HYPERTENSIVE VASCULAR DISEASE - JU Medicine...2018/01/05  · HYPERTENSIVE VASCULAR DISEASE Arteriolosclerosis Hypertension(HTN) • Cutoffs in diagnosing hypertension in clinical

HYPERTENSIVEVASCULARDISEASE

Arteriolosclerosis

Hypertension(HTN)

• Cutoffsindiagnosinghypertensioninclinicalpracticeè sustaineddiastolicpressures>90mmHg,and/orsustainedsystolicpressures>140mmHg

• Malignanthypertensionà 5%ofHTNpatientspresentwitharapidlyrisingbloodpressurethat,ifuntreated,leadstodeathwithin1to2years.è systolicpressures>200mmHgordiastolicpressures>120mmHgà associatedwithrenalfailureandretinalhemorrhagesàmostcommonlyissuperimposedonpreexistingbenignhypertension

Hypertension(HTN)hasthefollowingpotentialcomplications:

• stroke(CVD)• multi-infarctdementia• atheroscleroticcoronaryheartdisease• cardiachypertrophyandheartfailure(hypertensiveheartdisease)

• aorticdissection• renalfailure

Typesofhypertension

1- essential(idiopathic)hypertension (95%)2- secondaryhypertension:Mostareduetorenaldisease,orrenalarterynarrowing

(=renovascular hypertension),andtoalesserdegreeareduetomanyotherconditions….

1- EssentialHTNAccountsfor90%to95%ofallcases

2- Secondary HTN:

Renal(mostcommonofsecondary)AcuteglomerulonephritisChronicrenaldiseasePolycysticdiseaseRenalarterystenosisRenalvasculitisRenin-producingtumors

EndocrineAdrenocortical hyperfunction (Cushingsyndrome,primaryaldosteronism,CAHlicoriceingestion)Exogenoushormones(glucocorticoids,estrogensympathomimeticsmonoamineoxidase inhibitors)PheochromocytomaAcromegalyHypothyroidism(myxedema)Hyperthyroidism(thyrotoxicosis)Pregnancy-induced(pre-eclampsia)

CardiovascularCoarctation ofaortaPolyarteritis nodosaIncreasedintravascularvolumeIncreasedcardiacoutputRigidityoftheaorta

NeurologicPsychogenicIncreasedintracranialpressureSleepapneaAcutestress,includingsurgery

• Pathogenesisofessential HTN• ?Geneticfactors• ?familialclusteringofhypertension• angiotensinogen polymorphismsandangiotensin IIreceptorvariants;polymorphismsoftherenin-angiotensin system.

• ?Susceptibilitygenesforessentialhypertension:genesthatcontrolrenalsodiumabsorption,etc.

PathogenesisofessentialHTN

• Environmentalfactors• stress,obesity,smoking,physicalinactivity,andhighlevelsofsaltconsumption,modifytheimpactofgeneticdeterminants.

• Evidencelinkingdietarysodiumintakewiththeprevalenceofhypertensionindifferentpopulationgroupsisparticularlystrong.

Morphology

• HTNisassociatedwitharteriolosclerosis(smallarterialdisease)

• Twoformsofsmallbloodvesseldiseasearehypertension-related:

1- hyalinearteriolosclerosis2- hyperplastic arteriolosclerosis

1- Hyalinearteriolosclerosis• withbenign hypertension.• homogeneous,pinkhyalinethickeningofthearteriolarwalls;luminalnarrowing.

• leakageofplasmacomponentsacrossinjuredendothelialcells intovesselwallsandincreasedECMproductionbysmoothmusclecellsinresponsetochronichemodynamicstress.

• Hyalinearteriolosclerosis:Complications- Mostsignificantinkidneysènephrosclerosis (glomerularscarring).

• Othercauseshyaline arteriolosclerosis:1- elderlypatients(normo-tensive)2- diabetis mellitus

2- Hyperplastic arteriolosclerosis

• Withsevere(malignant) hypertension.• "onionskin"concentriclaminatedthickeningofarteriolarwallsàluminal narrowing.

• =smoothmusclecellsandthickened,reduplicatedbasementmembrane.

• Inmalignanthypertensionà fibrinoid vesselwallnecrosis(necrotizingarteriolitis),whichareparticularlyprominentinthekidney

A,Hyalinearteriolosclerosis.Thearteriolarwallisthickenedwiththedepositionofamorphousproteinaceous material,andthelumenismarkedlynarrowed.B,Hyperplastic arteriolosclerosis("onion-skinning")(arrow)causingluminalobliteration

EDEMA

EDEMA 60% of lean body wt. = water

à(2/3) intracellular. à(1/3) extracellular (interstitial fluid) waterà5% blood plasma.

edema = accumulation of interstitial fluid within tissues.

Edema ≠ Extravascular fluid collection in body cavities:- pleural cavity (hydrothorax)- the pericardial cavity (hydropericardium)- peritoneal cavity (hydroperitoneum, or ascites).

Increased Hydrostatic PressureImpaired Venous ReturnCongestive heart failure; Constrictive pericarditis; Ascites (liver cirrhosis); Venous obstruction or compression; Thrombosis; External pressure (e.g., mass); Lower extremity inactivity with prolonged dependency

Arteriolar DilationHeat; Neurohumoral dysregulation

Reduced Plasma Osmotic Pressure (Hypoproteinemia)Protein-losing glomerulopathies (nephrotic syndrome)Liver cirrhosis (ascites); Malnutrition; Protein-losing gastroenteropathy

Lymphatic ObstructionInflammatory; Neoplastic; Postsurgical; Postirradiation

Sodium RetentionExcessive salt intake with renal insufficiencyIncreased tubular reabsorption of sodium

Renal hypoperfusionIncreased renin-angiotensin-aldosterone secretion

InflammationAcute inflammation; Chronic inflammation; Angiogenesis

Mechanisms of edema

Clinical Correlation of edema Subcutaneous edema: - the most common; - important to recognize as it signals potential underlying cardiac or

renal disease- Can impair wound healing or the clearance of infections. ------------- --------- ---------- Brain edema: - life-threateningà brain herniation (extrude) e.g. through the

foramen magnum.

Pulmonary edema: ØCommon causes:- left ventricular failure - renal failure - ARDS- inflammatory and infectious disorders of the lung. Øcan cause death by interfering with normal ventilatory

function & impeding oxygen diffusionØcreates a favorable environment for infections