What values designate hypertension?

> 140/90

This must be a sustained value. Blood pressures can fluctuate depending on activity and stressors.

BP = CO x TPR

CO is dependent upon blood volume and by extension sodium homeostatsis (CO = SV x HR)

TPR =  total peripheral Resistance

Outline the Renin-Angiotensin System:

Atrial Natriuretic Peptide

Released by the atrial and ventricular myocardium. This is in response to increased blood pressure and stretching of the heart walls. ANP works on the collecting tubules, decreasing sodium retention. It also has a vasodilatory effect on the afferent artery feeding a glomerulus. This along with an increase in heart rate, also caused by ANP, increased fluid filtration and excretion to lower blood pressure.

Considered an endogenous inhibitor of the renin-angiotensin system.

Pressure Natriuresis

This mechanism is blunted in the kidneys of hypertensive people

Primary (essential/idiopathic)

95%

Exclusion

The other 5% are called 2ndary hypertension with an identifiable, and possible modifiable mechanism.

Single Gene disorders leading to primary hypertension (or even hypotension) are rare/common (choose).

These mutations generally affect what aspect of blood pressure control?

Rare

These mutations generally alter net sodium resorption by the kidney

A form of salt-sensitive hypertension.

It is caused by mutations in an epithelial Na+ channel protein.

When induced by aldosterone, sodium retention is increased.

decreased renal sodium excretion.

retained sodium keeps water in the system and leads to increased plasma volumes.

Oral contraceptives (estrogens cause increased hepatic production of angiotensinogen)

Glucocorticoids, cyclosporine, Erythropoietin, and sympathomimetic drugs (A1 and B1 agonists)

Cocaine and chronic alcohol use (increased sympathetic nerv. syst. activity -- bet you though alcohol was a depressant didn't you?)

Atherosclerosis

Fibromuscular dysplasia (narrowing of renal artery)

these decrease renal blood flow and initiate the renin-angiotensin system. not curative so the cycle repeats.

What is a pheochromocytoma?

What symptoms present clinically?

A catecholamine (NE and EPI) secreting tumor or neuroendocrine cells (adrenal medulla, usually). Causes intermittent or chronic vasoconstriction and tachycardia + other sympathetic effects.

Pt. may present with paroxysmal rises in BP and autonomic attacks: severe, ThRoBbInG headaches, profuse sweating, racing pulse.

Treat with surgical resection of the tumor. Have to nip it in the bud.

Cortisol is an example of a glucocorticoid, as in cushings syndrome (recall, Cushings disease is a pituitary tumor releasing excessive ACTH)

glucocorticoids stimulate production of components of the renin-angiotensin system. Excessive glucocorticoids also activate mineralocorticoid receptors.

BOTH!

1. induce sodium-potassium ATPases in heart and vessels
2. Increases blood volume
3. stimulate tissue metab. and O2 demand

Hyperthyroid via cardiac hyperactivity and increased blood flow

Hypothyroid via increase in peripheral resistance...diastolic hypertension (mediated through sympathetic and adrenal activation)

How does coarctation of the aorta produce hypertension?

The narrowing of the aorta creates an obstruction to reduce blood flow. While blood pressue is high in the upper limbs and head, below the coarctation blood pressure is low. The Kidneys sense this and respond with activation of the renin-angiotensin system. This increased blood volume and peripheral resistance.

The constant higher BP in the aortic arch and cortid sinuses causes them to stiffen and suffer accelerated atheroclerosis. This blunts the normal baroreceptor response (resets the set point)

HTN causes degenerative changes in the walls of _____ and ______ sized arterie.

Hyaline arteriosclerosis

Hyperplastic arteriosclerosis

What is the cause of Hyaline thickening in arterioles?

What disease states might you see these in?

Hyalinization comes from an increase in plasma leakage across damaged endothelial cells. Also, chronic hemodynamic stress causes smooth muscles to lay down extra ECM around the blood vessel.

This is also seen in diabetic microangiography due to hyperglycemic damage to endothelial cells. Not that it's a disease, but these are also seen in the elderly (normo or hypertensive)

What conditions elicit hyperplastic arteriosclerosis?

What is characteristic about this condition?

Severe, Malignant hyperstension causes this from of vascular hyperplasia. This produces a characteristic "onion skin" appearance around the vessel from the proliferation of smooth muscle cells.

This proliferation causes a narrowing of the vessel lumen, obstructing blood flow.

Also, this is accompanied by fibrinoid deposits and vessel wall necrosis  -- fibrinoid necrosis(necrotizing arteriolitis)

What are the abnormalities accumulated by the vasculature, in general terms, due to HTN?

Think just about overall structural changes (3)

1. Smooth muscle hypertrophy
2. Endothelial dysfunction
3. Fatigue of elastic fibers

Effects of HTN on the Heart:

Left Ventricular Hypertrophy (LVH)--->

High arterial pressure increases afterload and hypertrophies the wall.

__________ hypertrophy (without dilation), is the normal compensation.

__________ hypertrophy, caused by increased blood volume. Also causes ventricular dilation.

LVH yields increased stiffness, diastolic disfuntion (less pumped out so filling results in backflow), increased LV filling pressure, and ______________

Concentric Hypertrophy

Eccentric Hypertrophy

Pulmonary congestion

The degree of heart hypertrophy correlates with the development of...

It's kind of random but just trying to struggle to make this short, vague list might help.

(5)

HTN, of course.

Leads to degenerative changes in the aortic valve, which may open up and allow blood inbetween the aortic layers.

Lacunar Infarct:

Affects DEEP, PENETRATING arteries within the brain.

may develop arteriolar sclerosis and occlude.

Consequence is the development of single or multiple small cavitary infarcts...hence lacunae

Lake-like spaces <15mm

tissue loss with scattered lipid-laden macro's and surroundig gliosis (to perhaps encapsulate the area)

Small-caliber (diameter) penetrating vessels develop small slits through which blood hemorrhages.

These hemorrhages resorb with time, leaving a brownish discoloration in their wake.

Brain Parenchymal Hemorrhage

Larger hemorrhages withing the brain.

most common cause of these hemorrhages is hypertension, accounting for more than 50% of clinically significant hemorrhages.

Minute aneurysms which may rupture, or simply stay as small dilations of blood vessels within the brain. These are particularly found in HTN patients.

Careful not to confuse these with sacular/berry aneurysms which affect larger blood vessels. Note the key word for these types is "minute" -- <300 micrometers

They are most commonly found in the lenticulostriate vessels of the basal ganglia (coming from middle cerebral artery) and are common causes of stroke

Acute form is a clinicopathologic syndrom arising from malignant hypertension.

Characterized by diffuse cerebral dysfunction, including headaches, confusion, vomiting, and convulsion...sometimes coma

requires rapid intervention to reduce intracranial pressure...edema.

Autopsy may reveal petechiae and fibrinoid necrosis of arterioles.

a benign (chronic) nephrosclerosis

HTN leads to vascular changes including hyaline arteriosclerosis, medial and intimal thickening. Thickening causes a narrowing of the lumen and tissue ischemia. Ischemia leads to glomerulonecrosis and chronic injury with decreasing function. Scarring and shrinking

Surface of kidney will resemble grainy leather.

associated with malignant/accelerated HTN

causes vascular damage with fibrinoid necrosis of arterioles and small arteries...hyperplastic arteriosclerosis

leads to kidney ischemia...rupture of arterioles and capillaries.

Kidney appears with small pinpoint petechial hemorrhages (burst capillaries) and is described as "flea bitten".

Also called accelerated hypertension

1. severe hypertension: systolic over 200 mmHg, diastolic over 120 mmHg (either, or)
2. Renal Failure
3. Retinal hemorrhages and exudates
4. May or may not include papilledema

It is most often imposed on a pre-existing HTN

Contrast the effects of chronic hypertension on the retina against the effects of malignant hypertension.

Chronic:

vasoconstriction causes arterial narrowing and intimal thickening (hypertrophy). There may be "nicks" crossing the veins.

Severe chronic HTN leads to accelerated sclerosis and an unusual reflection of light from a fundoscope. "copper" or "silver wire" appearance of the vessels.

No papillary edema

Malignant:

small retinal hemorrages and exudates of plasma lipids. May show papilledema.