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 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 % of population <35% aware Complications bring to diagnosis but late…

Classifying Blood Pressure Readings Category Systolic Diastolic Normal <120 < 80 Prehypertension Stage 1 Hyper Stage 2 Hyper =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

ENVIRONMENTAL FACTORS

Table Types and Causes of Hypertension Essential Hypertension Secondary Hypertension Renal Endocrine Cardio Vascular Neurologic

Pathogenesis- Essential Hypertension: ? Pathogenesis - Multifactorial Exact not known Various Hypotheses

Control of Blood Pressure: BP Cardiac Output Peripheral Resistance Blood Volume Na+, Aldosterone Vasoconstrictors Angiotensin II Catecholamines Vasodilators Pg & Kinins Local Factors pH, Hypoxia Neural Factors  Adrenergic – Cons ß Adrenergic - Dil Cardiac Factors Rate & Contract.. Humoral Factors

MECHANISM OF ESSENTIAL HYPERTENSION Homeostasis

SECONDARY HYPERTENSION - CAUSES Endocrine Renal diseases Coarctation of aorta Drugs Alcohol Pregnancy (pre – eclampsia)

ENDOCRINE CAUSES Cushing Syndrome Hyperaldosteronism Pheochromocytoma High BP

ATHEROMA COARCTATION OF AORTA VASCULAR CAUSES:

RENAL DISEASES Renal Artery stenosis

Pathogenesis of Renovascular HTN:  GFR Renin by JGA Angiotensin II Vasoconstriction  P. Resistance Sodium Retention  Blood Volume Aldosterone Hypertension

Target Organ Damage: Blood Vessels Heart Kidney Eyes Brain

Hyperplastic Arteriolosclerosis: Onion Skin Thickening Of arterioles. Narrow Lumen

Hyaline Arteriolosclerosis: Narrow Lumen Hyaline deposition

BLOOD VESSELS A T H E R O MA AORTIC DISSECTION

Heart Attack- Myocardial Infarction

Left Ventricular Hypertrophy: Left Ventricular Hypertrophy

Subarachnoid Haemorrhage:

Cerebral Infarction - Stroke:

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

T Y P E S & S I T E S OF A N E U R Y S M S

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, 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% 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

THORACIC AORTIC ANEURYSM SITE TEAR TRANSVERS OR OBLIQUE10 CM AORTIC VALVES 1-5 CM LONG MIDDLE AND OUTER 1/3

SYPHILITIC ANEURYSM TERTIARY STAGE THORACIC AORTA OBLITERATIVE END ARTERITIS OF VASA VASORUM MEDIAL DESTRUCTION DUE TO ISCHAEMIA TREE BARKING CAR BOVINUM COMPRESSION EFFECTS

DeBakey Classification

Dissection