Chapter 18

Disorders of Blood Flow and

Blood Pressure

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Artery Structure

Tunic externa: collagen fibers

Tunica media: smooth muscle and elastin

Tunica intima: endothelium

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Artery Structure (cont.)

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Question

Which vessel layer can expand to accommodate pressure

changes?
A. Tunica intima
B. Tunica media
C. Tunica adventitia
D. Tunica externa

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Answer

B. Tunica media

Rationale: The tunica media is composed of smooth

muscle, which can stretch/expand to accommodate
changes in blood pressure.

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Vascular Endothelium

Food and O2 pass into tissues from blood.

Wastes and CO2 pass from tissues into blood.
Creates compounds that stimulate:
Vasodilation or vasoconstriction
Inflammation
Promote clot formation in injured areas
Smooth muscle

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Lipoproteins

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Lipoprotein Structure

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Lipid Transport in the Body

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Lipid Transport in the Body (cont.)

Dietary lipids absorbed as chylomicrons.

Adipose, muscle cells take up lipids from chylomicrons
remnants are IDLs.
IDLs become LDLs (bad cholesterol).
LDLs deliver cholesterol to the liver and other tissues.
LDL receptors are necessary for cell internalization.
Some LDLs taken up by scavenger cells (macrophages).

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Lipoproteins

LDLlow-density lipoproteins
Lower density: less protein, more cholesterol
Transports cholesterol from the liver to cells
Can be oxidized and deposited

HDLhigh-density lipoproteins
Higher density: more protein, less cholesterol
Transports cholesterol from cells to the liver

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Question

Is the following statement true or false?

LDL is considered to be good cholesterol.

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Answer

False

Rationale: LDL (low-density lipoproteins) has more lipids

and less proteinits the bad cholesterol. HDL (high
density) has more protein and less fatits considered
good cholesterol.

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Fatty Streaks and Atherosclerotic Plaques

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Atherosclerosis

Monocytes attach to the endothelium macrophages.

Macrophages release free radicals oxidized LDL.

Macrophages ingest oxidized LDL foam cells.

WBCs, platelets, and vascular endothelium release

chemicals that promote plaque formation.

Plaques block the arteries.

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Scenario

A man has several genetic defects in his lipoprotein

receptors.

His liver lacks LDL receptors.

His muscle cells lack receptors for the apoproteins on

chylomicrons.

His scavenger cells have extra LDL receptors.

Question:

Why might he develop atherosclerosis?

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Unstable Plaques

Have thin fibrous caps

Plaque can rupture clot forms (thrombus)

May completely block the artery

May break free and become an embolus

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Question

What immediate threat do unstable plaques present?

A. Clot formation will increase pressure in the vessel.
B. Plaque may lead to angina (chest pain).
C. Clots may break loose and block blood flow to key
organs.
D. All of the above constitute immediate threats.

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Answer

C. Clots may break loose and block blood flow to key

organs.

Rationale: If a clot breaks loose, becoming an embolus, it

may lodge in a blood vessel to the brain, heart, or
lungs. When blood flow is significantly decreased or
blocked altogether, the result is tissue deathin the
examples here, stroke, heart attack, or pulmonary
embolus. The other choices represent more long-
term/chronic problems.

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Peripheral Vascular Disorders
Peripheral Arterial Disease (PAD)atherosclerotic
blockages
Large arteries (not coronary, aortic arch, brain)
Thromboangitis Obliterans (Buerger disease)
nonatherosclerotic inflammation and thrombosis
Small- and medium-sized arteries and veins
Raynaud Phenomenonintense vasospasm
Arteries, arterioles in the fingers and toes

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Scenario
A woman complains of pain in her left leg.
Her foot is cool and pale.
She reports that it is often red and warm when she is
sitting down.
The pain occurs when she is walking to church.
The skin on her left leg is shinier than on the right leg.
Questions:
What could have caused all this? How?

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Aneurysms

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Aneurysms (cont.)

Wall of the vessel weakens and stretches

True aneurysm, false aneurysm
Berry aneurysm, fusiform aneurysm, saccular
aneurysm, dissecting aneurysm
Aortic aneurysm, abdominal aortic aneurysm,
aortic dissection
Risk of rupture, hemorrhage, clot formation

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Arterial Blood Pressure

Systolic pressureventricle contracts

Diastolic pressureventricle relaxes
Pulse pressure = systolic diastolic
Mean arterial pressure = 1/3 systolic + 2/3 diastolic
Cardiac output (CO) = heart rate stroke volume
Blood pressure = CO total peripheral resistance

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Blood Pressure Regulation

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ReninAngiotensinAldosterone Pathway

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Hypertension
Primary or essential
Genetics, race, age, insulin resistance, diet,
obesity, alcohol

Secondary
Renal hypertension, adrenocortical hormones,
pheochromocytoma, aortic coarctation, oral
contraceptives

Hypertensive crisis, urgency, emergency

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Discussion
How would each of the following affect blood pressure?
Vasodilation
Decreased stretching of baroreceptors
Hypoxemia
Inhibiting angiotensin-converting enzyme
Beta-blockers
2-agonists
Calcium channel blockers

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Question

A patient takes a drug that is a sympathetic agonist. Which

of the following would you expect to occur?
A. Increased heart rate and blood pressure
B. Increased heart rate and decreased blood pressure
C. Decreased heart rate and increased blood pressure
D. Decreased heart rate and blood pressure

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Answer

A. Increased heart rate and blood pressure

Rationale: The sympathetic nervous system stimulates

b1-adrenergic receptors on the heart to increase
heart rate. Increased heart rate increases cardiac
output, which increases blood pressure. Sympathetic
agonists will also stimulate other adrenergic
receptors to result in increased blood pressure.

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Hypertension in Pregnancy

Preeclampsiaeclampsia
Hypertension after 20 weeks, proteinuria, elevated
serum creatinine and liver enzymes, decreased
platelets
Gestational hypertension
After 20 weeks, resolves by 12 weeks postpartum
Chronic hypertension
Preeclampsia superimposed on chronic hypertension

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Blood Pressure Control When Standing

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Veins and Varicosities

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