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  1. 1. Hypertension Ahmed A. Ajeebi 4’th Y, Faculty of Medicine, Jazan University
  2. 2. Qs. What’s HTN ?! Who at risk ? How is’t occur ? Pt. , How present ? Emergency HTN ! How to approach ? What about management ?
  3. 3. What’s HTN ? Chronic medical condition in which blood pressure elevated. Blood pressure is force which exerted by blood against the wall of the blood vessels, which is adequate to maintain perfusion during activity and rest. Blood pressure; A. Maximum systolic pressure in the artery when left ventricle contract to force the blood into aorta & other arteries. B. Minimum diastolic pressure in the artery when ventricle relaxed & filling up, blood receiving from veins.
  4. 4. What’s HTN ? Regulation of blood pressure; A. Baroreceptor reflex in medulla “localization in Rt. & Lt. carotid sinus and Aortic arch” B. Renin angiotensin system “for long term” • Kidney - composition • Endogenous vasoconstriction - angiotensin I C. Aldosterone release “adrenal cortex” • Stimulate sodium retention & potassium execration by kidney • Increases fluid retention
  5. 5. What’s HTN ? Arterial blood pressure maintained by cardiac output and systemic vascular resistance, so the relation between systemic arterial pressure and morbidity appear to be quantitative rather than qualitative
  6. 6. What’s HTN ? Background; A. Hypertension is one of the most common worldwide diseases afflicting humans and is a major risk factor for stroke, myocardial infarction, vascular disease, and chronic kidney disease. B. Despite extensive research over the past several decades, the etiology of most cases of adult hypertension is still unknown, and control of blood pressure is suboptimal in the general population. C. Hypertension is the most important modifiable risk factor for coronary heart disease (the leading cause of death in North America), stroke (the third leading cause), congestive heart failure, end-stage renal disease, and peripheral vascular disease, Therefore, health care professionals must not only identify and treat patients with hypertension but also promote a healthy lifestyle and preventive strategies to decrease the prevalence of hypertension in the general population.
  7. 7. What’s HTN ? JNC-8 classification ! ! ! The classification is based on the average of 2 or more readings taken at each of 2 or more visits after initial screening. Stage Systolic pressure Diastolic pressureNormal < 120 mmHg < 80 mmHg Pre - hypertensive 120 - 139 mmHg 80 - 89 mmHg Grade I hypertension 140 - 159 mmHg 90 - 99 mmHg Grade II hypertension > 160 mmHg > 100 mmHg
  8. 8. What’s HTN ? Prehypertension, emphasizes that patients with prehypertension are at risk for progression to hypertension and that lifestyle modifications are important preventive strategies. Hypertension may be categorized as either essential “primary” or secondary.
  9. 9. Who at risk ? Tobacco use, particularly cigarettes, including chewing tobacco Elevated LDL cholesterol (or total cholesterol ≥240 mg/dL) or low HDL cholesterol: component of metabolic syndrome Diabetes mellitus: component of metabolic syndrome Obesity (BMI ≥30 kg/m2): component of metabolic syndrome Age greater than 55 years for men or greater than 65 years for women: increased risk begins at the respective ages; the Adult Treatment Panel III used earlier age cut points to suggest the need for earlier action Estimated glomerular filtration rate less than 60 mL/min Microalbuminuria Family history of premature cardiovascular disease (men < 55 years; women < 65 years) Lack of exercise
  10. 10. How is’t occur ? Hypertension may be primary, which may develop as a result of environmental or genetic causes, or secondary, which has multiple etiologies, including renal, vascular, and endocrine causes. Primary or essential hypertension accounts for 90-95% of adult cases, and a small percentage of patients (2-10%) have a secondary cause. Hypertensive emergencies are most often precipitated by inadequate medication or poor compliance.
  11. 11. How is’t occur ? Primary (essential) hypertension is diagnosed in the absence of an identifiable secondary cause. Risk factor family Hx. of HTN or heart disease, a high sodium diet, smoking, obesity, ethnicity “black>white”, and advanced age. Pt. asymptomatic until complication develop, so pt. should evaluated for end organ damage to the brain”stroke, dementia”, eye “cotton wall exudate, hemorrhage” , heart “LVH” and kidney “chronic kidney disease, proteinuria & artery stenosis”
  12. 12. How is’t occur ? Secondary forms of hypertension, for identifiable causes, such as primary hyperaldosteronism, account for 20% of resistant hypertension (hypertension in which BP is >140/90 mm Hg despite the use of medications from 3 or more drug classes, 1 of which is a thiazide diuretic). other causes; A. Renal causes 2.5-6% “Chronic renal disease, polycystic kidney disease, urinary tract obstruction, renin producing tumor, liddl syndrome” B. Renovascular hypertension “RVHT” causes .2-4% of cases. C. Vascular causes “Coarctation of aorta, vasculitis, collagen vascular disease” D. Endocrine causes account for 1-2% include, exogenous causes include administration of steroids. Another endocrine causes oral contraceptive use oral contraceptive use in association with mild renal disease, family Hx., female older than 35 year
  13. 13. How is’t occur ? E. Exogenous administration of the other steroids used for therapeutic purposes also increases blood pressure (BP), especially in susceptible individuals, mainly by volume expansion, they blocks both “COX-1” and “COX-2” which can inhibit natriuretic effect, which in turn increase sodium retention, also inhibit vasodilation of prostaglandins and produce vasoconstriction enzyme endothelin-1 F. Endogenous hormonal causes; 1. Primary hyperaldosteronism 2. Cushing syndrome 3. Pheochromocytoma 4. Congenital adrenal hyperplasia
  14. 14. How is’t occur ? G. Drugs and toxin; 1. Alcohol 2. cocaine 3. NSAIDs H. Other causes; 1. Hyperthyroidism & hypothyroidism 2. Hypercalcemia 3. Hyperparathyroidism 4. Obstructive sleep apnea 5. Pregnancy induced hypertension
  15. 15. How is’t occur ? I. Neurogenic causes, include; 1. Brain tumor 2. Bulbar poliomyelitis 3. Intrcranial hypertension
  16. 16. How is’t occur ? Environmental and genetic/epigenetic causes; A. Hypertension develops secondary to environmental factors, as well as multiple genes, whose inheritance appears to be complex. Furthermore, obesity, diabetes, and heart disease also have genetic components and contribute to hypertension. B. In an attempt to elucidate the genetic components of hypertension, multiple genome wide association studies (GWAS) have been conducted, revealing multiple gene loci in known pathways of hypertension as well as some novel genes with no known link to hypertension as of yet
  17. 17. How is’t occur ? C. Epigenetic phenomena, such as DNA methylation and histone modification, have also been implicated in the pathogenesis of hypertension. For example, a high salt diet appears to unmask nephron development caused by methylation. D. Despite these genetic findings, targeted genetic therapy seems to have little impact on hypertension. In the general population, not only does it appear that individual and joint genetic mutations have very small effects on BP levels, but it has not been shown that any of these genetic abnormalities are responsible for any applicable percentage of cases of hypertension in the general population
  18. 18. Pt. how present ? Asymptomatic, pt. unaware they have HTN until complicate Non-specific symptom, mild symptom Headache Confusion Morning headache Fatigue SOB Nausea
  19. 19. Pt. how present ? Anxiety Nose bleeding Heart palpitation Chest pain Pale skin Change of vision
  20. 20. • Complication - Stroke - Coronary artery disease - Arterial Fibrillation - Renal Failure. - Erectile Dysfunction - Renovascular HTN - Pheochromocytoma
  21. 21. Emergency HTN The most common hypertensive emergency is a rapid unexplained rise in BP in a patient with chronic essential hypertension, which lead to end organ damage Most patients who develop hypertensive emergencies have a history of inadequate hypertensive treatment or an abrupt discontinuation of their medications Other causes of hypertensive emergencies include the use of recreational drugs, abrupt clonidine withdrawal, post pheochromocytoma removal, and systemic sclerosis, as well as causes of secondary HTN that listed before.
  22. 22. Emergency HTN Pt. with end organ damage revealed by renal disease, chest pain “MI or ischemia”, back pain “aortic dissection”, or change in mental status “hypertensive encephalopathy”
  23. 23. How to approach ? Obtain a history of the patient’s use of over-the-counter medications; herbal medicines such as herbal tea containing licorice, ephedrine/ ephedra, current and previous unsuccessful antihypertensive medication trials; oral contraceptives; ethanol; and illicit drugs such as cocaine The patient’s lifestyle factors should also be included, such as changes in weight, dietary intake of sodium and cholesterol, exercise level, and psychosocial stressors The historical and physical findings that suggest the possibility of secondary hypertension are a history of known renal disease, abdominal masses, anemia, and urochrome pigmentation
  24. 24. How to approach ? A history of sweating, labile hypertension, and palpitations suggests the diagnosis of pheochromocytoma A history of cold or heat tolerance, sweating, lack of energy, and bradycardia or tachycardia may indicate hypothyroidism or hyperthyroidism A history of obstructive sleep apnea may be noted A history of weakness suggests hyperaldosteronism. Kidney stones raise the possibility of hyperparathyroidism
  25. 25. How to approach ? Physical examination revealed elevated blood pressure Routine investigation of the HTN pt include; A. ECG B. Urine dipstick test for protein and blood C. Fasting blood for lipids “total and HDL cholesterol” and glucose D. Serum urea, creatine and electrolyte
  26. 26. How to approach ? If the urea or creatinine is elevated, more specific are renal investigation are indicated A low serum potassium may indicate an endocrine disorder (primary hyperaldosteronism or glucocorticoid excesses)
  27. 27. What about management ? Drugs 1. ACEIs; arterial & venous vasodilation, has advantage in HTN pt. with CHF & diabetic nephropathy. 2. beta-blocker; which decrease heart rate, cardiac out put, ideal in HTN pt. with angina. 3. CCBs; which cause arterial vasodilation. 4. alpha-blocker; cause relaxation of smooth muscle, which has advantage in pt. w/ BPH 5. ARBs; Has benefit of ACEs apart form side its effect “cough”. 6. Diuretics; decrease plasma volume, useful in CHF, smoker & chronic urinary disease. Surgical intervention Life style modification
  28. 28. What about management ? Stage Systolic pressure Diastolic pressure Life style modification Drug therapy Normal < 120 mmHg < 80 mmHg Encourage - Pre - hypertensive 120 - 139 mmHg 80 - 89 mmHg Yes No indication Grade I hypertension 140 - 159 mmHg 90 - 99 mmHg Yes Thiazide Diuretic, ACEIs, beta blocker, CCBs Grade II hypertension > 160 mmHg > 100 mmHg Yes 2 drugs combination, Diuretic + ACEIs, ARB,
  29. 29. What about management ? Treatment of primary HTN ! ! ! Population Agent Uncomplicated Diuretics, beta-blocker, ACEIs CHF Diuretics, beta-blocker, ACEIs, ARBs, Aldosteron antagonist Diabetic Diuretics, beta-blocker, ACEIs, ARBs, CCBs Post- MI beta-blocker, ACEIs, ARBs, aldosteron antagonist Chronic kidney dosease ACEIs, ARBs
  30. 30. What about management ? Etiology Management 1ْ Renal disease ACEIs Renal artery stenosi May treated with angioplasty or stinting OCP user Discontinue “may delayed” Pheochromocytoma alpha agonist & beta blocker, then removal of tumor Conn’s syndrome “hyper aldosteronism” Removal of tumor Cushing’s syndrome Removal of tumor & exogenous steroids Aortic Coarctation Surgical repair
  31. 31. What about management ? Treatment of Emergency HTN ! ! ! Status Management Hypertensive urgency oral hypertensive “beta blocker, clonidine, ACEIs”, with goal lowering BP within 24h Hypertensive emergency IV medication “labetalol, nitroprusside, nicardipine”, with goal lowering BP 25% over first 2 hour to prevent cerebral hypo
  32. 32. I hope it was helpful presentation