21f total cholesterol 325 HDL 210 TG 180 LDL 79 VLDL 36 currently lactational amenorrhoea ho malignant hypertension with PRES during post partum period with convulsions GTC with prolongation of PT raised INR ,marginally raised SGPT SGOT...initially thought of post partum eclampsia..after controlling BP patient improved well...after few months she developed malignant hypertension bp 180/140 mmhg p 140/min with profuse sweating headache..all episodic in nature.. provisional diagnosis was made of pheochromocytoma dd paragnaglioma TFT was normal later on lipid profile hyperalphalipoproteinemia (HALP) was diagnosed...after controlling her Bp she was discharged , all other investigation done in view of above provisional diagnosis was normal..later antihypertensives were tapered down according to her Bp? was maintained on metoprolol amlodipine 25/2.5 mg but later few months again developed hypertension bp 150/120 p 130 my question is how to approach this case??


The various findings enlisted are related to the stages in the pathogenesis of malignant hypertension while other findings are incidental but not contributory to malignant hypertension. First we deal with incidental/ non contributory findings. First is the post partem settingsetting. Development of malignant hypertension in this setting lead to considering.cause and effect . Since it recurred beyond pP period this cause is ruled out. Secondly the HALP . This is obvious from high HDL and very low VLDL - HALP being the only cause to reckon with to explain this pattern of didlipidemia. HALP is no way related to malignant hypertension.So excusion from mainsream these two entities resolves some cofusion atleast. Now the findings stages in the pathogenesis of M .htn. Raised PT, and INR to be explained on one hand and ac. raise in bp with sweating which simulated pheochromocytoma but investigations tuling out the same. Umresponsiveness of metaprolol+amlodepine after initial response has also to be explained. 1) The raised PT / INR are indicative of activated coagulation system. This is due to endothelial damage consequent to sustained bp which leads to deposition of platlets and fibrin in the vessel wall leading to activation of coagulation profile. This can cause ' fibrinoid necrosis' of the vessel walls the actual pathology behing M htn .The same effect could be achieved through imtra vascular coagulation defect caused by deposition of coagulation a tivators cited above. When fibrinoid necrosis of blood vessels is seen, established M.htn has already ushered in. Thus the raised PT / INR are evolutionary findings leadind to the end result. The convusive episode in the clinical sprectrum is mis interpreted as GTCS/ eclampsi. Actually it is a nurological sequele of M .htn ie ' hypertensive encephalopathy ' .if CT brain should haemorrage it could have been even due to ' intracerebral haemorrhage/thrombosis due to activated coagulatuon profile. Now the confusion of oheochromocytoma which has been ruled out. The other effect of sustained high BP is vasoconstriction resultinv in activation of rein- angiotensin, vasopressin and catacholamines. The raise in later is the source of confusion by causing diaphoresis which is the only lead available to think of pheochromocytoma. So the findings in the evolution of final stage of M htn are explained. Now only thing to be explained is ineffectiveness of metaprolol+amlodepine after initial effectiveness. Now a distinction has to be drawn between ' accelerated hypertension ' and ' malignant hypertension ' in both bp criteria is same ie greater than 180/ 120. But the former is characterised by grade e fundus and the later by grade r fundus findings. As the disease progresses, the antihupertensuve dose has to be up graded. Bjut the crucial step in management i use of quick acting vasodilators like sodium nitro prusside, labetolol, etc during ' hypertensive crisis ' . Another point is target orgon damage prevention by regular screening. The cause is more often cryptic ( primary) than secondery. Still the secondery causes should be ruled out as they are remidiable. 80% causes are re al parenchymal like AGN, Chr.pyelonepritis etc and 2p % are due to tubulo interstitial causes. Collagen diseases like SLE, SSand poly ateritis nodosa are to be ruled out. R/o Renovascular hypertension. This is the course of action in my view.

If possible to find out "renal artery" pathology???

Renal arterial doppler is normal

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