NEET MDS Lessons
General Pathology
Anemia (Disorder of Hematopoietic System) - Probably the most common effect of nutritional deficiency. Any factor that decreases hematopoiesis can cause an anemia.
A. Iron deficiency - Widely recognized as the most important cause of anemia, It is indicated that ½ of all pregnant women and infants are affected, as are ~13% of all adult women.
1. Dietary factors - Availability of iron from different food sources and mixtures.
2. Malabsorption – One third of patients with inflammatory bowel disease (IBD) have recurrent anemia and 30% or more of patients who have had partial gastrectomy will develop iron deficiency anemia.
3. Blood loss - Menses, gastrointestinal bleeding
4. Increased demand - Pregnancy, growth in children.
5. Congenital - Atransferrinemia
6. Importance of multiple factors.
7. Pathophysiology - Initially iron is mobilized from reticuloendothelial stores and increased intestinal absorption occurs. Total iron stores are depleted, serum iron levels fall. In severe cases in peripheral blood, the red cells become smaller (microcytic) and their hemoglobin content is reduced (hypochromic).
B. Megaloblastic anemias- Characterized by the presence of abnormal WBCs and RBCs. In severe cases, megaloblasts (abnormal red cell precursors) may be present. These anemias are a consequence of disordered DNA synthesis.
1. Folate deficiency - Can be caused by:
a. Dietary deficiency
b. Malabsorption (celiac disease)
c. Increased demand (pregnancy & lactation)
d. Drugs - methotrexate, anticonvulsants, oral contraceptives, alcoholism.
e. Liver disease
2. Cobalamin (vitamin B12) deficiency - Almost always a secondary disorder that can be caused by:
a. Intrinsic factor deficiency (pernicious anemia due to autoimmune destruction of the gastric mucosa)
b. Malabsorption
3. Pyridoxine (vitamin B6) deficiency- most commonly associated with alcoholism.
C. Other factors known to be frequently associated with anemia would include protein-calorie malnutrition, vitamin C deficiency, and pyridoxine deficiency (usually associated with alcoholism).
D. Other anemias not particularly associated with nutritional disease would include hemolytic anemia
(decreased red cell life span) and aplastic anemia (failure of marrow to produce new cells).
Monocytosis:
Causes
-Infections causing lymphocytosis, especialy tuberculosis and typhoid.
-Monocytic leukaemia.
-Some auto immune diseases.
THE PITUITARY GLAND
This is a small, bean-shaped structure that lies at the base of the brain within the confines of the sella turcica. It is connected to the hypothalamus by a "stalk," composed of axons extending from the hypothalamus. The pituitary is composed of two morphologically and functionally distinct components: the anterior lobe (adenohypophysis) and the posterior lobe (neurohypophysis). The adenohypophysis, in H&E stained sections, shows a colorful collection of cells with basophilic, eosinophilic or poorly staining ("chromophobic") cytoplasm.
Immunohistochemistry
This is a method is used to detect a specific antigen in the tissue in order to identify the type of disease.
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)
OEDEMA
Excessive accumulation of fluid in the extra vascular compartment (intersttitial tissues). This includes ascites (peritoneal sac), hydrothorax (pleural cavity) hydropericardium (pericardial space) and anasarca (generalised)
Factors which tend to accumulate interstitial fluid are:
- Intravascular hydrostatic pressure
- Interstitial osmotic pressure.
- Defective lymphatic drainage.
- Increased capillary permeability.
Factors that draw fluid into circulation are:
- Tissue hydrostatic-pressure (tissue tension).
- Plasma osmotic pressure,
Oedema fluid can be of 2 types:
A. Exudate.
It is formed due to increased capillary permeability as in inflammation.
B. Transudate
Caused by alterations of hydrostatic and osmotic pressures.
|
|
Exudate |
Transudate |
|
Specific Gravity |
>1.018 |
1.012 |
|
Protein Content |
High |
Low |
|
Nature of Protein |
All Plasma Protein |
Albumin mostly |
|
Spontaneous Clotting |
High(Inflammatory Cells) |
Low |
Local Oedema
1. Inflammatory oedema. Mechanisms are.
- Increased capillary permeability.
- Increased vascular hydrostatic pressure.
- Increased tissue osmotic pressure.
2.Hypersensitivity reactions especially types I and III
3. Venous obstruction :
- Thrombosis.
- Pressure from outside as in pregnancy, tourniquets.
4. Lymphatic obstruction:
- Elephantiasis in fillariasis
- Malignancies (Peau de orange in breast cancer).
Generalized Oedema
1. Cardiac oedema
Factors :Venous pressure increased.
2. Renal oedema
- Acute glomerulonephritis
- Nephrotic syndrome
3. Nutritional (hypoproteinaemic) oedema. it is seen in
- Starvation and Kwashiorkor
- Protein losing enteropathy
4. Hepatic oedema (predominantly ascites)
Factors:
- Fall in plasma protein synthesis
- Raised regional lymphatic and portal venous pressure
5. Oedema due to adrenal corticoids
As in Cushing's Syndrome
Pulmonary oedema
- Left heart failure and mitral stenosis.
- Rapid flv infusion specially in a patient of heart failure.
THROMBOPHLEBITIS AND PHLEBOTHROMBOSIS
- The deep leg veins account for more than 90% of cases (DVT)
- the most important clinical predispositions are: congestive heart failure, neoplasia, pregnancy, obesity, the postoperative state, and prolonged bed rest or immobilization
- local manifestations: distal edema, cyanosis, superficial vein dilation, heat, tenderness, redness, swelling, and pain
- migratory thrombophlebitis (Trousseau sign): hypercoagulability occurs as a paraneoplastic syndrome related to tumor elaboration of procoagulant factors