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HYPERTENSION - systolic blood pressure greater than or equal to 140 mmHg or diastolic blood pressure greater than or equal to 90 mmHg or taking hypertensive medication
American Cardiac society and American heart association - Grades
Elevated arteriolar pressure
Normal - 120/80
Elevated; systolic btwn 120-129 diastolic Less than 80
Stage 1- systole 130-139 or diastole 80-89
Stage 2 systole at least 140, diastole at least 90
Hypertensive Crisis/ malignant hypertension - systolic over 180, diastole over 120,. Patient needing prompt change in medication
Clinical features
Asymptomatic
Headache
Blurred vision
Dizziness
Epidemiology
Age standardized prevalence - 24.5%
Only 15.7% were aware
Factors associated - older age, higher BMI, harmful alcohol use, being male
Classification
Essential/ primary hypertension
Unknown causes but genetics and environmental influences
Secondary
Cardiovascular ( coarctation of aorta, polyarteritis nodosa, high intravascular volume, high CO, rigidity of aorta)
Endocrine
Adrenal hyperfunction eg Cushing, hyperaldosteronism
Exogenous hormones eg glucocorticoids, estrogen, MAO inhibitor, tyramine foods eg chocolate
Physiology
Eg increase in growth hormone
Hyperthyroidism
Pregnancy
Renal- acute glomerulonephritis, chronic glomerulonephritis, polycystic kidney, renal artery stenosis, renal vasculitis, reninomas
Neurogenic
Acute stress eg surgery
Psychogenic
High ICP
Sleep
Pathogenesis of essential hypertension
Genetic factors
As determined by monozygotic and dizygotic twins
Hypertension within families
Polygenic and heterogenic traits
Several mutation or gene polymorphism
Eg aldosterone synthetase - 11 beta hydroxylase
17- alpha hydroxylase
Lead to high secretion of aldosterone, salt water retention, increase plasma volume
Angiotensin II and I receptor altered to increase
Na resorption mutations eg liddle syndrome - salt sensitive hypertension
Environmental - Chinese American
Pathogenicity mechanism
1.Vasoconstriction or arteriosclerosis/ hypertrophy
a. Neurogenic factors increase BP in stress
b. Increase in vasoconstrictor- renin angiotensin aldosterone system, catecholamines, endothelin
c. Arteriosclerosis
2. Sodium retention
Angiotensin- angiotensin I - angiotensin II- Adlosterone- increased mineral corticosteroids- increase Na resorption
Gilelman syndrome- NaCl co transporter
Liddle syndrome- beta and alpha ENAC
Pseudohyperaldosteronism - alpha and beta subunits of ENAC
Result
Vasoconstriction- peripheral resistance
Increased ECF/ intravascular fluid volume
Increased Co
Hypertension
Pathological change
Hyaline arteriosclerosis - in old age, diabetic
Hyaline thickened arterioles wall, luminal narrowing
Chronic BP create turbulence with endothelial damage, leakage of plasma cells across endothelium and hyaline deposit
Hypertrophic arteriosclerosis
Concentric laminated thickening of arterioles wall, onion skin appearance, luminal narrowing
Necrotizing arteriolitis
Focal fibrinoid necrosis in hypertrophic vessels
Complications of hypertension
Hypertensive heart disease
Atherosclerosis
Cerebrovascular accident
Retinopathy
Nephropathy
IUFD/IUFGR
Clinical presentation
Asymptomatic - silent killer
Palpitation
Nausea
Vomiting
Difficulty in breathing
Poor vision
Loss of pregnancy
HYPERTENSIVE HEART disease
Heart muscle disease complicating systemic arteriole hypertension leading to concentric hypertrophy of Left ventricle and Ischemia in absence of ather condition that can cause LV hypertrophy
History of systemic arteriole hypertension
Pathogenesis
Myocyte hypertrophy in response to increased workload due to increased peripheral resistance
Hypertrophic myocardum reduce LV compliance, impairing diastolic filling
Individual myocyte hypertrophy increase the distance for oxygen and nutrient diffusion from adjacent capillaries
Associated coronary artery atherosclerosis accompany hypertension further cause Ischemia
Morphology
Concentric Left ventricle hypertrophy Great than 20mm
Weight 500+ g
Narrow lumen
Microscopy - increased transverse diameter of myocardum, irregular nuclei enlargement, variation in myocyte size , fibrosis, irregular myocardiocytes
Complications of HYPERTENSIVE HEART disease
Heart failure
Pulmonary oedema
Arrythmias - atrial fibrillation
CVAs complicating atrial fibrillation
HYPERTENSIVE retinopathy
Malignant hypertension leads to acute vasospasm and narrowing
Onion skin appearance
Grade I II III
Flame hemorrhages; dot and blot , cotton wool appearance, hard waxy exudate
HYPERTENSIVE nephropathy
Long standing essential hypertension
Endothelial damage
Arteritis
Increased permeability - fibrin
Intravascular thrombosis
Platelets growth factor lead to Intimal smooth muscle hyperplasia
Ischemia to kidney
Angiotensin renin mechanism triggered
Vicious cycle
Gross
Fleas bitten appearance, due to hemorrhage, larger kidney initially, shrunken kidney later with uniform granular surface and capsular adhesion
Microscopy
Fibrinoid necrosis, inflammatory cells infiltrate, hyperplastic arteriolitis ( onion skin) , necrotizing glomerulonephritis - thrombosed capillaries , inflammatory cells infiltrate, infarct
Uncontrollable 60% die in 3. Months
90%. Die in one year
Accelerated
Thrombotic microangiopathy eg HUS, TTP
Intimal edema, RBC fragmentations, onion skin fibrosis
Effects due to placental changes
Abruptio placenta - IUFD, Intrauterine hypoxia
Placental insufficiency -. Small for gestational age, IUFGR, IUFD
Placental changes in hypertension
Infarct
Increased syncytial knots
Hypovascularity of villi
Cytotrophoblastic proliferation
Thickening of trophoblastic basement membrane
Obliterative enlarged endothelial cells in fetal capillaries
Atherosis of spiral arteries in placental bed
Effects
Placental insufficiency
Fetal growth retardation
Due to occlusion of uteroplacental vasculature and placental Ischemia
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