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Hypertension. Diseases of arterias. C. Hypertensive Vascular Disease TYPES . essential hypertension . About 90-95% of hypertension is idiopathic and apparenly primary, secondary 5-10% is to renal disease or other causes
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Diseases of arterias C. Hypertensive Vascular Disease TYPES . essential hypertension. About 90-95% of hypertension is idiopathic and apparenly primary, secondary 5-10% is to renal disease or other causes About 5% of hypertensive persons show a rapidly rising blood pressure, which, if untreated, leads to death within 1 or 2 years – malignant hypertension.
Diseases of arterias C. Hypertensive Vascular Disease One of the most important risk factors coronary heart disease and cerebrovascular accidents. cardiac hypertrophy with heart failure, aortic dissectin, renal failure.
Diseases of arterias C. Hypertensive Vascular Disease Morphology hyaline arteriolosclerosis (in elderly patients, more severe in patients with hypertesion and diabetes, a homogenous, pink, hyaline thickening of the walls of arterioles with narrowing of the lumen) and hyperplastic arteriolosclerosis(in patients with more severe elavation of blood pressure, there is typical onion-skin, concentric thickening of the walls of arterioles with progressive narrowing of the lumens).
Hypertension - Introduction • Silent Killer – painless – late symptoms • dizziness, headache and visual difficulties • 15- 20 % of population • <35% aware • Complications bring to diagnosis but late…
Classifying Blood Pressure Readings Category Systolic Diastolic Normal <120 < 80 Prehypertension 120-139 80-89 Stage 1 Hyper 140-159 90-99 Stage 2 Hyper < =160 > =100 Malignant Hyper > 210 > 120
Types of Hypertension: • Primary or Essential Hypertension (90-95%) • Secondary Hypertension (5-10%) SUBTYPES • Benign • Malignant
Factors Influencing Essential Hypertension • Genetic • Environmental
Factors Influencing Essential Hypertension Genetic: Genes – • Aldosteron metabolism 17 alpha hydroxylase • Plymorphism- Renin agiotensen loci, recepter • Liddle syndrome- mut –protiens( Na channels) • Mendalian rare • Susceptibility genes unknown • Genes- Na load, sooth muscles constriction, growth, pressor subs level
Risk Factors • Major diet and hyperlipidemia, hypertension, cigarette smoking, diabetes • Minor obesity, lack of exercise, age, male, family history, stress, BCP, High CHO intake, hyperhomocysteinemia
Table 11-3. Types and Causes of Hypertension Essential Hypertension Secondary Hypertension • Renal • Endocrine • Cardio Vascular • Neurologic
Pathogenesis- Essential Hypertension: • ? Pathogenesis - Multifactorial • Exact not known • Various Hypotheses
Cardiac Output Peripheral Resistance BP Control of Blood Pressure: Humoral Factors Vasoconstrictors Angiotensin II Catecholamines Vasodilators Pg & Kinins Blood Volume Na+, Aldosterone Cardiac Factors Rate & Contract.. Local Factors pH, Hypoxia • Neural Factors • Adrenergic – Cons ß Adrenergic - Dil
MECHANISM OF ESSENTIAL HYPERTENSION Homeostasis
ENDOCRINE CAUSES High BP Hyperaldosteronism Pheochromocytoma Cushing Syndrome
VASCULAR CAUSES: ATHEROMA COARCTATION OF AORTA
RENAL DISEASES Renal Artery stenosis
Pathogenesis of Renovascular HTN: GFR Renin by JGA Aldosterone Angiotensin II Sodium Retention Blood Volume Vasoconstriction P. Resistance Hypertension
Target Organ Damage: • BloodVessels • Heart • Kidney • Eyes • Brain
Hyperplastic Arteriolosclerosis: Narrow Lumen Onion Skin Thickening Of arterioles.
Hyaline Arteriolosclerosis: Hyaline deposition Narrow Lumen
BLOOD VESSELS A T H E R O MA AORTIC DISSECTION
Left Ventricular Hypertrophy: Left Ventricular Hypertrophy
Renal Artery stenosis - Atrophy
Benign Nephrosclerosis: Leathery Granularity due to minute scarring
Hypertensive Retinopathy: Hemorrhages (Flame shape) Papilloedema Narrowing of arterioles
HYPERTENSION: INVESTIGATION OF ALL PATIENTS • Urinalysis for blood protein and glucose • Blood urea electrolytes and creatinine Hypokalaemic alkalosis may indicate primary hyperaldosteronism but is usually due to diuretic therapy • Blood glucose • Serum total and high-density lipoprotein (HDL) cholesterol • 12-lead ECG (left ventricular hypertrophy, coronary artery disease)
ANEURYSM • DEFINITION “It is localized, permanent, abnormal dilatation of blood vessels that occurs mostly in the aorta or the heart”
ANEURYSM • DEFINITION TYPES • ETIOLOGYcongenital/ aquired: • MACROSCOPIC: saccular/ fusiform TRUE OR FALSE
ANEURYSM (Contd) • CAUSES : congenital • BERRY ANEURYSM
ANEURYSM (Contd) • CAUSES Aquired INFECTIONS (MYCOTIC) • SYPHILIS TERTIARY- endarteritis of vasavasorum media injury, aortic valve annulusl • TRAUMA • ATHEROSCLEROSIS • CYSTIC MEDIAL DEGENERATION • IMMUNOLOGIC • SUPPURATIVE PROCESS • SEPTIC EMBOLI
ANEURYSM • DEFINITION TYPE • MACROSCOPIC: • Saccular: • Portion of the wall, • thrombus, • 5- 20 cm • Fusiform : cicumferential • 20 cm
ANEURYSM T TRUE: intact vessel wall(thinned) At rosclerosis Syphilis Congenital Ventricular aneurysm FALSE: Ventricular rupture Hematoma extra vascular Arterial dissection
Aneurysms • Abdominal aorta frequently affected • Natural history is to rupture • Ischemic intima and media? • Male caucasians • Early detection
ANEURYSM (Contd) • PATHOGENESIS: • (1)QUALITY OF CT • (2) IMBALANCE OF DEGRADATION AND SYN • OF COLLAGEN • (3) SMOTH MUSCLE AND ECM LOSS(OTHER • THAN COLLAGEN)
ANEURYSM (Contd) PATHOGENESIS: (1) QUALITY OF CT • Marfans syndrome –fibrillin- TGF-b • Loeys Dietz synd – TGF-b • Ehlars Danlos syn – collagen III • Vit C def
ANEURYSM (Contd) • PATHOGENESIS: • (2) IMBALANCE OF DEGRADATION AND SYN • OF COLLAGEN: • Inflammatory infiltrate -MMP-macrophages • atheromatous plaque and vasculitis • TIMMP dec • Genetic predisposition- polymorph ism in • MMP/ TIMMP
ANEURYSM (Contd) • PATHOGENESIS: • (3) SMOTH MUSCLE AND ECM LOSS(OTHER • THAN COLLAGEN) Inappropriate syn • ischemia- degeneration of media, • increased syn of glycosaminoglycan • Atherosclerosis • Hypertention ath
ABDOMINAL AORTIC ANEURYSM • > 50 YEARS, MALE • BELOW RENAL ARTERIES AND ABOVE BIFURCATION OF AORTA • ATHEROSCLEROSIS: plahin thin media, mural thrombi: • MYCOTIC- Salmonella destroys media, • HYPERTENSION • FAMILIAL • CONNECTIVE TISSUE COMPONENT DEFECT • METALLOPROTEINASES (MMPs)
COURSE OF DISEASE • RUPTURE & HAEMORRHAGE OCCLUSION OF BRANCH VESSELS; renal, ilial, meseteric • EMBOLISATION • COMPRESSION OF NEARBY STRUCTURES • PULSATING MASS
COURSE OF DISEASE • RUPTURE & HAEMORRHAGE Nil-less 4 cm 1% - 4-5 cm 11%- 5-6 cm 25%- more 6 cm Expands .2-.3 cm/ yr
TREATMENT OF DISEASE • RUPTURE & HAEMORRHAGE 5cn or more- aggreorssive anti hypertensive surgery stents Mortality: Timely surgery-5% Emergency surgery 50%
THORACIC AORTIC ANEURYSM • CAUSES • MARFANS SYN • LOEYS DIETZ SYN • HYPERTENTION • TERTIARY SYPHILIS • COMPLICATIONS • RESPIRATORY DISTRESS • SWALLOWING DIFF • RUPTURE-CORONARIES