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HYPERTENSION- DEFINITION,CLASSIFICATION, ETIOLOGY HYPERTENSION- DEFINITION,CLASSIFICATION, ETIOLOGY

HYPERTENSION- DEFINITION,CLASSIFICATION, ETIOLOGY - PowerPoint Presentation

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HYPERTENSION- DEFINITION,CLASSIFICATION, ETIOLOGY - PPT Presentation

DR CHAITHRA K JR1 MEDICINE HYPERTENSION IS ONE OF THE LEADING CAUSES OF GLOBAL BURDEN OF DISEASE ID: 1047600

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1. HYPERTENSION- DEFINITION,CLASSIFICATION, ETIOLOGY DR CHAITHRA K JR1 MEDICINE

2. HYPERTENSION IS ONE OF THE LEADING CAUSES OF GLOBAL BURDEN OF DISEASEIT DOUBLES THE RISK OF CARDIOVASCULAR DISEASES, ISCHEMIC AND HEMORRHAGIC STROKE , RENAL FAILURE AND PERIPHERAL ARTERIAL DISEASELARGE SEGMENTS OF HYPERTENSIVE POPULATION ARE EITHER UNTREATED OR INADEQUATELY TREATED

3. CLINICALLY HYPERTENSION DEFINED AS THAT LEVEL OF BP AT WHICH THE INSTITUTION OF THERAPY REDUCES BP RELATED MORBIDITY AND MORTALITYIT IS THE PRODUCT OF CARDIAC OUTPUT AND PERIPHERAL RESISTANCEIT IS BASED ON THE AVERAGE OF TWO OR MORE SEATED BP READINGS DURING EACH OF TWO OR MORE OUT PATIENT VISITS

4. SBP IS MORE IMPORTANT THAN DBP IN THE MEASUREMENT OF CARDIOVASCULAR RISK EXCEPT IN YOUNG PATIENTSPULSE PRESSURE(PP)=SBP-DBPMEAN ARTERIAL PRESSURE=DBP+1/3PPISOLATED SYSTOLIC HYPERTENSIONSBP>140 WITH DBP<90ARTERIOSCLEROSIS/AR/FEVER/THYROTOXICOSIS/AV FISTULA

5. AHA CLASSIFICATIONCATEGORYSYSTOLICDIASTOLICNORMAL<120<80ELEVATED120-129<80HYPERTENSIONSTAGE 1130-13980-89STAGE 2>140>90

6. ESC CLASSIFICATIONCATEGORYSYSTOLICDIASTOLICOPTIMAL<120<80NORMAL120-12980-84HIGH NORMAL130-13985-89GRADE 1140-15990-99GRADE 2160-179100-109GRADE 3>180>110

7. SBPDBPOFFICE/CLINIC>_14090SELF/HOME BP>_13585AMBULATORY(24HR AVG)>_13585

8. HOME BLOOD PRESSURE MEASUREMENT-TO IDENTIFY WHITE COAT HTN-INCREASES ADHERENCE TO MEDICATION-DETECT MASKED HTNTHE BLADDER LENGTH OF BP CUFF SHOULD BE 80% CIRCUMFERENCE AND IDEAL WIDTH IS 40%

9. AMBULATORY BP MEASUREMENTOVER A PERIOD OF 24-48 HRDETECT EPISODIC HTNHYPOTENSIVE EPISODESAUTONOMIC DYSFUNCTIONEVALUATION OF SLEEP APNEAEVALUATE ANTIHYPERTENSIVESRESISTANT HTN

10. CATEGORYNORMALHTN24 HRS AVG130/80135/85DAY /AWAKE135/85140/90ASLEEP /NIGHTTIME120/70125/75

11. PATHOPHYSIOLOGYINCREASED CARDIAC OUTPUT INCREASED PERIPHERAL RESISTANCEESTABLISHED HTN- INCREASED PERIPHERAL RSISTANCE AND NORMAL CARDIAC OUTPUT

12. INCREASED COINCREASED FLUID VOLUME-EXCESS SODIUM INTAKE INCREASES FLUID VOLUME AND PRELOADRENAL SODIUM RETENTIONRENIN ANGIOTENSIN SYSTEMSYMPATHETIC NERVOUS SYSTEM OVERACTIVITY-

13. INCREASED PERIPHERAL VASCULAR RESISTANCEINCREASED INTRACELLULAR CALCIUMANGIOTENSIN 2, IGF,PROSTAGLANDINS,ENDOTHELINSTRUCTURAL VASCULAR REMODELLING AND HYPERTROPHY

14.

15. PRIMARY HYPERTENSION80-95% HTN PATIENTS ARE DIAGNOSED AS HAVING PRIMARY OR ESSENTIAL HYPERTENSION INCLUSIVE OF PATIENTS WITH OBESITY AND METABOLIC SYNDROMEFAMILIALPREVALENCE INCREASES WITH AGEOBESITY(BMI>30 kg/m2) HAVE LINEAR CORRELATION WITH BP

16. METABOLIC SYNDROME-INSULIN RESISTANCE ,ABDOMINAL OBESITY,HTN, DYSLIPIDEMIAHERITABLE AS A POLYGENIC CONDITIONEXPRESSION IS MODIFIED BY ENVIRONMENTAL FACTORSHYPERINSULINEMIA- MARKER OF INSULIN RESISTANCE-PREDICT THE DEVELOPMENT OF HTN AND CARDIOVASCULAR DISEASEINSULIN- ANTINATRIURETIC EFFECT

17. SECONDARY CAUSES OF HTN

18. RENALPARENCHYMAL DISEASES, RENAL CYSTS( POLYCYSTIC KIDNEY DISEASE)RENAL TUMOURS(RENIN SECRETING TUMOURS),OBSTRUCTIVE UROPATHYRENOVASCULARARTERIOSCLEROTIC, FIBROMUSCULAR DYSPLASIAADRENALPRIMARY ALDESTERONISM, CUSHINGS SYNDROME,PHEOCHROMOCYTOMA,17 ALPHA HYDROXYLASE DEF,11 BETA HYDROXYLASE DEFAORTIC COARCTATIONOBSTRUCTIVE SLEEP APNEAPREECLAMPSIA/ECLAMPSIANEUROGENICDIENCEPHALIC SYNDROME,FAMILIAL DYSAUTONOMIA,POLYNEURITIS(A/C PORPHYRIA,LEAD POISONING)RAISED ICT,A/C SPINAL CORD SECTION

19. ENDOCRINEHYPOTHYROIDISM, HYPERTHYROIDISM,HYPERCALCEMIA,ACROMEGALYMEDICATIONSHIGH DOSE ESTROGENS,ADRENAL STERIODS,DECONGESTANTS,AMPHETAMINES,CYCLOSPORINE,TCA, ATYPICAL ANTIPSYCHOTICS,MAO-INHIBITORS ,NSAIDS,ALCOHOL,COCAINEMENDELIAN FORMS OF HTNLIDDLES SYNDROME,PCKD,PHEOCHROMOCYTOMA,GORDONS SYNDROME,11BETA HYDROXYLASE DEF17ALPHA HYDROXYLASE DEF

20. RENAL PARENCHYMAL DISEASESM/C/C OF SECONDARY HYPERTENSIONHTN IS MORE SEVERE IN GLOMERULAR DISEASES THAN IN INTERSTITIAL HTN CAUSES NEPHROSCLEROSIS

21. RENOVASCULAR HYPERTENSIONHTN DUE TO AN OCCLUSIVE LESION OF RENAL ARTERYCURABLEPLAQUE OSTRUCTING RENAL ARTERY, FIBROMUSCULAR DYSPLASIACONSIDERED IN PATIENTS WITH OTHER EVIDENCE OF ATHEROSCLEROTIC VASCULAR DISEASEFT

22. SEVERE OR REFRACTORY HTN /RECENT LOSS OF HTN CONTROL/CAROTID OR FEMORAL ARETERY BRUIT/FLASH PULMONARY EDEMA/UNEXPLAINED DETERIORATION OF RFT/DETERIORATION ASSOCIATED WITH ACE INHIBITORDOPPLER ULTRASOUND / GADOLINIUM CONTRAST MR ANGIOGRAPHYFUNCTIONALLY SIGNIFICANT IF STENOSIS IS >70%/ PRESENCE OF COLLATERALS/RENAL VEIN RENIN RATIO>1.5 OF AFFECTED SIDE/CONTRALATERAL SIDE

23. INTERVENTIONS-PTRA, PLACEMENT OF STENT,SURGICAL RENAL REVASCULARIZATIONBP ADEQUATELY CONTROLLED +RFT STABLE- NO INTERVENTION NEEDEDFIBROMUSCULAR D/S -YOUNG AGE ,FAVOURABLE OUTCOME

24. PRIMARY ALDOSTERONISMINDEPENDENT OF RENIN ANGIOTENSIN SYSTEMSODIUM RETENTION, HTN, HYPOKALEMIA, LOW PRA,KIDNEY DAMAGE AND CVS DISEASESDIAGNOSED AT 3RD OR 4TH DECADEASYPTOMATICPOLYURIA,POLYDYPSIA,PARESTHESIA ,MUSCLE WEAKNESS DUE TO HYPOKALEMIC ALKALOSIS

25. REFRACTORY HTN/ HTN WITH UNPROVOKED HYPOKALEMIAPATIENTS ON DIURETICS- S POTASSIUM<3.1 SCREENING TESTPA/PRA >30:1 PA>550 pmol(20ng/dl)ARB & ACEI AFFECT THIS RATIO- SHOULD BE STOPPED 4-6 WKS BEFORE TESTINGALDOSTERONE BIOSYNTHESIS IS K+ DEPENDENT- HYPOKALEMIA CORRECTED WITH ORAL SUPPLEMENTS

26. PATIENTS WITH ELEVATED PA/PRA RATIO –DIAGNOSIS CONFIRMED WITH FAILURE TO SUPRESS PA BYORAL SODIUM LOADING/SALINE INFUSIONFLUDROCORTISONE/CAPTOPRIL

27. SPORADIC / FAMILIALSPORADIC- ADENOMA/ BILATERAL ADRENAL HYPERPLASIA/ADRENAL CARCINOMA/ECTOPIC MALIGNANCYIMAGING- HIGH RESOLUTION CT/ADRENAL SCINTIGRAPHYB/L ADRENAL VENOUS SAMPLING- HIGH SENSITIVITY AND SPECIFICITYTO DIFFERENTIATES U/L & B/L

28. ADENOMA- SURGICAL MX-U/L ADRENELECTOMYHYPERPLASIA –MEDICAL MX- ALDOSTERONE BLOCKERS SPIRONOLACTONE, EPLERENONE

29. GLUCOCORTICOID REMEDIABLE HYPERALDOSTERONISM-AD/ MOD TO SEVERE HTN AT YOUNG AGEOVER PRODUCTION OF BOTH ALDOSTERONE AND STEROIDRx- SUPRESSION OF ACTH BY LOWDOSE GLUCOCORTICOIDS

30. CUSHING’S SYNDROMEM/C/C- IATROGENIC STEROIDSACTH DEPENDENT-PITUTARY ADENOMA/ ECTOPIC ACTHACTH INDEPENDENT- ADRENAL TUMOURSOVERNIGHT DEXAMETHASONE SUPRESSION TEST OR 24 HOUR URINARY CORTISOL OR LATE NIGHT SALIVARY CORTISOLRx – SURGICAL AND MEDICAL

31. PHEOCHROMOCYTOMACATECHOLAMINE SECRETING TUMOURS IN ADRENALSIN EXTRA ADRENAL PARAGANGLION TISSUE –PARAGANGLIOMAHEADACHE/PALPITAION/SWEATING/EPISODIC HTN/ORTHOSTSIC HYPOTENSIONINV-24HR FRACTIONATED METANEPHRINS/PLSMA FREE METANEPHRINSCT/MRIRx-ALPHA BLOCKERS- BETA BLOCKERS-SURGERY

32. OBSTRUCTIVE SLEEP APNEAHTN DUE TO SYMPATHETIC ACTIVATION CAUSED BY INTERMITTENT HYPOXIA AND FRAGMENTED SLEEPBP REMAIN ELEVATED DURING NIGHT TIME- REVERS DIPPERSCPAP VENTILATION IS THE TREATMENTIT ABOLISHES APNEA,PREVENTS INTERMITTENT BP SURGES,RETORES NORMAL DIPPING PATTERN

33. THANK YOU