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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.


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.

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
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)

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 (150-
160/100mmhg) 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
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
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.


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
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

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?


Exposure to mercury?
Panic attack?
pheochromocytoma: pounding headaches, problems bending over, EPISODIC!
Primary hypertension is sustained HT

Who is the patient?

Mother with 3 kids
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.


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)



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.