NEET MDS Lessons
General Pathology
Staphylococcal Infection
Staphylococci, including pathogenic strains, are normal inhabitants of the nose and skin of most healthy people
Virulence factors include coagulase (which clots blood), hemolysin, and protein A (which ties up Fc portions of antibodies). Although we have antibodies against staphylococci, they are of limited usefulness.
Staphylococci (and certain other microbes) also produce catalase, which breaks down H2O2, rendering phagocytes relatively helpless against them.
The coagulase-positive staphylococcus (Staphylococcus pyogenes var. aureus) is a potent pathogen. It tends to produce localized infection
It is the chief cause of bacterial skin abscesses. Infection spreads from a single infected hair (folliculitis) or splinter to involve the surrounding skin and subcutaneous tissues
Furuncles are single pimples
carbuncles are pimple clusters linked by tracks of tissue necrosis which involve the fascia.
Impetigo is a pediatric infection limited to the stratum corneum of the skin -- look for honey-colored crusts
Staphylococcal infections of the nail-bed (paronychia) and palmar fingertips (felons) are especially painful and destructive
These staph are common causes of wound infections (including surgical wounds) and of a severe, necrotizing pneumonia. Both are serious infections in the hospitalized patient.
Staph is the most common cause of synthetic vascular graft infections. Certain sticky strains grow as a biofilm on the grafts
Staph aureus is pathogenic, β-hemolytic, and makes coagulase.
Staph epidermidis are non-pathogenic strains that don’t make coagulase. Often Antibiotics resistant, and can become opportunistic infections in hospitals.
Staph aureus is normal flora in the nose and on skin, but can also colonize moist areas such as perineum. Causes the minor infections after cuts. Major infections occur with lacerations or immune compromise, where large number of cocci are introduced.
While Staph aureus can invade the gut directly (invasive staphylococcal enterocolitis), it is much more common to encounter food poisoning due to strains which have produced enterotoxin B, a pre-formed toxin in un-refrigerated meat or milk products
Staph epidermidis (Coagulase-negative staphylococci)
Universal normal flora but few virulence factors. Often antibiotic resistant.
Major cause of foreign body infections such as prosthetic valve endocarditis and IV line sepsis.
Staph saprophyticus
Common cause of UTI in women.
Pathogenicity
Dominant features of S. aureus infections are pus, necrosis, scarring. The infections are patchy. Serious disease is rare because we are generally immune. However, foreign bodies or necrotic tissue can start an infection. Staph infections include wound infections, foreign body sepsis, pneumonia, meningitis.
Occassionally, S. aureus can persist within cells.
Major disease presentations include:
--Endocarditis
--Abscesses (due to coagulase activity)
--Toxic Shock
--Wound infections
--Nosocomial pneumonia
Prevention of Staph aureus infections
S. aureus only lives on people, so touching is the main mode of transmission. Infected patients should be isolated, but containment is easy with intense hand washing.
THE PITUITARY GLAND
This is a small, bean-shaped structure that lies at the base of the brain within the confines of the sella turcica. It is connected to the hypothalamus by a "stalk," composed of axons extending from the hypothalamus. The pituitary is composed of two morphologically and functionally distinct components: the anterior lobe (adenohypophysis) and the posterior lobe (neurohypophysis). The adenohypophysis, in H&E stained sections, shows a colorful collection of cells with basophilic, eosinophilic or poorly staining ("chromophobic") cytoplasm.
Hepatic failure
Etiology. Chronic hepatic disease (e.g., chronic active hepatitis or alcoholic cirrhosis) is the most common cause of hepatic failure although acute liver disease may also be responsible.
- Widespread liver necrosis may be seen with carbon tetrachloride and acetaminophen toxicity. Widespread steatosis is seen in Reye's syndrome, a cause of acute liver failure most often seen in children with a recent history of aspirin ingestion for an unrelated viral illness.
- Massive necrosis may also be seen in acute viral hepatitis, after certain anesthetic agents, and in shock from any cause.
Clinical features. Hepatic failure causes jaundice, musty odor of breath and urine, encephalopathy, renal failure (either by simultaneous toxicity to the liver and kidneys or the hepatorerial syndrome), palmar erythema, spider angiomas, gynecomastia , testicular atrophy
Eczematous Dermatitis
Eczematous dermatitis includes a large category of skin lesions characterized by severe pruritus and distinctive gross and microscopic features.
- type I hypersensitivity is involved with atopic dermatitis in patients who have an allergic history.
- type IV hypersensitivity is involved in contact dermatitis (poison ivy).
- acute eczematous dermatitis is characterized by a weeping, pruritic rash, while a chronic eczematous dermatitis presents with dry, scaly, plaque-like thickening of the skin, a process called lichenification.
Congenital heart defect
Congenital heart defects can be broadly categorised into two groups,
o acyanotic heart defects ('pink' babies) :
An acyanotic heart defect is any heart defect of a group of structural congenital heart defects, approximately 75% of all congenital heart defects.
It can be subdivided into two groups depending on whether there is shunting of the blood from the left vasculature to the right (left to right shunt) or no shunting at all.
Left to right shunting heart defects include
- ventricular septal defect or VSD (30% of all congenital heart defects),
- persistent ductus arteriosus or PDA,
- atrial septal defect or ASD,
- atrioventricular septal defect or AVSD.
Acyanotic heart defects without shunting include
- pulmonary stenosis, a narrowing of the pulmonary valve,
- aortic stenosis
- coarctation of the aorta.
cyanotic heart defects ('blue' babies).
obstructive heart defects
cyanotic heart defect is a group-type of congenital heart defect. These defects account for about 25% of all congenital heart defects. The patient appears blue, or cyanotic, due to deoxygenated blood in the systemic circulation. This occurs due to either a right to left or a bidirectional shunt, allowing significant proportions of the blood to bypass the pulmonary vascular bed; or lack of normal shunting, preventing oxygenated blood from exiting the cardiac-pulmonary system (as with transposition of the great arteries).
Defects in this group include
hypoplastic left heart syndrome,
tetralogy of Fallot,
transposition of the great arteries,
tricuspid atresia,
pulmonary atresia,
persistent truncus arteriosus.
ESOPHAGUS Pathology
Congenital malformations
1. A tracheoesophageal fistula (the most prevalent esophageal anomaly) occurs most commonly as an upper esophageal blind pouch with a fistula between the lower segment of the esophagus and the trachea. It is associated with hydramnios, congenital heart disease, and other gastrointestinal malformation.
2. Esophageal atresia is associated with VATER syndrome (vertebra1 defects, anal atresia, tracheoesophageal fistula, and renal dysplasia)
3. Stenosis refers to a narrowed esophagus with a small lumen. lt may be congenital or acquired, e.g., through trauma or inflammation.
Inflammatory disorders
Esophagitis
most often involves the lower half of the esophagus. Caused by the reflux of gastric contents (juices) into the lower esophagus. One of the most common GI disorders.
Clinical features.
Patients experience substernal burning associated with regurgitation, mild anemia, dysphagia, hematemesis, and melena. Esophagitis may predispose to esophageal cancer.
Etiology
- Reflux esophagitis is due to an incompetent lower esophageal sphincter that permits reflux of gastric juice into the lower esophagus.
- Irritants such as citric acid, hot liquids, alcohol, smoking, corrosive chemicals, and certain drugs, such as tetracycline, may provoke inflammation.
- Infectious etiologies include herpes, CMV, and C. albicans. The immunocompromised host is particularly susceptible to infectious esophagitis.
Although chronic or severe reflux disease is uncommon, consequences of these conditions can lead to Barrett’s esophagus, development of a stricture, or hemorrhage.
Pathology
-Grossly, there is hyperemia, edema, inflammation, and superficial necrosis.
Complications include ulceration, bleeding, stenosis, and squamous carcinoma.
Treatment: diet control, antacids, and medications that decrease the production of gastric acid (e.g., H blockers).
Barrett's esophagus,
gastric or intestinal columnar epithelium replaces normal squamous epithelium in response to chronic reflux.- A complication of chronic gastroesophageal reflux disease.
- Histologic findings include the replacement of squamous epithelium with metaplastic columnar epithelium.
- Complications include increased incidence of esophageal adenocarcinoma, stricture formation, or hemorrhage (ulceration).
Motor disorders.
Normal motor function requires effective peristalsis and relaxation of the lower esophageal sphincter.
Achalasia is a lack of relaxation of the lower esophageal sphincter (LES), which may be associated with aperistalsis of the esophagus and increased basal tone of the LES.
Clinical features. Achalasia occurs most commonly between the ages of 30 and 50. Typical symptoms are dysphagia, regurgitation, aspiration, and chest pain. The lack of motility promotes stagnation and predisposes to carcinoma.
Hiatal hernia is the herniation of the abdominal esophagus, the stomach, or both, through the esophageal hiatus in the diaphragm.
Scleroderma is a collagen vascular disease, seen primarily in women, that causes subcutaneous fibrosis and widespread degenerative changes. (A mild variant is known as CREST syndrome which stands for calcinosis. raynaud's phenomenon , esophageal dysfunction, sclerodactyly and telengectseia. esophagus is the most frequently involved region of the gastrointestinal tract.
Clinical features are mainly dysphagia and heartburn due to reflux oesophagitis caused by aperlistalsis and incompetent LES.
Rings and webs
1. Webs are mucosal folds in the upper esophagus above the aortic arch.
2. Schatzki rings are mucosal rings at the squamocolumnarjunction below the aortic arch.
3. Plummer Vinson Syndrome consist of triad of dysphagia, atrophic glossitis, and anemia. Webs are found in the upper esophagus. The syndrome is associated specifically with iron deficiency anemia and sometimes hypochlorhydria. Patients are at increased risk for carcinoma of the pharynx or esophagus.
Mallory-Weiss syndrome
Mallory-Weiss tears refers to small mucosal tears at the gastroesophageal junction secondary to recurrent forceful vomiting. The tears occur along the long axis an result in hematemesis (sometimes massive).
- Characterized by lacerations (tears) in the esophagus.
- Most commonly occurs from vomiting (alcoholics).
- A related condition, known as Boerhaave syndrome, occurs when the esophagus ruptures, causing massive upper GI hemorrhage.
Esophageal varices
- The formation of varices (collateral channels) occurs from portal hypertension.
Causes of portal hypertension include blockage of the portal vein or liver disease (cirrhosis).
- Rupture of esophageal varices results in massive hemorrhage into the esophagus and hematemesis.
- Common in patients with liver cirrhosis.
Diverticula
are sac-like protrusions of one or more layers of pharyngeal or esophageal wall.
Tumors
- Benign tumors are rare.
- Carcinoma of the esophagus most commonly occurs after 50 and has a male:female ratio of 4.1.
Etiology: alcohal ingestion, smoking, nitrosamines in food, achalasia , web ring, Barrettes esophagus, and deficiencies of vitamins A and C , riboflavin, and some trace minerals
Clinical features include dysphagia (first to solids), retrosternal pain, anorexia, weight loss, melena, and symptoms secondary to metastases.
Pathology
- 50% occur in the middle third of the esophagus, 30% in the lower third, and 20% in the upper third. Most esophageal cancers are squamous cell carcinomas.
Adenocarcinomas arise mostly out of Barrett's esophagus.
Prognosis
is poor. Fewer than 10% of patients survive 5 years, usually because diagnosis is made at a late stage. The most common sites of metastasis are the liver and lung. The combination of cigarette smoking and alcohol is particularly causative for esophageal cancer (over l00% risk compared to nondrinkers/nonsmokers).
Cholecystitis
It is inflammation of the gall bladder. It may be acute or chronic.
In 80-90% of cases, it is associated with gall stones (Calcular cholecystis).
Causes and pathogenesis:-
Obstruction of cystic or common bile duct- By stones, strictures, pressure from the outside, tumors etc.
Obstruction , chemical irritation of the gall bladder, Secondary bacterial infection, stone formation, trauma to the wall of gall
bladder
Secondary bacterial infection
Usually by intestinal commensals E.coli, streptococcus fecalis. They reach the gall bladder by lymphatics.
S.typhi reaches the gall bladder after systemic infection
Acute cholecystitis
Gall bladder is enlarged edematous and fiery red in color.
- Wall is edematous, hyperemic, may show abscesses or gangrenous dark brown or green or black foci which may perforate.
Serous covering show fibrinosuppurative inflammation and exudation. Mucosa is edematous, hyperemic and ulcerated.
- If associated with stones, obstruction results in accumulation of pus leading to Empyaema of the gall bladder.
Fate:- Healing by fibrosis and adhesions.
Complications:-
- Pericholecystic abscess.
- Rupture leading to acute peritonitis.
- Ascending suppurative cholangitis and liver abscess
Chronic cholecystitis
May follow Acute cholecystitis or starts chronic. Gall stones are usually present.
Pathology
1. If associated with obstruction: Gall bladder is dilated. Wall may be thickened or thinned out. Contents may be clear, turbid or purulent.
2. If not associated with obstruction: - Gall bladder is contracted, wall is markedly thickened.
3. Serosa is smooth with fibrous adhesions. Draining lymph nodes are enlarged.
4. Wall is thickened, opaque and gray-white with red tinge.
5. Mucosa is gray- red with ulcerations and pouches.
6. Stones are usually present