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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
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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
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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 Headache 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 |
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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 |
