more common in men - associated with fibrosis and distortion of
the main pancreatic duct.
- Protein material secreted by the acinar cells blocks the tiny acinar
ducts.
- This eventually leads to the formation of encapsulated cysts, which
are a feature of acute and chronic pancreatitis.
- Causes – Infection of pancreas, Injury to the abdomen, Obesity,
Pancreatic cancer, Gallstones, Alcohol consumption, etc.
- Symptoms – Upper abdominal pain, Rapid pulse, Tenderness in the
abdomen, Abdominal pain that worsens after eating, etc.
- Risks – Excessive alcohol consumption, Obesity, Family history of
pancreatitis, Smoking, etc.
- Complications – Pseudocyst, Kidney failure, Diabetes, Malnutrition,
Pancreatic cancer, etc.
References:-
1. Harsh Mohan,Textbook of Pathology,
Published by Jaypee Brothers Medical
Publishers Pvt. Ltd. , New Delhi, 7th
Edition.
2. Ross andWilson, Anatomy & Physiology
in Health and Illness by Anne Waugh and
Allison Grant Published by Churchill
Livingstone, 12th Edition.
3. Gerard J.Tortora & Bryan Derrickson,
Principles of Anatomy & Physiology,
Published by John Wiley and Sons, Inc.,
14th Edition.
4. www.mayoclinic.org
5. www.healthline.com
6. https://my.clevelandclinic.org

More Related Content

What's hot

Biliary tract Disease.ppt
Biliary tract Disease.pptBiliary tract Disease.ppt
Biliary tract Disease.ppt
Shama
 
General pathology lecture 1 introduction & cell injury
General pathology lecture 1 introduction & cell injuryGeneral pathology lecture 1 introduction & cell injury
General pathology lecture 1 introduction & cell injury
Huang Yu-Wen
 
Liver pothology
Liver pothologyLiver pothology
Liver pothology
raj kumar
 

What's hot (20)

Topic laboratory and instrumental methods of studying the kidneys and urinar...
Topic  laboratory and instrumental methods of studying the kidneys and urinar...Topic  laboratory and instrumental methods of studying the kidneys and urinar...
Topic laboratory and instrumental methods of studying the kidneys and urinar...
 
Liver & liver diseases
Liver & liver diseasesLiver & liver diseases
Liver & liver diseases
 
Peptic ulcer
Peptic ulcerPeptic ulcer
Peptic ulcer
 
Renal pathology
Renal pathologyRenal pathology
Renal pathology
 
Pathophysiology of leukopenia
Pathophysiology of leukopeniaPathophysiology of leukopenia
Pathophysiology of leukopenia
 
Diseases of the liver
Diseases of the liverDiseases of the liver
Diseases of the liver
 
Pathology of the digestive system
Pathology of the digestive systemPathology of the digestive system
Pathology of the digestive system
 
Pathophysiology of liver
Pathophysiology of liverPathophysiology of liver
Pathophysiology of liver
 
Introduction of pathology
Introduction of pathologyIntroduction of pathology
Introduction of pathology
 
Steatorrhea, Chyluria, Gallstone (Cholelithiasis), Pancreatitis (Chronic and ...
Steatorrhea, Chyluria, Gallstone (Cholelithiasis), Pancreatitis (Chronic and ...Steatorrhea, Chyluria, Gallstone (Cholelithiasis), Pancreatitis (Chronic and ...
Steatorrhea, Chyluria, Gallstone (Cholelithiasis), Pancreatitis (Chronic and ...
 
Biliary tract Disease.ppt
Biliary tract Disease.pptBiliary tract Disease.ppt
Biliary tract Disease.ppt
 
Chronic hepatitis
Chronic hepatitis Chronic hepatitis
Chronic hepatitis
 
General teaching about disease
General teaching about diseaseGeneral teaching about disease
General teaching about disease
 
General pathology lecture 1 introduction & cell injury
General pathology lecture 1 introduction & cell injuryGeneral pathology lecture 1 introduction & cell injury
General pathology lecture 1 introduction & cell injury
 
Cardiovascular Pathophysiology
Cardiovascular PathophysiologyCardiovascular Pathophysiology
Cardiovascular Pathophysiology
 
Cell injury and degenerations
Cell injury and degenerationsCell injury and degenerations
Cell injury and degenerations
 
Liver pothology
Liver pothologyLiver pothology
Liver pothology
 
Stomach pathology
Stomach pathologyStomach pathology
Stomach pathology
 
Diseases of the pancreas csbrp
Diseases of the pancreas csbrpDiseases of the pancreas csbrp
Diseases of the pancreas csbrp
 
Lect.no(6)
Lect.no(6)Lect.no(6)
Lect.no(6)
 

Similar to Pathophysiology of Gastrointestinal tract

Gngival enlargement
Gngival enlargement Gngival enlargement
Gngival enlargement
Parth Thakkar
 
E.N.T. COM.(dr.hewa)
E.N.T. COM.(dr.hewa)E.N.T. COM.(dr.hewa)
E.N.T. COM.(dr.hewa)
student
 

Similar to Pathophysiology of Gastrointestinal tract (20)

Diseases of salivary glands
Diseases of salivary glandsDiseases of salivary glands
Diseases of salivary glands
 
Oral manifestations of gastrointestinal disorders
Oral manifestations of gastrointestinal disordersOral manifestations of gastrointestinal disorders
Oral manifestations of gastrointestinal disorders
 
Bacterial infections of mouth
Bacterial infections of mouthBacterial infections of mouth
Bacterial infections of mouth
 
Diseases of the mouth
Diseases of the mouthDiseases of the mouth
Diseases of the mouth
 
Oral pathology en-lecture-6
Oral pathology en-lecture-6Oral pathology en-lecture-6
Oral pathology en-lecture-6
 
Salivary Gland Diseases.pptx
Salivary Gland Diseases.pptxSalivary Gland Diseases.pptx
Salivary Gland Diseases.pptx
 
Fmd
FmdFmd
Fmd
 
Foot and Mouth Disease
Foot and Mouth DiseaseFoot and Mouth Disease
Foot and Mouth Disease
 
Fmd
FmdFmd
Fmd
 
Gngival enlargement
Gngival enlargement Gngival enlargement
Gngival enlargement
 
lecture one.pptx
lecture one.pptxlecture one.pptx
lecture one.pptx
 
Intestinal obstruction
Intestinal obstructionIntestinal obstruction
Intestinal obstruction
 
21ss_diseases of digestive system_new.ppt
21ss_diseases of digestive system_new.ppt21ss_diseases of digestive system_new.ppt
21ss_diseases of digestive system_new.ppt
 
NCM 116_diseases of digestive system_new.ppt
NCM 116_diseases of digestive system_new.pptNCM 116_diseases of digestive system_new.ppt
NCM 116_diseases of digestive system_new.ppt
 
gingival and periodontal diseases
gingival and periodontal diseasesgingival and periodontal diseases
gingival and periodontal diseases
 
Abdominal radiology pattern recognition
Abdominal radiology pattern recognitionAbdominal radiology pattern recognition
Abdominal radiology pattern recognition
 
Alimentary tract (clinical anatomy)
Alimentary tract (clinical anatomy)Alimentary tract (clinical anatomy)
Alimentary tract (clinical anatomy)
 
EAR INFECTIONS-1.ppt
EAR INFECTIONS-1.pptEAR INFECTIONS-1.ppt
EAR INFECTIONS-1.ppt
 
PULP AND PERIAPICAL DISEASES-2 / oral surgery courses  
PULP AND PERIAPICAL DISEASES-2 / oral surgery courses  PULP AND PERIAPICAL DISEASES-2 / oral surgery courses  
PULP AND PERIAPICAL DISEASES-2 / oral surgery courses  
 
E.N.T. COM.(dr.hewa)
E.N.T. COM.(dr.hewa)E.N.T. COM.(dr.hewa)
E.N.T. COM.(dr.hewa)
 

More from pharmacampus

More from pharmacampus (17)

Type II- diabetes mellitus
Type II-  diabetes mellitusType II-  diabetes mellitus
Type II- diabetes mellitus
 
Diabetes: treatment and management
Diabetes: treatment and management Diabetes: treatment and management
Diabetes: treatment and management
 
Diagnostic tests for GI disorders
Diagnostic tests for GI disordersDiagnostic tests for GI disorders
Diagnostic tests for GI disorders
 
Anatomy & Physiology of GIT
Anatomy & Physiology of GITAnatomy & Physiology of GIT
Anatomy & Physiology of GIT
 
Rheumatoid arthritis- diagnosis and treatment
Rheumatoid arthritis- diagnosis and treatment Rheumatoid arthritis- diagnosis and treatment
Rheumatoid arthritis- diagnosis and treatment
 
ACE inhibitors- How do they work?
ACE inhibitors- How do they work? ACE inhibitors- How do they work?
ACE inhibitors- How do they work?
 
Methods of improving bioavailability
Methods of improving bioavailabilityMethods of improving bioavailability
Methods of improving bioavailability
 
Methods for Measurement of bioavailability
Methods for Measurement of bioavailability Methods for Measurement of bioavailability
Methods for Measurement of bioavailability
 
Which are the Factors affecting bioavailability?
Which are the Factors affecting bioavailability?Which are the Factors affecting bioavailability?
Which are the Factors affecting bioavailability?
 
What are the applications of Biostatistics in Pharmacy?
What are the applications of Biostatistics in Pharmacy?What are the applications of Biostatistics in Pharmacy?
What are the applications of Biostatistics in Pharmacy?
 
Bio-equivalence study of drugs
Bio-equivalence study of drugsBio-equivalence study of drugs
Bio-equivalence study of drugs
 
What are Bioequivalence studies?
What are Bioequivalence studies?What are Bioequivalence studies?
What are Bioequivalence studies?
 
Introduction to Bio-availability study
Introduction to Bio-availability study Introduction to Bio-availability study
Introduction to Bio-availability study
 
Keywords in brand management
Keywords in brand managementKeywords in brand management
Keywords in brand management
 
Introduction to indian pharma industries
Introduction to indian pharma industriesIntroduction to indian pharma industries
Introduction to indian pharma industries
 
Indian Pharma Industry- Government of India’s initiatives
Indian Pharma Industry- Government of India’s initiativesIndian Pharma Industry- Government of India’s initiatives
Indian Pharma Industry- Government of India’s initiatives
 
Growth drivers in Indian Pharma Industry
Growth drivers in Indian Pharma Industry Growth drivers in Indian Pharma Industry
Growth drivers in Indian Pharma Industry
 

Recently uploaded

College Call Girls in Haridwar 9667172968 Short 4000 Night 10000 Best call gi...
College Call Girls in Haridwar 9667172968 Short 4000 Night 10000 Best call gi...College Call Girls in Haridwar 9667172968 Short 4000 Night 10000 Best call gi...
College Call Girls in Haridwar 9667172968 Short 4000 Night 10000 Best call gi...
perfect solution
 
Call Girls Aurangabad Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Aurangabad Just Call 8250077686 Top Class Call Girl Service AvailableCall Girls Aurangabad Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Aurangabad Just Call 8250077686 Top Class Call Girl Service Available
Dipal Arora
 

Recently uploaded (20)

Premium Bangalore Call Girls Jigani Dail 6378878445 Escort Service For Hot Ma...
Premium Bangalore Call Girls Jigani Dail 6378878445 Escort Service For Hot Ma...Premium Bangalore Call Girls Jigani Dail 6378878445 Escort Service For Hot Ma...
Premium Bangalore Call Girls Jigani Dail 6378878445 Escort Service For Hot Ma...
 
Call Girls Ludhiana Just Call 9907093804 Top Class Call Girl Service Available
Call Girls Ludhiana Just Call 9907093804 Top Class Call Girl Service AvailableCall Girls Ludhiana Just Call 9907093804 Top Class Call Girl Service Available
Call Girls Ludhiana Just Call 9907093804 Top Class Call Girl Service Available
 
Top Rated Bangalore Call Girls Richmond Circle ⟟ 9332606886 ⟟ Call Me For Ge...
Top Rated Bangalore Call Girls Richmond Circle ⟟  9332606886 ⟟ Call Me For Ge...Top Rated Bangalore Call Girls Richmond Circle ⟟  9332606886 ⟟ Call Me For Ge...
Top Rated Bangalore Call Girls Richmond Circle ⟟ 9332606886 ⟟ Call Me For Ge...
 
Call Girls Ooty Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Ooty Just Call 8250077686 Top Class Call Girl Service AvailableCall Girls Ooty Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Ooty Just Call 8250077686 Top Class Call Girl Service Available
 
Call Girls Faridabad Just Call 9907093804 Top Class Call Girl Service Available
Call Girls Faridabad Just Call 9907093804 Top Class Call Girl Service AvailableCall Girls Faridabad Just Call 9907093804 Top Class Call Girl Service Available
Call Girls Faridabad Just Call 9907093804 Top Class Call Girl Service Available
 
Call Girls Haridwar Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Haridwar Just Call 8250077686 Top Class Call Girl Service AvailableCall Girls Haridwar Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Haridwar Just Call 8250077686 Top Class Call Girl Service Available
 
VIP Service Call Girls Sindhi Colony 📳 7877925207 For 18+ VIP Call Girl At Th...
VIP Service Call Girls Sindhi Colony 📳 7877925207 For 18+ VIP Call Girl At Th...VIP Service Call Girls Sindhi Colony 📳 7877925207 For 18+ VIP Call Girl At Th...
VIP Service Call Girls Sindhi Colony 📳 7877925207 For 18+ VIP Call Girl At Th...
 
Night 7k to 12k Navi Mumbai Call Girl Photo 👉 BOOK NOW 9833363713 👈 ♀️ night ...
Night 7k to 12k Navi Mumbai Call Girl Photo 👉 BOOK NOW 9833363713 👈 ♀️ night ...Night 7k to 12k Navi Mumbai Call Girl Photo 👉 BOOK NOW 9833363713 👈 ♀️ night ...
Night 7k to 12k Navi Mumbai Call Girl Photo 👉 BOOK NOW 9833363713 👈 ♀️ night ...
 
♛VVIP Hyderabad Call Girls Chintalkunta🖕7001035870🖕Riya Kappor Top Call Girl ...
♛VVIP Hyderabad Call Girls Chintalkunta🖕7001035870🖕Riya Kappor Top Call Girl ...♛VVIP Hyderabad Call Girls Chintalkunta🖕7001035870🖕Riya Kappor Top Call Girl ...
♛VVIP Hyderabad Call Girls Chintalkunta🖕7001035870🖕Riya Kappor Top Call Girl ...
 
Best Rate (Patna ) Call Girls Patna ⟟ 8617370543 ⟟ High Class Call Girl In 5 ...
Best Rate (Patna ) Call Girls Patna ⟟ 8617370543 ⟟ High Class Call Girl In 5 ...Best Rate (Patna ) Call Girls Patna ⟟ 8617370543 ⟟ High Class Call Girl In 5 ...
Best Rate (Patna ) Call Girls Patna ⟟ 8617370543 ⟟ High Class Call Girl In 5 ...
 
Top Quality Call Girl Service Kalyanpur 6378878445 Available Call Girls Any Time
Top Quality Call Girl Service Kalyanpur 6378878445 Available Call Girls Any TimeTop Quality Call Girl Service Kalyanpur 6378878445 Available Call Girls Any Time
Top Quality Call Girl Service Kalyanpur 6378878445 Available Call Girls Any Time
 
Manyata Tech Park ( Call Girls ) Bangalore ✔ 6297143586 ✔ Hot Model With Sexy...
Manyata Tech Park ( Call Girls ) Bangalore ✔ 6297143586 ✔ Hot Model With Sexy...Manyata Tech Park ( Call Girls ) Bangalore ✔ 6297143586 ✔ Hot Model With Sexy...
Manyata Tech Park ( Call Girls ) Bangalore ✔ 6297143586 ✔ Hot Model With Sexy...
 
Call Girls Cuttack Just Call 9907093804 Top Class Call Girl Service Available
Call Girls Cuttack Just Call 9907093804 Top Class Call Girl Service AvailableCall Girls Cuttack Just Call 9907093804 Top Class Call Girl Service Available
Call Girls Cuttack Just Call 9907093804 Top Class Call Girl Service Available
 
💎VVIP Kolkata Call Girls Parganas🩱7001035870🩱Independent Girl ( Ac Rooms Avai...
💎VVIP Kolkata Call Girls Parganas🩱7001035870🩱Independent Girl ( Ac Rooms Avai...💎VVIP Kolkata Call Girls Parganas🩱7001035870🩱Independent Girl ( Ac Rooms Avai...
💎VVIP Kolkata Call Girls Parganas🩱7001035870🩱Independent Girl ( Ac Rooms Avai...
 
The Most Attractive Hyderabad Call Girls Kothapet 𖠋 6297143586 𖠋 Will You Mis...
The Most Attractive Hyderabad Call Girls Kothapet 𖠋 6297143586 𖠋 Will You Mis...The Most Attractive Hyderabad Call Girls Kothapet 𖠋 6297143586 𖠋 Will You Mis...
The Most Attractive Hyderabad Call Girls Kothapet 𖠋 6297143586 𖠋 Will You Mis...
 
College Call Girls in Haridwar 9667172968 Short 4000 Night 10000 Best call gi...
College Call Girls in Haridwar 9667172968 Short 4000 Night 10000 Best call gi...College Call Girls in Haridwar 9667172968 Short 4000 Night 10000 Best call gi...
College Call Girls in Haridwar 9667172968 Short 4000 Night 10000 Best call gi...
 
Call Girls Aurangabad Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Aurangabad Just Call 8250077686 Top Class Call Girl Service AvailableCall Girls Aurangabad Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Aurangabad Just Call 8250077686 Top Class Call Girl Service Available
 
Best Rate (Hyderabad) Call Girls Jahanuma ⟟ 8250192130 ⟟ High Class Call Girl...
Best Rate (Hyderabad) Call Girls Jahanuma ⟟ 8250192130 ⟟ High Class Call Girl...Best Rate (Hyderabad) Call Girls Jahanuma ⟟ 8250192130 ⟟ High Class Call Girl...
Best Rate (Hyderabad) Call Girls Jahanuma ⟟ 8250192130 ⟟ High Class Call Girl...
 
Call Girls Bangalore Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Bangalore Just Call 8250077686 Top Class Call Girl Service AvailableCall Girls Bangalore Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Bangalore Just Call 8250077686 Top Class Call Girl Service Available
 
VIP Call Girls Indore Kirti 💚😋 9256729539 🚀 Indore Escorts
VIP Call Girls Indore Kirti 💚😋  9256729539 🚀 Indore EscortsVIP Call Girls Indore Kirti 💚😋  9256729539 🚀 Indore Escorts
VIP Call Girls Indore Kirti 💚😋 9256729539 🚀 Indore Escorts
 

Pathophysiology of Gastrointestinal tract

  • 1.
  • 2. Diseases of Mouth - Since mouth is the entry point of various pathogens and microorganisms, be it with food or as such, there are chances of a number of diseases to occur in the mouth. • Thrush (Oral Candidiasis) - Thrush acute fungal infection is caused by the yeast Candida albicans, which occurs when the commensal microbe grows in white patches on the tongue and oral mucosa. - Caused by – Candida albicans (Yeast) - Symptoms – Itching and rash at the infected site. - Risks - In adults it causes opportunistic infection mainly in those whose immunity is lowered by, e.g., steroids, antibiotics or cytotoxic drugs. In children it occurs most commonly in bottle-fed babies. - Diagnosis – Physical examination of the lesions in mouth; Blood test – Candida specific antibody test is used to detected candidiasis – IgM, IgA & IgG. - Treatment – Antifungals (Clotrimazole, Fluconazole, etc.), Antiseptics, etc.
  • 3. • Gingivitis - This is inflammation of the gums. - May be Acute or Chronic. - It occurs in response to accumulation of bacterial plaque around the teeth. - It gradually destroys the tissues supporting the teeth. - Symptoms – Swollen gums, bleeding gums. - Risks – Poor oral hygiene, Smoking or chewing tobacco, Older age, etc. • Dental Caries - Dental caries cause destruction of the calcified tissues of the teeth. - If untreated - microorganisms may invade the pulp, causing inflammation and infection. - Bacteria - produce acids that demineralize the enamel. - Dextran, a sticky polysaccharide produced from sucrose, causes the bacteria to stick to the teeth. - Masses of bacterial cells, dextran, and other debris adhering to teeth constitute dental plaque. - Root canal treatment helps to treat the decay of pulp caused due to the infection.
  • 4. Diseases of Pharynx • Tonsilitis - This is the inflammation of palatine tonsils, palatine arches and walls of the pharynx caused byViruses and Streptococcus pyogenes. - There may be production of abscess at the site of infection. - The infection, if untreated may spread to the neck and cause cellulitis. - Repeated infection may lead to chronic inflammation, fibrosis and permanent enlargement. - Surgical removal of the tonsils (Tonsillectomy) can help to reduce the pain and inflammation. - NSAIDs, analgesics and antibiotics can be used.
  • 5. • Diphtheria - Causative agent - Corynebacterium diphtheriae - This is a bacterial infection of the pharynx – extends to the nasopharynx and trachea, caused by a bacteria in which thick fibrous membrane forms over the area and may obstruct the airway. - The microbe produces powerful exotoxins that may severely damage cardiac and skeletal muscle, the liver, kidneys and adrenal glands. - It may be treated by using antitoxin to diphtheria toxin. - Vaccination with diphtheria toxoid is the best way to prevent its occurrence.
  • 6. Diseases of Salivary Glands • Mumps - Caused by - Mumps virus - This is an acute inflammatory condition of the salivary glands, especially the parotids. - The virus is spread by inhalation of infected droplets. - Viruses multiply elsewhere in the body before spreading to the salivary glands. - Complications may affect: a. the brain, causing meningitis or meningoencephalitis b. the testes, causing orchitis (testicular inflammation) c. Pancreatitis, Heart problems, miscarriage, etc. Risks – Unvaccinated individuals are at a high risk, children between 2-12 years, etc. Symptoms – Pain while swallowing, Fever, Loss of appetite, etc.
  • 7. • Tumor of Salivary Glands 1. Salivary adenoma - This benign tumor occurs mainly in the parotid gland and is the most common tumor of the salivary glands. - A second tumor may develop in the same gland several years - malignant type. 2. Carcinoma - Malignant tumors most commonly affect the parotid glands. - Some forms have a tendency to infiltrate nerves in the surrounding tissues, causing severe pain. • Symptoms – Swelling near the jaw or in neck or mouth, difficulty swallowing, numbness in part of the face, etc. • Causes – Genetic mutations (predominantly), smoking, tobacco chewing, etc.
  • 8. Diseases of Esophagus • Gastro-esophageal reflux disease (GERD) - This disease is characterised by the reflux of gastric juice and acids from the stomach into the esophagus. - It may be due to a fault in the lower esophageal sphincter to close and prevent the gastric contents from entering into the esophagus. - It results in inflammation of the lower esophagus. - It the reflux persists, fibrous tissues form at the site of inflammation. - Reflux of gastric contents is associated with: • increase in the intra-abdominal pressure, e.g. in pregnancy, constipation and obesity. • low levels of secretion of the hormone gastrin, leading to reduced sphincter action at the lower end of the oesophagus. • the presence of hiatus hernia.
  • 9. Symptoms – Heartburn, nausea, regurgitation, discomfort in upper abdomen, etc. Cause – Failure of the lower Oesophageal sphincter to constrict properly. • Barrett’s oesophagus - This disease is actually a consequence of Reflux Oesophagitis. - In this stratified squamous epithelium of the lower oesophagus is replaced by columnar epithelium (columnar metaplasia). - If not treated on time, may progress to Carcinoma of Oesophagus followed by Adenocarcinoma. - Symptoms – Difficulty in swallowing food, Chest pain, heartburn and regurgitation. - Causes – Not know, but is thought to be a consequence of Reflux disease. - Risk – Family history, Gender (Men are more likely to develop it), Smoking, GERD, Obesity, etc.
  • 10. • Achalasia - Achalasia of the oesophagus is a neuromuscular dysfunction due to which the cardiac sphincter fails to relax during swallowing and results in progressive dysphagia and dilatation of the oesophagus. - It occurs when the intramural neurons in the wall of the oesophagus are damaged. - Symptoms – Heartburn, regurgitation of food, belching, chest pain, vomiting, etc. - Causes – Loss of nerve cells from oesophagus. - Risk – Allgrove syndrome, Herpes infection, Measles, Autoimmune diseases, etc.
  • 11. • Oesophageal Diverticula - These are the protrusions or pouches of oesophageal wall at the point of weakness. 1. Congenital diverticula occur either at the upper end of the oesophagus or at the bifurcation of trachea. 2. Acquired diverticula may be of 2 types: a) Pulsion (Zenker’s) type—It is seen in the region of hypopharynx and occurs due to oesophageal obstruction such as due to chronic oesophagitis, carcinoma etc. The mucosa and submucosa herniate through the weakened area or through defect in the muscularis propria. • b) Traction type—It occurs in the lower third of oesophagus from contraction of fibrous tissue such as from pleural adhesions, scar tissue of healed tuberculous lesions in the hilum, silicosis etc. • Complications of diverticula include obstruction, infection, perforation, hemorrhage and carcinoma. Oesophageal Diverticula Congenital Acquired
  • 12. • Carcinoma of Oesophagus - Although exact etiology of carcinoma of the oesophagus is not known, a number of conditions and factors have been implicated as under: 1. Diet and personal habits: - i) Heavy smoking - ii)Alcohol consumption 2. Oesophageal disorders: - i) Oesophagitis (especially Barrett’s oesophagus in adenocarcinoma) - ii)Achalasia - iii) Hiatus hernia - iv) Diverticula 3. Other factors: - i) Family history—association with tylosis (keratosis palmariset plantaris). - ii) Genetic factors—predisposition with coeliac disease, epidermolysis bullosa, tylosis. - iii) HPV infection—is a recent addition in etiologic factors.
  • 13. - Abnormality of p53 tumor suppressor gene is found to be associated with the onset of the disease. • Carcinoma of the oesophagus is mainly of 2 types— A. Squamous cell carcinoma - 90% of primary oesophageal cancers are of this type. - Majority of the squamous cell carcinoma occur in the middle third, followed by lower third, and the upper third of oesophagus in that order of frequency. - 3 types of patterns are recognized (Fig. 18.4,B): i) Polypoid fungating type—is the most common form. It appears as a cauliflower-like friable mass protruding into the lumen. ii) Ulcerating type—is the next common form. It looks grossly like a necrotic ulcer with everted edges iii) Diffuse infiltrating type—appears as an annular, stenosing narrowing of the lumen due to infiltration into the wall of oesophagus. Oesophageal Carcinoma Squamous cell carcinoma Adenocarcinoma
  • 14. B. Adenocarcinoma - 10% of primary oesophageal cancers are of this type. - The common locations are lower and middle third of the oesophagus. - Oesophageal adenocarcinoma appears as nodular, elevated mass in the lower oesophagus. - Three patterns recognized: 1. Intestinal type—is the adenocarcinoma with a pattern similar to that seen in adenocarcinoma of intestine or stomach. 2. Adenosquamous type—is the pattern in which there is an irregular admixture of adenocarcinoma and squamous cell carcinoma. 3. Adenoid cystic type—is an uncommon variety and shows a cribriform appearance in an epithelial tumour.
  • 15. Diseases of Stomach ❖Congenital and Acquired Condition:- • Pyloric Stenosis - In this disease, there is narrowing of the pyloric opening especially in male children as a congenital defect (infantile pyloric stenosis). - It is rarely observed in adults – may be due to acquired inflammatory fibrosis or by invasion of tumors - Causes: 1. For infantile pyloric stenosis – Genetic and environmental factors responsible. 2. For adult pyloric stenosis – related to antral gastritis, and tumors in the region (gastric carcinoma, lymphoma, pancreatic carcinoma, etc.)
  • 16. - In both the types, there is hypertrophy as well as hyperplasia of the circular layer of muscularis in the pyloric sphincter accompanied by mild degree of fibrosis. - Symptoms – Vomiting after feeding/eating, Stomach contractions, Dehydration, Changes in bowel movement, etc. - Risks – Gender (More seen in males), Premature birth, Family history, Smoking during pregnancy, etc. - Complications – Jaundice (rare), Stomach irritation, etc. ❖Inflammatory Conditions:- • Gastritis - It is a condition in which the lining of the stomach becomes inflamed which may be cause upper abdominal discomfort like indigestion or dyspepsia. - In worst cases, it may progress to peptic ulcer or gastric cancer.
  • 17. • Types: A. Acute Gastritis - Acute gastritis is a transient acute inflammatory involvement of the stomach, mainly mucosa, and is usually a response to irritant drugs (NSAIDs like Aspirin, etc.) or alcohol. - Causes- 1. Diet and personal habits: - Highly spiced food, Excessive alcohol consumption, Malnutrition, Smoking. 2. Infections: - Bacterial infections e.g. Helicobacter pylori, diphtheria, salmonellosis, pneumonia, staphylococcal food poisoning, etc. 3. Drugs:- Intake of drugs like NSAIDs, aspirin, cortisone, phenylbutazone, indomethacin, preparations of iron, chemo therapeutic agents. Gastritis Acute Chronic
  • 18. 4. Severe stress:- Emotional factors (like shock, anger), Extensive burns,Trauma, Surgery. • Mechanism of Injury: B. Chronic Gastritis - Chronic gastritis is a milder but longer-lasting condition. - It is usually associated with Helicobacter pylori but is sometimes due to autoimmune disease or chemical injury. 1. Reduced blood flow 2. Increased acid secretion and its accumulation 3. Decreased production of bicarbonate buffer.
  • 19. 1. Helicobacter-associated gastritis. Helicobacter pylori is a bacterium that can survive in the gastric mucosa and is commonly associated with gastric conditions, especially chronic gastritis and peptic ulcer disease. 2. Autoimmune gastritis - It is called autoimmune gastritis due to the presence of circulating antibodies and is sometimes associated with other autoimmune diseases such as Hashimoto’s thyroiditis and Addison’s disease. - Antibodies against parietal cells and intrinsic factor are produced, as a result there is depletion of parietal cells and impaired secretion of intrinsic factor. - May lead to significant gastric atrophy where intestinal metaplasia may occur. • Consequences include: - pernicious anemia due to lack of intrinsic factor - increased risk of cancer of the stomach
  • 20. - Symptoms- Nausea, Vomiting, Burning ache or pain in upper abdomen, etc. - Risks – Bacterial infection, Frequent use of pain relievers, Stress, Excessive alcohol use, Autoimmune disease, etc. - Complications – If left untreated, may lead to stomach ulcers and bleeding. - Prevention – Frequent washing of hands with soap and water, consuming completely cooked food.
  • 21. • Peptic Ulcer Disease (PUD) - Peptic ulcers are the areas of degeneration and necrosis of gastrointestinal mucosa exposed to acid-peptic secretions. - These are basically open sores that develop on the inner lining of the stomach and duodenum. - They can occur in any part of the GIT which are exposed to HCl and Pepsin, but majority occur in Stomach and Duodenum. A. Acute Peptic Ulcer - These are a result of severe stress. - These are multiple, small mucosal erosions, seen most commonly in the stomach but occasionally involving the duodenum.
  • 22. - Causes - B. Chronic Peptic Ulcer - If not specified – chronic peptic ulcers would mean gastric and duodenal ulcers – the two major forms of peptic ulcer disease of the upper GI tract. - More common in duodenum than in stomach. - H. pylori infection is found associated in 90% of duodenal and 70% of stomach ulcer cases. Causes Physiological stress Severe trauma Extensive burns Septicaemia Local irritants (e.g. alcohol) Psychological stress
  • 23. - Three distinct causes of PUD are recognized: - the bacterium Helicobacter pylori - (2) nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin - (3) hypersecretion of HCl - Causes - Helicobacter pylori gastritis, NSAIDs-induced mucosal injury, Psychological factors, Genetic factors, etc. • Symptoms – Burning stomach pain, Bloating, Intolerance to fatty food, Heartburn, etc. • Risks – Smoking,Alcohol consumption, Consuming spicy food, Stress, etc. • Complications - 1. Haemorrhage 2. Perforation 3. Anaemia 4. Gastric outflow obstruction 5. Gastric cancer
  • 24. • Tumors A. Polyps 1. Hyperplastic (Inflammatory) Polyps - regenerative, nonneoplastic lesions which are the most common type (90%). - Often located in the pyloric antrum. 2. Hamartomatous Polyps - not true neoplasms but are malformations. B. BenignTumor 1. Adenomas - true benign epithelial neoplasms and are much rare in the stomach than in the large intestine. 2. StromalTumors - Firm, circumscribed nodules, that appear as submucosal nodules.
  • 25. B. BenignTumor Gastric Carcinoma - Carcinoma of the stomach is responsible more than 90% of all gastric malignancies. • Causes - H. pylori infection, Genetic factors, Pre-malignant changes in the gastric mucosa, etc. • Symptoms - Digestion, Heartburn, Stomach pain, Difficulty swallowing,Vomiting, etc. • Risks – GERD, Obesity, Smoking, Stomach polyps, Familial history, H. pylori infection, etc. • Prevention – Stop smoking, consume lots of fruits and vegetables, reduce the amount of salty food, etc.
  • 26. • Classification:- 1. Early gastric carcinoma (EGC) Types: Type I : Polypoid type Type IIa : Superficial elevated Type IIb : Superficial flat Type IIc : Superficial depressed Type III : Ulcerated type 2. Advanced gastric carcinoma Types: i) Ulcerative carcinoma ii) Fungating (Polypoid) carcinoma iii) Scirrhous carcinoma iv) Colloid (Mucoid) carcinoma v) Ulcer-cancer
  • 27. Diseases of Small Intestine ❖Congenital Abnormality: • Meckel’s Diverticulum - Meckel’s diverticulum is an outpouching containing all the layers of the intestinal wall in their normal orientation. - It is more common in males. - Causes – It occurs as a result of incomplete absorption of the vitelline duct by the foetus during the 7th week of pregnancy. - Symptoms – GI bleeding, Abdominal pain, Obstruction of the bowels, diverticulitis (swelling of the intestinal wall), etc. • Other congenital conditions: 1. Intestinal atresia (congenital absence of intestinal lumen) 2. Intestinal stenosis (congenital narrowing of the intestinal lumen) 3. Intestinal malrotation (failure of normal rotation of midgut)
  • 28. • Hernia - Protrusion of an organ or part of an organ through a weak point or aperture in the surrounding structures. - External hernia - protrusion of the bowel through a defect or weakness in the peritoneum. - Internal hernia - herniation that does not present on the external surface - Most common type – Inguinal hernias; followed by femoral and umbilical hernias. Factors involved in formation of Hernia Increased intra- abdominal pressure Local weakness
  • 29. - Inguinal hernias may be of 2 types: ➢ Direct when hernia passes medial to the inferior epigastric artery and it appears through the external abdominal ring. ➢ Indirect when it follows the inguinal canal lateral to the inferior epigastric artery. - Strangulated hernia - blood flow in the hernial sac is obstructed; results in infarction or gangrene of the affected loop of intestine. • Sites of Hernias:- 1. Inguinal hernia – Inguinal canal; occurs more commonly in males. 2. Femoral hernia - femoral canal through which the femoral artery passes. 3. Umbilical hernia – umbilicus, where the umbilical blood vessels from the placenta enter the fetus before birth. 4. Incisional hernia - repeated stretching of fibrous (scar) tissue formed after previous abdominal surgery. 5. Hiatus hernia - protrusion of a part of the fundus of the stomach through the esophageal opening in the diaphragm. (Types – Rolling & Sliding) (Figures: A. Common sites of herniation. B. Strangulated hernia formation.)
  • 30. - Causes – Congenital, Aging, Damage from injury, Pregnancy, Previous surgery, Obesity, etc. - Symptoms – Bulge or Lump in the affected area (which disappears on lying down), Pain, Heartburn, Difficulty in swallowing,Chest pain (in case of Hiatus hernia), etc. - Risks – Family history, Pregnancy, Smoking, Premature birth, Cystic fibrosis, etc. Figure: Hiatus hernia
  • 31. • Inflammatory Bowel Disease (IBD) - This is a term used to describe disorders that involve chronic inflammation of the digestive tract. - It basically includes 2 conditions: 1. Crohn’s disease 2. Ulcerative colitis A. Crohn’s disease - It is characterized by inflammation of the lining of the digestive tract, often involving deeper layers of the digestive tract. - There is chronic patchy inflammation with oedema – causing partial obstruction of the lumen – skip lesions. - Complications - Fistula formation, Malabsorption, Development of malignancy, Bowel obstruction, etc.
  • 32. B. Ulcerative colitis - Involves inflammation and ulcers along the lining of the colon and rectum. - Ulcerative colitis begins in the rectum, and extends upwards into the sigmoid colon, descending colon, transverse colon, and sometimes may involve the entire colon. • Complications - Fulminant colitis (Toxic megacolon), Perforated colon, Perianal fistula, Colon cancer, Severe dehydration, etc. • Symptoms for both: - Diarrhoea, Blood in stools, Reduced appetite,Weight loss, etc. • Risks for both: - Smoking, Familial history, Excessive use of NSAIDs, etc. • Causes – Mostly Idiopathic; may be due to immune system malfunction, hereditary, etc.
  • 33. • Enteric Fever (Typhoid & Paratyphoid) - Causative agents – Salmonella typhi (Typhoid) and S. paratyphi A or B (Paratyphoid). Typhoid: - The incubation period is about 10–14 days during which time bacteria invade the lymphoid tissue of the small intestine, especially the aggregated lymph follicles (Peyer’s patches). - The bacilli invade the bloodstream causing bacteremia, and the characteristic clinical features of the disease like continuous rise in temperature and rose spots on the skin are observed. - Eventually, the bacilli are localized in the intestinal lymphoid tissue, in the mesenteric lymph nodes, in the liver, in the gallbladder, and in the spleen. Paratyphoid: - Paratyphoid fever follows a similar course but is usually milder and of shorter duration although the onset can be more sudden; complications are less frequent.
  • 34. - Causes – Ingestion of food or water contaminated with Salmonella typhi and S. paratyphi A or B. - Mode of spread - Through typhoid carriers, Fecal-oral transmission route. - Symptoms – High fever, Stomach pain, Constipation or Diarrhoea, Rashes, etc. - Risks – Close contact with an infected person, Drinking contaminated water,Travelling to affected areas, etc. - Complications- Myocarditis, Endocarditis, Pneumonia, Pancreatitis, etc. - Prevention – Washing hands properly, Avoid drinking untreated water, Avoid raw fruits and vegetables, Consumption of hot food, Getting vaccinated, etc.
  • 35. • Dysentery - The term refers to a condition in which diarrhoea is accompanied with abdominal cramps and passage of mucus in the stools. - Types: 1. Bacillary dysentery 2. Amoebic dysentery A. Bacillary dysentery - Causative agent - Shigella species - Vector - common housefly - Infection caused by Shigella species: S. dysenteriae, S. flexneri, S. boydii and S. sonnei. - Superficial transverse ulcerations of mucosa of the bowel wall occur in the region of lymphoid follicles. - The mucosa overlying the lymphoid follicles become necrosed and the surrounding mucosa shows congestion and oedema. Shigella dysenteriae
  • 36. - Complications - The complications of bacillary dysentery are haemorrhage, perforation, stenosis. B. Amoebic dysentery - Causative agent - Entamoeba histolytica - Vector - common housefly, rodents, cockroaches - The disease primarily affects the large intestine. - Infection occurs from ingestion of cyst form of the parasite. - The cyst wall is dissolved in the small intestine from where the liberated amoebae pass into the large intestine. - Here, they invade the epithelium of the mucosa, reach the submucosa and produce the characteristic flask-shaped ulcers. - Complications - amoebic liver abscess, amoebic hepatitis, perforation, haemorrhage. Entamoeba histolytica
  • 37. - Symptoms – Loose water stools, Blood in stools, Fever, Mucus in stools, Bloating, etc. - Risks – Contaminated food, Poor hand washing, Swimming in contaminated water - lakes, etc. - Complications – Excessive thirst, Dry mouth, Dark coloured urine, etc. - Prevention – Wash hands frequently and properly, Use hand sanitizer, etc.
  • 38. Diseases of Large Intestine • Appendicitis - It refers to acute inflammation of the appendix (a narrow, worm-like pouch at some distance away from the junction of ileum – caecum i.e. ileocecal junction). - A diet with low bulk or cellulose and high protein intake more often causes appendicitis. - It causes intense pain in the lower right abdomen. - It is common is people between 10-30 years of age. - Causes – Blockage in the lining of appendix, Obstructive (Faecolith, Calculi, Tumor, etc.), Low bulk or cellulose and high protein intake diet, Bacterial infections, etc. - Symptoms – Sudden pain in the right side of the lower abdomen, Nausea and Vomiting, Loss of appetite, Constipation or Diarrhoea, Bloating, Flatulence, etc. - Complications – Ruptured appendix, Appendix abscess, Mucocele, etc.
  • 39. • Hemorrhoids (Piles) - These are varicosities of the hemorrhoidal veins in the anus and lower rectum. - Internal piles - dilatation of superior hemorrhoidal plexus covered over by mucous membrane; inside the rectum. - External piles - involve inferior hemorrhoidal plexus; under the skin around the anus. - Causes - Portal hypertension, Chronic constipation and straining at stool,Cardiac failure, Venous stasis of pregnancy, Hereditary predisposition,Tumors of the rectum, Eating low fiber diet, etc. - Symptoms: ➢External hemorrhoids – Itching or irritation in anal region, Bleeding, Swelling around anus, Pain, etc. ➢Internal hemorrhoids – Painless bleeding during bowel moment, Pain, Irritation, etc. ➢Thrombosed hemorrhoids – Severe pain, Swelling, Inflammation, Hard lump in anus, etc.
  • 40. - Risks – Aging, Pregnancy, etc. - Complications – Anemia, Strangulated hemorrhoid, Blood clot, etc. - Prevention – Eat high fiber foods, Drink plenty of fluids, Exercise, Avoid long periods of sitting, etc.
  • 41. Diseases of Liver • Jaundice - It refers to the yellow pigmentation of the skin or sclerae of the eye by bilirubin. - Bilirubin is derived from degradation of hemoglobin from the worn out RBCs. - Jaundice is the result of elevated levels of bilirubin in the blood termed hyperbilirubinaemia (serum bilirubin exceeds 2 mg/dl). - Types: 1. Pre-hepatic jaundice - Occurs as a result of increased hemolysis of red blood cells that results in production of excess bilirubin. - Because the excess bilirubin is unconjugated (unconjugated bilirubin is fat soluble) it cannot be excreted in the urine, which therefore remains normal in colour. - Neonatal haemolytic jaundice - high rate of hemolysis coupled with a shortage of conjugating enzymes in the hepatocytes of the still immature liver in the neonates.
  • 42. 2. Intra-hepatic jaundice - This is the result of damage to the liver itself by: Viral hepatitis, Toxic substances, such as drugs, Amoebiasis, Cirrhosis, etc. - Excess bilirubin accumulates in the liver. - Because it is mainly in the conjugated form, it is water-soluble and excreted in the urine making urine dark in colour. 3. Post-hepatic jaundice - Causes of obstruction to the flow of bile in the biliary tract include: Gallstones in the common bile duct, Tumor of the head of the pancreas, Fibrosis of the bile ducts, following cholangitis or injury by the passage of gallstones. - In this situation excess bilirubin is also conjugated and is therefore excreted in the urine. - The effects of raised serum bilirubin include: Pruritus (itching), Pale feces due to absence of stercobilin, Dark urine due to the presence of increased amounts of bilirubin.
  • 43. - Causes – High rate of synthesis of bilirubin, gall stones, Liver damage,Alcoholism, etc. - Symptoms – Fever, Chills, Abdominal pain. Dark coloured urine, Yellowing of skin, etc. - Complications – Bloating, Stomach pain, Diarrhoea, Vomiting, etc. - Prevention – Avoid alcohol consumption, Maintain healthy weight, Manage cholesterol levels, etc. - Risks- Liver infections like hepatitis, cirrhosis, etc.
  • 44. • Gilbert’s Syndrome - It is a familial, genetically-determined, autosomal disease of the liver. - It is characterised by mild, benign, unconjugated hyperbilirubinaemia which is not due to haemolysis. - It may be due to reduced conjugation of bilirubin or impaired hepatic uptake of bilirubin. - Causes – Genetically inherited disease due to an abnormal gene. - Symptoms – Occasional yellowing tinge of the skin and whites of the eyes due to slightly elevated levels of bilirubin as seen in Jaundice, - Risks – Gender (Males are at a high risk), Both the parents carry the abnormal gene for the disorder. - Complications – Low levels of the enzyme (UDP-glucuronosyl transferase) causing Gilbert’s syndrome may increase the side effects of other drugs (like Irinotecan, etc.) that are metabolized by the same enzyme.
  • 45. • Hepatic failure - May develop from severe acute liver injury with massive necrosis of liver cells (acute hepatic failure), or from advanced chronic liver disease (chronic hepatic failure). - It occurs when liver function is markedly impaired. - Liver failure has serious effects on other parts of the body. - Manifestations: 1. Jaundice 2. Hepatic encephalopathy (Hepatic coma) 3. Hyperkinetic circulation 4. Hepatorenal syndrome 5. Hepatopulmonary syndrome 6. Oedema and ascites 7. Jaundice 8. Endocrine changes
  • 46. - Causes – Certain medicines (like Paracetamol), Viral hepatitis, Toxins, Certain autoimmune disease, etc. - Symptoms – Loss of appetite, Jaundice, weight loss, bruising or bleeding, Itching, Edema, Ascites, etc. - Complications – Cerebral edema, Bleeding disorders, infections, Kidney failure, etc. - Prevention – Get vaccinated for HBV, HAV, avoid alcohol consumption, etc.
  • 47. • Viral Hepatitis - It refers to the infection and inflammation of the liver by hepatotropic viruses. - Currently there are 5 main varieties of these viruses causing distinct types of viral hepatitis: ➢ Hepatitis A virus (HAV) - causing a faecally-spread self-limiting disease. ➢ Hepatitis B virus (HBV) - causing a parenterally transmitted disease that may become chronic. ➢ Hepatitis C virus (HCV) - involved chiefly in transfusion-related hepatitis. ➢ Hepatitis delta virus (HDV) - associated as superinfection with hepatitis B infection. ➢ Hepatitis E virus (HEV) - causing water-borne infection. - Only HBV is a DNA virus, all other human hepatitis viruses are RNA viruses.
  • 48. Hepatitis A - It affects mainly children, causing a mild illness although it is often asymptomatic. - Infection is spread by the fecal– oral route, e.g. via contaminated hands, food, water and fomites. - Hepatitis A is usually a benign, self-limiting disease and has an incubation period of 15-45 days. - Most frequently affected age group is 5-14 years; adults are often infected by spread from children. - Serologic and viral markers: IgM anti-HAV antibody, IgG anti-HAV antibody. - Causes – Infection from Hepatitis A virus. - Symptoms – Vomiting, Low-grade fever, Clay-coloured bowel movement, Dark urine,Yellowing of eyes, Intense itching, etc. - Risks – HIV positive, Clotting factor disorders, Physical contact with infected person, etc. - Complications – Loss of liver function, etc. - Prevention – Hepatitis AVaccine. Fig: Structure of hepatitis A virus
  • 49. Hepatitis B (serum hepatitis) - It is transmitted parenterally, such as in recipients of blood and blood products, patients treated by renal dialysis and hospital workers exposed to blood. - The virus has a longer incubation period - 30-180 days. - The infection causes more severe form of illness that includes: acute hepatitis B, chronic hepatitis, progression to cirrhosis. - It leads to the development of hepatocellular carcinoma. - Serologic and viral markers: HBsAg Anti-HBs HBeAg Anti-Hbe HBcAg Anti-HBc HBV-DNA
  • 50. - Causes – Infection from Hepatitis B virus. - Symptoms – Abdominal pain, Dark urine, Fever, Loss of appetite,Weakness, Jaundice, etc. - Risks – Unprotected sex with infected person, Sharing of needles, Infant born to an infected mother, etc. - Complications –Cirrhosis, Liver cancer, Liver failure, etc. - Prevention – Hepatitis B vaccine. Fig: Structure of hepatitis B virus
  • 51. Hepatitis C - This disease is acquired by blood transfusions, blood products, hemodialysis, parenteral drug abuse and accidental cuts and needle-pricks in health workers. - Acute HCV hepatitis is milder than HBV hepatitis but HCV has a higher rate of progression to chronic hepatitis than HBV. - The infection is asymptomatic and infection is usually diagnosed later in life when cirrhosis or chronic liver failure becomes evident. - Currently, HCV is considered more important cause of chronic liver disease worldwide than HBV. - Serologic and viral markers: Anti-HCV antibodies, HCV-RNA. - Causes – Infection from Hepatitis C virus. - Symptoms – Dark urine, Fluid buildup in abdomen, Swelling of legs, Bruising and bleeding easily, Jaundice, Poor appetite, etc. - Risks – HIV, Piercing or tattoo, Infant born to an infected mother, etc. - Complications – Cirrhosis, Liver cancre, Liver failure, etc. - Prevention – Practice safe sex, Hepatitis C vaccine. Fig: Structure of hepatitis C virus
  • 52. Hepatitis D - HDV is a defective virus for which HBV is the helper; hepatitis D develops when there is concomitant hepatitis B infection. - Co-infection – HDV infection and hepatitis B occur simultaneously. - Superinfection – HDV infects a chronic HBsAg carrier. - Serologic and viral markers: HDV identification in the blood and in the liver cell, HDAg, Anti-HD antibody. - Causes – Infection from Hepatitis D virus - Symptoms – Abdominal pain, Loss of appetite, Vomiting, Dark urine, Fatigue, etc. - Risks – Unprotected sex, Infant born to an infected mother, HVB infected individuals, etc. - Complications – Cirrhosis, Liver cancer, Liver diseases, etc. - Prevention – Get vaccinated, Practice safe sex, Cautious about Piercing or tattoo, etc. Fig: Structure of hepatitis D virus
  • 53. Diseases of the BiliaryTract • Gallstones (Cholelithiasis) - Gallstones consist of deposits of the constituents of bile, most commonly cholesterol. - Many small stones or one or more large stones may form but they do not necessarily produce symptoms. - Types of Gall stones: a. Pure gallstones – Pure cholesterol gallstones, Pure pigment gallstones, Pure calcium carbonate gallstones. b. Mixed gallstones – contain more than 50% cholesterol monohydrate plus an admixture of calcium salts, bile pigments and fatty acids. c. Combined gallstones – has a pure gallstone nucleus and outer shell of mixed gallstone; or a mixed gallstone nucleus with pure gallstone shell.
  • 54. - Causes – Too much cholesterol in bile, Too much bilirubin in bile, obstruction of bile duct, etc. - Symptoms – Sudden and rapidly intensifying pain in upper right portion of the abdomen, Pain in right shoulder, Back pain between shoulder blades, etc. - Risks – Gender (Females are more prone), Age above 40, Low fiber diet, Familial history, Diabetes, Liver disease, etc. - Complications – Cholecystitis, Blockage of common bile duct, Blockage of pancreatic duct, Gallbladder cancer, etc. - Prevention – Don’t skip meals, Consume high fiber food, etc. Fig: Effects of gallstones in different locations
  • 55. • Cholecystitis - This is usually accompanied with Gallstones. A. Acute cholecystitis - In this there is acute inflammation of the gall bladder that occurs when a gallstone becomes stuck in the cystic duct. - It does not cause jaundice because bile from the liver can still pass directly into the duodenum. - It may be complicated by bacterial infection and distension of the gall bladder, which carries the risk of perforation and peritonitis. B. Chronic cholecystitis - Chronic cholecystitis is the commonest type of clinical gallbladder disease. - The onset is usually insidious, sometimes following repeated acute attacks. - Gall stones are present and there may be accompanying biliary colic. - This condition is associated with cancer of the gall bladder.
  • 56. - Causes – Gallstones,Tumor, Bile duct blockage, Infection, etc. - Symptoms – Severe pain in upper right abdomen, Tenderness in abdomen,Vomiting, Fever, etc. - Risks – Gallstones - Complications – Infection within gallbladder, Necrosis or gallbladder, etc. - Prevention – Healthy diet, Maintain a healthy wait, etc.
  • 57. Diseases of Pancreas • Pancreatitis - Pancreatitis is inflammation of the pancreas. - Proteolytic enzymes produced by the pancreas are secreted in inactive forms, which are not activated until they reach the intestine – this protects the pancreas from digestion by its own enzymes. - If these precursor enzymes are activated while still in the pancreas, pancreatitis results. A. Acute pancreatitis - The onset is sudden and lasts for a few days. - The severity of the disease is dependent on the amount of pancreatic tissue involved. - The condition occurs in adults between the age of 40 and 70 years and is commoner in females than in males. - There is elevation of serum amylase level within the first 24 hours and elevated serum lipase (specific for pancreatic disease) level after 3 to 4 days.
  • 58. B. Chronic pancreatitis - The condition is either due to repeated attacks of acute pancreatitis or may arise gradually without evidence of pancreatic disease. - It is more common in men - associated with fibrosis and distortion of the main pancreatic duct. - Protein material secreted by the acinar cells blocks the tiny acinar ducts. - This eventually leads to the formation of encapsulated cysts, which are a feature of acute and chronic pancreatitis. - Causes – Infection of pancreas, Injury to the abdomen, Obesity, Pancreatic cancer, Gallstones, Alcohol consumption, etc. - Symptoms – Upper abdominal pain, Rapid pulse, Tenderness in the abdomen, Abdominal pain that worsens after eating, etc. - Risks – Excessive alcohol consumption, Obesity, Family history of pancreatitis, Smoking, etc. - Complications – Pseudocyst, Kidney failure, Diabetes, Malnutrition, Pancreatic cancer, etc.
  • 59. References:- 1. Harsh Mohan,Textbook of Pathology, Published by Jaypee Brothers Medical Publishers Pvt. Ltd. , New Delhi, 7th Edition. 2. Ross andWilson, Anatomy & Physiology in Health and Illness by Anne Waugh and Allison Grant Published by Churchill Livingstone, 12th Edition. 3. Gerard J.Tortora & Bryan Derrickson, Principles of Anatomy & Physiology, Published by John Wiley and Sons, Inc., 14th Edition. 4. www.mayoclinic.org 5. www.healthline.com 6. https://my.clevelandclinic.org