L14- Hypertension Year 4 Internal Medicine Notes OmpathStudy

L14- Hypertension Year 4 · Internal Medicine Collection: 4TH YEAR ALL NOTES / IMED / I MED BEAUTIFUL NOTES / CVS -- Lecture 13 \nEditing file\n\n Hypertension \n★ To be able to recognize the definition of hypertension.\n★ To be able to identify the stages of hypertension ( ACC/AHA\n-European society of cardiology/European society of\nhypertension (ESC/ESH).\n★ To find out the complication of hypertension.\n★ To learn how to measure blood pressure.\n★ To acquire knowledge on how to treat hypertension.\n\n Color index: Color index:\nOriginal text Females slides Males slides\nDoctor’s notes Text book Important Golden notes Extra \n\n Introduction 2\n\n Hypertension is a condition in which arterial BP is chronically elevated. BP occurs\nDefinition within a continuous range, so cutoff levels are defined according to their effect on\npatients’ risk.\n\n ◄ Epidemiology of Hypertension:\n● The global prevalence of hypertension was ● The overall prevalence of hypertension in\nestimated to be 1.13 billion in 2015 Saudi is 25.5-31.4%.\n● The 4th most common cause of death ● More common with advancing age.\nworldwide. ● Prevalence of 60% in people aged 60 years.\n● 20% of deaths worldwide are related to ● Only 72% are aware of their disease2.\nhypertension. ● 55% of participants on medication for\n● The overall prevalence of hypertension in hypertension had their blood pressure\nadults is around 30 - 45%. uncontrolled3.\n● The onset of primary hypertension ranges\nbetween 25 to 55 years, mainly in 40 to 50.1.\n\n ◄ Mechanism of Blood Pressure:\nStroke Volume Salt and Water Retention\n\n HR\nBlood Pressure\n\n Elasticity\n●\nSympathetic ●\n●\nParasympathetic ●\n● Angiotensin II\n(vasoconstrictor)\nHormonal\n●\n●\nEndothelium\n\n - Recall from cardio physiology: BP= CO (SV x HR) x SVR. So increasing CO or SVR will increase BP.\nWhat are the determinants of SVR?\n1. Loss of Elasticity: Vessels in old ppl are stiff and rigid due to loss of elasticity so it doesn’t Vasodilate → ↑BP\n2. Sympathetic activation: e.g. Anxiety and stress → ↑BP\n3. Parasympathetic activation: When baroreceptors in carotid are stimulated → Activate Beta-receptors → vasodilation → ↓BP\n4. Hormones: Think of adrenal gland hormone and angiotensin II. Angiotensin II is the most important hormone and has the\nstrongest effect.\n5. Endothelial factors: Release endothelin-1 (vasoconstrictor) in response to damage of blood vessels. It also releases NO (Vasodilator)\n\n1: if patient is younger than 40 year old, HTN is usually secondary. 2: Because HTN is a silent killer, mostly asymptomatic 3: Either due to noncompliance because of the side effects of the drugs, or the fact that they need more than one drug to control it. \n\n Types of Hypertension 3\n\n A. Primary (Essential) Hypertension (90-95%):\n● No cause can be found. \nRisk Factors \nModifiable Non-Modifiable \n● Obesity-metabolic syndrome ● Family history of essential HTN\n● Unhealthy diet: ● Aging\n○ Excessive salt intake1 ● Race (African american) & genetic\n○ low potassium intake2\n● Excessive alcohol intake\n● Polycythemia → High blood volume (↑SV)\n● Lack of exercise3\n● Non-steroid anti-inflammatory drugs4 \nCaffeine and smoking increase the BP acutely but are not risk factors for the development of chronic\nessential HTN. Hence why you shouldn’t drink coffee or smoke for at least half an hour before measuring\nBP (Bc it will temporarily raise BP)\n\n B. Secondary Hypertension (5-10%): C’s \nPrimary renal disease Renovascular disease Oral contraceptives\n\n As they ↑salt and water retention,\ne.g. Chronic kidney disease (CKD), e.g. Renal artery stenosis\n↑weight and ↑production of\nPolycystic kidney disease (PCKD), (RAS). In RAS you will hear\nangiotensinogen.\nGlomerulonephritis abdominal bruits on\nOther drugs: corticosteroids,\nauscultation. sympathomimetic agents, NSAIDs and\nCarbenoxolone \nSleep apnea syndrome Primary hyperaldosteronism Cushing’s syndrome\nHighly recommend you read about this topic!!\nClick here\n\n Breathing-related sleep disorder and is AKA Conn’s syndrome. Excess of aldosterone due Typical clinical features include\ntypically associated with obesity. Have an to adrenal hyperplasia or adrenal adenoma. central obesity, thin, easily bruisable\nAldosterone causes Na-water retention and skin, abdominal striae, secondary\nincreased risk of hypertension, heart hypertension, hyperglycemia, and\nhypokalemia. often asymptomatic and found to\nfailure, myocardial infarction and stroke. proximal muscle weakness.\nhave hypertension at routine health checks. \nPheochromocytoma Coarctation of the aorta Other endocrine\n\n Narrowing of aorta. e.g. Hyperparathyroidism,\nIncrease production of adrenaline\nSigns and Symptoms: Difference in Thyrotoxicosis, Acromegaly, primary\nfrom adrenal gland\nradio-radial artery, BP in leg will be hypothyroidism, congenital adrenal\nSigns & Symptoms: Episodic Sudden\nlower than the arm (Normally leg has hyperplasia (CAH) due to\nattack, anxiety, tac