NEET MDS Lessons
General Pathology
TOXOPLASMOSIS
Infection with Toxoplasma gondii, causing a spectrum of manifestations ranging from asymptomatic benign lymphadenopathy to life-threatening CNS disease, chorioretinitis, and mental retardation.
Symptomatic infections may present in several ways
Acute toxoplasmosis may mimic infectious mononucleosis with lymphadenopathy, fever, malaise, myalgia, hepatosplenomegaly, and pharyngitis. Atypical lymphocytosis, mild anemia, leukopenia, and slightly abnormal liver function tests are common. The syndrome may persist for weeks or months but is almost always self-limited.
A severe disseminated form characterized by pneumonitis, myocarditis, meningoencephalitis, polymyositis, diffuse maculopapular rash, high fevers, chills, and prostration. Acute fulminating disease is uncommon.
Congenital toxoplasmosis usually results from a primary (and often asymptomatic) acute infection acquired by the mother during pregnancy. The risk of transplacental infection increases from 15% to 30 to 60% for maternal infections acquired in the 1st, 2nd, or 3rd trimester of gestation, respectively
Nephrolithiasis, urolithiasis
Formation of calculi (calcium stones) in the kidney (nephrolithiasis) or urinary tract (urolithiasis).
Commonly associated with hyperparathyroidism.
Signs and symptoms
urinary tract obstruction, severe pain, and pyelonephritis.
Note: an enlarged prostate can also cause urinary tract obstruction in males.
The Specific Immune Response
Definition
The immune response comprises all the phenomenon resulting from specific interaction of cells of the immune-system with antigen. As a consequence of this interaction cells appear that mediate cellular immune response as well cells that synthesis and secrete immunoglobulins
Hence the immune response has 2 components.
1. Cell mediated immunity (CMI).
2:. Humoral immunity (antibodies)
(I) Macrophages. Constituent of the M. P. S. These engulf the antigenic material.
(i) Most of the engulfed antigen is destroyed to' prevent a high dose paralysis of the Immune competent cells.
(ii) Some of it persists in the macrophage, retaining immunogenecity for continued stimulus to the immune system.
(iii)The antigenic information is passed on to effectors cells. There are two proposed mechanisms for this:
(a) As messenger RNA with code for the specific antibody.
(b) As antigen-RNA complexes.
(2) Lymphocytes. There are 2 main classes recognized by surface characteristics.
(A) T-Lymyhocytes (thymus dependant) :- These are responsible for cellular immunity . On exposure to antigen
- They transform to immunoblasts which divide to form the effectors cells.
- They secrete lymphokines These are
- Monocyte migration inhibition factor
- Macrophage activation factor
- Chemotactic factor
- Mitogenic factor
- Transfer factor
- Lymphotoxin which kills target cell
- Interferon.
- Inflammatory factor which increases permeability. .
- Some remain as 1onglived memory cell for a quicker recognition on re-exposure
- They also modify immune response by other lymphocytes in the form of “T – helper cells “ and “T-suppressor” cells
- They are responsible for graft rejection
(B) B-Lymphocytes (Bursa dependent). In birds the Bursa of Fabricious controls
these cells. In man, its role is taken up by," gut associated lymphoid tissue)
(i) They are responsible for antibody synthesis. On stimulation they undergo blastic transformation and then differentiation to plasma cells, the site of immunoglobulin synthesis.
(ii) They also form memory cells. But these are probably short lived.
(C) In addition to T & B lymphocytes, there are some lymphocytes without the surface markers of either of them. These are 'null' cells-the-natural Killer (N,K.) cells and cells responsible for antibody dependent cellular-cytotoxicity.
(3) Plasma cells. These are the effectors cells of humoral immunity. They produce the immunoglobins, which are the effector molecules.
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.
Infections caused by gonorrhea
1. Acute urethritis. Mostly in males. Generally self-limiting. Dysuria and purulent discharge.
2. Endocervical infection. Purulent vaginal discharge, abnormal menses, pelvic pain. Often co-infection with other STD’s. Some women are asymptomatic.
3. Pelvic Inflammatory Disease (PID). Consequence of ascending endocervical infection. Causes salpingitis, endometriosis, bilateral abdominal pain, discharge, fever. May lead to sterility, chronic pain, and ectopic pregnancy because of loss of fallopian cilia.
4. Anorectal inflammation. Mostly in homosexual men. Pain, itching, discharge from anus.
5. Dermatitis/arthritis. Occurs after bacteremia. Skin will have papules on an erythematous base which develop into necrotic pustules. Asymmetric joint pain. These infections are susceptible to penicillin.
6. Neonatal infections. Ophthalmia neonatorum is a conjunctival infection from going through infected vagina. After one year of age, suspect child abuse.
Lymphomas
A. Hodgkin’s disease
1. Characterized by enlarged lymph nodes and the presence of Reed-Sternberg cells (multinucleated giant cells) in lymphoid tissues.
2. Disease spreads from lymph node to lymph node in a contiguous manner.
3. Enlarged cervical lymph nodes are most commonly the first lymphadenopathy observed.
4. The cause is unknown.
5. Occurs before age 30.
6. Prognosis of disease depends largely on the extent of lymph node spread and systemic involvement.
B. Non-Hodgkin’s lymphoma
1. Characterized by tumor formation in the lymph nodes.
2. Tumors do not spread in a contiguous manner.
3. Most often caused by the proliferation of abnormal B cells.
4. Occurs after age 40.
5. Example: Burkitt’s lymphoma
a. Commonly associated with an EpsteinBarr virus (EBV) infection and a genetic mutation resulting from the translocation of the C-myc gene from chromosome 8 to 14.
b. The African type occurs in African children and commonly affects the mandible or maxilla.
c. In the United States, it most commonly affects the abdomen.
d. Histologically, the tumor displays a characteristic “starry-sky” appearance.
Paroxysmal nocturnal haemoglobinuria (PNH).
Feature:
- Acquired RBC rnembrane defect rendering it susceptible to complement lysis.
- Features of intravascular haemolysis.
- Blood picture of haemolysis anemais with pancytopenia.
- Ham’s acid serum test (lysis at 37COin acid pH) + ve