Medicine Hack

 DEFINITION  Edema is an abnormal presence of excessive fluid in the interstitial space.  PATHOPHYSIOLOGY  The movement of water and low molecular weight solutes such as salts between the intravascular and interstitial spaces is controlled primarily by the opposing effect of vascular hydrostatic pressure and plasma colloid osmotic pressure. Normally the outflow of fluid from the arteriolar end of the microcirculation into the interstitium is nearly balanced by inflow at the venular end. A small residual amount of fluid may be left in the interstitium and is drained by the lymphatic vessels, ultimately returning to the bloodstream via the thoracic duct. Either increased capillary pressure, diminished colloid osmotic pressure or inadequate lymphatic drainage can result in an abnormally increased interstitial fluid i.e. edema. An abnormal increase in interstitial fluid within tissues is called edema, while fluid collections in the different body cavities are variously

In a classical lesion, dilated and destroyed respiratory bronchioles coalesce in series and in parallel to produce sharply demarcated emphysematous spaces. They are separated from the acinar periphery (the  lobular septa) by intact  alveolar ducts and sacs of normal size, as shown by the diagram below.  The lesions vary in quality and quantity even within the same lung. There is striking irregularity of involvement of lobules, and even within the same lobule. The lesions are usually more common and become more severe in the upper than in the lower zones of the lung. Most affected are the upper lobe, particularly the posterior and apical segments, and the superior segment of the lower lobe as depicted below.  This type of emphysema is commonly seen in chronic cigarette smokers. For classification of emphysema, follow this link:  Emphysema

Pathology: In some cases, the scarring process remains in the remodelling phase for longer than usual. These hypertrophic scars are more cellular and more vascular than mature scars.  There is increased collagen production and collagen breakdown but the balance is such that excess collagen is produced.  Clinical features: The hypertrophic scars are red, raised, itchy and tender. They will eventually mature to become pale and flat, and it is this spontaneous resolution which distinguishes hypertrophic scars from keloid scars.  Cause: Hypertrophic scars typically occur in wounds where healing was delayed, e.g. in cases where infection or dehiscence has occurred.  Incidence: They are more common in children and where skin tension is high such as the tip of the shoulder or any scar that runs across relaxed skin tension lines. Prevention and treatment: The risk of developing a hypertrophic scar can be minimised by ensuring quiet primary healing. Where hypertrophy

Hyperemia and congestion both indicate a local increased volume of blood in a particular tissue. Hyperemia is an active process that result from augmented blood flow due to arteriolar dilation (e.g. at sites of inflammation or in skeletal muscle during exercise). The affected tissue is redder than normal because of engorgement with oxygenated blood. Congestion, on the other hand, is a passive process resulting from impaired venous return out of a tissue. It may occur due to systemic causes like cardiac failure or a local cause like isolated venous obstruction. The tissue is cyanosed because the worsening congestion leads to accumulation of deoxygenated hemoglobin in the affected tissues. 

It is a Fab fragment of a humanized monoclonal antibody directed against the glycoprotein IIb/IIIa. The latter is a platelet surface integrin. It is a receptor for fibrinogen which binds platelets to each other causing aggregation. By inhibiting the receptor, abciximab acts as a potent antiplatelet agent.  Indications: 1) myocardial ischemia, 2) percutaneous coronary intervention. Dose: 1) For M.I - initially an I.V bolus of 0.25 mg/kg over 5 min followed by 0.125 µg/kg/min (to a maximum of 10 µg/min) for 12 hours. 2) For P.C.I - initially, 0.25 mg/kg I.V bolus over 5 min 20-60 min prior to angioplasty followed by 0.125 µg/kg/min (to a maximum of 10 µg/min) for next 12 hours. Contraindications: 1) bleeding disorder or use of anticoagulant within 7 days, 2) CVA within 2 years, 3) known allergy to this product, 4) major trauma or surgery within 6 weeks, 5) severe uncontrolled hypertension, 6) active internal bleeding, 7) thrombocytopenia i.e pla

Recent studies have found that allergic people tend to have more symptoms at the beginning of the season. This is regardless of the medications taken. The following are the proposed explanations: 1) Sufferers get used to the symptoms and are therefore not bothered by them. So they did not report the symptoms. 2) Allergen-specific regulatory T cells may down regulate the inflammatory response after high exposure to the pollen at the beginning of the season. 3) Pollen at the later part of the season are less allergenic.

It is a diarrheal disease and is commonly seen in cases of food poisoning. Pathogenesis: Man acquires this infection by ingesting contaminated water or food. Water is usually infected by feaces from an infected animal or human. Poultry and eggs also comprise an important source of salmonella. The organisms may be present on the outer shell or even in the yolk. The clinical syndromes that can occur in man includes gastroenteritis, enteric fever and septicaemia. In the case of enterocolitis, the salmonella bacilli attach themselves to the microvilli of the ileal mucosa by means of adhesins and then invade the cells. They cause massive efflux of fluids and electrolytes. Clinical presentaion: There is large volume watery diarrhea, fever, headache, chills, abdominal pain and tenesmus. In simple uncomplicated cases, the diarrhea will last for 3-7 days. Diagnosis is made by stool culture. The disease is self limited. Treatment consists only of correcting any fluid and electrolyte

Virchow's triad refers to the 3 primary influences for thrombus formation and it includes: 1) Endothelial injury 2) Stasis, turbulence or abnormal blood flow 3) Blood hypercoagulability. Endothelial injury Physical loss of endothelium leads to exposure of subendothelial extra-cellular matrix, adhesion of platelets, release of tissue factor, and local depletion of PGI 2 and plasminogen activators. Abnormal blood flow Turbulence can cause endothelial injury which is in itself a major influence for thrombosis. Apart from that abnormal blood flow can: 1) Disrupt laminar flow and bring platelets into contact with the endothelium 2) Prevent dilution of activated clotting factors by fresh-flowing blood 3) Retard the inflow of clotting factor inhibitors and permit the buildup of thrombi 4) Promote endothelial cell activation, resulting in local thrombosis, leukocyte adhesion, etc.  Hypercoagulability It can be primarily due to a genetic disorder and secondarily due to some acqui