NEET MDS Lessons
General Pathology
N. meningiditis
Major cause of fulminant bacteremia and meningitis. Has a unique polysaccharide capsule. It is spread person to person by the respiratory route. Frequently carried in nasopharynx, and carriage rates increased by close quarters. Special risk in closed populations (college dorms) and in people lacking complement. Sub-saharan Africa has a “meningitis belt.”
Pathogenesis is caused by adherence factors that attach to non-ciliated nasopharyngeal epithelium. These factors include pili which promote the intial epithelial (and erythrocyte) attachment, and Opa/Opc surface binding proteins.
Adherence stimulates engulfment of bacteria by epithelial cells. Transported to basolateral surface.
The polysaccharide capsule is a major virulence factor that prevents phagocytosis and lysis.
A lipo-oligosaccharide endotoxin also contributes to sepsis.
EMBOLISM
Definition: transportation of an abnormal mass of an abnormal mass of undissolved material from one part of circulation to another. The mass transported is called embolus.
Types
I .Thrombi and clots.
2. Gas or air.
3. Fat
4.Amniotic fluid.
5.Tumour
Thromboembolism
This is the commonest type of embolus and may be formed of the primary thrombus or more often of propagated clot region which is loosely attached.
Emboli from venous thrombi can result In impaction in the pulmonary arteries and result in sudden death.
Embolism from cardiac or arterial thrombi results in systemic embolism causing infraction and gangrene.
Gaseous
This occurs when gas is introduced into the circulation:
• Accidental opening of large veins during surgery.
• Mismanaged transfusion. .
As air is readily absorbed into blood only sudden introduction or large quantities of air produces effects
Caisson’s Disease bubbling of nitrogen from the blood during sudden decompression as seen during deep sea diving.
Fat Embolism
Causes
• Fractures especially of long bones and multiple
• Crush injuries.
Sites of impaction:
o Lungs.
o Systemic: causing -
→ petechial skin haemorrhages.
→ Embolism to brain leading to coma and death.
→ Conjunctival and retinal haemorrhages
Tumor Embolism.
Invasion of vascular channe1.s is a feature of malignant neoplasms and this leads to:
• Metastatic deposits,
• DlC
Q Fever
An acute disease caused by Coxiella burnetii (Rickettsia burnetii) and
characterized by sudden onset of fever, headache, malaise, and interstitial
pneumonitis.
Symptoms and Signs
The incubation period varies from 9 to 28 days and averages 18 to 21 days. Onset
is abrupt, with fever, severe headache, chills, severe malaise, myalgia, and,
often, chest pains. Fever may rise to 40° C (104° F) and persist for 1 to > 3
wk. Unlike other rickettsial diseases, Q fever is not associated with a
cutaneous exanthem. A nonproductive cough and x-ray evidence of pneumonitis
often develop during the 2nd wk of illness.
In severe cases, lobar consolidation usually occurs, and the gross appearance of
the lungs may resemble that of bacterial pneumonia
About 1/3 of patients with protracted Q fever develop hepatitis, characterized
by fever, malaise, hepatomegaly with right upper abdominal pain, and possibly
jaundice. Liver biopsy specimens show diffuse granulomatous changes, and C.
burnetii may be identified by immunofluorescence.
Acne vulgaris is a chronic inflammatory disorder usually present in the late teenage years characterized by comedones, papules, nodules, and cysts.
- subdivided into obstructive type with closed comedones (whiteheads) and open comedones (blackheads) and the inflammatory type consisting of papules, pustules, nodules, cysts and scars.
- pathogenesis of inflammatory acne relates to blockage of the hair follicle with keratin and sebaceous secretions, which are acted upon by Propionibacterium acnes (anaerobe) that causes the release of irritating fatty acids resulting in an inflammatory response.
- pathogenesis of the obstructive type (comedones) is related to plugging of the outlet of a hair follicle by keratin debris.
- chocolate, shellfish, nuts iodized salt do not aggravate acne.
- obstructive type is best treated with benzoyl peroxide and triretnoin (vitamin A acid)
- treatment of inflammatory type is the above plus antibiotics (topical and/or systemic; erythromycin, tetracycline, clindamycin).
DIPHTHERIA
An acute, contagious disease caused by Corynebacterium diphtheriae, characterized by the formation of a fibrinous pseudomembrane, usually on the respiratory mucosa, and by myocardial and neural tissue damage secondary to an exotoxin.
Cutaneous diphtheria (infection of the skin) can occur when any disruption of the integument is colonized by C. diphtheriae. Lacerations, abrasions, ulcers, burns, and other wounds are potential reservoirs of the organism. Skin carriage of C. diphtheriae is also a silent reservoir of infection.
Pathology
C. diphtheriae may produce exotoxins lethal to the adjacent host cells. Occasionally, the primary site is the skin or mucosa elsewhere. The exotoxin, carried by the blood, also damages cells in distant organs, creating pathologic lesions in the respiratory passages, oropharynx, myocardium, nervous system, and kidneys.
The myocardium may show fatty degeneration or fibrosis. Degenerative changes in cranial or peripheral nerves occur chiefly in the motor fibers
In severe cases, anterior horn cells and anterior and posterior nerve roots may show damage proportional to the duration of infection before antitoxin is given. The kidneys may show a reversible interstitial nephritis with extensive cellular infiltration.
The diphtheria bacillus first destroys a layer of superficial epithelium, usually in patches, and the resulting exudate coagulates to form a grayish pseudomembrane containing bacteria, fibrin, leukocytes, and necrotic epithelial cells. However, the areas of bacterial multiplication and toxin absorption are wider and deeper than indicated by the size of the membrane formed in the wake of the spreading infection.
Amyotrophic lateral sclerosis (Lou Gehrig’s disease)
a. Characterized by the rapid degeneration of motor neurons in the spinal cord and corticospinal tracts.
b. More common in men in their 50s.
c. Clinically, the disease results in rapidly progressive muscle atrophy due to denervation. Other symptoms include fasciculations, hyperreflexia, spasticity, and pathologic reflexes. Death usually occurs within a few years from onset, usually by respiratory failure or infection.
Aplasticanaemia and pancytopenia.
Aplastic anaemia is a reduction in all the formed elements of blood due to marrow hypoplasia.
Causes
- Primary or Idiopathic.
- Secondary to :
1 Drugs :
Antimetabolites and antimitotic agents.
Antiepileptics.
Phenylbutazone.
Chloramphenicol.
2 Industrial chemicals.
Benzene.
DDT and other insecticides.
TNT (used in explosives).
3 Ionising radiation
- Familial aplasia
Pancytopenia (or reduction in the formed elements of blood) can be caused by other conditions also like:
-Subleukaemic acute leukaemia.
-Megaloblastic anaemia
-S.L.E.
-hypersplenism.
-Marrow infiltration by lymphomas metastatic deposits, tuberculosis, myeloma etc
Features:
- Anaemia.
- Leucopenia upper respiratory infections.
- Thrombocytopenis :- petechiae and bruising.
Blood picture:
- Normocytic normochromic anaemia with minimal anisopoikilocytosis in aplastic anaemia. Other causes of pancytopenia may show varying degrees of anisopoikilocytosis
- Neutropenia with hypergranulation and high alkaline phosphatase.
- Low platelet counts
Bone marrow:
- Hypoplastic (may have patches of norm cellular or hyper cellular marrow) which may -> dry tap. .
- Increase in fat cells , fibroblasts , reticulum cells, lymphocytes and plasma cells
- Decrease in precursors of all three-Series.
- Underlying cause if any, of pancytopenia may be seen