📖 General Pathology
Eczematous Dermatitis
General PathologyEczematous 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.
Chemical Mediators In Inflammation
General PathologyChemical Mediators In Inflammation
Can be classified as :
A. Neurogenic
Also called the Triple Response of Lewis. It involves neurogenic vasodilatation of arterioles due to antidromic axon reflex arc. The constituents of the response are:
1. arteriolar vasoconstriction followed by
2. arteriolar vasodilatation
3. swelling
B. Chemical
1. Amines: Histamine and 5 hydroxytryptamine. Released from platelets and mast cells.
Actions: Immediate and short lived.
Dilatation of arterioles.
Increased capillary premeability.
Kinins: Bradykinin and kallidin These are present in inactive from and are activated by kinin forming proteases
Actions:
Arteriolar dilatation.
Increased vascular permeability
Pain
Kinin forming proteases Plasmin and Kallikrein. Present as inactive precursors.
Cleavage products of complement C3a und C5a are called anaphylatoxins
Actions:
Histamine release from mast cells
Chemotaxis (also C567 )
Enhance phagocytosis.
Polymorph components
Cationic: proteins which cause
Increased permeability
Histamine release.
Chemotaxis of monocytes
Neutral proteases which:
Cleave C3 and C5 to active form
Convert Kininogen to Kinin
Increase permeability.
Acid proteases which liberate leucokinins
Slow reacting. substance of anaphylaxis: (SRS-A) is a lipid released from mast cell.
Action --Increases vascular permeability
Prostaglandins: E1 + E2 .
Platelets are rich source
Action:
Platelets are a rich source.
Vasodilatation.
Increased permeability.
Pain.
VIII. Miscellaneous: like
Tissue lactic acid.
Bacterial toxins.
Parkinson’s disease
General PathologyParkinson’s disease
a. Characterized by the degeneration of neurons in the basal ganglia, specifically the substantia nigra and striatum.
b. Histologic findings in affected neurons include Lewy bodies.
c. Clinically, the disease affects involuntary and voluntary movements. Tremors are common. Symptoms include pin-rolling tremors, slowness of movements, muscular rigidity, and shuffling gait.
VIRAL DISEASES -RABIES
General PathologyVIRAL DISEASES
RABIES (Hydrophobia)
An acute infectious disease of mammals, especially carnivores, characterized by CNS pathology leading to paralysis and death.
Etiology and Epidemiology
Rabies is caused by a neurotropic virus often present in the saliva of rabid animals
Pathology
The virus travels from the site of entry via peripheral nerves to the spinal cord and the brain, where it multiplies; it continues through efferent nerves to the salivary glands and into the saliva.
microscopic examination shows perivascular collections of lymphocytes but little destruction of nerve cells. Intracytoplasmic inclusion bodies (Negri bodies), usually in the cornu Ammonis, are pathognomonic of rabies, but these bodies are not always found.
Sign/Symptoms
In humans, the incubation period varies from 10 days to > 1 yr and averages 30 to 50 days.
Rabies commonly begins with a short period of depression, restlessness, malaise, and fever. Restlessness increases to uncontrollable excitement, with excessive salivation and excruciatingly painful spasms of the laryngeal and pharyngeal muscles. The spasms, which result from reflex irritability of the deglutition and respiration centers, are easily precipitated Hysteria due to fright
Prognosis and Treatment
Death from asphyxia, exhaustion, or general paralysis usually occurs within 3 to 10 days after onset of symptoms