NEET MDS Lessons
General Pathology
STOMACH
Congenital malformations
1. Pyloric stenosis
Clinical features. Projectile vomiting 3-4 weeks after birth associated with a palpable "olive" mass in the epigastric region is observed.
Pathology shows hypertrophy of the muscularis of the pylorus and failure to relax.
2. Diaphragmatic hernias are due to weakness in or absence of parts of the diaphragm, allowing herniation of the abdominal contents into the thorax.
Inflammation
1. Acute gastritis (erosive)
Etiology. Alcohol, aspirin and other NSAIDs, smoking, shock, steroids, and uremia may all cause disruption of the mucosal barrier, leading to inflammation.
Clinical features. Patients experience heartburn, epigastric pain, nausea, vomiting, hematemesis, and even melena.
2. Chronic gastritis (nonerosive) may lead to atrophic mucosa with lymphocytic infiltration.
Types
(1) Fundal (Type A) gastritis is often autoimmune in origin. It is the type associated with pernicious anemia and, therefore, achlorhydria and intrinsic factor deficiency.
(2) Antral (Type B) gastritis is most commonly caused by Helicobacter pylori and is the most common form of chronic gastritis in the U.S. H. pylori is also responsible for proximal duodenitis in regions of gastric metaplasia.
Clinical features. The patient may be asymptomatic or suffer epigastric pain, nausea, vomiting, and bleeding. Gastritis may predispose to peptic ulcer disease, probably related to H. pylori infection.
3. Peptic ulcers
Peptic ulcers are usually chronic, isolated ulcers observed in areas bathed by pepsin and HCI; they are the result of mucosal breakdown
Common locations are the proximal duodenum, the stomach, and the esophagus, often in areas of Barrett's esophagus.
Etiology. There are several important etiologic factors.
Duodenal ulcers occur predominantly in patients with excess acid secretion, while gastric ulcers usually occur in patients with lower than average acid secretion.
Other predisposing conditions include smoking, cirrhosis, pancreatitis, hyperparathyroidism, and H. pylori infection. Aspirin, steroids, and NSAlDs are known to be assoicated with peptic ulcer disease. Next to H. pylori colonization, aspirin or NSAID ingestion is the most common cause of peptic ulcer.
Clinical features. Patients experience episodic epigastric pain. Duodenal and most gastric ulcers are relieved by food or antacids. Approximately one-fifth of gastric ulcer patients get no relief from eating or experience pain again within 30 minutes.
Pathology. Benign peptic ulcers are well-circumscribed lesions with a loss of the mucosa, underlying scarring, and sharp walls.
Complications include hemorrhage, perforation, obstruction, and pain. Duodenal ulcers do not become malignant .Gastric ulcers do so only rarely; those found to be ma1ignant likely originated as a cancer that ulcerated.
Diagnosis is made by upper gastrointestinal Series , endoscopy, and biopsy to rule out malignancy or to demonstrate the presence of H. pylori.
4. Stress ulcers
are superficial mucosal ulcers of the stomach or duodenum or both. Stress may be induced by burns, sepsis shock, trauma, or increased intracranial pressure.
Tumors
1. Benign
a. Leiomyoma, often multiple, is the most common benign neoplasm of the stomach. Clinical features include bleeding, pain, and iron deficiency anemia.
b. Gastric polyps are due to proliferation of the mucosal epithelium.
2. Malignant tumors
a. Carcinoma
Etiology. Primary factors include genetic predisposition and diet; other factors include hypochlorhydria, pernicious anemia, atrophic gastritis, adenomatous polyps, and exposure to nitrosamines. H. pylori are also implicated.
Clinical features. Stomach cancer is usually asymptomatic until late, then presents with anorexia, weight loss, anemia, epigastric pain, and melena. Virchow's node is a common site of metastasis.
Pathology. Symptomatic late gastric carcinoma may be expanding or infiltrative. In both cases the prognosis is poor (approximately 10% 5-year survival), and metastases are frequently present at the time of diagnosis.
Adenocarcinomas are most common.
b. Gastrointestinal lymphomas may be primary In the gastrointestinal tract as solitary masses.
c. Sarcoma is a rare, large, ulcerating mass that extends into the lumen.
d. Metastatic carcinoma. Krukenberg's tumor is an ovaria metastasis from a gastric carcinoma.
e. Kaposi's sarcoma. The stomach is the most commonly involved GI organ in Kaposi's sarcoma. It primarily occurs in homosexual men, appearing as hemorrhagic polypoid, umbilicated nodular lesions, typically in a submucosal location. It rarely causes symptoms
Psoriasis
1. Characterized by skin lesions that appear as scaly, white plaques.
2. Caused by rapid proliferation of the epidermis.
3. Autoimmune pathogenesis; exact mechanism is unclear.
Chronic lymphocytic leukaemia
Commoner in middle age. It starts insidiously and often runs a long chronic course
Features:
- Lymphnode enlargement.
- Anaemia (with haemolytic element).
- Moderate splenomegaly.
- Haemorrhagic tendency in late stages.
- Infection.
Blood picture:
- Anaemia with features of haemolytic anaemia
- Total leucocytic count of 50-100,OOO/cu.mm.
- Upto 90-95% cells are lymphocytes and prolymphocytes.
- Thrombocytopenia may be seen.
Bone marrow. Lymphocytic series cells-are seen. Cells of other series are reduced,
Glycogen storage diseases (glycogenoses)
1. Genetic transmission: autosomal recessive.
2. This group of diseases is characterized by a deficiency of a particular enzyme involved in either glycogen production or degradative pathways.
Diseases include:
on Gierke disease (type I)
(a) Deficient enzyme: glucose-6-phosphatase.
(b) Major organ affected by the buildup of glycogen: liver.
Pompe disease (type II)
(1) Deficient enzyme: α-glucosidase(acid maltase).
(2) Major organ affected by the buildup of glycogen: heart.
Cori disease (type III)
(1) Deficient enzyme: debranching enzyme (amylo-1,6-glucosidase).
(2) Organs affected by the buildup of glycogen: varies between the heart, liver, or skeletal muscle.
Brancher glycogenosis (type IV)
(1) Deficient enzyme: branching enzyme.
(2) Organs affected by the buildup of glycogen: liver, heart, skeletal muscle, and brain.
McArdle syndrome (type V)
(1) Deficient enzyme: muscle phosphorylase.
(2) Major organ affected by the buildup of glycogen: skeletal muscle.
Nevus
1. Commonly known as moles.
2. A benign, pigmented tumor of melanocytes, found deep within connective tissue.
3. Types of skin nevi:
a. Junctional nevus—found in the epidermis.
It is the only type of nevus that may be considered to be premalignant.
b. Compound nevus—found in both the epidermis and underlying dermis.
c. Intraepidermal nevus—found in the dermis.
Nephritic syndrome
Characterized by inflammatory rupture of the glomerular capillaries, leaking blood into the urinary space.
Classic presentation: poststreptococcal glomerulonephritis. It occurs after a group A, β–hemolytic Streptococcus infection (e.g., strep throat.)
Caused by autoantibodies forming immune complexes in the glomerulus.
Clinical manifestations:
oliguria, hematuria, hypertension, edema, and azotemia (increased concentrations of serum urea nitrogen
and creatine).
General chromosome abnormalities
The normal human cell contains 46 chromosomes, including 22 homologous pairs of autosomes and one pair of sex chromosomes (XX for female and XY for male). A somatic cell is diploid, containing 46 chromosomes. Gametes are haploid, containing 23 chromosomes.
Aneuploidy
(a) Any deviation in the number of chromosomes, whether fewer or more, from the normal haploid number of chromosomes.
(b) Nondisjunction—a common cause of aneuploidy. It is the failure of chromosomes to pass to separate cells during meiotic or mitotic cell division.
(c) Often seen in malignant tumors.
Deletion: loss of a sequence of DNA from a chromosome.
Translocation: the separation of a chromosome and the attachment of the area of separation to another chromosome.