NEET MDS Lessons
General Pathology
SHOCK
Definition. It is a clinical state of acute inadequacy of perfusion to tissues due to fall in effective circulating blood volume.
This inadequacy can be caused by :
- Increased vascular capacity
- Decreased blood volume
- Altered distribution of available blood
- Defective pumping system
Causes:
(1) Hypovolemic
- Massive hamorrhage (external or internal).
- Loss of plasma as in bums.
- Dehydration due to severe vomiting, diarrhea diabetic coma.
- Generalized capillary permeability as in anaphylaxis.
(2) Cardiogenic
- Myocardial infarction.
- Pulmonary embolism.
- Cardiac tamponade
(3) Peripheral pooling:
- Endotoxic shock.
- Disseminated intravascular coagulation (DIC).
(4) Neurogenic:
- Syncope.
- Contributory factor in trauma, bums etc.
Metabolic changes in shock
- Hyperglycaemia due to glycogenolysis.
- Increased blood lactate and pyruvate due to anaerobic glycolysis. This results in metabolic acidosis.
- Protein catabolism and increased blood urea.
- Interference with enzyme systems.
Organs involved in shock
(1) Kidneys:
- Renal tubular necrosis.
- Cortical necrosis.
(2) Lungs:
- Oedema, congestion and haemorrhage.
- Microthrombi.
(3) G.I.T. :
- Mucosal oedema.
- Ulceration and haemorrhage
(4) Degeneration and focal necrosis in:
- Heart.
- Liver.
- Adrenals
(5) Anoxic encephalopathy
A dermatofibroma is a benign tumor of the dermis, MC located on the lower extremity, where it has a nodular, pigmented appearance.
- composed of benign histiocytes.
Seborrheic dermatitis is a scaly dermatitis on the scalp (dandruff) and face.
- due to Pitysporium species
- can be seen in AIDS as an opportunistic infection
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).
NECROSIS
Definition: Necrosis is defined as the morphologic changes caused by the progressive degradative
action of enzymes on the lethally injured cell.
These changes are due to
I. Autolysis and
2. Heterolysis.
The cellular changes of necrosis i.e. death of circumscribed group of cells in continuity with living tissues are similar to changes in tissues following somatic death, except that in the former, there is leucocytic infiltration in reaction to the dead cells and the lytic
enzymes partly come from the inflammatory cell also. (Heterolysis). Cell death occurs in the normal situation of cell turnover also and this is called apoptosis-single cellular dropout.
Nuclear changes in necrosis
As cytoplasmic changes are a feature of degeneration ,similarly nuclear changes are the hallmark of necrosis. These changes are:
(i) Pyknosis –condensation of chromatin
(ii) Karyorrhexis - fragmentation
(iii) Karyolysis - dissolution
Types of necrosis
(1) Coagulative necrosis: Seen in infarcts. The architectural outlines are maintained though structural details are lost. E.g, myocardial infarct.
(2) Caseous necrosis: A variant of coagulative necrosis seen in tuberculosis. The architecture is destroyed, resulting in an eosinophilic amorphous debris.
(3) Colliquative (liquifactive). Necrosis seen in Cerebral infarcts and suppurative necrosis.
Gangrenous necrosis: It is the necrosis with superadded putrefaction
May be:
a. dry - coagulative product.
b. Wet - when there is bacterial liquifaction.
Fat necrosis
May be:
a. Traumatic (as in breast and subcutaneous tissue).
b Enzymatic (as in pancreatitis). It shows inflammation of fat with formation of lipophages and giant cells.
This is often followed by deposition of calcium as calcium soaps.
Hyaline necrosis: Seen in skeletal muscles in typhoid and in liver ceIs in some forms of hepatitis.
Fibrinoid necrosis: In hypertension and in immune based diseases.
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.
Actinic keratosis
1. Dry, scaly plaques with an erythematous base.
2. Similar to actinic cheilosis, which occurs along the vermilion border of the lower lip.
3. Caused by sun damage to the skin.
4. Dysplastic lesion, may be premalignant.