Lecture 15 Nov 8th-cv

1DDX Lecture November 8th, 2006 Hypertension Case: A 45 year-old African American man is seen in the outpatient department complaining of 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 HT primary or secondary.? Will come back to case at the end of class. (THIS CASE WAS DISCUSSED IN NOVMEBER 10TH CLASS) To treat pt., have to come up with definitive Dx. Need history! Number 1! Always. Data from Physical Examination Investigations: what tests are needed to confirm Dx? Interpretation of lab tests. What is going on? How do you read reports? After getting all of info together, will get assessment, differentiate to get Dx. Need much knowledge to make Dx. Clinical sciences are interconnected, interdependent. Lab Dx, path, ddx. PAGE 1 What is hypertension (HT)? SUSTAINED elevation of systolic or diastolic blood pressure. After 1 measurement that is high, can’t diagnose HT. Have to take subsequent readings. The length of time between follow-ups depends on the reading that you receive.

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Why so important to know about HT? Affects 50 million people in US. 7.1 million deaths per year. HT is called a “silent killer”. No symptoms in early stages, does not seek treatment. Elevated BP is unrecognized. **magnification of Classification of Blood pressure included in note package. Go through this. Normal: <120, <80. Prehypertension: not a disease, but to ID patients at high risk to develop HT. Can help to prevent disease from developing. 2 stages of disease itself. Different BP measurements for both stages. Isolated systolic hypertension: increase in systolic BP, but diastolic BP may still be in normal range. Most often in elderly patient with incompliant arterial tree. HT linked to stroke, heart failure, premature death (esp. in pregnant women). Suboptimal blood pressure: if pt. with suboptimal BP: 115, but has an accumulation risk factors, they are still at risk. Even if the pt. has just suboptimal pressure, but have accumulation of risk factors, they are still at risk (unclear if “suboptimal” it WHO definition of HT which is 160, not >120) PAGE 2 See Recommendations for Follow Up chart (MAGNIFICATION IN NOTE PACKAGE). Base follow up on assessment of individual patient. HT: most common cause for visit to physician. Can affect all ages. Treatable at early stages, important for us to be able to recognize it. What is BP? • result of cardiac output and peripheral vascular resistance. • Have to wait at least 2 minutes before taking blood pressure a second time. Will get false result if you do it again right away. • After inflating cuff to occlude radial pulse, wait 2 minutes before taking BP or you will get a false reading. Could also switch arms, but this may be more awkward for patient. • If you take BP on both sides and you get different readings, take the higher one, or record both, esp. if patient is at risk. PAGE 3 Have to be careful with label of HT, careful with measurement of BP -may medicate pt. Unnecessarily (if you diagnose HT and their BP is normal) -may become hypotensive (as a result of unnecessary medication) -insurance (we are liable!)

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-Inaccurate measurement of blood pressure: may miss dx of ht: hypertensive pt. may think their bp is accurate, but it isn’t normal Magnification of “Patient’s initial BP is out of normal range” Never ask pt. to support their own arm. Their arm must be totally relaxed when you take bp. Shouldn’t take BP at beginning of appt.: white coat syndrome, may have rushed to get to appointment. What is normal for 1 patient may be an “at risk” reading for another patient. Determined by other risk factors. If you ID patient in pre-hypertensive state, have to follow up with them, don’t just let them go. Co-management: most patients will need this, will probably have involvement of MD Severe elevation : immediate referral. Can’t wait until next day. >200 SBP, 120 DBP. Risk Factors: • Why age? Hardened arteries, decreased elasticity, increased resistance • Smoking: vasoconstriction. Have higher incidence of malignant hypertension. Quickly developing complications, refractory (non-responsive) to treatment • Male • Obesity: increased peripheral resistance, increased blood volume, stroke volume. Increased weight contributes to hyperlipidemia • Family history: there is a genetic predisposition to HT. Also want to know personal history: drug (NSAIDs may increase BP), smoking • Sodium intake: leads to retention of water. 1 molecule of sodium retains 2 of water. • Alcohol use: will interfere with metabolism of drugs. Vasoconstrictor • Psychological stress: eg. Exams, family circumstances, finances, etc.) Sympathetic activation, (early vasodilation, but later –> vasoconstriction, elevated blood pressure. • Race: more cases among African Americans, increased sensitivity to sodium • Contraceptive pills: activates renin-angiotensin-aldosterone system. Same risk factors play role in dev. of other CV diseases. Diabetes, stroke, transient ischemic attacks. PAGE 4 Exact pathogenesis of HT is unknown. Know renin-angiotensin-aldosterone system. Activation increases BP, therapies interrupt system. Renin, proteolytic. Released by juxtaglomerular cells under stress of decreased bp. Renin catalyses conversion of Angiotensinogen produced by liver, and becomes AT1 (inactive), converted to AT2 (active) Strong vasoconstrictor. AT2 also stimulates aldosterone production. This causes sodium retention, and water is therefore retained, BP is increased. DDX LECTURE 15, NOVEMBER 8TH – PAGE 3

Need to know if the HT is primary or secondary: this will determine treatment. Primary is a DIAGNOSIS OF EXCLUSION! You have to rule out all possible secondary causes of HT. Secondary HT: has to be ruled out. There is an underlying disease that causes the HT. This only causes 5% of hypertensive conditions. Even seeing this in people less than 20 years of age. Very severe: numbers tend to be very high. Red flag: no family history of hypertension. Unresponsive to treatment because there is another cause of the HT. PAGE 5 For any hypertensive patient, see recommended work-up. Kidney: one of the target organs being affected by HT. Kidney have parenchyma and vasculature that can be affected. **change neuropathy to nephropathy in notes*** Parenchyma is being destroyed: filtration compromised. Renovascular: something is going on with the blood flow to kidney. Could be atherosclerotic plaque: increased production of renin. Coarctation fo aorta: narrowing, could be due to atherosclerosis. Endocrine diseases: • Hyperaldosteronism • Cushing’s disease • Pheochromocytoma Adrenal glands: have cortex. Produce mineralocorticoids: excessive production leads to hyperaldosteronism. Could be due to a tumor of adrenal medulla. If tumour is detected and removed, patient may be cured and HT is stopped. Glucocorticoid excess: Cushing’s disease/syndrome. Increased production of renin substrates. Cushing’s syndrome may also come form hormone therapy, Adrenal medulla: produces catecholamines: excessive production of these hormones is pheochromocytoa. Tumour in adrenal medulla. BP will be elevated. Cannot be treated until tumour is surgically removed. Acromegaly: excessive production of growth hormone promotes moderate retention of sodium. Retain fluid, increase BP. DDX LECTURE 15, NOVEMBER 8TH – PAGE 4

How do we know kidney is involved? 24 hour urine collection. Look at creatinine and protein excretion. Creatinine measures glomerular function. PAGE 6 Normal renal arteriogram: aorta is in the middle of slide. Renal arteries originate from aorta. To Dx renal artery stenosis, listen for bruit over renal artery. Must refer to specialist for renal arteriogram. Could be the cause of hypertention. Renal arteriogram of a nonsmoking white man with hypertension see stenosis of renal artery. Kidney is very sensitive to changes in blood pressure, delivery of blood. Renal arteriogram in a white woman with hypertension see twisted renal arteries causing extreme hypertension. Coarctation of the aorta. Claudication: pain in a large muscle group due to insufficient blood supply. Sign of peripheral arterial disease. Complication of coarcation: dissection of the aorta. Covered in pathology too. **pulses are asymmetric. (Can use this as example for PCD exam) PAGE 7 Cushings: excessive production of glucocorticoids. Weight gain, central trunk edema. Have to treat for Cushing’s first, the HT will disappear. Striae (stretch marks) in Cushing’s are purplish, not silvery like those that follow pregnancy, growth. (**can use all of these as abnormalities for PCD exam) Acromegaly: can ask pt. to bring picture from several years ago to compare. For Ddx: see chart called “clinical features of other secondary causes of hypertension” PAGE 8 Clinical manifestations: no pathoneumonic (SP) signs of ht. Can have many different sys. Target organs: the organs that HT will affect sooner or later. We want to avoid these consequences through treatment.

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Heart: Left ventricular hypertrophy because ht pumps against resistance. Angina (chest pain due to damaged coronary circulation) see list.MI, Coronary art. Disease Kidney: chronic renal failure retinopathy damage to vessels PAGE 9-10 Eye: check Bates for pictures of abnormalities One of first areas to be affected by increased blood pressure is the eye. Grade 1 vascular spasm Grase 2 vascular sclerosis Grade 3 hermlrrages and /or exudates grade 4 papilledema.: edema of optic disk shows the beginning of edema of the brain -how will patient feel if they present with this? Will feed heaviness, blurred vision** (brain tumor, viruses can also cause blurred vision) Brain: very sensitive! Every part resp. for very specific function. Pressure on brain tissue Transient Ischemic attack or stroke may happen 2 types of risk factors for stroke: Modifyable, non-modifyable. 2 types of stroke: ischemic: lack of blood due to blockage, vasoconstriction hemorrhagic: bleeding due to increased permeability (contriction of bv plus high bp, increased permeability: blood goes into blood tissue. Tissue is now under pressure, will damage function of brain. Can assess damage through function. SUDDEN ONSET: key. Transient ischemic attack, it comes and goes. Dt constriction, spasm of bv. Lasts for 15-30 minutes.

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