Disorders of blood vessels and blood pressure Flashcards

1
Q

What is hyperlipidemia?

A

elevated lipids (cholesterol, phospholipids, triglycerides) in the blood

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2
Q

What is an apoprotein?

A

a protein that transports lipids in blood because lipids are not water-soluble

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3
Q

What is a lipoprotein?

A

when lipids bind to an apoprotein they are called lipoproteins, they vary in density (influenced by protein content)

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4
Q

What is HDL?

A

high density lipoprotein, it has a high density because of a high protein content

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5
Q

What is LDL?

A

low density lipoprotein, it has a low density due to a lower protein content, it therefore has a higher lipid content, this type is bad

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6
Q

Define atherosclerosis.

A

formation and deposition of a soft paste in the ateries

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7
Q

What does atherosclerosis cause?

A
  • atherosclerosis causes the formation of fibrofatty lesions called atheromas in the intima of larger arteries
  • as lesion grows, the patency of the artery is decreased
  • this decreases perfusion of the tissue the artery supplies
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8
Q

Define ischemia.

A

local inadequacy of perfusion due to an obstructed blood vessel

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9
Q

Define infarction.

A

Cell death related to ischemia.

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10
Q

Atherosclerosis is a process that occurs over decades and the lesions change over time. Name and describe the 3 different lesions seen in atherosclerosis.

A

1) fatty streak - yellowish discolouration
2) fibrous atheromatous plaque - further deposition of cells, lipids and smooth muscle cells
3) complicated lesion - there are changes in the lumen of the blood vessel and a build up in the lumen which now has the potential to be dislodged

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11
Q

What is the pathophysiology of atherosclerosis.

A
  • begins with endothelial injury (risk factors)
  • this allows lipids to enter/accumulate into the intima, triggers inflammation
  • inflammatory cells migrate into the tissue (monocytes bind and enter endothelium, become macrophages, oxidize lipids, releasing free radicals, engulf oxidized lipids and become foam cells, free radicals cause injury, foam cells release growth hormone causing smooth muscle to proliferate)
  • foam cells degenerate, release contents forming an atheroma (formation of necrotic core)
  • in later stages, endothelium ruptures, collagen is exposed - platelets contact and begin the clotting cascade… form a thrombus
  • the thrombus can break off and cause problems
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12
Q

Which blood vessels are most often affected by atherosclerosis?

A

1) abdominal aorta and iliac arteries
2) proximal coronary arteries
3) thoracic aorta, femoral and popliteal arteries
4) internal carotid arteries

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13
Q

What is hypertension?

A

persistently elevated blood pressure that does not return to normal, clinically persistent blood pressure more than 140/90 mmHg

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14
Q

Why is hypertension bad?

A
  • heart must work harder, requires more oxygen, more susceptible to injury/disease
  • high pressure can damage endothelium, causing atherosclerosis
  • high pressure can damage capillaries in retina, glomerulus
  • high pressure makes it more likely a plaque will break off… PE, CVA
  • high pressure also increases likelihood that vessels break, causing hemorrhagic stroke
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15
Q

What are 4 major ways that blood pressure is controlled?

A

1) arterial baroreceptors (in carotid and aorta to protect brain and coronary circulation)
2) RAAS
3) vascular autoregulation
4) blood volume (regulation of fluid volume by the kidney with the help of ADH and aldosterone)

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16
Q

What is normal blood pressure?

A

under 120/80 mmHg

17
Q

What are the categories and related ranges of hypertension?

A

high normal:
120-139 systolic and/or 80-90 diastolic

stage 1/mild:
140-159 systolic and/or 90-99 diastolic

stage 2/moderate:
160-179 systolic and/or 100-109 diastolic

stage 3/severe:
over 180 systolic or over 110 diastolic

18
Q

What is the difference between primary and secondary hypertension?

A

primary or essential hypertension is idiopathic (90% of cases)

secondary hypertension has an identifiable cause… like renal disease

19
Q

In most hypertension, both systolic and diastolic pressures are elevated. Explain who might be affected by systolic hypertension and why they would only experience elevated systolic pressure.

A
  • people over 50 years old because of vessel degeneration and atherosclerosis
  • vessel compliance is reduced, can no longer stretch to accommodate the increased pressure during systole
20
Q

What are three other types of hypertension?

A

1) white coat hypertension - hypertension in clinical setting
2) gestational hypertension - elevated blood pressure during pregnancy
3) malignant hypertension - sudden, marked elevations in blood pressure with diastolic pressure over 120 mmHg

21
Q

Hypertension is usually asymptomatic except for one sign - what is it?

A

elevated blood pressure

22
Q

When hypertension does have signs and symptoms, what are they? What do they indicate?

A
  • fatigue
  • palpitations
  • am headaches
  • blurred vision
  • dizziness

signs of long-term damage from hypertension on other organs and tissues

23
Q

What is target organ damage?

A

complications associated with hypertension that affect the heart, brain, kidneys, eyes, and blood vessels

24
Q

What is a palpitation?

A

sensation of a forceful, irregular heart beat

25
Q

How is hypertension treated?

A

1st - lifestyle modifications
2nd - if this doesn’t work after a few months, add diuretic medication
3rd - if this doesn’t work, add a second medication: calcium channel blocker, angiotensin II receptor blocker, ACEI

26
Q

What is peripheral vascular disease?

A

disorder of the circulation of the extremeties

27
Q

What are the two types of PVD?

A

1) acute arterial occlusion - when there is an acute disruption to perfusion, usually from a thrombus or embolus
2) atherosclerotic occlusive disease - the gradual development of an atheroma impedes perfusion, can lead to ischemia and tissue damage

28
Q

How does PVD manifest?

A

acute arterial occlusion: sudden onset of 5 p’s = pulselessness, palor, polar, pain, paraesthesia

atherosclerotic occlusive disease: intermittent claudication (pain from ischemia when walking), edema caused by venous or lymphatic stasis (fluid and wast accumulates)

29
Q

Who has increased incidence of atherosclerotic occlusive disease? Why?

A
  • increased incidence in elderly and those with diabetes mellitus
  • atherosclerosis manifests later in life
  • vascular damage is a chronic complication of DM
30
Q

How does the body react/compensate for peripheral vascular disease? Is it effective?

A
  • vasodilating (doesn’t work)
  • switching to anaerobic metabolism (good if short term)
  • form new blood vessels around the occlusion - collateralization (takes time)
31
Q

What happens if PVD is not treated?

A

ulceration and gangrene… amputation

32
Q

What is an aneurysm?

A

A localized dilation in an artery that does not return to normal/is permanent.

33
Q

What causes an aneurysm?

A

degenerative changes in a vessel wall

34
Q

What are some risk factors for aneurysms?

A

hypertension, atherosclerosis, congenital defects

35
Q

What are the three types of aneurysms? Describe them?

A

1) fusiform - bulge around entire circumference of vessel
2) saccular - bulge on 1 side of the vessel only
3) dissecting - blood flows between 2 layers of the blood vessel to cause a bulge

36
Q

Where do aneurysms commonly (generally) occur and why?

A
  • bend in a vessel
  • bifurcation in a vessel
  • where vessel lacks external support

why? because the vessel is subject to higher pressure in these areas

37
Q

What are common sites of aneurysms?

A
  • abdominal and thoracic aorta
  • femoral artery
  • iliac artery
  • popliteal artery
38
Q

What are the complications associated with aneurysms?

A
  • rupture and hemorrhaging
  • applies pressure to adjoining structures
  • thrombosis
  • embolism