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Hypertension according to harrison

harrison hypertension

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Hypertension according to harrison

  1. 1. HYPERTENSION DETECTION, AND NON-PHARMACOLOGIC INTERVENTION
  2. 2. According to the Joint National Committee based on the averagethe average of two or more properly measured BP readings. On each of two or more office visits. DEFINITION
  3. 3. The patient must be properly prepared and positioned and seated quietly for at least 5 minutes in a chair. The auscultatory method should be used. Caffeine, exercise, and smoking should be avoided for at least 30 minutes before BP measurement. An appropriately sized cuff should be used. ACCURATE BLOOD PRESSURE MEASUREMENT
  4. 4. Isolated systolic hypertension is considered to be present when the blood pressure is ≥140/<90 mmHg  isolated diastolic hypertension is considered to be present when the blood pressure is <140/≥90 mmHg ISOLATED HYPERTENSION
  5. 5. White coat hypertension defined as blood pressure that is consistently elevated by office readings but does not meet diagnostic criteria for hypertension based upon out-of-office readings. Masked hypertension — Masked hypertension is defined as blood pressure that is consistently elevated by out-of-office measurements but does not meet the criteria for hypertension based upon office readings 0 0.5 1 1.5 2 2.5 Normal BP White coat hypertension Masked Hypertension Hypertension prognosis OddsRatioofa CardiovascularEvent
  6. 6. referstopatientswithbloodpressurespersistently>140/90mmHg despitetaking three ormore antihypertensiveagents, including adiuretic, in a reason- ablecombinationandatfulldoses Secondary causes of hypertension should be considered RESISTANT HYPERTENSION
  7. 7. MALIGNANT HYPERTENSION Moderate to severe hypertensive retinopathy (formerly called "malignant hypertension") The absolute level of blood pressure is not as important as its rate of rise. usually associated with diastolic pressures above 120 mmHg. However, it can occur at diastolic pressures as low as 100 mmHg in previously normotensive patients. Clinically; -progressive retinopathy (arteriolar spasm, hemorrhages, exudates,papilledema), -deteriorating renal function with proteinuria, -microangiopathic hemolytic anemia -encephalopathy.
  8. 8. Hypertensive Urgencies: severe hypertension (diastolic pressure usually >120 mmHg) in asymptomatic patients with no acute target- organ damage Hypertensive Emergencies: severe hypertension (diastolic pressure usually >120 mmHg) in patients with acute ongoing target-organ damage HYPERTENSIVE CRISES
  9. 9. FOLLOW-UP BASED ON INITIAL BP MEASUREMENTS FOR ADULTS* *Without acute end-organ damagewww.nhlbi.nih.gov
  10. 10. Ibrahim: I think systolic pressure is much more important that the diastolic. Naisam: no my friend, you are so wrong! they are both important but the diastolic pressure is more important as a CVD risk factor QUESTION
  11. 11. Systolic BP is more important cardiovascular risk factor after age 50. Diastolic BP is more important before age 50. ANSWER
  12. 12. BENEFITS OF TREATING HYPERTENSION Younger than 60 (reducing BP 10/5-6 mmHg)  reduces the risk of stroke by 42%  reduces the risk of coronary event by 14% Older than 60 (reducing BP 15/6 mmHg)  reduces overall mortality by 15%  reduces cardiovascular mortality by 36%  reduces incidence of stroke by 35%  reduces coronary artery disease by 18% Lancet 1990;335:827-38 Arch Fam Med 1995;4:943-50
  13. 13. TREATMENT
  14. 14. LIFESTYLE INTERVENTIONS
  15. 15. PHARMACOLOGIC THERAPY
  16. 16. Low-dose Thiazide inhibittheNa+/Cl− pumpin thedistalconvolutedtubuleand henceincreasesodiumexcretion Inthelong term,theymayactasvasodilators additiveeffectswhencombinedwith beta blockers, ACEIs, ARBs Incontrast,additionofa diuretictoa calciumchannelblockerislesseffective. side effects:  Hypokalaemia – muscle pain and fatigue–tosades de pointes  Hyperglycemia: insulin resistance  Hyperlipidemia: rise in total LDL level – risk of stroke  Hyperurecaemia: inhibition of urate excretion-gout DIURETICS
  17. 17. Loop diuretics Less effective that thiazide in treating HTN Abrupt effect (uncomfortable) reservedforhypertensivepatientswith reducedglomerularfiltration reflectedin serumcreatinine>2.5mg/dL CHF,or sodiumretention andedemafor someother reason DIUERITICS
  18. 18. decreasetheproduction ofangiotensinII, increasebradykinin levels reducesympatheticnervoussystemactivity. ACEIsandARBshavebeenshown toimprove insulin action anddiminish theadverse effectsofdiureticson glucosemetabolism. decreaseintraglomerularpressureandproteinuria andmayretardthe rateofprogression ofrenalinsufficiency, Adverse effects: functional renalinsufficiencyina kidneywitha stenoticlesionofthe renalartery. Drycoughoccursin ~15%ofpatients, angioedema occursin<1% swelling of lips, mouth, nose BLOCKERS OF THE RENIN-ANGIOTENSIN SYSTEM
  19. 19. nonselectivealdosteroneantagonist maybe aparticularlyeffective agentinpatientswithlow-reninessentialhypertension,resistanthypertension, andprimaryaldosteronism. InpatientswithCHF,low-dosespironolactonereducesmortalityandhospitalizations sideeffects gynecomastia, impotence menstrual abnormalities, Eplerenone whichisa selectivealdosteroneantagonist circumvented] thesesideeffects ALDOSTERONE ANTAGONISTS (SPIRONOLACTONE)
  20. 20. lowerbloodpressurebydecreasing cardiacoutput particularlyeffectiveinhypertensivepatientswithtachycardia, Carvedilol andlabetalolblockboth receptorsandperipheralβ α adrenergicreceptors. Thepotential advantagesofcombined - and -adrenergicblockadeβ α in treating hypertensionremain tobedetermined • Carvedilol Does not affect the embryo in pregnant women  Side effectsimpotence,braddycardia(SSd) fatigue BETA BLOCKERS
  21. 21. lowerbloodpressurebydecreasing peripheralvascular resistance has not beenshowntoreducecardiovascularmorbidityandmortalityortoprovideasmuchprotectionagainstCHFasotherclassesofantihypertensive agents effectiveintreatingBPHsymptomsinmen Side effect orthostatic hypotension -Α ADRENERGIC BLOCKERS
  22. 22. reducevascularresistancethroughL-channelblockade->reducesintracellularcalciumandbluntsvasoconstriction sideeffects flushing, headache, andedema *edema isdue toan increaseintranscapillarypressuregradients,. CALCIUM CHANNEL BLOCKERS VERAPAMIL DILTIAZEM NIFEDIPINE-LIKE
  23. 23. decreaseperipheralresistance not consideredfirst-line agentsbutaremosteffectivewhen addedto a combinationthatincludesa diuretic Minoxidilisaparticularlypotentagentandisusedmostfrequentlyin patientswithrenalinsufficiencywhoarerefractorytoall otherdrugs. sideeffectsofminoxidil hypertrichosisandpericardialeffusion. DIRECT VASODILATORS HYDRALAZINE MINOXIDIL
  24. 24. whenusedasmonotherapy: thiazidediuretics, beta blockers, ACEIs, ARBs, calciumantagonists,andα 2 blockers.On average, standarddosesofmostanti- hypertensiveagentsreduce bloodpressureby8–10/4–7 mmHg; Youngerpatientsmaybemoreresponsiveto beta blockers andACEIs, whereaspatientsoverage50 maybe moreresponsive to diureticsandcalcium antagonists. ACEIsprovidebetter coronaryprotection thando calciumchannel blockers, whereascalciumchannelblockers provide more strokeprotection Aftera stroke,combination therapywithan ACEIanda diuretic, butnotwithan ARB,reducestherate ofrecurrentstroke COMPARISON
  25. 25. for the general hypertensive population under the age of 60 years <140/90 patients of all ages with diabetes or chronic kidney disease who do not have proteinuria<140/90 for the general hypertensive population aged 80 years and older.Goal blood pressure is <150/90 mmHg The choice between these two goal blood pressures depends upon the patient's general health, comorbid conditions, postural blood pressure changes, the number of medications needed to reach the goal, and upon individual values and preferences. GOAL BLOOD PRESSURE
  26. 26. hypertensive patients who are less than 20/10 mmHg above goal can initially be treated with monotherapy. the major classes of drugs that have been used for monotherapy are a low-dose thiazide diuretic, long-acting angiotensin-converting enzyme (ACE) inhibitor/angiotensin II receptor blocker (ARB), or a long-acting dihydropyridine calcium channel blocker. MONOTHERAPY
  27. 27. recommended therapy with the combination of a long-acting ACE inhibitor/ARB plus a long-acting dihydropyridine calcium channel blocker Among nonobese patients who are already being treated with an ACE inhibitor/ARB plus a thiazide diuretic and have attained goal blood pressure, we suggest stopping the thiazide and switching to a long-acting dihydropyridine calcium channel blocker COMBINATION THERAPY
  28. 28. Although bloodpressure should beloweredrapidlyin patientswithhypertensiveencephalopathy,therearerisksofoverlyaggressivetherapy. In hypertensiveindividuals, theupperandlower limitsofautoregulation ofcerebralblood flowareshifted to higherlevelsofarterialpressure, andrapid lowering ofbloodpressuretobelow thelowerlimitofautoregulationmayprecipitate cerebral ischemia orinfarction asa consequenceofdecreasedcerebral bloodflow. Theinitialgoaloftherapyistoreducemean arterial blood pressurebynomorethan 25%within minutesto2hortoa bloodpressurein therangeof 160/100–110mmHg. IVnitroprusside, a short-acting vasodilator allowsforminute-to-minutecontrol ofbloodpressure TREATING MALIGNANT HYPERTENSION
  29. 29. Primary HTN: also known as essential HTN. accounts for 95% cases of HTN. no universally established cause known. Secondary HTN: less common cause of HTN ( 5%). secondary to other potentially rectifiable causes. TYPES OF HYPERTENSION
  30. 30. SECONDARY HYPERTENTION
  31. 31. CAUSES OF SECONDARY HTN
  32. 32. Onset: at age < 30 yrs ( Fibromuscular dysplasia) or > 55 (atherosclerotic renal artery stenosis), sudden onset (thrombus or cholesterol embolism). Episodic, headache and chest pain/palpitation (pheochromocytoma, thyroid dysfunction). Morbid obesity with history of snoring and daytime sleepiness (sleep disorders) Abdominal bruit especially with a diastolic component (renovascular) Truncal obesity, purple striae, buffalo hump (hypercortisolism SECONDARY HTN-CLUES IN MEDICAL HISTORY
  33. 33. Increased creatinine, abnormal urinalysis (renovascular and renal parenchymal disease) Unexplained hypokalemia (hyperaldosteronism) Impaired blood glucose ( hypercortisolism) Impaired TFT (Hypo-/hyper- thyroidism) SECONDARY HTN-CLUES ON ROUTINE LABS
  34. 34. AutoantibodiesAnti-GBMandANCAmaybepositivewithglomerulonephritis. ANAforconnectivetissue diseases. Plasma catecholaminesElevatedin phaeochromocytoma.Urinarycatecholamines, metanephrinesandvanillylmandelicacid Elevatedin phaeochromocytoma. 24-hoururinarycortisol; Excesscortisolin Cushing’ssyndrome. Low-dosedexamethasonesuppression testFailureofsuppressionofcortisoloccursin Cushing’ssyndrome. OralglucosetolerancetestFailureofsuppressionofserumgrowthhormoneoccursin acromegaly. Plasma renin andaldosteroneHypersecretion ofaldosteronein thepresenceoflowplasma renin levelsconfirmsautonomoussecretioninConn’s syndrome. USabdomenPolycystickidneys.DuplexDoppler can screenforrenalarterystenosis. RenalangiographyRenalarterystenosis. SPECIFIC INVESTIGATIONS
  35. 35. PRIMARY HYPERALDOSTERONISM • Idiopathic – 60%, hyperplasia. • Neoplasm – adenoma (rarely carcinoma) – 35%. Conn syn. F:M-2:1 • Glucocorticoid suppressible –Fusion between CYP11B1 and aldosterone synthase –Aldosterone secretion under regulation of ACTH
  36. 36. Plasma aldosterone to renin ratio — An elevated plasma aldosterone concentration to PRA ratio (PAC/PRA) and an increased PAC are both required for the diagnosis of primary aldosteronism.
  37. 37. APPARENT MINERALOCORTICOID EXCESS
  38. 38. Common cause of secondary HTN (2-5%) HTN is both cause and consequence of renal disease Multifactorial cause for HTN including disturbances in Na/water balance, vasodepressors/ prostaglandins imbalance Renal disease from multiple etiologies. RENAL PARENCHYMAL DISEASE
  39. 39. Prostaglandins produced by the COX- 2 isoenzyme have diuretic and natriuretic effects. NSAIDS
  40. 40. ANY QUESTIONS?

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