NEET MDS Lessons
General Pathology
Chronic hepatitis
Chronic hepatitis occurs in 5%-10% of HBV infections and in well over 50% of HCV; it does not occur in HAV. Most chronic disease is due to chronic persistent hepatitis. The chronic form is more likely to occur in the very old or very young, in males, in immunocompromised hosts, in Down's syndrome, and in dialysis patients.
a. Chronic persistent hepatitis is a benign, self-limited disease with a prolonged recovery. Patients are asymptomatic except for elevated transaminases.
b. Chronic active hepatitis features chronic inflammation with hepatocyte destruction, resulting in cirrhosis and liver failure.
(1) Etiology. HBV, HCV, HDV, drug toxicity, Wilson's disease, alcohol, a,-antitrypsin deficiency, and autoimmune hepatitis are common etiologies.
(2) Clinical features may include fatigue, fever, malaise, anorexia, and elevated liver function tests.
(3) Diagnosis is made by liver biopsy.
8. Carrier state for HBV and HCV may be either asymptomatic or with liver disease; in the latter case, the patient has elevate transaminases.
a. Incidence is most common in immunodeficient, drug addicted, Down's syndrome, and dialysis patients.
b. Pathology of asymptomatic carriers shows "ground-glass"" hepatocytes with finely granular eosinophilic cytoplasm.
Bacterial meningitis (pyogenic, suppurative infections)
1. Common causes include:
a. Escherichia coli in newborns.
b. Haemophilus influenzae in infants and children.
c. Neisseria meningitides in young adults.
d. Streptococcus pneumoniae and Listeria monocytogenes in older adults.
Clinical findings include severe headache, irritability, fever, and a stiff neck.
a. A spinal tap shows CSF fluid that is cloudy or purulent and is under increased pressure. There is also an increase in protein and a decrease in glucose levels.
3. Can be fatal if left untreated.
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.
Diseases from Str. pyogenes (Group A strep)
1. Streptococcal pharyngitis. Most frequent Group A infection. Throat has gray-white exudate. Infection may become systemic into blood, sinuses, jugular vein, meninges. In less than a week the M-protein and capsule production decrease, and transmission declines.
2. Skin infections, such as impetigo. Especially in children. Different M-proteins than in pharyngitis. Skin infections associated with edema and red streaking (characteristic).
3. Necrotizing fasciitis/myositis. Infection of deeper tissue advances despite antibiotics.
4. Scarlet fever. Caused by phage-associated erythrogenic toxin-producing strains. Toxins cause cardiac, renal, and other systemic failures. Rash is very red with a sand-papery feel and shedding of superficial skin.
5. Toxic Shock Syndrome. Parallels the toxic shock caused by TSST-carrying Staph. aureus.
6. Non-suppurative, post-infection diseases.
Rheumatic fever (myocarditis, cardiac valve disease, polyarthralgia, rashes. Occurs two weeks after a pharyngeal infection)
Glomerulonephritis (Occurs two weeks after pharyngeal or skin infections. Often due to immunologic reaction to M-protein type 12)
Parkinson’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.
SPIROCHETAL DISEASE
Syphilis
A contagious systemic disease caused by the spirochete Treponema pallidum, characterized by sequential clinical stages and by years of latency.
ACQUIRED SYPHILIS
T. pallidum is a delicate spiral organism about 0.25 µm wide and from 5 to 20 µm long, identified by characteristic morphology and motility with a darkfield microscope or fluorescent techniques
In acquired syphilis, T. pallidum enters through the mucous membranes or skin, reaches the regional lymph nodes within hours, and rapidly disseminates throughout the body. In all stages of disease, perivascular infiltration of lymphocytes, plasma cells, and, later, fibroblasts causes swelling and proliferation of the endothelium of the smaller blood vessels, leading to endarteritis obliterans.
In late syphilis, T. pallidum elicits a granulomatous-like (gummatous) reaction causing masses, ulcerations, and necrosis. Inflammation may subside despite progressive damage, especially in the cardiovascular and central nervous systems.
The CNS is invaded early in the infection. During the secondary stage of the disease, > 30% of patients have abnormal CSF and may have symptoms of meningitis
Symptoms, Signs, and Course
The incubation period of primary syphilis can vary from 1 to 13 wk but is usually from 3 to 4 wk. The disease may present at any stage and long after the initial infection
Primary stage: The primary lesion, or chancre generally evolves and heals within 4 to 8 wk in untreated patients. After inoculation, a red papule quickly erodes to form a painless ulcer with an indurated base that, when abraded, exudes a clear serum containing numerous spirochetes
The regional lymph nodes usually enlarge painlessly and are firm, discrete, and nontender. Chancres occur on the penis, anus, and rectum in men and on the vulva, cervix, and perineum in women. Chancres may also occur on the lips or the oropharyngeal or anogenital mucous membranes.
Secondary stage: Cutaneous rashes usually appear within 6 to 12 wk after infection and are most florid after 3 to 4 mo.
Frequently, generalized, nontender, firm, discrete lymphadenopathy and hepatosplenomegaly are palpable. Over 80% of patients have mucocutaneous lesions, 50% have generalized lymphadenopathy, and about 10% have lesions of the eyes (uveitis), bones (periostitis), joints, meninges, kidneys (glomerulitis), liver, and spleen.
Acute syphilitic meningitis may develop, with headache, neck stiffness, cranial nerve lesions, deafness, and, occasionally, papilledema.
Condyloma lata--hypertrophic, flattened, dull pink or gray papules at the mucocutaneous junctions and in moist areas of the skin--are extremely infectious. Hair often falls out in patches, leaving a moth-eaten appearance (alopecia areata).
Latent stage
In the early latent period (< 2 yr after infection), infectious mucocutaneous relapses may occur, but after 2 yr contagious lesions rarely develop, and the patient appears normal. About 1/3 of untreated persons develop late syphilis
Late or tertiary stage: Lesions may be clinically described as (1) benign tertiary syphilis of the skin, bone, and viscera, (2) cardiovascular syphilis, or (3) neurosyphilis.
The typical lesion is a gumma, an inflammatory mass that evolves to necrosis and fibrosis and that is frequently localized but may diffusely infiltrate an organ or tissue
Benign tertiary syphilis of the bones results in either periostitis with bone formation or osteitis with destructive lesions causing a deep, boring pain, characteristically worse at night. A lump or swelling may be palpable.
Cardiovascular syphilis: A dilated, usually fusiform aneurysm of the ascending or transverse aorta, narrowing of the coronary ostia, or aortic valvular insufficiency usually appears 10 to 25 yr after the initial infection
Neurosyphilis
In meningovascular neurosyphilis, brain involvement is signaled by headache, dizziness, poor concentration, lassitude, insomnia, neck stiffness, and blurred vision. Mental confusion, epileptiform attacks, papilledema, aphasia, and mono- or hemiplegia may also occur
Diagnosis:
Two classes of serologic tests for syphilis (STS) aid in diagnosing syphilis and other related treponemal diseases: screening, nontreponemal tests using lipoid antigens detect syphilitic reagin and include the Venereal Disease Research Laboratory (VDRL) and the rapid plasma reagin (RPR) tests. Specific treponemal tests detect antitreponemal antibodies and include fluorescent treponemal antibody absorption (FTA-ABS) test, microhemagglutination assay for antibodies to T. pallidum (MHA-TP), and Treponema pallidum hemagglutination assay (TPHA).
In darkfield microscopy, light is directed obliquely through the slide so that rays striking the spirochetes cause them to appear as bright, motile, narrow coils against a dark background
Plasma Cell Pathology
A. Multiple myeloma
1. Plasma cell neoplasm that results in the proliferation of monoclonal plasma cells. These tumor cells produce nonfunctional immunoglobulins.
2. Laboratory findings include:
a. Monoclonal IgG spike.
b. Bence-Jones proteins found in urine.
3. Radiographic findings: characteristic “punched-out” radiolucencies in bones.