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General Pathology

HERPES SIMPLEX

An infection with herpes simplex virus characterized by one or many clusters of small vesicles filled with clear fluid on slightly raised inflammatory bases.

The two types of herpes simplex virus (HSV) are HSV-1 and HSV-2. HSV-1 commonly causes herpes labialis, herpetic stomatitis, and keratitis; HSV-2 usually causes genital herpes, is transmitted primarily by direct (usually sexual) contact with lesions, and results in skin lesions

Primary infection of HSV-1 typically causes a gingivostomatitis, which is most common in infants and young children. Symptoms include irritability, anorexia, fever, gingival inflammation, and painful ulcers of the mouth.

Primary infection of HSV-2 typically occurs on the vulva and vagina or penis in young adults

Herpetic whitlow, a swollen, painful, and erythematous lesion of the distal phalanx, results from inoculation of HSV through a cutaneous break or abrasion and is most common in health care workers.

DEGENERATION

Definition:   Reversible cell injury.

(1) Water accumulation in the form   of 

(i)          Cloudy   swelling.

(ii)         Vacuolar   degeneration.

.(ill)        Hydropic   degeneration.

This change  is commonly   seen  in parenchymal   cells  e.g.  kidneys.

Gross appearance: The organ is swollen, soft and pale.

Microscopic appearance: Cells show varying degrees of swelling. Cytoplasm may be granular, vacuolated, homogenously pale and ballooned out.     

(2)  Fatty   change An excessive,   demonstrable accumulation of fat  is common   in  parenchymal cells of liver  and heart

In the liver, it can be due to:   .

(i) Excess  fat  entry  into  the  liver  as occurs  in  starvation  and  in  steroid excess due to mobilization from stores.

(ii) Excess triglyceride formation

(iii) Reduced phosphorlyation  of fat.  

(iv) Decreased release as lipoprotein due to protein deficiency.

Causes

(i) Hypoxia  as  in severe  anaemia  and  venous  stasis

(ii) Protein  malnutrition.

(iii) Hepatotoxins like CCl4.

(iv) Alcoholism

(v) Metabolic defects like Diabetes mellitus

(vi) Infections.

Gross appearance: The organ is enlarged, soft and greasy, with a pale yellowish colour. It may involve the organ uniformly or patchily ( thrush breast or tabby cat heart)

Microscopic appearance: The cells contain clear vacuoles (stainable by fat-sudan  stains on frozen sections). These may be small and dispersed or large, displacing the nucleus peripherally. Several such cells may fuse to form fat cysts.

(3) Hyaline degeneration

In alcoholic liver damage, the cytoplasmic organelles are damaged and give the cytoplasm a deep eosinophilic staining-Mallory hyaline.

Polycystic kidney disease

Characterized by the formation of cysts and partial replacement of renal parenchyma.
Genetic transmission: autosomal dominant.
Clinical manifestations:

 hypertension, hematuria, palpable renal masses, and progression to renal failure. Commonly associated with berry
aneurysms. 

Hepatitis D virus—can only infect cells previously infected with hepatitis B. 
 Delta hepatitis (HDV) is associated with a 35-nm RNA virus composed of a delta antigen-bearing core surrounded by HBV's Ag coat;

HDV requires HBV for replication.

Delta hepatitis can cause quiescent HBV states to suddenly worsened . Its transmission is the same as that of HBV.
 
 Hepatitis E virus—a high mortality rate in infected pregnant women.

Hepatitis E (HEV) is caused by a single-stranded RNA virus. The disease is typically self-limited and does not evolve into chronic hepatitis; it may, however, be cholestatic.

Pregnant women may develop fulminant disease.

Transmission is by the fecal oral route.

HEV occurs mainly in India, Nepal, Pakistan, and Southeast Asia.
 

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).

Nephrolithiasis, urolithiasis

Formation of calculi (calcium stones) in the kidney (nephrolithiasis) or urinary tract (urolithiasis).
Commonly associated with hyperparathyroidism.
Signs and symptoms 

urinary tract obstruction, severe pain, and pyelonephritis.

Note: an enlarged prostate can also cause urinary tract obstruction in males.

Peutz-Jeghers syndrome
1. Lesions appear as small, melanotic, and freckle-like. They can be found on the skin, oral mucosa, lips, feet, and hands. 
2. May also present with intestinal polyps, which may develop into a gastrointestinal carcinoma. 
3. Genetic transmission: autosomal dominant.

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