+ All Categories

Hypertension

Date post: 07-May-2015
Category:
Upload: marta-r-gerasymchuk-md-phd-associated-professor-ivano-frankivsk-national-medical-university
View: 4,852 times
Download: 0 times
Share this document with a friend
Description:
Prepared by md, PhD., Associate Professor Marta R. Gerasymchuk, pathophysiology department

of 67

Click here to load reader

Transcript
  • 1.Hypertension

2. ActualityActuality Arterial hypertension is a very commonArterial hypertension is a very common condition. Cerebral, coronary and renal vesselscondition. Cerebral, coronary and renal vessels are mainly affected byare mainly affected by the deleterious effect ofthe deleterious effect of this condition, and both acute and chronic organthis condition, and both acute and chronic organ failure may ensue.failure may ensue. Exacerbation of underlyingExacerbation of underlying pathophysiologicpathophysiologic conditions or new precipitating factors can leadconditions or new precipitating factors can lead to hypertensive crisis, either urgencies orto hypertensive crisis, either urgencies or emergencies.emergencies. During hypertensive emergencies, a quick raiseDuring hypertensive emergencies, a quick raise in arterial pressure may lead to acute andin arterial pressure may lead to acute and significant organ dysfunction,significant organ dysfunction, such as aorticsuch as aortic dissection, acute myocardial infarction,dissection, acute myocardial infarction, intracranial bleeding or acute renal failure.intracranial bleeding or acute renal failure. PerioperativePerioperative hypertension often takes thehypertension often takes the shape of a crisis and it can be related toshape of a crisis and it can be related to hypothermia, pain, neuro-hormonal response tohypothermia, pain, neuro-hormonal response to surgical trauma or antihypertensive drugssurgical trauma or antihypertensive drugs withdrawal.withdrawal. 3. CONTENTCONTENT 1. Factors which predetermine the level of blood pressure for a1. Factors which predetermine the level of blood pressure for a man, basal tone of vessels.man, basal tone of vessels. 2. Pressor and depressor systems of organism, their description.2. Pressor and depressor systems of organism, their description. 3. Arterial hypertensions: kinds, classification. Degrees of high3. Arterial hypertensions: kinds, classification. Degrees of high arterial pressure.arterial pressure. 4. Nephrogenic hypertensions: reasons, kinds, pathogenesis.4. Nephrogenic hypertensions: reasons, kinds, pathogenesis. 5. Etiology and pathogenesis of endocrinal hypertension.5. Etiology and pathogenesis of endocrinal hypertension. 6. A role of the sympathetic nervous system in pathogenesis of6. A role of the sympathetic nervous system in pathogenesis of nerogenic hypertension.nerogenic hypertension. 7. Salt hypertension: etiology, mechanisms of development.7. Salt hypertension: etiology, mechanisms of development. 8. Etiology and pathogenesis of essential hypertension.8. Etiology and pathogenesis of essential hypertension. 9. Complication of essential hypertension.9. Complication of essential hypertension. 10. Reasons and mechanisms of arterial hypotension.10. Reasons and mechanisms of arterial hypotension. 4. Determinants of Blood Pressure Components of B/P Pressure of blood against the walls of the arteries The elasticity of the artery walls The volume and thickness of the blood 5. Systolic Blood Pressure (SBP) pressure measured in brachial artery during systole (ventricular emptying and ventricular contraction period) Diastolic Blood Pressure (DBP) pressure measured in brachial artery during diastole (ventricular filling and ventricular relaxation) Mean Arterial Pressure (MAP) "average" pressure throughout the cardiac cycle against the walls of the proximal systemic arteries (aorta) estimated as: .33(SBP - DBP) + DBP Total Peripheral Resistance (TPR) - the sum of all forces that oppose blood flow length of vasculature (L) blood viscosity (V) vessel radius (r) Definitions TPR = ( 8 ) ( V ) ( L ) ( p ) ( r 4 ) 6. Physiological factors affecting Arterial Blood pressurePhysiological factors affecting Arterial Blood pressure AgeAge:: New born: 80/40 mmHgNew born: 80/40 mmHg 4 years: 100/65 mmHg.4 years: 100/65 mmHg. Adults: 120/80 mmHgAdults: 120/80 mmHg After that: Gradually increase due to increase elasticity of arteries.After that: Gradually increase due to increase elasticity of arteries. SexSex:: Children: have equal Blood pressure.Children: have equal Blood pressure. Adults before 45 years: male more than female.Adults before 45 years: male more than female. Adults after 45 years: the diastolic B.P. is more in female than males.Adults after 45 years: the diastolic B.P. is more in female than males. RaceRace:: ABP in oriental is less than in European and American.ABP in oriental is less than in European and American. GravityGravity:: B.P. in upper parts of the body is more than the lower partsB.P. in upper parts of the body is more than the lower parts especially during standing.especially during standing. Meals:Meals: Digestion increases the arterial blood pressure.Digestion increases the arterial blood pressure. Emotions and exerciseEmotions and exercise:: increase the arterial blood pressure.increase the arterial blood pressure. SleepSleep:: Deep quiet sleep decrease A.B.P., while sleep with dreamsDeep quiet sleep decrease A.B.P., while sleep with dreams increase A.B.P.increase A.B.P. 7. Measurements of Blood PressureMeasurements of Blood Pressure 1- Direct Method1- Direct Method The most accurate means for measuring bloodThe most accurate means for measuring blood pressure is directly within an artery (intra-arterial)pressure is directly within an artery (intra-arterial) using a catheter.using a catheter. But because this method is invasive, it is neitherBut because this method is invasive, it is neither practical nor appropriate for repeated measurementspractical nor appropriate for repeated measurements in non-hospital settings, or for large-scale publicin non-hospital settings, or for large-scale public health screenings.health screenings. 2- The mercury-filled sphygmomanometer2- The mercury-filled sphygmomanometer The usual method of measurement, therefore, is aThe usual method of measurement, therefore, is a noninvasive means that uses a sphygmomanometer,noninvasive means that uses a sphygmomanometer, which includes either a column of mercury orwhich includes either a column of mercury or pressure-registering gauge.pressure-registering gauge. 8. Cardiovascular Hemodynamic Basics Flow (Q) Pressure (MAP) P aorta P vena cava = = Resistance (TPR) (8) (V) (L) (p) (r 4 ) Flow (Q) = () (Pa Pv) (r 4 ) (8) (V) (L) V = viscosity of fluid (blood) flowing through the pipe L = length of pipe (blood vessel) r = radius of the pipe (blood vessel) Pa = aortic pressure Pv = venous pressure Normally Resting Q is about 5 - 6 liters / minute BP = CO x PRBP = CO x PR 9. RA RV LUNGS LA LV AORTA ARTERIOLES SYSTEMIC ARTERIES VEINS (CAPACITANCE VESSELS) (100) (92) (40) low compliance 13% of blood volume high compliance 64% of blood volume PO2 = 40 PCO2 = 46 (0) (2) PO2 = 100 PCO2 = 40 PO2 = 160 PCO2 = .3 CAPILLARY BEDS 7% of blood volume 9% of blood volume (7) (13) (3) Ohms Law: Flow (Q) = upstream pressure downstream pressure resistance Systemic Circulation = 100 mmHg 0 mmHg = 100 ml / sec = 6 liters / min Flow (Q) 1 mmHg sec / ml The Closed Cardiovascular Hemodynamic System Mean arterial pressures in red (20) 10. Blood Pressure RegulationBlood Pressure Regulation Systemic arterial pressure is a function ofSystemic arterial pressure is a function of stroke volume, heart rate, and totalstroke volume, heart rate, and total peripheral resistanceperipheral resistance The major organs involved in regulation ofThe major organs involved in regulation of blood pressure are the heart (HR & SV),blood pressure are the heart (HR & SV), the SNS (TPR-total peripheral resistance),the SNS (TPR-total peripheral resistance), and the kidneys (ECF extracellular fluidand the kidneys (ECF extracellular fluid volume & secretion of renin).volume & secretion of renin). (Wynne, Woo, & Olyaei, 2007, p. 1093)(Wynne, Woo, & Olyaei, 2007, p. 1093) 11. Factors Influencing BPFactors Influencing BP CardiacCardiac Heart rate Inotropic state Neural (pons and medulla) Humoral (hormones) CardiacCardiac Heart rate Inotropic state Neural (pons and medulla) Humoral (hormones) Cardiac OutputCardiac Output Renal Fluid Volume ControlRenal Fluid Volume Control Reninangiotensin Aldosterone Atrial natriuretic factor Copyright 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved. 12. Regulative systemsRegulative systems Sympathetic Nervous SystemSympathetic Nervous System BaroreceptorsBaroreceptors Nerve cells in carotid artery & aortic archNerve cells in carotid artery & aortic arch Maintain BP during normal activitiesMaintain BP during normal activities React to increases & decreases in BPReact to increases & decreases in BP BP impulse to brain to inhibit SNS; HR &BP impulse to brain to inhibit SNS; HR & force of contraction; vasodilation of arteriolesforce of contraction; vasodilation of arterioles BP activates SNS; vasoconstriction ofBP activates SNS; vasoconstriction of arterioles; HR & heart contractilityarterioles; HR & heart contractility 1. Barroreceptors of aorta arch and sinus caroticus 13. Sites of Cardiorespiratory Control 14. Increased BP send inhibitory impulse to sympathetic vasomotor center in brainstem; In long-standing hypertension, baroreceptors adjust to elevated BP and reads it as normal; doesnt make adjustments; also becomes less responsive in some older adults 15. On standing up venous return fallsOn standing up venous return falls Cardiac output diminishesCardiac output diminishes Arterial blood pressure is reducedArterial blood pressure is reduced Baroreceptor afferent firing reducedBaroreceptor afferent firing reduced Medullary centres inhibition reducedMedullary centres inhibition reduced THE BARORECEPTOR REFLEX - AN EXAMPLETHE BARORECEPTOR REFLEX - AN EXAMPLE CORRECTION OF POSTURAL HYPOTENSIONCORRECTION OF POSTURAL HYPOTENSION Effect of gravity onEffect of gravity on venous returnvenous return Preload diminishedPreload diminished - Starlings Law- Starlings Law Subject possibly feels faintSubject possibly feels faint as cerebral flow is reducedas cerebral flow is reduced Due to reduced arterial B.P.Due to reduced arterial B.P. VasoconstrictionVasoconstriction TachycardiaTachycardia Raised stroke workRaised stroke work Tend to restore arterial blood pressure Increased sympathetic tone toIncreased sympathetic tone to arteriolesarterioles Reduced vagal tone to s.a.Reduced vagal tone to s.a. nodenode Increased myocardial sympathetic toneIncreased myocardial sympathetic tone 16. Sympatetic activitySympatetic activity Increase BP Increases heart rate and contractility Increase cardiac output Vasoconstriction increasing peripheral vascular resistances Increases sodium and water reabsorption Increases vascular tone at precapillary level Induces vascular remodelling Increase diastolic pressure Chronic Ischemia and AMI Increased left ventricular hypertrofy and oxygen consumption 17. Blood pressure regulation by the renin-angiotensin systemBlood pressure regulation by the renin-angiotensin system and the central roles of sodium metabolism in specificand the central roles of sodium metabolism in specific causes of inherited and acquired forms of hypertension.causes of inherited and acquired forms of hypertension. Components of theComponents of the systemic renin-angiotensinsystemic renin-angiotensin system are shown in black.system are shown in black. Genetic disorders thatGenetic disorders that affect blood pressure byaffect blood pressure by altering activity of thisaltering activity of this pathway are indicated inpathway are indicated in red;red; arrowsarrows indicate sitesindicate sites in the pathway altered byin the pathway altered by mutation. Genes that aremutation. Genes that are mutated in these disordersmutated in these disorders are indicated inare indicated in parentheses. Acquiredparentheses. Acquired disorders that alter blooddisorders that alter blood pressure through effectspressure through effects on thison this pathway arepathway are indicated in blue.indicated in blue. (From Lifton RP, et al: Molecular genetics of human blood pressure variation. Science 272:676, 1996.) 18. Increase BPIncrease BP Renin Angiotensin II AldosteroneAldosterone VasoconstrictionVasoconstriction on systemic andon systemic and renal vasselsrenal vassels Left ventricularLeft ventricular hypertrophyhypertrophy andand myocardialmyocardial ischemiaischemia Increase leftIncrease left ventricularventricular wallwall tensiontension Alteration of renalAlteration of renal arterial andarterial and capillarycapillary vessels wallvessels wall Glomeruar ischemia,Glomeruar ischemia, parenchymal damage,parenchymal damage, proteinuria, end-stageproteinuria, end-stage renal failurerenal failure ADHADH Sodium andSodium and water renalwater renal retentionretention HHypervolemiaypervolemia Effect of renin-angiotensin systemEffect of renin-angiotensin system on cardiovascular homeostasison cardiovascular homeostasis 2.2. ReninReninangiotensinangiotensin systemsystem 19. Mutations altering blood pressure in humans.Mutations altering blood pressure in humans. A diagram of a nephron, the filtering unit of the kidney, is shown. The molecular pathways mediating NaCl reabsorption in individual renal cells in the thick ascending limb of the loop of Henle (TAL), distal convoluted tubule (DCT), and the cortical collecting tubule (CCT) are indicated, along with the pathway of the renin-angiotensin system, the major regulator of renal salt reabsorption. Single gene defects that manifest as inherited diseases affecting these pathways are indicated, with hypertensive disorders in red and hypotensive disorders in blue. Abbreviations: Al, angiotensin I; ACE, angiotensin converting enzyme; All, angiotensin II; MR, mineralocorticoid receptor; GRA, glucocorticoid-remediable aldosteronism; PHA1, pseudohypoaldosteronism, type 1; AME, apparent mineralocorticoid excess; 11b-HSD2, 11b-hydroxysteroid dehydrogenase-2; and DOC, deoxycorticosterone. (From Lifton RP, et al: Molecular mechanisms of human hypertension. Cell 104:545, 2001.) 20. Regulative systems 3. Reninangiotensin-aldosteron system Renin Actination of suprarenal glangs (cortical layer) Na reabsorbtion in kidney increase Angiotensin 2 Aldosteron excretion Na concentration in blood increase, blood osmotic pressure increase Move of extravascular fluid inside the vessels Increase of circulative blood volume (CBV) C increase 21. Mechanism of Action of AldosteroneMechanism of Action of Aldosterone Increases CO by increasing blood volume . 22. BP Regulation: EndotheliumBP Regulation: Endothelium Nitric oxideNitric oxide is secreted by endothelial cellsis secreted by endothelial cells which results in relaxation of blood vesselswhich results in relaxation of blood vessels It also produces local vasodilators, suchIt also produces local vasodilators, such asas prostacylcinprostacylcin andand endothelium-derivedendothelium-derived hyperpolarizing factorhyperpolarizing factor EndothelinEndothelin is an extremely potentis an extremely potent vasoconstrictor and also stimulatesvasoconstrictor and also stimulates vascular smooth muscle growthvascular smooth muscle growth (Wynne, Woo, & Olyaei, 2007, p. 1094)(Wynne, Woo, & Olyaei, 2007, p. 1094) 23. Healthy LifestyleHealthy Lifestyle Maintain a Healthy Blood Pressure: Blood PressureBlood Pressure ClassificationClassification Systolic BPSystolic BP (mm Hg)(mm Hg) Diastolic BPDiastolic BP (mm Hg)(mm Hg) NormalNormal < 120< 120 < 80< 80 PrehypertensionPrehypertension 120 139120 139 80 8980 89 Stage 1 HypertensionStage 1 Hypertension 140 159140 159 90 9990 99 Stage 2 HypertensionStage 2 Hypertension 160 179160 179 100 109100 109 Stage 3 HypertensionStage 3 Hypertension (Hypertensive crisis)(Hypertensive crisis) 180180 110110 Source: Clinical Practice Guidelines Management of Hypertension, 3rd Ed. 2008 February;MOH/P/PAK/156.08(GU) 24. Hypertension:Hypertension: DefinitionDefinition Persistent elevation ofPersistent elevation of Systolic bloodSystolic blood pressurepressure 140 mm Hg140 mm Hg oror Diastolic blood pressureDiastolic blood pressure 90 mm Hg90 mm Hg Worldwide an estimatedWorldwide an estimated 1 billion1 billion peoplepeople have hypertension; about 1 in 3have hypertension; about 1 in 3 Americans affectedAmericans affected Direct relationship between hypertensionDirect relationship between hypertension and cardiovascular disease (CVD)and cardiovascular disease (CVD) 25. ClassificationClassification Arterial hypotensionArterial hypotension Arterial hypertensionArterial hypertension AcuteAcute ChronicChronic SecondarySecondary AP above 139/89 mm HgAP above 139/89 mm Hg PrimaryPrimary AP less than 100/60 mm HgAP less than 100/60 mm Hg 26. Primary HypertensionPrimary Hypertension Etiological TheoriesEtiological Theories Inability of kidneys to excrete sodiumInability of kidneys to excrete sodium Overactive renin/angiotensin systemOveractive renin/angiotensin system Overactive sympathetic nervous systemOveractive sympathetic nervous system Decreased vasodilatory reactionDecreased vasodilatory reaction Resistance to insulin actionResistance to insulin action Genetic Inheritance (polygenic)Genetic Inheritance (polygenic) 27. Risk Factors R/T PrimaryRisk Factors R/T Primary HypertensionHypertension Age/HeredityAge/Heredity SexSex RaceRace ObesityObesity StimulantsStimulants SodiumSodium AlcoholAlcohol StressStress HyperlipidemiaHyperlipidemia DiabetesDiabetes SocioeconomicSocioeconomic StatusStatus 28. Risk Factors forRisk Factors for -- Primary HypertensionPrimary Hypertension Age (>55) Alcohol Cigarette smoking Diabetes mellitus Elevated serum lipids Excess dietary sodium Gender SBP rises with age Alcohol excessive use strongly correlated to hypertension Smoking increases risk for CV disease ; vasoconstriction Diabetes along with hypertension greater risk for target organ disease and usually more severe Hyperlipidemia elevated in people with hypertension; increases risk of atherosclerosis Some pts Na sensitive Males have higher rates of hypertension 55 29. Risk Factors forRisk Factors for Primary HypertensionPrimary Hypertension Family historyFamily history ObesityObesity EthnicityEthnicity Sedentary lifestyleSedentary lifestyle StressStress 30. Primary HypertensionPrimary Hypertension Water and sodium retentionWater and sodium retention AA high sodium intake may resulthigh sodium intake may result in water retentionin water retention Some people are Na sensitiveSome people are Na sensitive (about 20%) ; not everyone(about 20%) ; not everyone with high salt diet developswith high salt diet develops hypertensionhypertension 31. Pathophysiology ofPathophysiology of Primary HypertensionPrimary Hypertension Water and sodium retentionWater and sodium retention Certain demographics areCertain demographics are associated with saltassociated with salt sensitivitysensitivity ObesityObesity Increasing ageIncreasing age African American ethnicityAfrican American ethnicity People with diabetes, renalPeople with diabetes, renal diseasedisease 32. Pathophysiology ofPathophysiology of Primary HypertensionPrimary Hypertension Stress and increased SNS activityStress and increased SNS activity Produces increased vasoconstrictionProduces increased vasoconstriction HRHR Renin releaseRenin release Angiotensin II causes direct arteriolarAngiotensin II causes direct arteriolar constriction, promotes vascularconstriction, promotes vascular hypertrophy and induces aldosteronehypertrophy and induces aldosterone secretionsecretion 33. Pathophysiology ofPathophysiology of Primary HypertensionPrimary Hypertension Insulin resistance & hyperinsulinemia High insulin concentration stimulates SNS activity and impairs nitric oxidemediated vasodilation Not present in secondary hypertension and dont improve when hypertension is treated 34. Risk factors and aetiological influences in hypertensionRisk factors and aetiological influences in hypertension Risk factor or aetiologicalRisk factor or aetiological influenceinfluence Possible rationale and commentPossible rationale and comment MajorMajor Family historyFamily history Inherited tendency probably polygenicInherited tendency probably polygenic Dietary Na highDietary Na high Fluid retention; vascular wall oedema; ion pump defectFluid retention; vascular wall oedema; ion pump defect ObesityObesity Possible artefact of measurement (problem with arm cuff)?Possible artefact of measurement (problem with arm cuff)? Greater perfusion demands of increased body massGreater perfusion demands of increased body mass Reducing weight can reverse borderline HPTReducing weight can reverse borderline HPT AlcoholAlcohol Unknown mechanism; possibly 30% of HPT related to alcohol abuseUnknown mechanism; possibly 30% of HPT related to alcohol abuse Sedentary lifeSedentary life Unknown mechanism; regular exercise lowers BPUnknown mechanism; regular exercise lowers BP Renal diseaseRenal disease Overt or occult renal disease often implicated: cause or effect?Overt or occult renal disease often implicated: cause or effect? MinorMinor AgeAge Stress or type A personalityStress or type A personality Overactive sympathetic nervous system vasoconstriction and/or raised COOveractive sympathetic nervous system vasoconstriction and/or raised CO Difficult to quantify; effect may have been exaggeratedDifficult to quantify; effect may have been exaggerated DietaryDietary Ca, K, Mg Ca, K, Mg Saturated fatSaturated fat Animal productsAnimal products Some evidence,Some evidence, May induce vasoconstriction via endothelial interactionsespecially for KMay induce vasoconstriction via endothelial interactionsespecially for K Vegetarians may have lower BPVegetarians may have lower BP Glucose intoleranceGlucose intolerance Complex interaction between insulin resistance, hyperlipidaemia and HPTComplex interaction between insulin resistance, hyperlipidaemia and HPT RaceRace Increased average BP in urban Blacks: response to stress or dietary salt?Increased average BP in urban Blacks: response to stress or dietary salt? SmokingSmoking NoNo sustained effect on BP itself but greatly exacerbates atheroscleroticsustained effect on BP itself but greatly exacerbates atherosclerotic complicationscomplications BP, blood pressure; Ca, calcium; CO, cardiac output; HPT, hypertension; K, potassium; Mg, magnesium; Na, sodium.BP, blood pressure; Ca, calcium; CO, cardiac output; HPT, hypertension; K, potassium; Mg, magnesium; Na, sodium. 35. HypertensionHypertension Clinical ManifestationsClinical Manifestations Referred to as the silent killerReferred to as the silent killer Frequently asymptomatic until targetFrequently asymptomatic until target organ disease occursorgan disease occurs Or recognized on routine screeningOr recognized on routine screening 36. HypertensionHypertension Clinical ManifestationsClinical Manifestations often secondary to target organ disease Can include: Fatigue, reduced activity tolerance Dizziness Palpitations, angina Dyspnea 37. Target Organ DamageTarget Organ Damage Caused by damage to the bodys blood vesselsCaused by damage to the bodys blood vessels which particularly affect the following organs:which particularly affect the following organs: Blood VesselsBlood Vessels HeartHeart KidneysKidneys BrainBrain EyesEyes 38. HypertensionHypertension ComplicationsComplications Target organ diseases occur mostTarget organ diseases occur most frequently in:frequently in: HeartHeart BrainBrain Peripheral vasculaturePeripheral vasculature KidneyKidney EyesEyes 39. Hypertension-Hypertension-ComplicationsComplications Cerebrovascular diseaseCerebrovascular disease Stroke Peripheral vascular diseasePeripheral vascular disease Nephrosclerosis Retinal damageRetinal damage AtherosclerosisAtherosclerosis most common cause of cerebrovascular disease; hypertension major risk factor for cerebral atherosclerosis and stroke AtherosclerosisAtherosclerosis in peripheral blood vessels too; can lead to PVD, aortic aneurysm, aortic dissection Hypertension one of leading causes of end-stage renal disease, esp. in African-Americans; some degree of renal dysfunction usual in person with even mild BP elevations RetinaRetina is only place blood vessels can be directly visualized; if see damage there then indicates damage in brain, heart, & kidney too; Can cause blurring, retinal hemorrhage and blindness 40. Accelerated-malignant HTAccelerated-malignant HT Fundoscopic changesFundoscopic changes Retinal hemorrhagesRetinal hemorrhages ExudatesExudates PapilledemaPapilledema 41. Wong, T. Y. et al. N Engl J Med 2004;351:2310-2317 Examples of Mild Hypertensive Retinopathy AV nicking Focal narrowing AV nicking Copper wiring 42. Secondary HypertensionSecondary Hypertension It is caused by another diseaseIt is caused by another disease process such as:process such as: Renal FailureRenal Failure Diabetes MellitusDiabetes Mellitus Cushings SyndromeCushings Syndrome Primary AldosteronismPrimary Aldosteronism Coarctation of the AortaCoarctation of the Aorta PheochromocytomaPheochromocytoma Sleep ApneaSleep Apnea 43. Secondary hypertension representSecondary hypertension represent symptoms of such diseasessymptoms of such diseases 1. Diseases of kidneys: glomerulonephritis (14 %), pielonephritis, interstitial nephritis due to abusing analgetics, hereditary nephritis (syndrome Alports), polycytosis kidney. 2. Stenosis of renal artery (1 %). Hypertension arises not in each stenosis. The most often reason of stenosis, caused atherosclerotic platelits(at 70-80 of %), which damage usually proximal third of renal artery on the one hand. Other reason of stenosis with hypertension its fibromuscular hyperplasia of an average third of renal artery. It, as a rule, double-side and more often happens at the women. The mechanism of hypertension in stenosis of renal artery hyperproduction of renin. 44. Secondary hypertension representSecondary hypertension represent symptoms of such diseasessymptoms of such diseases 3. Primary aldosteronism (Cnn syndrome)3. Primary aldosteronism (Cnn syndrome) in 1 % in 1 % of cases. The reasons unilateral adenomaof cases. The reasons unilateral adenoma glomerular zone adrenal glands or double-sideglomerular zone adrenal glands or double-side diffuse hyperplasia of adrenal glands.diffuse hyperplasia of adrenal glands. 4. Paraganglioma (1 %)4. Paraganglioma (1 %) tumour from chromaffin tumour from chromaffin cells of medullarcells of medullar layer adrenal glands or sympatheticlayer adrenal glands or sympathetic nerves, as a rule nerves, as a rule benighnbenighn. In paraganglioma is. In paraganglioma is increased both cardiac output, and peripheralincreased both cardiac output, and peripheral resistance.resistance. 5. Coarctation of the aorta is an anatomic defect5. Coarctation of the aorta is an anatomic defect, in, in which aorta in pectoral or abdominal department iswhich aorta in pectoral or abdominal department is narrowed to such extend, that it represents seriousnarrowed to such extend, that it represents serious barrier for blood circulation. In all vessels, whichbarrier for blood circulation. In all vessels, which depart from the aorta proximal of narrowing, thedepart from the aorta proximal of narrowing, the resistance increases and is increased arterialresistance increases and is increased arterial pressure.pressure. 45. Pheochromocytoma A pheochromocytoma is a tumor of chromaffin tissue, which containsA pheochromocytoma is a tumor of chromaffin tissue, which contains sympathetic nerve cells.sympathetic nerve cells. The tumor is most commonly located in the adrenal medulla but canThe tumor is most commonly located in the adrenal medulla but can arise in other sites, such as sympathetic ganglia, where there isarise in other sites, such as sympathetic ganglia, where there is chromaffin tissuechromaffin tissue. Although only 0.1% to 0.5% of persons with. Although only 0.1% to 0.5% of persons with hypertension have an underlying pheochromocytoma, the disorder canhypertension have an underlying pheochromocytoma, the disorder can cause serious hypertensive crises.cause serious hypertensive crises. Eight percent to 10% of the tumors are malignant.Eight percent to 10% of the tumors are malignant. Like adrenal medullary cells, the tumor cells of a pheochromocytomaLike adrenal medullary cells, the tumor cells of a pheochromocytoma produce and secrete the catecholaminesproduce and secrete the catecholamines epinephrine andepinephrine and norepinephrine.norepinephrine. TheThe hypertensionhypertension that develops is the result of a massive release ofthat develops is the result of a massive release of these catecholamines. Their release may be paroxysmal, rather thanthese catecholamines. Their release may be paroxysmal, rather than continuous, causing periodic episodes of headache, excessivecontinuous, causing periodic episodes of headache, excessive sweating, and palpitations.sweating, and palpitations. HeadacheHeadache is the most common symptom and can be quite severe.is the most common symptom and can be quite severe. Nervousness, tremor, facial pallor, weakness, fatigue, and weight lossNervousness, tremor, facial pallor, weakness, fatigue, and weight loss occur less frequently. Marked variability in blood pressure betweenoccur less frequently. Marked variability in blood pressure between episodes is typical.episodes is typical. Some persons with pheochromocytoma have paroxysmal episodes ofSome persons with pheochromocytoma have paroxysmal episodes of hypertension, sometimes to dangerously high levels; others may havehypertension, sometimes to dangerously high levels; others may have sustained hypertension; and some may even be normotensive.sustained hypertension; and some may even be normotensive. 46. Peripheral Arterial DiseasePeripheral Arterial Disease (PAD)(PAD) PAD is equivalent in risk to ischemic heart disease.PAD is equivalent in risk to ischemic heart disease. Any class of drugs can be used in most PAD patients.Any class of drugs can be used in most PAD patients. Other risk factors should be managed aggressively.Other risk factors should be managed aggressively. Aspirin should be used.Aspirin should be used. 47. Hypertension in OlderHypertension in Older PersonsPersons More than two-thirds of people over 65 have HTN.More than two-thirds of people over 65 have HTN. This population has the lowest rates of BP control.This population has the lowest rates of BP control. Treatment, including those who with isolated systolic HTN,Treatment, including those who with isolated systolic HTN, should follow same principles outlined for general care ofshould follow same principles outlined for general care of HTN.HTN. Lower initial drug doses may be indicated to avoid symptoms;Lower initial drug doses may be indicated to avoid symptoms; standard doses and multiple drugs will be needed to reach BPstandard doses and multiple drugs will be needed to reach BP targets.targets. 48. Postural HypotensionPostural Hypotension Decrease in standing SBP >10 mmHg, when associatedDecrease in standing SBP >10 mmHg, when associated with dizziness/fainting, more frequent in older SBPwith dizziness/fainting, more frequent in older SBP patients with diabetes, taking diuretics, venodilators, andpatients with diabetes, taking diuretics, venodilators, and some psychotropic drugs.some psychotropic drugs. BP in these individuals should be monitored in the uprightBP in these individuals should be monitored in the upright position.position. Avoid volume depletion and excessively rapid doseAvoid volume depletion and excessively rapid dose titration of drugs.titration of drugs. 49. Hypertension in WomenHypertension in Women Hypertensive disorders complicate 6% to 8% ofHypertensive disorders complicate 6% to 8% of pregnancies.pregnancies. They are the second leading cause, after embolism, ofThey are the second leading cause, after embolism, of maternal mortality in the United States, accounting formaternal mortality in the United States, accounting for almost 15% of such deaths.almost 15% of such deaths. Hypertensive disorders also contribute to stillbirths andHypertensive disorders also contribute to stillbirths and neonatal morbidity and mortality.neonatal morbidity and mortality. The incidence of hypertensive disorders of pregnancyThe incidence of hypertensive disorders of pregnancy increases with maternal age and is more common inincreases with maternal age and is more common in African-American women.African-American women. 50. Classification of High Blood Pressure inClassification of High Blood Pressure in PregnancyPregnancy Classification Description GestationalGestational hypertensionhypertension Blood pressure elevation, without proteinuria, that isBlood pressure elevation, without proteinuria, that is detected for the first time during midpregnancy anddetected for the first time during midpregnancy and returns to normal by 12 weeks postpartum.returns to normal by 12 weeks postpartum. ChronicChronic hypertensionhypertension Blood pressure 140 mm Hg systolic or 90 mm HgBlood pressure 140 mm Hg systolic or 90 mm Hg diastolic that is present and observable before the 20thdiastolic that is present and observable before the 20th week of pregnancy. Hypertension that is diagnosed forweek of pregnancy. Hypertension that is diagnosed for the first time during pregnancy and does not resolvethe first time during pregnancy and does not resolve after pregnancy also is classified as chronicafter pregnancy also is classified as chronic hypertension.hypertension. Preeclampsia-Preeclampsia- eclampsiaeclampsia Pregnancy-specific syndrome of blood pressure elevationPregnancy-specific syndrome of blood pressure elevation (blood pressure >140 mm Hg systolic or >90 mm Hg(blood pressure >140 mm Hg systolic or >90 mm Hg diastolic) that occurs after the first 20 weeks ofdiastolic) that occurs after the first 20 weeks of pregnancy and is accompanied by proteinuria (urinarypregnancy and is accompanied by proteinuria (urinary excretion of 0.3 g protein in a 24-hour specimen).excretion of 0.3 g protein in a 24-hour specimen). PreeclampsiaPreeclampsia superimposedsuperimposed on chronicon chronic hypertensionhypertension Chronic hypertension (blood pressure 140 mm Hg systolicChronic hypertension (blood pressure 140 mm Hg systolic or 90 mm Hg diastolic prior to 20th week ofor 90 mm Hg diastolic prior to 20th week of pregnancy) with superimposed proteinuria and with orpregnancy) with superimposed proteinuria and with or without signs of the preeclampsia syndromewithout signs of the preeclampsia syndrome 51. 1st period functional violations (heart hypertrophy) 2d period Pathological changes in arteries and arterioles (dystrophy): - Arterioles sclerosis - Arterioles wall infiltration by plasma (leads to dystrophy) - Arterioles necrosis (hypertonic crisis arises in clinic) - Veins wall thickening Arterial hypertension after-effects 52. 33dd periodperiod Secondary changes in organs and systemsSecondary changes in organs and systems KidneyKidney ((nephrosclerosisnephrosclerosis andand chronicchronic kidneykidney insufficiencyinsufficiency)) KidneyKidney ((nephrosclerosisnephrosclerosis andand chronicchronic kidneykidney insufficiencyinsufficiency)) CNSCNS brain hypoxiabrain hypoxia neurons destructionneurons destruction apoplexyapoplexy ((because vessels destruction and rupturebecause vessels destruction and rupture leads toleads to brain hemorrhagesbrain hemorrhages and brainand brain destructiondestruction)) CNSCNS brain hypoxiabrain hypoxia neurons destructionneurons destruction apoplexyapoplexy ((because vessels destruction and rupturebecause vessels destruction and rupture leads toleads to brain hemorrhagesbrain hemorrhages and brainand brain destructiondestruction)) HeartHeart Decompensate heart failureDecompensate heart failure HeartHeart Decompensate heart failureDecompensate heart failure Organs of visionOrgans of vision - retinopathyretinopathy ((retinasretinas vessels injuryvessels injury)) - hemorrhages and separation (exfoliation) ofhemorrhages and separation (exfoliation) of retinaretina,, that leads to blindnessthat leads to blindness Organs of visionOrgans of vision - retinopathyretinopathy ((retinasretinas vessels injuryvessels injury)) - hemorrhages and separation (exfoliation) ofhemorrhages and separation (exfoliation) of retinaretina,, that leads to blindnessthat leads to blindness Endocrine systemEndocrine system Glands atrophy and sclerosisGlands atrophy and sclerosis Endocrine systemEndocrine system Glands atrophy and sclerosisGlands atrophy and sclerosis Arterial hypertension after-effectsArterial hypertension after-effects 53. Hypertensive crisisHypertensive crisis DefinitionDefinition Severe elevation in BP ( >220/120 mmHg)Severe elevation in BP ( >220/120 mmHg) Sub classified into emergency and urgencySub classified into emergency and urgency Hypertensive emergencyHypertensive emergency Require an immediate reduction in BP ( 1 hr )Require an immediate reduction in BP ( 1 hr ) Rx IV therapy and in ICURx IV therapy and in ICU Hypertensive urgencyHypertensive urgency No evidence of progressive end-organ injuryNo evidence of progressive end-organ injury Require only gradual reduction in BP in 24-48 hrRequire only gradual reduction in BP in 24-48 hr 54. Laboratory TestsLaboratory Tests Routine Tests Electrocardiogram Urinalysis Blood glucose, and hematocrit Serum potassium, creatinine, or the corresponding estimated GFR, and calcium Lipid profile, after 9- to 12-hour fast, that includes high- density and low-density lipoprotein cholesterol, and triglycerides Optional tests Measurement of urinary albumin excretion or albumin/creatinine ratio More extensive testing for identifiable causes is not generally indicated unless BP control is not achieved 55. Collaborative CareCollaborative Care Lifestyle ModificationsLifestyle Modifications Wt. reduction 10 kg (22 lb) loss; SBP by 5-20 mm Hg DASH eating plan (dietary approaches to stop hypertension) Na reduction


Recommended