Hypertension Lecture Notes PDF

pathology - CVS Hypertension LECTURE (4) hypertension Dr. M. Shalaby pathology - CVS Hypertension DEFINITION  Persistent elevation of systemic blood pressure above 140/90....

pathology - CVS Hypertension LECTURE (4) hypertension Dr. M. Shalaby pathology - CVS Hypertension DEFINITION  Persistent elevation of systemic blood pressure above 140/90. ACCORDING TO ACCORDING TO CAUSE SEVERITY, COURSE & PROGNOSIS CLASSIFICATION ① Primary (essential) HTN. ① Benign ② Secondary HTN. ② Malignant (accelerated) PRIMARY HYPERTENSION SECONDARY HYPERTENSION INCIDENCE Most common (95% of cases). Less common (5% of cases). UNKNOWN CAUSE. SECONDARY TO OTHER DISEASE AS:  Genetic factors: ① Renal: renal diseases, renal ischemia. ① Gene defects affecting enzymes ② Endocrine: hyperaldosteronism, involved in aldosterone metabolism pheochromocytoma, Cushing $. →↑ secretion of aldosterone →↑ ③ Coarctation of the aorta. renal salt & water reabsorption. ④ Polycythemia rubra vera. ② Mutation in proteins affecting ⑤ Toxemia of pregnancy. renal sodium reabsorption. ⑥ Contraceptive pills. ETIOLOGY  Liddle syndrome mutation in protein in epithelial Na channel →↑ renal Na reabsorption.  Environmental factors:  Increased dietary sodium intake.  Stress, obesity  Smoking, physical inactivity. Dr. M. Shalaby pathology - CVS Hypertension  Blood pressure is the function of cardiac output & vascular peripheral resistance. BP = COP x PR  Increased through: ① Increased blood volume. CARDIAC OUTPUT ② Increased heart rate. ③ Increased cardiac contractility.  Determined mainly at level of arterioles.  Regulated through: ① Humoral vasoconstrictors (angiotensin II, catecholamine, endothelin) ② Humoral vasodilators (kinin, prostaglandins, NO). PERIPHERAL ③ Neural factors: through arterial baroreceptors. In primary RESISTANCE hypertension, the baroreceptors & their reflexes become less sensitive to elevated BP. ④ Auto regulation: increased blood flow → VC to protect tissues from over perfusion. EARLY KEY  Salt & water retention → ↑ blood volume & cardiac output. INITIATING EVENT  Additional sodium is excreted by kidneys to equal the intake & ESTABLISHED prevent further fluid retention. HYPERTENSION  Cardiac output returns to normal.  Increased peripheral resistance (increased arteriolar tone). Dr. M. Shalaby pathology - CVS Hypertension BENIGN HYPERTENSION MALIGNANT HYPERTENSION INCIDENCE 90-95% 5-10% Age  Starts after 40 years.  30-40 years.  Pressure rises gradually to  Pressure rises rapidly over 200/120. Onset 180/100.  It can develop in normotensive individuals or superimposed on preexcisting benign HTN. Course  Prolonged for many years.  Short for months or 1-2 years. ① CARDIAC CHANGES  Compensated stage:  Concentric left ventricular hypertrophy with bulge of inter ventricular septum.  Decompensated stage:  Left ventricle is dilated with thin wall.  Hypertrophy of left atrium then dilation, pulmonary hypertension & right sided heart failure. BENIGN HYPERTENSION MALIGNANT  Minimal effect: HYPERTENSION  Due to no time to occur unless it occurs on top of benign hypertension. Dr. M. Shalaby pathology - CVS Hypertension ② VASCULAR CHANGES ① Hyaline arteriolosclerosis. BENIGN ② Elastosis. ARTERIOLOSCLEROSIS  Atheroma is more severe. ① Necrotising arteriolitis (fibrinoid necrosis) MALIGNANT ② Cellular hyperplasia (hyperplastic arteriolosclerosis with onion skin ARTERIOLOSCLEROSIS appearance of the vessels.  Atheroma is less severe. BENIGN ARTERIOLOSCLEROSIS MALIGNANT ARTERIOLOSCLEROSIS ③ RENAL CHANGES BENIGN NEPHROSCLEROSIS MALIGNANT NEPHROSCLEROSIS GROSS SIZE  Small (primary contracted kidney).  Normal or enlarged.  Adherent.  Strips easily and shows areas of CAPSULE subcapsular hemorrhage.  Reduced cortex and medulla  Areas of hemorrhage  Not demarcated from each other  Arteries at the base of pyramids C/S  Arteries at the base of the pyramids are are and dilated. thick and dilated MICROSCOPIC BLOOD  Hyaline arteriolosclerosis of the  Necrotising arteriolitis of the VESSELS afferent arterioles. afferent arterioles.  Non-functioning: atrophy, fibrosis &  Non-functioning: necrosis & hyalinosis. fibrosis. NEPHRONS  Functioning: compensatory  Functioning: mild compensatory hypertrophy. dilatation. INTERSTITISL  Fibrosis & few lymphocytes  Minimal fibrosis & hemorrhage. TISSUE thick Dr. M. Shalaby pathology - CVS Hypertension ④ BRAIN CHANGES  Intracerebral microaneurysms BENIGN  Related to small vessels of basal ganglia. HYPERTENSIVE  Multiple, small ENCEPHALOPATHY  May rupture to give massive spontaneous cerebral hemorrhage.  Arterial spasm, leads to MALIGNANT ① Cerebral edema. HYPERTENSIVE ② Papilledema. ENCEPHALOPATHY ③ Encephalomalcia, liquafactive necrosis due to ischemia. ④ Massive spontaneous cerebral hemorrhage. Dr. M. Shalaby pathology - CVS Hypertension ⑤ RETINAL CHANGES BENIGN HYPERTENSIVE  Retinal hemorrhage & exudate. RETINOPATHY MALIGNANT  Retinal hemorrhage, edema & necrosis. HYPERTENSIVE  May lead to blindness. RETINOPATHY BENIGN HYPERTENSION MALIGNANT HYPERTENSION ① Left ventricular failure. ① Progressive uremia. ② Cerebral hemorrhage. ② left ventricular failure. ③ Chronic uremia. ③ Cerebral hemorrhage. Dr. M. Shalaby