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End of Hypertension
Atherosclerosis and Coronary Artery Disease
Clinical Symptoms (see class notes from last day) for each organ system affected
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!
Case#1:
A 45 year-old African American man is seen in the outpatient department complaining of
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)
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)
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.
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.
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.
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.
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.
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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.
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.