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General Pathology - NEETMDS- courses
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General Pathology

PERTUSSIS (Whooping Cough)

An acute, highly communicable bacterial disease caused by Bordetella pertussis and characterized by a paroxysmal or spasmodic cough that usually ends in a prolonged, high-pitched, crowing inspiration (the whoop).

Transmission is by aspiration of B. pertussis

Symptoms and Signs

The incubation period averages 7 to 14 days (maximum, 3 wk). B. pertussis invades the mucosa of the nasopharynx, trachea, bronchi, and bronchioles, increasing the secretion of mucus, which is initially thin and later viscid and tenacious. The uncomplicated disease lasts about 6 to 10 wk and consists of three stages: catarrhal, paroxysmal, and convalescent.

Pathology

The branch of medicine dealing with the essential nature of disease, especially changes in body tissues aorgans that cause or are caused by disease. Pathology is the structural and functional manifestations of disease.

 


Anatomic pathology  the anatomical study of changes in the function, structure, or appearance of organs or tissues,including postmortem examinations and the study of biopsy specimens.

Cellular pathology  - Cytopathology is a diagnostic technique that examines cells from various body sites to determine the cause or the nature of disease.

Clinical pathology  pathology applied to the solution of clinical problems, especially the use of laboratory 

methods inclinical diagnosis.

Comparative pathology  that which considers human disease processes in comparison with those of other 

animals.

Oral pathology  that treating of conditions causing or resulting from morbid anatomic or functional changes in thestructures of the mouth.

Surgical pathology  the pathology of disease processes that are surgically accessible for diagnosis or treatment.

Enterococci

Most common are E. fecalis and E. fecium.  Cause inflammation at site of colonization.

Serious resistance to antibiotics.  E. fecium is now a vancomycin resistant enterococcus (VRE)

Acute pericarditis

1. Characterized by inflammation of the pericardium.
2. Causes include:
a. Viral infection.
b. Bacterial infection, including Staphylococcus, Pneumococcus.
c. Tuberculosis.
d. MI.
e. Systemic lupus erythematosus.
f. Rheumatic fever.

3. Signs and symptoms include:
a. Pericardial friction rub on cardiac auscultation.
b. Angina.
c. Fever.

4. Consequences include constrictive pericarditis,which results from fusion and scarring of the pericardium. This may lead to the restriction of ventricular expansion, preventing the heart chambers from filling normally.

NECROSIS

Definition: Necrosis is defined as the morphologic changes caused by the progressive degradative
action of enzymes on the lethally injured cell.

These changes are due to
I. Autolysis and
2. Heterolysis.

The cellular changes of necrosis i.e. death of circumscribed group of cells in continuity with living tissues are similar to changes in tissues following somatic death, except that in the former, there is leucocytic infiltration in reaction to the dead cells and the lytic
enzymes partly come from the inflammatory cell also. (Heterolysis). Cell death occurs in the normal situation of cell turnover also and this is called apoptosis-single cellular dropout.

Nuclear changes in necrosis

As cytoplasmic changes are a feature of degeneration ,similarly nuclear changes are the hallmark of necrosis. These changes are:
(i) Pyknosis –condensation of chromatin
(ii) Karyorrhexis - fragmentation
(iii) Karyolysis - dissolution


Types of necrosis

(1) Coagulative necrosis: Seen in infarcts. The architectural outlines are maintained though structural details are lost. E.g, myocardial infarct.
(2) Caseous necrosis: A variant of coagulative necrosis seen in tuberculosis. The architecture is destroyed, resulting in an  eosinophilic amorphous debris.
(3) Colliquative (liquifactive). Necrosis seen in Cerebral infarcts and suppurative necrosis.

Gangrenous necrosis: It is the necrosis with superadded putrefaction

May be:
a. dry - coagulative product.
b. Wet - when there is bacterial liquifaction.

Fat necrosis

May be:
a. Traumatic (as in breast and subcutaneous tissue).
b Enzymatic (as in pancreatitis). It shows inflammation of fat with formation of lipophages and giant cells.

This is often followed by deposition of calcium as calcium soaps.

Hyaline necrosis: Seen in skeletal muscles in typhoid and in liver ceIs in some forms of hepatitis.

Fibrinoid necrosis: In hypertension and in immune based diseases.
 

 Staphylococcal aureus
 - cutaneous infections
  
 - furuncles (boils)
    - carbuncles (more complicated furuncle with multiple sinuses)
    - impetigo (often mixed with Streptococcus and has a more bullous appearance than crusted)
    - hidradenitis suppurative (abscess of apocrine glands→e.g., axilla)
    - nail bed (paronychial infection) 
    - postoperative wound or stitch abscess
    - postpartum breast abscesses 
 
toxin related skin rashes

 - infants and young children develop toxic epidermal necrolysis or Ritter's syndrome (scalded baby syndrome)→large, red areas of denuded skin and generalized bulla formation.
 - toxic shock syndrome (TSS) is due to a toxin producing strain of Staphylococcus aureus (bacteriophage induced) usually, but not exclusively in tampon wearing (hyperabsorbent type), menstruating women; 1-4 day prodrome of high fever, myalgias, arthralgias, mental confusion, diarrhea and on erythematous rash that occurs during or soon after menses; rash predominantly on hands and feet with eventual desquamation in 5-12 days. 

CONGESTION

Congestion or hyperaemia means an increase in the content of blood in an organ. It may be :

A. Active - due to increased arterial flow to the organ with dilatation of micro vessels as in

  • Inflammation.
  • Increased metabolic activity.
  • Neurogenic blushing.

B. Passive - due to decreased venous drainage resulting in pooling of blood. There is always an associated element of oedema.

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