Scibug

Increased cardiac output co is not equal to increased BP.
Increased Co does not lead to sustained BP unless renal compensatory mechanism fails.
Increased peripheral vascular resistance PVR = increased BP (most important factor for sustained increased BP)
Increased cardiac output co → increased Renal blood flow → increased Renal Interstitial hydrostatic pressure → Pressure natriuresis → BP normal.

As per European society of hypertension: reducing the systolic blood pressure by 10 mm of Hg and diastolic blood pressure by 5 mm of Hg lowers the risk of CAD death by 40-50% and risk of stroke death by 50-60%.

Lupus erythromatosus (LE) cell is___
The LE cell is a phagocytic neutrophil or macrophage Nuclei of damaged cells react with Anti Nuclear Antibodies (ANAS), lose their chromatin pattern and become homogeneous to produce LE bodies or hematoxylin bodies. Related to this phenomenon is the LE cell. These cells engulf the denatured nucleus of an injured cell. Demonstration of LE cells in vitro was used in the past for diagnosis of SLE.
hence hematoxylin bodies may be seen in lymphnodes in sle.

Rheumatic fever  lead to acute rheumatic heart diasese:
Which have
1. Precardial component: pericarditis
2. Myocardial component:myocarditis
3. Endocardial component: endocarditis mitral valve becomes inflammed during acute phase transiently then if blood passing from the atria to ventricle during this period during acute rheumatoid endocarditis mitral valve transiently inflammed= leading to when blood passing through it from atrium to ventricle = soft rumbling murmur as transiently will disappear as inflammation with disease disappears= called carry coombs murmur= mid diastolic murmur = during acute rheumatic endocarditis= mitral valve severely inflammed= soft rumbling murmur= when acute phase terminated fever resolves then this murmur goes away but when this person suffers repeatedly with rheumatic heart disease acutely several time = recurrent attack of rheumatic process = chronic rheumatic endocarditits= endocardium inflamed is healed by fibrosis and vegetation again and again  healed with fibrosis and stenosis = now as chronic eventually person develops not transient but permanent fibrosis and stenosis = so now valve have permanent murmur= don’t goes away mid diastolic murmur= soft rumbling murmur chronic phase classical middiastolic mitral stenosis murmur. So rheumatic heart disease can produce 2 types of mid diastolic murmur =during the acute phase is carry coombs murmur while in chronic phase classical middiastolic mitral stenosis murmur murmur = these 2 characteristics are mentioned above.

why there is opening snap in mitral stenosis ?
Answer:
When ventricular relaxation starts  S2 occurs. And ventricular diastole = will cause the mitral valve now to open = noramlly when valve is healthy = then open silently, but incase of mitral stenosis will open with difficulty = and already left atrial pressure higher (as in last cycle all the blood cant be ejected into ventricle because of the mitral stenosis) so during left ventricular diastole = when the thick fibrosed stenotic valve trying to open under high pressure from atria will not completely open will abruptly stops as stenotic doesn’t completely open and due to this abruptly stopage the valve custps from convex towards the atrium turns concave towards the atrium leading to reverse of its curvature of the cusps of the mitral valve= = this curvature change from convex towards the atrium to concave towards the atrium = leading to this opening snap sound during ventricular diastole just after S2 in early diastole part. So this mitral valve unfortunately doesn’t open properly still producing opening snap

The frontiers were inked and the time is ticking