NEET MDS Lessons
General Pathology
Viral meningitis
1. Can be caused by many different viruses, including cytomegalovirus, herpes virus, rabies, and HIV.
2. CSF fluid from a spinal tap differs from that seen in a bacterial infection. It shows mononuclear cells, higher levels of protein, and normal levels of glucose.
ANAEMIA
Definition. Reduction of the hemoglobin level below the normal for the age and sex of the patient
Classification
1. Blood loss anaemia:
- Acute.
- Chronic (results in iron deficiency).
2. Deficiency anaemia:
- Iron deficiency.
- Megaloblastic anaemia-BI2 and Folic acid deficiency.
- Protein deficiency.
- Scurvy-Vitamin C deficiency.
3. Marrow dysfunction:
- Aplastic anaemia.
- Marrow infiltration.
- Liver failure.
- Renal failure.
- Collagen diseases.
4 Increased destruction (Heamolysis)
- Due to corpuscular defects.
- Due to extra corpuscular defects
Lymphopenia:
Causes
-As part of pancytopenia.
-Steroid administration.
Blastomycosis (North American Blastomycosis; Gilchrist's Disease)
A disease caused by inhalation of mold conidia (spores) of Blastomyces dermatitidis, which convert to yeasts and invade the lungs, occasionally spreading hematogenously to the skin or focal sites in other tissues.
Pulmonary blastomycosis tends to occur as individual cases of progressive infection
Symptoms are nonspecific and may include a productive or dry hacking cough, chest pain, dyspnea, fever, chills, and drenching sweats. Pleural effusion occurs occasionally. Some patients have rapidly progressive infections, and adult respiratory distress syndrome may develop.
LUNG ABSCESS Lung abscess is a localised area of necrosis of lung tissue with suppuration.
It is of 2 types:
- Primary lung abscess that develops in an otherwise normal lung. The commonest cause is aspiration of infected material.
- Secondary lung abscess that develops as a complication of some other disease of the lung or from another site
ETIOPATHOGENESIS.
The microorganisms commonly isolated from the lungs in lung abscess are streptococci, staphylococci and various gram-negative organisms. These are introduced into the lungs from one of the following mechanisms:
1. Aspiration of infected foreign material.
2. Preceding bacterial infection.
3. Bronchial obstruction.
4. Septic embolism.
5. Miscellaneous (i) Infection in pulmonary infarcts, (ii) Amoebic abscesses, (iii) Trauma to the lungs. (iv) Direct extension from a suppurative focus.
Abscesses may be of variable size from a few millimeters to large cavities, 5 to 6 cm in diameter. The cavity often contains exudate. An acute lung abscess is initially surrounded by acute pneumonia and has poorly-defined ragged wall. With passage of time, the abscess becomes chronic and develops fibrous wall.
Microscopic Examination
The characteristic feature is the destruction of lung parenchyma with suppurative exudate in the lung cavity. The cavity is initially surrounded by acute inflammation in the wall but later there is replacement by exudate of lymphocytes, plasma cells and macrophages. In more chronic cases, there is considerable fibroblastic proliferation forming a fibrocollagenic wall.
Chemical 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.
Systemic Candidiasis (Candidosis; Moniliasis)
Invasive infections caused by Candida sp, most often C. albicans, manifested by fungemia, endocarditis, meningitis, and/or focal lesions in liver, spleen, kidneys, bone, skin, and subcutaneous or other tissues.
Infections due to Candida sp account for about 80% of all major systemic fungal infections.
Symptoms and Signs
Esophagitis is most often manifested by dysphagia. Symptoms of respiratory tract infections are nonspecific, such as cough. Vaginal infections cause itching, burning, and discharge. Candidemia usually causes fever, but other symptoms are typically nonspecific. Sometimes, a syndrome develops resembling bacterial sepsis, with a fulminating course that may include shock, oliguria, renal shutdown, and disseminated intravascular coagulation.
Hematogenous endophthalmitis starts as white retinal plaques that can cause blindness as destructive inflammation progresses, extending to opacify the vitreous and causing potentially irreversible scarring. Most often, there are no symptoms in early stages of Candida endophthalmitis. If treatment is not begun before symptoms appear, significant or even total loss of vision is likely to occur in the affected eye. In neutropenic patients, eye involvement is more often manifested by retinal hemorrhages; papulonodular, erythematous, and vasculitic skin lesions may also develop.