Lecture 16 Nov 10th-cv

1DDX: NOVEMBER 10TH, 2006 End of Hypertension Atherosclerosis and Coronary Artery Disease Review of last class: For the test, we will be tested on clinical presentation: primary, secondary, risk factors (most important factors for secondary), target organs. Clinical Symptoms (see class notes from last day) for each organ system affected 2 types of stroke: ischemic, hemorrhagic stroke Early signs of stroke Classification/categories of blood pressure and treatments for different levels. Family history/personal history is very important: gather as much info as possible DDX of secondary hypertention: know this chart for exam. Be able to differentiate between different types of hypertension. END OF NOTE PACKAGE Go over Hypertension Evaluation – Algorithm: understand this chart. Good for future clinical practice. Also Hypertension Management – Algorithm. We may not know everything on the management chart: gives an overview. Don’t need to memorize the chart. Take home message: SEVERE HYPERTENSION MUST BE REFERRED! We can do a lot with non-pharmacologic treatment: lifestyle modification. Antihypertensive drug therapy: major classes: SE= side effects of drugs 1. Diuretics 2. Prevents excess production of catecholamines Beta blockers: SE= bronchioconstriction. Cough may be due to medication, not pathology. 3. Vasodilators 4. Calcium channel blockers: calcium causes constriction of arteries 5. ACE inhibitors 6. Angiotensin II antagonist **see Renin-angiotensin-aldosterone pathway, posted on ecollege.** Best treatment: combination of diuretics and beta blockers If diuretic alone doesn’t work within 6 months, introduce beta blockers (making sure this is primary) Case#1: A 45 year-old African American man is seen in the outpatient department complaining of DDX LECTURE 16, NOVEMBER 10TH – PAGE 1

intermittent throbbing headaches that have occurred every morning for 2 weeks. He has a history of untreated, asymptomatic, sustained high blood pressure (150160/100mmhg) of 10 years’ duration. He has no history of palpations, sweating, tremor, or periodic paralysis. His father was also hypertensive and died from a stroke at age 67. The patient has smoked cigarettes, tow packs per day, for 30 years. His physical examination reveals a blood pressure of 180/120 mmHg and a heart rate of 90 beats per minute and regular. Fundal examination reveals the presence of arterial vasoconstriction. Cardiac examination reveals a laterally displaced PMI (Point of Maximal Impulse), S4, no S3, and no murmur. During abdominal examination, no bruit or mass is found and the neurologic and other systems are unremarkable. After 2 weeks of treatment, the patient is lost to follow-up. Five years later, he presents to the ER complaining of blurring vision and severe headaches. His physical examination at that time reveals a blood pressure of 270/140 mmHg and a heart rate HR 100 bpm. His sensorium and orientation are normal, but fundal examination reveals retinal hemorrhage, exudates and papiledema. Heart examination shows left ventricular lift and S4. On a chest x-ray film, mild to moderate cardiomegaly is noted. His creatinine level is 2.4 mg/dl. (Normal is 1.5) Is this primary or secondary? Risk factors: African American Heavy smoker Male He is 45 years old: secondary tends to affect younger people Family history: father was hypertensive, died of stroke. **Patient has multiple risk factors. What are abnormal results of PE? Stage III hypertension: severe hypertension: THIS PATIENT NEEDS IMMEDIATE ATTENTION. HR: 90 (this is within normal range: Good sign.) Heart is still able to compensate Fundal examination reveals arterial vasoconstriction: ABNORMAL: this is an early sign of HT. Narrowing of the arteries. How do you know if they are arteries or veins? Arteries are brighter, veins are darker.. Displaced PMI: Enlargement of left ventricle. INDICATES CHRONIC HYPERTENSION. Re: heart sounds. Normal is S1 (closure of mitral/tricuspid valve) “lub”, and S2 (closure of aortic and pulmonary valves) “dub”. These are high-pitched sounds. Abnormal are S3, S4. These are low-pitched sounds. S4:Caused by vibrations of atria after closure of valve. Pathological sounds (see Bates: to be discussed in PCD on Nov 13th). Could indicate MI, HT, impending heart failure. S3: sign of impending CHF (patient does not have signs of CHF) Arterosclerosis, narrowing of lumen by atherosclerotic plaque. This will cause a bruit. DDX LECTURE 16, NOVEMBER 10TH – PAGE 2

No signs of constriction in abdominal aorta or renal arteries. This could be a sign of secondary hypertension (ruled out by his physical exam.) He was lost to follow-up: he didn’t come back. His hypertension was unmanaged and continued to get worse. Presented with retinopathy (pathologies of retina) Papiledema: edema of the optic nerve. Vasoconstriction hemorrhage 270/140: sudden elevation to extreme numbers = hypertensive crisis: may accompany stroke, MI, other damage to target organs. In his case, no stroke, MI yet. Damage to eyes. Sensorium and orientation are normal. Sensorium: evaluation of neurological function: no evidence of paralysis. This patient may be on the verge of having a stroke. Hard exudate: accumulation of lipids. Left ventricular lift: due to hypertrophy of left ventricle Cardiomegaly: enlarged heart: reliable sign of chronic hypertension. Elevated creatinine levels: damage to kidneys, compromised filtration. What target organs are involved? Eyes, brain (to some extent), kidney, heart. What is prognosis? Poor if patient is again lost to follow-up. Have to monitor this patient regularly. Drugs and lifestyle modifications are required. Why does HT affect the kidney? High pressure of blood damages kidney. Can compensate for some elevation, but in end stages, there is damage to kidney. This is primary hypertension. We are seeing the presentation of complications from primary hypertension. Case #2 A 28 year-old woman presents to her GP complaining that for the past nine months she has been experiencing episodes consisting of severe pounding headaches, sweating, palpitations and intense anxiety lasting for about 20 minutes. These attacks have been increasing in frequency and now occur on an almost daily basis. They seem to be triggered by bending or laughing. She has not lost weight and her appetite is good. She has had no previous medical illnesses. She is a dental assistant and is married with three children. She is a non-smoker and drinks alcohol occasionally. She is on no medication. On examination, she looks healthy. Her pulse rate is 72/min regular, and blood pressure 156/94. Fundoscopy shows silver-wiring and arteriovenous nipping. Her examination is otherwise normal. The GP orders investigations. Blood work is normal. What is the problem?

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Exposure to mercury? Panic attack? Migraines hypertension pheochromocytoma: pounding headaches, problems bending over, EPISODIC! Primary hypertension is sustained HT Who is the patient? Mother with 3 kids Female 28 years old Hypertension is life-threatening. Think of this first. Primary or secondary? (See Bates for “silver wiring”. Look up for next week) She was tested for catecholamines. She was DX with right adrenal pheochromocytoma, (tumour): more pressure on the abdomen/tumour made the condition worse. Her hypertension was cured when the tumour was removed. White blood cell counts were not elevated because it was not an inflammatory tumour. Second set of class notes: Atherosclerosis and coronary artery disease We can’t observe the pathological mechanisms inside the patient: have to assume they are going on. Ischemia is the key word for coronary artery disease. All clinical presentations will be based on ischemia. Atherosclerosis and hypertension go hand-in-hand. –> means “results in” When coronary arteries are affected by atherosclerosis –> ischemia –> MI Physical activity increases the needs of the body: the heart pumps faster, and if vessels are normal, there is adequate compensation by the coronary tree. However, if the arteries are hard, diminished elasticity, there is an imbalance. The heart needs more oxygen, but the arteries can’t compensate. We won’t see this but we will observe the clinical presentation. Accumulation of waste products (we have to look these up: CO2, lactate): will give signals to nerve fibres, pain. Ischemic pain due to insufficient oxygen supply. PAGE 2 5 types of hyperlipidemia, just understand, don’t need to memorize. Within the plaque formation, also signs of inflammatory process. (She asked us to just read this on our own)

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PAGE 3 Risk Factors: They are the same as for hypertension Age: increased arteriosclerosis Gender: Males more at risk than women. After menopause, decrease of estrogen, women no longer have this advantage. Estrogen has a protective effect on the vessels. HRT can help protect vessels. Low HDL (the GOOD lipoprotein) Hypertension: high BP damages the intima of the arteries: predisposition to athrosclerotic plaques forming. Elevated BP is associated with insulin resistance, glucose intolerance, dyslipidemia. Controlling BP is of paramount importance. High incidence in Canada. • • • • • • • •

Metabolic syndrome: very high risk of developing complications: have to manage these symptoms. Smokers 60% more likely to develop coronary artery disease. Smoking increases carbon monoxide in blood, damages arteries (second hand smoke too) Smoking increases platelet reactivity, adhesiveness, increases chance of thrombus formation. Decreases HDL, increases LDL, increases plasma fibrinogen concentration (more likely to form clots, increases viscosity of blood.) Positive family history: any sudden death? (Usually due to coronary disease) Personal history: type A personality, low physical activity, alcohol. Risk factors may be reversible: can prevent fatal outcome. Reversible: (at pre-hypertensive stage) diet, smoking, obesity

Non-reversible: age, family/personal history, gender Pathogenesis of ischemic heart disease: 2 hypotheses: Lipid hypothesis Chronic endothelial injury Stable plaque: it is there already. Our goal is to keep it stable. Prevent any fissure. Symptom will be stable angina. Unstable plaque (fissure, rupture etc.) With ulceration, plaque becomes more fragile. Elevation of blood pressure, trauma, piece of it may break off. Will see unstable angina (medial emergency): lumen is not blocked completely in angina.

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