NEET MDS Lessons
General Pathology
Pulmonary embolism
A pulmonary embolism (thromboembolism) occurs when a blood clot, generally a venous thrombus, becomes dislodged from its site of formation and embolizes to the arterial blood supply of one of the lungs.
Clinical presentation
Signs of PE are sudden-onset dyspnea (shortness of breath, 73%), tachypnea (rapid breathing, 70%), chest pain of "pleuritic" nature (worsened by breathing, 66%), cough (37%), hemoptysis (coughing up blood, 13%), and in severe cases, cyanosis, tachycardia (rapid heart rate), hypotension, shock, loss of consciousness, and death. Although most cases have no clinical evidence of deep venous thrombosis in the legs, findings that indicate this may aid in the diagnosis.
Diagnosis
The gold standard for diagnosing pulmonary embolism (PE) is pulmonary angiography
An electrocardiogram may show signs of right heart strain or acute cor pulmonale in cases of large PEs
In massive PE, dysfunction of the right side of the heart can be seen on echocardiography, an indication that the pulmonary artery is severely obstructed and the heart is unable to match the pressure.
Treatment
Acutely, supportive treatments, such as oxygen or analgesia
In most cases, anticoagulant therapy is the mainstay of treatment. Heparin or low molecular weight heparins are administered initially, while warfarin therapy is given
Leukaemias
Uncontrolled proliferation of leukocyte precursors (may be with associated red cell and platelet series proliferation).
Factors which may playa causal role are.
- Viral
- Radiation.
- Genetic.
Classification
1. Acule leukaemia:
a. Lymphocytic (lymphoblastic).
b. Myelocytic and promyelocytic (myeloblastic).
c. Monocytic.
d. Myelomonocytic.
e. Undifferentiated (Stem cell).
2. Chronic leukaemia:
a. Lymphocytic
b. Myelocytic
3. Miscellaneous:
a. Erythroleukaemia (De Guglielmo's disease).
b. Eosinophilic leukaemia.
c. Megakaryocytic leukaemia.
Lymphangitis
is the acute inflammation due to bacterial infections spread into the lymphatics most common are group A β-hemolytic streptococci.
lymphatics are dilated and filled with an exudate of neutrophils and monocytes.
red, painful subcutaneous streaks (the inflamed lymphatics), with painful enlargement of the draining lymph nodes (acute lymphadenitis).
subsequent passage into the venous circulation can result in bacteremia or sepsis.
INFLAMMATION
Response of living tissue to injury, involving neural, vascular and cellular response.
ACUTE INFLAMMATION
It involves the formation of a protein .rich and cellullar exudate and the cardinal signs are calor, dolor, tumour, rubor and function loss
The basic components of the response are
Haemodynamic changes.
Permeability changes
Leucocyte events.
1. Haemodynamic Changes :
- Transient vasoconstriction followed by dilatation.
- Increased blood flow in arterioles.
- More open capillary bed.
- Venous engorgement and congestion.
- Packing of microvasculature by RBC (due to fluid out-pouring)
- Vascular stasis.
- Change in axial flow (resulting in margination of leucocytes)
.2. Permeability Changes:
Causes.
- Increased intravascular hydrostatic pressure.
- Breakdown of tissue proteins into small molecules resulting in
- increased tissue osmotic pressure.
- Increased permeability due to chemical mediators, causing an
- immediate transient response. .
- Sustained response due to direct damage to microcirculation.
3. White Cell Events:
.Margination - due to vascular stasis and change in axial flow.
Pavementing - due to endothelial cells swollen and more sticky.
Leucocytes more adhesive.
Binding by a plasma component
Emigration - of leucocytes by amoeboid movement between endhothe1ial cells and beyond the basement membrane. The passive movement of RBCs through the gaps created during emigration is called diapedesis
Chemotaxis - This is a directional movement, especially of polymorphs and monocytes towards a concentration gradient resulting in aggregation of these cells at the site of inflammation. .Chemotactic agents may be:
- Complement components. (C3and C5 fragments and C567)
- Bacterial products.
- Immune complexes, especially for monocyte.
- Lymphocytic factor, especially for monocyte.
Phagocytosis - This includes recognition, engulfment and intracellular degradation. It is aided by .Opsonins., Specific antibodies., Surface provided by fibrin meshwork.
Functions of the fluid and cellular exudate
1. Dilution of toxic agent.
2. Delivers serum factors like antibodies and complement components to site of inflammation.
3. Fibrin formed aids In :
- Limiting inflammation
- Surface phagocytosis
- Framework for repair.
4. Cells of the exudate:
Phagocytose and destroy the foreign agent.
Release lytic enzymes when destroyed, resulting in extracellular killing of organisms- and digestion of debris to enable healing to occur
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
THE THYROID GLAND
The thyroid gland develops embryologically from the developing pharyngeal epithelium that descends from the foramen cecum at the base of the tongue to its normal position in the anterior neck. This pattern of descent explains the occasional presence of ectopic thyroid tissue, most commonly located at the base of the tongue (lingual thyroid) or at other sites abnormally high in the neck.
Hepatitis
Hepatitis viruses—this group of viruses causes hepatitis, a disease affecting the liver.
1. General characteristics of hepatitis.
a. The general presentation of hepatitis is the same regardless of the infecting virus; however, the time and severity of symptoms may differ.
b. Symptoms of hepatitis include fever, anorexia, malaise, nausea, jaundice, and brown-colored urine.
c. Complications of a hepatitis infection include cirrhosis, liver failure, and hepatorenal failure.